LESSON: “GASTRORESECTIONAL SYNDROMES”

Figure 1. Anatomy of the stomach

Figure 2. Blood supply of the stomach

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Figure 3. Lymphatic drainage of the stomach

Figure 4. Anatomy of the vagus nerves

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Figure 5. Anatomic structure of a mammalian gastric gland from fundic mucosa.

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Classification of postgastroresectional syndrome:
I. Organic affections:
- recidivant peptic ulcer
- jejunal peptic ulcer
- gastroenterocolic fistula

II. Postgastroresectional syndromes:

- small remnant syndrome
- early Dumping syndrome
- tardive Dumping syndrome (hypoglycemic)
- alkaline reflux gastritis, reflux esophagitis
- acute afferent loop syndrome
- chronic afferent loop syndrome

III. Postvagotomy syndromes:

- disfagia
- gastrostasis
- duodenostasis
- diarrhea

IV. Malabsorbtion, maldigestion

I. Organic affections.

1. Recidivant peptic ulcer –in 95-98% of cases are represented by

patients which underwent surgery for duodenal ulcer. The
frequency of recidivant peptic ulcer depend of the type of
performed surgical intervence /FIGURE 6/.

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Fig.6 Corellation between frequency of peptic ulcer and type of performed surgical intervences

Tipul operaţiei Frecvenţa (%)

Rezecţie gastrică 2/3 1–7

VT + rezecţie gastrică economă 0–4

VT + operaţie de drenaj gastric 8 – 12

VSP 6 – 10

Causes of recidivant peptic ulcer are various, but more frequent is /FIGURE 7/:
- keeping of the antrum at the end of afferent loop
- incomplete vagotomy
- stenosis of gastroduodenoanasthomosis
- Zollinger-Ellison syndrome (gastrinoma)
- primary hyperparathireasis (parathireoidian adenoma)

Fig.7 Causes of recidivant peptic ulcer

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 Clinical manifestations.Peptic ulcer
recidived, as a rules, durind first two postoperative
years. Epigastral pains are permanent and more
intensive (penetration in pancreas), resistant to
antacids drogs, associated by diarrhea.
Complications – ulcerous bleeding (20% of cases);
anemic status (in 50% of cases resulting from
Fig.8. Radiography of stomach. oculte bleeding and absorbtion disorders);
Peptic ulcer of
gastroenteroanasthomosis. penetration with gastrojejunocolic fistula;
perforation (in 1-9% of cases).
Diagnostic studies – radiologic contrast exploration of stomach /FIGURE 8/.
Endoscopia is the method of choice – localization of the ulcer, dimensions, biopsy
for the diagnosis of carcinoma or H. pylori infection,
which appears to be a significant factor in peptic ulcer and gastritis.
Treatment. Preoperative conservative therapy is indicated to diminish
periulcerous inflammatory tumefication. The aim of surgical reintervence is to
eliminate the cause of recidive of peptic ulcer.
After Bilroth-I resection is necessary to perform reresection Bilroth-II or
truncal vagotomy (diminish hypersecretion of HCl) /FIGURE 9/.

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 The
causes of
recidive
of peptic
ulcer
after
Bilroth-II
resection
Fig.10 Peptic ulcer of GEA or residual antral mucosa. Reconstruction of GEA Bilroth-II in
Bilroth-II in ”Y”-loop /a la Roux/.
Fig.9 Surgical treatment of peptic ulcer are
A – gastroduodenoanasthomosis
B – reresection Roux ecomomical gastric resection, residual antral
C – reresection Balfour
mucosa above duodenal stump, gastrinoma.
In these cases is necessary to perform gastric reresection or resection of antrum
portion above duodenal stump /FIGURE 10/, to
appreciate serum gastrin.

Fig.11 Peptic ulcer of jejunum

Ulcer peptic jejunal.

2. Peptic ulcer of jejunum – apaire after Bilroth-II gastric

resection /FIGURE 11/. Causes of peptic ulcer of jejunum are high secretion of the
mucosa of gastric stump, residual antral mucosa above duodenal stump, elevated
sensibility of jejunal mucosa to peptic action of gastric juice.

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 Clinical manifestations – permanent pains localized in left epimesogastrium,
irradiating in left lombar region and left hemithorax, muscular reaction and
sensibility in the point of proiection of gastroenteroanasthomosis.

