ANAESTHETIC MANAGEMENT OF AIO patients

1. DR ZIKRULLAH
1

2. INTRODUCTION
 The term intestinal obstruction refers to any form
of impedance to the normal passage of the bowel
contents through the small or large intestine.

3. CLINICAL PICTURE
 Colicky abdominal pain
 Abdominal distension
 Vomiting
 Decreased passage of stool or flatus

4. ABDOMINAL PAIN
 Pain is the first symptom to develop.
 Initially colicky & intermittent later continous.
 Diffuse persistent pain after initially colicky- strangulation ?
 Small bowel obs- crampy, recurrent & short episodes. (30 secs)
 Large bowel obs- longer episodic pain.
 Adynamic obs- diffuse & mild.
 A/I- pain leads to increased CA levels & stress hormones,
even leads to splinting of respiration & basal atelectasis

5. VOMITING
 Is a sign of early obstruction i.e. small bowel obstruction.
 In large bowel obstruction it is a late feature.
 Duodenal and ileal obstruction- vomitus is billous.
 Large bowel obstruction -if it is its feculent.
 A/I – recurrent vomiting- suspect fluid & electrolyte
abnormality.

6. DISTENSION
 Sign of large bowel obstruction.
 Absent or minimal in duodenal or jejunal obs.
 Ileal obs- visible intestinal peristalsis k/a step
ladder peristalsis.

7. RADIOLOGICAL INVESTIGATION
 X ray abdomen supine & erect if perforation is suspected.
-Air fluid levels- distal the obs more the a/f levels
-Normal is 3 a/f level- stomach, duodenum & caecum.
 - When dilated- small bowel >3 cm, proximal large bowel >9cm,
tranverse colon >5.5 cm & sigmoid >5cm.
 Barium – is contradicated in acute obs.
 CT scan- high senstivity & specificity.
can identify strangulation, oedema & ischemia.
 USG abdomen
 Xray is the gold standard inv.

8. CLASSIFICATION
 Type – dynamic or adynamic
 Site- small bowel or large bowel
 Etiology- extra luminal, intraluminal or intramural
 Partial vs. complete
 Simple vs. strangulated
 Congenital or acquired

9. DYNAMIC OBSTRUCTION: mechanical blockage of normal
propulsion of intestinal contents.
ADYNAMIC ILEUS : Functional failure of normal intestinal
transit.
Paralytic ileus
Spastic ileus
Ileus of vascular occlusion.

10.  Paralytic ileus is the most common type postoperatively.
 Post operative ileus affects small bowel for 24hrs, gastric
motility for 48hrs, while colonic motility for 3-5days.
 Other causes are-
metabolic- hypokalemia, hyponatremia etc.
drugs- narcotics, antacids, anticoagulants etc.
others like intraperitoneal inflammation.
 Treatment – treat the cause, nasogastric decompression,
treat metabolic & fluid abn & nutritional support.

11. Mechanical Obstruction
11

12. Adynamic Ileus
12

13. CAUSES OF OBSTRUCTION
Outside the wall(extraluminal)
Adhesions (usually postoperative)
• Hernia
• Neoplastic
• Intra-abdominal abscess/ diverticulitis
• Volvulus (sigmoid, cecal)
• Inside the wall(Intraluminal): Gallstone :Enterolith ,Bezoar
,Foreign body
• Inside the lumen(intramural ):-Congenital
- Traumatic
- Infections-Tuberculosis
- Neoplastic
-Inflammatory- Crohn's disease
-Intussusception

14. ADHESIONS
14

15. EXTERNAL HERNIA
15

16. Simple v/s strangulation
strangulation is associated with compromised blood supply
leads to ischemia & gangrene.
 4 Cardinal Signs
fever, tachycardia, abdominal tenderness,
leukocytosis.
 Mortality increases from 3% to 30%.
 Associated with increased chances of complications e.g.
perforation, toxemia, septicemia etc.
 Closed loop & volvulus obs has got higher chances to
strangulate.
16

17. Strangulation
17
Impaired venous
return
Bowel distension Congestion & edema
of bowel wall
Decreased arterial supplyStrangulation
& gangrene
Bacterial
translocation
perforation
Peritonitis, bacteremia, toxemia &
septicemia

