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Year : 1999  |  Volume : 47  |  Issue : 1  |  Page : 51--4

Non-traumatic acute rhabdomyolysis.

AB Taly, KP Nair, GR Arunodaya, S Das, R Christopher, C Mohan, HS Swamy 
 Departments of Neurology, Neuropathology and Neurochemistry, National Institute of Mental Health and Neuro Science (NIMHANS), Bangalore, Karnataka, 560029 India., India

Correspondence Address:
A B Taly
Departments of Neurology, Neuropathology and Neurochemistry, National Institute of Mental Health and Neuro Science (NIMHANS), Bangalore, Karnataka, 560029 India.


A boy developed sudden severe generalized muscle stiffness, bulbar weakness and passed dark coloured urine. Laboratory tests revealed marked elevation of creatinine kinase(CK) levels and myoglobinuria. Histopathology of quadriceps muscle showed features of acute rhabdomyolysis. Patient made complete clinical recovery over a period of three weeks and CK returned to normal level. The possible aetiologies of non-traumatic rhabdomyolysis are discussed and the relevant literature reviewed.

How to cite this article:
Taly A B, Nair K P, Arunodaya G R, Das S, Christopher R, Mohan C, Swamy H S. Non-traumatic acute rhabdomyolysis. Neurol India 1999;47:51-4

How to cite this URL:
Taly A B, Nair K P, Arunodaya G R, Das S, Christopher R, Mohan C, Swamy H S. Non-traumatic acute rhabdomyolysis. Neurol India [serial online] 1999 [cited 2023 Mar 31 ];47:51-4
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  ::   IntroductionTop

Rhabdomyolysis denotes acute necrosis of striated muscles and often follows crush injury. Lately, it has been recognized that acute rhabdomyolysis can occur without trauma.[1] Non-traumatic acute rhabdomyolysis has been associated with congenital muscle enzyme deficiencies, exposure to drugs and toxins, malignant hyperthermia, physical exertion, status epilepticus, polymyositis and muscular dystrophies.[2] While myalgia, myoglobinuria and elevated levels of serum creatinine kinase (CK) are the cardinal features, acute renal failure, compartment syndrome and cardiac arrest are the major complications of this entity.[3] The clinical spectrum may vary from fulminant rhabdomyolysis with coma to exercise induced myalgia and weakness.[4] In this communication, a patient with acute non-traumatic rhabdomyolysis is reported and the relevant literature is briefly reviewed.

  ::   Case summaryTop

A 13 year old boy woke up at night due to breathlessness, abdominal pain and swelling of face and neck. On his way to hospital he had one brief generalized tonic clonic seizure and vomiting. He was treated with adrenaline, chlorphenaramine maleate, crystalline penicillin and gentamicin at a nearby hospital for presumed anaphylactic reaction. Within two hours from the onset of symptoms he had difficulty in opening the mouth, dysphagia, dysphonia, nasal twang and stiffness of both lower limbs. Later, he passed very dark coloured urine. There was no history of fever, injury, loose motions, oliguria or overt snake or insect bite. He had no prior history of systemic disease, fever, recurrent abdominal pain, neuro-muscular dysfunction or allergic disorder. However, he had a history of solitary unprovoked generalized tonic clonic seizure three weeks prior to the present episode for which he did not receive any treatment. Family history for any systemic or neurologic disease was negative.

A day later, he was transferred to this Institute. Examination revealed mild oedema of face and anaemia. There was no skin rash, insect bite mark or oedema of limbs. His vital parameters and systemic examination were otherwise normal. He was conscious, alert and had no cognitive deficits. There was no ptosis, ophthalmoplegia or facial paresis. He had marked stiffness of jaw muscles and could open the mouth only with great difficulty. His voice was of low volume and had nasal twang. The palatal and gag reflexes were sluggish. Motor functions in upper limbs were normal but lower limbs were very stiff and as such the power could not be assessed in a formal manner. He had difficulty in sitting or getting up due to his inability to flex the stiff muscles, but when helped to stand, he could walk unaided. His sensations were normal but muscles in lower limbs were tender. Muscle stretch reflexes were brisk but plantar response was flexor. There were no features of autonomic dysfunction.

Normal laboratory test included blood triglyceride, serum sodium, potassium, calcium, phosphorus, alkaline phosphatase and bilirubin, bleeding and clotting time, X-ray chest, electrocardiogram, electroencephalogram and CT scan of head. Results of the other tests were : Haemoglobin-11.4gm% (n=>14.0 gm%), total leukocyte count-14,000/cm, neutrophils-94%, lymphocytes-6%. Peripheral smear revealed normochromic normocytic red blood cells with no features of haemolysis. Serum proteins - 5.6gm% (n = > 7.0 gm%) and serum albumin -3.6 gm% (n = > 3.5 gm%). Serum CK, SGOT, SGPT and LDH were markedly elevated [Table I]. Urine when passed was burgundy red and did not change in colour on further standing. It was acidic, negative for sugar, urobilinogen, porphobilinogen and positive for protein (++++) and benzidine test. Microscopic examination showed a few epithelial cells but no RBCs or casts.

Nerve conduction studies of common peroneal, median and sural nerves were normal. Electromyography of biceps and quadriceps revealed normal insertional activity. There was no spontaneous activity. Motor unit potentials were of small amplitude and normal duration. Recruitment was complete even with submaximal effort.

