Hyponatremia, defined as a serum sodium concentration of <135 mmol/L, often develops as a consequence of elevated levels of arginine vasopressin (AVP) hormone. AVP elevation can occur in a number of common clinical conditions, including syndrome of inappropriate secretion of AVP, volume depletion, postoperative states, heart failure, cirrhosis, neuroendocrine disorders and trauma. A history of concurrent illness and medication use, assessment of extracellular fluid volume as well as measurement of serum and urine osmolality and urine sodium concentration will help to establish the primary underlying causes. Presence or absence of significant neurologic signs and symptoms must guide treatment. Symptomatic hyponatremia must be treated promptly with 3% hypertonic saline to increase the serum sodium by 1-2 mmol/L per hour until symptoms abate, or a total magnitude of correction of 12 mmol/L in 24 hours or 18 mmol/L in 48 hours is achieved. Initial infusion rate (ml/kg per hour) can be estimated by body weight (kg) x desired rate of increase in sodium (mmol/L per hour). An overly rapid increase in sodium (>12 mmol/L per 24 hours) may result in serious neurologic injury. Fluid restriction and loop diuretic are frequently employed to treat volume overload. Vasopressin receptor antagonists provide prompt and effective water diuresis and increase in serum sodium concentration in both euvolemic and hypervolemic hyponatremia. In this review article, the author introduces a problem-solving approach to dissect the different clinical cases with hyponatremia and presents simple algorithms for the evaluation and management of hyponatremia that are useful at the bedside to improve quality, safety and cost-effectiveness of the patient's care.