Septic Shock - Ongoing Management After Resuscitation in Children - UpToDate

11/14/2016
Septic shock: Ongoing management after resuscitation in children - UpToDate
Official reprint from UpToDate

www.uptodate.com 2016 UpToDate
Septic shock: Ongoing management after resuscitation in children

Authors: Scott L Weiss, MD, Wendy J Pomerantz, MD, MS
Section Editors: Susan B Torrey, MD, Adrienne G Randolph, MD, MSc, Sheldon L Kaplan, MD
Deputy Editor: James F Wiley, II, MD, MPH
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Oct 2016. | This topic last updated: Jan 19, 2016.
INTRODUCTION Sepsis is a clinical syndrome complicating severe infection that is characterized by
systemic inflammation, immune dysregulation, microcirculatory derangements, and end-organ dysfunction.
There is a continuity of severity ranging from sepsis to severe sepsis and septic shock. Severe sepsis and
septic shock are characterized by dysfunction of 2 organ systems and cardiovascular dysfunction,
respectively [1]. With increased attention to rapid recognition, aggressive fluid administration, and early
administration of vasoactive agents and antibiotics, pediatric mortality from severe sepsis and septic shock
has decreased markedly [2-7].
The management of severe sepsis and septic shock in children after the first hour of resuscitation is
reviewed here. The rapid recognition and initial resuscitation of pediatric septic shock and the definitions,
epidemiology, and clinical manifestations of sepsis in children are discussed separately. (See "Septic
shock: Rapid recognition and initial resuscitation in children" and "Systemic inflammatory response
syndrome (SIRS) and sepsis in children: Definitions, epidemiology, clinical manifestations, and diagnosis".)
RESUSCITATION The key interventions in the initial resuscitation of children from septic shock are
discussed in detail separately. (See "Septic shock: Rapid recognition and initial resuscitation in children".)
OVERVIEW Repeated, frequent assessment of the patient in septic shock is essential. In children who
have responded to therapy with resolution of hypotension, ongoing monitoring, antimicrobial therapy, and
optimal respiratory support are essential.
In patients with fluid-refractory hypotension, ongoing aggressive resuscitation should continue after the
initial resuscitation of pediatric septic shock according to the principles of goal-directed therapy (algorithm
1). (See "Septic shock: Rapid recognition and initial resuscitation in children", section on 'Physiologic
indicators and target goals'.)
Whenever possible, children requiring resuscitation for septic shock should receive ongoing management
by a pediatric critical care specialist or pediatrician with similar expertise in a pediatric intensive care unit
(PICU).
Priorities for continued management of children with septic shock include:
Control the infection by identifying the optimal choice of antimicrobial therapy based upon culture
results and by ensuring that the source of infection is controlled
Ongoing monitoring of respiratory status and provision of optimal respiratory support
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Ongoing monitoring of tissue perfusion and blood pressure

