Journal of Postgraduate Medicine
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Year : 2002  |  Volume : 48  |  Issue : 2  |  Page : 158  

Intracranial bleeding in Weil's disease.

KV Murali, R Sujay, S Pavithran, M Thomas 

Correspondence Address:
K V Murali

How to cite this article:
Murali K V, Sujay R, Pavithran S, Thomas M. Intracranial bleeding in Weil's disease. J Postgrad Med 2002;48:158-158

How to cite this URL:
Murali K V, Sujay R, Pavithran S, Thomas M. Intracranial bleeding in Weil's disease. J Postgrad Med [serial online] 2002 [cited 2022 Jun 30 ];48:158-158
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A 45-year-old male presented with history of fever, generalised myalgia and high coloured urine of one week’s duration. He developed obtundation with generalised tonic-clonic seizures on the previous day of admission. There was no history of any significant medical illness in the past. He was drowsy, icteric, with bilateral subconjunctival haemorrhages and conjunctival congestion. Blood pressure was 140/84 mm Hg. There was anisocoria with the left pupil being larger, bilateral brisk deep tendon reflexes and bilateral extensor plantar responses. There were no signs of meningeal irritation and the ocular fundi were normal. He had hepatomegaly of 2 cms and mild ascites. There was no evidence of haematuria or bleeding from intravenous access sites. The total leucocyte count was 11,500/mm3 with 75% polymorphs, ESR 100mm/h, serum bilirubin 8.1mg/dL, blood urea 193mg/dL and creatinine 7.3mg/dL with a normal platelet count and liver enzymes. Weil’s IgM antibody by ELISA was > 20 panbio units. Prothrombin time (13, control 12 seconds) and activated partial thromboplastin time (32, control 30 seconds) were normal. FDP was <10. CT scan head showed intracerebral haematoma in the right deep parietal lobe with intraventricular, subarachnoid, subdural and extradural haematomas and midline shift. The patient succumbed, 9 hours after admission despite treatment with crystalline penicillin, anti-oedema measures and platelet transfusion.

Weil’s syndrome is characterised by jaundice, renal dysfunction, haemorrhagic diathesis and a high mortality. Common haemorrhagic manifestations include petechiae, purpura and ecchymosis. Pulmonary, gastrointestinal and intracranial bleeding occurs less commonly. Reports of primary intracranial haemorrhages (ICH) are few.[1],[2],[3],[4]

Coagulation abnormalities are well recognised in patients with Weil’s disease: abnormal bleeding and clotting times, prolonged prothrombin time, reduced factor V concentration, shortening or prolongation of thrombin time and features of disseminated intravascular coagulation.[5] Thrombocytopaenia occurs in up to 50% of Weil’s disease patients.[5] Other mechanisms that play a role in the bleeding diathesis are vasculitis and direct vascular invasion by the organism. Mortality is high in patients with ICH associated with Weil’s disease. A high index of suspicion is called for in the recognition of the condition as the physician is often led astray by the hepatic dysfunction and uremia which are much more common causes of obtundation.


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