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Pediatric Shock REVIEW Pediatric shock Usha Sethuraman† & Pediatric shock accounts for significant mortality and morbidity worldwide, but remains Nirmala Bhaya incompletely understood in many ways, even today. Despite varied etiologies, the end result †Author for correspondence of pediatric shock is a state of energy failure and inadequate supply to meet the metabolic Children’s Hospital of Michigan, Division of demands of the body. Although the mortality rate of septic shock is decreasing, the severity Emergency Medicine, is on the rise. Changing epidemiology due to effective eradication programs has brought in Carman and Ann Adams new microorganisms. In the past, adult criteria had been used for the diagnosis and Department of Pediatrics, 3901 Beaubien Boulevard, management of septic shock in pediatrics. These have been modified in recent times to suit Detroit, MI 48201, USA the pediatric and neonatal population. In this article we review the pathophysiology, Tel.: +1 313 745 5260 epidemiology and recent guidelines in the management of pediatric shock. Fax: +1 313 993 7166 [email protected] Shock is an acute syndrome in which the circu- to generate ATP. It is postulated that in the face of latory system is unable to provide adequate oxy- prolonged systemic inflammatory insult, overpro- gen and nutrients to meet the metabolic duction of cytokines, nitric oxide and other medi- demands of vital organs [1]. Due to the inade- ators, and in the face of hypoxia and tissue quate ATP production to support function, the hypoperfusion, the body responds by turning off cell reverts to anaerobic metabolism, causing the most energy-consuming biophysiological acute energy failure [2]. This energy failure process, namely the mitochondria [3]. results in the cell being unable to maintain In the initial stages of anemic and ischemic homeostasis, the disruption of ionic pumps, shock, compensation occurs by tachycardia, accumulation of intracellular sodium, efflux of tachypnea and peripheral vasoconstriction, potassium, accumulation of cytosolic calcium which maintains flow to the vital organs. How- and eventual cell death. Widespread cell death ever, when the shock state persists, hypotension results in multi-organ dysfunction. occurs, and the shock becomes a decompensated one. In children, this occurs much later in the Pathophysiology course. Anion gap acidosis occurs in the later Shock can result from lack of oxygen delivery, a stages due to reversion to anaerobic metabolism lack of glucose delivery or mitochondrial dys- and conversion of pyruvate to lactate. An anion function [2]. DO2 is the amount of oxygen deliv- gap of greater than 16 mEq/l is a surrogate ered to the tissues per minute, and is dependent marker of ischemic shock [2]. on the amount of blood pumped by the heart Shock due to impaired glucose delivery presents per minute (cardiac output [CO]) and the as anion gap acidosis, and presence of hypo- oxygen content of that blood (CaO2), that is: glycemia, euglycemia or hyperglycemia. In this case, the acidosis is due to the organic acids that DO = CO× CaO 2 2 are produced during catabolism of fat and protein Oxygen content is measured by the following as a result of the lack of glucose substrate [2]. formula: Thus, clinical findings of shock are directly CaO2 = 1.36 (% hemoglobin) (% oxygen saturation) related to the abnormalities seen at the tissue, cel- + 0.003 (PaO ) lular and biochemical levels [1]. All types of shock 2 have underlying maldistribution of capillary Keywords: cardiogenic, distributive, early Thus, oxygen delivery can be impaired by ane- blood flow. Local sympathetic activity and circu- goal-directed therapy, mia (low hemoglobin), hypoxia (decreased oxygen lating vasoactive and inflammatory mediators hypovolemic, infection, saturation) or ischemia (decreased CO). Glucose cause smooth muscle contraction in the precapil- multiple-organ dysfunction, pediatric, sepsis, septic, shock, delivery can be impaired during states of hypogly- lary sphincters and arterioles. Such mediators are SIRS cemia or insulin resistance. Mitochondrial dys- released by the host in response to endotoxins function results from the cellular hypoxia [2]. It is and cell injury. Mechanical obstruction of the part of well known that mitochondria consume more capillaries occurs due to blockage by debris that than 90% of the total body oxygen consumption forms due to a fall in hydrostatic pressures, 10.2217/14750708.5.4.405 © 2008 Future Medicine Ltd ISSN 1475-0708 Therapy (2008) 5(4), 405–423 405 REVIEW – Sethuraman & Bhaya making it difficult for leukocytes to squeeze is no tricuspid valve stenosis) and can be easily through the microvessels. Activation of the com- assessed clinically. Similarly, in the absence of plement system causes further