DISCUSSION
The adverse effects of recreational drugs such as MDMA and cocaine resulting in rhabdomyolysis are usually acute in onset. MDMA has been postulated to cause rhabdomyolysis in acute settings via hyperpyrexia, increased activity such as dancing and crush injury as the patients are prone to being unconscious6. Ambient temperature, motor activity, metabolic regulation, autonomic vascular changes, and central disturbances in thermoregulation all contribute to profound MDMA-induced elevations in core body temperature.7Delayed rhabdomyolysis has been reported to be caused by some mushroom poisonings and anabolic androgenic steroid use8,9. In a case with delayed rhabdomyolysis and neuroleptic malignant syndrome, a novel RYR1 mutation was detected10. Acute tubular necrosis induced by pigment as a result of non-traumatic rhabdomyolysis (myocyte necrosis brought on by a sharp increase in intracellular calcium) is the most significant cause of acute kidney damage. In such cases, creatinine phosphokinase concentrations can exceed 100,000 U/l.
Previously reported delayed onset rhabdomyolysis had occurred at 30 hours 11, 55 hours 7and 510 days. As our patient presented after 8 days, a new study into the mechanism of metabolism of MDMA and pathophysiology of rhabdomyolysis may be required. The patient also presented with significantly high creatinine kinase values in the range of 300,000 U/L. Similarly, high creatinine values were reported in another case ultimately requiring hemodialysis and high creatinine kinase value is indicative of the severity of renal iniury12. Few cases have been reported where patients have survived a massive overdose. It was hypothesized that MDMA toxicity may be increased by an interaction of direct pharmacological effects of the drug and the prevailing environmental conditions at administration. Other factors (e.g., immune mechanisms, genetic variants of CYP2D6, idiosyncrasy) cannot be excluded as influencers13. It is evident that severe acute sickness is relatively rare despite widespread MDMA use. However, when difficulties do arise, they can be fatal, necessitating the execution of a well-thought-out plan based on the clinical situation and knowledge of the physiological effects and toxicity profile of MDMA14.
Long periods of dancing, convulsions, or overheating can result in non-traumatic rhabdomyolysis. Arrhythmias may result from rhabdomyolysis-related hyperkalemia. Treatment modalities include hydration-force diuresis, monitoring and optimization of the fluid and electrolyte situation, including intake and removal, and kidney function tests15. For hyperkalemia, hemodialysis can be used. Urine alkalization is not recommended, as it would lessen the kidneys’ ability to remove MDMA16.
CT scan without IV contrast is preferred as contrast may further deteriorate the kidney injury Non-contrast CT scan of Abdomen and Pelvis showed loss of cortico-medullary differentiation in our case. In another case report where rhabdomyolysis resulted in AKI, CT findings were striate nephrogram, perinephric collection and nephromegaly17. However, in other reported cases of rhabdomyolysis associated with illicit drug use, MRI and CT scan was primarily used to identify the muscles affected and the extent of disease. MRI was preferred over CT scan for early diagnosis of rhabdomyolysis18. Even though the MRI findings are non-specific, the sensitivity in the detection of muscle involvement is higher than CT or US.19
Upon 3 months follow up, our patient still had demonstrated elevated levels of serum creatinine and now can be labeled as chronic kidney disease. The progression of AKI to CKD in illicit drug users has not been studied extensively and those few studies that are available present contrasting conclusion. In the majority of patients admitted to an ICU with severe rhabdomyolysis, AKI develops, and RRT is necessary in 35% of cases. The serum myoglobin and phosphate levels upon admission appear to be substantially linked to the long-term renal prognosis; these two molecules could be eliminated utilizing specialized devices to lower the risk of AKI to CKD development. In a large multicentre retrospective study, where 259 patients of rhabdomyolysis were evaluated for AKI and CKD, 80 had eGFR data available at 3 months20. Among them, 23/80 patients (28.8%) had an estimated GFR below 60 mL/min/1.73 m2 at month 3 (CKD KDIGO stage 3 to 5), compared to 9/80 (11.2%) before hospital admission for rhabdomyolysis. This shows that rhabdomyolisys can be a significant contributor to the risk of CKD20. Similarly, in a study of over 5861 persons with CKD (defined as GFR< 60 ml/dk/1.73 m2 or for micro-albumin: male >17 mg/g creatinine, and female >25 mg/g creatinine), 1202 were reported to have used illicit drugs. However, CKD presence, kidney function and albuminuria were not found to be significantly associated with the use of cocaine, methamphetamine and heroin.21. Another study by Vuputturi et al documented that documented a significant, positive, and independent association between illicit drug use and risk for mild kidney function decline.22
On long term follow-up, the patient’s kidney function improved and the renal parameters were within normal range. This can be attributed to aggressive monitoring, early initiation of renal replacement therapy and a multi-disciplinary team involvement in an intensive care set-up. Similar recovery was reported in other studies where it was found that early therapeutic intervention improves prognosis, such cases should be promptly referred and managed in centers where aggressive supportive therapy can quickly be instituted3