Septic Shock Rapid Recognition and Initial Resuscitation in

Septic shock: Rapid recognition and initial resuscitation in children
19-05-2013
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Septic shock: Rapid recognition and initial resuscitation in children Authors Scott L Weiss, MD Wendy J Pomerantz, MD, MS Disclosures All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Apr 2013. | This topic last updated: Feb 19, 2013. Section Editors Adrienne G Randolph, MD, MSc Susan B Torrey, MD Sheldon L Kaplan, MD Deputy Editor James F Wiley, II, MD, MPH
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 early recognition and initial management of severe sepsis and septic shock in children during the first hour of resuscitation are reviewed here. The definitions, epidemiology, and clinical manifestations of sepsis in children and ongoing management of children with septic shock are discussed separately. (See "Systemic inflammatory response syndrome (SIRS) and sepsis in children: Definitions, epidemiology, clinical manifestations, and diagnosis" and "Septic shock: Ongoing management after resuscitation in children".) DEFINITION Septic shock refers to sepsis with cardiovascular dysfunction (ie, hypotension, reliance on vasoactive drug administration to maintain a normal blood pressure, or two of the following: prolonged capillary refill, oliguria, metabolic acidosis, or elevated arterial lactate) that persists despite the administration of 40 mL/kg of isotonic fluid in one hour. (See "Systemic inflammatory response syndrome (SIRS) and sepsis in children: Definitions, epidemiology, clinical manifestations, and diagnosis", section on 'Severity'.) RAPID RECOGNITION A clinical diagnosis of septic shock is made in children who have signs of inadequate tissue perfusion, two or more criteria for the systemic inflammatory response syndrome (table 1), and suspected or proven infection [8]. Rapid recognition of hemodynamic abnormalities and early suspicion of infection are essential to achieve favorable outcomes. As an example, in a prospective cohort study of 91 infants and children presenting to community hospitals with septic shock (defined by hypotension or delayed capillary refill), each hour delay in initiation of appropriate resuscitation or persistence of hemodynamic abnormalities was associated with a clinically significant increased risk of death (OR 1.5 and 2.3, respectively) [4]. (See "Systemic inflammatory response syndrome (SIRS) and sepsis in children: Definitions, epidemiology, clinical manifestations, and diagnosis", section on 'Definitions' and "Systemic inflammatory response syndrome (SIRS) and sepsis in children: Definitions, epidemiology, clinical manifestations, and diagnosis", section on 'Severity'.) Inadequate tissue perfusion Seriously ill patients should undergo urgent evaluation for the following signs of impaired perfusion or shock [8,9]: Fever Tachycardia or bradycardia Decreased peripheral pulses compared with central pulses Mottled or cool extremities Flash or >3 second capillary refill Dry mucus membranes, sunken eyes, and decreased urine output Tachypnea, bradypnea, or apnea Hypotension Altered mental status (irritability, anxiety, confusion, lethargy, somnolence, apnea) Hypothermia (especially neonates) Tachycardia and tachypnea are common and non-specific findings in young pediatric patients and may be due to fever, anxiety, dehydration, pain/discomfort, anemia, or agitation. However, persistent tachycardia is a sensitive indicator of circulatory dysfunction and should not be overlooked. If a question exists as to whether tachycardia is due to circulatory impairment, a fluid bolus is recommended unless there is evidence for cardiac dysfunction (eg, hepatomegaly, jugular venous distention, S3 gallop, cardiomegaly). Hypotension is a late sign of cardiovascular dysfunction and shock in pediatric patients and is not necessary to diagnose septic shock. Infants and children with sepsis often maintain blood pressure despite the presence of septic shock through an increase in heart rate, systemic vascular resistance, and venous tone but have a limited capacity to augment myocardial stroke volume. As a result, infants and children are also more likely to exhibit cold shock in sepsis compared to the classic presentation of warm (or hyperdynamic or vasodilated) shock in adults. (See "Systemic inflammatory response syndrome (SIRS) and sepsis in children: Definitions, epidemiology, clinical manifestations, and diagnosis", section on 'Shock'.) Signs of infection Patients should be simultaneously evaluated for an infectious source to distinguish non-infectious from septic shock. Fever, cough or congestion, dyspnea, hypoxemia, rash, abdominal pain, myalgias, immunocompromising condition (eg, chemotherapy, sickle cell disease, or other known conditions associated with splenic dysfunction or primary immune deficiency), leukocytosis, or leukopenia with thrombocytopenia should raise suspicion for infection (table 2). Other factors concerning for specific infections, such as dysuria (urinary tract infection), hematochezia (gastroenteritis), headache and neck stiffness (meningitis), bone or joint inflammation (Staphylococcus aureus), conjunctival suffusion/injection (toxic shock syndrome), ecthyma (Pseudomonas species) and petechiae/purpura (meningococcemia), should also be quickly ascertained. (See "Systemic inflammatory response syndrome (SIRS) and sepsis in children: Definitions, epidemiology, clinical manifestations, and diagnosis", section on 'Infection'.) If an infection is suspected or a non-infectious etiology of shock is not clear, current guidelines recommend obtaining blood, urine, and, as indicated, other cultures and administering empiric broad-spectrum antibiotics within one hour of presentation [10]. Antibiotic therapy should not be delayed beyond one hour in order to obtain cultures if there is a concern for severe sepsis or septic shock. Patients with a recent history of an immunocompromising condition (eg, neutropenia, chemotherapy, sickle cell disease, or primary immune deficiency) are at highest risk for sepsis and severe complications and their outcome is highly dependent on rapid antimicrobial treatment. (See 'Initial antimicrobial therapy' below.)
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Suggestive laboratory findings Suggested laboratory studies for children with sepsis and septic shock are discussed in detail separately and include (see "Systemic inflammatory response syndrome (SIRS) and sepsis in children: Definitions, epidemiology, clinical manifestations, and diagnosis", section on 'Laboratory studies'): Rapid blood glucose Arterial or venous blood gas Complete blood count with differential Blood lactate Serum electrolytes Blood urea nitrogen and serum creatinine Ionized blood calcium Serum total bilirubin and alanine aminotransferase Prothrombin and partial thromboplastin times (PT and PTT) International normalized ratio (INR) Fibrinogen and D-dimer Blood culture Urinalysis Urine culture Other cultures as indicated by clinical findings Diagnostic serologic testing as indicated to identify suspected sources of infection Inflammatory biomarkers (eg, C-reactive protein, procalcitonin) in selected cases The following laboratory findings support the diagnosis of septic shock: Lactic acidosis indicated by metabolic acidosis on blood gases and elevation of arterial blood lactate (>3.5 mmol/L) (see "Systemic inflammatory response syndrome (SIRS) and sepsis in children: Definitions, epidemiology, clinical manifestations, and diagnosis", section on 'Laboratory studies') Age-specific leukocytosis or leukopenia (table 1) Platelet count <80,000/microL or a decline of 50 percent from highest value recorded over the past three days Disseminated intravascular coagulopathy (decreased fibrinogen with increased D-dimer, international normalized ratio, prothrombin time, or partial thromboplastin time) (see "Disseminated intravascular coagulation in infants and children", section on 'Diagnosis') Renal insufficiency suggested by a serum creatinine 2 times upper limit of normal for age or twofold increase in baseline creatinine Liver dysfunction implied by a total bilirubin 4 mg/dL (not applicable to newborn) or alanine aminotransferase (ALT) >2 times upper limit of normal for age Pyuria indicating an urinary tract infection PHYSIOLOGIC INDICATORS AND TARGET GOALS Restoration of tissue perfusion, such as reversal of shock, should be targeted to the following therapeutic endpoints (goals in parentheses) (algorithm 1) [8-10]: Quality of central and peripheral pulses (strong, distal pulses equal to central pulses) Skin perfusion (warm, with capillary refill <2 seconds) Mental status (normal mental status) Urine output (1 mL/kg per hour, up to 40 mL per hour, once effective circulating volume is restored) Blood pressure (systolic pressure at least fifth percentile for age: 60 mmHg <1 month of age, 70 mmHg + [2 x age in years] in children 1 month to 10 years of age, 90 mmHg in children 10 years of age or older); however, blood pressure by itself is not a reliable end point for assessing the adequacy of resuscitation Lactate (<4 mmol/L or 10 percent decrease per hour until normal) Central venous oxygen saturation (ScvO2), (70 percent), if