18. PATHOPHYSIOLOGY
18
Intestinal obstruction
Increased peristalsis
Obstruction not relieved
Peristalsis ceases.
Flaccid dilated bowel

19. Pathophysiology contd.
19
Decreased
absorption
Increased
secretion
Fluid
sequestration Bowel distention.
Edema, congestion &
inflammatory response
Bacterial
growth
Intramural hypoxia
Disrupt mucosal
barier
septicemia

20. Decreased
absorption
Increased
secretion
Fluid
sequestration
Decreased
intake
Increased
vomiting
Dehydration & electrolyte
abnormalities
Pathophysiology contd.
20

21. SYSTEMIC DERANGEMENTS
 Hemodynamic changes
 Profound dehydration
 Hypovolaemia and pre renal ARF
 Sepsis
 Respiratory compromise
 Electrolyte abnormalities
 Disturbances in acid-base balance

22. HEMODYNAMIC CHANGES
 The distended abdomen significantly affects venous return
by two mechanisms.
 First, distension decreases negative intrathoracic pressure
and thereby decreases venous return.
 The second is due to direct venacaval compression from
intraperitoneal tension.

23. Fluid and electrolytes
 Two types of clinical presentation
23
-Mid or high bowel obs.
-Major absorptive &
secretory site.
-Increased rate of
complications
-Lower or large bowel obs.
-Major chunk of fluid are
absorbed above
-Less incidence of comp.

24. ELECTROLYTE ABNORMALITIES
 The extent of extracellular fluid loss may be monitored by
serial hematocrit determinations.
 A rise in the hematocrit is proportionate to the amount of
fluid loss.
 For example, if the hematocrit has risen to 55%,
approximately 40% of plasma and extracellular fluid
volume has been lost.

25.  As the obstruction continues, there is a gradual decrease in
the plasma sodium and chloride concentrations.
 Hyponatremia will aggravate hypovolemic hypotension,
and confusion and somnolence will develop.
 Hypokalemia will be manifested in delayed ventricular
conduction, ST-T segment changes, and ventricular
arrhythmias.

26. ACID BASE ABNORMALITIES
 The most common occurrence is metabolic acidosis
because of the effects of dehydration, starvation, ketosis,
and loss of alkaline secretions.
 Metabolic alkalosis is rare and is the result of marked loss
of acidic gastric fluid.

27. METABOLIC ACIDOSIS
 The symptoms of metabolic acidosis include Kussmaul
respiration, decreased cardiac output, disorientation,
lethargy, dehydration, vasodilation, hypotension,
bradycardia, and increased susceptibility to ventricular
dysrhythmias.
 Decreased hepatic and renal blood flow.
 Acidosis directly reduces the activity of the extrinsic and
intrinsic coagulation pathways
 These adverse effects are generally not seen until pH
decreases below 7.2.

28. METABOLIC ACIDOSIS
 When the acidosis is mild (pH >7.2) a rightward
shift in the oxyhemoglobin dissociation curve partially
compensates for the decreased cardiac output by
increasing the unloading of oxygen to the tissues.
 Pre op ABG is important to evaluate the PaO2 & pH.
 Therapy for metabolic acidosis remains directed toward
correcting the underlying hypoperfusion.
 Resuscitation endpoints include normalization of arterial
pH, base deficit, and lactate.

29.  Bicarbonate administration should be deferred until
the pH persists below 7.15, despite optimal fluid
loading and inotropic support.
 Used with extreme caution when the patient has an
associated respiratory acidosis.
 The amount of base required to achieve full correction
of the metabolic component of an acidosis is
calculated as follows:
mEq base required = 0.4 × base deficit × body weight
(kg)
29

30. METABOLIC ALKALOSIS
 Occurs relatively infrequently ; however, it may be life-
threatening when severe.
 It consists of the triad of (1) increased pH, (2) increased
HCO3 and (3) decreased serum chloride concentration.
 Prolonged emesis, gastric suction ,use of diuretics and
volume depletion are the most common causes in surgical
patients.
 All results in the loss of chloride and protons from the
stomach, producing alkalosis and volume contraction.

