Shock in Pediatrics Medication
- Author: Adam J Schwarz, MD; Chief Editor: Timothy E Corden, MD more...
Medication Summary
A variety of therapeutic treatments may be required for pediatric patients in shock. Possible therapies may include the following (see the image below):
- Inotropic medications - To enhance cardiac contractility
- Dextrose - To maintain glycogen stores
- Electrolytes and calcium stabilization - To decrease risk of arrhythmias
- Prostaglandin E1
- Corticosteroids
Definitions of shock include the following: Cold or warm shock: Decreased perfusion including decreased mental status, capillary refill more than 2 seconds (cold shock) or flash capillary refill (warm shock) and diminished (cold shock) or bounding (warm shock) peripheral pulses; mottled, cool extremities (cold shock) or decreased urine output less than 1mL/kg/h. Fluid-refractory, dopamine-resistant shock: Shock persists despite more than 60mL/kg fluid resuscitation in the first hour and dopamine infusion to 10mg/kg/min. Catecholamine-resistant shock: Shock persists despite use of catecholamines epinephrine or norepinephrine. Refractory shock: Shock persists despite goal-directed use of inotropic agents, vasopressors, vasodilators, and maintenance of metabolic (glucose and calcium) and hormonal (thyroid and hydrocortisone) homeostasis.
Inotropic agents
Class Summary
Inotropic agents increase myocardial contractility and have variable effects on peripheral vascular resistance. Some inotropic agents may be vasoconstrictors (eg, epinephrine, norepinephrine), whereas others are vasodilators (eg, dobutamine, milrinone).
Which inotropic agents are indicated and are effective in patients with any given etiology of shock depends on the clinical volume and contractile state of the patient's cardiovascular system. Indications for the use of such cardiotropic medications include cardiogenic shock that requires pharmacologic improvement of contractile function and decompensated shock refractory to volume expansion alone.
Dopamine
Dopamine is a naturally occurring endogenous catecholamine that stimulates beta1- and alpha1-adrenergic and dopaminergic receptors in a dose-dependent fashion. It stimulates the release of norepinephrine.
In low doses (2-5mcg/kg/min), dopamine acts on dopaminergic receptors in renal and splanchnic vascular beds, causing vasodilatation in these beds. In midrange doses (5-15mcg/kg/min), it acts on beta-adrenergic receptors to increase heart rate and contractility, improve cardiac output (CO), and enhance conduction (ie, increasing sinoatrial [SA] rate) in the heart. In high doses (15-20mcg/kg/min), it acts on alpha-adrenergic receptors to increase systemic vascular resistance and raise blood pressure.
After initiating therapy, increase the dose by 1-4mcg/kg/min every 10-30 minutes until an optimal response is obtained. More than 50% of patients are satisfactorily maintained on doses of less than 20mcg/kg/min.
Dobutamine
Dobutamine is a sympathomimetic amine with stronger beta than alpha effects. It is, therefore, almost a pure inotropic agent, with primarily beta1-agonist effects. It also provides some relatively weak beta2-mediated peripheral vasodilation that may reduce systemic vascular resistance and afterload and improve tissue perfusion. Therefore, dobutamine is an appropriate drug to provide to a patient with cardiogenic shock in order to help augment myocardial contractility. Dobutamine is less likely to precipitate ventricular dysrhythmias than epinephrine. A typical dose begins with 5mcg/kg/min IV and is gradually increased to 20mcg/kg/min IV.
Epinephrine (Adrenalin)
Epinephrine is used for hypotension refractory to dopamine. Its alpha-agonist effects include increased peripheral vascular resistance, reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. Its beta2-agonist effects include bronchodilation, chronotropic cardiac activity, and positive inotropic effects.
Norepinephrine (Levophed)
Norepinephrine is used for protracted hypotension following adequate fluid-volume replacement. This agent stimulates beta1- and alpha-adrenergic receptors, in this way increasing cardiac muscle contractility and heart rate, as well as vasoconstriction. As a result, systemic blood pressure and coronary blood flow increase. Once norepinephrine produces a therapeutic response, the dose should be adjusted and maintained at a low-normal blood pressure, such as 80-100mm Hg systolic, sufficient to perfuse vital organs.
Phosphodiesterase Enzyme Inhibitor
Class Summary
Inamrinone (formerly amrinone) and milrinone are phosphodiesterase inhibitors that work via a different mechanism than that of the catecholamines. They produce an increase in intracellular cyclic adenosine monophosphate (cAMP), which raises intracellular calcium levels, improving cardiac inotropy and peripheral vasodilation. They may be useful for the treatment of shock in patients who have adequate intravascular volume but who need increased cardiac contractility and better peripheral perfusion.