available Heart rate is an important physiologic indicator of circulatory status that should also be monitored closely (table 3). However, many other factors (ie, fever, drugs, anxiety) influence heart rate. Although trends in response to treatment should be carefully monitored, specific target goals for heart rate are difficult to define and may not be useful. Children with persistently elevated heart rate unresponsive to repeated fluid boluses should be evaluated for cardiac dysfunction. (See 'Inadequate tissue perfusion' above.) Several studies have demonstrated that lactate and ScvO2 can correlate with severity of shock and prognosis in sepsis [11-13]. Persistently elevated lactate >4 mmol/L or failure to decrease by at least 10 percent every one to two hours and ScvO2 <70 percent may indicate persistence of abnormal end-organ perfusion. However, an ScvO2 70 percent can also be falsely reassuring in sepsis due to hyperdynamic cardiac function, microcirculatory shunting, or mitochondrial dysfunction [14,15]. Blood lactate can be obtained by bedside testing. When measuring ScvO2 in pediatric patients, pulmonary artery catheters are rarely used. Instead, changes in central venous oxygen saturation (ScvO2) are obtained from a catheter with its tip in the superior vena cava (ScvO2) [16]. Identifying physiologic indicators to monitor the effectiveness of resuscitation for children with septic shock is challenging. Noninvasive ultrasonic determination of cardiac index, cardiac output, systemic vascular resistance, and stroke volume is feasible in healthy children, and age-based normative values have been published. Although not widely available, bedside Doppler ultrasound shows promise as a noninvasive method to guide vasoactive therapy by calculating cardiac output (CO) and systemic vascular resistance (SVR) from measurements of blood flow over the pulmonary artery or aorta. (See "Initial management of shock in children", section on 'Physiologic indicators and target goals'.) Regardless of the method used to measure vascular pressures, clinical signs of end organ perfusion must also be monitored in order to accurately determine the severity of shock and response to treatment. These indicators can be readily monitored noninvasively during the initial management of shock and, since many children in shock respond well, invasive monitoring can often be avoided. Mean arterial pressure can be measured with a blood pressure cuff. Clinical experience suggests that quality of central and peripheral pulses, skin perfusion, mental status, and urine output are useful signs for assessing response to
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therapy. Limited observational evidence suggests that capillary refill time may correlate with ScvO2. (See "Initial management of shock in children", section on 'Physiologic indicators and target goals'.) RESUSCITATION Early goal-directed therapy Goal-directed therapy for septic shock refers to an aggressive systematic approach to resuscitation targeted to improvements in physiologic indicators of perfusion and vital organ function within the first six hours. Effective treatment of septic shock requires rapid correction of circulatory dysfunction with continuous monitoring and re-evaluation at frequent intervals and early administration of empiric broad-spectrum antimicrobial therapy [10]. We suggest that children with septic shock receive treatment according to the 2007 American College of Critical Care Medicine (ACCM) guidelines with emphasis on early goal-directed therapy (algorithm 1) [8]. These guidelines are also largely compatible with the algorithm for pediatric septic shock promoted in the Pediatric Advanced Life Support (PALS) course (algorithm 2). However, the ACCM guidelines provide a tighter time frame for optimal delivery of initial intravenous fluid boluses. The timing of therapeutic actions in the ACCM guidelines should be viewed as best practices for resuscitation of a child with septic shock. However, meeting the time targets may not always be possible within the first hour of illness depending upon patient factors and available pediatric expertise. This recommendation is supported by one trial and observational studies that show a marked reduction in mortality among children with severe sepsis after wide dissemination of the 2002 ACCM guidelines on which the 2007 guidelines are based as follows: In a trial of goal-directed therapy in 102 children with severe sepsis or fluid-refractory septic shock treated in two pediatric intensive care units, 28-day mortality was lower in patients who received goal-directed therapy versus therapy guided by blood pressure (12 versus 39 percent, respectively) primarily due to the marked benefit of goal-directed therapy among the children with central venous oxygen saturation (ScvO2) <70 percent [17]. Patients managed according to goal-directed therapy received a clinically significantly greater volume of crystalloid, more blood transfusions, and more vasoactive drug therapy. Although patients with ScvO2 >70 who received goal-directed therapy also had lower mortality than controls (12 versus 22 percent), this difference was not statistically significant. Institution of timely goal directed interventions by a mobile intensive care team compatible with the ACCM 2002 guidelines, including early and aggressive bolus colloid administration, endotracheal intubation and mechanical ventilation, and vasoactive therapy in conjunction with regionalization of care for 331 children with meningococcemia in the United Kingdom was associated with a decrease in the case fatality rate from 23 to 2 percent over five years (annual reduction in the odds of death 0.41, 95% CI: 0.27-0.62) [18]. Analysis of the case fatality rate among children treated for sepsis and purpura (primarily caused by Neisseria meningitidis, serogroup C) over 20 years in a childrens hospital demonstrated a drop in annual mortality from approximately 20 to 1 percent with no deaths after 2002, corresponding to release of the ACCM guidelines and a nation-wide meningococcal C vaccination campaign [19]. In the United States, the annual death rate from severe sepsis was estimated as 4 percent (2 percent in healthy children and 8 percent in children with prior chronic illness) in 2003 compared with 9 percent in 1999 [2,3]. Airway and breathing All patients with septic shock should initially receive 100 percent supplemental oxygen to optimize blood oxygen content and, thus, oxygen delivery to tissues. Oxygenation should be monitored using continuous pulse oximetry (SpO2). Once adequate perfusion has been restored, supplemental oxygen should be titrated to avoid SpO2 >97 percent to prevent the adverse effects (eg, lung injury and microcirculatory vasoconstriction) associated with hyperoxia and free radical generation [20]. (See "Continuous oxygen delivery systems for infants, children, and adults" and "Basic airway management in children".) Endotracheal intubation using rapid sequence intubation (RSI) is frequently necessary in children with septic shock to protect the airway, assist with ventilation, and/or promote oxygenation. In addition, endotracheal intubation and sedation reduces the work of breathing which may avoid diversion of cardiac output to the muscles of respiration and may improve perfusion to other organs. A rapid overview of RSI in children is provided in the table (table 4). Emergent endotracheal intubation in children and pediatric rapid sequence intubation (RSI) are discussed in detail separately. (See "Emergent endotracheal intubation in children" and "Rapid sequence intubation (RSI) in children".) Key actions when performing RSI in children with septic shock include: Patients with hemodynamic instability should receive appropriate support with fluid and/or catecholamines (see below) prior to or during intubation. Ketamine, if available and not contraindicated, is preferable for sedation prior to endotracheal intubation. (See "Sedation or induction agents for rapid sequence intubation in adults", section on 'Ketamine'.) Etomidate inhibits cortisol formation and should not be used routinely. If etomidate is used, we suggest the following: It is important to evaluate for signs of adrenal insufficiency sometimes evidenced by refractory shock [21,22]. (See "Rapid sequence intubation (RSI) in children", section on 'Etomidate' and "Septic shock: Ongoing management after resuscitation in children", section on 'Address adrenal insufficiency'.) Emergency clinicians should inform the physicians assuming care for the patient in the intensive care unit when etomidate has been used for induction. Etomidate should not be used as an infusion or in repeated bolus doses for maintenance of sedation after intubation. Thiopental and propofol are associated with hypotension and should be avoided in children with septic shock. When performing rapid sequence intubation in a child with septic shock, it is important to choose agents that do not worsen cardiovascular status. Previously, etomidate was a common choice because it typically does not compromise hemodynamic stability. However, small observational studies in children with sepsis and septic shock undergoing intubation with or without etomidate indicate that one dose of etomidate is associated with lower levels of serum cortisol, cortisol to 11-deoxycortisol ratios, and higher adrenocortical hormone levels for up to 24 hours [21,23]. In one case series of 31 children with meningococcal sepsis who required endotracheal intubation, of the eight children who died, seven received etomidate [23]. The 2007 update to the Clinical Guidelines for Hemodynamic Support of Neonates and Children with Septic Shock from the American College of Critical Care Medicine states that etomidate is no longer recommended to sedate children with septic shock [8]. The 2010 advanced life support recommendations provided by the American Heart Association and the International Liaison Committee on Resuscitation on which the Pediatric Advanced Life Support course is based also suggest that etomidate not be used routinely in children with septic shock [9].