aggregation of mitral valve disease, the pulmonary artery platelets and granulocytes and damage to the wedge pressure reflects the LVEDP. It is often endothelium. not possible to evaluate the LVEDP by clinical The damaged endothelium promotes pro- assessment alone. coagulant activity, while superoxide radicals, Compliance is the change in ventricular vol- metabolites of cells and cytokines of macrophages ume for a given change in pressure [4]. Thus, that the body produces to kill bacteria, add to the administration of fluids to a patient with a com- damage. The end result of all this is tissue pliant ventricle may increase the stroke volume, ischemia, which is common to all types of shock. while producing a minimal change in VEDP. This ischemia results in decreased ATP pro- Conversely, in a stiff ventricle, administration of duction (2 M of ATP per 1 M of glucose instead even a small amount of fluid can cause a signifi- of the normal 38 M of ATP) and reversion to cant increase in VEDP, and hence judicious use anaerobic metabolism. Glycogen stores are fur- of fluids with close monitoring is important [4]. ther depleted by the anaerobic metabolism, caus- Cardiac output is also defined by the follow- ing accumulation of lactate. Sodium and water ing equation, where MAP is the mean arterial enter the cell, resulting in cellular swelling and pressure, CVP is the central venous pressure and clinically apparent edema. SVR is the systemic venous resistance: With prolonged states of low flow, thrombosis CO = MAP– CVP/SVR and hypofibrinolysis occur due to activation of the endothelium by systemic inflammation This equation guides clinical management. mediators [2]. The activated endothelium causes During fluid resuscitation, the increase in MAP consumption of both procoagulant and anti- must be more than the increase in CVP, or the coagulant proteins, thus explaining the presence perfusion pressure would be reduced [2]. Hence, of both bleeding and thrombosis in patients with at this point, vasopressors would be indicated severe shock. Prompt resuscitation with fluids, rather than fluids [2]. ionotropes and vasodilators reverses and prevents It is also important to note that CO can fall if disseminated intravascular coagulation [2]. the SVR increases, even in the presence of nor- mal MAP – CVP. Perfusion pressure is main- Cardiovascular physiology tained, even in the presence of low CO states, by Cardiac output is the volume of blood ejected by increased SVR [2]. Hence, patients with a poor the heart per minute, and is a product of heart CO can have a normal blood pressure, as the sys- rate and stroke volume. In childhood, the heart temic vascular tone is high. These patients may rate is higher and the stroke volume is smaller benefit from the addition of vasodilators and than in adults. The stroke volume can be altered inotropes [2]. by conditions that affect ventricular preload, Ventricular contractility is the speed and compliance, contractility and afterload [4]. force of ventricular contraction. With improved Ventricular preload is the presystolic stretch contractility, the speed of ejection improves, of ventricular fibers, which, according to the thus increasing the time for refill of the ventri- Frank–Starling Law of the Heart, has a linear cles, and hence increasing the stroke volume. relationship with the tension generated by myo- The contractility is best evaluated by an cardial fibers (Figure 1) [4]. As the fiber length echocardiographic evaluation of the left ven- increases, the tension generated by the myo- tricular shortening fraction (LVSP). The normal cardial fibers, and hence the stroke volume, LVSP is approximately 28–44%, and a reduced increase up to a point. LVSP is associated with reduced contractility. Since the length of the myocardial fiber can- Other measures of the contractility include the not be measured clinically, right or left ventricu- ejection fraction and the rate of peak ventricular lar end-diastolic pressure (VEDP) is measured pressure development [4]. Patients with inade- to help evaluate the ventricular preload. Increas- quate stroke volume despite adequate volume ing the VEDP causes increased stroke volume loading have reduced contractility and have a and CO. However, at one point, when the ven- flat curve on the Frank–Starling curve [2]. Treat- tricle is overfilled, the stroke volume falls again. ment with inotropes, vasodilators and volume in Central venous pressure (CVP) or right atrial these patients moves the curve upwards and to pressure is equal to the RVEDP (provided there the left. 406 Therapy (2008) 5(4) futurefuture sciencescience groupgroup Pediatric shock – REVIEW Figure 1. Frank–Starling curve. shock is likely to show cardiac dysfunction, poor intravascular volume and maldistribution
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