Corrosive Poisoning

Ram E. Rajagopalan, MBBSAB (Int Med) AB (Crit Care)

Department of Critical Care MedicineSUNDARAM MEDICAL FOUNDATION

Chennai

So What’s the Difference?

Definition of CorrosiveA corrosive poison is one that causes tissue injury by a chemical reaction

Most commonly: Strong acids & alkalisConcentrated weak acids & alkalisOxidizers (with neutral pH)Alkylating agentsDehydrating agentsHalogens & organic halidesOther organic chemicals (phenol)

Common AgentsAcids:Car battery fluid : H2SO4

De-scalers: HClMetal cleaners: HNO3

Rust removers: HFDisinfectants: Phenol

Alkali:Household cleaners: Ammonia-basedDisinfectants; Bleach (hypochlorite) Drain cleaners; NaOH

Factors Determining Corrosiveness

Solid particulate: deep local burnsLiquids; diffuse/ circumferential

Food may buffer

Pyloric spasm from acid transit time

Titrable acid/alkali reserve (TAR)(amount needed to normalize pHof corrosive)

Mechanism of Injury

Acid

Coagulation (desiccate / denature protein)

Eschar formed

Delayed eschar loss (> 3 days): perforation / bleeding

Fibrosis & cicatrization is subsequently seen

Alkali

Liquefaction (saponify fat / solubilize protein)

Collagen swelling

Small vessel thrombosis

Heat

Myth: “Acid is ‘good’, Alkali is evil”

Intuitively alkali has greater effect on tissue necrosis; but strong acids also cause full thickness injury

“Oesophageal sparing” by acids is not true45-85% of acid ingestions show damage@

Strong acid ingestion is an independent predictorof death in corrosive poisoning (OR 7.9)*

@Int Care Med Update 2008;*Endoscopy 2002; 34(4): 304-310

Which is more dangerous?

Clinical Approach

Identify immediate life threatsMortality ~10-15% reported in hospitalized patients

Mainly due to:Airway injury:Mucosal edema obstructionInhalation ALI / ARDS

Gastro-esophageal injury:Perforation sepsisHaemorrhage

Airway Concerns (1)Supraglottic edema acute airway obstructionUnpredictable progression

If compromised (Stridor, dyspnea, CNS):

1. Consider fibre-optic visualization / intubation

2. Balance the risks of NMB (Rapid Sequence Induction vs. propofol)

3. Anticipate surgical airway (Cricothyrotomy)

Avoid blind “awake” naso-tracheal attempts

Airway Concerns (2)Medical management:

Poorly definedExtrapolated from other series in adults (epiglottitis)

Unpredictable progression warrants close watch

No role for adrenaline IV / nebulized in reducingthe risk of endotracheal intubation

Undefined role of systemic steroids in edemaAJRCCM 2004; 169: 1273-77

Normal respiration +

Drooling Dysphonia / aphonia Hoarseness Stridor

Haemodynamic Issues

Acute compromise usually from hypovolemiaHaemorrhageVomitingThird-space sequestration

Sepsis occurs later in hospital course

No unique issues in haemodynamic Rx: Crystalloid fluid resuscitation: Invasive monitoring in unstable patients

Decontamination?Almost any attempt to gastric emptying / dilutionis CONTRAINDICATED in corrosive poisoning

NO emetics (ipecac): injury & perforation riskNO Ewald / NG tube: Esophageal perf. ; aspirationNO Activated charcoal; No adsorption / interferes

NG tube aspiration may be considered early(<90 minutes) in large volume ingestions

Dilution & Neutralization?