Correction of electrolyte and metabolic derangements (eg, hypoglycemia, hypocalcemia)
In the subpopulation of children with fluid-refractory septic shock requiring continued vasopressor support,
additional priorities include:
Placement of invasive monitoring devices (eg, central venous catheter, arterial line, bladder catheter)
to accurately assess blood pressure and to deliver vasopressor infusions safely
Continued fluid resuscitation and vasopressor delivery targeted to principles of goal-directed therapy
Administration of blood products, when needed, to treat anemia and coagulopathy
Treatment of adrenal insufficiency and evaluation of other potential underlying causes (eg,
hypothyroidism)
Provision of advanced therapies in patients who do not respond to conventional therapy
If physiologic goals have been achieved, indicating that perfusion is improved, the patient should continue
to receive supportive treatment and careful monitoring. The goals of treatment include achieving a normal
blood pressure, improved mental status and good perfusion for the patient who is hypotensive. For
children with compensated shock and normal blood pressures, therapeutic endpoints based upon
noninvasive indicators are reasonable targets but may be unreliable. (See "Septic shock: Rapid
recognition and initial resuscitation in children", section on 'Physiologic indicators and target goals'.)
Eradicate infection Prompt identification and treatment of the source of infection are essential to
successful management of septic shock and constitute critical interventions that can reverse septic shock.
In contrast, other therapies (eg, fluid administration, vasoactive drug infusion, or mechanical ventilation)
are purely supportive in nature [8-10].
A careful history and physical examination may yield clues to the source of sepsis and help guide
subsequent microbiologic evaluation (table 1). Gram stain of suspicious fluids may give early clues to the
etiology of infection while cultures are incubating. In addition to cultures of specific sites, blood should be
drawn and inoculated into standard blood culture media. Blood cultures should be incubated both
aerobically and anaerobically. (See "Blood cultures for the detection of bacteremia".)
Eradication of the inciting infection is essential for the successful treatment of septic shock. This includes
prompt administration of antimicrobial therapy and source control. Initial antimicrobial therapy should
provide broad spectrum coverage tailored to host factors, such as age and underlying medical conditions,
and be administered as soon as possible after presentation. (See "Septic shock: Rapid recognition and
initial resuscitation in children", section on 'Initial antimicrobial therapy'.)
Source control (physical measures undertaken to eradicate a focus of infection, to eliminate ongoing
microbial contamination, and to render a site inhospitable to microbial growth and invasion) should be
undertaken when possible because localized foci of infection (ie, abscess) may not respond to antibiotics
alone (table 1). As examples, potentially infected foreign bodies should be removed and abscesses,
infected fluid collections, or tissues should be percutaneously or surgically drained and dbrided. (See
"Necrotizing soft tissue infections", section on 'Treatment'.)
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Continue respiratory support Oxygenation should be monitored using continuous pulse oximetry
(SpO2). Patients should continue to receive supplemental oxygen to maintain oxygen saturation at 100
percent (patients with continued shock) or 97 percent (patients with restored perfusion and blood
pressure).
In patients with continued shock, endotracheal intubation should be performed if not already accomplished.
Mechanical ventilation should be performed with the following goals in mind [11,12]:
Keep plateau pressure 30 cmH2O.
Keep tidal volume under 10 mL/kg ideal body weight. Tidal volume may need to be decreased as low
as 4 to 6 ml/kg in patients with very low lung compliance using lung protective ventilation strategies to
achieve a plateau pressure 30 cmH2O [13,14].
Maintain arterial pH between 7.30 and 7.45.
Titrate fraction of inspired oxygen (FiO2) and positive end-expiratory pressure to maintain arterial
oxygen concentration (PaO2) between 60 and 80 mmHg (8 to 10.7 kPa) or pulse oximetry 90 to 97
percent in patients with hypoxia who require FiO2 50 percent.
Maintain hemoglobin 10 g/dL. (See 'Blood transfusion' below.)
Ongoing and invasive monitoring During initial management, monitoring of tissue perfusion using
physiologic indicators and target goals continues. (See "Septic shock: Rapid recognition and initial
resuscitation in children", section on 'Physiologic indicators and target goals'.)
In addition, the clinician should determine the need for invasive monitoring via intraarterial and central
venous cannulas:
Intraarterial cannula placement Although noninvasive blood pressure measurement is
acceptable in patients who have markedly improved or had total reversal of septic shock, automated
blood pressures overestimate systolic blood pressure relative to intraarterial or Doppler ultrasound
measurements in hypotensive children and underestimate systolic blood pressure among
hypertension patients [15]. Thus, insertion of an intraarterial catheter is suggested if blood pressure is
labile or if restoration of arterial perfusion pressures is expected to be a protracted process. However,
efforts to obtain intraarterial access should not interfere with the resuscitation of septic shock.
Procedures for obtaining intraarterial access in children are discussed separately. (See "Arterial
puncture and cannulation in children", section on 'Arterial cannulation'.)
Central venous access Central venous access is indicated for patients with catecholamineresistant septic shock because these patients frequently are dependent upon uninterrupted
vasoactive medication administration to prevent further decompensation and, if they also have poor
perfusion, are at a greatly increased risk of extravasation and significant local tissue damage.
Furthermore, central venous access permits monitoring of central venous pressures (CVP) and
central venous oxygen saturation (ScvO2) in these unstable patients and helps guide ongoing
therapy.
Central venous access is also appropriate in patients who have reversal of shock after initiation of
vasoactive drugs, although patients who rapidly improve after receiving vasoactive medications and in
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whom a rapid weaning of support is expected, may not require central venous line placement.
In the absence of an elevated intraabdominal pressure, the correlation between femoral vein pressure
and CVP is good, though absolute values may differ slightly [16,17]. Changes in ScvO2, which
provides reliable information regarding tissue oxygenation should also be frequently monitored [18]. If
direct measure of ScvO2 is not available, limited evidence suggests that a capillary refill time 2
seconds is associated with a ScvO2 70 percent. However, capillary refill time can be brisk despite
significant hemodynamic derangement in children with septic shock. (See "Initial management of shock
in children", section on 'Physiologic indicators and target goals'.)
Continue fluid administration The need for aggressive administration of fluids to optimize tissue
perfusion and to achieve physiologic goals typically continues beyond the first hour of care in children with
septic shock. In patients with persistent poor perfusion or hypotension, boluses of fluids should continue
until the central venous pressure is 8 to 12 cmH2O (12 to 15 cmH2O in mechanically ventilated patients) or
evidence of cardiac insufficiency (eg, pulmonary edema, enlarged heart) occurs. The volume per bolus
and types of fluid are as for the resuscitation period (algorithm 1). Fluid input and output should be
carefully monitored on an hourly basis. (See "Septic shock: Rapid recognition and initial resuscitation in
children", section on 'Intravenous fluid therapy'.)
Fluid overload Interstitial edema is common in sepsis due to increased vascular permeability. In
patients with clinical findings of significant fluid overload (eg, pitting edema, anasarca, or pulmonary
edema), early initiation of diuretic therapy (eg, furosemide) may be appropriate in patients with hypoxia and
pulmonary edema after a period of 12 to 24 hours of sustained hemodynamic stability off vasoactive
infusions. Patients in whom urine output remains insufficient may warrant renal replacement therapy (eg,
continuous veno-venous hemofiltration or intermittent hemodialysis). Observational studies in critically ill
children, including children with sepsis who received renal replacement therapies, indicate that more than
10 percent fluid overload is associated with mortality [19,20]. However, the evidence is not sufficient to
determine whether or not fluid overload has an independent deleterious effect on survival. Nonsurvivors
may have had more severe septic shock and therefore, required greater amount of fluid and were more
likely to develop renal insufficiency.
Blood transfusion Hemoglobin is the primary determinant of blood oxygen carrying capacity and,
therefore, of tissue oxygen delivery. Thus, maintaining adequate hemoglobin levels is a critical aspect of
managing children with septic shock. We suggest a hemoglobin goal of 10 g/dL (equivalent to 30 percent
hematocrit) as a target to maintain with blood transfusion during treatment of unstable children with septic
shock (eg, profound hypotension despite high levels of vasopressor support or profound hypoxia) [12].
Evidence is lacking to support the safety of tolerating a lower hemoglobin in such patients.
We typically use a hemoglobin of 7 g/dL instead of 10 g/dL as the threshold for blood transfusion in stable
patients recovering from septic shock instead of 10 g/dL. Limited evidence suggests that this lower
hematocrit threshold for blood transfusion is likely to be safe [21]. As an example, in a multicenter
unblinded trial of 137 stabilized children with sepsis (mean systemic arterial pressure was not below two
standard deviations of normal for age and cardiovascular support was not increased for at least two hours
before enrollment) that compared restrictive transfusion (transfusion for hemoglobin <7.0 g/dL) with liberal
transfusion (transfusion for hemoglobin <9.5 g/dL), no clinically significant differences were found for the
occurrence of new or progressive multiple organ dysfunction syndrome (18.8 versus 19.1 percent), PICU
length of stay (13 days in both groups), or PICU mortality (7 versus 3 percent, respectively) [21]. However,
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two additional patients died in the restrictive transfusion group after discharge from the PICU.
Treat disseminated intravascular coagulation Patients with septic shock frequently have
