Acid-Base Physiology

Case 19 : A young man who ingested barium carbonate


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 report from Schorn et al (1991)

Arterial Blood Gases

pH 7.23

pCO2 34 mmHg

pO2 69 mmHg

HCO3 12.1 mmol/l


First: Initial clinical assessment

The high lactate indicates a lactic acidosis though there is no evidence of shock. A respiratory acidosis due to respiratory muscle failure and hypoventilation is a likely disorder in this settimng. The diarrhoea is unlikely to have caused a hyperchloraemic metabolic acidosis due the short duration.

Second: The acid-base diagnosis

Proceeding systematically:

  1. pH: The acidaemia indicates an acidosis is present.
  2. Pattern: The combination of a low bicarbonate and 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) indicating a high anion gap metabolic acidosis. The high lactate levels confirms a lactic acidosis. There is no evidence of another high anion gap disorder. The glucose is low. The Delta ratio is 2 (ie 36-12/24-12) and not helpful here.
  4. Compensation: The expected arterial pCO2 at maximal compensation is 26 mmHg (ie 1.5 x 12 + 8).
  5. Formulation: An acute high anion gap metabolic acidosis which is minimally compensated due to the short time since ingestion. A respiratory acidosis due to ventilatory failure associated with the muscle weakness was considered likely but there was no blood-gas evidence of this. Respiratory muscle weakness will make it difficult for increased ventilation (compensation) to occur over the following hours so the result may be a respiratory acidosis. The delta ratio of 2 is higher then the average value found in lactic acidosis (1.6) but not remarkably so. This delta ratio 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), but the brief duration and presumed previous good health in a young person does not provide any support for this additional diagnosis. There is also no support for a hyperchloraemic acidosis due to diarrhoea.
  6. Confirmation: No further compensation of the acid-base disorder is required. Urinalysis to exclude ketouria is simple to perform and should be done.

Finally: the Clinical Diagnosis

Acute self-inflicted poisoning with barium carbonate resulting in muscle paralysis (due to hypokalaemia) and acute lactic acidosis. The cause of this lactic acidosis is not clear. There is no evidence of circulatory failure.

Reported treatments include gastric lavage (only if soon after ingestion), instillation of magnesium sulphate (to precipitate the barium in the bowel), a KCl infusion at 25 mmol/hr via a central line (to correct the hypokalaemia), sodium bicarbonate (see comment below) and 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. Administration of NaHCO3 may worsen hypokalaemia and precipitate arrhythmias. This probable contribution of the NaHCO3 infusion to a worsening of the hypokalaemia and the subsequent life-threatening arrhythmias was not commented upon in this published 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.

Barium suphate is an insoluble salt of barium which is widely used as a radiological contrast and people think that "barium" is safe to use. Of course barium sulphate is an insoluble barium salt and is safe to use. However all soluble barium salts are extremely toxic.

A 2012 case report of barium toxicity due to barium sulphide discusses treatment options. Barium carbonate can be added to, or mistaken for, flour and accidentally ingested. In one report in 2009, 12 of 27 people died.

Further Reading

  1. Bradberry S and 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