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Preoperative Case Presentation & Sharing of Information on Vomiting

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, consultRx: 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-ERDx: UGIB 2 PUDR/O Gastric MalignancyCBC, PC, BT, CXR electrolytes done(+) Saline loading testBT, 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

Systemic Mechanical

NeurologicInfectious

UGIT LGIT

Stomach Small BowelEsophagus Duodenum Colon

Sphincter Fnxn

Mechanical Obstruction

Mechanical ObstructionA. StrictureB. Mass

Clinical Diagnosis:

Diagnosis Certainty Treatment

Gastric outlet obstruction 2 stenosis 2 PUD

70% Medical/Surgical

Gastric Outlet obstruction 2 to gastric mass

30% Surgical

Do I need a para-clinical diagnostic procedure?Yes.• To increase the certainty of my primary

diagnosis.• To determine my treatment plan

Para-clinical Diagnostic ProcedureBenefit Risk Cost Availability

UGIS Sn rate: 80-85%

SP rate: 82%

radiation 2k /

Endoscopy with Biopsy

Sn rate: 95%

SP rate: 98%

perforation 5k /

CT scan Sn rate: 88%

SP rate: 85%

radiation 3k /

Endoscopy Result:

Gastric Outlet Obstruction; pyloric channel, secondary to healed pyloric ulcer, 98% obstructing

No Biopsy done

Pre-Treatment Diagnosis:

Diagnosis Certainty Treatment

Gastric outlet obstruction 2 stenosis 2 healed PUD

95% Surgical

Gastric Outlet obstruction 2 to stenosis 2 malignancy

5% Surgical

Goals of Treatment:

• Resolution of the obstruction• Maintenance of bowel continuity • No recurrence• No complications

TREATMENT OPTIONS BENEFIT RISK COST AVAILABI

LITY

Resolution of obstruction

Bowel continuity Local recurrence

Vagotomy + Antrectomy

/// /// MR: 5%

RR: 2%

3k /

Vagotomy + Jaboulay gastroduodenostomy

/// /// MR:1%

RR: 10%

3k /

Vagotomy + gastrojejunostomy*

/// /// MR: 1%

RR: 1%

3k /

Endoscopic baloon dilatation

/ /// MR: 1%

RR: 50%

15k x

*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

Mobilization of left lateral segment of the liver

Division of triangular ligament

Exposure of esophagogastric junction

Exposure of anterior vagus nerve

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

Drainage via Gastrojejunostomy

Anastomotic site

Posterior serosal suture

Gastric incision

Posterior mucosal suture

Anterior mucosal suture

Completion of anastomotic defect

Post-op Care

• 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

Sharing of information

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

Epidemiology  

Gastric ulcer Duodenal ulcer

Age 40 – 60 20 – 45

Sex M : V = 1.5 : 1 M : V = 3 : 1

Socio-economic Lower Higher

Blood group A O

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

Clinical Picture

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

2)    Different degrees of nausea and vomiting

3)    Weight gain ( Pain relieved by ingestion of food)

4)    Epigastric tenderness just to the right of the midline, may be absent.

GASTRIC ULCER

1)    Epigastric pain – Brought on by meals often within 30 minutes

2)    Nausea and vomiting

3)    Weight loss

4)    Epigastric tenderness

Complications

1)    Bleeding

2)    Perforation

3)    Gastric outlet obstruction

4)    Penetration

Management

• Surgery is indicated and for the following:

1)    Non-healing ulcer ( 8 – 12 weeks for GU, DU can be managed conservatively for longer since the risk for malignancy is low)

2)    Complications • a) Perforation

b)  Bleeding if massive,

c)  Gastric outlet obstruction that does not clear up on conservative management.

Surgical principle for definitive ulcer surgery

Definitive ulcer operations for GU

• Type 1 GU partial gastrectomy. Vagotomy not done.

• Type 2 and 3 GU treated as DU. HSV contra-indicated due to high ulcer recurrence with prepyloric ulcers.

• Type 4 GU treated with partial gastrectomy and excision of a long tongue of lesser curvature including the ulcer(Pauchet procedure).

Gastric outlet obstruction

• Cycles of inflammation and repair may cause obstruction at the gastroduodenal junction as a result of edema, muscular spasm and fibroses.

• Edema and spasm can resolve with medical treatment.

• Obstruction is mainly caused by DU and prepiloric GU.

• Malignant tumors is the other important cause of gastric outlet obstruction.

• normal pylorus is about 20 mm in diameter and can distend to 25 mm

• gastric outlet obstruction occur when the diameter of the antroduodenal segment is below 10 mm

• A saline load test can be utilized in the objective measurement of outlet obstruction or gastric atony and the assessment of response to therapy

• The major benign causes of GOO are PUD, gastric polyps, ingestion of caustics, pyloric stenosis, congenital duodenal webs, gallstone obstruction (Bouveret syndrome), pancreatic pseudocysts, and bezoars

Clinical picture

• Longstanding history of PUD

• Progressive worsening of ulcer pain and early satiety.

• Vomiting after meals of partially digested food without bile ( food eaten earlier the day or the previous day).

• Dehydration and severe weight loss.

• Visible peristalses of the dilated stomach (rarely).

• Succussion splash audible with to and fro movement of abdomen.

• Tetany in cases of advanced alkaloses.

• Develop hyponatremic, hypokalemic, hypochloremic metabolic alkaloses

Management

1)    Resussitation initially with 0.9% sodium chloride. Potassium supplementation only after good urine output is established.

2)    Gastric lavage with thick stomach tube ( 32 F) to remove food residue.

