Clinical Details
A 22 year old man was admitted to hospital 1.5 hours after ingestion of about 10G of barium carbonate dissolved in hydrochloric acid. Symptoms included abdominal pain, generalised areflexic muscle paralysis, increased salivation and diarrhoea. BP 180/110. Pulse 92/min.

Initial biochemistry (in mmol/l) was: Na⁺ 140, K⁺ 2.1, Cl 92, glucose 2.2 and plasma lactate 10.2.
[This case reported by Schorn et al (1991).]

Assessment
Firstly, initial clinical assessment (on the first gas results):
The clinical suspicions are:

• Lactic acidosis (high lactate levels)

• Respiratory acidosis due to respiratory muscle failure (muscle paralysis)

• Hyperchloraemic metabolic acidosis due to diarrhoea (but considered very unlikely in view of the short duration)

Secondly, the acid-base diagnosis:  
1. pH:  An acidaemia indicates the presence of an acidosis
2. Pattern:  The combination of a low bicarbonate & a low pCO2 indicates either a metabolic acidosis or a respiratory alkalosis. In this case with a known acidosis, a metabolic acidosis must be present.
3. Clues:  The anion gap is 36 (ie 140 - 92 - 12) which indicates the presence of a hign anion gap metabolic acidosis. The high lactate levels confirms a lactic acidosis. There is no evidence presented of another high anion gap disorder. The glucose is low. The Delta ratio is 2 (ie 36-12/24-12).
4. Compensation:  The expected paCO2 at maximal compensation is 26 mmHg (ie 1.5 x 12 + 8). Only a short time has passed since the ingestion and this is insufficient time for the maximal amount of compensation to have been reached so our analysis cannot use this prediction of what would be expected at maximal compensation other than as a lower bound.
5. Formulation: The acid-base diagnosis is an acute lactic acidosis with partial respiratory compensation. Respiratory compensation is not yet maximal because of the short time since ingestion. 

A respiratory acidosis due to ventilatory failure associated with the muscle weakness was considered a clinical possibility but there was no blood-gas evidence of this. 

 The delta ratio of 2 is higher then the average value found in lactic acidosis (1.6) but not remarkably so. A ratio this high suggests we should consider the possibility of a pre-existing high bicarbonate level (due to metabolic alkalosis or in compensation for a chronic respiratory acidosis). The brief duration and presumed previous good health in a young person do not provide any support for this additional diagnosis. There is also no support for a hyperkalaemia acidosis due to diarrhoea which fits with the clinical expectation given the very short duration between ingestion and presentation.

It is noted that the anion gap is the difference between unmeasured anions and unmeasured cations. The [K⁺ ] has decreased from its normal range and this accounts for a small amount of the rise in anion gap.

6. Confirmation: No further confirmation of the acid-base diagnosis is required.

Finally, the Clinical Diagnosis:
Acute self-inflicted poisoning with barium carbonate resulting in muscle paralysis (due to hypokalaemia) and acute lactic acidosis. The immediate cause of the lactic acidosis is not clear as their is not evidence of circulatory failure.

Comment
Reported treatment included:

• gastric lavage

• instillation of magnesium sulphate (to precipitate the barium in the bowel)

• KCl infusion at 25 mmol/hr via a central line (to correct the hypokalaemia)

• sodium bicarbonate (see comment below)

• haemodialysis.

The patient developed ventricular tachycardia after the sodium bicarbonate. The arrhythmia resolved but respiratory failure required intubation soon after. Ventricular fibrillation occurred during intubation and required 30 minutes of resuscitation before a stable rhythm was achieved. 

The K⁺ just before resuscitation was 1.5 mmol/l. Bicarbonate may worsen hypokalaemia and precipitate arrhythmias. The probable contribution of the NaHCO3 infusion to a worsening of the hypokalaemia and the subsequent life-threatening arrhythmias was not commented upon in the case report.

The hypokalaemia on presentation was due to the barium. Barium causes a large transfer of K⁺ from the ECF to the ICF in muscle cells due to a marked reduction in passive permeability of the membrane to K⁺ (minimising K⁺ loss from the cell) without initially affecting the Na⁺-K⁺ ATPase (allowing continued uptake of K⁺ by the cell). In this patient, barium levels fell rapidly with haemodialysis. This patient survived. 
[A recent article from New Zealand reports a case of barium intoxication & discusses the usefulness of early haemodialysis.]

References
1. Bradberry S & Vale J. Disturbances of potassium homeostasis in poisoning. J Toxicol Clin Toxicol 1995;33(4):295-310
2. Schorn T et al.  Barium Carbonate Intoxication. Intensive Care Med. 1991;17:60-62.
3. Thomas M et al. Acute barium intoxication following ingestion of ceramic glaze.  R.Postgrad Med J 1998 Sep;74:545-6

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