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home - Oesophagus - Miscellaneous - Perforation Necrosis and Fistulae 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.

Perforation Necrosis and Fistulae

Pathogenesis of acute oesophageal necrosisProbably two ‘hits’ are needed.Ischaemia often happens in the lower third which has a worse blood supply which then allows damage as the underlying cause. Endoscopy: Distal esophageal involvement -can extend proximally; ends sharply at the GOJ Histology: Diffues and severe necrosis of mucosa and submucosa with no stratified squamous cells, occasional deranged muscle fibers, hyperemia and scattered thrombosed vessels without specific causative agents. Clin Presentation Acute upper GI bleeding. DiagnosisThe lesion is initally black then progresses to white slough with sharp demarkation at GOJ. TreatmentsNBM for 24 hours.iv PPI.Sucralfate.Treat underlying illness.Avoid NG.Antibiotics as required.No need for repeat OGD. Prognosis Death is from underlying illness, not black oesophagus (mortality 20-35%). Epidemiology Incidence is 1: 10,000. It is more common in men. Acute esophageal necrosis (black oesophagus) Differential diagnoses of blackened oesophagus:Melanosis.Pseudomelanosis.Melanoma.Acanthosis nigricans.Coal dust and exogenous dye ingestion.Pseudomembranous oesophagitis. Free perforation on CT Early (<24hrs) Late Healthy oesophagus- primary closure Diseased oesophagus- resection Diversion and delayed reconstruction Causes of acute oesophageal necrosis:Broad spectrum antibiotics.Hyperglycemia.Underlying malignancy.Herpetic infection.Gastric volvulus.Stevens-Johnson syndrome.After prolonged vomiting following alcohol binging.Alcoholic lactic acidosis.Following OGD and esophageal manometry/pHmetry.Paresophageal hernia.Alcoholic hepatitis. Boerhaave syndrome FeaturesIt usually occurs in the distal oesophagus in left postero-lateral aspect.30% get Mackler's triad (emphysema/vomiting/chest pain).40% are alcoholics.Gastroduodenal ulcer disease is present in 40%.Pain occurs in 83%.Vomiting is a presentation in 79%.The initial CXR is always abnormal in Boerhaave’s. Treatment Endoclips. Covered, self-expanding metal stent. Fibrin sealant. Endoclips. Written by Dr Sebastian Zeki

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