Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Necrotizing Enterocolitis (NEC) of the new-born is a serious syndrome characterized by bilious vomiting, gastric retention, abdominal distention and bloody stools. Furthermore, the general condition of the neonate is frequently compromised. The pathogenesis is multi-factorial; however, most authors state that the primary cause of this syndrome is due to ischemia of the intestinal wall. The most serious complication in babies with NEC is perforation of the necrotic bowel, a condition which must always be treated surgically. We present a case of NEC that has a particularly interesting clinical course and, as well, an interesting approach to treatment, which involved the placement of a peritoneal drain. This drain was subsequently utilized for peritoneal lavage once the diagnosis of NEC was confirmed, because we felt that the patient's general condition was so serious that he could not tolerate surgery at this time.
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PMID:[Treatment of necrotizing enteritis using peritoneal drainage. Presentation of a clinical case (author's transl)]. 730 14

Iloprost is a synthetic stable analogue of prostacyclin (PGI2), which shares its antiaggregating and vasodilating properties. Iloprost has been administered by i.v. route to patients with critical limb ischaemia (CLI) of different origin (maximal dosage: 2 ng/kg/min 6 hours/day infusion for 14-28 days). In patients with claudicatio intermittens (Fontaine stage II) iloprost improved the time to claudication and the maximal walking distance on treadmill, with an effect still lasting 60 days after suspension. This benefit was not related to a significant improvement in blood flow. Five multicentric, perspective, randomized versus placebo studies in patients with more severe CLI (Fontaine stage III-IV) susceptible to surgical treatment, showed that iloprost was able to reduce pain and ulcer dimensions. Furthermore, tha amputation rate of the ischemic limb was significantly lower in patients treated with iloprost during a 6 month follow-up (p < 0.01). Iloprost was also more effective than aspirin in causing pain relief and ulcer healing in patients with thromboangiitis obliterans and more effective than nifedipine in reducing frequency, intensity and duration of ischemic episodes in patients with Raynaud's phenomenon. Minor side effects of iloprost administration are represented by facial flushing, tachycardia, headache, nausea, vomiting, abdominal cramping, diarrhoea, whose frequency ranges from 16% to 70%; major collateral effects, occurring in less than 5% of patients, are above all represented by severe hypotension and angina pectoris. Clinical data indicate therefore that iloprost treatment can allow to improve the clinical conditions and the prognosis in patients with critical ischemia of the limbs, not candidate to surgical revascularization, by causing a relief of pain, a reduction in ulcer dimensions and deferring amputation.
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PMID:[The role of iloprost in the treatment of critical ischemia of the limbs]. 750 14

Besides classical necrotizing enterocolitis (in neonates), which is seen in India as elsewhere in the world, we observe sporadic cases of tropical enterocolitis, i.e. segmental jejunitis, ileitis or colitis and rarely duodenitis. This is a distinct clinico-pathological entity presenting as "acute abdomen", with pain, bilious vomiting, constipation or bloody diarrhoea. The clinical course is not as fulminating as neonatal necrotizing enterocolitis. Most cases are salvaged by conservative treatment especially after the confidence brought by laparoscopic vision of the abdomen, thus excluding perforation or gangrene of the bowel involved. Without laparoscopy, most of the cases end up in laparotomy. The pathology appears to be a kind of local hyperimmune reaction in the segment of bowel involved, ranging from punctate haemorrhages in the seromuscular layer of the bowel to a generalized red fiery look or perforation due to mucosal ulceration. Whatever the causative agent, the pathogenesis is of local vasculitis leading to ischemia and various patterns of disease.
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PMID:Tropical enterocolitis in children. 808 96

A 67-year-old woman experienced a severe headache and vomiting. A computed tomographic (CT) scan showed a mild subarachnoid hemorrhage. Cerebral angiography revealed a saccular aneurysm at the apex of the basilar artery. Several days later, she noticed mild hemiparesis of the left extremities. She underwent a clipping operation on the aneurysm by approaching from the right temporal love. Postoperatively, she developed diplopia and dilatation of the left pupil. Cerebral angiography revealed an occlusion of the left posterior cerebral artery. She was admitted to another hospital in order to continue rehabilitation. General physical examination was normal. Neurological examination revealed paralysis of the left medial and left inferior rectus muscles and palsy of the left inferior oblique muscle. The pupil of the left eye was dilated, measuring 5 mm in diameter, and it did not constrict to any stimuli. The left superior rectus and levator palpebrae superioris functioned normally. Visual acuity and visual fields were normal except for the influence of a senile cataract. She had a mild left hemiparesis, slight left ataxia and slurred speech. She had numbness of the left half of the body. A CT scan showed small low density areas in the right thalamus and left cerebellar hemisphere. Her ophthalmologic findings were compatible with the inferior branch palsy of the oculomotor nerve. The ophthalmoplegia of this case seems to be due to partial damage of the oculomotor nerve induced by ischemia of vascular supply. It is supposed to be caused by a vasospasm of the left posterior cerebral artery following a clipping operation of the basilar apex aneurysm.
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PMID:[Inferior branch palsy of the oculomotor nerve following clipping of basilar apex aneurysm]. 831 94

