Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Heroin lung is the most frequent complication of heroin intoxication. In September 1991 and January 1993, two young men aged 19 and 22 years presented with a sudden loss of consciousness and cyanosis after injecting heroin. They were both brought to our emergency department in the night and were immediately intubated and given 100% oxygen. Following intravenous naloxone, they both regained consciousness. The first patient's chest X ray revealed increased bilateral perihilar lung markings and mild patchy alveolar edema while the second patient showed a bat's wing shaped confluent alveolar edema. The blood gases in both cases revealed hypoxemia and hypercapnia. Follow-up chest roentgenograms on the second hospital day in case 1 and the third hospital day in case 2 revealed partial clearing of the lung fields. Fever developed on the second hospital day and they both received two weeks of antibiotics prior to discharge. Case 1 had normal pulmonary function testing, but case 2 developed mild restrictive lung changes. Review of the literature shows that heroin can cause a fulminant but rapidly reversible form of pulmonary edema. The treatment for this noncardiogenic pulmonary edema is adequate ventilation, good pulmonary toilet, and naloxone to reverse the respiratory and central nervous system depression. Diuretics, digitalis and morphine are not recommended in the treatment of heroin lung.
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PMID:Heroin lung: report of two cases. 791 90

This report is of two adult patients who were scheduled for excision of carotid body tumours. One of the patients had bilateral tumours, while the second had a unilateral tumour. In the first, anaesthesia was maintained by nitrous oxide:oxygen and halothane 1-2%. Postoperatively, the intramuscular injection of meperidine 75 mg resulted in apnoea, cyanosis, and loss of consciousness. In the second, anaesthesia was maintained by nitrous oxide:oxygen, supplemented by fentanyl 2 micrograms.kg-1 and incremental doses of vecuronium. Following complete reversal of neuromuscular block, the patient became wide awake but spontaneous breathing was resumed at a rate of only two to three breaths per minute, and the oxygen saturation as monitored by pulse oximetry decreased to 50%. Naloxone 0.4 mg iv increased the respiratory rate to 14 per minute and the oxygen saturation to 98%. The report suggests that surgical excision of carotid body tumours, whether unilateral or bilateral, can be followed by severe postoperative respiratory depression. The complication may be attributed to opioid administration in the absence of peripheral chemoreceptor drive.
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PMID:Postoperative respiratory depression following excision of carotid body tumours. 800 36

In normal erythrocytes, small quantities of methaemoglobin are formed constantly and are continuously reduced, almost entirely by the reduced nicotine adenine dinucleotide (NADH) diaphorase system, rather than the reduced nicotine adenine dinucleotide phosphate (NADPH) diaphorase system. Methaemoglobinaemias are usually the result of xenobiotics, either those that may directly oxidise haemoglobin or those that require metabolic activation to an oxidising species. The most clinically relevant direct methaemoglobin formers include local anaesthetics (such as benzocaine and, to a much lesser extent, prilocaine) as well as amyl nitrite and isobutyl nitrite, which have become drugs of abuse. Indirect, or metabolically activated, methaemoglobin formation by dapsone and primaquine may cause adverse reactions. The clinical consequences of methaemoglobinaemia are related to the blood level of methaemoglobin; dyspnoea, nausea and tachycardia occur at methaemoglobin levels of > or = 30%, while lethargy, stupor and deteriorating consciousness occur as methaemoglobin levels approach 55%. Higher levels may cause cardiac arrhythmias, circulatory failure and neurological depression, while levels of 70% are usually fatal. Cyanosis accompanied by a lack of responsiveness to 100% oxygen indicates a diagnosis of methaemoglobinaemia, which should be confirmed using a CO-oximeter. Pulse oximeters do not detect methaemoglobin and may give a misleading impression of patient oxygenation. Methaemoglobinaemia is treated with intravenous methylene blue (methyl-thioninium chloride; ;1 to 2 mg/kg of a 1% solution). If the patient does not respond, perhaps because of glucose-6-phosphate dehydrogenase (G6PD) deficiency or continued presence of toxin, admission to an intensive care unit and exchange transfusion may be required. Dapsone-mediated chronic methaemoglobin formation can be reduced by coadministration of cimetidine to aid patient tolerance. Increasing knowledge and awareness of drug-mediated acute methaemoglobinaemia among physicians should lead to prompt diagnosis and treatment of this potentially life-threatening condition.
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PMID:Drug-induced methaemoglobinaemia. Treatment issues. 882 17

