Pediatric Shock
May 1, 2009 21 minutes read
Pediatric Shock
Author: Wendalyn K. Little, MD, MPH, Assistant Professor of Pediatrics and Emergency Medicine, Emory University School of Medicine, Atlanta, GA; Associate Medical Director, CHOA Hughes Spalding Emergency Department, Atlanta, GA.
Peer Reviewer: S. Margaret Paik, MD, Assistant Professor of Pediatrics, Associate Medical Director, The University of Chicago, Comer Children's Hospital, Chicago, IL.
By simplest definition, shock is a state of inadequate substrate delivery at the cellular level. In clinical practice, shock is the manifestation of often complex and multifactorial disturbances in cardiorespiratory function that results in inadequate delivery of oxygen and nutrients to meet metabolic needs. If unrecognized and untreated, shock leads to cellular death followed by multiple organ failure and, ultimately, death of the organism. Timely recognition and intervention can reduce the morbidity and mortality for patients presenting with shock. The recognition and management of shock in infants and children presents unique challenges to practitioners because of size, developmental and physiologic differences from adult patients.
This article will review the presentation, classification, treatment, and management controversies for various shock states in pediatric patients.
The Editor
Background and Epidemiology
The 19th century surgeon Samuel Gross described shock as "the rude unhinging of the machinery of life."1 This is an apt description, as shock is a common pathway to death for all living creatures. Emergency medicine providers frequently encounter patients presenting in various shock states. Worldwide, infections are the leading cause of death for children. In the United States and other industrialized nations, trauma is the leading cause of death for children, but infectious causes are consistently in the top 10 causes of pediatric mortality. Trauma and infection are therefore the leading causes of shock in pediatric patients and contribute substantially to morbidity, mortality, and healthcare utilization amongst children.2 Practitioners caring for children must, therefore, know how to recognize and treat various shock states in pediatric patients if they are to impact the outcome and survival of seriously ill and injured children.3
Definition and Classification
Shock is a state of acute cellular oxygen deficiency. The causes of shock are many. Indeed, any serious injury or illness can cause a state of shock if circulatory function is significantly impaired. Shock is a dynamic process; the presentation and clinical course depends upon the nature and severity of injury or illness, the compensatory capability of the patient, time elapsed and treatment provided. Shock may be classified by physiologic state or by cause, as described below.
Physiologic classification
Unrecognized and untreated (or inadequately treated), shock follows a progression of physiological derangement that may be classified as compensated, uncompensated and finally, terminal shock. In compensated shock, autonomic reflex mechanisms are activated including endogenous catecholamine release. These responses lead to increased heart rate, cardiac contractility, and systemic vascular resistance and may maintain vital organ perfusion and function for a period of time. These compensatory mechanisms are particularly active in previously healthy children and young adults and may make early phases of shock difficult to recognize. If unrecognized and untreated, compensated shock progresses to a state of uncompensated shock in which cellular function deteriorates and leads to progressive metabolic acidosis and signs of organ dysfunction such as altered mental status, decreased urine output and myocardial dysfunction. The development of systemic hypotension also signifies transition to an uncompensated shock state. Finally, terminal or irreversible shock implies organ damage to a degree that death is inevitable.4-7
Classification by Cause
Hypovolemic Shock. Characterized by inadequate circulating intravascular volume, hypovolemic shock is the most common cause of shock in pediatric patients. Hypovolemic shock may be caused by hemorrhage (trauma, GI bleed), plasma loss (burns, capillary leak syndrome), gastrointestinal losses (vomiting, diarrhea), or excessive renal loss (diabetic ketoacidosis, diuretic use, diabetes insipidus).
Distributive Shock. Characterized by systemic vasodilation leading to a state of functional or relative hypovolemia, distributive shock may be caused by anaphylaxis, spinal cord injury, or administration of vasodilatory medications.
