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Figure 95-2. Upper extremity splints. A. Coaptation

splint. B. Sugar-tong splint. C. Long arm posterior

splint. D. Gutter splints. E. Dorsai "Ciam digger" splint.

F. Thumb splint and th umb spica splint. G. Finger

splint. Reprinted with permission from Simon RR,

Sherman SC. Spli nts, Casts, and Other Techniques. In:

Simon RR, Sherman sc, eds. Emergency Orthopedics.

6th ed. New York: McGraw-Hill, 201 1.

Finger Splints

These splints can be rapidly placed using commercially

available malleable padded materials (Figure 95-2G).

Finger splints are used to protect the digits after phalangeal

fractures. Alternatively, a dynamic finger splint can be used

when a minor ligamentous sprain occurs at a proximal

interphalangeal joint. Apply this functional splint by taping

the proximal and middle phalanx of the injured digit to an

uninjured neighboring finger (buddy taping).

CONTRAINDICATIONS

There are no absolute contraindications to splinting. Ensure

proper wound care for all lacerations or open wounds before

splint application. When re-evaluating such a patient, remove

the splint to inspect for subsequent wound infection.

EQUIPMENT

Supplies include stockinette, cotton padding, fiberglass or

plaster splint material, scissors, warm water, and elastic

bandages.

PROCEDURE

Place a stockinette on the involved extremity extending

beyond the proximal and distal limits of where the splint

will be applied (optional). Use the patient's noninjured

extremity to measure the correct length of necessary

material. Cut either prefabricated fiberglass or approxi ­

mately 1 0-15 sheets of plaster to the proper length.

..... Fiberglass

Most EDs use fiberglass splinting material as its application

is both easy and quick. It comes prefabricated with a layer

of padding wrapped around the fiberglass. It should be

placed on the injured extremity after lightly wetting the

fiberglass component with warm water. Important tips

when using fiberglass splint material include:

1. When working with fiberglass rolls, clamp the unused

end of the protective covering immediately after cutting the splint material. This prevents prolonged air

exposure and subsequent hardening of the entire roll.

2. Some prefabricated fiberglass splint material has a

padded side and a nonpadded side. Remember to place

the padded side against the skin.

3. Stretch the padding longitudinally to ensure that it

covers the cut ends of the fiberglass, as exposed edges

that remain in direct contact with the skin after

hardening can induce skin injury (Figure 95-3 ).

...,._ Plaster

When applying a plaster splint, start by circumferentially

wrapping several layers of cotton padding around the affected

extremity. Take special care to apply extra layers of padding

over bony protuberances ( eg, the malleoli) where excessive

pressure might induce underlying skin necrosis. Finally,

remember to place extra padding between all involved digits.

Briefly soak the premeasured plaster in a bath of warm

water. Remove excess water by wringing the plaster between

the hands and smooth out the sheets by holding them up

with one hand while the thumb and index finger of the other

SPLINTING

Figure 95-3. Skin injury due to a fiberglass splint

that was appl ied improperly. The padding should be

stretched longitudinally to avoid contact between the

hard, dried plaster and the skin.

hand gently squeeze out any folds and/or air pockets. As the

calcium sulfate in the plaster reacts with the water it will

produce heat as it cures, which the patient will notice as the

splint is applied. Place the splint on the appropriate extremity and add an additional layer of cotton padding over the

plaster (optional). This will prevent the final layer of the

splint (elastic bandage) from adhering to the drying plaster.

Circumferentially wrap the extremity and splinting material (whether fiberglass or plaster) with an elastic bandage,

taking care to ensure that the splint remains in the desired

position when finished. Avoid over-tightly wrapping the

extremity to prevent the development of a secondary com partment syndrome. Instruct the patient to not move the extremity

until the splint has adequately hardened (5-10 minutes).

COMPLICATIONS

Circumferential bandages, especially when applied too

tightly, may produce an iatrogenic compartment syndrome.