A case of severe accidental hypercapnia during anesthesia is presented. A 44-year-old woman underwent laparotomy under general anesthesia. Forty minutes after the start of the operation, BP rose slightly and HR increased from 110 to 140 x min-1. Then ST segment depression was noted on ECG monitor. Therefore, nitrous oxide was discontinued for 20 minutes. Frequent oxygen supply with oxygen flush was needed to inflate the collapsed bag. The operation was concluded without additional clinical problems. The patient remained unconscious after the anesthetics were discontinued. Cyanosis was observed despite the delivery of 100% oxygen. Cardiac arrest occurred following abrupt bradycardia, but she responded immediately to resuscitation. She was in a deep comatose state and did not respond to painful stimuli. The pupils were fully dilated with absent light reflex. Arterial blood gas analysis revealed; pH 6.720, PaCO2 277 mmHg, PaO2 159 mmHg, and BE-16.2. Disconnection of anesthetic circuit was noted, thereafter, and hyperventilation was performed. Then, the pupils became promptly constricted and the response to painful stimuli appeared within 30 minutes. Her level of consciousness recovered completely after 4.5 hours of hyperventilation. She suffered from refractory hypotension (BP70-85 mmHg in systolic pressure) in spite of catecholamine administration, tachycardia (HR 140-160 x min-1) and ARDS in the ICU, but all the symptoms disappeared by the 16 hours after ICU admission.
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PMID:[A patient who manifested various symptoms following severe accidental hypercapnia]. 899 34

A sudden death syndrome was induced in chicks and poults fed diets containing Fusarium fujikuroi, formulated to contain 0-330 mg/kg moniliformin (M) with or without the maximum recommended therapeutic concentration of monensin. Lesions of monensin toxicosis were not observed. Clinical signs were referable to cardiac dysfunction (sudden death, dyspnea, cyanosis, depression). Poults and chicks dying early in the study had no gross lesions or had lesions of right ventricular dilation. Treated poults and chicks dying late in the study or euthanatized at termination of the study had lesions of bilateral myocardial hypertrophy, usually concentric. Absolute heart weights and relative heart weights, expressed as a percentage of body weight, were significantly greater in treated birds than controls (P < 0.05), whereas body weights were significantly less (P < 0.05). Microscopically, lesions progressed from acute myocardial degeneration to necrosis, fibrosis, and hypertrophy. Ultrastructural findings were consistent with the gross and microscopic lesions. Serum pyruvate concentrations were a useful indicator of M-induced cardiotoxicosis. Concentrations of serum pyruvate increased with increased concentration of dietary M, but were not affected by addition of monensin to the diet. In chicks ingesting 40-300 mg/kg M, serum pyruvate concentrations were significantly greater (P > 0.05) than those in controls (controls, 0.28 +/- 0.08 mmol/liter; exposed 0.38 +/- 0.11-0.55 +/- 0.13 mmol/liter). Poults ingesting 80-330 mg/kg M had significantly greater serum pyruvate concentrations than controls (controls 0.33 +/- 0.09 mmol/liter; exposed 0.43 +/- 0.13-1.00 +/- 0.006 mmol/liter). The Vetronics System was used to evaluate electrocardiographic alterations in a limited number of chicks and poults surviving to the end of the feeding trial. Electrocardiographic alterations in poults and chicks fed diets containing > or = 40 mg/kg and > or = 160 mg/kg M, respectively, were consistent with ventricular hypertrophy, myocardial injury, and hypoxia. Electrocardiographic alterations were more striking in poults than in chicks. Altered myocardial metabolism due to M toxicosis, in conjunction with the unusual susceptibility of domestic poultry to altered cardiac metabolism, is believed to be the cause of the organ-specific lesions in these birds. These findings suggest that cardiac injury with subsequent alterations in cardiac electrical conductance may be a cause of the sudden deaths observed in poultry chronically intoxicated with dietary M.
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PMID:A sudden death syndrome induced in poults and chicks fed diets containing Fusarium fujikuroi with known concentrations of moniliformin. 908 17

The most important complications from tonsillectomy and adenoidectomy are bleeding, stridor, and laryngospasm. This controlled, double-blind study was designed to investigate the effects of topical and intravenous lidocaine on stridor and laryngospasm. A total of 134 patients scheduled for elective tonsillectomy and/or adenoidectomy were randomly separated into four groups. In the topical lidocaine group 4 mg/kg of 2% lidocaine was applied to subglottic, glottic, and supraglottic areas before endotracheal intubation. Normal saline solution was used topically for the first control group. In the intravenous lidocaine group, patients were given 1 mg/kg of 2% lidocaine before extubation, and the same amount of 0.9% NaCl was given to the second control group. Postoperative stridor, laryngospasm, cyanosis, bleeding, sedation degree, and respiratory depression were observed, and plasma lidocaine levels were measured. Both topical and intravenous lidocaine groups revealed less stridor and laryngospasm than the control groups, and no difference was found between the topical and intravenous lidocaine groups except the higher sedation scores in the early postoperative period for the intravenous lidocaine group.
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PMID:The use of preoperative lidocaine to prevent stridor and laryngospasm after tonsillectomy and adenoidectomy. 962 58

