1/34. Predicting outcome from coma: man-in-the-barrel syndrome as potential pitfall.The glasgow coma scale motor score is often used in predicting outcome after hypoxic-ischemic coma. Judicious care should be exerted when using this variable in predicting outcome in patients with coma following hypotension since borderzone infarction can obscure the clinical picture. We describe a patient who underwent skull base surgery for a schwannoma of the left facial nerve. The operation, which lasted for 10 h, was conducted under controlled hypotension. After the intervention the patient remained comatose with absent arm movements upon painful stimuli. An absent motor score usually carries a poor prognosis. However, magnetic resonance inversion recovery imaging of the brain showed bilateral hyperintense lesions in the arm-hand area indicative of borderzone ischemic damage. The patient received optimal supportive care and after 17 days he regained consciousness with 'man-in-the-barrel syndrome', which also further improved over time.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
2/34. Coma as an acute presentation of adrenoleukodystrophy.X-linked adrenoleukodystrophy is a metabolic disorder with broad clinical variations. A 4-year-old male admitted to the hospital with fever, hypotension, and coma as the presenting signs of adrenoleukodystrophy is reported. The initial presentation followed by rapidly developing disseminated intravascular coagulopathy and multiorgan failure suggested an initial diagnosis of septic shock. However, bronze skin pigmentation and a cranial computed tomography scan demonstrating posterior demyelination consistent with adrenoleukodystrophy led to the final diagnosis. The diagnosis was confirmed by the findings of elevated very-long-chain fatty acid levels and an elevated C24/C16 ratio in plasma and fibroblast cultures. Atypical presentations of the disease require a high index of suspicion to initiate treatment before the appearance of irreversible sequelae.- - - - - - - - - - ranking = 0.125keywords = coma (Clic here for more details about this article) |
3/34. Perioperative stroke associated with postoperative epidural analgesia.A patient with an epidural catheter for postoperative analgesia developed a stroke in association with a hypotensive episode resulting from a bolus of local anesthetic. After undergoing resection for femoral chondrosarcoma under epidural anesthesia, the patient received a continuous infusion of epidural morphine for postoperative analgesia. lidocaine 1% (10 mL in divided doses) was administered through the catheter for breakthrough pain. The patient experienced a hypotensive episode and was noted to have a motor and cortical sensory deficit of the left arm and leg 8 hours after the hypotensive episode. Clinical presentation and subsequent workup were consistent with a watershed infarction. The patient recovered full neurologic function before discharge. Postoperative hypotension from epidural analgesia may be associated with stroke; however, a cause-and-effect relationship usually cannot be established with certainty.- - - - - - - - - - ranking = 0.125keywords = coma (Clic here for more details about this article) |
4/34. Hypotensive hemorrhagic necrosis in basal ganglia and brainstem.Hypotensive hemorrhagic necrosis of the basal ganglia and brainstem has only occasionally been described. Three such cases are reported. Cardiac arrest had occurred in all cases, and it took at least 1 hour to restore adequate circulation. The patients remained comatose for 2 days to 2 weeks until death. Persistent hypotension causing ischemia in the distribution of deep perforating arteries is considered to have been the key underlying mechanism. Hemorrhage is thought to have been caused by extravasation of red blood cells through damaged blood vessels.- - - - - - - - - - ranking = 0.125keywords = coma (Clic here for more details about this article) |
5/34. Postoperative hypoglycaemic coma associated with chlorpropamide.A 72-year-old male being treated with chlorpropamide for diabetes mellitus had an emergency operation for a perforated gastric ulcer. Hypoglycaemic coma occurred after the operation.- - - - - - - - - - ranking = 0.625keywords = coma (Clic here for more details about this article) |
6/34. hypotension and bradycardia in infants after the use of topical brimonidine and beta-blockers.Brimonidine is a selective alpha-2 adrenergic agonist used to treat glaucoma. There have been several reports of central nervous system depression after its use in infants. We observed rapid-onset bradycardia and decreased blood pressure in addition to central nervous system depression in 2 infants who received concomitant topical brimonidine and beta-blockers.- - - - - - - - - - ranking = 0.125keywords = coma (Clic here for more details about this article) |
7/34. Hypotensive and bradycardiac responses to thyrotropin-releasing hormone in a comatose patient.A 46-year-old female motorcyclist, who suffered injuries to the brain stem in a traffic accident, showed hypotensive and bradycardiac responses to thyrotropin-releasing hormone (TRH) given to counter consciousness disturbance. The cardiodepressive responses to TRH were reduced with i.v. pretreatment with atropine sulfate, suggesting an involvement of the vagal nervous system in the development of the responses. Furthermore, this patient had complicated impairments in the sympathetic nervous system, which were revealed by the results of testing baroreceptor reflex sensitivity to pharmacological alterations in blood pressure. We thus speculate that the hypotensive and bradycardiac effects of TRH observed in this patient may result from derangements of the sympathetic nervous system caused by the injuries. This case report is believed to be a novel description of the cardiodepressive effects of TRH.- - - - - - - - - - ranking = 0.5keywords = coma (Clic here for more details about this article) |