Instruct the patient to return to the ED with the development

of any worsening pain or new numbness or tingling of the

extremity. Additionally, plaster splints will produce a significant amount of heat as they dry, which can result in thermal

injuries when insufficient cotton padding is used .

SUGGESTED READING

Menkes JS. Initial evaluation and management of orthopedic

injuries. In: Tintinalli JE, Stapczynski JS, Ma OJ, Cline DM,

Cydulka RK, Meckler GD. Tintinalli's Emergency Medicine: A

Comprehensive Study Guide. 7th ed. New York, NY: McGrawflill, 20 l l, pp. 1 783-1796.

Simon RR, Sherman SC. General principles and appendix. In:

Simon RR, Sherman SC. Emergency Orthopedics. 6th ed. New

York, NY: McGraw-flill, 201 1, pp. 1-3 1 and 563-579.

Life-Th reatening

Dermatoses

Henry z. Pitzele, MD

Chad 5. Kessler, MD

Key Points

• Rapid identification of life-threatening rashes and

immed iate treatment can be life-saving.

INTRODUCTION

Cutaneous lesions can be the first clinical sign of a serious

systemic illness. It is important to recognize and treat these

illnesses early. Life-threatening dermatoses can be grouped

into 3 distinct categories: erythrodermas (diffuse red rashes),

vesiculobullous lesions, and hemorrhagic lesions.

� Erythrodermas

Staphylococcal scalded skin syndrome (SSSS) is an exotoxinproducing Staphylococcal infection that causes shedding

of the superficial layer of the epidermis. SSSS is most common in children and neonates; 98% of patients are <6 years

of age.

Toxic shock syndrome (TSS) causes a diffuse red

macular rash associated with fever, hypotension, and

malfunction of at least 3 organ systems. It was originally

diagnosed in menstruating women using vaginal tampons,

but can also be seen in patients with surgical wounds

and nasal packings. Incidence is about 10-20 cases per

100,000 persons. TSS is most often caused by a variant of

Staphylococcus aureus, which produces the exotoxin TSST -1,

which mediates the clinical effects. Streptococcus pyogenes

may more rarely cause a similar syndrome.

Kawasaki disease is thought to be an immunologic

disorder triggered by infection or toxin, leading to a generalized vasculitis. It causes nearly 3,000 hospital admissions annually and usually appears in children <9 years

of age, with a peak incidence in children 1 8-24 months

• If there is any uncerta inty of etiology in a given case,

treat presumptively for the most serious etiology,

especially meningococcemia.

of age. Epidemics occur primarily in the late winter and

early spring. Approximately 20% of patients develop

cardiovascular complications, and the most common

cause of death is myocardial infarction secondary to

coronary artery aneurysm, which can develop 2-8 weeks

after fever.

� Vesiculobul lous Lesions

Erythema multiforme (EM), as the name implies, presents

with many simultaneous types of skin lesions, including

macules, papules, and bullae. EM accounts for as many as

1% of dermatologic outpatient visits and is more common

in spring and fall. The etiology is a hypersensitivity reaction

precipitated by medications, infections, sarcoidosis, collagen

vascular diseases, or malignancies. About 50% of cases are

idiopathic.

Stevens-Johnson syndrome (SJS) is a more severe

form of EM that involves ;:::2 mucosal surfaces such as

eyes, lips, mouth, urogenital area, or anus. SJS can progress to toxic epidermal necrolysis (TEN), with large bullae and sloughing of the epidermis in sheets. Frequency is

up to 6 cases per 1 million persons annually. The etiology

is similar to EM, but medications are more commonly

associated with SJS.

TEN is the most severe end of the EM spectrum, with

TEN affecting > 30% of the body surface area. There is

approximately 1 case per 1 million persons annually, with

adults most commonly affected. TEN desquamates the

entire thickness of the epidermis; therefore, mortality rates

41 8

LIFE-THREATENING DERMATOSES

are 30-40% from hypovolemia and infection. TEN is

thought to be provoked by drugs such as phenytoin, sulfas,

penicillins, and nonsteroidal anti-inflammatory drugs.

