Dengue and rhabdomyolysis.

Sir,

I read the article “Acute dengue myositis with rhabdomyolysis and ARF” with interest.[1] I would like to make the following comments.

The clinical significance of myoglobinuric acute renal failure and other serious sequalae is attributable to often subtle initial clinical manifestations of rhabdomyolysis.[2] The authors suggest that the incidence is rare, in contrast to the literature indicating underreporting and underrecognition of such a complication by physicians for many reasons.[34] Secondly, the authors also presume that vigorous manual labor, 2 days after the fever onset, might have led to the persistent inflammation in this professional casual laborer. In general, a CK rise above 10,000 IU/L after exercise is not the common. The paper does not give the serial CK results to suggest the second spike in CK is secondary to this exertional rhabdomyolysis trigger. Factors such as impaired sweating, exertion in extremely humid conditions, dehydration,[5] (through hyperthermia), sleep deprivation, fasting; common drugs, such as ibuprofen, paracetamol, diazepam; emotional stress; nutritional supplements (especially in hot/humid conditions through severe hypokalaemia and hypomagnesemia);[6] and hemoglobinopathy (sickle cell trait in those who exert at a high altitude); enzymatic deficiencies[7-9] associated with this condition, particularly impaired sweating and humid condition, might have triggered rhabdomyolysis.[8-10] If this was an exercise-, fasting- or febrile illness-induced episode in an adult, the metabolic myopathies, particularly carnitine palmitoyl transferase II deficiency should have been included near the top of the differential. If this is the cause, then there is a risk of recurrence. Lastly, the adoption of serum CK, serum and urine myoglobin, and histopathology in addition to the signs and symptoms to confirm muscle trauma in this case sends a signal to the readers that these are mandatory to confirm rhabdomyolysis and its clinical sequalae.

It is important to recognize rhabdomyolysis early in order to prevent acute renal failure and electrolyte disturbances[9]. When rhabdomyolysis is suspected (e.g. dengue viral infection), measuring the initial serum CK level at admission and the second at 12 h after the suspected onset of the insult can indicate early rhabdomyolysis.[8] If both (the first at admission & the 2nd at 12h) CK levels are less than 30 times the upper limit of the local reference range (established by the lab), provided the specimens are taken within the first 3 days after the suspected insult, impending ARF unlikely as per the currently available evidences.[268] If either admission or 12-h CK is above the value just quoted, the patient is at risk from the consequences of rhabdomyolysis and regular monitoring of serum potassium and creatinine are indicated with maintenance of good urine output with a correct fluid balance appropriate to the clinical condition.

When suspiciously pigmented urine is encountered, the recommendation is to use dipsticks for heme, and the result of a positive heme test in urine with no RBCs should be followed by the measurement of serum CK to establish the diagnosis of rhabdomyolysis. If serum CK is within the reference range, causes of hematuria/hemoglobinuria must be investigated. The high serum levels of creatine kinase, potassium, and phosphorus; low levels of serum albumin, dehydration and sepsis can predict ARF in rhabdomyolysis.[910]

It is important to educate the patients to report any new muscular symptoms and to monitor serum CK levels at regular interval.The urine myoglobin may not be more informative than serum CK and there's no evidence that urine myoglobin level can reliably detect rhabdomyolysis or predicting acute renal failure following rhabdomyolysis.- The learning point from this case is the heightened awareness of this silent killer and performing CK to enable the diagnosis even when physical signs and symptoms may be minimal.