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MANAGEMENT OF CAUSTIC AGENT INGESTION Gilbert Oporto, M.D. February 24, 2010.

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Presentation on theme: "MANAGEMENT OF CAUSTIC AGENT INGESTION Gilbert Oporto, M.D. February 24, 2010."— Presentation transcript:

1 MANAGEMENT OF CAUSTIC AGENT INGESTION Gilbert Oporto, M.D. February 24, 2010

2 Introduction Caustic agents may induce a rapidly progressive, devasting injury to the GIT and mediastinal structures Accidental – usually among children Non-accidental – suicide attempts among adults

3 Common Chemical Exposures Alkaline (pH > 7)) – Sodium hypochlorite (weak base) Bleaches – Ammonia base (weak base) Toilet bowl cleaner, hair dyes, glass cleaners – Sodium hydroxide (weak base) Detergents, laundry powders, paint removers – Sodium borates, phosphates, carbonates Electric dishwasher, detergents

4 Common Chemical Exposures Acid (pH < 7) – Hydrochoric acid – swimming pool cleaners, metal and toilet bowl cleaners – Hydrofluoric acid – anti rust products – Sulfuric acid – car battery fluids

5 Mechanism of injury Extent of injury depends on: – Type of agent – Quantity – Duration of contact – Contration / strength of agent

6 Mechanism of injury Acid – Coagulation necrosis – Penetration is limited until the agent reaches the stomach where the acidic pH heightens the effect of the agent causing more extensive injuries – Strong odor and bitter taste induces rapid emetic response – Likely to produce skip lesions with distal perforation

7 Mechanism of Injury Alkali – Liquefaction necrosis – Deeper penetration to tissues – Injuries at the upper esophageal or oropharyngeal tract

8 Mechanism of injury Phase I – occurs within seconds – Edema, erythema – Shallow ulcers Phase II – progression of injury – 2 – 7 days -necrosis and sloughing off of tissues – Esophageal or gastric wall weakness – 3 rd to 4 th week – granulation – critical window for perforation

9 Mechanism of injury Phase III – scar formation – Fibroblast proliferation, cicatrization, stricture formation – Scar formation is complete within 8 weeks in 80% of patients but can continue up to 6 - 8 months

10 Mechanism of injury Mucosal sloughing (4-7 days after initial injury) – bacterial invasion, inflammatory response Collagen deposition may not begin until the 2 nd week, tensile strength of healing tissue is low during the first 3 weeks Scar retraction begins by the 3 rd wk, may continue for several months Many people advocate avoiding endoscopy between 5 to 15 days

11 Clinical presentation Symptoms – Oropharyngeal pain – Odynophagia – Dysphagia – Salivation – Chest pain – Abdominal pain

12 Danger signs Stridor / hoarseness – Epiglottal edema – Intubation Dysphagia and hematemesis – Esophageal injury Retrosternal pain radiating to the back – Impending mediastinitis Acidosis / worsening hemodynamic instability Fever, tachycardia, altered mental status

13 Clinical presentation REMEMBER! – Absence of abdominal pain does not rule out GIT injury – Perforation can occur anytime during the first two weeks of ingestion – Significant tissue destruction occurs within the first 24 hours

14 Clinical presentation 10 – 30% of patients with esophageal burns have no oropharyngeal damage 70% of patients with oropharyngeal burns do not have damage to esophagus Injuries to oropharynx are not a reliable index of damage to esophagus

15 Immediate Therapy Key to successful management – Identify the severity of injury – Minimize extension Type and amount of agent must be identified Airway must be the primary goal Intubation, direct visualization of oropharynx

16 Management Diagnosis – History and PE Early endoscopy (within first 24 hrs – gold standard) – Indications: – Stridor – Intended suicidal ingestions – Symptomatic children – Oropharyngeal burns CXR – Detect infiltrates – possible aspiration – Detect perforation

17 Management – GS 1 Protocol Airway IV fluid resuscitation NO NGT Medications: PPI or H2 Blocker started, prophylactic antibiotics Diagnostics: CXR, EGD, ABG Referral: Toxicology, Psychiatry Feeding progression Follow-up = EGD q 2 wks up to 8 wks

18 Classification of injury

19 Surgical intervention Evidence of perforation – Presence of peritoneal signs – Radiographic signs of perforation – Endoscopic stigmata of full-thickness injury – Increasing severity of condition Operative field – From mandible to pelvis

20 Surgical intervention Options – Esophagectomy with cervical esophagostomy and tube jejunostomy – Gastrectomy with abdominal esophagostomy and tube jejunostomy – Esophagogastrectomy with cervical esophagostomy and tube jejunostomy

21 Post-operative care Pain control Pulmonary toilette Feeding Follow-up – After 7 to 10 days – Every 3 months – Prepare for reconstruction Gastric pull-up, Colonic interposition, Jejunal free flap


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