3. STOMACH
SAC-LIKE ORGAN LOCATED MOSTLY IN THE LEFT
UPPER PART OF THE ABDOMEN
HAS 2 SURFACES (ANTERIOR & POSTERIOR), 2
CURVATURES (GREATER & LESSER), & 4 REGIONS
(CARDIA, FUNDUS, PYLORUS,& ANTRUM
The gastric wall is made up of 4 layers: mucosa,
submucosa, muscularis propria, and serosa
4. STOMACH
The mucosa forms thick longitudinally oriented folds
or rugae which flatten with distention.
The muscularis propria is a combination of 3 muscle
layers: inner oblique, middle circular and outer
longitudinal
8. STOMACH
It functions primarily as a reservoir to store large quantities
of recently ingested food
Its volume ranges from about 30ml in a neonate to 1.5 to 2L
in adulthood.
The gastroesophageal junction generally lies to the left of
the 10th thoracic vertebral body, 1-2cm below the
diaphragmatic hiatus.
The gastroduodenal junction lies at L1 and generally to the
right of the midline, but may be lower
9. STOMACH
ANTERIOR RELATIONS – DIAPHRAGM, ANTERIOR
ABDOMINAL WALL, LEFT COSTAL MARGIN, & THE
LEFT LOBE OF THE LIVER
POSTERIOR RELATIONS – LESSER SAC, PANCREAS,
LEFT SUPRARENAL GLAND, LEFT KIDNEY, SPLEEN,
SPLENIC ARTERY, & THE TRANVERSE COLON
SUPERIOR RELATIONS – LEFT DOME OF THE
DIAPHRAGM
11. STOMACH
BLOOD SUPPLY: FROM THE COELIAC AXIS – LEFT
GASTRIC, SPLENIC (SHORT GASTRIC & LEFT
GASTROEPIPLOIC), HEPATIC
(GASTRODUODENAL[SUPERIOR
PANCREATICODUODENAL & RIGHT EPIPLOIC],
CYSTIC, & RIGHT GASTRIC)
13. STOMACH
NERVE SUPPLY: VAGUS (ANTR & POSTR) The vagus
constitutes the motor and secretory nerve supply for
the stomach. When divided, in the operation of
vagotomy, the neurogenic (reflex) gastric acid
secretion is abolished but the stomach is, at the same
time, rendered atonic so that it empties only with
difficulty
14. STOMACH
; because of this, total vagotomy must always be
accompanied by some sort of drainage procedure, either a
pyloroplasty (to enlarge the pyloric exit and render the
pyloric sphincter incompetent) or by a gastrojejunostomy
(to drain the stomach into the proximal small intestine).
Drainage can be avoided if the nerve of Latarjet is
preserved, thus maintaining the innervation and function
of the pyloric antrum (highly selective vagotomy).
15.
16. STOMACH
The sympathetic innervation is derived from
preganglionic fibers arising predominantly from T6 to
T8 spinal nerves.
20. DUODENUM
DUODENUM
25cm LONG, C-SHAPED CURVE AROUND THE HEAD OF THE PANCREAS,
DIVIDED INTO 4 PARTS
1ST PART
5cm LONG, ASCENDS FROM THE GASTRODUODENAL JUNCTION,
OVERLAPPED BY THE LIVER & GALL BLADDER
IMMEDIATELY POSTR ARE THE PORTAL VEIN, COMMON BILE DUCT &
GASTRODUODENAL ARTERY SEPARATING IT FROM THE INFERIOR VENA
CAVA
• 2nd PART
7.5CM LONG, DESCENDS IN A CURVE AROUND THE HEAD OF
PANCREAS, CROSSED BY THE TRANSVERSE COLON & LIES ON THE
RIGHT KIDNEY AND URETER
21. DUODENUM
3rd PART
10cm LONG, RUNS TRANSVERSELY TO THE LEFT
CROSSING THE INFERIOR VENA CAVA, AORTA & L3
VERT
• 4th PART
ASCENDS UPWARDS & TO THE LEFT TO END AT THE
DUODENOJEJUNAL JUNCTION
• BLOOD SUPPLY – THE SUPERIOR & INFERIOR
PANCREATICODUODENAL ARTERIES
22. DUODENUM
The luminal surface of the duodenum is lined with
mucosa, forming circular folds known as the plicae
circulares or valvulae conniventes
The duodenal bulb has smooth, featureless mucosa
The duodenal wall is composed of outer longitudinal and
inner circular muscle layers
The first few centimeters of the duodenum are
intraperitoneal, whereas the remainder is retroperitoneal
27. INTRODUCTION
Gastric outlet obstruction is not a single entity.
