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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of acute pancreatitis with diabetic ketoacidosis associated with increased serum myoglobin concentration, acute renal failure, and disseminated intravascular coagulation. A 49-year-old man suffering from diarrhea, vomiting, and somnolence was admitted to the hospital. He had had flu-like symptoms for 4 days prior to the onset of these symptoms. He was a habitual drinker and had been consuming 360 ml-900 ml of the drink "shochu" (distilled spirits containing 28% alcohol) daily for 30 years. Laboratory data on admission revealed elevated serum levels of pancreatic enzymes, including amylase, trypsin, lipase, pancreatic secretory trypsin inhibitor (PSTI), phospholipase A2 (PLA2), and elastase-1, as well as elevated levels of glucose (373 mg/dl), ketone bodies (3675 mumol/l), and myoglobin (229.8 ng/ml). Treatment with subcutaneous insulin and intravenous administration of electrolyte fluid and the systemic protease inhibitor, gabexate mesilate, was begun immediately. Early after the initiation of treatment, there was an increase in serum creatinine (4.9 mg/dl), and thromobocytopenia (15000/microliters) was observed. The patient completely recovered from renal failure and acute pancreatitis, but required insulin therapy. Alcohol ingestion and dehydration are thought to have played a major role in the triggering of the acute pancreatitis. We examined the relationship among acute pancreatitis, diabetic ketoacidosis, and hypermyoglobinemia in the literature.
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PMID:Acute pancreatitis with diabetic ketoacidosis associated with hypermyoglobinemia, acute renal failure, and DIC. 884 91

A 51-year-old man presented with headache, vomiting and exophthalmus. Neurological examination revealed anosmia, papilledema, decrease in visual acuity, and disability in ocular movement. MRI showed a huge mass which occupied the whole nasal cavity and compressed the frontal lobe upwards and the eyes laterally. CT revealed an extensive bony destruction of the frontal base and bilateral orbits. The mass was biopsied transnasally, and was histologically diagnosed as olfactory neuroblastoma. It was highly radiosensitive and disappeared with a local irradiation of 40 Gy. Three months later the patient complained of a pain radiating from the neck to the right arm. MRI demonstrated a metastasis at the vertebral body of C5. Local irradiation of 30 Gy was performed. The metastatic lesion was removed, and a bone graft taken from the iliac bone was transplanted via an anterior cervical approach. Three weeks later, however, a hard mass appeared in the right of his neck and was surgically removed. By histological examination, it was also identified as a metastatic neuroblastoma to the cervical lymph node. A week after the removal of the cervical metastatic lesion, the metastasis extended rapidly to the left cervical and the bilateral hilar lymph nodes of the lungs. Chemotherapy was performed with a total doses of 800mg of cyclophosphamide, 1.5mg of vincristine, 40mg of pirarubicin, and 80mg of cisplatin. The lesions disappeared within 7 days. However, the patient died from disseminated intravascular coagulation 10 months after the onset. Olfactory neuroblastoma is usually an intranasal neoplasm, but it rarely extends intracranially and intraorbitally as is shown in our case. Basically, olfactory neuroblastoma is a relatively slow-growing tumor though it has a tendency to develop local recurrences over long periods even after aggressive primary treatment, and accompanied with distant metastases. However, our patient showed a very short survival time. Invasive extension and multiple metastases occurred during a short period, followed by disseminated intravascular coagulation. Combined chemotherapy at the initial treatment may be recommended in such an extensive case.
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PMID:[A case of olfactory neuroblastoma with intracranial, intraorbital extension and multiple metastases]. 902 94

Individuals with Prader-Willi syndrome (PWS) have excessive appetite with the ability to consume large quantities of food. Absence of vomiting and a high pain threshold are considered manifestations of the disorder. We present 6 patients with PWS with acute dramatic gastric distention. In 3 young adult women with vomiting and apparent gastroenteritis, clinical course progressed rapidly to massive gastric dilatation with subsequent gastric necrosis. One individual died of overwhelming sepsis and disseminated intravascular coagulation. In 2 children, gastric dilatation resolved spontaneously. Gastrectomy specimens--in 2 cases subtotal and distal, in the other with accompanying partial duodenectomy and pancreatectomy--showed similar changes. All cases demonstrated signs of ischaemic gastroenteritis. All specimens showed diffuse mucosal infarction with multifocal transmural necrosis. Vascular dilatation and small bifrin thrombi were apparent within the infarcted areas. These 6 women with PWS had acute idiopathic gastric dilatation. It is possible that a predisposition to acute gastric dilatation may be related to abnormal gastric homeostasis on a genetic basis. Understanding the mechanisms responsible for this event could increase the understanding of gastrointestinal and appetite regulation in individuals with PWS.
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PMID:Acute idiopathic gastric dilation with gastric necrosis in individuals with Prader-Willi syndrome. 941 71

