Cerebral Venous Thrombosis

Introduction

In India incidence of puerperal venous thrombosis is 40 -50 /10,000 deliveries.

Case Report

Twenty six year old primigravida with 8 weeks amenorrhoea was admitted for hyperemesis gravidarum.

She responded within 48 hours to four pints of ringer lactate and antiemetics. Patient was symptomatically better.We were planning to discharge her on day 4. On that day early morning patient had generalised tonic clonic convulsions about 8 episodes for which she was shifted to intensive care unit. Intravenous diazepam 10 mg IV was givan as a loading dose. Emergency investigations were Hb 10.5 gm%, total count 10,500, N74 L26 platelets adequate, RBS 104 mg%, BUN 12 mg% Na 140 mg%, K 4 meq/liter, SGOT 74 IU/lit, SGPT 33 IU/lit, Alkaline phosphatase 73 mg% Bilirubin normal Total protin 68 mg%, Alb 3.5 mg%.

Patient had persistent convulsions inspite of IV loading dose therefore 40 mg of IV diazepam was given over a period of 6 hours. within an hour after admission to MIC, patient had developed weakness in left upper and lower extremities. Power in left upper and lower extremity was 3/5 and therefore immediate CT brain with contrast was advised. Rapid eptonisation was done with 600 mg phenytoin Na in a 200 ml of normal saline over a period of one hour. CT scan showed superior sagittal, sigmoid sinus, internal jugular venous thrombosis. Intravenous injection Heparin 5000 IU bolus followed by 1000 IU/hr was given. Coagulation profile after starting Heparin was PT 14.9 with control of 11, PTTK 30.2 with control of 32, serum homocystine 9(Normal 5-15 umol/lit). Magnetic resonance venogram was done after 36 hours of which showed left transverse and sigmoid and superior sagittal sinus thrombosis and right high frontal lobe venous infarct.

Next day patient had one more episode of convulsion.Treatment with Phenytoin Na was continued in view of the MRI findings a joint decision to terminate the pregnancy was taken by obstetrician, physician and Neurophysician.

Heparin was omitted six hours prior to MTP. Medical termination of pregnancy was done by suction and evacuation under controlled general anaesthesia after necessary high risk consent. Prior to MTP PT was 22 with control of 12, INR was 2.4. After 6 hours of termination of pregnancy patient was restarted on inj Heparin .

She was then started on oral anticoagulation with an overlap of Heparin therapy over 5 days. Dose of warfarin being 5 mg HS and Tablet Phenytoin Na 100 mg three times a day Patient was advised to followup with coagulation profile. Patient was counselled regarding high risk for future pregnancy and was informed that there will be 12% risk of developing pulmonary embolism and deep vein thrombosis and advised planned pregnancy in future under anticoagulation cover. Her future pregnancy need to be supervised by team approach, i.e. Obstetrician, Physician and Neurophysician.

Discussion

Pregnancy is a hypercoagulable state. All the coagulation factors increases in pregnancy more so after first trimester of pregnancy . On the balance it seems likely that both thrombosis and fibrinolysis increases in pregnancy.

Association of cerebral venous thrombosis with oral contraceptive pill and during puerperium is known. It is rare in Western Europe and North America with incidence of perhaps 1 per 10,000 deliveries. In India incidence of puerperal venous thrombosis is 40 -50 /10,000 deliveries. It typically presents in second or third week postpartum. Aetiological factors being dehydration, hypercoagulable state, antiphospholipid antibody, protein C deficiency homocystinuria and paroxysmal noctunal haemoglobinuria.

Venous sinuses of cranial cavity are situated between layers of dura matter. Their main function is

1) To receive blood from the brain through cerebral vein and CSF from subarachnoid space through the arachnoid villi. The blood in the dural sinuses ultimately drains into internal jugular vein in the neck. Superior sagittal sinus occupies the upper fixed borders of falx cerebri.

Clinical presentation depends on which vein occluded and how fast the clot propagates.

Usually persistent headache or a seizures demand evaluation. In cortical vein thrombosis increasingly severe headache preceeds focal or generalised convulsions which are followed by aphasia, weakness and other focal neurological signs.

The propagation of clot through the cortical vein provoke more seizures and neurological deficits. Faster the progression poorer the prognosis because collateral circulation is obstructed and the risk of venous infarction and intracerebral bleeding increases.

Increased intracranial pressure may be caused by either mass effect of intracranial bleeding or the obstruction of cerebrospinal fluid absorption by clot in the superior sagittal sinus.

In superir sagittal sinus thrombosis headache is due to intracranial hypertension sometimes clots spreads into parasagittal motor cortex causing primarily leg weakness a focal convulsions into occipital cortex causing hemianopia or on occasion cortical blindness if both occipital lobes are affected.

Diagnosis is mainly by computed tomography, magnetic resonant imaging or by a digital subtraction angiography.

Treatment includes hydration, anticonvulsant and anticoagulation and thrombolytic therapy is contraindicated in pregnancy because;¹ they cross the human placenta;² it can cause uterine atony because of interference of FDP with uterine contractions.

References

1. Puerperal Cerebral Venous Thrombosis : Therapeutic Benefit of Low Dose Heparin D Nagaraja, T Haridas, AB Taly, M Veerendrakumar, DK SubbuKrishna Department of Neurology, National Institute of Mental Health and Neurosciences, Hosur Road, Bangalore, India.

2. J Neurol Neurosurg Psychiatry 2003 Jun;74(6):814-6. Related Articles, Links Risk of recurrence of cerebral venous and sinus thrombosis during subsequent pregnancy and puerperium

SUPERIMPOSED ACUTE HEPATITIS E INFECTION IN PATIENTS WITH CHRONIC LIVER DISEASE

Superinfection with HEV in patients with CLD causes severe liver decompensation, which is frequently complicated with hepatic encephalopathy and renal failure. Acute hepatitis E in these patients has a protracted course with high morbidity and mortality.

To summarize, superinfection with HEV in patients with underlying CLD causes severe liver decompensation that is frequently complicated with hepatic encephalopathy and renal failure. Hepatitis E infection in this setting has a protracted course with high morbidity and mortality. With the future availability of an effective HEV vaccine, patients with CLD may be among the group of prime beneficiaries, along with pregnant women and travellers.

Indian Society of Gastroenterology, 2004; 23 : 50-51.