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Multiple-organ failure is generally attributed to bacterial infection, although a correlation with positive blood cultures is not consistently found. Consequently, we studied the effects of a local nonbacterial inflammatory stimulus on distant organ functions and metabolism. Wistar rats were inoculated intraperitoneally with zymosan. Heart and ventilatory rates, oxygen consumption, and body temperature were measured. Survivors were killed at day 12 for blood analysis, weighing of organs, and microscopy. Intraperitoneal zymosan resulted in an early hyperdynamic "septic" response with a 35% mortality. After a few days, oxygen consumption decreased, serum lactate levels increased, and the function of multiple organs deteriorated, while blood cultures remained sterile. The experiment was repeated in germ-free rats with similar results but a lower mortality. We concluded that a severe inflammatory response in itself is capable of inducing multiple-organ failure with "sepsis."

A review of the recent literature concerning the Adult Respiratory Distress Syndrome (ARDS) and Multiple Organ Failure (MOF) is presented. We hypothesize that the two syndromes probably have a common pathophysiology, with ARDS as the first occurring organ failure. The clinical situations that may cause ARDS and MOF are characterized by massive and prolonged activation of the complement system. This results in activation of granulocytes with ensuing release of lysosomal enzymes, toxic oxygen products and prostaglandins, which collectively cause endothelial damage and permeability changes. In the lungs interstitial and alveolar edema develops, with an impaired alveolo-capillary gas exchange. Oxygen diffusion in the peripheral tissues is impeded by the same mechanism, ultimately resulting in organ failure. Hypoxia may cause additional microvascular lesions, as toxic oxygen radicals are produced during reoxygenation. The implications of this hypothesis for the prevention and therapy of ARDS and MOF are discussed.

A patient with dysphagia caused by a sessile polyp in the lower esophagus is reported. Histologic examination showed ectopic gastric mucosa. Of the benign tumors of the esophagus, only leiomyoma is seen regularly. The remaining tumors are so rare that the consequences of this diagnosis are unclear. When symptoms make treatment necessary, local excision is preferred.

As multiple-organ failure (MOF) has been generally associated with sepsis, the importance of bacterial sepsis was evaluated retrospectively in 55 trauma and 37 intra-abdominal-sepsis patients with MOF. The severity of MOF was graded, and an analysis was made of day of onset, incidence, severity, sequence, and mortality of organ failures. No difference was found between groups in sequence, severity, or mortality of organ failures. In contrast, bacterial sepsis was found in 65% of intra-abdominal-sepsis patients but only in 33% of trauma patients. It is concluded that sepsis is probably not the essential cause of MOF. Instead, an alternative hypothesis is presented involving massive activation of inflammatory mediators by severe tissue trauma or intra-abdominal sepsis, resulting in systemic damage to vascular endothelia, permeability edema, and impaired oxygen availability to the mitochondria despite adequate arterial oxygen transport.

It has been suggested that generalized endothelial damage and permeability changes, induced by prolonged activation of the complement system and ensuing release of lysosomal enzymes, prostaglandins and toxic oxygen products, underlie the genesis of the Adult Respiratory Distress Syndrome (ARDS) and Multiple Organ Failure (MOF). The effects in New Zealand white rabbits were investigated of a 4 h infusion of activated complement and its combination with a short hypoxic episode on respiratory function, leukocyte count, platelet count and morphology of the lungs, heart, liver, kidney and spleen. Prolonged activation of the complement system induced hyperventilation with respiratory alkalosis and hypocapnia, depletion of granulocytes (PMN), and a variable accumulation PMN in the capillaries of all organs examined, in combination with interstitial, and, in the liver, cellular oedema. Electron microscopy of the lungs revealed degranulation of PMN, endothelial swelling and widening of the alveolar septa. The combination of hypoxia and systemic complement activation appeared to aggravate this microvascular injury with the occurrence of protein rich alveolar oedema and haemorrhage in the lungs and accumulation of PMN debris containing macrophages in the spleen. The alterations in respiratory function and pulmonary morphology in these rabbits, imitate the clinical and morphological characteristics of the early phase of ARDS. The inflammatory reaction, found in all other organs examined, might represent the early phase of MOF. If so, ARDS and MOF -- clinically closely interconnected syndromes -- might be interpreted as manifestations of the same syndrome and as the clinical expression of an uncontrolled whole body inflammation.