Phosphodiesterase inhibitors may be used together with catecholamines to further increase myocardial contractility while reducing systemic vascular resistance and afterload. They are often a useful adjunct after heart surgery in patients who have myocardial impairment. They may also be useful in improving perfusion in patients who remain in compensated shock with poor peripheral perfusion but a normal central blood pressure and adequate intravascular volume.
Typical doses of inamrinone in children are a loading dose of 0.75mg/kg IV over 2-3 minutes, followed by a continuous IV infusion of 5-10mcg/kg/min. Most pediatric dosing recommendations for milrinone are derived from adult data. Milrinone may be initiated with a loading dose of 25-50mcg/kg over 10 minutes, followed by a continuous IV infusion of 0.375-0.75mcg/kg/min. Many practitioners forgo the loading dose and begin a continuous infusion only.
Adverse effects of inamrinone and milrinone may include arrhythmias and thrombocytopenia.[33] Care must be taken when choosing to start phosphodiesterase inhibitors, because of their vasodilator effects and long half-life.
Inamrinone
Inamrinone is a phosphodiesterase inhibitor with positive inotropic and vasodilator activity. It produces vasodilation and increases the inotropic state. It is more likely than dobutamine to cause tachycardia and may exacerbate myocardial ischemia.
Milrinone
Milrinone is a positive inotrope and vasodilator with little chronotropic activity. It induces peripheral vasodilation and provides inotropic support. It is different in mode of action from either cardiac glycosides (digoxin) or catecholamines. Milrinone selectively inhibits phosphodiesterase type III (PDE III) in cardiac and smooth vascular muscle, resulting in reduced afterload, reduced preload, and increased inotropy.
Prostaglandins, Endocrine
Class Summary
Neonates who present with shock associated with a large liver, enlarged cardiac silhouette, or heart murmur may have obstructive shock that develops because of closing of the ductus arteriosus. Prior to closure, the ductus arteriosus allows sufficient systemic blood flow to bypass the obstructive lesion. In such patients in whom the ductus arteriosus has closed, initiation of prostaglandin E1 to maintain or reestablish its patency may be lifesaving.
The recommended dose is 0.05-0.1mcg/kg/min IV as a continuous infusion. Adverse effects may include fever, apnea, or hypotension due to vasodilation. Evaluation of cardiac anatomy with echocardiography, performed by a pediatric cardiologist, should be obtained as soon as possible.
Alprostadil IV (Prostin VR)
Alprostadil is identical to naturally occurring prostaglandin E1 and possesses various pharmacologic effects, including vasodilation and inhibition of platelet aggregation.
It is a first-line medication used as palliative therapy to temporarily maintain patency of the ductus arteriosus before surgery.
This agent is beneficial in infants with congenital defects that restrict pulmonary or systemic blood flow and in patients who depend on a patent ductus arteriosus for adequate oxygenation and lower body perfusion. It produces vasodilation and increases cardiac output. Each 1mL ampule contains 500mcg/mL.
Corticosteroid
Class Summary
The use of corticosteroids in shock is controversial. However, it is possible that patients in severe septic shock have inadequate levels of circulating glucocorticoids and may benefit from an infusion of corticosteroids.
Hydrocortisone (Solu-Cortef, Cortef)
Hydrocortisone is the corticosteroid of choice in shock because of its mineralocorticoid activity and glucocorticoid effects.
Fisher JD, Nelson DG, Beyersdorf H, Satkowiak LJ. Clinical spectrum of shock in the pediatric emergency department. Pediatr Emerg Care. Sep 2010;26(9):622-5. [Medline].
Tobin JR, Wetzel RC. Shock and multi-organ system failure. In: Rogers MC, ed. Textbook of Pediatric Intensive Care. Baltimore, Md: Lippincott, William & Wilkins; 1996:555-605.
.
Ackerman AD, Singhi S. Pediatric infectious diseases: 2009 update for the Rogers' Textbook of Pediatric Intensive Care. Pediatr Crit Care Med. Jan 2010;11(1):117-23. [Medline].
American Heart Association. Recognition of respiratory failure and shock. In: Chameides L, Hazinski MF, eds. Pediatric Advanced Life Support. Dallas, Tx: American Heart Association; 1997.
Saavedra JM, Harris GD, Li S, Finberg L. Capillary refilling (skin turgor) in the assessment of dehydration. Am J Dis Child. Mar 1991;145(3):296-8. [Medline].
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. Nov 2008;36(11):3030-7. [Medline].
Domico M, Liao P, Anas N, Mink RB. Elevation of brain natriuretic peptide levels in children with septic shock. Pediatr Crit Care Med. Sep 2008;9(5):478-83. [Medline].
