Saudi Journal of Kidney Diseases and Transplantation

: 1995  |  Volume : 6  |  Issue : 3  |  Page : 294--297

Rhabdomyolysis and Acute Renal Failure in Head Injury Patients

Mahmoud Ghallab1, Bassam Bernieh2, Salem Jamjoum3, Mohamed Allam3,  
1 Department of ICU, King Fahd Hospital, Madina Al-Munawarah, Saudi Arabia
2 Department of Nephrology, King Fahd Hospital, Madina Al-Munawarah, Saudi Arabia
3 Department of Laboratories, King Fahd Hospital, Madina Al-Munawarah, Saudi Arabia

Correspondence Address:
Bassam Bernieh
Department of Nephrology, King Fahd Hospital, Madina Al-Munawarah
Saudi Arabia


Rhabdomyolysis is a known complication of crush injuries, but is not known to complicate the course of the patients with head injuries without other apparent skeletal muscle injuries. The frequency of renal failure may be high in such group of patients. We conducted a prospective study to evaluate such incidence on twenty patients with head injuries. Ten patients (50%) had other injuries in addition, but none of the patients had crush injury. All the patients were investigated daily for serum electrolytes, urea, creatinine, creatinine phosphokinase (CPK) and myoglobulinuria. All these patients were on a dehydrating protocol to prevent brain edema, including administration of dopamine infusion (1-3 µg/kg/min), intravenous bolus doses of mannitol, and sodium bicarbonate. Nine patients (45%) developed renal impairment, three of them had no other apparent skeletal muscle injuries, but none of them required dialysis. Rhabdomyolysis is not uncommon in head injury patients in the absence of apparent skeletal muscle injuries, and may precipitate renal failure. This may have therapeutic implications to prevent the incidence of acute renal failure in such group of patients.

How to cite this article:
Ghallab M, Bernieh B, Jamjoum S, Allam M. Rhabdomyolysis and Acute Renal Failure in Head Injury Patients.Saudi J Kidney Dis Transpl 1995;6:294-297

How to cite this URL:
Ghallab M, Bernieh B, Jamjoum S, Allam M. Rhabdomyolysis and Acute Renal Failure in Head Injury Patients. Saudi J Kidney Dis Transpl [serial online] 1995 [cited 2019 Dec 7 ];6:294-297
Available from:

Full Text


Rhabdomyolysis is a clinical and bioche­mical syndrome, resulting from skeletal muscle injury, with release of muscle cell contents into the circulation [1] . This syndrome is increasingly recognized as a cause of acute renal failure ARF [1] . Rhabdomyolysis is not well known as a complication in head injury patients without apparent skeletal muscles injury. In a pilot retrospective study done over one year in our intensive care unit (ICU), it was found that 31.4% of the head injury patients developed renal impairment, Hemodialysis was needed in 20% of them, The cause of renal failure was rhabdomyolysis in all the dialysed patients. The aim of this prospective study was to evaluate the frequency of rhabdomyolysis and renal function impairment in patients with head injury in the absence accompanying skeletal muscle injuries.

 Patients and Methods

This study was conducted over a period of three months. The total number of patients admitted to the ICU during that period was 114 patients. Forty two of these patients (37%) had head injuries. The criteria of inclusion were: rise of serum creatinine phosphokinase (CPK) more than three folds the normal, with the presence of myoglobin in the urine. Twenty of these head injury patients (47%) fulfilled the criteria of entry to the study. Of these patients 17 were males and 3 were females, with a mean age of 28.5 + 15.3 years. These patients were classified into two groups: Group I: 10 patients with apparently isolated head injury without apparent skeletal muscle injuries; Group II: 10 patients who had other trauma (simple fracture of ribs or limbs) in addition to the head injury. None of the patients had crush injury. Renal impairment was defined as serum creatinine level 0110 µmol/L (Normal 53-97 µmol/L). The patients of both groups were monitored by continuous electrocardio­gram, noninvasive arterial blood pressure (every 30 minutes), central venous pressure, temperature, urine output (hourly) and urine pH (every 6 hours). Laboratory investigations included daily: serum electrolytes, blood urea, creatinine, CPK, random blood sugar and urine myoglobin. Moreover, serum, calcium, phosphorus, magnesium and liver function tests, were monitored twice weekly. The management protocol consisted of forced diuresis by intravenous (i.v.) mannitol 0.25gm/kg, and furosemide 0.3mg/ kg every 8 hours, to allow negative fluid balance for 4-5 days to prevent brain edema in the study group as dictated by the neurologic condition of the patient. Furosemide was discontinued after that, and the dose of mannitol was reduced to 10-20 gm/ day to maintain diuresis. Alkalinization of the urine was achieved by i.v. bolus doses of sodium bicarbonate to keep urine pH > 6.5. In addition, dopamine i.v. infusion, in a dose of 1-3 /µg/ kg/min was given to induce intrarenal vaso­dilatation. Rehydration was started when the neurologic status of the patients allowed.

 Statistical Analysis

Data were analyzed for statistical signi­ficance using the "t"-test. All the values were given as means ± standard deviation (SD); p Group I: (Apparently isolated Head Injury)

All the patients in this group [Table 1] had high serum CPK (1773 + 2964 IU/L) on the admission day, and it took 1-5 days to reach its maximum value (3754 + 2904 IU/L). Three of these patients developed second elevation of serum CPK level (1328 + 4801 IU/L) after it had considerly decreased. Serum creatinine and blood urea were elevated in 3 patients (224 + 150 µmol/L, and 16 + 6.9 mmol/L respectively.