disseminated intravascular coagulopathy that may warrant treatment. Thus, baseline measures of clotting
status should be routinely obtained in children with septic shock. (See "Septic shock: Rapid recognition
and initial resuscitation in children", section on 'Suggestive laboratory findings'.)
There have been no trials to study the efficacy of platelet, fresh frozen plasma (FFP), or cryoprecipitate
transfusions in children with sepsis and DIC. Nevertheless, the use of these agents seems rational in
patients with significant bleeding (melena, or prolonged bleeding from venipuncture sites) due to
thrombocytopenia and clotting factor consumption or significant risk of bleeding (eg, pre- or postoperative
patients). (See "Disseminated intravascular coagulation in infants and children", section on 'Replacement
therapy'.)
The goal of replacement therapy is to reduce or stop significant bleeding. Although replacement therapy
should not be used to normalize laboratory tests (which often is impossible), a reasonable guide for the
judicious use of blood components in the setting of significant bleeding includes maintaining platelet counts
>50,000 per mm and fibrinogen concentration >100 mg/dL (1 mol/L). (See "Disseminated intravascular
coagulation in infants and children", section on 'Replacement therapy'.)
Clotting factors can be replaced by either FFP or cryoprecipitate. FFP provides both procoagulant and
anticoagulant proteins and is administered every 12 to 24 hours at a dose of 10 to 15 mL/kg per infusion.
Cryoprecipitate has higher concentrations of factor VIII and fibrinogen, and can be used to correct
hypofibrinogenemia. It is administered every six hours as needed at a dose of 10 mL/kg per infusion.
Platelet transfusions are administered with a goal of maintaining the platelet counts >50,000 per mm. (See
"Disseminated intravascular coagulation in infants and children", section on 'Replacement therapy'.)
Although initial observational studies indicated that children with sepsis frequently have low circulating
levels of activated protein C, administration of recombinant human activated protein C (drotrecogin alfa)
has shown no benefit and may be harmful. As an example, in a multicenter randomized trial comparing
drotrecogin alpha with placebo for the treatment of children with severe sepsis, interim analysis
demonstrated no benefit for treatment with drotrecogin alpha and an increased incidence of central
nervous system bleeding, particularly in those younger than 60 days [22]. As a result, this trial was
discontinued. A systematic review that included this trial concluded that recombinant human activated
protein C should not be used for any children or for adults who are not severely ill [23]. In October 2011,
drotrecogin alpha was voluntarily removed from the worldwide market by Eli Lilly due to a negative second
trial in adults with severe septic shock.
Observational and dose finding studies of protein C concentrate in selected children with severe
meningococcal septic shock, and purpura fulminans have shown potential promise. Protein C concentrate
is not biologically active on administration (requires conversion to activated protein C by thrombin or
thrombin bound to endothelial thrombomodulin) and is used mainly in patients with severe congenital
protein C deficiency. (See "Treatment and prevention of meningococcal infection", section on 'Protein C
concentrate' and "Protein C deficiency".)
Manage glucose abnormalities Hypoglycemia remains a concern during the initial management
phase of septic shock. Children have limited glycogen stores and may develop profound hypoglycemia
during periods of stress. Thus, blood glucose should be monitored frequently upon admission and at least
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every six hours while the patient is unstable and corrected (table 2). (See "Septic shock: Rapid recognition
and initial resuscitation in children", section on 'Treat hypoglycemia and hypocalcemia'.)
Once tissue perfusion is restored and shock is resolved, children should receive intravenous fluid that
contains dextrose sufficient to maintain euglycemia. This therapy typically consists of 5 to 10 percent
dextrose in electrolyte solution appropriate to the patients ongoing sodium and potassium requirements.
The glucose dose is determined by age: 8 mg/kg per minute (neonates), 4 mg/kg per minute (children), 2
mg/kg per minute (adolescents) [24].
Hyperglycemia is commonly present in children with septic shock. Data regarding exogenous insulin as a
means to maintain euglycemia in these patients is as follows:
In one small observational study of 57 children with septic shock, children who died had higher peak
serum glucose levels than survivors (262 versus 168 mg/dL) [25].
In one small series of 16 children with meningococcal sepsis or septic shock, hyperglycemia reflected
hypoinsulinemia rather than insulin resistance in those patients with septic shock [26].
In a trial of 700 critically ill infants and children admitted to a PICU that compared conventional versus
intensive control of serum glucose, duration of PICU stay was shortest in the intensive versus
conventional treatment group (5.5 versus 6.2 days). However, hypoglycemia (defined as blood
glucose 40 mg/dL [2.22 mmol/L]) was more common in children receiving intensive glucose control
(25 versus 1 percent, respectively). Nine (3 percent) patients died in the intensively treated group
versus 20 (6 percent) in the conventional group (p = 0.038) [27]. At a median of four years of followup, children who had been treated with tight glycemic control during their ICU admission did not have a
worse measure of intelligence than those who had received usual care [28].
In a trial of 980 children (0 to 36 months of age), undergoing surgery with cardiopulmonary bypass
randomized to either tight glycemic control (with the use of an insulin-dosing algorithm) targeting a
blood glucose level of 80 to 110 mg/dL (4.44 to 6.12 mmol/L) or standard care in the cardiac intensive
care unit, no difference was found in the rate of health care-associated infections (8.6 versus 9.9 per
1000 patient-days) or other secondary outcomes [29]. This study used continuous glucose monitoring
to guide the frequency of blood glucose measurement and to detect impending hypoglycemia, with
only 3 percent of the patients in the tight glycemic control group exhibiting severe hypoglycemia (blood
glucose <40 mg/dl [2.22 mmol/L]).
Taken together, the evidence suggests that there are no clear benefits to tight glycemic control in critically
ill children. Until further data are available, insulin therapy is warranted to avoid long periods of
hyperglycemia >180 mg/dL (9.99 mmol/L) while also avoiding hypoglycemia. We do not advocate tight
glycemic control. However, there is no universally accepted insulin regimen, and the optimal approach to
hyperglycemia in children with septic shock awaits further study.
Glycemic control in adults with critical illness is discussed separately. (See "Glycemic control and intensive
insulin therapy in critical illness", section on 'Glycemic control'.)
Avoid hypocalcemia Adequate calcium stores are essential for maintaining myocardial contractility.
Thus, ionized blood calcium levels should be monitored every one to two hours during initial management
of septic shock. Patients with persistent shock and an ionized calcium <1.1 mmol/L (4.8 mg/dL) or those
with symptomatic hypocalcemia (eg, positive Chvostek or Trousseau signs, seizures, prolonged QT interval
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on EKG, or cardiac arrhythmias) in association with a an ionized calcium <1.1 mmol/L (4.8 mg/dL) should
undergo correction with calcium gluconate 10 percent solution in a dose of 50 mg/kg (0.5 mL/kg), maximum
dose 2 g (20 mL) by slow intravenous or intraosseous infusion over five minutes. This suggested dose is
equivalent to elemental calcium 5 mg/kg (0.15 mmol/kg), up to 180 mg elemental (4.5 mmol) per single
dose.
Calcium should be administered in a larger vein or, preferably, a central line. Sodium bicarbonate should
not be introduced into the IV or IO without flushing before and after administration because of potential
precipitation.
Calcium chloride 10 percent in a dose of 10 to 20 mg/kg (0.1 to 0.2 mL/kg), maximum dose 1 g (10 mL)
provides an equivalent dose but should only be administered through a central line. Patients receiving a
calcium infusion warrant continuous cardiac monitoring.
Treat known hormonal deficiencies Patients with septic shock who are receiving replacement
therapy for adrenal insufficiency should receive stress doses of glucocorticoids. (See 'Address adrenal
insufficiency' below.)
Similarly, children with septic shock and hypothyroidism should continue to receive thyroid replacement
with levothyroxine [24]. (See "Treatment and prognosis of congenital hypothyroidism", section on 'Dose of
L-T4' and "Acquired hypothyroidism in childhood and adolescence", section on 'T4 dose'.)
REFRACTORY SEPTIC SHOCK The initial treatment of septic shock including management
recommendations for fluid-refractory septic shock are described in the algorithm and discussed in detail
separately (algorithm 1).
Fluid-refractory, catecholamine-resistant shock is defined as cardiovascular dysfunction despite at least 60
mL/kg of fluid resuscitation and dopamine 10 mcg/kg/min and/or direct-acting catecholamines
(epinephrine, norepinephrine). Principles of management for children with refractory septic shock include
treatment of reversible etiologies, stress dose glucocorticoid therapy for patients with absolute adrenal
insufficiency, and combination vasoactive drug therapy targeted to maintaining central venous oxygen
saturation 70 percent and normalizing blood lactate levels.
Although cardiac index targets are mentioned in previous pediatric septic shock guidelines [24], evidence
of improved outcomes from routine measurement of cardiac index is lacking (algorithm 1). If performed, the
target range is 3.3 to 6.0 L/min/m2.
Treat reversible etiologies Pneumothorax, pericardial tamponade, and intra-abdominal hypertension
(eg, peritonitis or ascites) comprise mechanical causes of shock that can be reversed by chest tube
thoracostomy, pericardiocentesis, or abdominal decompression surgery, respectively. (See "Placement
and management of thoracostomy tubes", section on 'Tube thoracostomy' and "Emergency
pericardiocentesis", section on 'Technique overview'.)
Drainage or debridement of infection sites (eg, necrotizing fasciitis) or broadening of antimicrobial
coverage are additional actions that may be warranted. (See 'Eradicate infection' above and "Necrotizing
soft tissue infections", section on 'Treatment'.)
Uncontrolled hemorrhage, typically caused by spontaneous bleeding secondary to disseminated
intravascular coagulopathy warrants timely administration of blood and blood products. (See 'Treat
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disseminated intravascular coagulation' above.)

