Br. J. Surg. Vol. 68 (1981) 19-20 Printed in Great Britain

Traumatic renal artery occlusion producing hypertension D A V I D E R N S T A N D C O L I N W. 0. W I N D S O R *

SUMMARY Traumatic renal artery occhsion is relatively rare. Prior to 1974 there were only 38 cases reported in the literature (1). The true incidence, however, is greater and the diagnosis is frequently missed at the time of the original injury. Less than 50 per cent of cases will develop hypertension. Early diagnosis is essential if this compli- cation is to be avoided. Two cases of traumatic renal artery occlusion producing hypertension are described.

Case reports Case 1: A 39-year-old woman was admitted as an emergency after being forcibly jabbed in her left upper abdomen by a broom handle. She complained of severe left-sided upper abdominal pain. On examination she was not shocked. There were superficial abrasions in the left hypochondrium and epigastrium and superficial tenderness without signs of signific- ant intra-abdominal injury. There was no haematuria. She was admitted for observation and treated conservatively. Abdominal X-rays showed a paralytic ileus with gas in the stomach and small bowel and a suggestion of a retroperitoneal haematoma. Within 2 days her symptoms had settled almost completely and she was discharged 4 days later. She was

reviously known to be normotensive and at discharge her glood pressure was 130/80 mmHg. Three months later she was readmitted to a medical ward with severe headaches associated with nausea and vomiting, which had gradually developed since her original discharge. On examination there was little to find clinically, but her blood pressure was found to be 180/120 mmHg. She remained hypertensive and an intraven- ous pyelogram showed a non-functioning kidney on the left side. A renogram failed to show left renal blood flow and a left retrograde pyelogram confirmed the presence of a left ureter with normal calyceal system. The left kidney was accordingly explored through the bed of the twelfth rib. She was found to have a small fibrotic kidney adherent to surrounding structures and there was no pulsation in the renal artery. There were islands of vascularized tissue in an otherwise ischaemic kidney. Nephrectomy was performed. Postoperatively her blood pressure fell immediately to within normal limits. Follow-up to 5 years later confirmed normotension.

Case 2: A 22-year-old male motorcyclist was admitted as an emergency having been involved in a road traffic accident. Clinically he was conscious but shocked with a pulse of 130/min and a systolic blood pressure of 80 mmHg. He complained of severe abdominal pain and loss of sensation and movement in his left arm. On examination he had superficial cuts and grazes to his upper abdominal wall and a rigid, distended abdomen. There was marked rebound tenderness and bowel sounds were absent. His left arm showed signs of acute injury to his brachial plexus. A clinical diagnosis of a ruptured viscus was made and he was resuscitated and taken to theatre. He was found to have a ruptured spleen, a large tear in the base of the jejunal mesentery, superficial tears in both lobes of the liver and a sizeable retroperitoneal haematoma on the left side. Splenectomy was performed, the bleeding mesenteric vessels were ligated and the abdomen closed. He was transfer- red to the intensive care unit for 36 h. His initial postoperative recovery was satisfactory, but on his return to the general ward his blood pressure was found to be consistently between I 0 0 and 110 diastolic. He was known to be normotensive before his accident. After 24 h he was found on routine ward testing to have microscopic haematuria, which gradually became ob- vious clinically over the ensuing 4 days. Over the same period

his blood pressure had risen to 210/130 mmHg. He was treated with beta-blocking agents. An emergency intravenous pyelo- gram showed a non-functioning kidney on the left side. A renogram showed no renal flow on the left side. A left retrograde ureterogram confirmed a normal ureter and caly- ceal system. Accordingly the kidney was explored through the bed of the twelfth rib. There was no evidence of specitic renal trauma, but the kidney was found to be grossly avascular with only small islands of vascularized tissue. The renal artery was not pulsating and, when opened, there was a small circumferen- tial dissection of the intima with super-added thrombus and complete occlusion. A left nephrectomy was performed and the

atient recovered quickly from the operation. However, his g lood pressure remained elevated and he needed beta-blocking agents to control it. Four weeks later the blood pressure was still 130/100 mmHg but it subsequently returned to normal, and when seen 3 months later the patient was normotensive.

Discussion Traumatic renal artery occlusion was first described by Von Recklinghausen in 1861 (2). The majority of cases result from rapid deceleration-type blunt injuries. I t is thought that sudden displacement of the kidney from a relatively immobile aorta stretches the vascular pedicle producing a tear in the somewhat inelastic intima with resultant subintimal dissection and/or thrombosis, as in Case 2 (3,4). Alternatively, direct blows to the abdomen may compress the renal artery against the vertebral column, as in Case 1 (5).

Diagnosis is often delayed as there are other more obvious injuries present. Even a t laparotomy it may not be possible t o diagnose the problem because of retro- peritoneal haematoma (6), as in Case 2. Eighty per cent of cases present with haematuria in association with non-specific loin pain. The diagnosis is suspected if a non-functioning kidney is found on IVP and established by isotope renography or arteriography.

Attempts a t revascularization have been sporadically performed with some success (1 ,4 , 6-8), but in most cases the treatment of choice is nephrectomy, princi- pally t o avoid the possible consequence of hypertension, which may be severe, fulminating, prolonged and resistant t o drug therapy (9).