GOO is the clinical and pathophysiological
consequence of any symptom complex that produce a
mechanical impediment to gastric emptying.
It usually follows chronic PUD
29. Epidemiology
Incidence of GOO has been reported to be less than
5% in patients with PUD
Though is the leading benign cause GOO
Peri-pancreatic malignancy is the leading malignant
cause
FMC Owerri (jan 2011 – oct 2012)
7 cases of GOO
3 – PUD, all male
4 – gastric ca
30. Etiology
The factors predisposing to chronicity of PUD may
include:
- persistent imbalance between the
aggressive and defensive factors
- non eradication of H. pylori infection
- non compliance to anti PUD
medication etc.
31. Etiology contd
However, GOO usually occur at the pyloro-duodenal
area.
It is caused by:
- cicatrization
- edema
- pyloro-duodenal spasm
32. Pathogenesis/ pathophysiology
Obstruction of the stomach
hypertrophy of the stomach
Dilatation
Gastritis &
depressed acid secretion
35. HISTORY
AGE:20-45 years with peak 30-35 years
Known or suspected case of chronic pud
Epigastric and Lt hypochondrial pain :
-relieved by alkali, milk +/- food.
-gnawing/biting
-periodic (spontanous healing)
-association with food and time of day
-radiates to the back (?pancrease
penetration
-Generalised (perforation)
36. Anorexia,nausea.
Easy satiety
Vomiting: -characteristic unpleasant
-copious
-projectile
-Non bilous
-Food taken several days ago.
37. Feeling of unwell
Appetite is maintained but fear of pain often prevent
patient from eating
Weight loss.
Abdominal swelling
41. investigation
2)To confirm diagnosis
Plain x-ray of abdomen:shows large gastric shadow
and a large amount of gastric fluid.
Gastric aspiration:a wide bore stomach tube is placed
early in the morning and the stomach is aspirated of
resting juice.if >400ml of juice is obtained a
presumptive diagnosis of GOO can be made.
42. investigation
Esophagogastroduodenoscopy + biopsy(histology and
bacterioloical investigation).
Aim is to viualise the stomach mucosa and any
ulcer.
Barium meal:
-markely dilated stomach with a lot of residue
-presence of an ulcer crater
-trifoil deformity of the duodenal cap.
43. .
-Hour glass deformity
-Tea cup deformity
-Abrupt obstruction to barium
53. Intro…definitions.
PUD:
Break in acid secreting GIT
mucosa; exposed to acid and
pepsin secretn; more than 5mm in
diameter;heals by granulation
tissue formation.
Erosion:
Break in GI mucosa;not penetrating musclaris
mucosa;<5mm in diameter;occuring in both acid
secreting and non-acid secreting mucosa; heals rapidly
by epithelial bridging.
54. Intro…
Chronic PUDx is characterized by
-Presence of chronic inflam cells
-Reactive mucosal epithlial changes
-Attempt at healing
+-malignant changes.
55. Intro..
GOO 2* Chronic PUDx is a surgically
amenable obstructive complication of
PUDx.It includes pathologic entities such
as:
-Chronic PUDx with active edematous ulcer;
-Chronic PUDx with antral cicatrisation;
-Chronic PUDx with Pyloric stenosis;
-Hour glass stomach;
-Teapot stomach.
56. PRINCIPLES.
Guiding Principles lies in the
recognition of GOO as an emergency,
as such, GOAL of treatment include:
-1)Resuscitation/stabilization.;
-2)Relieve obstruction;
-3)Patient selection/categorization;
-4)Offer definitive curative care;
-5)Prevent recurrence/Follow up care.
57. Principles…Factors
Factors Influencing Choice Of Tx:
Patient-specific Factors
i).Stability:Shock,Fluid and
electrolyte imbalance.
ii)Obesity:DVT prophylaxis,
concomitant bariatric surgery
iii)Age:Better outcome in younger
age
iv)Comorbidities:Dm,Htn.
