1/11. A Japanese case of congenital hyperinsulinism with hyperammonemia due to a mutation in glutamate dehydrogenase (GLUD1) gene.We describe a Japanese case of neonatal hyperinsulinism due to a de novo mutation (Gly446Asp) in glutamate dehydrogenase gene (GLUD1). A boy suffered from hypoglycemic coma with relative hyperinsulinemia on day 1 after birth, and received subtotal pancreatectomy. Examination of the resected pancreas revealed a diffuse increase in endocrine cells, consistent with 'nesidioblastosis'. He is now 15 years old and has exhibited mild but persistent hyperammonemia, which is a very unique feature of the disorder caused by GLUD1 activating mutations. He has also been suffering from seizures and mental retardation. Thus, GLUD1 mutations can be a cause of congenital hyperinsulinism in Japanese.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
2/11. serotonin syndrome presenting as hypotonic coma and apnea: potentially fatal complications of selective serotonin receptor inhibitor therapy.OBJECTIVE: To describe a patient who developed serotonin syndrome on four separate occasions as a result of monotherapy with two different selective serotonin receptor inhibitors (fluoxetine and cetalopram). DESIGN: Case report. SETTING: Community hospital. patients: Single patient with four episodes of serotonin syndrome. MEASUREMENTS AND MAIN RESULTS: The syndrome was characterized by coma/unresponsiveness (four episodes), dilated pupils (four episodes), salivation (two episodes), dryness of mouth (two episodes), myoclonus like activity of eyelids (four episodes), oculogyric crisis (four episodes), flaccid paralysis of all extremities (four episodes), tremors (two episodes), apnea (two episodes), restlessness (one episode). Recovery occurred within 24 hrs, although muscle pain and weakness persisted for 2 months after stopping fluoxetine. apnea occurred in both episodes associated with fluoxetine therapy. CONCLUSION: apnea and coma may occur in serotonin syndrome.- - - - - - - - - - ranking = 6keywords = coma (Clic here for more details about this article) |
3/11. Second place winner. absorption of topical ophthalmic medications presenting as lethargy and apnea in an infant.The case of a previously healthy 3-week-old infant with lethargy and apnea resulting from topical absorption of ophthalmic antiglaucoma medications is described. This case illustrates the importance of including topical drugs in medication histories and considering them as potential causes of systemic toxicity. It also emphasizes the high level of vigilance that is needed in monitoring infants and small children when prescribing concentrated topical medications that are usually given to adults.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
4/11. Insomnia-coma and auto-electrocution complicating general anesthesia. Incidental factors which also cause cerebral, respiratory and cardiac arrest.Whatever induces general anesthesia, i.e. cerebral arrest, tends to cause respiratory and cardiac arrest also. However, general anesthesia does not necessarily exclude nor block all other mechanisms which can provoke one or more of these three phenomena. Amongst many such more or less equipotent factors are intracranial, intrapleural, intra-abdominal and intratracheal pressures. These mechanical factors occurring but unrecognized in surgical patients cause puzzling complications including, insomnia, coma and unexpected sudden death.- - - - - - - - - - ranking = 5keywords = coma (Clic here for more details about this article) |
5/11. brain death and persistent vegetative states.patients who suffer severe brain damage may be brain dead, even though their cardiorespiratory function is supported by mechanical ventilation. According to criteria established in the United Kingdom and the united states, if these patients meet the preconditions of apneic coma that is attributable to diagnosed irreversible cause, and the presence of drug intoxication, hypothermia, or metabolic coma is excluded, then documentation of absent brainstem reflexes and apnea despite a PaCO2 of 50 mm Hg or greater will confirm the presence of brain death. If the brain is dead, the patient is dead, regardless of the state of his circulation, and he should be declared dead and removed from the ventilator. If the patient has lost higher cortical function but brainstem function is preserved, he may be in the persistent vegetative state and live for years with apparent sleep-wake cycles but no awareness of any external or internal stimuli. As the prognosis for recovery from the persistent vegetative state is absent, there is no ethical responsibility to continue treatment other than to provide basic nursing care to maintain the dignity of the patient.- - - - - - - - - - ranking = 2keywords = coma (Clic here for more details about this article) |
