Pediatr Nephrol (2006) 21:289–291DOI 10.1007/s00467-005-2045-z

B R I E F R E P O R T

Shruti Agrawal · Vinay Agrawal · Arvind Taneja

Hypokalemia causing rhabdomyolysis resultingin life-threatening hyperkalemia

Received: 3 March 2005 / Revised: 23 June 2005 / Accepted: 25 June 2005 / Published online: 27 October 2005� IPNA 2005

Abstract Hyperkalemia is commonly associated withrenal failure and is rare if renal function is normal. It israrely caused by rhabdomyolysis and can be life threat-ening if unrecognized. Rhabdomyolysis is caused bymany disorders, including hypokalemia. The availableliterature, both for human beings and experimental ani-mals, contains evidence of hypokalemia causing rhabdo-myolysis and rhabdomyolysis leading to hyperkalemia.Hypokalemia as a cause of rhabdomyolysis often goesunnoticed, because of the counteracting effect of rhab-domyolysis on serum potassium. There are no pediatricreports showing hypokalemia as a cause of rhabdomyol-ysis leading to life-threatening hyperkalemia. This caseemphasizes the vigilance required toward the occurrenceof rhabdomyolysis, which if not detected promptly mayprove fatal.

Keywords Hypokalemia · Rhabdomyolysis ·Hyperkalemia · Normal renal function

Introduction

Raised serum potassium levels in pediatric practice areusually associated with renal failure. The other rarecauses are pseudohyperkalemia, hyperkalemic renal tu-bular acidosis, and adrenocorticoid deficiency. Rhabdo-myolysis can result in acute renal failure with associatedhyperkalemia, hyperkalemia without renal failure, andmyoglobinuria. Rhabdomyolysis is rarely diagnosed. Theonly report in the pediatric literature of a 12-year-old girlwith rhabdomyolysis is in the setting of hypokalemia

associated with celiac disease. Hypokalemia is a rela-tively common event in pediatric practice. This case re-port emphasizes the high index of suspicion required fordiagnosing rhabdomyolysis in this clinical situation.

Case report

A 5-month-old male infant was referred to our medical center withpossible diagnosis of Bartter’s syndrome. The patient had beenadmitted, two days before referral, to a local hospital with gastro-enteritis and abdominal distension. Repeated investigations therehad shown hypokalemia (K+ 2.8/2.2/2.6/2.0 meq L�1), (Cl� 92/94/92/95 meq L�1), metabolic alkalosis (pH 7.5–7.58, HCO3

� 38–42 mmol L�1, and base excess +8 to +14 meq L�1). The patient hadbeen treated with IV fluids and potassium replacement. Resultsfrom other investigations were: urea 10.0 mg dL�1, creatinine0.3 mg dL�1, Hb 10.1 g dL�1, TLC 9700 mm�3, and platelets3.12�106 mm�3; abdomen ultrasound revealed normal-sized kid-neys and no abnormality.

The patient had been born at term with a birth weight of 2.8 kgand had an uneventful perinatal period. The patient thrived well onbreast feeds and formula milk feeds until approximately sevenweeks of age. The patient then started to suffer from repeatedepisodes of watery diarrhea and was diagnosed as milk protein/lactose intolerant and switched to soya-based formula. The patientwas thriving well on this formula until 15 days before this illnesswhen his parents switched to ordinary formula milk feeds. Devel-opment was normal for his age.

Examination revealed an active, 5.5-kg male (growth 25thcentile), length 61.5 cm (25th centile), head circumference 40 cm(25th centile) with stable hemodynamics, mild dehydration, ab-dominal distension, and reduced bowel sounds. Investigations re-vealed K+ 2.0 meq L�1 with pH 7.59, pCO2 52 mm Hg, pO2 73 mmHg, HCO3

� 48 meq L�1, BE +28 meq L�1, Na+ 129 meq L�1, Cl�

95 meq L�1, Hb 9.2 g dL�1, WBC 6400 mm�3, P40L58M2, platelets2.1�106 mm�3, urea 16.0 mg dL�1, creatinine 0.3 mg dL�1. Plain X-ray abdomen was suggestive of adynamic ileus. Simultaneous urineelectrolytes were K+ 3 meq L�1 and Na+ 40 meq L�1. A provisionaldiagnosis of pseudo-Bartter’s Syndrome was made and the patientwas started on intravenous hydration and potassium supplementa-tion (K+ 30 meq: deficit+maintenance, over 24 h). Sixteen hoursafter starting the treatment potassium was 3.8 meq L�1 with bloodpH 7.36, HCO3

� 32 meq L�1, and BE +2 meq L�1. Diarrhea andabdominal distension improved and the patient was started on soya-based formula.

On the 3rd day after admission the patient became irritable andwas sweating more than his usual. He was otherwise sucking well,had infrequent loose motions, passed urine freely, and was afebrile.

