Anaesthetic considerations in emergency intestinal obstruction Dr . S. Parthasarathy

1. Anaestheticconsiderations in emergency intestinal obstruction • Dr. S. Parthasarathy • MD., DA., DNB, MD (Acu), • Dip. Diab. DCA, Dip. Software statistics • PhD (physio) • Mahatma Gandhi medical college and research institute , puducherry – India

2. Incidence • Intestinal obstructions • account for about 20 percent of admissions to the hospital for abdominal disorders.

3. Features of intestinal obstruction • Abdominal pain • Abdominal distension • Obstipation • vomiting

4. Possible causes • Hernia, • Adhesions, • Intussusption • Ascaris • Gangrene, • Volvulus • Growth. • Stricture.

5. Mechanical obstruction – correction usually surgical Laparotmy discussed now Laparoscopy later separate

6. Preop problems • Normal secretions • Saliva - 1.5 litres • Stomach – 2.5 litres. • Succusentericus - 1.5 to 3 litres • Pancreas – 750 ml • Bile - 300 ml • Total – 7 – 8 litres

7. Clinically what is the loss? • Early small bowel – 1.5 litres • Well established with vomiting – 3 litres. Hypotension and hemodynamic instability -- 6 litres.

8. Small and large • Fluid derangement fast – small gut • Slow in large gut • Electrolyte imbalance slow in large gut Systemic derangement is progressive Except volvulus – no gangrene in large gut

9. Where – obstruction – what happens? • Pyloric obstruction causes a loss of H+ and Cl- (and Na+ and K+) due to vomiting acidic gastric secretions. • Alkaline pancreatic and duodenal secretions are retained and the result is a hypochloraemic metabolic alkalosis

10. Mid or high small bowel obstruction presents a different picture. Large volumes of fluid are lost (Na+, K+ and water) • combination of alkaline intestinal secretions and acidic gastric secretions prevents the development of a metabolic alkalosis.

11. In low small bowel obstruction and large bowel obstruction fluid loss tends to be less initially as much of the water and solute • sepsis leads to circulatory collapse and metabolic acidosis.

12. preop • Fluid loss • ------ shock • Chloride loss • Hypokalemia • Hyponatremia • May lead on to starvation, ketosis and acidosis

13. preop • If in shock and acidosis • Possible intubation and ventilation • Correct fluid deficits ,electrolytes and acidosis • RL and NS with KCl – monitor CVP and urine output and correct

14. The aim should be • to correct the dehydration over 24 hours, • giving half the calculated amount in the first 8 hours • second half over the following 16 hours. • If the patient is very hypernatremic (Na+ > 155mmol/ l) rehydration should be over 48 hours because of the risk of cerebral oedema

15. Don’t look at the heroine alone

16. Look at others also

17. OTHERS ---- ROUTINE • Airway • CVS • RS • CNS • Spine • etc

18. preop • Gut mucosa – impermeable to bacteria • Once strangulated , barrier breaks, toxins absorbed – septic shock • Increased permeability also leads to loss of red cells into bowel and peritoneal cavity. • Hence anemia

19. To see • Pulse • BP • CVP, acid base • Routine blood , electrolytes • ECG , urine output

20. Hematocrit • If hematocrit is 55 % then fluid loss is 40 % • Hematocrit may be a guide to assess fluid infusion

21. narcotics • Narcotics • Slow gastric emptying • Affect peristalsis • We can add anticholinergics to combat.

22. INTRA ABDOMINAL HYPERTENSION • The normal intra-abdominal pressure ranges from slightly sub-atmospheric to 6.5 mmHg, and varies with the respiratory cycle • above 12 mmHg constitutes intra-abdominal hypertension(IAH).

23. IAH ON CVS • Haemodynamic compromise is due to complex alterations in preload, afterload and intra-thoracic pressure. A decrease in cardiac output is both due to : • Increase in afterloadsecondary to mechanical compression of the abdominal vascular beds • Decrease in preload due to direct compression of IVC and portal vein

24. IAH • INTRATHORACIC PRESSURE • IMPEDES VENOUS RETURN • ALSO GIVES • FALSE CVP VALUES (BEWARE!)

25. Respiratory effects • Distended bowel and IAH • Pressure on the diaphragm • Inadequate ventilation • Increase PCo2 decrease PO2 • Increased risk of regurgitation • HPV • Increased plat. And peak pressures.

26. Renal • Oliguria is observed at intra-abdominal pressures between 15 and 20 mmHg, which can progress to anuria when pressures exceed 30 mmHg • splanchnic • decreased blood flow, microcirculatory abnormalities, ---- tissue hypoxia • Except adrenals –blood flow Decrease • Increased ICT

27. premed • Narcotics, benzo. and anticholinergics • Preexisting tachycardia ? • Acid aspiration prophylaxis • Metoclopramide, • Ryles tube aspiration • Indwelling catheter. • Monitors.

28. Anaesthesia • Controlled GA – ideal • Epidural catheter with controlled GA is ok in selected cases

29. Anaesthesia • Ketamine?? If hemdynamically unstable • Rapid sequence induction • Precurarize before suxa ?? • ET tube

30. Anaesthesia • Inhalational agents • Rocuronium if possible?? • N2O : O2 ? • Air : O2 : inh. agent √

31. Problems of N2O • bowel gas volume increases approximately 75–100% after 2 hours of 70–80% N2O, and by 100–200% after 4 hours.

32. Intraop Monitoring • Pulse, BP, • CVP, • ECG, • Temperature, • NMJ • Urine output • Blood loss, blood gases • Think of sudden decompression

33. sepsis • Antibiotics • And antifungal SOS

34. Reversal • Suggamadex -cyclodextrin -4 mg/kg. dose. • Neostigmine can worsen anastomosis • Atropine can cause undue hemodynamic disturbance • Post op ventilation

35. suggamadex

36. suggamadex

37. High spinal or epidural anaesthesia • promotes hyper peristaltic activity - blockade of sympathetic innervation.s • The unopposed parasympathetic activity may cause nausea and vomiting • anastomotic breakdown, especially in • colon surgery?? • More theoritical?

38. Postop • Pain relief • Tramadol, epidural drugs. • Other narcotics. • Atelectasis (AU 93) • ILEUS • Fluids and urine output

39. In short, • 6 litres fluid • Electrolytes K +, Cl - , acid base • Preop. vent. • Controlled GA (with epidural) • No N2O • Blood SOS. • Post op pain relief ,fluid

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