Onset is usually within the first 8 weeks of therapy.

Pemphigus vulgaris (PV) is characterized by flaccid

bullae that begin in the mouth and spread to involve the

skin. Frequency is approximately 3 cases per 100,000 persons. Peak age of onset is 50-60 years. The etiology is an

autoimmune blistering reaction characterized by autoantibodies directed against keratinocyte cell surfaces; some

cases are drug-induced. Bullous pemphigoid (BP) is a

similar autoimmune blistering disease, but it usually only

affects the elderly. Unlike PV, the bullae of BP are tense

rather than flaccid, and oral involvement is uncommon .

..... Hemorrhagic Lesions

Patients with disseminated gonococcal infection (DGI) are

usually young, sexually active females with fever, skin

lesions, arthritis, arthralgias, or migratory tenosynovitis.

DGI occurs after approximately 1% of gonococcal genital

infections. Certain subtypes of Neisseria gonorrhoeae are

more likely to lead to disseminated infection.

Another Neisseria species, Neisseria meningitidis, can

cause meningococcemia. Cutaneous manifestations are part

of a hemorrhagic cascade resulting from systemic sepsis. The

frequency is approximately 2 cases per 100,000 persons annually, although sporadic outbreaks with higher prevalence

occur frequently. The mortality rate varies between 10% and

50%, depending on the severity of the systemic infection.

CLINICAL PRESENTATION

..... Erythrodermas

SSSS generally begins on the face (perioral area) as red

patches that are warm and tender. The erythema spreads

and becomes flaccid clear bullae, which then desquamate

in large sheets. The mucous membranes usually are not

involved. Nikolsky sign is positive and can be elicited when

gentle stroking of the skin produces peeling (Figure 96- 1 ).

Exfoliation begins on day 2 of the illness, and healing

occurs within 1 0-14 days.

The TSS patient will present with fever, hypotension,

and multisystem organ dysfunction. In addition to diffuse

erythroderma, patients will have a strawberry-appearing

tongue, red conjunctiva, and edema of the face, hands, and

feet. The rash fades within 72 hours and is followed by

acral desquamation within 1-2 weeks.

The rash of Kawasaki disease is erythematous and

similar in morphology to Scarlet Fever. The clinical diagnosis of Kawasaki disease includes fever greater than

5 days' duration, plus 4 of 5 of the following criteria: conjunctivitis, oral mucous membrane involvement (straw ­

berry tongue, cracked lips), edema/ erythema of extremities,

diffuse maculopapular rash, and cervical lymphadenopathy (usually > 1 .5 em and unilateral). Patients often present

with arthralgia and irritability and can have peripheral

.&. Figure 96-1 . Nikolsky sign. Reprinted with

permission from Suurmond D. Section 24. Bacterial

I nfections Involving the Skin. In: Suurmond D, ed.

Fitzpatrick's Color Atlas Er Synopsis of Clinical

Dermatology. 6th ed. New York: McGraw-Hill, 2009.

leukocytosis and elevated levels of acute-phase reactants

and transaminases.

..... Vesiculobul lous Lesions

The typical lesion of EM is the "target lesion;' described as

erythematous plaques with dusky centers and bright red

borders resembling the "hull's eye" of a target (Figure 96-2).

The lesions are symmetric and are usually found on the

extremities, palms, and soles and may also involve the oral

mucosa. A burning sensation is present, and pruritus is

notably absent.

Stevens-Johnson syndrome presents with lesions similar

to those of EM, but has additional findings of blistering of

<10% of the skin and mucosal involvement. Fever, malaise,

myalgias, and arthralgias are common. Lesions begin on the

dorsal surfaces of the hands and feet and spread centrally.

Toxic epidermal necrolysis begins with a prodrome of

constitutional symptoms including fever, malaise, and

myalgias. After 1-2 weeks, the skin becomes painful with

hot red blisters and large areas of sloughing (>30% of

skin), progressing to diffuse exfoliation and acute skin

failure (Figure 96-3).

