A 75 year old man with a history of chronic alcohol abuse
presented with bleeding per rectum. He was diagnosed to have bleeding
haemorrhoids and was admitted in the hospital and given intravenous fluids. A
day later he became confused and agitated. He was suspected to have delirium
tremens and was treated with parenteral Thiamine. His agitated behaviour
subsided but he became drowsy and lethargic. At this point his serum sodium was
noted to be 168mmol/L. His blood urea was elevated but his serum creatinine was
within normal limits.
About hypernatremia
Hypernatremia should be considered a water-problem and not a
salt-problem. People develop hypernatremia only when there is an impairment of
the thirst mechanism or when there is limited access to water. This elderly man
developed hypernatremia in the hospital in the setting of an alcohol-related change
in behaviour and sensorium. We can assume that his hypernatremia reflects
impaired release of vasopressin from the brain (diabetes insipidus) along with
insufficient fluid intake. There is evidence that alcohol can damage the
supraoptic and paraventricular nuclei in the brain. (Reference)
The diagnosis of diabetes insipidus is suspected when a person has polyuria (more than 3 litres of urine in a day) with hypotonic urine (urine osmolality less than 300mOsm/kg). As a general rule, in all patients who have polyuria with hypotonic urine, we must suspect three possibilities: compulsive polydipsia, central diabetes insipidus and nephrogenic diabetes insipidus. The fluid deprivation test can help us confirm or rule out compulsive polydipsia. The desmopressin stimulation test will help us identify nephrogenic diabetes insipidus.
Treating hypernatremia
Hypernatremia is dangerous because it dehydrates brain cells
and damages them. Before treating hypernatremia, we should know the duration of
hypernatremia. If the condition has been present for less than 24 hours, rapid
correction is safe. In this patient we have to assume that the hypernatremia
was present for more than 24 hours. Hence his hypernatremia should be corrected
slowly. Rapid correction can lead to cerebral edema. Slow correction means
reducing the sodium levels by not more than 10 to 12 mmol/L per day.
Correcting elevated
serum sodium
In correcting hypernatremia we use 5 percent dextrose which
does not contain any sodium at all. To know how much the serum sodium will fall
by giving 1 litre of 5 percent dextrose, there is a formula:
(Amount of sodium in the infusate minus the serum sodium)
divided by (total body water plus 1) is equal to the amount by which the serum sodium will fall.
His total body water = 50 percent of body weight = 30
litres because his body weight was estimated to be 60kg.
The calculated fall in serum sodium by infusing one litre of
5 percent dextrose will be: (0 – 168) divided by (30+1) = 5.4mmol/L
A fall of 10mmol/L in serum sodium needs: 10 divided by 5.4
= 1.85 litres of 5 percent dextrose.
Now we must add in the insensible and obligatory losses of
fluid from the body per day. This depends on factors like urine output, body
temperature, ambient temperature and respiratory rate. As an approximation, if
his urine output is 900 ml per day, and insensible losses are 600ml per day, we
have to add (900+600) = 1.5 L to the daily fluid requirement.
Hence he should be given (1.85 + 1.5) = 3.15 L of 5 percent
dextrose per day in order to reduce serum sodium by 10mmol/day.
This means
infusing the fluid at the rate of approximately 130ml per hour. This is a rough
guide only. We must check the serum sodium every 1 to 2 hours and adjust our
infusion rate accordingly. At all costs, we must avoid a rapid fall in serum
sodium.
What predisposed this
patient to develop a confusional state in hospital?
There are two possibilities. Delirium tremens and acute
onset of beriberi.
Delirium tremens is a severe clinical manifestation of
alcohol withdrawal and shows itself as a confusional state with features of
sympathetic over-activity. It generally occurs 3 to 10 days after stopping
alcohol intake. It is important to treat it urgently because cardiovascular
collapse can occur. Benzodiazepines in adequate doses should always be used.
Beta blockers can be added if necessary. Attention must be paid to fluid and
electrolyte balance and management of other medical / surgical conditions in the
patient.
Beriberi can present as a confusional state – Wernicke’s
encephalopathy and Korsakoff psychosis. People who chronically abuse alcohol
may have low levels of Vitamin B1 or thiamine in their bodies. When such people
are given dextrose containing fluids, they can develop acute thiamine
deficiency because whatever little thiamine is present in them is used up for
the metabolism of glucose.
References:
1. Diabetes insipidus. http://emedicine.medscape.com/article/117648-overview
2. Delirium tremens. http://emedicine.medscape.com/article/166032-overview
