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Unusual early presentation of puerperal cerebral venous thrombosis
lntrrnurional
Journal c,f’ Obsterw
0 1994 Longman
Group
Anesfhrsiu
(1994)
3. 227-228
Ltd
International
-
‘8K%$ Anesthesia
CASE REPORT Unusual early presentation of puerperal cerebral venous thrombosis S. Mallaiah, C. H. Tailby Department of Anaesthesia, Mill Road Maternity Hospital, Liverpool, UK
tory. Prochlorperazine 12.5 mg was given intramuscularly. When she had recovered it was decided that this episode was unrelated to the epidural and it was deemed safe to proceed with epidural analgesia. A single bolus of 8 ml of 0.375% bupivacaine was administered. However, no significant analgesic benefit was apparent from this and she refused further epidural top-ups. She became increasingly unreasonable and extremely uncooperative. This was considered by the midwives to be in keeping with her behaviour especially during her latter antenatal admissions. Four hours after siting the epidural catheter, she was delivered vaginally of a live female infant weighing 3.26 kg with Apgar scores 6 and 9 at 1 and 5 min respectively. During suturing of a perineal tear, she complained of a severe frontal headache. She was found to be quite unwell and irritable with persistent nausea and vomiting and an altered level of consciousness. She was photophobic with a painful stiff neck but no focal neurological deficit was demonstrable and the fundi were normal. Her pulse and blood pressure were within normal limits. The possibility of a post dural puncture headache was raised by the obstetric staff although there had never been any reason to suspect a dural puncture. Due to the temporal relation of the onset of these symptoms to the possibly violent expulsive efforts of spontaneous vaginal delivery, subarachnoid haemorrhage had to be excluded. Neurological observations were commenced while a CT scan was being arranged for her at the regional neurological unit. In the ensuing halfhour two grand ma1 seizures were observed. The CT scan failed to demonstrate any haemorrhage or masses but the patient was detained in the neurological unit as the grand ma1 seizures continued with increasing frequency and she required intensive care for control of status epilepticus. No firm diagnosis was made. Eclampsia was suggested by the neurologists but the obstetric team felt this was unlikely.
Hypercoagulability of blood in pregnancy is a well recognised phenomenon. Plasma fibrinogen levels rise from about 200-450 mg% in the non pregnant state to about 400-650 mg% in late pregnancy. Coagulation factors VII, VIII, IX and X are increased and antithrombin III activity and fibrinolytic activity are decreased during pregnancy.’ Deep vein thrombosis and pulmonary embolism are frequently seen and are well recognised. The less common problem of cerebral venous thrombosis is more difficult to recognise and the symptoms may be mistaken for other disorders such as eclampsia, subarachnoid haemorrhage or post dural puncture headache.2*3 Rarely the clinical symptoms may suggest focal intracranial space occupying lesions,4 and the early use of an appropriate CT or MRI scan may avoid diagnostic errors and unnecessary surgery.
CASE HISTORY
A Caucasian 19-year-old primigravida was admitted at 39 weeks’ gestation following spontaneous rupture of membranes at home. She was well known to the hospital following a stormy pregnancy. She had been admitted to the hospital on 8 occasions during the previous 20 weeks for treatment of recurrent severe urinary tract infections. On this occasion she was found to be in labour and requested epidural analgesia. An epidural catheter was sited at L4/5 level after appropriate counselling. There was no suggestion of a dural puncture or intravenous placement. Following administration of a test dose of 3 ml of 0.375% plain bupivacaine, she became nauseated and vomited about 100 ml of bile stained fluid and was observed to have a brief syncopal episode. This was not accompanied by any alteration of blood pressure and fetal observations were satisfacCorrespondence to S. Mallaiah. Liverpool Maternity Hospital. Oxford
Consultant Anaesthetist, Street, Liverpool. UK. 221
228
International Journal of Obstetric Anesthesia
She improved gradually with supportive treatment and 3 days later a contrast enhanced CT scan was performed which demonstrated bilateral swollen hemispheres and probable cortical venous thrombosis. Phenytoin therapy was continued and an MRI scan on the eleventh day showed a patent sagittal sinus but persistent evidence of cortical venous infarction. By this time she was well enough to be discharged home. It was planned to exclude systemic lupus erythematosis as a possible contributory factor for her thrombosis at her postnatal follow up visit but she defaulted repeatedly. After several months it was confirmed by her general practitioner that she remained well at home without residual disability.