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Treat hypoglycemia and hypocalcemia Children with septic shock are at risk for hypoglycemia and hypocalcemia Rapid blood glucose and ionized calcium should be measured as intravenous access is obtained. Hypoglycemia Hypoglycemia should be corrected by rapid intravenous infusion of dextrose as described in the rapid overview (table 5). After initial hypoglycemia is reversed, the clinician should provide a continuous infusion of dextrose to maintain blood glucose in a safe range (70 to 150 mg/dL [3.89 to 8.33 mmol/L]) for children whose condition does not permit oral intake. Hypoglycemia may also be an indicator of adrenal insufficiency in predisposed children and those with refractory septic shock. (See 'Corticosteroids' below and "Septic shock: Ongoing management after resuscitation in children", section on 'Address adrenal insufficiency'.) In normoglycemic young children, a continuous maintenance infusion of dextrose 10 percent is a reasonable option to prevent the occurrence of hypoglycemia and is suggested by the American College of Critical Care Medicine [8]. Hyperglycemia should be avoided. Hypocalcemia Children with persistent shock in association with an ionized calcium <1.1 mmol/L (4.8 mg/dL) or symptomatic hypocalcemia (eg, positive Chvostek or Trousseau signs, seizures, prolonged QT interval on EKG, or cardiac arrhythmias) should undergo correction with calcium gluconate 10 percent solution in a dose of 50 to 100 mg/kg (0.5 to 1 mL/kg), up to 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 an intravenous or intraosseous cannula 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. Hypocalcemia is a common finding in critically ill patients with sepsis likely due to changes in the hormonal milieu, though the exact pathophysiology remains unclear [24-26]. Intracellular calcium is necessary for cardiac and smooth muscle contraction. Infants under 12 months of age may rely more heavily on extracellular calcium to maintain adequate cardiac contractility than older patients. Animal models and observational studies have suggested improved physiologic outcomes when hypocalcemia is treated [27,28]. Although definitive evidence to support improved clinical outcomes in humans receiving intravenous calcium for low ionized calcium levels is lacking [29], current guidelines recommend correcting ionized hypocalcemia in patients with septic shock even in the absence of clinical manifestations of hypocalcemia (eg, seizures, cardiac arrhythmias) [8]. Intravenous fluid therapy Relative intravascular hypovolemia is common in septic shock (due to vasodilation and capillary leak) and may be severe. Observational evidence suggests that vigorous fluid resuscitation may have a major role in preventing end-organ damage and improving survival. (See "Initial management of shock in children", section on 'Benefits'.) Thus, guidelines emphasize rapid restoration of intravascular volume when treating children with septic shock as follows (algorithm 1 and algorithm 2) [8-10]: Rapid intravenous (IV) access IV access (preferably two sites and of the largest caliber that can be reliably inserted) should be established within five minutes. If a peripheral IV cannot be obtained in this time, guidelines advise placement of an intraosseous needle. (See "Vascular (venous) access for pediatric resuscitation and other pediatric emergencies", section on 'Peripheral access' and "Intraosseous infusion", section on 'Indications' and "Intraosseous infusion", section on 'Fluid and drug administration'.) Initial IV fluid bolus In resource-rich settings and when not contraindicated by comorbidities (eg, severe anemia, diabetic ketoacidosis, heart failure, severe malnutrition), initial therapy should begin with a bolus of 20 mL/kg of isotonic crystalloid solution (ie, 0.9 percent normal saline or lactated Ringer solution) infused over five minutes or as rapidly as possible, preferably with a manual push-pull technique or rapid infuser. After the initial infusion, the child should be quickly reassessed for signs of inadequate end-organ perfusion to determine if additional fluid is needed (see 'Inadequate tissue perfusion' above and "Initial management of shock in children", section on 'Risks'). Repeated IV fluid bolus Repeated 20 mL/kg fluid boluses should be given until tissue perfusion, oxygen delivery, and blood pressure are adequate, or signs of fluid overload (rales, gallop rhythm, enlarged liver) develop. Experience suggests that patients may require volumes of 60 mL/kg or more in the first hour and up to 120mL/kg or more during the first several hours of fluid administration [30]. Establish ongoing monitoring of tissue perfusion Once effective circulating volume has been restored, ongoing fluid requirements are guided by monitoring of tissue perfusion, including capillary refill time; urine output; serial blood lactate levels; and, if available and appropriate, measurement of radial arterial blood pressure, central venous pressure, and central venous oxygen saturation. (See "Septic shock: Ongoing management after resuscitation in children", section on 'Ongoing and invasive monitoring'.) Other fluids The use of colloid for fluid resuscitation for children with septic shock is controversial. Nevertheless, colloid infusion with albumin 5 percent is a reasonable option for children who have not improved following >60 mL/kg of crystalloid fluid, have hypoalbuminemia (albumin <3 g/dL), or who develop a hyperchloremic metabolic acidosis. Although the findings are not consistent and multiple preparations are available, synthetic colloids, such as hydroxethylstarch solutions, have been shown to increase the risk of acute kidney injury, coagulopathy, and death in adults with severe sepsis or septic shock, especially with administered volumes >15 mL/kg and should be avoided. (See "Treatment of hypovolemia (dehydration) in children", section on 'Crystalloid versus colloid' and "Evaluation and management of severe sepsis and septic shock in adults", section on 'Intravenous fluids'.) Preliminary evidence in one small pediatric trial suggests that administration of hypertonic saline may achieve hemodynamic stability with a lower volume of fluid, but its impact on other outcomes relative to normal saline are uncertain [31]; thus, we do not advocate use of hypertonic saline outside of an experimental protocol. Resource-limited settings In resource-limited settings, fluid resuscitation according to emergency triage assessment and treatment guidelines developed by the World Health organization is suggested for children with signs of shock. (See "Initial management of shock in children", section on 'Resource limited settings'.) In resource-limited settings that cannot provide advanced airway and circulatory support, children with signs of shock and severe febrile illness but without dehydration or hemorrhage who receive rapid bolus administration of albumin or normal saline may have increased mortality. Thus, rapid fluid infusion according to the American College of Critical Care Medicine as described above should be avoided in this special population of patients. (See "Initial management of shock in children", section on 'Risks'.) Initial antimicrobial therapy Intravenous antimicrobial therapy should be initiated immediately after obtaining appropriate cultures with the goal of completing administration within one hour of presentation. Each hour delay in antibiotic administration has been associated with an approximately 8 percent
