Shock
Pankaj B. Agrawa
I. DEFINITION.
Shock is an acute, complex state of circulatory dysfunction resulting in insufficient oxygen and nutrient delivery to the tissues relative to their metabolic demand leading to cellular dysfunction that may eventually cause cell death. Initially, shock may be compensated with reduction in blood supply to the skin, muscle, and splanchnic vessels and adequate blood flow to the vital organs. This may be followed by an uncompensated phase when signs of poor perfusion are accompanied by hypotension. In premature neonates, extremely low systemic perfusion can occur with normal blood pressure (BP). Lowest acceptable normal BPs are not well established, particularly for premature infants. Recent studies indicate that a mean arterial pressure (MAP) <30 mm Hg in extremely low birth weight neonates is associated with reduced cerebral blood flow and lack of cerebral autoregulation, which, in turn, may lead to white matter injury and cerebral hemorrhage.
II. ETIOLOGY.
In the immediate postnatal period, abnormal regulation of peripheral vascular resistance with or without myocardial dysfunction is the most frequent cause of hypotension underlying shock, especially in preterm infants. Hypovolemia must also be considered as an underlying cause of shock in the setting of fluid loss (blood, plasma, excessive urine output, or transepidermal water losses).
Distributive shock secondary to:
Abnormal peripheral vasoregulation in neonates secondary to:
Increased or dysregulated endothelial nitric oxide (NO) production in the perinatal transitional period, particularly in the preterm neonate
Immature neurovascular pathways
Sepsis-related with release of proinflammatory cascades that lead to vasodilation
Rare causes include anaphylactic and neurogenic shock in neonates
Hypovolemic shock. Common scenarios of fluid loss in the neonatal period include the following:
Placental hemorrhage, as in abruptio placentae or placenta previa
Fetal-to-maternal hemorrhage (diagnosed by the Kleihauer-Betke test of the mother’s blood for fetal erythrocytes)
Twin-to-twin transfusion
Intracranial hemorrhage
Massive pulmonary hemorrhage (often associated with patent ductus arteriosus [PDA])
Disseminated intravascular coagulation (DIC) or other severe coagulopathies
Plasma loss into the extravascular compartment, as seen with low oncotic pressure states or capillary leak syndrome (e.g., sepsis)
Excessive extracellular fluid losses, as seen with volume depletion from excess insensible water loss or inappropriate diuresis, as commonly seen in extremely low birth weight infants
Cardiogenic shock due to myocardial dysfunction. Although an infant’s myocardium usually exhibits good contractility, various perinatal insults, congenital abnormalities, or arrhythmias can result in heart failure.
Intrapartum asphyxia can cause poor contractility and papillary muscle dysfunction with tricuspid regurgitation, resulting in low cardiac output.
Myocardial dysfunction can occur secondary to infectious agents (bacterial or viral) or metabolic abnormalities such as hypoglycemia. Cardiomyopathy can be seen in infants of diabetic mothers (IDMs) with or without hypoglycemia.
Obstructive shock. Obstruction to blood flow resulting in decreased cardiac output. Types of obstructions to blood flow include:
Inflow obstructions
Cardiac anomalies including total anomalous pulmonary venous return, cor triatriatum, tricuspid atresia, and mitral atresia
Acquired inflow obstructions can occur from intravascular air or thrombotic embolus, or from increased intrathoracic pressure caused by high airway pressures, pneumothorax, pneumomediastinum, or pneumopericardium.
Outflow obstructions
Cardiac anomalies including pulmonary stenosis or atresia, aortic stenosis or atresia, and coarctation of the aorta or interrupted aortic arch
Hypertrophic subaortic stenosis seen in IDMs with compromised left ventricular outflow
Arrhythmias, if prolonged
III. DIAGNOSIS
Clinical presentation. Clinical presentation is based on the compensatory mechanisms that are activated to maintain oxygen delivery to tissues. The shock is initially compensated when clinical findings are consistent with inadequate tissue perfusion but systolic BP is within normal range. Clinical findings during compensated shock include tachycardia to maintain cardiac output; increased systemic vascular resistance (SVR) presenting as cold, pale skin, delayed capillary refill, and weak peripheral pulses with narrow pulse pressure (raised diastolic BP); and increased splanchnic vascular resistance manifesting as oliguria and ileus.
The physiologic response of increased SVR is altered in septic shock with release of inflammatory mediators causing vasodilation and increased capillary permeability. In such cases, hypotension and wide pulse pressure are early indicators of shock.
When inadequate tissue perfusion is associated with systolic hypotension, the infant is noted to be in hypotensive shock. This indicates that physiologic attempts to maintain systolic BP and perfusion are no longer effective, and this may signal irreversible organ injury or impending cardiac arrest. As brain perfusion declines, the infant becomes lethargic. In preterm infants, the associated decrease in brain blood flow and oxygen supply during hypotension
predisposes to intraventricular/cerebral hemorrhages and periventricular leukomalacia with long-term neurodevelopmental abnormalities. In addition, in extremely low birth weight infants, the vasculature of the cerebral cortex may respond to transient myocardial dysfunction/shock with vasoconstriction rather than vasodilation, further diminishing cerebral perfusion and increasing the risk of neurologic injury.
