Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Shock in Pediatrics Treatment & Management

  • Author: Eric A Pasman, MD; Chief Editor: Timothy E Corden, MD  more...
 
Updated: Mar 03, 2015
 

Approach Considerations

Early goal-directed therapy (EGDT) is targeted at maintaining and restoring an adequate airway, oxygenation, ventilation, and circulation within the first hour of shock onset. Adequate circulation is further defined by adequate perfusion, normal blood pressure for age, and normal or threshold heart rate.

As the initial principles of shock treatment are largely the same regardless of etiology, the 2007 American College of Critical Care Medicine (ACCM) clinical practice parameters for the treatment of pediatric and neonatal septic shock are appropriate to utilize for the initial treatment of pediatric shock.[14]

Pediatric shock management algorithm. ACTH = adren Pediatric shock management algorithm. ACTH = adrenocorticotropic hormone; CI = cardiac index; ECMO = extracorporeal membrane oxygenation; MAP-CVP = mean arterial pressure-central venous pressure; PALS = Pediatric Advanced Life Support; PDE = phosphodiesterase; PICU = pediatric intensive care unit; SVC O2 = superior vena cava oxygen saturation.

Additionally, the 2012 Surviving Sepsis Campaign update provides supplemental considerations for pediatric shock management.[15]

Appropriate therapeutic goals for the treatment of pediatric shock should, therefore, include the following:

  • Normal mental status
  • Normal blood pressure for age
  • Normal or threshold heart rate for age
  • Normal and equal central and peripheral pulses
  • Warm extremities with capillary refill of 2 seconds or less
  • Urine output greater than 1 mL/kg/h
  • Normal serum glucose levels
  • Normal serum ionized calcium levels
  • Decreasing serum lactate levels

As an additional therapeutic goal, the ACCM guidelines also recommend resuscitating children with septic shock to a central venous oxygen saturation (ScvO2) of more than 70%.[14] One randomized controlled trial of EGDT in septic children that compared continuous monitoring ScvO2 to unmonitored ScvO2 demonstrated a significant reduction in 28-day mortality (from 39.2% to 11.8%) and fewer new organ dysfunctions.[23] A follow-up prospective cohort study also compared intermittent ScvO2 monitoring versus no monitoring in children with fluid refractory shock; it further showed a 39% decrease in mortality and improved organ dysfunction.[24] These studies support the use of ScvO2 monitoring and EGDT to guide resuscitation beyond basic clinical measures, such as vital signs, central venous pressure (CVP), and urine output alone.

Next

Initial Resuscitation

Regardless of the cause of shock, the ABCs (airway, breathing, circulation) must be immediately evaluated and stabilized without delay for further diagnostic workup or imaging studies. Place the patient on appropriate noninvasive monitors, such as a pulse oximeter and cardiorespiratory monitor.

The patient's airway must be patent, and the patient must be adequately oxygenated and ventilated. Initially, administer 100% supplemental oxygen at a high flow rate via a face mask or, if respiratory distress is present, via high flow nasal cannula or noninvasive continuous positive airway pressure (CPAP). If the patient is in respiratory failure, consider intubating and providing mechanical ventilation. If the airway can be maintained and oxygenation supported without immediate intervention, delay intubation to allow for initiation of aggressive fluid resuscitation. This is recommended because of the negative—and potentially catastrophic—effect of positive pressure ventilation on venous return and cardiac stability in the hypovolemic patient.

Once the airway has been stabilized and adequate ventilation and administration of oxygen have been ensured, immediately focus on improving circulation and systemic oxygen delivery. Circulatory improvement is achieved via volume expansion and, if necessary, pharmacologic therapy with vasopressors and cardiac inotropic agents.

Previous
Next

Glucose and Calcium Stabilization

Children in shock, particularly when due to sepsis, are at risk for both hypoglycemia and hypocalcemia. These conditions should be rapidly identified and corrected to improve survival and minimize morbidities.