This report describes a 12-year-old girl who developed vaccine-type pneumococcal septicemia (type 4, Danish nomenclature) 2 years after splenectomy for recurrent idiopathic thrombocytopenia despite vaccination with the 23-valent vaccine 4 weeks before surgery and antibiotic prophylaxis with penicillin V. The disease presented as high fever with shivering and vomiting followed by disseminated petechiae and a deteriorated general condition. Initial laboratory studies showed severe sepsis with leucocytopenia and thrombocytopenia, a markedly elevated CRP, and disseminated intravascular coagulation. Despite antibiotic treatment, which was initiated with clindamycin, cefotaxime and trimethoprim/sulfamethoxazole and was switched to cefotaxime and penicillin after the result of the blood culture had been obtained, the patient had to be ventilated, and hemofiltration became necessary because of acute renal insufficiency. Furthermore, she required amputation of all her toes because of severe necrosis. No type-specific pneumococcal antibody titers were detected during and after infection. It remains unclear whether the susceptibility to Streptococcus pneumoniae was due to primary failure of antibody production or a decline in antibody levels after vaccination. Patients and/or their relatives should be informed that neither vaccination nor continuous antibiotic prophylaxis can guarantee full protection against infection with S. pneumoniae in patients after splenectomy.
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PMID:Overwhelming postsplenectomy infection with vaccine-type Streptococcus pneumoniae in a 12-year-old girl despite vaccination and antibiotic prophylaxis. 942 57

A 29-year-old woman with a triplet pregnancy received emergency caesarean section in the 33rd week of pregnancy. She lost 2 babies, one of whom was a fetal death and the other a neonatal death. Three weeks before delivery, she was admitted to hospital suffering from vomiting, diarrhea and polyuria. There were no laboratory abnormalities such as a slightly elevated levels of liver enzymes, nor any clinical symptoms of preeclampsia. At the end of the operation, disseminated intravascular coagulation (DIC) occurred and HELLP syndrome was diagnosed. However, the hemoglobin level was in the normal range at this point. On the 2nd postoperative day, hemolytic anemia developed in spite of the resolution of other problems. We suggested that the hemolysis, which may have been caused by a latent hemoconcentration and a membrane disorder of the red cells, was an osmotic hemolysis. This case was unique for the following reasons; 1) a lack of symptoms of hypertension, proteinuria and edema, 2) complications due to diabetes insipidus, 3) postpartum severe hemolysis following latent hemoconcentration, and 4) slow progress of the condition after onset. Early detection of HELLP syndrome is difficult. It should be considered in the management of patients with unrecognizable hemoconcentration and nonspecific complications.
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PMID:[HELLP syndrome in triplet pregnancy complicated by DIC and transient diabetes insipidus]. 951 34

Clinical Confusion between human babesiosis and malaria is often reported in the literature. Headache, fever, chills, nausea, vomiting, myalgia, altered mental status, disseminated intravascular coagulation, anaemia with dyserythropoiesis, hypotension, respiratory distress, and renal insufficiency are common to both diseases. This remarkable similarity is not restricted to the human host. In the mouse, for example, the histological changes wrought by fatal malaria (Plasmodium vinckei) and babesiosis (Babesia rhodaini) are identical, and parasites of both genera cross-protect. Malarial disease pathogenesis is now generally associated with excessive production of pro-inflammatory cytokines , such as tumour necrosis factor. While this concept has not yet been examined in babesiosis, indirect evidence arises from noting the parasite density at which illness occurs in primary infections caused by either organism. Naive mice tolerate high loads of malarial or babesial parasites before they become ill, and are also tolerant to endotoxicity, which is mediated by these same cytokines. In contrast, humans require very much smaller loads of Plasmodium or Babesia spp. before becoming ill, and likewise are very sensitive to endotoxin, the harmful effects of which are mediated by the pro-inflammatory cytokines. For these reasons, as discussed in this review, the diseases caused by these two genera of intra-erythrocytic protozoan parasites will probably prove to be conceptually identical.
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PMID:Do babesiosis and malaria share a common disease process? 968 99

