Underlying prothrombotic states in pregnancy associated cerebral venous thrombosis.
BACKGROUND
The exact pathogenesis of pregnancy associated cerebral venous thrombois is still unsettled. Aims : To identify possible inherited and acquired prothrombotic risk factors and also identify the factors associated with mortality in pregnancy associated CVT.


METHODS
Prospective cohort study to identify prothrombotic risk factors and case control study of influence of local traditional practice of puerperal water restriction on postpartum CVT.


METHODS
Consecutive patients with pregnancy associated CVT seen over a period of three years. Thrombotic workup included genetic markers, protein assays, and other factors.


METHODS
Univariate and chi-square analysis.


RESULTS
Of the 41 patients studied during the study period, 71% of patient had a single and 34% had multiple prothrombotic risk factors. Methylene tetrahydro-folate reductase (MTHFR) heterozygosity (19.5%) and factor V Leiden heterozygous (7.3%) were the commonest genetic markers. Hyperhomocysteinemia (34%) and elevated factor VIII levels (14.6%) were the other important risk factors. In this cohort the mortality was 17%. Mortality increased by odds of 1.3 for every additional prothrombotic marker. The factors associated with increased mortality included: status epileptics (P = 0.05, OR 13.2, 95% CI 1.002 - 173), deep venous system involvement (P = 0.016, OR 9.64, 95% CI 1.53 - 60.6), presence of midline shift (P = 0.012, OR 24.7, 95% CI 2.05 - 29.8) and diffuse cerebral edema (P = 0.006, OR 14.5, 95% CI 2.18- 96.4). The traditional practice of decrease intake of water during puerperium was significant in woman with pregnancy associated CVT when compared to control subjects (P < 0.02).


CONCLUSIONS
In patients with pregnancy associated CVT, prothrombotic markers can be multiple and are associated with increased odds of mortality. Deep venous system involvement, presence of midline shift and diffuse cerebral edema increased mortality. Peuperial water restriction may be a modifiable risk factor.
Aaron
S
S
Department of Neurological Sciences, Neurology Unit, Christian Medical College, Vellore, Tamil Nadu, India.
Alexander
M
M
Maya
T
T
Mathew
V
V
Goel
M
M
Nair
S C
SC
Mammen
J
J
Vikram
M
M
D000328:Adult; D000704:Analysis of Variance; D016009:Chi-Square Distribution; D015331:Cohort Studies; D005165:Factor V / Q000378:metabolism; D005260:Female; D005343:Fibrinolytic Agents / Q000627:therapeutic use; D006493:Heparin / Q000627:therapeutic use; D006801:Humans; D020767:Intracranial Thrombosis / Q000209:etiology* / Q000378:metabolism* / Q000628:therapy; D042965:Methylenetetrahydrofolate Reductase (NADPH2) / Q000378:metabolism; D011247:Pregnancy; D011250:Pregnancy Complications, Hematologic / Q000378:metabolism; D011516:Prothrombin / Q000378:metabolism*; D012307:Risk Factors; D020246:Venous Thrombosis / Q000209:etiology* / Q000378:metabolism* / Q000628:therapy; D014868:Water Deprivation / Q000502:physiology; D055815:Young Adult
D005343:Fibrinolytic Agents; C095381:factor V Leiden; D005165:Factor V; D011516:Prothrombin; D006493:Heparin; D042965:Methylenetetrahydrofolate Reductase (NADPH2)