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 »  Case report
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Year : 2000  |  Volume : 48  |  Issue : 3  |  Page : 292-4

Cortical sinovenous thrombosis in a child with nephrotic syndrome and iron deficiency anaemia.

Department of Neurology, Nizam's Institute of Medical Sciences, Panjgutta, Hyderabad, 500082, India.

Correspondence Address:
Department of Neurology, Nizam's Institute of Medical Sciences, Panjgutta, Hyderabad, 500082, India.

  »  Abstract

Cortical sinovenous thrombosis in a child with nephrotic syndrome and iron deficiency anaemia is described. The most probable mechanism for the hypercoagulable state was thrombocytosis associated with iron deficiency anaemia. The other possible contributing factor might have been the diuretic therapy during the phase of relapse.

How to cite this article:
Meena A K, Naidu K S, Murthy J M. Cortical sinovenous thrombosis in a child with nephrotic syndrome and iron deficiency anaemia. Neurol India 2000;48:292

How to cite this URL:
Meena A K, Naidu K S, Murthy J M. Cortical sinovenous thrombosis in a child with nephrotic syndrome and iron deficiency anaemia. Neurol India [serial online] 2000 [cited 2022 May 19];48:292. Available from: https://www.neurologyindia.com/text.asp?2000/48/3/292/1515

   »   Introduction Top

Hypercoagulable state is a well recognised complication of nephrotic syndrome. Both arterial and venous thrombosis have been recognised.[1],[2],[3],[4] Among the venous thrombosis, renal vein thrombosis is more common.[5] Cortical sinovenous thrombosis (CSVT) is a rare complication of hypercoagulable state in nephrotic syndrome.[5],[6],[7] This report describes cortical sinovenous thrombosis in a child with nephrotic syndrome and iron deficiency anaemia, and discusses the possible mechanisms.

   »   Case report Top

A 4 year old boy, a known case of nephrotic syndrome due to minimal change nephritis, on intermittent course of steroids and diuretics, was admitted with history of headache, vomiting and generalized tonic clonic seizures of 10 days duration. One month before admission, he had third relapse of nephrotic state. He was put on corticosteroids (20 mg/day) and frusemide (10 mg/day). He lost 3 kg of weight. On examination he was normotensive. He had puffy face and mild pedal oedema. Neurological examination revealed an alert child with bilateral papilloedema. Motor, sensory, and cerebellar systems were normal. Urinary analysis showed proteinuria (+), however, no casts were seen. Haemoglobin was 8.3 gm/dl with packed cell volume of 28.2%. Total leukocyte count was 9,200/mm3, and platelets were 11.94 lakhs/mm3. Peripheral blood smear showed microcytic hypochromic anaemia and thrombocytosis. Erythrocyte sedimentaion rate was 35 mm during the first hour. Prothrombin time and activated partial thromboplastin time were similar to control values. Serum fibrinogen level was 196 mg/dl, blood urea 22 mg/dl and serum creatine 0.6 mg/dl. Total proteins were 6.7 gm/dl with 3.7 gm/dl albumin. The serum levels of protein C was 82% (control 70-130%), protein S was 88% (control 65-140%), and antithrombin III was 106% (control 96-112%). Collagen vascular disease profile and anticardiolipin antibodies were negative. Total cholesterol was 146 mg/dl, triglycerides 90 mg/dl, low density lipoproteins and high density lipoproteins were 93 mg/dl and 335 mg/dl (normal 35-55 mg/dl) respectively. Tests for collagen profile and anti cardiolipin antibodies were negative. Contrast CT scan of the brain done in the third week of illness showed 'empty delta' sign, suggesting superior sagittal sinus thrombosis [Figure - 1].
The patient was given intravenous heparin for 7 days and later was shifted to acitrom 1.5 mg/day for 3 months. In addition he was also given iron supplements. During follow-up, platelet count showed steady improvement with the improvement in the level of haemoglobin. By 5th week, platelet count was 2.2 lakhs/cumm and haemoglobin 13.3 gm/dl. Papilloedema completely regressed over a period of 9 to 10 weeks. His nephrotic state was also in remission.

