Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eighty-two patients were hospitalized following an accidental exposure to chlorine. All patients presented with dyspnoea and cough. The other symptoms included irritation of throat (53.6%), irritation of eyes (42.3%), headache (29.2%), abdominal pain (26.8%), vomiting (24.3%) and giddiness (9.7%). All of them had bronchospasm and 5 (6%) had cyanosis at the onset. An x-ray of the chest revealed patchy infiltrates in 3 (3.85%) and hilar congestion in 2 (2.44%). Pulmonary function tests showed an obstructive pattern in 27.4%, restrictive in 3.25% and mixed in 53.2%. Pulmonary functions were normal in 16.1% of the patients. Bronchoscopy revealed tracheobronchial mucosal congestion in all cases, hemorrhagic spots in 35.7%, erosions and ulcers in 12.5%. All patients were treated with oxygen, aminophylline, hydrocortisone and antibiotics. Haematemesis (n = 1) and pulmonary oedema (n = 2) developed 12 hours after the admission. Two other patients developed pneumonia 48 hours later. All patients recovered satisfactorily. On follow-up 16 patients had no sequelae after one year. Pulmonary functions were normal in 5 patients after 3 years of follow-up.
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PMID:Acute accidental exposure to chlorine fumes--a study of 82 cases. 145 67

Two cases are reported of acute respiratory failure occurring during sickling crises. In the first one, the crisis was characterised by priapism, and in the other one, by abdominal pain. The different causes of these respiratory effects are discussed: infection, fat embolism, pulmonary infarct, haemodynamic pulmonary oedema, as was probably the case in the first patient, or non haemodynamic pulmonary oedema due to sickling, as during conventional treatment of a sickling crisis (oxygen, antibiotics, blood transfusion, cytapheresis). Invasive investigations may contribute to keeping up the clinical picture, because of hypoxic sickling. The water equilibrium of these patients must be monitored with great care. Worsening of the patient's condition despite 48 h of correct treatment must lead to the search for a specific cause.
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PMID:[Acute respiratory insufficiency in sickle cell disease]. 150 96

During her pregnancy (29 weeks) a 29-year-old woman complained of pain in the right upper quadrant of her abdomen. Gallbladder stones were demonstrated by ultrasonography. Because of recurrent pain attacks cholecystectomy was performed. Continuous intravenous tocolytic therapy, fenoterol bromide (Parusisten), was given during and following surgery. Two days after this first laparotomy she underwent a second laparotomy because of unexplained abdominal pain and blood loss. A subhepatic haematoma was found without a specific origin for the blood loss. Shortly after this second operation she developed clinical signs and abnormalities on the chest X-ray compatible with severe pulmonary oedema. She needed artificial ventilation for 15 days. There appears to be a pathophysiological relationship between the development of pulmonary oedema and tocolytic therapy. Probably, pulmonary oedema may develop during tocolytic therapy as a result of several factors such as increased hydrostatic pressure, decreased oncotic pressure and perhaps capillary leakage.
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PMID:[A patient with pulmonary edema following use of beta-sympathomimetics (tocolytic agents)]. 203 83

Simple cardiopulmonary functions were studied serially in 26 mountaineers between sea level and an altitude of 25,200 ft. Up to 12,000 ft there was no altitude sickness, though there were complaints of leech bite (26.9%) and blisters (3.8%). One member died of exhaustion, two developed pulmonary oedema, one "flu" (at 15,600 ft) and one pleural rub (at 21,000 ft). Up to 16,000 ft altitude, 4 to 7.7% developed diarrhoea or epistaxis only, but at higher levels 25 to 50% subjects developed several symptoms, besides excessive dyspnea. These included diarrhoea (35-60%), vomiting (30%) abdominal pain (35-60%), rectal bleeding (15%), chest pain (10-40%), dry cough (40-60%), giddiness (30%) and poor memory (7.7%). A small rise in blood pressure was seen (for systolic at lower and diastolic at greater altitudes). After 18,200 ft the steady increase seen in VE slowed and the rise in heart rate and respiratory rate (f) became steeper. After a small rise at 7,800 ft, FVC and FEV1 showed a gradual decline at higher altitudes. After a large initial increase in PEFR up to 12,000 ft, a gradual decline was seen. The mean weight loss during the expedition was 8 +/- 2.7 kg. These changes seem to be due to an incomplete acclimatisation, which future mountaineering teams should take into consideration to avoid health problems and improve performance.
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PMID:Cardiopulmonary functional changes in acute acclimatisation to high altitude in mountaineers. 225 31