A 72-year-old male developed shock syndrome after a single dose of bromocriptine. He had undergone uncomplicated subtotal removal of an invasive prolactinoma in our department. The patient had normal ranges of pituitary hormones apart from hyperprolactinemia (167.7 ng/ml) after surgery. An acute suppression test with bromocriptine (2.5 mg per os) was done in the supine position 6 days following surgery. Three and a half hours after bromocriptine administration, he suddenly complained of anterior chest discomfort in bed. Cyanosis and profuse diaphoresis were noted. His blood pressure was 80/60 mmHg. Electrocardiography revealed sporadic premature contractions and slight depression in the ST segments. He recovered in about 10 hours after a rapid infusion of corticosteroid and lactic Ringer solution, and was discharged without sequelae. This is a very rare complication of bromocriptine, but the cardiovascular function of patients taking bromocriptine for therapeutic and diagnostic purpose should be monitored carefully.
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PMID:Shock syndrome induced by bromocriptine test in a patient with prolactinoma--case report. 986 53

The suggested role of oxidative stress in the pathogenesis of heart failure is largely based on utilizing left heart failure models. The present study on rats evaluated changes in antioxidants as well as oxidative stress in relation to hemodynamic function subsequent to the right heart failure induced by monocrotaline (50 mg/kg, i.p.). During the post-injection period, monocrotaline (MCT)-treated rats demonstrated a persistent growth depression. Two to three weeks after the injection, MCT-treated rats showed signs of fatigue, peripheral cyanosis and dyspnea. In these rats, right heart hypertrophy was confirmed by a significant increase in right ventricular weight as well as right ventricle to body weight ratio. In MCT-treated rats, there was also a significant increase in right ventricular systolic as well as end diastolic pressures. No change in lung and liver wet/dry weight ratios between MCT-treated and control animals was observed. Based on the hemodynamic data as well as other clinical observations, the functional stage achieved was compensated heart failure. Myocardial antioxidant enzymes, catalase, glutathione peroxidase and superoxide dismutase, in the MCT-treated rats were not different compared to control rats. Vitamin E levels were significantly depressed in the RV and there was no change in retinol levels. There was a significant increase in lipid hydroperoxide concentrations in MCT-treated rats as compared to the control group. These data provide evidence that right heart failure is associated with an increase in oxidative stress.
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PMID:Myocardial oxidative stress changes during compensated right heart failure in rats. 1044 2

Hypoxaemia is a common complication of acute lower respiratory tract infections in children. In most developing countries, where the majority of deaths from pneumonia occur, facilities for early detection of hypoxaemia are lacking and oxygen is in short supply. This review examines the usefulness of different clinical signs and symptoms in the prediction of hypoxaemia associated with acute respiratory infections in children. Several respiratory signs were found to be associated with hypoxaemia. These include very fast breathing (with a respiratory rate of more than 60 or 70 breaths per minute), cyanosis, grunting, nasal flaring, chest retractions, head nodding and auscultatory signs, as well as signs of general depression of the child, such as inability to feed or lethargy. The sensitivity and specificity of these signs, as described in the reviewed studies, is presented, and combination rules are discussed. Through appropriate combination of several physical signs, which can be used by peripheral health workers and be taught to mothers, it is possible to predict hypoxaemia in children with acute respiratory tract infections with reasonable accuracy.
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PMID:Clinical signs of hypoxaemia in children with acute lower respiratory infection: indicators of oxygen therapy. 1140 75

Neonatal diabetes mellitus (NDM) is defined as hyperglycemia occurring in the first few weeks of life. It can be either transient (TNDM) or permanent (PNDM). A 25 days old newborn was brought to the hospital with restlessness, respiratory depression and cyanosis. He was born at term with a birth weight of 2,000 g. There was no consanguinity between his parents. His physical examination findings were as follows: Weight and height were under 3th percentile, he was hypoactive and dehydrated. Serum glucose level was 800 mg/dl; C-peptide was 0.41 ng/ml. Upon investigation for dyslipidemia in association with his neonatal diabetes, hyperchylomicronemia was found both in the patient and his father. Pancreatitis, anemia and cholestasis were also observed. Insulin treatment was started for his diabetes together with a special diet for dyslipidemia. At the end of 28 months of follow-up, dyslipidemia has resolved but the need for insulin therapy was still existing. However, TNDM was considered in differential diagnosis because he was small for gestational age (SGA) at birth and his symptoms had started at the 25th day of the neonatal period. Delayed recovery from insulin dependency brought out the possibility of PNDM. Furthermore, neonatal diabetes combined with hypechylomicronemia is a rare clinical picture. Reported cases of NDM with different clinical evaluation will help to better understanding of this disorder.
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PMID:Neonatal diabetes with hyperchylomicronemia. 1255 65


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