Treatment. As the direct application of medicines to the inflamed mucous membrane can only be of a momentary character, treatment is confined to administering emollient, anodyne, and slightly astringent drinks, the action of which is assisted by feeding with milk, farinaceous or mucilaginous foods. Under these circumstances recovery occurs in ten to fifteen days. The application of stimulant or blistering ointments along the jugular furrow may have a good effect.
When the general condition of the patient becomes aggravated, and the formation of an abscess appears certain, it is best to recommend slaughter. In the case of a submucous abscess the passage of the probang may, however, predispose or cause the abscess to open into the œsophagus, and thus lead rapidly to recovery, but this is exceptional. The “pointing” of the abscess and its opening towards the jugular furrow may be followed by temporary improvement, but at a later stage is followed by fistula formation, or by contraction of the œsophagus itself. From an economic standpoint it is better to slaughter.
STRICTURE OF THE ŒSOPHAGUS.
Under normal conditions the cavity or lumen of the œsophageal tube is, so to speak, imaginary: the walls of the tube lie flatly together, and the mucous membrane is in folds. During the act of swallowing the tube becomes dilated to a degree varying with the size of the bolus of food, and again retracts as soon as deglutition is effected. Whenever the dilatability of the tube is markedly diminished by changes in its walls, and, in a much higher degree, when this dilatability has disappeared, true stricture exists. In the former case small boluses of food and liquids alone succeed in passing the stricture; in the latter, liquids alone can pass.
Causation. Strictures are never primary. They result from intense attacks of œsophagitis, ending in sclerosis of the mucous coat, extensive ulceration consequent on scalding, or interstitial inflammation affecting the muscular coats, which then become thickened or sclerosed.
Internal injuries due to attempts to withdraw or propel foreign bodies along the œsophagus may also cause strictures.
Lesions. In simple strictures the lesions are confined to the development in the depths of the mucous membrane and in the muscular layers of inflammatory tissue, which becomes denser with lapse of time. This alters the character of the walls and the structure of the tissues, and causes them to lose their elasticity. After extensive ulceration the tissue of the cicatrix contracts and hardens to a very varying degree.
Symptoms. The apparent symptoms are very clearly marked; the appetite is good, and the animal masticates as usual, but in the act of deglutition is seen to extend the head on the neck, and to make efforts to swallow, which prove unavailing when the contraction is too marked. A reflex antiperistaltic movement often causes the substances ingested to be at once rejected. These violent efforts, however, in time provoke dilatation above the stricture. A quantity of food accumulates in this dilatation, and the symptom so characteristic of œsophageal stricture then appears—viz., regular regurgitation. The second constant symptom associated with compression or obstruction of the œsophagus is tympanites after feeding, however trifling may be the amount swallowed. Rumination is suspended, and even eructation of gas is difficult. Finally, the characteristic sign of stricture is noted on passing the probang, which reveals the existence of the condition, indicates its position, and suggests its degree of development.
Fig. 65.—Schema of recent and old-standing contraction of the œsophagus. R, simple contraction; D, secondary dilatation.