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Query: UMLS:C0021843 (bowel obstruction)
 9,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intestinal malrotation presenting beyond the neonatal period is associated with a multiplicity of symptoms, which are often non-specific and, consequently, are associated with delays in diagnosis. Pseudo-Bartter's syndrome, which mimics the manifestations of Bartter's syndrome, can be caused by a severe chloride deficiency secondary to vomiting, diarrhea, perspiration, diuretic abuse and so on. We describe a 6 year old boy who had been admitted to hospital three times during the preceding year. The patient lapsed into a critical condition with profound hypochloremia and hypokalemic metabolic alkalosis induced by extremely massive vomiting. The attacks of vomiting were spasmodic and self-limited. During the episodes of vomiting he fulfilled the criteria of pseudo-Bartter's syndrome, including hyperreninemia, hyperaldosteronism and normal blood pressure, but in the intervals between attacks he was completely asymptomatic. At the third admission, examination supported an overall clinical picture of bowel obstruction, which was confirmed by radiographic examination. Laparotomy revealed a midgut volvulus with intestinal malrotation. After surgery he made a good recovery and was symptom-free. In this patient, the high degree of hypochloremia and hypovolemia activated the renin-angiotensin-aldosterone system, then aldosterone promoted intensive reabsorption of sodium and excretion of potassium into the urine. Consequently the diagnosis of pseudo-Bartter's syndrome was establish on the basis of an extreme decrease in urinary chloride and an increase in urinary potassium concentration. It is relatively rare for vomiting due to intestinal malrotation to induce pseudo-Bartter's syndrome. The importance of considering this rare diagnosis in such cases is discussed.
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PMID:A case of pseudo-Bartter's syndrome due to intestinal malrotation. 816 99

Although the dehydration-rehydration problem in end-of-life care is one of the most important issues, clinical indications of hydration therapy have not been clarified because the pathophysiology is poorly understood. To explore the physiological changes of fluid status in terminally ill cancer patients, a prospective observational study was performed. We obtained 9 pairs of blood samplings from hospice inpatients with irreversible bowel obstruction who underwent two or more laboratory examinations during the admission periods. The plasma renin activity (PRA) and brain natriuretic peptide (BNP) were measured, in addition to basic laboratory tests performed as clinically required. A chart review evaluated the degree of fluid retention symptoms. In 7 patients receiving intravenous rehydration of 700-2200 ml/day, the mean PRA level significantly increased from 3.5+/-2.5 ng ml(-1) h(-1) to 11+/-8.2 ng ml(-1) x h(-1) ( P=0.047), and the mean BNP level significantly decreased from 52+/-34 pg/ml to 22+/-14 pg/ml ( P=0.047). Edema, ascites, and pleural effusion/pulmonary edema deteriorated in 5, 3, and 5 patients, respectively. In 2 patients without rehydration therapy, peripheral edema deteriorated with increased PRA levels (0.5 to 20 ng ml(-1) x h(-1), 0.4 to 8.7 ng ml(-1) x h(-1), respectively). In conclusion, intravenous volume depletion with fluid retention symptoms was observed in terminally ill cancer patients with intestinal obstruction both receiving and not receiving intravenous hydration. The pathological mechanism hypothesized is the fluid shift from the intravascular compartment to the interstitial spaces.
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PMID:Fluid status of terminally ill cancer patients with intestinal obstruction: an exploratory observational study. 1235 26

Encapsulating peritoneal sclerosis (EPS) is a life-threatening complication of long-term peritoneal dialysis (PD), which may even occur after patients have switched to hemodialysis (HD) or undergone kidney transplantation. The incidence of EPS varies across the globe and increases with PD vintage. Causative factors are the chronic exposure to bioincompatible PD solutions, which cause long-term modifications of the peritoneum, a high peritoneal transporter status involving high glucose concentrations, peritonitis episodes, and smoldering peritoneal inflammation. Additional potential causes are predisposing genetic factors and some medications. Clinical symptoms comprise signs of intestinal obstruction and a high peritoneal transporter status with incipient ultrafiltration failure. In radiological, macro-, and microscopic studies, a massively fibrotic and calcified peritoneum enclosed the intestine and parietal wall in such cases. Empirical treatments commonly used are corticosteroids and tamoxifen, which has fibrinolytic properties. Immunosuppressants like azathioprine, mycophenolate mofetil, or mTOR inhibitors may also help with reducing inflammation, fibrin deposition, and collagen synthesis and maturation. In animal studies, N-acetylcysteine, colchicine, rosiglitazone, thalidomide, and renin-angiotensin system (RAS) inhibitors yielded promising results. Surgical treatment has mainly been performed in severe cases of intestinal obstruction, with varying results. Mortality rates are still 25-55% in adults and about 14% in children. To reduce the incidence of EPS and improve the outcome of this devastating complication of chronic PD, vigorous consideration of the risk factors, early diagnosis, and timely discontinuation of PD and therapeutic interventions are mandatory, even though these are merely based on empirical evidence.
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PMID:Encapsulating Peritoneal Sclerosis: Pathophysiology and Current Treatment Options. 3174 97