Hypoglycemia

Hypoglycemia is common as a result of inadequate glycogen stores, increased glucose consumption, and metabolic failure. Neonates and infants have limited glycogen stores, which may become rapidly depleted during shock and lead to hypoglycemia. Alternatively, high levels of endogenous and exogenous catecholamines may cause a relative insulin-resistant state that can result in serum hyperglycemia.

Because glucose is the major metabolic substrate, a rapid bedside glucose test should be performed on all patients who present in shock. If the glucose level is low, replacement therapy is provided with intravenous (IV) dextrose. The dose of dextrose is 0.5-1 g/kg. It can be given as follows:

  • 5-10 mL/kg of D10W
  • 2-4 mL/kg of D25W
  • 1-2 mL/kg D50W

Following correction of hypoglycemia, if oral intake is contraindicated, a continuous dextrose infusion is recommended as part of maintenance IV fluids for pediatric patients.

Hypocalcemia

Shock may also cause alterations in available levels of serum ionized calcium, despite normal total serum calcium levels. Hypocalcemia in the shock state is due to impaired parathyroid hormone function, decreased hepatorenal vitamin D hydroxylation, and end-organ resistance. Furthermore, administered blood products (which contain citrate) may bind free available calcium, thereby additionally decreasing the available ionized calcium levels.

Calcium mediates excitation-contraction coupling in muscle cells, including cardiac muscle; low levels of ionized calcium have been shown to be associated with cardiac dysfunction and more severe organ dysfunction.[25] The availability of functioning ionized calcium also depends on the patient's serum acid-base status; an acid environment favors the dissociation of calcium from proteins, making it available as a cofactor in cell function. Calcium is also indicated for treating shock caused by arrhythmias that are precipitated by hyperkalemia, hypermagnesemia, or calcium channel blocker toxicity.

Calcium may be provided either as calcium gluconate or calcium chloride. However, calcium chloride has been shown to produce higher and more consistent levels of available calcium and, therefore, is recommended in the acute resuscitation of a child in shock.[26] The recommended calcium chloride (10%) dose is 10-20 mg/kg (0.1-0.2 mL/kg) IV, administered at an IV infusion rate that does not exceed 100 mg/min. Further therapy may be guided by repeat plasma ionized calcium measurements. Calcium should not be given empirically during active cardiopulmonary resuscitation (CPR) without clear indication because this has been associated with increased mortality.[27]

Previous
Next

Fluid Resuscitation

The major physiologic abnormality in most forms of pediatric shock is either an absolute or a relative intravascular hypovolemia. Children with hypovolemic shock who receive appropriate aggressive fluid resuscitation within the first hour of resuscitation have the most optimal chance of survival and recovery.[28, 29] In one study, a higher mortality rate was demonstrated in children who received less than 40 mL/kg of fluid resuscitation in the first hour and those whose treatment was not initiated within the first 30 minutes after the diagnosis.[30] Therefore, the therapy of choice is rapid and aggressive fluid resuscitation.

If possible, place a minimum of two large-bore, free-flowing IV catheters. If vascular access is not easily and readily achieved, then an intraosseous (IO) needle may be placed into the bone marrow for rapid fluid administration. Such an IO line can be considered as good as an IV line for the purpose of any fluid or medication administration that is necessary for the acute resuscitation of a compromised infant or child in shock.[31]

Administer 20 mL/kg of an isotonic crystalloid infusion, such as 0.9% isotonic sodium chloride or lactated Ringer solution, over 5 minutes or less. This may be most rapidly achieved by a disconnect-reconnect technique using large volume syringes. In this technique, one provider prepares syringes of normal saline or lactated Ringer solution while the other pushes the fluid filled syringe into an IV or IO catheter.[32]

As soon as the initial bolus of fluid (20 mL/kg) has been infused, reevaluate the patient. If the patient retains the clinical appearance of shock, immediately infuse another 20 mL/kg of fluid and repeat the cycle. Additional boluses are titrated to clinical improvement with improved mental status, hemodynamics, perfusion, and urinary output. Ultimately, a child with severe hypovolemia or sepsis should receive 60 mL/kg of volume in the first 15 minutes of early goal-directed therapy (EGDT).

