Spontaneous Bilateral Basal Ganglia Haemorrhage Secondary to Methanol Poisoning.

Methanol toxicity remains as major problem in the medical field.[1],[2],[3] With its active metabolite, formic acid often leads to severe metabolic acidosis and to some extend brain damaged.[4],[5],[6] We are reporting a case of brain hemorrhage at the right external capsule and left basal ganglia with mass effect and obstructive hydrocephalus in a methanol poisoning patient. A confused 29-year-old gentleman was brought into hospital. Initial investigation showed severe metabolic acidosis with raised anion gap. Initial brain CT scan was normal. Subsequently, serum methanol was reported to be high (112 mg/dL). Intravenous (IV) ethanol 10% was given without any delayed. As there was no improvement in his consciousness level, a repeat brain CT was performed and it showed multiple cerebral hemorrhage with obstructive hydrocephalus. Hence, clinicians should have high index of suspicion for cerebral hemorrhage in a patient with methanol toxicity, who presented with altered mental status and severe metabolic acidosis.

Hematoma location and morphology of anticoagulation-associated intracerebral hemorrhage.

OBJECTIVE: To study hematoma location and morphology of intracerebral hemorrhage (ICH) associated with oral anticoagulants (OAC) and delineate causes and mechanism. METHODS: We performed a systematic literature research and meta-analysis of studies comparing neuroimaging findings in patients with OAC-ICH compared to those with ICH not associated with OAC (non-OAC ICH). We calculated pooled risk ratios (RRs) for ICH location using the Mantel-Haenszel random-effects method and corresponding 95% confidence intervals (95% CI). RESULTS: We identified 8 studies including 6,259 patients (OAC-ICH n = 1,107, pooled OAC-ICH population 17.7%). There was some evidence for deep ICH location (defined as ICH in the thalamus, basal ganglia, internal capsule, or brainstem) being less frequent in patients with OAC-ICH (OAC-ICH: 450 of 1,102/40.8% vs non-OAC ICH: 2,656 of 4,819/55.1%; RR 0.94, 95% CI 0.88-1.00, p = 0.05, I 2 = 0%) while cerebellar ICH location was significantly more common in OAC-ICH (OAC-ICH: 111 of 1,069/10.4% vs non-OAC ICH: 326 of 4,787/6.8%; RR 1.45, 95% CI 1.12-1.89, p = 0.005, I 2 = 21%) compared to non-OAC ICH. There was no statistically significant relationship to OAC use for lobar (OAC-ICH: 423 of 1,107/38.2% vs non-OAC ICH: 1,884 of 5,152/36.6%; RR 1.02, 95% CI 0.89-1.17, p = 0.75, I 2 = 53%, p for heterogeneity = 0.04) or brainstem ICH (OAC-ICH: 36 of 546/6.6% vs non-OAC ICH: 172 of 2,626/6.5%; RR 1.04, 95% CI 0.58-1.87, p = 0.89, I 2 = 59%, p for heterogeneity = 0.04). The risk for intraventricular extension (OAC-ICH: 436 of 840/51.9% vs non-OAC ICH: 1,429 of 3,508/40.7%; RR 1.26, 95% CI 1.16-1.36, p < 0.001, I 2 = 0%) was significantly increased in patients with OAC-ICH. We found few data on ICH morphology in OAC-ICH vs non-OAC ICH. CONCLUSION: The overrepresentation of cerebellar ICH location and intraventricular extension in OAC-ICH might have mechanistic relevance for the underlying arteriopathy, pathophysiology, or bleeding pattern of OAC-ICH, and should be investigated further.

Large Amount of Cannabis Ingestion Resulting in Spontaneous Intracerebral Hemorrhage: A Case Report.

Although multiple cases of cannabis-associated ischemic stroke have been reported, there are only 2 reported cases of hemorrhagic stroke with an associated cerebral vasoconstriction. To our knowledge, we present the first case of basal ganglia hemorrhage after a large-volume oral ingestion of cannabis without other identified risk factors. In our case, cerebral digital subtraction angiography within 24 hours of presentation did not reveal vasoconstriction leading to a possible alternative explanation for hemorrhagic stroke, including cannabis-induced transient arterial hypertension and autoregulation disruption.

Basal Ganglion Hemorrhage as Delayed Complication of Diethylene Glycol Ingestion.

Diethylene glycol (DEG), an organic compound (HOCH2CH2)2O is a commonly used solvent. Mass poisoning outbreaks have been reported because of frequent contaminations. A PubMed search for diethylene resulted in 795 publications with 151 specifically discussing the toxicity. Of the 151 reported toxicity reviews/case reports, only 6 publications discussed the long-term neurological effects of diethylene toxicity. We report a fatal case of oral ingestion of DEG with complications from delayed toxicity. She died 7 days after the second admission. Autopsy disclosed a right basal ganglia hemorrhage within the brain and microscopic deposits of polarizable crystals into small cerebral blood vessels. Both kidneys illustrate tubular necrosis with scattered tubular deposition of polarizable calcium oxalate crystals. PubMed search leads to only 2 reported cases of basal ganglia hemorrhage (based on radiological findings) after ethylene glycol intoxication. Our case is the first reportable case of basal ganglia hemorrhage after DEG ingestion.

Bipallidal haemorrhage after ethylene glycol intoxication.

Acute or subacute bipallidal lesion, an uncommon radiological feature produced by metabolic disorders or poisoning, has never been attributed to ethylene glycol (EG) intoxication. This 50-year-old Afro-Caribbean alcoholic man had unexplained loss of consciousness. Blood tests showed osmolar gap. Drug screening was positive for EG at 6.06 mmol/l. Brain CT revealed bilateral pallidal haemorrhage. Pallidal haematoma, which could be related to deposition of oxalate crystals issued from EG metabolism, should lead to toxicological screening.

Early computed tomography hypodensity predicts hemorrhage after intravenous tissue plasminogen activator in acute ischemic stroke.

Parenchymal hypodensity is a proposed risk factor for hemorrhage after recombinant tissue plasminogen activator (TPA) thrombolysis for ischemic stroke. In Buffalo, NY, and Houston, TX, the authors reviewed 70 patients who were treated with intravenous TPA for acute middle cerebral artery (MCA) stroke. Two observers blinded to clinical outcome analyzed initial noncontrast head computed tomography (CT) scans. Basal ganglia CT hypodensity was quantitated in Hounsfield units (HUs). Contralateral-ipsilateral difference in density was calculated using the asymptomatic side as a control. Ictus time to TPA averaged 2.5 hours. Six patients developed symptomatic intraparenchymal hematomas (2 fatal). The hemorrhage group had more severe basal ganglia hypodensity (mean 7.5 +/- 1.4, range 6-10 HU) than the nonhemorrhage group (2.2 +/- 1.4, range 0-9 HU) (P < .0001). The hemorrhage group had hypodensity of > 5 HU; the nonhemorrhage group had hypodensity of < or = 4 HU, except 1 patient with hypodensity of 9 HU. In predicting hemorrhage, the positive predictive value of hypodensity > 5 HU was 86%; the negative predictive value was 100%. Prethrombolysis NIH Stroke Scale (NIHSS) deficit (P = .0007) and blood glucose (P = .005) were also higher in the hemorrhage group. Age, gender, smoking, hypertension, and ictus time to TPA infusion did not differ between the 2 groups. Logistic regression indicated that basal ganglia hypodensity was the best single predictor of hemorrhage. Hypodensity and NIHSS score together predicted all cases of hemorrhage. The authors conclude that basal ganglia hypodensity quantified by CT may be a useful method of risk stratification to select acute MCA stroke patients for thrombolytic therapy.