This document summarizes a seminar on anesthesia considerations for morbid obesity. It discusses the physiological effects of obesity including changes to the respiratory, cardiovascular and endocrine systems. It notes increased risks of difficult intubation and ventilation. Pre-anesthetic evaluation and preparation is emphasized, including assessing airway difficulty, optimizing medical conditions, counseling on smoking cessation and weight loss, and providing prophylaxis for thrombosis.

1. SEMINAR ON
DEPARTMENT OF ANESTHESIOLOGY AND CRITICAL CAREDEPARTMENT OF ANESTHESIOLOGY AND CRITICAL CARE
J.J.M.MEDICAL COLLEGEJ.J.M.MEDICAL COLLEGE
DAVANGEREDAVANGERE
““Anaesthesia for Morbid Obesity”Anaesthesia for Morbid Obesity”
Presented by:Presented by:
Dr. TanmoyDr. Tanmoy
RoyRoy
Moderator:Moderator:
Dr. RamappaDr. Ramappa
M.D.M.D.
Date : 30th
March

2. Introduction and Definition
Physiological aspect: Regulation of Body weight
Etiology of Obesity
Systemic Pathophysiology associated with Morbid Obesity
Anaesthetic considerations in Morbid Obesity
Treatment of Obesity
Complication in Obesity: The Obstructed Sleep Apnoea and Hypopnoea Syndrome
Conclusion
References

3. “O besity is a metabolic disease in
which adipose tissue comprises a
greater than normal proportion of
body tissue and amount of fatty
tissue is increased beyond a point
compatible with physical and
mental health and normal life
expectancy”
Derived from the Latin word OBESUS meaning
“Fattened by eating”.

4. “DEURENBERG EQUATION”: - Estimation of body fat.
1.2 X BMI + 0.23 X Age – 10.8 X Sex – 5.41.2 X BMI + 0.23 X Age – 10.8 X Sex – 5.4
 age is in years
 sex is 1 for male and 0 for female
>25% in males and >33% in females is considered as obesity

5. Excessive abdominal fat is
defined as:
•>40 inches in Males
•>35 inches in Females
OVERWEIGHT: Excess of total body weight including muscle,
bone, water and fat.

8. Ideal Body Weight is the weight which is associated with lowest
mortality for a given height and gender, and is estimated by
BROCA’s index
Ideal Body Weight (IBW) in Kg =Ideal Body Weight (IBW) in Kg =
Height(cm) – 100 (Males)/105 (Females)Height(cm) – 100 (Males)/105 (Females)

10.  Centrally regulated mechanism
 Satiety center in ventomedial hypothalamic nuclei and
Feeding center in lateral hypothalamus are involved in
the regulation of body weight
 Long term signals informing about energy stores and
endocrine status of the body are mediated by
predominantly humoral mechanisms
 Short term signals are mediated by the gut hormones
and neural signals from the brain and they signal the gut
for meal initiation and termination

11.  Arcuate nucleus integrates these signals
 Neuropeptides in the hypothalamus are classified as:

12. Complex and multifactoral.
Occurs when net energy intake exceeds net energy
expenditure over prolonged period.
Genetic Predisposition – Familial and contributed by diet
and lifestyle
Medical Disorders – Endocrine diseases like Cushing’s
disease, hypothyroidism, drugs like corticosteroids,
antidepressants, antihistamines
Energy balance – Imbalance between energy intake and
expenditure

13.  Psychological factors – Depression
 Ethnic influences – Africans, Mexicans, and Asians with
central fat distribution are at higher risk
 Socioeconomic Factors – More in poor strata in
developed countries and rich in developing world

14. 1. Airway: -
• Deposit of adipose tissue in the lateral pharyngeal walls ,
uvula, tonsillar pillars, tongue and aryepiglottic folds,
causing a decreases in pharyngeal area.
• Deposit of adipose tissue external to the upper airway,
extrinsically compressing the airway.
• Presence of hypopharyngeal adipose tissue not evident
on external examination that acts as a ball valve,
obstructing the upper airway and interfering with the
line of sight at direct laryngoscopy.

15. • Presence of pretracheal adipose tissue, which pushes the
hyoid bone posteriorly into a less favorable position ,
causing epiglottis to partially override the glottis
entrance, worsening laryngoscopic view.
 Alteration in the shape of the pharynx from an ellipse
with the long axis lateral transverse to an ellipse with the
long axis anterior – posterior.
 Decreased efficiency of the anterior pharyngeal dilator
muscles (tensor palatine, genioglossus, hyoid muscles)
which promotes snoring.

