A 52-year-old male with a history of chronic alcohol abuse was brought to the Emergency Department with a reported change in his mental state for 3 - 4 days. He was drowsy and lethargic but communicated appropriately when roused. He did not appear dehydrated . The following are his blood results on presentation:
|
Parameter |
Patient Value |
Normal Adult Range |
||
|
Sodium |
116 mmol/L* |
135 - 145 |
||
|
Potassium |
2.9 mmol/L* |
3.5 - 5.0 |
||
|
Chloride |
67 mmol/L* |
95 - 110 |
||
|
Bicarbonate |
14 mmol/L* |
22 - 32 |
||
|
Urea |
2.9 mmol/L* |
3.0 - 8.0 |
||
|
Creatinine |
46 umol/L |
45 - 90 |
||
|
Glucose |
6.8 mmol/L |
3.5 - 7.8 |
||
|
Phosphate |
0.60 mmol/L* |
0.65 - 1.45 |
||
|
Maqnesium |
0.51 mmol/L* |
0.70 - 1.05 |
||
|
Calcium adjusted |
2.31 mmol/L |
2.10 - 2.60 |
||
|
Albumin |
34 q/L* |
36 - 52 |
||
|
Bilirubin total |
13 umol/L |
< 18 |
||
|
Alanine aminotransferase |
67 U/L* |
< 35 |
||
|
Asoartate transaminase |
80 U/L* |
< 40 |
||
|
Alkaline phosphatase |
148 U/L* |
30 - 110 |
||
|
y-Glutamyl transferase |
480 U/L* |
< 40 |
||
|
Lipase |
492 U/L* |
< 95 |
||
|
Amylase |
189 U/L* |
< 130 |
||
|
Free T4 |
14.2 omol/L |
12.0 - 31.0 |
||
|
Thyroid stimulatinq hormone |
0.65 mU/L |
0.50 - 5.00 |
||
|
Cortisol |
1440 nmol/L* |
150 - 700 |
||
|
B-Hvdroxvbutyrate |
4.4 mmol/L* |
< 0.4 |
||
|
Osmolality |
254 mOsm/L* |
275 - 295 |
||
|
Urine Chemistrv |
||||
|
Sodium |
< 20 mmol/L |
|||
|
Potassium |
37 mmol/L |
|||
|
Osmolality |
198 mOsm/L |
|||
a) Give the likely diagnosis with the rationale for your decision. (25% marks)
b) Briefly outline your management of the hyponatraemia in this patient. (20% marks)
a) Beer potomania (alcoholic intoxication / ketoacidosis acceptable)
History
Abnormal LFTs with predominantly raised GGT
Acidosis with elevated BOHB with normal glucose Low urine osmolality
Normal endocrine profile
b) Likely chronic hyponatraemia so replace slowly < 10 mmol/24 hrs Stop non-essential fluids
At risk of seizures from alcohol withdrawal
Let us analyse the results in some detail.
This guy is a drinker, and his GGT is elevated, so... he has been drinking.
After a few days of decreased level of consciousness he is not dehydrated, so ... he has been drinking a lot.
The bloods demonstrate hypoosmolar hyponatremia with a low usine osmolality and a low urine sodium. There are only a few conditions which can give rise to this:
Beer potomania is a case of dietary solute deficiency. Your water intake is excessive, but you eat virtually nothing containing salt. Lets say you are a degenerate beer-fiend, and your total nutritional intake consists of carbohydrate-rich, sodium-poor beer. Vast volumes are happily ingested. The carbohydrate from the beer is metabolised preferentially, leading to a suppression of protein catabolism. Low protein catabolism results in low urea levels, and with the sodium dropping, what solute can you excrete? None. The volume of urine drops. Each day you will excrete as little as 4 litres of maximally dilute urine. Obviously if you drink more than 4 litres of beer a day, hyponatremia will ensue. This phenomenon is not limited to American college students; ovolactovegetarians and people trying to lose weight too fast are also susceptible.
Hariprasad MK, Eisinger RP, Nadler IM, Padmanabhan CS, Nidus BD. Hyponatremia in psychogenic polydipsia. Arch Intern Med. 1980 Dec;140(12):1639-42.
Hilden T, Svendsen TL. Electrolyte disturbances in beer drinkers. A specific "hypo-osmolality syndrome". Lancet. 1975 Aug 9;2(7928):245-6.
Thaler SM, Teitelbaum I, Berl T. "Beer potomania" in non-beer drinkers: effect of low dietary solute intake. Am J Kidney Dis. 1998 Jun;31(6):1028-31.
Fox BD.Crash diet potomania. Lancet. 2002 Mar 16;359(9310):942.