31. METABOLIC ALKALOSIS
 Alkalemia acts as a negative inotrope .
 The increased pH also decreases the fraction of ionized
serum calcium and reduces the arrhythmia threshold.
 The leftward shift of the oxyhemoglobin dissociation curve
reduces the amount of oxygen unloaded and may
contribute to tissue hypoxia.
 Metabolic alkalosis should be treated with hydration.
Once normal renal function returns, potassium
replacement is begun.
 This therapy increases the GFR and causes the excretion of
bicarbonate.

32.  In severe cases, or when the alkalosis is not responsive to
saline, acetazolamide(carbonic anhydrase inhibitor),
arginine hydrochloride,
or even 0.1 N HCl may be used.
 Acetazolamide results in renal loss of bicarbonate,
potassium, water, and sodium.
 The drug typically takes 2–3 days to produce an effect and is
normally begun intravenously at a dose of 5 mg/kg once
daily.

33. Respiratory compromise
33
Increased abdominal
pressure
Splinting due to pain
Increased abdominal
distension
1. Increased work of breathing
2. Decreased FRC
3. Decreased TV
4. Basal atelectasis.
5. Decreased PaO2
6. Increased PaCO2
*Decreased oxygen reserve, so desaturates rapidly, preoxygenate (denitrogenate) adequately.

34. IMPLICATIONS OF TENSE
ABDOMINAL WALL
 Higher incidence of reverse peristalsis
 Requires deeper anaesthesia and more muscle relaxant to
provide adequate operating conditions
 Distended abdomen significantly affects venous return
 At the time of surgical incision, care must be taken to
prevent the fluid from escaping rapidly from the abdomen
to minimize severe hypotension.

35. FLUID SHIFT DURING SMALL BOWEL
OBSTRUCTION
 Normally, approximately 7 to 9 L of fluid are secreted daily
into the upper gastrointestinal tract.
 In early small bowel obstruction, 1,500 mL of fluid
accumulates in the bowel.
 Once intestinal obstruction is well established and
vomiting occurs, 3,000 mL of fluid may be present.
 When the patient exhibits hypotension and tachycardia,
indicating circulatory instability, as much as 6,000 mL of
fluid is in the gut.
 Lastly, vomiting and/or nasogastric suctioning further
increase fluid losses.

36. Common problems
Cardiovascular Hypovolaemia, Dehydration,Sepsis and septic shock
Respiratory Hypoxia, Tachypnoea, Atelectasis
Blood Anaemia, If septic - potential coagulopathy
Renal Oliguria or anuria due to acute renal failure
CNS Decreased level of consciousness, confusion
Anxiety, Pain, Possibility of intoxication
Gastro-intestinal Full stomach, Abdominal distension
Bowel perforation or obstruction
Metabolic Pyrexia, Hypothermia, Acidosis, Electrolyte disturbance,
Hypoglycaemia
36

37. Management of Bowel Obstruction
NEVER LET THE SUN RISE OR FALL ON A PATIENT
WITH
BOWEL OBSTRUCTION
37

38.  OPERATIVE INDICATION:
 Incarcerated or strangulated hernia
 Peritonitis
 Pneumopertioneum
 Suspected strangulation
 Closed loop obstruction
 Complete obstruction
 Large bowel obstruction
 NOT SAFE TO OPERATE:
 postoperative ileus
 partial small bowel obstruction,
 intestinal obstruction resulting from inflammation

39. 39

40. ANAESTHETIC CONSIDERATIONS
 4 things to be kept in mind
1) Full stomach
2)Respiratory complication
3)Fluid and hemodynamics
4)Electrolytes

41. Anaesthetic approach
postoperative
41
preoperative
intraoperative

42. 42

43. PREOPERATIVE
 The main purpose of the preoperative treatment is to
optimise the patient’s condition and maximise their
chance of survival.
 Early effective resuscitation improves oxygen delivery to
the tissues and reduces mortality in this group of patients.
43

44.  Patient presentation
 Patients presenting with abdominal emergencies for
laparotomies often come to hospitals very late.
 They have often been sick for some days with a perforated
or obstructed bowel.
 It is extremely important to establish the duration of their
disease, as this can give some idea of the degree of
dehydration and electrolyte imbalance.
44

45. Dehydration
Reasons for dehydration include:
 No oral intake especially in children
 Vomiting/ diarrhoea
 Fever
 High environmental temperature
 Third space loss (fluid in the body which is not available to
the circulation for example oedema, ascites or other
collections).
45

46. 46
 When taking the history enquire specifically about the
oral intake,vomiting/diarrhoea,fever and also the colour
and amount of urine over the last day as profound
dehydration and hypovolaemia will result in oliguria or
even anuria.

