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Case report: Rhabdomyolysis following grand mal seizures presenting as a delayed and increasingly dense nephrogram
Clinical Radiology (1993) 47, 139-140
Case Report: Rhabdomyolysis Following Grand Mal Seizures Presenting as a Delayed and Increasingly Dense Nephrogram C. P. W A L K E R , M. J. DUDDY and G. SAGAR
Department of Radiology, Dudley Road Hospital, Birmingham Rhabdomyolysis as a result of major trauma is a well recognized cause of acute renal failure. Non-traumatic rhabdomyolysis causing transient renal impairment may occur following generalized convulsions. We present a case in which rhabdomyolysis following epilepsy was first indicated at urography by a delayed and increasingly dense persistent nephrogram. Walker, C.P., Duddy, M.J. & Sagar, G. (1993). Clinical Radiology 47, 139-140. Case Report: Rhabdomyolysis Following Grand Mal Seizures Presenting as a Delayed and Increasingly Dense Nephrogram.
CASE REPORT A 53-year-old man without relevant past medical history was admitted with left-sided abdominal pain. A provisional diagnosis of renal colic was made and an IVU requested. Initial investigations included normal urea and creatinine estimations (Fig. 1). On Day 2 the patient had a generalized tonic-clonic seizure, witnessed by medical staff, lasting approximately 2 min and stopping spontaneously. Two hours later a further grand mal seizure, lasting approximately 8 min, occurred. He was given i.v. diazepam and started on phenytoin. On Day 3 the patient had i.v. urography 0VU). Following injection of 50ml of Urografin 325 (sodium diatrizoate (0.4g/ml) and meglumine diatrizoate (0.18g/ml); Schering AG), immediate films and early tomography showed no nephrograms. The patient's blood pressure was normal. By 20 rain faint nephrograms were visible and these became increasingly dense over 8 h (Fig. 2) and persisted for at least 24 h. Ultrasound examination was performed during the early stages of the IVU to exclude bilateral obstruction and bilateral renal vein thrombosis (Fig. 3). Both kidneys were slightly enlarged and demonstrated hyperechoic cortices resulting in exaggerated corticomedullary differentiation (i.e. type 1 renal parenchymal disease). There was no evidence of obstruction and duplex Doppler examination of both renal arteries and veins was normal. Over the subsequent 72 h renal function showed marked deterioration with serum creatinine peaking at 448 #mol/1 before returning to normal (Fig. 1). His acute renal failure was managed by fluid restriction without recourse to haemodialysis. A clinical diagnosis of acute renal failure, secondary to rhabdomyolysis as a result of muscle spasm during his seizures, was confirmed by a serum creatine kinase (CK) of 5095 u (upper limit of normal 150 u).
14
N o underlying cause for his seizure was revealed by subsequent investigation which included cranial computed tomography (CT). An abdominal radiograph taken following contrast administration for the CT 10 days after admission demonstrated normal nephrograms and pyelograms bilaterally.
DISCUSSION
Acute renal failure due to rhabdomyolysis as a result of major trauma is well recognized. There have been several reports of instances of reversible acute renal failure due to
500
12
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10
0
300 ~
'200 '~ :~ 4 = 2
~e -<>- Urea - e - Creatinine
..~ I
1 Fitsl
I
2
I
3 I IVU
1
4
I
5
I
6
I
7
100 o I
8
I
9
0
10
Day
Fig. 1 - Transient renal impairment secondary to rhabdomyolysis. Correspondence to: Drs C. P. Walker and G. Sagar, Department of Radiology, Dudley Road Hospital, Dudley Road, Birmingham BI8 7QH, UK.
Fig. 2 - Bilateral dense persistent nephrograms at 8 h following contrast medium injection.