Cardiogenic Shock. Cardiogenic shock is caused by myocardial dysfunction leading to inadequate cardiac output to meet tissue needs. Myocardial dysfunction may be secondary to dysrhythmia, cardiomyopathy (infectious, metabolic, or toxin mediated), trauma (myocardial contusion), or congenital heart disease.
Obstructive Shock. Obstructive shock is caused by mechanical obstruction of cardiac output. Causes include pericardial tamponade, tension pneumothorax, hypertension (pulmonary or systemic), or congenital heart disease with ventricular outflow tract obstruction.
Septic Shock. Meriting individual attention, the presentation of septic shock may involve features of several other shock classifications, depending on the individual patient and the stage of the disease process. In early septic shock, a hyperdynamic circulatory state may exist with increased cardiac output and decreased systemic vascular resistance. Patients in this state may mimic distributive shock with a relative intravascular hypovolemia secondary to vasodilatation. As septic shock progresses, compensatory mechanisms lead to vasoconstriction and increased systemic vascular resistance. These mechanisms, as well as intrinsic myocardial depression, may lead to decreased cardiac output and a component of cardiogenic shock. At the same time, capillary leak syndrome, fever and increased respiratory rate may contribute to a component of hypovolemic shock.8
Recognition of Shock
Rapid recognition of shock, especially early or compensated shock, is crucial to preventing progression to a state of uncompensated or terminal shock. Early recognition may be difficult, especially in previously healthy, young patients in whom compensatory mechanisms may maintain vital organ function and blood pressure despite significant reduction in circulating blood volume.
Keys to prompt diagnosis of shock include a high index of suspicion in patients with a history of trauma, extremes of age, immunodeficiency, and underlying medical problems. Careful and repeated physical examination is also extremely important in diagnosis and management of patients in shock, and may give valuable information as to the nature and cause of shock. (See Table 1.) Physical exam should start with an observation of the patient's state of alertness and responsiveness to the surrounding environment. Agitation, restlessness, and inability to be consoled by parents or known caregivers may be an early sign of shock in infants and children. Even more ominous is a quiet, withdrawn child who does not make eye contact with caregivers or respond to painful stimulus such as venipuncture. Patients with such an appearance warrant immediate evaluation and treatment. Close attention should next be paid to issues of airway and breathing. Effortless tachypnea is often an early sign of hypovolemic, distributive, or septic shock as the patient attempts to compensate for an increasing metabolic acidosis through respiratory elimination of carbon dioxide. In contrast, patients in cardiogenic shock often have increased work of breathing, grunting, and crackles heard on lung auscultation secondary to pulmonary venous congestion.4,5,9
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The next step in the rapid assessment of patients in shock is to evaluate the circulatory status. Heart rate and pulse quality are another element of the cardiovascular assessment. Tachycardia is one of the earliest signs of shock. It is important to remember that heart rate may be affected by fear, agitation or fever, and must also be interpreted in context to age-specific normal values. (See Table 2.) Quality of pulses is also important. Hypovolemic or cardiogenic shock leads to narrow pulse pressure with thready pulses. Initially the patient may have weak distal pulses with more normal central pulses; as the shock state worsens central pulse quality also weakens and peripheral pulses may become difficult or impossible to palpate. In contrast to this, patients in early distributive or septic shock may have widened pulse pressure with bounding pulses. As shock state worsens however, pulse pressure will eventually narrow and pulses will weaken and become undetectable.4,5 Attention should be paid to skin perfusion, temperature, and capillary refill time. Healthy patients in a warm environment should have pink, warm skin with brisk (< 2 seconds) capillary refill time. A cold environment or the presence of fever may cause peripheral vasoconstriction in infants and young children and make evaluation more difficult. Patients with hypovolemic shock may have cool distal extremities and prolonged capillary refill. These changes may be minimal at first but will progress with worsening shock. Patients with distributive shock may have flushed skin and brisk capillary refill. They may also have urticaria in cases of anaphylactic shock or petechiae in early septic shock. Patients in cardiogenic shock often have cool, mottled skin, and delayed capillary refill. Urine output reflects renal perfusion. Diminished urine output may be an early sign of intravascular volume depletion and steadily decreases to a state of anuria in patients with severe shock.4,5,7,9,10