58. Principles…..Factors cont’d
Lesion-related Factors:
i)Nature:e.g edema Lavage+H.pylori rx
ii)Location:Duodenal/Pyloric antral/
Body/Fundus/cardia.
iii)Associated Deformity:Resections
iv)Presence of malignant
transformation:Resections
Surgeon’s expertise/Materials and
manpower available
59. ……Patient selection/category
Acutely Obstructed/Chronically
Obstructed group:Nonop Tx for
acutely obstructed.
Frail Elderly:Low life expectant
group:Nonop e.g. balloon dilation.
Stable/Unstable group:Limited
surgical time,extent of resection e.t.c
Low/High lying lesion/Deformity.
60. GENERAL MEASURES.
Resuscitation: (Wide bore canular)
i).Antishock Therapy:IVF NS/Ringer’s
@25ml/kg over 1st 30mins then
repeated and reassess
ii).Urethral catheter:Input/output
monitor@30-50ml/hr.(CVP@10-15cmH20)
iii).NGT-Decompress,lavage and
aspirate
61. General Measures…cont’d
Iv)Correction of electrolyte
Imbalance: K+ correction,ensuring
urine output,
ideally under ECG monitoring.
V)Correction of anemia.
Vi)Renal challenge after adequate
fluid volume resuscitation.
Vii)Renal dialysis(resuscitative) in
uremia.
62. General measures..
Viii)Calorie-Maintaining with fluid
@ 100ml/kg first 10kg,50ml/kg 2nd
10kg, 25ml/kg subsequent kgs.
Ensuring at least 100g of glucose is
delivered(in 2liters of 5%Dw)
Ix)TPN:With period of inanition
>7days, marked weight loss
64. SPECIFIC/DEFINITIVE MEASURES
NONOPERATIVE MEASURES:
i)Warm Saline Lavage+H.Pylori
Eradication(usu for acute
edematous active ulcer)Recurrence
high in chronic active edematous
ulcers.
ii)Endoscopic Balloon dilation.May
be useful in elderly frail patients
unfit for surgery.Repeat necessary.
65. SPECIFIC/DEFINITIVE MEASURE.
OPERATIVE MEASURES:
Operative Principle:
i-Surgically achieving physiologic
control of acid production;
ii-Ensuring normal gut
continuity(Resection and
Reconstruction);
iii-Minimizing Postgastrectomy
&Postvagotomy sequalae.
67. SPECIFIC MEASURES…
1)Antral Oedema with Failure Of
Lavage or Recurrence:
a)Parietal Cell Vagotomy+ GJ+H.Pylori
Eradication.
(It maintains antral innervation,
prevents ductal motility problems and
lesser sequalae).
Nb:Criminal nerve of Grassi must be
identified and severed.
72. Completeness Test(Postvagotomy)
Intraop Tests
I)Burge Test-Manometer passed via
esophagogastric balloon and pylorus is
stimulted.Any change in pressure
indicates incomplete vagotomy.
II)Grassi Test-Glass electrode inserted
through an gastrostomy to measure P.H
and MAO.A p.H 1.2-2 surrounded by
area of 5.5-7,indicate actual area of
incomplet.
73. Postop Test
i)Pentagastrin test -Peak acid
output reduction of >/50% is
indicative of completeness.
ii)Insulin (Hollander’s )test. Largely
prognostic.Done 1week post
vagotomy.If positve in a short time,
recurrence risk is high.
75. Postgastrectomy Synd(Related
to Resection)
i)Early dumping -Results from
disruption of the pyloric sphincter
mechanism>Hyperosmolar chyme
transit>rapid shift of fluid>luminal
distension>autonomic responses.
Occurs 20-30mins after ingestion
of meal. Characterized by both GI
and cardiovascular symptoms.
76. Cardiovascular symptoms-
flushing, diaphoresis,
palpitations,dizziness,
fainting,blurring of vision.GI-
nausea, vomiting,explosive
diarrhea, cramping abd.pain.
Mgt-Patient informed preop
-Spontaneous relief.
-Dietary(less sugar),freq. small
meals(Most will resolve).
