Caustics and Corrosives Exam 1 Flashcards
acid burn
produce a coagulation necrosis by denaturing proteins, forming a coagulum (also known as an eschar)
alkali burn
cause liquefaction necrosis -> Fats in the tissue are saponified, and an eschar does not form
When assessing for gastric burn….
the absence of oropharyngeal burns does not reliably exclude esophageal or gastric burns
Clinical complications of chemical burns: Vital Signs
Tachypnea
Clinical complications of chemical burns: HEENT
effects range from corneal burns to opacification and blindness
Clinical complications of chemical burns: Dermatologic
Dermal toxicity ranges from irritation to full‐thickness burns
Clinical complications of chemical burns: Cardiovascular
Cardiovascular collapse is a rare complication of severe exposure
Clinical complications of chemical burns: Pulmonary
- bronchospasm, upper airway edema or obstruction, or laryngospasm
- Upper airway edema may develop abruptly after inhalation or aspiration
- In severe cases adult respiratory distress syndrome may develop
- Young children are at greater risk of severe upper airway edema after ingestion
Clinical complications of chemical burns: Gastrointestinal (with acid)
- Esophageal injury is usually maximal in the middle and lower thirds of the esophagus; gastric burns are more common
- Gastrointestinal bleeding or perforation may occur acutely after grade III (full‐thickness) injury
Clinical complications of chemical burns: Gastrointestinal (with alkali)
- Esophageal burns are most common, occurring in 5 to 35% of patients
- Exposure to concentrated alkalis may cause esophageal burns in up to 100% of patients, even after accidental ingestion
- Gastric burns are less common, and intestinal burns are unusual except after large ingestions
Clinical complications of chemical burns: Gastrointestinal (in general)
vomiting, drooling, and stridor
Clinical complications of chemical burns: Renal
Renal failure is a rare complication of severe burns, generally caused by hypotension due to shock.
Clinical complications of chemical burns: Fluids and Electrolytes
- Metabolic acidosis may develop in patients with severe GI bleeding or massive tissue necrosis after corrosive ingestion.
- Extensive gastrointestinal injury may result in massive fluid loss.
- Hyperphosphatemia has occurred secondary to phosphoric acid ingestion
Clinical complications of chemical burns: Hematologic
- Hemolysis has occurred after severe formic, acetic, or sulfuric acid exposure
- Disseminated intravascular coagulation (DIC) is a rare complication in severe cases
treatment for chemically-burned patient
- Initial treatment should focus on hemodynamic support and evaluating the injury.
- Aggressive airway management after aspiration or inhalation exposure is indicated because airway edema may develop rapidly.
- Emergency surgical evaluation is needed for patients with signs of perforation
- small amounts of fluid only; too much fluid can stimulate N/V