1294

MALLORY WEISS THROUGH THE ENDOSCOPE

VOMITING is a natural reflex in man and many othermammals though it is absent in a few, such as the rat.It requires us to put normal physiology into reversegear-something that the wisdom of the body finds diffi-cult. What is involved is an integration of glottic closureto protect the lungs; contraction of the abdominalmusculature to increase intra-abdominal pressure; andrelaxation of the oesophagogastric muscular complexwhich is called the lower oesophageal sphincter. Failureof coordination may result in inhalation of vomit (parti-cularly common in heavy drinkers, in whom it is a majorcause of lung abscess); oesophageal rupture (the syn-drome first described by Boerhaave and one whichseems, because of its association with indulgence and theRoman habit of auto-emesis, to have captured the medi-cal imagination); and, with a lesser degree of the sameproblem, a serosal-submucosal tear with disruption ofmajor intramural blood-vessels and massive gastrointes-tinal bleeding. The last was described by Mallory andWeiss in 19191 on necropsy evidence and until lately wasregarded as a rarity.The introduction of fiberoptic endoscopy has radically

altered this view. When barium contrast studies were the

only court of appeal, much gastrointestinal bleeding wasput down to alcoholic or acute gastritis. Now, the abilityto see the oesophagus, stomach, and duodenum hasbrought Mallory Weiss syndrome into much greater nu-merical prominence and has partly removed it from theclinical context of the original workers’ description of along and intense alcoholic debauch.2,3 True, we are like-ly to see the lesion more frequently in those who over-indulge, and, because memory is ablated by alcohol, ahistory of retching and vomiting cannot always beobtained. However, these social stigmas apart, aesophago-gastric tearing short of rupture is now third commonestcause of hxmatemesis and/or melaena in some communi-ties. However, the clinical diagnostic rate remains low.4Two recent communications emphasised these points. Itmay not be fortuitous that both come from communitieswith a reputation for bouts of heavy drinking. At GrooteSchuur in Cape Town, South Africa,4 Clain and others4have found that about 8% of patients admitted withgastrointestinal hxmorrhage have Mallory Weiss syn-drome and that there is an association with alcohol in-

gestion and retching; and at the Queen Elizabeth Hospi-tal in Adelaide, South Australia,5 the incidence is almostidentical though the frequency of alcohol consumptionand of vomiting and retching is higher. Common to bothgroups, and in contradistinction to the experience ofothers,3 was the fact that surgery was almost neverneeded to control the bleeding. Doubtless the certaintyof diagnosis made the clinicians more confident aboutnon-operative management.Two general conclusions can be drawn. Firstly, Mal-

lory Weiss syndrome should be in the mind of all wholook after patients with gastrointestinal bleeding-

1. Mallory, G. K., Weiss, S. Am. J. med. Sci. 1929, 178, 506.2. Cotton, P. B., Rosenberg, M. T., Waldram, R. P. L., Axon, A. R. T. Br med.

J. 1973, ii, 505.3. St. John, D. J. B., Masterton, J. P., Yeomans, N. D., Dudley, H. A. F. ibid.

1974, i, 140.4. Clain, J. E., Novis, B. H., Barbezat, G. O., Bank, S. S. Afr. med. J. 1978,

53, 596.5. Kerlin, P., Bassett, D., Kerr Grant, A., Paull, A. Med. J. Aust. 1978, i, 471.

hxmatemesis in particular, but also melaena withouth2ematemesis .4 A story of vomiting or retching shouldput the endoscopist on the alert. Secondly, if the diag-nosis is established-and it must be remembered thatother lesions are often present in the group of patientswho have Mallory Weiss syndrome-initial conservativemanagement is very much in order. A small placeremains for transgastric underrunning of a tear. The in-dications are the same as for any other cause of gastro-intestinal bleeding: failure to keep the patient stable andevidence of continuing important blood-loss.

ACUTE EPIGLOTTITIS

ACUTE epiglottitis is often mistaken for laryngo-tracheobronchitis, but its pathology and clinical courseare quite different. It arises mainly in children aged 2-7years,’ and they may be dead within a few hours.Because the mucous membrane is firmly attached to thevocal cords, inflammation above this point tracks

rapidly upwards and is accommodated in the loose sub-mucosa of the epiglottis, aryepiglottic folds, and hypo-pharynx.2 The result is a red and swollen ring round thelaryngeal inlet, obstructing respiration and swallowing.Septicxmia is invariably present, the usual organismbeing Haemophilus influenzae type b. Hence the clinicalpicture of a toxic child, with a fulminating history ofdysphagia and respiratory distress, and a thick muffledvoice, drooling saliva. Complete respiratory obstructionmay rapidly supervene.

All the management protocols3-5 agree that the doctormust remain with the patient all the time until the air-way is secure. Few conditions demand expert hospitalcare more urgently. As a first-aid measure, the child maybe sat up leaning slightly forward with his chin thrustout: this is the posture adopted by older children, andhelps to relieve the obstruction. Humidification mayproduce dramatic benefit. Addy et al. advise immediateadministration of intramuscular ampicillin by the familydoctor, although this may upset the child and make theobstruction worse. In an emergency, mouth-to-mouth

respiration may be effective, even if obstruction seemscomplete. No attempt should be made to examine thepharynx with a tongue depressor, which may precipitatecomplete obstruction. Once in the emergency room, thechild with severe obstruction should immediately be in-tubated under general anaesthesia, by an expert anaathe-tist with full back-up. The epiglottis, swollen and

usually (though not always) red, is seen at the same

time, confirming the diagnosis. Blanc et al. favour inha-lational induction and recommend avoidance of keta-

mine, since the associated restlessness during recoveryincreases the risk of accidental extubation. Muscle relax-ants are not needed.3,6

If the child is not in immediate danger, the diagnosiscan be made from posteroanterior and lateral soft-tissueX-rays of the neck.7 If supraglottic swelling is then

visible, many clinicians advocate prophylactic insertion

1. Addy, M. G., Ellis, P. D. M., Turk, D. C. Br. med. J. 1972, i, 40.2. Morus Jones, H. Practitioner, 1975, 215, 732.3. Oh, T. H., Motoyama, E. K. Anesthesiology, 1977, 46, 214.4. Blanc, V. F., et al. Can. anœsth. Soc. J. 1977, 24, 1.5. Johnson, G. K., Sullivan, J. L., Bishop, L. A. Archs Otolar. 1974, 100, 3336. Heldtander, P., Lee, P. Acta Otolar. 1973, 75, 379.7. Rapkin, R. H. J Pediat. 1972, 80, 96.