Gastropathy on the basis of mesenteric arterial ischemia can be masked in presentation as the typically more benign entities of gastritis, gastric ulceration, or gastric atony. Gastritis and ulceration are commonly associated with stress, hyperacidity, Helicobacter pylori infection, or medication injury. Gastric atony is less commonly seen and usually attributable to diabetes mellitus, vagotomy, or mechanical gastric outlet obstruction. Gastric ischemia as a cause of gastropathy is an underappreciated phenomenon with a particularly poor prognosis in which early diagnosis is essential to potentially successful intervention. Seven patients with ischemic gastropathy are described; all are women, aged 41 to 71 years, smokers, with hypertension. Nausea, vomiting, weight loss, and gastrointestinal bleeding were the common presenting symptoms. All patients had endoscopic or autopsy-proven gastric ulcerations or necrosis, and two patients had proven gastroparesis. Four of five patients with ischemic gastritis died within 3 months of diagnosis despite vascular reconstruction. The two patients with gastroparesis underwent aorto-celiac bypass and are well 9 and 20 months, respectively, after operation. Treatment results were distressingly unsatisfactory, especially in those patients in whom gastritis rather than gastroparesis was the presenting problem. Although the high mortality of mesenteric ischemia is well described, little documentation of gastric ischemia exists in the literature. This entity is generally not considered in the differential diagnosis of gastritis, ulceration, or gastroparesis. Empirically, an early diagnosis and treatment may improve the survival in this select patient group.
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PMID:Lethal nature of ischemic gastropathy. 848 53

Endotoxemia occurs when intestinal ischemia allows bacterial lipopolysaccharide to translocate from colonic flora into the bloodstream, which triggers release of cytokines that can cause hypotension, rigors, fever, shock, and even death. Recently, blood endotoxin levels were shown to be higher in athletes needing medical attention (330 pg.ml-1) than in their competitors with similar performances (81 pg.ml-1). Though there were no data showing that these athletes had elevated core temperatures or severe illness, speculation followed that endotoxin may play a causal role in heat stroke. We examined the relationship between endotoxemia and mild post-exertional illness in 39 cyclists after a 100-mile ride. Thirteen cyclists had at least one of the following: orthostatic hypotension, rigors, nausea, vomiting, diarrhea, or syncope. Only 2/26 case-controls had any of these symptoms. Data were collected on vital signs, hemoglobin, sodium, creatine kinase, creatinine, and uric acid. Endotoxin titer was determined by chromogenic assay; tumor necrosis factor alpha (TNF-alpha) titer was determined by ELISA. One ill cyclist had an endotoxin level of 330 pg.ml-1, one control had an endotoxin level of 150 pg.ml-1, but endotoxin level was < or = 64 pg.ml-1 in all others. Comparison of pre- and post-ride data showed that controls increased creatine kinase activity (154 +/- 34 vs 561 +/- 191 IU.dl, P < 0.05), creatinine concentration (1.5 +/- 0.0 vs 1.6 +/- 0.0 mg.dl-1, P < 0.05), and uric acid concentration (5.4 +/- 0.3 vs 6.3 +/- 0.3 mg.dl-1, P < 0.05). Ill cyclists had lower serum sodium than post-ride controls (138 +/- 2 vs 142 +/- 0.6 mEq.l-1, P < 0.05), but there were no differences between groups in CK, creatinine, or uric acid. These findings suggest that endotoxemia may complicate, but does not cause mild post-exertional illness in cyclists.
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PMID:Exercise-associated collapse in cyclists is unrelated to endotoxemia. 853 21

We present the first reported case of vision loss due to tension orbital emphysema associated with tension pneumocephalus resulting from blunt trauma. In the setting of trauma, intraorbital air indicates paranasal sinus-orbital communication. Tension orbital emphysema may cause vision loss through optic nerve compression, ischemia, or contusion; or central retinal artery occlusion. Vision impairment after craniofacial injury should prompt urgent computed tomography. Tension orbital emphysema with associated vision impairment requires treatment including direct decompression and, in some cases, high-dose steroids to preserve vision. Increases in sinus pressure from coughing, nose-blowing, or vomiting should be avoided until definitive treatment can be instituted.
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PMID:Tension pneumocephalus and tension orbital emphysema following blunt trauma. 883 34