8/34. hypotension due to interaction between lisinopril and tizanidine.OBJECTIVE: To report a case in which significant hypotension occurred after initiation of tizanidine in a patient using the antihypertensive agent lisinopril. CASE SUMMARY: A 48-year-old woman was admitted due to cerebral hemorrhage at the midbrain and pons, with extension to the fourth ventricle. consciousness disturbance (glasgow coma scale 4) with a decerebrate posture improved 5 days after stroke onset. As the BP was fairly high, antihypertensive agents, including lisinopril, were initiated. Three weeks later, the decerebrate rigidity and high BP remained, and tizanidine was initiated to see whether the decrease in muscle tone could facilitate hypertension control and motor recovery. However, the BP dropped dramatically within 2 hours after the first dose of tizanidine. The tizanidine and all of the antihypertensive medications were withdrawn. Tizanidine was used again after her BP had stabilized, but did not produce similar problems. DISCUSSION: A similar event was reported in 2000. The reaction in our patient appeared after tizanidine initiation and improved after both lisinopril and tizanidine were discontinued. According to the Naranjo probability scale, this was classified as a possible drug interaction. This kind of reaction is seldom mentioned as occurring during co-administration with tizanidine. With its characteristics, tizanidine has the potential to compromise hemodynamic stability during concomitant angiotensin-converting enzyme inhibitor use. CONCLUSIONS: Based upon the literature review, the hypotension in this patient was possibly due to the interaction between tizanidine and lisinopril.- - - - - - - - - - ranking = 0.125keywords = coma (Clic here for more details about this article) |
9/34. Case of fulminant hepatic failure due to unrecognized peripartum cardiomyopathy.OBJECTIVE: To describe a postpartum patient who presented with fulminant hepatic failure and hepatic coma as a result of unrecognized peripartum cardiomyopathy. DESIGN: Case report. SETTING: Medical intensive care unit of a tertiary care academic medical center. PATIENT: A 35-yr-old woman 5 wks postpartum from an uneventful spontaneous vaginal delivery who was transferred to our institution with fulminant hepatic failure and worsening hepatic encephalopathy of unknown etiology for consideration of liver transplantation. INTERVENTIONS: An echocardiogram was obtained as part of an evaluation for refractory shock and the patient was found to have severe global hypokinesis with an ejection fraction of approximately 15%. She was diagnosed with peripartum cardiomyopathy and treatment with digoxin and afterload reduction was initiated. MEASUREMENTS AND MAIN RESULTS: After initiation of appropriate treatment for dilated cardiomyopathy, the patient's hepatic failure resolved and she made a full recovery. CONCLUSIONS: Congestive heart failure is one of the few treatable causes of fulminant hepatic failure. Congestive heart failure must always be included in the differential diagnosis of fulminant hepatic failure of unknown pathogenesis.- - - - - - - - - - ranking = 0.125keywords = coma (Clic here for more details about this article) |
10/34. Near-fatal amitraz intoxication: the overlooked pesticide.Amitraz is commonly used in agricultural industries throughout the world as a farm-animal insecticide. Despite its widespread use, amitraz intoxication is extremely rare and mainly occurs through accidental ingestion by young children. Severe, life-threatening amitraz intoxication in adults is very rarely recognized and reported. Described herein is a previously healthy 54-year-old patient who accidentally ingested a mouthful of liquid amitraz concentrate, and rapidly developed life-threatening clonidine-like overdose syndrome, manifested as nausea, vomiting, hypotension, bradycardia, bradypnoea, and deep coma. Supportive treatment, including mechanical ventilation, and atropine administration resulted in full recovery within 48 hr. Very few cases of near-fatal amitraz poisoning in adults have been described in the medical literature, leading to low awareness of physicians in general practice to the potential toxicity of amitraz. As a consequence, cases of amitraz poisoning are not recognised and therefore erroneously treated as the much more commonly recognized organophosphate and carbamate intoxication. In our discussion, we review the clinical and laboratory manifestations of amitraz poisoning, including clinical hints that aid in the recognition of this often-overlooked diagnosis. Differentiation of amitraz intoxication from the much more commonly seen pesticide-related organophosphate and carbamate intoxication is of utmost importance, in order to avoid erroneous, unnecessary, and often dangerous treatment.- - - - - - - - - - ranking = 0.125keywords = coma (Clic here for more details about this article) |
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