47.  Keypoint
 Every patient with an ‘acute abdomen’ is severely
dehydrated unless proven otherwise.
47

48. Physical examination
 The ABCD framework should be used for both examination and
initial management.
 Airway can be a problem so should be checked in every patient.
Rapid Airway Assessment
 LEMON law
 1,2,3 rule
 Breathing - an increased respiratory rate (RR) is an early
warning sign caused by acidosis or hypoxia and is often ignored.
 Tachypnoea can also be caused by pain, anxiety or pyrexia.
 Check the oxygen saturation and record respiratory rate
regularly.
48

49.  Circulation - the cardiovascular system is usually
significantly compromised due to hypovolaemia. Assess:
 heart rate (HR)
 blood pressure (BP)
 pulse - is it weak or well filled?
 capillary refill time; make sure it is done properly - press
for 5s (count to 5) then release the pressure and count refill
time.
This sign is very accurate in children and young adults, less
reliable in very anaemic or old patients.
49

50.  core - peripheral temperature gradient –
 check the difference between the temperature of the trunk,
which is usually hot (pyrexia) and the extremities which are
cold (vasoconstriction).
 This is a very good indicator of the intravascular volume;
especially useful to observe the trend - the difference
should reduce during resuscitation.
50

51.  degree of dehydration –
 severe thirst, decreased skin turgor, dry tongue,
sunken eyes, sunken fontanelle in a newborn.
 However, decreased skin turgor or sunken eyes may be
masked by oedema resulting from hypoalbuminaemia.
51

52.  Disability - assess the mental status; adult patients can
be apathetic occasionally agitated; children can
fluctuate between being apathetic and agitated.
 Document all of your findings on an appropriate chart.
52

53.  Key point
 it is important to realise that these patients do not only
have an abdominal problem, but multiple organ
impairment.
53

54. What are the electrolyte
abnormalities
Decreased
absorption
54
vomiting Fluid
sequestration
hypovolemia
Hyponatremia
Hypokalemia
Hypochremia

55.  In all cases of dehydration due to bowel obstruction there
is a total body deficit of Na+ and water and therefore
whatever the Na+ concentration (i.e. whether the patient is
hyponatremic or hypernatremic) replacement needs to be
with a fluid with a high Na+ content (0.9% saline or ringer
lactate).
 Correct fluid deficit according to U.O., CVP, Vitals etc to
achieve normovolemia.

56. 56
 K+ should be added to the fluid if necessary (usually 20-
40mmol/l provided the patient is not anuric or
hyperkalaemic).
 The aim should be to correct the dehydration over 24
hours, giving half the calculated amount in the first 8
hours and the second half over the following 16 hours.
 If the patient is very hypernatremic (Na+ > 155mmol/ l)
rehydration should be done slowly because of the risk of
cerebral oedema.

57.  Fluid losses can be calculated knowing that the body turns
over 17 to 18 L of fluid a day.
 There is tremendous fluid loss into the gut, which may
amount to 4,500 to 9,000 mL of functional fluid loss,
including loss resulting from vomiting and nasogastric
suctioning.
 If there is significant bowel wall edema and leakage of
fluid into the peritoneal cavity because of peritonitis , an
additional 7 L of fluid may be sequestered in the peritoneal
space.

