age in the 2015 Pediatric Advanced Life Support guidelines
less than 60 mm Hg in term neonates (0–28 days)
less than 70 mm Hg in infants (1–12 months)
less than 70 mm Hg + (2 × age in years) in children 1 to 10 years of age
less than 90 mm Hg in children older than or equal to 10 years of age
Fluid resuscitation should be continued until clinical improvement is clear or there
is clinical evidence of hypervolemic state as evidenced by rales, a gallop rhythm, or
hepatomegaly. Further discussion of the management of hypovolemia and dehydration
in children can be found in Chapter 103, Pediatric Fluid, Electrolytes, and Nutrition.
M.M. should receive a bolus 120 mL normal saline IV infused over 5 minutes,
followed by assessment of perfusion status to ascertain improvement. If he has not
demonstrated significant improvement, the fluid bolus should be repeated until
adequate perfusion is seen and blood pressure is stable at greater than 70 mm Hg.
CASE 106-3, QUESTION 3: As noted earlier in the case, M.M. is hypoglycemic with a blood glucose of
Hypoglycemia often develops in infants during episodes of stress, including shock,
seizures, and sepsis. Infants have high glucose needs and low glycogen stores, which
make hypoglycemia a risk in a critically ill infant, especially one with poor enteral
intake. Point-of-care glucose testing should be performed in any critically ill infant
with a history of poor oral intake. One should not wait to obtain serum chemistries.
Aggressive fluid resuscitation recommended for hypovolemia and shock will only
exacerbate hypoglycemia. Most importantly, hypoglycemia needs to be prevented
during cardiopulmonary and trauma resuscitation because it may cause seizures and
has been linked with poor neurologic outcome.
3,13 Hypoglycemia in pediatric patients
must always be promptly identified and treated. After diagnosis, the patient should be
managed with a bolus of 0.5 to 1 g/kg of glucose or 5 to 10 mL/kg of a 10% dextrose
solution as required to achieve a serum glucose greater than 100 mg/dL. Neonates,
especially premature neonates, are more prone to intraventricular hemorrhage with
rapid changes in serum osmolarity than older infants and children; therefore, 0.2 g/kg
or 2 mL/kg of 10% dextrose is recommended in this population until the target serum
glucose is achieved. M.M. should be given 30 mL (5 mL/kg) of 10% dextrose IV for
1 to 2 minutes, followed by reassessment of his serum glucose. Treatment may be
continued until his serum glucose is within the normal range for his age (60–105
mg/dL). After stabilization, maintenance therapy should be initiated with fluids
SEPSIS AND SEPTIC SHOCK IN INFANTS AND
Septic shock can be a mixture of hypovolemic, cardiogenic, and distributive shock. In
a recent population-based study of children in the United States with severe sepsis
(defined as bacterial or fungal infection with at least one acute organ dysfunction),
reported an increase in the incidence of severe sepsis from 2000 to
2005 and from 0.56 to 0.89 cases per 1,000 children. The increase reported in
newborns was from 4.5 to 9.7 cases per 1,000. This increase was led by sepsis in
very low birthweight neonates. The second increase was reported in children from
15 to 19 years of age with a reported increase from 0.37 to 0.48 cases per 1,000. The
mortality rate in this study was 8.9%, unchanged from 2000, but significantly lower
than that reported for adult patients with severe sepsis and septic shock
(approximately 30% and 50%, respectively). This dramatic improvement in outcome
has been attained through a better understanding of the physiology of shock. The use
cardiovascular, renal, and nutritional support, and improved antibacterial, antiviral,
and antifungal therapy, has resulted in improved survival in infants and children with
septic shock and the resultant multisystem organ failure.
Infants and young children are at a higher risk of severe systemic illness after
infection than adults. Despite new developments in vaccine technology, rates of
sepsis have not declined. This phenomenon is most likely as a result of cases
occurring in infants before complete immunization. Infants are particularly vulnerable
to infections for several reasons.
20 Passive immunity is normally conveyed from the
mother to the fetus through transmission of immunoglobulins during the last trimester.