3)    Diagnostic tests after gastric lavage : Gastroscopy with biopsies with or without barium meal to rule out malignancy.

4)    IV H2-blockers or proton pump inhibitors.

5)    A nasogastric tube is passed. The patient may drink water. The amount of oral intake and drainage is charted. This gives an impression whether the obstruction is resolving.

6)    Balloon dilatation of pyloric channel is possible but seldom produces a final solution.

7)   Surgery is indicated if the obstruction does not resolve after one week of conservative treatment. Mostly a truncal vagotomy and antrectomy is done although truncal vagotomy with a drainage procedure is sometimes performed.

Complications of PUD surgery

Complications due to vagotomy

• Intraoperative complications can occur with injury to adjacent structures.

• Early post-operative complication – delayed gastric emptying – dysphagia and lesser curve necroses( lesser

curve necroses specific to HSV).

• Late complications include postvagotomy diarrhea, reflux esophagitis and gallstones

Complications of gastrectomy

• Early complications – bleeding– anastomotic leakage– obstruction – hepatobiliary-pancreatic complications

(pancreatitis, bile duct injury)

• Late complications are classified as follows :

– 1)    Ulcer recurrence

a) Recurrent ulcer (anastomotic,stomal,marginal)

b) gastrojejenocolic fistula

2)    Mechanical problemsa)    Chronic afferent loop obstruction after BII

anastomoses – abdominal pain relieved by vomiting , vomit mainly bile without food.

b)    Chronic efferent loop obstruction

c)    Internal herniation, jejenogastric intussusception and late gastroduodenal obstruction

3)   Pathophysiologic problemsa)    Alkaline reflux gastritis – reflux of bile into stomach.

Pain not relieved with vomiting. Vomitus contains food and bile.

b)    Dumping(I)Early dumping – symptoms within 20 minutes after meal. Gastro-intestinal : Abdominal cramps, satiety, nausea, vomiting and explosive diarrhea. Cardiovascular : sweating, dizziness, weakness,dyspnea, palpitations and flushing.

– Due to sudden release of high osmolality chyme into duodenum with fluid shifts and release of gastro-intestinal hormones.

• (II) Late dumping – only vasomotor symptoms. Caused by enteroglucagon secretion which leads to increased and prolonged insulin secretion with resultant hypoglycaemia.

4)   Malabsorption and Nutritional problems

a)    Malabsorption of protein, carbohydrates and fat

b)   Early satiety

c)   Anemia : Fe, folate and B12 deficiency. B12 problems mostly after total or near total gastrectomy.

d)   Osteopmalacia

References:1. Csendes A. Maluenda F. et al. Prospective randomized controlled trial

comparing three surgical techniques for the treatment of gastric outlet obstruction secondary to duodenal ulcer. Am J Surg. 1993 Jul 166:45-49

2. Edwards LW, Herrington JL Jr. Vagotomy and gastroenterostomy—vagotomy and conservative gastrectomy. Ann Surg, 1953; 137: 873– 83.

3. Emas S, Fernstrom M. Prospective, randomized trial of selective vagotomy with pyloroplasty and selective proximal vagotomy with and without pyloroplasty in the treatment of duodenal, pyloric and prepyloric ulcers. Am J Surg, 1985; 149: 236–43.

4. Fischer AB. Twenty-five years after Billroth II gastrectomy for duodenal ulcer. World J Surg, 1984; 8: 293–302.

5. Kuwada, S et al. Long-term outcome of endoscopic dilation of nonmalignant pyloric stenosis. Gastrointestinal Endoscopy 1995; 41(1) 15-17.

6. Gibson JB, Behrman SW, Fabian TC: Gastric outlet obstruction resulting from peptic ulcer disease requiring surgical intervention is infrequently associated with Helicobacter pylori infection. J Am Coll Surg 2000 Jul; 191(1): 32-7[Medline].

7.Millat B, Fingerhut A et al. surgical treatment of complicated duodenal ulcer. Controlled trial. World J Surg. 2000 Mar. 24(3) 299-306.

8. Siu WT, Tang CN, Law BK, et al: Vagotomy and gastrojejunostomy for benign gastric outlet obstruction. J Laparoendosc Adv Surg Tech A 2004 Oct; 14(5): 266-9[Medline].

9. Haglund UH, Jansson RL, Lindhagen JG, Lundell LR, Svartholm EG, Olbe LC.Primary Roux-Y gastrojejunostomy versus gastroduodenostomy after antrectomy and selective vagotomy.Am J Surg. 1992 Apr;163(4):457-8.

Questions

1. Gastric Outlet Obstruction secondary to healed pyloric ulcer may present with which of the following?

a. vomiting

b. hyponatremia

c. hypochloremia

d. epigastric pain

e. All of the above

2. What is the most common complication of peptic ulcer disease?

a. bleeding

b. perforation

c. intractability

d. obstruction

3. The following statements is/are true regarding gastric outlet obstruction.

1. Cycles of inflammation and repair may cause obstruction at the gastroduodenal junction as a result of edema, muscular spasm and fibroses.

2. Edema and spasm can resolve with medical treatment.3. Obstruction is mainly caused by DU and prepiloric GU. 4. Malignant tumors is the other important cause of

gastric outlet obstruction.

4. Which of the following choices is/are late complication/s of vagotomy?

1. postvagotomy diarrhea,

2. reflux esophagitis and

3. Gallstones

4. Delayed gastric emptying

5. Which of the following is/are not early complication of gastric surgery ?

6. Bleeding

7. anastomotic leakage

8. hepatobiliary-pancreatic complications (pancreatitis, bile duct injury)

9. gastrojejenocolic fistula

Thank you!