In rare instances, persistent shock may reflect anaphylaxis to administered antibiotic agents. These
patients warrant treatment with antihistamines, epinephrine, glucocorticoids, and removal of the inciting
agent (table 3). (See "Anaphylaxis: Emergency treatment", section on 'Immediate management'.)
Obtain cardiac evaluation Patients with refractory septic shock warrant an electrocardiogram to
assess for signs of myocardial ischemia or infarction and heart failure. Pediatric cardiology consultation
and echocardiography is also advised to assess for signs of myocarditis or, especially in neonates and
young infants, signs of congenital heart disease.
Patients with myocarditis diagnosed by endomyocardial biopsy may benefit from intravenous gamma
globulin, although evidence is very limited. Glucocorticoids or other immunosuppressive agents may be
appropriate for patients with myocarditis caused by systemic autoimmune disease in addition to infection.
(See "Treatment and prognosis of myocarditis in children", section on 'Immunomodulatory therapy'.)
Address adrenal insufficiency Adrenal insufficiency is a clinical condition frequently associated with
fluid- and catecholamine-resistant septic shock [24,30,31]. We suggest that children with fluid-refractory,
catecholamine-resistant septic shock receive stress dose glucocorticoids (eg, hydrocortisone 50 to 100
mg/m2 per dose or 1 to 2 mg/kg [maximum 100 mg] per dose followed by 50 to 100 mg/m2 or 1 to 2 mg/kg
[maximum 100 mg] per day either given continuously or divided every four or six hours) [12,24,32-35].
Glucocorticoid therapy should be discontinued when the patient becomes hemodynamically stable and no
longer requires vasoactive medication administration. Practice varies regarding whether glucocorticoids
are abruptly discontinued or tapered in children with septic shock. Adult guidelines suggest tapering of
glucocorticoids but there is insufficient data in children. However, tapering is suggested if duration of
glucocorticoid use is long enough to potentially have caused adrenal suppression or adrenal suppression
is identified by provocative testing. (See "Glucocorticoid therapy in septic shock", section on
'Administration'.)
Stress-dose glucocorticoids should not be given to children with septic shock who never required or who
no longer require vasopressor support unless the patient has pre-existing known adrenal insufficiency.
Whether to use baseline cortisol measurements, adrenocorticotropin stimulation testing, or persistent
hemodynamic instability alone as indicators for initiating and continuing glucocorticoid therapy in children
with refractory septic shock is debated and evidence for the best approach is lacking.
Adrenal insufficiency (AI) is often defined in the critically ill pediatric population by an insufficient response
to an adrenocorticotropic hormone (ACTH) stimulation test with a change in cortisol from baseline to one
hour after the intravenous cosyntropin of <9 mcg/dL. Using this definition, one multicenter study showed
that 30 percent of 381 critically ill children met criteria for AI during the first day of intensive care with a
similar frequency occurring in the 59 patients with sepsis [36]. Patients receiving catecholamines had a
higher rate of AI (43 percent). The median baseline cortisol was 28.6 mcg/dL in the children with AI, versus
16.7 in those without AI. Among patients who did not receive glucocorticoids and were re-tested 24 hours
later, <20 percent met criteria for AI. Thus, AI can exist in critically ill patients with a relatively high random
cortisol level, and AI can resolve without specific treatment. These findings have led some experts to
suggest the use of stress dose glucocorticoids in children with refractory septic shock without specific
testing for AI.
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Glucocorticoids are not without risk and should not be routinely used in children with septic shock. In an
observational study of 6693 children with severe sepsis treated in childrens hospitals, glucocorticoid
treatment was associated with clinically significantly increased mortality (adjusted odds ratio 1.9 [95% CI
1.7, 2.1]) [37]. Neonates who received 2 days of glucocorticoids had a greater absolute increase in
mortality than older patients (12 versus 6 percent increased mortality). Thus, further evidence is needed to
better guide the use of glucocorticoid administration in children with septic shock, including those patients
who are most likely to benefit or experience adverse effects.
Combination vasoactive drug therapy The ongoing management of vasoactive drug therapy in
children with septic shock should be performed by clinicians with pediatric critical care expertise whenever
possible. The approach provided here is for patients with septic shock who have already received a rapid
infusion of at least 40 to 60 mL/kg of crystalloid and initial infusions of epinephrine or dopamine requiring
addition of epinephrine (patients with cold shock) or norepinephrine (patients with warm shock) (algorithm
1).
The physical findings of cold and warm shock are discussed separately. (See "Systemic inflammatory
response syndrome (SIRS) and sepsis in children: Definitions, epidemiology, clinical manifestations, and
diagnosis", section on 'Shock'.)
Additional vasoactive therapy should be based upon the type of persistent shock (cold or warm shock) and
the central venous oxygen saturation (ScvO2) as follows (algorithm 1) [24]:
Warm shock with low blood pressure, ScvO2 <70 percent Norepinephrine is suggested for
children with warm shock who do not respond to fluid resuscitation. (See "Septic shock: Rapid
recognition and initial resuscitation in children", section on 'Warm shock'.)
Patients who do not respond to norepinephrine infusion may receive vasopressin or its long-acting
formulation, terlipressin, if available, although use of these agents is controversial [24]. Case reports,
case series, and one trial indicate that administration of either vasopressin or terlipressin is associated
with an increase in mean arterial blood pressure and urine output in children with fluid-refractory,
catecholamine-resistant septic shock [38-40]. However, in a multicenter trial of 65 children with
vasodilatory shock, low-dose vasopressin did not decrease the time to hemodynamic stability off
vasopressor agents versus placebo (49.7 versus 47.1 hours) [41]. Patients receiving low-dose
vasopressin had higher mortality (30 versus 16 percent) although this difference was not statistically
significant.
Cold shock with normal or low blood pressure, ScvO2 <70 percent Epinephrine is suggested
as the initial vasopressor for patients with cold shock. If the patient is initially receiving dopamine and
not responsive to escalating doses, then the addition of an epinephrine infusion is warranted. (See
"Septic shock: Rapid recognition and initial resuscitation in children", section on 'Cold shock'.)
If ScvO2 remains below 70 percent despite escalating doses of epinephrine, the addition of agents
with inotropic properties and afterload reduction (eg, dobutamine, milrinone) or rapid-acting
vasodilators for afterload reduction (eg, nitroprusside) may be helpful (algorithm 1) [12]. Since
hypotension could be exacerbated by addition of vasodilating agents, these should be titrated
carefully with close attention to hemodynamic changes. Vasodilators should be discontinued if
hypotension worsens.
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In a small trial of 12 children with refractory catecholamine-resistant shock, administration of milrinone