77. -Long acting somatostatin analogue
(octreotide) is highly effecttive for both
GI and CV symptoms in longstanding
cases.Its expensive.
-<1% fail to respond to conservative tx:
+Jejunal 20cm Isoperistaltic loop
Interposition(dilates overtime,reservoir
fxn)
+Jejunal 10cm antiperistaltic loop
interpositn(substitute pylorus,delaying
emptying)
78. ii)Late Dumping -Result from rapid
gastric emptying too but specifically
for CH2O meal being delivered>
quickly absbd>Hyperglycemia> large
amt of insulin release>OVERSHOOT
> Profound hypoglycemia.
Adrenaline release-diaphoresis,
tremor ,giddiness ,confusion
Mgt-Small meals,less CH2O.
-Antiperistaltic loop.
79. Complications…cont’d
Postgastrectomy Synd(Related to
Reconstruction):
iii)Affarent loop synd :May occur
within few days of op or years after.Usu
when>30-40cm.Xterised by a).RUQ
abd.pain radiating to interscapular
area.
b)Projectile bilious vomiting not
containing food and relieves
symptoms.
80.
81. Mgt(a surgical emergency).
-A high index of suspicion.
-Convert BillrothII to I.
-Enteroenterostomy (e.g Braun,
easier) below the stoma.
-Creation of a Roux-en-Y
82. iv)Efferent loop synd: Quite rare.
>50% occur within 1st mth postop.
Usu from herniation of limb
behind anastomosis (R-L fashion).
Mgt-Reduce retroanastomosis
hernia
-Close retroanastomosis space.
83. v)Duodenal Blow out: Usu occurs
4-5th day postop.Life threatening.
Mgt-Control fistula and sepsis
-Enteroenterostomy later.
84. Vi)Postvagotomy
diarrhoea:Occurs in >30% of
px.Part of Dumping synd. Usu
disappears after 3-4 mths.
Mgt-self limiting
-Cholestyramine(4g tds)
-<1% lasting >1year,Jejunal
Interposition.
85. Vii)Postvagotomy Gastroparesis:
Occurs in both TV&SV, not in PCV.
Paresis allows liquid(loss of receptive
relaxation) not solid(dependent on
antral pump mech)
Mgt-Prokinetics
[Metochlopramide(cholinergic
enhancing) and Erythromycin(motilin
receptor binding)].Usu suffices.
87. ix)Alkaline Reflux Gastritis:
severe epig pain+bilious
vomiting+wgt loss. Usu ffng
Billroth II.
Diagnosis largely clinical but HIDA
scan shows bile reflux into
stomach/esoph endoscopy show
beefy red ,friable mucosa.
Mgt-BillrothII to a Roux-en-Y GJ.
88. X)Blind Loop synd.:Bacterial
overgrowth in static loop causing bind
B12 and deconjugate bile acid with
resultant Megaloblastic anemia.
Xi)Retained Antrum synd:From
retained terminal antrum in the duod
stump,continually bathed in alkaline
secretion>increased gastrin
release>increased acid secretion>
recurrent ulcer.
89. FOLLOW UP.
Events in the follow up period
i-H.Pylori Eradication
ii-H.pylori screening(to document
eradication)-serology
-CLUB test(4weeks after)
iii-BAO output monitoring
iv-Yearly upper GI endoscopy+biopsy.
v-Nutritional supplementation.
vi-Life style
modification(alcohol,smoking)
90. PROGNOSIS
Factors affecting Prognosis:
i)Age/Physiologic reserve-H.pylori
infection load increases by about
1%/year(more in elderly and they
present more severe
complication.Less physiologic resrve
to tolerate homeostatic changes from
GOO.
ii)Duration of illness:Longer the poorer
early presentation is better outcome.
92. CHALLENGES
i)Poor patient knowledge
base/compliance to medical therapy.
ii)Substandard medications for HPE
iii)Poor status of health facility(
screening test,endoscopy)
Iv)Financial constraints HPE(PPI)
V)Poor life style/socioeconomic status
93. CONCLUSION:
Though PUDx is largely medically
managed with the place of the
surgeon gradually being relegated
to the background following
improved medical therapy.
However, considering our third
world and its attendant
constraints,the surgeon’s place can
not be overemphasized.