Less than 50 per Cent of cases develop hypertension, the mechanism of which appears to be sustained renin release from the ischaemic kidney. This has been demonstrated in experimental animals following Goldblatt’s pioneering work on renal ischaemia (lC12). In rats hypertension is produced if one renal artery is partially clipped rendering the kidney is- Chaemic (1 3). The renin concentration in the ischaemic kidney is high with compensatory inhibition of renin from the contralateral normal kidney (14). The high renin output is maintained both in the initial and established phases of hypertension (1 5).

In man, high renin output can be demonstrated in the renal vein in patients with renal artery stenosis, but little

* Worcester Royal Infirmary, Ronkswood Branch, Newtown Road, Worcester WR5 IHN. Correspondence to: Colin W. 0. Windsor.

20 D. Ernst and C. W. 0. Windsor

work has been done in this regard in patients with hypertension secondary to traumatic renal artery occlu- sion, because of its rarity. In 1958, however, McDonald (1 6) cured hypertension by nephrectomy following accidental surgical damage to a renal artery leading to thrombosis. He noted that the renin concentration in the ischaemic kidney was thirty-four times normal.

The renin mechanism in all its undoubted complexity explains why only a proportion of patients develop hypertension. For renin to be produced there must be surviving renal parenchyma. It follows that hyperten- sion will only occur if the occlusion to the renal artery is incomplete and collateral flow is sufficient to maintain viability of part of the renal parenchyma. Where the occlusion iscomplete or collateral flow is insufficient, no hypertension will develop.

The development of hypertension would therefore indicate that part of the kidney is viable. The viability of the rest of the kidney, and therefore the possibility 0.f revascularization, will depend on the nature of the injury to the renal artery and the speed of onset of ischaemic damage. Early diagnosis is therefore essen- tial. In this context it might have been possible to attempt revascularization in our second patient, but we should not have adopted the posterior surgical ap- proach as this is suitable only for nephrectomy.

References I . FAY R., BROSMAN s., LINDSTROM R. et al.: Renal artery

thrombosis: a successful revascularization by auto- transplantation. J . Urol. 1974; 111: 572-7.

2. VON RECKLINGHAUSEN F.: Hamorrhagische Niereninfarkei. Virchows Arch. Pathol. Anat. 1861: 20: 205.

3. COLLINS H. A., and JACOBS J . K.: Acute arterial injuries due to blunt trauma. J . Bone Joint Surg. 1961; 43A: 193.

4. MORTON J. R., and CRAWFORD E. s.: Bilateral traumatic renal artery thrombosis. Ann. Surg. 1972; 176: 62-7.

5 . SULLIVAN M. J. et al.: Renal artery occlusion secondary to blunt abdominal trauma. J . Trauma 1972; 12: 509.

6. STABLES u. P., FOUCHE R. F., DE VILLIERSVAN NIEKERK J. R. et al.: Traumatic renal artery occlusion: 21 cases. J . Urol. 1976; 115: 229-33.

7. KOHL L.: Vascular surgery in urology. Proc. R . Soc. Med. 1971: 64: 589.

8. SKINNER D. G.: Traumatic renal artery thrombosis: a successful thrombectomy and revascularization. Ann. h u g . 1973; 177: 264-7.

9. PATEL s. c.: Renal artery thrombosis following minor trauma. J . R . CON. Surg. Edinb. 1970; 15: 337.

10. GOLUBLATT H., LYNCH J., HANZAL R. F. et al.: Experimental hypertension due to renal ischaemia. Bull. A-cad. Med. Clev. 1932; XVI: 6.

11. COLDBLATT H., LYNCH J. et al.: Studies on experimental hypertension: I , 11, and 111. J . Exp. Med. 1934; 5 9 347, 1937; 65: 223, 1937; 65, 671.

12. GOLDBLATT H.: Studies on experimental hypertension. Ann. Intern. Med. 1937; 11: 69.

13. WILSON C. and BYRON F. B.: Renal changes in malignant hypertension. Lancet 1939; 1: 136.

14. GROSS F.: The renin-angiotensin system in hypertension. Ann. Intern. Mrd . 1971; 7 5 771.

15. MOHRING J., MOHRING B., NAUMANN H. J. et a].: Salt and water balance and renin activity in renal hypertension of rats. Am. J . Physiol. 1975; 288: 1847.

16. MCDONALD R. T., SZILAGYI E., and SMITH R. F.: Nephrogenic hypertension (Goldblatt kidney) .following operative trauma to the renal artery. Circulation 1958: 18: 71.

Paper accepted 19 May 1980.

Statistics in The British Journal of Surgery It is part of the clinical scientist’s stock-in-trade to use statistical methods. In many instances, and by most readers, these can be taken on trust, but in that there is a wide variety of tests and, on occasion, disagreement amongst both amateurs and professionals on the best choice, it is always wise that authors quote the method used. It is indeed journal policy to quote methods, the reason for their choice and, in the case of clinical trials, the confidence or tolerance limits of the observed results. Delay in acceptance may occur if contributors do not include these details.