CORRECT ANSWER IS A

Acute life-threatening pulmonary edema (APO) can occur in endurance athletes with Exercise induced hyponatremia (EAH) as the primary sole manifestation or in conjunction with other evidence of cerebral encephalopathy. EAH develops in susceptible endurance athletes after excess hypotonic fluid ingestion. Stimulants for increased ADH secretion in endurance athletes include volume depletion, pain and nausea, possibly interleukin-6 from muscle breakdown during exercise. Impaired renal diluting ability and metabolic water production from the breakdown of glycogen, Natriuresis promoted by atrial natriuretic peptide secreted in response to atrial stretch induced by plasma volume expansion could be contributory factors. Acute symptomatic EAH management involves administration of hypertonic saline should be promptly employed to reduce brain oedema. The use of isotonic or hypotonic intravenous fluids is contraindicated, as circulating ADH increases the retention of free water, aggravating the hyponatremia.

The possible mechanisms by which APO develops in association with exercise induced hyponatremia include compression and distortion of the medulla and cervical spinal cord from raised intracranial pressure resulting in profound sympathetic activation. Increased catecholamine release likely causes pulmonary vasoconstriction, elevated capillary hydrostatic pressure resulting in capillary wall injury and increased permeability.

Other differential diagnosis for APO in this endurance athlete include myocardial infarction, Takotsubo’s cardiomyopathy and acute post viral myocarditis. An elevated BNP and raised troponin can occur with left ventricular stretch secondary to increased end diastolic volumes associated with exercise and do not necessarily imply acute CHF/MI. Takotsubo cardiomyopathy (left ventricular apical ballooning syndrome) presents similar to myocardial infarction with chest pain and dyspnea but can be associated with heart failure. It tends to follow an emotionally or physiologically stressful event predominantly in women. Echo done in this patient did not show characteristic appearance of apical ballooning of the left ventricle with hyperdynamic basal segments on echocardiogram.  viral myocarditis in less likely in absence of recent viral upper respiratory tract infection.

IV lasix plus hypertonic saline can be used to achieve an acute rise in serum sodium in an emergency situation resulting in reversal of pulmonary edema and hyponatremia and should be started emergently with close monitoring of serum sodium to achieve standard recommended rate of serum sodium correction. Alternate choices mentioned are not reliable for acute hyponatremia treatment in an emergency situation.

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