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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 23-year-old male was admitted to hospital with severe dehydration and hypokalemic myopathy due to secondary aldosteronism. On admission serum sodium and chloride were markedly elevated to 198 mEq/l and 169 mEq/l, respectively, and serum potassium was down to 2.3 mEq/l. Serum electrolytes were normalized by transfusion therapy, but subsequently rhabdomyolysis grew worse due to metabolic abnormalities such as dehydration, hypothermia, oppressive ischemia and metabolic acidosis, at the same time transient polyuria and the elevation of serum myoglobin and enzymes originating in muscle tissue were observed. Serum CPK went up to 26,532 IU/l on the sixth day and other enzymes reached a peak following CPK. Dexamethasone was administered when the increase in enzyme levels caused the patient to fall into a stupor. He rapidly regained consciousness from the 15th day after admission, and he was able to stand up on the 29th day. Serum enzymes originating in muscle tissue decreased gradually to the normal range by the 30th day and no renal failure occurred.
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PMID:A case of severe dehydration with marked rhabdomyolysis. 402 Dec 12

There is a type of cerebral lesion, which kills neuronal cells at a later stage (greater than 48 hrs) post CA, while the systemic circulation is functioning normally. Although this lesion is probably dependent on multiple factors (----multiple therapies), a keyfactor in the pathogenesis is the loss of autoregulation and "finetuning" of the cerebral bloodflow according to local tissue metabolic needs. Although beneficial effect of almost none of the following therapies has been documented in randomised clinical studies, the following suggestions are made: a) In the CA-CPR phase: efficient respiratory care and external cardiac compressions (ECC), especially during bicarbonate administration; consider open chest CPR early, especially in cases of long arrest time and ineffective ECC. The socalled new CPR does not improve neurological outcome. b) In the post CPR phase: The non-autoregulated brain (cfr. focal ischemia) is kept preferentially at pCO2 values 25-30 mmHg, pO2 values greater than 100 mmHg, and normotension. Some form of stress, seizure and hyperthermia control prevents further imbalance metabolism/bloodflow. Relative dehydration, oncotic balance, steroids, early control of sepsis and uremia, early CT scan and measurement/control of ICP. All the above is currently grouped under "standard neuro-intensive therapy". Some other therapies, presently suggested by animal research are not very obvious, need first randomised clinical studies and are not suggested at this stage for clinical use: barbiturate coma, diphantoine, streptokinase, multifaceted therapy including hemodilution-brainflushing, Ca++ influx blocking drugs (lidoflazine). One such "innovative" therapy, barbiturate coma, has already been proven to be relatively ineffective (BRCT I) (Acta anaesth. belg., 1984, 25, suppl., 219-226).
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PMID:Brain protection in the immediate post-resuscitation phase. 651 33

The effects of longlasting dehydration on total and local renal blood flow and glomerular filtration rate have not been studied previously in the laboratory rat. We therefore determined zonal renal blood flow (ZRBF) in cortical and medullary zones by the 125I-iodoantipyrine and H2 gas washout techniques. After 8 days of water deprivation renal blood flow (RBF) was reduced by 65% and renal vascular resistance (RVR) had increased by 110%. Half the RVR increase could be ascribed to increased blood viscosity as reflected by increased hematocrit (42 to 60%). Fractional ZRBF decreased by 5% in the outer half and increased by 5% in the inner half of the cortex. Measurements of the relative single nephron glomerular filtration rate (sngfr) of superficial and deep nephrons, determined by the 14C-ferrocyanide technique, indicated no detectable changes in filtrate distribution. Both ZRBF and sngfr heterogeneity had increased in dehydrated as compared to control rats. In one rat studied with the H2 gas washout method, local ischemia and intermittent blood flow occurred. Similarly, cortical patches of nonfiltering nephrons were observed in another rat. These findings suggest that the increased heterogeneity of intrarenal flow and filtration may involve, and in part be due to, intermittent local changes in blood flow.
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PMID:The effect of water deprivation on local renal blood flow and filtration in the laboratory rat. 664 Aug 59