As a result, premature neonates are immunoglobulin-deficient. Even the full-term
neonate has decreased polymorphonuclear leukocyte (PMN) function and small PMN
storage pools compared with older children and adults, as well as decreased ability
to synthesize new antibodies. Lastly, neonates cannot make and deliver adequate
amounts of phagocytes to sites of infection. Low immunoglobulin levels also make
the infant susceptible to viral infections. Stores of maternal immunoglobulin are
depleted at approximately 2 to 5 months of age. Adult levels of immunoglobulin are
not typically achieved until 4 to 7 years of age. As the result of these physiologic
differences, as well as differences in bacterial resistance patterns, the list of most
likely pathogens in children with sepsis differs from those of adults. Table 106-5
lists common pediatric pathogens and appropriate empiric antibiotic coverage.
Antibiotics should be administered within 1 hour of diagnosis, after the collection of
As in adults, baseline health status also affects the likelihood of a child exhibiting
severe sepsis. Watson et al. found that 49% of cases of sepsis occurred in children
who had underlying illnesses which may place them at risk of higher morbidity and
14 At the Children’s Hospital of Pittsburgh, the mortality rate for children
who were previously healthy was 2% compared with 12% in children with chronic
QUESTION 1: J.B., a 6-year-old, 20-kg girl, presented to the pediatric emergency department in acute
laboratory values are notable for a white blood cell count of 21 × 10
3 μL. Her parents report that she has not
urinated since the previous evening. Does J.B. meet the criteria for septic shock?
In an effort to develop a consensus definition of the pediatric sepsis continuum
including systemic inflammatory response syndrome (SIRS), infection, sepsis, severe
sepsis, septic shock, and multisystem organ dysfunction syndrome, a group of
international experts in the fields of adult and pediatric sepsis and clinical research
gathered in 2002. A panel was chosen consisting of published pediatric critical care
physicians and scientists with clinical research experience in pediatric sepsis.
Because the clinical variables used to define SIRS and organ dysfunction are greatly
affected by the normal physiologic changes that occur as children age, the group first
defined six clinically and physiologic age categories for defining SIRS criteria
(Table 106-6). Premature infants were not included because their care occurs
primarily in neonatal intensive care units and not in PICUs. Before discussing
treatment, it is important that the practitioner should understand the terms used to
define sepsis. In 1992, SIRS was proposed by the American College of Chest
Physicians and the Society of Critical Care Medicine (SCCM) to describe the
nonspecific inflammatory process occurring in adults after trauma, infection, burns,
pancreatitis, and other diseases.
22,23 Sepsis was defined as SIRS associated with
infection. The SIRS criteria were developed for use in adults; it was not until 2005
that a consensus definition was published for SIRS in children (Table 106-7).
separate pediatric definition for SIRS was essential. Tachycardia and tachypnea,
pivotal to the adult definition of SIRS, are common presenting symptoms of many
pediatric disease processes. To better distinguish SIRS from other diseases, the
pediatric definition also includes temperature and leukocyte abnormalities as
criteria. Numeric values for each criterion were also established to account for the
different physiology in children. Table 106-8 gives the age-specific cutoffs for each
Causative Pathogens and Recommended Treatments for Pediatric Sepsis
Age or Risk Factor Microorganism Empiric Antibiotic Coverage
Age <30 days Listeria monocytogenes
Ampicillin + aminoglycoside or
acyclovir (if patient presents with seizures,
Age 1 to 3 months L. monocytogenes
Immunocompromised child Pseudomonas aeruginosa
cefepime or piperacillin/tazobactam +
Child with a ventriculoperitoneal
aDosed to maintain trough vancomycin serum concentrations of 15 to 20 mcg/mL.
Pediatric Age Group Definitions for Severe Sepsis
Toddler and preschool 2–5 years
Adolescent and young adult 13–<18 years
for sepsis and organ dysfunction in pediatrics. Pediatr Crit Care Med. 2005;6(1):3.
Temperature is one of the main criteria of the pediatric SIRS definition. A core
temperature greater than 38.5°C or less than 36°C may indicate serious infection.
Hypothermia is more likely to occur in infants. A core temperature is the one
measured by either rectal, bladder, oral, or central catheter probe. Temperatures
taken via the tympanic, toe, or another auxiliary route are not sufficiently accurate.
Temperature may also be documented by a reliable source at home within 4 hours of
presentation to the hospital or physician’s office. If environmental overheating, such
as that produced by overbundling, is suspected, the child should be returned to a
neutral temperature environment, unbundled, and the temperature retaken in 15 to 30
Meeting the SIRS criteria in children requires the presence of an abnormal
temperature, either hypothermia or hyperthermia, or an abnormal leukocyte count in
the presence of tachypnea and tachycardia. Sepsis is defined as the proven or
suspected infection in the setting of SIRS. Severe sepsis is defined as sepsis in the
setting of acute respiratory distress syndrome, cardiovascular organ dysfunction, or
two or more acute organ dysfunctions (respiratory, renal, hematologic, neurologic, or
hepatic). The definitions of organ dysfunction have also been modified for children
(Table 106-9). Carcillo et al.