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increase in mortality [32]. In patients in septic shock, effective delivery of antimicrobials usually requires two ports or sites for intravenous access: one devoted to fluid resuscitation and one for antimicrobial delivery. Antimicrobials should not be withheld for children in whom lumbar puncture cannot be performed safely due to hemodynamic instability or coagulopathy (algorithm 3). The choice of antimicrobials can be complex and should consider the child's age, history, comorbidities, clinical syndrome, Gram stain data, and local resistance patterns. Consultation with an expert in pediatric infectious disease is strongly encouraged for all children with septic shock. General principles for initial antimicrobial coverage for children who are critically ill with sepsis include the following: All children with septic shock should receive coverage for methicillin-resistant Staphylococcus aureus (MRSA). Coverage for enteric organisms should be added whenever clinical features suggest genitourinary (GU) and/or gastrointestinal (GI) sources (eg, perforated appendicitis or bacterial overgrowth in a child with short gut syndrome). Treatment for Pseudomonas species should be included for children who are immunosuppressed or at risk for infection with these organisms (ie, those with cystic fibrosis). Listeria monocytogenes and herpes simplex virus are important pathogens in infants 28 days of age. When treating empirically, antibiotics which can be given by rapid intravenous bolus (eg, beta-lactam agents or cephalosporins) should be administered first followed by infusions of antibiotics, such as vancomycin, that must be delivered more slowly. Ongoing antimicrobial therapy should be modified based upon culture results, including antimicrobial susceptibility and the patients clinical course. Suggested initial empiric antimicrobial regimens based upon patient age, level of immunocompetence, and previous antibiotic administration include: Children >28 days of age who are normal hosts: Vancomycin (15 mg/kg, maximum 1 to 2 g, for the initial dose) PLUS cefotaxime (100 mg/kg, maximum 2 g, for the initial dose) OR ceftriaxone (75 mg/kg, maximum 2 g, for the initial dose) Consider adding an aminoglycoside (eg, gentamicin) for possible GU source and/or piperacillin with tazobactam, clindamycin or metronidazole for possible GI source Children >28 days who are immunosuppressed or at risk for infection with Pseudomonas species: Vancomycin (15 mg/kg, maximum 1 to 2 g, for the initial dose) PLUS cefepime (50 mg/kg, maximum 2 g, for the initial dose) OR ceftazidime (50 mg/kg, maximum 2 g, for the initial dose) PLUS an aminoglycoside (eg, gentamicin, amikacin) or carbapenem (eg, imipenem, meropenem) in settings where bacterial organisms with extended-spectrum beta-lactamase (ESBL) resistance are prevalent. For patients who have been recently (within two weeks) treated broadspectrum antibiotics (eg, third-generation cephalosporin, aminoglycoside, or fluoroquinolone), the addition of a carbapenem is favored over an aminoglycoside. Children who cannot receive penicillin or who have recently received broad-spectrum antibiotics: Vancomycin (age appropriate dose) PLUS Meropenem (<3 months: 20 mg/kg for the initial dose, 3 months: 20 mg/kg, maximum 2 g, for the initial dose) Aztreonam OR ciprofloxacin PLUS clindamycin may be used instead of meropenem Patients at increased risk of fungal infection (eg, identified fungal source, immunocompromised with persistent fever on broad spectrum antibiotics) Add liposomal Amphotericin B or an echinocandin (eg, caspofungin, micafungin) to the antimicrobial regimen [33] Patients with risk factors for rickettsial infection (eg, travel to or reside in an endemic region): Add a tetracycline antibiotic (eg, doxycycline) to the antimicrobial regimen Infants 0 to 28 days of age: Vancomycin (15 mg/kg for the initial dose) PLUS cefotaxime (50 mg/kg for the initial dose) PLUS gentamicin (2.5 mg/kg for the initial dose) PLUS ampicillin (50 mg/kg for the initial dose) Add acyclovir (20 mg/kg per dose) for suspicion of HSV infection For neonates with clinical features concerning for herpes simplex virus (HSV) infection who may receive acyclovir, viral cultures of vesicles if present, cerebrospinal fluid and surface (mouth, nasopharynx, eye, and anus can be obtained from one swab ending with the anal swab) and polymerase chain reaction testing (from cerebrospinal fluid and blood) for HSV should be obtained whenever possible. Concerning clinical features include family members with HSV infection, respiratory collapse, elevated transaminases, thrombocytopenia, and/or abnormal cerebrospinal fluid suggestive of HSV infection (table 6). (See "Neonatal herpes simplex virus infection: Clinical features and diagnosis", section on 'Clinical manifestations'.) Fluid-refractory shock Vasoactive agents are frequently necessary in the initial resuscitation of children with septic shock to sustain perfusion pressure while hypovolemia is corrected. Based upon expert opinion, the American College of Critical Care Medicine guidelines suggest the initiation of vasoactive therapy in children with septic shock who have not improved after 40 to 60 mL/kg of isotonic crystalloid along with continued fluid administration [8]. Although central venous access is preferred for vasopressor administration (eg, dopamine, epinephrine, dobutamine, or norepinephrine), peripheral intravenous (IV) access or intraosseous needle is acceptable while central venous access is being obtained. The initial choice of vasoactive agents is guided by physical findings [8,34].
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Cold shock The American College of Critical Care Medicine (ACCM) guidelines suggest that patients with cold shock (eg, poor perfusion, cold extremities) that do not respond to initial boluses of 40 to 60 mL/kg of fluid receive dopamine infusions (starting dose 5 mcg/kg per minute, titrate to response up to 10 mcg/kg per minute) (algorithm 1)[8]. At lower doses, dopamine improves splanchnic and renal blood flow and, at higher doses, it provides both inotropic and vasopressor support. Unlike adults, dopamine is still a first-line agent in children because of its wide availability and practitioner familiarity, and no evidence has correlated dopamine use with increased mortality in children with septic shock. However, infants younger than one year of age may be less responsive to dopamine [8]. Of note, in the Pediatric Advanced Life Support guidelines, low-dose dopamine is suggested for patients with septic shock but normal blood pressures and epinephrine is suggested for patients with cold shock (algorithm 2) [9]. No trials have directly compared dopamine to epinephrine for the treatment of cold shock in children. Thus, the optimal approach is debated and awaits further study. If cold shock is resistant to dopamine infusion at a dose of 10 mcg/kg per minute, epinephrine infusion at a rate between 0.05 to 0.3 mcg/kg per minute may be added [8]. At doses exceeding 0.1 mcg/kg/minute (and possibly lower in some patients), alpha-adrenergic effects of epinephrine are more pronounced and systemic vasoconstriction may be more evident. Examples of how to prepare an epinephrine infusion for a 10 kg or 20 kg child are provided in the tables (table 7 and table 8). Warm shock For patients with warm shock (eg, bounding pulses, pink extremities, and flash capillary refill) the American College of Critical Care Medicine and Pediatric Advanced Life Support guidelines suggest norepinephrine infusion starting at 0.03 to 0.05 mcg/kg/minute as the first-line drug (algorithm 1 and algorithm 2) [8]. If dopamine infusion has already been started then norepinephrine can be added to dopamine. Corticosteroids Patients who persist with shock in spite of rapid fluid administration and continuous infusions of epinephrine or norepinephrine may have adrenal insufficiency. Risk factors include purpura fulminans, recent or chronic treatment with corticosteroids, hypothalamic or pituitary abnormalities, or adrenal insufficiency (congenital or acquired). When adrenal insufficiency is suspected, administration of hydrocortisone in stress doses (50mg/m2/day or 2 mg/kg per day, intermittent or continuous infusion, maximum dose 50 mg/kg per day) is suggested [8]. Although evidence is lacking regarding the best method to identify adrenal insufficiency in children with refractory septic shock, assessment of adrenal status (either baseline serum cortisol or adrenocorticotropin hormone stimulation testing) is advised prior to corticosteroid administration. (See "Septic shock: Ongoing management after resuscitation in children", section on 'Address adrenal insufficiency'.) Transfer to definitive care After resuscitation, children with septic shock should be managed by clinicians with pediatric critical care expertise in a setting that has the necessary resources to provide pediatric intensive care. Children with septic shock who present to facilities without the necessary clinical expertise or resources should undergo timely transfer to an appropriate facility. Use of a pediatric specialized team is associated with improved patient survival and fewer adverse effects during transport. Thus, the use of pediatric specialized teams for transport of children with septic shock is recommended whenever it is available. (See "Prehospital pediatrics and emergency medical services (EMS)", section on 'Inter-facility transport'.) SUMMARY AND RECOMMENDATIONS A clinical diagnosis of septic shock is made in children who have signs of inadequate tissue perfusion, two or more criteria for the systemic inflammatory response syndrome (table 1), and suspected or proven infection. (See 'Rapid recognition' above and "Systemic inflammatory response syndrome (SIRS) and sepsis in children: Definitions, epidemiology, clinical manifestations, and diagnosis", section on 'Diagnosis'.) All patients with septic shock should initially receive 100 percent supplemental oxygen to optimize blood oxygen content and, thus, oxygen delivery to tissues. Once adequate perfusion has been restored, supplemental