If more than 2-3 volumes of crystalloid have been infused into a patient at risk for hemorrhage (eg, from trauma), administer blood or packed red blood cells (PRBCs). If rales or hepatomegaly develop at any point during the volume resuscitation, the resuscitation should transition from volume administration to inotropic therapy initiation.

Precautions

Cardiogenic shock

An exception to repetitive volume resuscitation in a child with shock is the child who presents with cardiogenic shock. During the initial infusion of fluid for volume expansion, the child can be evaluated for the possibility of cardiogenic shock. If the cause of shock is cardiogenic in etiology, judicious fluid boluses of 5-10 mL/kg should be utilized and balanced with the potential need for early inotropic support to prevent fluid overload.

Global management variation

Of note, a large study in African children presenting with apparent sepsis to resource-limited facilities demonstrated a worse outcome for children treated with what would be considered standard fluid resuscitation by Western practice. These results should be considered when treating children in the region of the world studied. The authors suggest that further study is warranted regarding volume expansion and fluid effects on septic children in different settings and with various etiologies.[33]

Stratification of initial mortality risk

Providing additional insight into the role of fluid status, one large study in the United States showed that when stratified for mortality risk, increased volume fluid resuscitation and positive fluid balance in patients with a low initial mortality have worse outcomes, with persistence of multisystem organ failure and death. Patients with a moderate to high initial mortality risk did not show increased mortality with aggressive fluid management.[34]

Previous
Next

Antibiotics and Source Control

If septic shock is a concern, initial coverage with empiric antibiotics is essential to eliminating the precipitating cause of shock. The current standard of care is to initiate empiric antibiotics within the first hour of the diagnosis of severe sepsis. Delayed antimicrobial therapy, specifically greater than 3 hours after recognition of sepsis, has been associated with increased mortality and prolonged organ dysfunction.[35]

Blood cultures should be obtained before antibiotic administration if possible, or as soon as clinical stability permits. Early source control is also recommended.

Management of significant septic shock should be multidisciplinary and should involve the resources of infectious disease specialists when available.[15, 36, 37] The choice of antibiotics may vary, depending on the patient’s age, comorbidities, epidemiologic disease prevalence, and previous antibiotic exposures. Neonates are often started on a combination of ampicillin and gentamicin. Older infants and children may be covered with a third-generation cephalosporin, possibly along with expanded gram-positive organism coverage with vancomycin initially. Intravenous immunoglobulin (IVIG) has not shown any benefit in treating pediatric patients with septic shock.[38]

Due to the global burden caused by septic shock, multiple international groups have worked to produce sepsis guidelines, bundles, and checklists, including The Surviving Sepsis Campaign[15] and the World Federation of Pediatric Intensive and Critical Care Societies.[39]

Previous
Next

Blood Therapies

During the resuscitation of the pediatric patient in shock with a central venous oxygen saturation (ScvO2) that is less than the goal of 70%, transfusion of packed red blood cells (PRBCs) to a threshold of 10 g/dL may be beneficial to increase arterial blood oxygen content (CaO2).

In the hemodynamically stable pediatric patient with resolving shock, a similar restricted transfusion threshold of 7 g/dL (as in adults) is targeted. If the cause of shock is hemorrhage from trauma, then ongoing bleeding may need to be surgically addressed.

Previous
Next

Vasoactive Agents

Following the initial fluid resuscitation, if shock persists, then it is described as fluid-refractory shock. In this situation, the early initiation of inotropic catecholamine infusions is recommended to potentially help restore sufficient total arterial flow of oxygen (DO2) through improved perfusion and cardiac function.

Initial administration of inotropic agents via peripheral vascular access is recommended until central venous access is obtained. The specific inotropic agent used depends on the hemodynamics, cardiac output (CO), and systemic vascular resistance (SVR) of the patient in shock. For the patient in cold shock with high SVR, dopamine and epinephrine are first-line agents. For the patient with warm shock and low SVR, norepinephrine is recommended. Based on clinical measures to include the central venous oxygen saturation (ScvO2) and potentially directly or indirectly measured cardiac index (CI), vasodilators such as milrinone may also be used to treat low cardiac output states.

