MSC - F. Surgery Answers 2025

18. Conservative treatment of ulcer gastroduodenal bleeding. Endoscopic hemostasis, its capabilities and methods.

Medical Therapy:

Proton Pump Inhibitors (PPI):

o IV pantoprazole/esomeprazole → reduces rebleeding.

oHigh-dose PPI (80 mg bolus + 8 mg/hr infusion).

H. pylori eradication: If positive (PPI + antibiotics).

Supportive:

oBlood transfusion (if Hb <7 g/dL).

o NPO initially → gradual diet reintroduction.

Endoscopic Hemostasis Methods:

1. Injection Therapy:

oEpinephrine (1:10,000) → vasoconstriction + mechanical tamponade.

oSclerosants (ethanol, polidocanol) → vessel fibrosis.

2.Mechanical Methods:

oHemoclips (best for visible vessels).

oBand ligation (rarely used in ulcers).

3.Thermal Coagulation:

oBipolar electrocoagulation (BICAP).

oArgon Plasma Coagulation (APC).

4.Topical Hemostatics:

oFibrin glue, Hemospray (temporary control).

Success Rate:

90% for initial hemostasis.

Rebleeding risk: 10–20% (higher in Forrest Ia-IIa).

19. Surgical treatment of ulcer gastroduodenal bleeding.

Indications for Surgery:

Failed endoscopic hemostasis.

Hemodynamic instability despite resuscitation.

Large ulcer (>2 cm) with visible vessel.

Recurrent bleeding after initial control.

Surgical Options:

1. Duodenal Ulcer:

oUnder-running suture (ligation of gastroduodenal artery) + Truncal Vagotomy & Pyloroplasty.

oBancroft procedure (if ulcer is non-resectable).

2.Gastric Ulcer:

oPartial Gastrectomy (Billroth I/II) (ulcer excision + reconstruction).

o Wedge resection (for high-risk patients).

Postoperative Care:

PPI continuation.

Monitor for rebleeding, sepsis, anastomotic leak.

Key Takeaways

Diagnosis: Endoscopy is gold standard (Forrest classification guides therapy).

Medical: PPI + H. pylori eradication.

Endoscopic: Clips, coagulation, epinephrine injection.

Surgical: Reserved for failure of conservative/endoscopic methods.

Acute intestinal obstruction

1. Definition of the concept and etiopathogenesis of acute intestinal obstruction.

Definition

Acute Intestinal Obstruction (AIO) is a surgical emergency characterized by the complete or partial blockage of intestinal lumen, leading to:

Failure of intestinal contents to pass (gas, fluids, feces).

Proximal bowel distension → vascular compromise → ischemia/perforation.

Systemic toxicity due to bacterial translocation, fluid loss, and shock.

Mortality: 10–15% (higher in strangulating obstruction).

Etiopathogenesis

1. Causes of Intestinal Obstruction

A. Mechanical Obstruction (90%)

B.Functional (Paralytic) Obstruction (10%)

No physical blockage; failure of peristalsis due to:

oPostoperative ileus, electrolyte imbalances (hypokalemia), sepsis, spinal injury.

2. Pathophysiological Mechanisms

A.Local Changes in the Bowel

1.Proximal Distension:

oGas (swallowed air, bacterial fermentation) + fluid (secretions, ingested liquids) accumulate.

o↑ Intraluminal pressure → venous congestion → edema → arterial compromise → ischemia/necrosis.

2.Mucosal Barrier Breakdown:

oIschemia → bacterial translocation (E. coli, Bacteroides) → endotoxemia → septic shock.

B. Systemic Effects

1.Fluid & Electrolyte Losses:

oVomiting + sequestration in bowel

→ hypovolemia, hypokalemia, metabolic alkalosis (if proximal obstruction).

oDehydration → hypotension, tachycardia, oliguria.

2.Toxemia & Shock:

oNecrotic bowel releases cytokines (TNF-α, IL-6) → SIRS → multiorgan failure.

oStrangulation (e.g., volvulus, hernias) accelerates ischemia

→ peritonitis.

