Shock is a general term used to describe the clinical condition that results from damage to any or all tissue and/or organs in the body. The physiological response to such damage, often stemming from loss of blood volume or other trauma, results in a cascade of events that can lead to multiple organ system failure and, in some cases, death. Acutely ill children are particularly vulnerable to shock because their small body size limits the amount of reserve they have, which may be insufficient to meet the physiological demands of the trauma or illness.
1. Hypovolemic shock
Hypovolemic shock generally results from diarrhea, vomiting, poor fluid intake, hemorrhage, heat stroke or burns. The leading cause of shock worldwide is hypovolemia—or loss of blood volume—due to diarrhea. Accordingly, hypovolemic shock is a major cause of infant mortality.
Clinical signs of hypovolemic shock include rapid breathing and or heart rate, abnormally low blood pressure, weak peripheral pulses, cool pale skin, increased urine output and changes in mental status.
2. Distributive shock
When blood volume is not adequately distributed to the necessary organs and tissues, distributive shock occurs. It is most commonly associated with sepsis, a severe allergic reaction and head or spinal injury.
Signs of distributive shock in children may be similar to hypovolemic shock. In a child with a higher cardiac output and low systemic vascular resistance (more specific to distributive shock), additional signs indicative of a "warm shock" may be seen, including low blood pressure (with a narrow pulse), bounding peripheral pulses, brisk capillary refill and warm, flushed extremities.
3. Cardiogenic shock
The inadequate tissue perfusion that characterizes cardiogenic shock is due to myocardial dysfunction. The dysfunction may be caused by heart disease or an arrhythmia; however, congenital heart disease is the most common cause of cardiogenic shock among children.
Signs of cardiogenic shock in children and infants may include those associated with hypovolemic shock, but additional signs will likely also be present specific to the cardiogenic effects. These signs include hepatomegaly (enlarged liver), increased respiratory effort, cyanosis (a blue coloration of the skin and mucous membranes due to a lack of oxygen), cardiac murmurs and gallop and precordial heave. In tertiary stages of emergency assessment, cardiomegaly (enlarged heart) may be seen on a chest x-ray, while cardiac hypertrophy (thickening of the heart muscle) may be indicated by an echocardiograph.
4. Obstructive shock
Physical obstructions to the blood flow result in obstructive shock. Specific congenital heart diseases are causes of obstructive shock that may be seen in neonates within the first few weeks of life. These conditions usually first present through cyanosis (a blue coloration of the skin and mucous membranes due to a lack of oxygen), followed later by shock if the physical obstruction is not corrected.
Stages of shock
Early or Compensated Shock
In early compensated shock several compensatory mechanism are activated. In the face of impending hypoperfusion, sympathetic nervous system stimulation increases heart rate and systemic vascular resistance (SVR) through the release of catecholamines from adrenal glands. Renin-angiotensin-aldosterone system is also activated, contributing to vasoconstriction, maintenance of SVR, and fluid retention through concentration of urine.
In children, vascular tone is maintained in low flow states (7) of septic and cardiogenic shock. Therefore, children can often maintain their blood pressure until they are in profound shock. Compensatory vasoconstriction is often so pronounced that systemic blood pressure can be maintained within the normal range despite significant circulatory compromise. Hypotension is typically a late finding among children in shock. With vasoconstriction, blood flow is shunted away from the non-vital organs (skin and splanchnic bed) to brain, heart, and lungs. As a result, extremities are cold and mottled, capillary refill is prolonged, catecholamine-induced tachycardia occurs. If shock is left untreated, the compensatory mechanisms will fail and uncompensated shock develops. Failure of normalization of peripheral pulses, skin temp, and capillary refill with treatment predicts death from shock. (6)
Children are mostly dependent on their heart rate to increase cardiac output. Ability to increase contractility in response to catecholamine stimulation is limited due to insufficient muscle mass and "stiffness" of the young myocardium compared to the adult heart. (8) When the compensatory mechanisms are activated children become dependent on intravascular volume (preload) to maintain CO. (9) Since afterload is already increased in an effort to maintain SVR and BP, maintaining adequate intravascular volume is the key aspect of successful resuscitation.
Uncompensated shock
When the compensatory mechanisms fail to meet the increased metabolic demands at the tissue level uncompensated shock with hypotension will develop. Tissue hypoxemia and ischemia will trigger anaerobic metabolism resulting in lactate build-up and the development of metabolic acidosis. A number of other vasoactive metabolites such as adenosine, nitric oxide are also released and accumulate locally. Compensatory vasoconstriction fails as a result of hypoxia. Capillary blood flow becomes sluggish, leukocytes marginate, microthrombi form. The vasomotor paralysis and microcirculatory dysfunction escalate into end-organ hypoperfusion, organ dysfunction, and multi-organ failure. Organ hypoperfusion manifests itself as early organ dysfunction with altered mental status, tachypnea, tachycardia, lethargy, decreased or absent urine output, and mottled extremities. Once the blood pressure falls, the patient will progress into irreversible shock if the perfusion pressure to tissues is not restored. Irreversible shock, as the name implies, is the point of no return when the mortality rate is high irrespective of interventions.