DISCUSSION Cerebral venous thrombosis as a complication of pregnancy and the puerperium was first described in l888.6 It may occur as early as 7 weeks gestation7 and is also a recognised complication of oral contraception.’ In the puerperium the symptoms usually occur 48 h after delivery,2*3s5although presentation may be delayed for up to 10 days after delivery.4 Our patient developed overt symptoms and signs such as severe headache, photophobia and neck stiffness within an hour of a normal vaginal delivery, followed very quickly by repeated seizures. She had been described as being drowsy and uncooperative during the last admission which preceded her delivery by a few days. It is possible that this was actually the start of her symptoms which were unfortunately dismissed as being due to a difficult personality. She had required admission to hospital several times for urinary tract infections which may be significant in that she was febrile and vomiting requiring intravenous fluids on many of these occasions. This implies some degree of dehydration and immobilization which are predisposing factors. The initial emergency CT scan which was done without contrast did not demonstrate the pathology. A contrast enhanced CT scan is usually diagnostic but an MRI scan is more sensitive and may be preferred, especially in pregnancy. Once the diagnosis
is made, the treatment is mainly supportive aimed at controlling seizures with anticonvulsants and reducing intracranial pressure and cerebral oedema with mechanical ventilation and steroids. The role of heparin in this situation is controversial. Some authorities advocate caution because of the risk of intracranial haemorrhage in the presence of venous infarction9 Increasingly the evidence seems to suggest that this risk is overrated.4~7~10*” This is a serious condition with a reported incidence of about 1 in 3000 pregnancies carrying a mortality of about 25%. In the Report on Confidential Enquiries into Maternal Deaths in the United Kingdom 1988-1990 there were 6 deaths attributed to cerebral venous thrombosis. In those patients that survive, the prognosis is usually good with very little residual disability. References 1. Camann W R, Ostheimer G W. Physiologic adaptions in Pregnancy. In: Ostheimer G W, ed. Manual of Obstetric Anesthesia, 2nd Edn. New York: Churchill Livingstone, 1992: pp 4-5. 2. Ravindran R S, Zandstra G. Cerebral venous thrombosis vs postlumbar puncture headache. Anesthesiology 1989; 71: 478479. 3. Hubbert C H. Dural puncture headache suspected, cortical vein thrombosis diagnosed. Anesth Analg 1987; 66: 285. 4. Srinivasan K. Cerebral venous and arterial thrombosis in pregnancy and puerperium - study of 135 patients. Angiology 1983; 34: 731-746. 5. Krenz I, Power K J. Postpartum thrombosis of the great vein of Galen. Anaesthesia 1990; 45: 6433645. 6. Gowers W R. Thrombosis in cerebral veins and sinuses. In: A Manual of Diseases of the Nervous Svstem. Vol II. London: J. & A. Churchill. 1888: 4i6-417. I. Enevoldson T P, Ross Russell R W. Cerebral venous thrombosis: new causes for an old syndrome? Q J Med 1990; 77: 1255-1275. 8. Atkinson E A, Fairburn B, Heathfield K W G. Intracranial venous thrombosis as a complication of oral contraception. Lancet 1970; 1: 914-918. 9. Gettelfinger D M, Kokmen E. Superior sagittal sinus thrombosis. Arch Nemo1 1977; 34: 2-6. 10. Halpem J P, Morris J P, Driscoll G L. Anticoagulants and cerebral venous thrombosis. Aust NZ J Med 1984; 14: 643-648. 11. Vilringer A, Gamer C, Meister W, Haberl R, Pfister W, Einhaeupl K M. High dose heparin treatment in cerebral venous thrombosis. Stroke 1988; 19: 135.