Fig.12 Surgical treatment of peptic ulcer of jejunum

I – Reduodenization
II – Reduodenization by gastroduodenojejunoplastia

Diagnostic studies. pH-metria of gastric mucosa (hypersecretion of HCl),

serum gastrin. Radiography of gastric stump – ulcerous defect at the level of
jejunum. Endoscopia – ulcer of jejunal segment, implicated in
gastroenteroanasthomosis.
Treatment. Conservative therapy is ineffective. Surgical treatment – gastric
reresection with compromised jejunal loop, finished with restoration of digestive
tract’s integrity by reduodenization, gastroduodeno- and jejuno-
jejunoanasthomosis /FIGURE 12, I/ or by
gastrojejunoduodenoplastia /FIGURE 12, II/. In case of peptic ulcer of
jejunum, determined by Zollinger-Ellison syndrome, it is necessary to perform
excision of abenoma (isolated forms), corporal or caudal resection of the pancreas
(diffuse forms).

3. Gastrojejunocolic fistula – resulting from penetration of peptic ulcer of

jejunum into transverse colon /FIGURE 13/.

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Clinical manifestations – postprandial diarrhoea, aparison of indigested foods in
stool, fetid eructation, vomiting with fecal content, weight losses, cahexia, anemia,
disproteic periferic edema. In left epigastriu can be palpated fixed painfull
tumefication, muscular rigidity.
Diagnostic studies. Gastric radiography and passage will detect momentan
evacuation of contrast from stomach to colon. Irigofraphy – exaggerated gas bule
of stomach, adnormal penetration of the contrast into stomach. Chromoscopia -
coloured solution, administrated orally or by clyster, showed presence of fistula
(coloured gastric juice or stool).
Treatment is exclusive surgical – reresection with gastroduodeno-,
gastroduodenojejunoplastia or reresection by Roux technique. The integrity of
colon can be restored primary or in second stage – colostoma, reconversion of
digestive tube after 2-3 months by end-to-end colo-coloanasthomosis.
4. Recidivant peptic ulcer after vagotomy. Causes – incomplete vagotomy
with hypersecretion of HCl or inadecvate gastric drainage. Diagnostic studies –
gastric pH-metria, fibrogastroduodenoscopia.
Treatment – conservative therapy (H2-
blocators, inhibitors of protonic pump).
Surgery – truncal vagotomy +
piloroantrumectomia Bilroth-I or Bilroth-II, in
case of duodenostasis – reresection by Roux
technique.

Fig.13 Gastrojejunocolic fistula II. POSTGASTRORESECTIONAL

SYNDROMES

1. Small remnant syndrome – is caused by reduced gastric capacity.

Clinialc manifestations – postprandial discomfort in epigastrium, eructations,

nausea, vomiting. Diagnostic studies – gastric radiography will detected reduced
gastric capacity and the speed of emptying into duodenum or jejunum.

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 2. Dumping syndrome – the most characteristic complications after

surgical intervences on stomach (10-30% of cases). Surgical intervence is indicated

in 1-9% of patients with grave forms of Dumping syndrome (after gastric
resection by Bilroth-II technique females for 2-3 times more frequently).
Ethiopathogeny. Dumping syndrome is one pathologic state after
gastric resection, which apaire after ingestion of easy assimilated foods (especially,
carbohydrates), characterized by neurovegetative, vasomotor (diffusion of
intravascular and intercellular fluids in intestinal lumen) and intestinal
disorders /FIGURE 14/. Although the exact mechanism has eluded
definition, it appears to be related to the rapid emptying of hyperosmolar chyme,
particularly carbohydrate, into the intestine. This draws fluid into the intestine
and probably releases one or more vasoactive hormones, such as adrenalin,
serotonin and vasoactive intestinal polypeptide (VIP). This is associated with
epigastric distention, cramps, nausea, vomiting, dizziness, flushing, and
palpitations.
Pathophysiological aspects of Dumping syndrome:
- release of vasoactive amines → early vasomotor symptoms; dyspeptic
symptoms: nausea, diarrhea;
- hipovolemia → tahicardia, ↓ arterial pressure, ↓ circulant blood
volume with 15-20%, electrocardiographic changes, dizziness;
- hyperglycemia → hyperinsulinemia →
hypoglycemia;
- dismethabolic disorders → weight
losses, avitaminosis, anemia.