For the patient with persistent, catecholamine resistant shock despite appropriate volume and blood and electrolyte repletion, conduct additional evaluation to rule out alternate causes. Pericardial effusion, pneumothorax, and pulmonary embolism all should be ruled out. Any malignant arrhythmias should be converted to normal sinus rhythm as soon as possible. Consideration of a potential endocrine emergency, such as relative/absolute adrenal insufficiency or hypothyroidism is also necessary.

Previous
Next

Supportive Therapies

Corticosteroids

The use of corticosteroids in shock, particularly septic shock, is controversial. Many large-scale, controlled trials in animals and humans have not demonstrated improved outcome with corticosteroid use.[40, 41, 42] Nevertheless, a question remains as to whether patients in severe septic shock have adequate levels of circulating glucocorticoids to support their physiology when it is severely stressed.

Adrenocortical failure or infarction, known as Waterhouse-Friderichsen syndrome, may result in cardiovascular failure and hyporesponsiveness to catecholamines. In affected patients, initiation of stress-dose hydrocortisone, in the range of 50-100 mg/m2/day IV, may be beneficial and lifesaving. A serum cortisol level may be drawn prior to initiating the first dose of corticosteroids, and if this random serum cortisol level is low, then replacement doses may be beneficial. Moreover, some data suggest a potential role for corticosteroid replacement therapy in select patients with septic shock.

Furthermore, select patients may have adrenal insufficiency, rendering them fluid refractory and catecholamine resistant during resuscitation from shock. Some practitioners evaluate a baseline serum cortisol level in children with fluid-refractory, catecholamine-resistant shock and/or perform a corticotropin stimulation test with 250 mcg of corticotropin, and then treating the patient with hydrocortisone, although the use of such serum measurements has not been shown to result in improved outcomes.

Therapy is continued for patients who prove to have an absolute baseline cortisol level of less than 20 mcg/dL and/or a depressed response to the corticotropin stimulation test (ie, a rise of < 9 mcg/dL at 30 and 60 minutes after administration of corticotropin).[43]

Bicarbonate

Sodium bicarbonate use in the treatment of shock is also controversial. During shock, acidosis develops, which impairs myocardial contractility and optimal function of catecholamines. However, treatment with bicarbonate may worsen intracellular acidosis while it corrects serum acidosis. This occurs because bicarbonate is an ion that does not readily traverse semipermeable cell membranes. Hence, bicarbonate combines with acid in serum, resulting in the production of carbon dioxide and water, as defined by the Henderson-Hasselbalch equation.

If the increased carbon dioxide is not removed via ventilation, it readily enters the cell and drives the Henderson-Hasselbalch reaction in the opposite direction, thereby increasing intracellular acidosis. Worsened myocardial intracellular acidosis may result in a decrease in myocardial contractility.[44] In addition, bicarbonate administration may result in hypernatremia and hyperosmolality, thereby decreasing the availability of ionized calcium.

Finally, laboratory and clinical data have not demonstrated that bicarbonate administration improves the ability to defibrillate, improves total arterial flow of oxygen (DO2), or improves survival rates in shock and cardiac arrest.[45, 46] Studies in patients with cardiovascular arrest have not demonstrated improved survival rates associated with the use of bicarbonate. Thus, acidosis that results from shock should ideally be corrected with increased perfusion from volume supplementation and judicious use of inotropic medications in conjunction with optimal ventilation.

Previous
Next

Other Special Considerations

Other modalities of supportive care and multiple system organ support may be required. Lung-protective modes of ventilation should be utilized, such as allowing for permissive hypercapnia, low tidal volumes, and limiting peak plateau pressures. Nutrition should be optimized with early enteral feeds in children who will tolerate them and via IV nutrition in those who are unable to tolerate enteral feeds. Glycemic control should target glucose levels of 180 mg/dL or less. Fluid overload should be limited and reversed following the resolution of shock which may require diuretics and, potentially, renal replacement therapies such as continuous veno-venous hemofiltation (CVVH) or intermittent dialysis., For patients with refractory shock, extracorporeal membrane oxygenation (ECMO), if available, should be initiated.[47, 48, 49]

All of the therapies discussed here are aimed at restoring adequate perfusion to the tissues and organs of the body as soon as possible. Ongoing support offers the body the opportunity to repair the hypoxic and ischemic damage sustained, with the ultimate goal of functioning, intact patient survival.