Journal c,f’ Obsterw
0 1994 Longman
Group
Anesfhrsiu
(1994)
3. 227-228
Ltd
International
-
‘8K%$ Anesthesia
CASE REPORT Unusual early presentation of puerperal cerebral venous thrombosis S. Mallaiah, C. H. Tailby Department of Anaesthesia, Mill Road Maternity Hospital, Liverpool, UK
tory. Prochlorperazine 12.5 mg was given intramuscularly. When she had recovered it was decided that this episode was unrelated to the epidural and it was deemed safe to proceed with epidural analgesia. A single bolus of 8 ml of 0.375% bupivacaine was administered. However, no significant analgesic benefit was apparent from this and she refused further epidural top-ups. She became increasingly unreasonable and extremely uncooperative. This was considered by the midwives to be in keeping with her behaviour especially during her latter antenatal admissions. Four hours after siting the epidural catheter, she was delivered vaginally of a live female infant weighing 3.26 kg with Apgar scores 6 and 9 at 1 and 5 min respectively. During suturing of a perineal tear, she complained of a severe frontal headache. She was found to be quite unwell and irritable with persistent nausea and vomiting and an altered level of consciousness. She was photophobic with a painful stiff neck but no focal neurological deficit was demonstrable and the fundi were normal. Her pulse and blood pressure were within normal limits. The possibility of a post dural puncture headache was raised by the obstetric staff although there had never been any reason to suspect a dural puncture. Due to the temporal relation of the onset of these symptoms to the possibly violent expulsive efforts of spontaneous vaginal delivery, subarachnoid haemorrhage had to be excluded. Neurological observations were commenced while a CT scan was being arranged for her at the regional neurological unit. In the ensuing halfhour two grand ma1 seizures were observed. The CT scan failed to demonstrate any haemorrhage or masses but the patient was detained in the neurological unit as the grand ma1 seizures continued with increasing frequency and she required intensive care for control of status epilepticus. No firm diagnosis was made. Eclampsia was suggested by the neurologists but the obstetric team felt this was unlikely.
Hypercoagulability of blood in pregnancy is a well recognised phenomenon. Plasma fibrinogen levels rise from about 200-450 mg% in the non pregnant state to about 400-650 mg% in late pregnancy. Coagulation factors VII, VIII, IX and X are increased and antithrombin III activity and fibrinolytic activity are decreased during pregnancy.’ Deep vein thrombosis and pulmonary embolism are frequently seen and are well recognised. The less common problem of cerebral venous thrombosis is more difficult to recognise and the symptoms may be mistaken for other disorders such as eclampsia, subarachnoid haemorrhage or post dural puncture headache.2*3 Rarely the clinical symptoms may suggest focal intracranial space occupying lesions,4 and the early use of an appropriate CT or MRI scan may avoid diagnostic errors and unnecessary surgery.
CASE HISTORY
A Caucasian 19-year-old primigravida was admitted at 39 weeks’ gestation following spontaneous rupture of membranes at home. She was well known to the hospital following a stormy pregnancy. She had been admitted to the hospital on 8 occasions during the previous 20 weeks for treatment of recurrent severe urinary tract infections. On this occasion she was found to be in labour and requested epidural analgesia. An epidural catheter was sited at L4/5 level after appropriate counselling. There was no suggestion of a dural puncture or intravenous placement. Following administration of a test dose of 3 ml of 0.375% plain bupivacaine, she became nauseated and vomited about 100 ml of bile stained fluid and was observed to have a brief syncopal episode. This was not accompanied by any alteration of blood pressure and fetal observations were satisfacCorrespondence to S. Mallaiah. Liverpool Maternity Hospital. Oxford
Consultant Anaesthetist, Street, Liverpool. UK. 221
228
International Journal of Obstetric Anesthesia
She improved gradually with supportive treatment and 3 days later a contrast enhanced CT scan was performed which demonstrated bilateral swollen hemispheres and probable cortical venous thrombosis. Phenytoin therapy was continued and an MRI scan on the eleventh day showed a patent sagittal sinus but persistent evidence of cortical venous infarction. By this time she was well enough to be discharged home. It was planned to exclude systemic lupus erythematosis as a possible contributory factor for her thrombosis at her postnatal follow up visit but she defaulted repeatedly. After several months it was confirmed by her general practitioner that she remained well at home without residual disability.
