Anaesthetic considerations in
emergency intestinal obstruction
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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 - 1.5 litres
 Stomach – 2.5 litres.
 Succus entericus - 1.5 to 3 litres
 Pancreas – 750 ml
 Bile - 300 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
 Airway
 CVS
 RS
 CNS
 Spine

etc
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ROUTINE
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).
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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 :
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Increase in afterload secondary to
mechanical compression of the abdominal
vascular beds
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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
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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
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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
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
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