Clinical Surgery Pearls
• Fistulization with urinary bladder resulting in
pneumaturia
• Gastrocolic fistula
• Acu te appendicitis/appendicular abscess
(obstructive appendicitis as a result of the growth
in the cecum)
• Intussusceptions (always rule out a growth in all
cases of adult intussusception. There is no role for
hydrostatic reduction in adults).
Q 32. Having made the diagnosis of carcinoma
cecum, how do you manage the patient?
After doing investigationsin the form of X-ray chest
to rule out metastases in the lungs, ultrasound
abdomen to rule out metastases liver and free fluid,
the patient is prepared for resection.
Q 33. What are the preparations for surgery?
• Make the patient fit for anesthesia (evaluate
cardiac, respiratory status)
• Correction of anemia
• Correction of hypoproteinemia
• Dietary regulation
• Bowel preparation
• Prophylactic subcutaneous heparin
• Prophylactic antibiotics.
Q 34. What is the role of mechanical bowel
preparation?
• Dietary restriction in the form of liquid diet for
24 hours before surgery.
• The role of mechanical bowel preparation for
elective surgery is highly controversial. There
is enough evidence in the literature for safe
surgery without mechanical bowel preparation.
• Conventionally
– Bowel washes
– Laxativesin the form ofsodium picosulphate
– Cleansing agents like Polyethylene glycol
(PEG) orally are given the day before.
Q 35. What is the role of antibiotic prophylaxis in
colonic surgery?
The routine practice of Nichol’s regime by giving
3 doses of antibiotics 18, 17 and 10 hours preoperatively with neomycin and erythromycin is no
longer practised.
A single dose of ampicillin—sulbactam or
quinolone and metronidazole or parenteral cefoxitin
are recommended for antibiotic prophylaxis (1 hour
before skin incision).
Q 36. How will you assess the operability? (PG)
a. After laparotomy look for metastases in
peritoneum (small white seed-like), liver, pelvic
deposits, Krukenberg’s tumor (metastatic
ovarian tumor) ascites and lymph nodes
b. Look for tumor mobility and adjacent structure
involvement
c. Liver metastases if found are not biopsied—it
will cause tumor dissemination
d. Hepatic metastases resection is done as a staged
procedure later
e. Tumor dissemination is not a contraindication
for resection of the primary.
Q 37. What is the surgical procedure of choice
when there is a cecal growth?
Right hemicolectomy is the operation of choice, where
a radical resection of the involved colon along with its
lymphovascular drainage is done. Any devascularized
segment should be removed in addition. Suspicious
lymph nodes are taken for biopsy.
Q 38. How much is the clearance required in
colonic resection?
The clearance of a minimum of 5–10 cm on either
side is recommended.
Contd...
Suspected Carcinoma of the Cecum
141
Q 39. What are the vessels ligated for right
hemicolectomy?
The ileocolic, right colic, and right branch of the middle
colic vessels are ligated for right hemicolectomy.
Q 40. What are the technical precautions taken
during surgery and how much ileum is removed?
(PG)
• The cecum is mobilized by incising the lateral
peritoneum which is carried around the hepatic
flexure
• Take care not to injure the ureter, spermatic
vessels (in males) and duodenum
• The mesentery of last 30 cm of ileum isremoved
• The colon is divided as far as the proximal third
of transverse colon
• The anastomosis is done between the rest of
ileum and transverse colon in layers.
Q 41. What is non touch technique of Turnbull? (PG)
Its usefulness has been debated. Here early ligation
of vascular pedicle and control of proposed
resection edges is done before mobilization of the
tumor bearing area. It aims to prevent the luminal,
vascular and lymphatic pathways for tumor emboli
or tumor cells while handling the lesion.
Q 42. What are the anatomical peculiarities of the
colon from anastomotic point of view?
1. The content of the colon is fecal matter and
therefore there is more chance for infection after
resection and anastomosis
2. The wall—longitudinal muscle coat is thin and
therefore there is more chance for anastomotic
leak
3. The arterial supply—It is precarious and special
(Fig. 10.1).
Fig. 10.1: Colonic blood supply
142
Clinical Surgery Pearls
The colon is supplied by branches of the superior
mesenteric artery namely the ileocolic artery, the
right colic artery, and middle colic artery.
The inferior mesenteric artery arises from the
aorta opposite L3 vertebrae and the branches are
left colic artery and sigmoid arteries.
The marginal artery of drummond: It is present in
almost all patients. It is a single arterial trunk along
the concave part of large intestine from ileocecal
junction to rectosigmoid junction forming a
communicating channel between the superior and
inferior mesenteric artery. It gives off vasa recta
which run perpendicular to the colonic wall.
Meandering artery (Arc of Riolan):These are collateral
branches connecting proximal middle colic artery
to left colic artery. During colonic mobilization this
artery should be protected.
Griffith’s point: It is the weak point in the vascular
anastomosis between middle and left colic arteries.
Therefore it is important to avoid anastomosis at
the splenic flexure.
Sudek’s point: It is at the level of lowest sigmoid
and superior rectal artery. There is a higher chance
of avascularity if anastomosis is performed here.
Q 43. What is the lymphatic drainage of colon?
Lymph nodes are divided into four groups.
a. Epicolic—located on the bowel wall
b. Paracolic—located along the marginal artery
c. Intermediate—located along the colic vessels
d. Principal—located along SMA and IMA.
Q 44. What is white line of Toldt?
The ascending and descending colon has no
peritoneal covering on their posterior aspects but
has areolar tissue (fascia of Toldt), which represent
the embryonic fusion of mesentery to posterior
peritoneum. At the lateral parietal wall it reflects as
the white line of Toldt. This line is used as the plane
for avascular mobilization of the colon.
Q 45. Which part of the colon has the largest
diameter?
• Cecum—7.5 cm
• Narrowest part is rectosigmoid—2.5 cm.
Q 46. Which are the mobile portions of the colon?
Transverse colon and sigmoid colon. (The rest of
the colon is fixed).
Q 47. What are the ligaments attaching the
hepatic flexure of colon (which is fixed)?
• Nephrocolic ligament
• Hepatocolic ligament
• Duodenocolic ligament.
Q 48. What is the attachment of splenic flexure?
Phrenicocolic ligament.
Q 49. What is the extent of descending colon?
It extends from the splenic flexure to the brim of
the true pelvis.
Q 50. What is the attachment of transverse
mesocolon?
The transverse mesocolon is attached to the
descending part of duodenum, to the head and
lower aspect of the body of the pancreas, and to
the anteriorsurface ofthe left kidney—horizontally.
Q 51. What is the attachment of mesosigmoid?
It is inverted ‘V’ shaped, the apex of this peritoneal
attachment is at the bifurcation of the left common
iliac vessels over the left sacroiliac joint (at the left
ureter). The right limb, comes down to the third
piece of sacrum and the left limb traverses along
the brim of the left side of pelvis (Fig. 10.2).
Suspected Carcinoma of the Cecum
143
Q 52. What is the management of carcinoma colon
when there is obstruction? (PG)
a. If risk factors are present—Resection plus
exteriorization of the bowel ends is preferred.
b. Healthypatients(norisk factors)—Resectionplus
primary anastomosis. If primary anastomosis is
done always do a protective colostomy.
c. Unresectable cases—Ileo transverse anastomosis is done or ileostomy.
Note: Primary anastomosis is worrisome in left
sided lesions because of increased anastomotic
dehiscence seen in dilated and edematous
unprepared bowel.
Q 53. What is the management of unresectable
lesion with widespread metastases and severe
comorbidity? (PG)
• Colonic stenting (SEMS).
• Complications of stenting are stent migration
and restenosis.
Q 54. What is “On - Table - Lavage”?
This is done for unprepared bowel during
emergency surgery. In left sided obstructed colonic
growths presenting as emergency, a Foley catheter
is introduced via terminal ileum to the cecum or
directly to cecum through an appendectomy stump
and the colon is irrigated. The colon is transected
above the growth and the effluent is collected
through a tubing (Boyle’s apparatus tubing), until
the colon is clean.
Q 55. What is the treatment of synchronous
lesion? (PG)
• If lesions are in the same segment—segmental
resection
• Iftheyarewidelyseparated—subtotal colectomy.
Q 56. What is CEA (Carcinoembryonic antigen)?
CEA (Carcinoembryonic antigen)
• Itis a glycoprotein found in cell membrane of many
tissues including colorectal cancer
• Some antigen enters the circulation and this is
identified by radioimmunoassay
• Itis presentin other body fluidslike urine and feces
• CEA is not specific for carcinoma of colorectum
• It is present in other GI cancers, nonalimentary
cancers, and benign diseases
• It is high in 70% of carcinoma colon
• It is not useful as a screening investigation
• It is useful for detecting recurrence after a curative
surgery if the serial CEA values are rising after 6–9
months
• CEA level of > 2.5 ng/mL is significant
• CEA level of > 5 ng/mL indicates poor prognosis
• If preoperative elevated CEAdoes notfallto normal
within 2–3 weeks after resection, the resection is
incomplete or there is occult metastases
• CEAvalues are highestin lung and liver metastases.
Fig. 10.2: Mesosigmoid attachment
144
Clinical Surgery Pearls
Q 57. What is left hemicolectomy?
This is done for tumors of descending colon and
splenic flexure. Here resection of the colon from
splenic flexure to rectosigmoid is done.
Q 58. What is the treatment for sigmoid cancer?
Sigmoidectomy.
Q 59. What are the indications for total colectomy/
subtotal colectomy?
• Multiple primary tumors
• Completely obstructing sigmoid cancers
• HNPCC
• Transverse colon carcinoma.
Q 60. What is extended right hemicolectomy?
This is done for proximal transverse colon growth.
Q 61. What is extended left hemicolectomy?
This is done for distal transverse colon growth.
Note: For transverse colon growth subtotal
colectomy is another option.
Q 62. What are the surgical procedures of choice
for growth in various regions of the colon?
Surgical procedures of choice for growth in various
regions of the colon.
Site Surgical procedure
Cecum, ascending colon,
hepatic flexure
Right hemicolectomy
Proximal part of
transverse colon
Extended right
hemicolectomy
Distal transverse colon Extended left
hemicolectomy
Descending colon and
splenic flexure
Left hemicolectomy
Sigmoid colon Sigmoidectomy
Transverse colon, sigmoid
colon, multiple tumors,
HNPCC
Subtotal colectomy
Q 63. What are the peculiarities of cancer
secondary to ulcerative colitis?
• May occur at many sites
• May affect the colon more than rectum
• They are high grade tumors
• After 20 years the risk is 12%.
Q 64. What are the bad prognostic factors in
colonic cancer? (PG)
1. Depth of tumor invasion and nodal metastases
(most important)
2. Bowel obstruction—poor prognosis
3. CEA > 5 ng/mL
4. Right sided colon carry worse prognosis
5. Pathological variables
– Histological grade
– Signet ring type-poor prognosis
– Small cell carcinoma
– Lymphovascular invasion.
Q 65. What is the indication for adjuvant therapy
in colorectal cancer? (PG)
• In stage I lesion no further adjuvant therapy
• In stage II and III – adjuvant therapy has most
important impact
• In Stage II – 5FU and Leucoverin (folenic acid)
– Folenic acid is a potentiator of 5 FU
– (immunomodulator levamisole with 5 FU is
used less nowadays)
– Histopathologically positive lymph nodes is
an indication for chemotherapy.
• In Stage III – FOLFOX 4 regimen
– (Oxaliplatin and 5FU - 2 times a month for 12
cycles)
OR
– FOLFIRI regimen (folic acid, and 5FU and
Irinotecan).
Suspected Carcinoma of the Cecum
145
Q 66. What is the most effective single chemotherapeutic agent for adenocarcinoma?
5-Fluorouracil.
Q 67. What is the follow-up for carcinoma colon?
Clinical examination once in six months.
Annual examination of the following:
• CEA
• Chest X-ray
• Colonoscopy
• LFT
• CBC.
Q 68. What is fast track surgery?
It is a multimodal rehabilitation regimen for elective
colonic surgery for enhanced recovery consisting
of—
Fast track surgery
• Preoperative counseling and optimization
• Epidural catheter for pain control
• General anesthesia using propofol (no nitrous
oxide)
• No bowel preparation
• Transverse abdominal incision instead of vertical
• Continuous epidural analgesia for two days
• Oral feeding with protein drink (60–80 gm protein/
day) from the day of surgery
• Early mobilization
• Laxative and prokinetics for bowel function from
the day of surgery
• POP day 1 remove urinary catheter
• POP day 2 remove epidural catheter
• POP day 3 discharge after lunch.
For PG’s—What is new?
• Cancer of the descending colon with obstruction current treatment choice is endoscopic stenting followed by
elective surgery after two weeks or Hartmann’s procedure or colostomy
• All carcinomas arise from adenomas
• All adenomas need not produce carcinoma
• NSAIDs will reduce the number and size of polyps but will not prevent carcinoma
• Full colonoscopy is a must for all colonic carcinoma
• CEA – Indian patients are non secretors
• For metastatic disease FOLFOX 4 cycles followed by surgery followed by 4 cycles of FOLFOX
• Adjuvant—usually 8 cycles
• Cheaper OP Regimen—Cape OX Regimen – Oxaliplatin and Capecitabine orally for 15 days
• New agent for colonic cancer is Cetuximab—agent against Kras
• Forsynchronous metastasisin liver two approaches are there (a) Surgery of liver along with primary (b) Surgery
of liver later (majority of surgeons favor the second approach).
11 Appendicular Mass
Case
Case Capsule
A 25-year-old female patient presents with history
of abdominal pain of 4 days duration. Initially the
pain started as a vague central abdominal pain in
the early morning hours. This pain was preceded
by loss of appetite. The patient was constipated
for a few days. She felt nauseated and vomited
once on the first day of pain. Later the pain shifted
to the right iliac fossa. Her pain is aggravated by
moving and coughing. The patient is married and
has two children. Her menstrual cycles are regular
having normal blood flow. Her last menstrual period
was 6 days back. There is no history of discharge
from vagina. On examination the patient looks
pale. There is mild pyrexia. The tongue is furred
and there is fetor oris (halitosis). Her pulse rate is
90 per minute. Abdominal examination revealed
a tender mass of 16 × 9 cm size in the right iliac
fossa with overlying muscle guard and rigidity
confined to the right iliac fossa. There is no intrinsic
movement for the mass and all the borders are
well made out except the lateral border. The mass
is intra-abdominal and intraperitoneal. There is no
extension of the mass below the inguinal region.
The rest of the abdomen is soft and nontender.
There is no free fluid demonstrated. The bowel
sounds are normally heard. On digital rectal
examination, the patient complained of pain deep
in the pelvis and the mass is palpable per rectum.
On vaginal examination movement of the cervix did
not cause pain. Other systems are normal.
Read the checklist of previous case
Checklist with special reference to this case
• Acarefulgynecological history istaken inallwomen
• Last menstrual period—to find out whether it is a
mid-menstrual pain (mittelschmerz) and to rule out
pregnancy
• History of vaginal discharge—pelvic inflammatory
disease
• History of dysmenorrhea
• Pelvic examination to rule out adnexal and cervical
tenderness
• HighvaginalswabtoruleoutChlamydia trachomatis
• Urine for pregnancy test
• Ultrasound abdomen.
Q 1. What is the most probable diagnosis in this
case?
Appendicular mass.
Q 2. What are the differential diagnoses?
• Read the differential diagnosis ofrightiliac fossa
mass
Appendicular Mass
147
• The patient being a female, in addition to those
conditions consider the following:
– Torsion of ovarian cyst/tumor
– Tubo-ovarian mass
– Ectopic pregnancy
– Pelvic inflammatory disease
– Uterine swellings.
Q 3. What are the diagnostic points in favor of
appendicular mass?
1. History of Murphy’s triad of symptoms—
migratory pain, vomiting/anorexia, and fever
2. Short duration
3. Patient—ill looking and febrile
4. Tender mass in the right iliac fossa
5. The tender mass is indistinct, dull to percussion
and fixed to the right iliac fossa (unlike ovarian).
Q 4. What are the clinical point in favor of an
ovarian cyst?
Clinical points in favor of ovarian cyst
• Smooth, spherical with distinct edges
• You cannot get below the swelling (arisesfrom the
pelvis)
• It may be mobile from side to side (horizontally)
No up and down mobility
• It is dull to percussion
• The lower part of the swelling may be palpable
during pelvic examination
• The movement of the cyst per abdominally will be
transmitted to the examining finger in the pelvis.
Q 5. What are the clinical points in favor of fibroid
uterus?
• Fibroids can grow to enormous size and fill the
whole abdomen
• It arises out of the pelvis and so lower edge is
not palpable
• It is firm or hard
• Bosselated or knobby
• It is dull to percussion
• Slight transverse mobility will be present.
Q 6. What is appendicular mass?
It is a complication of acute appendicitis. As a result
of small perforation in the appendix, the policeman
of the abdomen, i.e. omentum will come and try
to seal the perforation, as a protective mechanism
leading to mass formation. The mass is a palpable
conglomerate consisting of the inflamed appendix
(usually perforated), adjacent viscera namely cecum
and ileum and greater omentum. This is also called
phlegmon.
Q 7. What is appendicular abscess?
One should suspect appendicular abscess
during the course of conservative treatment of
appendicular mass. The clinical criteria for the
diagnosis of appendicular abscess are:
1. A rising pulse rate
2. Increasing or spreading abdominal pain
3. Increasing size of mass
4. Patient looking ill.
Q 8. What are the differences between appendicular mass and abscess?
Appendicular mass Appendicular abscess
1. Mass forms around the
3rd day
Abscess around 5 – 10
days
2. Fever absent Fever present
3. Local signs subside with
antibiotics
Local signs aggravate
with antibiotics
4. Leukocytosis will return
to normal
Rising leukocyte count
5. Imaging—absence of
fluid inside
Imaging—presence of
fluid inside
6. Clinically patient is not sick Patient is very sick
148
Clinical Surgery Pearls
Q 9. What is initial management of appendicular
mass?
When a mass is diagnosed, the patient is not
operated but treated conservatively. It is a contraindication for appendicectomy. The classical
treatment is the so-called Ochsner-Sherren regimen
(conservative treatment). This consists of:
1. Bed rest (preferably hospitalized)
2. Fluid intake output chart
3. Mark out the limits of mass on the abdominal
wall (using a skin pencil)
4. Pulse, temperature and respiration chart (4th
hourly)
5. Initiate antibiotic therapy
6. Patientis given fluid diet only initially (ifrequired
IVfluidsmaybegiven—ifpatient cannottolerate
oral fluids)
7. Contrast enhanced CT is done to rule out abscess
inside.
Q 10. Why appendicectomy is contraindicated in
appendicular mass?
1. Immediate appendicectomy is technically more
difficult
2. Fear of disturbing the natural barrier present in
the mass
3. The mass will resolve without surgery (90% will
resolve with conservative treatment)
4. Operation can always be resorted to, should the
initial conservative trial fail.
Q 11. What is the indication for stopping the
conservative treatment and proceed to surgery?
1. Clinical deterioration
– rising pulse rate
– Febrile
2. Failure of the mass to resolve
3. Peritonitis.
Q 12. What is the management of appendicular
abscess?
• Traditionally appendicular abscess used to
be treated with surgery in the form of extraperitoneal drainage of the abscess.
• But now sono-guided percutaneous catheter
drainage is the option.
Q 13. What are the indications for CT scan in
appendicitis?
Indications for CT scan in appendicitis
1. Equivocal clinical findings
2. Diagnostic dilemma
3. Appendicular mass/abscess
4. Older patients in whom, acute diverticulitis, neoplasms are differential diagnoses.
Q 14. What are the CT finding in appendicitis?
What are the advantages and problems of CT?
• A distended appendix of more than 6 mm size
with intramural gas or with stranding of the
periappendiceal fat is indicative of inflammation.
• CT scan has been demonstrated to have a
sensitivity ranging from 96–100% for the
appendix.
• Utilization of CT has been associated with
decrease in the negative appendicectomy rate
[use of ultrasound is recommended for
evaluation of pelvic organs in women of childbearing age].
Note: A wholesale move to the routine use of spiral
CT for the diagnosis of appendicitis will emasculate
the clinical skills of the next generation of the
surgeons.
It is important not to substitute clinical
uncertainty for radiological ambivalence.
Appendicular Mass
149
Q 15. What is the CT classification of appendicular
abscess?
Group I – comprises phlegmons and abscesses
with maximum diameter smaller than
3 cm
Group II – Larger but well-localized abscesses
Group III – Includes extensive periappendicular
abscesses involving multiple intra or
extraperitoneal compartments.
Q 16. What is the management for each of these
CT groups?
Group I patients—antibiotic alone (identification of
pus collection alone is not an indication for drain)
Group II patients—percutaneous catheter drainage
Group III patients—surgical drainage.
Q 17. What are the complications of appendicular
abscess?
Complications of appendicular abscess
• Obscure subacute intestinal obstruction
• Formation of granulation tissue leading to frozen
pelvis
• Stricture ofthe rectum subsequentto frozen pelvis
• Pelvic abscess.
Q 18. What is the role of laparoscopy in
appendicular mass/abscess?
Appendicular abscess is considered a relative
contraindication for laparoscopy because of the
following reasons:
1. Spread of sepsis
2. Risk of injury to the bowel and mesentery
3. Periappendiceal adhesions.
Q 19. What is the sonological finding in acute
appendicitis?
Tense, tender, noncompressible tubular structure of
more than 6 mm size in the right iliac fossa.
Q 20. What is interval appendicectomy?
• After treating an appendicular mass conservatively by Ochsner-Sherren regimen,
conventionally the patient is advised to undergo
appendicectomy after 6–12 weeks of waiting
period. This is nowadays shortened to the time
required for complete resolution of the mass.
• However, now, many have questioned the
practice of interval appendicectomy, since
the recurrence rate of acute appendicitis after
management of the mass is only 10% (3–15%).
• Routine interval appendicectomy is unnecessary
in the majority of patients.
• An argument can be made in favor of interval
appendicectomy in patients who in the future,
may not have easy access to modern surgical
facilities.
Q 21. How to tackle the issue of missing or
missed diagnosis of a malignancy in cases of
appendicular mass?
It is recommended that patients over the age of
40 years undergo a barium enema examination
(double contrast) or a colonoscopy after successful
conservative treatment of appendicular mass.
Q 22. What is Alvarado score?
It is a clinical and laboratory based scoring system
devised to assist the diagnosis of acute appendicitis.
A score of 7 or more is strongly predictive of acute
appendicitis. A score of 5–6 is considered equivocal
and needs contrast enhanced CT examination to
reduce the rate of negative appendicectomy. In
Alvarado score, points are given for 3 symptoms,
3 signs, 2 laboratory findings. The mnemonic for
Alvarado score is—MANTRELS—migratory pain,
anorexia, nausea/vomiting, tenderness, rebound
tenderness, elevated temperature, leukocytosis,
shift to the left.
150
Clinical Surgery Pearls
Alvarado score
Score
Symptoms
• Migratory RIF pain 1
• Anorexia 1
• Nausea and vomiting 1
Signs
• Tenderness (RIF) 2
• Rebound tenderness 1
• Elevated temperature 1
Laboratory
• Leukocytosis 2
• Shift to left (increase in the number 1
of immature neutrophils) or banded
forms
Total score 10
Q 23. What is the acceptable negative appendicectomy rate?
• It should ideally be less than 20% (with the
introduction of CT for the diagnosis of acute
appendicitis the negative appendicectomy rate
should be less than 5%)
• If the rate is more it means we are over doing it
• If the rate is very less it means we are too much
waiting, so that perforation will occur.
Q 24. In the course of an operation for presumed
acute appendicitis, the appendix is found to be
engulfed in a mass of uncertain etiology. How
to proceed?
The safe approach is a segmental intestinal resection
with primary ileocolonic anastomosis. Whether
a limited resection through the same incision or
to have a formal right colectomy depends on the
likelihood of malignancy.
Q 25. What are the differential diagnoses of right
iliac fossa pain of acute onset? (Fig. 11.1)
The Attic (the nasopharynx and thorax)
• Tonsillitisin children (swallowed exudate causes
tonsil tummy)
• Lobar pneumonia and pleurisy.
Upper storey (diaphragm to the level of the umbilicus):
• Perforated peptic ulcer (the visceral content
passing along the paracolic gutter to the right
iliac fossa)
• Acute pancreatitis
• Acute cholecystitis
• Leaking aortic aneurysm
• Cyclical vomiting in children
• Ruptured liver abscess.
The ground floor (umbilicus to the brim of pelvis):
• Nonspecific mesenteric lymphadenitis
• Meckel’s diverticulitis
• Gastroenteritis
• Enterocolitis
• Intestinal obstruction
• Intussusception
• Carcinoma of the cecum
• Diverticulitis
• Torsion of appendix epiploicae
• Mesenteric infarction
• Leaking aortic aneurysm
• Regional ileitis
• Diverticulum of cecum (solitary)
• Rectus sheath hematoma.
The basement (the pelvis):
• Pelvic inflammatory disease
• Salpingitis
• Ectopic gestation
• Ruptured ovarian follicle (mittelschmerz)
Appendicular Mass
151
• Twisted right ovarian cyst
• Endometriosis.
The backyard (the retroperitoneal structures):
• Right ureteric colic
• Right sided acute pyelonephritis.
The electrical installation (central nervous system)
• Preherpetic pain ofthe righttenth and eleventh
dorsal nerves
• Tabetic crisis
• Spinal conditions
– Pott’s disease of the spine,
– Secondary carcinomatous deposits
– Senile osteoporosis
– Multiple myeloma.
Fuel supply (blood)
• Henoch-Schönlein purpura
• Blood dyscrasias
• Use of anticoagulants.
Other conditions:
• Abdominal crisis of porphyria
• Diabetic abdomen
• Leukemic ileocecal syndrome
• Clostridial septicemia.
Fig. 11.1: Appendicitis building
12 Obstructive Jaundice
Case
“Jaundice is the disease that your friends diagnose”
Sir William Osler (1849–1919)
Case Capsule
A 68-year-old male patient presents with epigastric
discomfort, anorexia and weight loss of 6 months
duration. Initially these complaints were dismissed
by his doctor. Later he noticed yellow discoloration
of urine and conjunctiva for the last two months.
The jaundice is painless and progressive. There is
no history of waxing and waning of symptoms.
At present he complaints of generalized itching
for the last 1 month. He passes clay-colored stools
for the last two months. He is a recently detected
diabetic. He is a heavy smoker for the last 50 years.
On examination he is ill built and cachexic. The
sclera is yellow orange in color (deeply jaundiced).
Scratch marks are seen in the abdomen and chest.
Abdominal examination revealed a globular mass
below the costal margin in the midclavicular line
impinging upon the examining hand on inspiration
of about 10 × 4 cm size. The mass is visible and
moving up and down with respiration. This mass
is better seen than felt and better palpated by
superficial palpation than deep palpation. The liver
is palpable about 4 cm below the costal margin.
It is firm in consistency, the edges are sharp and
the surface is smooth. There is no other palpable
mass in the abdomen. There is no free fluid. Digital
rectal examination is normal. There is a hard mobile
lymph node in the left supraclavicular area
between the two heads of sternomastoid muscle.
Read the checklist for abdominal examination
Checklist for history
• Family history of jaundice: Gilbert’s familial nonhemolytic hyperbilirubinemia, Crigler-Najjar’s
familial nonhemolytic jaundice, Dubin-Johnson’s
familial conjugated hyperbilirubinemia
• History of cigarette smoking: Carcinoma pancreas
• History of alcoholism: Acute alcoholic jaundice
• Highdietaryconsumption of meat: Carcinoma pancreas
• History of transfusion: Hepatitis B
• History of omphalitis: Infection of umbilicus →
incomplete obliteration of umbilical vein → jaundice
• History of drugs: Chlorpromazine, Methyl testosterone, etc.
• Historyofinjections, drug abuse, tattoos (hepatitis B)
• Past history of biliary surgery (postoperative
stricture)
Contd...
Obstructive Jaundice
153
• Family history of jaundice with anemia (hemolysis)
– Hereditary spherocytosis
• Back pain: 25% of patients with carcinoma pancreas
(relief of pain in sitting position)
• Whitish clay-colored stools: Suggestive of obstructive jaundice
• Melena: Periampullary carcinoma (silver paintstool)
• Waxing and waning of jaundice: Suggestive of CBD
stone and periampullary carcinoma
• Diabetes mellitus: Early manifestation of 25% of
carcinoma pancreas
• Charcot’s triad: Intermittent jaundice, pain and
intermittent fever.
Checklist for examination of a case of
obstructive jaundice
• Examination in daylight for yellow discoloration—
sclera, skin, nails bed, posterior part of the hard
palate, under surface of the tongue
• Look for presence of scratch mark in the lower limbs,
chest and abdomen—accumulation of bile salt
• Look for migratory thrombophlebitis (Trousseau’s
sign seen in carcinoma pancreas
• Look for spleen (hereditary spherocytosis)
• Look forstigmata of liver disease—liver palms, spider
angioma, ascites, collateral veins on the abdomen
and splenomegaly
• Look for a distended gallbladder → Courvoisier’s law
• Gallbladder is better seen than felt. Better palpated
by superficial palpation than by deep palpation
• Look for ascites
• Look forleg ulcers—Hereditary spherocytosis, sickle
cell disease
• Look for left supraclavicular nodes
• Rectal examination—rectal shelf of Blumer,
presence of primary growth, color of stool, and
blood stained finger stall.
Q 1. What are the physical findings of an enlarged
gallbladder?
Physical findings of an enlarged gallbladder
• It is better seen than felt
• It is better felt by superficial palpation than deep
palpation
• It appears from beneath the tip of the ninth rib on
the right side
• It is ovoid and smooth and moves with respiration
• It is dull to percussion
• You cannot feel a space between the lump and the
edge of the liver.
Q 2. What are your points in favor of obstructive
jaundice?
• It is a painless progressive jaundice
• Presence of itching and scratch marks
• Presence of palpable gallbladder
• Loss of weight.
Q 3. What is the definition of jaundice?
Jaundice is yellow staining of body tissues produced
by an excess of circulating bilirubin. Normal serum
concentration is 5–19 mmol/L (0.2–1.2 mg/dL)
Jaundice is detected clinically when the level rises
above 40 mmol/L (2.5 mg/dL).
Q 4. How bilirubin is formed and how is bile
pigments metabolized?
Bilirubin is formed from hem, a compound of iron
and protoporphyrin and about 85% of that produced
daily comes from the breakdown of hem from
mature RBC’sin the reticuloendothelialsystem. 15%
is derived from heme compounds in liver and bone
marrow. This bilirubin is unconjugated (which is
insoluble in water) and transported attached to the
plasma proteins to the liver cells. In liver, conjugation
occurs and the conjugated bilirubin is called bilirubin
glucuronide (which is water-soluble) and transported
Contd...
154
Clinical Surgery Pearls
to the bile ducts. Disturbance to the flow of bile
leads to stagnation and retention of conjugated
bilirubin. Therefore, in hemolytic anemia, liver is
overloaded with unconjugated bilirubin produced
from excessive breakdown of hem; hence the rise
in indirect bilirubin in prehepatic and hepatic
jaundice. In obstructive jaundice, the conjugated
bilirubin is raised (direct). Bacterial deconjugation of
bilirubin occurs in the colon to form stercobilinogen.
Part of this stercobilinogen is absorbed into the
circulation and re-excreted by the liver and kidneys
(urobilinogen). This stercobilinogen is partly
converted to stercobilin and excreted in the feces
(Fig. 12.1).
Q 5. What are the types of jaundice?
Jaundice is classified as:
A.
• Prehepatic (hemolytic)
• Hepatic
• Posthepatic (obstructive).
B.
• Intermittent
• Continuous
• Progressive.
C.
• Painful jaundice
• Painless jaundice.
Q 6. Can you differentiate the types clinically by
the color of jaundice?
Lemon yellow – Hemolytic jaundice
Orange – Hepatocellular jaundice
Deep and greenish – Obstructive jaundice
Q 7. Clinically what are the other differentiating
features of various jaundice?
Clinical features of various types of jaundice
Disease Symptoms Pain Jaundice
Hemolytic General
malaise,
loss of
weight
No pain Slow onset
and jaundice
persists
Infective
hepatitis
Loss of
appetite,
nausea,
malaise
Dull ache Gradual
onset and
disappearance
Gallstone Episodes
of flatulent
dyspepsia
Intermittent
severe pain
Sudden onset,
fades slowly in
days
Carcinoma
head of
pancreas
Loss of
weight,
loss of
appetite,
itching
Backache Progressive
jaundice
Fig. 12.1: Bile pigment metabolism
Obstructive Jaundice
155
Q 8. What are the causes for each type of jaundice?
Causes for prehepatic, hepatic and posthepatic jaundice
Prehepatic (hemolytic) Hepatic Posthepatic (obstructive)
• Hereditary spherocytosis
• Hereditary nonspherocytic anemia
• Sickle cell disease
• Thalassemia
• Acquired hemolytic anemia
• Hypersplenism
• Crigler-Najjar syndrome*
• Gilbert’s disease*
Hepatocellular—Acute viral hepatitis,
alcoholic cirrhosis
Dubin Johnson syndrome**
Cholestatic—Toxic drugs,
cholestatic jaundice of
pregnancy, postoperative cholestatic
jaundice, biliary cirrhosis
In the lumen—
• Gallstone
• Parasites (hydatid, liver fluke
roundworms)
• Foreign body—broken T tube
• Hemobilia
• Benign stricture
• Malignant stricture
In the wall—
• Congenital atresia
• Traumatic strictures
• Choledochal cyst
• Caroli’s disease
• Tumors of bile duct
• Klatskin’s tumor
• Sclerosing cholangitis
Outside the wall—
• Carcinoma head of pancreas
• Periampullary carcinoma
• Porta hepatis metastasis
• Pancreatitis
• Chronic duodenal diverticulum
• Pseudocyst of pancreas
• Metastatic carcinoma
*Crigler-Najjar and Gilbert’s disease are due to defective uptake and conjugation of bilirubin and
therefore the hyperbilirubinemia is of the unconjugated type. They are differential diagnoses for
hemolytic jaundice.
**Dubin Johnson’s familial conjugated hyperbilirubinemia is a condition where the hepatic excretion
of conjugated bilirubin into the biliary system is impaired and therefore a differential diagnosis for
obstructive jaundice (Fig. 12.2).
156
Clinical Surgery Pearls
Q 9. What is the problem of this classification?
Obstruction can occur without any evidence of a
lesion requiring surgical correction, e.g. intrahepatic
cholestasis due to drugs and early primary biliary
cirrhosis. A patient with viral hepatitis may have
considerable cholestasis suggesting obstruction.
A patient with obstructive jaundice may go on
to develop a degree of hepatocyte insufficiency
too. Hence, the classification has considerable
overlapping.
Q 10. How to differentiate the types of jaundice
biochemically?
There are two types of bilirubin—conjugated
(direct) and unconjugated (indirect).
The direct bilirubin is increased in obstructive
jaundice whereas the indirect bilirubin is increased
in hemolytic jaundice. In obstructive jaundice
conjugated bilirubin from the hepatocytes and
biliary radicles overflow into the bloodstream,
whereas in hemolytic jaundice, unconjugated
bilirubin overloads the liver and is detected as
elevated in blood.
• The serum bilirubin levelrarely exceeds 4–5 mg/
dL in hemolytic jaundice.
• The bilirubin exceed to 10–20 mg/dL in
obstruction due to neoplasm.
• In obstruction due to stones usually itranges up
to 5 mg, rarely does it exceed 15 mg.
Fig. 12.2: common causes of obstructive jaundice
Obstructive Jaundice
157
Q 11. What is the role of liver enzymes in the
diagnosis of jaundice?
The two most important enzymes are ALT, AST and
alkaline phosphatase (ALP).
• ALT above 1000 is suggestive of viral hepatitis
• In alcoholic liver disease AST israised (AST : ALT
is >2)
• Alkaline phosphatase is raised in obstructive
jaundice and infiltrative liver diseases like
tumor or granuloma.
Note: Normal values: ALT: 5 – 35 U/L
AST: 5 – 40 U/L
Q 12. What are the sources of alkaline phosphatase
and what are the conditions in which the enzyme
is increased?
There are three sources for alkaline phosphatase
1. Liver
Equal contribution 2. Bone
3. Intestine—Small contribution
• In the liver, it is a product of epithelial cells of
the cholangioles
• It is expressed in Bodansky units (previously
KA units)
Note: Normal value: 30 – 115 U/L.
Clinical conditions in which alkaline
phosphatase is increased
• Intrahepatic cholestasis
• Cholangitis
• Extrahepatic obstruction
• Focal hepatic lesions without jaundice
• Solitary metastases
• Pyogenic abscess
• Granulomas
• Bone tumors (primary and secondary).
Q 13. How to rule out alkaline phosphatase rise
because of bone pathology? (PG)
• Serum calcium and phosphorus (which will be
abnormal in bony pathology)
• 5’ nucleotidase and γ-glutamyl transpeptidase
which are specific for obstructive jaundice.
Q 14. What is acholuric jaundice?
It is nothing but the result of hereditary spherocytosis.
It is called acholuric because there is no excretion of
bilirubin in the urine. In this condition, because of the
hemolysis as a result of spherocytosis, the bilirubin
produced is insoluble (unconjugated). This is not
filtered by glomerulus. There will be family history
of jaundice. In addition you get—
• Pigmented stones in gallbladder
• Enlarged spleen
• Leg ulcers.
It produces hemolytic crisis—
• Pyrexia
• Abdominal pain
• Nausea and vomiting
• Extreme pallor.
The fragility of the RBC’s will be increased
because of the biconvex nature of the RBC in
contrast to the normal biconcave.
Q 15. What are the investigations for hemolytic
jaundice?
Investigations for hemolytic jaundice
1. Peripheral smear for spherocytosis
2. Osmotic fragility test for red cells (which will be
increased).
3. Reticulocyte count which will be increased
(compensatory hemopoesis)
4. Positive Coombs’ test.
158
Clinical Surgery Pearls
Q 16. What is surgical jaundice?
Surgical jaundice is a condition where the
jaundice can be corrected by surgery. The
posthepatic jaundice is mainly included in this
category. Hemolytic conditions like hereditary
spherocytosis require splenectomy as part of the
treatment, but are not referred to commonly as
surgical jaundice.
Q 17. Any other classification for surgical jaundice?
• Complete jaundice – Carcinomaheadof
pancreas
• Intermittent jaundice – Periampullary
carcinoma
• Chronic and incomplete – Biliary stricture
• Segmental – Traumatic
Q 18. What is Courvoisier’s law?
Courvoisier first drew attention to the association
of an enlarged gallbladder and a pancreatic tumor
in 1890 and this law states.
“When the gallbladder is palpable and the patient
is jaundiced, the obstruction of bile duct causing the
jaundice is unlikely to be a stone because previous
inflammation will have made the gallbladder thick
and nondistensible.”
• But he never said when the gallbladder is not
palpable, it is due to stones (that is, the converse
– jaundice without palpable gallbladder
certainly does not implicate stones).
• Gallbladder is palpable only in 30% of cases of
carcinoma head of the pancreas.
• There are exceptions to Courvoisier’s law
Exceptions to Courvoisier’s law
1. Stones, simultaneously occluding the cystic duct
and the distal CBD (Double impaction)
2. Pancreatic calculus obstructing the ampulla
3. Oriental cholangiohepatitis because of Clonorchis
sinensis (Ductal stones formed secondary to the
liver fluke infestation)
4. Mucocele/empyema of gallbladder
5. Carcinoma of the gallbladder with or without
jaundice—it’s although rare it can also cause a
palpable gallbladder (In 1 to 4 the gallbladder is
palpable in a jaundiced patient with stones)
6. Nodes in porta hepatis
7. Carcinoma gallbladder with multiple metastases in
liver.
Q 19. What is oriental cholangiohepatitis?
It is because of Clonorchis sinensis (Chinese liver fluke)
and in this condition, stones are formed primarily in
the bile ducts and therefore the gallbladder is often
palpable.
Q 20. What is choledochal cyst?
It is a dilation or diverticula of all or a portion of the
common bile duct. Women are more affected than
men and Asians are more affected than Western
people. The incidence is very high in Japan. Various
causes are postulated:
• Infectious agents
• Reflux of pancreatic enzymes via long common
channel
• Genetic
• Autonomic dysfunction.
Q 21. What are the types of choledochal cysts? (PG)
Types of choledochal cyst
Type 1 – Fusiform (85%)
Type 2 – Saccular
Type 3 – Choledochocele (wide mouth dilatation
of the common bile duct at its confluence
with duodenum)
Type 4 – Cystic dilatation of both intra and extrahepatic bile duct
Type 5 – Lakes of multiple intrahepatic cysts (Type 5
along with hepatic fibrosis is called Caroli’s
Contd... disease).
Contd...
Obstructive Jaundice
159
Alonso-Lej/Todani classification of choledochal cyst
Type I Classic cyst type characterized by cystic dilatation of CBD. Most common (50–85%) IA (Cystic); IB
(Fusiform); IC (Saccular)
Type II Simple diverticulum of extrahepatic biliary tree; located proximal to the duodenum (5%)
Type III Cystic dilatation of the intraduodinal portion of the extrahepatic CBD also known as choledochocele (5%)
Type IV Involve multiple cysts of intrahepatic and extrahepatic biliary tree
Type IV A Both intrahepatic and extrahepatic cysts (30–40%)
Type IV B Multiple extrahepatic cysts without intrahepatic involvement
Type V Isolated intrahepatic biliary cystic disease (Caroli’s disease) associated with periportal fibrosis or cirrhosis;
can be multilobar or confined to a single lobe.
