Rhabdomyolysis and acute renal failure in a child with para-influenza type 1 infection
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- Vrsalovic, R., Tesovic, G. & Mise, B. Pediatr Nephrol (2007) 22: 1369. doi:10.1007/s00467-007-0486-2
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We present a rare case of para-influenza type 1 virus-induced rhabdomyolysis, complicated by acute renal failure (ARF). The child underwent continuous venovenous haemofiltration and has shown full clinical and biochemical recovery. ARF due to rhabdomyolysis in para-influenza type 1 infection in a child has, to the best of our knowledge, not been previously reported.
KeywordsRhabdomyolysisPara-influenza type 1 virusAcute renal failureChildren
Rhabdomyolysis is a potentially life-threatening syndrome resulting from the breakdown of skeletal muscle fibres with leakage of muscle contents into the circulation . The most common causes of rhabdomyolysis in children are viral myositis, trauma, and connective tissue disease . Acute renal failure (ARF) due to rhabdomyolysis in para-influenza type 1 infection in a child has, to the best of our knowledge, not been previously reported. We report a case of ARF following rhabdomyolysis due to evident para-influenza type 1 virus infection in a 5-year-old boy.
Our patient was 5-year-old boy with psychomotor retardation and spastic quadriplegia who, 2 days before admission, developed rhinorrhoea, cough and vomiting. One day before admission he developed chills and a fever, with a temperature of up to 40.5°C. There was no family history of renal or musculoskeletal disease, nor had he experienced any trauma, drug abuse or a recent increase in his exercise level. His past medical history was remarkable for cerebral palsy due to perinatal asphyxia.
At the time of admission the patient was semi-comatose, dehydrated and dyspnoeic. He was febrile, with a temperature of 40.0°C, with a heart rate of 180 beats/minute, a respiratory rate of 40 breaths/minute and a blood pressure of 135/80 mmHg. Crackles were audible throughout both lung fields, but heart sounds were normal. Meningeal signs were not present.
The initial laboratory studies revealed: erythrocyte sedimentation rate 33 mm in the first hour; C-reactive protein 73 mg/l; white blood cell count 17.9 × 109/l with 83% neutrophils, 11% lymphocytes and 6% monocytes; haemoglobin 75 g/l; haematocrit 0.24; platelets 511 × 109/l; blood urea nitrogen (BUN) 6.1 mmol/l; creatinine 39 μmol/l and normal levels of electrolytes. D-dimer was 0.2 mg/l with prothrombin time of 16.4 s and partial thromboplastin time of 28.8 s. Arterial blood pH at admission was 7.342, base excess −6.9 mmol/l, PaCO2 34.7 mmHg, PaO2 57.3 mmHg, O2 saturation 86.9%. Serum bilirubin, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase, γ-glutamyl transpeptidase concentrations were normal. Urine analysis revealed protein 2+, ketone 1+; microscopic examination of the sediment revealed 5 white blood cells per high-power field but no red blood cells.
The patient’s cerebrospinal fluid (CSF) was clear, with white blood cells 11/3 mm3, protein 164 g/l and glucose 3.4 mmol/l. No organisms were isolated from blood and CSF cultures. Chest radiography revealed bilateral diffuse infiltration.
A nasopharyngeal swab specimen obtained on the first hospital day indicated sensitive Streptococcus pneumoniae. Para-influenza type 1 virus was identified from a nasopharyngeal aspirate sample taken on the first hospital day by direct immunofluorescence antibody assay (DFA).
During the first 12 hours of hospital stay the patient’s condition was stable. He was febrile, with a temperature of approximately 40°C, and tachydyspnoeic but well oxygenated following oxygen therapy.
The next day the patient’s condition deteriorated; he became extremely tachydyspnoeic (80–90 breaths/minute), with a heart rate of 200–216 beats/minute. Despite the oxygen therapy, hypoxia developed, and mechanical ventilation was initiated because of respiratory failure. On the third hospital day arterial hypotension unresponsive to crystalloid infusions occurred, and a continuous dopamine infusion (10 μg/kg per minute) was started. During the next day, there was a progressive decline in renal function, with a peak creatinine level of 214 μmol/l, blood urea nitrogen of 33 mmol/l, and hyperkalaemia of 6.8 mmol/l. Relevant laboratory values included a creatine phosphokinase (CPK) level of 22,242 IU/l, aspartate aminotransferase 1,040 IU/l, alanine aminotransferase 664 IU/l, and lactate dehydrogenase 2,995 IU/l, consistent with skeletal muscle necrosis. Metabolic acidosis was registered for the first time, with an arterial blood pH of 7.169, base excess −16.6 mmol/l and bicarbonates concentration of 12.2 mmol/l. Urinary pH was 5.5.