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Blood pressure should also be measured as part of the cardiovascular assessment. Many references differentiate compensated versus uncompensated shock by whether arterial blood pressure is maintained within an age-specific appropriate range. (See Table 2.) Over-reliance on blood pressure, however, may lead to missed cases of shock states, especially in previously healthy children and young adults with hypovolemic shock. Early in any shock state, compensatory mechanisms are activated and result in massive endogenous catecholamine release. This serves to increase cardiac output through increased heart rate and contractility. These compensatory mechanisms also lead to an increase in systemic vascular resistance (except in cases of distributive shock) and a shunting of blood flow away from the skin, muscles, and abdominal organs to preferentially maintain flow to vital organs such as the heart and brain.6 Because of these active compensatory mechanisms, some patients, especially previously healthy children and young adults, may be capable of maintaining normal blood pressure for quite some time even in the face of progressing shock. Infants and patients with pre-existing cardiac disease may have limited ability to increase cardiac output through increased contractility and therefore have less cardiac reserve than older, healthy children. In cases of hypovolemic shock, especially acute hemorrhagic states, blood pressure may be maintained in a normal range until approximately 30% of the circulating blood volume has been lost, at which point uncompensated shock ensues and may progress rapidly to terminal shock unresponsive to therapy.9,10 Therefore, it is important to realize that hypotension is a late and ominous sign of shock in pediatric patients and every effort should be made to recognize and treat shock states before such decompensation occurs.4,5,9,10
Laboratory studies may be a useful adjunct in diagnosing and treating shock, but cannot replace careful and repeated assessment of physical exam and vital signs. Rapid bedside assessment of electrolytes, especially serum glucose, may aid in treatment. Hypoglycemia should be quickly recognized and treated with intravenous dextrose. The hemoglobin level should be measured, especially if anemia or hemorrhage is suspected. It is important to remember, however, that hemoglobin values may initially be normal, or even increased through hemoconcentration, despite the presence of acute hemorrhage. Blood should be sent for type and cross match for any patient in whom hemorrhage or anemia is suspected. Measurement of serum pH, base deficit, and lactate levels may give an indication of severity of shock and may be useful in determining response to therapy and guiding resuscitation efforts. There is evidence to suggest that failure to normalize or significantly improve acidosis in the first 24 hours of therapy is indicative of more severe disease and poor prognosis. Finally, appropriate cultures should be obtained, if possible, before starting antibiotics in cases of suspected septic shock, but treatment should not be delayed if cultures cannot be promptly obtained.4,5,9,10
Treatment of Shock
Appropriate management of patients presenting in shock necessitates rapid recognition of the shock state and determination of the most plausible etiology for the shock. Certain treatment principles apply regardless of the etiology and should be instituted immediately for all patients presenting with signs of shock. Attention should first be directed toward airway and breathing. Even patients with a patent airway and spontaneous respirations may benefit from early intubation to reduce metabolic demand and assure adequate oxygenation and ventilation, especially in cases of severe or decompensated shock.11-13 All patients should be placed on supplemental oxygen, preferable by a high-flow mask.
