Recombinant factor VIIa in a case of pontine hemorrhage.

A 59-year-old lady presented with hypertensive hemorrhage involving the pons. Since she presented within 3 hours of onset of the stroke, recombinant factor VIIa was administered. From a state of altered sensorium there was a rapid recovery of consciousness followed by gradual improvement in limb weakness. Serial CT scans of the brain revealed no further expansion of the hematoma. The hematoma progressively resolved. Recombinant factor VIIa could be an attractive therapeutic option in treating hemorrhages at critical sites like brainstem where expansion of hematoma could be fatal.

Recurrent venous thrombosis with factor V Leiden mutation.

A patient who presented with recurrent venous thrombosis is reported. Following an episode of spontaneous deep vein thrombosis of the lower limb he was started on oral anticoagulant therapy, which he discontinued. He presented with cerebral venous thrombosis and improved partially with anticoagulant therapy. Evaluation for hypercoagulable states revealed factor V Leiden mutation by polymerized chain reaction method. Long-term anticoagulation has been planned. Evaluation for factor V Leiden mutation is always warranted in patients presenting with spontaneous thrombosis, especially if there is recurrent thrombosis.

Cardiac involvement in Wilson's disease--an electrocardiographic observation.

BACKGROUND: Wilson's disease is known for its protean manifestations; however electrocardiographic abnormalities have not received much attention. AIM: To evaluate the various electrocardiographic (ECG) changes in patients with Wilson's disease. METHOD: The resting ECGs of 50 patients with Wilson's disease were systematically analyzed independently by three observers after excluding other causes that could induce ECG abnormalities. RESULT: Fifteen patients had at least one abnormality in the ECG. Sinus tachycardia was seen in eight and sinus bradycardia in six. Other abnormalities included: bifid P wave (1), ST elevation (2), ST depression (2), T inversion (4), ventricular premature contraction - VPC (1) and prominent U waves (1). QRS axis, PR interval, QRS complex, R/S amplitude ratio and QT interval were normal in all. Ventricular premature beats were not recorded in any. None had features of ventricular hypertrophy. There was no statistically significant difference in ECG abnormalities with reference to age, gender, duration of illness or treatment, serum copper or ceruloplasmin, and severity of neurological impairment. CONCLUSION: ECG abnormalities are not uncommon in Wilson's disease and are presumably related to an underlying cardiomyopathy due to deposition of copper in heart.