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Barium carbonate intoxication: an electrophysiological study
  1. A KAKAR,
  2. I ANAND,
  1. Department of Neurology, Sir Ganga Ram Hospital, Rajinder Nagar, New Delhi 60, India
  1. Dr Atul Kakar, 31 South Patel Nagar, New Delhi 110008, India.

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Barium carbonate is an uncommon poisoning agent in India. This whitish coloured powder is available over the shelf from the chemists and is used mainly as a rodenticide (rat poison). We report an unusual case of barium carbonate poisoning. The nerve and muscle electrophysiological studies are reported for the first time in barium carbonate intoxication.

A 19 year old boy presented to a hospital emergency department with sudden onset tetraplegia. He was referred to our centre as a case of Guillian-Barré syndrome. The patient presented with tingling in the right upper arm, which was immediately followed by weakness in all four limbs. The weakness progressed and involved trunk muscles also within a few minutes. There was no history suggestive of bulbar or facial nerve involvement.

On examination, higher mental functions, cranial nerves, and sensory and cerebellar examination were normal. Examination of the motor system showed a power of 0/5 globally. No deep tendon reflex could be elicited. Surprisingly, with complete areflexic paralysis there was increased tone in the lower limbs. A diagnosis of Guillian-Barré syndrome was considered, but there were some pointers against this diagnosis. The onset and progression to complete tetraplegia was very rapid and the weakness started from the upper limbs followed by that of the lower limbs. Increased tone in the lower limbs was also not consistent with the diagnosis of Guillian-Barré syndrome.

Routine blood investigations at the time of admission, including serum electrolytes, were normal. Nerve conduction study showed normal distal latency of the compound muscle action potential and motor nerve conduction. Amplitude of the compound muscle action potential was low on proximal and distal stimulation. No conduction block, dispersion of compound muscle action potential, or F wave response was recordable. Sensory conduction studies on median and ulnar nerves at both sides of the body were normal for distal latency and amplitude of sensory nerve action potential. No H reflex was recordable on stimulation of posterior tibial nerves on both sides. The patient now disclosed that he had accidentally consumed barium carbonate (15 g) on the day before admission. He ingested barium salt by mistaking it for dieting food given to him by a slimming centre. Ingestion was followed immediately by profuse vomiting. One hour later, the patient had watery diarrhoea. Four hours later he was taken to hospital where his stomach was washed out with magnesium sulphate solution. Blood investigations repeated 8 hours after admission showed normal blood counts, blood gas analysis, and renal and liver function tests. Serum potassium was 2.8 m mol/l and sodium was 140 mmol/l. An ECG showed prominent U waves. Based on available history and investigations, a diagnosis of barium carbonate induced hypokalemic periodic paralysis was considered. The patient was moved to the intensive care unit and monitored for arrhythmias. He was started on intravenous potassium. On day 2, the patient had completely recovered clinically (power 5/5). Serum potassium was normal. Nerve conduction studies were performed as on day 1 with similar results except that the amplitude of compound muscle action potentials were in the normal range. The F waves and H-reflexes were still unrecordable. Electromyography was carried out with concentric needles in the biceps, deltoid, and quadriceps. It showed no abnormal insertional or spontaneous activity and motor unit action potentials were normal in amplitude and duration. The recruitment pattern was reduced. Visual evoked potential, EEG, and brain stem evoked potential were all normal. Nerve conduction velocity and EMG were repeated on day 7 and were normal in all aspects.

Most patients with barium intoxication have gastrointestinal and cardiac involvement with tetraplegia. Barium carbonate is a rare cause of hypokalaemic periodic paralysis.1 Diarrhoea and arrhythmias are due to direct stimulatory action of barium ions on smooth and cardiac muscles.2 Heart failure and hypertension may occur in a few cases. Barium blocks the potassium channels and thus potassium efflux from the muscle is reduced whereas the sodium-potassium pump is intact. This causes increased potassium in the muscle and decreased resting membrane potential.3Barium acts mainly at the neuromuscular junction by this mechanism.4 The fatal dose of barium carbonate is 0.8 g and death occurs within 2–12 hours.4

There is only one report of an EMG study done in four patients with paralysis because of barium carbonate poisoning. It was done within 1 week of admission and did not show any abnormality.4 In our case nerve conduction velocity studies and EMG were done on the first day and were sequentially repeated. Interpreting the nerve conduction velocity studies of day 1—namely, low amplitude of compound muscle action potentials— would indicate axonal neuropathy but similar findings can be found in profound muscle weakness because of neuromuscular junction blockade or myopathy. Loss of F waves and H reflexes on day 1 can be explained by the presence of lower amplitudes of compound muscle action potentials on distal nerve stimulation. Loss of F waves and H reflexes with normal distal nerve conduction velocity is suggestive of proximal demyelination or dysfunction at the spinal cord level. Loss of H reflexes and the F response has not been reported previously in patients with hypokalaemic periodic paralysis. As H reflex latency depends on several factors including the central delay in the cord involving conduction, synaptic transmission, and activation of anterior horn cells, any of these processes might be involved in barium carbonate poisoning. The exact mechanism for their absence is still unclear. These responses reverted back to normal on day 7. The concentric needle EMG study on the second day showed a reduced recruitment pattern which is found in neuropathies but has also been reported in hypokalaemic periodic paralysis.5

In most cases of barium ingestion the recovery from weakness occurs rapidly and uneventfully.4 Oral magnesium sulphate or sodium sulphate precipitate barium in the gut and thus reduce absorption. Large amounts of intravenous potassium are needed to restore the pump electrogenesis and to displace barium from potassium channels.1 Hypertension caused by barium cannot be reversed by this treatment. Haemodialysis is a useful therapeutic adjuvant in severe barium carbonate poisoning. Ventilatory support may be required due to respiratory muscle involvement.4

In summary, this is the first electrophysiological study done on day 1 in a case of barium carbonate poisoning with paralysis. Previously involvement of neuromuscular junctions has been considered as a cause for weakness. In our study, we found that barium acted at more than one level—that is, muscles, proximal segments of the reflex arc, and probably γ efferents as the tone was increased.