A young patient who was engaging in heavy
weightlifting presented to the ED with proximal muscle
weakness. The night before he had one hour of acute onset bilateral
leg and hip flexor cramps with stiffness and “hardened” muscles and
marked weakness that prevented him from standing or walking. This resolved
spontaneously. After an intense workout the next morning he noted cramping and
weakness in his legs and was unable to walk, therefore he presented to the ED.
He had been taking a thyroid supplement for several months but had stopped about three weeks prior. He was also taking lisinopril for hypertension. He was currently using a steroid supplement containing
designer steroids (10 mg androstenone and 10 mg androstan-one-azine) for
several months. He also took vitamin B5 and niacin. He was eating a high protein diet mainly consisting of
chicken and sauce (some sort of Teriyaki sauce) and some rice and very few
vegetables for several months averaging 4000 to 8000 calories on most of the
days of the week.
designer steroids (10 mg androstenone and 10 mg androstan-one-azine) for
several months. He also took vitamin B5 and niacin. He was eating a high protein diet mainly consisting of
chicken and sauce (some sort of Teriyaki sauce) and some rice and very few
vegetables for several months averaging 4000 to 8000 calories on most of the
days of the week.
Two days before presentation he started eating
“normally” again with high amounts of carbohydrates as a treat (cake and
sweets).
“normally” again with high amounts of carbohydrates as a treat (cake and
sweets).
In the ED:
K 2.0 mmol/L, PO4 1.0 mg/dl, glucose 197 mg/dl, Mg 2.0 meq/L, CK 5070 U/L, TSH 0.01, low normal total T3, low total T4 and low free T4
but normal free T3. Urine electrolytes at the time of presentation were notable
for a potassium of < 10 and an undetectable phosphorus level (Fractional
excretion Phos < 5%). His ECG showed slight abnormalities but troponins were negative x 3.
K 2.0 mmol/L, PO4 1.0 mg/dl, glucose 197 mg/dl, Mg 2.0 meq/L, CK 5070 U/L, TSH 0.01, low normal total T3, low total T4 and low free T4
but normal free T3. Urine electrolytes at the time of presentation were notable
for a potassium of < 10 and an undetectable phosphorus level (Fractional
excretion Phos < 5%). His ECG showed slight abnormalities but troponins were negative x 3.
Phosphate was repleted with 12 mmol NaPhosphate and normalized. Potassium was repleted with 40 meq KCl IV and 120 meq po
until normal. His leg weakness resolved and the CK started to trend down.
until normal. His leg weakness resolved and the CK started to trend down.
The question is: what caused his profound electrolyte
abnormalities?
abnormalities?
One possibility is refeeding syndrome as described in a previous post. The
sudden surge of carbohydrates following a long period of high protein, low carb
diet might have caused an increase in insulin driving potassium and phosphate
into the cells. Hypomagnesemia was, however, not present in this patient. The
time frame (within 4 days) would be consistent with refeeding syndrome. The
rhabdomyolysis occurred as a consequence of hypokalemia and hypophosphatemia with a contribution from heavy exercise. He responded quite fast to potassium and phosphate
supplementation and improved clinically within a day.
sudden surge of carbohydrates following a long period of high protein, low carb
diet might have caused an increase in insulin driving potassium and phosphate
into the cells. Hypomagnesemia was, however, not present in this patient. The
time frame (within 4 days) would be consistent with refeeding syndrome. The
rhabdomyolysis occurred as a consequence of hypokalemia and hypophosphatemia with a contribution from heavy exercise. He responded quite fast to potassium and phosphate
supplementation and improved clinically within a day.
Patients with the following conditions have traditionally
been at risk for refeeding syndrome: anorexia, chronic malnutrition (e.g.
in patients with cancer), alcoholism, prolonged fasting, after a duodenal switch operation for
obesity, hunger strikers and postoperative states. In these times of extreme dieting one should think outside
the box and ask about special diets such as high protein diets. The kidney on
the other side has been doing it’s duty and preserved whatever electrolytes
were still in the circulation by absolutely minimizing excretion of potassium and and phosphate.
Posted by Florian Toegel
been at risk for refeeding syndrome: anorexia, chronic malnutrition (e.g.
in patients with cancer), alcoholism, prolonged fasting, after a duodenal switch operation for
obesity, hunger strikers and postoperative states. In these times of extreme dieting one should think outside
the box and ask about special diets such as high protein diets. The kidney on
the other side has been doing it’s duty and preserved whatever electrolytes
were still in the circulation by absolutely minimizing excretion of potassium and and phosphate.
Posted by Florian Toegel