Types of Shock
Several types of shock syndrome can be recognized based on the etiology. Table 1 summarizes the types of shock seen in pediatric patients and below is a brief description of each type.
Hypovolemic shock
This is by far the most common type of shock seen in pediatric patients. Hypovolemia may be absolute with actual fluid losses (severe dehydration with gastrointestinal losses, renal losses in diabetes mellitus, etc) or frank loss of blood as in hemorrhagic shock. Nonhemorrhagic hypovolemic shock is the most common type seen in the developing world. Findings of dehydration are present on physical exam with dry mucous membranes, sunken eyes and fontanels, diminished skin turgor (table 1). (10) Table 2 summarizes the varying presentation of hemorrhagic shock in children based on blood loss.
Distributive Shock
Volume loss could also be relative - sometimes referred to as distributive shock seen in anaphylaxis or spinal shock. The mechanism involved here is not an absolute loss of intravascular volume but pathological and inappropriate vasodilatation, endothelial dysfunction with capillary leak, loss of vascular tone or a combination of these factors. Based on the underlying etiology intravascular fluid volume is "maldistributed" and signs of shock will appear. In septic and anaphylactic shock, intravascular fluid leaks into the interstitial space augmenting the hypovolemic state.
Septic shock
Sepsis remains a major cause of mortality and morbidity for children. Although mortality from pediatric sepsis and sepsis shock has decreased from over 95% in 1960s to nearly 10% in 1990s, data from a recent US survey suggests that more than 4,300 children die each year from severe sepsis and septic shock and the annual cost is approximately $ 2 billion. (11)
Definitions for pediatric systemic inflammatory response syndrome, sepsis, severe sepsis and septic shock were standardized at the international consensus conference in 2002. (12) Children have specific physiological changes that occur as part of normal growth and development. Normal values for vital signs and laboratory values are also age dependant. Accordingly, for the purposes of diagnosing sepsis syndromes, pediatric patients are divided into six different age groups (neonate, newborn, toddler, child and adolescent). According to the international consensus criteria systemic inflammatory response syndrome (SIRS) is defined as tachycardia or tachypnea with fever or high leukocyte count. Sepsis is defined as SIRS in the presence of suspected or proven infection; and severe sepsis is defined as sepsis with accompanying organ dysfunction. When cardiovascular failure occurs in the setting of severe sepsis then it is classified as septic shock. The consensus definition also provides specific criteria for diagnosis of organ dysfunction (respiratory, cardiovascular, hematologic, neurologic, renal, and hepatic). In adults the classic picture of septic shock is one of high cardiac output and low SVR (warm shock). (13,14) However pediatric vascular tone is maintained in septic shock (6,7,15) and sepsis-induced myocardial dysfunction is more common. Therefore, pediatric septic shock can occur as low CO/high SVR, high CO/low SVR, or low CO/low SVR. In fact, in one study where cardiac index was measured, the majority (80%) of septic shock cases had low cardiac index and only about 20% presented in the typical "warm shock" (bounding peripheral pulses and flash capillary refill). (7) This has important therapeutic implications as children have more myocardial dysfunction in the setting of septic shock compared to adults and might benefit from early inotropic support and even in some instances afterload reduction. In adults the ability to increase oxygen consumption as oxygen delivery is enhanced by clinical interventions is associated with better survival in septic shock. (16) No evidence in pediatrics exists that oxygen extraction decreases in septic shock. In children with septic or cardiogenic shock, the major determinant for oxygen consumption is oxygen delivery, not oxygen extraction (15); therefore, efforts should be aimed at improving CO and oxygen delivery.
Cardiogenic shock
This type of shock is simply a pump failure. Myocardial failure may be primary as in myocarditis, congenital heart disease or secondary as in myocardial dysfunction in the setting of toxins, ischemia. Early use of echocardiography should be considered. Judicious fluid administration might still be indicated as many patients might still be on the hypovolemic side with room on theirs Starling curve. However, the mainstay of treatment is pharmacological support of the failing myocardium. Extracorporeal therapies are increasingly being used as a bridge to transportation or to "rest" the myocardium to allow recovery.
Obstructive shock
This is the setting of circulatory deficiency where venous blood return to the heart (preload) is "obstructed" usually as a result of an intrathoracic catastrophe such as tension pneumothorax or cardiac tamponade.
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