   »   Discussion Top

Brathelemy et al reported dural sinus thrombosis complicating nephrotic syndrome for the first time.[8] CSVT complicating nephrotic syndrome can occur in both children[5],[6],[7],[9] and adults.[5],[10] Rarely it can be fatal.[11] Thrombotic complications of nephrotic state are related to hypercoagulable states. The possible mechanisms for hypercoagulable states in nephrotic syndrome are many. These include: a) loss of body's own anticoagulant factors like plasminogen, antithrombin III, protein C and protein S;[12] b) enhanced production of clotting factors like factor V, combined factor VII, X and fibrinogen;[12] c) hypercholesterolaemia;[2] and d) thrombocytosis and platelet hyperactivity.[13] In this child it appears that the nephrotic syndrome played only a minor role, if at all, as the screening for hypercoagulable states related to nephrotic syndrome was negative.
The possible mechanisms for hypercoagulable state in this child include: a) thrombocytosis related to iron deficiency and b) diuretic therapy. Temporal relation between the onset of symptoms and diuretic therapy during the phase of third relapse supports the later hypothesis. Diuretic therapy adds to the hypercoagulable state through volume depletion. Thrombocytosis can occur in severe anaemia of any type but is more common in iron deficiency anaemia.[13] Presence of microcytic hypochromic red blood cells in the peripheral smear and improvement in haemoglobin level with iron supplementation suggests that the anaemia in this child was probably due to iron deficiency. Iron deficiency anaemia coinciding with cerebral vein thrombosis has been reported. The hypercoagulable state is due to associated thrombocytosis.[14]

  »   References Top

1.Lisch F : Hypercoagulability, renal vein thrombosis, and other thrombotic complications of nephrotic syndrome. Kidney Int 1985; 28 : 429-439.   Back to cited text no. 1    
2.Fuh JL, Teng MMH, Yang WC et al : Cerebral infarction in young men with nephrotic syndrome. Stroke1992;23:295-297.   Back to cited text no. 2    
3.Kenall AG, Lohmann RE, Dossetor JB : Nephrotic syndrome: A hypercoagulable state. Arch Inter Med 1971; 127 : 1021-1027.   Back to cited text no. 3    
4.March EE III, Biller J, Adams HP Jr et al : Cerebral infarction in patients with nephrotic syndrome. Stroke 1991; 22 : 90-93.   Back to cited text no. 4    
5.Cameron JS : Clinical consequences of nephrotic syndrome. In Grunfeld J, Kerr D, Ritz E (eds), Oxford text book of nephrology clinical nephrology, Oxford University Press, Oxford. 1992; 276-297.   Back to cited text no. 5    
6.Lau SO, Bock GH, Edsop JR et al : Sagittal sinus thrombosis in the nephrotic syndrome. J Pediatr1980; 97 : 948-959.   Back to cited text no. 6    
7.Frycon MT, Richard O, Allard D et al : Intracranial venous sinus thrombosis in nephrotic syndrome. Pediatrics 1992; 47 : 513-516.   Back to cited text no. 7    
8.Barthelemy M, Bousser MG, Jacobe C : Cerebral venous thrombosis: complication of the nephrotic syndrome. Nouvelle Presse Medicale 1980; 9 : 367-369.   Back to cited text no. 8    
9.Fritech G, Ladurner G, Scheider G : Cerebrovascular diseases in childhood: etiology, clinical aspects and prognosis. Germ Foktschvitte der Neurologic Pschiatrie 1986; 54 : 47-53.   Back to cited text no. 9    
10.Purvin V, Dunn DW, Edwards M : MRI and cerebral venous thrombosis Comput Radiol 1987; 11 : 75-79.  Back to cited text no. 10    
11.Anonymous. Minimal change nephrotic syndrome in children: deaths during the first 5 to 15 years observation, Report of the International Study of Kidney Diseases in Children. Pediatrics1984; 73 : 497-501.   Back to cited text no. 11    
12.Panicucci F, Sagripanti A, Vispi M et al : Comprehensive study of hemostasis in nephrotic syndrome. Nephron 1983; 33 : 9-13.   Back to cited text no. 12    
13.Stuart M, Kelton JG : The platelet: Quantitative and qualitative abnormalities. In Nathan DG, Oski FA (eds), Hematology of infancy and children, Philadelphia, WB Saunders Co, 1987; 1395-1459.   Back to cited text no. 13    
14.Belman AL, Roque CT, Anocona R et al : Cerebral venous in a child with iron deficiency anemia and thrombosis. thrombocytosis. Stroke1990; 21 : 488-493.   Back to cited text no. 14    
15.Spontaneous Resolution of a Non-Functioning Pituitary Adenoma Following an Apoplexy   Back to cited text no. 15    
16.R. Kachhara, S. Nair, A.K. Gupta   Back to cited text no. 16    


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