Previous
 
 
Contributor Information and Disclosures
Author

Eric A Pasman, MD Resident Physician, Department of Pediatrics, National Capital Consortium, Walter Reed National Military Medical Center

Eric A Pasman, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics

Disclosure: Nothing to disclose.

Coauthor(s)

Christopher M Watson, MD, MPH Assistant Professor, Department of Pediatrics, Uniformed Services University of the Health Sciences; Adjunct Assistant Professor, Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine

Christopher M Watson, MD, MPH is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Medical Association, Association of Pediatric Program Directors, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Chief Editor

Timothy E Corden, MD Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin

Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, Wisconsin Medical Society

Disclosure: Nothing to disclose.

Acknowledgements

Barry J Evans, MD Assistant Professor of Pediatrics, Temple University Medical School; Director of Pediatric Critical Care and Pulmonology, Associate Chair for Pediatric Education, Temple University Children's Medical Center

Barry J Evans, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Adam J Schwarz, MD Consulting Staff, Critical Care Division, Pediatric Subspecialty Faculty, Children's Hospital of Orange County

Adam J Schwarz, MD is a member of the following medical societies: American Academy of Pediatrics and Phi Beta Kappa

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Acknowledgments

The views expressed are those of the authors and do not reflect the official policy or position of the US Navy, Department of Defense, or the US Government.

References
  1. Epstein D, Randall CW. Cardiovascular physiology and shock. Nichols DG, ed. Critical Heart Disease in Infants and Children. 2nd Ed. Philadelphia, PA: Mosby Elsevier; 2006. 17-72.

  2. Nadel S, Kissoon N, Ranjit S. Recognition and Initial Management of Shock. Nichols DG, ed. Roger’s Textbook of Pediatric Intensive Care. Philadelphia, PA: Lippincott, William & Wilkins; 2008. 372-383.

  3. Smith LS, Hernan LJ. Shock states. Fuhrman BP, Zimmerman J, eds. Pediatric Critical Care. 4th Ed. Philadelphia, PA: Elsevier Saunders; 2011. 364-378.

  4. American Academy of Pediatrics. Policy statement--child fatality review. Pediatrics. 2010 Sep. 126(3):592-6. [Medline].

  5. [Guideline] Simons FE, Ardusso LR, Dimov V, Ebisawa M, El-Gamal YM, Lockey RF, et al. World Allergy Organization Anaphylaxis Guidelines: 2013 update of the evidence base. Int Arch Allergy Immunol. 2013. 162(3):193-204. [Medline].

  6. Ackerman AD, Singhi S. Pediatric infectious diseases: 2009 update for the Rogers' Textbook of Pediatric Intensive Care. Pediatr Crit Care Med. 2010 Jan. 11(1):117-23. [Medline].

  7. Goldstein B, Giroir B, Randolph A. International pediatric sepsis consensus conference: definitions for sepsis and organ dysfunction in pediatrics. Pediatr Crit Care Med. 2005 Jan. 6(1):2-8. [Medline].

  8. Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013. Lancet. Jan 2015. 385:117-71. [Medline].

  9. Carcillo JA, Kuch BA, Han YY, Day S, Greenwald BM, McCloskey KA, et al. Mortality and functional morbidity after use of PALS/APLS by community physicians. Pediatrics. 2009 Aug. 124(2):500-8. [Medline].

  10. Fisher JD, Nelson DG, Beyersdorf H, Satkowiak LJ. Clinical spectrum of shock in the pediatric emergency department. Pediatr Emerg Care. 2010 Sep. 26(9):622-5. [Medline].

  11. Balamuth F, Weiss SL, Neuman MI, Scott H, Brady PW, Paul R, et al. Pediatric severe sepsis in U.S. children's hospitals. Pediatr Crit Care Med. 2014 Nov. 15(9):798-805. [Medline]. [Full Text].