16. 2. Respiratory System: -
• Pulmonary Mechanics –
Tidal volume(Vt)
=/ in obese; in Obesity Hypoventilation↑ ↓
syndrome(OHS)
Inspiratory Reserve
Volume(IRV)
↓
Expiratory Reserve
Volume(ERV)
↓↓, due to increased torso weight limiting normal
rib expansion
Residual Volume(RV) =
FRC(ERV+RV) ↓↓, due to decrease in ERV
VC(ERV+ Vt+IRV) ↓, due to decrease in ERV
TLC(RV+VC) ↓, due to decrease in ERV

17. • Diffusion capacity carbon monoxide(DLCO) –
Normal in obese individuals and reduced mildly in cases
of OHS, because the lung parenchyma is normal and the
changes in PFT are due to chest wall mechanics and
lower lung volumes.
• Compliance –
Total respiratory Compliance is decreased because of
the weight of the torso and abdominal contents.
Lung compliance is decreased when pulmonary and
circulatory abnormalities persist.

18. • Resistance –
Increase in both airway resistance and respiratory system
resistance at lower lung volumes due to reduced elastic
tension of the lung and chest wall respectively.
• Closing Capacity(CC) –
FRC is reduced in the morbidly obese and may be below
CC resulting in small airway closure, V/Q mismatch, R L→
shunt and possible hypoxaemia (Positional Ventilatory
Collapse).
Worsened by supine position, Trendelenberg position,
GA and muscle relaxants. Improved by PEEP and reverse
Trendelenberg position.

20. • Work of breathing(WOB) –
70% increase in WOB and a fourfold rise in oxygen
consumed by respiratory muscle.
• PaO2 and PaCO2 –
Hypoxaemia is the most common blood gas abnormality
in severe obese patient, mainly due to low V/Q ratio and
less commonly due to hypoventilation.
PaCO2 is variable and not related to lung disease , and
dependent on the alveolar ventilation.

21. 3. Cardiovascular System: -
• Circulating Blood Volume –
 Increase in body mass requires increased cardiac
output and increased IV volume.
 Increased Renin-Angiotensin activity Increased IV→
volume.
 Blood volume on weight basis is less than normal
(45ml/kg compared to 70ml/kg)
• Left Ventricular Changes –
Increased stroke volume and cardiac work leads to
increased LV load causing dilatation and compensatory
LV hypertrophy. This leads to subsequent decrease of LV
compliance and increased LV filling, which further
results in heart failure.

22. • Right Ventricular Changes –
 Increased right ventricular filling pressure.
 Right ventricular hypertrophy and dilatation.
• Cardiac arrhythmias –
 Sudden death.
 Causes include Myocardial hypertrophy, Hypercapnia,→
Coronary artery disease, Electrolyte imbalance. Etc
 Prevalent ECG changes are –
 P-wave, QRS, and T-wave axis are shifted leftward in obese
subjects, but still within normal limits.
 Diffuse low voltage (11%)

23.  Left ventricular hypertrophy (66%)
 Non-specific ST and T-wave abnormalities (11%)
 Flattened T-waves in the inferior (58%) and lateral (29%) leads
 Central obesity is associated with QT prolongation and potential
ventricular dysrhythmias
 Ventricular premature beats occur 30 times more frequently in
obese patients
 Atrial and ventricular dysrhythmias

24. • Coronary Artery disease –
It is a major risk factor for IHD manifested as angina,
myocardial ischaemia/ infarction and sudden death.
• Systemic vascular resistance –
 As cardiac output is increased in obese patients, so for
any given arterial pressure SVR is reduced.
 HR remains unchanged.
• Hypertension –
 D/t increased sympathetic tone, increased IV volume and
increased renin-angiotensin-aldosterone system
 For every 10 kg of weight gain, there is 3-4 mmHg rise in
systolic and 2 mmHg rise in diastolic b.p.

