Subperitoneal hemorrhage.

G F CUSHMANN

Home/Archive/PubMed

PubMed · 13009511

Subperitoneal hemorrhage.

G F CUSHMANN

View original source ↗Export metadata ↓

Abstract

Clinical diagnosis of subperitoneal hemorrhage can be made in a substantial percentage of cases by recognition of a quite constant syndrome-provided the possibility of bleeding is considered. Progressive anemia, as indicated by repeated counts of erythrocytes in the blood or by hematocrit determinations, is confirmation of the diagnosis. The majority of patients recover spontaneously under conservative management.Surgical intervention is indicated if repeated episodes of hemorrhage occur or if the volume of circulating blood cannot be maintained by repeated transfusions of whole blood.

Explore related subjects

Abdomen Abdominal Neoplasms Anemia Blood Transfusion Erythrocytes Hematocrit Hemorrhage Humans Neoplasms ABDOMEN/neoplasms HEMORRHAGE Journal Article

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

G F CUSHMANN. 1953. Subperitoneal hemorrhage.. https://pubmed.ncbi.nlm.nih.gov/13009511/

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

KEEP EXPLORING

Related citations

PubMed2007

A case of scirrhous gastric cancer with peritonitis carcinomatosa controlled by TS-1 + paclitaxel for 36 mo after diagnosis.

A 34-year-old female complaining of abdominal fullness was diagnosed as scirrhous gastric cancer (type 4') with peritonitis carcinomatosa in July 2002. A combined chemotherapy regimen was selected to control massive ascites; TS-1 80 mg/m(2) was given orally on d 1-14, 22-35, and paclitaxel 50 mg/m(2) was administered intravenously on d 1, 8, 22 and 29. After 2 courses of this regimen, the primary tumor was markedly reduced, and ascites completely vanished. Alopecia (grade 1, since d 30), leukocytopenia (grade 2, on d 34) and anemia (grade 2, on d 34) were the only adverse events throughout the following courses. The chemotherapy was effective for 28 mo, and then it was discontinued upon the patientos own request, and she survived for 36 mo after diagnosis.

Abdomen↗

PubMed2007

Endocrine role of the renin-angiotensin system in human adipose tissue and muscle: effect of beta-adrenergic stimulation.

The renin-angiotensin system has been implicated in obesity-related hypertension and insulin resistance. We examined whether locally produced components of the renin-angiotensin system in adipose tissue and skeletal muscle play an endocrine role in vivo in humans. Furthermore, the effects of beta-adrenergic stimulation on plasma concentrations and tissue release of renin-angiotensin system components were investigated. Systemic renin-angiotensin system components and arteriovenous differences of angiotensin II (Ang II) and angiotensinogen (AGT) across abdominal subcutaneous adipose tissue and skeletal muscle were assessed in combination with measurements of tissue blood flow before and during systemic beta-adrenergic stimulation in 13 lean and 10 obese subjects. Basal plasma Ang II and AGT concentrations were not significantly different between lean and obese subjects. Ang II concentrations were increased in obese compared with lean subjects during beta-adrenergic stimulation (12.6+/-1.5 versus 8.1+/-1.0 pmol/L; P=0.04), whereas AGT concentrations remained unchanged. Plasma renin activity increased to a similar extent in lean and obese subjects during beta-adrenergic stimulation (both P<0.01). No net Ang II release across adipose tissue and skeletal muscle could be detected in both groups of subjects. However, AGT was released from adipose tissue and muscle during beta-adrenergic stimulation in obese subjects (both P<0.05). In conclusion, locally produced Ang II in adipose tissue and skeletal muscle exerts no endocrine role in lean and obese subjects. In contrast, AGT is released from adipose tissue and muscle in obese subjects during beta-adrenergic stimulation, which may contribute to the increased plasma Ang II concentrations during beta-adrenergic stimulation in obese subjects.

Abdomen↗

PubMed2007

Absence of selective brain cooling in unrestrained baboons exposed to heat.

To test whether baboons are capable of implementing selective brain cooling, we measured, every 5 min, the temperature in their hypothalamus, carotid arterial bloodstream, and abdominal cavity. The baboons were unrestrained and exposed to 22 degrees C for 7 days and then to a cyclic environment with 15 degrees C at night and 35 degrees C during the day for a further 7 days. During the latter 7 days some of the baboons also were exposed to radiant heat during the day. For three days, during heat exposure, water was withheld. At no time was the hypothalamus cooler than carotid arterial blood, despite brain temperatures above 40 degrees C. With little variation, the hypothalamus was consistently 0.5 degrees C warmer than arterial blood. At high body temperatures, the hypothalamus was sometimes cooler than the abdomen. Abdominal temperature was more variable than arterial blood and tended to exceed arterial blood temperature at higher body temperatures. Hypothalamic temperature cooler than a warm abdomen is not evidence for selective brain cooling. In species that can implement selective brain cooling, the brain is most likely to be cooler than carotid arterial blood when an animal is hyperthermic, during heat exposure, and also dehydrated and undisturbed by human presence. When we exposed baboons to high ambient temperatures while they were water deprived and undisturbed, they never implemented selective brain cooling. We conclude that baboons cannot implement selective brain cooling and can find no convincing evidence that any primate species can do so.

Abdomen↗