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Table 9-5 Systemic Inflammatory Response Syndrome

Distributive Shock

Distributive shock occurs in a state of inappropriate oxygen utilization associated with the systemic

inflammatory response syndrome (SIRS). Classically, SIRS is triggered by sepsis, but SIRS is associated

with other immune processes including trauma, pancreatitis, and other types of tissue injuries.

However, other types of distributive disturbances can occur unrelated to inflammation that may be

directly due to loss of vascular tone from spinal cord injury, endocrine dysfunction, or anaphylaxis.

Septic Shock

5 Septic shock is defined as a SIRS response to infection in conjunction with arterial hypotension,

despite adequate fluid resuscitation.32 It occurs when bacterial products interact with cells of the

immune system, leading to elaboration of mediators that cause circulatory disturbances and direct and

indirect cell damage leading to the clinical manifestations of SIRS (Table 9-5).33 Hemodynamic changes

are defined as early (warm or hyperdynamic) or late (cold or hypodynamic). These stages are primarily

characterized by the degree of ventricular contractility and peripheral vasomotor impairment present,

but can be misclassified if not appropriately evaluated. Early septic shock is distinguished by peripheral

vasodilation, flushed and warm extremities, and a compensatory elevation in cardiac output. Although

an increase in venous capacitance diminishes venous return to the heart, cardiac output is maintained

via tachycardia and the decrease in afterload due to systemic vasodilation.

Late septic shock is characterized by impaired myocardial contractility due to local and systemic

release of cardiac depressants, worsening peripheral perfusion, vasoconstriction, extremity mottling,

oliguria, and hypotension. Peripheral oxygen utilization may be severely impaired by bacterial toxins,

such as lipopolysaccharide (LPS) and the inflammatory products of the host’s own immune response,

resulting in metabolic dysfunction and acidosis despite a high systemic oxygen delivery. This

inappropriate oxygen utilization and systemic shunting lead not only to confusion regarding the

adequacy of resuscitation but also to progressive cell death. Together, both systemic hypoperfusion and

the altered tissue metabolism create a vicious cycle that propagates the inflammatory response initiated

in reaction to the initial infectious challenge leading to progressive cellular injury.

Due to both volume deficits and cardiovascular dysfunction, persistent perfusion deficits are common

and contribute significantly to multiple organ failure and mortality. In fact, the fluid volume required

for treatment may exceed that required for treatment of other forms of shock due to persistent

microvascular endothelial capillary leak. As a result of this profound leak, interstitial and total-body

fluid balances become extreme, leading to the potential development of marked hypoxia and the

abdominal compartment syndrome (ACS).

Although appropriate early resuscitation and cardiovascular support are essential to the treatment of

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septic shock, as important are early infection source control and appropriate administration of

antimicrobials. In fact, numerous investigators have demonstrated that even a few hours delay in

initiation of antimicrobial therapy is associated with a significant increase in mortality.34

Traumatic Shock

The major contributor to shock after injury is hypovolemia due to hemorrhage. Even when hemorrhage

ceases or is controlled, patients can continue to suffer loss of plasma volume into the interstitium of

injured tissues and develop progressive hypovolemic shock. In addition, tissue injury evokes a broader

pathophysiologic immunoinflammatory response and a potentially more devastating degree of shock

than that produced by hypovolemia alone.

The degree to which direct tissue injury and an inflammatory response participate in the development

and progression of traumatic shock distinguishes it from purely hypovolemic shock. Thus, traumatic

shock results from direct tissue or bony injury, resulting in not only hypovolemia caused by fluid and

blood loss but also an immunologic and neuroendocrine response to tissue destruction and

devitalization. This combined insult complicates what might otherwise be straightforward hemorrhagic

shock by inducing a systemic response that utilizes many of the inflammatory mediators present in

septic shock.35 These mediators propagate and intensify the effects of the initial hypovolemia and make

subsequent multiple organ failure far more likely than occurs with hypovolemic shock alone.

Although this condition can lead to increased fluid requirements, common problems associated with

this condition such as rhabdomyolysis should be aggressively evaluated and treated with optimal

resuscitation.36 In addition, common patient characteristics are known to alter traumatic shock

resuscitation, in particular, morbid obesity that can result in delayed correction of metabolic acidosis

and increased risk for organ dysfunction.37

Thus, initial management of the seriously injured requires the assurance of an airway, breathing, and

circulation; later management requires appropriate volume resuscitation and control of ongoing losses.

Control of hemorrhage is a major concern and demands priority over attention to other injuries. After

resuscitation and control of volume losses, efforts become necessary to minimize the potentially lethal

postshock sequelae, including acute respiratory distress syndrome (ARDS) and multiple organ

dysfunction syndrome (MODS).

