Presentation on theme: "Anaesthetic considerations in emergency intestinal obstruction Dr. S. Parthasarathy MD., DA., DNB, MD (Acu), Dip. Diab. DCA, Dip. Software statistics."— Presentation transcript:
Anaesthetic considerations 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
Incidence Intestinal obstructions account for about 20 percent of admissions to the hospital for abdominal disorders.
Features of intestinal obstruction Abdominal pain Abdominal distension Obstipation vomiting
Mechanical obstruction – correction usually surgical Laparotmy discussed now Laparoscopy later separate
Preop problems Normal secretions Saliva litres Stomach – 2.5 litres. Succus entericus to 3 litres Pancreas – 750 ml Bile ml Total – 7 – 8 litres
Clinically what is the loss? Early small bowel – 1.5 litres Well established with vomiting – 3 litres. Hypotension and hemodynamic instability -- 6 litres.
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
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
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.
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.
preop Fluid loss shock Chloride loss Hypokalemia Hyponatremia May lead on to starvation, ketosis and acidosis
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
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
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
To see Pulse BP CVP, acid base Routine blood, electrolytes ECG, urine output
Hematocrit If hematocrit is 55 % then fluid loss is 40 % Hematocrit may be a guide to assess fluid infusion
narcotics Narcotics Slow gastric emptying Affect peristalsis We can add anticholinergics to combat.
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).
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 afterload secondary to mechanical compression of the abdominal vascular beds Decrease in preload due to direct compression of IVC and portal vein
Reversal Suggamadex -cyclodextrin -4 mg/kg. dose. Neostigmine can worsen anastomosis Atropine can cause undue hemodynamic disturbance Post op ventilation
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?