The next management priority should be establishing vascular access. This is best accomplished through the placement of a peripheral intravenous catheter of as large a caliber as is possible for the patient's size. Every effort should be made to have at least two functioning IVs in severely ill or injured patients. The rate of flow through a catheter is proportional to the diameter and inversely proportional to the length of the catheter; therefore short, large-caliber catheters are preferred over long, central venous lines for initial resuscitation.7,10 When IV access cannot be quickly established, consideration should be given to placement of an intraosseous (IO) access device.9,10 Historically, IO access was recommended only for infants and young children. Newer devices, however, allow the IO route to be used for older children and adults.14,15 Fluid therapy should be initiated immediately after access is established. The majority of patients presenting in shock have some degree of absolute or relative intravascular volume depletion and may benefit from intravenous fluids. Early, aggressive fluid resuscitation has been shown in multiple studies to improve survival and outcomes in adult and pediatric septic shock patients.9,11,13,16-19 Even patients presenting with suspected cardiogenic shock may benefit from fluid resuscitation, but fluids should be given in smaller amounts and patients should be carefully monitored for signs of worsening congestive heart failure. The following sections will review the general management principles for different types of shock. Medical personnel caring for patients in shock must remember that any given patient may have a mixture of etiologies causing the shock state, and treatment must be tailored to the individual patient's presentation.
While some patients in early shock state may be successfully resuscitated in the emergency department to the point of stability for hospitalization on a regular hospital ward, most patients presenting in shock will need ongoing care in an intensive care setting. During initial resuscitation, plans should be made for transfer to an appropriate level of care.
Treatment of Shock Hypovolemic Shock
As previously mentioned, hypovolemic shock is the most common shock state affecting pediatric patients. Leading causes of hypovolemic shock in these patients are hemorrhage from trauma and dehydration from gastrointestinal losses (vomiting and diarrhea). All patients presenting in hypovolemic shock require rapid vascular access (IV or IO) and volume resuscitation. Initial fluid therapy should consist of a 20 mL/kg bolus of isotonic crystalloid fluid such as normal saline or Ringer's lactate. This bolus should be given as quickly as possible. If the patient's heart rate, level of consciousness, and capillary do not improve, a second bolus of 20 mL/kg should be rapidly administered. Blood should be drawn for determination of electrolyte and hemoglobin levels and for type and crossmatch of red blood cells in trauma patients. Hypoglycemia should be corrected if present. Patients presenting with severe hypovolemic shock may need 40–60 mL/kg of crystalloid for initial resuscitation. In cases of trauma, if systemic perfusion does not respond to administration of 40–60 mL/kg of crystalloid, packed red blood cells should be transfused in 10–15 mL/kg aliquots. Blood transfusion may be repeated as needed. Type-specific crossmatched blood is preferred; however, Type O blood may be used in urgent circumstances until crossmatched blood is available. Emergent surgical consultation should be arranged for patients exhibiting signs of shock after trauma, as they may require surgical exploration to identify and correct ongoing hemorrhage.9,10,20
Treatment of Shock Distributive Shock
Distributive shock is the result of decreased vascular tone. Common causes are anaphylaxis and spinal cord injuries. This loss of vascular tone creates a state of relative vascular volume depletion. Therefore, initial treatment of distributive shock is similar to that of hypovolemic shock. Vascular access should be obtained and crystalloid boluses of 20 mL/kg should be delivered until systemic perfusion improves. If systemic perfusion does not improve after two or three such boluses, attention should be given to starting infusion of vasoactive medications, such as dopamine or norepinephrine. The alpha adrenergic properties of these medications cause systemic vasoconstriction and may improve perfusion in cases of distributive shock. Table 3 summarizes commonly used vasoactive medications.
