Caustic burn: Difference between revisions
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==Disposition== | ==Disposition== | ||
*All pts w/ symptomatic caustic ingestions should be admitted | *All pts w/ symptomatic caustic ingestions should be admitted | ||
==Ocular Exposure== | ==Special Situations== | ||
===Ocular Exposure=== | |||
*Alkali injuries are more severe than acidic injuries | *Alkali injuries are more severe than acidic injuries | ||
*Treatment | *Treatment | ||
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**Discharge w/ 24hr f/u if pt only has corneal epithelial injury (fluorescein uptake) | **Discharge w/ 24hr f/u if pt only has corneal epithelial injury (fluorescein uptake) | ||
==Dermal Exposure== | ===Dermal Exposure=== | ||
*Acidic injuries (except HF acid) | *Acidic injuries (except HF acid) | ||
**Respond well to copious saline or water irrigation | **Respond well to copious saline or water irrigation | ||
| Line 116: | Line 116: | ||
***Partial-thickness injuries >10-15% of BSA | ***Partial-thickness injuries >10-15% of BSA | ||
***All full-thickness burns | ***All full-thickness burns | ||
===Hydrofluoric Acid=== | |||
====Background==== | |||
*Uses | |||
**Glass etching, metal cleaning, petroleum processing | |||
**Found in chrome wheel cleaner, rust remover | |||
*Kills via calcium chelation, not via burn | |||
*Oral ingestion has a very high mortality rate | |||
====Diagnosis==== | |||
*Onset of symptoms (pain, erythema) correlated w/ concentration | |||
**Dilute solutions (<20%) may have delayed onset up to 24hr post-exposure | |||
**Moderate solutions (20-50%) develop symptoms w/in 1-8hr | |||
**Concentrated solutions (>50%) develop symptoms immediately | |||
***These pts are at risk for systemic toxicity/death | |||
***Pain immediately (even if wound appears minor) implies severe injury | |||
====Treatment==== | |||
*Minor injuries (<50 cm2 from dilute solutions <20%) | |||
#Copious irrigation | |||
#Application of gel paste of Ca gluconate or benzalkonium Cl | |||
##Rub into affected area for 10-15min w/ pain relief being used as end-point of tx | |||
##Calcium gel is commercially available (found in industrial first-aid kits) | |||
##Calcium gel can be made: | |||
###Mix calcium gluconate powder 3.5gm w/ 150mL water-soluble lubricant OR | |||
###Mix 25mL 10% calcium gluconate solution w/ 75mL water-soluble lubricant | |||
##Benzalkonium Cl is commercially available | |||
##If calcium gluconate is not available calcium chloride can be used | |||
*Severe injuries | |||
#Treat w/ intradermal injections of 5% calcium gluconate | |||
##Prepare by diluting conventional 10% Ca gluconate w/ sterile NS in 1:1 ratio | |||
##Inject in and around the burned area in amount not to exceed 0.5mL per cm2 | |||
*Refractory injuries | |||
#Treat w/ intra-arterial infusion of calcium gluconate | |||
##Deliver via arterial line placed proximal to injury in the same limb | |||
##Infuse 10mL of 10% Ca gluconate dilued in 40mL of NS or D5water over 4 hr | |||
*Ingestion | |||
#If <1hr of ingestion place NG tube, suction, gastric lavage | |||
##Follow lavage by 300mL 10% Ca gluconate down NGT | |||
##Provide aggressive IV supplementation if ECG signs of hypoCa or hyperK | |||
==See Also== | ==See Also== | ||
Revision as of 06:19, 26 July 2011
Background
- Substances that cause damage on contact with body surfaces
- Degree of injury determined by pH, concentration, volume, duration of contact
- Etiologies for shock include GI bleeding, perforation, volume depletion
- Intentional ingestion a/w higher grade injuries
- Esophageal injuries
- Mild injuries - normal function is restored
- Severe injuries - strictures
- Days 2-14 post-injury are a/w highest tissue friability / risk of perforation
- High-grade caustic burns a/w 1000x increase in esophageal SCC
Alkalis
- Hydroxide ion easily penetrates tissue causing immediate cellular destruction
- May cause deep penetration into surrounding tissues (e.g. abd/mediastinal necrosis)
- Examples
- Bleach, drain openers, oven cleaners, toilet cleaner, hair relaxers
- Household bleach rarely causes significant injury
Acids
- Hydrogen ion leads to cell death and eschar formation, which limits deeper involvement
- However, due to pylorospasm and pooling high-grade gastric injuries are common
- Mortality rate is higher compared to strong alkali ingestions
- However, due to pylorospasm and pooling high-grade gastric injuries are common
- Ingestion may be complicated by systemic absorption (met acidosis, hemolysis, ARF)
- Examples
- Auto batteries, drain openers, metal cleaners, swimming pool products, rust remover
Diagnosis
- All pts w/ serious esophageal injuries have some initial sign or symptom
- E.g. stridor, drooling, vomiting
- Exam eyes and skin (splash and dribble injuries may easily be missed)
- GI tract injury
- Dysphagia, odynophagia, epigastric pain, vomiting
- Laryngotracheal injury