58.  Preoperative resuscitation obviously takes time but long
delays before surgery should be avoided as early surgical
management improves the outcome in septic patients.
 The preoperative plan should be discussed between the
surgical and anaesthetic teams to achieve the right balance
between providing adequate resuscitation and the risk of
delaying surgery.
 Most patients will benefit from 2 - 4 hours preoperative
resuscitation.
 The best area to carry out resuscitation is ICU/HDU if
available. 58

59.  Make a management plan following the ABC framework.
 Airway and Breathing
 Provide oxygen with the face mask at 2-4 l/min
 Circulation
 insert iv cannula, preferably 16G or 2x 18G
 take a sample for Hb, electrolytes and consider
crossmatching (see below).
 Infuse first litre of normal saline or ringer lactate rapidly
over 15 min. During the following hour give
2000mls,watching clinical signs.
59

60.  Insert Foley catheter; measure and record the initial
amount and colour (concentration) of urine in the bag and
discard it.
 Crossmatching is essential as the patient may be severely
anaemic, and the “normal” Hb level is due to
haemoconcentration caused by severe dehydration &
hypovolemia.
60

61. Further treatment
 Request urgent surgical opinion.
 If abdominal X-ray requested by surgeon, and patient is
very sick make sure that he/she is transported to X- ray
department on a stretcher or wheel-chair and iv fluids are
continued.
 Antibiotics prescribed should be administered iv as soon
as possible
 Insert NG tube
 Check temperature
61

62.  Keypoint
 make sure that patients are not operated on while still
hypovolaemic, hypoxic, and oliguric.
62

63.  Further management
 Assess the patient after each 1 - 2 l of fluids. Whenever
possible warm the fluids even if patient is pyrexial. Use
either crystalloids and colloids, but avoid glucose 5 or 10%.
 Ringer lactate seems slightly better then normal saline as it
results in less hyperchloraemic acidosis.
 The correct volume of fluid is more important then the
type.
 When the initial resuscitation is completed, potassium
containing fluids (20mmol KCl /litre) may be used
providing there is an adequate urine output.
63

64. MONITORING
 Assessment of progress of resuscitation involves
assessment of:
 HR
 BP
 capillary refill time
 RR
 Improving peripheral temperature
 filling of neck veins
 urine output
 CVP monitoring 64

65.  After 4-5 l of IV crystalloid (or 1.5 - 2 l of colloid) it may be
worth repeating the Hb level to assess whether a blood
transfusion is likely to be required.
 In case of severe anaemia (Hb < 4g/dl), which is frequently
accompanied by hypoproteinaemia, there is a significant
risk of pulmonary oedema.
 In such cases blood should be transfused in early stages of
fluid resuscitation.
65

66.  What about inotropes?
 Noradrenaline & dopamine are frequently used in to
treat sick patients with abdominal emergencies.
66

67.  Patients who do not respond to fluid resuscitation and
require an inotrope infusion have a very high mortality and
are often in an irreversible clinical situation.
 Inotropes can also divert attention from providing
adequate fluid resuscitation by increasing the blood
pressure without adequate volume expansion.
 In cases of septic shock, adrenaline or noradrenaline can be
used provided adequate fluid administration has been
achieved.
67

68.  Electrolyte imbalance
 K+ levels are important as cardiac arrhythmias may result
from hypo or hyperkalaemia. Sick patients are normally
depleted due to K+ loss from diarrhoea and third space
losses.
 However, anuric patients are at risk of hyperkalaemia.
 After initial resuscitation, when the patient is passing good
volumes of urine, it is justified to add 20 -40mmol of KCl to
each litre of IV fluids.
68

69.  Anaesthesia
 The correct timing of anaesthesia and surgery depends on
the underlying problem.
 Resuscitation should be as complete as possible, but delay
dramatically increases the risk to the patient in cases of
peritonitis or bleeding.
69

70.  Ideally following resuscitation and before anaesthesia, the
patient will be stable with
 a pulse less than 100/min,
 a blood pressure greater than 90 systolic,
 established urine output and
 good capillary return.
70

71.  Patients require general anaesthesia with intubation and
ventilation. Diligent preparation is extremely important.
 On top of the usual routine preparation and equipment
check there is enough oxygen for a long case, adequate
amounts of IV fluids (warmed) and high volume suction.
 Empty the urine bag and suction NG tube.
71

72. Nasogastricstric decompression &
nasogastric tube
 Nasogastric sxning preoperatively
 What to do with the tube
 OR ???
72
Decreases aspiration riskDecreases respiratory
compromise,
Leave the tube
Allows gastric decompression
&
Removal may induce vomiting
Remove the tube
Doesn’t ensure empty stomach
&
Keeps LES patent
Difficulty in mask ventilation
& intubation.