Group II: (Head Injury with Other Trauma)

All these patients [Table 1] had high CPK (3742 ± 4445 IU/L) at admission, which reached the peak value (6220 ± 5081 IU/L) on 1-9 days. Two of these patients developed second rise of CPK level (295 + 584 IU/L). Serum creatinine and blood urea were elevated in 6 patients (241 +100 µmol/L and 24.8 + 15 mmol/L respectively.

The myoglobinuria was detected positive transiently (within the first 5 days) in all the patients. There were no appreciable changes in serum potassium, calcium and phosphorus. The mean serum creatinine at admission was (112 + 26 µmol/L) for all the patients with renal impairment, which was signi­ficantly higher than the patients with normal renal function (P 330 mosm/L).

No significant difference of serum CPK level was found between patients with and without renal impairment. None of the patients in any group was oligoanuric and none needed dialysis. One patient in group II died because of his nurologial condition.


Rhabdomyolysis is not a well recognized complication in head injury patients in the absence of other skeletal muscle injuries and to our knowledge has not been reported so far. Fifty percent of the patients in this study had "apparently isolated head injury, and the rest of the patients had other injuries in addition. However, none of them had crush injuries. Rhabdomyolysis in this category of patients might be explained by muscle compression caused by blunt trauma of the accident. Other factors played an important role in aggravating rhabdo­myolysis. These included dehydration (due to the therapeutic negative fluid balance, dictated by the neurologic condition), plasma hyperosmolality, coma and acute immobili­zation. The significance of these factors predisposing to rhabdomyolysis, and preci­pitating ARF has been reported by several authors [2][3][4] . The diagnosis of rhabdomyolysis could be established by simple parameters such as, high CPK level with the presence of myoglobin in urine [5],[6],[7],[8] . Elevated CPK level is the most sensitive indicator of muscle damage, and may continue to increase several days after admission [1] . Because the plasma half life of the myoglobin is relatively short (1-3 hours), it disappears from the plasma within 6 hours [9] , which explains the transient positivity of the myoglobinuria; which was noticed in the patients of this study. The results of this study were consistent with other studies which found ARF developing in 16.5% to 45% in patients with rhabdomyolysis [10],[11],[12] . However, all those patients had crush injuries as well. From the previous studies the suggested plan to prevent rhabdomyolysis induced ARF was an early volume replace­ment therapy, followed by forced alkaline diuresis by the use of mannitol and sodium bicarbonate infusion [1],[3],[13],[14] . This plan had to be modified to keep the patients in a negative fluid balance for 4-5 days as a therapeutic measure for brain edema to prevent increased intracranial pressure. This might have precipitated the acute renal insufficiency, especially that hyperosmolality developed in this group more than the group of patients with no renal insufficiency. In our study the CPK level was not significantly high in patients with renal impairment, and could not be used to predict the incidence of renal failure as was reported by Gabow et al [15] .

We conclude that rhabdomyolysis is not uncommon in head injury patients, despite the absence of crush injury. Early diagnosis by daily check up of serum CPK and myo­globin in the urine may detect rhabdomyo­lysis in the patients with head injuries in the absence of apparent skeletal muscle injuries. This may have therapeutic implications to prevent acute renal failure in this group of patients.


We would like to thank the ICU Staff in King Fahd Hospital, Madina Al-Munawarah for their appreciated help in this work. Also we would like to thank Ms. Dolores S. Antonio for her excellent secretarial assistance.


1Richard H. Rhabdomyolysis: Critical Care Secrets; Hanley and Belfus Inc. Philadelphia. 1992;216-19.
2Kung AW, Pun KK, Lam KS, Yeung RT. Rhabdo myolysis associated with cranial diabetes insipidus. Postgrad Med J 1991;67(792):912-3.
3Ellinas PA, Rosner F. Rhabdomyolysis: report of eleven cases. J Natl Med Assoc 1992;84(7):617-24.
4Jitsuka T, Koyama A, Kobayashi M, et al. Acute renal failure due to rhabdomyolysis clinical investigation on 6 cases. Nippon Jinzo Gakkai Shi. 1992;34(3):317-24.
5Lawza G, Marinoni V, Travaglino F, Fontana S. The rhabdomyolytic syndrome: a not uncommon occurance. Minerva Med 1990;81(3 Suppl):41-4.
6Nakano Y, Simizu K, Ando M, Nakano S, Koyanagi R. Investigation of etiologies for acute renal failure due to rhabdomyolysis in 6 patients. Nippon Jinzo Gakkai Shi 1990;32(H): 1221-7.
7Arany S, Rado J. (Rhabdomyolysis following acute muscular exertion.) Orv Hetil 1992;133(31):1965-7.
8Marcus EL, Rudensky B, Sonnenblick M. Occult elevation of CK as a manifestation of rhabdomyolysis in the elderly. J Am Geriatr Soc 1992;40:454-6.
9Rainford DJ, Stevens PE. Acute renal failure from Tubular Injury. Oxford textbook of clinical nephrology. Oxford University Press. 1992;1000-7.
10Briner V, Colombia A, Brunner W, Truniger B. Acute rhabdomyolysis. Schweiz Med Wochensch 1986;116(7):198-208.
11Hishida A, Kato A, Yamada M. Myoglobinuria and acute renal failure. Rinsho Byori 1991;39(2):110-4.
12Wand MM. Factors Predictive of acute renal failure in rhabdomyolysis. Arch Intern Med 1988;148(7):1553-7.
13Ron D, Taitelman U, Michaelson M, Bar Joseph G, Bursztein S, Better OS. Prevention of acute renal failure in traumatic rhabdomyolysis. Arch Inter Med 1984;144(2):277-80.
14Better OS. The crush syndrome revisited. Nephron 1990;55(2):97-103.
15Gabow PA, Kaehny WD, Kelleher SP. The spectrum of rhabdomyolysis. Medicine Baltimore 1982;61:141-52.