1/20. Metabolic acidosis and coma following a severe acetaminophen overdose.OBJECTIVE: To report a case of metabolic acidosis and coma in a severe acetaminophen overdose. CASE SUMMARY: A 29-year-old white woman was admitted to the emergency department with a diminished level of consciousness and metabolic acidosis. The toxicology screen revealed a serum acetaminophen concentration of 1072 microg/mL, and she was consequently treated with intravenous acetylcysteine. Despite the elevated concentration, the patient did not manifest signs of hepatotoxicity. DISCUSSION: Metabolic acidosis and coma are rare manifestations in acetaminophen overdoses. In published case reports, severe acetaminophen ingestion independently causes metabolic acidosis and coma in the absence of hepatotoxicity. The mechanism by which metabolic acidosis occurs is not clearly defined. Studies conducted on animals demonstrated that in severe overdoses, acetaminophen may cause lactic acidosis by inhibiting mitochondrial respiration. The mechanism by which acetaminophen can cause coma is still unknown. CONCLUSIONS: Severe acetaminophen overdoses can independently cause metabolic acidosis and coma in the absence of hepatotoxicity.- - - - - - - - - - ranking = 1keywords = white (Clic here for more details about this article) |
2/20. Suicidal poisoning with barium chloride.A 49-year-old male pharmacist suffering from depression phoned the emergency services telling of how he had ingested barium chloride. He was found semicomatose in bed and resuscitation attempts were to no avail and he died at the scene. A white plastic container labelled "barium chloride... Poison", and a book with a writing on a blank page... "give sulphate... SO(4)" were found.At autopsy, 1l of whitish-yellow fluid was found in the stomach.autopsy barium levels were: blood 9.9mg/l; bile 8.8mg/l; urine 6.3mg/l; gastric 10.0g/l.cause of death was given as cardiorespiratory arrest due to barium chloride poisoning.The issue of barium toxicity in a variety of itatrogenic and non itatrogenic situation is discussed together with the two only other cases of suicidal barium ingestion, and the feasibility of early intervention at the scene by an emergency team.- - - - - - - - - - ranking = 1keywords = white (Clic here for more details about this article) |
3/20. Reversible coma with raised intracranial pressure: an unusual clinical manifestation of cadasil.A 50-year-old woman presented with recurrent episodes of headache, nausea and disturbed consciousness that were fully reversible within a few days. Clinical and radiological findings suggested raised intracranial pressure, which on one occasion was confirmed by intracranial pressure monitoring. magnetic resonance imaging performed in the asymptomatic interval disclosed a diffuse leukoencephalopathy. Brain biopsy surprisingly revealed the typical vascular changes of cadasil and subtle endothelial alterations. The white matter showed edematous changes and reactive gliosis. Mutational analysis of the Notch3 gene revealed a previously unreported mutation. We suggest that a transient disturbance of the blood-brain barrier related to the underlying vascular pathology may have caused this unusual presentation of cadasil.- - - - - - - - - - ranking = 1keywords = white (Clic here for more details about this article) |
4/20. flumazenil and dialysis for gabapentin-induced coma.OBJECTIVE: To describe a case of gabapentin-induced coma that was reversed with flumazenil and hemodialysis. CASE SUMMARY: We describe an 83-year-old dialysis-dependent white man who became comatose after a single dose of gabapentin for phantom limb pain. The patient was successfully revived from the coma with administration of flumazenil, which was then followed by hemodialysis. serum concentration data before and 4 hours after dialysis document the effectiveness of hemodialysis for gabapentin toxicity. DISCUSSION: An objective causality assessment revealed that this adverse event was probably related to the gabapentin that the patient received. To our knowledge, this is the first documented case of not only gabapentin-induced coma, but also the effectiveness of flumazenil for treatment of this type of coma. Although therapeutic hemodialysis has been previously described, our case report is strengthened by the serum concentration monitoring accompanying it. CONCLUSIONS: This report underscores the importance of initiating gabapentin therapy at low doses in dialysis-dependent patients and introduces a novel treatment for those who experience toxicity.- - - - - - - - - - ranking = 1keywords = white (Clic here for more details about this article) |
5/20. MR imaging findings in cerebrospinal gnathostomiasis.Human gnathostomiasis is an infection caused mainly by gnathostoma spinigerum, a nematode. Infected humans can present with various clinical manifestations. serology is the criterion standard for diagnosing gnathostomiasis, whereas MR imaging represents a complementary tool for assessing severity and extent of disease. We report two definite cases of gnathostomiasis that were confirmed by the immunoblotting technique. MR imaging of the cervical cords showed cord enlargement and diffuse high signal intensity, mainly of the gray-white matter regions. MR imaging of the brain showed hemorrhagic tract and scattered deep intracerebral hemorrhage with diffuse, fuzzy white matter lesions with nodular enhancement. Severe gnathostomiasis was unresponsive to treatment.- - - - - - - - - - ranking = 2keywords = white (Clic here for more details about this article) |