73.  Very sick patients are frequently hypotensive immediately
after induction.
 Make sure there is a large bore IV line through which you
can infuse fluids fast.
73

74. Prepare “emergency” drugs:
 Vasopressor, ready and diluted in the syringe
 Atropine
 In case of high risk patients, also prepare diluted
adrenaline.
74

75. INVESTIGATIONS
 Hgb – anemia due to sequestration or carcinoma
 WBC- leukocytosis in strangulation
 RFT- renal failure due to complication
 Electrolytes – decreased K, Na etc.
 CVP & urine output- assess hypovolemia.
 Xray chest- ARDS
 ECG
 ABG- acidosis due to shock OR bowel ischemia or alkalosis
in SBO

76. INTRAOPERATIVE
76

77. POSITION OF PATIENT
SITTING OR SEMISITTING
Keeps gastric contents within
the stomach.
BUT
If vomits increased risk of
aspiration.
Difficult to ventilate &
intubate.
77
SUPINE OR HEAD DOWN
Easy to suction & decreased
risk of aspiration.
BUT
increased risk of regurgitation.
OR
Go for the conventional, you are confident in & expertise in i.e. supine
position.

78. FULL STOMACH
 Intestinal obstruction leads to:
 Accumulation of fluid and air.
 Increased intra-gastric pressure
 Persistent vomiting
 Loss of bowel motility.
 Increased risk of aspiration
 This increases both volume & acidity of aspirate.
 Give H2 blockers, antiemetics, nasogastric suctioning
and RSI.

79. PREMEDICATION
 Avoid premedications like opioids & BZD with resp.
depressant activity.
 Avoid using anticholinergics in pts with tachycardia or
hyperthermia.
 Antacids can stimulate vomiting.
 Avoid prokinetics.
 H2 blockers with antiemetics are preferred.

80.  Induction
 Preoxygenation is followed by rapid sequence induction
with cricoid pressure.
 Thiopentone or ketamine can be used. In hypotensive
patients, ketamine is a better choice.
 This should be followed by suxamethonium.
 The cricoid pressure is absolutely mandatory as
regurgitation is almost guaranteed.
80

81. MUSCLE RELAXANT
 Succinylcholine is preferred.
 it may increase IGT due to fasciculations.
 Defasciculating dose of NDMR can be used
 Rocuronium can be used in larger doses as part of rapid
sequence induction although it does not provide rapid
intubating conditions comparable to Suxamethonium.
 Make sure that anatomical abnormalities of the upper
airway that can pose difficulty, in laryngoscopy and
intubation, are ruled out before choosing nondepolarising
relaxants.

82.  Maintenance
 If hypotension follows induction of anaesthesia, it should
be treated with rapid infusion of fluids and ephedrine or
adrenaline boluses.
 If hypotension does not respond to vasopressor, adrenaline
is indicated.
 It has been suggested that keeping inspired oxygen level
around 80% intra-operatively and for 2 hours after surgery
might reduce the incident of wound infection and post
operative nausea and vomiting (PONV).
82

83. N₂0
Diffuse from blood to bowel
83
Nitrous is 35 times more
soluble than nitrogen in
bowel.
Distends the bowelIncrease intrabowel
pressure
Avoid nitrous, maintain with oxygen, inhalational, short acting opoids and muscle
relaxants.

84. ANALGESICS
 Simple analgesic should be given per-operatively and
prescribed regularly for 24-48 hours.
 Narcotics (e.g. morphine, meperidine (pethedine) or
pentazocine) as boluses or by infusion should be used
judiciously as they may cause hypotension especially in the
presence of hypovolaemia or sepsis.
 They can also result in postoperative respiratory
depression.
 Regional techniques like epidural catheters may be used
but are contraindicated if sepsis is suspected

85.  During anaesthesia make sure that the patient receives an
adequate amount of fluids and use ephedrine or adrenaline
as your second line of treatment.
 In septic patients who are unresponsive to inotropes,
hydrocortisone 2-3mg/kg should be considered.
85

