1. Caustics

2. Objectives: 1- Acquire the skills of taking focused history and physical examination of the patients presenting with caustic induced injury in the ED 2- Acquire the basic approach to this group of patient. 3- Understand the pahto physiological and pharmacological effects of caustics. 4- Understand the role of healthcare professionals in poison control and prevention.

3.  cause tissue injury on contact with mucosal surfaces.  Agents capable of causing chemical injury include alkaline and acidic corrosives. Perspective

4.  Alkalis accept protons, resulting in the formation of conjugate acids and free hydroxide ions.  Lye is an example of an alkali caustic and refers to both sodium hydroxide (NaOH) and potassium hydroxide (KOH).  Ammonia (NH 3 ) is another common alkaline corrosive. Perspective

5.  Acids are proton donors, as they dissociate into conjugate bases and free hydrogen ions in solution. Acidic caustics include  hydrochloric acid (HCl) Rust Removal or Toilet bowl cleaner  sulfuric acid (H 2 SO 4 ) acidic drain cleaners Perspective

6.  The severity of caustic agents typically increases with a pH less than 3 or greater than 11.  On the contrary, hydrofluoric acid (HF) is a relatively weak acid that can cause necrotizing injury and life- threatening systemic toxicity. Perspective HF burns, not evident until a day after rust removers, aluminum brighteners and heavy duty cleaners

7. Other chemicals that have caustic properties Phenol Formaldehyde Iodine concentrated hydrogen peroxide. Perspective

8. Factors that influence the extent of injury  Type of agent  Concentration of solution  Volume  Viscosity  Duration of contact  pH  Presence or absence of food in the stomach. PRINCIPLES

9.  Acidic compounds desiccate epithelial cells and cause coagulation necrosis.  An eschar is formed there by limiting further penetration.  Because of resistance of squamous epithelium to coagulation necrosis, acids are thought to be less likely to cause esophageal and pharyngeal injury, although severe esophageal and laryngeal burns may still occur.  Acids can be absorbed systemically, causing metabolic acidosis, as well as damage to the spleen, liver, biliary tract, pancreas, and kidneys. PRINCIPLES

10.  Alkaline contact causes liquefaction necrosis, fat saponification, and protein disruption, allowing further penetrance of the alkaline substance into the tissue.  A concentration of 30% NaOH in contact with tissue for 1 second results in a full-thickness burn. PRINCIPLES

11. Gastric mucosa after ingestion of 35% potassium hydroxide

12. Gastric serosa after ingestion of 35% potassium hydroxide.

13. Esophagus after ingestion of 35% potassium hydroxide.

14.  Classically, the damage occurs in four steps. Initially, necrosis occurs, with invasion by bacteria and polymorphonuclear leukocytes. Vascular thrombosis follows, increasing the damage.  Over the next 2 to 5 days, superficial layers of injured tissue begin to slough. PRINCIPLES

15.  First-degree burns (also known as grade 1) consist of edema and hyperemia.  Second-degree burns (grade 2) can be further divided into 2a, which are non-circumferential, and 2b, which are near-circumferential.  Overall, second-degree burns are characterized by superficial ulcers, whitish membranes, exudates, friability, and hemorrhage. PRINCIPLES

16.  Third-degree burns (grade 3) are associated with transmural involvement with deep injury, necrotic mucosa, or frank perforation of the stomach or esophagus. PRINCIPLES

17.  Airway edema and esophageal/gastric perforation are the most emergent issues.  Laryngeal edema occurs over a matter of minutes to hours.  Systemic toxicity; hypovolemic shock; and hemodynamic instability with hypotension, tachycardia, fever, and acidosis are ominous findings. CLINICAL FEATURES

18.  Patients present with oral pain (41%), abdominal pain (34%), vomiting (19%), and drooling (19%).  Many patients have wheezing and coughing. Others present with stridor and dysphonia.  Chest pain is common.  Peritoneal signs suggest hollow viscous perforation or contiguous extension of the burn injury to adjoining visceral areas. CLINICAL FEATURES

19. Lip burn after exposure to35% potassium hydroxide.

20.  Patients with chest and abdominal pain should have a chest radiograph and decubitus or upright abdominal studies to identify peritoneal and mediastinal air, denoting perforation or pleural effusion.  Any suggestion of abdominal involvement should prompt abdominal CT or US.  ABG to monitor systemic metabolic acidosis. DIAGNOSTIC STRATEGIES