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Patients presenting with a history suggestive of anaphylaxis, such as an insect envenomation or ingestion of potential allergens such as nuts, should be treated with epinephrine.9,21 Historically, epinephrine has been given subcutaneously; recent literature, however, suggests that an intramuscular route of delivery leads to faster and more consistent uptake and is the preferred delivery route.22,23 Anaphylaxis should also be treated with antihistamines (both H1 and H2 blocking drugs), and administration of systemic steroids.9,21
Treatment of Shock Obstructive Shock
Successful treatment of obstructive shock requires identification and specific therapy for the type of obstruction. Pericardial tamponade may present with muffled heart sounds, diminished pulses, and distended neck veins. There may be a history of connective tissue disease, malignancy, or trauma. Chest x-ray and bedside ultrasound, when available, may be helpful in making the diagnosis. If the patient's clinical condition permits, pericardial drainage under ultrasound guidance by an experienced practitioner is the preferred treatment. In patients with severe shock or cardiovascular collapse, emergent pericardiocentesis may be lifesaving and should be performed without delay. Likewise, tension pneumothorax may cause a picture of shock with hypotension, diminished pulses, diminished or absent breath sounds on the affected side, and distended neck veins and/or tracheal deviation. Chest x-ray may be helpful in making the diagnosis, but therapy should not be delayed in severely ill patients in whom there is a suspected tension pneumothorax. These patients should have immediate decompression of the pneumothorax by placement of an over-the-needle catheter in the second intercostal space in the mid-clavicular line followed by tube thoracostomy.7,9,10
Some forms of congenital heart disease, such as interrupted aortic arch or coarctation of the aorta, may cause cardiac outflow tract obstruction leading to obstructive shock. These infants may appear normal at birth only to present with signs of poor perfusion and shock when the ductus arteriosus constricts and closes. This may happen in the immediate neonatal period or be delayed for up to several weeks after birth. A high index of suspicion of congenital heart disease must be maintained when evaluating young infants presenting in shock. If congenital heart disease is suspected in such infants, it may be appropriate to start a continuous infusion of prostaglandin E1 while awaiting echocardiographic confirmation of congenital heart disease. Practitioners should be mindful of the potential side effects of prostaglandin infusion, which include respiratory depression and fever, and be prepared to intubate the infant, especially if the child must be transported for further evaluation and care. Concern for these side effects, however, should not delay the initiation of prostaglandin therapy in newborns with suspected congenital heart disease, as prostaglandin infusion may reopen a closing ductus arteriosus and be lifesaving in these patients.4,9,11
Treatment of Shock Septic Shock
Septic shock is perhaps the most studied, yet least understood and most controversial, type of shock. Sepsis may be defined as the systemic response to infection. This systemic response is independent of the type of invading microorganism (bacteria, virus, fungus) and is the result of the complex interaction of microbial agents and toxins and host inflammatory response. The outcome of this interaction is multiple organ system derangement and dysfunction at the cellular and subcellular level.11 Patients in septic shock manifest a variety of signs and symptoms reflective of this multiorgan system dysfunction. The early signs of septic shock are similar to those of other types of shock; patients may demonstrate tachycardia, anxiety or restlessness, and diminished capillary refill. Fever is often present in septic shock, but some patients, especially young infants, may present with hypothermia. Patients in early septic shock are often in a hyperdynamic cardiovascular state with bounding pulses and warm extremities. This state is sometimes referred to as "warm shock." Because of decreased systemic vascular resistance, these patients may be profoundly hypotensive despite overall increased cardiac output. As the shock state progresses, cardiac output falls as a result of increased systemic vascular resistance, decreased preload and intrinsic myocardial depression.8,24-26 On physical examination, these patients may have cool, clammy, or mottled skin with diminished or absent pulses and delayed capillary refill time. This state is sometimes referred to as "cold shock."
Initial treatment considerations in septic shock are the same as those for any type of shock. In 2003, evidence-based guidelines for the treatment of septic shock were prepared by a committee of critical care and infectious disease experts.13 Figure 1 summarizes these recommendations. Careful attention should be given to airway, breathing and oxygenation. Patients with evidence of real or impending respiratory arrest should be intubated as soon as safely possible. Consideration should be given to early, elective intubation of patients in septic shock, as this may decrease the metabolic demand caused by increased respiratory effort that often accompanies septic shock, and also ensure adequate oxygenation and ventilation.12 (See Table 4.) Patients not requiring intubation should be given high-flow supplemental oxygen. IV or IO access should be quickly obtained and fluid resuscitation begun immediately. Patients in septic shock may require in excess of 100 mL/kg of isotonic fluids in the first hours of treatment to restore adequate perfusion.12,19,27 Fluids should be delivered as 20 mL/kg boluses, each given rapidly with careful reassessment between boluses. Hepatomegaly or rales on lung auscultation may be signs of fluid overload and should prompt slower and more careful delivery of fluids. Patients may also require transfusion of blood products, such as packed red blood cells to treat anemia or platelets and fresh frozen plasma to correct consumptive coagulopathy which may develop as part of the sepsis syndrome.