26. 4. Endocrinal System :- Abnormalities seen are:
• Insulin resistance
• Hyperinsulinaemia
• Glucose intolerance
• High BP
• ↓ HDL-C level
• ↑ Triglycerides
• ↑ Cortisol production and metabolism
• ↑ risk of NIDDM
• ↑ risk of infertility and hypothyroidism

27. 5. Gastrointestinal System :- Risk of aspiration of gastric
contents(aspiration pneumonitis) due to:
• ↑ intra abdominal pressure
• High volume(>25 ml) and larger residual volume; low
pH(<2.5) of gastric contents
• Delayed gastric emptying
• High incidence of hiatus hernia and gastro-esophageal
reflux

28. 6. Genitourinary System :-
• GFR is increased as evident by the increased Renal Blood
Flow
• There is increased renal tubular resorption and decreased
natriuresis d/t:
 Thorough activation of the sympathetic and renin-
angiotensin system
 Physical compression of the kidney
7. Musculoskeletal System :-
Increased incidence of osteoarthritis of weight bearing
joints and back pain

29. 8. Venous Thrombosis:-
• Reduced mobility causing venous stasis
• Diminished circulatory anticoagulant – antithrombin III
• ↓ fibrinolytic activity

30. Pre-anaesthetic evaluation:
•Detailed history and examination with all the baseline
investigations
•Preoperative visit with proper explanation of the intended
anaesthetic procedure
•Evaluation of intubating conditions:
Mallampati Grading
Assessment of head and neck, jaw, TMJ, Teeth, mentohyoid distance
Inspection of oropharynx
Neck circumference- 40cms has 5% chance of difficult intubation; 60cms
has 35%
USG neck showing >2.5 cms of pretracheal adipose tissue at the level of
vocal cord is an independent indicator of difficult intubation

31. • In anticipated difficult intubation, awake intubation and
tracheostomy must be discussed and considered
• Pt should be advised to quit smoking(minimum 6-8 wks
prior) and weight reduction by diet control and exercise
Investigations:
• Hb%, BT, CT, Blood sugar-Fasting; Postprandial
• LFT and RFT
• Chest X-ray and Neck X-ray
• ECG and ECHO
• ABG studies
• Pulmonary Function Tests – Sitting; Supine
• Lipid Profile
• Thyroid function Tests and Adrenal Function test

32. Preoperative preparation:
•Important medical records pertaining to the relevance of the
case should be obtained and maintained
•H/O OSA or heavy snoring should have formal sleep study or
polysomnogram(PSG)
•Spirometry and incentive Spirometry
•Psychological preparation
•Preformed informed and written consent for getting
anaesthetized and operated
•Strong weight bearing shifting trolleys

33. • Prophylaxis for phlebothrombosis by LMWH, elastic stockings
and frequent leg lifts
• Appropriate sized equipments regarding Anaesthetic
technique
• PACU beds
• Well working BP cuffs with adequate length and breadth of
cuff, rechecking functionality of monitors
• A ventilator capable of generating high inspiratory pressure
• Continue medications of hypertension and shift from oral
hypoglycemics to insulin if possible

34. Premedication:
•Opoids and sedatives are to be best avoided as may cause
respiratory depression
•Avoid intramuscular and subcutaneous routes of injection – a
well secured and conveniently placed IV cannula is to be
instituted. Other preferred routes are oral and sublingual route
•If awake or fibreoptic intubation is considered, Atropine and
Glycopyrrolate is necessary
•Acid aspiration prophylaxis – (Ranitidine 150 mg);
(Metoclopramide 10 mg) p.o 12hrs and 2 hrs before surgery

35. • Low dose subcutaneous heparin as prophylaxis against deep
vein thrombosis
• Prophylactic antibiotics
• Dextrose – Insulin regimen is required for all diabetics except
short procedures. Insulin requirements may increase
postoperatively
Positioning:
• Two operating tables joined together may be needed
• Supine position decreases the chest wall compliance and
increases V/Q mismatch
• Left lateral decubitus or lateral position is safe as prevents
compression of IVC

36. • Patient to be strapped to
table
• Towels or folded blankets
under shoulder and head
can compensate for the
exaggerated flexed
position of posterior
cervical fat
• Chin to be kept at a higher
than the chest to facilitate
laryngoscopy and
intubation
TOWELS AND BLANKETS UNDER
SHOULDERS AND HEAD

37. • Head Elevated Laryngoscopy Position(HELP) - Here, the
obese patient’s head, upper body and shoulders are elevated
above the chest to the extent that an imaginary horizontal
line connects the sternal notch with the external auditory
meatus to better improve laryngoscopy and intubation
IMAGINARY HORIZONTAL LINE
POINT
CORRESPONDING TO
STERNAL NOTCH

38. Monitoring:
•Radial artery cannulation is preferable for continuous BP
monitoring. If non – invasive techniques are used, appropriate
cuff of proper size to be used
•Pulse oximetry, EtCO2, ECG, respiratory volumes
measurement(expiratory tidal volume), capnography are useful
•Nerve stimulator to assess degree of NM blockade during
procedure and to monitor reversal of NM blockade at
completion of surgery. Because of excess fat, surface electrodes
are inaccurate; needle electrodes are advisable.
•Pulmonary artery flotation catheters are considered in patients
undergoing extensive surgery or those with serious cardio
respiratory ailments.

