Article

Rhabdomyolysis after successful resuscitation of a patient with near-fatal asthma

Case Report

Rhabdomyolysis after successful resuscitation of a patient with near-fatal asthma

Acute rhabdomyolysis is an infrequent complication after severe acute asthma. We described a patient who developed rhabdomyolysis and acute renal failure after successful resuscitation from near-fatal asthma. We described the pathophysiologic relationship between severe asthma and rhabdomyolysis and discussed other potential causes of rhabdomyolysis in this specific situation. The case report highlights the importance of considering acute rhabdomyol- ysis in patients resuscitated from near-fatal asthma, which is a potentially remediable cause of renal failure if timely appropriate management is given.

Acute rhabdomyolysis is an infrequent cause of post- resuscitation renal failure unless massive cardioversion has been given. In this report, we describe a patient who developed rhabdomyolysis after resuscitation without car- dioversion. The patient experienced out-of-hospital cardiac arrest due to near-fatal asthma. There were only few case reports that described rhabdomyolysis after severe acute asthma attacks and none associated with resuscitation [1-6]. We discuss the association between severe asthma and rhabdomyolysis and other potential causes of rhabdomyol- ysis in this specific situation.

A 41-year-old woman presented to the emergency department (ED) with out-of-hospital cardiac arrest. She had a history of asthma without regular medical control. Her sister reported that 2 hours before ED admission, the patient complained of progressive dyspnea. One hour later, she was found unconscious, with apnea and cyanosis. The emergen- cy medical system was called. When the advanced life support team arrived, no vital signs could be measured, and automated external defibrillator showed asystolic rhythm. Immediate cardiopulmonary resuscitation with tracheal intubation was performed in the ambulance. After 5

minutes’ resuscitation and a total of 2 mg IV epinephrine, spontaneous circulation was restored. On arrival at the ED, her body temperature was 35.38C, pulse rate 134/min, blood pressure 64/37 mm Hg, pulse oxygen saturation 100%, and Glasgow Coma Scale score E1M1Vt. High airway pressure was noted on manual ventilation. Physical examination results disclosed diffuse wheezing over bilateral chest, and the remainder was not remarkable. Electrocardiogram showed sinus tachycardia without ST-T change. Chest roentgenogram revealed emphysematous change without pneumonic patch. The laboratory findings on admission were as follows: arterial blood gas, 100% Fio2; pH, 6.78; Paco2, 98.4 mm Hg; Pao2, 228.9 mm Hg; white blood cell count, 19680/lL; potassium, 5.1 mEq/L; creatinine, 114.9 lmol/L (1.3 mg/dL); blood urea nitrogen, 3.3 mmol/L (9.3 mg/dL); Creatinine kinase, 184 U/L; troponin I, 0.024 ng/mL; and lactate, higher than 12 mmol/L. The initial treatment included inhaled b-agonists, systemic cortico- steroids (prednisolone 40 mg), intravenous dopamine (20 lg d kg–1 d min–1), and oxygen (8 L/min). Despite initial treatment, brochoconstriction with high airway pressure persisted. Intravenous aminophylline (0.7 mg d kg–1 d h–1) was started. The wheezing symptoms then improved gradually. On the second day, deteriorated renal function was noted. Simultaneously, serum creatinine kinase level was noted to rise and peak at 114 150 U/L on the fifth day (Table 1). Acute rhabdomyolysis with renal failure was suggested. Considering the possibility of steroid myopathy or aminophylline toxicity, the dosage of these 2 drugs was reviewed. The cumulative steroid dosage was 13.6 mg/kg, and the peak serum level of aminophylline was 9.23 lg/mL (reference range, 10-20 lg/mL). Renal failure deteriorated to an anuric state on the eighth day, and Emergent hemodialysis was instituted. On the 13th day after admission, an episode of refractive ventricular fibrillation occurred, and the patient died.