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Patients not responding after 40-60 mL/kg of IV fluid should be considered to be in fluid refractory shock, and consideration should be given to vasopressor therapy.19,24,26,27 Dopamine is often the first vasopressor used in pediatric patients. Dopamine has combined alpha- and beta-adrenergic effects and therefore may increase both systemic vascular resistance through vasoconstriction and cardiac output through increased contractility and heart rate. Patients with continued hypotension and poor perfusion on dopamine therapy may benefit from norepinephrine or epinephrine infusions. Norepinephrine is primarily an alpha agonist, and as such causes systemic vasoconstriction. Norepinephrine is therefore most beneficial in situations such as anaphylaxis, spinal shock, and early septic shock in which hypotension and decreased perfusion are secondary to systemic vasodilation. Epinephrine has potent alpha and beta effects and may be useful in improving cardiac output in situations such as severe septic shock or post-cardiac arrest.8,11,19,25,27,28
In some situations, such as cardiogenic shock, septic shock with impaired cardiac contractility, or pulmonary hypertension, it may be useful to improve cardiac output by increasing cardiac contractility and simultaneously decreasing systemic vascular resistance.24 Dobutamine may be used in patients suspected of having a predominantly cardiogenic cause of shock; dobutamine is an inotropic agent and increases cardiac contractility through stimulation of beta agonist receptors.4,19,27 The phosphodiesterase inhibitors are another class of medications which may be used to improve cardiac output in shock states. The most commonly used drug in this class is milrinone.8 Milrinone may improve cardiac contractility and may be especially useful for decreasing pulmonary vascular resistance in patients with pulmonary hypertension.11
Treatment of infection is also important in the management of suspected septic shock, and should be undertaken during or immediately following initial resuscitation efforts. Appropriate cultures should be obtained before giving antibiotics whenever possible, although antibiotic therapy should not be withheld if cultures cannot be quickly obtained. For example, patients with suspected meningitis judged unstable for lumbar puncture should not have antibiotics withheld.12 Initial antimicrobial therapy should initially be broad spectrum, with attention given to potential infectious agents based on patient history and presentation (e.g., immunocompromise, recent travel, presence of abscess, rash, etc.).
Several controversies exist in the management of septic shock. One of these surrounds the use of steroids in fluid- and vasopressor-resistant hypotension and shock. In patients at risk for adrenal crisis, such as those with Addison's disease, congenital adrenal hyperplasia, ongoing or recent systemic steroid use, purpura fulminas with Friedrich–Waterhouse syndrome, and pituitary abnormalities, timely administration of systemic steroids may be lifesaving. Such patients should be provided "stress dose" steroids, usually in the form of hydrocortisone.8,27 The controversy surrounding steroid use revolves around the concept that some critically ill patients may exist in a state of relative adrenal insufficiency and that provision of systemic steroids to this population may improve hemodynamic parameters. This has led to interest in some intensive care units in conducting corticotropin stimulation testing and administering steroids when cortisol levels fail to rise to a pre-determined level after stimulation.13,19,29,30 Complete acceptance of this approach has been hampered by a lack of consensus as to what constitutes an appropriate cortisol level in patients with septic shock and lack of a clear-cut survival benefit in patients given systemic steroids.16,26,27,31 Perhaps more important to the emergency medicine physician is the controversy surrounding