oxygen should be titrated to avoid oxygen saturation by pulse oximetry of greater than 97 percent to prevent the adverse effects associated with hyperoxia and free radical generation (eg, lung injury and microcirculatory vasoconstriction). (See 'Airway and breathing' above.) Endotracheal intubation using rapid sequence intubation (RSI) is frequently necessary in children with septic shock to protect the airway, assist with ventilation, and/or promote oxygenation. When performing RSI in children with septic shock, ketamine, if available and not contraindicated, is preferable for sedation prior to endotracheal intubation. Etomidate should not be used routinely in patients with septic shock. A rapid overview of RSI in children is provided in the table (table 4). (See 'Airway and breathing' above.) We suggest that children with septic shock receive treatment according to the American College of Critical Care Medicine (ACCM) guidelines including goal-directed therapy which provides a systematic approach to resuscitation of septic shock targeted to specific improvements in physiologic indicators of perfusion and vital organ function (algorithm 1) (Grade 2C). For children in resource-rich settings, rapid infusion of isotonic fluid (eg, normal saline) and early administration of empiric broad-spectrum antimicrobial therapy are essential actions. (See 'Early goal-directed therapy' above and 'Physiologic indicators and target goals' above and 'Resuscitation' above.) The American College of Critical Care Medicine guidelines suggest the initiation of vasoactive therapy in children with septic shock who have not improved after 40 to 60 mL/kg of isotonic crystalloid along with continued fluid administration. Specific vasopressor agents (eg, dopamine, epinephrine, or norepinephrine) are given based upon whether the patient has clinical findings of cold or warm shock. (See 'Fluid-refractory shock' above.) Patients who persist with shock in spite of rapid fluid administration and continuous infusions of epinephrine or norepinephrine may have adrenal insufficiency. When adrenal insufficiency is suspected, administration of hydrocortisone in stress doses (50 to 100 mg/m2/day or 1 to 2 mg/kg per day, intermittent or continuous infusion, maximum dose 50 mg/kg per day) is suggested [8]. Assessment of adrenal status (either baseline serum cortisol or adrenocorticotropin hormone stimulation testing) is advised prior to corticosteroid administration. (See 'Corticosteroids' above.) After initial resuscitation, ongoing aggressive management of septic shock should continue according to the principles of goal-directed therapy for children in whom adequate circulation has not been restored (algorithm 1). This care should be provided by clinicians with pediatric critical care expertise in a setting that has the necessary resources to provide pediatric intensive care. (See 'Transfer to definitive care' above and "Septic shock: Ongoing management after resuscitation in children".) Use of UpToDate is subject to the Subscription and License Agreement. REFERENCES 1. Goldstein B, Giroir B, Randolph A, International Consensus Conference on Pediatric Sepsis. International pediatric sepsis consensus conference: definitions for sepsis and organ dysfunction in pediatrics. Pediatr Crit Care Med 2005; 6:2. 2. Odetola FO, Gebremariam A, Freed GL. Patient and hospital correlates of clinical outcomes and resource utilization in severe pediatric sepsis. Pediatrics 2007; 119:487.
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3. Watson RS, Carcillo JA, Linde-Zwirble WT, et al. The epidemiology of severe sepsis in children in the United States. Am J Respir Crit Care Med 2003; 167:695. 4. Han YY, Carcillo JA, Dragotta MA, et al. Early reversal of pediatric-neonatal septic shock by community physicians is associated with improved outcome. Pediatrics 2003; 112:793. 5. Weiss SL, Parker B, Bullock ME, et al. Defining pediatric sepsis by different criteria: discrepancies in populations and implications for clinical practice. Pediatr Crit Care Med 2012; 13:e219. 6. Jaramillo-Bustamante JC, Marn-Agudelo A, Fernndez-Laverde M, Bareo-Silva J. Epidemiology of sepsis in pediatric intensive care units: first Colombian multicenter study. Pediatr Crit Care Med 2012; 13:501. 7. Kutko MC, Glick RD, Butler LM, et al. Histone deacetylase inhibitors induce growth suppression and cell death in human rhabdomyosarcoma in vitro. Clin Cancer Res 2003; 9:5749. 8. 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. 9. Kleinman ME, de Caen AR, Chameides L, et al. Pediatric basic and advanced life support: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Pediatrics 2010; 126:e1261. 10. Dellinger RP, Levy MM, Rhodes A, et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med 2013; 41:580. 11. Dugas MA, Proulx F, de Jaeger A, et al. Markers of tissue hypoperfusion in pediatric septic shock. Intensive Care Med 2000; 26:75. 12. Nguyen HB, Rivers EP, Knoblich BP, et al. Early lactate clearance is associated with improved outcome in severe sepsis and septic shock. Crit Care Med 2004; 32:1637. 13. Arnold RC, Shapiro NI, Jones AE, et al. Multicenter study of early lactate clearance as a determinant of survival in patients with presumed sepsis. Shock 2009; 32:35. 14. Velissaris D, Pierrakos C, Scolletta S, et al. High mixed venous oxygen saturation levels do not exclude fluid responsiveness in critically ill septic patients. Crit Care 2011; 15:R177. 15. Fink MP. Bench-to-bedside review: Cytopathic hypoxia. Crit Care 2002; 6:491. 16. Dueck MH, Klimek M, Appenrodt S, et al. Trends but not individual values of central venous oxygen saturation agree with mixed venous oxygen saturation during varying hemodynamic conditions. Anesthesiology 2005; 103:249. 17. de Oliveira CF, de Oliveira DS, Gottschald AF, et al. ACCM/PALS haemodynamic support guidelines for paediatric septic shock: an outcomes comparison with and without monitoring central venous oxygen saturation. Intensive Care Med 2008; 34:1065. 18. Booy R, Habibi P, Nadel S, et al. Reduction in case fatality rate from meningococcal disease associated with improved healthcare delivery. Arch Dis Child 2001; 85:386. 19. Maat M, Buysse CM, Emonts M, et al. Improved survival of children with sepsis and purpura: effects of age, gender, and era. Crit Care 2007; 11:R112. 20. Asfar P, Calzia E, Huber-Lang M, et al. Hyperoxia during septic shock--Dr. Jekyll or Mr. Hyde? Shock 2012; 37:122. 21. den Brinker M, Joosten KF, Liem O, et al. Adrenal insufficiency in meningococcal sepsis: bioavailable cortisol levels and impact of interleukin-6 levels and intubation with etomidate on adrenal function and mortality. J Clin Endocrinol Metab 2005; 90:5110. 22. Menon K, Ward RE, Lawson ML, et al. A prospective multicenter study of adrenal function in critically ill children. Am J Respir Crit Care Med 2010; 182:246. 23. den Brinker M, Hokken-Koelega AC, Hazelzet JA, et al. One single dose of etomidate negatively influences adrenocortical performance for at least 24h in children with meningococcal sepsis. Intensive Care Med 2008; 34:163. 24. Sanchez GJ, Venkataraman PS, Pryor RW, et al. Hypercalcitoninemia and hypocalcemia in acutely ill children: studies in serum calcium, blood ionized calcium, and calcium-regulating hormones. J Pediatr 1989; 114:952. 25. Zaloga GP, Chernow B. The multifactorial basis for hypocalcemia during sepsis. Studies of the parathyroid hormone-vitamin D axis. Ann Intern Med 1987; 107:36. 26. Mller B, Becker KL, Krnzlin M, et al. Disordered calcium homeostasis of sepsis: association with calcitonin precursors. Eur J Clin Invest 2000; 30:823. 27. Kovacs A, Courtois MR, Barzilai B, et al. Reversal of hypocalcemia and decreased afterload in sepsis. Effect on myocardial systolic and diastolic function. Am J Respir Crit Care Med 1998; 158:1990. 28. Porcelli PJ Jr, Oh W. Effects of single dose calcium gluconate infusion in hypocalcemic preterm infants. Am J Perinatol 1995; 12:18. 29. Forsythe RM, Wessel CB, Billiar TR, et al. Parenteral calcium for intensive care unit patients. Cochrane Database Syst Rev 2008; :CD006163. 30. Carcillo JA, Davis AL, Zaritsky A. Role of early fluid resuscitation in pediatric septic shock. JAMA 1991; 266:1242. 31. Chopra A, Kumar V, Dutta A. Hypertonic versus normal saline as initial fluid bolus in pediatric septic shock. Indian J Pediatr 2011; 78:833. 32. Kumar A, Roberts D, Wood KE, et al. Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock. Crit Care Med 2006; 34:1589. 33. Pappas PG, Kauffman CA, Andes D, et al. Clinical practice guidelines for the management of candidiasis: 2009 update by the Infectious Diseases Society of America. Clin Infect Dis 2009; 48:503. 34. Pediatric Advanced Life Support Provider Manual, Ralston M. (Ed), American Heart Association, Subcommittee on Pediatric Resuscitation, Dallas 2006. p.102. Topic 85767 Version 7.0
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GRAPHICS
Pediatric systemic inflammatory response syndrome criteria
Heart rate (beats/min) Age group
Tachycardia New born (0 days to 1 w k) Neonate (1 w k to 1 mo) Infant (1 mo to 1 yr) Toddler and preschool (>1 to 5 yrs) School age (>5 to 12 yrs) Adolescent (>12 to <18 yrs) >180 >180 >180 >140 Bradycardia <100 <100 <90 NA
Respiratory rate (breaths/min)