From twenty six personal cases, the authors make a review of the literature. 92% of their cases are met in a post operative (28%), neurological (28%), general (24%) context, or in intensive care with assisted ventilation (36%). The major symptom is the meteorism (100%) with in one out of three cases, abdominal pain, vomiting, right iliac defense, absence of bowel sounds. Radiological distension involves mostly the right colon and the coecum (28%), right and transverse colon (40), sometimes the whole colon (32%). The mean diameter of the coecum reached 12 cm (9 to 25 cm). Early coloscopy was mandatory in 20 patients, of which 14 were cured, 13 patients were operated on, for suspicion of ischemia or perforation, because incertain diagnosis, or failure of colonoscopy. Ceocostomy or right hemicolectomy (55%) were performed rather than transverse colostomy. The surgical approach must be adapted to the anatomical lesions. Total mortality was 4% in this series. Early diagnosis of pseudo obstruction, early colonoscopy with intubation must allow to avoid surgery.
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PMID:[Ogilvie's syndrome or colonic pseudo-obstruction. Apropos of 26 cases]. 908 29

This review illustrates the changing paradigms in the understanding of the pathogenesis of pneumatosis intestinalis. Although many theories have been evoked, pragmatically there appear to be four major clinical and diagnostic imaging considerations. The most common and most emergent life-threatening cause of intramural bowel gas is the result of bowel necrosis due to bowel ischemia, infarction, necrotizing enterocolitis, neutropenic colitis, volvulus, and sepsis. In the stomach, intramural gas can be caused by emphysematous gastritis or ingestion of caustic agents. These situations represent surgical emergencies. Pneumatosis is found secondary to mucosal disruption presumably due to over-distention from peptic ulcer, pyloric stenosis, annular pancreas, and even to more distal obstruction. Disruption can also be caused by ulceration, erosions, or trauma, including the trauma of child abuse. Disruption can also be iatrogenic from intracatheter jejunal feeding tubes, stent perforation, sclerotherapy, or surgical or endoscopic trauma. In these cases, the gas may be focal or linear. Treatment depends on the extent of the disruption and the underlying cause. A more subtle form of mucosal disruption may occur due to mucosal erosions and also to defects in intestinal crypts secondary to acute and subclinical enteritides that allow intraluminal bacterial gas under pressure to percolate into the bowel wall layers, particularly the submucosa (29). Pneumatosis, often linear or cystic in appearance, is seen with increased frequency in patients who are immunocompromised because of steroids, chemotherapy, radiation therapy, or AIDS. In these cases, the pneumatosis may result from intraluminal bacterial gas entering the bowel wall due to increased mucosal permeability caused by defects in bowel wall lymphoid tissue. Clinical and imaging findings are important in the differentiation of this transient pneumatosis from fulminant life-threatening causes in this subset of patients. A pulmonary cause must still be considered in cases of chronic obstructive pulmonary disease, asthma, and cystic fibrosis. It can occur with barotrauma and after chest tube placement. It may relate to increased intrathoracic pressure associated with retching and vomiting. The possibility remains that occasionally the origin of pneumatosis intestinalis will remain cryptogenic--caused but unexplained.
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PMID:Pneumatosis intestinalis: a review. 953 Feb 94

A diagnosis based on the presumed mechanism of stroke onset is useful for management strategies in acute ischemic stroke. Ninety-two patients with embolic (cardiac or artery-to-artery) and 107 with non-embolic (thrombotic or hemodynamic) stroke were diagnosed on strict cerebral angiographic criteria alone. To clearly discriminate between these two groups, the neurological and computed tomographic (CT) findings were then compared. Rapidity of onset, vomiting, urinary incontinence, level of consciousness, cervical bruit, anisocoria, tongue deviation, sensory disturbance, and CT findings (location of hypodense area, findings of brain edema and hemorrhagic transformation) were discriminatory factors between the two groups (p<0.01). According to these 11 items, we prepared a numerical table for quantitative differential diagnosis. A diagnostic accuracy of 98.9% for embolic and 87.9% for non-embolic stroke in internal verification, and 90.0% and 82.9%, respectively, in external verification was observed. The differences in clinical features and CT findings between embolic and non-embolic stroke may reflect the pathophysiological mechanisms of the occlusive process of cerebral artery as well as the extent and severity of ischemia.
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PMID:Differences in clinical features and computed tomographic findings between embolic and non-embolic acute ischemic stroke: a quantitative differential diagnosis. 955 May 93


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