Q 22. What is the treatment of choledochal cyst?
(PG)
There is increased chance for malignancy, if part
of cyst is left behind. Therefore, complete excision
followed by hepaticojejunostomy is the treatment
of choice.
Q 23. What is Caroli’s disease? (PG)
It is a congenital cystic disease having saccular intrahepatic dilatation of the ducts. It may be isolated
or associated with:
– Congenital hepatic fibrosis
– Medullary sponge kidney
It may manifest as cholangitis or obstructive
jaundice.
Q 24. What is hemobilia? (PG)
It is a complication of hepatic trauma as a result
of bleeding from intrahepatic branch of the
hepatic artery into a duct. The triad of hemobilia
(Sandblom’s triad) consists of
– Biliary colic
– Obstructive jaundice
– Occult/gross intestinal bleeding.
Causes for hemobilia
• Trauma
• Oriental cholangiohepatitis
• Hepatic neoplasm
• Rupture of hepatic artery aneurysm
• Hepatic abscess
• Choledocholithiasis.
The diagnosisis by Technicum 99m labeled RBC
scan and arteriogram.
Q 25. What is the treatment of hemobilia? (PG)
Therapeutic embolization using:
• Stainless steel coils
• Gel foam
• Autologous blood clot.
Q 26. What are the causes for intermittent jaundice?
1. CBD stones
2. Periampullary carcinoma
3. Repeated hemolytic episode
4. Parasite
5. Hemobilia
6. Duodenal diverticula.
160
Clinical Surgery Pearls
Q 27. What are the symptoms of a patient with
carcinoma head of pancreas?
• Progressive jaundice 75% (it is possible to
get carcinoma head of the pancreas without
obstructive jaundice).
• Pain: Pain is frequent even though classical
description is painless.
• Hematemesis and melena in late cases.
• Chills and fever when there is cholangitis.
• Diabetes mellitus: Carcinoma pancreas induces
glucose intolerance resulting in diabetes
mellitus (25% of patients).
• Courvoisier sign: Palpable gallbladder noted
only in 25% of patients with resectable lesions.
Q 28. How will you proceed to investigate the
given case of jaundice?
A. Investigations for diagnosis and staging are (Flow
chart 12.1):
1. Ultrasound e x a m i n a t i o n — l o o k f o r
intrahepatic biliary radicle dilatation
– Size of the CBD normally should be less
than 8 mm sonologically
– Dilatation of pancreatic duct (dilatation of
CBD and pancreatic duct is suggestive of
carcinoma head of the pancreas)
– For biliary stones
– For free fluid
– For mass lesions (difficult to identify
pancreatic head malignancy in ultrasound because of the gas in intestines in
front of the organ)
– For liver metastases.
2. Contrast enhanced helical CT
– Can identify the tumor in the head of
pancreas (Central zone of decreased
Flow chart 12.1: Management of pancreatic cancer
Obstructive Jaundice
161
attenuation will be present). Pancreatic
duct and bile duct dilatations are strong
evidence of pancreatic carcinoma
– Note the size of the tumor
– Infiltration to the adjacent structures like
portal vein
– Nodal involvement.
3. Endoscopy/ERCP (Endoscopic retrograde
cholangiopancreatography)—useful for non
dilated ducts—in the absence of mass in the
CT, ERCP is indicated. It is the most sensitive
test for such situations.
– The periampullary carcinoma can be
visualized
– Biopsy can be taken from the periampullary
lesion
– The lower limit of the growth can be
identified by ERCP
– Stenting can be done to relieve the
jaundice
– Sphincterotomy can be done to remove
the bile duct stone.
4. Endoscopic ultrasound
– To assess the operability
– Size of the tumor
– To know the involvement of mesenteric
lymph nodes, para-aorticnodes and
superior mesenteric vein
– Hepatic metastases.
5. Percutaneous transhepatic cholangiography
(PTC)—useful for dilated ductal system.
– The coagulation profile is checked and
antibiotic coverage is given. In this
procedure a pliable needle is inserted
under local anesthetic and sonological
guidance into the dilated biliary duct.
Should decompression of the biliary tree
be desired preoperatively, then a fine bore
catheter may be left in the ducts to allow
continuous drainage of bile.
– I t i s a l s o p o s s i b l e t o i n s e r t a n
endoprosthesis to relieve the obstruction
for unresectable lesions.
– The PTC is ideal for demonstrating
the anatomy above an extrahepatic
obstruction and the upper limit of the
obstructing lesion can be identified by
injecting dye.
6. Upper GI series—to decide whether a
gastrojejunostomy is indicated or not. The
classical findings are (largely replaced by
Helical CT).
– Widening ofthe C-loop ofthe duodenum
in carcinoma head of the pancreas.
– Reverse3 sign in periampullary carcinoma.
B. Biochemical investigations
• Total bilirubin, direct and indirect (direct
is increased obstructive and indirect is
increased in hemolytic jaundice (total and
direct bilirubin raised in hepatic).
• Alkaline phosphatase—( o v e r 1 0 0
international unit is indicative of cholestasis
if bone disease is absent).
• Total protein, albumin and globulin
(albumin and globulin levels are reversed in
chronic hepatocellular damage). Globulin
level will be very high in biliary cirrhosis. In
biliary obstruction per se there won’t be any
change in the values.
• Serum transaminase levels are above normal
in viral hepatitis.
C. Coagulation profile—Prothrombin Time—normal
inhemolytic jaundice. Prolongedbut correctable
162
Clinical Surgery Pearls
with vitamin K in cholestatic jaundice (provided
their remains some functioning liver tissue).
This will be prolonged and not correctable in
advanced hepatocellular disease.
• Platelet count, bleeding time and clotting
time.
D. Urine examination
1. Absent urobilinogen indicates obstruction
to the common bile ducts.
2. Excess urobilinogen occurs in hemolytic
jaundice and sometimes in liver damage.
3. Absent bilirubin indicates hemolytic jaundice
(Bilirubin predominantly unconjugated).
4. Excess bilirubin is present in obstructive
jaundice.
E. Stool examination
1. Absence of bile pigment indicates biliary
obstruction (Clay-colored stool).
2. Positive occult blood indicates ampullary
carcinoma, bleeding esophageal varices and
alimentary carcinoma.
Q 29. What is the dose of vitamin K and how is
it given?
The dose of vitamin K is 10 mg and it is given IM
for 3 days.
The vitamin K1 (phytomenadione) is given
intravenously—10 mg daily for 3 days.
Q 30. What are the preoperative preparations if
you are planning for surgery?
1. Hydration
2. Nutrition
3. Correction of coagulation deficiency—vitamin
K, FFP, platelet transfusion, etc.
4. Correction of anemia.
Q 31. What are the indications for preoperative
biliary decompression? (PG)
Indications for preoperative biliary decompression
• Bilirubin > 12 mg
• Sepsis
• Hepatorenal failure
• Severe cardiopulmonary disease
• Severe malnutrition.
NB: Routine drainage is not recommended.
Q 32. What is the other simple option for drainage?
Simple cholecystostomy, if other options are not
available.
Q 33. What are the causes for fever in jaundice?
Causes for fever in jaundice
1. Cholangitis 2. Hemolysis
3. Septicemia 4. Hepatic abscess
Q 34. What are the 3 important special risks in
obstructive jaundice? (PG)
1. Hypocoagulability
2. Renal failure—may be because of increased
bile pigment load on the tubules, increased
postoperative distal tubular reabsorption
of water and failure of liver to trap enteric
nephrotoxins
3. Sepsis of bile with or without calculi.
Q 35. What are the signs of unresectability in
carcinoma head of the pancreas?
1. Hepatic metastases
2. Distant metastases (Distant lymph nodes from
pancreatic head)
3. Ascites (Peritoneal metastases)
4. Encasement of superior mesenteric, hepatic or
celiac artery by tumor.
Note: Nowadays the superior mesenteric artery is
approached from behind as the first step before
Obstructive Jaundice
163
contemplating Wipple’s resection and if the artery
is involved resection is abandoned.
Q 36. Should portal vein involvement preclude a
resection? (PG)
Involvement of a short segment (< 1.5 cm) of portal
vein is not a contraindication to a curative resection.
Q 37. What is the treatment of itching because of
obstructive jaundice? (PG)
a. Cholestyramine—It is an ion exchange resin,
usually provides relief by binding bile salts in the
intestinal lumen, thus, inhibiting their reabsorption
into blood.
b. Opiates.
Q 38. What is the role of percutaneous biopsy
(Aspiration) of pancreatic tumor? (PG)
• It is done under ultrasound/CT guidance
• It is contraindicated in candidatesforsurgery—
risk of spreading
• Done in patients with radiographic evidence of
unresectability
• It is also done preoperatively in operable cases
• Biopsy may miss the lesion because a variable
area of pancreatitis surround the tumor, leading
to sampling error.
Q 39. What are the complications of needle biopsy
of pancreatic tumor? (PG)
• Pancreatitis
• Fistula
• Hemorrhage
• Infection.
Q 40. What is the tumor marker for pancreatic
malignancy? (PG)
• CA 19-9 (Carbohydrate antigen)—It is useful in
following the results of the treatment
• CEA (Carcinoembryonic antigen).
Q 41. Perioperatively can you differentiate chronic
pancreatitis from carcinoma? (PG)
• It is very difficult.
• A hard noncystic mass in the head and
obstructive jaundice and dilatation of CBD is
more in favor of carcinoma.
• Ahard noncystic massin the retroampullarypart
and no jaundice and no dilatation is in favor of
chronic pancreatitis.
Q 42. What are the signs of inoperability in
carcinoma head of pancreas?
Signs of inoperability in carcinoma head
of pancreas
Clinically
• Supraclavicular nodes
• Ascites
• Rectal shelf of Blumer
• Liver metastases, etc.
Preoperatively
• Ascites
• Liver metastases
• Peritoneal metastases
• Rectal shelf of Blumer
• Involvement of the portal vein and superior
mesenteric vessels (preoperatively assess the
resectability after Kocherizing the duodenum and
passing the surgeon's finger between the pancreas
and the portal vein) – “Tunnel of love”.
Q 43. What are the surgical options for the
operable carcinoma head of the pancreas?
1. The classical Whipple’s p r o c e d u r e
(pancreaticoduodenectomy followed by
pancreaticojejunostomy/gastrostomy, choledochojejunostomy and gastrojejunostomy)
(Fig. 12.3).
164
Clinical Surgery Pearls
2. Pylorus preserving pancreaticoduodenectomy
(PPPD).
The second procedure is favored nowadays.
Note: Currently the pancreatic head is accessed
from behind to see invasion of mesenteric artery
as the first step and if it is found to be involved, it is
considered inoperable.
Q 44. What is the morbidity and mortality of this
procedure? (PG)
Mortality is 3 – 5% in high volume center
Morbidity is around—40%—pancreatic leak—
10%—infection.
Q 45. What are the surgical options for inoperable
cases?
To relieve jaundice
1. After ruling out a low insertion of cystic duct,
a cholecystojejunostomy is done to relieve
the jaundice. This may be combined with a
jejunojejunostomy.
2. If there is low insertion of cystic duct, a
choledochojejunostomy is done to relieve the
obstruction.
Relieve duodenal obstruction
1. If duodenal obstruction (15% of cases) is suspected
in addition, a gastrojejunostomy is done.
2. Self-expanding metal stent placed endoscopically, is an alternative to gastrojejunostomy.
Q 46. What is the management of pain in
inoperable cases?
Transthoracic splanchnicectomy (dividing the
splanchnic nerve transthoracically preferably
through thoracoscope).
Q 47. What percentage of pancreatic head
malignancy is resectable?
At the time of presentation 90% are unsuitable for
resection because of local spread to the superior
mesenteric vein, para-aortic and mesenteric nodes
and liver metastases.
Q 48. What is the role of chemotherapy in
pancreatic cancer?
Chemotherapeutic agent of choice is 5 fluorouracil
(5FU)
• A new drugGemcitabine produces remission in
15 – 25% of patients.
Q 49. What is the prognosis of carcinoma head of
the pancreas?
• The overall median survival is only 20 weeks
• Less than 3% of patients survive for 5 years
• In carcinoma of the ampulla ofVater, the 5 years
survival after resection is 40%.
OBSTRUCTIVE JAUNDICE DUE TO STONES
Q 50. What are the manifestations of CBD stones?
The classical presentation is Charcot’s triad
consisting of:
Fig. 12.3: View of pancreaticojejunostomy
Obstructive Jaundice
165
• Intermittent pain
• Intermittent fever
• Intermittent jaundice.
Q 51. What is cholangitis?
Obstruction of bile duct will lead on to bacterial
infection of the bile duct. Obstruction is synonymous
with infection. The obstruction may be partial or
complete. The causes for cholangitis are—
• Choledocholithiasis
• Biliary stricture
• Neoplasms (15%)
• Ampullary stenosis (less common)
• Chronic pancreatitis
• Pseudocyst
• Duodenal diverticulum
• Parasitic.
Q 52. What is the pathology of cholangitis ?
(PG)
• The ductal pressure increases when there is
obstruction
• Bacteria escape to the systemic circulation via
hepatic sinusoids
• Organism willreach the blood and blood culture
will positive.
Q 53. What are the common organisms for
cholangitis ? (PG)
Organisms causing cholangitis
• E. Coli
• Klebsiella
• Pseudomonas
• Enterococci
• Proteus
• Bacteroides.
Q 54. What is Reynold’s pentad?
It is a manifestation of acute toxic cholangitis as a
result of obstruction of the bile duct (It is also called
suppurative cholangitis). It is a life-threatening
condition and should be managed as emergency.
The Pentad consists of:
• Pain
• Fever
• Jaundice
• Mental confusion
• Shock.
Q 55. What is the management of acute toxic
cholangitis? (PG)
It is an emergency. The antibiotic of choice is
aminoglycoside and clindamycin/metronidazole.
The ductal system is decompressed by emergency
sphincterotomy or by transhepatic drainage. The
associated gallbladder pathology may be tackled
as an elective procedure later by laparoscopic
cholecystectomy.
Q 56. What is the management of obstructive
jaundice due to CBD stone?
The investigations and preparations are the same
as for obstructive jaundice. (which is given above).
There are 3 surgical options:
1. Endoscopic sphincterotomy initially, followed
by laparoscopic cholecystectomy preferably in
the same admission. (currently favored where
laparoscopic expertise is not available).
2. Laparoscopic cholecystectomy a n d
laparoscopic CBD exploration (if expertise is
available); the CBD exploration may be done
through the cystic duct or if the duct is more
than 1.5 cm through a choledochotomy.
3. Open—Laparotomy, cholecystectomy and CBD
exploration and stone removal.
166
Clinical Surgery Pearls
Q 57. What are the contraindications for sphincterotomy?
• Stone size more than 2 cm.
• Stenosis of bile duct proximal to the sphincter.
Q 58. What is the management of bile duct
tumor? (PG)
The bile duct tumors may be benign or malignant.
The benign tumors are rare and far less common. The
malignant tumors are called cholangiocarcinomas.
Cholangiocarcinoma is a term now applied to
malignant intrahepatic, perihilar and distal extra
hepatic tumors of the bile ducts. The incidence
of this condition is rising. The management may
be palliative stenting or surgery. Most patients
will receive only palliative surgery. The consensus
of surgical opinion is that the surgical treatment
is difficult and should be reserved for the fittest
patients getting 5 mm clearance, node and liver
resection if required. In all cases, reconstruction is
made using hepaticojejunostomy (Roux–en–Y).On
the right side an extended right hepatic lobectomy
is done because of anatomical reasons. The length
of right hepatic duct is smaller in contrast to the left
which has got significant length of extrahepatic duct.
Q 59. What are the risk factors for cholangiocarcinoma? (PG)
These include:
Risk factors for cholangiocarcinoma
• Sclerosing cholangitis
• Chronic intrahepatic gallstones
• Caroli’s disease
• Choledochal cyst
• Ulcerative colitis
• Liver flukes.
Possible association:
• INH (Inhibitor)
• Methyldopa
• Oral contraceptives
• Asbestos.
Q 60. What is Klatskin tumor? (PG)
The perihilar cholangiocarcinoma is called Klatskin
tumor. About 50% of all cholangiocarcinomas are
Klatskintumor.Ofthe reminder,half are intrahepatic
and half are related to extrahepatic bile ducts.
Q 61. Is there any role for fine needle aspiration
cytology? (PG)
Percutaneous fine needle aspiration cytology is
absolutely contraindicated in patients who may
be operable.
Q 62. What is the Bismuth classification of
cholangiocarcinoma? (PG)
Type I – involving the common hepatic duct.
Type II – the growth involving the proximal
common hepatic duct that extends
to the bifurcation, but both hepatic
ducts are free.
Type III – growth involving one hepatic duct.
Type IV – is the hilar involving both hepatic and
proximal common hepatic ducts.
Q 63. What are the contraindications for
surgery? (PG)
• Lymph node involvement
• Encasement of hepatic hilar vessels.
Q 64. What is Taj Mahal resection? (PG)
The technique of central liver resection for
cholangiocarcinoma is called Taj Mahal resection
owing to the shape of the defect in the liver. This
involves removal of segments 1, 4 and 5 and the
relevant bile ducts.
Obstructive Jaundice
167
Q 65. What is the palliative surgical treatment? (PG)
Palliative surgicaldrainage isdoneby anastomosing
a Roux loop to the segment III duct.
Q 66. Is there any role for surgery in hereditary
spherocytosis?
• Splenectomy is done
• Gallbladder stones, if present are managed by
cholecystectomy.
Q 67. What type of gallstone you get in hereditary
spherocytosis?
Pigment stone.
For PG’s—What is new?
• The imaging modality of choice for pancreatic malignancy is MDCT (Multi Detector Computed Tomography)
and angiography, MRI and MRCP
• Tumor marker CA 19-9 is measured routinely in pancreatic carcinomas and levels greater than 1000 units/mL
have been found to be linked to unresectable disease
• PTC—is an investigation done for proximal biliary obstruction and not routine
• There is no role for mannitol in the preoperative preparation of obstructive jaundice patient. In fact, it will worsen
the renal function
• Uncinate—First approach for pancreaticoduodenectomy—this approach issuitable forinfiltration ofthe superior
mesenteric vein or portal vein. It is also suitable for infiltration of the arterial axis
• SMA—First approach for pancreaticoduodenectomy—It comprises early dissection of superior mesenteric
artery after kocherization of the duodenum along with the posterior pancreatic capsule. The advantage of this
technique is that the tumor infiltration of SMV, portal vein, or tumor proximity to SMA can be handled at the
initial stage or resection can be abandoned. This will reduce the chances of margin positive pancreatic head
resection. It will also help improved lymph node yield
• The indications for preoperative biliary drainage are:- 1. Acute cholangitis (systemic sepsis of biliary origin is
called cholangitis), 2. Obstructive jaundice with secondary renal impairment, 3. Comorbidities delaying the
surgery
• Classic Whipple’s operation is reserved for duodenal cancers
• Removal oflymph nodes ofthe rightside ofthe hepatoduodenal ligament,posteriorpancreaticoduodenal nodes,
nodes to the right side of the superior mesenteric artery from the origin to the inferior pancreaticoduodenal
artery are important
• Neoadjuvant chemotherapy is beneficial
• For pancreatic leak irradiation of pancreas is useful
• R1 cases needs postoperative radiotherapy
• Multimodality treatment is now recommended for pancreatic carcinoma
• Chemotherapeutic agents are 5FU, Cisplatin and alpha interferon
• Gemcitabine alone or in combination with other drugs.
13 Varicose Veins
Case
Case Capsule
Middle-aged multiparous female patient presents
with dilated tortuous veins on both lower limbs of
10 years duration. She complains of dull ache felt
in the calves and lower leg that get worse through
the day especially during standing. It is relieved by
lying down for 30 minutes. She also complaints of
mild swelling of the ankle by the end of the day.
She does not give history of previous accidents,
major operations or prolonged illness. Her mother
and elder sister had similar complaints.
On inspection, large tortuous visible veins
are noted in the distribution of long saphenous
vein. Skin of the lower third of the medial side
of the right leg shows brown pigmentation and
there is an ulcer situated just above the medial
malleolus of the size of 7.5 × 5 cm. On palpation
there is pitting edema of the right ankle region.
The skin and subcutaneous tissue are thickened
over the area. Palpation along the course of the
long saphenous vein behind the medial border
of the tibia revealed three defects in the deep
fascia 5, 10 and 15 cm above the medial malleolus.
There is a palpable cough impulse in the groin at
the saphenous opening region. The veins collapse
when the patient lies down and the limb is elevated.
Trendelenburg test I and II are positive on the right
side and test I positive on left side. Modified Perthes
test is negative on both sides. Multiple tourniquet
test shows perforator incompetence in the right
leg corresponding to the fascial defects mentioned
above. Schwartz test is positive on right side. There
is no bruit heard over the veins.
The ulcer is of the size of 7.5 × 5 cm with a
sloping edge and the surrounding skin is purple
blue in color. The floor of the ulcer is covered with
pink granulation tissue. The base of the ulcer is fixed
to the deeper tissues. There is serous discharge
from the ulcer. Equinus deformity is present at the
ankle joint. Regional lymph nodes are enlarged,
firm in consistency and mobile (the vertical group
of inguinal nodes on right side). On abdominal
examination there is no vein seen crossing the
abdomen and there is no mass lesions. Per rectal
and per vaginal examination shows no pelvic cause
for the dilated tortuous veins. Examination of the
peripheral vascular system is normal.
Varicose Veins
169
Checklist for history
History of
• Major surgery
• Majorillness necessitating prolonged recumbency
• Recentlong airtravel (economy classsyndrome)—
deep vein thrombosis
• Sudden undue strain
• Drug intake—hormone containing pills (like
contraceptives)
• Computer professionals requiring long hours in a
sitting posture—E thrombosis
• Occupation demanding prolonged standing
• Family history of varicose veins.
Checklist for examination of varicose veins
• Examine the patient in standing position
• Expose the patient from umbilicus to the toes
• Examine the front and back of the limb
• Examine the limbs for inequality of circumference
• Know the anatomy of long saphenous and short
saphenous veins with its named tributaries
• Identify the anatomical distribution of the varicose
veins
• Feel the veins—tender/fibrous /thrombosed
• Examine the ankle—congestion, prominent veins,
pigmentation, eczema, ulcer
• Pelvic examination to rule out secondary causes
of varicose veins—intrapelvic neoplasms (uterus,
ovary and rectum)
• Examine the abdomen for dilated veins that will
be secondary to obstruction of inferior vena cava
(commonest cause—intra-abdominal malignant
disease)
• Always do abdominal examination—forintrapelvic
tumor such as ovarian cysts, fibroid, cancer cervix,
abdominal lymphadenopathy
• Look for large suprapubic veins and abdominal
varices which are present in cases of patients with
chronic iliac vein occlusion
• Digital rectal examination
• Auscultate the veinsto rule out continuous murmur
(for AV fistula)
• Always examine theperipheralpulses—venous and
arterial disease often coexist.
Contd...
Contd...
170
Clinical Surgery Pearls
Q 1. What are varicose veins?
By definition varicose veins are thin-walled,
tortuous, dilated, and lengthened veins with
incompetence of the contained valves. This
excludes the normal prominent and dilated veins
on healthy muscular legs in nonobese people.
Physiologically varicose vein is one that permits
reversal of flow through its faulty valves.
Q 2. What are the causes for varicose veins?
• Congenital—rare (congenital absence of valves)
• Primary varicose veins (cause not known, often
familial)—wall theory (weakness of walls) and
valve theory
• Secondary varicose veins:
– Post-thrombotic (destruction of valves)
– Post-traumatic
Varicose Veins
171
– Pregnancy
– Fibroids and ovarian cysts
– Abdominal lymphadenopathy
– Pelvic tumors
– Retroperitoneal fibrosis
– Ascites
– Iliac vein thrombosis
– High flow and pressure states, e.g. AV fistula.
Q 3. How can you distinguish primary varicose
veins associated with a normal deep venous system
from varicose veins secondary to a diseased deep
venous system (the postphlebitic syndrome)?
Primary varicose veins Secondary varicose veins
Seen in early
adolescence
Positive family history
Saphenous distribution
alone is involved
Positive Trendelenburg—
1— test
No stasis sequelae
(dermatitis and
ulceration)
No morning ankle edema
Patent deep veins in
doppler and duplex
History of varicose veins
of long duration without
any previous acute event
like edema
Older age group
No family history
In addition to the
saphenous, the
perforators and the deep
veins are involved
Trendelenburg—1 and 2
positive
Stasis sequelae present
Ankle edema present
Deep veins and
perforators are abnormal
in Doppler and duplex
The limb is normal until
swelling begins as a
sudden event. Varicose
veins develop later
Note: Primary varicose veins can ultimately lead to
stasis sequelae, even ulceration because with time,
retrograde flow down the superficial system and back
into the deep system can produce sustained venous
hypertension. At this end-stage the appearance may
be indistinguishable from postphlebitic syndrome, but
the history is very different.
Q 4. What is the incidence of varicose vein?
About 20% of the population suffer varicose veins.
Q 5. How much blood is there in the venous
system?
About 70% of the body’s blood is in the venous
system at any one time and there are at least 3 times
as many veins as arteries in the limbs.
Q 6. What percentage venous blood is carried by
the superficial system?
10%.
Q 7. What is the anatomy of veins in the lower
limb?
The venous system in the lower limb has three
portions.
Superficial: Long saphenous system and short
saphenous system with their tributaries (they
terminate at the saphenofemoral and saphenopopl
junctions respectively.
Deep veins: Three pairs below the knee each with its
associated artery—anterior tibial, posterior tibial,
and peroneal. In the upper third of calf they join to
form the popliteal vein which proximally becomes
the superficial femoral vein.
Perforating veins: In the case of long saphenous
vein four sets:
• Dodd’s perforator in relation to the subsartorial
canal.
• Boyd’s perforator in relation to the calf muscles
just below the knee.
• Cockett’s perforatorsjust above the ankle –5, 10,
and 15 cm above the malleolus.
• Ankle perforators of May or Kuster.
In the case of short saphenous vein:
• Bassi’s perforator—5 cm above the calcaneum
• Soleus point perforator
• Gastrocnemius point perforator.
172
Clinical Surgery Pearls
Q 8. What is the anatomy of long saphenous
system?
This is the biggest vein in the body, arises in front of
the medial malleolus. It ascends behind the medial
femoral condyle along the medial aspect of the
thigh and terminates in the common femoral vein
through the saphenous opening in the groin. The
important tributaries are:
• The posterior arch vein (Leonardo’s vein) (Fig
13.1)—starts behind the medial malleolus
and runs upwards to the long saphenous vein
joining it at the knee level. This vein is important
because it has 3–4 constant perforators—(the
cockett’s perforators) joining it at the posterior
border of the tibia linking the superficial with
the posterior tibial vein of the deep system. This
Fig. 13.1: Posterior arch vein
vein has a tendency to become varicose rather
than the long saphenous vein.
• Anterior superficial tibial vein—ascend along
the shin and joins the long saphenous system
again at knee level (Fig. 13.2).
• The medial andlateral accessory saphenous vein
(posteromedial and anterolateral) in the thigh
joining of the long saphenous vein at variable
levels near to the saphenofemoral junction.
• The saphenofemoral junction tributaries—
superficial inferior epigastric, superficial
circumflex iliac and superficial external pudendal
(Fig. 13.2).
Fig. 13.2: Long saphenous
Varicose Veins
173
Q 9. What is the anatomy of the short saphenous
system?
The vein starts behind the lateral malleolus and
ascends superficially through the posterior aspect
of the calf to terminate in the popliteal vein after
piercing the deepfascia. In about 50%ofindividuals
the short saphenous vein terminates above the
popliteal fossa (Fig. 13.3).
Q 10. What is ‘Blow out syndrome’? (PG)
This was described by Cockett. When the valves
of the perforating veins become incompetent,
contraction of the muscle will result in retrograde
flow of venous blood from the deep to the
superficial veins. The resultant high pressure reflux
is called venous hypertension (describedbyCockett
as blow out syndrome).
Q 11. What are the functions of veins?
There are three principal functions.
• Return of blood to the heart
• Blood storage
• Thermoregulation.
Q 12. What is the normal hemodynamics of venous
system in the lower limb? What is ambulatory
venous hypertension?
Normally the venous blood flow is from the superficial
to the deep system through the perforators if the
valves are competent. On standing the venous
pressure in the foot vein is equivalent to the height
of the column of blood extending from the heart
to the foot. Normally the pressure in the superficial
veins of the foot and ankle is around 80–100 mm
of Hg. The venous blood is pumped to the heart
from the limb by the series of muscle pumps in the
calf and thigh. They are called peripheral hearts.
In addition there is a foot pump that ejects blood
from the plantar veins during walking (there are
three pumps altogether— the foot pump, the calf
pumpandthighpump).Duringwalkingthepressure
within the calf compartment rises to 200–300 mm
of Hg and the blood is pushed up from the deep
system. During the relaxation of the calf muscle
the pressure within the calf falls to a low level and
the blood from the superficial veins flows through
the perforators to the deep veins. The pressure
in the superficial system will then automatically
fall to about 20 mm of Hg. When the perforators
are incompetent, the pressure in the superficial
system will not fall and eczema, skin damage and
leg ulceration develops. The failure of superficial
Fig. 13.3: Short saphenous vein venous pressure to fall during exercise is called
174
Clinical Surgery Pearls
ambulatory venous hypertension and is the main
cause of venous leg ulceration. Incompetence of the
deep veins has a more severe effect on the venous
physiology than superficial venous incompetence
because the deep veins are much larger than the
superficial veins. Persistently raised venous pressure
tracks back to the microcirculation of the skin and
causes skin damage, resulting in venous ulceration.
Q 13. What are the causes for venous ulcer?
Venous ulcers occur in the following situations:
1. In patients with deep vein thrombosis (DVT)—
post-thrombotic limb
2. Ankle perforator incompetence
3. Sometimes long-standing superficial varicose
veins.
Q 14. What is the pathophysiology of venous
ulcer?
1. The fibrin-cuff theory of Browse:
Persistently raised venous pressure
↓
Capillary proliferation and inflammation in the skin
and subcutaneous tissue (Like a glomerulus) ↓
increased capillary leakage
↓
Perivascular cuff of fibrin, collagen type IV and
fibronectin around the capillaries
↓
Fibrotic process affecting the skin and subcutaneous
fat (lipodermatosclerosis)
↓
Barrier to diffusion preventing nutrient exchange ↓
Ulcer
Note: This theory is no more accepted because it has
been found that there is no physical barrier to the
diffusion.
2. White cell trapping theory (Dormandy)—
presently accepted theory:
Venous hypertension
↓
Blood slows down in capillaries
↓
White cells marginate and are trapped
↓
Leukocyte sequestration
↓
Activation of trapped leukocyte
↓
Release of proteolytic enzymes
↓
Damage to capillary endothelium
↓
Leg ulcer
Q 15. What is venous claudication?
After deep vein thrombosis recanalization will
usually occur. When recanalization fails to occur
after iliofemoral venous thrombosis, venous
collaterals develop to bypass the obstruction
to the venous outflow. These collaterals usually
suffice while the patient is at rest. However, any
leg exercise induces increased arterial inflow to
the lower extremities along with a commensurate
increase in venous outflow requirements. This may
exceed the capacity of the venous collateral bed
resulting in venous hypertension. The pressure built
up is manifested as tight or bursting pain. Relief is
obtained with rest but not as prompt as in arterial
claudication. This pain is seen after walking and
towards the evening.
Varicose Veins
175
Q 16. What are thread veins (dermal flares)?
They are smaller veins of 0.5 mm diameter seen in
the skin in varicosity. They are `usually purple or
red in color. These tiny veins are associated with
superficial venous incompetence in 30% of cases.
Q 17. What are reticular veins?
Reticular veins are small vessels of 1—3 mm in
diameter lying immediately beneath the skin. They
may present as small varices. These tiny varices are
associated with superficial venous incompetence
in about 30% of cases.
Q 18. What are the symptoms of varicose veins?
Symptoms of venous insufficiency
1. Asymptomatic
2. Cosmetic problems
3. Aching
4. Heaviness and cramps
5. Itching—especiallyonstanding(thewhole lower
leg may itch)
6. Venous claudication
7. Ankle swelling - towards the end of the day
8. Pigmentation on the medial aspect of lower leg
9. Eczema
10. Ulcer—on the medial aspect of lower leg (gaiter
area)
Note:
1. Aching, swelling, cramps, heaviness, itching are
absent in the morning and become evident and
aggravates as the day goes by
2. The severity of the symptoms is unrelated to the
size of the veins and is often more severe during
the early stages of the development of varices.
Based on symptoms patients may be classified into
three groups:
Group I
(Cosmetic only)
Group II
(Symptomatic)
Group III
(Complications)
• Venous
telangiectasia
• Thread veins
(0.5 mm)
• Reticular
varices (1–3
mm)
• Visible
varicose
veins
• Ache/
cramps/
tenderness
• Heaviness/
swelling
• Champagne
bottle leg
• Itch/restless
legs/
paresthesia
• Bleeding from
trauma
• Superficial phlebitis
• Ankle venous flare/
edema
• Atrophie blanche
• Venous eczema
•Lipodermatosclerosis
• Venous ulcers
Q 19. What is the cause for ankle edema?
Ankle edema is a feature of persistent venous
obstruction. In some patients veins remain
permanently blocked following a deep vein
thrombosis. This causes symptoms which are worse
than venous valvular incompetence. The passage of
time will allow recanalization and the ankle edema
may become less. The recanalized veins are likely
to be incompetent and the features of venous
hypertension may then predominate.
Q 20. From the location of varicose veins can you
identify the system affected?
1. Varicosities of the medial calf and thigh →
originate from great saphenous vein.
2. Varicosities on the posterior and lateral calf and
popliteal fossa → short saphenous system.
3. Varicosities in the groin and along the anterior
abdominal wall → iliac vein obstruction.
176
Clinical Surgery Pearls
Q 21. What is Klippel-Trenaunay syndrome?
In this condition you get prominent veins along
the lateral aspect of thigh mostly present from very
young age, with dysplastic deep veins. The classical
clinical triad consists of:
a. Hemangiomas
b. Hypertrophy of soft tissue and over growth of
extremity
c. Varicose vein.
Q 22. What is postphlebitic syndrome?
It includes a chronically swollen limb with
hyperpigmentation, lipodermatosclerosis and
nonhealing ulcers with or without varicose veins
around the ankle. One of the common presentations
is a patient with chronic ulcer around the ankle. A
definite history of DVT may not be present in most
of these patients. Almost all of them will have
destroyed deep veins due to the previous DVT.
Q 23. What are the clinical tests to be done in a
patient suspected with varicose veins?
Tests for varicose veins
1. Morrissey’s cough impulse test
2. Brodie-Trendelenburg test—1 and 2
3. Modified Perthes’test
4. Multiple tourniquet test
5. Schwartz’s test—(tap sign)
6. Pratt’s test
7. Fegan’s test
8. Assessment of the short saphenous vein.
Q 24. What is Raju’s test? (PG)
This is a useful test for venous obstruction. With
patient lying supine, pressure is measured in the
veins of hand and foot. Normally the foot pressure is
equalto orslightly higher(by 5 mm ofHg)than the
hand pressure. In venous obstruction this difference
is more (10–15 mm of Hg).
Note: The venous pressure is measured by inserting
a cannula to the dorsal vein of foot and measuring
the pressure by a saline manometer with the help
of a three way.
Q 25. What is Morrissey’s cough impulse test?
In this test the patient is recumbent. The lower limb
is elevated and the veins are emptied. The limb is
elevated to about 30° and then the patient is asked
to cough. If there is saphenofemoral incompetence
expansile impulse is seen and felt at the saphenous
opening. One can also see retrograde filling of the
proximal part of the long saphenous vein.
Q 26. What is Brodie-Trendelenburg test?
The patient lies down on a couch and the limb
is raised to allow the blood to drain out of the
veins. The saphenous vein at the upper 3rd of the
thigh is then compressed with a tourniquet (the
saphenofemoral junction may be occluded with
the thumb). The patient is then asked to stand up.
The varices are observed for 30 seconds. Normally
the venous filling occurs from the periphery slowly
when the patient gets up and takes more than 20
seconds. When the tourniquet is released if the
veins fill rapidly from above, it indicates valvular
incompetence of the saphenofemoral junction. This
is a positive Trendelenburg-1 test.
If the veins fill rapidly from below despite the
applied tourniquet this indicates incompetence of
the perforating veins (here the tourniquet is not
released). This is a positive Trendelenburg-2 test.
Note:Test 1 is done first that is followed by the 2nd
test.
Q 27. How is the assessment for sapheno- popliteal
incompetence done? (short saphenous system).
This can be done in the same manner applying a
tourniquet around the calf below the popliteal fossa.
Varicose Veins
177
The long saphenous vein should simultaneously
be occluded at the upper thigh for accurate
interpretation.
Q 28. What is modified Perthes’ test?
This is a test for assessing the patency of the deep
veins. In this test, with the patient standing, a rubber
tourniquet is applied around the upper 3rd of thigh
tight enough to occlude the long saphenous vein
butnotthedeepveins(note—here the veins arenot
emptiedbefore the test).Nowthepatientis askedto
walk quickly for 5 minutes. If the patient complains
of bursting pain in the lower leg, it is proof that the
deep veins are occluded. The additional evidence
is that the superficial varicosities, if present, will
become more prominent as their exit is blocked
by the tourniquet.
In original Perthes’ test the affected limb is
wrapped with elastic bandage and then allowed
to walk.
Q 29. Is there any alternative test for assessing the
patency of deep veins ?
Apply a tourniquet at the upper third of the calf
with the patient in standing position. The patient is
asked to perform 10 repeated tip toe movements.
The patient will experience bursting pain.
Q 30. How is multiple tourniquet test done and
what is the purpose?
This is done for seeking the sites of perforators.
The patient is in the supine position. Elevate the
affected lower limb and empty the veins. The first
tourniquet is tied at the ankle, second one below
the knee, third one above the knee and the fourth
one below the saphenous opening. The purpose
of fourth tourniquet is to prevent retrograde filling
from above into the long saphenous vein.
Make the patient stand up, and ask the patient
to stand on toes. The resultant pumping action will
throw the blood from the deep system through the
perforators to the superficial. Now the tourniquets
are sequentially released from below upwards.
Look for varicosities at the ankle after releasing the
tourniquet at the ankle. Next release the tourniquet
at the calf below the knee. If the veins are prominent
here perforators in this region are incompetent.
Lastly release the tourniquet above the knee and
look for varicosities.
Q 31. What is Schwartz’s test? (Tap sign)
In standing position a tap is made on the long
saphenous varicose vein with the right middle
finger in the lower part of the leg after placing the
fingers of the left hand just below the saphenous
opening at the groin. A thrill (impulse) will be
felt in the left hand, if it is a varicosity of the long
saphenous system.
Q 32. What is Pratt’s test?
In this test Esmarch bandage is applied to the leg
from below upwards followed by tourniquet below
the saphenofemoral junction. Now the bandage is
released slowly keeping the tourniquet in position
to see the blow outs.
Q 33. What is Fegan’s test?
This is done for seeking the sites of perforators. In
the standing position mark the excessive bulges
within the varicosities. Now the patient lies down.
The affected limb is elevated to empty the varicose
veins, resting the heel against the examiners upper
chest. The examiner palpates along the line of the
marked varicosities carefully to find out gaps or
circular defects with sharp edges in the deep fascia
which transmit the incompetent perforators. They
are marked with an‘X’.
178
Clinical Surgery Pearls
Tests for varicose veins
Sl. No Test for varicose vein Purpose of the test
1. Trendelenburg-1 To identify saphenofemoral incompetence
2. Trendelenburg-2 To identify perforator incompetence
3. Morrissey’s cough impulse test To identify saphenofemoral incompetence
4. Modified Perthes’test For noting the patency of the deep veins and ruling out deep vein
thrombosis—Clinically identified as bursting pain during walking and
increase in the prominence of varicosities
5. Multiple tourniquet test Done to identify the segment of perforator incompetence when
Trendelenburg test 2 is found positive
6. Schwartz’s test Demonstrates incompetent saphenofemoral junction by tapping below
just above the ankle region
7. Pratt’s test To demonstrate “blow outs” at the site of perforators
8. Fegan’s test Demonstrate deep fascial defects at the site of incompetent perforators
Q 34. What is CEAP (American Venous Forum 1994)
classification? (PG)
This acronym CEAP stands for:
• C—Clinical classification
• E—Etiological classification
• A—Anatomic classification
• P—Pathophysiological classification
C—Clinical classification—7 clinical grades have
been identified
Class 0—No visible or palpable sign of venous
disease
Class 1—Telangiectasis or reticular veins
Class 2—Varicose veins
Class 3—Edema
Class 4—Skin changes (pigmentation, eczema or
lipodermatosclerosis)
Class 5—Skin changes defined above with healed
ulceration
Class 6—Skin changes defined above with active
ulceration
E—Etiological classification—3 etiologies
Ec—Congenital
Ep—Primary (undetermined cause)
Es—Secondary (post-thrombotic, post-traumatic,
other causes)
A—Anatomic classification — 18 anatomic segments
have been described in 3 anatomic regions
As—Superficial veins
Ad—Deep veins
Ap—Perforating veins
P—Pathophysiological classification—3 pathologic
mechanisms
Pr—Reflux
Po—Obstruction
Pro—Reflux and obstruction
Q 35. What is gaiter area?
