Corrosive Poisoning

Ram E. Rajagopalan, MBBS

AB (Int Med) AB (Crit Care)

Department of Critical Care Medicine

SUNDARAM MEDICAL FOUNDATION Chennai

So Whats the Difference?

Definition of Corrosive
A corrosive poison is one that causes tissue injury by a chemical reaction Most commonly:
Strong acids & alkalis Concentrated weak acids & alkalis Oxidizers (with neutral pH) Alkylating agents Dehydrating agents Halogens & organic halides Other organic chemicals (phenol)

Common Agents
Acids: Car battery fluid : H2SO4 De-scalers: HCl Metal cleaners: HNO3 Rust removers: HF Disinfectants: Phenol Alkali: Household cleaners: Ammonia-based Disinfectants; Bleach (hypochlorite) Drain cleaners; NaOH

Factors Determining Corrosiveness

Solid particulate: deep local burns Liquids; diffuse/ circumferential Food may buffer Pyloric spasm from acid J transit time Titrable acid/alkali reserve (TAR) (amount needed to normalize pH of corrosive)

Mechanism of Injury
Liquefaction
(saponify fat / solubilize protein)

Alkali

Collagen swelling Small vessel thrombosis Heat Coagulation

(desiccate / denature protein)

Acid

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

Fibrosis & cicatrization is subsequently seen

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 true 45-85% of acid ingestions show damage@
@Int

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

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

Which is more dangerous?

Clinical Approach
Identify immediate life threats Mortality ~10-15% reported in hospitalized patients
Mainly due to:

Airway injury: Mucosal edema obstruction Inhalation ALI / ARDS

Gastro-esophageal injury: Perforation sepsis Haemorrhage

Airway Concerns (1)

Supraglottic edema acute airway obstruction Unpredictable progression If compromised (Stridor, dyspnea, CNSD): 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:

Normal respiration + Drooling Dysphonia / aphonia Hoarseness Stridor

AJRCCM 2004; 169: 1273-77

Poorly defined Extrapolated from other series in adults (epiglottitis)

Unpredictable progression warrants close watch No role for adrenaline IV / nebulized in reducing the risk of endotracheal intubation

Undefined role of systemic steroids in K edema

Haemodynamic Issues
Acute compromise usually from hypovolemia Haemorrhage Vomiting Third-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 / dilution is CONTRAINDICATED in corrosive poisoning

NO emetics (ipecac): J injury & perforation risk NO Ewald / NG tube: Esophageal perf. ; J aspiration NO 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 aspiration No 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 ingestion b. Stratify the risk of patients for acute and long-term complications Mainly clinical assessment + radiography and Endoscopic grading of corrosive lesions

Symptoms & Clinical Signs

Oesophageal leak / rupture; mediastinitis Chest pain Subcutaneous emphysema Hammans sign (cardiac crunch)

Gastric leak / bleed; peritonitis Hematemesis; melena / bloody stool Abdominal pain Rigidity / rebound tenderness

Continuous Diaphragm
Routine evaluation of the patient with significant oral / airway burn should include chest & abdominal radiography

Mediastinal Air

The radiographic signs of early mediastinal Ds are usually subtle

CT; Pneumo-mediastinum
Subcutaneous air

Mediastinal air

Studies with water-soluble contrast will allow localization of 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 WBC count > 20,000 is an independent predictor of mortality* Hypocalcemia will occur with HF (industrial cleaner) Anion-gap, osmolar-gap to identify co-ingestion

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 / triage Planning nutritional support Planning long-term management

Upper Endoscopy: Who?

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

CAUTION: Avoid in haemodynamic compromise Avoid prior to ET tube in airway edema

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 reveal the 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: Findings
Grade 0 1 2a 2b 3a 3b Description Normal Erythema Sup. ulcer /erosion / friability haemorrhage / exudates + deep discrete / circumferential ulcers Scattered necrosis (black / grey discolouration) Extensive / circ. necrosis

Implications of Endoscopy
Initial 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
% Retrospective study 273 adults with caustic ingestion 1999-2006
BMC Gastroenterology 2008, 8:31 doi:10.1186/1471-230X-8-31

Multivariate Mortality Model

210 patients Retrospective analysis 6.2% had surgery 11.9% mortality
Factor Age (/10-years) Strong acid ingestion WBC 20,000 at admission Deep gastric ulcers (Gr. 2b)
Endoscopy 2002; 34: 304-10

OR 2.4; 7.9; 6.0; 9.7; 20.9;

95% CI 1.4 - 4.1 1.8 - 35.3 1.3 28 1.4 - 66.8 4.7 - 91.8

Gastric necrosis (Gr. 3a/b)

Rx of Questionable Value
Corticosteroids: Completely anecdotal experience Only one RCT* in 60 children with documented esophageal injury 2 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 inhibitors are more controversial than steroids Nutrition

Long term management of GI complications is beyond my scope!

I hope this corrosive talk didnt leave you itching for its end!