etomidate and adrenal insufficiency. Etomidate has found widespread use in emergency departments as an induction agent for rapid sequence intubation. Etomidate is known to cause adrenal suppression, but this phenomenon was believed to be short-lived and clinically insignificant. Recent literature, however, suggests a link between etomidate usage and prolonged adrenal insufficiency in patients with septic shock, leading some sources to suggest the use of alternative induction agents for patients with known or suspected septic shock and requiring intubation.32,33 Other areas of controversy and ongoing investigation in septic shock include immunomodulation through novel therapies such as activated protein C and less new but as yet unproved therapies such as plasmapheresis. Extracorporeal oxygen membrane oxygenation (ECMO) is also in use at some centers for severe or refractory septic shock.8,11,13,26
Determining response to therapy and therapeutic endpoints is another area of controversy in shock management, especially for septic shock. Improving mental status, blood pressure, urine output, and peripheral perfusion are obvious goals of fluid resuscitation and shock management. More controversial is monitoring and adjustment of therapy for patients in severe, ongoing shock states. Various sources suggest monitoring lactate levels, mixed venous oxygen saturation, base deficit, and invasive measurements of cardiac output, to name a few, to help predict mortality and to guide and determine response to therapy.20,34,35 Such goal-directed therapy has been shown in some series to improve survival in adult septic shock.1,6,19 The benefit of these measures has not been as well studied or proven for pediatric patients. Further investigation is needed in determining the optimal care of pediatric septic shock patients, especially in regards to the role of steroids, immunotherapy, and monitoring and treatment goals.
Summary
Shock states have many causes and presentations, but all represent acute failure of substrate delivery at the cellular level. While some general management principles apply to all forms of shock, practitioners must use all means at their disposal to determine the cause and appropriate therapy of shock in order to see improvement of morbidity and mortality. Pediatric patients may pose unique challenges to healthcare providers in terms of recognition and management of shock. Providers who care for children must be familiar with the recognition of early shock, age-specific vital sign parameters, and resuscitation skills, specifically vascular access and airway management skills, to provide timely and potentially life-saving care to these young patients.
References
1. Cairns CB. Rude unhinging of the machinery of life: Metabolic approaches to hemorrhagic shock. Curr Opin Crit Care 2001; 7:437-443.
2. Angus DC, Linde-Zwirble WT, Lidicker J, et al. Epidemiology of severe sepsis in the united states: Analysis of incidence, outcome, and associated costs of care. Crit Care Med 2001;29: 1303-1310.
3. Hamilton B, Arialdi M, Martin J, et al. Annual summary of vital statistics: 2005. Pediatrics 2007;119:345-360.
4. McConnell MS, Perkin RM. Shock states. In: Furman BP, Zimmerman JJ, editors. Pediatric Critical Care. St Louis: Mosby; 1998: 293-306.
5. Vanore M, Perks D. Early recognition and treatmentof shock in the pediatric patient. J Trauma Nurs 2006;13:18-21.
6. Hameed SM, Aird WC, Cohn SM. Oxygen delivery. Crit Care Med 2003;31:S658-S667.
7. Cheatham ML, Block EFJ, Smith HG, et al. Shock: An overview. In: Irwin RS, Rippe JM (eds). Irwin and Rippe's Intensive Care Medicine. Philadelphia, PA: Wolters Kluwer; 2007:1831.
8. Tabbutt S. Heart failure in pediatric septic shock: Utilizing inotropic support. Crit Care Med 2001;29:S231-S236.
9. American Heart Association. PALS Provider Manual. Dallas, TX: American Heart Association; 2002.
10. American College of Surgeons. Advanced Trauma Life Support for Doctors, 7th ed. Chicago, IL: American College of Surgeons; 2004.
