Water toxicity can occur due to numerous etiologies but is challenging to diagnose as it presents with vague symptoms of altered mental status, disorientation, confusion, nausea, and vomiting which may resemble psychosis. It may be misdiagnosed on presentation, due to the variability of symptoms. To avoid more serious outcomes like seizures and coma early detection is vital. Untreated cases may also lead to death.
Water toxicity in normal circumstances is rare as there is a precise regulation of the water content in the body. However, excessive water ingestion may occur in the following conditions:
Water intoxication can occur in a broad range of different clinical settings. It is uncommon and often associated with contests and alcohol intoxication.
The concentration of solutes is high inside cells as compared to the extracellular space. In water toxicity, with excessive ingestion of water, this excess water migrates to the site with increased solute concentration owing to diffusion. Thus the amount of intracellular water increases, causing the cells to swell. In the CNS, the swollen neurons increase the intracranial pressure which leads to the symptoms of confusion, lethargy, headache, and drowsiness. Further, an increase in ICP may cause bradycardia and hypertension.
Initial presenting symptoms may mimic psychosis which includes a hostile, delirious profile with delusions, hallucinations, confusion, and disorientation. Undertreatment or a delay in diagnosis may result in progression of symptoms to seizures, delirium, and coma.
With water toxicity, in clinical practice hyponatremia impacts the choice of treatment the most. For the evaluation of hydration status, various methodologies exist:
These principles encompass the following strategies:
This is the most important parameter in the evaluation of the severity and choice of treatment.
Plasma and urine osmolarity
It is not routinely considered as part of diagnostic evaluation but can be supportive for diagnosis.
Water intake and output
Estimation of water balance by the assessment of both water intake (input) and water losses (output) during a period. Water output includes losses in urine and stool.
Body weight changes are a sensitive, accurate and readily measured indicator of water balance when measured under standard conditions and if past data is available for comparison.
Goals of therapy:
Osmotic demyelination syndrome (ODS) can occur due to overly aggressive therapy for hyponatremia. It usually occurs when sodium level raises by a rate faster than 18 mEq/L in 48 hrs or more than 10 to 12 mEq/L in 24 hrs. A few cases also are known to develop ODS after correction rates as slow as 9 mEq/L in 24 hrs.
In acute conditions such as water intoxication causing hyponatremia, the goal to be achieved in the initial 24 hrs is achievable in the first few hours since it is the change per day, rather than the change per hour, in serum concentration of sodium which is responsible for ODS. Hence, the treatment can be more aggressive in the initial few hours of presentation for a case requiring emergency therapy.
The therapy provided on presentation or up to six hours of water ingestion is dependent on whether the patient is symptomatic.
Because water draws through the blood-brain barrier due to osmosis, acute hyponatremia can lead to cerebral edema which can be lethal. Thus a case in which there are even mild symptoms needs attention in the setting of hyponatremia and warrants prompt administration of hypertonic saline.
Asymptomatic cases - In asymptomatic patients with acute hyponatremia after having a serum concentration of sodium lower than 130 mEq/L, usually treatment is initiated by a 3 percent saline 50 ml bolus so that the serum concentration of sodium doesn't fall further. However, 3 percent saline is not given if the auto-correction for the hyponatremia is already underway owing to diuresis. Also, if the sodium concentration has been reversed, there is increased output of urine, and production of dilute urine (osmolality <200 mOsm/kg, specific gravity <1.005, or the sum of the urine sodium and potassium concentrations, i.e., the urine cation concentration is less than half the serum sodium) one might be inclined to suspect the role of auto-correction. Valuable and prompt information can be provided by a point-of-care sodium analyzer, about the trajectory of the serum sodium in such patients.
Monitoring of patients for signs and symptoms and measuring the serum sodium concentration must be done every couple of hours to decide if the patient needs further treatment. The serum sodium may continue to decline after hours of presentation, due to a delay in absorption of the water ingested. Increased sodium excretion can occur because of patients being volume expanded due to excessive water load. Sometimes, a stimulus unrelated to the etiology, e.g., vomiting, may cause loss of volume, which causes the ADH levels to remain high causing a phenomenon called 'desalination.'
Symptomatic (including minimally symptomatic patients) — In patients who are acutely hyponatremic and having a concentration of sodium in the serum <130 mEq/L who are symptomatic suggesting increased intracranial pressure, treatment is initiated with a 3 percent saline 100 ml bolus, followed by up to 2 additional 100 ml doses (total 300 ml); each bolus is infused over 10 minutes, if symptoms persist. Alternatively, treatment consisting of two 3 percent saline 150 ml boluses, each administered over 20 minutes and measuring the serum sodium between infusions.
Rapidly increasing the serum sodium by 4 to 6 mEq/L is preferred as the goal of therapy, over a period of a few hours. If the serum concentration of sodium is elevated by 4 to 6 mEq/L brain herniation could be prevented along with cessation of any symptoms.
According to the data from clinical experience, in a patient having a severe case of symptomatic hyponatremia, the only rapid method for raising the serum sodium concentration is the administration of 3 percent saline. It also improves neurologic symptoms and prognosis.
Vasopressin antagonists (e.g., vaptans) or mannitol are not preferred in such cases, even instead or on top of hypertonic saline. Mannitol is not preferred despite being used for cerebral edema as it is toxic to kidneys and can exacerbate hyponatremia. Therefore, controlling sodium level becomes more difficult. Vaptans vary in their efficacy and not preferred in acute hyponatremia for the delayed initiation of action.
Other precautions from keeping the serum concentration of sodium from falling further include water intake limitation and discontinuing any drug having a role in causing hyponatremia.
Due to the severity of the clinical scenario, patients with hyponatremia must be evaluated hourly for any change in mental status or evolution of symptoms. An elevation of sodium concentration by 4-6mEq/L should ensure the disappearance of symptoms.
It is imperative to rule out the reversible causes of polydipsia while evaluating the causes of water toxicity. Diabetes can be prevalent in patients with psychogenic polydipsia especially due to the tendency of antipsychotics to cause metabolic syndrome. In chronically mentally ill patients, anticholinergic induced dry mouth may play a measurable, but clinically insignificant, role in the disorder. Patients with primary polydipsia are frequently misdiagnosed as diabetes insipidus (low level or deficient activity of ADH) as polydipsia itself reduces the renal response to ADH due to the down-regulation of aquaporin-2 channels.
Water toxicity can occur due to numerous etiologies, and the diagnosis can be challenging. Because of the diverse presentation and high morbidity, the condition is best managed by a multidisciplinary team that includes a nurse, internist, endocrinologist, a nephrologist, and an intensivist. To prevent more serious outcomes including seizures and coma early detection is vital. Untreated cases may also lead to death.
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