DISCUSSION Cerebral venous thrombosis as a complication of pregnancy and the puerperium was first described in l888.6 It may occur as early as 7 weeks gestation7 and is also a recognised complication of oral contraception.’ In the puerperium the symptoms usually occur 48 h after delivery,2*3s5although presentation may be delayed for up to 10 days after delivery.4 Our patient developed overt symptoms and signs such as severe headache, photophobia and neck stiffness within an hour of a normal vaginal delivery, followed very quickly by repeated seizures. She had been described as being drowsy and uncooperative during the last admission which preceded her delivery by a few days. It is possible that this was actually the start of her symptoms which were unfortunately dismissed as being due to a difficult personality. She had required admission to hospital several times for urinary tract infections which may be significant in that she was febrile and vomiting requiring intravenous fluids on many of these occasions. This implies some degree of dehydration and immobilization which are predisposing factors. The initial emergency CT scan which was done without contrast did not demonstrate the pathology. A contrast enhanced CT scan is usually diagnostic but an MRI scan is more sensitive and may be preferred, especially in pregnancy. Once the diagnosis
is made, the treatment is mainly supportive aimed at controlling seizures with anticonvulsants and reducing intracranial pressure and cerebral oedema with mechanical ventilation and steroids. The role of heparin in this situation is controversial. Some authorities advocate caution because of the risk of intracranial haemorrhage in the presence of venous infarction9 Increasingly the evidence seems to suggest that this risk is overrated.4~7~10*” This is a serious condition with a reported incidence of about 1 in 3000 pregnancies carrying a mortality of about 25%. In the Report on Confidential Enquiries into Maternal Deaths in the United Kingdom 1988-1990 there were 6 deaths attributed to cerebral venous thrombosis. In those patients that survive, the prognosis is usually good with very little residual disability. References 1. Camann W R, Ostheimer G W. Physiologic adaptions in Pregnancy. In: Ostheimer G W, ed. Manual of Obstetric Anesthesia, 2nd Edn. New York: Churchill Livingstone, 1992: pp 4-5. 2. Ravindran R S, Zandstra G. Cerebral venous thrombosis vs postlumbar puncture headache. Anesthesiology 1989; 71: 478479. 3. Hubbert C H. Dural puncture headache suspected, cortical vein thrombosis diagnosed. Anesth Analg 1987; 66: 285. 4. Srinivasan K. Cerebral venous and arterial thrombosis in pregnancy and puerperium - study of 135 patients. Angiology 1983; 34: 731-746. 5. Krenz I, Power K J. Postpartum thrombosis of the great vein of Galen. Anaesthesia 1990; 45: 6433645. 6. Gowers W R. Thrombosis in cerebral veins and sinuses. In: A Manual of Diseases of the Nervous Svstem. Vol II. London: J. & A. Churchill. 1888: 4i6-417. I. Enevoldson T P, Ross Russell R W. Cerebral venous thrombosis: new causes for an old syndrome? Q J Med 1990; 77: 1255-1275. 8. Atkinson E A, Fairburn B, Heathfield K W G. Intracranial venous thrombosis as a complication of oral contraception. Lancet 1970; 1: 914-918. 9. Gettelfinger D M, Kokmen E. Superior sagittal sinus thrombosis. Arch Nemo1 1977; 34: 2-6. 10. Halpem J P, Morris J P, Driscoll G L. Anticoagulants and cerebral venous thrombosis. Aust NZ J Med 1984; 14: 643-648. 11. Vilringer A, Gamer C, Meister W, Haberl R, Pfister W, Einhaeupl K M. High dose heparin treatment in cerebral venous thrombosis. Stroke 1988; 19: 135.