Transcript Preoperative Case Presentation & Sharing of Information on Vomiting Jeffy G. Guerra, MD Level III Surgery Resident OMMC-Surgery.

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, consultadmitted 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
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•
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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:
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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:
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68F
Known case of PUD
Epigastric pain,
Gastrointestinal reflux, regurgitation
Vomiting
Slight tenderness Epigastric area
DRE: E/N
VOMITING
Mechanical
Systemic
Neurologic
Infectious
Esophagus
Sphincter Fnxn
Mechanical Obstruction
UGIT
Stomach
LGIT
Duodenum
Mechanical Obstruction
A. Stricture
B. Mass
Small Bowel
Colon
Clinical Diagnosis:
Diagnosis
Gastric outlet
obstruction 2
stenosis 2 PUD
Gastric Outlet
obstruction 2 to
gastric mass
Certainty
70%
Treatment
Medical/Surgi
cal
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 Procedure
Benefit
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
Gastric outlet
obstruction 2
stenosis 2 healed
PUD
Gastric Outlet
obstruction 2 to
stenosis 2
malignancy
Certainty
Treatment
95%
Surgical
5%
Surgical
Goals of Treatment:
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Resolution of the obstruction
Maintenance of bowel continuity
No recurrence
No complications
TREATMENT OPTIONS
BENEFIT
Resolution of
obstruction
Vagotomy +
Antrectomy
Vagotomy +
Jaboulay
gastroduod
enostomy
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RISK
COST
AVAILABI
LITY
Bowel continuity
Local recurrence
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MR: 5%
RR: 2%
3k
/
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MR:1%
RR: 10%
3k
/
Vagotomy +
gastrojejun
ostomy*
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MR: 1%
RR: 1%
3k
/
Endoscopic
baloon
dilatation
/
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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)
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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:
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Resolution of obstruction
Live patient
No complications
Satisfied patient
No medico-legal suit
Sharing of information
SURGERY FOR PEPTIC ULCER
DISEASE(PUD)
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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 nonsteroidal 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)
5)
Mucosal resistance
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
Epigastric pain – Brought on by meals
often within 30 minutes
2) Nausea and vomiting
3) Weight loss
4) Epigastric tenderness
1)
Complications
1)
2)
3)
4)
Bleeding
Perforation
Gastric outlet obstruction
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)
5)
IV H2-blockers or proton pump inhibitors.
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 problems
a)
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 problems
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.
a)
– 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): 2669[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.
b.
c.
d.
e.
vomiting
hyponatremia
hypochloremia
epigastric pain
All of the above
2. What is the most common complication of peptic ulcer
disease?
a.
b.
c.
d.
bleeding
perforation
intractability
obstruction
3. The following statements is/are true regarding gastric
outlet obstruction.
1.
2.
3.
4.
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.
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 ?
1.
2.
3.
Bleeding
anastomotic leakage
hepatobiliary-pancreatic complications (pancreatitis,
bile duct injury)
4. gastrojejenocolic fistula
Thank you!