>50 >40 >34 >22
Leukocyte count (leukocytes x 103 /mm3 )

>34 >19.5 or <5 >17.5 or <5 >15.5 or <6
Systolic blood pressure (mmHg)

<59 <79 <75 <74
>130 >110
NA NA
>18 >14
>13.5 or <4.5 >11 or <4.5
<83 <90
NA: not applicable. Originally published in: Goldstein B, Giroir B, Randolph A, et al. International pediatric spesis consensus conference: Definitions for sepsis and organ dysfunction in pediatrics. Pediatr Crit Care Med 2005; 6:2. Correction published in: Gebara BM. Values for systolic blood pressure. Pediatr Crit Care Med 2005; 6:500. Copyright 2005 Lippincott Williams & Wilkins.
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Evaluation of common sources of sepsis

Suspected site
Upper respiratory tract Low er respiratory tract
Symptoms/signs
Pharyngeal inflammation plus exudate sw elling and lymphadenopathy Productive cough, pleuritic chest pain, consolidative auscultatory findings
Microbiologic evaluation
Throat sw ab for aerobic culture Sputum of good quality, rapid influenza testing, urinary antigen testing (eg, pneumococcus, legionella), quantitative culture of protected brush or bronchoalveolar lavage Urine microscopy show ing pyuria Culture of blood (from the catheter and a peripheral site), culture catheter tip (if removed) Culture of pleural fluid (through catheter), culture of catheter tip (if removed) Gram stain and culture of draining pus, w ound culture not reliable Culture blister fluid or draining pus; role of tissue aspirates not proven CSF microscopy, protein, glucose, culture, bacterial antigen test Stool culture for Salmonella, Shigella, and Campylobacter Aerobic and anaerobic culture of percutaneously or surgically drained abdominal fluid collections Cell count and culture of PD fluid W omen: Endocervical and high vaginal sw abs onto selective media Men: Urine Gram stain and culture
Urinary tract Vascular catheters: arterial, central venous Indw elling pleural catheter W ound or burn Skin/soft tissue Central nervous system Gastrointestinal Intraabdominal
Fever, urgency, dysuria, loin pain Redness or drainage at insertion site
Redness or drainage at insertion site Inflammation, edema, erythema, discharge of pus Erythema, edema, lymphangitis Signs of meningeal irritation Abdominal pain, distension, diarrhea, and vomiting Specific abdominal symptoms/signs
Peritoneal dialysis (PD) catheter Genital tract
Cloudy PD fluid, abdominal pain, fever W omen: Low abdominal pain, vaginal discharge Men: Dysuria, frequency, urgency, urge incontinence, cloudy urine, prostatic tenderness
Joint
Pain, w armth, decreased range of motion
Arthrocentesis w ith cell counts, Gram stain, and culture
CSF: 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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Recommendations for stepwise management of hemodynamic support in infants and children with sepsis
Algorithm for time sensitive, goal-directed stepwise 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 O2 saturation >70 percent, and CI >3.3, <6.0 L/min/m2 in pediatric intensive care unit (PICU).
Hgb: hemoglobin; PICCO: pulse contour cardiac output; FATD: femoral arterial thermodilution; ECMO: extracorporeal membrane oxygenation; CI: cardiac index; CRRT: 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.
http://www.uptodate.com/contents/septic-shock-rapid-recognition-and-initial-resuscitation-in-children?topicKey=EM%2F85767&elapsedTimeMs=0&source=see_link&view=print&displayedView=full10 / 19
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Pediatric respiratory rate and heart rate by age*

Age group
0-3 months 3-6 months 6-9 months 9-12 months 12-18 months 18-24 months 2-3 years 3-4 years 4-6 years 6-8 years 8-12 years 12-15 years 15-18 years
Respiratory rate
Median (1st-99th percentile) 43 (25-66) 41 (24-64) 39 (23-61) 37 (22-58) 35 (21-53) 31 (19-46) 28 (18-38) 25 (17-33) 23 (17-29) 21 (16-27) 19 (14-25) 18 (12-23) 16 (11-22)
Heart rate
Median (1st-99th percentile) 143 (107-181); term new born at birth: 127 (90-164) 140 (104-175) 134 (98-168) 128 (93-161) 123 (88-156) 116 (82-149) 110 (76-142) 104 (70-136) 98 (65-131) 91 (59-123) 84 (52-115) 78 (47-108) 73 (43-104)
* The respiratory and heart rates provided are based upon measurements in aw ake, healthy infants and children at rest. Many clinical findings besides the actual vital sign measurement must be taken into account w hen determining w hether a specific vital sign is normal in an individual patient. Values for heart rate or respiratory rate that fall w ithin normal limits for age may still represent abnormal findings that are caused by underlying disease in a particular infant or child. Data from: Fleming S, Thompson M, Stevens R, et al. Normal ranges of heart rate and respiratory rate in children from birth to 18 years of age: a systematic review of observational studies. Lancet 2011; 377:1011.
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Pediatric Advance Lifes Support septic shock algorithm
* NOTE: Fluid refractory and dopamine- or norepinephrine-dependent shock defines patient at risk for adrenal insufficiency. Draw baseline cortisol; consider ACTH stimulation test if unsure of need for steroids. If adrenal insufficiency is suspected give hydrocortisone 2 mg/kg bolus IV; maximum 100 mg. Reprinted with permission from: American Academy of Pediatrics, American Heart Association. Management of Shock. In: Pediatric Advanced Life Support Provider Manual, Chameides L, Samson RA, Schexnayder S, Hazinski MF (Eds), American Heart Association, 2011. Copyright 2011 American Heart Association.
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Rapid overview of rapid sequence intubation in children