  12. American Heart Association. Part 2: Systematic approach to the seriously ill or injured child. Chameides L, Samson RA, Schexnayder SM, Hazinski MF, eds. Pediatric Advanced Life Support Provider Manual. Dallas, TX: American Heart Association; 2011.

  13. Carcillo JA. Capillary refill time is a very useful clinical sign in early recognition and treatment of very sick children. Pediatr Crit Care Med. 2012 Mar. 13(2):210-2. [Medline].

  14. [Guideline] Brierley J, Carcillo JA, Choong K, Cornell T, Decaen A, Deymann A, 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 Feb. 37(2):666-88. [Medline].

  15. [Guideline] Dellinger RP, Levy MM, Rhodes A, Annane D, Gerlach H, Opal SM, et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med. 2013 Feb. 41(2):580-637. [Medline].

  16. Ferrari M, Mottola L, Quaresima V. Principles, techniques, and limitations of near infrared spectroscopy. Can J Appl Physiol. 2004 Aug. 29(4):463-87. [Medline].

  17. Adcock LM, Wafelman LS, Hegemier S, Moise AA, Speer ME, Contant CF, et al. Neonatal intensive care applications of near-infrared spectroscopy. Clin Perinatol. 1999 Dec. 26(4):893-903, ix. [Medline].

  18. Ghanayem NS, Wernovsky G, Hoffman GM. Near-infrared spectroscopy as a hemodynamic monitor in critical illness. Pediatr Crit Care Med. 2011 Jul. 12(4 Suppl):S27-32. [Medline].

  19. Post F, Weilemann LS, Messow CM, Sinning C, Münzel T. B-type natriuretic peptide as a marker for sepsis-induced myocardial depression in intensive care patients. Crit Care Med. 2008 Nov. 36(11):3030-7. [Medline].

  20. Domico M, Liao P, Anas N, Mink RB. Elevation of brain natriuretic peptide levels in children with septic shock. Pediatr Crit Care Med. 2008 Sep. 9(5):478-83. [Medline].

  21. Wong HR, Salisbury S, Xiao Q, Cvijanovich NZ, Hall M, Allen GL, et al. The pediatric sepsis biomarker risk model. Crit Care. 2012 Oct 1. 16(5):R174. [Medline]. [Full Text].

  22. Wong HR, Weiss SL, Giuliano JS Jr, Wainwright MS, Cvijanovich NZ, Thomas NJ, et al. Testing the prognostic accuracy of the updated pediatric sepsis biomarker risk model. PLoS One. 2014. 9(1):e86242. [Medline]. [Full Text].

  23. [Guideline] de Oliveira CF, de Oliveira DS, Gottschald AF, Moura JD, Costa GA, Ventura AC, 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 Jun. 34(6):1065-75. [Medline].

  24. Sankar J, Sankar MJ, Suresh CP, Dubey NK, Singh A. Early goal-directed therapy in pediatric septic shock: comparison of outcomes "with" and "without" intermittent superior venacaval oxygen saturation monitoring: a prospective cohort study*. Pediatr Crit Care Med. 2014 May. 15(4):e157-67. [Medline].

  25. Dias CR, Leite HP, Nogueira PC, Brunow de Carvalho W. Ionized hypocalcemia is an early event and is associated with organ dysfunction in children admitted to the intensive care unit. J Crit Care. 2013 Oct. 28(5):810-5. [Medline].

  26. Broner CW, Stidham GL, Westenkirchner DF, Watson DC. A prospective, randomized, double-blind comparison of calcium chloride and calcium gluconate therapies for hypocalcemia in critically ill children. J Pediatr. 1990 Dec. 117(6):986-9. [Medline].

  27. Meert KL, Donaldson A, Nadkarni V, Tieves KS, Schleien CL, Brilli RJ, et al. Multicenter cohort study of in-hospital pediatric cardiac arrest. Pediatr Crit Care Med. 2009 Sep. 10(5):544-53. [Medline]. [Full Text].