Despite adequate hydration with normal saline and urine alkalization with sodium bicarbonate the patient developed oliguric acute renal failure requiring temporary continuous venovenous haemodiafiltration (CVVHD) 3 days after admission. He remained oliguric until day 17 of hospitalization. Haemodialysis was stopped on day 18. His condition and renal function continuously improved, and he required no further dialysis. CPK levels decreased until normalization on day 20. The patient’s respiratory status gradually improved, and 31 days after admission he was successfully weaned and extubated. The hospitalization course was further complicated by acquisition of post-transfusion cytomegalovirus (CMV) infection confirmed by CMV DNA polymerase chain reaction (PCR). The patient was discharged on day 50, with a serum creatinine concentration of 38 μmol/l and BUN of 4.0 mmol/l.
A wide variety of infections that could have caused the illness similar to that in our patient were considered at the outset and sought diagnostically, including bacterial sepsis, mycoplasma infection, legionellosis, influenza A or B, respiratory syncytial virus, adenovirus and para-influenza type 1, 2 or 3 virus, but an exhaustive workup excluded all with exception of para-influenza type 1 virus.
Three months after his discharge from hospital, the child was re-admitted because of bilateral bronchopneumonia (non-typable Haemophilus influenzae was isolated from the nasopharyngeal aspirate). Although he was hyperpyretic for 3 days, his CPK level, as well as his urine output, remained within normal ranges.
There has been no recurrence of rhabdomyolysis during the 11 months follow up.
The term rhabdomyolysis refers to disintegration of striated muscle, which results in the release of muscle cell constituents into the extracellular fluid and the circulation .
Rhabdomyolysis can be induced by numerous factors, including crush injury, skeletal muscle overuse, heat, alcohol abuse, myopathies, drugs, toxins and metabolic derangements (such as hypokalaemia, hyponatraemia or hypernataremia, and hypophosphataemia), as well as several types of viral and bacterial infections . Viral myositis causes more than a third of all rhabdomyolysis cases among paediatric patients, especially in their first decade of life . Virus-associated rhabdomyolysis follows infections caused by influenza virus (42% of cases of virus-mediated rhabdomyolysis) , coxsackie virus, enterovirus, human immunodeficiency virus, Epstein–Barr virus , varicella zoster virus  and cytomegalovirus . To date, three cases of para-influenza virus-induced rhabdomyolysis infection have been described in the literature, none with para-influenza type 1 [9–11]. In children rhabdomyolysis is usually a mild event, causing only elevation of muscle enzymes in asymptomatic patients . However, in some patients, complications occur. Complications of rhabdomyolysis are classified as early or late. Early complications include severe hyperkalaemia that causes cardiac arrhythmia and arrest . The most serious late complication is ARF, which occurs in approximately 5% of paediatric patients with this syndrome . The precise mechanism by which rhabdomyolysis causes renal failure remain unclear. The potential mechanisms may be renal vasoconstriction/hypoperfusion, renal tubular obstruction, due to cast formation, and myoglobin-mediated tubular cytotoxicity [1, 2, 4]. The contributing factors for the development of ARF in paediatric patients with rhabdomyolysis, besides the severity of muscle damage, are dehydration, metabolic acidosis, or multiple organ dysfunction syndrome (MODS) . In the patient that we describe here, the development of ARF coincided with MODS that occurred during the early hospital stay. According to Proulx criteria, our patient had primary MODS defined by dysfunction of cardiovascular and respiratory system as well as ARF . In our opinion the main, or maybe the only, cause of MODS in our patient was severe rhabdomyolysis caused by para-influenza type 1 virus. Although, hyperpyrexia at the beginning of the symptoms of viral disease could not be fully excluded as a contributor, we conclude that its influence was not crucial, because, 3 months after the present disease, the child experienced bilateral bronchopneumonia with hyperpyrexia as a symptom, but without signs of rhabdomyolysis and with normal urine output. Immobilization during the actual disease was also a less possible cause of the rhabdomyolysis in our patient, because, owing to his chronic condition, he had been bedridden for the majority of his life.
Finally, we can conclude that this is the first young child to be reported with para-influenza type 1 virus-induced rhabdomyolysis and development of ARF requiring continuous venovenous haemofiltration. The presence of MODS caused by rhabdomyolysis was probably the main (or only) factor that contributed to the development of ARF.
In conclusion, para-influenza type 1 virus infection must be considered as a possible cause of viral rhabdomyolysis and ARF in paediatric patients.