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J R Soc Med. 2002 June; 95(6): 300–301.
PMCID: PMC1279914

Acute renal failure after punishment beatings

Douglas M G Bowley, FRCS, Craig Buchan, BComm,1 Laurence Khulu, MBBCh, and Kenneth D Boffard, Bsc FRCS

In the face of soaring crime rates, South Africa has seen the growth of vigilante groups that seek to mete out summary justice. Punishment, described as ‘African medicine’, often involves beating of the suspect with a whip (or sjambok). Victims of sjambokking have characteristic patterns of injury.

CASE HISTORIES

Case 1

A man of 32 was surrounded by a mob and beaten with a sjambok, punched and kicked for several hours. Most of his body surface was covered with sjambok marks, contusions and lacerations (Figure 1). A urinary catheter was inserted and rosé-coloured urine was obtained, which tested positive for myoglobin. Treatment consisted of aggressive volume loading with monitoring of central venous pressure. Despite treatment, the patient developed acute renal failure (ARF) requiring haemodialysis. He slowly improved and at three-month follow-up his renal function had returned to normal.

Figure 1
Patient 1: extensive sjambok marks on the trunk

Case 2

A man aged 22 came to hospital two days after a severe sjambokking. On admission he was alert, with a pulse of 100, blood pressure of 100 mmHg and a respiratory rate of 20 breaths per minute. On admission arterial blood pH was 7.356 with a base excess of -16 and bicarbonate 9.8 mmol/L. Within seven hours he had deteriorated greatly; despite aggressive treatment he died before haemodialysis could be instituted. Serum potassium taken at the time of his cardiac arrest was 8.4 mmol/L.

COMMENT

The association between rhabdomyolysis and ARF was first reported in victims trapped during the London Blitz1. The syndrome is seen in earthquake survivors2, after excessive exercise,3 and when limbs have been forced into abnormal postures for long periods, such as during anaesthesia or coma induced by alcohol or drugs3. Rhabdomyolysis leading to ARF has been reported in victims of torture5 and severe child abuse6 and is well recognized in South Africa after beatings with the sjambok7,8,9.

Sjamboks are about one metre in length, originally constructed from rhino hide but now manufactured from synthetic material. This weapon produces extensive soft tissue injury which may not be apparent on initial assessment, since the skin is often intact and natural skin pigmentation can make the deep muscle bruising difficult to detect (Figure 2). In 1991, Muckart et al.7 reported a series of 42 sjambokked patients, of whom 3 (7.1%) died. After introducing a protocol stressing the importance of prompt volume replacement, the same group had only one death (1.6% mortality rate) in a later series of 64 patients8. Factors associated with poor outcomes, such as delay in presentation, heavy pigmenturia, acidosis, and abnormal admission creatinine, had low specificity and poor predictive value. Patients with adverse factors may respond to fluid loading and recover uneventfully while other patients with normal measurements on admission may develop acute renal failure9. The most accurate predictor of the risk for the development of ARF appears to be the initial venous bicarbonate. In one study, no patient with a venous bicarbonate > 17 mmol/L developed ARF, while 4 out of 5 patients with venous bicarbonate < 17 mmol/L went on to develop ARF8.

Figure 2
Patient 2: deep bruising on right arm and flank

ARF after rhabdomyolysis is multifactorial; injured muscle may sequester many litres of fluid, reducing the effective intravascular volume and activating both the sympathetic and the renin-angiotensin systems, with consequent renal vasoconstriction and ischaemia10. Muscle cell damage releases vasoactive mediators into the circulation, further reducing renal blood flow. Myoglobin precipitates in the tubule, leading to tubular obstruction. Precipitation is enhanced in acidic conditions; however, myoglobin initiates tubular injury in concentrations lower than are needed to cause precipitation. Tubular injury seems to be mediated by free radicals, which cause lipid peroxidation within the nephron. Free iron was initially implicated as the cause of this free radical generation; however, the haem group of myoglobin is now thought to cause lipid peroxidation directly10.

Compartment syndrome is uncommon after sjambok injury, though it must not be forgotten. If the skin is broken as a consequence of the sjambok injuries, sepsis may develop and occasionally progresses to necrotizing fasciitis. This aggressive soft-tissue sepsis may easily be overlooked in an already swollen limb and unless recognized and promptly treated may have fatal results9. The other common mode of death after rhadomyolysis is cardiac arrest due to uncontrolled hyperkalaemia9,10; thus, close monitoring and control of serum potassium is essential. Restoration of muscle blood flow may prevent more extensive muscle necrosis, but creates a reperfusion injury10. We surmise that the liberation of potassium and vasoactive mediators during muscle reperfusion precipitated cardiac arrest in our second patient.

The role of mannitol is controversial; it may have specific value in lessening high compartment pressures but routine use is not advocated10. Loop diuretics have the theoretical disadvantage of acidifying the urine11. Up to 10% of patients with sjambok injuries will require renal replacement therapy7,8,9. Alkalinization of the urine not only improves myoglobin washout from the kidney but also helps prevent renal vasoconstriction and lipid peroxidation10.

Sjambok injuries can be deceptive and aggressive treatment is required to prevent kidney failure; a urine dipstick detects myoglobinuria and may aid recognition of patients at risk, especially if natural skin colouring obscures the extent of the injury. Early intravenous fluids are essential and we recommend doses of alkali to keep the urine pH ≥ 7.0.

References

1. Bywaters EGL, Beall D. Crush injuries with impairment of renal function. BMJ 1941;i: 427-32 [PMC free article] [PubMed]
2. Oda Y, Shindoh M, Yukioka H, Nishi S, Fujimori M, Asada A. Crush syndrome sustained in the 1995 Kobe, Japan, Earthquake; treatment and outcome. Ann Emerg Med 1997;30: 507-12 [PubMed]
3. Teitjen DP, Guzzi LM. Exertional rhabdomyolysis and acute renal failure following the Army Physical Fitness Test. Mil Med 1989;154: 23-5 [PubMed]
4. Szewcyk D, Ovadia P, Abdullah F, Rabinovici R. Pressure-induced rhabdomyolysis and acute renal failure. J Trauma 1998;44: 384-8 [PubMed]
5. Bloom AI, Zamir G, Muggia M, Friedlaender M, Gimmon Z, Rivkind A. Torture rhabdomyorhexis—a pseudo-crush syndrome. J Trauma 1995;38: 252-4 [PubMed]
6. Mukerji SK, Siegel MJ. Rhabdomyolysis and renal failure in child abuse. AJR Am J Roentgenol 1987;148: 1203-4 [PubMed]
7. Muckart DJJ, Abdool-Carrim ATO. Pigment-induced nephropathy after sjambok injuries. S Afr J Surg 1991;29: 21-4 [PubMed]
8. Muckart DJJ, Moodley M, Naidu AG, Reddy ADR, Meineke KR. Prediction of acute renal failure following soft tissue injury using the venous bicarbonate concentration. J Trauma 1992;33: 813-17 [PubMed]
9. Knottenbelt JD. Traumatic rhabdomyolysis from severe beating—experience of volume diuresis in 200 patients. J Trauma 1994;37: 214-19 [PubMed]
10. Holt SG, Moore KP. Pathogenesis and treatment of renal dysfunction in rhabdomyolysis. Intensive Care Med 2001;27: 803-11 [PubMed]
11. Better OS, Stein JH. Early management of shock and prophylaxis of acute renal failure in traumatic rhabdomyolysis. N Engl J Med 1990;322: 825-9 [PubMed]

Articles from Journal of the Royal Society of Medicine are provided here courtesy of Royal Society of Medicine Press