11. Maar SP. Emergency care in pediatric septic shock. Pediatr Emerg Care 2004;20:617-624.
12. Welch SB, Nadel S. Treatment of meningococcal infection. Arch Dis Child 2003;88:608-614.
13. Parker MM, Hazelzet JA, Carcillo JA. Pediatric considerations. Crit Care Med 2004;32:S591-S594.
14. Buck ML, Wiggins BS, Sesler JM. Intraosseous drug administration in children and adults during cardiopulmonary resuscitation. Ann Pharmocother 2007;41:1679-1686.
15. Blumberg SM, Gorn M, Crain EF. Intraosseous infusion: A review of methods and novel devices. Pediatr Emerg Care 2008;24:50-59.
16. Carcillo JA, Han K, Lin J, et al. Goal-directed management of pediatric shock in the emergency department. Clin Pediatr Emerg Med 2007;8:165-175.
17. Dellinger RP, Carlet JM, Masur H, et al. Surviving sepsis campaign guidelines for management of severe sepsis and septic shock. Crit Care Med 2004;32:858-873.
18. Goldstein B, Giroir B, Randolph A. International pediatric sepsis consensus conference: Definitions for sepsis and organ dysfunction in pediatrics. Pediatr Crit Care Med 2005;6:2-8.
19. Hollenberg SM, Ahrens TS, Annane D, et al. Practice parameters for hemodynamic support of sepsis in adult patients: 2004 update. Crit Care Med 2004;32:1928-1948.
20. Kelley DM. Hypovolemic shock: An overview. Crit Care Nurs Q 2005;28:2-19.
21. Kobrynski L. Anaphylaxis. Clin Pediatr Emerg Med 2007;8: 110-118.
22. Simons F, Gu X, Simons K. Epinephrine absorption in adults with a history of anaphylaxis. J Allergy Clin Immunol 2001; 108:871-873.
23. Simons F, Roberts J, Gu X, et al. Epinephrine absorption in children with a history of anapylaxis. J Allergy Clin Immunol 1998;101:33-37.
24. Ceneviva G, Paschall JAP, Maffei F, et al. Hemodynamic support in fluid-refractory pediatric septic shock. Pediatrics 1998; 102:e19.
25. Dries DJ. Vasoactive drug support in septic shock. Shock 2006; 26:529-530.
26. Dellinger R. Cardiovascular management of septic shock. Crit Care Med 2003;31:946-955.
27. Carcillo J, Fields A. Clinical practice parameters for hemodynamic support of pediatric and neonatal patients in septic shock. Crit Care Med 2002;30:1365-1378.
28. Notterman D. Pharmacology of the cardiovascular system. In: Fuhrman BP, Zimmerman JJ, (eds). Pediatric Critical Care. St Louis: Mosby; 1998: 329-346.
29. de Jong MFC, Beishuizen A, Spijkstra JJ, et al. Relative adrenal insufficiency as a predictor of disease severity, mortality, and beneficial effects of corticosteroid treatment in septic shock. Crit Care Med 2007;35:1896-1903.
30. Annane D, Sebille V, Charpentier C, et al. Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock. JAMA 2002;288:862-871.
31. Zimmerman JJ. A history of adjunctive glucocorticoid treatment for pediatric sepsis: Moving beyond steroid pulp fiction toward evidence-based medicine. Pediatr Crit Care Med 2007; 8:530-539.
32. Cotton BA, Guillamondegui OD, Fleming SB, et al. Increased risk of adrenal insufficiency following etomidate exposure in critically injured patients. Arch Surg 2008;143:62-67.
33. Fengler BT. Should etomidate be used for rapid-sequence intubation induction in critically ill septic patients? Am J Emerg Med 2008;26:229-232.
34. Randolph LC, Takacs M, Davis KA. Resuscitation in the pediatric trauma population: Admission base deficit remains an important prognostic indicator. J Trauma 2002;53:838-847.
35. Engleharta MS, Schreiber MA. Measurement of acid–base resuscitation endpoints: Lactate, base deficit, bicarbonate, or what? Curr Opin Crit Care 2006;12:569-574.
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