21.  Endoscopy is contraindicated in patients with possible or known perforation.  Patients with signs and symptoms (vomiting, drooling, stridor, or dyspnea) of intentional ingestion should undergo endoscopy within 12 to 24 hours to define the extent of the disease.  Endoscopy performed too early may miss the extent or depth of tissue injury. DIAGNOSTIC STRATEGIES

22.  Early endotracheal intubation is warranted when airway compromise is suggested by hoarseness, throat pain, drooling, or edema.  Intubation should also be undertaken early if significant exposure is suggested, before edema and secretions both threaten the airway and make intubation difficult or impossible. MANAGEMENT

23.  IV access and vigorous fluid resuscitation.  In alert patients who are not vomiting and can tolerate liquids, small volumes (1–2 cups) of water or milk can be considered within the first few minutes after ingestion.  Because injuries occur almost immediately, later dilution is not warranted.  Forcing fluids is never indicated.  Do not neutralize the ingested corrosive with weak acids or alkalis due to possible thermal reactions and worsening injury. MANAGEMENT

24.  administering activated charcoal, and performing gastric lavage are not indicated. MANAGEMENT

25.  Immediate surgical exploration is indicated for free air, peritonitis, increasing and severe chest and abdominal pain, and hypotension.  Early and continuous hemodynamic monitoring is essential.  Contaminated clothing should be treated as hazardous waste and disposed of using proper precautions. MANAGEMENT

26.  Ocular alkali exposures are true ophthalmologic emergencies.  Immediate and aggressive lavage with at least 2 L of normal saline per eye is indicated in all cases except for frank perforation.  Dermal caustic exposures can also result in significant burn injuries. Clothing removal, copious irrigation, and local wound debridement are the most importantinitial treatment measures. SPECIAL CASES

27.  Povidone-iodine (Betadine)is used as a surgical scrub and is not a caustic agent, but ingestion of tincture of iodine can cause severe gastrointestinal injury and is potentially life- threatening.  Gastric irrigation with starch or milk in these cases may convert iodine to the much less toxic iodide.  Ingestion of phenol or formaldehyde can also cause severe caustic injury to the gastrointestinal tract. . SPECIAL CASES

28.  Systemic symptoms, including dysrhythmias, hypotension, seizures, and coma, may also result from phenol ingestion.  Acidosis may be quite prominent after formaldehyde ingestion due to its metabolism to formic acid.  Phenol is well absorbed through the skin, and dermal exposure may result in burns and systemic toxicity. SPECIAL CASES

29.  Button batteries are usually made of a metallic salt (lithium, mercury, nickel, zinc, cadmium, or silver) bathed in NaOH or KOH.  Obstruction can cause pressure necrosis, caustic injury due to leakage of alkaline medium, or electrical injury.  Ulceration, perforation, and possible fistula formation occur but are uncommon.  Heavy-metal toxicity in this setting has not been reported SPECIAL CASES

30.  Button (disk) batteries and conventional alkaline cylindrical batteries pose potential obstructive and chemical hazards if ingested. SPECIAL CASES

31.  Evaluation of button battery ingestions requires radiography to assess the position of the foreign body.  Batteries lodged in the airway or esophagus require expeditious removal.  Gastric or intestinal batteries can be treated with watchful waiting.  Checking the stool for passage of the batteries is recommended.  Follow-up radiographs should be obtainedin 1 week if the battery has not passed. SPECIAL CASES

33. True/False Patients with caustic ingestion may present with 1- Dysphagia 2-Wheezing and cough 3- Chest pain 4- Stridor 5- Vomiting

34. True/False Following are the signs of severe systemic toxicity with caustics 1- Systemic hypovolemia/ shock 2- Good skin colour & turgor. 3- Tachycardia 4- Fever 5- Acidosis

35. True/False Following are useful for the treatment of caustic poisoning, 1- 500cc milk to drink after 30 minutes of ingestion of the poison. 2- Gastric lavage 3- Activated charcoal 4- IV fluids 5- Neutralize the acid ingestion by weak oral alkali solution.