Neurogenic Shock

Neurogenic shock is defined as failure of the nervous system to provide effective peripheral vascular

resistance, resulting in inadequate end-organ perfusion. Warm, flushed, flaccid extremities; paraplegia;

confusion; oliguria; and hypotension are the classic clinical findings. Injury to the proximal spinal cord,

with interruption of the autonomic sympathetic vasomotor pathways, disrupts basal vasoconstrictor

tone to peripheral veins and arterioles. Profound vasodilation of all microvascular beds below the level

of cord injury diminishes venous return to the heart, reduces cardiac output, and precipitates

hypotension. Injuries at or above the fourth thoracic vertebrae may disrupt sympathetic enervation to

the heart, resulting in significant bradycardia and severe decompensation.

Similar to the initial therapy for shock resulting from hypovolemia, treatment of the relative

hypovolemia due to vasodilation of neurogenic shock requires intravenous volume resuscitation.

Restoration of the pathologically expanded intravascular space improves preload and cardiac output and

may reverse hypotension. However, maintenance of adequate hemodynamics often requires vasopressor

support in an effort to avoid the administration of excessive fluids. CVP monitoring to assess cardiac

preload should be considered as a means of determining adequate and nonexcessive filling pressures, as

loss of vasomotor capacity within the pulmonary circulation predisposes these patients to pulmonary

edema. As spinal cord injury is often associated with other traumatic injuries, the diagnosis of isolated

neurogenic shock must be a process of exclusion.

This condition should not be confused with spinal shock. Spinal shock is defined as a loss of sensation

accompanied by motor paralysis with initial loss but gradual recovery of spinal reflexes following spinal

cord injury. The reflexes caudal to the spinal cord injury are hyporeflexic or absent, while those rostral

are unaffected. No circulatory compromise is associated with this condition; thus, it should not be

considered a shock state.

Hypoadrenal Shock

The role of adrenocortical hormones in providing resistance to shock is well recognized. The reduction

in effective blood volume and changes in blood chemistry that occur after adrenalectomy are similar to

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those of shock and hemorrhage. Adrenalectomized animals have markedly diminished tolerance to both

trauma and hypovolemia. Adrenal cortical hormones also play a key role in maintaining normal

capillary tone and permeability. In recent years, the concept of functional or relative adrenal

insufficiency has received increasing attention as a cause of unrecognized shock and hypoperfusion.

Most critically ill patients have elevated cortisol levels, but some have low concentrations in relation to

the degree of stress imposed by their disease. Administration of physiologic doses of steroids to correct

this insufficiency may result in stabilization of hemodynamics and possible survival benefits.38

However, the concept of routine administration of physiologic doses of steroids has been questioned;

thus, routine and indiscriminate use is not recommended.39

Diagnosis of hypoadrenal shock is difficult, as classic signs of Addison disease are absent. The only

clinical clues may be unexplained hypotension and refractory response to high-dose vasopressors. An

isolated serum cortisol level is difficult to interpret because the range of values observed in critically ill

patients varies considerably. A cortisol level below 15 μg/dL suggests a high likelihood of adrenal

insufficiency, whereas a value above 35 μg/dL suggests adequate adrenal function.40 The

adrenocorticotropic hormone (ACTH) stimulation test may be used to identify hypoadrenal patients

when the diagnosis is unclear, but the utility of this test, particularly with an elevated baseline value, is

of questionable utility.

The utility of the ACTH stimulation test is especially questionable in patients with persistent evidence

of shock and elevated baseline levels of cortisol above 35 μg/dL. These patients actually demonstrate

evidence of inadequate systemic cortisol utilization with a significant risk of morality, and thus may

actually benefit from systemic administration of physiologic concentrations of corticosteroids.41

Although hypoadrenal shock may complicate various types of shock, there is conflicting evidence to

support the use of supplemental corticosteroids in patients with septic shock if there is biochemical

evidence of hypoadrenalism. Thus, supplemental corticosteroids should be used with extreme caution

until further evidence is available.32,41

Physiologic Response to Hypovolemia

Common to each shock state is usually an initial decrease in circulating intravascular volume. This

reduction is due directly to fluid loss or secondarily to fluid redistribution. This reduction in circulating

fluid volume initiates both a rapid and sustained compensatory response. Within minutes, a rapid

compensatory response occurs primarily due to adrenergic output. Sustained responses, in contrast,

occur slower and result in intravascular fluid reabsorption and renal conservation of water and

electrolytes (Algorithm 9-1).

Rapid Response

Hypovolemia results in the initial secretion of epinephrine and norepinephrine from the adrenal gland

due to decreased afferent impulses from arterial baroreceptors. Catecholamine release is acute and

limited to the first 24 hours following the onset of hypovolemia. This results in vasoconstriction,

tachycardia, and increased myocardial contractility. Adrenergic-induced vasoconstriction of the systemic

capacitance of small veins and venules shifts blood back to the central venous circulation, thus

increasing right-sided filling pressures. Left-sided filling and pressure are augmented by pulmonary

vasoconstriction. Concomitantly, vasoconstriction occurs in the skin, kidneys, and viscera, effectively

shunting blood to the heart and brain. Adrenergic-induced vasoconstriction increases cardiac filling and

causes increased contractility and reflex tachycardia, all of which combine to increase stroke volume

and cardiac output.

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