16 defined pediatric septic shock (SS) as the presence of
tachycardia and poor perfusion, including decreased peripheral pulses compared
with central pulses; altered alertness; capillary refill greater than 2 seconds; mottled
or cool extremities; or decreased urine output. This definition of pediatric SS does
not include hypotension as required in adults because children will often maintain
their blood pressure until they are severely ill. Shock may occur long before
hypotension occurs. J.B. exhibits the majority of the criteria for pediatric SS,
including lethargy, fever, tachycardia, decreased perfusion, and decreased urination.
CASE 106-4, QUESTION 2: What physiologic differences may need to be taken into account when
developing a management strategy for J.B.?
Definitions of Systemic Inflammatory Response Syndrome, Infection, Sepsis,
Severe Sepsis, and Septic Shock in Children
SIRS The presence of at least two of the following four criteria, one of which must be abnormal
temperature or leukocyte count:
Core temperature of >38°C or <36°C (must be measured by rectal, bladder, oral, or central
Tachycardia defined as at least two standard deviations above normal for age in the absence
of externalstimulus, chronic drugs, or painfulstimuli; or otherwise persistent elevation for a
0.5- to 4-hour time period OR for children <1 year old: bradycardia, defined as a mean heart
rate <10% percentile for age in the absence external vagalstimulus, β-blocker drugs, or
congenital heart disease; or otherwise unexplained depression in a half-hour period
Mean respiratory rate >2 standard deviations above normal for age or mechanical ventilation
for an acute process not related to underlying neuromuscular disease or receipt of general
Leukocyte count elevated or depressed for age (not secondary to chemotherapy-induced
neutropenia) or >10% immature neutrophils
infection caused by any pathogen OR a clinicalsyndrome associated with a high probability of
infection. Evidence of infection includes positive findings on clinical examination, imaging, or
laboratory tests (e.g., white blood cells in a normally sterile body fluid, perforated viscus, chest
radiograph consistent with pneumonia, petechial or purpuric rash, or purpura fulminans)
Sepsis SIRS in the presence of or as a result of suspected or proven infection
syndrome OR dysfunction of two or more other organs, as defined in Table 106-9
Septic shock Severe sepsis with cardiovascular dysfunction, as defined in Table 106-9
SIRS, systemic inflammatory response syndrome.
for sepsis and organ dysfunction in pediatrics. Pediatr Crit Care Med. 2005;6(1):4.
Age-Specific Vital Signs and Laboratory Variables
0 day to 1 week >180 <100 >50 >34 <65
2 to 5 years >140 n/a >22 >15.5 or <6 <94
6 to 12 years >130 n/a >18 >13.5 or <4.5 <105
13 to <18 years >110 n/a >14 >11 or <4.5 <117
and upper limits for the for the 95th percentile.
for sepsis and organ dysfunction in pediatrics. Pediatr Crit Care Med. 2005;6(1):4.
There are developmental differences in the hemodynamic response to sepsis in
newborns, children, and adults. Practitioners in the PICU may encounter all age
ranges and thus must be familiar with the clinical differences seen between age
groups because it may affect therapy. Adults and children have different adaptive
responses that must be considered when selecting therapeutic management.
Adolescent patients pose a unique challenge because they may present with either
types of symptoms. Among adult patients, the most common hemodynamic alterations
include diminished systemic vascular resistance (SVR) and elevated cardiac output
(CO). SVR is diminished due to decreased vascular responsiveness to
catecholamines, alterations in α-adrenergic receptor signal transduction, and the
elaboration of inducible nitric oxide synthase. In general, adults with SS have
myocardial dysfunction with a decreased ejection fraction; however, CO is
preserved or increased through two compensatory mechanisms: tachycardia and
Unlike SS in adults, pediatric SS is associated with severe hypovolemia, and
children frequently respond well to aggressive fluid resuscitation. Pediatric patients
demonstrate diverse hemodynamic profiles during fluid-refractory SS: 58% have low
cardiac indexes responsive to inotropic medications with or without vasodilators,
20% exhibit high cardiac index and low SVR responsive to vasopressor therapy, and
22% present both vascular and cardiac dysfunctions necessitating the use of
vasopressors and inotropic support.
