Corrosive Poisoning

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

Department of Critical Care Medicine


So What‟s 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) .

NaOH .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.

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

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 .

9)* .Myth: “Acid is „good‟. Alkali is evil” Intuitively alkali has greater effect on tissue necrosis. 34(4): 304-310 Strong acid ingestion is an independent predictor of death in corrosive poisoning (OR 7. *Endoscopy 2002. 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.

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 .

Balance the risks of NMB (Rapid Sequence Induction vs. Anticipate surgical airway (Cricothyrotomy) Avoid blind “awake” naso-tracheal attempts . propofol) 3. dyspnea. CNSD): 1. Consider fibre-optic visualization / intubation 2.Airway Concerns (1) Supraglottic edema  acute airway obstruction Unpredictable progression If compromised (Stridor.

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 .

J aspiration NO Activated charcoal.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. . 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 .

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 .Assessing the stabilized patient Initial evaluation of the stable / stabilized patient aims to a.

Symptoms & Clinical Signs Oesophageal leak / rupture. melena / bloody stool Abdominal pain Rigidity / rebound tenderness . peritonitis Hematemesis. mediastinitis Chest pain Subcutaneous emphysema Hamman‟s sign (cardiac crunch) Gastric leak / bleed.

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. osmolar-gap to identify co-ingestion .000 is an independent predictor of mortality* Hypocalcemia will occur with HF (industrial cleaner) Anion-gap.

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 .

necrosis .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.

Zargar SA. 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. Kochar R. 1 & 2a. 71% cicatrization in higher grades . Mehta S & Mehta SK 81 patients.Implications of Endoscopy Initial study* from PGI Chandigarh.

1186/1471-230X-8-31 .Confirmatory Study % Retrospective study 273 adults with caustic ingestion 1999-2006 BMC Gastroenterology 2008. 8:31 doi:10.

4 .4 . 95% CI 1.35.7 . mortality Factor Age (/10-years) Strong acid ingestion WBC ≥ 20. 7. 6.7. 20.8 4.8 .2% had surgery 11.000 at admission Deep gastric ulcers (Gr. 1.3 – 28 1. 3a/b) .Multivariate Mortality Model 210 patients Retrospective analysis 6.3 1. 34: 304-10 OR 2.8 Gastric necrosis (Gr. 2b) Endoscopy 2002.

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. 323: 637-40 . 11/ 29 in controls Systemic or intra-lesional? Claims for superiority of agents can be questioned *N Engl J Med 1990.

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” didn’t leave you itching for its end! .

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