39. Pharmacological considerations:
Greater than normal adipose tissue content
Increased lean body mass and altered tissue protein binding
Increased blood volume and cardiac output
Increased concentration of blood constituents such as FFA, TGs, cholesterol and α-
acid glycoprotein
OBESE
PEOPLE
Smaller than normal fraction of TBW

40. • Dosing of drugs done according to their lipophilicity:
 Highly lipophilic drugs have increased Vd for obese people compared to
normal people. Doses are calculated according to total body weight.
Eg – Thio, Propofol, BDZ, Fentanyl, Sufentanyl, Scoline, Atracurium and
Cisatracurium
 Weakly lipophilic/ lipophobic drugs have unchanged Vd. Doses are calculated
according to patients lean body weight (IBW+20%-40%IBW).
Eg – Alfentanyl, Ketamine, Vecuronium, Rocuronium, Pancuronium,
Morphine

41. • Renal clearance is increased due to increased renal flow,
increased GFR and tubular secretion
• Drug metabolism in liver is partly changed due to decreased
hepatic blood flow
• Halogenated anesthetics:
 Halothane and Enflurane are metabolized more resulting high serum and
urine level of Fluoride ions.
 Isoflurane and Desflurane appear to be volatile anaesthtics of choice

42. • Plasma pseudocholinesterase level and the volume of ECF
determine the activity of Scoline, both of them are increased in
obesity. So the dose of Scoline is higher than average patients
• Local anesthetics:
 Absolute volume of distribution of lignocaine is increased in obesity but not
changed when corrected for body weight
 IV lignocaine is to be given according to total body weight
 Greater extradural fat necessitates greater initial dose , it may prolong drug
effect and level of anaesthesia
 Engorged veins and large amount of fat constrict potential extradural space
thereby increased segmental drug distribution
 Dose requirement of LA for intrathecal and extradural anaesthesia in obese
people are reduced by 20-25%

43. Anaesthetic options:
a)Regional Anaesthesia – The preferred technique, with
supplemental oxygen support and minimal sedatives
(preferably Remifentanil)
Advantages are:
Airway intubation difficulties are avoided
Risk of gastric aspiration reduced
NM blockers and their potential problems avoided
Awake communicative patient
Lesser postoperative respiratory complications
Early ambulation
→Ultra short acting
Equally potent as Fentanyl
Short half life (8-20 mins)
Context sensitive half life of 4 minutes,
making it ideal for infusions

44. N.B –
•Regional anaesthesia can be technically difficult in an obese patient
due to difficulties in identifying landmarks
•Epidural and spinal anaesthesia preferably in sitting position and
using longer needles
•Use of USG to guide the Tuohy needle in position
•Preferable to put the epidural catheter beforehand in the previous
evening of surgery to save time the next day
•Use of nerve stimulators for nerve blocks
•Facilities to convert to GA should be there at hand

45. b) General Anaesthesia –
• Ideally two anaesthesiologists should be present.
• Potential management problems with GA include:
 Maintaining a proper fitting tight mask, maintaining airway and
performing other tasks simultaneously may be difficult
 Regurgitation and aspiration problems
 Limited range of head and neck mobility
 Short fat neck, suprasternal, presternal and post cervical fat
 Pendulous breasts
• Preoxygenation in the 25o
head up position achieves 23%
higher oxygen tensions allowing a clinically significant
increase in the desaturation safety period- greater time for
intubation and airway manipulation

46. • Towels or folded blankets under the shoulders and head can
compensate for the exaggerated flexed position from
posterior cervical fat. This is stacking, and facilitates
laryngoscopy and intubation
• Rapid IV induction with Thiopentone and Succinylcholine
combined with cricoid pressure is the safest method
• In anticipated difficult tracheal intubation, an awake
intubation with topical anaesthesia and sedation
with/without fibreoptic bronchoscope is preferred. After
confirming the position of the tube, patient is anaesthetized
with Sevoflurane

47. • NM blocking agents are administered only after confirming
acceptable chest wall mechanics.
• Higher Tidal Volumes of 15-20 ml/kg are required for
ventilation with minimal 5-10mm Hg PEEP
• Suboptimal intubation conditions call for use of LMAs, LMA
fasttrach, LMA C track, Glide scope. Tracheo-oesophageal
combitube is also useful