S. Agrawal ()) · V. Agrawal · A. TanejaDepartment of Paediatrics,Max Medcentre,New Delhi, Indiae-mail: shrutiagrawal2000@yahoo.comTel.: +447886500431

Present address:S. Agrawal, 37, Ranelagh Road, Swinton, Manchester,M274HG, UK

Repeat investigations revealed Hb 9.0 g dL�1, WBC 5700 mm�3,P43L55M2, platelets 2.56�106 mm�3, K+ 9.3 meq L�1, Na+

129 meq L�1, urea 18 mg dL�1, creatinine 0.4 mg dL�1, and normalblood gas (pH 7.34, pCO2 40 mm Hg, pO2 86 mm Hg, HCO3

�

23 meq L�1, BE 1.5 meq L�1), blood sugar 102 mg dL�1. Repeatsample ruled out any hemolysis. ECG showed tall-tented T waveswith broad QRS complex (0.12 s) and increased QTc (0.5) (Fig. 1).The patient was given one bolus of calcium gluconate (2 meq kg�1)intravenously over 15 min, which resulted in normalization ofECG. The patient was started on treatment for hyperkalemia withcontinuous intravenous calcium infusion (1 meq kg�1 h�1), oralresonium A (1 g kg�1/2 h), intravenous hydration (120 mLkg�1 day�1) and salbutamol nebulization (1 mg per dose every twohours).

Other investigations revealed urea 18 mg dL�1, creatinine0.3 mg dL�1, CPK 790 IU L�1 (normal reference range: 25–175 IU L�1), MB 71 IU L�1 (normal: <24 IU L�1), SGOT81 IU L�1, SGPT 71 IU L�1; calcium 8.2 meq L�1, bilirubin0.3 mg dL�1, pH 7.38, pCO2 36 mm Hg, pO2 123 mm Hg, HCO3

�

21 meq L�1, and BE 1.5 meq L�1. Provisional diagnosis of hypo-kalemia-induced rhabdomyolysis was made and the patient wasmanaged for hyperkalemia. Potassium levels gradually decreased tonormal by the end of 24-h treatment, maximum being 10.4 meq L�1

and 3.8 meq L�1 at the end of 24 h. The total potassium intake inthe 24 h preceding hyperkalemia was 4 meq kg�1 day�1. CPK de-creased to 490 IU L�1 after 24 h. Although the urine was notchecked for myoglobin, urine for hemoglobin was positive ondipstick and there were no RBCs in the urine, indicating likelypresence of myoglobin in the given clinical setting. A week later,the patient on follow-up was normal, abdominal distension haddecreased and serum potassium, CPK, and renal function tests werenormal.

Discussion

Rhabdomyolysis is defined as an acute increase in serumcreatinine phosphokinase to more than five times thenormal, with/without associated acute renal failure andhyperkalemia [1, 2]. Various causes of rhabdomyolysishave been identified and may be subdivided into traumatic,

exercise-induced, toxicological, environmental, meta-bolic, infectious, immunological, and inherited causes [3].Available literature shows hypokalemia as an establishedcause of rhabdomyolysis, both in human beings and inexperimental animals since the early nineteen-sixties [4,5, 6]. The occurrence of rhabdomyolysis in hypokalemiais found to be independent of the etiology and degree ofhypokalemia. It has been further suggested that sub-clinical rhabdomyolysis is a common complication ofhypokalemia, which is detected only as elevated muscleenzymes, and as a result, hypokalemia as a cause ofrhabdomyolysis goes unnoticed because of the counter-acting response of rhabdomyolysis on serum potassiumconcentration [7, 8, 9].

Clinical presentation of rhabdomyolysis varies be-tween patients. Muscle pain, discoloration of urine, etc.,are not always found on presentation. Laboratory studiesin an index case with high level of suspicion help toclinch the diagnosis. The usual laboratory features ofrhabdomyolysis are acute renal failure with or withouthyperkalemia, hyperkalemia without renal failure, andmyoglobinuria. Other uncommon features are hyper-phosphatemia, hypocalcemia, hyperuricemia, and DIC[3].

Hyperkalemia is an important feature of rhabdomyol-ysis [10]. Potassium is mainly an intracellular ion andeven a minor muscle injury may release enough potassi-um to cause severely elevated serum potassium levels [7,8].

The only literature reference to such a phenomenon inthe pediatric age group was to a 12-year-old girl withceliac disease leading to hypokalemia inducing rhabdo-myolysis [10]. The mechanism underlying this phenom-enon is the change in potential difference across musclecells, which blunts the vasodilatory response to exercise,

Fig. 1 ECG strip of the patient showing hyperkalemic changes

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and the decrease in muscle glycogen, which impairs en-ergy production [11]. These factors can cause musclenecrosis leading to rhabdomyolysis. The other mechanismexplained in the literature for hyperkalemia after hypo-kalemia in states of adrenergic stress response is the in-tracellular shift of potassium because of catecholamine-induced beta-2 stimulation of the sodium–potassiumpump. This leads to severe hypokalemia. When the surgedisappears, potassium levels may overshoot leading tohyperkalemia [12]. In our patient rhabdomyolysis was thecause of hyperkalemia. Evidence that rhabdomyolysiswas present were CPK levels extremely high and resultsfrom urine examination suggestive of myoglobinuria.There was no evidence of renal failure.

This case emphasizes the vigilance required to detectthe occurrence of rhabdomyolysis with hypokalemia,which if not detected promptly may prove fatal. It may bea condition which is rather under-diagnosed and can aptlybe called a “silent killer” [2].

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