86. Routine Intraoperative Fluid Administration
 Rate of fluid= CVE+Deficit+maintainance+loss+third
space
 Compensatory Intravascular Volume Expansion -must
be supplemented to compensate for the venodilation
and cardiac depression caused by anesthesia.
 It is 5 to 7 mL/kg of balanced salt solution must occur
before or simultaneous with the onset of anesthesia.
 Deficit - Maintenance fluid requirement multiplied by
the hours since last intake
 Maintenance - based on the 4-2-1 rule

87.  Losses - Blood loss is replaced initially with 3 mL of
balanced salt solution or 0.9% NaCl for each 1 mL of
blood loss. For each 1 mL of blood los t= 1 mL of colloid.
PRBC 1ml= 2ml of blood loss
 PRBC infused =E.B.V (Desired HCT – Observed HCT ) /
0.6
 Intra-abdominal procedures with small incisions (e.g.,
hysterectomy) may require an additional 2 mL/kg/hr,
whereas a major bowel resection requires an additional
4 to 6 mL/kg/hr.
87

88.  Normothermia during and after surgery improves
recovery, decreases oxygen consumption (increased by
shivering), reduces wound infection and decreases blood
loss.
 Intravenous fluids should be warmed.
 This can be achieved by putting the fluids into a simple
water bath.
 Using hot-water bottles (wrapped in cotton sheets) and
applying them to armpit and groins can also help to warm
up patients.
 Appropriate antibiotics should be administered pre- or
intra-operatively
88

89. POSTOPERATIVE
89

90. POST OPERATIVE CONCERNS
 Cardiovascular and respiratory monitoring and
stabilization
 Fluid and electrolyte balance
 Care of the wound and antibiotic prophylaxis when
indicated
 Commencement of enteral nutrition as soon as feasible
 Thromboembolism prophylaxis
 Adequate pain relief to facilitate physiotherapy and prevent
atelectasis and consolidation.

91. Respiratory compl.
91
Residual effects of
anaesthetics, muscle
relaxants
Splinting due to pain
residual abdominal
distension
1. Decreased FRC (15-20%)
2. Decreased TV, VC
3. Basal atelectasis.
4. Decreased PaO2
5. Increased PaCO2
*if suspected postop respiratory comp, keep on intubated patient for 1wk.
Abdominal surgery is a high risk case of post op resp comp.

92.  Post-operative period
 Patients are best managed in a recovery area, and then in
an Intensive Care Unit (ICU) or High Dependency Unit
(HDU) if possible.
 Supplementary oxygen (3-4 litres/minute) should be
continued for the first 24 hours if available.
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93.  Careful monitoring of basic physiological parameters (RR,
HR, BP, oxygen saturation, urine output, temperature) is
essential over next 24 hours.
 Signs such as tachypnoea, tachycardia, hypotension,
hypoxia, oliguria, changed mental state or hypothermia
should trigger immediate review by the medical staff.
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94.  Intravenous fluid requirements will remain high in the
immediate post-operative period.
 Patients will continue to have third space loss and residual
fluid deficit from the preoperative period.
 Therefore fluid requirements will be above the
maintenance amount of 3 litres per day.
 Often 4 - 6 litres are required in the first 24 hours and
should be given as Hartmanns or Normal Saline.
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95.  Although the calculated fluid balance will be positive,
increased insensible losses (fever, tropical environment),
fluid loss from drains and continuing third space losses
due to the underlying pathology result in continued fluid
deficit in the circulation.
 Adding 20mmol of potassium to each 1000ml bag of fluid
is recommended, providing the urine output is adequate.
 The daily requirement of potassium is 70 - 100mmol.
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96. POST OP PAIN
 The preoperative establishment of epidural analgesia aids
post-operative pain control.
 Epidural anesthesia improved splanchnic flow and may aid
recovery.
 Reduces the incidence of pulmonary morbidity.
 Opiod/ local anaesthetic combinations are more effective
and safer than either agents used alone.

97. BOWEL MOTILITY
 Bowel may not regain motility till third postop day.
 Distention persists, may accentuate resp comp.
 Keep on doing nasogastric decompression for 5-6
postoperative day.

98. Thank you
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