48. • Fluid management:- Intraoperative fluid requirements are
usually larger, upto 4-5 liters of crystalloid for an average of 2
hours long operation. This adds upto twice the calculated
maintenance fluid requirements plus a calculated deficit
based on 12 hours fasting for an average 70 kg patient for the
first hour by using the Holiday-Segar formula
• Extubation:- To be only extubated when patients are fully
awake with adequate cough reflex and have complete
reversal of NM blockers
“Combined regional and general balanced anaesthesia is
preferable as it enables better titration of anaesthetic drugs,
use of higher concentration of oxygen, optimal NM blockade
and decreased concentration of volatile anaesthetic agents”

49. Post-anaesthetic care:
•Transfer to PACU is done in semi-recumbent position
•Continue monitoring with supplemental oxygen; avoid shivering
•Increased incidence of atelectesis has been reported and
initiation of CPAP starting in the recovery room, continuing
overnight to prevent postoperative acute airway obstruction.
BiPAP can also be used as an option
•Early ambulation is to be encouraged to prevent
thromboembolism.DVT prophylaxis and LMWH are helpful

50. • Incentive Spirometry and physiotherapy to be started
• Postoperative analgesia:-
 Epidural local anaesthetic/narcotics via the thoracic route are
a safe and effective form of postop analgesia.
 Intrathecal narcotics are also being used.
 Patient controlled analgesia with Morphine provides a
superior quality of analgesia and shortens the duration of
postoperative ileus

51. Indications:
a)Medical Therapy:
•BMI>30 kg/m2
•BMI between 27-29.9 kg/m2
associated obesity related medical
complications
b)Bariatric surgery:
•BMI>40 kg/m2
•BMI>35 kg/m2
with severe co-morbidities
•Failure of medical therapy

52. Medical Therapy:
•Phentermine and Fenfluramine
•Sibutramine; inhibits the reuptake of nor epinephrine to
increase satiety after the onset of eating
•Orlistat; blocks the absorption and digestion of dietary fat
by binding lipases in the GIT
Surgical therapy:
•Malabsorptive procedures:
Jejuno-Ileal bypass
Biliopancreatic diversion
•Restrictive procedures:
Vertical banded gastroplasty
Adjustable gastric banding
Roux-en-Y gastric bypass

54. SPECTRUM OF OBESITY
INDUCED MORTALITY AND
MORBIDITY

55. Previously, OSA referred to both Obstructive Sleep Apnoea
(OSA) proper and to Obstructive Sleep Hypopnoea (OSH)
syndrome, a milder variant. Currently it is more precise to refer to
OSAHS, when naming the general condition.
OSA – Cessation of airflow for more than 10 seconds despite
continuing ventilatory effort, five or more times per hour of
sleep, associated with a decrease in SpO2 of greater than 4%.
OSH – Decrease in airflow of more than 50% for more than 10
seconds, 15 or more times per hour of sleep, associated with a
decrease in SpO2 of greater than 4%. Milder form of OSA.

56. Both forms are usually associated with:
Snoring
Sleep disruption from increased ventilation effort-induced
arousal
Hypersomnolence (day time sleepiness)
Altered CVS function
Pathophysiologic alterations
Primary: Hypoxemia and Hypercarbia
Secondary: Polycythemia, Systemic and pulmonary HTN,
arrhythmias, myocardial ischaemia, RVH & LVH, Heart failure

57. Risk factors: - Severe obesity, Male, Middle age, Alcoholism, Drug
induced sleep
In non obese people, craniofacial dysostoses, cartilaginous
abnormality, tonsillar hypertrophy and chronic nasal obstruction.
Types: - Usually of 2 types:
•Childhood OSA-
It starts as snoring and continues to upper airway resistance
syndrome till the fully expressed syndrome.
Peripheral origin; due to nocturnal airway blockage from nasal
physiology, hypertrophied tonsils, adenoids etc.
Symptomatology include snoring, rare daytime sleepiness and
frequent behavioral disturbances

58.  Polysomnogram diagnosis is not gold standard
 Distinguished from adult OSA by:
 Snoring being continuous
 No sex predilection
 Surgery is curative
• Adult OSA/ OSAHS-
• Continuum from asymptomatic to paroxysmal snoring to
severe nocturnal airway closure requiring the patient to sleep
in sitting position, and day time somnolence
• Pathophysiology is central, peripheral and mixed

