Page 91 - Edited - Webster HEAD AND NECK - part 2-Merge PDF

HN 284
i) press on the patient's cricoid cartilage (what do you mean, "What's that?", "Don't know how to find it", etc. etc.?) to compress the
upper oesophagus between the cartilage and the body of the sixth cervical vertebra and prevent the vomit entering the
hypopharynx (HN 287);
ii) keep your finger in place and immediately roll the patient onto his/her side, mouth as low as possible and remove your finger;

iii) shout "Help!". (If you have thoughtlessly rolled the patient towards you, watch out for your shoes.)

This is simple “antiperistaltic” vomiting - it is seen in the unconscious, and in unweaned infants with over-full stomachs (greedy
little pigs they are, most of them). However, vomiting also usually involves the abdomino-thoracic "squeeze" or “pump” mechanism which
means there must be spread of neural activity to the spinal cord (SI 21,86). This empties the stomach very rapidly and when the “squeeze”
is powerful, vomit may be flung forcefully from the mouth (“projectile vomiting”). Such vomiting may even be so violent as to rupture the
oesophagus, especially if opening of the crico-pharyngeal (upper) sphincter (HN 280; 285) is ill-coordinated. Continued rhythmical
contraction of the abdominal wall accompanied by operation of the pharyngo-laryngeal mechanism when the stomach is empty is known as
“retching”.

The triggers for vomiting are various. Poking the oropharynx has already been mentioned ("gagging"). Foul tastes are another
possibility (Vllth and IXth nerves to solitary nucleus - the synaptic interactions of the solitary nucleus must be different from those involved
in coughing: although opiate drugs act as antitussives, they promote vomiting.). Pathology of the stomach (e.g. inflammation or gastritis -
signalled to the brain by Xth nerve and sympathetic system but probably directly affecting the enteric plexus, too) is another. Abnormal
blood chemistry is also a trigger, as, for example, a marked and sudden acidosis caused by exercise (trackside vomiting is not unknown at
schools' athletics contests!). This is presumably signalled by the carotid and aortic arch bodies, but, like other metabolic disorders, perhaps
influences the vomiting pattern generator directly through a chemoreceptive part of the medulla, where the blood-brain barrier is defective
(c.f. control of respiration SI 82). There is also some evidence for the involvement of the gut APUD system in the genesis of vomiting. Some
causes seem quite bizarre and are due to either influence from the cerebrum (e.g. extreme anxiety, fear, intense pain - especially of sudden
6
onset; unpleasant sights and smells) or apparently unrelated parts of the brainstem (the vestibular nuclei in motion sickness ).
The metabolic consequences of prolonged vomiting are dealt with in the Gut/Renal handout (Sll 198).

K.E.W.

6 Note: The word "nausea" comes, via Latin, from the Greek word for "ship" (naus), cf. "nautical". A notable sufferer from sea-sickness was Horatio, Admiral Lord Nelson -
a spectacularly successful sailor who, in spite of this seemingly unlikely problem, worked his way up through the ranks and never took a "Whitehall desk job". (If
you don't know what Trafalgar Square commemorates ... ). Today, he would have been told he was "gastro-motionally challenged" and sent for counselling. Like
"nausea", "vomit" has a classical etymology (as does "emesis" - hence "emetic drugs", i.e. substances promoting vomiting). "Sick", "spew'' and "puke" are all plain
Anglo-Teuton.
\NewCMedPhysSc\20 HN SwallowVomit.