Diagnostic studies. Gastric radiography and

passage with barium mass detect accelerated
emptying of stomach (for 5 -6 times), diarrhea with
Fig.14 Pathoghenesis of
Dumping syndrome barium after 15 minutes of investigation. Test with

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intrajejunal administration of hyperosmolar glucosa (50% - 150 ml) – registred ↓
of arterial systolic pressure, tahicardia, dizziness etc.
Clinical manifestations. Main symptoms – epigastric distention, cramps,
nausea, vomiting, dizziness, flushing, and palpitations.
Classification of Dumping syndrome:
Grade I – easy – main symptoms persist for
15-20 minutes; PS is elevated with 10-15
per minute; arterial pressure is diminished
with 10-15 mm Hg; circulant volume of
blood is diminished with 200-300 ml;
weight losses about 5 kg. Work ability is
well. Dieta and medicamentous therapy
conduct to good results.
Grade II – medium – main symptoms
persist for 20-40 minutes; PS is elevated
Fig.15 Pathoghenesis of tardive Dumping
syndrome with 20-30 per minute; arterial pressure is
diminished with 15-20 mm Hg; circulant volume of blood is diminished with 300-
500 ml; weight losses about 5-10 kg. Work ability is reduced. Dieta and
medicamentous therapy temporary ameliorated general state of patient.
Grade III – severe – main symptoms persist for 1 -2 hours; PS is elevated with 20-
30 per minute; arterial pressure is diminished with 20-30 mm Hg; circulant volume
of blood is diminished more that 500 ml; weight losses more that 10 kg. Work
ability is absent. Dieta and medicamentous therapy are ineffective.
Tardive Dumping syndrome (hypoglycemic) – is manifested after 2-3 hours
from alimentation. Ethiopathoghenesis. Early Dumping syndrome →
hyperglycemia → hyperinsulinemia → hipoglycemia /FIGURE 15/. Clinical
manifestations – after 2-3 hours from alimentation apaire cold transpiration,
bulimia, dizziness, ↓ blood pressure, bradicardia, pallidity of skin. Diagnostic
studies – clinical picture and control of glycemia at the moment of exacerbation.

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Treatment of Dumping syndrome. Conservative treatment is indicated in easy
forms of disease – alimentation 5-6 times per day, diet containing 2800-3000 kkal
per day, milk and sweets will be excluded. Medicamentous therapy – gastric juice,
plasma, albuminum, vitamins, pancreatic enzymes, insuline before alimentation.
Surgical techniques in Dumping syndrome are divised:
1. Operations which stopped emptying of gastric stump:
- reduction of GEA dimensions
- striping of afferent loop
- reconversion of primary pyloroplastia by Gheineche-Mikulich
technique
- reversion of jejunal segmentum

2. Reduodenization:
- reconversion of Bilroth-I in Bilroth-II anasthomosis /FIGURE 16/
- isoperistaltic gastrojejunoplastia /FIGURE 17, A/
- antiperistaltic gastrojejunoplastia /FIGURE 17, B/

3. Operations on small intestine ant its nervous system:

- reversion of jejunal segmentum

- miotomy, miectomy

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 - vagotomy

3. Alkaline reflux gastritis, reflux esophagitis is installing after surgical

intervences on stomach with affection of pyloric and inferior esophageal

Fig.16 Reduodenization – conversion of Bilroth-I in Bilroth-II

anasthomosis
sphincters, which contribute to alteration of the mucosa of stomach and esophagus.

Fig.17 Surgical treatment of Dumping syndrome

A – Gastrojejunoduodenoplastia with isoperistaltic jejunal segmentum
B – Gastrojejunoduodenoplastia with antiperistaltic jejunal segmentum

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 Ethiopathoghenesis /FIGURE 18/. The bile washing mucus from the
mucosa of stomach. Biliary acids penetrating the mucosa and provocating cytolysis
of gastric epithelium. As a result are released histamine and acethylcholine → ↑ of
capillar permeability, edema, hemorrhagia per diapedesum → inverse diffusion of
anions H+ into gastric mucosa → erosions and ulcerations, atrophic gastritis (↓
Vit.B12, megaloblastic anemia). During 5-25 years increase the risc of gastric stump
carcinoma.

Clinical manifestations – acute epigastral pains, bilious vomiting,

regurgitation, dysphagia, weight losses.

Fig.18 Pathoghenesis of alkaline reflux gastritis

A – duodeno-gastral reflux
B – alteration of the mucosa of stomach

Diagnostic studies – pH-metria of gastric mucosa (alkaline stomach;

stimulated secretion can be hypo-, hyper- or normoacide); endoscopy – relevated
bile in esophagus, stomach; atrophy of mucosa, hyperemia and erosions.
Radiography of stomach and passage of barium mass → normal or Trendelenburg
position of patient → duodeno-gastral or gastro-esophageal reflux.
Treatment. Conservative therapy – cholestiramine, H 2-blokators, antacids,
carbenoxalon etc. Surgical treatment – the goals is to exclude duodeno-gastral
reflux. After Bilroth-I resection → gastroenteroanasthomosis on “Y”-loop (a la
Roux) or isoperistaltic gastrojejunoplastia. After vagotomy → gastric resection a la
Roux.