This is an area immediately above the medial
malleolus and less commonly above the lateral
malleolus where the changes of chronic venous
Varicose Veins
179
hypertension (venous stasis) are seen in the
form of lipodermatosclerosis, dermatitis, eczema,
pigmentation and ulceration.
Gaiter is a type of protective clothing for a
person’s ankles and legs below the knees. Gaiter
area is the area of lower extremity over which a
gaiter fits roughly from ankle to the proximal calf.
Q 36. What is champagne bottle leg (inverted beer
bottle appearance)?
The lipodermatosclerosis will present as palpable
induration in the gaiter area. Contraction ofthe skin
and subcutaneous tissue in this region will result in
narrowing of the ankle area. The combination of a
narrow ankle and prominent calf is referred to as
the champagne bottle.
Q 37. What is atrophie blanche?
In this condition the superficial veins are lost from
the skin and white patches develop. This is called
atrophie blanche. This indicate that the skin has
been severely damaged by the venous valvular
incompetence. Venous ulceration may develop in
these areas.
Q 39. What are the investigations for diagnosis?
Investigations for varicose veins
• Duplex ultrasound imaging
• Doppler ultrasound
• Photoplethysmography
• Venography (phlebography)—invasive
• Ambulatory venous pressure studies
• Raju’s test—arm foot venous pressure study
• Ultrasound of the abdomen.
1. Duplex ultrasound imaging—The examination is
performed with the patient in standing position.
The examiner steadily work his way from the
groin to the ankle.
This is the most important noninvasive
investigation for practically all venous disorders.
It produces high quality pictures using a
combination of B mode imaging and Doppler
ultrasound. Anatomical, physiological and
functional details can be obtained. Venous
lumen, flow, direction and reflux of blood can be
visualized. The site of perforator incompetence
can be located with accuracy. It has replaced the
venography. All patients with recurrent varices,
history of previous DVT and patients with skin
changes should be fully investigated by using
duplex ultrasonography or venography.
2. Doppler ultrasound—This investigation is also
done in the standing position. A bidirectional
flow probe will identify venous reflux. The
Doppler probe isfirst placed over the saphenofemoral junction. With one hand the examiner
squeezes the calf to produce an acceleration of
bloodflowinthe veins.Thisisheardas a‘whoosh’
from the speaker of the Doppler machine. The
calf compression is released and look for any
reverse flow in the veins. This procedure is
repeated over the saphenopopliteal junction
and over other areas. The saphenopopliteal
junction is inconstant. it can be identified and
markedwithDoppler.Doppler assessmentisthe
minimum investigation required before treating
a patient with venous disease. The arterial
disease can also be excluded.
• Four characteristics descriptions are patent,
augmented, spontaneous and phasic.
Patent – Flow is heard at the anatomical
level of the vein
– Rarely does the flow completely
disappear with DVT
180
Clinical Surgery Pearls
– D V T i s associated with
continuous, high pitched signal
Augmented – Firm, gentle compression ofthe
limb for a few seconds distal
to the vein should result in
augmentation of the flow
– Proximal compression followed
by release should also result in
augmentation
– Augmentation produced by
proximal compression before
release or distal compression
after release indicates valvular
incompetence
Spontaneous – DVTresultsinlossofspontaneous
flow
– Anything causing vasoconstriction also causes loss of
spontaneity
Phasic – Variation with respiration is
called phasicity
– A Valsalva maneuver should
decrease the signal and a deep
breath should augment the
signal with normal venous
physiology
– This is lost in DVT.
3. Venography (Phlebography)—invasive- not done
now-a-days. For identifying incompetence of
the valves a descending phlebography is done
where the dye is injected into the femoral vein
with the patient standing.
Forrulingoutdeepveinthrombosisanascending
phlebography is done by injecting the dye to the
foot vein after occluding the superficial veins
above the ankle by a tourniquet.
4. Ambulatory venous pressure study—is not done
routinely. It is considered by many to be the gold
standard venous function test (the significance
of the pressure is described earlier).
5. Raju’s test—arm foot venous pressure study—
(described earlier).
Ultrasound of the abdomen—to rule out abdominal
pathology in suspected cases of secondary varicose
veins.
Q 39. What are goals of treatment?
• Alleviation of pain
• Reduction of edema
• Healing of ulcers if present
• Prevention of recurrence.
Compression remains the cornerstone of treatment.
Q 40. What is the contraindication for surgery?
Deep venous thrombosis. Superficial varices
developing after a venous thrombosis may be the
only route of venous drainage in the lower limb
and should not be removed until the patency of the
deep veins of the limb has been shown.
Q 41. What are the treatment options available?
(Flow chart 13.1).
Treatment options for varicose veins
• Reassurance
• Elastic compression stockings
• Injection sclerotherapy—foamsclerotherapy, echosclerotherapy and microsclerotherapy
• Surgical treatment
• Laser therapy.
Q 43. What are the indications for treatment?
Better results are obtained with early treatment
before continuous reflux:
• Varicose veins that cause discomfort
Varicose Veins
181
• Cosmetic embarrassment
• Complications like venous ulcers.
Q 43. What is the role of compression stockings?
The symptoms of varicose veins may be relieved
by the use of compression stockings. Which are
available in 3 grades—Class 1, 2 and 3.
Q 44. What are the agents used for injection
sclerotherapy?
• STD—Sodium Tetradecyl Sulphate (3%)
• Polidocanol
• Ethanolamine oleate.
Q 45. What is the indication for sclerotherapy?
1. This is used to treat varicose veins in the
absence of junctional incompetence and
major perforating veins.
2. Used for smaller veins < 3 mm in size.
Q 46. What is the technique of injection sclerotherapy?
The sclerosant is injected into an empty vein and the
vein is compressed. The endothelial lining is destroyed.
If the vein is not compressed it will produce thrombosis
which will later get recanalized producing recurrence.
Flow chart 13.1: Management of varicose veins
182
Clinical Surgery Pearls
Q 47. What is foam sclerotherapy (by Tessari)?
In thistechnique the STD is drawn into one syringe
and air is taken in another syringe. Using a three
way, rapid too and fro movements of the piston
of the syringe, the foam is produced. This foam is
then injected into the long saphenous vein after
cannulation. The air is absorbed, the vein collapses
and the endothelial lining is destroyed. A much
larger volume can be injected into the vein with
a small quantity of sclerosant so that it will fill the
superficial varicosities. The patient is lying supine
with the leg elevated instead.
Q 48. What is echosclerotherapy? (PG)
When the procedure of foam sclerotherapy is done
under the guidance of duplex ultrasound imaging
it is called echosclerotherapy.
Q 49. What is the advantage of sclerotherapy?
The patients can undergo repeated treatment
sessions to ensure that all veins are removed.
Q 50. What are the complications of sclerotherapy?
Complications of sclerotherapy
• Skin pigmentation
• Injury to the skin and ulceration
• Allergic reaction
• Thrombophlebitis
• Deep vein thrombosis.
Q 51. What is microsclerotherapy? (PG)
The thread veins and reticular varices are injected by
inserting a 30 G needle. The solutions used are STD
and polidocanol. After the injection compression
bandage is given for a period of 1–5 days.
Q 52. What is the surgical treatment of saphenofemoral incompetence?
Trendelenburg’s operation and stripping ofthe long
saphenous vein.
Q 53. What is the contraindication for Trendelenburg’s operation?
Whendeep vein thrombosis is destroying the main
axial limb vein and the patient will depend on the
superficial veins for venous drainage.
Q 54. What is Trendelenburg’s operation?
An oblique incision is made in the groin and the
long saphenous vein is exposed. The procedure has
got two portions:
a. Saphenofemoral flush ligation
b. Ligation of the proximal five tributaries:
1. The superficial external pudendal vein
2. The superficial inferior epigastric vein
3. The superficial circumflex iliac vein
4. The posteromedial vein (medial accessory
saphenous vein)
5. Theanterolateral(lateralaccessorysaphenous
vein).
Note: It is important that the femoral vein is
inspected carefully at least 1cm above and below
the saphenofemoral junction(SFJ) andalltributaries
in this situation ligated and divided.
Q 55. Why it should be combined with stripping
of the long saphenous vein?
The main principle of the surgical treatment
is to ligate the source of venous reflux and to
remove the incompetent saphenous trunk. The
Trendelenburg procedure alone is associated with
high rate of recurrence. To ensure elimination of as
much reflux as possible it is necessary to remove
the long saphenous vein. Similarly in case of
saphenopopliteal incompetence the part of the
short saphenous vein must be removed.
Q 56. What type of stripping is recommended for
saphenous vein?
To avoid injury to the saphenous nerve the long
saphenous vein should not be removed below the
Varicose Veins
183
midcalf level. The conventional way of removing
the longsaphenous veiniswitha stripper(Babcock).
Here the stripper wire is passed down the long
saphenous vein. The end is identified in the upper
calf and a 2 mm incision is made to retrieve the
stripper. An olive of about 8 mm diameter is
attached to the upper end and the saphenous vein
is removed by firm traction on the wire in the calf.
Q 57. What is invaginating stripping (inverting)?
(PG)
The aim of this type of stripping is to reduce the
damage to the tissues around the vein. There will
be less pain and less bleeding in this operation. A
rigid metal pin stripper(Oesch) hasbeen developed
and this is passed down the inside of the saphenous
veinwhichisrecoveredfromtheupper calf.Astrong
suture is attached to the stripper and firmly ligated
to the proximal end of the vein. During pulling of
the stripper the long saphenous vein will invert and
can be delivered through a 2 mm incision in the
midcalf region. Here no olive is used.
Q 58. What are the nerves at risk during venous
surgery?
1. Saphenous nerve—this is likely to be injured
during stripping of the long saphenous vein
2. Sural nerve—this is likely to be injured during
stripping of the short saphenous vein.
Q 59. What is the peculiarity of the saphenopopliteal junction?
The saphenopopliteal junction is not constant. The
termination may lie from 2 cm below the knee to
15 cmabove the knee. Itis very importanttoidentify
the termination sonologically and mark it on the
skin before surgery.
Q 60. What is hook phlebectomy? (PG)
After stripping, the residual veins and tributaries
are left behind. These veins conventionally used
to be managed by incisions long enough to insert
artery forceps for ligating the veins. Now these
veins can be tackled by means of small hooks that
may be inserted through incisions of 1–2 mm size.
The closure of these small incisions is achieved
using adhesive strips. This gives excellent cosmetic
outcome.
Q 61. What is the postoperative management?
1. Compression bandaging is applied to the limb
at the end of the operation to prevent bruising.
2. Some surgeons apply compression to the limb
before stripping.
3. After two days the bandage may be replaced
with thigh length high compression stockings
(class 2).
Q 62. What is VNUS closure? (PG)
This is intraluminal destruction of the long and
short saphenous vein using ablation catheter under
ultrasound guidance.
Q 63. What are the complications of varicose vein
surgery? (PG)
Complications of varicose vein surgery
1. Pain, discomfort and bruising
2. Nerve injury—saphenous for long saphenous
surgery—Sural for short saphenous surgery
3. Venous thrombosis in residual varices
4. Deep vein thrombosis—1/1000 operations (give
prophylactic heparin when there is history of
previous DVT).
Q 64. What are the complications of varicose
veins?
Complications of varicose veins
• Hemorrhage
• Superficial thrombophlebitis
Contd...
184
Clinical Surgery Pearls
• Eczema
• Pigmentation
• Lipodermatosclerosis
• Deep vein thrombosis (rarely)
• Venous ulcer
• Marjolin’s ulcer
• Calcification
• Periostitis
• Talipes equinus.
Q 65. What are the causes for superficial
thrombophlebitis ?
Causes for superficial thrombophlebitis
• TAO (Buerger’s disease)
• Occult carcinoma (visceral malignancy)
• Varicose veins
• Polycythemia
• Iatrogenic—IV Injection.
Q 66. What is the classical location for venous
ulcer?
Just proximal to the medial and lateral malleolus
(gaiter area).
Q 67. What are the differences between venous
ulcer and varicose ulcer?
When the ulcer is secondary to deep venous
pathology or perforator incompetence producing
chronic venous hypertension, it is called venous
ulcer. When the ulcer is due to superficial
insufficiency alone, it is called varicose ulcer. It is
better to use the term venous ulcer because the
ulcer is not caused by the varicose veins but by the
disordered pattern of the venous blood flow.
Differences between varicose ulcer and venous ulcer
Varicose ulcer (40–50%) Venous ulcer
Due to pure superficial
venous insufficiency
(long standing SFJ
incompetence)
Due to incompetence of
the perforators and deep
venous incompetence. It
may be post-thrombotic
venous damage
History of long standing
superficial varicosity
History suggestive of
deep vein thrombosis
followed by lower limb
edema
Ankle edema may not be
there
Ankle edema, calf muscle
increase and narrow
ankle suggestive of deep
vein problem
Painless Painful
Does not penetrate deep
fascia
Penetrate deep fascia
Respond to surgical
treatment of the
superficial varicosity
Does not respond to
treatment
Q. 68. What are the most important causes for
leg ulceration?
Causes of leg ulcers
• Peripheral arterial disease
• Venous disease of the lower limb
• Diabetes
• Neuropathy
• Infective ulcers
• Traumatic ulcers
• Malignant ulcers
• Rheumatoid disease
• Autoimmune disease—systemic sclerosis, SLE.
Contd...
Varicose Veins
185
Q 69. What are the characteristic features of
venous ulcer?
Features of venous ulcer
1. Seen at the gaiter area (usually on the medial
side)—lower 3rd of the leg (never found above the
junction of middle and upper third of leg)
2. The surrounding tissues show signs of chronic
venous hypertension—pigmentation, eczema and
lipodermatosclerosis
3. Presence of obvious varicose veins (may not be
visible sometimes)
4. The ulcer can take any shape
5. The edge will be sloping
6. The floor will be covered with granulation tissue/
slough/white fibrous tissue
7. The tendons and bone may be sometimes exposed
8. The base of the ulcer is fixed to the deeper tissues
9. The movements of the ankle joint may be limited
by the scarring of the ulcer—equinus deformity.
Q 70. What are the investigations in venous ulcer?
1. Examine the peripheral pulses to rule out arterial
problem
2. Examine the sensation to rule out neuropathy
3. Doppler ankle blood pressure
4. Duplex ultrasonography ofthe veins andarteries
5. Blood examination to rule out SLE, rheumatoid
disease
6. Biopsy of the ulcer.
Q 71. What is the management of venous leg
ulcers?
This consists of :
1. Management of the ulcer
2. Surgery forthe superficial venousincompetence
3. In patients with deep venous insufficiency
surgery may not be effective.
Q 72. Is it necessary to delay surgery until the ulcer
has healed? (PG)
It is not necessary and surgery may be carried out
before the ulcer has healed. It is found that the ulcer
healing is rapid in this situation.
Q 73. What is the management of ulcer?
The standard old regimen is called Bisgaard regime
consisting of:
• Elevation of the limb
• Elastocrepe bandage (compression stocking)
• Exercise
• Education.
Note:Docultureandsensitivity andgiveappropriate
antibiotics.
Biopsy of the ulcer if nonhealing
Blood examination—Blood sugar
ESR
Rheumatoid factor, etc.
Q 74. What is Marjolin’s ulcer?
Malignant change may occur in long standing
venous ulcers. This should be suspected, when
there is evidence of raised or rolled out edge. They
are nothing but squamous cell carcinoma.
Q 75. Is there any role for topical applications and
topical antibiotics?
• No
• Topical applications will not speed up healing
• It will produce allergy and skin sensitization
• Topical antibiotics are ineffective
• If eczematousreaction isthere around the ulcer,
topical steroid may be useful.
Q 76. What is the role of compression?
• A pressure of 30–45 mm of Hg applied to the
ulcer is found to be effective for healing of the
ulcer.
186
Clinical Surgery Pearls
• Class III stockings exert about 30 mms of Hg
compression
• The compression is applied to the ulcer region
alone (below knee stockings)
• Those who cannot use compression stockings
use multilayer bandaging regimes (4 layer
bandage developed by Charing Cross Hospital,
London).This bandage is changed once ortwice
weekly.
Q 77. What is the principle of compression?
The exact mechanism by which compression is of
benefit is not known but the following physiological
alterations occur.
1. Relieves the leg edema
2. Controls the chronic venous insufficiency
3. Reduction in ambulatory venous pressure
4. Improvement in skin microcirculation
5. Increase in subcutaneous pressure preventing
transcapillary fluid leakage.
Q 78. What is the drug treatment for venous ulcer?
Drugs are inferior to compression bandaging. The
following drugs are used:
• Aspirin • Pentoxifylline
• Prostaglandin E • Calcium
Analog Dobesilate
• Diosmin • Flavonoids
Q 79. What is the role of systemic antibiotics in
venous ulcer?
• Antibiotics have no effect on ulcer healing
• Evidence of infection in the form of cellulitis and
fever, are indications for antibiotics.
Q 80. What is the treatment of deep venous
insufficiency? (PG)
The surgical treatment is difficult and being done
only in a few centers. The surgical options are:
a. Direct vein valve repair by valvuloplasty (Kistner)
b. Vein valve transposition
c. Transplantation of a segment of axillary vein.
Q 81. What is the indication for deep venous
surgery? (PG)
Those who have persisting swelling of the lower
limb after a previous venous thrombosis.
Q 82. What is the surgical treatment for deep
venous obstruction? (PG)
1. Palma operation: This involves mobilizing
the long saphenous vein in the opposite leg,
tunnelling the distal end of the LSV across
suprapubically and inserting it into the femoral
vein of the affected side below the obstruction.
2. May-Husni procedure: This is done for the
obstruction of the superficial femoral vein.
The long saphenous vein is connected to the
popliteal vein in the same limb allowing blood
to flow along the superficial vein.
Q 83. What is the treatment of perforator
incompetence?
1. Subfascial endoscopic perforatorsurgery (SEPS)
2. Foam sclerotherapy
3. Open subfascial ligation—Linton flap andDodd
and cocket procedure
4. Multiple perforator ligation.
Q 84. What are the new alternatives of treatment?
1. Radiofrequency ablation—a catheter is passed
up the saphenous vein from the lower leg and
withdrawn under ultrasound guidance while
radio frequency waves are used to destroy the
endothelial lining through a series of metal
prongs.
2. Endovenous laser ablation (EVLA)—A laser
probe is passed up inside a catheter inserted
into the lower part of the saphenous vein
Varicose Veins
187
under sono-guidance. Large amounts of
crystalloid fluid containing local anesthesia
are placed around the vein to separate the
skin from the laser probe to avoid cutaneous
burns. The laser probe is kept just below the
saphenofemoral junction and a set number of
joules are given to the endothelial lining. Flush
occlusion is not possible with radio-frequency
ablation and laser.
Poem on Varicose Veins
“Varicose vein disease is sometimes diagnosed
with ease,
But of the best attempts will meet with sad and
sorrowful defeat
So let us give you good advice
Examine once, Examine twice:
Examine from head to toes,
Before you dare to diagnose
More harm is done because you do not look
Than from not knowing what is in the book
Above all do not try to spot
Because you think you know a lot
Spot diagnosis you should hate
Until you are a surgeon great!
By then of course you will have learnt
Some lessons bitter and you daren’t”
14 Peripheral Occlusive
Vascular Disease
Case
Case Capsule
A 60-year-old male patient presents with left
calf muscle, thigh muscle and gluteal pain of 18
months duration. He gets a cramp-like pain only
while he walks and the pain disappears when he
stops walking. At the beginning of the walk he
gets numbness, pins and needles and paresthesia
in the skin of the foot. Initially the claudication
distance was about 200 meters. The walking
distance gradually shortened over a few months.
There is no history of chest pain, fainting, blurred
vision or weakness or paresthesia of the upper
limbs. For the last 3 weeks he gets continuous
severe pain aching in nature which is present at
rest throughout the day and night, mostly in the
foot and leg. After a few days he noticed black color
of the left big toe and ulcer in the left heel region.
The maximum pain he gets is at the junction of
black area of the big toe and the remaining normal
foot. He prefers to sleep sitting in a chair, if at all in
the bed, he hangs his leg over the side of the bed.
The patient is requesting for amputation of the leg.
On examination, the patient is found to be
hypertensive. The patient sits with the left knee
bent, holding the left foot still. He is unwilling
to lie flat. When the limb is kept horizontal the
foot is pale. The capillary filling is retarded. The
pulps of the toes show wasting. The veins of the
limb are empty and guttered. The entire left big
toe is gangrenous. A line of demarcation is seen
between the gangrenous area and the normal foot.
There is an ulcer of 4 × 3 cm size situated in the
left heel region. The floor of the ulcer is covered
with slough and the edge is punched out. The
surrounding area of the ulcer is very tender. The
skin temperature from midcalf downwards is cold.
The femoral, popliteal, dorsalis pedis and posterior
tibial pulses are absent on the left side. On the
right side all the pulses are present except dorsalis
pedis and posterior tibial. There is wasting of left
leg muscles. There is an audible bruit over the
right femoral artery. Cardiovascular system and
neurological examination are normal.
Checklist for history
• Character of the pain, severity aggravating and
relieving factors
• Claudication distance
• History of sudden onset or gradual onset
• History of smoking
• History of diabetes mellitus
• History of cardiac illness
Contd...
Peripheral Occlusive Vascular Disease
189
• History of cerebrovascular accidents/TIA
• History of dyslipidemias
• History of superficial phlebitis
• History of fainting, blurred vision, abdominal pain
• History of impotence
• Family history of atherosclerosis.
Checklist for examination
• Always examine theheartbecause vasculardiseases
are part of the cardiovascular system
• Listen for aortic, renal, celiac and iliac bruits
• Look forsigns of congestive cardiac failure—raised
JVP, edema, basal creps, pleural effusion, ascites
• Take blood pressure in both arms
• Look for palpable thrill over the vessels
• Examine all peripheral pulsesincluding both lower
limbs and upper limbs, common carotid arteries
and their bifurcation, facial and superficial temporal
vessels
• Assessthe mentalstatus and speech abnormalities
• Look for visual defects
• Examine for evidence of motor and sensory
disorders—(hemiplegia of the contralateral leg,
arm and face)
• Look for speech problems—aphasia
• Ipsilateral temporary visual loss (Atheromatous
fragments in retinal vessels)
• Look for nutritional changes (trophic changes)
of the toes, foot, fingertips and hands—thin and
atrophic skin, loss of pulp, brittle and deformed
nails, with loss of hair, wasting of muscles. Painful
cracks appear across the heel
Contd...
• Look for ulceration in the pressure points and bony
prominences—the heel, malleoli, tips of toes, 5th
metatarsal head region, and ball of the foot.
Contd...
Contd...
190
Clinical Surgery Pearls
Q 1. What is the most probable diagnosis in this
case?
• Peripheral occlusive arterial disease
• Probably atherosclerotic obstruction
• Level of obstruction being aortoiliac
• With gangrene of the left big toe
• Ischemic ulcer of left heel.
In all cases of peripheral occlusive vascular disease
ask the following questions
• Find outthe level of occlusion clinically and include
it in the diagnosis?
• Look for bruitin all arterial diseases overthe vessels
even if they are palpable—carotids, subclavian,
aorta, renal, celiac axis, and femoral
• Find out the nature of obstruction? Thrombosis/
embolism
• D ecid e whether patient needs invasive
investigations?
• Invasive investigations are done only if patient is
suitable for surgery?
• Assess the comorbid conditions?
Q 2. What are diagnostic points in favor of your
diagnosis?
• Intermittent claudication
• Ischemic rest pain
• Absent popliteal, dorsalis pedis and posterior
tibial pulsations with audible bruit over the left
femoral
• Ischemic ulcer (nonhealing heel ulcer)
• Pallor of foot on elevation and pink color on
dependency
• Gangrene of left big toe
• Low ankle brachial index.
Q 3. Why this is a case of atherosclerosis rather
than TAO (Buerger’s)?
The difference between atherosclerosis and
Buerger’s disease are given below: In the given
circumstances the diagnosis is atherosclerosis.
Differences between ASO and Buerger’s disease
Feature Atherosclerosis Buerger’s
Age of onset Above 40 years 20–40 years
Sex Male > female Rare in women
Smoking Can occur without smoking
Seen only in
smokers
Progression of
disease
Proximal to
distal
Distal to
proximal
Venous
involvement
Not seen Common
Thrombophlebitis Not seen Common
Inflammatory
reaction
Not seen Common
Layer of vessel
affected
Affects the
intima
Affects all
layers—panarteritis, periarteritis, and
panphlebitis
Contd...
Peripheral Occlusive Vascular Disease
191
Site of lesion Large and
medium sized
arteries (aorta,
iliac, femoral
and popliteal)
Small arteries
Arteriography Proximal lesion Distal lesion
Collateral in
arteriography
Extensive
collaterals
(tree root
appearance)
Poor
collaterals
(cork screw
appearance)
Distal run off in
arteriogram
Usually present Usually absent
Bypass surgery Possible Not possible
Note: Atherosclerotic obstructionn (ASO)
Q 4. What is claudication?
Claudication meanslimping (Claudio = I limp). The
term is now used to describe the cramp-like muscle
pain which appears following exercise as a result of
inadequate arterial blood flow. The three criteria
for claudication are:
1. It is a cramp-like muscle pain (usually calf)
2. Pain develops only when the muscle is
exercised—(not present on taking the firststep
in contrast to osteoarthritis)
3. The pain disappears when the exercise stops
(contrast lumbar intervertebral disk nerve
compression).
Q 5. What are the types of claudication?
There are three types of claudication
1. Arterial claudication
2. Venous claudication
3. Neurogenic claudication.
Q 6. What is the cause for paresthesia in the skin
of the foot?
The patient notices numbness, pins and needles
and other paresthesia in the skin of the foot at
the when muscle pain begins. This is as a result
of shunting of blood from the skin to the muscle.
Q 7. What is the cause for claudication pain?
The cause of the pain can be explained as a response
to the accumulation of acidic, anaerobic metabolite
(P - substance) due to inadequate blood and oxygen
supplies to meet the requirements of the increased
activity. On stopping the activity the blood supply is
replenished, the anoxia is abolished and the painful
metabolites are washed away.
Q 8. What is claudication distance?
The distance a patient can walk on normal ground and
at a normal speed without pain and having to stop.
Q 9. What are the sites of claudication pain?
Depending on the level of occlusion, the site of
claudication pain will differ. The following chart shows
the claudication sites for each level of occlusion.
Levels of occlusion with clinical features
Level of occlusion Site of claudication and
other clinical findings
1. Absent ankle pulses Claudication of calf and foot
2. Femoropopliteal obstruction (femoral pulse
present and popliteal
pulse absent)
Unilateral claudication in
calf
3. Iliac vessel obstruction
(the femoral and distal
pulses absent)
Unilateral claudication in
thigh and calf and some
times buttock. Bruit over
iliac or femoral vessel
4. Aortoiliac obstruction
(a l l p u l s a t i o n s f ro m
femoral down absent on
both sides)
Bilateral claudication of
both buttocks, thighs
and calves. Presence of
bruit over both femoral
Impotence-common
Contd...
192
Clinical Surgery Pearls
Q. 10. What is Leriche’s syndrome?
It occurs in men as a result of aortoiliac disease and
consists of:
• Claudication of the hip, thigh and buttock
muscles (Gluteal claudication)
• Atrophy of the leg muscles
• Sexual impotence
• Diminished/absent femoral pulses
• Tran sien t numbness of the extremity
accompanies the pain and fatigue of claudication.
Q 11. What is the cause for impotence in Leriche’s
syndrome?
It is due to the lack of blood supply to the penis. The
penis is getting blood supply through the internal
iliac vessels which is occluded in this conditions.
Q 12. What is rest pain? What is the site of rest pain?
• It is the continuous pain caused by severe
ischemia. This pain is present at rest throughout the day and night. The pain is relieved by
putting the leg below the level of the heart
(the patient hangs his legs over the side of the
bed and prefers to sleep sitting in a chair. In the
bed he often sits with the knee bent holding the
foot still to try and relieve the pain).
• Therestpainusuallyoccursinthemost distal part
of the limb. The toes and the fore foot. If there is
associated gangrene the patient feels the pain at
the junction of the living and dead tissue.
Q 13. What is Boyd’s grading of claudication?
Boyd’s grading of claudication
Grade I Patient experiences pain after walking
some distance. Pain disappears and patient
continues to walk
Grade II Pain persists and still the patient continues
to walk
Grade III Pain compels the patient to take rest.
Q 14. What is Fontaine classification for the
severity of chronic ischemia?
Fontaine classification of limb ischemia
Stage I Asymptomatic
Stage II Intermittent claudication limiting lifestyle
• IIa—Well compensated (> 200 meters)
more than 1 block
• IIb—Poorly compensated < 200 meters
Stage III Rest pain due to ischemia
Stage IV Ulceration or gangrene due to ischemia.
Q 15. What is ischemic ulcer? What are the features
of ischemic ulcer?
Ischemic ulcer is an ulcer caused by
inadequate blood supply
The features of ischemic ulcers
• They are usually found at the tips of toes/fingers
and over the pressure areas
• The ulcer and surrounding tissues are very tender
• The surrounding tissues are very cold
• The edge of ischemic ulceris punched out(because
there is no attempt at healing)
• Skinattheedgeoftheulcerisusuallybluegreyincolor
• The floor may contain slough
• Ischemic ulcers are very deep and penetrate down
to the bone and joints
• Thebaseofulcermaybebone, ligamentsortendons.
Q 16. What are the causes for ischemic ulcerations?
Causes for ischemic ulcers
• Large artery occlusion—Atherosclerosis
– Embolism
• Small artery occlusion
– Buerger’s disease
– Diabetes
– Embolism
Contd...
Peripheral Occlusive Vascular Disease
193
– Trauma
– Scleroderma
– Raynaud’s disease
– Physical agents—radiation, electric burns
• Systemic diseases affecting the vessels.
Q 17. How will you assess the skin temperature?
The skin temperature can be assessed reliably only
when both limbs are exposed to the same ambient
temperature for a full five minutes.Do not examine
immediately after pulling back the sheets. The
temperature assessment is done by back of the
fingers of the clinician because the palmar surface
of the hand is usually warm and moist and is not a
good temperature sensor as the cool dry back of
the fingers.
Q 18. What are the clinical tests to be carried out?
Clinical tests in a vascular case
• Assess the skin temperature of the affected limb
• Buerger’s vascular angle
• Capillary filling time
• Venous filling
• Capillary refilling
• Feel the peripheral pulsations
• Crossed leg test of Fuchsig
• Reactive hyperemia test
Test for upper limb
• Adson’s test
• Allen’s test
• Elevated arm stress test.
Note:
• Auscultate for bruit in all cases
• Measure blood pressure in all cases.
Q 19. What is Buerger’s vascular angle?
It is the angle to which the leg must be raised before
it becomes white (pallor). In a normal person the
straightened limb can be raised by 90° and the
toes and foot will remain pink. In an ischemic leg
elevation to 15–30° may cause pallor. The angle is
directly proportional to the pressure in the small
vessels of the foot. The height in cm, between the
sternum and heel at the elevation when it becomes
pale is equal to the pressure in the foot vessel in
mm of Hg. A vascular angle < 20° indicates severe
ischemia.
Q 20. What is capillary filling time?
After determining the vascular angle by elevating
the limb, ask the patient to sit up and hang his legs
down over the side of the couch. A normal leg will
remain pink in color. The ischemic leg will slowly
turn from white to pink which is caused by the blood
filling the dilated skin capillaries. The time taken for
the foot to become pink is the capillary filling time.
More than 20–30 seconds indicates severe ischemia.
Q 21. What is venous filling?
The limb should be elevated for 30 seconds and
then laid flat on the bed. The veins collapse when
the legs are raised above the level of the heart.
But if the circulation is normal they do not empty
completely. Normal venous filling occurs within
5 seconds. When there is ischemia, the veins
collapse and become guttered at 10–15° elevation.
Normally at room temperature, the veins are
relaxed and full of blood when the patient is lying
horizontal. In ischemia the veins will be collapsed
and some times look like blue gutters.
Q 22. What is capillary refilling?
Press the tip of nail or the pulp of a toe or a finger
for 2 seconds. Then observe the time taken for
Contd...
194
Clinical Surgery Pearls
the blanched area to turn pink after releasing the
pressure. This gives a crude indication of the rate of
blood flow in the capillaries.
Q 23. What are the peripheral pulsations to be
examined?
The arteries are palpated against a bone (where
it is crossing the bone). Diminution of a pulse can
be appreciated by comparing it with the pulse in
the other limb. The following arterial pulsations
are looked for against the areas mentioned below.
Pulsations Area to be examined
Dorsalis pedis
artery
Proximal intermetatarsal space on the dorsum of the foot, lateral to the tendon of extensor hallucis longus
The pulse is felt against the navicular bone and base of 1st metatarsal. Absent in 10% of populations
Posterior tibial
artery
Pulsation is felt against the medial aspect of the calcaneum, or against the back of the medial
malleolus
Peroneal artery 1cm medial to the lateral malleolus
Anterior tibial
artery
Midway between the malleoli against the lower end of the tibia just above the level of ankle at
the head of the talus
Popliteal
artery
(an easily
palpable
popliteal
artery may be
aneurysm)
Three methods:
1. Flex the knee to 135° with the heel resting on the couch. The thumb of the examiner is on the
tibial tuberosity and the fingers over the lower part of the popliteal fossa. Press the neurovascular
bundle against the posteriorsurface of the tibia (in the upper part of popliteal fossa it is difficult
to palpate the artery because it is deep between the condyles of the femur)
2. The most reliable method is perhaps the most inconvenient. Here the patient is examined in
the prone position. Flex the knee to relax the popliteal fossa and feel the artery with fingertips
of both hands in the lower part of the fossa over the posterior surface of the upper end of tibia
(medial tibial condyle)
3. With the leg straight, place one hand of the examiner around the knee with the fingertips on
the midline of popliteal fossa and hyperextend the knee against this hand and the couch with
the other hand
Femoral
artery
At the groin mid way between the symphysis pubis and the anterior superior iliac spine against
the neck of femur
Radial artery Is felt at the wrist in front of the lower end of the radius laterally, lateral to the flexor carpi radialis tendon
Ulnar artery Is felt at the wrist against the lower end of the front of ulna, lateral to the flexor carpi ulnaris tendon
Brachial artery Is felt against the lower part of humerus, medial to the biceps brachii tendon
Axillary artery Felt in the apex of the axilla against the neck of the humerus
Subclavian
artery
Felt against the first rib in the middle of supraclavicular fossa
Common carotid artery
Felt medial to the sternomastoid muscle at the level of the thyroid cartilage against the carotid
tubercle (Chassaigne tubercle) of the 6th cervical vertebra
Facial artery Felt against the body of the mandible where the masseter is attached
Superficial temporal artery
Felt in front of the tragus of the ear against the temporal bone.
Peripheral Occlusive Vascular Disease
195
Q 24. What is disappearing pulse?
In arterial occlusion with well-developed collateral
circulations, the distal pulses will be normal to
palpation. The patient is exercised to the point of
claudication, which may unmask the effect of an
arterial obstruction by disappearance of the pulse.
The pulse will reappear after a minute or two after
rest. The exercise produces vasodilatation below the
obstructing lesion and the arterial inflow cannot
keep pace with the increasing vascular space and
the pulse disappears.
Q 25. What is crossed leg test of Fuchsig?
This test is done for the assessment of the patency
of the popliteal artery. The patient sits with legs
crossed in a chair. Oscillatory movements of the
foot occur synchronously with the pulsation of the
popliteal artery, if the artery is patent. Attention of
the patient is distracted from the legs.
Q 26. What is Adson’s test (for cervical rib/scalenus
anticus syndrome)?
The patient will be sitting in a chair and the radial
pulse of the patient is felt. Patient is asked to turn
the face to the same side where the pulse is being
felt. Now ask the patient to take a deep breath to
narrow the cervicoaxillary channel. If the radial
pulse disappears or becomes feeble it is suggestive
of a cervical rib or a scalenus anticus syndrome.
The purpose of taking deep breath is for allowing
the rib cage to move upwards so that it will narrow
the cervicoaxillary channel. The purpose of turning
the face to the same side is to contract the scalenus
anterior muscle.
Q 27. What is Allen’s test (to look for completeness
of the palmar arch formed by radial and ulnar
artery)?
This test is done for assessing the patency of radial
and ulnar arteries and digital arteries. The patient
is asked to clench his fist tightly and then the
clinician will compress the radial and ulnar arteries
at the wrist. The patient opens and closes the fist
several times for venous return. After 1 minute ask
the patient to open his fist. The palm will be white.
Now release the compression on the radial artery
and watch the blood flow to the hand. Normally
the hand will become pink immediately, whereas
if there is obstruction to the artery or one of the
digital arteries the concerned area will remain pale.
Slow flow into one finger caused by digital artery
occlusion will be apparent from the rate at which
that finger turns pink. Now repeat the procedure
by releasing the pressure on the ulnar artery first.
Q 28. What is elevated arm stress test (for thoracic
outlet syndrome)?
This is a test for thoracic outlet syndrome. In this
test the patient is asked to keep both arms in
abducted position at 90°. The patient is then asked
to make fist and release it repeatedly on both sides
for 5 minutes. The patient will continue to do the
manoeuvre in the normal side. On the effected side
patient will get pain and paresthesia with difficulty
to continue the manuever.
Q 29. What is reactive hyperemia test?
This gives an indication of severity of the arterial
ischemia. Inflate sphygmomanometer cuff around
the limb to 250 mm ofHg forfive minutes and then
measure the interval between releasing the cuff and
appearance of red flush in the skin. In the normal
limb it appears within 1–2 seconds. In a severely
ischemic leg it may never appear.
Q 30. What is bruit?
It is the sound produced by the turbulent blood
flow through a stenotic arterial segment which is
transmitted distally along the course of artery.
When a bruit is heard over the peripheral vessel,
196
Clinical Surgery Pearls
stenosis is present at or proximal to that level. It
is heard loudest during systole and with greater
stenosis it may extend into the diastole. The pitch of
the bruit rises as the stenosis become more marked.
When the vessel become completely occluded, the
bruit may disappear. Absence of bruit does not
indicate absence of occlusion. You need a bell on
your stethoscope to listen along the line of an artery.
Do not press too hard over a superficial artery.
Q 31. What are the common sites to listen for
bruits?
Common sites to listen for bruit
Name of artery Where to look for
Subclavian artery Supraclavicular fossa
Carotid Behind the angle of mandible
Renal artery Posteriorly below the 12th rib
Celiac axis Epigastrium
Femoral artery In the groin—half way between
the anterior superior iliac spine
and the symphysis pubis and
over the adductor canal (a hand’s
breadth above the knee).
Note: The systolic bruits are conducted distally. A
bruit at the level of angle of mandible without any
supraclavicular bruit means a carotid artery stenosis.
When a bruit is heard over supra clavicular fossa and
angle of mandible, the origin may be more proximal
i.e. aortic valve, aortic arch, brachiocephalic or
subclavian arteries.
Q 32. What are the investigations for diagnosis?
1. Doppler ultrasound
2. Ankle brachial pressure index (ABPI) -
(Cornerstone of diagnosis)
3. Duplex imaging
4. Arteriography—if intervention is planned
5. DSA (if required)
6. Magnetic resonance angiogram (MRA)
7. Plethysmography
8. Photoplethysmography Not routinely done
9. Transcutaneous oximetry.
Q 33. What is Doppler ultrasound?
The Doppler signal indicates moving blood. It
does not indicate that the blood flow detected is
sufficient to prevent limb loss. A continuous wave
of ultrasound signal is transmitted from the probe
at an artery. The reflected beam is picked up by a
receiver within the probe itself in a case of hand held
Doppler. The Doppler ultrasound equipment can
be used as a sensitive stethoscope in conjunction
with sphygmomanometer to assess the systolic
pressure in small vessels. This is possible even at
sites where the arterial pulse can not be palpated. It
can be used to assess the difference in arterial blood
pressure between segments of the limb and hence
can identify the site of stenosis. In the leg the cuff
is commonly placed above the ankle, mid calf, and
mid thigh to provide segmental pressure.
Note: Christian Johann Doppler enunciated
Doppler principle in 1842.
Q 34. What is ankle brachial pressure index (ABPI)?
The ABPI is a quick screening test and is the cornerstone
of diagnosis in arterial occlusion. A blood pressure cuff
is applied above the ankle and the systolic pressure
is determined using a Doppler probe at the dorsalis
pedis or posterior tibial artery region. Similarly systolic
pressure is recorded in the brachial artery using
Doppler probe. The higher systolic BP at the ankle
is divided by the brachial pressure to give the ABPI.
Normally it is more than 1 or about 1 (100%). Vascular
disease is confirmed if it is less than 0.9. The test may
be repeated after exercise. Normally ABPI will rise after
exercise. In occlusive arterial disease it will fall.
Peripheral Occlusive Vascular Disease
197
Q 35. What is the relationship between ABPI and
vascular symptoms?
ABPI Symptoms
> 0.9 None
0.5 to 0.8 Claudication
0.3 to 0.5 Rest pain
< 0.3 Gangrene
Q 36. What is the fallacy of ABPI?
In elderly patients or diabetics the tibial artery may
be calcified. An elevated pressure is recorded even
though the intraluminal pressure is low, since such
a vessel cannot be compressed leading to falsenegative examination. Wall calcification should be
suspected when ABPI is more than 1.2 or when the
value is out of proportion to the patients clinical status.
