Shock is associated with a number of specific changes in organs, including acute tubular necrosis, acute respiratory distress syndrome, liver failure, depression of host defense mechanisms, and heart failure.

The Heart:

Grossly, the heart shows petechial hemorrhages of the epicardium, particularly on the posterior aspect, and of the endocardium, especially the left outflow tract.

Microscopically, there are necrotic foci in the myocardium, ranging from the loss of single fibers to large areas of necrosis.

The affected fibers stain a deep red with eosin and the nuclei become pyknotic.

Prominent contraction bands, although visible by light microscopy, are better seen by electron microscopy.

Ultrastructurally, flattened areas of the intercalated disk are a sign of cell swelling, and invagination of adjacent cells is considered a catecholamine-induced lesion.

The Kidney:

Acute renal failure has been divided into three phases:

- the initiation phase, from the onset of injury to the beginning of renal failure;

- the maintenance phase, from the onset of renal failure to a stable, reduced renal function; and

- the recovery phase. In survivors, the recovery phase begins about 10 days after an episode of severe systemic shock and lasts up to 8 weeks.

During acute renal failure, the kidney is large, swollen, and congested, although the cortex may be pale.

Cross section reveals blood pooling in the outer strip of the medulla.

Microscopically, fully developed acute tubular necrosis is manifested by dilatation of the proximal tubules and focal necrosis of cells.

Frequently, pigmented casts in the tubular lumina indicate leakage of hemoglobin or myoglobin.

Coarse, "ropy" casts are seen in the distal nephron and distal convoluted tubules.

Interstitial edema is prominent in the cortex and mononuclear cells accumulate within the tubules and surrounding interstitium.

Renal blood flow is restricted to one-third of normal following the acute ischemic phase, an effect that is even more severe in the outer cortex.

The constriction of arterioles reduces the filtration pressure, thus reducing the amount of filtrate and contributing to oliguria.

Interstitial edema occurs, possibly through process termed "backflow".

Excessive vasoconstriction is thought to be related to stimulation of the renin-angiotensin system.

The Lung:

Following the onset of severe and prolonged shock, injury to the alveolar wall results in focal or generalized interstitial pneumonitis (shock lung).

The sequence of changes is mediated by acute inflammatory cells and includes interstitial edema, necrosis of endothelial cells, microthrombi, and necrosis of the alveolar epithelium.

Grossly, the lung is firm and congested. Frothy fluid exudes from the cut surface. Interstitial edema is first seen around peribronchial connective tissue and lymphatics, subsequently filling the inter-alveolar connective tissue.

In this initial period a large fluid volume drains into the pulmonary lymphatics.

If removal of this fluid becomes insufficient, or if the balance of forces that keep the fluid in the interstitial space is disturbed, alveolar edema develops.

Edema of the lung is initiated by the loosening of intercellular junctions between the pulmonary capillary endothelial cells, a reaction that occurs at different speeds in different types of shock.

It occurs within 2 to 3 minutes following endotoxemia and can be traced to the activation of complement and production of C5, a substance that is chemotactic for polymorphonuclear leukocytes.

The significance of leukocyte trapping in the terminal vascular bed is not fully understood.

Possibly the release of lysosomal enzymes or activated oxygen species from neutrophils mediates endothelial injury.

A reversible accumulation of platelets in the terminal vascular bed is characteristic of both hemorrhagic and endotoxin shock.

Shock-induced lung injury leads to the appearance of hyaline membranes in the alveoli, which are frequently expelled into the alveolar ducts and terminal bronchioles.

These lung changes may heal entirely, but in half of the patients the repair processes progress and cause a thickening of the alveolar wall.

Type II pneumocytes proliferate and form a picket line of alveolar lining cells, interfering with gas exchange.

Fibrous tissue proliferation also leads to organization of the alveolar exudates.

The Intestines:

Injury to the gastrointestinal tract is one of the more serious consequence of shock, leading to pancreatitis, duodenitis, and duodenal ulcer and rupture of esophagus.

Insufficiency of the microcirculation has been thought to be the main cause of intestinal malfunction.

The microvasculature shows thrombosis and increased fibrinolysis, processes that lead to interruption of the vessels and diffuse gastric hemorrhage.

The high alpha adrenergic receptor activity in shock induces pronounced vasoconstriction and causes mucosal necrosis of varying degrees.

The mucosal surface of the ascending colon is frequently the target of milder degrees of ischemia.

Interruption of the barrier function of the intestine may be related to the development of septicemia.

More severe necrotizing lesions are responsible for the deterioration in the final phase of shock.

The Liver:

In patients who die in shock, the liver is heavy and enlarged and has a mottled cut surface that reflects marked centrilobular pooling of blood.

The most prominent histologic lesion is centrilobular zonal necrosis, although it is not clear how important it is clinically.

The cells in the centre of the lobule are the most distant from the blood supply that comes from the portal tracts and are, therefore, presumably more vulnerable to circulatory disturbances.

Hypoxia of the liver leads to the development of cytoplasmic vacuoles, which represent dilated cisternae of the endoplasmic reticulum.

An increase in intracellular fat is consistently noted in individuals who have survived shock for sometime - 2 to 24 hours, for example.

Evidence of disturbed microcirculation is best seen in the pooling of blood in the centrilobular region close to the central vein, although in severe cases the midzonal region is also involved.

However, the liver shows little indication of fibrin deposits, platelet aggregates, or microthrombi.

If the patient survives the shock for some time, large autophagic vacuoles develop.

Kupffer cells are prominent and are packed with cellular debris.

Exocrine Pancreas:

The splanchnic vascular bed, which supplies the exocrine pancreas, is particularly affected by impaired circulation during shock.

The resulting ischemic damage to the pancreas unleashes activated catalytic enzymes from exocrine pancreas and causes acute pancreatitis, a complication that further promotes shock.

Host Defenses:

The alteration of the immunologic system and the host defenses in shock is not well defined, although clinically it is common that patients who survive the acute phase succumb to subsequent overwhelming infection.

It may well be that several factors interact, namely ischemic colitis, tissue trauma, suppression of the immune system, and metabolic suppression of host defenses.

Humoral immunity and phagocytic activity by leukocytes and mononuclear macrophages are both depressed, but the mechanisms of these effects are not clear.

The Brain:

Brain lesions are rare.

Occasionally, microscopic hemorrhages are seen, but patients who recover do not display neurologic deficits.

In severe cases, particularly in individuals with cerebral atherosclerosis, hemorrhage and necrosis may appear in the overlapping region between the terminal distributions of major arteries, the so called watershed zone.

The Adrenals:

In severe shock the adrenal glands may exhibit conspicuous hemorrhage in the inner cortex. Frequently, this hemorrhage is only focal, but it can be massive and accompanied by hemorrhagic necrosis of the entire gland, as seen in the Waterhouse-Friderichsen syndrome.