Search PubMedSearch

PubMed · 4058181

[Multiorgan failure].

Abstract

The diagnosis of multiple organ failure is based upon the sequential occurrence of failure of vital organ functions within a short period of time (lung, kidney, circulatory system, gastrointestinal tract, liver, metabolism, hemostasis). Underlying diseases are polytrauma, high risk surgical procedures, acute abdominal complications. Sepsis is the main pathogenetic factor. The mortality is 60-80% and in patients with abdominal sepsis plus acute renal failure and dialysis plus acute lung failure and artificial ventilation up to 100%. Intensive care is therefore focussed upon prophylaxis, predominantly shock therapy and surgical treatment of sepsis.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

H P Schuster. 1985. [Multiorgan failure].. https://doi.org/10.1007/bf01836674

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

The abdominal diameter index and sudden coronary death in men.

Alternative anthropometric indexes were compared for their ability to discriminate between 35 Atlanta men with sudden coronary death and 81 male controls. With or without adjustments for age, race, and body mass index, the abdominal diameter index (supine sagittal abdominal diameter divided by midthigh circumference) was associated with sudden coronary death more strongly than the waist/hip ratio or waist/thigh ratio of circumferences.

Abdomen

Failure to detect connexin43 mutations in 38 cases of sporadic and familial heterotaxy.

BACKGROUND: Heterotaxy results from failure to establish normal left/right asymmetry during embryonic development. Typical manifestations include complex heart defects and malpositioning of abdominal organs. Missense base substitutions clustered in a 150-base pair region of the gap-junction gene connexin43 (cx43) have been implicated in the pathogenesis of heterotaxy. METHODS AND RESULTS: cx43 was studied in 38 cases of sporadic and familial heterotaxy. A 400-base pair region containing the previously reported mutation sites was amplified and directly sequenced in 19 patients. Nineteen additional patients were tested for restriction fragments predicted by two of the previously reported missense substitutions. No difference from normal control subjects was detected in any of the patients. CONCLUSIONS: Randomly selected cases of heterotaxy are unlikely to be the result of mutations in cx43.

Abdomen