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