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Preoperative Case Presentation & Sharing of Information on Vomiting. Jeffy G. Guerra, MD Level III Surgery Resident OMMC-Surgery 053006. General Data:. C.P., 68F SAB, Mla. Chief Complaint:. Vomiting. History of Present Illness:.
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Preoperative Case Presentation & Sharing of Information on Vomiting Jeffy G. Guerra, MD Level III Surgery Resident OMMC-Surgery 053006
General Data: C.P., 68F SAB, Mla
Chief Complaint: Vomiting
History of Present Illness: 8 years PTA epigastric pain, on/off, moderate, slightly relieved by antacid consult : ulcer
1 year PTA Persistence of Ssx, consult Rx: Cimetidine lost to follow-up
8 months PTA episodes of regurgitation, gastrointestinal reflux
1 month PTA (+) black tarry stool no consult
25 days PTA epigastric pain vomiting unrelieved by antacid, admitted: IV started, H2 block and BT, 2 units, apparently d/c well
2 days PTA vomiting, 3x, nonprojectile, postprandial, partially digested food
Few hours PTA persistence, consult- admitted IM-ER Dx: UGIB 2 PUD R/O Gastric Malignancy CBC, PC, BT, CXR electrolytes done (+) Saline loading test BT, 2 u PRBC ordered
Course in the Ward: IM • NPO, NGT • Meds: • FeSO4 tab, TID • Ranitidine 50mg TIV, q12 • No Subjective complaints • PPE: E/N • Plan: EGD • Referred to Surgery
Past Medical History: NSAID use Family History: no history of cancer in the family Personal Social History: non-smoker non-alcoholic beverage drinker
Physical Examination: • Conscious, coherent, ambulatory, NICRD • BP:110/70 CR:75 RR:21 T:37ºC • Pale palpebral conjunctiva, anicteric sclerae • Supple neck, (-) cervical LAD • Symmetrical chest expansion, clear breath sounds • Adynamic precordium, normal rate & regular rhythm • Flat, NABS, soft, (+) slight Direct tenderness, epigastric area, no mass • DRE: (+) yellow feces on tactating finger
Salient Features: • 68F • Known case of PUD • Epigastric pain, • Gastrointestinal reflux, regurgitation • Vomiting • Slight tenderness Epigastric area • DRE: E/N
VOMITING Mechanical Systemic Neurologic Infectious UGIT LGIT Esophagus Stomach Duodenum Colon Small Bowel • Mechanical Obstruction • Stricture • Mass Sphincter Fnxn Mechanical Obstruction
Do I need a para-clinical diagnostic procedure? Yes. • To increase the certainty of my primary diagnosis. • To determine my treatment plan
Endoscopy Result: Gastric Outlet Obstruction; pyloric channel, secondary to healed pyloric ulcer, 98% obstructing No Biopsy done
Goals of Treatment: • Resolution of the obstruction • Maintenance of bowel continuity • No recurrence • No complications
TREATMENT OPTIONS *Csendes A. et al. RCT on three techniques for GOO treatment. *Millat B. Surgical treatment of complicated Duodenal ulcer: RCT
Pre-op preparation: what I will do • Informed consent secured • Psychosocial support provided • Optimized patient’s physical health • Correction of anemia/electrolytes • Nutritional build-up • Patient screened for any health condition • Operative materials secured
Intra-op Management: How I will do It (Vagotomy, Gastrojejunostomy) • Patient supine under GETA • Asepsis and antisepsis technique • Sterile drapes place • Long vertical incision from xyphoid to supraumbilical area
Isolation/ligation of nerve trunk, anterior, posterior and esophageal branches • Anterior vagal trunk is encircled with hook and dissected sharply from esophageal musculature • Nerve trunk is ligated proximally and distally
Postoperative care: • Intravenous fluids • nasogastric decompression • Analgesics • hemodynamics • The nasogastric tube is removed upon return of gastrointestinal transit, and feeding is slowly begun.
Outcome: • Resolution of obstruction • Live patient • No complications • Satisfied patient • No medico-legal suit
SURGERY FOR PEPTIC ULCER DISEASE(PUD) • Ulcer in the GIT is characterized by an interruption in the mucosa stretching through the muscularis mucosa into the submucosa or deeper • Location - in order of decreasing frequency • Duodenum • Stomach • Esophagus
Classification of Gastric Ulcers(GU) ( Gaintree – Johnson ) • Type 1 = incisura on the lesser curvature. No increased acid secretion. Mucosal resistance problem. • Type 2 = Gastric and duodenal ulcer. Gastric ulcer secondary to gastric stases caused by duodenal ulcer. • Type 3 = Prepyloric ulcer within 2-3cm of the pylorus. Often acid hypersecretors. Association with blood group O. Treated like duodenal ulcer.
Type 4(Csendes) = High on lesser curvature near gastro-esophageal junction. As Type 1. • Type 5 = Secondary to chronic use of non-steroidal anti-inflammatory drugs (NSAID). Can occur anywhere in the stomach.
Pathogenesis • Still debated • Traditionally duodenal ulcers are seen as a problem with acid hypersecretion and gastric ulcers as a mucosal resistance problem
Gastric acid. Central in pathogenesis – no benign ulceration occurs without gastric acid Gastric stases. Delayed emptying of normal amounts of acid with increased exposure
Enviromental factors are very important. a) Helicobacter pylori infection. 90% of patients with DU and 50% of patients with GU b) NSAID use. The mucus gel layer contains bicarbonate. This layer adheres to the gastric mucosa. It protects the mucosa against back diffusion of hydrogen ions. NSAID’s suppress mucus cell function. c) Smoking
4) Mucosal resistance 5) Genetic predisposition
DUODENAL ULCER 1) Epigastric pain – Central or slightly to the right Burning or gnawing Can spread to the back Relieved by ingestion of food or anti-acid Pain occurs when patient is hungry