6/20. Multiple complications and withdrawal syndrome associated with quetiapine/venlafaxine intoxication.OBJECTIVE: To report a case of quetiapine/venlafaxine intoxication associated with multiple complications and to review their possible relationship with these 2 drugs. CASE SUMMARY: A 53-year-old white man was admitted to the hospital for loss of consciousness secondary to voluntary intoxication with venlafaxine and quetiapine. Several complications were attributable to this intoxication including seizures, prolonged coma, respiratory depression, neuroleptic malignant syndrome, prolonged QRS and QTc intervals, and a possible venlafaxine withdrawal syndrome. DISCUSSION: Quetiapine could be responsible for the neuroleptic malignant syndrome presented in this case. Moreover, venlafaxine intoxication, fever, autonomic instability, and myoclonus presented serotonin syndrome as a differential diagnosis. Potential causes of seizures and prolongation of the QRS and QTc intervals are reviewed. Finally, prolonged coma and late venlafaxine withdrawal are discussed with regard to the pharmacodynamics and pharmacokinetics of drug elimination in the context of intoxication. CONCLUSIONS: Clinicians should be aware of possible complications following intoxication with atypical antipsychotics and anti-depressants, including protracted altered mental status.- - - - - - - - - - ranking = 1keywords = white (Clic here for more details about this article) |
7/20. Fatal avian influenza A (H5N1) in a child presenting with diarrhea followed by coma.In southern vietnam, a four-year-old boy presented with severe diarrhea, followed by seizures, coma, and death. The cerebrospinal fluid contained 1 white cell per cubic millimeter, normal glucose levels, and increased levels of protein (0.81 g per liter). The diagnosis of avian influenza A (H5N1) was established by isolation of the virus from cerebrospinal fluid, fecal, throat, and serum specimens. The patient's nine-year-old sister had died from a similar syndrome two weeks earlier. In both siblings, the clinical diagnosis was acute encephalitis. Neither patient had respiratory symptoms at presentation. These cases suggest that the spectrum of influenza H5N1 is wider than previously thought.- - - - - - - - - - ranking = 1keywords = white (Clic here for more details about this article) |
8/20. carbon monoxide brain toxicity: clinical, magnetic resonance imaging, magnetic resonance spectroscopy, and neuropsychological effects in 9 people.carbon monoxide (CO) exposure is a common cause of toxic brain damage, whereby effects range from transient neurological dysfunction to coma and death. A spectrum of severity of magnetic resonance imaging (MRI) findings after CO brain toxicity, including globus pallidus and white matter lesions, is well documented. Reports of MR spectroscopy (MRS) findings re main sparse. This article reports 9 people exposed to CO because of an apartment house's faulty gas heater. Four, with transient loss of consciousness after chronic moderate level CO exposure, suffered intellectual impairment without MRI abnormalities. The MRS of 1 individual demonstrated decreased n-acetyl aspartase in the basal ganglia, bilaterally. Of 5 exposed to high levels for about 12 hours, 1 died prior to clinical and/or MRI evaluation. One who suffered coma recovered but was lost to evaluation. Three, who were unconscious for hours to days, exhibited T2 MRI white matter signal abnormalities. MRS showed decreased basal ganglia n-acetyl aspartase in 2. One of these suffers a Parkinsonian syndrome. All 3 are intellectually impaired. This study demonstrates that although MRI and MRS are useful markers of CO-induced brain damage, they are not always sensitive to resultant intellectual dysfunction.- - - - - - - - - - ranking = 2keywords = white (Clic here for more details about this article) |
9/20. Devic disease with brainstem lesions.We describe a patient who suffered from an unusually severe form of neuromyelitis optica with a hyperacute time-course evolution requiring mechanical ventilation within 3 days. The patient died after 72 days and autopsy showed major spinal cord, optic nerve, and brainstem necrosis, and multifocal necrotic lesions on the cerebellum and cerebral white matter.- - - - - - - - - - ranking = 1keywords = white (Clic here for more details about this article) |
10/20. Hypoglycemic encephalopathy with extensive lesions in the cerebral white matter.Here we report an autopsy case of hypoglycemic encephalopathy with prolonged coma. Laboratory data obtained when the patient lapsed into a coma showed that she had a low level of serum glucose (27 mg/dL). Although the level of glucose returned to within the normal range rapidly after glucose infusion, the patient remained in a coma for 22 months. It was presumed that the state of hypoglycemia persisted for about 4 h. There was no evidence of hypotension or hypoxia. magnetic resonance imaging was performed 3 h after glucose administration; diffusion-weighted images revealed hyperintensity in the cerebral white matter and in the boundary zone between the middle and posterior cerebral arteries. Post-mortem examination revealed superficial laminar necrosis throughout the cerebral cortex. Neuronal necrosis was also found in the hippocampus and dentate gyrus, although the CA3 region appeared normal. In addition to these lesions, which are consistent with hypoglycemia-induced brain damage, the cerebral white matter exhibited severe loss of myelin and axons with reactive astrocytosis and macrophage infiltration. Old infarcts were also present in the bilateral occipital lobes. Since the cerebral blood flow is reported to be decreased during severe hypoglycemia, the present findings suggest that white matter lesions and boundary-zone infarctions may develop primarily in uncomplicated hypoglycemia.- - - - - - - - - - ranking = 7keywords = white (Clic here for more details about this article) |
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