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| Year : 1982 | Volume
: 28
| Issue : 4 | Page : 223-4 |
Reversible malignant hypertension due to inferior vena cava thrombosis. (A case report).
Ravichandran RR, Desai SS, Acharya VN
How to cite this article:
Ravichandran R R, Desai S S, Acharya V N. Reversible malignant hypertension due to inferior vena cava thrombosis. (A case report). J Postgrad Med 1982;28:223 |
How to cite this URL:
Ravichandran R R, Desai S S, Acharya V N. Reversible malignant hypertension due to inferior vena cava thrombosis. (A case report). J Postgrad Med [serial online] 1982 [cited 2023 May 31];28:223. Available from: https://www.jpgmonline.com/text.asp?1982/28/4/223/5594 |
Post-thrombotic obstruction of inferior vena cava (IN.C.) has been recognised since Schenck,[7] in 1644, described 2 cases at autopsy. The clinical features were established by Welch (1899)[8] and Pleasants (1911)[6] in a classic review of 314 cases. Obstruction to I.V.C. can present itself with varying symptomatology such as cardiac failure, cirrhosis, nephrotic syndrome etc.[1], [4], [5] Here we are reporting a case who presented with malignant hypertension.
Mrs. K., a 35 year old multiparous patient hailing from Central India presented to us with a history of distention of abdomen and oedema of feet of 3 months' duration. The onset of distention of abdomen was fairly sudden and increased rapidly over the first two weeks. There was no history of fever or prolonged bed rest prior to the event. There was no history of jaundice or any urinary complaints. The patient had delivered a normal child at full term 2 years ago. She was not on oral contraceptives. There was no history of consumption of any herbal medicines.
On examination, she was found to be pale; there was bilateral pitting oedema of the feet, the pulse was 86/min. and the blood pressure 180/130 mm of Hg in the right upper limb. Her initial weight was 57 kg. Clinically, she had features suggesting a left pleural effusion and a massive, tense ascites. There were no prominent veins over the abdominal wall. Liver and spleen could not be palpated. The fundus examination showed arteriolar narrowing, bilateral papilloedema with haemorrhages and exudates.
On investigating, her haemoglobin was 9 gm% with a WBC count of 10,000 per mm3 with polymorphs 70% and lymphocytes 30%. The bleeding time was 2 minutes, clotting time 6½ minutes, prothrombin time-26 seconds (control: 16 seconds), and clot retraction 1 hour; platelet (count was 1.68 Macs/cumm. Fibrinogen-492 mg% and euglobin lysis time 3 hours. Her initial BUN was 17 mg% with a serum creatinine of 2.5 mg%; total protein was 6.5 gm% with albumia 3.5 gm%. The SGOT. SGPT, alkaline phosphatase and bilirubin were normal. Her urine examination showed albumin +++ with 24 hours' protein excretion of 2.5 gms. The culture did not show any growth. Both the pleural and ascitic fluids were transudates. An intravenous urogram failed to reveal any renal outlines or excretion. An inferior vena cavogram was done by transfemoral route which showed obstruction to the flow of dye in the upper segment (suprahepatic portion) of the I.V.C. The rest of the I.V.C. was entirely normal [Fig. 1A] & [Fig. 1B].
The patient was put on large doses of diuretics-frusemide, spironolactone and metalazone. Ascitic tapping was done on 4 occasions removing 1.5 litres of fluid each time. Initially, her blood pressure was controlled with a combination of methyldopa, propranolol and hydrallazine. Over a period of two and a half months, the oedema of feet, ascites and pleural effusion totally disappeared, the blood pressure returned to normal and the papilloedema and haemorrhages in the eyes disappeared. She did not require any diuretics or antihypertensives later. A repeat inferior vena cavogram showed recanalisation of the upper segment of I.V.C. [Fig. 2A] and [Fig. 2B]. Although her serum creatinine value returned to normal level, the proteinuria persisted and a kidney biopsy done showed normal glomeruli, with mononuclear infiltration and fibrosis of the interstitium with tubular atrophy, suggestive of a diagnosis of tubulo-interstitial disease. On a follow up after 6 months, her urine picture has become normal with the proteinuria disappearing.
Obstruction to the I.V.C. is not an uncommon disorder with variable clinical presentations.[1], [4], [5] The clinical features, to a certain extent, depend on the site of obstruction-upper, middle or lower segments of the I.V.C.[1], [5] Primary thrombosis of the upper segment is rare. Majority of the cases of upper segment obstruction are due to a membrane.[2] This patient, however, had primary thrombosis of the upper segment of the I.V.C. as shown by the spontaneous recanalisation in the inferior vena cavograms. The absence of any precipitating factor is well known 4, 6 Similarly, in acute obstruction of the I.V.C. the abdominal collaterals fail to develop. The most odd feature of the case is the malignant hypertension which has been reported so far only in one instance of lower segment I.V.C. block with unilateral renal vein thrombosis[5] and not in high I.V.C. block as in our case. The hypertension could have been due to two reasons:
(a) increase in the renal venous pressure.
(b) the tubulo interstitial involvement of the kidneys. It is possible that both the I.V.C. block and the renal pathology might have been produced by a singe toxic agent or the renal disease might have been secondary to high doses of diuretics given to the patient.[3]
| 1. | Chawla, A. K., Jindal, S. K., Singh, J. D., Sodhi, J. S., Pathak, I. C. and Wahl, P. L.: Clinical pattern of inferior vena cava obstruction. J. Assoc. Phys. India, 29: 85-88, 1981.  |
| 2. | Datta, D. V., Saha, S., Samanta, A. K. S., Singh, A., Gupta, B. B., Aikat, B. K. and Chuttani, P. N.: Clinical spectrum of Budd-Chiari syndrome in Chandigarh, with particular reference to obstruction of intra-hepatic portion of inferior vena cava. Ind. J. Med. Res., 60: 385-402, 1972. |
| 3. | Gilman, A. G., Goodman, L. S. and Gilman, A.: "The Pharmacological Basis of Therapeutics". 6th Edition, MacMillan Publishing Company Inc. New York, Collier MacMillan Canada Ltd., Toronto and Bailliere Tindall, London, 1980, 906. |
| 4. | Jackson, B. T. and Thomas, M. L. Post-thrombotic inferior vena caval obstruction-A review of 24 patients. Brit. Med. J., 1: 18-22, 1970. |
| 5. | Missal, M. E., Robinson, J. A. and Tatum, R. W.: Review: Inferior vena cava Obstruction: Clinical manifestations, diagnostic methods and related problems. Ann. Intern. Med., 62: 133-161, 1965. |
| 6. | Pleasants, J. H.: Obstruction of the inferior vena cava with a report of 18 cases. John's Hopk, Hosp. Report, 16: 363, 1911. Quoted by Jackson and Thomas.[4] |
| 7. | Schenck, (1944): Observationum Medicarum Rariorum Lugduni, Lib. 3, p. 399. suoted by Jackson and Thomas (1970).[1] |
| 8. | Welch, W. H.: In, "A System of Medicine". Vol. 6, Editor: T. C. Allbutt and H. D. Rolleston, MacMillan, London, 1899, p. 217. Quoted by :Jackson and Thomas (1970).[4] |
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