EMS Subspecialty Certification Review Course. Learning Objectives. Pathophysiology. Caustics

Transcription

1 EMS Subspecialty Certification Review Course Caustics Version Date: 2/6/2013 Learning Objectives Upon the completion participants will be able to: Define a caustic substance Describe difference in site and nature of injury with acid vs. alkali ingestion Describe the prehospital care priorities for patients with caustic ingestions 2 Pathophysiology Caustics and corrosives cause tissue injury by a chemical reaction. Vast majority of caustic chemicals are acidic or alkaline substances that damage tissue by accepting a proton (alkaline substance) or donating a proton (acidic substance) in an aqueous solution. 1

2 Pathophysiology Increased risk of severe injury with ph <3 or > 11 Severity of tissue injury also determined by the: Concentration and duration of contact Amount and state (liquid, solid) of the substance involved Physical properties such as tissue penetration and titratable reserve(how much acid/base to neutralize) Generally speaking: Solids increase risk of proximal injury (oropharynx/prox esophagus) Liquids increase risk of distal injury(dist esophagus/gastric) 4 Common acid containing sources Toilet bowl cleaning products Automotive battery liquid Rust removal products Metal cleaning products Cement cleaning products Drain cleaning products Soldering flux containing zinc chloride Common alkaline containing sources Drain and oven cleaning products Ammonia products(tub/tile cleaners) Swimming pool cleaning products Automatic dishwasher detergent Hair relaxers Clinitest tablets Bleaches(most common) Cement 2

3 Alkalis Cause injury by liquefaction necrosis, saponification of fats and solubilization of proteins Severe and deeper injury occurs rapidly after alkaline ingestion(min) Special attention paid to ocular injury Appear deceptively superficial First contact most severely affected oropharynx, hypopharynx, and esophagus (most common). stomach much less frequently Tissue edema occurs immediately, may persist for 48 hours, and may eventually progress sufficiently to create airway obstruction. Acids Acid ingestions cause tissue injury by coagulation necrosis causes desiccation/denaturation of superficial tissue proteins formation of an eschar preventing/delaying deeper injury If skin respond well to copious irrigation(except HF) The stomach is the most commonly involved organ following an acid ingestion pyloric and antral spasm causes pooling resulting in severe injury and may induce emesis some natural protection of the esophageal squamous epithelium. Small bowel exposure also occurs in about 20% of cases. Higher mortality compared to strong alkali ingestion Signs and symptoms The presence or absence of the following symptoms should be determined since the presence of any of these symptoms suggests the possibility of significant internal injury. However, their absence does not preclude significant injury. Dyspnea Dysphagia Oral pain and odynophagia Chest pain Abdominal pain Nausea and vomiting 3

4 Signs and symptoms Tachycardia Oropharyngeal burns these are important when identified, but significant esophageal involvement may occur in the absence of oropharyngeal lesions. Drooling Subcutaneous air Acute peritonitis Abdominal guarding, rebound tenderness, and diminished bowel sounds Signs of impending airway obstruction may include the following: Stridor Hoarseness Dysphonia or aphonia Respiratory distress, tachypnea, hyperpnea Cough Airway management Because of the risk of rapidly developing airway edema, immediate assessment of the patient s airway and mental status should be performed and continually monitored. Equipment for endotracheal intubation and cricothyrotomy should be readily available (consider difficult airway) Nasotracheal intubation and BIAD should be avoided due to the increased risk of soft tissue perforation Cricothyrotomy or percutaneous needle cricothyrotomy may be necessary in the presence of extreme tissue friability or significant edema. Treatment Dilution typically a home remedy for accidental (<30 min) Do not induce emesis or attempt to neutralize This induces an exothermic reaction, which can compound the chemical injury with a thermal injury. It may also induce emesis re exposing tissue to the caustic agent. NO NGT or charcoal Prompt evaluation of airway and vital signs as well as immediate cardiac monitoring and intravenous access. 4

5 Special Considerations Alkali eye injury More severe and deeply penetrating with continued liquefaction Copious and continuous irrigation Disc battery ingestion Most < 6yoa Leakage(rare) risks alkali injury and toxic metals If airway and esophagus is removed Past GE junction gets f/u x ray in hrs 13 Take home points Identify acid/base and consider injuries to contiguous organs Supportive care rather than specific antidotes is the mainstay Careful monitoring and management of airway considering friable/edematous tissues Rapid transport to the nearest ED EMS Subspecialty Certification Review Course Hydrofluoric acid Version Date: 2/6/2013 5

6 Learning Objectives Upon the completion of this program participants will be able to: 1. Understand the potential sources of HF exposure 2. Describe the pathophysiology of HF toxicity 3. List the signs and symptoms of HF exposure 4. Describe the treatment of HF exposure 16 Hydrofluoric acid (HF) Colorless gas or fuming liquid (hydrogen fluoride) When dissolved in water ishydrofluoric acid Used to make refrigerants, herbicides, aluminum, plastics, electrical components, fluorescent bulbs, etching, and metal/wheel cleaners, and rust removers 17 Pathophysiology HF dissociates and fluoride ions penetrate skin quickly and deeply without extensive coagulation necrosis (eschar formation) Fluoride ions react with calcium and magnesium Systemic toxicity due to depletion of total body stores of calcium and magnesium Majority of deaths result from cardiac dysrhythmias secondary to hypocalcemia, hypomagnesemia, hyperkalemia, acidosis 18 6

7 Hydrofluoric Acid Paradox Lower concentrations = more severe burns >50% immediate symptoms 20 50% delayed 1 8 hrs <20% up to 24 hrs Characteristic pain out of proportion to tissue injury Majority involve small areas usually fingers and upper extremities 19 Signs and symptoms Inhalation burns Hypoxemia Stridor Wheezing Rhonchi Skin burns Grade 1: a white burn mark and/or erythema and pain Grade 2: a white burn mark and/or erythema and pain + edema and blistering Grade 3: a white burn mark and/or erythema and pain + edema and blistering + necrosis 20 Prehospital Treatment PPE and rapid irrigation Bind fluoride Apply calcium gluconate gel if available Soak digits in a magnesium hydroxide (e.g. Mylanta ) SQ 5 10% CaGlu (0.5mL/cm2) if refractory Symptomatic management Pain control with opioid agents Apply ice packs (slows diffusion of the fluoride ion) With any evidence of hypocalcemia, administer 10% calcium gluconate 21 7

8 22 10 Take Home Points 1. HF may cause delayed symptoms 2. Treatment with topical and intravenous calcium is vital 3. Hypocalcemia is cause of lethal dysrythmias 24 8

9 Epidemiology The alkali drain cleaners and acidic toilet bowl cleaners are responsible for the most fatalities from corrosive agents. Approximately 10% of caustic ingestions result in severe injury requiring treatment. Between 1% and 2% of caustic ingestions results in stricture formation. Approximately 80% of caustic ingestions occur in children younger than 5 years. Most intentional ingestions occur in adults 26 Signs and symptoms Vast majority of HF cases involves only small areas of exposure, usually to the fingers High concentration (solutions > 14%) produce immediate symptoms Less concentrated solutions usually cause delayed symptoms of one to several hours Deeper penetration of un dissociated HF acid, with more severe burn Pain is disproportionate to apparent skin involvement 27 9