Q 37. What are the indications for Doppler and
ABPI? (PG)
1. For confirming the diagnosis.
2. Objective estimation of the degree of ischemia.
3. Follow-up of patients on conservative treatment.
4. Follow-up of patients after surgery (graft
surveillance). A successful bypass must demonstrate a significant increase in ABPI, even if the
distal pulse is not palpable.
5. For the diagnosis of diabetic vascular disease.
6. Prediction of healing of ischemic ulcers.
7. Deciding the level of amputation.
8. For intraoperative assessment of the Doppler
signal over the graft.
Q 38. What is duplex imaging?
The duplex imaging is a combination of B mode
ultrasound and Doppler. The B mode ultrasound
will image the vessels. The Doppler is then used to
insonate the imaged vessels and the Doppler shift
obtained is analyzed by a computer which will give
knowledge about the blood flow and turbulence.
The new machines are capable of color coding
indicating the direction of flow. High flow in a
segment suggest stenosis. The duplex imaging is
as accurate as arteriography.
Q 39. Do you recommend arteriography in all cases?
No. Arteriogram is undertaken only after deciding
intervention. This is because arteriography is
invasive and itis associatedwith risk (especially so in
the case of carotid arteries having the risk of stroke).
Q 40. What are the techniques available for
arteriography?
1. Translumbar method for aortography (not done
now-a-days)
2. The Seldinger technique.
Q 41. What is Seldinger technique?
It is a retrograde percutaneous catheter method
usually done through the femoral artery. It can also
be done through brachial and axillary vessels. The
catheter can be pushed up into the aorta and its
various branches depending on the requirement.
When vessels like superior mesenteric or inferior
mesenteric vessels are selectively cannulated and
dye is injected, it is called selective arteriography.
Through the radial artery or brachial artery the
coronary arteries can be cannulated and angiograms
obtained to search for coronary artery blocks.
Q 42. What are the complications of arteriogram?
(PG)
1. Allergic
2. Anaphylactic reactions
3. Thrombosis of the vessel
4. Hematoma formation
5. Arterial dissection
6. Neurological dysfunction
7. Renal dysfunction.
198
Clinical Surgery Pearls
Q 43. What are the dyes used for arteriography?
1. Meglumine diatrozoate
2. Ionohexal
3. Carbon dioxide
4. Gadolinium.
Q 44. What are the angiographic informations to
be looked for?
1. Site of the occlusion
2. Extent of the occlusion
3. Nature of occlusion
4. Run in—patency of the vessel proximal to the
occlusion
5. Distal run off—patency of the vessel distal to
the occlusion
6. State of collateral circulation.
Q 45. What is distal run-off?
It is the patency of the artery distal to the obstruction
demonstrated by arteriography. Arterial bypass
surgery is feasible only if a named distal artery is
open beyond the block where the anastomosis
can be done.
Q 46. What is run-in?
It is the state of arteries proximal to the stenosis
(whether it is normal or not). If the proximal artery
also is occluded the patient will not benefit from a
bypass. In a planned femeropopliteal bypass, it will
not function if the ipsilateral iliac artery has got a
significant stenosis.
Q 47. Is it possible to do arterial revascularization
in Buerger’s disease?
It is not usually possible because it is a disease of the
small arteries and distal run-off is absent.
Q 48. What is Digital substraction angiography (DSA)?
A computer system is used to digitize the
angiographic images. This allows precontrast
injection images to be substracted from the contrast
image, removing the extraneous background and
providing clarity. This can be carried out by injecting
the contrast intra-arterially or intravenously.
Intravenous injection of the contrast avoids arterial
puncture but the only problem is that large volumes
of contrast agent is required for the investigation.
Q 49. What is magnetic resonance angiography
(MRA)?
It is a multiplanar imaging without arterial puncture,
catheters, or ionizing radiation. The principle is
rearrangements of hydrogen atoms in a strong
magnetic field. We can image the vascular tree and
the soft tissue surrounding the vessel. The dye used
is called gadolinium (non-iodine containing). This
dye is not nephrotoxic and therefore can be used in
patients with compromised renal function.
Q 50. What is plethysmography? (PG)
It is a device to measure the volume of an organ
or extremity. The pulse volume recording, i.e. the
change in the volume of an extremity between
systole and diastole is a reflection of the pulsatile
blood flow. It is not routinely done.
Q 51. What is photoplethysmography? (PG)
It is a measurement of the blood in the cutaneous
microcirculation by detecting the reflection of
infra-red light.
Q 52. What is transcutaneous oximetry? (PG)
It is the measurement of intracutaneous oxygen
tension (PO2
) by placing the probe over the skin
surface. Normally it is 40–70 mm of Hg. When the
TCPO2
is less than 30 mm of Hg, the part will go in
for gangrene.
Q 53. What is gangrene? (See definitions)
Macroscopic death of tissue with putrefaction is
called gangrene.
Peripheral Occlusive Vascular Disease
199
Q 54. How will you classify gangrene according
to etiology?
Causes for gangrene
1. Secondary to arterial obstruction
• Atherosclerosis
• Buerger’s disease
• Embolism
• Diabetic arteriopathy
• Raynaud’s disease
• Iatrogenic—intra-arterialinjectionlikethiopentone
2. Infective gangrene
• Carbuncle
• Gas gangrene
• Fournier’s gangrene (gangrene of scrotum)
3. Traumatic
• Direct arterial injury—Crushinjury,pressure sores
• Indirect arterial injury—Injury to vessels atsome
distance from the site of gangrene, e.g. Injury to
popliteal artery by fractured lower end of femur
• Physical agents—burns, scalds, frost bite,
electrical, irradiation, etc.
• Chemical
4. Venous gangrene.
Note: Mnemonic for the secondary causes of
gangrene is BREASTED.
B – Buerger’s disease
R – Raynaud’s disease
E – Ergot intake
A – Arterial injection (Thiopentone)
S – Senile (Atherosclerosis)
T – Thrombosis
E – Embolism
D – Diabetes
Q 55. What is the clinical appearance of gangrene?
Gangrenous part lacks the following:
• Arterial pulsation
• Venous return
• Capillary response to pressure
• Sensation
• Warmth
• Function.
The color of the part varies from pallor, mottled
grey, dark brown, greenish black, and finally black.
Q 56. What is the cause for black appearance?
It is due to the formation of iron sulphide as a result
of disintegration of hemoglobin.
Q 57. What are the clinical types of gangrene?
a. Dry gangrene—slow arterial occlusion alone
—the affected part becomes dry and wrinkled.
b. Wet gangrene (moist gangrene)—arterial and
venous obstruction is present. Infection is
always present. The affected part is swollen
and discolored. The epidermis may be raised as
blebs. Crepitus may be palpated (gas forming
organisms).
Q 58. What is the line of demarcation?
It is zone of demarcation between the truly viable
and dead or dying tissues indicated on the surface
by a band of hyperemia and hyperesthesia. The
separation of the dead and living tissue is achieved
by the development of a layer of granulation tissue
which will advance into the dead tissue until it can
get nourishment.This is followed by ulceration and
final line of the demarcation.
In dry gangrene the separation is by aseptic
ulceration (final line of demarcation in a few days).
In moist gangrene the separation is by septic
ulceration (here there is more infection and
suppuration reaching the neighbouring living
tissues and the separation takes long time and will
be more proximal than dry gangrene). The moist
gangrene should be converted to dry gangrene.
200
Clinical Surgery Pearls
Q 59. What is skip lesion?
Appearance of black patches on the other side of
the foot or proximally in the calf is suggestive of
spreading of gangrene due to arterial occlusion and
a proximal amputation may be required.
Q 60. What is pre-gangrene?
The term pre-gangrene is used by clinicians to
describe the changes in tissues indicating that the
blood supply to the part is precarious and it will
soon be inadequate to keep the tissues alive. The
principle symptom is rest pain and the signs are:
1. Pallor on elevation
2. Congestion when dependent
3. Coldness
4. Tenderness.
Q 61. What is the treatment of gangrene?
• Exposure of gangrenous area for desiccation
• Protection of local pressure areas (the skin of
heel and malleoli)
• Removal of the hard desiccated skin for release
of pus in other areas
• The gangrenous part must be removed
• A limb saving attitude is required
• Thepoorblood supplyproximalto the gangrene
in the given case can be improved by surgery or
percutaneous angioplasty.
• General measures—control of diabetes
– Control of pain
– Treatment of cardiac failure
– Correction of anemia
– Improve tissue oxygenation.
Q 62. What is the difference between Raynaud’s
disease and Raynaud’s syndrome?
Raynaud’s disease is an idiopathic condition
occurring in young women due to abnormal
sensitivity of the arterioles to cold affecting upper
limbs more than the lower limbs.
Raynaud’s syndrome is a secondary phenomenon,
secondary to underlying systemic disorder often one
of the collagen diseases. The clinical features are
much more aggressive. It is seen in diseases like:
• Collagen diseases
Peripheral arterial manifestations of the diseases
like:
• Systemic lupus erythematosus (SLE)
• Rheumatoid arthritis(RA) manifestations of the
disease
• Vibration white finger (seen in those who are
using vibrating tools like pneumatic drills, chain
saws, etc.).
Q 63. What are the manifestations of Raynaud’s
disease?
Characteristically it is painful and paroxysmal and
the sequences are:
• Blanching—constriction of arterioles
• Dusky cyanosis—capillaries then dilate and fill
with deoxygenated blood
• Red engorgement—the arterioles relax and
oxygenated blood returns to the capillaries
Gangrene is usually uncommon.
Q 64. What is the treatment of Raynaud’s disease?
1. Protection from cold—Electricallyheatedgloves
in winter
2. Avoidance of pulp and nail bed infection
3. Calcium antagonists—Nifedipine
4. Sympathectomy.
Q 65. What is the treatment of Raynaud’s
syndrome?
1. Treatment of the primary condition
2. Gangrene will occur in secondary and may
require multiple amputations
3. Nifedipine
4. Steroids
5. Sympathectomy is ineffective.
Peripheral Occlusive Vascular Disease
201
Q 66. What is acrocyanosis?
It is painless and not paroxysmal affecting the
young females producing cyanosis of fingers and
legs accompanied by paresthesia. Sympathectomy
may be useful.
Q 67. How will you classify limb ischemia?
Can be classified as—
• Acute limb ischemia
• Chronic limb ischemia
• Acute on chronic limb ischemia.
Q 68. What is the basic difference between acute
and chronic limb ischemia? (PG)
Acute occlusion leads to gangrene unless
revascularization is done. Chronic occlusive
disease allows time for collateral arterial formation.
In chronic, mild ischemia gives rise to intermittent
claudication. But when the residual vessels are
unable to provide enough blood to support the
resting metabolic needs a state of critical ischemia
is reached accompanied by the symptoms of rest
pain and gangrene.
Q 69. What is critical limb ischemia? (PG)
Two criteria:
1. Recurring rest pain that persists for more than
2 weeks, requiring regular analgesics with ankle
systolic pressure of < 50 mm of Hg or toe systolic
pressure < 30 mm of Hg and ABPI < 0.5.
2. Ulceration or gangrene of the foot or toes with
similar hemodynamic parameters.
Q 70. What are the causes for chronic arterial
occlusion?
Common causes:
1. Atherosclerosis
2. Buerger’s disease
3. Arteritis—Takayasu’s disease, SLE
4. Post-traumatic—direct injury, radiation.
Rare causes:
1. External – Thoracic outlet syndrome
compression
– Popliteal entrapment
2. Developmental – Coarctation anomalies
3. Arterial wall – Fibromuscular dysplasia
disorders – Cystic medial necrosis.
Q 71. What is the management of the given case?
General measures
• Stop smoking (vascular bypasswill get occluded
earlier in smokers)
• Keep walking (exercise is to be encouraged,
walking within the limit of disability)
• Care of the foot – well fitting footwear
– heel raise—the claudication
distance can be improved
by 1cm heel raise
• Diet—weight reduction in obese patients
• Control of diabetes and hypertension.
Pharmacological therapy
• Analgesics—opioid should be avoided
• Antiplatelet agents—aspirin – 75–300 mg
daily—Clopidogrel
• Pentoxifylline 400–800 mg tablet 3 times daily
altersthe blood viscosity (useful in intermittent
claudication)
• Naftidrofuryl oxalate (Praxilene)—May alter the
tissue metabolism and increase the claudication
distance
• Prostaglandin E1 (Alpostin)—Useful in critical
limb ischemia in doses of 100 mg daily (over
10 hrs) for five days monthly × 6 months.
Surgical procedures
The given case needs above knee amputation
because of the nonhealing ischemic ulcer in the
heel with aortoiliac occlusion. His general condition
202
Clinical Surgery Pearls
and comorbid factors makes him unsuitable for
aorto femoral revascularization. If patient’s general
condition is good and there is no ischemic ulcer
of the heel the following surgical procedures are
recommended for him.
• Ray amputation of big toe
• Aortofemoral bypass graft orifthe contralateral
femoral is normal a femoro-femoral cross over
graft or an axillofemoral bypass graft may be
tried for revascularization of the limb.
Q 72. What is the role of surgery in peripheral
vascular disease?
Can be divided into 3 broad groups.
1. Direct arterial surgery
• Percutaneous transluminal angioplasty and
stenting
• Endarterectomy
• Bypass graft.
2. Lumbar sympathectomy
3. Amputations.
Q 73. What are the indications for direct arterial
surgery? (PG)
1. Critical limb ischemia
2. Severe intermittent claudication which is
incapacitating
3. To lower the level of the amputation.
Q 74. What is percutaneous transluminal angioplasty and where it is used?
It involves a femoral angiogram during which a
guide wire is inserted and a balloon catheter is then
inserted over the guide wire and positioned within
the stenosis. Now the balloon is inflated for 1minute
and then deflated. In cases where the vessels fail
to stay adequately dilated it may be possible to
hold the lumen using metal stent. The catheter is
removed. Now self-expanding stents are available.
It is used in the following situations.
• Coronary artery (widely used)
• Iliac vessels
• Vessels of the lower limb
• Vessels of the upper limb
• Renal arteries
• Mesenteric vessels.
Q 75. What is endarterectomy?
The occluded intima and a part of the media are
removed by coring them out through an artificial
plane created in the media. This is usually done for
large arteries like aorta. Nowadays it is rarely done.
Q 76. What is bypass graft? (PG)
Anative vein (usually saphenous vein) or a prosthetic
material is used for bypassing the obstruction in the
vessel.The bypass procedures can be classified as—
• Anatomic, e.g. femoropopliteal bypass
• Extra anatomic—femoro-femoral crossovergraft.
– iliofemoral crossover graft
– Axillobifemoral.
Q 77. What are the materials used for bypass graft?
• Reversed long saphenous vein (the most useful
and successful conduit)—ifthe long saphenous
vein is not available short saphenous vein or arm
vein may be used.
• PTFE (Poly Tetra Fluro Ethylene)
• Dacron-twotypes—WovenandKnitted(Knitted
prosthesis are sealed with gelatin or collagen)
• Humanumbilical vein(Glutaraldehyde—tanned,
Dacron supported).
Q 78. How will you choose the prosthetic
material? (PG)
It depends on the site of disease and the type of
operation.
The patients own saphenous vein gives the
best results when used either as a reversed conduit
or as in situ after valve disruption.
Peripheral Occlusive Vascular Disease
203
Q 79. What are the bypass operations done for
peripheral vascular disease?
Bypass operations depending on the
level of occlusion
Site of disease Type of operation
1. Aortoiliac
occlusion
Aortobifemoral bypass surgery.
2. Unilateral Iliac
occlusion alone
Percutaneous transluminal
angioplastyalone (PTA) with or
without stent or endarterectomy
I n p a t i e n t s u n a b l e t o
withstand abdominal surgery
femorofemoral or iliofemoral
crossover bypass graft (8 mm
PTFE or dacron graft tunnelled
subcutaneously above the pubis)
3. Bilateral iliac
occlusion with
pregangrenous
limb on one side
Axillofemoral graft to the
affected side with 8 mm PTFE
4. Superficial
femoral with
profunda femoris
occlusion
Femoropopliteal graft artery
using autogenoussaphenous
vein or human umbilical vein
Note:
• For long distance claudication conservative
treatment is wise.
• Salvage operationsshould not be performed for
intermittent claudication alone. Gangrene and
loss of limb may occur if the operation fails.
• Any vein used for anastomosis requires a
diameter of at least 3 mm.
• The size ofsuture material used for anastomosis
from groin down is 4/0–5/0 polypropylene.
• Femoro-distal bypasses are usually carried out
using long saphenous vein preferably in situ.
Q 80. What is in situ bypass graft? (PG)
This is done for femoropopliteal bypass graft. The
long saphenous vein is not removed and reversed in
this operation. Instead it isleft in place (in situ) and
the valves disrupted with a valvulotome. The vein is
then anastomosed to the femoral artery proximally
and to the popliteal vessel distally.
Q 81. What is profundaplasty? (PG)
The common femoral artery and its branches are
exposed. After giving heparin IV and clamping the
vessel an incision is made into the common femoral
artery and carried down into the profunda dividing
the stenotic profunda origin. The arteriotomy
is then closed with a patch of vein to widen the
narrowed segment.
Q 82. What is the role of lumbar sympathectomy?
This should only be done if there is no chance for
direct arterial surgery or angioplasty. It has no role
in the treatment of intermittent claudication. The
indications are:
• Nonhealing ischemic ulcers
• Ischemic rest pain
• Vasospastic conditions
• Hyperhidrosis
• Causalgia.
Q 83. What is lumbar sympathectomy?
In lumbar sympathectomy the second, third and
fourth lumbar sympathetic ganglia are removed.
The removal of bilateral first lumbar ganglia will
result in retrograde ejaculation. The operation can
be done either by open or laparoscopic method.
The open method is done by extra-peritoneal
approach using a loin incision. The sympathetic
trunk lies on the side of the bodies of the lumbar
vertebrae on the right side overlapped by IVC. Care
is taken not to mistake and remove small lymph
204
Clinical Surgery Pearls
nodes and tendinous strip of psoas minor. It is also
important to avoid the genitofemoral nerve.
Q 84. What is chemical sympathectomy?
Under radiographic fluoroscopic control with
the patient in the lateral position after giving local
anesthesia a long spinal needle is inserted to seek
the side of vertebral body to reach the lumbar
sympathetic chain. 5 mL of phenol in water (1:16)
is injected after confirming the needle position
by injecting contrast agent. It is carried out in two
sites beside the bodies of second to fourth lumbar
vertebrae. It is important to avoid aorta, IVC and
ureters. It is contraindicated in patients taking
anticoagulants.
Q 85. What is the role of amputation?
Amputation is inevitable when the arterial surgery
and conservative treatment fail. The commonly
performed amputations are:
1. Ray amputations for gangrene of toes
2. Transmetatarsal for fore foot gangrene
3. Below knee (BK) amputation—if the gangrene
is limited to foot
4. AK (above knee) amputation—if the gangrene
is approaching to the leg.
Note:The BK amputation isfunctionally farsuperior
to AK amputation provided the popliteal is patent.
Discussion on Acute Lower Limb Ischemia
Q 1. What are the causes for acute limb ischemia?
The causes may traumatic or non-traumatic.
Non-traumatic
Common causes:
1. Embolism(commonestindevelopingcountries)
2. Thrombosis of a native artery—atsitesofarterial
stenosis due to disorders like atherosclerosis,
buerger’s disease, etc. Thrombosis of an
artery can occur in hypercoagulable states
like malignancy, protein C, protein S, and
antithrombin III deficiency.
3. Thrombosis of a bypass graft (commonest in
developed countries).
Rare causes:
1. Thrombosed popliteal artery aneurysm
2. Aortic dissection
3. Popliteal artery entrapment syndrome.
Q 2. What are the clinical features of acute
embolism?
Six Ps
• Pain
• Pallor
• Pulseless ness
• Paresthesia
• Paralysis
• Poikilothermia (cold limb).
Clinically important features are:
• Sudden loss of previously palpable pulse
• Coldness of the limb
• Severe continuous pain
• Sensory disturbances like tingling, numbness
and complete loss of sensation
• Paralysis of the limb—which is usually a late
feature.
Q 3. What is the critical period for revascularization. (PG)
Ischemia of the tissues distal to the site of occlusion
begins from the moment of occlusion. The extent
of damage to various tissues depends on the cell
type and their metabolic rate. In the limb the
peripheral nerves are most sensitive to ischemia
Peripheral Occlusive Vascular Disease
205
followed by muscles, subcutaneous tissue and
skin. Reversible ischemia will occur after 6 hours.
Histological changes can develop by 4 hours of
warm ischemia. Pre-existing collaterals may delay
this event. By 12 hours ischemic muscles undergo
irreversible changes. Muscle rigidity will occur over
the next 12–24 hours.
Q 4. What are the clinical differences between
acute thrombosis and embolism?
Differences between thrombosis and embolism
Feature Thrombosis Embolism
Onset Gradual Sudden
History of
claudication
Common None
Contralateral
pulse
Often absent Normal
Source of
embolus
None Usually heart showing
either valvular disease
or fibrillation
Temperature
changes
Less marked More marked
Loss of
function
Slow - because
collaterals are
there
Rapid loss of function
(4–6 hrs)
Angiography Diffuse disease Minimal disease
“ Tapered and
irregular cut off
Sharp cut off
“ Collaterals welldeveloped
Few collaterals
Q. 5. What are the causes for peripheral arterial
embolism?
It is classified as cardiac, noncardiac and cryptogenic.
Cardiac—(80–90%)
• Atrial fibrillation
• Myocardial infarction
• Cardiac valvular prosthesis
• Rare causes like atrial myxoma.
Noncardiac
• Atherosclerotic disease (plaques in proximal
arteries)
• Aneurysm in proximal arteries
• Noncardiac tumors
• Foreign bodies—broken cannula.
Cryptogenic—Unknown inspite of investigation
(5–10% of cases).
Q 6. What is the classification for severity of acute
limb ischemia? (PG)
Class 1 (viable) – No persisting pain
– No motor and sensory deficits
– Doppler signals audible
Class 2a (marginally threatened)
– Numbness/paresthesia
– Digital sensory loss
– No audible Doppler signals
Class 2b (immediately threatened)
– Above and persistent ischemic pain
– Sensory and motor deficit
Class 3 (irreversible)
– Profound anesthesia and paralysis
may be early and late.
Q 7. What is the management of acute limb
ischemia? (PG)
Once the diagnosis is made patient should be
heparinized.
Contrast angiography is still considered the gold
standard investigation of choice.
C-arm facility and peroperative angiograms are
necessary.
The site of entry for angiogram should be
preferably the contralateral limb.
206
Clinical Surgery Pearls
In case of bilateral lower limb problem the
brachial artery should be the entry point.
Immediate revascularization is required
either by surgical (embolectomy by Fogarty or
open thrombectomy with or without bypass
procedures) or endovascular procedures.
Class 1 and 2 – Angiography and
thrombolysis
Class 2b and 3 early – Emergency surgery
Class 3 late – Delayed amputation
For distal embolism thrombolytic therapy is
preferred.
Q 8. What is embolectomy?
• The femoral artery is exposed under general
anesthesia or local anesthesia.
• Longitudinal arteriotomy is made after placing
vascular clamps.
• A Fogarty catheter of appropriate size is passed
proximally, the bulb inflated, and catheter gently
pulled down to extract the blood clot. This is
repeated until a good antegrade flow is obtained.
• The same procedure is repeated in the distal
artery until good back flow is obtained.
• Heparin is given IV. (5000 units) and anticoagulation is continued postoperatively.
• Arteriotomy is closed by continuoussuture with
5/0 or 6/0 polypropelene.
• Fasciotomy ofthedistal muscle isrecommended
if the ischemic time has exceeded 6 hours.
Q 9. What is thrombolytic therapy? (PG)
This will bring about lysis of fibrin by stimulating
the plasmin system. It cannot be done in a limb
threatened with gangrene. It may take upto 48
hours to lyse the thrombus. Old clots cannot be lysed
by thrombolytic therapy.Duration ofthe procedure
is lengthy. The commonly used agents are:
• Streptokinase (Abacterial enzyme)—Cheap but
antigenic—Anaphylaxis is a problem.
• Urokinase (Extracted from renal parenchymal
cells).
• Tissue plasminogen activator (TPA-Synthetic).
Q 10. What are the contraindications for Thrombolytic therapy? (PG)
• Recent stroke
• Recent surgery
• History of GI hemorrhage
• Pregnancy
• Uncontrolled hypertension
• Allergy to the agent.
15 Lymphoma
Case
Case Capsule
A 20-year-old male patient presents with weight loss,
malaise, pyrexia of unknown origin and drenching
night sweats that require change of cloths for the
last 9 months. There is neither history of pruritus,
nor alcohol intolerance. There is no abdominal pain
after drinking alcohol. He also complains of bilateral
supraclavicular swellings for the last 7 months which
is painless. There is no history of bone pain.
On examination the patient is febrile and
pale. There is a 10 × 6 cm size swelling in the right
supraclavicular region and 12 × 8 cm size swelling in
the left supraclavicular region. On palpation, there is
neither local rise of temperature nor tenderness over
the swelling. It appears to be a group of lymph nodes
on either side. It is possible to define individual
nodes and they are ovoid, smooth and discrete.
The nodes are having rubbery consistency. These
nodes can be moved from side to side. There is
no fixity of the nodes. The abdominal examination
revealed enlargement of the liver, about 4 cm
below the costal margin, firm in consistency and
the surface is smooth and edge is sharp. The spleen
is also enlarged. No palpable abdominal nodes
detected. There is no free fluid in the abdominal
cavity. Examination of other lymph node areas like
axillary and inguinal is normal. There is no evidence
of collaterals veins across the chest wall suggestive
of mediastinal mass. There is no venous congestion
of the neck. Examination of the genitalia is normal.
Read the checklist for examination of abdomen.
Checklist for lymph node examination in
section on short cases
Mnemonics for lymph node examination –‘PALS’ (short
case section)
P – Primary (examine the drainage area of the lymph
node for a primary lesion)
A – Another node (always look for another node when
one group is palpable)
L – Liver (always examine the ab domen for
enlargement of liver)
S – Spleen
Remember the 3 lymphatic water sheds of the skin
(on each side):
A vertical line through the sagittal plane of the body
divides the lymphatic drainage of the skin into 3
areas on each side. There is some communications
across the midline. The 3 areas on each side of
the body are demarcated from each other by two
horizontal lines one at the level of the clavicle,
the other at the level of the umbilicus. These lines
208
Clinical Surgery Pearls
are the lymphatic water sheds and the skin lymph
flows in a direction away from them. Each line also
represents the meeting place of adjacent territories,
so that the cancer situated in one of these lines may
spread by two routes along the lymphatics running
away from the water shed, e.g. cancer situated
at the umbilicus may spread in four directions.
Viz: towards both axillae and both groins, as
lymphatics draining to these glands come into
communication at the umbilicus. Similarly a cancer
situated anywhere in the midline of the surface
of the body may spread in at least two directions
because of the lymphatic communication across
the midline. Thus, we get 3 groups of lymph nodes
draining the three areas.
1. Cervical lymph nodes
2. Axillary lymph nodes
3. Inguinal lymph nodes
• The lymphatic above the clavicle will drain to
the cervical nodes.
• The lymphatics below the clavicle up to the
level of umbilicus will drain to the axilla (both
front and back).
• The lymphatics below the level of umbilicus
will drain to the inguinal nodes.
• If axillary node is enlarged, examine the
following drainage areas—breast, front of
the chest and upper abdomen up to the
umbilicus, back of the chest down up to the
level of umbilicus, and the entire upper limb.
• If the inguinal lymph node is enlarged,
examine the following drainage areas—the
lower abdomen from the level of umbilicus,
the corresponding area in the back, the
gluteal region, natal cleft, perineum, genitalia,
the lower part of the anal canal and the entire
lower limb. The lower limb lymphatics will
drain to the vertical group of nodes. The
remaining areas will drain to the horizontal
group of inguinal nodes. A digital rectal
examination must be done in all cases of
horizontal inguinal lymph node enlargement.
• Whenthecervical lymphnodeisenlargedthe
drainage areas to be examined will start from
the scalp down to the level of the clavicle,
including examination of the oral cavity,
pharynx (oral and nasal) nasal sinuses and
the hidden areas.
Checklist for history
• H/o weight loss(> 10% loss of weight in 6 months)
• H/o fever occurring in a periodic fashion (PelEbstein fever)
• H/o pruritus
• Alcohol-induced nodal pain
• Bone pain (lymphomatous infiltration)
• Pallor
• Family history of leukemias and similar illness.
Checklist for examination
• Look for other groups of lymph nodes
• Look for liver and spleen
• Look for anemia
• Look for jaundice
• Look for venous congestion of the neck and upper
chest—superior venacaval obstruction produced
by mediastinal masses
• Look for edema of both legs—abdominal masses
obstruct the inferior vena cava
• Examine the skin for scaly elevated reddened
patches of skin—mycosis fungoides (dermatological manifestations of lymphoma).
Lymphoma
209
Q 1. What are the physical signs of an enlarged
spleen?
Physical signs of enlarged spleen
• It appears from below the tip of the 10th rib
• It enlarges along the line of the rib towards the
umbilicus
• Definite notch will be felt (splenic notch)
• One cannot get above it
• Moves with respiration
• It is dull to percussion
• It is not bimanually palpable.
Contd...
Contd...
210
Clinical Surgery Pearls
Q 2. How many times the spleen must be enlarged
for clinical palpation?
Traditionally it was taught that the spleen must
be enlarged 2–3 times before it become palpable.
According to Blackburn, spleen must be 1½ times
larger than normal, before it can be detected by
clinical methods.
Q 3. What is Kenawy’s sign?
This sign is seen in splenomegaly associated with
bilharzial cirrhosis of liver (Egyptian splenomegaly). It is also seen in portal hypertension
secondary to the above condition. The stethoscope is
applied beneath the xiphoid process. This will reveal
a venous hum which is louder on inspiration. This is
because of the engorgement of the splenic vein and
the hum is louder during inspiration because the
spleen is compressed during inspiration.
Q 4. What are the causes for splenomegaly?
The causes for splenomegaly can be classified as
follows:
Splenomegaly
Cause Conditions
Neoplastic • Benign c o n d i t i o n s l i k e
hemangioma (commonest)·
• Malignant
- Hodgkin’s lymphoma
- Non-Hodgkin’slymphoma(NHL)
- Myelofibrosis(abnormalproliferation of mesenchymal
elements in the bone marrow,
spleen, liver and lymph nodes)
- Metastatic disease
Hematologic
malignancies
• Acute leukemia
• Chronic leukemia
Hemolyticnemias • Hereditary spherocytosis
• Autoimmune hemolyticnemia
• Thalassemia (cooley’s anemia,
Mediterranean anemia)
• Sickle cell disease
Other blood
diseases
• Idiopathic thrombocytopenic
purpura
• Pernicious anemia
• Polycythemia vera
• Erythroblastosis fetalis
Tropical
splenomegaly
• Malaria
• Kala-azar
• Schistosomiasis
• Tropical splenomegaly
• Trypanosomiasis
Infective • Bacterial
- Typhoid, paratyphoid, tuberculosis, splenic abscess and
septicemia
• Viral
- Infectious mononucleosis,
HIV related, psittacosis.
• Spirochaetales
- Weil’s disease, syphilis
• Parasitic—Hydatid cyst
Metabolic • Porphyria (hereditary error of
hemoglobin catabolism in which
porphyrinurea occurs— the
orange colored urine turns to a
port-wine color after exposure
to the air)
• Gaucher’s disease (Lipid storage
disease)
• Amyloid
Collagen disease • Felty syndrome
• Still's disease
Nonparasitic cysts • True cyst—(lined by flattened
epithelium) dermoid and
mesenchymal inclusion cyst
• False cyst—(pseudocyst)
Circulatory disease • Portal hypertension
• Segmentalportal hypertension
of pancreatic carcinoma Contd...
Contd...
Lymphoma
211
Q 5. What is hypersplenism?
Hypersplenism is an indefinite clinical syndrome
characterized by splenic enlargement, any
c o m b i n a t i o n o f a n e m i a , l e u k o p e n i a o r
thrombocytopenia, compensatory bone marrow
hyperplasia and improvement of the condition
after splenectomy.
Q 6. What are the clinical characteristics of lymph
nodes in lymphoma?
• They cause lymphadenopathy in the posterior
triangle
• The nodes are ovoid, smooth and discrete
• Possible to define individual nodes even when
they are large (in contrast to tuberculosis)
• The nodes are solid and rubbery
• The nodes can be moved from side-to-side and
are rarely fixed to the surrounding structures.
Q 7. What is lymphoma?
It is a primary malignant neoplasm originating from
lymphoid tissue of the lymphatic system. There are
two types:
1. Hodgkin’s disease
2. Non-Hodgkin’s disease (NHL).
Q 8. What is lymphoid neoplasm?
Lymphoid neoplasm consists of the following:
• Hodgkin’s
• Non-Hodgkin’s lymphoma (NHL)
• Lymphatic leukemia
• Plasmacytoma.
Q 9. Why this new nomenclature of lymphoid
neoplasm is preferred over lymphoma?
Traditionally, neoplasms that typically present with an
obvious tumor or mass of lymph nodes or extra nodal
sites are called lymphomas and neoplasms that
typically involve the bone marrow and peripheral
blood without tumor mass are called leukemias.
However, we now know that many B and T/NK
– cell neoplasms may have both tissue masses and
circulating cells, either in the same patient or from
one patient to another. Thus, it is artificial to call
them different diseases, when in fact, they are just
different stages or phases of the same disease.
• Neoplasmsthattypically produce tumor masses
are called lymphomas.
• Neoplasms that typically have only circulating
cells are called leukemias.
• Those that have both solid and circulating
phases are designated lymphoma/leukemia.
• Plasma cell neoplasms including multiple
myelomas and plasmacytoma have their
origin from B cell are also now included under
lymphoid neoplasms.
B cell chronic lymphocytic leukemia and B cell
small lymphocytic lymphoma are simply different
manifestations of the same neoplasm. (Similarly,
lymphoblastic lymphoma and acute lymphoblastic
leukemia are different manifestations of the same
neoplasm).
Q 10. What is the classic cell of Hodgkin’s disease?
The Hodgkin’s lymphoma is defined by the
histological finding of Reed-Sternberg cells. They
are binucleate cells. The binucleate cell is having
vesicular nuclei and prominent eosinophilic
neucleoli (pennie on plate appearance or owl eye
appearance). The subtype is decided by the pattern
of lymphocyte infiltrate.
Q 11. What are the clinical features of mediastinal
lymph nodes?
When the nodes are large in the mediastinum,they
occlude the superior vena cava, causing venous
congestion in the neck and the development of
collateral veins across the chest wall. This is called
superior vena cava syndrome. It may also produce
212
Clinical Surgery Pearls
dysphagia or hoarseness of voice. This is one of
the classic presentations for nodular sclerosis in
Hodgkin’s.
Q 12. What is the clinical feature of intraabdominal lymph node mass?
Large nodal masses in the abdomen can obstruct
the inferior vena cava and iliac veins producing
edema of both lower limbs.
Q 13. Can you differentiate Hodgkin’s lymphoma
from non-Hodgkin’s lymphoma (NHL) clinically?
What are the differences between Hodgkin’s and
NHL?
Clinically it is difficult to differentiate these
conditions. The differences are given in table 15.1.
Q 14. What is the probable diagnosis in this case?
Hodgkin’s disease.
Q 15. What are the points in favor of Hodgkin’s
disease?
• Cervical and axillary lymph node enlargement
with hepatosplenomegaly
• Clinical nature ofthe lymph nodes as mentioned
earlier
• The age group of patient(younger age isin favor
of Hodgkin’s rather than NHL).
Q 16. What are the differential diagnoses?
• NHL
• Leukemias
• Myeloproliferative disorders.
Q 17. Why cannot this be tuberculosis?
• Tuberculosis will produce usually matting of
lymph nodes.
• It will not produce hepatosplenomegaly.
Q 18. What are the causes for matting of lymph
nodes?
1. Acute lymphadenitis
2. Tuberculosis (Read tuberculosis of lymph nodes)
3. Late stages of lymphoma
4. Late stages of metastasis.
Q 19. What is the WHO Classification of lymphoma
(REAL classification)?
Revised European-American classification of
Lymphoid neoplasms).
It is a list of distinct disease entities, which are
defined by combination of morphology, immunophenotype and genetic features and which have
distinct clinical features. The classification includes
all lymphoid neoplasms: Hodgkin’s lymphoma,
non-Hodgkin’s lymphoma, lymphoid leukemias and
plasma cell neoplasms.
B Cell Neoplasms
Precursor B-cell Neoplasm
• Precursor B-lymphoblastic leukemia/lymphoma
(precursor B-cell acute lymphoblastic leukemia).
Mature (peripheral) B-cell neoplasms
• B-cell chronic lymphocytic leukemia/small
lymphocytic lymphoma
• B-cell pro lymphocytic leukemia
• Lymphoplasmacytic lymphoma
• Splenic marginal zone B-cell lymphoma (with or
without villous lymphocytes)
• Hairy cell leukemia
• Plasma cell myeloma/plasmacytoma
• Extra nodal marginal zone B-cell lymphoma of
MALT type
• Nodal marginal zone B-cell lymphoma (with or
without monocytoid B cells)
• Follicular lymphoma
• Mantle cell lymphoma
• Diffuse large B-cell lymphoma
• Burkitt lymphoma/Burkitt cell leukemia.
Lymphoma
213
T Cell and NK Cell Neoplasms
Precursor T-Cell Neoplasm
• PrecursorT-lymphoblastic lymphoma/leukemia
(precursor T-cell acute lymphoblastic leukemia).
Mature (peripheral) T/NK-cell neoplasms
• T-cell pro lymphocytic leukemia
• T-cell granular lymphocytic leukemia
• Aggressive NK-cell leukemia
• Adult T-cell lymphoma/leukemia (HTLVI +)
• Extra nodal NK/T cell lymphoma, nasal type
• Enteropathy—type T-cell lymphoma
• Hepatosplenic T-cell lymphoma
• Subcu taneous panniculitis-like T- cell
lymphoma
• Mycosis fungoides/Sezary syndrome
• Anaplastic large cell lymphoma, T/null cell,
primary cutaneous type
• Peripheral T-cell lymphoma, not otherwise
characterized
• Angioimmunoblastic T-cell lymphoma
• Anaplastic large cell lymphoma, T/null cell,
primary systemic type.
Q 20. What is the staging of Hodgkin’s lymphoma?
Ann-Arbor staging
Stage Description
Stage I Involvement of a single lymph node
region (I) or localized involvement of a
single extra lymphatic organ or site in the
absence of any lymph node involvement
(1E) (rare in Hodgkin’s lymphoma)
Stage II Involvement of two or more lymph
node regions on the same side of the
diaphragm (II); or localized involvement
of a single extralymphatic organ or site
in association with regional lymph node
involvement with or without involvement
of other lymph node regions on the same
side of the diaphragm (IIE). The number
of regions involved may be indicated by
a subscript, as in, for example, II3
Stage III Involvement of lymph node regions on
both sides of the diaphragm (III) which
also may be accompanied by extra
lymphatic extension in association with
adjacent lymph node involvement (IIIE)
or by involvement of the spleen (IIIS) or
both (III E, S)
Stage IV Diffuse or disseminated involvement
of one or more extralymphatic organs,
with or without associated lymph node
involvement or isolated extralymphatic
organ involvement in the absence of
adjacent regional lymph node involvement,
but in conjunction with disease in distant
site (s). Any involvement of the liver or
bone marrow or nodular involvement of
the lung (s). The location of stage IV disease
is defined further by specifying the site
according to the notation.
Note:Allstages are havingA/B stagesdepending on
the absence or presence of B symptoms.
Q 21. What are B symptoms?
The B symptoms are:
• Weightloss—unexplained weightloss of > 10%
of the usual body weight in 6 months prior to
diagnosis Contd...
Contd...
214
Clinical Surgery Pearls
• Fever—unexplained fever with temperature >
38°C
• Drenching night sweats—that require change
of bedclothes.
Note:PruritusalonedoesnotqualifyforBclassification
nor does alcohol intolerance, fatigue or a short febrile
illness associated with suspected infection.
Q 22. What are the pathological types of Hodgkin’s
disease?
Major categories of Hodgkin’s lymphoma are:
• Nodular lymphocyte predominance Hodgkin’s
lymphoma (NLPHL)
• Classic Hodgkin’s lymphoma (CHL)—further
divisions given below:
Classic Hodgkin’s lymphoma
Sub type Characteristics
1. Lymphocyte rich
classic Hodgkin’s
lymphoma (LRCHL)
Uncommon-6%. Few
Reed-Sternberg cells
Diffuse lymphocytes –
excellent prognosis
2. Lymphocyte depletion
Hodgkin’s lymphoma
(LDHL)
Older males affected
Aggressive
Rare-2% Abundant ReedSternberg cells
Paucity of lymphocyte
3. Mixed cellularity
Hodgkin’s lymphoma
(MCHL)
Common 20 – 25%
often presents with
disseminated disease
4. Nodular sclerosis
Hodgkin’s lymphoma
(NSHL)
Commonest – 70%
Fibrosis present, ReedSternberg cells and
lymphocytes seen. Young
women affected Cervical
and Mediastinal disease
Q 23. What are the features of the lymphocyte
predominant Hodgkin’s lymphoma?
• Considered to be an indolent B-cell lymphoma
• More common in young men and old ages
• Infradiaphragmatic disease common than
Hodgkin’s disease
• Bulky disease and splenic involvement
uncommon
• Natural history like low grade NHL
• Can have delayed relapses
• Can progress to large B-cell lymphomas.