was associated with improved cardiac index and increased oxygen delivery although improved survival
was not demonstrated [42]. Milrinone is a phosphodiesterase inhibitor that provides both increased
cardiac contractility and vasodilation with afterload reduction. However, long-term use of milrinone is
associated with an increased frequency of ventricular arrhythmias, including torsade des pointes.
Patients receiving milrinone warrant close monitoring for hypotension, given its long half-life.
Alternatively, use of a vasodilator (eg, nitroprusside) for afterload reduction may be beneficial in
selected patients. If nitroprusside is used, the medication should be protected from light, and doses in
excess of 1.8 mcg/kg per minute should be avoided. Concomitant administration of thiosulfate to
scavenge the cyanide produced by nitroprusside metabolism is suggested, either prophylactically or if
cyanide levels are elevated.
Advanced therapies
Extracorporeal membrane oxygenation (ECMO) We and the American College of Critical Care
Medicine (ACCM) suggest that children with persistent catecholamine-resistant shock in whom physiologic
targets (eg, ScvO2 70 percent) cannot be attained with fluid repletion, vasoactive infusion, and hormonal
therapy; who do not have an immediately reversible cause, such as myocarditis, pneumothorax, or
pericardial effusion; and who have a high likelihood of mortality, be evaluated for ECMO support, if
available (algorithm 1) [12]. If ECMO is not available at the facility in which the child is receiving care then
the potential benefits of ECMO must be weighed against the likelihood that the patient can tolerate
transfer.
Severe sepsis and septic shock were previously considered to be contraindications to ECMO [24].
However, more recent data suggest that for patients who receive ECMO, survival to hospital discharge
approaches 50 percent in pediatric refractory septic shock and 80 percent for neonatal refractory septic
shock. As an example, in a small case series of 23 children with refractory septic shock in which central
cannulation was used to achieve higher blood flow rates, 18 (78 percent) patients survived to be
decannulated off ECMO and 17 (74 percent) children survived to hospital discharge [43]. Our experience
suggests that the chances of survival in such patients with conventional therapy alone are otherwise very
remote.
Intravenous immune globulin Adjuvant therapy with intravenous immune globulin (IVIG) has been
proposed but evidence for benefit in children with septic shock remains inconclusive. A trial of polyclonal
IVIG in 100 children with pediatric sepsis syndrome showed a significant reduction in mortality (28 versus
44 percent), length of stay (six versus nine days), and less progression to complications (8 versus 32
percent) [44]. However, a more recent multicenter trial of polyclonal IVIG in 3493 neonates receiving
antibiotics for suspected or proven serious infection found no significant difference in the rate of the
primary outcome of death or major disability at the age of two years (relative risk [RR], 1.00; 95% CI, 0.91.1) [45]. Evidence in adult patients with septic shock suggests that IVIG has no benefit in this population.
(See "Investigational and ineffective therapies for sepsis", section on 'Intravenous immune globulin'.)
For patients with toxic shock syndrome, IVIG may have clinical utility. IVIG for this indication is discussed
separately. (See "Staphylococcal toxic shock syndrome", section on 'Intravenous immune globulin'.)
EXPERIMENTAL THERAPIES
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11/14/2016
Plasma exchange or plasmapheresis There has been considerable interest in extracorporeal

