A shocking finish of the 'Dam tot Damloop'
Douma, J.A.J., Loffeld, R.J.L.F.
Voorzitter(s): dr. B.J. Looij, Geleen & dr. Y.W.J. Sijpkens, Den Haag
Locatie(s): Zaal 2.1
Categorie(ën):
Case report: A 32-year old female was admitted to our hospital. After the finish line of the “Dam tot Dam loop” she collapsed, without signs of epileptic activity. The patient was admitted and didn’t had any complaints. Blood pressure was normal, with a pulse rate of 112, her core temperature was 37.8 oC. Shortly after arrival the patient became unconscious, with rhythmic movement of the eye lids and extremities. An epileptic seizure was diagnosed and intravenous benzodiazepines were given, with only partial and shortlasting effect. The patient was admitted to the ICU-department and treated with phenytoin, sedation and ventilator support. Laboratory investigation showed mild renal insufficiency with a creatinin of 113 umol/l, a maximum creatinin kinase of 1695 U/l, a corrected calcium of 2.06 mmol/l and a severe hypophosphatemia of 0.30 mmol/l. Arterial blood gas examination revealed a metabolic acidosis, with a pH of 7.31, pCO2 35 mmHg, bicarbonate 17.6 mmol/l and a lactate of 2.6 mmol/l. Intravenous administration of phosphate was initiated. The next day the patient was doing well and did not show any signs of epileptic activity. A MRI-scan of the brain showed no abnormalities. An EEG showed no focal abnormalities and no signs of epileptic activity. Vitamin D level was normal. Three months later, calcium and phosphate levels in blood and urine were normal. The final diagnosis was a severe exercise-induced hypophosphatemia, with epileptic seizures.
Discussion: Hypophosphatemia as a result of exercise is rarely reported in the literature. In one study participants with collapse after a running competition had a significant hypophosphatemia compared with runners who did not collapse. The cause is unknown. Rapid absorption of inorganic phosphate into the muscles to replenish the depleted stores of phosphocreatinin after heavy exercise is one of the possible mechanisms. Also some of the inorganic phosphate is sequestered in the hexophosphates and triose-phosphates of the glycolytic pathway. Another factor could be the high level of circulating catecholamines during severe exercise, what can cause a phosphate shift from extracellular tot intracellular. Hypophosphatemia is related to different forms of neurologic dysfunction, like confusion, generalized weakness, neuropathy, seizures and coma. The mechanism that leads to neurological dysfunction in hypophosphataemic patients is unclear. Maybe it is caused by diminished oxygen delivery in neurologic tissue, as a consequence of lower concentrations of 2,3-DPG and ATP in red blood cells. In conclusion, heavy exercise can cause severe hypophosphatemia with serious neurological dysfunction.