  28. Carcillo JA, Davis AL, Zaritsky A. Role of early fluid resuscitation in pediatric septic shock. JAMA. 1991 Sep 4. 266(9):1242-5. [Medline].

  29. Ranjit S, Kissoon N, Jayakumar I. Aggressive management of dengue shock syndrome may decrease mortality rate: a suggested protocol. Pediatr Crit Care Med. 2005 Jul. 6(4):412-9. [Medline].

  30. Oliveira CF, Nogueira de Sá FR, Oliveira DS, Gottschald AF, Moura JD, Shibata AR, et al. Time- and fluid-sensitive resuscitation for hemodynamic support of children in septic shock: barriers to the implementation of the American College of Critical Care Medicine/Pediatric Advanced Life Support Guidelines in a pediatric intensive care unit in a developing world. Pediatr Emerg Care. 2008 Dec. 24(12):810-5. [Medline].

  31. Voigt J, Waltzman M, Lottenberg L. Intraosseous vascular access for in-hospital emergency use: a systematic clinical review of the literature and analysis. Pediatr Emerg Care. 2012 Feb. 28(2):185-99. [Medline].

  32. Cole ET, Harvey G, Urbanski S, Foster G, Thabane L, Parker MJ. Rapid paediatric fluid resuscitation: a randomised controlled trial comparing the efficiency of two provider-endorsed manual paediatric fluid resuscitation techniques in a simulated setting. BMJ Open. 2014 Jul 3. 4(7):e005028. [Medline]. [Full Text].

  33. Maitland K, Kiguli S, Opoka RO, Engoru C, Olupot-Olupot P, Akech SO, et al. Mortality after fluid bolus in African children with severe infection. N Engl J Med. 2011 Jun 30. 364(26):2483-95. [Medline].

  34. Abulebda K, Cvijanovich NZ, Thomas NJ, Allen GL, Anas N, Bigham MT, et al. Post-ICU admission fluid balance and pediatric septic shock outcomes: a risk-stratified analysis. Crit Care Med. 2014 Feb. 42(2):397-403. [Medline]. [Full Text].

  35. Weiss SL, Fitzgerald JC, Balamuth F, Alpern ER, Lavelle J, Chilutti M, et al. Delayed antimicrobial therapy increases mortality and organ dysfunction duration in pediatric sepsis. Crit Care Med. 2014 Nov. 42(11):2409-17. [Medline]. [Full Text].

  36. [Guideline] Kleinman ME, Chameides L, Schexnayder SM, Samson RA, Hazinski MF, Atkins DL, et al. Pediatric advanced life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Pediatrics. 2010 Nov. 126(5):e1361-99. [Medline].

  37. Hanna W, Wong HR. Pediatric sepsis: challenges and adjunctive therapies. Crit Care Clin. 2013 Apr. 29(2):203-22. [Medline]. [Full Text].

  38. Alejandria MM, Lansang MA, Dans LF, Mantaring JB 3rd. Intravenous immunoglobulin for treating sepsis, severe sepsis and septic shock. Cochrane Database Syst Rev. 2013 Sep 16. 9:CD001090. [Medline].

  39. Kissoon N, Carcillo JA, Espinosa V, Argent A, Devictor D, Madden M, et al. World Federation of Pediatric Intensive Care and Critical Care Societies: Global Sepsis Initiative. Pediatr Crit Care Med. 2011 Sep. 12(5):494-503. [Medline].

  40. Zimmerman JJ, Williams MD. Adjunctive corticosteroid therapy in pediatric severe sepsis: observations from the RESOLVE study. Pediatr Crit Care Med. 2011 Jan. 12(1):2-8. [Medline].

  41. Atkinson SJ, Cvijanovich NZ, Thomas NJ, Allen GL, Anas N, Bigham MT, et al. Corticosteroids and pediatric septic shock outcomes: a risk stratified analysis. PLoS One. 2014. 9(11):e112702. [Medline]. [Full Text].

  42. Menon K, McNally D, Choong K, Sampson M. A systematic review and meta-analysis on the effect of steroids in pediatric shock. Pediatr Crit Care Med. 2013 Jun. 14(5):474-80. [Medline].