Q 24. What is nodal/extra nodal disease?
For the purpose of coding and staging, lymph
nodes, Waldeyer’s ring, and spleen are considered
nodalor lymphatic sites.
Extra nodal or extra lymphatic sites include the
following:
• Bone marrow
• Gastrointestinal tract
• Skin
• Bone
• Central nervous system
• Lung
• Gonads
• Ocular adnexa
• Liver
• Kidneys and uterus.
Note:
• Hodgkin’s lymphoma rarely presents in extranodal site
• About 25%ofNHL is extra nodal at presentation
• Mycosis fungoides (a type of NHL affecting the
skin) and MALT lymphomas are virtually always
extra nodal.
Lymphoma
215
Q 25. What is the ‘E Lesion’ for Hodgkin’s
lymphoma?
• The Ann-Arbor system defined E as extra
lymphatic.
• Disease in sites such as Waldeyer’s ring, the
thymus, and the spleen although extra nodal
is not extra lymphatic and therefore not
considered to be ‘E Lesion’.
According to the revised AJCC system the E
Lesion is defined as disease that involves extra
lymphatic sites (s) adjacent to site (s) of lymphatic
involvement but in which direct extension is not
necessarily demonstrable. Examples of E lesions
include extension into:
• Pulmona ry parenchyma from adjacent
pulmonary hilar/mediastinal nodes
• Extension into the anterior chest wall and into
the pericardium from mediastinal mass
• Involvement of iliac bone from adjacent lymph
node
• Involvement of lumbar vertebral body from
para-aortic nodes
• Involvement of pleura from internal mammary
nodes
• Involvement of thyroid from adjacent cervical
lymph nodes.
Note 1: It is proposed that for NHL, the E designation
should indicate the presentation of lymphoma in extra
nodal sites and the lack of an E designation should
indicate lymphoma presenting in lymph nodes.
Note 2: Liver is designated as H; bone marrow
designated as M and spleen is designated as S.
Q 26. In which core nodal region, the infraclavicular
nodes are included (Read core nodal regions in
NHL section)?
It is considered as part of the axilla.
Q 27. What are the other lymphatic structures
other than lymph nodes?
The lymphatic structures in the body:
• Lymph nodes
• Spleen
• Appendix
• Peyer’s patches
• Waldeyer’s ring
• Thymus.
Q 28. What is splenic involvement in Hodgkin’s
disease?
• Evidence of one or more nodules in the spleen
of any size on imaging evaluation
• Histologic involvement documented by biopsy
or splenectomy.
Note: Splenic enlargement alone is insufficient to
support a diagnosis of splenic involvement.
Q 29. What is hepatic involvement in Hodgkin’s?
• One or more nodules in the liver of any size on
imaging
• Histological involvement documented by
biopsy.
Note: Hepatic enlargement alone is insufficient.
Q 30. What is bone marrow involvement?
Bone marrow involvement must be documented
by biopsy from a clinically/radiographically
uninvolvedarea ofbone. Bonemarrowinvolvement
is designated by the letter M. Bone marrow
involvement is always considered as diffuse extra
lymphatic disease (stage IV).
Q 31. What are the unfavorable types of Hodgkin’s
disease?
1. The presence of B symptoms
2. Unfavorable histology—mixed cellularity and
lymphocyte depleted.
216
Clinical Surgery Pearls
Q 32. What is the most important confirmatory
investigation for this case?
Lymph node biopsy.
Q 33. Is there any role for FNAC of the lymph node?
For the diagnosis of lymphoma a node biopsy is a
must in order to study the histological background
and architecture of the lymph node. FNAC can be
done as a screening investigation if more than one
node is palpable. The needle aspiration will produce
anomalies in the node and it will be difficult for the
histopathologist to interpret this node, if it is taken
for biopsy later.
Q 34. Which lymph node is taken for biopsy and
what are the precautions for lymph node biopsy?
• The largest and most central node in a group is
most likely to be diagnostic.
• The inguinal nodes are avoided because they
often show changes of chronic infection (if other
enlarged nodes are available).
• A cervical node is preferred to the axillary or
inguinal group.
• Always take an intact node for biopsy.
• Biopsied node should be handled gently.
• Imprint of freshly cut node may be done if this
is available (imprint cytology).
• Avoid nodes which are aspirated for biopsy.
• For imprint cytology purpose the node should
be send in a bottle containing saline.
Q 35. What is the staging work up?
Clinical staging includes:
• Careful recording of medical history
• Physical examination
• Imaging of chest, abdomen and pelvis
• Complete blood count
• Blood chemistry
• Bone marrow biopsy
Recommendations for the diagnostic evaluation
of patients with lymphoma.
A. Mandatory procedure
1. Biopsy,withinterpretationbyaqualifiedpathologist
2. History, with special attention to the presence and
duration of fever, night sweats, and unexplained
loss of 10% or more of body weight in the previous
6 months
3. Physical examination
4. Laboratory tests
a. Complete blood cell count and platelet count
b. Erythrocyte sedimentation rate
c. Liver function tests
5. Radiographic examination
a. Chest X-ray
b. CT of chest, abdomen and pelvis
c. Gallium scan
6. Bone marrow biopsy.
B. Ancillary procedures
1. Laparotomy andsplenectomy ifdecisionsregarding
management are likely to be influenced
2. Liver biopsy (needle), if there is a strong clinical
indication of hepatic involvement
3. Radioisotopic bone scans, in selected patients with
bone pain
4. CT of head and neck in extra nodal or nodal
presentation to define disease extent
5. Gastroscopy and/or GI series in patients with GI
presentations
6. MRI of spine in patients with suspected spinal
involvement
7. CSF cytology in patients with Stage IV disease and
bone marrow involvement, testis involvement, or
parameningeal involvement.
Q 36. What are the indications for bone marrow
biopsy?
• B symptoms
• Anemia
Lymphoma
217
• Leukopenia
• Thrombocytopenia.
Q 37. What is the role of staging laparotomy?
(PG)
Staging laparotomy is not done nowadays after
CT has become part of the staging work up where
by most of the nodal status and disease process
can be ascertained. 40% of the patients require
chemotherapy because of the reasons mentioned
below and therefore, a staging laparotomy is
omitted.
• It has got significant morbidity in 10% of
patients.
• It is considered when the results are likely to
alter the treatment strategy (chemotherapy
vs radiation). If the chemotherapy will be
used regardless of the finding on laparotomy,
there is no need for staging laparotomy.
Hodgkin’s disease that is localized may be
curable by radiation therapy if all involved
nodes are included in the treatment field.
Non-Hodgkin’s lymphomas are usually treated
with chemotherapy because of wide-spread
nodal and extra-nodal involvement especially
of the bone marrow. Therefore, laparotomy is
unnecessary in NHL.
• Considered only in specialsituations ofstage IIa
or less in which mantle radiation is planned.
• In children, splenectomy will produce
overwhelming postsplenectomy sepsis(OPSI)—
0.1%/year
• In 20% of the cases, the stage is upstaged by
staging laparotomy and therefore, will require
chemotherapy
• About 20% of the patients will develop relapse
requiring chemotherapy.
Q 38. What are the important steps in staging
laparotomy? (PG)
In staging laparotomy the following procedures
are done:
• Splenectomy
• Wedge biopsy of liver
• Biopsy—nodes of the paraaortic, splenic hilar,
hepatic, portal, and iliac nodes—the suspicious
nodes are clipped
• Oophoropexy in women (childbearing age)
which will allow radiation therapy to be given to
the inverted ‘Y’ field which covers the iliac and
inguinal nodes without radiation damage to the
ovaries.
Q 39. Which are the nodal regions affected by
Hodgkin’s disease?
Mediastinal – 60%
Pure infradiaphragmatic – 3%
Extra nodal – 5 – 10%
Splenomegaly – 10%
Q 40. What are the etiological factors for Hodgkin’s
disease? (PG)
1. Siblings with Hodgkin’s disease
2. HLA antigens
3. Patients who have undergone tonsillectomy
4. Immunodeficiency states
5. Autoimmune disorders
6. Oncogenic viruses
7. Epstein-Barr virus(EBV)—Nuclearproteinin 40%
of Hodgkin’s
8. Lymphotropic viruses.
Q 41. What is the antigen in Hodgkin’s disease?
(PG)
It is CD 30 positive, which is a surface antigen seen
in Reed-Sternberg cells.
Other CD markers:
218
Clinical Surgery Pearls
• NK cell—CD 54
• Leukocyte antigen—CD 45
• Stem cells—CD 34
• T cells—CD 3, 4, 5, 15 and 30
• B cells—CD 19, 20, 21, 22
Rituximab is a Monoclonal antibody against CD 20.
Q 42. What is the stage of the disease in the given
case?
Stage III because of the infradiaphragmatic
involvement.
Q 43. What is early stage disease?
• Stage IA and IIA
• Nonbulky disease.
Q 44. What is bulky disease? (PG)
• 10 cm diameter mass or more
• Mediastinal disease with transverse diameter
exceeding 1/3rd of the transverse thoracic
diameter is defined as bulky disease.
Q 45. What is the treatment of Hodgkin’s disease?
The treatment is classified as:
• Radiotherapy—curative radiation therapy is
given to 3 major fields known as:
– Mantle
– Para-aortic
– Pelvic (inverted Y fields)
• The lungs, heart, larynx, kidneys, gonads and
iliac crest are protected by shields
• The dose ofradiotherapy is approximately 40-45
grey delivered at the rate of 10 Gy/week
• When used with chemotherapy the dose of
radiation is reduced.
Chemotherapy
Combined modality—Radiation and Chemotherapy
Q 46. What is the indication for radiotherapy?
Localized disease—I A and II A.
Q 47. What is the indication for chemotherapy?
Stages III and IV are generally treated with
combination chemotherapy.
Q 48. What is the management of B symptoms
of I and II?
Even if the disease seems to be localized, B symptoms
and unfavorable histology (mixed cellularity and
lymphocyte depletion), usually calls for the use
of chemotherapy with or without radiation. The
relapse rates are high after radiation therapy alone.
Q 49. What is Mantle radiation?
Irradiation of -
• Cervical
• Axillary
• Mediastinal
• Hilar lymph nodes.
Q 50. What is Subtotal Lymphoid Irradiation
(STLI)? (PG)
Irradiation of Mantle area and upper abdominal and
para-aortic and splenic bed nodes.
Q 51. What is Total Lymphoid Irradiation (TLI)?
(PG)
Irradiation of the pelvic field in addition to STLI is
given.
Q 52. What is the indication for chemotherapy for
early stage Hodgkin’s disease? (PG)
Chemotherapy is given to eradicate subclinical
disease outside the radiotherapy ports.
The ABVDregimen is used because ofthe better
toxicity profile and effectiveness.
Q 53. What is combined modality therapy?
(PG)
This is done to prevent relapse, where radiation is
combined with chemotherapy. The indications are:
• Unfavorable disease (Stage III and IV)
Lymphoma
219
• Unfavorable histology (mixed cellularity and
lymphocyte depletion type)
• Extensive splenic involvement
• Children who cannot tolerate full dose of
radiotherapy.
Q 54. What is the chemotherapeutic regime for
Hodgkin’s disease (HD)?
There are two regimes:
• ABVD regime
• MOPP regime.
Q 54. What is ABVD regime?
(6 – 8 cycles)
It is a widely used regimen for Hodgkin’s disease.
The drugs used are:
• Adriamycin
• Bleomycin
• Vinblastin
• Dacarbazine.
Q 56. Why ABVD is preferred over MOPP?
• Better disease free survival and over all survival
• Better toxicity profile.
Q 57. What is MOPP regime?
The drugs used in this regime for the treatment of
Hodgkin’s disease are:
• Nitrogen mustard
• Vincristine (Oncovin)
• Procarbazine
• Prednisolone.
Q 58. What is high dose chemotherapy? (PG)
Chemotherapeutic drugs are given in high doses
with stem celltransplant(Bone marrow transplant).
Q 59. What are the problems of chemotherapy?
• Infertility
• Second cancers—leukemia, solid tumors like
breast and thyroid
• Cardiopulmonary complications.
Q 60. What is radioimmunotherapy? (PG)
• Thisisusuallygivenforrelapseforwhich131I labeled
anti CD30 Monoclonal antibodies are used
• Dendritic cell vaccines against EB virus
• Antibodies against CD3, CD28, CD25 are also
available.
Q 61. What are the bad prognostic factors?
Bulky disease
Anemia
High ESR
Inflammatory signs
Inguinal node involvement
Tissue eosinophilia
High serum LDH
Pathological grade
Sex: Male
Age > 45
WBC > 15000/cumm
Serum albumin < 4 gm
Stage 4 disease
Lymphocyte count < 600/cumm
NON-HODGKIN’S LYMPHOMA
Q 62. What is the definition of NHL?
It is a heterogenous group of B and T cell
malignancies having diversity in — cellular origin,
morphology, cytogenetic abnormalities, response
to treatment and prognosis.
Q 63. What are the features of NHL?
These are neoplasms of the immune system usually
presenting as disseminated and extra-nodal disease
of the old age. The peculiarities are:
1. Multicentricity
2. Wide spreading
3. Showing malignant cell in the blood
4. Leukemic transformation may occur in 10–15%
of patients.
220
Clinical Surgery Pearls
Q 64. What are the clinical features of NHL?
1. Asymptomatic
2. B symptoms
3. Enlarged lymph nodes
4. Abdominal mass
5. GI symptoms—pain, vomiting, bleeding
6. Loss of weight.
Q 65. What are the predisposing factors?
(PG)
The following predisposing factors are attributed:
1. Immunosuppression
2. Autoimmune diseases
– Hashimoto’s disease
– Sjogren’s syndrome.
3. Infective agents
– EB virus – African Burkitt’s
– AIDS related
– Nasopharyngeal lymphoma
– Transplant lymphoma
– Lymphoma after infectious mononucleosis
– HTLV-I infection – (Human T cell Lymphotropic Virus)
– HTLV -II – T cell lymphoma and Leukemia
– H. pylori – Gastric lymphoma
– Hepatitis C virus – 8 and 6
– Human herpes virus
4. Prior chemotherapy
5. Prior radiotherapy.
Q 66. What are the congenital disorders having
increased incidence of NHL? (PG)
• Ataxia telangiectasia
• Wiskott-Aldrich syndrome
• Celiac disease.
Q 67. What are the core nodal regions?
They are as follows:
• Right cervical(includingcervical,supraclavicular,
occipital and preauricular lymph nodes)
• Left cervical nodes
• Right axillary
• Left axillary
• Right infraclavicular
• Left infraclavicular
• Mediastinal lymph nodes
• Hilar lymph nodes
• Para-aortic lymph nodes
• Mesenteric lymph nodes
• Right pelvic lymph nodes
• Left pelvic lymph nodes
• Right inguinofemoral lymph nodes
• Left inguinofemoral lymph nodes.
Q 68. Can NHL involve any other nodes other than
the core nodal regions?
Yes. NHL may involve the following nodes in
addition:
• Epitrochlear lymph nodes
• Popliteal lymph nodes
• Internal mammary lymph nodes
• Occipital lymph nodes
• Submental lymph nodes
• Preauricular lymph nodes
• Many other small nodal areas.
Q 69. What is the E designation for NHL?
For NHL the E designation should indicate the
presentation of lymphoma in extra nodal site
and the lack of E designation should indicate
lymphomas presenting in lymph nodes. For
example, lymphoma presenting in thyroid gland
with cervical lymph node involvement should be
staged as IIE. Lymphoma presenting only in cervical
node is Stage I.
Lymphoma
221
Q 70. What are the extra nodal sites?
Extra nodal sites
• Paranasal sinuses
• Thyroid
• GI tract
• Liver
• Testicles
• Skin
• Bone marrow
• Bone
• CNS
• Lung
• Gonads
• Kidneys
• Uterus
• Ocular adnexa.
Q 71. What are the classifications for NHL?
1. Rappaport
2. Working classification
– Low grade: B cell lymphomas
– In te rmedia te grade: B cell o r T cell
(lymphoblastic group)
– High grade.
3. REAL (Revised European - American Lymphoma)/
WHO classification
• B cell — precursor B cell cancers
—peripheral B cell neoplasms – Burkitt’s
• T cell and natural killer cells (NK)
– Precursor T-cell neoplasm
– Peripheral T-cell and NK cell neoplasm –
Mycosis fungoides
– Intestinal T-cell lymphoma.
4. Functional classification (for treatment
purposes).
• Indolent—smaller cells, differentiated cells
– Low grade, very difficult to cure
– Progress to more aggressive type
• Aggressive—larger cells, less differentiated
— Better chance for cure
• Highly aggressive.
Q 72. Since low grade lymphomas can progress
to aggressive type, what are the criterion for
suspecting a disease transformation? (PG)
1. Increased LDH
2. Rapid enlargement of the nodes
3. Constitutional symptoms
4. Extra nodal disease.
Q 73. What is Burkitt’s lymphoma?
It is a B-cell tumor.
Q 74. What is Mycosis fungoides?
It has a T cell and NK cell origin and will manifest
as skin lesion. Skin is followed by lungs and lymph
node involvement (Cezary syndrome—circulating
T and NK cells).
Q 75. What is the staging of NHL?
The Ann-Arbor classification is used for staging (see
Hodgkin’s disease).
Q 76. What is stage IV disease?
By convention, any involvement of the following
calls for classification as stage IV disease.
Stage IV disease
• Bone marrow
• Liver
• Pleura
• CSF.
Q 77. What are the investigations required for
diagnostic evaluation of NHL?
Read the chart for Hodgkin’s lymphoma.
Q 78. What is the treatment of NHL?
Chemotherapy is the primary modality of treatment
in NHL, because NHL spreads widely and there is
222
Clinical Surgery Pearls
early hematogenous spread. For localized disease
radiotherapy may be useful.
Indolent lymphoma—treatment
a. Localized—Radiotherapy
Disseminated—rarely curative
b. Palliation—watch and wait until they progress
to more aggressive type.
The quality of life is better here.
Aggressive
– Stage I and II—Radiation alone
– Stage III and IV—CHOP regimen
– High dose chemotherapy—with autologous
marrow transplantation.
Q 79. What is the chemotherapeutic regime for
NHL?
NHL is generally treated with CHOP regimen, which
is combination chemotherapy of the following
drugs.
• Cyclophosphamide
• Adriamycin (is designated H – Hydroxydaunorubicin or Doxorubicin)
• Oncovin
• Prednisolone.
Q 80. What is CD - 20? (PG)
It is a cell surface protein involved in the
development and differentiation of natural B cells.
Q 81. What is Rituximab? (PG)
It is a monoclonal antibody that binds to the B cell
surface antigen CD-20.The dose is 375 mg/m2
slow
IV infusion once weekly for 4 doses.
Q 82. What is the chemotherapeutic agent for CNS
lymphoma? (PG)
The CHOP therapy has poor penetration to the
blood brain barrier (BBB) and therefore it is
ineffective. It can be treated with whole brain
irradiation. Methotrexate is effective and it may
be given systemically or intrathecally.
Q 83. What is international prognostic index (IPI)
for NHL?
Five pretreatment characteristics were found to
be independent statistically significant factors for
prognosis.
International Prognostic Index
• Age > 60 years
• Ann-Arbor stage III or IV
• Increased LDH
• Reduced performance status (ECOG > 2)
• Extra nodal site-one or more.
Q 84. What are the extra nodal sites which are
more aggressive?
1. GIT
2. Nasopharynx
3. Testis.
Q 85. What are the lymphomas having predilection
for CNS metastasis? (PG)
• Testis
• Paranasal sinuses
• AIDS related.
Note: Prophylactic intrathecalmethotrexate is given
in such situations.
Q 86. What is the role of surgery in NHL?
1. For establishing the diagnosis
2. For resection of extra nodal GI lesions.
Q 87. What is the treatment of NHL of stomach
and small bowel?
It is controversial, whether to treat it with
chemotherapy or surgery. Resection is recommended because of the following reasons:
Lymphoma
223
• Risk of perforation
• Risk of fatal bleeding (with chemotherapy)
Stage 1 and 2 non bulky—H. pylori eradication
– if it disappears surveillance for three years.
Stage 1 and 2 bulky—Chemotherapy and
surveillance for three years.
Stage 3 and 4—Chemotherapy
Q 88. What is paraneoplastic syndrome? (PG)
Many tumors develop the ability to elaborate
hormones or cytokines that can have deleterious
consequences for the host. The effects may be
affecting a single organ system or systemic. The
common cancer sequelae like hypercoagulation,
cachexia, fever and anemia of chronic disease are
due to this syndrome.
16 Renal Swelling
Case
Case Capsule
A 55-year-old male patient presents with fever,
hematuria, flank pain and mass abdomen of 8
months duration. He also complains of loss of
weight. He noticed recently that his left side of the
scrotum and testes are hanging too low than what
it used to be. He is found to be hypertensive recently.
On examination his blood pressure is 166/110
mm of Hg. He is febrile and there is pitting edema of
both lower limbs. On examination of the abdomen,
distended subcutaneous veins are seen in the
anterior abdominal wall. The shape of the abdomen
is normal and it moves with respiration. On palpation
there is no local rise of temperature and tenderness.
There is a mass in the left lumbar region of about
15 × 12 cm size which moves with respiration (Fig.
16.1). The mass is firm in consistency and the surface
is smooth. All the borders of the mass are welldelineated. One can get above the swelling. The mass
is ballotable and bimanually palpable. Percussion
over the mass revealed that it is resonant. There is
no mass lesion on the right side. The supraclavicular
lymph nodes are not enlarged. Examination of
the genitalia revealed left sided varicocele. On
examination of the spine, there is no scoliosis. The
left renal angle is full and it is dull to percussion.
There is no bruit at the lumbar area adjacent to the
lumbar spine. Examination of the chest is normal.
There is no evidence of bony metastasis. (The mass
is intra-abdominal and retroperitoneal).
Fig. 16.1: Left lumbar mass
Renal Swelling
225
Read the checklist for abdomen.
Checklist for examination of suspected
renal swelling
1. Always check the blood pressure reading—
hypertension can be a cause or consequence of
renal disease (renal artery stenosis)—patient may
present with headache
2. Remember the triad of renal cell carcinoma—flank
pain, hematuria, and flank mass
3. Examine the genitalia for varicocele—tumor
thrombus in the renal vein
4. Examine for lower limb edema—tumor thrombus
in the inferior vena cava
5. Gross distension of the abdominal veins as a result
of venacaval obstruction Examine the contralateral
flank for bilateral renal swellings
6. Examine the renal angle—for fullness, tenderness
and dullness
7. Look for scoliosis—inflammatory conditions will
produce scoliosis with concavity towards the side
of the lesion
8. Auscultation for a bruit at the lumbar areas
adjacent to the lumbar spine at the level of L2
(renal artery stenosis)
9. Always examine the chest for pulmonary
metastasis
10. Always examine the bones for pain and
pathological fractures.
Q 1. What are the physical signs of an enlarged
kidney?
Physical signs of an enlarged kidney
1. It moves with respiration
2. It is resonant on percussion (because it is covered
by colon in front)
3. Fingers can be insinuated between the mass and
costal margin
4. Bimanual palpable
5. Ballotable.
Q 2. Why the kidney is moving up and down with
respiration?
Upper posterior aspect of the kidney is related to
the diaphragm (diaphragmatic area) and therefore
it will move up and down with respiration.
Q 3. What is Ballottement?
This sign is useful for the diagnosis of the following
conditions.
a. This is a sign used for the confirmation of
pregnancy of more than 3 months standing
b. For ballottement of kidneys
c. It is also used for mobile intraperitoneal fluid
filled swellings like ovarian cyst
d. Ballottement of swellings rising out of the pelvis
where one hand is laid over the hypogastrium
and the other inserted to vagina or rectum.
Q 4. What is renal ballottement?
The patient is supine and one hand of the examiner
is laid flat upon the abdomen, so that the greater
part of the flexor surfaces of the fingers overlies the
swelling. This hand is called the watching hand.
The slightly flexed fingers of the other hand are
insinuated behind the loin so that they contact
the area lateral to the sacrospinalis muscle. This
hand is the displacing hand. Short, quick, forward
thrusts are made by the displacing hand (posterior).
If these movements impart a bouncing sensation
to the anteriorly placed watching hands, the sign
is positive.
Q 5. What is the significance of a bimanually
palpable swelling?
It is a palpation done by both hands, right
hand placed anteriorly and the left hand placed
posteriorly. All the big abdominal masses in the loin
are bimanually palpable. Therefore, it is important to
decide with which hand the mass is better felt. If it
226
Clinical Surgery Pearls
is better felt with the anterior hand, it is likely to be
arising from colon or one of the viscera. If it is better
felt with the posterior hand, it is likely to be kidney.
Q 6. What is the significance of scoliosis of lumbar
spine in a renal mass?
Scoliosis of lumbar spine with concavity towards
the affected side is a constant sign in inflammatory
conditions of the kidney like perinephric abscess.
Bending the trunk away from the side of lesion is
likely to cause more pain in such conditions.
Q 7. What is renal angle? What is the significance
of examination of renal angle?
It is the angle formed by the lateral border of the
sacrospinalis muscle and the last rib. The renal
angle is normally resonant to percussion because
of the colonic flexure in front of the kidneys. The
renal angle is dull, when there is enlargement of
the kidney.
The renal angle is checked for:
Fullness—when there is mass lesion/enlargement.
Tenderness—in inflammatory pathology.
Dullness—when there is mass lesion/enlargement.
Q 8. What is Murphy’s kidney punch? (The renal
angle test)
The patient sits up and folds his arms in front of
him. The thumb is then placed under the 12th rib
to the lateral side of the sacrospinalis muscle. Sharp
and jabbing movements are made with the thumb.
Initially the movements are very gentle and if the
patient is not experiencing pain, the strength is
increased. This test is useful for demonstration of
deep-seated tenderness.
Q 9. What is renal pain?
It is a persistent fixed ache situated mainly in the
costovertebral angle. If there is significant renal
enlargement, stretching of the peritoneum may
localize the pain more anteriorly to the upper and
outer quadrants of the abdomen. The pain is not
strictly lumbar.
Q 10. What is the triad of renal cell carcinoma (RCC)?
Triad of renal cell carcinoma
Hematuria—40%
Flank pain—30%
Palpable flank mass—20%
Note: Only 10% of patients have all these symptoms.
Q 11. What is the most probable diagnosis in this
case?
The first diagnosis will be a renal tumor.
Q 12. What are the differential diagnoses?
Clinically carcinoma of the descending colon can
have a clinical presentation like this.
The points against colon are:
• Ballottementis positive thatisin favor of kidney
• Renal angle is obliterated and dull
• There are no bowel symptoms
• In colon, the swelling will be better felt with
the anterior hand in bimanual palpation and
ballottement will be negative.
The other differential diagnoses of a renal mass are:
Differential diagnoses of renal mass other than colon
1. Hydronephrosis
2. Adult polycystic kidney disease
3. Tuberculosis
4. Adrenal tumors
5. Retroperitoneal tumors
6. Angiomyolipoma
7. Benign renal tumors
8. Xanthogranulomatous pyelonephrosis
9. Solitary cyst of the kidney
10. Abscess (Perinephric).
Renal Swelling
227
Q 13. What is the definition of hydronephrosis?
Aseptic dilatation of pelvicalyceal system because
of partial or intermittent obstruction.
Q 14. What are the causes for unilateral
hydronephrosis?
Causes for unilateral hydronephrosis
1. Pelviureteric obstruction—
a. Congenital pelvi-ureteric junction stenosis
b. Stones in the renal pelvis
c. Tumors in the renal pelvis
d. Pressure from aberrant arteries
2. Ureteric obstruction
a. Stones
b. Tumor infiltration of the ureter—carcinoma
colon, rectum, cervix and prostate
c. Tumors of the ureter
d. Bladder tumors
e. Ureterocele.
Q 15. What are the causes for bilateral hydronephrosis?
Causes for bilateral hydronephrosis
• Prostatic enlargement—benign or malignant
• Urethral strictures and valves
• Carcinoma of the bladder
• Retroperitoneal fibrosis
• Phimosis
Q 16. What is the most common tumor in this
age group?
Renal cell carcinoma (RCC) is the correct terminology.
The older names are:
• Grawitz’s tumor
• Hypernephroma
• Adenocarcinoma
• Clear cell tumor
The most common of the neoplasm of the kidney is RCC.
Q 17. Why is it called hypernephroma?
Hypernephroma means above the kidney. Grawitz
initially thought that they arose from adrenal rests
within the kidneys. Later on, Lubarsch stated that
these tumors are definitely adrenal in origin leading
to the term hypernephroma.
The tumors usually occupy the poles most
commonly the upper pole. The tumors of the hilum
are less common.
Q 18. Why is it called the ‘golden tumor’ and what
is the cut section appearance?
The tumor is yellowish because of the abundance of
lipids including cholesterol. It is also rich in glycogen
and exhibits areas of necrosis and hemorrhage.
Cut section appearance:
The tumors are irregular in shape with central
hemorrhage and necrosis. It is semitransparent.
The tumor is often divided into lobules by fibrous
septa, some of which are cystic.
Q 19. What is the histology of RCC?
Histologically it is an adenocarcinoma containing
clear, granular and spindle cells in varying
proportions.
Q 20. What are the pathological types of RCC?
• Clear cell
• Granular cell
• Spindle cell
• Sarcomatoid
• Papillary
• Chromophilic.
Q 21. What are the methods of spread of RCC?
1. Local
2. Lymphatic spread—lymph nodes of hilum and
later on to the para-aortic nodes.
3. Tumor thrombus into the veins—renal vein,
inferior vena cava and then up to the right heart—
228
Clinical Surgery Pearls
pieces of growth may end up in the lungs where
they grow to form cannon ball secondary deposits.
4. Metastases to bone—they are highly vascular
and may pulsate (pulsatile bony metastasis DD
follicular carcinoma thyroid metastasis).
Q 22. What is the cause for hypertension in renal
tumors?
The renal cell carcinoma produces renin and thus
causes hypertension.
Q 23. What is the cause for erythrocytosis in renal
cell carcinoma (RCC)?
About 60% of the tumors will produce raised level
of erythropoietin. This will result in erythrocytosis
(not polycythemia).
Q 24. What is paraneoplastic syndrome?
Nonendocrine tumor producing ectopic hormone
inappropriate for the tissue of origin.
Q 25. What are the paraneoplastic syndromes
produced by renal cell carcinoma (RCC)? (PG)
1. Hypertension
2. Parathyroid hormone like substances—Hypercalcemia
3. Adrenocorticotropic hormone—Cushing
4. Human chorionotropic hormone
5. Kinin substances—fever (renal tumors may present as
pyrexia of unknown origin). Persistence of fever after
nephrectomy suggests the presence of metastasis
6. Thrombocytosis
7. Anemia
8. Erythrocytosis
9. Coagulopathy
10. Vasculopathy
11. Amyloidosis
12. Nephrotic syndrome
13. Stauffer’s syndrome (Hepatopathy)
14. Polymyalgia rheumatica
15. Cachexia
16. Skin rash.
Q 26. What is Stauffer’s syndrome? (PG)
It is a nonmetastatic liver dysfunction seen in cases
of hypernephroma.
Q 27. What is the importance of genitalia
examination in cases of renal tumors?
Renal carcinoma has a predilection for producing
occlusive thrombi in the renal vein and the inferior
vena cava. When the left renal vein is occluded it will
produce acute varicocele on the left side.
Q 28. Why varicocele is seen only on left side in
case of renal tumors?
The left renal vein is the vein of three paired organs
namely—the kidneys, the adrenal and the testis.
The right testicular vein joins the inferior vena cava
directly instead of the renal vein. On the left side
the left testicular vein joins the renal vein at right
angles. When there is tumor thrombus in the left
renal vein, the resultant pressure is transmitted to
the left testicular vein resulting in varicocele.
Q 29. What is the cause for lower limb edema in
renal tumors?
As mentioned earlier tumor thrombus will occlude
the inferior vena cava and manifest as lower limb
edema.
Q 30. What are the ectopic hormones produced
by RCC? (PG)
1. Parathyroid hormone like substances
2. Adrenocorticotropic hormone
3. Human chorionotropic hormone
4. Kinin substances.
Q 31. What are the causes for hematuria?
Causes for hematuria
Site Cause
Urethra Trauma
Contd...
Renal Swelling
229
Urethritis
Stricture
Stone
Carcinoma of the urothelium
Prostate Benign prostatic hyperplasia (BPH
Carcinoma of the prostate
Prostatitis
Bladder Cystitis
Carcinoma
Stone
Trauma
Schistosomiasis
Ureteric Stone
Carcinoma of the urothelium
Renal Carcinoma of the kidney
Stone
Polycystic kidney
Tuberculosis
Carcinoma of the renal pelvis
Trauma
Glomerulonephritis
Note: Frank hematuria indicates a urological
malignancy until proven otherwise.
Q 32. What is clot colic?
When the patient is having hematuria, the clot will
obstruct the ureter and will present with clinical
features of ureteric colic.
Q 33. What are the investigations for this patient?
Investigations can be classified as:
• Investigations for diagnosis
• General investigations
• Staging investigations.
General Investigations
1. Urine analysis—may reveal hematuria
2. ESR – may be increased but nonspecific
3. Hematocrit—elevated in RCC
4. Hb—anemia is present in RCC—with or without
hematuria (anemia unrelated to blood loss occur
in 20-40% of patients
5. Serum calcium—elevated in RCC
6. Alkaline phosphatase—increased.
Investigations for Diagnosis and Staging
1. X-ray chest—reveal ‘cannon balls’—it is the
metastatic lesions in the lungs from RCC.
2. Plain X-ray abdomen—Reveal calcified renal
mass and distortion of renal outline—only
20% contain demonstrable calcification (20%
of the masses with peripheral calcification are
malignant and 80% with central calcification
are malignant).
3. IVU—(initial technique for workup of
hematuria) the calyces may be stretched and
distorted. The typical ‘spider leg’ deformity
occupying the upper or lower pole (splaying of
calyceal system) is seen. It is important to know
the function of the contralateral kidney.
4. Ultrasonography—Can define solid and cystic
lesions. The ultrasound will reveal solid mass
within the renal parenchyma in RCC. It can also
identify venacaval tumor thrombus.
5. CT scan and CT urography (contrast enhanced)—
it is the diagnostic procedure of choice when
a solid renal mass is identified in ultrasound
(delineates RCC in 95% of cases) RCC will show
heterogeneous enhancing lesion (in 80%).
In addition to diagnosis, CT is also useful for:
• Local staging
• Involvement of perinephric fat
• Hilar lymph nodes
• Tumor thrombus in renal vein and IVC.
Contd...
230
Clinical Surgery Pearls
6. MRI — It is the investigation of choice for renal
vein and venacaval thrombi. MR angiography
is useful for mapping the blood supply of the
tumor and the relationship of the tumor to
adjacent structures.
7. Isotope bone scanning—It is indicated in patients
with bone pain, elevated alkaline phosphatase
and known metastasis cases.
8. Renal angiography—It is not done nowadays
after the CT became available. The practice of
preoperative embolization has also waned.
Q 34. What are the risk factors for RCC? (PG)
• Cigarette smoking
• Coffee drinking
• Cadmium exposure
• Von Hippel-Lindau disease (Cerebellar hemangioblastoma, retinal angiomatosis, bilateral renal cell
carcinoma)
• Adult polycystic kidney disease
• Acquiredrenalcysticdiseaseinendstagerenaldisease.
Q 35. What is the tumor suppressor gene in Von
Hippel-Lindau renal cancer? (PG)
Suppressor gene on 3p
Q 36. What is Robson’s staging?
Stage 1 Tumor confined within the renal
parenchyma
Stage 2 Extracapsular extensions into the
perinephric fat or the adrenal but within
Gerota’s fascia
Stage 3 Spread to the regional nodes and
lymphatics within the Gerota’s layer and
or tumor thrombus invasion of the wall of
the renal vein or IVC
Stage 4 Adjoining organ invasion—colon,
posterior muscle wall or distant metastasis.
Q 37. What is the TNM Staging as per AJCC 7th
edition? (PG)
Primary Tumor (T)
TX Primary tumor cannot be assessed
T0 No evidence of primary tumor
T1 Tumor 7 cm or less in greatest dimension,
limited to the kidney
T1a Tumor 4 cm or less in greatest dimension,
limited to the kidney
T1b Tumor more than 4 cm but not more than
7 cm in greatest dimension limited to the
kidney
T2 Tumor more than 7 cm in greatest dimension,
limited to the kidney
T2a Tumor more than 7 cm but less than or equal
to 10cm in greatest dimension, limited to the
kidney
T2b Tumor more than 10 cm, limited to the kidney
T3 Tumor extends into major veins or perinephric
tissues but not into the ipsilateral adrenal
glands and not beyond Gerota’s fascia
T3a Tumor grossly extends into the renal vein or
its segmental (muscle containing) branches,
or tumor invades perirenal and/or renal sinus
fat but not beyond Gerota’s fascia
T3b Tumor grossly extends into the vena cava
below the diaphragm
T3c Tumor grossly extends into the vena cava
above the diaphragm or invades the wall of
the vena cava
T4 Tumor invades beyond Gerota’s fascia
(including contiguous extension into the
ipsilateral adrenal gland).
Regional Lymph Node (N)
NX Regional lymph nodes cannot be assessed
N0 No regional lymph node metastasis
N1 Metastasis in regional lymph node (s)
Renal Swelling
231
Distant Metastasis (M)
M0 No distant metastasis
M1 Distant metastasis
Anatomic stage/prognostic groups
Renal cell carcinoma
Stage T N M
I T1 N0 M0
II T2 N0 M0
III T1 or T2 N1 M0
T3 N0 or N1 M0
IV T4 Any N M0
Any T Any N M1
Q 38. This patient is having stage II RCC. What is
the management?
Stage I, II and IIIA are best treated by radical
nephrectomy.
Q 39. What is radical nephrectomy?
This is an en-block removal of the following
structures.
• Kidney
• Surrounding Gerota’s fascia (including the
ipsilateral adrenal)
• Renal hilar lymph nodes
• Proximal half of the ureter.
Q 40. What are the approaches for nephrectomy?
(PG)
The kidney may be approached by the following
routes:
1. Loin incisions (Retroperitoneal)
– Transcostal starts from the angle of 12th rib
and goes for 8–15 cm beyond the tip of the
12th rib
– Subcostal – from the renal angle downwards
and forwards between the12th rib and iliac
crest and stops 4–5 cm above the anterior
superior iliac spine
– Supracostal – between the 11th and 12th rib
– Lumbotomy – the incision starts from
the upper border of the 12th rib vertically
downwards along the lateral border of the
erector spinae and then forwards to the iliac
crest for 10 cm
– Nagamatsu is used for better renal artery
control—this incision starts at the angle of
11th rib down to the 12th rib angle and then
along the 12th rib to the umbilicus. This is an
extrapleural retroperitoneal approach.
2. Abdominal (Transperitoneal) — this approach
has as the advantage that the renal pedicle and
inferior vena cava can be widely exposed.
– Midline
– Paramedian
– Transverse abdominal (for bilateral renal
tumors).
3. Thoracoabdominal
For lesions of the upper pole, and lesions
invading the inferior vena cava.
Q 41. What are the precautions to be taken in
radical nephrectomy? (PG)
• The vascular pedicle should ligated before the
kidney is mobilized (malignant cells will be
released into the circulation)
• Initially the renal artery is ligated in continuity
(massive bleeding during mobilization is less
likely)
• Palpate the renal vein gently to rule out tumor
thrombus (renal vein extension may embolize to
the pulmonary circulation during nephrectomy).
If it is empty, it is divided between ligatures
232
Clinical Surgery Pearls
• The renal artery is then divided and the kidney
mobilized
• Theureteristhentraceddownwards anddivided
and ligated at appropriate level.
Q 42. If the renal vein or inferior vena cava is
invaded what is the procedure? (PG)
• The surgeon must obtain control of the cava
above and below
• Cardiac bypass may be required, if there is
extension into the thorax (Get the cardiac team)
and the tumor thrombus may be removed from
the right side of the heart.
Q 43. Is there any role for partial nephrectomy
(nephrone sparing surgery)?
Yes. Partial nephrectomy is recommended in the
following situations:
• Patients with tumors in solitary kidney
• Those with diabetes mellitus
• Patients with renal insufficiency
• Tumors under 4 cm size (Even with normal
opposite kidney)
(In patients with negative surgical margins the
prognosis will be the same as that of the radical
nephrectomy).
Q 44. What is the role of laparoscopic nephrectomy?
It is becoming the gold standard in institutions with
appropriate expertise. Laparoscopic radical or partial
nephrectomy has been advocated as a method equal
to the open approach with the following advantages:
• Less blood loss
• Shorter hospitalization
• Less pain
• Earlier return to normal activity.
Q 45. What is the treatment for a patient with
solitary pulmonary metastasis? (PG)
Joint surgical removal of both the primary lesion
and metastatic lesion is recommended.
Q 46. Is there any role for preoperative arterial
embolization? (PG)
This will not improve survival rate. It is recommended
as a single treatment in symptomatic patients with
nonresectable primary lesions.
Q 47. What is the role of radiotherapy?
It is useful only for the treatment of symptomatic
bone metastases.
Q 48. What are the chemotherapeutic agents used
in RCC? (PG)
Vinblastine
Medroxy progesterone—for metastatic RCC.
