1- What are your differential diagnoses for the patient?
Acute renal failure due to other causes: any underlying asymptomatic renal disease (chronic kidney disease, asymptomatic glomerulonephritis) could have become exacerbated and evident after a marathon. Tumor lysis syndrome may also produce similar laboratory findings, but the clinical data do not support this diagnosis.
2- What’s your final diagnosis?
3- What additional tests would be helpful in confirming the diagnosis?
Measurement of creatine phosphokinase (CPK) levels. Slight elevations in CPK levels occur in acute renal failure, minor trauma or even after intramuscular injections. However, CPK levels are expected to be at least over 1000 in patients with rhabdomyolysis. In this typical case, I would expect CPK levels above 10000. AST, ALT, and LDH are non-specific enzymes that could be elevated in any type of tissue necrosis and are not necessarily required for the diagnosis of rhabdomyolysis.
4- Based on the information provided, what is the most likely etiology of this patient’s main problem?
Strenuous exercise (marathon) is the most likely etiology for this patient.
5- What EKG abnormalities are associated with hyperkalemia?
Tall peaked tented T waves with a shortened QT interval are usually the first findings. As the hyperkalemia gets more severe, there is progressive lengthening of the PR interval and QRS duration, the P wave may disappear, and ultimately the QRS widens further to a sine wave pattern. Ventricular standstill with a flat line on the ECG ensues with complete absence of electrical activity.
6- How would you acutely manage the hyperkalemia in this patient?
The main question would be: “does this patient need calcium gluconate?”
Calcium is given to antagonize the cardiotoxicity of hyperkalemia. It does not lower serum potassium levels. The fastest acting potassium lowering therapy is insulin+glucose (a bolus infusion of 10 units of regular insulin with 50 mL of glucose 50%). The effect of insulin begins in 10 to 20 minutes, peaks at 30 to 60 minutes, and lasts for four to six hours.
Therefore, we must ask ourselves: “does this patient have 30 minutes time before insulin+glucose reaches its peak effect?” I would not administer calcium gluconate for this patient.
Calcium infusions are indicated only for severe manifestations of hyperkalemia (as with widening of the QRS complex or loss of P waves, but not necessarily for peaked T waves alone), in whom it would be potentially dangerous to wait the 30 to 60 minutes for insulin and glucose to act.
Other rapidly acting treatments are not indicated in this patient (salbutamol, bicarbonate).
Hemodialysis should be considered for the renal failure of this patient (Cr= 10 mg/dL, decreased urine output) and when performed, would also decrease serum potassium levels.
7-This patient has hyperkalemia, hypocalcemia and hyperphosphatemia. What factors are responsible for these derangements?
Hyperkalemia, hyperphosphatemia and severe hyperuricemia result from the release of potassium and phosphorus from damaged muscle cells. Hypocalcemia, which can be extreme, occurs in the first few days because of both deposition of calcium salts in damaged muscle and decreased bone responsiveness to parathyroid hormone.
All answers were good. Dr. Mirreza provided complete answers to all questions.