SMALL ANIMAL MEDICINE
Peripheral Neuropathy and Aspiration Pneumonia
Liesel L van der Merwe, BVSc MMed Vet (Med) Small Animals
Senior lecturer: Outpatients
A predisposition to aspiration only occurs in patients with any neuromuscular disease which impairs unconscious
protection of the airways such as laryngeal paralysis, myasthenia gravis, polyradiculoneuritis, organophosphate
poisoning and neurotoxic snake bites .
The neuromuscular junction is a synapse connecting peripheral motor nerves to skeletal/striated muscle fibres.
The neurotransmitter is acetylcholine (ACh) and the ACh receptors on the muscle membrane are nicotinic.
Calcium is required for effective neurotransmission. ACh esterase is also required to remove and recycle the
ACh from the receptor to prevent overstimulation.
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Botulsim is a disruption with the release of ACh vesicles, myaesthenia gravis or MG-like syndrome is from
antigens to the post- synaptic receptors which blocks them, and weakness and paralysis in organophosphate
poisoning occurs due to overstimulation and down-regulation of nicotinic ACh receptors due to toxin
binding to cholinesterase.
Interference with any aspect of impulse transmission across this synapse leads to weakness with several
possible clinical manifestations:
Acute flaccid tetraparesis: botulism, neurotoxic snake envenomation, fulminant myaesthenia gravis, and tick
paralysis. These cases present with weakness and hypotonia, reduced or absent segmental spinal reflexes
and muscle atrophy. Cranial nerve deficits may also present as dysphonia, dysphagia inspiratory stridor,
megaoesophagus and reduced or absent gag and palpebral reflexes. Acute polyradiculoneuritis is a major
differentia diagnosis. Voluntary tail movement and anal tone are often preserved despite the absence of
voluntary movement anywhere else in the body.
Episodic weakness exacerbated by activity: Myaesthenia gravis. Also consider metabolic disease (hypothyroidism,
addisons disease), cardiac disease, polyneuropathies and myopathies.
Megaoesophagus
With idiopathic/congenital megaoesophagus a defect in the afferent neural pathway responsive to oesophageal
distension is suspected as the underlying cause. Acquired secondary megaoesophagus may result from many
diseases affecting the neuromuscular function.
In the dog the upper oesophageal sphincter (cricopharyngeus muscles) and the entire body of the oesophagus
is made up of striated muscle and the lower oesophageal sphincter is smooth muscle. In the cat the last third
of the oesophagus is smooth muscle.
Idiopathic megaoesophagus is easily visualised radiographically as the oesophageal dilation is severe and
obvious. With acquired oesophageal dysfunction there is often very little, to no oesophageal distension visible
radiographically. However these are the patients that are MOST prone to aspiration pneumonia. The reason for
this is that all the small muscles controlling laryngeal and pharyngeal function are striated, thus they will be
affected by anything affecting the neuromuscular junction.
Often not obviously dysphagic, these dogs can aspirate if force fed or allowed to eat ad lib as the muscles tire
easily and their function can become choppy and asynchronous.
I advise withholding food until you are sure the patient can eat/swallow properly using water as a test medium.
In cases with neurotoxic snakebite paralysis I withhold food for the day or two required for recovery. In cases
poisoned with organophosphates be very sure that there is no problem with swallowing before treating with
activated charcoal. If there is any doubt – place a naso-oesophageal tube. Additionally, don’t use large volumes
of fluid/food laced with activated charcoal as the upper oesophageal sphincter function is compromised and
reflux may occur.
Source: Textbook of Veterinary Internal Medicine, 7 th ed. Stephen J. Ettinger, Edward C. Feldman
Issue 05 | NOVEMBER 2018 | 21