The clinical features of an inner-city population of 304 patients presenting with acute myocardial infarction (MI) with and without typical chest pain, were studied retrospectively. This population consisted of 172 men and 132 women; 155 (51%) were black, 88 (29%) hispanic, and 61 (20%) white, by self-identification. Typical ischemic chest pain was the presenting symptom in 85% (258); 15% (46) presented with nonchest symptoms, most frequently shortness of breath, abdominal pain, and dizziness. But the frequency of such nonchest symptoms was similar in both groups. When patients were grouped by the presence or absence of chest pain, the proportions of those without chest pain were significantly higher for blacks (22.7%) than hispanics (9.1%, P = 0.001) or whites (4.9%, P less than 0.01). Patients without chest pain also had higher admission systolic (P less than 0.01) and diastolic (P less than 0.01) blood pressures and more frequent histories of congestive heart failure (P less than 0.05), and more often presented with pulmonary edema (P = 0.001) than those with chest pain. Both groups were similar in age, sex, history of hypertension, and presence of hypertension on admission, defined as greater than or equal to 160/95 mmHg, prevalence of diabetes, history of smoking, previous MI, type of MI, history of angina, and mortality rates. Patients without chest pain were characterized by black race, history of congestive heart failure, elevated blood pressure and pulmonary edema than those with typical ischemic chest pain. Thus significant delays in the diagnosis and treatment of this important clinical entity may be reduced by alerting clinicians to these features and by educating selected patient groups.
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PMID:Clinical features of patients with acute myocardial infarction presenting with and without typical chest pain: an inner city experience. 252 Aug 50

High doses of cytosine arabinoside (ara-C) were administered by continuous infusion to 24 patients with acute leukemia in relapse or blast phase of chronic myelogenous leukemia (CML). Ara-C was infused at a dose rate of 250 mg/M2/hr for 36 to 72 hr. The major toxicities were myelosuppression, diarrhea, and abdominal pain. Other toxicities included pulmonary edema, neurotoxicity, and liver function abnormalities. The gastrointestinal toxicity was dose-limiting and a phase II dose was established at 250 mg/M2/hr for 60-72 hr. Four patients treated with this dose schedule had objective responses. Two patients with CML in blast phase returned to chronic phase and have remained stable without maintenance therapy for 12 and 18 months. Two patients with acute myelogenous leukemia in relapse entered complete remissions which continued unmaintained for 4 and 6 months. Steady-state plasma ara-C levels ranged between 7 and 24 x 10(-6) M, while ara-U levels were as high as 4.5 x 10(-4) M. There was no detectable accumulation of ara-C or ara-U during the infusion period. These findings would suggest that the continuous infusion of high dose ara-C may be useful in the treatment of acute leukemia and CML in blast crisis.
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PMID:Prolonged high dose ARA-C infusions in acute leukemia. 328 17

A 54 year old man, hospitalised for thoraco-abdominal pain resulting from a septicemia which gives positive hemocultures for streptococcus D Bovis, is diagnosed to have a splenic abscess which will require splenectomy. At the same time, an endocarditis develops and gets worse, with auriculo-ventricular blockade and, especially, major aortic insufficiency, which is the cause of death by a brutal and massive pulmonary oedema. In the progression of an endocarditis, the occurrence of a splenic abscess, primary localisation of the initial septicemia or the secondary of an arterial septic embolism, is a rare contingency compared to the frequency of splenomegaly or splenic infarction: less than 2 percent of the cases in the literature. This very atypical and exceptional case serves as a reminder, on the one hand, of the diagnostic inadequacy of echocardiography which cannot visualise vegetation in the course of progressive endocarditis, and, on the other, of the prognostic importance of auriculoventricular blockade in septal and aortic endocardial lesions.
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PMID:[Splenic abscess disclosing endocarditis]. 393 91