25 Pediatric patients such as J.B. are different
from adults with SS in that low CO, not low SVR, is associated with increased
mortality. In fact, studies suggest that the majority of children showed some degree of
cardiac dysfunction on presentation after fluid resuscitation.
change in their inotropic and vasopressor management, or the addition of another
agent during the first hours of treatment, emphasizing that the hemodynamic status in
Despite administration of isotonic intravenous fluid bolus 40 mL/kg in 1 hour
Need for vasoactive drug to maintain BP in normal range (dopamine >5 mcg/kg/minute or dobutamine,
epinephrine, or norepinephrine at any dose) OR
Unexplained metabolic acidosis: base deficit >5 mEq/L
Increased arterial lactate >2 times upper limit of normal
Oliguria: urine output <0.5 mL/kg/hour
Prolonged capillary refill: >5 seconds
Core to peripheral temperature gap >3°C
/FIO2 <300 in absence of cyanotic heart disease or preexisting lung disease OR
PaCO2 >65 torr or 20 mm Hg over baseline PaCO2 OR
to maintain saturations >92% OR
Need for nonelective invasive or noninvasive mechanical ventilation
Glasgow Coma Scale (see Table 106-12) <11 OR
Acute change in mentalstatus with a decrease in Glasgow Coma Scale ≥3 points from abnormal baseline
(for chronic hematology/oncology patients) OR
International normalized ratio of >2
Serum creatinine >2 times upper limit of normal for age or twofold increase in baseline creatinine
Total bilirubin ≥4 mg/dL (not applicable for newborn) OR
ALT 2 times upper limit of normal for age
bAcute respiratory distress syndrome must include a Pao2
ratio <200 mm Hg, bilateral infiltrates, acute onset,
and no evidence of left heart failure. Acute lung injury is defined identically except the Pao2
cProven need assumes oxygen requirement was tested by decreasing flow if required.
infectious process in the lungs that prevents him or her from being extubated.
ALT alanine transaminase; BP, blood pressure.
for sepsis and organ dysfunction in pediatrics. Pediatr Crit Care Med. 2005;6(1):5.
SS in the neonatal patient differs from that seen in older children. The relative
ability of infants and children to augment CO through increased heart rate (HR), as
seen in adults, is limited by their preexisting elevated HR, which precludes
proportionate increases in HR without compromising diastolic filling time. In adults,
ventricular dilation is a compensatory response used to maintain CO. However, the
increased connective tissue content of the infant’s heart and diminished content of
actin and myosin limits the potential for acute ventricular dilation. Neonatal SS can
be further complicated by the physiologic transition from fetal to neonatal circulation.
Sepsis-induced acidosis and hypoxia can increase pulmonary vascular resistance and
thus arterial pressure, thereby maintaining the patency of the ductus arteriosus. This
results in persistent pulmonary hypertension (PPHN) of the newborn and persistent
fetal circulation. Neonatal SS with PPHN will increase the workload on the right
ventricle, leading to right-ventricular failure, tricuspid regurgitation, and
hepatomegaly. Therefore, therapies directed at reversing right-ventricular failure by
Based on her mottled dry skin, sluggish capillary refill, and decreased urination, it
is evident that J.B. has inadequate perfusion. She should receive aggressive fluid
resuscitation, beginning with a fluid bolus of 400 mL (20 mL/kg) normal saline or
lactated Ringer’s solution IV administered over 5 minutes. She should be reassessed
immediately after the bolus to evaluate perfusion status as described previously. The
400-mL fluid bolus should be repeated until adequate perfusion has been established.
INITIAL MANAGEMENT OF PEDIATRIC SEPTIC
Because the landmark study by Rivers in 2001 demonstrated a 33% reduction in
mortality in adult patients with sepsis when they were aggressively treated with fluid
resuscitation, blood transfusion, and inotropic therapy within 6 hours of admission,
goal-directed therapy has been advocated for all patients who present in SS.
components of early goal-directed therapy include respiratory support along with
prompt resuscitation of poor perfusion through administration of IV fluids and
appropriately targeted inotropic and vasopressor therapy, early empiric
antimicrobial therapy, drainage of the infection whenever possible, and continuous
monitoring of the patient’s hemodynamic status.
CASE 106-4, QUESTION 3: J.B. has received one bolus of normal saline in the pediatric emergency
agents be considered to maximize perfusion and oxygenation?
