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home - Oesophagus - Miscellaneous - Foreign Bodies And Caustics Written by Dr Sebastian Zeki
Nausea and Vomiting:
Understands the pathophysiology of vomiting.
Appreciates the gastrointestinal conditions that cause nausea and
vomiting as well as the range of extra-intestinal causes

Recognises the influence of neurological conditions and metabolic
derangements such as diabetes

Understands the physiology of gastric emptying and how this is
affected by disease, toxins and drugs

Abdominal Pain:
Knows the causes of acute and chronic abdominal pain that arise
from upper gastrointestinal, biliary and pancreatic diseases

Understands the clinical presentations of the various conditions
causing pain and the means by which they can be diagnosed and
treated

Weight Loss:
Knows the significance of weight loss as a consequence of upper
gastrointestinal disease, knows those conditions that present with
loss of weight and how they are managed

Skills
Makes a detailed clinical assessment of patients presenting with
symptoms indicating possible upper gastrointestinal disease,
construct a management plan and be aware of the various avenues
of treatment

Behaviours
Evaluates patients in a structured and timely manner, carries out
appropriate investigations and formulates management plan.

Foreign Bodies And Caustics

Caustic Ingestion Written by Dr Sebastian Zeki ManagementPatients should be surgically or ITU managed.If low volume acid or alkali and no symptoms can be followed as outpatient without endoscopy otherwise NBM and iv PPI.Management involves mangement of airway damage.Do NOT use emetics/ neutralizers (exothermic reaction) or NG’s acutely.Endoscopy should be done as soon as possible after admission.Prophylactic stenting to prevent strictures is not recommended.Oesophagectomy with colonic interposition may be required for patients with severe strictures. Patients with grades 2B and 3A develop strictures in 75% Grade 3B carries a 65% early mortality and the need for esophageal resection with colonic or jejunal interposition in most cases. Patients with grades 1 and 2A have an excellent prognosis / no complications Esophageal squamous carcinoma — Risk is 1000 higher with lye ingestion Latency of around 41 yearsLye induced cancer present earlier and respond better because1. The esophageal becomes less distensible so earlier dysphagia. 2. The scar tissue prevents spreadSurveillance should begin 20 years after the caustic ingestion. Repeat endoscopy every 2 years Pyloric stenosis- The development of early satiety and postprandial vomiting months or years after ingestion suggest pyloric stenosis esp. with acids Stricture-1/3rd get strictures primarily in those with grade 2B or 3 injury The peak incidence of stricture-related is 2m, although it can occur as early as two weeks or as late as years after ingestion.Should wait three to six weeks after the initial injury before attempting dilation. Perforation occurs in 0.5% of procedures, and surgical correction is required in 70% The goal is to dilate the esophageal lumen to 15 mm and to completely relieve dysphagia Long and eccentric strictures may require endoscopic dilation under fluoroscopic guidance in order to minimize the risk of perforation.If pharyngoesophageal corrosive strictures is more complex. and cant dilate antegradally a retrograde approach with a mini-laparotomy and gastrostomy should be attempted with retrograde dilatationIn severe cases, elective esophageal resection with esophago-gastric anastomosis or colonic interposition is required.Temporary placement of a self-expanding plastic stent can be useful Dysmotility- due to scarred segment Management of damage:Patients with mild or no injury may be discharged.No therapy required for grade 1 or 2A damage.Start liquid diet with regular diet at 48hrs for minimal damageNasoenteric tube feeding should be initiated after 24 hours for severe damage.Oral liquids are allowed after the first 48 hours if the patient is able to swallow saliva.Observe for signs of perforation over at least a one-week period. Grading Of DamageGrade 0 — Normal Grade 1 — Mucosal edema and hyperemia Grade 2A — Superficial ulcers, bleeding, exudates Grade 2B — Deep focal or circumfer-ential ulcersGrade 3A — Focal necrosisGrade 3B — Extensive necrosis Damage usually in antrum as pylorus goes into spasm Food in the stomach tends to provide a protective effect. Amount of acid ingested tends to be limited as painful to swallow, and passes into stomach quickly Acid ingestion typically produces a superficial coagulation necrosis that thromboses the underlying mucosal blood vessels and consolidates the connective tissue, thereby forming a protective eschar. Acid(toilet bowl or swimming pool cleaners, antirust compounds, or in battery fluid ) Less common chance of duodenal injury (30%) Partially neutralised in the stomach so much less injury Causes liquefactive necrosis of oesophagus within seconds. Lasts 3-4 daysOver the ensuing two weeks, the esophageal wall becomes progres-sively thinner because of sloughing and the development of granulation tissue and fibrosis. Re-epithelialization is usually complete one to three months later. Alkali (drain cleaners, other household cleaning products, or disc batteries. ) =Lye CHECK THIS Late sequelae Leading cause of esophageal strictures in children.Ingestion is usually accidental in children <5y and intentional in adults and adolescents. Liquid household bleach (5 % sodium hypochlorite) ingestion rarely causes severe esophageal injury.Both cause laryngeal and tracheo-bronchial injury.Outcomes worse for acid ingestion Alkali Ingestion Acid Ingestion

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