140
CLINICAL RADIOLOGY
Fig. 3 - Hyperechoicrenal cortex and a trace of peritoneal fluid.
non-traumatic rhabdomyolysis [1-3]. Nielsen e t al. [1] described a transient reduction in renal function in nine out of 13 consecutive patients admitted following generalized convulsions These all recovered in 5 days. The increasingly dense nephrogram has a wide differential diagnosis and rhabdomyolysis is an u n c o m m o n cause. This I V U pattern is usually associated with stasis, secondary either to ureteric obstruction or intratubular block, but more rarely occurs in acute tubular necrosis and ischaemia [4]. The commonest example is the increasingly dense nephrogram seen in m a n y patients with acute ureteric obstruction due to calculus or blood clot, which m a y increase in density for 6-8 h. The renal failure in rhabdomyolysis is generally considered to be due to acute
tubular necrosis. H u n n a m and Sherwood [5] described a case ofrhabdomyolysis, demonstrating a striated nephrogram, which is seen in tubular obstruction, and suggested that tubular obstruction by myoglobin casts plays a part. The ultrasound appearance in our case is non-specific. Bisset and K h a n [6] list 20 causes o f type 1 renal parenchymal disease on ultrasound of which myoglobinuric renal failure is ranked number 15. Epilepsy is a c o m m o n condition, affecting 1% of the population, and it has been shown that a degree o f rhabdomyolysis commonly occurs in generalized seizures [1]. As in our case, the history o f seizures may not be given when urography is requested but should be considered in the differential diagnosis of bilateral delayed increasingly dense nephrograms. It is possible that under some circumstances i.v. contrast m a y exacerbate acute renal failure. CT scanning with i.v. contrast is frequently used in the investigation o f epilepsy. It m a y be prudent, therefore, not to perform the examination within 5 days of a generalized seizure, unless there is a clinical urgency, because unrecognized, transient renal impairment may be aggravated.
REFERENCES
1 Nielsen HV, Garsdal, P, Hansen PB, Rasmussen KT, Jensen H. Impairment of renal function after generalised seizures. Lancet 1987;i:1043. 2 Murray AN, Riordan G, Swanepoel CR, Eastman RW. Myoglobinuric renal failure after generalized tonic-clonic seizures: a case report. South African Medical Journal 1988;74:236-237. 3 0 s I, Lyngdal PT. General convulsions and rhabdomyolysis: case reports. Acta Neurologica Scandinavica 1989;79:246-248. 4 Fry IK, Cattell WR. Radiological investigation of renal disease. In: Black DAK & Jones N, eds. Renal disease. Blackwell, 1979:257-261. 5 Hunnam GR, Sherwood T. Striated nephrogram in rhabdomyolysis. British Journal o f Radiology 1985;58:682-683. 6 BissetRAL, Khan AN. Differentialdiagnosis in abdominal ultrasound. London: Bailliere Tindall, 1990:168.
Case Report: Rhabdomyolysis Following Grand Mal Seizures Presenting as a Delayed and Increasingly Dense Nephrogram C. P. W A L K E R , M. J. DUDDY and G. SAGAR
Department of Radiology, Dudley Road Hospital, Birmingham Rhabdomyolysis as a result of major trauma is a well recognized cause of acute renal failure. Non-traumatic rhabdomyolysis causing transient renal impairment may occur following generalized convulsions. We present a case in which rhabdomyolysis following epilepsy was first indicated at urography by a delayed and increasingly dense persistent nephrogram. Walker, C.P., Duddy, M.J. & Sagar, G. (1993). Clinical Radiology 47, 139-140. Case Report: Rhabdomyolysis Following Grand Mal Seizures Presenting as a Delayed and Increasingly Dense Nephrogram.
CASE REPORT A 53-year-old man without relevant past medical history was admitted with left-sided abdominal pain. A provisional diagnosis of renal colic was made and an IVU requested. Initial investigations included normal urea and creatinine estimations (Fig. 1). On Day 2 the patient had a generalized tonic-clonic seizure, witnessed by medical staff, lasting approximately 2 min and stopping spontaneously. Two hours later a further grand mal seizure, lasting approximately 8 min, occurred. He was given i.v. diazepam and started on phenytoin. On Day 3 the patient had i.v. urography 0VU). Following injection of 50ml of Urografin 325 (sodium diatrizoate (0.4g/ml) and meglumine diatrizoate (0.18g/ml); Schering AG), immediate films and early tomography showed no nephrograms. The patient's blood pressure was normal. By 20 rain faint nephrograms were visible and these became increasingly dense over 8 h (Fig. 2) and persisted for at least 24 h. Ultrasound examination was performed during the early stages of the IVU to exclude bilateral obstruction and bilateral renal vein thrombosis (Fig. 3). Both kidneys were slightly enlarged and demonstrated hyperechoic cortices resulting in exaggerated corticomedullary differentiation (i.e. type 1 renal parenchymal disease). There was no evidence of obstruction and duplex Doppler examination of both renal arteries and veins was normal. Over the subsequent 72 h renal function showed marked deterioration with serum creatinine peaking at 448 #mol/1 before returning to normal (Fig. 1). His acute renal failure was managed by fluid restriction without recourse to haemodialysis. A clinical diagnosis of acute renal failure, secondary to rhabdomyolysis as a result of muscle spasm during his seizures, was confirmed by a serum creatine kinase (CK) of 5095 u (upper limit of normal 150 u).