- Dysphonia, stridor, respiratory distress
- Occurs via aspiration of caustic or vomitus or inhalation of acidic fumes
Work-Up
Labs
Only necessary in pts w/ significant injury
- CBC
- Chemistry
- VBG
- Anion gap acidosis due to lactate production (tissue injury) or from the acid itself
- May also have non-anion gap acidosis (e.g. HCl)
- Anion gap acidosis due to lactate production (tissue injury) or from the acid itself
- Lactate
- LFTs
- Coags
- Type and screen
- Calcium level
- If HF acid exposure
- ECG
- Screens for coingestants in suicidal pts
- May show QT-prolongation if hypocalcemic 2/2 HF acid
Imaging
- Upright CXR
- Detect peritoneal and mediastinal air
- Left-side down CXR
- Indicated if unable to tolerate upright CXR
- CT
- Consider when perforated viscus is suspected or after intentional ingestion
Treatment
- Prevent personal exposure to the caustic agent
- Airway
- Should be considered as a difficult airway
- Blind nasotracheal intubation is contraindicated
- First-line is awake oral intubation w/ direct visualization
- LMAs, combitubes, bougies are probably unsafe; should be used as last resort
- Surgical back-up is recommended
- Steroids
- Some toxicologists recommend single dose of dexamethasone 10mg IV (06mg/kg in peds)
- Decontaminate in usual manner
- Activated charcoal
- Only consider when coingestants pose a risk for severe systemic toxicity
- Endoscopy
- Should be performed <12hr after ingestion and no later than >24hr after ingestion
- Indications:
- Intentional ingestion
- Unintentional ingestion with signs of:
- Stridor
- Significant oropharyngeal burns
- Vomiting
- Drooling
- Food refusal
- Surgery
- Indicated for peritoneal signs, free intraperitoneal or mediastinal air
- No evidence to support prophylactic abx
Disposition
- All pts w/ symptomatic caustic ingestions should be admitted
Special Situations
Ocular Exposure
- Alkali injuries are more severe than acidic injuries
- Treatment
- Copious irrigation in 15min intervals followed by pH check
- LR, NS, or 3% saline works best
- Treat until pH is 7.5-8.0
- Severe exposures may require anterior chamber irrigation
- Avoid testing pH of the irrigation fluid (wait few min before checking ocular fluid)
- After irrigation perform complete eye exam
- Prognosis determined by extent of injury at limbus and area/depth of injury to cornea
- Disposition
- Admit all pts w/ corneal haziness or opacity or limbal ischemia (paleness at limbus)
- Discharge w/ 24hr f/u if pt only has corneal epithelial injury (fluorescein uptake)
Dermal Exposure
- Acidic injuries (except HF acid)
- Respond well to copious saline or water irrigation
- Alkali injuries
- May appear superficial but often are deeper w/ ongoing burn
- Treat w/ copious irrigation and local wound debridement to remove residual compound
- Disposition
- Admit the following:
- Injuries that cross flexor or extensor surfaces
- Facial injuries
- Perineum injuries
- Partial-thickness injuries >10-15% of BSA
- All full-thickness burns
- Admit the following:
Hydrofluoric Acid
Background
- Uses
- Glass etching, metal cleaning, petroleum processing
- Found in chrome wheel cleaner, rust remover
- Kills via calcium chelation, not via burn
- Oral ingestion has a very high mortality rate
Diagnosis
- Onset of symptoms (pain, erythema) correlated w/ concentration
- Dilute solutions (<20%) may have delayed onset up to 24hr post-exposure
- Moderate solutions (20-50%) develop symptoms w/in 1-8hr
- Concentrated solutions (>50%) develop symptoms immediately
- These pts are at risk for systemic toxicity/death
- Pain immediately (even if wound appears minor) implies severe injury
Treatment
- Minor injuries (<50 cm2 from dilute solutions <20%)
- Copious irrigation
- Application of gel paste of Ca gluconate or benzalkonium Cl
- Rub into affected area for 10-15min w/ pain relief being used as end-point of tx
- Calcium gel is commercially available (found in industrial first-aid kits)
- Calcium gel can be made:
- Mix calcium gluconate powder 3.5gm w/ 150mL water-soluble lubricant OR
- Mix 25mL 10% calcium gluconate solution w/ 75mL water-soluble lubricant
- Benzalkonium Cl is commercially available
- If calcium gluconate is not available calcium chloride can be used
- Severe injuries
- Treat w/ intradermal injections of 5% calcium gluconate
- Prepare by diluting conventional 10% Ca gluconate w/ sterile NS in 1:1 ratio
- Inject in and around the burned area in amount not to exceed 0.5mL per cm2
- Refractory injuries
- Treat w/ intra-arterial infusion of calcium gluconate
- Deliver via arterial line placed proximal to injury in the same limb
- Infuse 10mL of 10% Ca gluconate dilued in 40mL of NS or D5water over 4 hr
- Ingestion
- If <1hr of ingestion place NG tube, suction, gastric lavage
- Follow lavage by 300mL 10% Ca gluconate down NGT
- Provide aggressive IV supplementation if ECG signs of hypoCa or hyperK
See Also
Source
Tintinalli
