Acute adynamic neuromuscular state of small intestine with dilatation i.e ileus

In this presentation I have explained acute adynamic neuromuscular state of small intestine with dilatation called as ileus.It cantains all information you need to know about ileus from risk factors to etiology investigation anf management.

1. Acute adynamic
neuromuscular state of
small intestine with
dilatation ( ileus)
Dr. Laila
Ghaffar Surgical
Resident

2. At the end of presentation audience will
able to learn:
*Definition
*Risk Factors
*Diagnosis

*Management
*Prevention

3. Classification of Intestinal Obstruction
▪Dynamic = in which intestinal peristalsis occuring against a
mechanical obstruction
▪Adynamic = in which there is no mechanical obstruction , pseudo-
obstruction

4. " Disruption of normal propulsive
Disruption of normal propulsive ability of the intestine due to malfunction of contractile
Activity in the absence of mechanical obstruction
This definition excepts meconium ileus and gallstone ileus that are technically misnomer
Because there is mechanical obstruction
Definition

5. Functional diseases of intestine
due to change in function of intestine
rarther than due to diseas affecting
structure of intestine

6. Signs and Symptoms
▪Abdominal distention
•Vomiting
•Distension increas pain from wound
•Absent bowel sounds

7. Risk Factors
▪*Recent surgery i.e POI occurs in 10-20% of major abdominal
surgery and defined as failure to tolerate oral intake or pass stool 72
hrs after surgery
▪*Local inflammation ( pritonitis, severe acute pancreatitis)
▪*Systemic inflammation by any cause e.g sepsis , trauma
▪*Electrolyte disturbance eg hypokalemia , hypercalcemia
▪*Acute edocrine disturbance ( hypothyroidism ,DKA)
▪*Medications eg Opiods
▪*Acute CNS disease ( high spinal transection )
▪Intestinal Ischaemia ( mesenteric vascular disease)

8. Innervation of GIT
ANS of GIT comprises extrinsic and intrinsic nervous system
Extrinsic ANS = PNS usually excitatory on function of GIT ( increase motility,secretion) consist of vagus
nerve innervate esophagus ,stomach ,pancreas and upper large intestine And pelvic splanchnic nerves (
greater, lesser and least ) innervate lower large intestine ,rectum and anus
SNS = is usually inhibitory on function of GIT ( decrease motility ,secretion)
Consist of thoracolumber i.e T8-L2 from spinal cord

9. Intrinsic nervous system
*Coordinate and relay informationfrom PNS and SNS to the GIT
*Use local reflexes to relay information within GIT
*Control functions of GIT even in absence of extrinsic innervation
Myenteric nervous system (Auerbach plexus) located between circular and
longitudnal layer of muscularis externa controls motility
Meissner plexus located in submucosa control secretions

10. E

11. Motility of Intestine
▪Fed Stat = Segmentation ( mixing and absorbtion)
▪ Peristalsis ( rythmic involentary contraction and relaxation of smooth muscle of gut to propel content forward in the gut .It
starts and travel few centimeter of gut and dies away
▪Fasting stat =
▪ MMC ( migratory motility complex) husekeeper of gut clear residuals nutrients , bacteria to prevent overgrowth and secretions .It start at
one point in git
▪and travel throughout length of intestine cycle repeats every 90 mints
Motilin produce by small intestine strengthen MMC
Pacemaker of intestine= Interstitial cells of cajalfibroblastic cells in muscularis externa
Produce slow waves that are oscillating RMP
Frequency = 3/mint in stomach
12/mint in duodenum
8-9 /mint in ileum

13. Pathophysiology

14. Diagnosis
•Clinical Evaluation (history + examination)
•* Biochemical tests ( FBC ,serum electrolytes ,serum calcium ,Mg
,LFT
Radiological Investigations
•*Ultrasound of abdomen
•Plain x –ray ( multiple air fluid levels throughout the abdomen with
dilatation of both large and small intestine
•*small bowel function test ( barium follow through , breath hydrogen
small bowel transit test ,wireless motility capsule small bowel
transit study )

15. CT is required to exclude mechanical obstruction and any local cause of
ileus eg pancreatitis , abscees

16. X-ray abdomen

17. CT abdomen

18. Management
▪*NPO restrict oral intake untill there is improvement
▪*NG aspiration
•*fluid and electrolyte replacement
▪*specific treatment is directed toward the cause
▪*laprotomy when bowel inactivity persists ,particularly if lasts >7
days or if bowel activity recommences following surgery and then
stops again

19. Prevention
•*Minimal invasive surgical approaches eg laproscopic techniques
•*Enhance recovery program ( start oral fluids and diet soon after
surgery)
•*Avoidance of opoid containg drugs
•* Suppresion of inflammation