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Anaesthetic Management of Obese Patient
Anaesthetic Management of Obese Patient
Dr ABHISHEK
OBESITY means
excessive body fat
Obesus fattened
by eating
Weight (Kg)
Height in m2
W.H.O classification of overweight by cut – off
points of the BMI
25.0 – 29.9 Over weight
30.0 – 34.9 Grade I Obesity
35 - 39.9 Grade II
40- 49.9 Grade III
>50 super obese
Aetiology
Genetic Predisposition :
- 25-30 % of human variations
in BMI are genetic and the
rest are due to environment
factors (70%)
- Tends to be familial
1. Cardiovascular :
3. Endocrine :
DM, Hypothyroidism, Cushings
disease.
4. Gastrointestinal :
Hiatus hernia, gall stones,
inguinal hernia
5. Malignancy :
Breast, Prostate, Colorectal,
Cervical Endometrial
6. Musculo Skeletal :
Osteo artrihtis, Back pain
Distribution of body fat and health risk
a. Central or android type of distribution
- MC in males
- Fat predominally distributed in upper body
Deposits of intraabdominal or visceral fat
- Metabolically more active
- Associated with dyslipidaemias, glucose intolerance
and DM
b. Peripheral or gynaecoid type :
- Fat distributed around hips, buttocks or
thighs
- Female pattern of distribution
- Metabolically less active
- Associated with less metabolic
complications
Physiological changes associated with obesity :
Respiratory system :
Obstructive sleep apnoea – 5%
→ frequent episodes of apnoea or hypoapnoea
→ snoring
→ daytime sleepness
Apnoea → complete cessation of airflow for atleast 10
sec.
Hypoapnoea → reduction in airflow associated with
arrosal or O2 desaturation
Residual volume N or
O2 consumption and CO2 production Both are
as a result of metabolic activity of excess fat
and increased work load on supportive
tissues.
Compliance and Resistance:
Chest wallcompliance – due to fat
lung compliance Work of breathing
Total respiratory
resistance
Work of Breathing:
- 30% increased in WOB
- Hypoventilation – 4 times increased WOB
Cardiovascular System: -
1. HTN – Mild to moderate
HTN – 60-70% Severe
HTN – 5- 10%
2. IHD – Increased central
Obesity
3. Increased extracellular
volume
- Increased Blood vol.
and Cardiac output
Obesity induced hypertension
,
4. Concentric hypertrophy of
the left ventricle – cardiac
failure
5. Splanchnic blood flow – increased by 20%
Renal and cerebral blood flow are normal
6. Cardiac arrhythmias – hypoxia, hypercarbia,
electrolyte imbalance, diuretic therapy or fatty
infiltration of the conducting tissue.
7. Cardiac function – left ventricle systolic and
diastolic function are affected.
Obesity induced cardiomyopathy
Co increased by 20-30% ml/kg of excess body
fat
- exercise tolerance is poor
Co is by increased HR
Obesity & diabetes:
Type II DM is an
independence risk factor
- insulin resistance
syndrome – metabolic
syndrome
Thromboembolic disease:
- DVT – Twice as common obese patient
- 2.4% to 4.5% - Bariatric surgery
- Prolonged immobilization that leads to venous
stasis and polycythemia
- Increased abdominal pressure – increased
pressure on the deep veins
- Decrease fibrinolytic activity with increased
fibrinogen concentration.
Obesity and GI disorders:
1. Increased intraabdominal pressure
2. High volume and low PH of gastric contents
3. Delayed gastric emptying
4. Increased incidence of gastro oesophageal
reflex
High risk for aspiration Pneumonia
DRUGS, PHARMCODYNAMICS &
KINETICS
- Alteration in the distribution binding and
elimination of many drugs.
- Drug dose should be calculated keeping the
lean body mass in view
Volume of distribution:
* VD is influenced by number of factors
1. The size of the fat organ
2. in lean body mass
3. in blood volume & cardiac output
4. Reduced total body water
5. Alterations in plasma protein binding
6. Lipophilicity of the drug
* Highly lipophilic drugs have an increased
volume of distribution
* Thiopentone, Benzodiazepines and potent
inhalation agents may persist for longer time
after discontinuation
Elimination:
Clearance is reduced
Cardiac failure and liver blood flow may slow
elimination of midazolam and lignocaine
Renal clearance is increased & renal blood flow
& GFR
Inhalational agents:
Hepatic metabolism Reductive metabolism of
halothane is more liver injury
Nephrotoxicity High fluoride Halothane
enfluane
Isoflurane does not increase fluoride
concentration and remain agent of choice in the
obese
Sevoflurane
lower blood solubility which will
Desflurane speed the anesthetic uptake
distribution and also recovery.
Anaesthetic Implications:
- Preoperative :
Thorough clinical examination
Serial
ABG analysis should be used to
assess adequacy of minute ventilation