There are no data to suggest a significant difference in survival rates in pediatric
patients after resuscitation with colloids, including blood products, compared with
26 The choice of fluid is less important than the volume
administered. Adequate volume is necessary to sustain cardiac preload, increase
stroke volume, and improve oxygen delivery. Both crystalloids and colloids,
specifically packed red blood cells (PRBC), have equal effects on improving stroke
volume. In addition, both restore tissue perfusion to the same degree if they are
titrated to the same level of filling pressure.
Administration of blood products also differs among institutions. The optimal
hemoglobin for infants and children in SS has not been established. In the early
management of sepsis in adults, maintaining hemoglobin of 7 to 9 g/dL to improve
oxygen carrying capacity has been documented to improve sepsis survival by
improving tissue perfusion. Anemia in sepsis has been associated with increased
mortality, but so has the administration of blood products.
available, SCCM has recommended that hemoglobin concentrations in adults be
13 As pediatric data are even more limited, it is necessary to
extrapolate from the adult literature suggesting maximizing tissue oxygen delivery if
there is evidence of poor tissue perfusion. Once tissue hypoperfusion, acute
hemorrhage, or lactic acidosis has resolved, PRBC transfusion should be considered
only when the hemoglobin is less than 7 g/dL.
13,28 At this time, there is no indication
for administration of blood products to J.B. Fresh frozen plasma may be infused to
correct abnormal prothrombin time (PT) and partial thromboplastin time (PTT)
values, but should not be rapidly infused because of the risk for acute hypotensive
effects caused by vasoactive kinins and high citrate concentration. There is no
literature to suggest that 5% albumin administration improves outcome in regard to
sepsis mortality. Albumin administration may be considered in patients who are
hypoalbuminemic, but routine use of albumin is not recommended.
As described previously for the management of hypovolemic shock, patients with
SS should be reassessed for signs of improved perfusion using clinical criteria such
as reduction in heart rate, improvement of blood pressure, capillary refill, quality of
pulses, and mental status with each fluid bolus. If the clinical signs of shock persist,
another 20 mL/kg of isotonic fluid should be administered reaching, if necessary, 60
mL/kg within the first 15 to 30 minutes of treatment.
require as much as 200 mL/kg in the first hour.
17 Patients remaining in shock despite
fluid resuscitation are given inotropic support to attain normal blood pressure for age
and capillary refill time of less than 2 seconds. Every hour that goes by without
implementing these therapies is associated with a 1.5-fold increased risk of
mortality. Patients who do not respond rapidly to initial fluid boluses or those with
insufficient physiologic reserve should be considered for invasive hemodynamic
monitoring. Invasive monitoring of central venous pressure (CVP) is instituted to
ensure that the satisfactory right-ventricular preload is present, typically using a goal
of 10 to 12 mm Hg, and that oxygen carrying capacity is optimized by PRBC
transfusion to correct anemia to a goal hemoglobin concentration greater than 7
Up to 40% of a child’s CO may be required to support the work of breathing
during SS; therefore, in the presence of respiratory distress, elective intubation and
mechanical ventilation can be used to allow redistribution of blood flow from
respiratory muscles toward other vital organs. Intubation is not without adverse
effects; it is imperative that patients receive adequate fluid resuscitation before
intubation because the change from spontaneous breathing to positive-pressure
ventilation will decrease the effective preload to the heart, further decreasing cardiac
output. Ventilation may reduce left-ventricular afterload that may be beneficial in
patients with low cardiac index and high SVR. In addition, it may provide an
alternative method to alter acid base balance. If sedatives and analgesics are used for
intubation, choice of agents that do not cause further vasodilation is critical.
Although laboratory studies rarely affect the management of SS in the first hour of
therapy, patients should have laboratory studies sent routinely assessing for
hematologic abnormalities, metabolic derangements, or electrolyte abnormalities that
may contribute to morbidity. A peripheral white blood count may aid in the choice of
broad-spectrum antibiotics and hemoglobin and platelet count will help in assessing
the need for early blood transfusion. A type and screen should be sent to the blood
bank to prepare for any necessary transfusions. Electrolyte abnormalities are
common in sepsis; recognition and treatment of metabolic abnormalities such as
hypoglycemia and hypocalcemia will improve outcome. A disseminated
intravascular coagulation panel, including PT, PTT, and fibrinogen, will aid in
assessing the severity of illness. If abnormalities exist, they may need to be corrected
before performing invasive procedures. Lastly, an arterial or venous blood gas will
determine the adequacy of ventilation, oxygenation, and severity of acidemia.