Preoxygenation
Begin preoxygenation as soon as the decision to intubate is considered. Administer oxygen at the highest concentration available.
Preparation
Identify conditions that w ill affect choice of medications. Identify conditions that w ill predict difficult intubation or bag-mask ventilation. Assemble equipment and check for function. Develop contingency plan for failed intubation.
Pretreatment
Atropine: All children 1 year, children <5 years receiving succinycholine, and older children receiving a second dose of succinylcholine. Dose: 0.02 mg/kg IV (maximum single dose 0.5 mg, minimum 0.1 mg; if no IV access, can be given IM). Lidocaine: Optional for increased intracranial pressure. Dose: 1.5 mg/kg IV (maximum dose 100 mg). Give 2 to 3 minutes before intubation.
Sedation
Etomidate: Safe w ith hemodynamic instability, neuroprotective, transient adrenal corticosuppression. Do not use routinely in patients w ith septic shock. Dose: 0.3 mg/kg IV. Ketamine: Safe w ith hemodynamic instability if patient is not catecholamine depleted. Use in patients w ith bronchospasm and septic shock. Use w ith caution in patients w ith increased intracranial pressure. Dose: 1 to 2 mg/kg IV. (If no IV access, can be given IM dose: 3 to 7 mg/kg). Midazolam: Time to clinical effect is longer, inconsistently induces unconsciousness. May cause hemodynamic instability at doses required for sedation. Dose: 0.2 to 0.3 mg/kg IV (maximum dose 2 mg, onset of effect requires 2 to 3 minutes). Thiopental: Neuroprotective. Do not use w ith hemodynamic instability. Dose: 3 to 5 mg/kg IV.*
Paralytic
Succinycholine: Do not use w ith chronic myopathy or denervating neuromuscular disease; 48 to 72 hours after burn, crush, or denervating injury; malignant hyperthermia; or pre-exisiting hyperkalemia. Dose: infants and young children: 2 mg/kg IV, older children: 1 to 1.5 mg/kg IV. (If IV access unobtainable, can be given IM, dose: 3 to 5 mg/kg). Rocuronium: Use for children w ith contraindication for succinylcholine. Suggested dose: 1 mg/kg IV (range 0.6 to 1.2 mg/kg).
Protection and positioning

Maintain manual cervical spine immobilization during intubation in the trauma patient. If cervical spine injury is not potentially present, put the patient in the "sniffing position" (ie, head forw ard so that the external auditory canal is anterior to the shoulder and the nose and mouth point to the ceiling). Apply cricoid pressure w hen the child is unconscious. Remove cricoid pressure if it causes airw ay obstruction or difficulty view ing the larynx. If used, maintain cricoid pressure until tracheal tube position is verified.
Positioning, with placement

Confirm tracheal tube placement w ith end-tidal CO2 detection and auscultation.
Postintubation management
Chest radiograph for tracheal tube placement; provide ongoing sedation (eg, midazolam), analgesia (eg, fentanyl 1 mcg per kilogram), and, if indicated, paralysis.
If IV access unobtainable, intraosseous administration of drugs listed is feasible (no data for ketamine).
* Not available in the United States and Canada. Vecuronium may be used in children w ith contraindications to succinylcholine and w hen rocuronium is not available. Suggested dose for RSI: 0.15 to 0.2 mg/kg. Patients may experience prolonged and unpredictable duration of paralysis at this dose. If decompensation after successful intubation use DOPE mnemonic to find cause: - D: Dislodgement of the tube (right mainstem or esophageal) - O: Obstruction of tube - P: Pneumothorax - E: Equipment failure (ventilator malfunction, oxygen disconnected or not on).
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Rapid overview for hypoglycemia in adolescents and children, other than neonates
Clinical features
Any patient w ith 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 - Cyanosis - Apnea - Seizures Older children and adolescents - Autonomic response (tends to occur w ith blood glucose <50 to 65 mg/dL)
Sweating Tachycardia Palpitations Tremor Nervousness Hunger Paresthesias Pallor
- Neuroglycopenia
Irritability C onfusion Uncharacteristic behavior Weakness Seizures C oma Occasionally, transient focal neurologic deficits
Diagnosis
Obtain rapid bedside blood glucose concentration Confirm the presence of hypoglycemia w ith a simultaneously draw n plasma glucose Treat, as outlined below , if the bedside value is low (<70 mg/dL [3.89 mmol/L]) in symptomatic patients 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 w ho are not being treated for diabetes mellitus or do not have a know n cause for hypoglycemia
Treatment
Do not delay treatment if symptomatic hypoglycemia is suspected. How ever, 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:
Administer 0.3 grams/kg (10 to 20 grams) of a rapidly-absorbed carbohydrate (eg, 2 to 3 glucose tablets, a tube of gel with 15 grams, 4 oz (120 mL) sweetened fruit juice, non-diet soda, or a teaspoon (5 mL) of honey or table sugar. May repeat in 10 to 15 minutes.
Altered mental status, unable to swallow, or does not respond to oral glucose administration within 15 minutes:
Give an initial IV bolus of glucose of 0.25 grams/kg of dextrose (maximum single dose 25 grams). The volume and concentration of glucose bolus is infused slowly at 2 to 3 mL per minute and based upon age: 2.5 mL/kg of 10 percent dextrose solution (D10W) in infants and children up to 12 years of age (10 percent dextrose is 100 mg/mL) 1 mL/kg of 25 percent dextrose (D25W) or 0.5 mL/kg of 50 percent dextrose (D50W) in adolescents (25 percent dextrose is 250 mg/mL; 50 percent dextrose is 500 mg/mL)
Unable to receive oral glucose and unable to obtain IV access:

Give glucagon 0.03 mg/kg IM or SQ (maximum dose 1 mg): Perform blood glucose monitoring every 10 to 15 minutes as the effects of glucagon may be transient
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Establish vascular access as soon as possible
After initial hypoglycemia is reversed, provide additional glucose and treatment based upon suspected etiology: - Give children and adolescents w ith type I diabetes mellitus a normal diet - Give patients w ith an unknow n cause of hypoglycemia intravenous infusion of dextrose 10 percent (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, w ho 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 w ith hypoglycemia of unknow n cause Obtain medical toxicology consultation for patients w ith ingestion of oral hypoglycemic agents by calling the United States Poison Control Netw ork at 1-800-222-1222 or access the W orld Health Organizations list of international poison centers (w w w .w ho.int/gho/phe/chemical_safety/poisons_centres/en/index.html) Admit the follow ing patients: - Cannot maintain normoglycemia w ith oral intake - Hypoglycemia of unknow n cause - Ingestion of long-acting hypoglycemic agents - Recurrent hypoglycemia during the period of observation IV: intravenous; IM: intramuscular; SQ: subcutaneous; D10W : 10 percent dextrose in w ater; D25W : 25 percent dextrose in w ater; D50W : 50 percent dextrose in w ater. * These findings may also occur in infants w ith sepsis, congenital heart disease, respiratory distress syndrome, intraventricular hemorrhage, other metabolic disorders, and in children and adolescents w ith a variety of underlying conditions. Specific laboratory studies to obtain in children include blood samples for glucose, insulin, C-peptide, beta-hydroxybutyrate, lactate (free flow ing blood must be obtained w ithout a tourniquet), plasma acylcarnitines, free fatty acids, grow th hormone, and cortisol. Higher doses of glucose (eg, 0.5 to 1 g/kg [5 to 10 mL/kg of 10 percent dextrose in w ater OR 2 to 4 mL/kg of 25 percent dextrose in w ater]) may be needed to correct hypoglycemia caused by sulfonylurea ingestion. (For more detail, refer to UpToDate topic on sulfonylurea agent poisoning). Glucagon w ill reverse hypoglycemia caused by excess endogenous or exogenous insulin and w ill not be effective in patients w ith 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 w hich 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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Management algorithm for infants (1 month) and children with suspected bacterial meningitis
STAT: intervention should be performed emergently; CBC: complete blood count; PT: prothrombin time; PTT: partial thromboplastin time; BUN: blood urea nitrogen; CSF: cerebrospinal fluid. * Antimicrobial therapy should not be delayed if lumbar puncture cannot be performed or is unsuccessful. Decisions regarding the administration of dexamethasone should be individualized depending on careful analysis of the risks and benefits as discussed in the text. (See "Treatment and prognosis of acute bacterial meningitis in children"). Empiric antibiotic therapy and dexamethasone (if w arranted) should be administered immediately after cerebrospinal fluid is obtained; if dexamethasone is to be administered, it should be given before, or immediately after, the first dose of antimicrobial therapy. Adapted from: 1. Tunkel AR, Hartman BJ, Kaplan SL, et al. Practice guidelines for the management of bacterial meningitis. Clin Infect Dis 2004; 39:1267 2. Fleisher GR. Infectious disease emergencies. In: Textbook of Pediatric Emergency Medicine, 5th ed, Fleisher GR, Ludwig S, Henretig FM (Eds), Lippincott Williams & Wilkins, Philadelphia 2006. p.792.
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Cerebrospinal fluid (CSF) patterns and diagnosis of viral meningitis in children