  43. Pizarro CF, Troster EJ, Damiani D, Carcillo JA. Absolute and relative adrenal insufficiency in children with septic shock. Crit Care Med. 2005 Apr. 33(4):855-9. [Medline].

  44. Schotola H, Toischer K, Popov AF, Renner A, Schmitto JD, Gummert J, et al. Mild metabolic acidosis impairs the ß-adrenergic response in isolated human failing myocardium. Crit Care. 2012 Aug 13. 16(4):R153. [Medline]. [Full Text].

  45. Mathieu D, Neviere R, Billard V, Fleyfel M, Wattel F. Effects of bicarbonate therapy on hemodynamics and tissue oxygenation in patients with lactic acidosis: a prospective, controlled clinical study. Crit Care Med. 1991 Nov. 19(11):1352-6. [Medline].

  46. Aschner JL, Poland RL. Sodium bicarbonate: basically useless therapy. Pediatrics. 2008 Oct. 122(4):831-5. [Medline].

  47. Paden ML, Rycus PT, Thiagarajan RR. Update and outcomes in extracorporeal life support. Semin Perinatol. 2014 Mar. 38(2):65-70. [Medline].

  48. DiCarlo JV, Dudley TE, Sherbotie JR, Kaplan BS, Costarino AT. Continuous arteriovenous hemofiltration/dialysis improves pulmonary gas exchange in children with multiple organ system failure. Crit Care Med. 1990 Aug. 18(8):822-6. [Medline].

  49. Foland JA, Fortenberry JD, Warshaw BL, Pettignano R, Merritt RK, Heard ML, et al. Fluid overload before continuous hemofiltration and survival in critically ill children: a retrospective analysis. Crit Care Med. 2004 Aug. 32(8):1771-6. [Medline].

  50. Vogt W, Laer S. Prevention for pediatric low cardiac output syndrome: results from the European survey EuLoCOS-Paed. Paediatr Anaesth. 2011 Dec. 21(12):1176-84. [Medline].

  51. Hoffman TM. Newer inotropes in pediatric heart failure. J Cardiovasc Pharmacol. 2011 Aug. 58(2):121-5. [Medline].

  52. Hoffman TM, Wernovsky G, Atz AM, Kulik TJ, Nelson DP, Chang AC, et al. Efficacy and safety of milrinone in preventing low cardiac output syndrome in infants and children after corrective surgery for congenital heart disease. Circulation. 2003 Feb 25. 107(7):996-1002. [Medline].

  53. Meyer S, Gortner L, Brown K, Abdul-Khaliq H. The role of milrinone in children with cardiovascular compromise: review of the literature. Wien Med Wochenschr. 2011 Apr. 161(7-8):184-91. [Medline].

  54. Bassler D, Kreutzer K, McNamara P, Kirpalani H. Milrinone for persistent pulmonary hypertension of the newborn. Cochrane Database Syst Rev. 2010 Nov 10. CD007802. [Medline].

 
Previous
Next
 
Chest radiograph in a patient with cardiomegaly, which may accompany cardiogenic shock.
Determinants of cardiac function and oxygen delivery to tissues. FiO2 = fraction of inspired oxygen. Adapted from Strange GR. APLS: The Pediatric Emergency Medicine Course. 3rd ed. Elk Grove Village, Ill: American Academy of Pediatrics; 1998:34.
Hemodynamic response to shock hemorrhage model (based on normal data). Adapted from Schwaitzberg SD, Bergman KS, Harris BH. A pediatric trauma model of continuous hemorrhage. J Pediatr Surg. Jul 1988;23(7):605-9.
Pediatric shock management algorithm. ACTH = adrenocorticotropic hormone; CI = cardiac index; ECMO = extracorporeal membrane oxygenation; MAP-CVP = mean arterial pressure-central venous pressure; PALS = Pediatric Advanced Life Support; PDE = phosphodiesterase; PICU = pediatric intensive care unit; SVC O2 = superior vena cava oxygen saturation.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.