14
N o underlying cause for his seizure was revealed by subsequent investigation which included cranial computed tomography (CT). An abdominal radiograph taken following contrast administration for the CT 10 days after admission demonstrated normal nephrograms and pyelograms bilaterally.
DISCUSSION
Acute renal failure due to rhabdomyolysis as a result of major trauma is well recognized. There have been several reports of instances of reversible acute renal failure due to
500
12
4OO
10
0
300 ~
'200 '~ :~ 4 = 2
~e -<>- Urea - e - Creatinine
..~ I
1 Fitsl
I
2
I
3 I IVU
1
4
I
5
I
6
I
7
100 o I
8
I
9
0
10
Day
Fig. 1 - Transient renal impairment secondary to rhabdomyolysis. Correspondence to: Drs C. P. Walker and G. Sagar, Department of Radiology, Dudley Road Hospital, Dudley Road, Birmingham BI8 7QH, UK.
Fig. 2 - Bilateral dense persistent nephrograms at 8 h following contrast medium injection.
140
CLINICAL RADIOLOGY
Fig. 3 - Hyperechoicrenal cortex and a trace of peritoneal fluid.
non-traumatic rhabdomyolysis [1-3]. Nielsen e t al. [1] described a transient reduction in renal function in nine out of 13 consecutive patients admitted following generalized convulsions These all recovered in 5 days. The increasingly dense nephrogram has a wide differential diagnosis and rhabdomyolysis is an u n c o m m o n cause. This I V U pattern is usually associated with stasis, secondary either to ureteric obstruction or intratubular block, but more rarely occurs in acute tubular necrosis and ischaemia [4]. The commonest example is the increasingly dense nephrogram seen in m a n y patients with acute ureteric obstruction due to calculus or blood clot, which m a y increase in density for 6-8 h. The renal failure in rhabdomyolysis is generally considered to be due to acute
tubular necrosis. H u n n a m and Sherwood [5] described a case ofrhabdomyolysis, demonstrating a striated nephrogram, which is seen in tubular obstruction, and suggested that tubular obstruction by myoglobin casts plays a part. The ultrasound appearance in our case is non-specific. Bisset and K h a n [6] list 20 causes o f type 1 renal parenchymal disease on ultrasound of which myoglobinuric renal failure is ranked number 15. Epilepsy is a c o m m o n condition, affecting 1% of the population, and it has been shown that a degree o f rhabdomyolysis commonly occurs in generalized seizures [1]. As in our case, the history o f seizures may not be given when urography is requested but should be considered in the differential diagnosis of bilateral delayed increasingly dense nephrograms. It is possible that under some circumstances i.v. contrast m a y exacerbate acute renal failure. CT scanning with i.v. contrast is frequently used in the investigation o f epilepsy. It m a y be prudent, therefore, not to perform the examination within 5 days of a generalized seizure, unless there is a clinical urgency, because unrecognized, transient renal impairment may be aggravated.
REFERENCES
1 Nielsen HV, Garsdal, P, Hansen PB, Rasmussen KT, Jensen H. Impairment of renal function after generalised seizures. Lancet 1987;i:1043. 2 Murray AN, Riordan G, Swanepoel CR, Eastman RW. Myoglobinuric renal failure after generalized tonic-clonic seizures: a case report. South African Medical Journal 1988;74:236-237. 3 0 s I, Lyngdal PT. General convulsions and rhabdomyolysis: case reports. Acta Neurologica Scandinavica 1989;79:246-248. 4 Fry IK, Cattell WR. Radiological investigation of renal disease. In: Black DAK & Jones N, eds. Renal disease. Blackwell, 1979:257-261. 5 Hunnam GR, Sherwood T. Striated nephrogram in rhabdomyolysis. British Journal o f Radiology 1985;58:682-683. 6 BissetRAL, Khan AN. Differentialdiagnosis in abdominal ultrasound. London: Bailliere Tindall, 1990:168.