Water intoxication

Introduction Water poisoning is a poisoning symptom of dehydration and hyponatremia caused by excessive intake of water by the human body. Although the chance of death from water poisoning is very low, it is still possible. The maximum diuresis rate of the human kidney is 16 ml per minute. Once the rate of ingestion of water exceeds this standard, excess water will cause the cells to swell, causing dehydration and hyponatremia. When drinking too much water, the electrolyte in the blood is reduced to a concentration lower than the safe water due to the excretion of water, which affects the operation of the brain and may be fatal.

Cause

Excessive ADH secretion

Can be seen in fear, blood loss, shock, acute infections (such as pneumonia, toxic dysentery, etc.), the use of analgesics (such as morphine, pethidine), or painful injuries, surgery and other stress stimuli. The time to increase ADH secretion after surgery usually lasts 12-36 h, or longer. In this case, excessive input of a solution containing no electrolyte such as glucose is likely to cause water poisoning. In addition, patients with late-stage edema of hypothyroidism can also increase the secretion of ADH through the stimulation of baroreceptors, and abnormal release of ADH when the adrenal insufficiency is present.

Renal dysfunction

In the oliguria and anuria period of acute renal failure, the diluting and concentrating functions of the kidneys are all obstacles. At this time, excessive water intake is likely to cause water poisoning. In addition, for any reason, the renal blood flow is insufficient or the glomerular blood perfusion is severely reduced, and excessive water cannot be discharged. In the case of combined hypotonicity, water poisoning is likely to occur.

Water and sodium metabolism disorder

In patients with severe sodium deficiency (hyponatremia) or hypotonic dehydration, the extracellular fluid is already in a hypotonic state, and the body has compensated. The absorption of water and sodium by the renal tubules has increased. Into, water poisoning can occur. It is even suggested that in the case of hypertonic dehydration, water poisoning sometimes occurs due to cell dehydration, such as rapid, large-volume input of salt-free liquid. Therefore, hyperosmotic dehydration, no matter how high it is, can only be input into low-tension solution during treatment.

Insufficient drainage

In acute and chronic renal insufficiency and oliguria, the renal drainage function is drastically reduced. If the water intake is not limited, it can cause water retention in the body, severe heart failure or cirrhosis, due to effective circulating blood volume and renal blood flow. Reduced, kidney drainage is also significantly reduced, if increased water load is also likely to cause water poisoning.

Hypotonic dehydration

In the late stage, extracellular fluid is transferred to the cells due to hypotonic extracellular fluid. It can cause intracellular edema, so when you input a lot of water, it can cause water intoxication.

an examination

Related inspection

Cortisone water test urine specific gravity (SG) urine specific gravity

Physical examination

Patients with acute or severe water poisoning have a rapid onset, and brain function dysfunction is the most prominent, so brain dysfunction is the main manifestation. Patients with headache, extremely weak, and then loss of orientation, confusion, drowsiness, sometimes agitation, or alternating sleepiness and agitation, followed by convulsions or epileptic seizures, and finally coma chronic or mild water poisoning patients, the onset is generally hidden, Slow progress, general symptoms such as fatigue, headache, and lethargy. Often accompanied by digestive symptoms such as loss of appetite, nausea and vomiting. A small number of patients have symptoms such as tendon, saliva or tear secretion and diarrhea.

Signs are often not very obvious, the body surface may have edema, severe cases may have depressed edema, weight gain, disorientation, unconsciousness, convulsions, coma, Babinski sign can be positive.

Laboratory inspection

The most important test indicators for water intoxication are reduced plasma osmotic pressure and reduced dilution of serum sodium. Because the cation that maintains the plasma osmotic pressure is primarily sodium, the changes in the two are often consistent. For the onset of water poisoning, the rate of decrease in plasma osmotic pressure and serum sodium concentration is more important than the value of the decrease. For example, the serum sodium concentration of patients with acute water intoxication rapidly decreased from 140 mmol/L to 120 mmol/L in l-2 d, and the degree of water toxicity was much more serious than that of chronic water poisoning patients whose serum sodium was maintained at 115 mmol/L for a long time. Severe hyponatremia can be reduced to less than 110mmol/L, but a rapid decrease in blood sodium concentration of 30 mmol/L can cause death.

Differential diagnosis

Although water poisoning is produced on the basis of hypoosmotic edema, it is significantly different from hypotonic edema. In acute attacks, there are often induced factors such as stress stimulation, renal excretion dysfunction and excessive water intake. Therefore, it is not difficult to identify simple water and electrolyte metabolism disorders such as hypoosmotic edema. It is worth noting that acute renal failure is similar to the onset of this disease, including prerenal and renal acute renal failure, and brain diseases. Such as cranial trauma, dural hematoma, subarachnoid hemorrhage, encephalitis, meningitis and other increased intracranial pressure and brain edema.

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