Q 49. What is the role of immunotherapy? (PG)
• Interferon alpha—15 – 20% response rate
• IL-2 (interleukin)
• Combination of interferon alpha and IL-2.
Q 50. What is the prognosis of RCC? (PG)
Removal of even the largest neoplasm may cure
the patient. In operable cases, 70% are well after 3
years and 60% after 5 years.
Q 51. What are the bad prognostic factors? (PG)
• Tumor invasion beyond the capsule
• Macroscopic involvement of renal vein and IVC
• Lymph node involvement.
Q 52. What is congenital polycystic kidney disease?
It is a hereditary condition transmitted by autosomal
dominant trait affecting both kidneys (one kidney
may contain larger cysts than the contralateral).
The disease manifests in 2nd or 3rd decade of life
and usually does not manifest before the age of 30
years. The etiology is uncertain. In 18% of cases,
there is associated congenital cystic liver disease.
The pancreas and lungs are occasionally affected.
The disease is more common in women. The most
important theory is failure of fusion between the
secretory part and collecting system during the
Renal Swelling
233
development (the secretory part is developed from
the meta-nephrogenic tissue cap, and collecting
part from the ureteric bud).
Q 53. What is the genetic abnormality in polycystic
kidney disease? (PG)
There are two types:
1. Autosomal recessive polycystic kidney disease
(ARPKD)—Previously called infantile. In this
condition small cysts arise from collecting ducts
resulting in bilateral symmetrical enlargement.
Occurs in 1/14000 births and may be detected in
utero. Infants usually die of respiratory failure.
2. Autosomal dominant polycystic kidney disease
(ADPKD)—The gene located on chromosome 16p.
Another gene responsible is PKD 2gene located in
chromosome 4q 21-23. ADPKD occurs in 1/1000
individuals.
Q 54. What is the median age for end stage renal
disease?
In PKD1—54 years
In PKD2—74 years
Q 55. What are the manifestations of polycystic
disease?
Manifestations of polycystic disease of kidney
• Uppe r abdominal mass (bilateral knobby
enlargement)
• Hypertension—present in 75% of patients above
20 years
• Loin pain—becuase of the weight of the organ or
stretching of the capsule
• Uremia—large volumes of urine of low specific
gravity (10:10 or less)—chronic renal failure
(headache, drowsiness, vomiting and anorexia)
• Infection—pyelonephritis
• Hematuria—rupture of cyst into the renal pelvis.
Q 56. What is the gross appearance of polycystic
disease?
The gross appearance is that of a collection of
bubbles beneath the renal capsule. The renal
parenchyma is riddled with cysts of varying sizes
containing clear fluid, thick brown material or blood.
Q 57. What are the investigations for polycystic
disease of the kidney?
• IVU—Enlarged kidneys with marked elongation
of the calyces which are compressed by the cysts.
The spider leg deformity or bell-like appearance
• Ultrasound multiple cystsin both kidneys,some
times in liver and other organs
• CT.
Q 58. What are the treatment options for polycystic
disease of the kidney?
• Medical—Low protein diet, treatment of
infection, anemia and renal failure
• Dialysis
• Renal transplantation is the ideal treatment
• Rovsing’soperation—(deroofingthecysts)—This
is a palliative procedure for relieving the pressure
on the parenchyma, and for reducing the pain.
The open operation is not done nowaday. If
required, it can be done laparoscopically.
Q 59. What is Dietl’s crisis?
This is seen in intermittent hydronephrosis. After
an attack of acute renal pain, swelling appears in
the loin. After a few hours following the passage
of a large volume of urine, the pain is relieved and
the swelling disappears. This is called Dietl’s crisis.
Causes for disappearing mass:
1. Dietl’s crisis
2. Intussusception
3. Choledochal cyst
234
Clinical Surgery Pearls
4. Communicating pseudocyst
5. Worm mass
6. Fecal impaction.
Q 60. What are the clinical features of
hydronephrosis due to idiopathic pelviureteric
junction obstruction?
• Renal colic
• Renal mass
• Intermittent hydronephrosis.
Q 61. What is the IVU finding in hydronephrosis?
• The minor calyces lose their normal cupping
• They become flattened
• Finally the classical clubbing is seen
• In very advanced cases the thin rim of poorly
functioning renal parenchyma may give a faint
nephrogram around the dilated calyces—the
soap bubble appearance.
Q 62. What is the most helpful test to establish the
dilatation because of obstruction?
Isotope renography using DTPA (Diethylene
Triamine Penta Acetic acid) 99Tc – DTPA is used for
this investigation.
Q 63. What is the principle behind 99Tc - DTPA?
The DTPA is injected intravenously, which is filtered
by the glomeruli and not absorbed. When the DTPA
is labeled with 99Tc it will emit gamma rays. The
passage of this technetium labeled DTPA through
the kidneys can be tracked using a gamma camera.
When the ureter is obstructed, the marker is trapped
in the renal pelvis and will not be washed out, even
if the flow of urine is increased by administering
frusemide.
Q 64. What is Whitaker test?
A percutaneous puncture of the kidney is made
through the loin and fluid is infused at a constant
rate with monitoring of intrapelvic pressure. An
abnormal rise in pressure confirms obstruction. This
test is done occasionally.
Q 65. What is RGP (Retrograde pyelogram)?
After cystoscopy, the affected ureter is cannulated
and dye is injected, which will reveal the anatomy
of obstruction. This is done when the kidneys are
not functioning in IVU in order to get an idea about
the site of obstruction before surgery.
Q 66. What are the indications for surgery in
idiopathic pelviureteric junction obstruction
(PUJ)?
• Increasing hydronephrosis
• Bouts of renal pain
• Parenchymal damage
• Infection.
Q 67. What are the operations available for PUJ?
The operations are classified into dismembered
Pyeloplasty and nondismembered pyeloplasty.
The example of nondismembered is Foley’s VY
– Pyeloplasty.
Anderson-Hynes is dismembered pyeloplasty, is
the most commonly performed operation (it can be
done laparoscopically or by open method).
Endoscopic pyelolysis—The disruption of the
pelviureteric junction is done by specially designed
balloon passed up the ureter under radiographic
control.
Q 68. What is the indication for nephrectomy in
hydronephrosis?
Conservation of renal parenchyma is the aim.
Nephrectomy is considered only when the renal
parenchyma has been largely destroyed. If renal
function is adequate (> 10% of total renal function
surgical repair of the stenosis is done.
17 Pseudocyst of Pancreas
Case
Case Capsule
A 45-year-old male patient presents with history of
upper abdominal pain, epigastric fullness, nausea
and occasional vomiting of 6 weeks duration. He
is a chronic alcoholic and gives history of hospital
admission for acute abdominal pain two months
back. For the last one week he gives history of
severe pain over the epigastric region with mild
fever and rigors. There is no history of trauma.
On general examination, there is mild icterus
and pallor. On abdominal examination the upper
abdomen shows fullness. The abdomen moves
with respiration and the umbilicus is normal. There
are no dilated veins seen in the abdominal wall. On
palpation of the abdomen there is a firm, tender
mass of 20 × 16 cm size (20 cm horizontal and 16
cm vertical) in the epigastrium extending to both
hypochondriums. The lower border of the swelling
is indistinct. The upper limit is not palpable. On
both sides the mass goes beneath the costal margin.
It does not move with respiration and there is
no intrinsic mobility. The surface of the swelling
is smooth. The mass is resonant to percussion.
The plane of the swelling is intra-abdominal and
retroperitoneal. The rest of the abdomen is normal.
There is no free fluid demonstrated and normal
bowel sounds are heard. Digital rectal examination
revealed no abnormality. The hernial orifices and
genitalia are normal. The left supraclavicular nodes
are not enlarged. The renal angles are normal.
Read the checklist for abdominal examination
Checklist for history in the case of
pseudocyst examination
• Historyof acute abdominalpainsuggestiveof acute
pancreatitis
• History of trauma
• History of chronic abdominal pain
• History of alcoholism
• History of jaundice—because of pressure from
pseudocyst.
Q 1. What are the physical features of pseudocyst
of pancreas?
Physical features of pseudocyst of pancreas
1. Epigastric mass with indistinct lower edge
2. The upper limit may or may not be palpable
3. It is resonant to percussion (because of the
overlying stomach)
4. There is no movement with respiration (minimal
movement may be there)
5. The mass will be firm or soft but it is not possible to
elicit fluctuation or fluid thrill
6. The mass may be tender.
236
Clinical Surgery Pearls
Q 2. What is pseudocyst?
This is a collection of pancreatic juice enclosed in
a wall of fibrous or granulation tissue that arises
following an attack of acute pancreatitis (old
definition is collection of fluid in the lesser sac).
Q 3. Why it is called pseudocyst?
It denotes absence of an epithelial lining. The true
cyst is lined by epithelium.
Q 4. What is the time gap between the attack of
acute pancreatitis and pseudocyst?
Usually it is four weeks.
Q 5. What are the types of pseudocyst?
The pseudocysts may be:
Acute pseudocyst or Chronic pseudocyst.
Another classification is
• Postnecrotic: Following an attack of necrotizing
pancreatitis (Confined to the lesser sac or into
the retroperitoneal space or to the mesentery
of small or large bowel)
• Peripancreatic: Associated with chronic
pancreatitis
• Intrapancreatic cyst: In advanced chronic
pancreatitis(majority intheheadofthepancreas).
Q 6. What is acute pseudocyst?
It is a fluid collection arising in association with an
episode of acute pancreatitis of > 4 weeks duration
and surrounded by well-defined wall of granulation
or fibrous tissue.
Q 7. What constitutes the fibrous tissue in the
wall of the cyst?
It is constituted by the inflammatory fibrosis of the
following:
• Peritoneum
• Mesentery
• Serous membrane.
Q 8. What are the locations of the pseudocyst?
• Lesser sac
• Neck
• Mediastinum
• Pelvis
Q 9. What is the incidence of acute pseudocyst?
It develops in about 2% of cases of acute pancreatitis.
Q 10. Can you get multiple pseudocysts?
Yes. The cysts are single in 85% cases and multiple
in the remainder.
Q 11. What is chronic pseudocyst?
Chronic pseudocyst is a collection with a welldefined wall that arises in a patient with chronic
pancreatitis, without antecedent episode of acute
pancreatitis. It may also occur in trauma victims
(after a blow) and alcoholics. The mechanism
consists of ductal obstruction and formation of a
retention cyst that loses its epithelial lining as it
goes beyond the confines of the gland. It may also
occur sometimes as iatrogenic after splenectomy.
Q 12. What is pancreatic abscess?
It is a circumscribed peripancreatic collection of pus
occurring late (more than 4 weeks) after the onset
of acute pancreatitis. Infected collections identified
earlier are classified as either infected acute fluid
collection or infected pancreatic necrosis.
Q 13. What is the difference between pseudocyst
and acute fluid collection?
The acute fluid collection occurs early in the course
of acute pancreatitis (less than 4 weeks) and is
lacking a wall of fibrous or granulation tissue and is
located in or near the pancreas (in pseudocyst there
is a wall of fibrous or granulation tissue).
Q 14. What is the nature of fluid in acute pseudocyst?
It is a collection enzyme rich pancreatic juice and
may contain small amounts of necrotic debris.
Pseudocyst of Pancreas
237
Q 15. What are the investigations for the diagnosis
of pseudocyst?
• Serum amylase—elevated (ifthe serum amylase
remains elevated for 3 weeks, about half will
have pseudocyst).
• Leukocytosis—(about 50% of patients).
• Bilirubin—elevated (suggestive of biliary
obstruction).
• CT scan is the diagnostic study of choice (the
size, shape of the cyst and its relationship to
other viscera can be seen).
Acute cysts are irregular in shape, chronic cysts
are circular.
An enlarged pancreatic duc t may be
demonstrated in chronic pancreatitis.
A dilated CBD would suggest biliary obstruction
either from the cyst or as a result of pancreatitis.
• Ultrasound—to follow changes in size of acute
pseudocyst and to study the gallbladder
• ERCP—not done routinely (If CT shows ductal
abnormalities and if LFT is abnormal)
• Upper GI series—to look for site of gastric or
duodenal obstruction. The cyst will push the
stomach wall anteriorly (the retrogastric space
will be increased).
Q 16. What is the role of ERCP in pseudocyst?
The ERCP will reveal the communication of the
cyst to the pancreatic duct. Based on this, the
pseudocysts are classified as—
• Communicating—communicating to the
pancreatic duct
• Noncommunicating.
Q 18. What are the differential diagnoses in
pseudocyst?
Differential diagnoses of pseudocyst of pancreas:
• Pancreatic abscess
• Pancreatic carcinoma (if gallbladderis palpable)
• Neoplastic cyst—cystadenoma or cystadenocarcinoma (about 5% of all cases of cystic
pancreatic masses)
• Other epigastric masses.
Q 18. What are the complications of pseudocyst?
The complications are—
1. Pancreatic pseudocyst hemorrhage—resulting
from autodigestion of the pancreas leading
to erosion of splenic, gastroduodenal, or
pancreaticoduodenal artery. This will result in
false aneurysm of the artery in the cyst wall.
The clinical presentations of hemorrhage in
the cyst are:
• Increasing epigastric pain
• Increase in the size of abdominal mass
• Shock
2. Hematemesis and melena—cyst eroding into
the stomach
3. Rupture of the cyst into the peritoneal cavity—
peritonitis and shock—emergency surgery with
irrigation of the peritoneal cavity and drainage
for the pseudocyst.
4. Infection—high fever, chills and leukocytosis
(percutaneous drainage or internal drainage is
the treatment).
Q 19. What are the indications for intervention in
pseudocyst?
Indications for intervention in pseudocyst
• Persisting pain
• Pressure effects caused by increasing size
• Cysts of > 6 cm size
• Cysts of > 6 weeks duration.
Q 20. Why the procedure is done after 6 weeks?
The cyst wall is mature enough only after 6 weeks
to hold sutures for anastomosis of the gut.
238
Clinical Surgery Pearls
Q 21. Why 6 cm size is taken as cut off for
treatment?
Thechanceforspontaneousresolutionistherein40%
of cases if the cysts are smaller and therefore expectant
management is recommended in smaller cyst.
Q 22. What is the cause for jaundice in a patient
with pseudocyst?
It is usually caused by pressure from the cyst on the
bile duct—Wadsworth syndrome.
Q 23. What are the therapeutic options for the
management of pseudocyst?
See the algorithm for the management of
pseudocyst (Flow chart 17.1).
Q 24. What are the internal drainage procedures
available for pseudocyst?
The internal drainage may be:
• Endoscopic—endoscopic cystogastrostomy or
cystojejunostomy
• Laparoscopic
• Open.
Q 25. What are the viscera to which internal
drainage procedures are carried out?
• Cys togas t ros tomy— technically simpler
(Recurrence and GI hemorrhage occur after
this procedure)
• Cystojejunostomy (Roux-en-Y)—is the most
versatile
• Cystoduodenostomy—risk of biliary injury.
Q 26. What is the prerequisite for the internal
drainage?
Cyst wall should be sufficiently mature for
anastomosis (usually 4–6 weeks).
Q 27. What is external drainage?
The external drainage is done when the wall
surrounding the fluid collection is too fragile for
internal drainage. It can be done under sonological
guidance. This is also called percutaneous catheter
drainage.
Q 28. What is the incidence of recurrence of
pseudocyst after catheter drainage? (PG)
The recurrence is 4 times greater after external
drainage than after internal drainage.
Q 29. What are indications for external drainage
(nonsurgical drainage)? (PG)
• Critically ill patients
• Infected pseudocyst
• Uncomplicated pseudocyst
• To shrink a huge pseudocyst occupying half of
the abdominal cavity.
Q 30. What is the complication of external
drainage? (PG)
Pancreaticocutaneousfistula in 20–30%of patients.
Q 31. Is there any other method of external
drainage? (PG)
A percutaneous drainage where a catheter is passed
through the anterior abdominal wall, the anterior wall
of the stomach and through the posterior stomach into
the cyst. After several weeks the catheter is removed.
Q 32. What are the essential steps of cystogastrostomy?
• Upper midline incision
• Anterior gastrotomy (longitudinal incision in the
anterior wall of stomach)
• Identify an area where the cyst wall is maximum
bulging to the lumen of the stomach
• A 4 cm longitudinal window is created in the
posterior wall along with the cyst wall (evacuate
the contents of the cyst)
• A fullthickness mattresssuture is used to suture
the edge of the posterior gastrotomy and cyst
wall together
Pseudocyst of Pancreas
239
Flow chart 17.1: Management of pseudocyst of pancreas
240
Clinical Surgery Pearls
• The anterior gastrotomy is closed
• The abdomen is closed.
Q 33. What are the important things to be done
with the pseudocyst during surgery? (PG)
Aspirate the cyst fluid and send for culture and
sensitivity.
Send the cyst fluid for CEA (> 400 ng/mL
suggestive of mucinous neoplasm) and amylase
estimation.
Take biopsy from the cyst wall (this will rule out
a cystic tumor).
Q 34. What will happen to the passage of food
after cystogastrostomy? (PG)
Surprisingly the food will not go to the cyst cavity
and the cystogastrostomy will get obliterated
within a few weeks and heal in due course of time.
Q 35. What is the recurrence rate for pancreatic
pseudocyst? (PG)
Its 10% (Recurrence is more frequent after external
drainage).
Q 36. What is the postoperative complication of
cystogastrostomy? (PG)
Hemorrhage occurs rarely.
Q 37. What is excision for pseudocyst? (PG)
This is the most definitive treatment. Usually this is
done for chronic pseudocysts in the tail of gland.
This is usually recommended for cysts following
trauma.
Q 38. What is the treatment of pseudocyst
hemorrhage? (PG)
• Angiographic embolization
• Subsequen t elective treatment of the
pseudocysts (after several weeks)
• Emergency laparotomy and ligation of the
bleeding vessel after opening the cyst, and
drainage of pseudocyst
• For lesions in the pancreatic head, pancreaticoduodenectomy may be required.
Q 39. What is Degidio and Schein classification? (PG)
Type I Type II Type III
Occurrence Acute Acute in
chronic
Chronic
Pancreatic duct Normal Diseased
but no
stricture
Stricture
present
Communication
with duct
No No With
communication
18 Retroperitoneal Tumor
Case
Case Capsule
A 55-year-old male patient presents with backache
and pain radiating down the left lower limb of
6 months duration. He in addition complains of
anorexia and loss of weight. For the last 3 months
he complains of distension of abdomen. There is
no history of therapeutic irradiation. There is no
family history of swelling all over the abdomen.
On examination, the patient is afebrile; the
blood pressure is 140/86 mm of Hg. There is pitting
edema of the left lower limb. On examination of
the abdomen, there is distension of abdomen
which is more towards the left half. A big
bosselated mass of 25 × 15 cm (25 cm vertically
and 15 cm horizontally) is felt in the left half of
the abdomen occupying the left lumbar region,
left hypochondrium and left iliac fossa. The mass
is firm in consistency and does not move with
respiration. All the borders except the lateral
border are well-defined. Medially it is not crossing
the midline. It is bimanually palpable, but not
ballotable. It is intra-abdominal as demonstrated
by the cough test. The mass is not falling forwards
as demonstrated by examination in the knee elbow
position and therefore retroperitoneal. There is
no intrinsic mobility for the mass. On percussion
there is resonance over the mass. The rest of the
abdomen is normal. There is no free fluid in the
abdomen and there is no organomegaly. Normal
bowel sounds are heard on auscultation. There is
no evidence of varicocele. The hernial orifices are
normal. The left lower limb pulsations are normal
and there is no neurological deficit in the left lower
limb. Chest examination is normal.
Read the checklist for abdominal examination.
Checklist for history
• History of therapeutic radiation
• History of exposure to vinyl chloride family
• History of Gardner’s syndrome
• Family history of Gardner’s
• Familial retinoblastoma
• Risk factorssuch asNeurofibromatosis, Li-Fraumeni
syndrome
• Historyofhypertension—becauseof catecholamine
production
• History of back pain and leg pain
• History of hypoglycemia—liposarcoma produces
insulin
• History of precocious puberty
• History of myoclonus in children.
242
Clinical Surgery Pearls
Checklist for examination
• Take the temperature—RP tumors produce fever
• Take the blood pressure—tumors produce
catecholamines
• Check the plane and remember the clinical points
for retroperitoneal tumors given below:
• Look for dilated abdominal veins—because of the
pressure on vena cava
• Look for lower limb edema
• Look for varicocele
• Look for ascites(nonmalignant ascites of RP tumor)
• Look for features of Costello syndrome.
Q 1. What is the most probable diagnosis in this
case?
Retroperitoneal tumor.
Q 2. What are the clinical points in favor of
retroperitoneal tumor?
Clinical points in favor of retroperitoneal tumor
• The mass is intra-abdominal as demonstrated by
head raising test (Carnet’s test)
• The mass is not falling forwards in the knee
elbow position (suggesting the plane to be
retroperitoneal)
• Th e re i s no movement with respiration
(retroperitoneal swelling will not move)
• The mass is fixed (no intrinsic movement)
• The massisresonant on percussion because of the
intestinal loops in front
• Themassisnot crossingthemidline (retroperitoneal
swellings usually will not cross the midline).
Q 3. What is the most probable diagnosis in this
case?
Malignant retroperitoneal tumor, most probably
liposarcoma.
Q 4. Why liposarcoma?
It is the most common retroperitoneal sarcoma
in adults.
Q 5. What is the age group affected in liposarcoma?
Usually 40–70 years and they are asymptomatic in
early stages.
Q 6. What is the cause for left lower limb edema
and pain in this patient?
These are symptoms of compression on the iliac
veins. The backache and lower limb pain in this
case is due to stretching of the lumbar and pelvic
nerves.
Q 7. What are the symptoms and signs of
liposarcoma?
Symptoms and signs of liposarcoma
• Mass abdomen (91%)
• Mass pelvis (21%)—DD ovarian malignancy
• Abdominal pain and discomfort (71%)
• Anorexia, vomiting, fatigue
• Weight loss
• Caval compression—limb edema, varicocele,
ascites (nonmalignant), dilated abdominal veins
• Back pain and leg pain—compression and
stretching of lumbar and pelvic nerves
• Fever.
Q 8. What is retroperitoneum?
According to Ackerman retroperitoneum is defined
as:
A region of the trunk covered—
• Anteriorly by the parietal peritoneum
• Superiorly by the 12th rib and diaphragm
• Inferiorly by the pelvic diaphragm and fascia of
the levator ani and coccygeus
• Posteriorly by the fascia of the muscles of the
anterior abdominal wall.
Retroperitoneal Tumor
243
Q 9. Is it a real space?
It is an actual or potential space.
Q 10. What are the contents?
The contents are structures of mesodermal and
endodermal origin with their embryonic remnants.
This consists of loose connective tissue, fat, nerves,
lymphatics and lymph nodes.
Q 11. What about the retroperitoneal organs?
Tumors of the retroperitoneal organs are not
included in the retroperitoneal tumors traditionally
(like kidneys, adrenals, pancreas and ureters).
Q 12. What is the incidence of retroperitoneal
tumors?
They are uncommon heterogeneous group of tumors
arising either primarily in the retroperitoneum or
metastasisfromelsewhere.The incidence is 0.3 to3%.
Q 13. What is the classification?
Classification
Retroperitoneal Retroperitoneal
tumors tumors
Cystic Solid Benign Malignant
• Cystic swelling is usually benign
• Majority are accidentally discovered
• Majority ofthe solid tumors are malignant(75–95%)
Q 14. What are the benign swellings?
Classification of benign tumors
• Lipomas
• Neurofibromas, neurilemmomas
• Leiomyomas
• Extra-adrenal chromaffinomas (pheochromaftinomas may be malignant)
• Mucinous cystadenomas
• Hemangiopericytomas
• Paragangliomas.
Q 15. What is Costello syndrome? (PG)
It is a syndrome consisting of mental retardation
and benign tumors usually papillomata. Children
with Costello syndrome develop embryonal
rhabdomyosarcoma.
Q 16. What is Paraganglioma? (PG)
Features of paraganglioma
• They are tumors of embryonal origin from the
neural crest
• May arise from any location along the aorta or the
sympathetic chain
• Theymaybe functioningornonfunctioning(secrete
norepinephrine)
• 20% are catecholamine secreting
• May be multiple
• Malignant paragangliomas can occur
• 0.1 – 0.5% cases produce hypertension
• Mayproducesyndromesimilartopheochromocytoma
• May be familial (hereditary paragangliomas)
• Associatedwith vonHippel-Lindau disease and RET
proto-oncogene.
Q 17. What is the pathology in paraganglioma?
(PG)
The paraganglioma may arise from type I or type
II cells.
Type I cells are chromogranin A positive (NSE
positive).
Type II cells are S 100positive (withgoodprognosis).
Q 18. What are the features of retroperitoneal
neurilemmomas? (PG)
They are well-demarcated round or oval mass in
CT with heterogeneous contrast enhancement.
Nonenhancement of the lesion may be due to cyst
formation or tumor calcification.
Q 19. What is mucinous cyst adenoma? (PG)
Mucinous cyst adenoma and cyst adenocarcinoma
are similar to ovarian mucinous tumors.
244
Clinical Surgery Pearls
Q 20. What is hemangiopericytoma? (PG)
They are vascular benign tumors derived from
pericytes. They are very bulky and silent tumors.
Treatment is excision.
Q 21. What are the malignant retroperitoneal
tumors?
They may be Primary or Secondary.
Primary Secondary (metastatic)
Sarcomas
Lymphomas
Malignant variety of germ
cell tumors (common in
children and are benign)
Teratocarcinoma
Endodermal sinus tumor
Tumors of embryonal origin
Urogenital ridge tumors
Adenocarcinoma
Endometrium
Prostate
Pancreas
Lung
GIT
Squamous cell carcinoma
(SCC) cervix, vagina and
lung
Chordoma
Q 22. What is the origin of malignant retroperitoneal tumors?
They may originate from mesodermal, neurectodermal or embryonic remnant
• 75% mesodermal in origin
• 24% neurectodermal
• 1% embryonic remnant
The most common malignancy is sarcoma.
Q 23. What is the most common retroperitoneal
malignancy?
Sarcoma.
Q 24. What is the most common sarcoma?
Liposarcoma isthe most common sarcoma in adults.
• Liposarcoma – 50%
• Leiomyosarcoma – 29%
• Malignant fibrous histiocytoma (MFH).
[In children the most common sarcoma is
Rhabdomyosarcoma:
• 18% present with neurological deficit
• 37% with distant metastasis.
Q 25. What are the etiological factors for retroperitoneal sarcoma? (PG)
Etiological factors for retroperitoneal sarcoma
• Idiopathic
• History of therapeutic radiation
• Exposure to vinyl chloride
• Thorium dioxide
• Familial disorders
• Gardner’s syndrome
• Familial retinoblastoma
• Neurofibromatosis
• Li-Fraumeni syndrome
• Germ line mutations of p53 (chapter 17)
Q 26. What is the origin of liposarcoma?
About 1/3rd of the liposarcoma originate from
perinephric fat.
Q 27. What is the cause of death in liposarcoma?
• Local treatment failure is the cause of death
• Distant metastasis is rare (30% of cases)—liver
and lungs.
Q 28. What is the pathology of liposarcoma?
They may be well-differentiated or highly aggressive
and undifferentiated. The tumor grows along the
fascial planes and envelops rather than directly
invading the nearby organs. Histologically they
exhibit meningothelial like whorls. Metaplastic
bone is seen in these whorls. Myofibroblastic or
osteoblastic differentiation may occur.
Q 29. What are the sarcomas which will spread to
the lymph nodes?
Lymph node spread is rare (< 5%). The following
sarcomas spread to the lymph nodes.
Retroperitoneal Tumor
245
Q 33. What are the MRI findings in various
sarcomas? (PG)
Liposarcoma—decrease in signal in T1 W increase
in signal in T2 W
MFH – Heterogeneous signal pattern
Hemangiopericytoma is multiloculated, cystic
mass with areas of solid tissue.
Q 34. What is the role of retroperitoneoscopy? (PG)
It is not established for routine use. The sensitivity
of this investigation for lymphoma is 84%, for
Hodgkin’s is 94%, for metastasis 95% and for
retroperitoneal tumors 100%. In future this may
replace CT guided biopsy.
Q 35. What is the metastatic evaluation for RP
sarcoma?
CT scan of the chest.
Q 36. Why CT scan of the chest is preferred over
X-ray chest? (PG)
The X-ray chest may not show metastasis because
sarcoma metastasizes to the periphery of the lung
which may be missed in X-ray chest.
Q 37. What is the TNM staging (AJCC 7th edition)?
(PG)
TNM Staging
Primary Tumor (T)
Tx – Primary tumor cannot be assessed
T0 – No evidence of primary tumor
T1 – Tumor 5 cm or less greatest dimension
T1a – Superficial tumor
T1b – Deep tumor
T2 – Tumor more than 5 cm in greatest dimension
T2a – Superficial tumor
T2b – Deep tumor
Regional Lymph Node (N)
Nx—Regional lymph nodes cannot be assessed
N0—No regional lymph node metastasis
N1—Regional lymph node metastasis
Sarcoma with lymph node metastasis
• Rhabdomyosarcoma
• Lymphangiosarcoma
• Epitheliod sarcoma.
Q 30. What are the paraneoplastic syndromes of
the retroperitoneal tumors? (PG)
1. Liposarcoma/Lipoma –Intermittent hypoglycemia
(Insulin like substance production or rapid use of
glucose by metabolically active sarcoma)
2. Paragangliomas – Catecholamine excess
3. Germ cell tumors – Precocious puberty
4. Neuroblastoma – Myoclonus in children
Q 31. How will you proceed to investigate?
Investigations in a case of retroperitoneal tumor
• Helical CT with contrast enhancement
• MRI
• CT scan of the chest/X-ray chest—to rule out
metastasis
• PET scan
• Retroperitoneal core needle biopsy under CT/USG
guidance
• IVU
• Retroperitoneoscopy
• Laboratory investigations –
Alpha - fetoprotein
HCG
Liver function tests
Renal function tests
• Role of FNAC – Recurrence
Metastasis
Lymph node involvement.
Q 32. What are the advantages of MRI over CT? (PG)
• Greater accuracy than CT (100% vs 80%)
• Extent of recurrence can be identified
• Points out areas of desmoplastic reaction.
246
Clinical Surgery Pearls
Distant Metastasis (M)
M0 – No distant metastasis
M1 – Distant metastasis
Gx – Grade cannot be assessed
G1 – Grade 1
G2 – Grade 2
G3 – Grade 3
Q 38. What is the staging as per AJCC 7th edition?
(PG)
AJCC Staging
Stage of
the disease
T
stage
N
stage
M
stage
Grade of
tumor
Stage IA T1a N0 M0 G1, GX
T1b N0 M0 G1, GX
Stage IB T2a N0 M0 G1, GX
T2b N0 M0 G1, GX
Stage IIA T1a N0 M0 G2, G3
T1b N0 M0 G2, G3
Stage IIB T2a N0 M0 G2
T2b N0 M0 G2
Stage III T2a,T2b N0 M0 G2
Any T N1 M0 Any G
Stage IV Any T Any N M1 Any G
Q 39. What is the grading as per AJCC 7th edition?
(PG)
The AJCC 7th edition incorporates a three tiered
grading system determine by three parameters—
mitotic activity, extent of necrosis and differentiation.
Each parameter is scored: differentiation (1–3),
mitotic activity (1–3) and necrosis (0–2). The scores
are summed to designate grade.
Grade 1 2 or 3
Grade 2 4 or 5
Grade 3 6 to 8
Q 40. What is the significance of nodal involvement?
Nodal involvement has very poor prognosis.
Outcome of the N1 is similar to M1 disease.
Q 41. What is the treatment of retroperitoneal
liposarcoma?
Complete en-block surgical excision at first
laparotomy is the treatment of choice. This is
possible only in 30% of cases.
Q 42. What are the preoperative preparations and
precautions?
• Bowel preparation
• Consent for removal of whole or part of the
adjacent organs
• Consent for fecal or urinary diversion
• Arrange adequate blood
• Operation is undertaken at a tertiary referral
center.
Q 43. What anesthesia is used for surgery? (PG)
Hypotensive anesthesia.
Q 44. What are the incisions recommended?
Midline incision for pelvic level tumors and
thoracoabdominal for upper level tumors.
Q 45. What is the clearance required for en-block
excision?
Best results are seen in which a surgical margin of
3 cm or more can be obtained beyond the tumor.
Q 46. What is the most difficult area for clearance?
(PG)
If a plane of dissection is there posteriorly, the
clearance will be adequate. Decide whether the
tumor has traversed along a spinal nerve root into
the spinal canal and its cord.
Q 47. What is the role of radiotherapy?
Radiotherapy has a definite role in lowering
the incidence of local recurrence. The dose
recommended is 5500 cGy. Radiotherapy will delay
Retroperitoneal Tumor
247
the progression of the disease but does not improve
the survival.
Q 48. What is the role of IORT (Intraoperative
radiotherapy)? (PG)
The IORT reduces local recurrence and reduces
radiation enteritis.
Q 49. What is the chemotherapeutic agent of
choice for RP sarcoma? (PG)
Adriamycin—as a single agent—15–35%response.
This may be combined with granulocyte macrophage colony stimulating factor (GM-CSF). There
are three important regimes.
1. AIM—Adriamycin, Iphosphamide, Mesna
2. AD—Adriamycin and Dacarbazine
3. MAID—Mesna, Adriamycin, Ifosfamide and
Dacarbazine.
Q 50. What are the important prognostic factors?
(PG)
The two most important factors are:
• Histological grade
• Completeness of surgical excision (R0).
Q 51. What is the prognosis of RP sarcoma? (PG)
A 5-year-survival of 62–92% for well-differentiated
tumor afterradical excision. 16–48%in undifferentiated tumors.
Q 52. What is the local recurrence rate? (PG)
About 40–82% with median time of 15 monthsto 44
months.
Q 53. What is the follow-up? (PG)
• Physical examination every 2–3 months
• If symptoms occur do CT/MRI
• Asymptomatic patients—CT/MRI to be done at
every 6 months for first 3 years.
Retroperitoneal Cystic Lesions
Q 54. What are the cystic lesions of the retroperitoneum?
Cystic lesions of the retroperitoneum
• Cystic lesions from the developmental remnants
(Wolffian) of urogenital tract situated near the
kidney
• Retroperitoneal mesenteric cyst
• Teratomatous and dermoid cysts
• Abdominal cystic lymphangioma (lymphogenous
cyst)
• Parasitic cysts.
Q 55. What are the clinical features of the abdominal cystic lymphangioma?
This is usually seen in infants and children (3 months
to 5 years). The most common presentation is
abdominal pain. 30% of the children present with
mass abdomen. 90%ofthe cysts are intraperitoneal.
10%are retroperitoneal. Children may present with
complications like intestinal obstruction.
Q 56. What is the diagnostic investigation?
USG abdomen.
Q 57. What is the treatment of the abdominal
cystic lymphangioma?
Surgical excision.
Q 58. Can you get abdominal cystic lymphangioma
in adults?
Yes. There will be a history of long duration. Acute
presentations are rare in adults.
19 Testicular Malignancy
Case
Case Capsule
A 40-year-old male patient presents with lower
abdominal pain, loss of appetite and loss of
weight of 6 months duration. The right testis
was absent from the scrotum from childhood. He
developed a swelling in the right inguinal region
at the age of 15 years which was operated, the
nature of surgery is not known. He gives history of
infertility since 10 years. There is no history of chest
pain, dyspnea or hemoptysis.
On examination there is pallor. There is no jaundice
and no generalized lymphadenopathy. Abdominal
examination revealed fullness in the right side of
the hypogastrium and right iliac fossa-region. On
palpation, there is a firm mass of 18 × 12 cm (18 cm
horizontal and 12 cm vertical) occupying the right
side of the hypogastrium and right iliac fossa. All the
borders of the mass except the lower border are well
defined. One cannot get below the mass. The mass
is fixed and the surface is nodular. The rest of the
abdomen is normal. Liver is not palpable. There is
no free fluid in the abdomen. The supraclavicular
lymph nodes are not enlarged.
On examination of the genitalia, the right
scrotal sac is found to be empty with absence of
rugae. The left testis is small and atrophic. The
left vas is normally palpated. Pubic hair and other
secondary sexual characteristics are normal. There
is no gynecomastia (Fig. 19.1).
Testicular Malignancy
249
Read the checklist for abdominal examination.
Checklist for history
• History of trauma
• Undescended testis
• Scrotal surgery
• Nausea and vomiting—retroduodenal metastasis
• Cough and dyspnea—pulmonary metastasis
• Backache—retroperitoneal metastasis
• Bone pain—skeletal metastasis.
Checklist for examination
• Look for empty hemiscrotum with absent rugae
• Look forlowerlimb edema (unilateral or bilateral)—
Pressure from the retroperitoneal nodes
• Gynecomastia—seen in 5% of cases
• Supraclavicular lymph nodes, iliac lymph nodes
• Look for secondary hydrocele
• Palpate the abdomen in the supraumbilical region
for retroperitoneal nodes
• Rule out liver metastasis
• Examine the chesttoruleoutpulmonarymetastasis
• Look for pallor (in advanced cases).
Q 1. What is the most probable diagnosis in this
case?
Malignant tumor arising from the undescended
testis. Most probably seminoma.
Q 2. Why seminoma?
That is the most common tumor in the undescended
testis.
Age group is also in favor of seminoma.
Q 3. What is the clinical sign for undescended
testis?
Emptyhemiscrotumwithabsentrugaeissuggestive
of undescended testis.
Q 4. What is “sign of the vas”?
In testicular neoplasm the vas deferens is normal,
whereas it is thickened in inflammatory lesions of
the testis and epididymis. In order to differentiate
tumor from inflammation, this clinical sign is used.
Q 5. What will happen to the undescended testis?
Degenerative changes will occur in the seminiferous
tubules. The lining cells become progressively
atrophic and hyalinized with peritubal fibrosis.
Degenerative changes begin to occur at 2 years of
age. If not corrected all bilaterally, cryptorchidism
in adult males becomes sterile.
Q 6. What is the chronology of descent of testis?
The testis is formed in front of the kidneys from
the genital fold medial to the mesonephros
Fig. 19.1: Hypogastric mass (undescended right testis)
Contd...
Contd...
250
Clinical Surgery Pearls
(Wolffian body) in early fetal life. They lie in the
retroperitoneum below the developing kidneys.
The primitive testis is attached to the posterior
abdominal wall by the mesorchium. Its descent
is a complicated process, which depends on
the gubernaculum testis, steroid hormones
and maternal gonadotropins. The testis is intraabdominal up to 7 months of intrauterine life.
Shortly before birth the testis reaches the bottom
of the scrotum being invaginated into a tube
of peritoneum—the processus vaginalis. The
chronology of descent is as follows:
Chronology of descent of testis
3rd month of – from loin to iliac fossa
intrauterine life
4–7 months of – rest at the site of internal ring
intrauterine life
7th month of – it is travelling through the
intrauterine life inguinal canal
8th month of – lies at the external ring
intrauterine life
9th month of – it enters the scrotum, reaching
intrauterine life its base at or after birth
Note: The descent may continue after birth, 50%
reaching the scrotum during the first month of life.
Q 7. What are the complications of undescended
testis?
Mnemonic—MAT SHOP
M – Malignancy
A – Atrophy – because of recurrent minor trauma
T – Torsion
S – Sterility – in bilateral cases
H – Hernia – in 95% there is patent processus
vaginalis and 25% develop clinical hernia
O – Orchitis (epididymo – orchitis)
P – Pain – because of trauma.
Q 8. What are the positions of undescended testis?
1. Intra-abdominal—(33%) lying extra peritoneal
just above the internal ring
2. In the inguinal canal—(50%) it may or may not
be palpable there
3. In the superficial inguinal pouch—(50%) it must
be distinguished from retractile testis.
Q 9. What is superficial inguinal pouch?
Failure of the testis to descend into the scrotum
may be caused by the presence of a dense layer of
subcutaneous tissue at the neck of the scrotum. As a
result of this, the testis turns upwards to lie in a pouch
just above and superficial to the external inguinal
ring. The testis is therefore felt in the subcutaneous
tissue just above and lateral to the pubic tubercle.
Q 10. What is the difference between ectopic testis
and incompletely descended testis?
An incompletely descended testis will lie along the
line of the normal descent at the neck of scrotum,
over the external ring to the canal and on the
posterior abdominal wall. In this situation, the
testis is palpable only when it is at or outside the
external ring. The ectopic testis is always palpable
in contrast to incompletely descended testis and it
is not in line of the normal descent.
Q 11. What are the common positions of ectopic
testis?
Common positions of ectopic testis
1. Femoral triangle—confused with lymph node
2. Base of the penis
3. Perineum
4. Superficial inguinal pouch.
Q 12. What is the timing of surgery for undescended
testis?
It is usually done between 6 months to 1 year of age
(the degenerative changes will start at the age of 2 years).
Testicular Malignancy
251
Q 13. What is the fertility after orchidopexy?
• Unilateral orchidopexy—fertility rate is 80%
• Bilateral orchidopexy—fertility rate is 50%.
Q 14. What is retractile testis?
During childhood the testis are mobile. In children
< 3 years with very active cremasteric reflex due
to the small size of testis the gonad will retract
into the external ring or within the canal. It can be
manipulated back into the mid or lower scrotum.
No treatment is required in this condition.
Q 15. What is ‘vanishing’ testis?
It is a condition where the testis develops but
disappears before birth. The most likely cause is
prenatal torsion.
Q 16. What is true agenesis?