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 4. Chronic afferent loop syndrome – caused by stenosis of
afferent /FIGURE 19, A/ or efferent /FIGURE 19, B/ loop after gastric resection
Bilroth-II. Frequency – 13-15%.

Pathoghenesis of chronic afferent loop syndrome: strictures, torsions, reflux

Fig.19 Causes of chronic afferent loop syndrome

in afferent loop; denervation of the duodenum → alimentary and biliary stasis →

duodeno-biliary reflux (cholecystitis, pancreatitis, hepatic cirrhosis); gastro-
esophageal reflux (gastritis, esophagitis) → malabsorbtion, maldigestion.
Clinical manifestations – postprandial epigastric pain (especially after
ingeration of fast foods) irradiating in the right thorax, distention, nonbilious
vomiting that is then relieved by projectile bilious vomiting, weight losses.
Diagnostic studies. Radiography of the stomach → excessive quantity of
liquid in the stomach, retention of barium mass into afferent loop, duodenum.
Treatment. Reresection a la Roux, gastrojejunoduodenoplastia. In case of
associated Dumping syndrome – reconversion of gastroenteroanasthomosis in
gastroduodenoanasthomosis.
Acute afferent loop syndrome – acute, vital important complication, caused
by invagination, torsion, kinking, anastomotic narrowing, or adhesion of afferent
loop. Acute obstruction of afferent loop conduct to vascular disorders, nechrosis of
duodenum and peritonitis. Duodenal hypertension conduct to duodeno-biliar reflux
and acute cholangitis or pancreatitis.

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 Clinical manifestations – superior gastrointestinal obstruction, duodenal
perforation, peritonitis, acute cholangitis and pancreatitis.
Treatment – urgent surgical intervence – duodenojejunostomia or
reconversion of gastroenteroanasthomosis by Roux technique.

III. POSTVAGOTOMIC SYNDROMES /FIGURE 20/

1. Dysphagia – apaire in early postoperative period and is caused by

denervation of esophagus. Don’t need special treatment.
2. Gastrostasis – is caused by postvagotomic atonia, inadequate drainage of
the stomach. Clinic manifestations - epigastric distention, nausea,
vomiting. Conservative treatment - cerucal, benzohexonium. Surgical
treatment – gastric resection Bilroth-I or Bilroth-II.
3. Duodenostasis – distension in right hipocondrium, periodic colicative pain,
nausea, bilious vomiting. Radiography – retention of barium mass
in duodenum. Tratament – gastric resection by Roux or Bolfour
techniques.
4. Postvagotomy diarrhea – 3-4 times per day. Frequency – 10-40%.
Ethiopathoghenesis – reduced gastric secretion, dismotilities of digestive
tract, pancreatic insuficience, exacerbation of intestinal hormones,
accelerated passage of alimentar chime, metabolic perturbations of biliary
acids, disbacteriosis. Conservative treatment – diet without milk,
cholesteramine, cerucal, motilium, antibiotics. Surgical treatment – reversion
of intestinal segmentum: malabsorbtion of proteins, hydrocarbonates – 120
cm from flexura duodenojejunale; malabsorbtion of water, lipids – inversion
of ileal segmentum.

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 Fig.20 Types of vagotomy. A. Vagal anatomy. B. Truncal vagotomy. C. Selective vagotomy. D. Highly
selective vagotomy.

V. SYNDROMES OF INTESTINAL MALABSORBTION

Are caused by absorbtion disorders of many ingredients of foods –
enzymatic defficience, ileitis, jejunitis, dismotilities, disbacteriosis, disorders in

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specific transport mechanisms of intestinal mucosa. Postoperative
malabsorbtion – gastrogenic, pancreatogenic, hepatogenic, enterogenic,
endocrine.
Clinical manifestations – decreased work ability, weight losses, cahexia,
steatorrhea, creatorrhea, defficience of vitamins B, Ca 2+, Fe3+. Malabsorbtion of
hydrocarbonates – flatulence, intestinal colic, diarrhea; of aminoacids –
hipoproteinemia, disorders of central nervous system; of lipids – steatorrhea, ↓
serum cholesterol and lipidic derivatives; of vitamine B 1 – pain in inferior
members, paraesthesia; of vitamine B2 – heilitis, stomatitis; of nicotinic acid –
glositis; of vitamine C – gingival hemorrhagia; of vitamine K – multiple
petehia. Disorders of hydro-electrolitic absorbtion conduct to hiponatriemia,
arterial hipotonia, tahicardia.
Treatment is very difficult, prognosis is unclaire.

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