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Correspondence

Indian Pediatr 2009;46: 538-539

Post Varicella Thrombosis


Padmasani Venkat Ramanan and Kanav Anand

Department of Pediatrics, Sri Ramachandra Medical College, 
Porur, Chennai 600 116,
India.  
 


We report a case of extensive thrombosis in a 12 year old boy, who had varicella 15 days earlier. The child presented with headache and generalized tonic clonic seizures for 2 hours. On examination, he had healed scars of varicella. Neurological examination revealed a Glasgow Coma Score of 9/15. CSF analysis, complete blood counts, RFT, LFT, blood sugar, serum electro-lytes, PT and APTT were normal. CT Brain revealed multiple areas of hemorrhage with perilesional edema involving bilateral parietal and left frontal region. The child was started on anticonvulsants. Magnetic resonance venography of brain revealed superior sagittal and bilateral transverse sinus thrombosis. Prothrombotic screen (Protein S, Protein C levels, Factor V Leiden Mutation, Anti-thrombin III levels and anti-cardiolipin antibodies) was planned, but could not be done due to financial constraints.

The child was started on LMW heparin along with oral anticoagulants. The child’s sensorium improved gradually over 5 days. On day five of admission, he developed left leg pain with swelling. Doppler study revealed extensive thrombosis of left external iliac, femoral and popliteal veins. He improved with limb elevation and analgesics. He was discharged on anticonvulsants and oral anticoagulants maintaining an INR of 2-3. On follow up there are no neurologic sequelae or subsequent episodes of thrombosis. Fresh frozen plasma was not used in child as the response to the above treatment was satisfactory.

The incidence of serious complications after varicella infection is 8.5/1 lakh population(1). Thrombotic complications are known especially involving the cerebral vasculature(2). Eidelberg, et al.(3) suggested that virus mediated endothelial injury promotes local thrombosis but transient deficiency of protein S activity (due to induction of anti-protein S auto antibodies) is also a causal factor(4,5). These antibodies persist for only a few months. The frequency with which antibodies to proteins S are induced in children during varicella infection is unknown. Thrombosis is more common in individuals with Factor V Leiden, which is a factor V variant resulting from a single point mutation. It increases the risk for thrombosis as it confers resistance to activated protein C [5]. Prognosis in post varicella thrombosis is good. A prothrombotic screen after recovery, to diagnose  hereditary prothrombotic states that need life long anticoagulants, is advisable.

References

1. Ziebold C, Von Kries R, Lang R, Weigl J, and HJ. Schmitt. Severe complications of varicella in previously healthy children in Germany: a 1-year survey. Pediatrics 2001; 108: e79.

2. Bodensteiner JB, Hille MR, Riggs JE. Clinical features of vascular thrombosis following varicella. Am J Dis Child 1992; 146: 100-102.

3. Eidelberg D, Sotrel A, Horoupian DS, Neumann PE, Pumarola-Sune T, Price RW. Thrombotic cerebral vasculopathy associated with herpes zoster. Ann Neurol 1986 ;19 :7-14 .

4. Ganesan V, Kirkham FJ . Mechanisms of ischaemic stroke after chickenpox. Arch Dis Child 1997; 76: 522-525.

5. Charles R. Woods, Johnson CA. Varicella purpura fulminans associated with heterozygosity for factor V leiden and transient protein S deficiency. Pediatrics 1998; 102: 1208- 1210.
 

 

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