MSC - F. Surgery Answers 2025
.pdf
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
6.Intestinal intussusception. Concept, etiopathogenesis, clinical picture.
Definition
Intussusception is the telescoping of a segment of the intestine (intussusceptum) into an adjacent distal segment (intussuscipiens), leading to mechanical intestinal obstruction, vascular compromise, and eventually necrosis if untreated.
Etiology
1.Idiopathic (most common, ~90%)
Typically seen in infants <1 year.
Triggered by hypertrophy of Peyer’s patches due to: o Viral infections (e.g., adenovirus, rotavirus).
o Immunological stimulation during weaning.
2.Secondary (Pathological lead point)
>1 year old, higher likelihood of underlying lesion: o Meckel’s diverticulum.
o Polyps (e.g., Peutz-Jeghers syndrome). o Lymphoma, rhabdomyosarcoma.
o Intestinal duplication, heterotopic tissue.
o Hematoma (e.g., Henoch-Schönlein purpura, hemophilia). o Cystic fibrosis, typhoid, yersiniosis.
Mechanism (Pathophysiology)
Mechanical Process
Antegrade telescoping of proximal bowel into distal bowel.
Mesentery is dragged along, leading to:
o Venous and lymphatic obstruction.
o Congestion, edema → arterial compromise → ischemia and necrosis.
Peristaltic Disruption
Imbalance between spasm of leading segment and paresis of distal bowel.
Often triggered by:
o Introduction of solid foods.
o Irritation (e.g., fruit juices with preservatives).
Anatomy of Intussusception
Most common site: Ileocecal junction (~91–94%).
Structures involved:
o Outer cylinder: Intussuscipiens (receiving segment). o Middle cylinder: Serosa of intussusceptum.
oInner cylinder: Mucosa of intussusceptum.
Cervix: Transition point from outer to inner layer.
Head: Leading edge of invaginated bowel.
Progression
Initial phase: Venous congestion → mucosal edema.
Intermediate: Hemorrhage into lumen, lymphatic obstruction.
Late: Ischemia → necrosis of bowel wall.
Time to necrosis: 24–48 hours.
Clinical Picture of Intussusception
Age: Commonest in infants 6–18 months.
Classic Triad (seen in <40% but highly suggestive):
1.Colicky abdominal pain – sudden, severe, episodic; child draws up legs and cries.
2.Vomiting – initially non-bilious, may become bilious.
3."Currant jelly" stool – blood and mucus, appears later.
Other Key Signs:
Lethargy between pain episodes (early sign of systemic involvement).
Palpable sausage-shaped mass, usually in right upper quadrant.
Abdominal distension, reduced bowel sounds in late phase.
Shock/peritonitis in advanced cases.
Rectal exam:
May reveal blood-stained mucus or low-lying mass.
7.Clinical picture of strangulated intestinal obstruction.
A surgical emergency caused by compromised blood supply to a loop of bowel due to obstruction (e.g. volvulus, hernia, intussusception).
Key Clinical Features:
Sudden, severe, constant pain (not colicky)
Rapid deterioration: tachycardia, hypotension, signs of shock
Peritonitis signs: guarding, rigidity, rebound tenderness
Systemic toxicity: fever, leukocytosis, dehydration
No flatus or feces passed
High-pitched or absent bowel sounds
Possibly bloody vomiting or rectal bleeding if advanced
Red flags: Severe pain out of proportion to exam + systemic toxicity = suspect strangulation.
8. Clinical picture of obstructive intestinal obstruction.
Occurs due to mechanical blockage without vascular compromise.
Key Clinical Features:
Colicky abdominal pain – waves of pain
Abdominal distension – more marked in distal obstructions
Vomiting:
o Early in high/small bowel obstruction
oLate or feculent in low/colonic obstruction
Obstipation – absence of stool/gas in complete obstruction
Visible peristalsis (especially in thin patients)
Generally slower progression than strangulated type. No systemic toxicity unless delayed.
10. Clinical diagnosis of mechanical intestinal obstruction. Based on history + physical exam:
History:
Sudden or gradual onset of colicky pain
Vomiting (progressive, may become feculent)
No bowel movement or gas
History of hernia, surgery (adhesions), tumors, gallstones
Physical Exam:
Distension
Tympanic percussion
Visible peristalsis
Auscultation:
o High-pitched "tinkling" bowel sounds (early)
oAbsent (late/strangulation)
Digital rectal exam: empty rectum or bloody mucus
If strangulation suspected: tenderness, rebound, rigidity, systemic signs →
Immediate surgery.
11. Instrumental diagnostics of mechanical intestinal obstruction.
1.Plain Abdominal X-ray (Upright & Supine):
Air-fluid levels with step-ladder pattern
Dilated loops of bowel (>3 cm small bowel; >6 cm colon)
Absence of gas distally
"Coffee bean" sign in sigmoid volvulus
2.Ultrasound:
Useful in children (e.g., intussusception: "target sign")
Detects free fluid, masses, peristalsis
Good for identifying hernias, tumors
3.CT Abdomen with contrast (gold standard in adults):
Localizes level and cause of obstruction
Identifies strangulation (e.g., bowel wall thickening, lack of enhancement, mesenteric edema, pneumatosis)
4.Contrast Studies:
Gastrografin enema or upper GI follow-through
Diagnostic & therapeutic in partial obstruction or intussusception
5.Colonoscopy or Sigmoidoscopy:
In large bowel obstruction (diagnosis, biopsy, stenting in cancer)
9. Types and etiopathogenesis of dynamic intestinal obstruction.
I. Classification
Dynamic intestinal obstruction is a non-mechanical form of obstruction, characterized by disrupted intestinal motility (peristalsis) rather than a physical blockage.
