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|Example of Acute Exposure data from MEDITEXT.|
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Example Content from MEDITEXT for Potassium carbonate:
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ACUTE EXPOSURE INFORMATION
- USES: Potassium carbonate is used in manufacturing soap, glass, and pottery; in process engraving and lithography; tanning and finishing leather; liquid shampoos; for removal of water from organic liquids; in analytical chemistry; and as a general-purpose food additive.
- PHARMACOLOGY: As an alkaline corrosive, potassium carbonate may cause liquefaction necrosis. It can saponify the fats in the cell membrane, destroying the cell and allowing deep penetration into mucosal tissue. In gastrointestinal tissue, an initial inflammatory phase may be followed by tissue necrosis (sometimes resulting in perforation), then granulation and finally stricture formation.
- EPIDEMIOLOGY: Exposure is unusual; potassium carbonate is generally available for industrial use only.
- WITH POISONING/EXPOSURE
- Limited data regarding specific human toxicity following potassium carbonate exposure is available. The following effects could be expected to occur, based on exposure data of other alkaline corrosives.
- MILD TO MODERATE ORAL TOXICITY: Patients with mild ingestions may only develop irritation or grade I (superficial hyperemia and edema) burns of the oropharynx, esophagus or stomach; acute or chronic complications are unlikely. Patients with moderate toxicity may develop grade II burns (superficial blisters, erosions and ulcerations) and are at risk for subsequent stricture formation, particularly esophageal. Some patients (particularly young children) may develop upper airway edema.
- Alkaline corrosive ingestion may produce burns to the oropharynx, upper airway, esophagus and occasionally stomach. Spontaneous vomiting may occur. The absence of visible oral burns does NOT reliably exclude the presence of esophageal burns. The presence of stridor, vomiting, drooling, and abdominal pain are associated with serious esophageal injury in most cases.
- PREDICTIVE: The grade of mucosal injury at endoscopy is the strongest predictive factor for the occurrence of systemic and GI complications and mortality.
- SEVERE ORAL TOXICITY: May develop deep burns and necrosis of the gastrointestinal mucosa. Complications often include perforation (esophageal, gastric, rarely duodenal), fistula formation (tracheoesophageal, aortoesophageal), and gastrointestinal bleeding. Upper airway edema is common and often life threatening. Hypotension, tachycardia, tachypnea and, rarely, fever may develop. Stricture formation (esophageal, less often oral or gastric) is likely to develop long term. Esophageal carcinoma is another long term complication. Severe toxicity is generally limited to deliberate ingestions in adults in the US, because alkaline products available in the home are generally of low concentration.
- INHALATION EXPOSURE: Mild exposure may cause cough and bronchospasm. Severe inhalation may cause upper airway edema and burns, stridor, and rarely acute lung injury.
- OCULAR EXPOSURE: Ocular exposure can produce severe conjunctival irritation and chemosis, corneal epithelial defects, limbal ischemia, permanent visual loss and in severe cases perforation.
- DERMAL EXPOSURE: Mild exposure causes irritation and partial thickness burns. Prolonged exposure or high concentration products can cause full thickness burns.
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