CASE REPORT A 15-year-old Chinese boy with a known history of bronchial asthma since age 2 years was admitted with a short history of wheezing and dyspnoea. His asthma had always been well- controlled, requiring only occasional inhaled salbutamol. He was diagnosed as having acute myeloid leukaemia at the age of 13 years, for which he had received 18 months of chemo- therapy. He had been in complete remission without chemo- therapy for 2 months prior to this admission. Corticosteroid was not part of the chemotherapy regime. His family history was unremarkable and the past medical history was not suggestive of any metabolic or muscular diseases. There was no recent history of severe physical exer- tion, heat exposure, trauma, alcohol consumption or illicit drug use. He presented to hospital with a 2-day history of coryzal symptoms that had progressed to wheezing and mild dyspnoea. On admission, he was comfortable in room air and afebrile. Blood pressure was 128/84 mmHg; heart rate 110 b.p.m; respiratory rate 16 breaths/min; oxygen saturation 94% in air. Examination of the chest revealed good air entry bilaterally, a prolonged expiratory phase and widespread polyphonic expira- tory rhonchi. The rest of his systemic examination was unre- markable. His chest X-ray on admission showed hyperinflation, but neither consolidation nor pneumothorax. Initial laboratory investigations, including full blood count, serum electrolytes, renal and liver function tests, were normal except for a mild leucocytosis (white blood count 15.6 × 10 9 /L). He was initially treated with regular nebulized salbutamol at 2 hourly intervals. However, his condition failed to improve and 30 mg of oral prednisolone was given 2 h after admission, followed by intravenous (i.v.) hydrocortisone (100 mg q.i.d.) started at 7 h after admission because he was becoming more dyspnoeic, with recruitment of his accessory respiratory muscles, and was requiring an increasing amount of supple- mental oxygen. His condition continued to deteriorate and at 18 h post admission, he began to show signs of respiratory muscle fatigue. While he was receiving 5 L of supplemental oxygen given through a face mask, his arterial blood gas showed a pH of 7.29, P a CO 2 8.25 kPa and P a O 2 10.5 kPa. He was intubated after an i.v. dose of etomidate and suxametho- nium and transferred to the intensive care unit (ICU). Induced paralysis with i.v. vecuronium was needed to facilitate mechan- ical ventilation. He was started on i.v. aminophylline infusion (0.9 mg/kg per h) and continuous nebulized salbutamol shortly after the transfer. Despite an initial prolonged period of respiratory acidosis (pH < 6.7 and P a CO 2 > 30 kPa for 4 h), his respiratory con- dition slowly improved, but approximately 6 h after he was admitted to the ICU, he began to pass dark-brown urine. Urinalysis by dipstick was positive for blood, but there were no red cells seen on microscopy. Urine testing for myoglobin was strongly positive. His serum creatine phosphokinase (CPK) had been 361 IU/L on admission and increased by almost three- fold to 1074 IU/L in 24 h, subsequently reaching a peak of 22 879 IU/L (with 99.1% CPK-MM, skeletal muscle band) at 56 h post-admission. With the working diagnosis of rhabdomy- olysis, vecuronium was stopped and he was treated aggres- sively with i.v. hydration. Although there was biochemical evidence of renal impairment with a peak creatinine level of 303 μmol/L, he did not require renal dialysis as he was able to maintain a satisfactory urine output and his serum potassium level was not elevated. The rest of his progress in the ICU was unremarkable except for an episode of pyrexia on day four for which antibiotics (cefoperazone and sulbactam 4 g daily) were given for 7 days. Sputum, blood and urine cultures and virology screening were all negative. After the endotracheal tube was removed on day 13, he complained of widespread myalgia and there was evidence of generalized muscle weakness on physical examination. Electrophysiological studies showed diffuse myopathic changes. He also developed dysphonia as a result of bilateral vocal cord palsy. His subsequent course in hospital was uneventful. His renal function and CPK level returned to normal by day 10 and 15, respectively. With daily physiotherapy and occupational therapy, he regained most of his muscle power and voice by day 50. He was discharged home after 60 days of hospitalization. J. Paediatr. Child Health (2001) 37, 409–410 Rhabdomyolysis following status asthmaticus AM LI, CK LI, KW CHIK, MMK SHING and TF FOK Department of Paediatrics, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong SAR, China Abstract: A 15-year-old Chinese boy developed rhabdomyolysis with myoglobinuria and marked elevation of serum creatine phosphokinase following a prolonged and severe attack of asthma. He recovered after vigorous hydration and supportive treatment. Clinicians should be aware of this potentially fatal, albeit rare, complication of status asthmaticus. Key words: creatine phosphokinase; rhabdomyolysis; status asthmaticus. Correspondence: Dr AM Li, Department of Paediatrics, 6th Floor, Clinical Sciences Building, Prince of Wales Hospital, Shatin, Hong Kong SAR, China. Fax: (852) 2636 0020; email: Albertm68mcli@yahoo.com Accepted for publication 16 October 2000.