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SEMINAR ON
DEPARTMENT OF ANESTHESIOLOGY AND CRITICAL CAREDEPARTMENT OF ANESTHESIOLOGY AND CRITICAL CARE
J.J.M.MEDICAL COLLEGEJ.J.M.MEDICAL COLLEGEDAVANGEREDAVANGERE
““Anaesthesia for Morbid Anaesthesia for Morbid Obesity”Obesity”
Presented Presented by:by:
Dr. Tanmoy Dr. Tanmoy RoyRoy
Moderator:Moderator:Dr. Ramappa Dr. Ramappa M.D.M.D. Date : 30th
March 2010
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
“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”.
“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
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.
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)
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
Arcuate nucleus integrates these signals
Neuropeptides in the hypothalamus are classified as:
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
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
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.
• 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.
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
• 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.
• 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.
• 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.
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.
• 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%)
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
• 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.
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
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
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
8. Venous Thrombosis:- • Reduced mobility causing venous stasis• Diminished circulatory anticoagulant – antithrombin
III• ↓ fibrinolytic activity
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 GradingAssessment of head and neck, jaw, TMJ, Teeth, mentohyoid distanceInspection of oropharynxNeck 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
• 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
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
• 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
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
• 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
• 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
• 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
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.
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
• 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
• 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
• 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%
Anaesthetic options:
a)Regional Anaesthesia – The preferred technique, with supplemental oxygen support and minimal sedatives (preferably Remifentanil)
Advantages are: Airway intubation difficulties are avoidedRisk of gastric aspiration reducedNM blockers and their potential problems avoidedAwake communicative patientLesser postoperative respiratory complicationsEarly 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
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
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 difficultRegurgitation and aspiration problemsLimited range of head and neck mobilityShort fat neck, suprasternal, presternal and post cervical fatPendulous 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
• 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
• 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
• 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”
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
• 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
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
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 bypassBiliopancreatic diversion•Restrictive procedures:Vertical banded gastroplastyAdjustable gastric bandingRoux-en-Y gastric bypass
SPECTRUM OF OBESITY INDUCED MORTALITY AND
MORBIDITY
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.
Both forms are usually associated with:SnoringSleep disruption from increased ventilation effort-induced arousalHypersomnolence (day time sleepiness)Altered CVS functionPathophysiologic alterationsPrimary: Hypoxemia and HypercarbiaSecondary: Polycythemia, Systemic and pulmonary HTN, arrhythmias, myocardial ischaemia, RVH & LVH, Heart failure
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
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
• 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
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.
Diagnosis: - Suspected by history, physical examination, comorbiditiesPatient characteristics typically associated with OSA are a higher BMI, HTN and cephalometric measurementsIn 90% cases, BMI is excess of 28 kg/m2
Definitive diagnosis is made by a formal sleep study or a polysomnogramResults are reported in as total number of apneas and hypopneas per hour of sleep or the Apnoea-Hypopnea Index(AHI)Mild OSA= AHI of 6-20Moderate OSA= AHI of 21-40Severe OSA= AHI of >40
Arousal Index(AI)= arousals/hour Respiratory Disturbance Index(RDI)=AHI+AI
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.
d) 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.
e) Of the potent inhalational anaesthetics; Desflurane combines the quickest wake-up, fastest return of airway reflex, lowest solubility and the lowest percentage of hepatometabolization
f) Intravenous agents should be either lipophobic, spontaneous degraded in vivo, or ultra short acting.
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.
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…………
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