Six patients with severe and complicated falciparum malaria (6.7 +/- 2.7 WHO criteria) were admitted to our Intensive Care Unit. All patients acquired the disease while travelling in tropical Africa without appropriate chemoprophylaxis. The clinical manifestations included hyperpyrexia (all patients), chills (4), sweating (2), asthenia (3), anorexia (2), headache (1), arthralgias (1), vomiting (4), diarrhoea or abdominal discomfort (3), jaundice (2) and disturbances of consciousness (4). All patients had anemia, thrombocytopenia, hyponatremia, hypoproteinemia, hypoalbuminemia, hypocalcemia and acute renal failure, in one case associated with anuria. A low grade parasitemia was observed in two patients and a high grade parasitemia (20%-58% of erythrocytes) in four. Exchange transfusion was performed only in high parasitemic patients and all of them survived. All patients were treated with quinine, a sulfonamide and pyrimethamine. Additionally, five patients received oxytetracycline, doxycycline or clindamycin. Three patients required hemodyalisis. Five patients had delirium, coma or seizures. All patients had at least one sign of hepatic impairment: liver enlargement, jaundice or increased bilirubin or aminotransferase levels. Two patients had spleen enlargement. Laboratory findings suggested disseminated intravascular coagulation in four patients. Four patients developed pulmonary changes and three of them required mechanical ventilation. A Swan-Ganz catheter was placed in four patients. In three of them (two with pulmonary edema) the pulmonary capillary wedge pressure was initially increased, which suggested a cardiogenic or hypervolemia mechanism, but soon returned to normal level. One patient with low grade parasitemia died because of adult respiratory distress syndrome after 18 days. In our series, the degree of parasitemia was not related to the severity of the disease.
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PMID:[Severe and complicated malaria. Report of six cases]. 977 80

Massive bee envenomation can produce both immediate and delayed toxic reaction. Signs and symptoms of immediate toxic reaction are fatigue, nausea, vomiting, hemolysis, kidney failure, and disseminated intravascular coagulation. The label "delayed toxic reaction" refers to a patient who is asymptomatic after a massive bee envenomation, with normal initial laboratory results, but later demonstrates laboratory evidence of hemolysis, coagulopathy, thrombocytopenia, rhabdomyolysis, liver dysfunction, and disseminated intravascular coagulation. The subject of this case report, a 66-year-old man, was stung more than 125 times in an attack by Africanized bees. He was initially asymptomatic, except for pain, and his laboratory findings were normal. The first signs of his fatal multi-organ-system failure were not apparent until 18 hours after envenomation. This experience has led the Good Samaritan Regional Poison Center in Phoenix, AZ, to recommend a 24-hour hospitalization for pediatric patients, older patients, and patients with underlying medical problems who are asymptomatic or who are experiencing only pain after an envenomation of 50 or more stings. Such patients have an increased risk of tissue injury, which may be delayed and which may be more effectively treated if identified early rather than on 12- to 24-hour follow-up. All other envenomated, asymptomatic patients or envenomated patients experiencing only pain who become symptomatic or who belatedly exhibit laboratory values consistent with hemolysis, thrombocytopenia, rhabdomyolysis, liver dysfunction, kidney failure, and disseminated intravascular coagulation within a 6-hour emergency department observation period should be admitted. Intravenous fluids, blood products, dialysis, and other intensive measures should be initiated if necessary.
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PMID:Delayed toxic reaction following massive bee envenomation. 1046 Jan 41

A 32-year-old woman was admitted with a diagnosis of impending premature delivery. In the 37th week of pregnancy, vaginal examination was performed. After ten minutes, vomiting, whole body flushing, and cold sweat appeared suddenly. Because fetal heart rate became 60-70 beats.min-1, emergency caesarean section was scheduled. When she arrived at the operating room, blood pressure was 75/45 and heart rate was 122 beats.min-1. Five minutes later, anesthesia was induced with thiopental and vecuronium, and operation was instituted concomitantly. After the delivery, pentazocine and midazolam were administered. During the operation, premature separation of normally implanted placenta or pressed cord was not observed. Hydrocortisone was administered for circulatory collapse. Gabexate mesilate was administered for the prevention of DIC. The scratch test, performed ten days later, revealed that latex was positive but lidocaine was negative. Therefore, it was concluded that anaphylaxis induced by latex gloves caused shock after internal examination.
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PMID:[A case of emergency caesarean section as a result of anaphylaxis to latex]. 1003 99

A 34-year-old obese woman with human immunodeficiency virus (HIV) infection diagnosed a year earlier was seen because of nausea, vomiting, and intermittent diarrhea for 3 weeks. Her current medications included zidovudine. Physical examination revealed tachypnea and tender hepatomegaly. Computed tomography of the abdomen showed hepatomegaly with fatty infiltration. Liver enzymes were within normal range except for elevated lactate dehydrogenase (LDH). The serum bicarbonate value was low, with a lactate level three times normal. The tachypnea and dyspnea worsened as lactate concentrations rapidly increased to 15 times normal. Although her Po2 and cardiac index were initially adequate, the patient had acute respiratory failure. She died with multiorgan dysfunction, including hepatic failure, severe lactic acidemia, disseminated intravascular coagulation, and renal failure. Autopsy revealed hepatomegaly and massive steatosis. Physicians should consider lactic acidosis in patients taking zidovudine and having unexplained tachypnea, dyspnea, and low serum bicarbonate concentrations.
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PMID:Zidovudine-associated type B lactic acidosis and hepatic steatosis in an HIV-infected patient. 1021 65


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