Definition: deep inflammation tending to abscess. Causes: invasion by pus microbes, infectious diseases, parasitism, traumas. Symptoms: hyperthermia, colic, tenderness, icterus, coincident disease, hæmatemesis. Lesions: submucous or subperitoneal abscess, parasites, peritonitis, exudation, thickening, neoplasm of mucosa, catarrhal complications. Treatment: careful diet, antiseptics, bitters, laxatives.
Definition. This is a gastric inflammation affecting the membranous layers, and tending to submucous or subperitoneal abscess. It is much less frequent than the catarrhal form.
Causes. It may be attributed to invasion of the gastric walls by pus microbes, and appears as secondary abscess in pyæmia and above all in strangles. The microbes are introduced more directly through the wounds inflicted by the larvæ of œstrus, or by the burrowing of these (Argus, Schlieppe, Schortmann), or of spiroptera (Argus). Wounds by sharp pointed bodies taken in with the food, furnish other infection—atria, and in their turn ulcers connected with catarrhal or toxic inflammation may furnish a means of entrance.
Symptoms. These resemble those of catarrhal inflammation, but are usually attended by greater hyperthermia, and the colicy symptoms are more marked. There is also greater tenderness in the epigastrium and left hypochondrium, and icterus is more marked. When it occurs as an extension of strangles or pyæmia the symptoms of these affections elsewhere are pathognomonic. When the abscess bursts into the stomach there may be vomiting of bloody mucus (hæmatemesis) which is not necessarily followed by a fatal result.
Lesions. As these are seen only in fatal cases, the presence of an abscess is the characteristic feature. This is usually submucous, or less frequently subperitoneal, and may vary in size from a hazelnut upward. The tendency appears to be to open into the stomach, though it may burst into the peritoneum and cause general infection of that membrane. In case of parasites, the spiroptera or œstrus larva may be found in the abcess cavity having a narrow opening into the stomach. In certain cases the abscess on the pyloric sac has been found opening into the duodenum. Congestion, thickening, puckering into rugæ and laceration of the adjacent mucosæ may be a marked feature, a circumscribed catarrhal gastritis complicating the local phlegmon.
Treatment. This is less hopeful than in catarrhal gastritis, but should be conducted along the same lines. The same careful diet, with daily antiseptics and bitters may prove valuable in limiting the inevitable suppuration, and, if the pus should escape into the stomach, in healing the lesion. Sulphites of soda, sulphide of calcium, chamomile, and quinia, are to be commended and pepsin may be added to secure at once proteid digestion and antisepsis. Laxatives may be required to counteract constipation or expel irritants, and these may be combined with the antiseptics already named or with salol, eucalyptol, sodium salicylate or other non-poisonous agent of this class.
TOXIC GASTRITIS IN SOLIPEDS.
Causes: caustics or irritants acting on mucosa, accidently, or maliciously. Symptoms: colics, pinched face, small rapid pulse, hurried breathing, hyperthermia, sometimes salivation, color of buccal mucosa, odor, congestion of tongue, thirst, urination, icterus, albuminuria, analysis of urine or vomited matter. Lesions: congestion, corrosion, necrosis or ulceration of gastric mucosa, discoloration. Treatment: antidote, stomach pump, demulcents, coagulants.
Causes. Toxic gastritis in solipeds is peculiar in this that it must be due to one or other of the more caustic or irritant agents, which act chemically on the tissues, while those agents that require to be absorbed to establish a physiological irritation are comparatively harmless. This depends on the fact that few or none of the poisonous agents are absorbed by the gastric mucosa of the soliped, and if ingested they must pass on into the duodenum before they can be absorbed into the tissues and blood-vessels. Hence the horse is injured mainly by actual caustics like mercuric chloride, zinc chloride, ferric or cupric sulphate, the caustic alkalies or earths, or alkaline carbonates, and the mineral acids. These may be taken accidently or administered maliciously, or as medicines.
Symptoms. Morbid symptoms vary according to the agent swallowed. There are colics, anxious countenance, small accelerated pulse, rapid breathing, hyperthermia, and salivation, especially marked with mercuric chloride. The buccal mucosa may give valuable indications, becoming white with muriatic acid, or zinc, or antimony, or mercuric chloride, yellow with nitric acid, and white changing to black with sulphuric acid or silver nitrate. Ferric or cupric sulphate may give their respective colors to the saliva, and the former will darken the fæces.