Twenty-eight peritoneovenous shunts were placed to relieve ascites in 26 patients with a variety of underlying malignancies. Nine of the patients had documented liver metastases and hyperbilirubinemia. Severe thrombocytopenia with laboratory evidence of disseminated intravascular coagulation (DIC) occurred in four of these nine patients following shunt placement. Relative or absolute thrombocytopenia was also commonly observed in this series. Other complications included pulmonary edema, ventricular tachycardia, culture-negative fever, pneumonia, and late shunt occlusion. Good palliation, with relief of abdominal pain or respiratory compromise, was achieved in 57% of these patients. Our experience suggests that DIC following peritoneovenous shunts in patients with malignancy may be more common than previously reported, although not as frequent as the incidence of DIC associated with shunt placement for cirrhotic ascites. Platelet aggregation or Factor X activation by ascitic fluid and failure of the liver to inactivate activated clotting factors may play a role in this coagulopathy. Because of the risk of potentially fatal DIC, palliative peritoneovenous shunts should be considered with caution in patients with liver metastases and hyperbilirubinemia.
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PMID:Thrombocytopenia and laboratory evidence of disseminated intravascular coagulation after shunts for ascites in malignant disease. 399 80

A review of the prelegal abortion scene in the US precedes discussion of the effect of injected soap, phenol, cresol, and their compounds. The latter is based on a review of 4 toxicology books. There is little difference in the symptoms after the instillation of phenols, cresols, or soaps. Any one of those agents can cause vaginal bleeding, abdominal pain and distension, nausea, vomiting, and cramps. The damage produced by the use of Lysol thus is due to both the phenol and soap components of the compound. Following instillation into the uterus, there is coagulation necrosis of the decidua and placental site. The toxin will invariable cause thrombosis of the intrauterine and parametrial veins. The thrombosis may spread to the entire pelvic vein plexus and paravaginal, paracervical, and ovarian veins. The liver and kidney are affected by the toxin. Icterus and bile pigments in the urine and clinical evidence of liver damage are seen often. Pulmonary edema has been described as have microscopic to massive pulmonary oil emboli and thrombosis. Depression of all bone marrow elements due to toxin has been reported. The red blood cells are further depressed in number because of hemolysis. Cerebral changes include oil emboli, cerebral coagulation, necrosis, and petechial hemorrhages. Until Studdiford and Douglas described gram-negative sepsis causing shock, patients admitted with hypotension accompanying septic abortion were thought to have concealed blood loss. Studdiford and Douglas showed that gram-negative septicemia could produce hypotension. With the advent of massive antibiotic therapy for septic abortion and septic shock, most of these patients could be saved. The kidneys, after exposure to phenolic-soap comounds, show mainly lower nephron changes. As long as the toxin is in the system those changes continue until irreversible renal damage occurs. It is essential to remove the source of the poison (the affected uterus) and then remove the circulating toxins. the main problem is removal of the circulating toxin. In addition to the problems produced by fixed and circulating toxin, it has been shown that most phenol-soap induced abortions are infected. Thus it is necessary to employ the optimal antibiotic therapy for septic incomplete abortion. The initial management phase moves along classic lines. First is monitoring the vital state and supporting the systems. This includes maintaining an intravenous solution with a large-bore needle, monitoring central venous pressure, measuring urinary output, monitoring the vital signs, maintaining adequate oxygenation, and supporting the blood pressure with blood vasopressors or other agents, as needed. Second is diagnosing the extent of the illness. Third is the initial treatment, which includes reestablishment of the blood volume with blood transfusions; aggressive coverage with double or triple antibiotic therapy; correction of hypofibrinogenemia with cryoprecipitate, fresh whole blood or fresh frozen plasma, as indicated; and avoidance of overhydration in the presence of actual or suspected renal failure. After antibiotic coverage has been established, removal of retained products of conception is indicated.
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PMID:Treatment of women who have undergone chemically induced abortions. 404 35

Intravenous injection of crude marijuana extract led to development of an acute illness with multisystem involvement. Gastrointestinal manifestations consisted of severe vomiting, diarrhea, and crampy abdominal pain. Hypotension, tachycardia, and peripheral vasodilation constituted the main cardiovascular manifestations of the disease. Moderate azotemia and oliguria, presumed to be of prerenal origin, were present and rapidly resolved with administration of intravenous fluids. Hematologic manifestations consisted of leukocytosis with a left shift, thrombocytopenia, prolonged partial thromboplastin time, increased fibrin degradation products, and positive protamine sulfate test. The observed coagulation abnormalities may suggest intravascular coagulation. C3, C4, and total hemolytic complement were reduced, suggesting possible activation of the complement system. Hyperventilation, hypoxemia, pulmonary edema, obstructive, and restrictive pulmonary function abnormalities and bilateral pleural effusions highlighted the pulmonary manifestations of the disease. Rhadbomyolysis and mild hepatic function abnormalities were also present. All observed abnormalities reversed in a few days with no significant sequelae.
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PMID:Toxicity with intravenous injection of crude marijuana extract. 723 64


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