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I completed my medical school and background EM training from India (Christian Medical College, Vellore and Apollo Hospitals, Hyderabad) where I worked for 4 years. Following this, I devoted (with all my heart) about 1.5 years to do US Medical Licensing Exams. My stint towards an EM Residency in States did not work but it took me to places and it has been quite a journey. I then relocated to London, England to work as a Registrar (Non-Trainee) in A&E. This gave me an opportunity to better understand NHS, EM training pathways and more importantly the EM Mindsets in the United Kingdom. 

Currently, I am pursuing Higher Specialist Training in Emergency Medicine at South East Scotland Deanery where I have the honour and privilege of training under some of the most innovative brains in the field of Emergency Medicine. Over the past few years, I have realised that LEARNING and UNLEARNING (which can be challenging!) is equally important to deliver cutting edge care to our patients.And through this blog, I aspire to disseminate knowledge, assist trainees with exams and stay up to date with contemporary EM literature. I have always been an avid FOAMed supporter because FOAMed has always played an indispensable role during my training. 


Lakshay Chanana
ST4 EM Trainee 
Edinburgh, Scotland
drlakshayem@gmail.com

Monday, June 8, 2015

Corrosive Poisoning

Corrosive poisoning is a common emergency as corrosive agents are easily available for household use. Corrosives can injure the GI tract by causing tissue necrosis, perforation, fibrosis, stricture formation and malignancy years after the exposure. These compounds include acids, bases, salts, heavy metals, iodine tincture etc. 




Acids
  • Car battery fluid (sulfuric acid)
  • Descalers (hydrochloric acid)
  • Metal cleaners (nitric acid)
  • Rust removers (hydrogen fluoride) 
Alkalis
  • Bleach (hypochlorite)
  • Sodium hydroxide (liquid lye) 

Pathophysiology
Alkali ingestion: Causes liquefaction necrosis. This process includes protein dissolution, collagen destruction, fat saponification, cell membrane emulsification, submucosal vascular thrombosis and cell death.

Acid ingestion: Causes coagulation necrosis. In this process, hydrogen (H+) ions desiccate epithelial cells producing an eschar. This process leads to edema, erythema, mucosal sloughing, ulceration and necrosis of tissues.

Both acids and alkalis cause fibrosis and stricture formation 



Signs and Symptoms

Clinical presentation varies and depends on the type/quantity of the agent ingested, timing of ingestion, presence of food in the stomach. Burns to the lips, mouth, and oropharyx may be seen but this does not necessarily correlate to the degree of injury tothe esophagus or stomach. Patients with airway deem may present with stridor, aphonia, hoarseness, or dyspnea. Other presenting symptoms include abdominal or chest pain, nausea/vomiting, GI bleed, dysphagia, odynophagia, drooling. 

If there is GI perforation, it may result in fluid loss causing renal failure, altered mental status, lethargy, arrythmias, respiratory distress and seizures.

Investigations
CBP
Basic Metabolic Profile
ABG
CXR (look for free air)
Type and Cross Match 
CT Scan (for suspected perforation despite negative X-Rays and to assess oesophageal wall thickness)
Endoscopy (for direct evaluation and management of strictures)

Esophagogastroduodenoscopy should be performed in the first 12 to 24 hours post-ingestion with great care, to avoid iatrogenic perforation. The grade and extent of the lesions of the upper gastrointestinal tract can be determined and classified according to the Zargar’s modified endoscopic classification of burns due to corrosive ingestion

Grade Description
  1. 0  Normal mucosa
  2. 1  Erythema/Hyperemia
  1. 2a  Superficial ulcer/erosion/friability/hemorrhage/ exudates
  2. 2b  Findings in 2a + deep discrete/circumferential ulcers
  1. 3a  Scattered necrosis (black/grey discoloration)
  2. 3b  Extensive/circumferential necrosis of mucosa 

Severe hypopharyngeal burns are an absolute contraindication for esophagogastroduodenoscopy.

Management 

1. If only a small amount is ingested: Observe and discharge from the ED if tolerating orallly, asymptomatic and normal intra oral examination. 

