Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 19-year old woman ingested an unknown amount of sodium azide (NaN3). The earliest symptoms were nausea and loss of vision. Within a few hours her clinical features were dominated by central nervous system signs, acute pulmonary edema, lactic acidosis, and hypothermia. The patient died within 12 hours, hypotension and shock occurring as preterminal events. This was the first recorded case in which antidotal methemoglobin production was attempted. Sodium nitrite administration resulted in methemoglobinemia but did not appreciably alter the clinical course and may not be of major benefit. Gross examination post-mortem showed marked pulmonary edema, visceral hemorrhage and congestion, and slight cerebral edema. Microscopically, the lungs showed alveolar and interstitial edema and a polymorphonuclear infiltrate. There were petechial hemorrhages and severe nonspecific changes in the brain.
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PMID:Fatal self-administration of sodium azide. 114 58

11 cases of cerebral venous thrombosis in adults are reported. Main clinical signs are: intracranial hypertension (headache, nausea, papilledema in 7 cases, loss of consciousness in 6 cases, neurological deficit in 6 cases, seizure in 4 cases. 1 patient is dead, who did not receive heparin treatment. Delay before diagnosis is between 2 and 20 days, and is shortened when arteriography or MRI are available and prescribed. At least one (or several) CT examination was performed in 10 patients. Direct signs of thrombosis are uneasily detected without contrast injection, seen here in 4 cases. Empty delta sign is observed in 7 patients, lately in 4 cases, and once only afterwards. Cerebral infarction is visualized in 7 cases over 10. Its features frequently seem evocative for cerebral venous thrombosis: triangularin 4 cases or nodular shape in 3 cases with hemorragic infarct in 7 cases, with bilateral topography in 6 cases, in frontal or central areas in 7 cases. 6 patients had a MRI examination. All cerebral infarctions appeared haemorragical, even at early stages. During subacute period, venous thrombosis is constantly and easily detected by the mean of methemoglobin high signal intensity on T1 weighted images. The prediagnosis delay is short, without necessity of arteriography. MRI should take the place of CT and arteriography in investigation of a clinically suspected cerebral venous thrombosis.
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PMID:[Thrombosis of the cerebral veins. X-ray computed tomography and MRI imaging. 11 cases]. 160 50

Among the potential hazards of laparoscopic surgery using electrocautery is the release of chemical by-products of incomplete tissue combustion into the pneumoperitoneum with subsequent transperitoneal absorption into the bloodstream and/or release into the operating room. The purpose of this study of patients undergoing laparoscopic cholecystectomy (LC) was twofold: (1) to assess the relationship between intraperitoneal concentration of carbon monoxide (CO) and blood levels of carboxyhemoglobin (COHb) and methemoglobin (MetHb), and (2) to assess the surgeon's inhalation of CO resulting from ambient smoke exposure. During LC with monopolar electrocautery, 21 patients were evaluated intraoperatively for intraperitoneal [CO] by sampling gas from a trocar, whereas arterial [COHb) and [MetHb] were determined perioperatively. The surgeon's venous blood was drawn pre- and postoperatively to assay [COHb] and [MetHb]. Patients completed visual analogue questionnaires 6 hours and 24 hours postoperatively to assess for adverse symptoms. Mean (+/- SEM) patient age and weight were 45 +/- 3 years and 84 +/- 4 kg, respectively. Mean duration of the operation was 69 +/- 5 minutes, and electrocautery was used for 3.0 +/- 0.3 minutes. Intraperitoneal [CO] rose to peak levels of 209 +/- 19 ppm at 50 minutes, whereas systemic [COHb] and [MetHb] were unchanged. The surgeon's systemic [COHb] and [MetHb] did not increase postoperatively. Nausea, abdominal pain, and fatigue scores decreased significantly between 6 and 24 hours postoperatively; however, there were no correlations between these symptoms and peak intraperitoneal [CO]. Although LC using electrocautery increases intraperitoneal [CO] to "hazardous" levels, systemic [COHb] and [MetHb] are not elevated by generation of intraperitoneal smoke. The surgeon's exposure to CO by the evacuation of smoke through laparoscopic ports is negligible. Production of smoke during LC using monopolar electrocautery, therefore, does not appear to pose a threat to either the patient or the surgeon.
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PMID:Production and systemic absorption of toxic byproducts of tissue combustion during laparoscopic cholecystectomy. 984 98

We describe the case of an adolescent girl who received high-dose metoclopramide in combination with oral N-acetylcysteine therapy for acute acetaminophen toxicity. Whole blood-sample analysis for abnormal hemoglobin pigments established the diagnosis of sulfhemoglobinemia. Metoclopramide has been shown to cause sulfhemoglobinemia, particularly when used in repeated high doses. Although N-acetylcysteine alone has not been associated as the cause, we suggest that sulfhemoglobine-mia is a potential complication in patients treated with metoclopramide for the nausea that often accompanies oral N-acetylcysteine therapy for acetaminophen toxicity. Cyanosis without respiratory distress should suggest this diagnosis.
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PMID:An adolescent case of sulfhemoglobinemia associated with high-dose metoclopramide and N-acetylcysteine. 1049 55