Glomerular visceral epithelial cells (podocytes) undergo flattening and spreading of major processes detectable by scanning electron microscopy in early postischemic acute renal failure in both animals and man. The authors examined the kinetics of development of these epithelial cell changes in the renal pedicle-clamping model of ischemic renal failure in the rabbit. They found that these changes develop progressively, increasing with increasing length of ischemia, and occur while the pedicle clamp is still in place. To assess the possible role of angiotensin II and vasopressin in producing the epithelial changes, the authors compared glomerular morphology before and during pedicle clamping in hydrated rabbits and in dehydrated rabbits. Dehydration alone produced changes in glomerular epithelial cells comparable to those seen in the postischemic kidney. The angiotensin-converting enzyme inhibitor captopril did not prevent the podocyte changes in either group. In vitro incubation studies confirmed that both angiotensin II and vasopressin produce glomerular epithelial cell changes with a threshold between 10(-7) M and 10(-8) M, a concentration that may be physiologically significant for angiotensin II, which is synthesized at the glomerulus and may have local paracrine effects. Such local synthesis may not be inhibited by systemic administration of captopril. Angiotensin II may play a role in producing podocyte alterations during renal ischemia, as well as in the dehydrated state.
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PMID:Glomerular epithelial cell changes after ischemia or dehydration. Possible role of angiotensin II. 669 12

An 11 year old boy was admitted to the Department of Pediatrics Medical School of Vienna with 2nd and 3rd degree burns covering 30% of his body. He presented with complications--high fever, vomiting, diarrhea and dehydration--which had led to acute renal failure. After 6 hemodialyses renal function recovered after two weeks and the patient entered a polyuric phase. In connection with a transient dehydration the patient showed a sudden bilateral cortical blindness. The computerized tomogram (CT) showed vague evidence of an occipital cortical ischemia. We assume that several factors have played a role in this sudden occurrence. As a result of hypovolemia and coincident anemia and electrolyte inbalance, cerebral edema and cortical tissue hypoxia with emphasis in the occipital cortical region developed in the brain possibly already damaged by burn injury. A complete reversal of the clinical state was achieved. The patient was discharged with normal vision and normalized renal function.
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PMID:[Acute cortical blindness: a reversible complication of acute kidney failure in a child with burns]. 683 79

Acute colonic ischemia is the most common form of intestinal ischemia. Nonocclusive ischemic colitis contributes to some of these disorders. Heart disease, such as congestive heart failure, myocardial infarction, arrhythmias, aortic valve disease, and atherosclerotic cardiovascular disease, account for many of its risk factors. The majority of cases are associated with severe congestive heart failure with low cardiac output, or disease states resulting in dehydration, or the splanchnic vasoconstrictive effect of some medications. Reactive splanchnic vasoconstriction is responsible for nonocclusive ischemic colitis. Ischemic colitis induced by a cleansing enema has been reported once before. The authors present a case of coronary artery disease complicated by colonic ischemia following glycerin enema in preparation for coronary bypass surgery. Reactive inferior mesenteric artery spasm in response to the enema was noted in this case, rather than diffuse mesenteric artery spasm in response to low cardiac output state and vasoconstrictive drugs.
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PMID:Nonocclusive ischemic colitis following glycerin enema in a patient with coronary artery disease. A case report. 763 24

We induced cerebral complete ischemia (CCI) by "four-vessel" model. The changes of Na+,K(+)-ATPase, Ca2+, Mg(2+)-ATPase, phospholipase A2 (PLA2), total phospholipids on brain cellular membrane (BCM) at 30, 180, 360 min of reperfusion following 30 min CCI were observed. The effects of selective head cooling (SHC, 28C, surface cooling method), mannitol dehydration (MD), and selective head cooling-dehydration combined therapy (SHCDCT) on these changes were also investigated. Compared with non-ischemic, during reperfusion activities of Na+, K(+)-ATPase, Ca2+, Mg(2+)-ATPase decreased while PLA2 increased (P < 0.001), phospholipids decreased at 180 and 360 min of reperfusion (P < 0.01). SHC and SHCDCT blocked all above changes, MD had no effect. These results suggest that SHCDCT after starting reperfusion do promote recruitment of BCM function by blockade of the successive reperfusion damage on BCM.
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PMID:[Study of mechanism of selective head cooling-dehydration combined therapy for brain resuscitation: effect on function of brain cellular membrane]. 777 12