Pathogen
Enterovirus
WBC (cells/mm3)
100-1000 None
RBC
Glucose (mg/dL)
NL/SL
Protein (mg/dL)
<160
Viral diagnosis
Cell culture: NP, rectal, CSF; PCR: CSF Cell culture: skin or mucosal lesion; PCR: CSF, blood PCR: CSF Serum serology
Herpes simplex virus Epstein Barr virus
~100
None or
~100 or higher
None
NL
Cytomegalovirus
None
Cell culture and CSF PCR Serology, cell culture and PCR
Lymphocytic choriomeningitis virus Influenza
None
NL/SL
NL/SL
NL/SL
None
NL
NL/SL
NP cell culture, antigen testing and PCR CSF PCR
Arboviruses
Eastern equine encephalitis Western equine encephalitis (WEE) West Nile virus St. Louis encephalitis virus
<200
400-4000 2000 <200 <200
None
NL
Serum and CSF serology testing Cell culture: research laboratories
Up to 900 ~200
W EE virus: PCR: CSF
NL: normal; SL: slightly; NP: nasopharyngeal aspirate; CSF: cerebrospinal fluid; PCR: polymerase chain reaction; : decrease; : increase. Data from: 1. Feigin RD, Shackelford PG. Value of repeat lumbar puncture in the differential diagnosis of meningitis. N Engl J Med 1973; 289:571. 2. Negrini B, Kelleher KJ, Wald ER. Cerebrospinal fluid findings in aseptic versus bacterial meningitis. Pediatrics 2000; 105:316. 3. Rotbart HA. Viral meningitis. Semin Neurol 2000; 20:277. 4. Sawyer MH. Enterovirus infections: diagnosis and treatment. Pediatr Infect Dis J 1999; 18:1033. 5. Simko JP, Caliendo AM, Hogle K, Versalovic J. Differences in laboratory findings for cerebrospinal fluid specimens obtained from patients with meningitis or encephalitis due to herpes simplex virus (HSV) documented by detection of HSV DNA. Clin Infect Dis 2002; 35:414.
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Example of epinephrine infusion - pediatric 10 kg

Example of preparation of epinephrine infusion for refractory symptoms of anaphylaxis for pediatric patient of 10 kg body weight for emergency/critical care units
Epinephrine 10 micrograms/mL (0.01 mg/mL) Add 1 mg (1000 micrograms) of epinephrine to 100 mL of 5 percent dextrose water (D5W). Resulting concentration is 10 micrograms per milliliter (mL). Preparation 1. CHECK vial strength. 2. To prepare epinephrine infusion for a final concentration of 10 micrograms per mL, dilute 10 mL of 0.1 mg/mL epinephrine (also labeled 1:10,000) in 100mL of D5W OR 1 mL of 1 mg/mL epinephrine (also labeled 1:1000) in 100 mL of D5W .* Administration Infuse an initial dose of 0.1 micrograms per kg per minute using a programmable infusion pump and titrate as needed w hile continuously monitoring the patient's cardiac rhythm and blood pressure. Administration rate Pediatric dose for 10 kg child 1 milligram epinephrine diluted in 100 mL D5W 10 micrograms per milliliter
Micrograms per kg per minute Micrograms per minute mL per minute for 10 kg child mL per hour for 10 kg child
0.05 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1
Multiply by patient weight (10 kg)
0.5 1 2 3 4 5 6 7 8 9 10
0.05 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1
Multiply by 60 minutes
3 6 12 18 24 30 36 42 48 54 60
To reduce the risk of making a medication error, w e suggest that centers have available an institutionally approved protocol for epinephrine infusion that includes steps on how to prepare and administer the infusion and standard concentration(s) The above table is provided as an example; there are other acceptable concentrations Intravenous epinephrine, like all vasopressors, can cause life-threatening hypertension, cardiac ischemia, and ventricular arrhythmias. It should be administered ONLY by clinicians trained and experienced in dose titration of intravenous epinephrine using continuous non-invasive electronic monitoring of heart rate and blood pressure. Epinephrine is an ischemia causing agent and peripheral venous irritant. Monitor infusion site for extravasation. See Lexicomp drug reference for information on managing extravasation including infiltration of phentolamine. Central line administration is preferred w hen available. * Unused diluted solutions should be discarded w ithin 24 hours or less of preparation depending on local standards. References: Gahart BL, Nazareno AR; Intravenous Medications 28th ed. Elsevier-Mosby 2012 St. Louis, MO; Lieberman P, et al. J Allergy Clin Immunol 2010; 126(3):477.
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Example of epinephrine infusion - pediatric 20 kg

Example of preparation of epinephrine infusion for refractory symptoms of anaphylaxis for pediatric patient of 20 kg body weight for emergency/critical care units
Epinephrine 10 micrograms/mL (0.01 mg/mL) Add 1 mg (1000 micrograms) of epinephrine to 100 mL of 5 percent dextrose water (D5W). Resulting concentration is 10 micrograms per milliliter (mL). Preparation 1. CHECK vial strength. 2. To prepare epinephrine infusion for a final concentration of 10 micrograms per mL, dilute 10 mL of 0.1 mg/mL epinephrine (also labeled 1:10,000) in 100mL of D5W OR 1 mL of 1 mg/mL epinephrine (also labeled 1:1000) in 100 mL of D5W .* Administration Infuse an initial dose of 0.1 micrograms per kg per minute using a programmable infusion pump and titrate as needed w hile continuously monitoring the patient's cardiac rhythm and blood pressure. Administration rate Pediatric dose for 20 kg child 1 milligram epinephrine diluted in 100 mL D5W 10 micrograms per milliliter
Micrograms per kg per minute Micrograms per minute mL per minute for 10 kg child mL per hour for 10 kg child
0.05 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8

Multiply by patient weight (20 kg)
1 2 4 6 8 10 12 14 16
0.1 0.2 0.4 0.6 0.8 1 1.2 1.4 1.6

Multiply by 60 minutes
6 12 24 36 48 60 72 84 96
To reduce the risk of making a medication error, w e suggest that centers have available an institutionally approved protocol for epinephrine infusion that includes steps on how to prepare and administer the infusion and standard concentration(s) The above table is provided as an example; there are other acceptable concentrations Intravenous epinephrine, like all vasopressors, can cause life-threatening hypertension, cardiac ischemia, and ventricular arrhythmias. It should be administered ONLY by clinicians trained and experienced in dose titration of intravenous epinephrine using continuous non-invasive electronic monitoring of heart rate and blood pressure. Epinephrine is an ischemia causing agent and peripheral venous irritant. Monitor infusion site for extravasation. See Lexicomp drug reference for information on managing extravasation including infiltration of phentolamine. Central line administration is preferred w hen available. * Unused diluted solutions should be discarded w ithin 24 hours or less of preparation depending on local standards. References: Gahart BL, Nazareno AR; Intravenous Medications 28th ed. Elsevier-Mosby 2012 St. Louis, MO; Lieberman P, et al. J Allergy Clin Immunol 2010; 126(3):477.

Septic Shock Rapid Recognition and Initial Resuscitation in

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Septic shock: Rapid recognition and initial resuscitation in children

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