Key Pathological Stages

1. Early Obstruction (6–12 hrs):

o Colicky pain, vomiting, distension.

oHyperactive bowel sounds (mechanical) / absent sounds (paralytic).

2.Intermediate (12–24 hrs):

oBowel wall edema → third-space fluid loss.

oMetabolic acidosis (lactic acid from ischemia).

3.Late (>24 hrs):

oPerforation → peritonitis, septic shock.

oDeath from circulatory collapse or MODS.

2.Classification of acute intestinal obstruction.

Acute intestinal obstruction (AIO) is classified based on morphofunctional nature, degree of obstruction, and clinical progression. Below is a structured breakdown:

I. Classification by Morphofunctional Nature 1. Dynamic (Functional) Obstruction

No physical blockage; caused by impaired peristalsis.

2. Mechanical Obstruction

Physical blockage of the intestinal lumen.

II. Classification by Degree of Obstruction

1. Small Bowel Obstruction (SBO) (70% of cases)

2. Large Bowel Obstruction (LBO) (30% of cases)

III. Classification by Clinical Progression

1. Stages of AIO

2.By Completeness of Obstruction

Complete obstruction: No passage of gas/feces → absolute constipation.

Partial obstruction: Intermittent passage (e.g., chronic strictures).

3.By Clinical Course

Acute obstruction: Sudden onset (e.g., volvulus, hernia).

2. Stage II: Vascular Compromise of the Bowel Wall

oIn strangulation, mesenteric vessels are compressed leading to:

Venous congestion → edema, cyanosis, hemorrhage

Arterial occlusion → ischemia and transmural necrosis within 1–6 hours

oIn obstruction without strangulation, ischemia occurs later due to increased intraluminal pressure and capillary stasis

oBowel wall becomes permeable → absorption of bacteria, endotoxins

3.Stage III: Peritonitis and Systemic Toxicity

oBowel perforation, spilling contents into the peritoneal cavity

o Bacterial peritonitis and profound systemic toxicity

o Consequences: septic shock, multi-organ failure, death

Pathophysiology: Strangulation vs. Obturative Obstruction

Strangulation Obstruction

Early vascular compromise — venous stasis followed by arterial ischemia

Transudation of fluid, gas, bacteria into peritoneal cavity

Rapid necrosis of bowel wall with high risk of perforation

Intense pain, signs of shock, peritonism

Systemic effects: hypovolemia (due to third-spacing of up to 12L/day), electrolyte loss, metabolic acidosis, endotoxemia

Hypokalemia worsens ileus, compounding the obstruction

Obturative Obstruction

No early vascular compromise, but prolonged obstruction leads to: o Progressive distension of proximal bowel

o Increased wall tension → capillary compromise o Mucosal ischemia → bacterial translocation

Common in left-sided colonic tumors, especially endophytic ones

Symptoms evolve more gradually than in strangulation

Bowel function preserved initially, but risk of closed-loop features if ileocecal valve is competent

Summary of Key Factors in Pathogenesis

Losses: Fluids (up to 12 L/day), electrolytes (Na , K , Cl ), proteins

Consequences: Hypovolemia, hemoconcentration, ileus, metabolic acidosis

Systemic effects: Endotoxemia, multiorgan failure, death without timely intervention

4.Etiopathogenesis of obstructive intestinal obstruction.

Obturative Obstruction

No early vascular compromise, but prolonged obstruction leads to: o Progressive distension of proximal bowel

o Increased wall tension → capillary compromise o Mucosal ischemia → bacterial translocation

Common in left-sided colonic tumors, especially endophytic ones

Symptoms evolve more gradually than in strangulation

Bowel function preserved initially, but risk of closed-loop features if

ileocecal valve is competent

5. Etiopathogenesis of strangulated intestinal obstruction.

Strangulation Obstruction

Early vascular compromise — venous stasis followed by arterial ischemia

Transudation of fluid, gas, bacteria into peritoneal cavity

Rapid necrosis of bowel wall with high risk of perforation