59. • Peripheral disease is due to excess adipose tissue in the upper
airway , in the setting of severe obesity, sometimes with a
superimposed craniofacial dystosis
• Symptomatology consists of intermittent snoring, apnoeic
episodes and daytime somnolence
• Obesity – Hypoventilation Syndrome (OHS):
Severe OSA with chronic daytime hypoventilation, super
obesity and hypercapnia not related to pulmonary disease
• Pickwickian Syndrome: OHS + cor pulmonale

60. Association of Obesity with OSA:- 60% - 90% patients with
OSAHS are obese.
Increased deposition of pharyngeal adipose tissue results in likelihood of
collapse of the oropharynx during relaxation of the upper airway muscles.
The long axis of the elliptical pharynx shifts from transverse to antero-
posterior plane; the muscles that open the collapsible pharynx on expiration
during sleep in response to the stretch receptors in the pharynx are located
in the anterior pharynx, and do not function well with a remodeled pharynx.
In a normal human being, patency of the pharynx depends on the
transmural pressure (difference between extra luminal and intra luminal
pressure) and the compliance of the wall. Obese patients , owing to their
excessively deposited adipose tissue around the neck, have increased extra
luminal pressure and thus compressed upper airway.

61. Diagnosis: - Suspected by history, physical examination,
comorbidities
Patient characteristics typically associated with OSA are a
higher BMI, HTN and cephalometric measurements
In 90% cases, BMI is excess of 28 kg/m2
Definitive diagnosis is made by a formal sleep study or a
polysomnogram
Results are reported in as total number of apneas and
hypopneas per hour of sleep or the Apnoea-Hypopnea
Index(AHI)
Mild OSA= AHI of 6-20
Moderate OSA= AHI of 21-40
Severe OSA= AHI of >40

62.  Arousal Index(AI)= arousals/hour
 Respiratory Disturbance Index(RDI)=AHI+AI

63. Anaesthetic Implication:-
Points to be kept in mind during anesthetizing these patients:
a)These patients are extremely sensitive to minimal doses of CNS
depressants and may exhibit prolonged sedation, resedation, apnoea,
upper airway obstruction. So BDZ or narcotics are sparingly used and
sedation is usually reserved for painful or unpleasant situations.
b)13%-24% OSAHS patients may present with difficult intubation
situation. Usually recommended strategy is an anaesthetic procedure
with safe induction, deep maintenance anaesthetic with muscle
relaxants, and a smooth emergence with rapid offset devoid of active
metabolites or trace anaesthetic.

64. c) The only weak inhalational agent, N2O, has the advantage of
being relatively insoluble (BG coeff. 0.46); but it causes intestinal
inflation and is contraindicated in pulmonary HTN, a condition
more common in morbid obesity.
d) Of the potent inhalational anaesthetics; Desflurane combines the
quickest wake-up, fastest return of airway reflex, lowest solubility
and the lowest percentage of hepatometabolization
e) Intravenous agents should be either lipophobic, spontaneous
degraded in vivo, or ultra short acting.

65. f) When feasible, regional anaesthesia is useful. Tracheal extubation
is considered when patients are fully awake with intact upper
airway reflexes. Episodic arterial hypoxaemia may occur early in
the first 24 hrs or late from the 2nd to the 5th day postoperatively
g) Discharge from the PACU may be made in the morbidly obese OSA
after they have been started on CPAP or BiPAP and have been
observed for minimum 30 minutes without any respiratory arrests.
One attack of respiratory arrest demands extension of the PACU
stay for additional 3 hours
h) Intravenous patient controlled analgesia appears to be well
tolerated by these patients. Dosing is based on ideal body weight.
Most common drug used is Morphine Sulfate starting at 20µg/kg
every 10 minutes with a 4 hour maximum dose of 80% of the
calculated dose. Hydromorphone is the second line agent.

66. Good health is a God gifted privilege and it mandates us to maintain
it in its proper way. Obesity is a recognized potential threat to any
individual, regardless of the situation whether in undergoing any
surgery or pursuing the daily chores of life. Recognizing this threat at
an early stage and taking proper steps to prevent it ensures a long
and healthy life; both physically and psychologically.
AND
FINALLY…………

67.  MILLER’S ANAESTHESIA 7TH
EDITION
 CLINICAL ANAESTHESIA (PAUL
G. BARASH) 4TH
EDITION
 CLINICAL ANAESTHESIOLOGY
(EDWARD MORGAN) 4TH
EDITION
 YAO’S ANAESTHESIOLOGY 6TH
EDITION
 ISACON-2009
 INTERNET