Gastric perforation

The GI stimulants are contraindicated in patients witii known hypersensitivity to the drug, GI obstruction, gastric perforation or hemorrhage, or epilepsy. These drugs are secreted in breast milk and should not be used during lactation. 

Skin contact with the solid hypochlorite pentahydrate or its concentrated solution can cause irritation. Ingestion may cause corrosion of mucous membranes and gastric perforation. 

If the patient has ingested a corrosive poison, such as a strong acid or alkali (e.g., drain cleaners), emesis increases the likelihood of gastric perforation and further necrosis of the esophagus. 

Five cases of gastric perforation (rather than the more common duodenal perforation) have been reported in young male smokers of crack, all of whom had only brief histories of prodromal symptoms and none of whom had long-standing peptic ulcer disease (196). 

Reuben SS, Steinberg R. Gastric perforation associated with the use of celecoxib. Anesthesiology 1999 91(5) 1548-9. 

Copper toxicity is uncommon and is most usually due to administration of copper sulphate. solutions. Oral copper sulphate may lead to gastric perforation. Serum copper concentrations may be greatly elevated. Copper is toxic to many organs, but renal tubular damage is the major concern. Treatment is by chelation with penicillamine. 

Human Toxicity Ingestion may cause corrosion of mucous membranes, esophageal or gastric perforation, laryngeal edema. Inhalation may produce severe bronchial irritation, pulmonary edema. Prolonged skin contact may result in irritation, cf Clinical Toxicology of Commercial Products, R. E. Gosselin et at. Eds. (Williams Sc. Wilkins, Baltimore, 4th ed.. 1976) Section HI, pp 174-176. 

Recently, eertain selective COX-2 inhibitors e.g., Celecoxib, Rofecoxib, Parecoxib, and Valdecoxib have been introduced that usually possess identical efficacy to non-selective COX-inhibitors, but they are virtually sueeessful in lowering upto 50% the incidence of bleeding, obstmction, and gastric perforation efficaciously. ... 

Hypochlorites are an irritant to skin. Acnte oral toxicity is low for the calcinm salt. The oral LD50 value in rats is 850 mg/kg. Ingestion of sodinm hypochlorite may canse gastric perforation and corrosion of mncons membranes. Toxicity of metal hypochlorites is attribnted to the toxicity of the metal cations present in the salts. 

B. Other useful laboratory studies include electrolytes, glucose, methemoglo-bln level (for potassium permanganate exposure), and upright chest x-ray (for suspected gastric perforation). 

B. X-rays of the chest and abdomen will usually reveal impacted button batteries. X-rays may also demonstrate air in the mediastinum from esophageal perforation or free abdominal air from gastric perforation. 

Peptic ulcer disease is much less common in the pediatric population than in adulthood. The classification of peptic ulcers is based on the region of involvement (gastric versus duodenal ulcers) and on the presence or absence of a known etiology (primary or secondary due to an underlying disease). Primary peptic ulcers are associated with H. pylori infection. Gastric ulcers are mostly seen in neonates (with or without the development of gastric perforation) while duodenal ulcers are much more common after the neonatal period. 

Gastric perforation beyond infancy in the pediatric population is also rare. It can be seen in cases of iatrogenic trauma (tubes and catheters), after Nissen or other fundoplications in patients with distal small bowel instruction, after caustic ingestion or in patients with blunt trauma to a distended stomach. Gastric rupture can also be seen in patients with perforated peptic ulcer and dermato-... 

Ibach JR, Inouye WY (1965) Neonatal gastric perforation secondary to annular pancreas. Am J Surg 110 985-987 Itha S, Yachha SK (2006) Endoscopic outcome beyond esophageal variceal eradication in children with extrahepatic portal venous obstruction. J Ped Gastroenterol Nutr 42 196-200... 

Human health Sulfuric acid is corrosive to all body tissues. Inhalation can paralyze the respiratory system, contact with eyes may result in loss of vision, and skin contact may result in severe bums and necrosis. Swallowing may cause severe injury or death. Between one teaspoonful and half an ounce of the concentrated acid may be fatal if swallowed, and an even smaller quantity may be fatal if inhaled. Chronic exposure may cause tracheobronchitis, stomatitis, conjunctivitis, and gastritis. Gastric perforation and peritonitis may occur and may be followed by collapse of the circulatory system. Pulmonary fibrosis, bronchiectasis, and emphysema have been reported from acute exposure to fuming sulfuric acid and sulfuric acid mist. Chronic exposure usually results in erosion of the teeth, particularly the incisors. 

NSAIDs, such as aspirin, IND, ketoprofen, ibuprofen, naproxen, sulindac and flurbiprofen, are widely used in treatment of chronic inflammatory diseases. Recent studies have also shown that they have activity in retardation of colonic tumor growth [89-91]. However, oral administration of NSAIDs usually generates gastrointestinal side effects (e.g. gastric ulcers and gastric perforation) [92]. Therefore, colon-specific and controlled release of NSAIDs are important to achieve sustained pharmacologic effects and reduce the side effects. 

F arrand, R. J. (1975) Enteric-coated aspirin ovcrdosagc and gastric perforation. Brit. med. J., 4,409. 

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