filtration of circulating inflammatory mediators in sepsis. Although multiple studies in adults have been
published on plasma exchange and plasmapheresis in sepsis, most are limited by small sample size at
single institutions with considerable variability in the protocols utilized. Thus, current evidence is conflicting
as to clinical benefit. (See "Investigational and ineffective therapies for sepsis", section on 'Hemofiltration'.)
In addition, the practical limitations of inserting a large catheter for plasma exchange in young children
(often with disseminated intravascular coagulopathy and increased risk of bleeding), the intensive
resources necessary to perform plasma exchange or plasmapheresis, and the potential to worsen
hypotension in hemodynamically unstable patients has limited this therapy in pediatric sepsis.
One small trial of 10 children demonstrated a survival benefit in patients with the clinical phenotype of
thrombocytopenia-associated multiple organ failure or TAMOF receiving plasmapheresis versus standard
therapy (five of five versus one of five surviving) [46]. In this study, low levels of the von Willebrand factor
cleaving protease, ADAMTS-13, activity were reversed with daily plasma exchange, which the authors
suggested as the potential benefit of this therapy. Until further data becomes available, plasma exchange
for pediatric patients with sepsis, including TAMOF with decreased ADAMTS-13 activity, remains an
experimental therapy.
Other therapies A variety of therapies have been investigated or are being evaluated to improve
clinical outcomes in sepsis. Those therapies that appear promising as well as ones that have been proven
to be ineffective are discussed in detail separately. (See "Investigational and ineffective therapies for
sepsis".)
GUIDELINE IMPLEMENTATION The early recognition and management of pediatric severe sepsis and
septic shock can be improved through the establishment of institutional care guidelines. As an example, in
an observational study of the impact of guidelines for sepsis management in a childrens hospital
emergency department versus baseline actions before implementation, significant gains were documented
for several key therapeutic actions including more timely fluid resuscitation (70 versus 43 percent receiving
20 mL/kg of normal saline in the first hour), antibiotic administration (90 versus 53 percent receiving
antibiotics within three hours), and blood lactate determination (measured in 70 versus 10 percent of
patients with possible septic shock) [47]. Median length of hospital stay decreased clinically significantly
after implementation of the guidelines (181 to 140 hours). Mortality was not significantly different (6 versus
7 percent).
PROGNOSIS Factors related to the host, site of infections, and microbiology may influence the
progression from systemic inflammatory response syndrome to severe sepsis to septic shock and provide
predictors of mortality. Severity of illness, progression to multiple organ failure, and treatment requirements
are also important prognostic indicators:
Host factors Case fatality rates in children with severe sepsis are highest for infants 1 to 12 months
of age (approximately 11 percent) and are higher across all age groups for children with comorbidities,
especially in children with cancer or human immunodeficiency virus infection (12 to 16 percent) [3,48].
Site of infection Children with endocarditis, central nervous system infection, and primary
bacteremia have high case fatality rates (15 to 20 percent) [3]. The case fatality rate is lowest for
genitourinary tract infections (approximately 4 percent).
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Microbiology Case fatality is increased in children with pneumococcal and fungal infections (15
and 13 percent, respectively) [3]. Infection with organisms resistant to antibiotics (eg, methicillinresistant Staphylococcus aureus or vancomycin-resistant enterococcus species) is associated with a
marked increased mortality from sepsis. (See "Sepsis syndromes in adults: Epidemiology, definitions,
clinical presentation, diagnosis, and prognosis", section on 'Type of infection'.)
Severity of illness Mortality increases markedly depending upon the severity of illness in children
with sepsis. As an example, in a multicenter observational study of 1051 children between one month
and 18 years of age treated for sepsis in pediatric intensive care units, mortality increased from 1
percent in children with sepsis to 6 and 34 percent in children with severe sepsis and septic shock,
respectively [6].
Multiple organ failure The development of multiple organ dysfunction indicates an increased
severity of illness in patients with sepsis and is associated with a higher mortality estimated as 0 to 7
percent for patients with one affected organ system and 20 to 50 percent with two or more failing
organ systems [3,48-50]. (See "Systemic inflammatory response syndrome (SIRS) and sepsis in
children: Definitions, epidemiology, clinical manifestations, and diagnosis", section on 'Sepsis'.)
Treatment requirements The need for multiple vasoactive infusions predicts a poor prognosis. As
an example, in an observational study of 96 episodes of pediatric septic shock in 80 patients, mortality
was significantly higher for patients receiving multiple rather than one vasoactive agent (43 versus 0
percent, respectively) [48].
SUMMARY AND RECOMMENDATIONS
The rapid recognition and initial resuscitation of children with septic shock is discussed separately.
(See "Septic shock: Rapid recognition and initial resuscitation in children".)
Ongoing aggressive resuscitation should continue after the initial resuscitation of pediatric septic
shock according to the principles of goal-directed therapy, especially when managing children in whom
adequate circulation has not been restored (algorithm 1). (See 'Overview' above.)
Whenever possible, children requiring resuscitation for septic shock should receive ongoing
management by a pediatric critical care specialist or pediatrician with similar expertise in a pediatric
intensive care unit (PICU). (See 'Overview' above.)
Eradication of infection can reverse septic shock. Antimicrobial treatment should be optimized based
upon culture results. Source control (physical measures undertaken to eradicate a focus of infection,
to eliminate ongoing microbial contamination, and to render a site inhospitable to microbial growth and
invasion) should be undertaken when possible because localized foci of infection (ie, abscess) may
not respond to antibiotics alone (table 1). (See 'Eradicate infection' above.)
During initial management, continuation of respiratory support, monitoring of tissue perfusion using
physiologic indicators and target goals, aggressive administration of fluids, and titration of vasoactive
infusions continue. In addition, the clinician should determine the need for invasive monitoring via
intraarterial and central venous cannulas. (See 'Ongoing and invasive monitoring' above and "Septic
shock: Rapid recognition and initial resuscitation in children", section on 'Physiologic indicators and
target goals' and 'Continue fluid administration' above.)
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Maintaining adequate hemoglobin levels is a critical aspect of managing children with septic shock. We
and the American College of Critical Care Medicine (ACCM) guidelines suggest a hemoglobin goal of
10 g/dL (equivalent to 30 percent hematocrit) as a target to maintain with blood transfusion during
resuscitation and ongoing management of unstable children with septic shock (Grade 2C). Once
shock has resolved, a lower hematocrit threshold for blood transfusion may be safe. (See 'Blood
transfusion' above.)
Platelets, fresh frozen plasma, and/or cryoprecipitate should be provided to patients with disseminated
intravascular coagulopathy and significant bleeding. (See 'Treat disseminated intravascular
coagulation' above.)
Other important interventions include management of glucose abnormalities, treatment of symptomatic
hypocalcemia, and replacement therapy for known adrenal insufficiency or hypothyroidism. (See
'Manage glucose abnormalities' above and 'Avoid hypocalcemia' above and 'Treat known hormonal
deficiencies' above.)
Principles of management for children with refractory septic shock include (see 'Refractory septic
shock' above):
Treatment of reversible causes (eg, pneumothorax, pericardial tamponade, hemorrhage)
Assessment for and treatment of adrenal insufficiency
Combination vasoactive therapy targeted to central venous oxygen saturation and other
measures of tissue perfusion (eg, capillary refill time, urine output, mental status, and serum
lactate levels)
We suggest that children with refractory catecholamine-resistant septic shock receive stress dose
glucocorticoids (eg, hydrocortisone 50 to 100 mg/m2 per dose or 1 to 2 mg/kg [maximum 100 mg] per
dose followed by 50 to 100 mg/m2 or 1 to 2 mg/kg [maximum 100 mg] per day either given
continuously or divided every four or six hours) (Grade 2C). Whether to use baseline cortisol
measurements, adrenocorticotropin stimulation testing, or persistent hemodynamic instability alone as
indicators for continued therapy is debated and evidence for the best approach in children is lacking.
Glucocorticoid therapy should be discontinued when the patient becomes hemodynamically stable.
Stress-dose glucocorticoids should not be given to children with septic shock who never required or
who no longer require vasopressor support unless the patient has pre-existing known adrenal
insufficiency. (See 'Address adrenal insufficiency' above.)
We and the ACCM guidelines suggest that children with persistent catecholamine-resistant shock in
whom physiologic targets (eg, ScvO2 70 percent) cannot be attained with fluid repletion, vasoactive
infusion, and hormonal therapy; who do not have a reversible cause, such as myocarditis,
pneumothorax, or pericardial effusion; and who have a high likelihood of mortality, be evaluated for
extracorporeal membrane oxygenation (ECMO) support, if available (algorithm 1) (Grade 2C). If the
patient is an ECMO candidate and ECMO is not available at the facility in which the child is receiving
care then the potential benefits of ECMO must be weighed against the likelihood that the patient can
tolerate transfer. (See 'Extracorporeal membrane oxygenation (ECMO)' above.)
Use of UpToDate is subject to the Subscription and License Agreement.
11/14/2016
Topic 86881 Version 10.0
11/14/2016
GRAPHICS
Recommendations for stepwise management of hemodynamic support in
infants and children with sepsis
The guideline and algorithm for the management of pediatric septic shock are undergoing review
11/14/2016
by the American College of Critical Care Medicine. Please refer to the UpToDate topics on the
recognition and management of septic shock in children for the latest recommendations.
Algorithm for time sensitive, goal-directed stepw ise management of hemodynamic support in
infants and children. Proceed to next step if shock persists. (1) First hour goalsRestore and
maintain heart rate thresholds, capillary refill 2 sec, and normal blood pressure in the first
hour/emergency department. Support oxygenation and ventilation as appropriate. (2)
Subsequent intensive care unit goalsIf shock is not reversed, intervene to restore and maintain
normal perfusion pressure (mean arterial pressure [MAP]-central venous pressure [CVP]) for age,
central venous O 2 saturation >70 percent, and CI >3.3, <6.0 L/min/m 2 in pediatric intensive care
unit (PICU).
Hgb: hemoglobin; PIC C O: pulse contour cardiac output; FATD: femoral arterial thermodilution; EC MO:
extracorporeal membrane oxygenation; C I: cardiac index; C RRT: continuous renal replacement therapy;
IV: intravenous; IO: interosseous; IM: intramuscular.
Reproduced with permission from: Brierley J, Carcillo JA, Choong K, et al. Clinical practice parameters for
hemodynamic support of pediatric and neonatal septic shock: 2007 update from the American College of
Critical Care Medicine. Crit Care Med 2009; 37:666. Copyright 2009 Lippincott Williams & Wilkins.
Graphic 80923 Version 15.0
11/14/2016
Evaluation of common sources of sepsis

