Published on 06/06/2015 by admin
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Last modified 06/06/2015
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2 Shock
Kari R. Posner, Aaron Donoghue
Shock is an acute clinical syndrome of circulatory dysfunction in which there is failure to deliver sufficient oxygen and substrate to meet metabolic demand. All practitioners who care for children must understand and identify shock promptly to initiate an effective treatment plan. This, in turn, can help prevent the progression and poor outcomes that characterize the natural clinical course of shock. The goal is to prevent end-organ damage; failure of multiple organ systems; and, ultimately, death.
Normal circulatory function is maintained by the interplay between the heart and blood flow with the purpose of delivering oxygen and nutrients to the tissues. Cardiac output is calculated by multiplying the stroke volume (volume of blood ejected by the left ventricle in a single beat) by the heart rate (ejection cycles per minute). Stroke volume is dependent on the filling volume of the ventricle (preload), resistance against which the heart is pumping blood (afterload), and myocardial contractility. During childhood, the heart rate is faster, and the stroke volume is smaller than during adulthood. In children, increasing the heart rate is the primary means to increase the cardiac output.
Shock develops as the result of conditions that cause decreased intravascular volume, abnormal distribution of intravascular volume, or impaired cardiovascular function. Children effectively compensate for circulatory insufficiency by increasing their heart rate, systemic vascular resistance (SVR), and venous tone. Children can therefore maintain normal blood pressures despite significantly compromised tissue perfusion. Thus, in pediatric patients, it is especially important to recognize that hypotension is not part of the definition of shock.
The clinical manifestations of shock can be directly related to the abnormalities seen on the tissue, cellular, and biochemical levels. Microcirculatory dysfunction; tissue ischemia; and release of biochemical, vasoactive, and inflammatory mediators are all part of the spectrum of pathophysiologic aberrations seen in shock. Poor perfusion of vital organs results in impaired function. For example, inadequate perfusion of the brain and kidneys results in depressed mental status and decreased urine output, respectively. As poorly perfused cells switch to anaerobic metabolism to generate energy, lactic acid accumulates resulting in a metabolic acidosis that further interferes with cell function. Hypoperfusion also initiates inflammatory events, such as the activation of neutrophils and release of cytokines, that cause cell damage and microischemia.
The prevalence of causes of shock varies by patient age, as well as region of the world. Hypovolemic shock from diarrheal illness is the leading cause of pediatric mortality worldwide, but is very rare in the United States. Congenital lesions (including heart disease) and complications of prematurity are most common in neonates and infants. Malignant neoplasms (for whom infectious complications are prevalent), infectious causes, and unintentional injuries are more common in older children and young adolescents. Injury, homicide, and suicide become more prevalent in older adolescents.
In compensated shock, homeostatic mechanisms have temporarily balanced metabolic supply and demand. In this state, the systolic blood pressure is normal in the presence of inadequate tissue perfusion. The earliest symptoms of shock result from an effort to maintain cardiac output and perfusion of vital organs (heart, brain, and kidneys). The body’s initial mechanism to maintain cardiac output and compensate for low stroke volume is to increase heart rate (tachycardia). Other compensatory mechanisms include increasing SVR, cardiac contractility, and venous tone. As shock continues, the early compensatory mechanisms fail to meet the metabolic demands of the tissues, and uncompensated shock ensues. Here, as the microcirculation is affected, the child shows signs of brain, kidney, and cardiovascular compromise.
Uncompensated shock occurs when attempts to maintain blood pressure and perfusion are no longer successful, resulting in hypotension. When hypotension develops, the child’s condition may deteriorate rapidly to cardiovascular collapse and subsequent cardiac arrest. Eventually, the child in uncompensated shock develops multiple organ dysfunction syndrome (MODS) secondary to ongoing shock and exaggerated inflammatory responses. Irreversible shock implies irreversible damage to vital organs resulting in death, regardless of therapy.
The most common type of shock in children is hypovolemic shock. Hypovolemia is defined as a decrease in circulating blood volume. The most common cause of hypovolemic shock is fluid loss associated with diarrhea and vomiting. Other causes include blood losses (e.g., trauma and gastrointestinal disorders), plasma losses (peritonitis, hypoproteinemia, burns), and water losses (osmotic diuresis, heatstroke). In hypovolemic shock, preload is decreased, SVR may be increased as a compensatory mechanism, and cardiac contractility is typically normal or may be increased.
Distributive shock is the result of abnormal distribution of blood volume (i.e., poor flow to the splanchnic circulation with excessive flow to the skin) caused by vasodilatation from changes in vasomotor tone and peripheral pooling of blood, resulting in inadequate tissue perfusion. SVR can be low, producing increased blood flow to the skin that keeps the extremities warm (warm shock), as well as a widened pulse pressure and bounding peripheral pulses. Conversely, SVR may be increased, resulting in decreased blood flow to the skin, resulting in cool extremities, with a narrowed pulse pressure and weak pulses (cold shock). Generally, cardiac output is normal or increased. Distributive shock commonly occurs in anaphylaxis; central nervous system or spinal injuries; drug ingestions; and most commonly in children, sepsis.
Cardiogenic shock results from myocardial dysfunction and can usually be distinguished from other forms of shock because of associated signs of congestive heart failure (i.e., rales, gallop rhythm, hepatomegaly, jugular venous distension). Pump failure, arrhythmias, and congenital heart disease may all contribute to the inadequate perfusion seen in cardiogenic shock. A patient may exhibit tachycardia, increased SVR, and signs of decreased cardiac output as a result of a decrease in myocardial contractility. Causes of cardiogenic shock in children include viral myocarditis, arrhythmias, drug ingestions, complications of cardiac surgery, trauma, metabolic derangements, and congenital heart disease. Cardiogenic shock can also occur with obstruction of blood flow, as seen with a tension pneumothorax, massive pulmonary embolism, or critical coarctation of the aorta or other obstructive vascular lesions. A patient may also show evidence of both intrinsic cardiac disease and obstruction of blood flow with a cardiac tamponade or ductal-dependent congenital abnormality. It is important to recognize that infants that present with shock caused by a ductal-dependent cardiac lesion require blood flow through the ductus arteriosus to maintain adequate oxygen delivery.
Neurogenic shock may occur in the setting of pediatric trauma. Spinal cord injury may produce hypotension caused by a loss of sympathetic tone. The classic picture of neurogenic shock is hypotension without tachycardia or cutaneous vasoconstriction. The pulse pressure is usually widened. Patients sustaining spinal injuries often have concurrent torso trauma. Therefore, patients with known or suspected neurogenic shock should be treated initially for hypovolemia.
Sepsis is defined as the presence of the systemic inflammatory response syndrome (SIRS) caused by a presumed or confirmed infection (Box 2-1
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