It is very rare. Laparoscopy is useful in distinguishing
true agenesis from cryptorchidism with intraabdominal testis.
Q 17. What are the anomalies associated with
cryptorchidism?
Thisisseen in 15%of cryptorchidism.The following
are the associated anomalies:
Anomalies associated with cryptorchidism
• Klinefelter’s syndrome
• Hypogonadotropic, hypogonadism
• Prune belly syndrome
• Horse shoe kidney
• Renal agenesis or hypoplasia
• Exstrophy of the bladder
• Ureteral reflux
• Gastroschisis
• Cloacal exstrophy.
Q 18. What is the incidence of undescended testis?
• 4% of full-term infants
• 30% in premature babies.
Q 19. Can the unilateral cryptorchid develop malignancy in the normally descended contralateral testis?
Yes. 10% of patients with history of cryptorchidism
develop malignancy in contralateral testis.
Q 20. What is the risk of malignancy according to
the position of the testis in undescended testis?
The relative risk for malignancy in:
Intra-abdominal testis – 1 in 20
Inguinal testis – 1 in 80.
Q 21. What is the most common pathological type
of malignancy seen in undescended testis?
Seminoma
Embryonal carcinoma—It is seen nowadays in
patients in whom the testis has been brought down.
Q 22. Will orchidopexy change the malignant
potential of the cryptorchid testis?
No. It facilitates examination and tumor detection.
Q 23. What are the factors responsible for the
malignant change in cryptorchidism?
Factors responsible for malignant change in
cryptorchidism
1. Abnormal germ cell morphology
2. Gonadal dysgenesis
3. Elevated temperature
4. Interference of blood supply
5. Endocrine dysfunction.
Q 24. What are the differential diagnoses of a solid
swelling in the testis?
Differential diagnoses of solid swelling in the testis
1. Testicular tumor
2. Acute and chronic epididymo-orchitis
3. Hematocele
4. Gumma
5. Orchitis (mumps).
252
Clinical Surgery Pearls
Q 25. What is ‘billiard ball’ testis? Histopathological Classification
Syphilisin adultswill cause interstitial inflammation
turning the testis into a round, hard and insensitive
mass, which is called‘billiard ball testis’.
Q 26. What is Gumma of the testis?
Gumma of the testis is due to syphilis. The testis is
painless and therefore presents as a lump on the
surface of the testis or enlargement of the whole
organ. The testicular sensation is lost early. H/o
exposure will be there. A search is made for stigmata
of syphilis like Clutton’s joint, interstitial keratitis,
etc. It is indistinguishable from tumor. If untreated
it will breakdown to form Gummatous ulcer.
Q 27. What is the relationship of testicular tumor
and trauma?
Many patients attribute the symptoms of the
swelling to trauma. But thisisto be ignored. We do
not know whether the lump is due to the hump
or the hump is due to the lump!!
Q 28. What is the most common starting point of
the tumor in the testis?
Lower pole of the body of the testis, later they
occupy the whole of the testis.
Q 29. What is the classification for testicular
tumors?
Various classifications are there:
• Dixon and Moore
• WHO
• British tumor panel
• Histopathological classification.
The testis is composed of actively dividing germ
cells, the supporting cells and connective tissue
stroma. The tumors of the testis arise from the
actively dividing germ cells. Comprising 90 – 95%
and the rest contributed by nongerminal neoplasms.
The histopathological classification is given below:
Q 30. What is teratoma? What is the classification
of teratoma?
Teratoma arises from totipotent cells in the rete
testis and contains a variety of cell types with
predominance of one or more cells. The usual
variety is yellowish in color with cystic spaces
containing gelatinous fluid. Cartilaginous areas
Testicular Malignancy
253
are often present. The tumor may be as small as a
peanut or as large as a coconut.
Testicular Panel Classification of Teratoma
• Teratoma differentiated (TD)—Uncommon.
• Even though there is no histologically recognizable malignant component, it cannot be
considered benign. It may contain cartilage,
muscle and glandular tissue.
• Malignant teratoma intermediate or Teratocarcinoma (MTI) (most common) (A and BType).
Contains definitely malignant and incompletely
differentiated components.
• Malignant teratoma anaplastic or Embryonal
carcinoma (MTA). The cells are presumed to be
derived from yolk sac and are responsible for
elevation of AFP.
• Malignant teratoma trophoblastic (MTT)—
Uncommon
It contains syncytial cell mass with malignant villous
or papillary cytotrophoblast (choriocarcinoma). It
produceschorionicgonadotropin(hCG).Itisoneofthe
most malignant tumors having spread by bloodstream
and lymphatics early.
Q 31. What are the differences between seminoma
and teratoma?
No. Seminoma Teratoma
1. Age group: 35 – 45
(older age group)
20 – 35 (younger age
group)
2. Cut surface is
homogeneous and
pinkish in color
Yellowish in color with
cystic spaces containing
gelatinousfluid. Cartilages
are often present
3. Origin: histologically
arising from seminiferous tubules
Originate from totipotent
cells in the rete testis
containing variety of cell
types
4. Cell type: Oval cells
with clear cytoplasm
and prominent acidophilic neucleoli
Cell type depends on the
type of teratoma – TD,
MTI, MTA, MTT
5. Main spread by
lymphatics
Spread by bloodstream
6. Sensitive to
radiotherapy
Not sensitive to
radiotherapy
Note: The non seminomatous tumors are classified
into three groups – Good risk, Intermediate risk
and bad risk
• TheHCGvalue will be >50,000 for bad risk and <
50,000 for good risk. The intermediate risk values
are in between.
Q 32. What is Leydig cell tumor?
It is an interstitial cell tumor arising from Leydig cells,
which masculinizes. They are prepubertal tumors
causing sexual precocity and extreme muscular
development. The regression of the symptoms
is incomplete after orchidectomy because of the
hypertrophy of the contralateral testis.
Q 33. What is Sertoli cell tumor?
They are interstitial cell tumor arising from Sertoli
cells, which produces feminizing hormones. This will
produce gynecomastia, loss of libido and aspermia.
These tumors are benign and orchidectomy is curative.
Q 34. What are the testicular tumors producing
gynecomastia?
• Teratoma
Contd... • Feminizing tumors (Sertoli).
Contd...
254
Clinical Surgery Pearls
Q 35. What is the cause for gynecomastia in
testicular tumor?
Raised β-hCG is responsible for gynecomastia.
Q 36. What are the etiological factors for testicular
tumors?
Etiological factors for testicular tumors
• Congenital—Cryptorchidism (3–14 times greater
incidence than normal)
• Acquired
• Trauma
• Viral—Mumps (Atrophy of testis)—atrophic testis
is more prone for malignancy
• AIDS
• Hormones—Estrogen administration results in
Leydig cell tumor—Testicular tumor in children of
mother’s treated with diethyl stilbestrol
• Ethnic factors
• Environmental factors
• Klinefelter’s syndrome.
Q 37. What are the modes of spread of testicular
tumor?
1. Local – Local involvement to epididymis and
cord is hindered by tunica albuginea
2. Lymphatic
3. Hematogenous.
Q 38. What is the lymphatic drainage of testis?
From the testis several lymphatic vessels emerge
from the mediastinum testis and accompany the
gonadal vessels in the spermatic cord. Where the
spermatic vessels cross ventral to the ureter, some
of these lymphatics diverge medially and drain
into the retroperitoneal lymph nodes, while others
follow the spermatic vessels to their origin and
reach the para-aortic nodes.
Lymphatics from the medial side of the testis
may run with the artery to the vas and drain into a
node at the bifurcation of the common iliac artery
(common iliac nodes).
The inguinal lymph nodes are affected when
the scrotal skin is involved.
Q 39. What you mean by landing zones for
lymphatics?
The primary landing zones for right testicular
tumor lies in the interaortocaval nodes immediately
below the renal vessels. (At the level of L2 lumbar
vertebrae). The ipsilateral lymphatics will also go
to paracaval, preaortic and right common iliac and
external iliac nodes.
For the left testicular tumor it lies in the true paraaortic nodes just below the left renal vessels. (Left
renal hilum). The ipsilateral distribution also includes
para-aortic, preaortic and left common iliac nodes.
The metastasis reach the common iliac, external
iliac and inguinal nodes usually secondary to
retrograde spread because of large volume disease.
Q 40. Clinically what is the level of retroperitoneal
nodes?
Above the umbilicus in the abdomen.
Q 41. What is the spread beyond the regional
nodes?
The retroperitoneal lymphatics empty into the
cisterna chyli via the right and left lumbar trunks.
From here, it will reach the left supraclavicular nodes.
From the para-aortic nodes, the lymphatics
will reach the retrocrural nodes and from there
it will reach the mediastinal nodes (posterior
mediastinum). Involvement of the anterior
mediastinum is rare.
Q 42. What is the method of contralateral spread?
(PG)
The contralateral spread is usually seen with right
sided tumors especially in large volume tumors
Testicular Malignancy
255
(rare with left sided tumors). If the patient has
undergone herniorrhaphy, vasectomy or other trans
scrotal procedures unrelated to the tumor, pelvic
and inguinal nodes may get enlarged.
Q 43. What is the mechanism of inguinal node
metastasis?
This will occur only if the tunica albuginea has been
invaded by the tumor or as a result of previous surgical
procedures like orchidopexy or herniorrhaphy.
Q 44. What are the sites of extranodal metastasis?
Sites of extranodal metastasisin order of decreasing
frequency are:
Lung
Liver
Brain
Bone
Kidney
Adrenal
GI tract
Spleen.
Q 45. Can testicular tumor occur bilaterally? (PG)
Yes. About 2–3% of testicular tumors are bilateral.
They may occur simultaneously or successively.
Primary bilateral tumors occur synchronously or
asynchronously.
Q 46. What is the most common cause for bilateral
testicular tumor? (PG)
• Testicular lymphoma
• Seminoma isthemost commonbilateralprimary
tumor.
Q 47. How will you size the testis? (PG)
They can be sized according to Prader orchidometer.
Q 48. When examining the testes, which side is
examined first?
The normal side is examined first.
Q 49. What is the incidence of testicular tumor? (PG)
• They make up 1–2% of the male cancers
• The life time probability of developing a tumor
of the testis is 0.2%
• The highest incidence is seen in Scandinavia
• Lowest incidence is in Africa and Asia
• Highersocioeconomic classhashigherincidence
• Incidence is 4 timesinwhites comparedtoblack.
Q 50. Why testicular tumor is more common on
the right side?
There is increased incidence of cryptorchidism on
the right side and therefore tumor is more common
on the right side.
Q 51. What are the clinical features of testicular
tumor?
Painless enlargement of the testis 90% (Dull ache,
sensation of heaviness in the lower abdomen,
anal area or scrotum) acute testicular pain due to
infarction or intratesticular hemorrhage is seen in
about 10% of cases.
Extra testicular manifestations
• Cough and dyspnea—pulmonary metastasis
• Anorexia,nausea,vomiting(retroduodenalmetastasis)
• Supraclavicular lymph node metastasis
• Back pain—retroperitoneal metastasis
• Lower extremitiesswelling—venacaval obstruction
(unilateral or bilateral limb)
• Metastaticpara-aortic lymphnodes(presentbehind
and above the umbilicus)
• Gynecomastia (5% of cases)
• Bone pain (skeletal metastasis)
• CNS involvement (spinal cord/root involvement)
• Asymptomatic (10%)—identified incidentally.
Q 52. What is the incidence of secondary hydrocele
in testicular tumors?
Its 10%. The secondary hydrocele is usually lax.
256
Clinical Surgery Pearls
Q 53. What is the cause for thickening of the
spermatic cord? (PG)
This is a late feature and it is because of the
cremasteric hypertrophy and the enlargement of
the testicular vessels.
Q 54. What is the importance of testicular
sensation in tumors?
The testicular sensation is lost completely in the
early stage of the tumor. This sign is better not
demonstrated because of the fear of dissemination. Palpation of the tumor also should be
avoided to the minimum.
Q 55. What is “hurricane tumor”?
It is a ferocious type of malignancy that kills the
patients in a matter of weeks because of the rapid
spread of the tumor.
Q 56. Can you feel the epididymis separately in
testicular tumor?
Epididymis is normal during initial stages. But it
becomes more difficult to feel as it is flattened and
incorporated in the growth in later stages.
Q 57. What are the tumor markers?
Tumor markers for testicular tumors
1. α - Fetoprotein (AFP)
2. b - Human chorionic gonadotropin (b-hCG)
3. Lactate dehydrogenase (LDH).
Q 58. What is the significance of serum tumor
markers? (PG)
In 85% of patients at least 1 marker is raised.
Markers are used for assessment of tumor regression
and recurrence.
Remember!!Tumoris possiblewithout elevation
of the tumor marker.
Q 59. What is the significance of LDH? (PG)
Itisincreased in 60%of nonseminomatousGCT and
80% of patients with advanced seminoma.
It has independent prognostic significance in
patients with advanced germ cell tumor.
Increase in the serum concentration is a reflection
of tumor burden, growth rate and proliferation.
Q 60. What is the significance of AFP? (PG)
• AFP is elevated in 70%of nonseminomas(notin
pure seminomas)—restricted to embryonal cell
carcinoma and endodermal sinus tumor (yolk
sac tumor).
• If AFP is elevated in seminoma, suspect nonseminoma elements in either the primary or
metastasis.
• The normal adult concentration is usually
< 15 ng/mL.
• The physiological half-life is 5–7 days.
Q 61: What is the significance of b-hCG? (PG)
• It is a glycoprotein produced by 65% of nonseminomas and 10% ofseminomas(all patients
with choriocarcinoma and 40% patients with
embryonal carcinoma).
• It is produced by syncytiotrophoblasts.
• Half-life of b-hCG is 24–48 hours
Q 62. What are the investigations in a patient with
suspected testicular tumor?
Investigations in testicular tumor
1. Blood—radioimmunoassay of tumor markers
2. Chest—radiograph – for pulmonary metastasis
3. Ultrasound—ofthe affected testis and abdomen—
abdomen for lymph nodes and liver metastasis
4. CT/MRI—for intra-abdominal and intrathoracic
secondaries
5. IVU—deviated or obstructed ureters as a result of
the retroperitoneal nodes will be demonstrated
6. High orchidectomy.
Testicular Malignancy
257
Q 63. What is the sonological finding in testicular
tumor? (PG)
Sonologically the tumor will appear as hypoechoic
lesion. It may also reveal secondary hydrocele.
Q 64. Why high orchidectomy is included along
with investigations?
Orchidectomy is considered as the basic
investigation in testicular tumors. It is essential to
remove the primary tumor to obtain the histological
type of malignancy. The pathological knowledge is
important for the AJCC staging because the tumor
status in this staging is always PT0, PT1, etc.
Q 65. What is the incision for high orchidectomy?
Transinguinal incision.
Q 66. Why not transscrotal incision?
If a transscrotal incision is made in testicular tumor,
the tumor will spread to the lymphatic territory of
the inguinal nodes (testis will normally drain to
para-aortic nodes). Therefore, if transscrotal incision
is made, the inguinal nodes also must be tackled by
radiotherapy. This must be avoided. There are three
things to be avoided in testicular tumors:
Three Nos in testicular tumors
• No transscrotal incision
• No transscrotal aspiration
• No transscrotal biopsy.
Q 67. What is high orchidectomy (inguinal
orchidectomy)? (PG)
Through a transinguinal incision the spermatic
cord is displayed by dividing the external oblique
aponeurosis. A soft clamp is placed across the
cord as the initial step to prevent dissemination of
malignant cells as the testis is mobilized into the
wound. The cord is then doubly ligated at the level
of the deep inguinal ring and divided, so that the
testis can be removed.
Q 68. What is Chevassu maneuver? (PG)
During the above procedure when the testis is
brought to the inguinal wound, if there is doubt
regarding the diagnosis, the testis should be
bisected along its anterior convexity so that its
internal structure can be examined by frozen
section. If a tumor is ruled out the bisected testis
can be closed and returned to the normal position.
Q 69. If the patient is explored by transscrotal
route already what is the course of action? (PG)
Hemiscrotectomy and radiation of inguinal nodes
is recommended.
Q 70. What is the clinical staging?
Clinical staging of testicular tumors
Stage 1—Tumor confined to the testis
Stage 2—Nodes below the level of the diaphragm—
spread to regional lymph nodes—
retroperitoneal, para-aortic
Stage 3—Nodes above the level of the diaphragm—
spread beyond the retroperitoneal nodes,
to the mediastinum or extra lymphatic
metastasis
Stage 4—Pulmonary or hepatic metastasis
Q 71. What is the TNM staging (AJCC 7th Edition)?
(PG)
T stage
*The extent of primary tumor is usually classified
after radical orchiectomy and for this reason; a
Pathological Stage is assigned using the prefix P
*pTX Primary tumor cannot be assessed
pTO No evidence of primary tumor(e.g. histologic
scar in testis)
pTis Intratubular germ cell neoplasia (carcinoma
in situ)
pT1 Tumor limited to the testis and epididymis
without vascular/lymphatic invasion, tumor
258
Clinical Surgery Pearls
may invade into the tunica albuginea but not
the tunica vaginalis
pT2 Tumor limited to the testis and epididymis
with vascular/lymphatic invasion, or tumor
extending through the tunica albuginea with
involvement of the tunica vaginalis
PT3 Tumor invades the spermatic cord with or
without vascular/lymphatic invasion
pT4 Tumor invades the scrotum with or without
vascular/lymphatic invasion
Note: Except for pTis and pT4, extent of primary
tumor is classified by radical orchiectomy. TX may be
used for other categories in the absence of radical
orchiectomy.
N Stage (Clinical)
NX Regional lymph nodes cannot be assessed
N0 No regional lymph node metastasis
N1 Metastasis with a lymph node mass 2 cm
or less in greatest dimension; or multiple
lymph nodes, not more than 2 cm in greatest
dimension
N2 Metastasis with a lymph node mass more
than 2 cm, but not more than 5 cm in greatest
dimension; or multiple lymph nodes, any one
mass greater than 2 cm but not more than 5
cm in greatest dimension
N3 Metastasis with a lymph node mass more
than 5 cm in greatest dimension.
Pathological N Stage (pN)
pNX Regional lymph nodes cannot be assessed
pN0 No regional lymph node metastasis
pN1 Metastasis with a lymph node mass 2 cm or
less in greatest dimension and less than or
equal to 5 nodes positive, not more than 2
cm in greatest dimension
pN2 Metastasis with a lymph node mass more
than 2 cm but not more than 5 cm in
greatest dimension; or more than 5 nodes
positive, not more than 5 cm; or evidence of
extranodal extension of tumor
pN3 Metastasis with a lymph node mass more
than 5 cm in greatest dimension
M stage
MX Distant metastasis cannot be assessed
M0 No distant metastasis
M1 Distant metastasis
M1a Non regional nodal or pulmonary metastasis
M1b Distant metastasis other than to non- regional
lymph nodes and lungs
Serum Tumor Markers (S)
SX Markerstudiesnot availableornotperformed
S0 Marker study levels within normal limits
S1 LDH<1.5 XN* and hCG(mIU/mL) <5000 and
AFP (ng/ml) < 1000
S2 LDH 1.5 – 10 X N or hCG (mIU/mL) 5000 –
50,000 or AFP (ng/mL) 1000 – 10,000
S3 LDH > 10 X N or hCG (mIU/mL) > 50,000 or
AFP (ng/mL) > 10,000
*Nindicates upperlimit of normalforthe LDHassay.
Q 72. What is the management of testicular
tumors?
The management of seminomas and nonseminomatous germinal cell tumors is different.
Q 73. What is the management of seminoma?
After high orchidectomy seminoma is treated with
radiotherapy (because seminoma is a radio sensitive
tumor) for stage 1 and nonbulky for stage 2.
• Over a 3-week-period administer 2500 cGy
hockey stick field including the following nodes
• Para-aortic,paracaval,bilateral commoniliac and
external iliac nodal regions
Testicular Malignancy
259
• Recently the radiation is confined to the paraaortic area alone
• With history of herniorrhaphy and orchidopexy
include the contralateral inguinal region
shielding the contralateral testis
• Mediastinal radiation is currently avoided
(chemotherapy is more effective).
Q 74. Is there any role for semen banking? (PG)
If the function of the contralateral testis is in
question, this should be considered. The semen of
the patient may be collected and preserved if the
patient is desirous of having children.
Q 75. What are the indications for chemotherapy
in seminoma? (PG)
• Bulky abdominal disease
• Metastasis.
Q 76. What is the chemotherapeutic regimen? (PG)
It is treated with four cycles of chemotherapy with
BEP regimen
• Bleomycin
• Etoposide
• Cisplatin.
Q 77. What is the treatment of residual abdominal
mass after chemotherapy? (PG)
Residual tumor of more than 3 cm is treated by
surgery.
Q 78. What is the management of nonseminomatous germ cell tumor?
After high orchidectomy, patients are treated with
Retroperitoneal Lymph Node Dissection (RPLND)
except bulky disease or distant metastasis.
Q 79. What are the approaches for RPLND? (PG)
• Transabdominal
• Thoracoabdominal.
Q 80. What is bulky disease? (PG)
All patients with retroperitoneal mass > 5 cm (high
burden disease).
Q 81. What is the most important problem of
RPLND? (PG)
Retrograde ejaculation.
Q 82. What is the extent of RPLND? (PG)
The standard RPLND is a bilateral dissection from
renal vessel down to aortic bifurcation, along the
external iliac artery to the deep inguinal ring on
the affected side. The following lymph nodes are
removed on both sides.
Lymph nodes removed in RPLND
Paracaval
Interaortocaval
Para-aortic
Preaortic
Common iliac nodes.
Q 83. What is the contraindication for RPLND? (PG)
Choriocarcinoma. Here the disease issystemic and
the treatment is multi agent chemotherapy.
Q 84. What are the indications for withholding
RPLND? (PG)
• Normal serum markers
• No nodes in abdominal CT
• No distant metastasis.
The rationale behind this policy is that only 20%
of such patients will develop disease and in such a
situation patient should be ready for regular follow-up.
Q 85. What is the follow-up of such a patient? (PG)
• Physical examination
• CT abdomen 3 monthly for first two years, 6
monthly thereafter
• Tumor markers.
260
Clinical Surgery Pearls
They are done monthly for the first year, every 2
monthly for the second year and 3–6 months thereafter.
Q 86. What is modified RPLND (Nerve sparing
RPLND)? (PG)
This involves bilateral dissection above the origin
of the inferior mesenteric artery and unilateral
dissection confined to the side of the tumor below
the origin of the inferior mesenteric artery. This
preserves the important sympathetic fibers from
the contralateral side thus, maintaining ejaculation.
Q 87. What is the treatment of extensive retroperitoneal nodes with chest metastasis? (PG)
High orchidectomy and multi agent chemo
followed by excision of the persistent mass in the
retroperitoneum.
Q 88. What are the alternative drugs for chemotherapy? (PG)
Ifosfamide/Doxorubicin.
Q 89. What is the prognosis of nonseminomatous
germ cell tumor? (PG)
Stage II – 90%cure rate at 5 years
Stage III – 70%cure rate at 5 years
Choriocarcinoma – 35% at 5 years
Q 90. What is the management of the given
case?
In this patient the tumor is arising from intraabdominal testis. It should be removed transabdominally and the further management depends
on the histopathology. Considering his age, the
pathology is likely to be seminoma and therefore
he requires radiotherapy.
20 Portal Hypertension
Case
Case Capsule
A 55-year-old male patient presents with melena
of one week duration. He is a chronic alcoholic
and gives history of three bouts of hematemesis
in the last 2 months. He complains of distension
of the abdomen, abdominal discomfort, and
lethargy for the last 6 months. He gives history
of jaundice in the childhood. His sleep pattern is
not altered. There is no history of treatment with
NSAIDs, paracetamol and anti- tuberculous drugs.
There is no history of omphalitis in the newborn
period. There is no history of chronic pancreatitis or
history of convulsions.
On general examination, the patient is ill
looking, poorly nourished and there is obvious
muscle wasting. He is fully oriented. There is no
memory impairment. The speech is normal. There
is pallor and mild icterus. Both lower limbs show
pitting type of edema. Clubbing of the fingers
and toes are seen. About 10 spider nevi spots are
present in the front of the chest, face and arms
(1 mm size bright red spots with radiating small
branches spreading to 2 mm diameter. They fade
completely when compressed with finger and
refill as soon as the pressure is released). Patient
has got bilateral gynecomastia. There is loss of
pubic and axillary hair. There is no evidence of
palmar erythema. Skin bruising is noted in the right
forearm of about 5 × 4 cm size. There is no flapping
tremor and there is no fetor hepaticus.
On examination of the abdomen, there is
generalized distension of the abdomen and
the umbilicus is everted. There are no caput
medusae. There is shifting dullness and fluid
thrill demonstrated. Dipping palpation revealed
splenomegaly. On auscultation a venous hum is
heard in the epigastrium that is louder on inspiration.
On examination of the genitalia, both testes are
found to be small and soft suggestive of testicular
atrophy. Central nervous system examination
showed no evidence of encephalopathy. The
cardiovascular system is normal and there are no
features suggestive of constrictive pericarditis or
tricuspid valve incompetence.
Read the checklist for abdominal examination.
Checklist for history
• History of alcoholism
• Previous jaundice
• Schistosomiasis
• Valvular heart disease, constrictive pericarditis
• Abdominal tumors—extrinsic compression
• Hematemesis and melena.
262
Clinical Surgery Pearls
Checklist for examination
• Stigmata of liver disease (refer chapter on liver)
• Triad of portal hypertension namely esophageal
varices, ascites and splenomegaly
• Look for jaundice
• Features of encephalopathy
• Look for anemia
• Look for pitting edema of lower limbs
• Look for ascites
• Look for hepatosplenomegaly
• Look for caput medusae
• Look for testicular atrophy
• Look for gynecomastia
• Look for Kenawy’s sign—venous hum, heard
louder on inspiration in the epigastrium in portal
hypertension
• Look for Cruveilhier-Baumgarten syndrome—loud
venous hum at umbilicus in case of portal hypertension.
Q 1. What is the probable diagnosis in this case?
Cirrhosis of liver with portal hypertension.
Q 2. What are the points in favor of portal hypertension?
1. History of alcoholism
2. History of upper GI bleed
3. Melena
4. Hepatosplenomegaly on examination
5. Mild icterus
6. Presence of ascites.
Q 3. What are the causes for ascites?
Causes for ascites are:
Hepatic causes
– Cirrhosis with portal hypertension
– Hypoalbuminemia of any cause
Malignant ascites
– Secondary to any primary or metastatic malignancy
Infective
– Tuberculous peritonitis
– Bacterial peritonitis
– Primary peritonitis
Congestive
– Right sided heart failure
– Budd-Chiari syndrome
– Constrictive pericarditis
Miscellaneous causes
– Pancreatic ascites
– Chylous ascites
– Meig’s syndrome
– Pseudomyxoma peritonei.
Q 4. What are the causes for general fullness of
the abdomen?
It may be due to:
• Fat
• Fluid
• Flatus
• Feces
• Fetus.
Q 5. What is the minimum amount of fluid required
to demonstrate free fluid in the abdominal cavity?
The minimum amount of fluid to demonstrate
clinical ascites is 1500 mL.
Q 6. What is the minimum amount required
radiologically to demonstrate fluid within the
peritoneal cavity?
The minimum amount required radiologically to
demonstrate ascites is 150 mL.
Q 7. What are the types of ascitic fluid?
Contd... May be transudate or exudates.
Portal Hypertension
263
Q 8. What are the differences between transudate and exudates?
Differences between transudate and exudate
Transudate Exudates
Protein Low—most of which is albumin < 1gm/dL High—(2.5 – 3.5 gm/dL)
High content of fibrinogen
Specific gravity < 1.012 > 1.020
Glucose content Same as plasma Low < 60 mg/dL
pH > 7.3 < 7.3
LDH Low High
Cellular debris Few cells More cells
Cause Obstruction to the venous outflow
from liver (ultrafiltrate of blood plasma
and results from imbalance across the
vascular endothelium) permeability of
endothelium—normal
Inflammatory extravascular fluid formed by
the escape of fluid, proteins and blood cells
from the vascular system into the interstitial
tissue or body cavities because of increased
vascular permeability
SAAG (Serum ascites
albumin gradient)
> 1.1 (Ascitic fluid has less albumin than
serum)
< 1.1 (Ascitic fluid has more albumin than
serum)
Q 9. What are the signs of ascites?
Signs of ascites
• Puddle sign—mild ascites
• Shifting dullness—moderate ascites
• Fluid thrill—severe ascites
• Tanyon sign—the umbilicus is pushed upwards in
ovarian cyst and downwards in ascites
Q 10. What is puddle sign?
This is a clinical method to demonstrate minimum
amount of fluid in the peritoneal cavity. The patient
is positioned in the knee elbow position and the
abdomen is percussed around the umbilicus that
will reveal dullness.
Q 11. How will you demonstrate shifting dullness?
Ask the patient to turn on to his left side, wait for a
minute so that the fluid gravitates. Start percussion
from the right side to the left noting where the
resonant area becomes dull and then mark the
spot on the abdominal wall. Then the patient is
asked to turn slightly on to his right side and after
1 minute if shifting dullness is present, the dull area
will become resonant and vice versa.
Q 12. How will you demonstrate fluid thrill?
An assistant places the edge of his hand firmly on
the center of the abdomen in order to damp down
a fatthrill.The abdominal wall on one side isflicked
and the hand on the other side of the abdomen
feels the thrill.
264
Clinical Surgery Pearls
Q 13. How will you differentiate ascites from
ovarian cyst (Pelvic mass)?
Differences between ascites and ovarian cyst
Ascites Ovarian cyst
• Dullness* Is dull in the
flanks and hypogastrium
Pelvic mass is
dull in the hypogastrium only
and flanks are
resonant
• Ruler test—a
flat ruler is
placed on
the abdomen
just above
the anterior
superior iliac
spine and
pressed firmly
backwards
Negative In the case of
ovarian cyst,
the pulsations
of the aorta are
transmitted
to the fingers
through the
ruler
• Position of
umbilicus
The umbilicus
is displaced
downwards
The umbilicus
is displaced
upwards
Note: *Mechanism of dullness—The ovarian cyst
displaces the loops of intestine to the flanks and
occupies the middle of the abdomen. Hence, the
dullness is felt over the mass in the hypogastrium
while the flanks are resonant. Ascitis fluid displaces
the loops of intestines to the middle of the abdomen.
The flanks are occupied by the ascitic fluid that on
percussion shows dullness while the floating loops of
intestine are resonant over the middle of the abdomen
(around the umbilicus).
Q 14. What is dipping palpation?
It is a special technique to palpate organs or tumors
in cases of ascites. The pads of fingers are placed
on the abdomen and then by a quick push, the
abdominal wall is depressed. By this method an
enlarged liver is felt easily so also a tumor mass.
Q 15. What is the definition of upper GI bleed?
Upper GI bleed is a bleeding located between
the oropharynx and the ligament of Treitz (lower
GI bleeding is a bleeding arising from distal to
ligament of Treitz).
Q 16. What is hematemesis?
Vomiting of blood thatis eitherfresh and unaltered
or digested by gastric secretion.
Q 17. What is melanemesis?
Vomiting of altered blood is called melanemesis.
Q 18. What is the cause for coffee ground vomitus?
It is due to vomiting of blood that has been in the
stomach long enough for gastric acid to convert
hemoglobin to acid hematin.
Q 19. What is hematochezia?
Passage of bright red blood per rectum is called
hematochezia. The bleeding source may be from
colon, rectum or anus. If the intestinal transit is
rapid during brisk bleeding in the upper intestine,
bright red blood may be passed unchanged in
the stool.
Q 20. What is melena?
It is defined as the passage of a black, tarry stool.
Usually it is because of bleeding from the upper GI
tract. But it can be produced by blood entering the
bowel at any point from mouth to the cecum. The
black color is because of the formation of hematin
that is a product of oxidation of heme by intestinal
and bacterial enzymes.
Q 21. What is the minimum amount of intestinal
bleeding required to produce melena?
About 50 to 100 mL of blood in the stomach.
Q 22. How long it will take to clear a melena of a
bleed of about 1000 mL of blood in the GI tract?
Three to five days.
Portal Hypertension
265
Q 23. What is the minimum amount of blood
required in the stool for a positive occult blood
test?
More than 10 mL (normal subjects lose about
2.5 mL of blood per day in their stool from minor
mechanical abrasion.
Q 24. What are the causes for upper GI bleeding?
Causes for upper GI bleeding
Common causes
1. Peptic ulceration—gastric ulcer, duodenal ulcer,
stomal ulcer
2. Esophagogastric varices
3. Gastritis
4. Mallory-Weiss syndrome
5. Acute mucosal lesions—(erosions)—they do
not extend through the muscularis mucosa and
therefore called erosions, not ulcers
6. Stress ulceration (secondary to shock, sepsis
following operation,trauma, etc.)—itis because of
decreased splanchnic blood flow and not because
of increased gastric secretion.
Uncommon causes
7. Reflux esophagitis
8. Gastric neoplasms
9. Curling’s ulcer—erosion of stomach and
duodenum in burns
10. Cushing ulcer—after head injury and cranial
operations
11. Steroid induced—steroid ulcers
12. Hiatal hernia
13. Duodenal diverticulum
14. Miscellaneous
– vascular lesions such as
– Angioma
– Rendu-Osler-Weber syndrome
– Aortoenteric fistula
– Hematobilia.
Q 25. What is the most important investigation
for diagnosis in this case?
Esophagogastroduodenoscopy: It can be done in
emergency situations when the patient’s general
condition is stabilized.
Q 26. What is the endoscopy finding for varices?
Varices appear as 3 or 4 large tortuoussubmucosal
bulging vessels running longitudinally in the distal
esophagus. The bleeding site may be identified. The
lesion may be obscured by blood.
Q 27. What is the endoscopic grading of
esophageal varices?
Grade 1—visible, nontortuous
Grade 2—tortuous, nonprotruding
Grade 3—protruding (normal mucosa in between
the columns)
Grade 4—like grade 3, no normal mucosa.
Q 28. What is “varices upon varices”?
The small vessels seen on the surface of varices
endoscopically are called varices upon varices.
Q 29. What are the endoscopic signs of prediction
for bleeding?
Endoscopic signs of prediction for bleeding
• Varices upon varices
• Red wale marking
• Cherry red spot
• Hematocystic spot
• Blue varices
• Erosions on mucosa.
Q 30. Any role for upper GI barium series?
Barium studies are neither sensitive nor specific.
A barium swallow outlines the varices in 90% of
the cases. But they are difficult and dangerous in
bleeding patients.
266
Clinical Surgery Pearls
Q 31. Is it possible to have bleeding duodenal
ulcer in patients with esophageal varices?
Yes. It isto be stressed that even in known patients of
esophageal varices, it is important to repeat the upper
GI endoscopy so as to exclude a bleeding peptic ulcer.
Q 32. What are the important investigations in
upper GI bleeding?
Important investigations in upper GI bleeding
1. Endoscopy
2. LFT—bilirubin is usually elevated, serum albumin
is often decreased
3. Hemoglobin—anemia may be as a result of
bleeding, hypersplenism or nutritional deficiency
4. Coagulation profile—PT, APTT, INR, platelet count
may be deranged in cirrhosis
5. Ultrasound abdomen—for identifying the size of
portal vein, the status of liver (cirrhotic or not), for
ascites, the amount of collaterals, etc.
6. Splenoportography—for identifying the site of
obstruction
7. Ascitic fluid study
8. Liver biopsy—for confirming the cause of portal
hypertension.
Q 33. What are the peculiarities of portal vein?
• Itis unique in thatitstarts and endsin capillaries
• It has no valves.
Q 34. What is the normal portal pressure? What is
the pressure in portal hypertension?
Normally it ranges from 7–10 cm of saline. In portal
hypertension the portal pressure exceeds 10 cm of
saline averaging around 20 cm of saline.
Q 35. How portal vein is formed?
It is formed in front of the inferior vena cava (IVC)
and behind the neck of the pancreas by union of
the superior mesenteric and splenic vein. This union
occurs at the level of the second lumbar vertebrae.
The vessel is 5–8 cm long and passes up and to the
right in the gastrohepatic omentum (lesser) to enter
the hilum of liver where it immediately divides into
right and left branches. In the liver right branch is
short and supplies the caudate lobe of the liver and
then divides into anterior and posterior branch. The
longer left branch of the portal vein runs to the left
in the porta hepatis.
Q 36. What is the mechanism of development of
collateral circulation in portal hypertension?
The obstruction to the flow of portal venous
blood in the liver promotes expansion of collateral
channels between the portal and systemic venous
system. When the portal pressure reaches around
40 cm of water (30 mm of Hg) the hepatic resistance
reaches a point of occlusion of the portal vein
and diverts the flow through collaterals without
significantly increasing in pressure.
Q 37. What are the sites of portosystemic
anastomosis?
Sites of portosystemic anastomosis and the
resulting manifestations are:
Sl. No Site Portal Systemic Manifestation
1. Lower end of esophagus Coronary vein from
stomach
Esophageal vein
draining to azygos
and vena cava
Esophageal var ices and
hematemesis
2. Around the umbilicus Veins along the
falciform ligament
Epigastric veins Radiating veins from
umbilicus—caput medusae
Contd...
Portal Hypertension
267
3. At the lower end of rectum Superior rectal vein Middle and inferior
rectal veins
Anorectal varices (they are
submucosal veins extending
upwards well above the level
of hemorrhoids and are easily
compressible)
4. In front of the kidney at the
back of the colon
Vesselsof peritoneum
and colon
Vessels of the kidney
(Veins of Retzius)
5. Bare area of the liver Liver veins Diaphragmatic veins –
(See Fig. 20.1)
Contd...
Fig. 20.1: Portosystemic anastomotic sites
This place is rich in the submucosal veins that
expands disproportionately in patients with portal
hypertension.
Q 39. What is the pathogenesis of rupture of
varices?
There are two theories.
1. Erosion from without (esophagitis)
2. Explosion from within (by increased pressure).
Q 40. Can you get isolated gastric varices without
esophageal varices?
Yes. Isolated thrombosis of the splenic vein causes
localized splenic venous hypertension. This will
result in development of large collaterals from
spleen to gastric fundus. From there the blood
returns to the main portal system through the
gastric coronary vein.
Q 41. How will you assess the functional status of
the liver disease?
Many scoring systems are available. The Child - Pugh
classification is one of the standard systems to
assess the functional status in liver disease.
Q 38. What are the sites of spontaneous bleeding
in portal hypertension?
It is seen only from gastroesophageal junction.
268
Clinical Surgery Pearls
Child-Turcotte-Pugh classification of functional
status in liver disease
Parameter Numerical
score
1 2 3
Class – A
[Risk - Low]
Class – B [Risk
- Moderate]
Class – C
[Risk- High]
Ascites Absent Slight to
Moderate
Tense
Encephalopathy
None Grade I - II Grade III
- IV
Serum albumin
(g/dL)
> 3.5 2.8 – 3.5 < 2.8
Serum bilirubin
mg/dL
< 2 - 0 2.0 – 3.0 > 3.0
Prothrombin
time (seconds
above control)
< 4.0 4.0 – 6.0 > 6.0
Total Child - Turcotte-Pugh Risk
score classification
5 – 6 A Low risk
7 – 9 B Moderate risk
10 – 15 C High risk
Q 42. What is Child’s classification?
Child’s classification of hepatocellular function in
cirrhosis.
Q 43. What are the causes for portal hypertension?
A. May be because of increased resistance to flow:
• Prehepatic
• Hepatic
• Posthepatic.
B. Increased portal blood flow—(because of the
tremendous reserve capacity of the liver to
accommodate increased blood flow, this is
uncommon).
• Banti’s syndrome
• Tropical splenomegaly
• Myeloid metaplasia.
Prehepatic causes
• Thrombosis of portal vein
• Thrombosis of splenic vein
• Congenital stenosis or atresia
• Extrinsic compression by tumors.
Hepatic causes
• Cirrhosis—portal, postnecrotic, biliary, Wilson’s
disease, hemochromatosis
• Congenital hepatic fibrosis
• Idiopathic portal hypertension
• Schistosomiasis
• Chronic active hepatitis
• Acute alcoholic liver diseases.
Posthepatic causes
• Budd-Chiari syndrome (hepatic vein thrombosis)
• Veno-occlusive disease
• Cardiac diseases—constrictive pericarditis, valvular
heart disease, right heart failure, etc.
Q 44. What are the important common causes for
portal hypertension?
Common causes for portal hypertension
1. Cirrhosis
a. Cirrhosis (alcoholic)—85%
b. Postnecrotic cirrhosis
c. Biliary cirrhosis
2. Extrahepatic portal venous thrombosis (children
and younger patients)
3. Idiopathic portal hypertension (Southern Asia)
4. Schistosomiasis (Egypt).
Portal Hypertension
269
Q 45. What is the cause of abnormal resistance in
the portal system in cirrhosis?
The resistance is predominantly postsinusoidal
thought to be because of:
• Distortion of the hepatic veins by degenerating
nodules
• Fibrosis of perivascular tissue around the
sinusoids and hepatic veins
• Centrilobular swelling and fibrosis produce
portal hypertension in acute alcoholic hepatitis
in the absence of cirrhosis.
Q 46. What is wedged hepatic vein pressure?
A catheter is wedged in a tributary of the hepatic
veins that will permit estimation of the pressure in
the afferent veins to sinusoids.
Q 47. What is the site of obstruction in
schistosomiasis?