Muscle biopsy from left quadriceps done on 14th day of iless showed widespread muscle necrosis in each of the fascicles [Figure1a] [Figure1b] [Figure1c] [Figure1d]. A large number of fibers showed coagulative necrosis with or without myophagocytosis. The inflammatory cells comprised histiocytes, plasma cells and lymphocytes. In several foci, interstitial and perivascular infiltration by chronic inflammatory cells was seen. Regenerating fibers were also observed in most of the fascicles. PTAH preparation revealed loss of cross striations in the necrotic fibers. Endomyseal collagen was not affected. On enzyme histochemistry, was observed in both type I and type II fibers, with significant type II fibre atrophy. Necrotic fibers had focal condensation of reaction products in oxidative enzyme preparations. The histological changes were suggestive of acute rhabdomyolysis. Myophagocytosis, interstitial inflammatory infiltration and presence of regenerating fibers suggested muscle fibers.

Patient was given corticosteroids (initially hydrocortisone 300 mg/day for three days and later dexamethasone 12 mg/day for seven days), intravenous fluids, ibuprofen and nasogastric feeding. He showed gradual improvement, initially in the stiffness of lower limbs and later in swallowing and voice. He was ambulant by fifth day and had normal bulbar function by eighth day. Muscle stiffness and teerness improved by 10th day. Throughout the period of hospital stay, the daily urinary out put ranged from 1,100 ml to 1,500 ml. The colour became amber yellow by eighth day. Biochemical tests also returned to normal by 15th day [Table I]. To exclude the possibi of drug induced rhabdomyolysis the patient was given injections of chlorpheneramine maleate, crystalline penicillin and gentamicin. However, there was no change in clinical or laboratory parameters. He was asymptomatic when discharged, three weeks after the onset of symptoms. Three months after discharge, the serum enzyme levels were : CK - 101, SGOT-30 U/L, SGPT-16 U/L and LDH-840 IU/L. Repeat electrophysiological studies revealed normal motor unit potentials and recruitment pattern. He was asymptomatic till last follow-up at four years.

  ::   DiscussionTop

Criteria for the diagnosis of rhabdomyolysis in an alert patient are myalgia or weakness, myoglobinuria and elevated serum CK and other sarcoplasmic enzyme levels which may rise by more than 100 folds during an acute episode. There may be no signs of muscle involvement if the patient is comatosed. However, in these subjects the sarcoplasmic enzyme levels should be 100 times the normal with evidence of acute renal failure.[2]

Our patient manifested with acute onset of myalgia, muscle stiffness, bulbar weakness and pigmenturia. Pigmenturia may occur due to myoglobin, haemoglobin or porphyria. The combination of a positive benzidine test, golden brown pigmented casts and absence of erythrocytes in urine, colourless serum and normal heptoglobulin level confirm myoglobinuria. However, immunologic technique, using specific antibodies against myoglobin is perhaps the most sensitive test for detecting myoglobin in urine and serum.[4] In the present case the urine was negative for porphobilinogen. The cellulose acetate electrophoresis of urine showed an abnormal protein of the molecular weight of 16,000-18,000, which is similar to myoglobulin. The muscle biopsy showed evidence of severe myonecrosis. The clinical and laboratory tests thus confirmed the diagnosis of acute rhabdomyolysis.

The aetiology of rhabdomyolysis in this boy is not clear. Acute polymyositis including viral polymyositis and tropical pyomyositis can cause a similar picture.[1],[2] Presence of palatal palsy suggested a possibility of acute polymyositis. However, sudden onset of clinical symptoms with hypotension, marked stiffness and rapid recovery within 10 days are against polymyositis. There was no evidence of focal muscle abscess to suspect tropical myositis. Status epilepticus can result in rhabdomyolysis[5] but this child had only a brief generalized tonic-clonic seizure and that too after the onset of symptoms. Thus, it is rather unlikely that the rhabdomyolysis was secondary to seizure. Severe muscular exertion can cause rhabdomyolysis. Chugh et al[6] reported a patient with acute rhabdomyolysis following vigorous contraction of respiratory muscles due to status asthmaticus. However, in the present case there was no history of undue physical exertion. Hereditary causes of rhabdomyolysis include disorders of glycogen and lipid metabolism, myoadenylate deaminase deficiency, malignant hyperthermia and `idiopathic' disorders.[4] Tonin et al[2] observed that half of the patients with idiopathic rhabdomyolysis had specific enzyme defects and usually manifest with exercise induced pigmenturia and myalgia. Our patient did not give any past history of exercise related symptoms or pigmenturia. However, detailed biochemical evaluation for all the muscle enzymes was not done. A number of drugs can cause acute myonecrosis.[2] This boy received adrenaline, gentamicin, penicillin and chlorphenaramine maleate. None of these drugs are known to cause rhabdomyolysis. Moreover, challenge with these drugs after recovery did not produce the symptoms. Acute rhabdomyolysis can occur due to envenomation following snake bite and insect stings.[7] Phospholipase present in the venom of insects of hymenoptera order can cause muscle membrane destruction.[7] This patient did not have history of snake bite or insect sting prior to the onset of symptoms and no bite marks or localized urticarial rashes were visible. However, in view of acute onset of bronchospasm, facial oedema and hypotension possibility of anaphylactic reaction to undetected insect bite was considered in our patient.

Rhabdomyolysis is not rare. Severe muscle necrosis can cause life threatening cardiac and renal complications. The diagnosis should be confirmed by measuring serum creatinine kinase activity and detection of myoglobin in urine. The treatment consists of adequate hydration to prevent renal complications and withdrawal of toxic drugs, if any. These patients may present to neurologists with clinical features ranging from myalgia to coma. Prompt diagnosis and treatment may help in preventing lethal complications. Further search for provocative factors and underlying metabolic defects may be rewarding.


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