Suspected site
Symptoms/signs
Microbiologic evaluation
Upper respiratory tract
Pharyngeal inflammation plus

exudate swelling and
lymphadenopathy
Throat swab for aerobic culture
Lower respiratory tract
Productive cough, pleuritic chest

pain, consolidative auscultatory
findings
Sputum of good quality, rapid

influenza testing, urinary antigen
testing (eg, pneumococcus,
legionella), quantitative culture of
protected brush or
bronchoalveolar lavage
Urinary tract
Fever, urgency, dysuria, loin pain
Urine microscopy showing pyuria
Vascular catheters: arterial,

central venous
Redness or drainage at insertion

site
C ulture of blood (from the

catheter and a peripheral site),
culture catheter tip (if removed)
Indwelling pleural catheter
Redness or drainage at insertion

site
C ulture of pleural fluid (through

catheter), culture of catheter tip
(if removed)
Wound or burn
Inflammation, edema, erythema,

discharge of pus
Gram stain and culture of draining

pus, wound culture not reliable
Skin/soft tissue
Erythema, edema, lymphangitis
C ulture blister fluid or draining

pus; role of tissue aspirates not
proven
C entral nervous system
Signs of meningeal irritation
C SF microscopy, protein, glucose,

culture, bacterial antigen test
Gastrointestinal
Abdominal pain, distension,

diarrhea, and vomiting
Stool culture for Salmonella,

Shigella, and C ampylobacter
Intraabdominal
Specific abdominal
symptoms/signs
Aerobic and anaerobic culture of

percutaneously or surgically
drained abdominal fluid
collections
Peritoneal dialysis (PD) catheter
C loudy PD fluid, abdominal pain,

fever
C ell count and culture of PD fluid
Genital tract
Women: Low abdominal pain,

vaginal discharge
Women: Endocervical and high

vaginal swabs onto selective
media
Men: Dysuria, frequency,

urgency, urge incontinence,
cloudy urine, prostatic tenderness
Joint
Pain, warmth, decreased range of

motion
Men: Urine Gram stain and

culture
Arthrocentesis with cell counts,
Gram stain, and culture
C SF: cerebrospinal fluid; PD: peritoneal dialysis.

Adapted from: Cohen J, Microbiologic requirements for studies of sepsis. In: Sibbald WJ, Vincent JL (eds),
Clinical Trials for the Treatment of Sepsis, Springer-Verlag, Berlin, 1995, p.73.
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Rapid overview for hypoglycemia in adolescents and children, other than

neonates
Clinical features
Any patient with acute lethargy or coma should have an immediate measurement of blood glucose to
determine if hypoglycemia is a possible cause
Other findings of hypoglycemia are nonspecific* and vary by age:
Infants
- Irritability
- Lethargy
- Jitteriness
- Feeding problems
- Hypothermia
- Hypotonia
- Tachypnea
- C yanosis
- Apnea
- Seizures
Older children and adolescents
- Autonomic response (tends to occur with blood glucose <50 to 65 mg/dL)
Swe a ting
T a chyca rdia
P a lpita tio ns
T re m o r
Ne rvo usne ss
Hunge r
P a re sthe sia s
P a llo r
- Neuroglycopenia
Irrita bility
C o nfusio n
Uncha ra cte ristic be ha vio r
W e a k ne ss
Se izure s
Com a
O cca sio na lly, tra nsie nt fo ca l ne uro lo gic de ficits
Diagnosis
Obtain rapid bedside blood glucose concentration (and -hydroxybutyrate, if available as a point-ofcare measurement)
C onfirm the presence of hypoglycemia with a simultaneously drawn plasma glucose
Treat, as outlined below, if the bedside value is low (<70 mg/dL [3.89 mmol/L]) in symptomatic
patients
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Obtain a blood sample for additional diagnostic studies prior to glucose administration, if possible, and
collect the first voided urine after the hypoglycemic event in all infants and young children who are not
being treated for diabetes mellitus or do not have a known cause for hypoglycemia
Treatment
Do not delay treatment if symptomatic hypoglycemia is suspected. However, every reasonable effort
should be made to obtain a rapid blood glucose measurement prior to administering glucose.
Give glucose based upon the patients level of consciousness and ability to swallow safely
(ie, alert enough to do so and with intact gag reflex) as follows:
Conscious and able to drink and swallow safely:
Adm iniste r 0.3 g/k g (10 to 20 g) o f a ra pidly-a bso rbe d ca rbo hydra te . 15 g is supplie d by 3
gluco se ta ble ts, a tube o f ge l with 15 g, 4 o z (120 m L) swe e te ne d fruit juice , 6 o z no n-die t so da ,
o r a ta ble spo o n (15 m L) o f ho ne y o r ta ble suga r. Ma y re pe a t in 10 to 15 m inute s.
Altered mental status, unable to swallow, or does not respond to oral glucose
administration within 15 minutes:
Give a n initia l IV bo lus o f gluco se o f 0.25 g/k g o f de x tro se (m a x im um single do se 25 g). T he
vo lum e a nd co nce ntra tio n o f gluco se bo lus is infuse d slo wly a t 2 to 3 m L pe r m inute a nd ba se d
upo n a ge :
2.5 m L/k g o f 10% de x tro se so lutio n (D10W ) in infa nts a nd childre n up to 12 ye a rs o f a ge
(10% de x tro se is 100 m g/m L)
1 m L/k g o f 25% de x tro se (D25W ) o r 0.5 m L/k g o f 50% de x tro se (D50W ) in a do le sce nts
(25% de x tro se is 250 m g/m L; 50% de x tro se is 500 m g/m L)
Unable to receive oral glucose and unable to obtain IV access:

Give gluca go n 0.03 m g/k g IM o r SQ (m a x im um do se 1 m g) :
P e rfo rm blo o d gluco se m o nito ring e ve ry 10 to 15 m inute s a s the e ffe cts o f gluca go n m a y
be tra nsie nt
Esta blish va scula r a cce ss a s so o n a s po ssible
After initial hypoglycemia is reversed, provide additional glucose and treatment based upon suspected
etiology:
- Give children and adolescents with type I diabetes mellitus a normal diet
- Give patients with an unknown cause of hypoglycemia intravenous infusion of dextrose 10% (6
to 9 mg/kg per minute) titrated to maintain blood glucose in a safe and appropriate range (70 to
150 mg/dL [3.89 to 8.33 mmol/L])
- Give patients, who have ingested a sulfonylurea and have recurrent hypoglycemia, octreotide
(dose: 1 to 1.5 mcg/kg IM or SQ, maximum dose 150 mcg every 6 hours) in addition to glucose.
(Refer to UpToDate topic on sulfonylurea poisoning).
Measure a rapid blood and plasma glucose 15 to 30 minutes after the initial IV glucose bolus and then
monitor every 30 to 60 minutes until stable (minimum of four hours) to ensure that plasma glucose
concentration is maintained in the normal range (>70 to 100 mg/dL [>3.89 to 5.55 mmol/L])
Obtain pediatric endocrinology consultation for patients with hypoglycemia of unknown cause
Obtain medical toxicology consultation for patients with ingestion of oral hypoglycemic agents by calling
the United States Poison C ontrol Network at 1-800-222-1222
or access the World Health
Organization's list of international poison centers
(www.who.int/gho/phe/chemical_safety/poisons_centres/en/index.html)
Admit the following patients:
- C annot maintain normoglycemia with oral intake
- Hypoglycemia of unknown cause
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- Ingestion of long-acting hypoglycemic agents