On rare occasions benzocaine has produced methemoglobinemia from oral, rectal and dermal exposures. There is disagreement whether this is an idiosyncratic event or a dose-related event. To gain a better perspective on this problem we retrospectively reviewed cases at 4 large regional poison centers of children <18-y of age from 1993-1996. One hundred and eighty-eight benzocaine exposures were reported. Mean and median ingested dosage were 86.8 (+/- 89.5) mg/kg and 50 mg/kg, respectively. Fifty-eight patients (30%) were managed in the emergency department; 8 patients had methemoglobin levels determined. One child had a methemoglobin level of 19%; all others were <1%. One hundred and seventy-three patients (92%) remained asymptomatic. Other symptoms were minor: oral numbness (8), vomiting (3), and 1 each of oral irritation, dizziness and nausea. In this series of accidental ingestions of benzocaine-containing products cyanosis was rare and apparently not dose related. These cases may be safely managed at home with telephone follow up for at least 2 h. If there is evidence of cyanosis, dusky pallor, shortness of breath, or change in mental status direct medical evaluation should be recommended.
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PMID:Multi-center retrospective evaluation of oral benzocaine exposure in children. 1092 90

Posttransplant lymphoproliferative disorder (PTLD) is a serious complication after solid organ transplantation. An elevated serum lactate dehydrogenase (LDH) is a marker of PTLD activity. We report the case of a 58-year-old female renal transplant patient with a prior history of extranodal PTLD, which developed 19 years after a second transplant. She was successfully treated with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) and maintained subsequently on sirolimus and prednisone. She presented 3 years later with fever, dyspnea, cough, lung infiltrates and elevated serum LDH concerning for recurrence of PTLD. Bronchoscopy revealed Pneumocystis carinii (jiroveci) pneumonia. The patient was treated with trimethoprim-sulfamethoxazole, but developed nausea and was converted to dapsone. The patient was readmitted 4 weeks later with increasing dyspnea and hypoxemia and found to have a methemoglobin level of 16%. Dapsone was discontinued with resolution of all symptoms. We discuss the diagnostic and clinical challenges in this complex case.
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PMID:Didactic lessons from the serum lactate dehydrogenase posttransplant: a clinical vignette. 1829 52

There is a long list of prescribed and over the counter oxidizing agents that can induce methemoglobinemia. We report a case of methemoglobinemia in a 46-year-old man with a mayor depression disorder who ingested 30 pills of diphenhydramine, 30 pills of haloperidol, 20 pills of dolagesic, 20 pills of cyclobenzaprine, 20 pills of naproxen, 14 pills of cephalexin, and 48 pills of chlorzoxazone. On admission, he was on mechanical ventilation, and responded only to painful stimuli. Five hours later his face, hands and feet became cyanotic. The pulse oximetry revealed a Sp02 of 85%. The dark chocolate color arterial blood showed a Pa02 of 290.8 mm Hg and oxygen saturation (Sa02) of 99%. The chocolate color arterial blood and unchanged Sp02 suggested the diagnosis of methemoglobinemia. One mg per Klg of intravenous methylene blue was administered in 5 minutes. Twenty minutes later, the cyanosis began to fade and one hour later, it had disappeared and the Sp02 was 99%. Early treatment of methemoglobinernia is crucial in preventing tissue hypoxia. Methylene blue is the treatment of choice in symptomatic patients. The initial dose of methylene blue is 1-2 mg/kg of a 1% solution administered over 5 minutes. Reduction of methemoglobin is usually complete within 1 hour. If methemoglobinernia persists, a second dose not to exceed a total dose of 5-7 mg/kg may be administered. Because headache, nausea, vomiting, diarrhea, and angina may occur with therapeutic doses, methylene blue should only be administered to those patients with symptoms or signs of hypoxia.
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PMID:Methemoglobinemia: life-threatening hazard of multiple drug ingestions. 1960

We describe the case of an adolescent girl who received high-dose metoclopramide in combination with oral N-acetylcysteine therapy for acute acetaminophen toxicity. Whole blood-sample analysis for abnormal hemoglobin pigments established the diagnosis of sulfhemoglobinemia. Metoclopramide has been shown to cause sulfhemoglobinemia, particularly when used in repeated high doses. Although N-acetylcysteine alone has not been associated as the cause, we suggest that sulfhemoglobinemia is a potential complication in patients treated with metoclopramide for the nausea that often accompanies oral N-acetylcysteine therapy for acetaminophen toxicity. Cyanosis without respiratory distress should suggest this diagnosis.
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PMID:An adolescent case of sulfhemoglobinemia associated with high-dose metoclopramide and N-Acetylcysteine. 2814 71