Katz RW, Pollack MM, Weibley RE. Pulmonary artery catheterization in pediatric intensive care. Adv Pediatr. 1983;30:169-90. [Medline].
Pollack MM, Fields AI, Ruttimann UE. Distributions of cardiopulmonary variables in pediatric survivors and nonsurvivors of septic shock. Crit Care Med. Jun 1985;13(6):454-9. [Medline].
Sibbald WJ, Calvin J, Driedger AA. Right and left ventricular preload and diastolic ventricular compliance: implications for therapy in critically ill patients. In: Shoemaker WC, Thompson WL, eds. Critical Care-State of the Art. Fullerton, Calif: Society of Critical Care Medicine; 1982.
[Guideline] 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. Feb 2009;37(2):666-88. [Medline].
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. Jun 2008;34(6):1065-75. [Medline].
Ferrari M, Mottola L, Quaresima V. Principles, techniques, and limitations of near infrared spectroscopy. Can J Appl Physiol. Aug 2004;29(4):463-87. [Medline].
Adcock LM, Wafelman LS, Hegemier S, et al. Neonatal intensive care applications of near-infrared spectroscopy. Clin Perinatol. Dec 1999;26(4):893-903, ix. [Medline].
Ghanayem NS, Wernovsky G, Hoffman GM. Near-infrared spectroscopy as a hemodynamic monitor in critical illness. Pediatr Crit Care Med. Jul 2011;12(4 Suppl):S27-32. [Medline].
[Guideline] Dellinger RP, Levy MM, Carlet JM, et al. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: 2008. Intensive Care Med. Jan 2008;34(1):17-60. [Medline].
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. Feb 2012;28(2):185-99. [Medline].
Carcillo JA, Davis AL, Zaritsky A. Role of early fluid resuscitation in pediatric septic shock. JAMA. Sep 4 1991;266(9):1242-5. [Medline].
Maitland K, Kiguli S, Opoka RO, et al. Mortality after fluid bolus in African children with severe infection. N Engl J Med. Jun 30 2011;364(26):2483-95. [Medline].
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. Dec 1990;117(6):986-9. [Medline].
Cingolani HE, Mattiazzi AR, Blesa ES, Gonzalez NC. Contractility in isolated mammalian heart muscle after acid-base changes. Circ Res. Mar 1970;26(3):269-78. [Medline].
Pannier JL, Leusen I. Contraction characteristics of papillary muscle during changes in acid-base composition of the bathing-fluid. Arch Int Physiol Biochim. Sep 1968;76(4):624-34. [Medline].
Arieff AI. Indications for use of bicarbonate in patients with metabolic acidosis. Br J Anaesth. Aug 1991;67(2):165-77. [Medline].
Walley KR, Cooper J, Baile EM. Bicarbonate does not improve left ventricular contractility during resuscitation from hypovolemic shock in pigs. J Crit Care. 1992;7:14-21.
Mäkisalo HJ, Soini HO, Nordin AJ, Höckerstedt KA. Effects of bicarbonate therapy on tissue oxygenation during resuscitation of hemorrhagic shock. Crit Care Med. Nov 1989;17(11):1170-4. [Medline].
Cronin L, Cook DJ, Carlet J, et al. Corticosteroid treatment for sepsis: a critical appraisal and meta-analysis of the literature. Crit Care Med. Aug 1995;23(8):1430-9. [Medline].
Bollaert PE, Charpentier C, Levy B, Debouverie M, Audibert G, Larcan A. Reversal of late septic shock with supraphysiologic doses of hydrocortisone. Crit Care Med. Apr 1998;26(4):645-50. [Medline].
[Best Evidence] Pizarro CF, Troster EJ, Damiani D, Carcillo JA. Absolute and relative adrenal insufficiency in children with septic shock. Crit Care Med. Apr 2005;33(4):855-9. [Medline].
Carcillo JA, Fields AI. Clinical practice parameters for hemodynamic support of pediatric and neonatal patients in septic shock. Crit Care Med. Jun 2002;30(6):1365-78. [Medline].
McCune S, Short BL, Miller MK, Lotze A, Anderson KD. Extracorporeal membrane oxygenation therapy in neonates with septic shock. J Pediatr Surg. May 1990;25(5):479-82. [Medline].
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. Aug 1990;18(8):822-6. [Medline].
Ramamoorthy C, Anderson GD, Williams GD, Lynn AM. Pharmacokinetics and side effects of milrinone in infants and children after open heart surgery. Anesth Analg. Feb 1998;86(2):283-9. [Medline].
Print