- Recurrent hypoglycemia during the period of observation
IV: intravenous; IM: intramuscular; SQ: subcutaneous; D10W: 10% dextrose in water; D25W: 25% dextrose in
water; D50W: 50% dextrose in water.
* These findings may also occur in infants with sepsis, congenital heart disease, respiratory distress syndrome,
intraventricular hemorrhage, other metabolic disorders, and in children and adolescents with a variety of
underlying conditions.
Specific laboratory studies to obtain in children include blood samples for glucose, insulin, C -peptide, betahydroxybutyrate, lactate (free flowing blood must be obtained without a tourniquet), plasma acylcarnitines, free
fatty acids, growth hormone, and cortisol.
Higher doses of glucose (eg, 0.5 to 1 g/kg [5 to 10 mL/kg of 10% dextrose in water or 2 to 4 mL/kg of 25%
dextrose in water]) may be needed to correct hypoglycemia caused by sulfonylurea ingestion. (For more detail,
refer to UpToDate topic on sulfonylurea agent poisoning).
Glucagon will reverse hypoglycemia caused by excess endogenous or exogenous insulin and will not be
effective in patients with inadequate glycogen stores (prolonged fasting), ketotic hypoglycemia, or are unable to
mobilize glycogen (glycogen storage diseases). Of note, children may exhaust their glycogen stores in as little
as 12 hours. Other conditions in which glycogen cannot be effectively mobilized include ethanol intoxication in
children, adrenal insufficiency, and certain inborn errors of metabolism (eg, a disorder of glycogen synthesis
and glycogen storage diseases).
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Rapid overview: Emergent management of anaphylaxis in infants and children*

Diagnosis is made clinically:
The most common signs and symptoms are cutaneous (eg, sudden onset of generalized urticaria,
angioedema, flushing, pruritus). However, 10 to 20% of patients have no skin findings.
Danger signs: Rapid progression of symptoms, evidence of respiratory distress (eg,
stridor, wheezing, dyspnea, increased work of breathing, retractions, persistent cough,
cyanosis), signs of poor perfusion, abdominal pain, vomiting, dysrhythmia, hypotension,
collapse.
Acute management:
The first and most important therapy in anaphylaxis is epinephrine. There are NO absolute
contraindications to epinephrine in the setting of anaphylaxis.
Airway: Immediate intubation if evidence of impending airway obstruction from angioedema. Delay
may lead to complete obstruction. Intubation can be difficult and should be performed by the most
experienced clinician available. C ricothyrotomy may be necessary.
IM epinephrine (1 mg/mL preparation): Epinephrine 0.01 mg/kg should be injected
intramuscularly in the mid-outer thigh. For large children (>50 kg), the maximum is 0.5 mg per dose. If
there is no response or the response is inadequate, the injection can be repeated in 5 to 15 minutes (or
more frequently). If epinephrine is injected promptly IM, patients respond to one, two, or at most, three
injections. If signs of poor perfusion are present or symptoms are not responding to epinephrine
injections, prepare IV epinephrine for infusion (see below).
Place patient in recumbent position, if tolerated, and elevate lower extremities.
Oxygen: Give 8 to 10 L/minute via facemask or up to 100% oxygen, as needed.
Normal saline rapid bolus: Treat poor perfusion with rapid infusion of 20 mL/kg. Re-evaluate and
repeat fluid boluses (20 mL/kg), as needed. Massive fluid shifts with severe loss of intravascular volume
can occur. Monitor urine output.
Albuterol: For bronchospasm resistant to IM epinephrine, give albuterol 0.15 mg/kg (minimum dose:
2.5 mg) in 3 mL saline inhaled via nebulizer. Repeat, as needed.
H1 antihistamine: C onsider giving diphenhydramine 1 mg/kg (max 40 mg) IV.
H2 antihistamine: C onsider giving ranitidine 1 mg/kg (max 50 mg) IV.
Glucocorticoid: C onsider giving methylprednisolone 1 mg/kg (max 125 mg) IV.
Monitoring: C ontinuous noninvasive hemodynamic monitoring and pulse oximetry monitoring should
be performed. Urine output should be monitored in patients receiving IV fluid resuscitation for severe
hypotension or shock.
Treatment of refractory symptoms:

Epinephrine infusion : In patients with inadequate response to IM epinephrine and IV saline, give
epinephrine continuous infusion at 0.1 to 1 mcg/kg/minute, titrated to effect.
Vasopressors : Patients may require large amounts of IV crystalloid to maintain blood pressure.
Some patients may require a second vasopressor (in addition to epinephrine). All vasopressors should
be given by infusion pump, with the doses titrated continuously according to blood pressure and cardiac
rate/function monitored continuously and oxygenation monitored by pulse oximetry.
IM: intramuscular; IV: intravenous.
* A child is defined as a prepubertal patient weighing less than 40 kg.
All patients receiving an infusion of epinephrine and/or another vasopressor require continuous noninvasive
monitoring of blood pressure, heart rate and function, and oxygen saturation. We suggest that pediatric centers
provide instructions for preparation of standard concentrations and also provide charts for established infusion
11/14/2016
rate for epinephrine and other vasopressors in infants and children.

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Official reprint from UpToDate

Septic shock: Ongoing management after resuscitation in children

Septic shock: Ongoing management after resuscitation in children - UpToDate

Ongoing monitoring of tissue perfusion and blood pressure

Septic shock: Ongoing management after resuscitation in children - UpToDate

Septic shock: Ongoing management after resuscitation in children - UpToDate

Septic shock: Ongoing management after resuscitation in children - UpToDate

Septic shock: Ongoing management after resuscitation in children - UpToDate

Septic shock: Ongoing management after resuscitation in children - UpToDate

Septic shock: Ongoing management after resuscitation in children - UpToDate

disseminated intravascular coagulation' above.)

Septic shock: Ongoing management after resuscitation in children - UpToDate

Septic shock: Ongoing management after resuscitation in children - UpToDate

In a small trial of 12 children with refractory catecholamine-resistant shock, administration of milrinone

Septic shock: Ongoing management after resuscitation in children - UpToDate

Plasma exchange or plasmapheresis There has been considerable interest in extracorporeal

Septic shock: Ongoing management after resuscitation in children - UpToDate

Septic shock: Ongoing management after resuscitation in children - UpToDate

Septic shock: Ongoing management after resuscitation in children - UpToDate

Topic 86881 Version 10.0

Septic shock: Ongoing management after resuscitation in children - UpToDate

Septic shock: Ongoing management after resuscitation in children - UpToDate

Septic shock: Ongoing management after resuscitation in children - UpToDate

Evaluation of common sources of sepsis

Upper respiratory tract

Pharyngeal inflammation plus

Throat swab for aerobic culture

Lower respiratory tract

Productive cough, pleuritic chest

Sputum of good quality, rapid

Fever, urgency, dysuria, loin pain

Urine microscopy showing pyuria

Vascular catheters: arterial,

Redness or drainage at insertion

C ulture of blood (from the

Indwelling pleural catheter

Redness or drainage at insertion

C ulture of pleural fluid (through

Inflammation, edema, erythema,

Gram stain and culture of draining

Erythema, edema, lymphangitis

C ulture blister fluid or draining

C entral nervous system

Signs of meningeal irritation

C SF microscopy, protein, glucose,

Abdominal pain, distension,

Stool culture for Salmonella,

Aerobic and anaerobic culture of

Peritoneal dialysis (PD) catheter

C loudy PD fluid, abdominal pain,

C ell count and culture of PD fluid

Women: Low abdominal pain,

Women: Endocervical and high

Men: Dysuria, frequency,

Pain, warmth, decreased range of

Men: Urine Gram stain and

C SF: cerebrospinal fluid; PD: peritoneal dialysis.

Septic shock: Ongoing management after resuscitation in children - UpToDate

Rapid overview for hypoglycemia in adolescents and children, other than

Septic shock: Ongoing management after resuscitation in children - UpToDate

Unable to receive oral glucose and unable to obtain IV access: