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Query: UMLS:C0000727 (acute abdomen)
 3,084 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The diagnosis of acute superior mesenteric artery occlusion in the dog has been achieved in every case by isotope scanning of the abdomen using technetium-labelled red cells or technetium-labelled human serum albumin. The white cell count is also significantly elevated, but the changes in the levels of the enzymes CPK, LDH, AST and serum amylase are not specific for actue mesenteric ischaemia. In the human the presence of a normal gut circulation can be demonstrated by isotope scanning provided that the patient is not severely shocked. The presence of a normal gut circulation as shown on the scintigram conclusively eliminates the possibility of acute main trunk occlusion of the superior mesenteric artery. This should be of help in differentiating acute occulusive mesenteric ischaemia from other causes of the acute abdomen. Abdominal scintiscanning is complementary to angiography, which still remains the most precise means of diagnosing acute mesenteric ischaemia. Although the abdominal scintigram is more limited in its application and is not as accurate as angiography, it is quicker to perform, non-invasive, and entirely safe. Abdominal scintiscanning is an excellent screening test to be used in patients suspected of suffering from acute occlusive mesenteric ischaemia.
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PMID:The early diagnosis of acute occlusive mesenteric ischaemia: experimental results and clinical applications. 28 87

HELLP syndrome continues to be a clinical entity of difficult diagnosis. Weinstein first defined it in 1982 giving the practicing obstetrician a sequence of useful initials (H = hemolysis; EL = elevated liver enzymes; LP = low platelets). Since then a lot has been written and it has become clear that the syndrome is a form of severe preeclampsia. The American College of Obstetrics and Gynecology does not include HELLP in the description of severe pre-eclampsia as such but does accept each of its components as being part of severe pre-eclampsia. The case presented deals with a 33 year old white female, admitted at 27 weeks gestation with nausea, epigastric pain resembling acute abdomen, nose bleeding and mild hypertension. The analysis revealed an abnormal liver profile with elevated GOT, GPT and LDH, heavy proteinuria (14.4 g/day), decreased platelet count (92000/mm3) and elevated total bilirubin. Pregnancy was terminated by cesarean section 24 hours after admission because the patient's condition was deteriorating. Obviously in pre-eclampsia/eclampsia there is a systematic injury to all tissues. Proof of this is the hypertension as a consequence of vascular spasm and proteinuria due to glomerular injury. In HELLP the sequence of events is probably altered; hepatic injury precedes vascular and renal injury of conventional preeclampsia. The syndrome results from many clinical and pathological symptoms derived from endothelial microvascular injury which determine a rapid platelet activation causing vascular spasm, platelet aggregation and further endothelial injury through a feedback mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Massive proteinuria and HELLP syndrome]. 130 8

A retrospective analysis of 140 cases with amebic liver abscess (ALA) seen at the AUNL University Hospital was done to see if patients with complications can be identified earlier in order to decrease morbidity and mortality. Sixteen patients (11.4%) presented complications and six patients died (4.2%). Patients with complications presented jaundice, large or multiple abscesses, acute abdomen, liver failure and sepsis more often than patients without complications. Hemoglobin, hematocrit, prothrombin time, total proteins, albumin, LDH, and BUN were more altered in patients who presented complications. The titer of antibodies against E. histolytica was higher in this group of patients. The six patients who died had been operated on. The causes of death were septic shock in two, sepsis in one, peritonitis in one, liver failure in one and colon perforation in one patient. Pleural effusion, jaundice and acute abdomen were seen in three patients, respectively (50%), two cases had multiple abscesses (33.3%), one patient had a ruptured abscess (16.7%). Patients who died exhibited more alterations in six laboratory examinations at admission: partial prothrombin time, total bilirubin, albumin, BUN, LDH, and leukocytes. Clinical data together with the severe alterations in laboratory examinations at admission for patients with ALA should alert the clinician to suspect complications earlier in order to decrease morbidity and mortality.
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PMID:Early detection of complications in amebic liver abscess. 134 Mar 6

The most important diagnostic step in the management of patients with severe acute pancreatitis is discrimination between interstitial-edematous pancreatitis and necrotizing pancreatitis. In this respect, laboratory measures like CRP, LDH, and antiproteases, and the application of contrast-enhanced CT are highly sensitive methods. Surgical decision-making should be based on clinical, bacteriological and contrast-enhanced CT data. Persistent or progressive systemic or local organ complications occurring despite ICU treatment for a minimum of three days are indicators for surgical management of necrotizing pancreatitis. Patients suffering from sepsis syndrome, cardiovascular shock, multisystemic organ failure syndrome, or surgical acute abdomen should be treated surgically early in the course of the disease. The use of a major pancreatic resection for the surgical management of necrotizing pancreatitis should be excluded from treatment protocols. Carefully performed necrosectomy or debridement, in combination with continuous or repeatedly applied surgical evacuation techniques for necrotic tissue, bacteria, and biologically active compounds, has proved to be very effective in experienced treatment centers. Necrosectomy and postoperative continuous local lavage is a well-adapted, safe, and atraumatic procedure. It results in a hospital mortality of less than 10% in patients with necrotizing pancreatitis.
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PMID:Surgery in acute pancreatitis. 185 79