Table 1 Laboratory data of the patient

Hospital days

1

2

3

4

5

6

7

CK (IU/L)

184

28796

78800

77390

114150

80601

32000

Creatinine (lmol/L)

114.9

114.9

300.6

592.3

707.2

839.8

963.6

Potassium (mmol/L)

5.1

4.8

3.6

2.9

3.3

3.6

4.7

Urine output (mL)

210

110

50

60

80

40

50

CK indicates creatinine kinase.

0735-6757/$ – see front matter D 2007

736.e4 Case Report

Rhabdomyolysis is a rare complication of acute severe asthma. To date, only 6 patients have been described to exhibit such an association. The first case report was approximately 3 decades ago, when Chugh et al [1] reported an episode of acute renal failure in a 25-year-old man after Status asthmaticus. In the following years, 5 other patients with ages ranging from 15 to 71 years have been described [2-6]. In 4 of the described cases, the authors ascribed the cause of rhabdomyolysis to vigorous exertion of the respiratory muscles, generalized muscle hypoxia, and metabolic and respiratory acidosis [1-4]. In 2 other cases, on the other hand, the authors thought the cause of rhabdomyolysis might be related to steroid or myorelaxant myopathy [5,6]. In our case, the patient did not receive a Muscle relaxant, and the Cumulative dose of steroid (13.6 mg/kg) was far lower than those reported to cause steroid myopathy. Currently, no definite dose has been validated to develop myopathy. Although some case reports describe the development of muscle weakness after a single low dose of corticosteroid, most studies suggest that acute-type steroid myopathy may occur after high-dose intravenous cortico- steroids for approximately 1 week [5,6].

In addition to the mentioned causes, others that may induce acute rhabdomyolysis in the context of asthmatic exacerbations include severe hypokalemia after aggressive b-agonist inhalation, myositis induced by Mycoplasma and Legionella infection, and Theophylline intoxication [7]. In our patient, repeated measurement of potassium level throughout the hospitalization course showed that it was within normal limits. Serologic tests for Mycoplasma and Legionella infection were also negative. As for aminophyl- line toxicity, the peak serum level of aminophylline in the patient was within the normal limits. According to previous case reports [8-10], most theophylline-related rhabdomyol- ysis occurred on Large doses of theophylline; therefore, aminophylline-related rhabdomyolysis was not favored in our patient.

Differently from those in previous case reports, our patient underwent cardiopulmonary resuscitation before acute rhabdomyolysis developed. Hence, more possible causes of rhabdomyolysis should be clarified. Severe acute renal failure requiring renal replacement therapy is a rather infrequent observation in patients after CPR [11]. Reports of postresuscitational rhabdomyolysis were even rarer. There were only 2 case reports describing postresuscitational rhabdomyolysis in the literature. One patient developed postresuscitational rhabdomyolysis due to inadvertent intra- arterial administration of excessive amounts of epinephrine (40 mg), and the other’s postresuscitational rhabdomyolysis was attributed to massive cardioversion and prolonged CPR [11,12]. In our patient, only 4 mg epinephrine was given through either intravenous or inhalational route, and no cardioversion was attempted. Therefore, we thought the most likely etiology of rhabdomyolysis in our patient was vigorous and repeated contractions of respiratory muscles with muscular hypoxia.

In summary, our case report serves to highlight the importance of considering acute rhabdomyolysis as a cause of acute renal failure in patients resuscitated from near-fatal asthma. Acute rhabdomyolysis is potentially remediable if proper management is instituted early. We suggest routine screening of serum level of creatinine kinase in patients who undergo resuscitation because of near-fatal asthma, which may help with the early detection of such complications.

Yi-Jung Chen MD Shih-Heng Chang MD Ang Yuan MD, PhD Chien-Hua Huang MD

Department of Emergency Medicine National Taiwan University Hospital

Taipei 100, Taiwan

Chien-Chang Lee MD, MSc Department of Emergency Medicine National Taiwan University Hospital

Taipei 100, Taiwan Graduate Institute of Epidemiology College of Public Health

National Taiwan University Hospital

Taipei 100, Taiwan E-mail address: [email protected]

doi:10.1016/j.ajem.2007.01.004

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