Resuscitation of the brain after a period of global ischemia is limited by two classes of post-ischemic pathologies: hemodynamic disturbances which prevent the adequate re-oxygenation of the ischemic brain, and metabolic disturbances which may lead to delayed neuronal death in so-called selectively vulnerable brain regions. The hemodynamic disturbances can be classified into the no-reflow phenomenon and the post-ischemic hypoperfusion syndrome. The no-reflow phenomenon results from a combination of increased blood viscosity and perivascular edema; the severity increases with the duration of ischemia, and the treatment is by combining arterial hypertension with dehydration and anticoagulation. The post-ischemic hypoperfusion syndrome is independent of the duration of ischemia, it develops after a delay and is due to an impairment of the metabolic/hemodynamic coupling mechanisms; there is no specific treatment at the present. The most important metabolic disturbance leading to delayed neuronal death is prolonged inhibition of protein synthesis. The injury is manifested already after 5 min ischemia but it progresses little if ischemia is prolonged to 1 h. Inhibition occurs at the translation level due to selective inhibition of polypeptide chain initiation. After brief periods of ischemia, the disturbance can be reversed by various anesthetics and hypothermia but there is no treatment if ischemia is prolonged. Exitotoxity, free radical-mediated reactions, disturbances of polyamine metabolism, acidosis and selective disturbances of gene expression may also be involved but are probably of lesser importance.
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PMID:Ischemia-mediated neuronal injury. 813 1

A 15-year-old girl with ischemic stricture of the jejunum, probably due to microangiopathy caused by diabetes mellitus is presented. Laparotomy revealed two circular strictures in the proximal jejunum, and histology showed ischemic enteritis with ulceration, granulation with microvascular proliferation, inflammatory cell infiltration, marked fibrosis, and hemosiderin deposition. Uncontrolled diabetes mellitus often causes ketoacidosis, increased blood viscosity and platelet aggregation, dehydration in addition to hyperglycemia, and occasionally results in occlusive or non-occlusive vascular disease of the intestine. Ischemic stricture of the bowel in the diabetic state is probably related to moderate ischemia resulting in ulceration and scar formation in the intestine.
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PMID:Ischemic jejunal stricture developing after diabetic coma in a girl: a case report. 832 18

This study was undertaken to prospectively assess all morbidity and mortality associated with temporary loop ileostomy. Eighty-three consecutive patients of a median age of 45 years required temporary fecal diversion after either ileoanal or low colorectal anastomosis (n = 72), for perianal Crohn's disease (n = 5), or for other reasons (n = 6). All loop ileostomies were supported with a rod, and fecal diversion was maintained for a mean of 10 weeks. To date, 67 patients have had re-establishment of intestinal continuity. Stoma closure was affected through a parastomal incision in 64 patients; in three, a laparotomy was required. The closure was stapled side to side in 49 patients, while a hand-sewn anastomosis was done in the other 18 patients; all skin wounds were left open. The mean length of surgery for ileostomy closure was 56 minutes, and the mean hospital stay was five days. Nine patients (10.8 percent) developed 10 complications, nine of which required hospitalization. Specifically, four patients developed dehydration and electrolyte abnormalities secondary to high stoma output, and two had anastomotic leaks that spontaneously healed following conservative management. One patient developed a superficial wound infection that spontaneously drained itself. One patient developed a partial small bowel obstruction that resolved without surgery after a four-day hospitalization. One stoma retracted after supporting rod removal and prompted premature closure. There was no stomal ischemia, hemorrhage, prolapse, or mortality in this series. Thus, loop ileostomy is a safe way to achieve fecal diversion.
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PMID:Loop ileostomy is a safe option for fecal diversion. 845 60


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