Schistosomiasis produces presinusoidal obstruction
because of deposition of parasite ova in small portal
venules. This produces inflammation followed by
fibrosis.
Q 48. What is Budd-Chiari syndrome?
This is a condition affecting mainly young females.
The obstruction is in the hepatic veins as a result of
hepatic vein thrombosis or congenital webs (venous
web). The liver becomes congested as a result of
obstruction, resulting in impaired liver function
and portal hypertension. The patient also develops
ascites and esophageal varices. If chronic, the liver
progresses to cirrhosis. It is important to rule out the
cause for venous thrombosis such as:
• Procoagulantstatessuch as protein C, protein S
and antithrombin III, deficiencies
• Myeloproliferative disorders.
Q 49. What is the CT finding in Budd-Chiari
syndrome? (PG)
• Ascites
• Large congested liver (early)
• Small cirrhotic liver(late)withgross enlargement
of segment I (caudate lobe).
Q 50. What is the cause for enlargement of
segment? (PG)
Segment I is having direct venous drainage to the
IVC(inferior vena cava).When there is atrophy ofthe
rest of the liver because of hepatic vein obstruction,
there will be gross enlargement of this segment.
Q 51. How will you confirm the diagnosis of BuddChiari syndrome? (PG)
This is done by hepatic venography through a
transjugular approach. This will reveal occlusion of
the hepatic veins.
Q 52. What is the treatment of Budd-Chiari
syndrome? (PG)
• If cirrhosis is not established—TIPSS or shunt
surgery
• If cirrhosisis established—Livertransplantation
• Lifelong anticoagulation with warfarin may be
required.
Q 53. What is TIPSS?
Transjugularintrahepaticportosystemic stentshunt
(TIPSS) was introduced 1988 as an emergency
treatment for variceal hemorrhage not responding
to medical management and endoscopic
sclerotherapy. The procedure is done under
local anesthesia and sedation using fluoroscopic
guidance and ultrasonography. A guide wire is
inserted through the internal jugular vein and
then via the superior vena cava, hepatic veins and
hepatic parenchyma to a branch of the portal vein.
The track in the parenchyma is then dilated with a
balloon catheter and a metallic stent is inserted.
This will produce satisfactory drop in portal venous
pressure, by shunting blood from portal system to
the inferior vena cava directly.
270
Clinical Surgery Pearls
Q 54. What are the complications of TIPSS? (PG)
• Perforation of liver capsule and fatal intraperitoneal hemorrhage
• TIPSS occlusion—further variceal hemorrhage
• Post-shunt encephalopathy (40%)
• Stenosis of the shunt (50% at one year).
Q 55. What is the cause for post-shunt encephalopathy after TIPSS? What is the incidence? (PG)
The portal blood bypassing the detoxification
effects of the liver will enter the systemic circulation
resulting in a confusional state. It occurs in 40%
of patients similar to the surgical shunts. The
early manifestations are subtle and mental and
personality changes may be overlooked in the
postoperative period. Restlessness, irritability and
insomnia are common. Neuromuscular signs of
unsustained clonus, increased tendon reflexes
and extensor plantar are seen. Blood ammonia
determination is unreliable. Finally more obvious
confusion, drowsiness, stupor and coma develop.
Q 56. What is Banti’s syndrome? (PG)
It is defined as a liver disease secondary to primary
splenic disease. It was erroneously considered as the
cause of portal hypertension but now it is known
that it is as a result of cirrhosis.
Q 57. What are the criteria by which you categorize
a patient to low-risk category in upper GI bleed?
(PG)
Low-risk—upper GI bleed
1. Age < 75 years
2. No unstable comorbid illness
3. No ascites evident on physical examination
4. Normal PT (prothrombin time)
5. Systolic BP above 100 within 1 hour after admission
(with or without fluid resuscitation)
6. Nasogastric aspirate free of fresh blood.
Q 58. What is the management of variceal
bleeding? (flow chart 20.1)
Emergency admission and following management
is carried out.
1. Monitor the patient for BP, pulse, CVP, hematocrit,
hourly urine output
2. Peripheral and central venous access
3. Arrange adequate blood (initially 10 units)
4. Serial hematocrit determination—is best for
monitoring continued blood loss and appropriate
replacement of the lost blood
5. Nasogastric aspiration—look for the color of the
aspirate (blood or altered blood is present or not)
6. Stabilize the patients
7. Endoscopy within 24 hours after admission (in
80% the bleeding source can be identified).
Two lesions are identified in 15% of patients
8. Upper GI series if endoscopy is equivocal
9. Medical management—vasopressin, terlipressin,
somatostatin analog (octreotide)
10. Mechanical—balloon tamponade
11. Interventional—endoscopic sclerotherapy/
banding
12. Prevent encephalopathy
13. Injection vitamin K to correct emergent coagulopathy (fresh frozen plasma may be required to
correct coagulopathy).
14. Maintain fluid and electrolyte balance
15. Surgical—emergency shunt
– Esophageal transection and anastomosis
– Devascularization procedures.
Q 59. What is the initial therapy of choice?
• Endoscopic sclerotherapy or banding
• Vasopressin or propranolol may or may not be
included
Portal Hypertension
271
• Balloontamponade (nolongerusedroutinely)—
reserved for special situations.
Q 60. What is sclerotherapy?
Through the fiberoptic endoscope 1–2 mL of the
sclerosant solution is injected into the varix either
intravariceally or paravariceally in a circumferential
pattern at the gastroesophageal junction and
subsequently also injected 3–4 cm proximal to the
junction. Following the injection, the endoscope is
advanced into the stomach and is keptthere for 4–5
minutes in order to compress the varices. It may be
done as emergency procedure or elective procedure.
Methods of sclerotherapy
a. Intravariceal—obliteration of varices
b. Paravariceal—perivascular cicatrization
c. Combined method of injection.
Flow chart 20.1: The management of portal hypertension
272
Clinical Surgery Pearls
Q 61. What are the sclerosants used? (PG)
The commonly used sclerosants
• Fatty acid derivatives
– Sodium morrhuate (5%)
– Ethanolamine oleate (5%)
• Synthetic products
– STD (Sodium Tetradecyl Sulphate)—1–3%
– Polidocanol (Hydroxy Polyethoxy dodecan (HPD
also called aethoxysklerol - 1%
• Other agents—Butyl cyanoacrylate
• Mixture of sclerosants.
Q 62. What is the mechanism of sclerotherapy? (PG)
It will cause:
• Intimal injury
• Thrombosis ofsubmucosal vessels(in 24 hours)
• Superficial and deep ulceration (5–7 days)
• Submucosal fibrosis (1month).
Q 63. How often sclerotherapy is repeated? (PG)
During active bleeding:
• It is repeated on 3rd day and 7th day
• Afterresolving edema repeatthe procedure 3–4
weeks after the last injection
• 5 to 6 procedures may be required for total
obliteration
• Endoscopic evaluation is done 3 to 6 months
after this.
Q 64. What is a successful sclerotherapy? (PG)
• If the aspirate is clear within 12 hours, it is
considered successful
• If unsuccessful repeat sclerotherapy 3 times at
an interval of 12 hours.
Q 65. What is the success rate of sclerotherapy? (PG)
Sclerotherapy controls bleeding in 80–95% of
patients.
Q 66. What is prophylactic sclerotherapy? (PG)
• When sclerotherapy is given for a patient with
esophageal varices without history of bleeding,
it is called prophylactic sclerotherapy
• When sclerotherapy is given during bleed free
intervals, it is called chronic sclerotherapy
• When it is given during hemorrhage, it is called
acute sclerotherapy.
Q 67. What are the complications of sclerotherapy?
(PG)
Complications may be classified as:
1. Minor
– Substernal pain
– Esophagitis (48 hours)
– Fever—25%
2. Major
Esophageal
– Ulceration—(7 days)
– Perforation (5 – 19 days)
– Stricture (4 months)
Pulmonary and mediastinal
– Pleural effusion right side
– Atelectasis
– Chylothorax right side
– ARDS
3. Rare—Superior mesenteric vein thrombosis.
Q 68. What is the treatment of gastric fundal
varices? (PG)
• Injection sclerotherapy with butyl cyanoacrylate
or
• Endoscopic banding.
Q 69. What is endoscopic banding?
The varix is lifted with suction tip and a small rubber
band is slipped around the base. The varix necroses
leaving behind a superficial ulcer. The rebleeding
episodes are less in banding, so also the morbidity
compared to sclerotherapy.
Portal Hypertension
273
Q 70. What is the role of vasopressin?
The vasopressin will lower the portal blood flow
and portal pressure by directly constricting
splanchnic arterioles. This will reduce the portal
flow. Vasopressin alone controls acute bleeding in
80% of patients and this is increased to 95% when
used in combination with balloon tamponade.
Q 71. What are the complications of vasopressin?
Complications of vasopressin
1. Myocardial infarction
2. Cardiac arrhythmias
3. Intestinal gangrene
4. Reduction in cardiac output
5. Reduces hepatic blood flow
6. Reduces renal blood flow.
Q 72. How can one prevent the complications of
vasopressin?
Simultaneous administration of nitroglycerin or
isoproterenol along with vasopressin.
Q 73. What is the dose of vasopressin?
It is given as an IV infusion in the dose of 0.4 units/
mt. The infusion is better than bolus injection. The
nitroglycerinecanbegivenIVorsublingually(20units
in 10 mL of 5% dextrose IV over 10 minutesinitially).
Q 74. What is Terlipressin?
It is a synthetic vasopressin analog. It undergoes
gradual conversion to vasopressin in the body. It
causes fewer cardiac side effects than vasopressin.
Dose 2 mg bolus injection IV 6th hourly.
Q 75. What is the role of octreotide acetate?
It is a long-acting synthetic somatostatin analog.
The action is similar to vasopressin but without
significant side effects. This is the drug of choice
for the pharmacological control of acute bleeding
varices.
Dose: 100 µg initial bolus, followed by continuous
infusion of 25 µg/h for 24 hours.
Q 76. What is the effectiveness of pharmacological
control?
• Vasopressin alone is superior to placebo
• Vasopressin and nitroglycerine is superior to
vasopressin alone.
Q 77. What is the role of Sengstaken-Blakemore
tube?
It is used for temporary hemostasis initially (balloon
tamponade). It has got 3 lumens with 2 balloons
which can be inflated (esophageal balloon and
gastric balloon). The balloons are inflated in the
lumen of gut (gastric balloon is inflated with 250
ml of air, and esophageal balloon to a pressure of
40 mm of Hg). The third lumen is for aspiration of the
gastric contents. The tube is introduced transorally.
After inflating the two balloons, traction is applied
to the tube so that gastric balloon compresses the
collateral veins at the cardia of the stomach. The
contribution of esophageal balloon compression
is negligible. The balloon should be temporarily
deflated after 12 hours to prevent pressure necrosis
of the esophagus.
Q 78. What are the complications of this tube?
• Aspiration of pharyngeal secretions and
pneumonia
• Esophageal rupture (this balloon is therefore
infrequently used)
• Pressure necrosis of the esophagus.
Q 79. What is the success rate of balloon
tamponade?
Above 75% of the actively bleeding patients can be
controlled by balloon tamponade. When bleeding
has stopped, it should be left in place for another
24 hours.
274
Clinical Surgery Pearls
Q 80. What is Minnesota tube?
This tube has got a 4th lumen to aspirate the
esophagus proximal to the balloon.
Q 81. What is the role of TIPSS in the management
of portal hypertension (read the answer in the
initial part of this chapter)? (PG)
• It is useful for the control of acute bleeding and
to prevent rebleeding (the portal hypertension
also is controlled)
• Patients with advanced liver disease are
considered for TIPSS
• TIPSS is used as a bridge to transplantation
• It should not be regarded for definitive therapy
(the shunt remains open for up to a year)
• Less severe cirrhosis patients—consider for
shunt surgery/devascularization.
Q 82. What are the surgical options? (Flow Chart 20.1)
• Surgical procedures may be classified as:
– Emergency procedures
– Elective surgical procedures.
Q 83. What are the emergenc y surgical
procedures? (PG)
• Surgical procedures are rarely considered for
the acute management of variceal hemorrhage,
since the morbidity and mortality are high
• The increasing availability of TIPSS and liver
transplantation is another factor
• Initial bleeding is usually controlled with
sclerotherapy/banding
• The main indication for surgery is a Child’s
grade—Acirrhoticpatientinwhomthebleeding
has been controlled by sclerotherapy
1. Emergency shunt operations
2. Emergency esophageal transection (stapled
transection)
3. Emergency devascularization.
Note:All these procedures are usually done as
elective procedures.
Q 84. What is the principle of shunt surgery and
what are the types of shunt surgery?
They reduce the pressure in the portal circulation by
diverting the blood into the low-pressure systemic
circulation. The different types of shunts are:
Nonselective (portacaval)
1. Side-to-side—portacaval, mesocaval, renosplenic, etc.
2. End-to-side—portacaval (total)
3. Mesocaval (H)
Selective
1. Distalsplenorenal (lienorenal) (Warren shunt)—
it is time consuming in emergency situations
2. Left gastric vena caval (Inokuchi).
Q 85. What are the advantages of selective
shunt? (PG)
• They preserve blood flow to the liver while
decompressing the left side of the portal
circulation, that is responsible for esophageal
and gastric varices.
• Selective shunts are associated with lower
incidence of portosystemic encephalopathy (PSE).
Q 86. What is total shunt (Eck fistula)? (PG)
This is an end-to-side shunt that completely
disconnects the liver from the portal system. The
portal vein is transected near its bifurcation in the
liver hilum and anastomosed to the side of the
inferior vena cava. The hepatic stump of the vein
is over sewn. This type of shunt gives immediate
and permanent protection from variceal bleeding
and somewhat easier to perform than side-to-side
portacaval shunt. Encephalopathy is less compared
to side-to-side shunt.
Portal Hypertension
275
Q 87. What is mesocaval shunt?
A segment of prosthetic graft or internal jugular
vein is anastomosed between the inferior vena cava
and the superior mesenteric vein. It is useful in cases
of portal vein thrombosis. The portal flow to the liver
is lost in this procedure. The portal flow to the liver
can be preserved by reducing the diameter of the
graft to 8 mm (from 12–20 mm). This will decrease
the incidence of encephalopathy, still preventing
variceal hemorrhage.
Q 88. What is central splenorenal shunt? (PG)
Here splenectomy is performed and the splenic vein
is anastomosed to the renal vein.
Q 89. What are the emergency shunt surgical
procedures commonly performed? (PG)
1. End-to-side portacaval
2. H - mesocaval shunt.
Q 90. What is the contraindication for shunt
procedure? (PG)
A good transplantation candidate should not be
subjected to portosystemic shunt or other shunt.
Generally, Child’s class A, patients are candidates
for portal decompression and class C patients are
candidates for transplantation.
Q 91. How will you select a shunt procedure? (PG)
• For elective portal decompression—distal
splenorenal shunt (Warren)
• If ascitesispresent—end-to-sideportacavalshunt
• Severe ascites—side-to-side shunt
• Budd-Chiari syndrome
• Emergency decompression—end-to-side or H
mesocaval.
Q 92. What are the results of portosystemic
shunts? (PG)
• Incidence of recurrent variceal bleeding—10%
• 5-year-survival for alcoholic liver disease—45%
• Encephalopathy15–25%(severeencephalopathy
in 20% of alcoholic after total shunt)
• Patency of shunt—90%.
Q 93. What is esophageal transection (stapled
transection)?
In many surgical units, it is the first choice when
nonsurgical methods fail. It must be done as soon
as a second attempt at sclerotherapy has failed. It
must be viewed as an emergency procedure and
not a definitive treatment.
Circular stapling device is used for resecting and
reanastomosing a ring of the lower esophagus. This
procedure is being replaced by TIPSS in centers
where it is available.
Q 94. What are the devascularization procedures?
(PG)
The devascularization procedures reduce proximal
gastric blood flow.
These procedures are not done nowadays.
1. Gastroesophageal decongestion and splenectomy
of Hassab—Allthe vessels exceptthe left gastric
vessels are ligated.
2. Sugiura procedure—it is done in two stages. The
first stage is transthoracic and the dilated venous
collaterals between esophagus and adjacent
structures are divided. The esophagus is then
transected and reanastomosed. The second
stage is done by laparotomy after the first stage
ifthepatientisbleeding (butdeferred 4–6weeks
in the elective cases). The upper 2/3rds of the
stomach is devascularized, selective vagotomy,
pyloroplasty and splenectomy are performed.
Q 95. What is the definitive treatment for portal
hypertension because of cirrhosis?
In cirrhosis the basic pathology is failing liver
cells and none of these procedures will rectify
276
Clinical Surgery Pearls
the problem. Therefore, the definitive treatment
is liver transplantation. Any young patient with
cirrhosis who has survived an episode of variceal
hemorrhage should be considered a candidate for
liver transplantation. Any other form of treatment
carries a much higher mortality rate within the
subsequent 1–2 years.
Q 96. What are the contraindications for liver
transplantation? (PG)
Contraindications for liver transplantation
1. Age > 65 years
2. Ischemic heart disease
3. Cardiac failure
4. Chronic respiratory disease
5. Continued alcohol use
6. Previous surgical shunt (relative).
Q 97. What is the procedure of choice during the
preparation period for transplantation? (PG)
Transjugular intrahepatic protosystemic shunt
(TIPSS).
Q 98. What is the treatment of nonbleeding
varices (prophylactic therapy)?
There is a 30% chance for bleeding at some point
for this group of patients. Of those who bleed
50% die. Patients who have bled once from
varices have a 70% chance of bleeding again. The
treatment of patients with varices that have never
bled is referred to as prophylactic therapy. Thus,
we have prophylactic sclerotherapy, prophylactic
propranolol, etc. The therapy of patients who
have bled before is referred to as therapeutic. The
prophylactic therapy consists of the following:
a. Prophylactic sclerotherapy
b. Prophylactic propranolol.
Q 99. What is the action of propranolol?
This beta-adrenergic blocking agent decreases
cardiac output and splanchnic blood flow and
therefore reduces the portal blood pressure.
Chronic propranolol therapy in a dose of 20–160 mg
twice daily decreases the frequency of rebleeding
by 40%. It also reduces the overall mortality.
Q 100. What is left sided portal hypertension?
It is caused by isolated splenic vein thrombosis.
Q 101. What are the causes of ascites in portal
hypertension?
• Decreased colloid osmotic pressure (decreased
proteins)
• Increased hydrostatic pressure
• Lymphatic blockage.
Q 102. What are the complications of ascites?
Complications of ascites
• Umbilical hernia
• Spontaneous bacterial peritonitis
• Respiratory embarrassment.
Q 103. What is the treatment of ascites in portal
hypertension?
1. Medical
– Spironolactone 25 mg bd orally
– Limit sodium intake.
2. Ascitic tap—slow gradual tapping is done
3. Shunt operations
– Leveen shunt (peritoneovenous shunt—
peritoneal cavity to internal jugular vein)
– Denver shunt—Peritoneal cavity to internal
jugular vein with a subcutaneous chamber
that can be milked when blocked.
Portal Hypertension
277
Q 104. What is the management of encephalopathy?
1. Protein-free diet
2. Oral Lactulose—30 mL tid
3. Oral neomycin—1–2 g 6th hourly (not given in
renal impairment)
4. Parenteral nutrition—(calories from carbohydrate sucrose is preferred over glucose)
5. Administration of 50% glucose in central vein.
Q 105. What is hepatorenal syndrome?
Acute renal failure without apparent cause may
occur in patients with liver disease at any time
during hospitalization. This is due to impaired renal
perfusion. Other possible causes include infection,
drug toxicity, etc. They usually succumb to hepatic
failure.
21 Mesenteric Cyst
Case
Case Capsule
A 15-year-old girl presents with abdominal
distension and recurrent colicky type of abdominal
pain of two months duration. There is no associated
vomiting and no other complaints. There is no
history of respiratory infection preceding the attack.
There is no alteration in bowel habits.
On general examination, she is afebrile, not ill
looking. There is no generalized lymphadenopathy
and no icterus. There is no circumoral pallor. On
examination of the abdomen, a central abdominal
fullness is noticed on inspection. A spherical
swelling of 15 cm diameter is situated in the
umbilical region, all the borders of which are welldefined. The surface of the swelling is smooth.
The swelling moves freely at right angles to the
line of attachment of the mesentery. It is dull to
percussion, however, the surrounding areas are
resonant. On fixing the swelling with the help of
the patient’s hand, it appears to be fluctuant. The
swelling cannot be pushed to the pelvis. There is
neither shifting dullness nor fluid thrill. There is
no organomegaly. The hernial orifices are normal.
On digital rectal examination, it is not possible to
feel the swelling from below. The supraclavicular
nodes are not enlarged.
Read the checklist for abdominal examination.
Checklist for history
Checklist for examination
Look for
• Circumoral pallor—mesenteric adenitis
• Cervical lymph nodes—seen in mesenteric
lymphadenitis
• Shifting tenderness, which is a sign of mesenteric
adenitis
• Free movement in a plane at right angles to the
attachment of mesentery (from left of the umbilicus
to the right iliac fossa)
• A zone of resonance around the swelling.
Q 1. What is the probable diagnosis in this case?
Mesenteric cyst.
Q 2. What are the differential diagnoses?
Differential diagnoses of central abdominal
cystic swelling
• Ovarian cyst
• Omental cyst
• Cyst of the mesocolon
• Tuberculous abscess in the mesentery
• Hydatid cyst of the mesentery
Contd...
Mesenteric Cyst
279
• Pancreatic pseudocyst
• Inflammatory cyst
• Serosanguinous cyst—may be traumatic in origin
• Retroperitoneal cyst.
Q 3. What are the characteristics of mesenteric
cyst?
1. A cystic swelling in the center of the abdomen
2. It moves at right angles to the line of attachment
of the root of the mesentery, but only slightly,
parallel to the root of the mesentery
3. Fluid thrill will be present
4. It is dull to percussion
5. One can get below the swelling (unlike ovarian cyst)
6. There is a zone of resonance around the cyst.
Q 4. What is the line of attachment of mesentery?
It is attached to the posterior abdominal wall to
the left of the 2nd lumbar vertebrae and passes
obliquely to the right and inferiorly to the right
sacroiliac joint and is 15 cm long.
Surface marking in the abdomen:
An oblique line starting 2.5 cm to the left of the
midline and 2.5 cm below the transpyloric plane and
extending downwards and to the right for about 15
cm.
Direction of movement of mesenteric cyst is
showing in Figure 21.1.
Q 5. What is the “sign of mesenteric cyst”?
Tillaux Triad
1. Soft swelling at the level of umbilicus
2. Movement perpendicular to mesentery
3. Dull note over the swelling surrounded by
resonance.
The lump moves in a plane from the right
hypochondrium to the left iliac fossa, but not in
the plane at right angles to this.
Q 6. What is mesenteric cyst and what is the
classification?
• They are developmental lesions
Classification of mesenteric cyst
• Chylolymphatic (commonest variety)
• Enterogenous
• Urogenital remnant
• Dermoid (teratomatous cysts).
Q 7. What is the age group affected by mesenteric
cyst?
• Most frequently in the second decade
• Less often 1 – 10 years
• Exceptionally in infants under 1year.
Contd...
Fig. 21.1: Mesentery (small intestine) attachment
direction of movement of mesenteric cyst
280
Clinical Surgery Pearls
3. Hemorrhage into the cyst
4. Infection
5. Peptic ulceration (when it contains ectopic
gastric mucosa)
6. Perforation
Q 11. How will you differentiate it from omental
cyst?
A lateral radiograph or ultrasound or CT scan will
show the cyst in front of the intestines, if it is an
omental cyst.
Q 12. What are the investigations in a suspected
case of mesenteric cyst?
1. Plain X-ray will show calcified lymph nodes in
tuberculous mesenteric lymph nodes
2. Barium meal and follow through hollow viscera
will be found to be displaced around the cyst or
lumen of the intestine may be seen narrowed
3. Ultrasoundabdomenwillrevealthe cysticnature
and the origin of the cyst
4. IVU to rule out hydronephrosis if ultrasound is
not done
5. CT scan
6. Needle aspiration and instillation of radio-paque
water-soluble contrast media.
Q 13. What is the treatment of chylolymphatic
cyst?
• Enucleation in toto
• After major portion of the cyst has been
dissected free, a portion abutting on the
intestine or a major blood vessel can be left
attached after destroying its lining.
Q 14. What is the treatment of enterogenous cyst?
• Enucleation is contraindicated
• Resection of the cyst with adherent portion of
the intestine followed by intestinal anastomosis
Q 8. What are the differences between
chylolymphatic cyst and enterogenous cysts?
Differences between chylolymphatic cyst and
enterogenous cysts
Chylolymphatic cyst Enterogenous cysts
• Arises from congenitally
misplaced lymphatic
tissue with no efferent
communication with
lymphatic system
• Arisesfromadiverticulum
of the mesenteric border
of the intestine which has
become sequestrated
from the intestinal canal or
duplication of the intestine
• Wall is thin—connective
tissue lined by endothelium
• Thicker wall—lined by
m u c o u s m e m b r a n e
(sometimes ciliated)
• Filled with clearlymph or
chyle (milky)
• Content is mucinous
(colorless or yellowish
brown)
• Blood supply is independent of that of the
adjacent intestines
• Common blood supply
with intestine
• Usually enucleation is
possible without resection of the gut
• Removal always entails
resection of the related
portion of intestine
Q 9. What is the cause for recurrent attacks of
abdominal pain?
It may be due to—
1. Torsion of the mesentery
2. Temporary impaction of food bolus in the
intestine narrowed by the cyst.
Q 10. What are the complications of the cyst?
Complication of mesenteric cyst
1. Torsion of the cyst
2. Rupture of the cyst
Contd...
Contd...
Mesenteric Cyst
281
• If a very large segment of small intestine is
implicated, an anastomosis should be made
between the apex of the coil of small intestine
and the cyst wall (the cyst wall will hold sutures
well).
Q 15. What is the role of marsupialization?
This is an old form of treatment not recommended
nowadays because of the fear of fistula and
recurrence.
Q 16. What is the surgical treatment if it is an
omental cyst?
Omentectomy.
Q 17. What are the neoplasms of the mesentery?
They are classified as benign and malignant.
Benign Malignant
• Lipoma • Lymphoma
• Fibroma • Secondary carcinoma
• Fibromyxoma
Q 18. What is the management of benign
neoplasms?
Benign tumors are excised in the same way as
mesenteric cyst, along with resection of the
adjacent intestine.
Q 19. What is the management of malignant
neoplasms?
• Biopsy confirmation
• Chemotherapy for lymphoma
• Chemotherapy for secondary carcinoma.
Q 20. How does tuberculous lymphadenitis occur?
The tubercle bacilli are usually ingested and they
enterthe mesenteric lymph node by way of Peyer’s
patches. The organism may be human or bovine. It
can occur after ingestion of raw milk. It may affect
a single lymph node or multiple lymph nodes
presenting as massive abdominal swelling.
Q 21. What is pseudomesenteric cyst?
When tuberculous mesenteric lymph nodes breakdown, the tuberculous pus may remain between
the leaves of the mesentery and cystic swelling
similar to mesenteric cyst is formed. When such
a situation is found the pus is evacuated without
soiling the peritoneal cavity and anti tuberculous
treatment is instituted.
Q 22. What is the cause for yellow-colored lymph
nodes in the ileocecal region?
Metastasis from carcinoid of the appendix will give
rise to yellow color for the lymph nodes.
Q 23. What are the causes for calcified shadows in
the plain radiograph of the abdomen?
Causes for radiopaque shadow in
plain X-ray abdomen
1. Renal or ureteric stone (renalstones are uniform in
density, take the shape of pelvicalyceal system and
lies superimposed on the shadows of the vertebral
column in the lateral view)
2. Gallstones are (less dense in the center and in front
of the vertebral bodies on the lateral view)
3. Pancreatic calculi
4. Calcified tuberculous lymph node—usually in
the ileocecal region and line of attachment of the
mesentery—outline isirregular and the nodes are
mottled like black berry
5. Phlebolith
6. Calcified costal cartilage
7. Fecolith
8. Stone in the appendix
9. Calcified renal artery
10. Calcified aneurysm of the abdominal aorta
11. Chip fracture of the transverse process of the
vertebrae.
282
Clinical Surgery Pearls
Q 24. How long it will take for calcification to occur
in tuberculous lymph nodes?
Eighteen months.
Q 25. Will the nodes be noninfective in such a
situation?
No. The node need not be defunct. So infection is
still possible.
Q 26. What is the cause for acute non specific
ileocecal mesenteric adenitis?
The etiology of this condition is unknown, it
affects children and unusual after puberty. Some
cases are associated with Yersinia infection of
the ileum. In other situations unidentified virus is
blamed. Respiratory infection precedes an attack of
mesenteric adenitis. This is a self-limiting disease. It
is called nonspecific in order to distinguish it from
tuberculous mesenteric adenitis.
Q 27. What are the clinical manifestations of
nonspecific mesenteric adenitis?
• Central abdominal pain lasting for 10–30 minutes
• Associated circumoral pallor
• Vomiting is common
• No alteration in bowel habits
• Intervals of complete freedom from pain
• The patient seldom looks ill
• Temperature may be elevated but never exceeds
38.5
• Tenderness along the line of mesentery
• Shifting tenderness(afterthe patientlies on the left
side for a few minutes the tenderness shift to the
left side)
• Pelvic peritoneum is tender to palpation.
Q 28. What will be the total leukocyte count like?
There is often leukocytosis in contrast to
tuberculosis.
Q 29. What is the treatment of nonspecific
mesenteric adenitis?
• Bed rest for a few days (if the diagnosis can be
made with certainty).
• If appendicitis cannot be excluded do
laparoscopy followed by appendectomy if
requir
clinical surgery pearls
clinical surgery pearls 3rd edition pdf
clinical surgery pearls 3rd edition pdf free download
clinical surgery pearls dayananda babu pdf
clinical surgery pearls pdf
clinical surgery pearls pdf google drive
clinical surgery pearls latest edition
clinical surgery pearls 2nd edition pdf free download
clinical surgery pearls pdf free download
clinical surgery pearls 3rd edition free pdf
clinical surgery pearls and co
clinical surgery pearls and beauty
clinical surgery pearls and skin
clinical surgery pearls clinic
clinical surgery pearls canada
clinical surgery pearls course
clinical surgery pearls clinical
clinical surgery pearls clinical trials
clinical surgery pearls dayananda babu pdf free download
clinical surgery pearls pdf download
clinical surgery pearls hotel
clinical surgery pearls hospital
clinical surgery pearls harvard
clinical surgery pearls harris
clinical pearls surgery
clinical surgery pearls journal
clinical surgery pearls japan
clinical surgery pearls jewellery
clinical surgery pearls jewelry
clinical surgery pearls kit
clinical surgery pearls ksa
clinical surgery pearls ks
clinical surgery pearls meaning
clinical surgery pearls mdpi
clinical surgery pearls medical
clinical surgery pearls md
clinical surgery pearls mcgill
clinical surgery pearls near me
clinical surgery pearls ncbi
clinical surgery pearls nursery
general surgery pearls of wisdom pdf
clinical surgery pearls qatar
clinical surgery pearls questions
clinical surgery pearls quiz
clinical surgery pearls review
clinical surgery pearls reviews
clinical surgery pearls spain
clinical surgery pearls spa
clinical surgery pearls sc
clinical surgery pearls st
clinical surgery pearls test
clinical surgery pearls therapy
clinical surgery pearls thesis
clinical surgery pearls video
clinical surgery pearls vessel
clinical surgery pearls valley
clinical surgery pearls xl
clinical surgery pearls youtube
clinical surgery pearls yellow
clinical surgery pearls yahoo finance
clinical surgery pearls yahoo
clinical surgery pearls yugioh
clinical surgery pearls zambia
clinical surgery pearls zurich
clinical surgery pearls zone
clinical surgery pearls zanzibar
can clinical surgery pearls and co
can clinical surgery pearls and beauty
can clinical surgery pearls and skin
can clinical surgery pearls benefits
can clinical surgery pearls before and after
can clinical surgery pearls before swine
can clinical surgery pearls black
can clinical surgery pearls canada
can clinical surgery pearls clinic
can clinical surgery pearls cost
can clinical surgery pearls costco
can clinical surgery pearls co
can clinical surgery pearls experience
can clinical surgery pearls free
can clinical surgery pearls for sale
can clinical surgery pearls for dogs
can clinical surgery pearls guide
can clinical surgery pearls good
can clinical surgery pearls growth
can clinical surgery pearls good or bad
can clinical surgery pearls guidelines
can clinical surgery pearls hospital
can clinical surgery pearls harvard
can clinical surgery pearls how to use
can clinical surgery pearls inc
can clinical surgery pearls in india
can clinical surgery pearls in china
can clinical surgery pearls in canada
can clinical surgery pearls journal
can clinical surgery pearls jobs
can clinical surgery pearls job description
can clinical surgery pearls job
can clinical surgery pearls journals
can clinical surgery pearls kit
can clinical surgery pearls kopen
can clinical surgery pearls ksa
can clinical surgery pearls meaning
can clinical surgery pearls mdpi
can clinical surgery pearls medical
can clinical surgery pearls md
can clinical surgery pearls mcgill
can clinical surgery pearls near me
can clinical surgery pearls ncbi
can clinical surgery pearls nursery
can clinical surgery pearls online
can clinical surgery pearls of the world
can clinical surgery pearls quotes
can clinical surgery pearls questions
can clinical surgery pearls quiz
can clinical surgery pearls quora
can clinical surgery pearls review
can clinical surgery pearls reviews
can clinical surgery pearls reddit
can clinical surgery pearls test
can clinical surgery pearls thesis
can clinical surgery pearls uk
can clinical surgery pearls uses
can clinical surgery pearls us
can clinical surgery pearls use
can clinical surgery pearls up
can clinical surgery pearls video
can clinical surgery pearls valley
can clinical surgery pearls work
can clinical surgery pearls worth
can clinical surgery pearls worth it
can clinical surgery pearls with
can clinical surgery pearls works
can clinical surgery pearls xl
can clinical surgery pearls xray
can clinical surgery pearls youtube
can clinical surgery pearls yellow
can clinical surgery pearls you
can clinical surgery pearls zurich
can clinical surgery pearls zambia
can clinical surgery pearls zanzibar
how clinical surgery pearls are
how clinical surgery pearls are made
how clinical surgery pearls benefits
how clinical surgery pearls before and after
how clinical surgery pearls canada
how clinical surgery pearls cost
how clinical surgery pearls cancer
how clinical surgery pearls come from
how clinical surgery pearls experience
how clinical surgery pearls experiment
how clinical surgery pearls free
how clinical surgery pearls foundation
how clinical surgery pearls good
how clinical surgery pearls grow
how clinical surgery pearls goodreads
how clinical surgery pearls good or bad
how clinical surgery pearls goods
how clinical surgery pearls have
how clinical surgery pearls harvard
how clinical surgery pearls inc
how clinical surgery pearls is
how clinical surgery pearls journal
how clinical surgery pearls jewellery
how clinical surgery pearls job description
how clinical surgery pearls journals
how clinical surgery pearls jewelry
how clinical surgery pearls kit
how clinical surgery pearls ksa
how clinical surgery pearls ks
how clinical surgery pearls knowledge
how clinical surgery pearls meaning
how clinical surgery pearls mean
how clinical surgery pearls means
how clinical surgery pearls made
how clinical surgery pearls make
how clinical surgery pearls near me
how clinical surgery pearls needed
how clinical surgery pearls norway
how clinical surgery pearls open
how clinical surgery pearls on
how clinical surgery pearls out
how clinical surgery pearls opened
how clinical surgery pearls of the world
how clinical surgery pearls questions
how clinical surgery pearls quiz
how clinical surgery pearls quotes
how clinical surgery pearls quora
how clinical surgery pearls quizlet
how clinical surgery pearls review
how clinical surgery pearls start
how clinical surgery pearls soap
how clinical surgery pearls started
how clinical surgery pearls test
how clinical surgery pearls thesis
how clinical surgery pearls use
how clinical surgery pearls uses
how clinical surgery pearls up
how clinical surgery pearls used
how clinical surgery pearls video
how clinical surgery pearls valley
how clinical surgery pearls work
how clinical surgery pearls works
how clinical surgery pearls worth
how clinical surgery pearls worked
how clinical surgery pearls worth it
how clinical surgery pearls xl
how clinical surgery pearls xray
how clinical surgery pearls youtube
how clinical surgery pearls you
how clinical surgery pearls yellow
how clinical surgery pearls yeast
how clinical surgery pearls zurich
how clinical surgery pearls zap
how clinical surgery pearls zundert
how to do clinical surgery pearls
which clinical surgery pearls are best
which clinical surgery pearls are made
which clinical surgery pearls are the same
which clinical surgery pearls benefits
which clinical surgery pearls before and after
which clinical surgery pearls better
which clinical surgery pearls canada
which clinical surgery pearls cost
which clinical surgery pearls come from
which clinical surgery pearls everyday
which clinical surgery pearls end
which clinical surgery pearls fit
which clinical surgery pearls foundation
which clinical surgery pearls found
which clinical surgery pearls fellow
which clinical surgery pearls fellows
which clinical surgery pearls good
which clinical surgery pearls grow
which clinical surgery pearls have
which clinical surgery pearls is best
which clinical surgery pearls is good
which clinical surgery pearls journal
which clinical surgery pearls jewellery
which clinical surgery pearls joint
which clinical surgery pearls killed
which clinical surgery pearls mean
which clinical surgery pearls made
which clinical surgery pearls means
which clinical surgery pearls make
which clinical surgery pearls needed
which clinical surgery pearls near me
which clinical surgery pearls need
which clinical surgery pearls open
which clinical surgery pearls on
which clinical surgery pearls offer
which clinical surgery pearls of the world
which clinical surgery pearls on a plane
which clinical surgery pearls quora
which clinical surgery pearls quiz
which clinical surgery pearls quality
which clinical surgery pearls questions
which clinical surgery pearls quote
which clinical surgery pearls review
which clinical surgery pearls real
which clinical surgery pearls replacement
which clinical surgery pearls reviews
which clinical surgery pearls support
which clinical surgery pearls start
which clinical surgery pearls started
which clinical surgery pearls test
which clinical surgery pearls the same
which clinical surgery pearls use
which clinical surgery pearls uses
which clinical surgery pearls valley
which clinical surgery pearls work
which clinical surgery pearls works
which clinical surgery pearls worth it
which clinical surgery pearls worth
which clinical surgery pearls xl
which clinical surgery pearls x ray
which clinical surgery pearls you
which clinical surgery pearls youtube
which clinical surgery pearls zurich
which clinical surgery pearls zap
which clinical surgery pearls zen
surgical examination
asmbs clinical pearls for emergency care of the bariatric surgery patient
clinical pearls for emergency care of the bariatric surgery patient
surgery examination
kaplan obstetrics and gynecology videos
طبيب سوداني باثولوجي
best of clinical surgery pearls
best and clinical surgery pearls
clinical surgery pearls شرح
clinical surgery pearls مترجم
clinical surgery pearls arabic
clinical surgery pearls download
clinical surgery pearls en arabe
clinical surgery pearls egybest
clinical surgery pearls greek
clinical surgery pearls gel شرح
clinical surgery pearls how to use in hindi
clinical surgery pearls hindi
clinical surgery pearls in hindi
clinical surgery pearls in شرح
clinical surgery pearls in arabic
clinical surgery pearls kurdish
clinical surgery pearls plus شرح
clinical surgery pearls review شرح
clinical surgery pearls uses in hindi
clinical surgery pearls uses in urdu
clinical surgery pearls us شرح
clinical surgery pearls white شرح
clinical surgery pearls x شرح
clinical surgery pearls xl شرح
can clinical surgery pearls arabic
can clinical surgery pearls download
can clinical surgery pearls egybest
can clinical surgery pearls greek
can clinical surgery pearls gel شرح
can clinical surgery pearls how to use in hindi
can clinical surgery pearls in hindi
can clinical surgery pearls in شرح
can clinical surgery pearls in arabic
can clinical surgery pearls like شرح
can clinical surgery pearls pdf
can clinical surgery pearls para que sirve
can clinical surgery pearls turkish
can clinical surgery pearls uses in hindi
can clinical surgery pearls uses in urdu
can clinical surgery pearls white شرح
can clinical surgery pearls x شرح
can clinical surgery pearls yapımı
how clinical surgery pearls arabic
how clinical surgery pearls download
how clinical surgery pearls does شرح
how clinical surgery pearls egybest
how clinical surgery pearls greek
how clinical surgery pearls gel شرح
how clinical surgery pearls hindi
how clinical surgery pearls how to use in hindi
how clinical surgery pearls in hindi
how clinical surgery pearls in hindi شرح
how clinical surgery pearls in شرح
how clinical surgery pearls in arabic
how clinical surgery pearls kurdish
how clinical surgery pearls like شرح
how clinical surgery pearls pdf
how clinical surgery pearls uses in hindi
how clinical surgery pearls uses in urdu
how clinical surgery pearls use in hindi
how clinical surgery pearls works شرح
how clinical surgery pearls work شرح
how clinical surgery pearls x شرح
how clinical surgery pearls zinc شرح
which clinical surgery pearls arabic
which clinical surgery pearls download
which clinical surgery pearls egybest
which clinical surgery pearls in hindi
which clinical surgery pearls pdf
which clinical surgery pearls quail
which clinical surgery pearls uses in hindi
which clinical surgery pearls use in hindi
which clinical surgery pearls uses in urdu
No comments:
Post a Comment
اكتب تعليق حول الموضوع