Dilution of ingestants by NGT lavage generates heat & increases risk of aspirationNo proven benefit

Attempts at neutralization have similar effects Small volume dilution with water may be rarely considered early (<30 minutes) with particulate agents

Assessing the stabilized patient

Initial evaluation of the stable / stabilized patient aims to

a.Identify acute complications of corrosive ingestionb.Stratify the risk of patients for acute and long-term complications

Mainly clinical assessment + radiographyandEndoscopic grading of corrosive lesions

Symptoms & Clinical Signs Oesophageal leak / rupture; mediastinitis

Chest painSubcutaneous emphysemaHamman’s sign (cardiac crunch)

Gastric leak / bleed; peritonitisHematemesis; melena / bloody stoolAbdominal painRigidity / rebound tenderness

Continuous Diaphragm

Routine evaluation of the patient with significant oral / airway burn should includechest & abdominal radiography

Mediastinal Air

The radiographicsigns of early mediastinal sare usually subtle

CT; Pneumo-mediastinum

Subcutaneous air

Mediastinal air

Studies with water-soluble contrast will allow localizationof leak

Air under the Diaphragm

Patients with documented mediastinal or peritoneal leaks require surgical intervention

Laboratory Tests?Arterial Blood Gas @: pH & base deficit correlate with severity & adverse outcome

Hypocalcemia will occur with HF (industrial cleaner)

Anion-gap, osmolar-gap to identify co-ingestion

WBC count > 20,000 is an independent predictor of mortality*

Upper Endoscopy: Why?Complications of corrosive injury:

Early (perforation / bleed) Late (cicatrization & obstruction)

The risk for complications is logically proportional to the depth & extent of tissue damage

Direct evaluation by endoscopy will be useful in Severity grading / triagePlanning nutritional supportPlanning long-term management

Upper Endoscopy: Who?

CAUTION:Avoid in haemo-dynamic compromise

Avoid prior to ET tube in airway edema

Small children Symptomatic older children & adults Patients with altered mental status Patients with intentional ingestions Ingestion of large volumes Ingestion of concentrated products

Not contributory in peritonitis / mediastinitis

No value in mild ingestions (asymptomatic; normal oral / upper airway exam)

Upper Endoscopy: When?

Very early endoscopy (<6 hours) may not revealthe full extent of injury

The landmark study on endoscopy performed the procedure <96 hours (4 days)*

Eschar destabilization & bleed can occur ~ day 3 Commonest practice is day 1-2

? Re-look at day 5

GI Endoscopy: FindingsGrade Description0 Normal

1 Erythema

2a Sup. ulcer /erosion / friability haemorrhage / exudates

2b + deep discrete / circumferential ulcers

3a Scattered necrosis (black / grey discolouration)

3b Extensive / circ. necrosis

Implications of EndoscopyInitial study* from PGI Chandigarh;Zargar SA, Kochar R, Mehta S & Mehta SK

81 patients; 88 early endoscopy (<96 hours)+ follow up at 3-9 weeks and as needed

Modified grading as described

All deaths occurred with grade 3a/ 3b injury

No long-term complications in grades 0, 1 & 2a;71% cicatrization in higher grades

Confirmatory Study

BMC Gastroenterology 2008, 8:31doi:10.1186/1471-230X-8-31

Retrospective study

273 adults with causticingestion

1999-2006

%

Multivariate Mortality Model

210 patientsRetrospective analysis

6.2% had surgery11.9% mortality

Endoscopy 2002; 34: 304-10

Factor OR 95% CI

Age (/10-years) 2.4; 1.4 - 4.1

Strong acid ingestion 7.9; 1.8 - 35.3

WBC ≥ 20,000 at admission 6.0; 1.3 – 28

Deep gastric ulcers (Gr. 2b) 9.7; 1.4 - 66.8

Gastric necrosis (Gr. 3a/b) 20.9; 4.7 - 91.8

Rx of Questionable ValueCorticosteroids: Completely anecdotal experience

Only one RCT* in 60 children with documented esophageal injury2 mg/Kg prednisone parenteral oral for 3 weeks

10/31 strictures in steroid group vs. 11/ 29 in controls

Systemic or intra-lesional?Claims for superiority of agents can be questioned*N Engl J Med 1990; 323: 637-40

Other Treatments’Medicine Sans Evidence!

Antibiotics

H2-blockade / Proton pump inhibitorsare more controversial than steroids

’

Nutrition

Long term managementof GI complications isbeyond my scope!

I hope this “corrosivetalk” didn’t leave you

itching for its end!