Pemphigus vulgaris may present with multiple scattered vesicles and bullae (scalp, face, chest, mucous membranes). However, since the bulla rupture easily, patients

may present only with painful erosions. Almost all patients

have mucosal involvement.

CHAPTER 96

Figure 96-2. The typica l target lesions of

eryth ema multiforme. Repri nted with permission

from Hardin J. Chapter 13. Cutaneous Co nditions. In:

Knoop KJ, Stack LB, Storrow AB, Thurman RJ, eds.

The Atlas of Emergency Medicine. 3rd ed. New York:

McGraw-Hill, 201 0. Photo contributor: Michael

Redman, PA- C.

� Hemorrhagic Lesions

DGI skin lesions are described as hemorrhagic gray

necrotic pustules on an erythematous base, numbering

between 10 and 30, and appearing on the extremities and

resolving rapidly. The classic rash of meningococcemia can

be petechial or macular, with pale gray vesicular centers,

and may progress to a hemorrhagic rash (Figure 96-4).

Fever, headache, and vomiting are present, although men ­

ingitis may or may not be present. It is rapidly progressive,

with a 1 00% mortality rate without treatment.

DIAGNOSTIC STUDIES

Unfortunately, there are no diagnostic studies that can aid

the emergency department (ED) diagnosis of these

diseases. Patients with significant to severe systemic illness

will receive routine blood tests and sometimes cultures,

Figure 96-3. Large surface skin sloug hing in toxic

epidermal necrolysis. Reprinted with permission from

Suurmond D. Section 8. Severe and Life-Threatening Skin

Eruptions in the Acutely Ill Patient. In: Suurmond D, ed.

Fitzpatrick's Color Atlas & Synopsis of Clinical

Dermatology. 6th ed. New York: McGraw-Hill, 2009.

immunoassays, and other specific testing. However, the

results of none of these tests will be available or useful to

guide the initial diagnosis in the ED.

MEDICAL DECISION MAKING

The initial diagnosis should be made clinically and will be

centered on the evaluation for specific life-threatening conditions. It is easiest to first attempt to classify the patient's

presenting skin lesion-erythroderma, vesiculobullous, or

hemorrhagic lesion-and, once subclassified, to attempt to

use a few clinical features to rule in or rule out specific

diagnoses (Figure 96-5). However, because it is sometimes

difficult to make a certain diagnosis in the initial presentation, the key to early treatment is to have a very high index

of suspicion for the most immediately lethal of the syndromes, especially meningococcemia.

LIFE-THREATENING DERMATOSES

Figure 96-4. The petechial rash of meningococcemia.

Reprinted with permission from Suurmond D. Section 24.

Bacterial Infections Involving the Skin. In: Suurmond D,

ed. Fitzpatrick's Color Atlas & Synopsis of Clinical

Dermatology. 6th ed. New York: McGraw-Hill, 2009.

Erythroderma?

No

Vesiculobul lous?

No

Hemorrhagic? Febri le?

TREATMENT AND DISPOSITION

..... Erythrodermas

Patients with SSSS should be treated with intravenous (IV)

antistaphylococcal antibiotics (nafcillin or vancomycin)

and IV fluids. They should be admitted to the hospital.

Patients with TSS should first have the source (tampon,

nasal packing) identified and removed. IV immunoglobulin

G (IVlG) has been shown to be effective in neutralizing the

TSS toxin and aids in recovery. These patients should also

receive IV antibiotics ( eg, nafcillin/vancomycin) and be

admitted to an intensive care unit (ICU). When Kawasaki

disease is diagnosed, high-dose aspirin therapy and IVlG

should be administered. Patients should be admitted to the

hospital for further monitoring and echocardiography .

..... Vesiculobul lous Lesions

Erythema multiforme is generally a benign, self-limited

rash that resolves within 2-4 weeks. It requires no

specific treatment except cool compresses and an

attempt to identify and remove the precipitating cause.

Yes

Yes

Yes

Yes

Yes

Yes