2. Major Ingestion
  • Pay special attention to the Airway/Oxygenation
  • IV Fluids
  • Add PPIs (reduce exposure of injured esophagus to gastric acid, which may result in decreased stricture formation.)
  • Antibiotics if there is evidence of perforation
  • Don't forget to add pain relief 
  • Keep Nil by Mouth 
Activated charcoal is relatively contraindicated in caustic ingestions because of poor adsorption and endoscopic interference. Emergency surgical intervention is indicated in case of perforation or peritonitis, or if uncontrolled massive hematemesis occurs. 

DO NOT
  • Induce Emesis (risk of mucosal injury and perforation)
  • Insert NG Tube (may cause esophageal perforation and increase the risk of aspiration)
  • Do Lavage (risk of damage to oesophagus and aspiration)
  • Try to neutralise the substance (risk of heat production resulting from this exothermic reaction
  • Administer systemic steroids


Nutrition: Endoscopic grade of lesions needs to be assessed for planning nutritional support in patients with caustic ingestion. Patients with Grade 1/2a lesions on endoscopy can tolerate oral feeds, while those with Grade 2b/3a lesions will need nasoenteral feeding. Patients with Grade 3b lesions require gastrostomy for enteral feeding and rarely need total parenteral nutrition (TPN). 

Acute presentation 
Within 48-72 hours of corrosive ingestion: Upper GI endoscopy should be performed on Day 1-2. (ideally between 12-24 hours of ingestion). If endoscopy reveals only mild lesions, then the patient can be discharged and clinical follow-up should be done at one month. If severe lesions are found on endoscopy, then surgical gastrostomy is indicated, which should be followed by repeat endoscopy and dilatation after three weeks.

Delayed Admission
Within 72 hours to three weeks of corrosive ingestion: No endoscopy is indicated here. Gastrostomy should be done if there is severe dysphagia. Endoscopy and dilatation of stricture (if present) should be done three weeks after ingestion.


Late Admission
More than three weeks of ingestion: Requires endoscopy and dilatation of stricture. If the procedure is successful, then follow-up endoscopy should be done at one month. If the procedure is unsuccessful, then surgical gastrostomy is performed, which is followed by retrograde dilatation of stricture after 10 days of operation.


Complications of the Disease and/or Management
Aspiration of corrosive substances into the respiratory tree may cause endotracheal or bronchial necrosis with mediastinitis. Acute kidney injury, disseminated intravascular coagulation, acid-base disturbances and pneumonia. Oesophageal stricture formation is the most feared long-term complication; stenosis gastric antrum or pylorus may also occur, as may fistula formation.

Stricture formation begins weeks to months after injury and is the most important consequence of corrosive poisoning. Procedures used for prevention and treatment of strictures are:

  1. Dilatation therapy: This is done 3-6 weeks after injury, progressively larger bougies are passed over endoscopically placed guide wires for dilatation. 
  2. Surgery: Esophageal strictures resistant to dilatation therapy may require surgery that includes resection of stricture surgically and esophageal bypass surgery. 
Key Points:
1. Both acids and Alkalis can cause strictures.
2. Endoscopy performed in the first 12 to 24 hours following ingestion is the gold standard  to assess the GI tract.
3. Pay attention to Airway, Hydration, Nutrition.
4. Say no to NG tube, gastric lavage, emetics, dilution and neutralisation, systemic steroids and activated charcoal.


For further reading:


  1. In: Critical Care Toxicology: Diagnosis and Management of the Critically Poisoned Patient. 1st edition, Brent, Wallace, Burkhart, Phillips, Donovan (Eds.) 2005:p. 1035-44.
  2. Caustics. In: Goldfrank’s Toxicologic Emergencies. 8th edition.
  3. Zargar SA, Kochhar R, Mehta S, Mehta SK. The role of fiberoptic endoscopy in the management of corrosive ingestion and modified endoscopic classification of burns. Gastrointest Endosc 1991;37(2):165-9.
  4. Anderson KD, Rouse TM, Randolph JG. A controlled trial of corticosteroids in children with corrosive injury of the esophagus. N Engl J Med 1990;323(10):637-40.
  5. Acids and alkalis. The Poisoning and Toxicology Handbook. 4th edition, Jerrold B. Leikin, Frank P. Paloucek Informa Healthcare, USA 2007:p.713-9.
  6. Alkali injury. In: Clinical Management of Poisoning and Drug Overdose. 3rd edition, Lester M. Haddad, Michael W. Shannon, and James F. Winchester (Eds.) 1998: p.817-20. 
  7. http://medind.nic.in/iaa/t12/i8/iaat12i8p131.pdf 


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