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

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

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

Don’t look at the heroine alone

Look at others also

OTHERS ---- ROUTINE  Airway  CVS  RS  CNS  Spine  etc

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

IAH  INTRATHORACIC PRESSURE  IMPEDES VENOUS RETURN  ALSO GIVES  FALSE CVP VALUES (BEWARE!)

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.

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

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

Anaesthesia  Controlled GA – ideal  Epidural catheter with controlled GA is ok in selected cases

Anaesthesia  Ketamine?? If hemdynamically unstable  Rapid sequence induction  Precurarize before suxa ??  ET tube

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

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

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

sepsis  Antibiotics  And antifungal SOS

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

suggamadex

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?

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

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