Discussion
Seizures have the ability to increase CK levels and even increase the
rate of in-hospital mortality [2, 12, 13]. Bosch et al. proposed
that less severe RM with few symptoms and no renal failure could be
designated hyperCKemia [2]. No patient developed renal failure or
needed renal replacement therapy in the present study. Therefore, in
this study, it was appropriate to define elevated CK as hyperCKemia.
In the current study, patients did not experience any trauma, metabolic
disorders, alcohol abuse, exposure to drugs or toxins, infection or
sepsis, myocardial infarction, or other diseases associated with
hyperCKemia [2, 7]. However, significant electrolyte disorders
caused by bowel preparation, vomiting, and diarrhea were observed in
patient 4 (hyponatremia and hypomagnesemia) and patient 6 (hypokalemia
and hypomagnesemia). Among the different electrolyte disorders,
hypokalemia and hypophosphatemia are known to cause damage to myocytes
[1], but hypophosphatemia was not observed in our cases.
Some studies indicated that a potassium level less than 2.0 mmol/L
observed in the initial evaluation could potentially cause RM [1,
16-18]. In the present study, it appeared that hypokalemia was not the
primary cause of hyperCKemia in patient 6, who exhibited a potassium
level of 2.66 mmol/L. No causal association has been established between
desmopressin acetate-induced hyponatremia and muscle injury in animal
studies [19]. In a clinical study, asymptomatic hyperCKemia was
associated with hyponatremia caused by diuretics and polydipsia, which
may have been complicated by AKI [20]. Compared to ultra-athletes
with normonatremia, exercise-associated hyponatremia is prone to develop
into exercise-associated RM [21]. Severe hyponatremia was observed
in patient 6, and we considered that hyponatremia might promote the
development of hyperCKemia. Hypomagnesemia was observed in two patients,
which may have been due to gastrointestinal losses as they had a history
of bowel preparation, vomiting, and diarrhea [22]. There was less
possibility of other causes of hypomagnesemia because these patients did
not have any history of hypomagnesemia, and their serum magnesium
gradually recovered after supplementation. Therefore, for these two
patients, hyperCKemia might have been caused synergistically by
electrolyte disorders and seizures.
Consequently, it was likely that the seizures experienced by the
patients in the present study caused the hyperCKemia. Other factors
might have been involved in the pathophysiological process associated
with muscle damage, especially the electrolyte disorders. Thus, we
recommend performing serial testing for levels of CK and electrolytes
after seizure onset.
Early and aggressive repletion of several liters of fluid to restore
renal perfusion and increase the urine flow rate is the primary
management for AKI [1, 2, 23]. We administered normal saline at
1,500 ml/day to the majority of patients with kidney function impairment
in the cases in this study. Fluid was administered at a rate of 2,500
ml/day to patient 6 due to his history of vomiting and diarrhea. Only
patient 6 had a lower eGFR (55.65 ml/min/1.73m2).
However, patient 6 did not report any history of kidney function
impairment, such as renal disease, toxin exposure, or sepsis [24].
Unfortunately, we could not investigate the reason for this outcome, as
patient 6 did not have a follow-up examination.
Urinary alkalization and diuretic agents were administrated to the
patients in this study. Alkaline urine might prevent lipid peroxidation,
redox-cycling, and myoglobin cast formation [2, 23]. Diuresis might
prevent the accumulation of debris in the renal tubules, increase renal
perfusion, and improve myoglobin excretion [1, 24]. Mannitol should
be avoided in anuric patients, and electrolytes should be monitored if
loop diuretics are used [1, 25]. Fortunately, no patient in this
study developed renal failure or required continuous renal replacement
therapy, probably due to the rate for renal failure was lower in
exertional RM or generalized tonic-clonic seizures [10, 12]. The
eGFR for all patients increased after treatment even though the recovery
level was less than 90 mL/min/1.73m2 at the time of
discharge. It might be necessary to conduct a follow-up examination.