6/11. Apneic spells associated with timolol therapy in a neonate.A 2-week-old premature child with congenital glaucoma secondary to anterior cleavage syndrome was treated with timolol maleate and cyclocryotherapy. The patient had apneic spells of up to 30 seconds that stopped soon after timolol maleate therapy was discontinued. No apnea was seen before timolol maleate administration, and no further spells were noted after subsequent cyclocryotherapy without timolol maleate treatment. Possible central nervous system toxicity of timol maleate or its metabolic by-products in neonates with immature blood-brain barriers was noted.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
7/11. Hazards of succinylcholine administration during electrotherapy.We describe prolonged apnea following electrotherapy in a patient who was also being treated with a topical organophosphate anticholinesterase, ecothiophate iodide (phospholine iodide), for glaucoma. The increased duration of action of succinylcholine resulted from low levels of serum cholinesterase that had been caused by the organophosphate. attention is called to other drugs that directly or indirectly (by lowering serum cholinesterase) interact with succinylcholine chloride resulting in prolonged apnea. Other potential hazards of succinylcholine administration, such as hyperkalemia and cardiac arrhythmias, are also discussed.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
8/11. Massive clonidine ingestion with hypertension in a 9-month-old infant.The antihypertensive drug clonidine has a double and antagonistic effect on arterial blood pressure. As a result of activation of peripheral alpha-adrenergic receptors, it causes a transient increase in blood pressure; by a central action it decreases sympathetic tone which results in sustained bradycardia and hypotension. Both central and peripheral effects are experimentally blocked by tolazoline, an alpha-adrenergic blocking agent. The toxic symptoms seen in clonidine poisoning are usually produced by the central effect. A case of severe clonidine poisoning in a 9-month-old infant is reported. The clinical picture included coma, miosis, apneic spells, bradycardia, and hypertension. Rapid and complete recovery was obtained with supportive treatment that included assisted ventilation. No adrenergic blockers or antihypertensive drugs were given. Use of tolazoline in cases of clonidine overdose in children remains controversial. Supportive measures alone may be adequate for even the most severe cases.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
9/11. risk of hypotension during apnea testing.OBJECTIVE: To determine the safety of apnea testing. DESIGN: Prospective, consecutive study. SETTING: Inner-city trauma center. patients: A total of 70 apnea tests were performed on 61 comatose patients as part of the determination of brain death. RESULTS: Only 43 examinations (61%) were well tolerated. During 27 examinations (39%) patients either developed marked hypotension (> or = 15% drop in mean arterial pressure) (n = 23) or required prophylactic vasopressor manipulation (n = 4). Of the 27 examinations in which hypotension developed, 14 were aborted, two were tolerated despite marked hypotension, four were tolerated after administration of prophylactic epinephrine (n = 1) or dopamine hydrochloride (n = 3), and seven were successfully completed after increases in the rate of dopamine infusion during the test. CONCLUSIONS: hypotension can pose a significant risk to patients undergoing apnea testing. Constant monitoring of vital signs throughout the test is essential to its safe completion.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
10/11. Preserved cortical somatosensory evoked potentials in apnoeic coma with loss of brain-stem reflexes: case report.A comatose patient suffering from diffuse cerebellar haemorrhage developed apnoea and brainstem areflexia, i.e. the clinical signs of brain death. However, median nerve somatosensory evoked potential testing 2.5 h and 22 h after the onset of this clinical syndrome showed cortical potentials partly preserved; these were abolished 46 h after the beginning of the clinical signs of brain death. This case report underlines the need for electrophysiological confirmation of brain death in patients with primarily infratentorial lesions.- - - - - - - - - - ranking = 5keywords = coma (Clic here for more details about this article) |
| | Next -> |