Unfortunately, clinical response to fluid resuscitation is a relatively insensitive
indicator for the completeness of restoration of microvascular blood flow. Success
of adequate fluid resuscitation can be guided by additional parameters: invasive
blood pressure monitoring, CVP, measurement of mixed venous oxygen saturation
), measurement of blood lactate, and urine output. An elevated serum lactate
level suggests tissue is inadequately perfused and undergoing anaerobic metabolism,
even in patients who are not hypotensive. Because low CO is associated with
increased O2 extraction, SvO2 can be used as an indirect indicator of whether CO is
adequate to meet tissue metabolic demand. If tissue oxygen delivery is adequate, then
SvO2 should be greater than 70%.
In the goal-directed study by Rivers, maintenance
of SvO2 was greater than 70% by use of blood transfusion to a hemoglobin of 10 g/dL
and inotropic support to increase CO resulted in a 40% reduction in mortality
compared with patients where only mean arterial pressure and CVP were
reproduced this finding in children with SS, reducing
mortality from 39% to 12% when directing therapy to a goal SvO2 saturation greater
Pharmacologic support in children with SS must be individualized because different
hemodynamic abnormalities exist in pediatric patients, and the primary hemodynamic
abnormalities may change with time and progression of the patient’s disease (Table
106-10). Twenty percent (20%) of children present with predominant vasodilatory
shock, referred to as “warm” shock. This form of shock is associated with
vasodilation and capillary leak, but normal or elevated CO. The patients have strong
pulses, warm extremities, good capillary refill, and tachycardia. In warm shock,
using a vasopressor such as dopamine, norepinephrine, phenylephrine, or
vasopressin to promote vasoconstriction would provide the most benefit. Fifty-eight
percent (58%) of children present with “cold shock” or a poor CO state. These
patients have vasoconstriction, increased cardiac afterload, and a high SVR. This is
clinically manifested as weak pulses, cool extremities, slow capillary refill, and
hepatic and pulmonary congestion. Using an inotrope with or without a vasodilator
would be most beneficial in cold shock (e.g., dobutamine, epinephrine, or milrinone).
Careful assessment of clinical response is critical because a combination of warm
and cold shock, with a low SVR and poor CO, occurs in approximately 22% of
Summary of Selected Vasoactive Agents
Agent Dose Range Peripheral Vascular Effects Cardiac Effects
Dobutamine 2–20 mcg/kg/minute 1+ 3–4+ 1–2+ Less chronotrophy and
Dopamine 2–4 mcg/kg/minute 0 0 0 Splanchnic and renal
>10 mcg/kg/minute 2–4+ 1–2+ 2+
0.2–0.5 mcg/kg/minute 4+ 2+ 3+
Nitroprusside 0.5–8 mcg/kg/minute Donates nitric oxide to
Nitroglycerine 0.5–10 mcg/kg/minute As a nitric oxide donor
Milrinone 50 mcg/kg load; then
Potent vasoconstrictor No direct effect None known
between 72 and 79 mm Hg (normal for age, >84 mm Hg). What would be an appropriate next step for the
Vasopressors are required in shock unresponsive to initial fluid resuscitation.
In pediatric SS, the initial agent of choice has typically been dopamine.
mechanisms of dopamine action is enhancement of endogenous catecholamine
release. In severe septic states, presynaptic vacuoles may be depleted of
norepinephrine, which may explain why dopamine may have diminished activity. In
addition, infants younger than 6 months of age may not have developed their
component of sympathetic innervations; therefore, they have reduced releasable
Some studies have raised the concern of increased mortality with the use of
dopamine. One possible explanation is the ability of dopamine to reduce the release
of hormones from the anterior pituitary gland, such as prolactin, through stimulation
receptor, thus reducing cell-mediated immunity and inhibition of
thyrotropin-releasing hormone release, worsening impaired thyroid function known
to occur in critical illness. Although most clinicians continue to use dopamine as
hypotensive hyperdynamic shock.
J.B. should be started on dopamine at a rate of 5 mcg/kg/minute, with further
titration of the dose in increments of 2.5 mcg/kg/minute every 3 to 5 minutes until the
goal of improved perfusion and/or a normal blood pressure for age is achieved.
maximum recommended dose of dopamine is 20 mcg/kg/minute; higher doses may
contribute to increased myocardial oxygen demand without much improvement in
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