It is classified into:
1.Paralytic (Adynamic) Ileus – most common.
2.Spastic Ileus – much rarer.
II. Etiopathogenesis
1.Paralytic Obstruction (Adynamic Ileus)
Pathophysiology:
o Suppression or cessation of peristalsis.
o Venous congestion in intestinal walls → impaired absorption.
oRisk of ischemia and necrosis with severe distention (rare).
Main Mechanism:
o↑ Sympathetic tone → ↓ peristalsis.
oRelaxation of pyloric sphincter & Bauhin’s valve (ileocecal).
Causes:
A. Neurological Disruption at 3 Levels:
oIntestinal Wall (Autonomous Plexus):
Inflammation (e.g., peritonitis).
Iatrogenic trauma (e.g., surgery).
Ischemia due to compression/distention.
oRetroperitoneal Plexus (e.g., celiac, Auerbach, Meissner):
Pancreatitis, pancreatic necrosis, retroperitoneal hematomas.
“Watchdog loop” sign: local ileus of upper GI.
oSpinal Nerves:
Vertebral fractures, hematomas affecting spinal roots.
B.Reflex Mechanisms:
oIrritative stimuli from other organs:
Rib fractures, torsion of testis or ovary, omentum twist.
C.Metabolic/Electrolyte Imbalances:
oHypokalemia – affects Na /K pump → muscle paralysis.
D.Toxins and Drugs:
oToxemia (e.g., burns).
oOpiate overdose.
E. Miscellaneous:
oUremia, pneumonia, meningitis.
2.Spastic Obstruction
Rare, may precede paralytic ileus.
Etiology:
1.Heavy metal poisoning (e.g., lead colic).
2.Hysteria or psychiatric syndromes (esp. young women).
3.Idiopathic colic or visceral neural hyperexcitability.
Mechanism:
o Localized intense intestinal contraction → lumen obstruction.
oMay progress to paralytic ileus if spasm leads to ischemia or nerve disruption.
12.Clinical picture and diagnostics of dynamic intestinal obstruction.
Paralytic Obstruction:
Onset: Gradual.
Pain: Dull, non-colicky, or absent.
Distension: Generalized and progressive, not segmental.
Bowel Sounds: Absent – “deathly silence.”
Vomiting: Late feature.
Signs of Dehydration/Toxemia: May appear after 1–2 days.
On Palpation:
o Abdomen: Soft, non-tender.
oMetallic “splash” on movement.
Rectal Exam: Empty rectum.
Imaging (X-ray/CT):
Diffuse gas throughout bowel.
Kloiber's cups (fluid levels), but gas > fluid.
No progression over days (unlike mechanical obstruction).
Elevated diaphragm on X-ray.
Spastic Obstruction:
Onset: Sudden.
Pain: Severe, colicky, often generalized.
Behavior: Restless, writhing.
Bowel movement: Cessation of stools and flatus.
Abdominal Findings:
o Navicular abdomen (retracted).
oNo guarding or rebound.
Vital signs: Stable; no intoxication signs.
Labs: Normal.
Imaging: Often normal or few small air-fluid levels.
Response to antispasmodics: Dramatic relief (diagnostic clue).
15.Principles of treatment of dynamic intestinal obstruction.
1. Paralytic Obstruction
Conservative Management – Primary Line of Therapy
Surgery only if underlying cause (e.g., peritonitis, hemorrhage) mandates.
Treatment Steps:
1.Treat underlying cause (e.g., pancreatitis, peritonitis).
2.Stimulate Peristalsis:
o Proserin (neostigmine), pituitrin.
oEpidural anesthesia for sympathetic inhibition.
3.Correct Electrolytes:
oK repletion, polarizing solution (glucose + insulin + KCl).
4.Decompression:
oNasogastric tube, rectal venting tube.
5.Enemas:
oCleansing, hypertonic (e.g., 10% NaCl), siphon enemas.
6.Fluids & Support:
oIV hydration, monitor for sepsis/organ failure.
2.Spastic Obstruction
Surgery contraindicated unless diagnostic uncertainty exists.
Treatment:
1. Antispasmodics:
oPapaverine, drotaverine, hyoscine.
2.Analgesics – cautious use.
3.Electrolyte correction – especially K.
4.Warmth – local heating pads.
5.Enemas – relieve irritation.
6.IV Fluids & Detoxification – if toxic/metabolic component suspected.
V. Mixed Forms: Special Notes
Adhesive Disease:
oMay present initially as paralytic due to inflammation of adhesions.
oTreat conservatively with:
Hydrocortisone, polarizing solution, proserin, hypertonic enemas.
oCan later evolve into mechanical obstruction → surgery needed.
Worm Infestation (Ascariasis):
oPhysical mass of worms + paralytic toxins.
o Rare; mostly in endemic areas.
o Requires antihelminthics + supportive care.
In Summary |
|
|
|
||
Type |
Mechanism |
Key Features |
Diagnostics |
Treatment |
|
Approach |
|||||
|
|
|
|
||
|
↓/Absent |
Painless |
Uniform gas, |
|
|
|
distension, silent |
Conservative |
|||
Paralytic peristalsis |
unchanged X-ray |
||||
|
|
abdomen |
|
|
|
Spastic |
Intestinal |
Severe pain, no |
Normal or |
Antispasmodics, |
|
|
|
||||
|
distension, |
minimal X-ray |
|||
|
|
|
|||