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MORBID OBESITY -
ANAESTHETIC MANAGEMENT
Prof. S. Manimala Rao MD, DA (London), FCCP, Head, Department of
Anaesthesiology & Intensive Care,
Nizam's Institute of Medical
Sciences, Hyderabad.
Obesity
means excessive body fat. The term obese, derived from Latin word means
fattened by eating. The amount of fat tissue may increased to such an
extent that mental and physical health is affected and life expectancy
is reduced.
Body
mass index (BMI) or Quetelet's index is calculated from subjects' height
and weight. It is used to indicate obesity. Obesity is indicated by BMI ³
30.0 (M), ³
28.6 (F). Morbid obesity is when BMI is more than 40 kg/m2. Many
clinical parameters depict women, as pear shaped, accumulating fat at
bottom and is regarded as safe, fat is stored between skin and body
wall. In men the classic beer belly look compared to a rounded apple,
here the fat is stored to internal organs.
Prevalence
and Epidemiology
There is a slow but steady increase in obesity. In
UK, in 1980 - 6% males and 8% females were obese. In 1987 - 8% males and
12% females were regarded obese. Obesity in children is also on the
rise. Prevalence varies with socioeconomic status. In developed
countries poverty is associated with greater prevalence whereas in
developing countries it is the affluent that carry higher prevalence.
Obesity is complex, wherein the net energy intake exceeds the net energy
expenditure over a prolonged period of time.
Pathophysiology
Brain controls appetite by means of signals triggered
by dietary breakdown products and by autonomic signals produced by
disturbance of the stomach and intestines. The multiple signals
generated are processed by complex interactions between neuronal
networks and neuro transmitters. Most important of them are
cholecystokinin 8 (CCK 8), which act at gut and brain. It induces
satiation, is released at beginning of a meal and promotes pancreatic
secretion of insulin, which lowers blood sugar and increases appetite.
Insulin crosses blood brain barrier and triggers hypothalamus, which in
turn juggles many other signals. Therefore the complexity of weight
maintenance is evident. 25-30% of human variations in BMI are genetic
and rest is due to environmental factors. It is a complex picture how
normal weight is maintained. The pathways regulating weight form series
of redundant regulatory loops. If one loop is weakened or attenuated,
the other can take over. It is this redundancy that regulates calorie
storage, but at the same time the redundancy makes it hard to get a
handle on how to prevent and treat obesity. It is an imbalance between
food intake and energy expenditure. The balancing act involves neural
and endocrinal signalling. These operate both by central and peripheral
mechanism. Problems can occur any where in this complex system.
Genetic
Predisposition
Tends to be familial. Children of two obese parents
have a 70% chance to become obese. The genetic issue plays 30% and
linked to at least 6 genes. 70% is dependent on environmental factors.
Genetic susceptibility may predispose and environmental issues may add
on.
Ethnic
Influences
In USA, the African Americans and Mexicans have
higher rate of obesity than the Whites. Asian migrates have more central
distribution of fat, which is associated with increased risk of diabetes
and Coronary Artery Disease. 0:P>
Medical
Diseases
Cushing's disease, hypothyroidism, medications like
steroids, antidepressants and antihistamines may also have a role to
play in obesity.
Obesity
Associated Medical Conditions
Diabetes,
hypertension, hyperlipidemia, heart diseases, infertility, hepatobilary
diseases, cerebrovascular disease, degenerative joint disease, chronic
back pain, gallstones, increased rates of colon and breast cancer
and asthma are also linked to rising levels of obesity. A BMI >29
kg/m2 increases the prevalence of pulmonary embolism. Risk of coronary
artery diseases is doubled if BMI is > 25kg/m2. A BMI 35kg/m2 leads
to a 40-fold increase in developing diabetes, respiratory diseases,
sleep apnoea and osteoarthritis. Risk of death increases with body
weight. Mortality rises exponentially with increasing body weight.
CHANGES
IN VARIOUS SYSTEMS
Obesity and Respiratory System
5% of morbidly obese have Obstructive Sleep Apnoea (OSA)
characterized by frequent episodes of apnoea or hypercapnia, snoring and
daytime sleepiness. Recurrent apnoea leads to hypoxia, hypercapnia,
pulmonary and systemic vascular hypertension, which in turn leads to
right ventricle failure. Loss of pharyngeal muscle tone in obese person
during sleep and significant narrowing of airway increases airflow
turbulence resulting in OSA.
Risk
Factors For OSA
Male gender, middle age, night sedation, evening alcohol can compound
the problem. Other features which can help identify OSA are BMI > 30
kg/m2, hypertension, observed episodes of apnoea during sleep,
hypoxemia, hypercapnia, changes in ECG and ECHO. Definite diagnosis is
made by polysomnography in sleep laboratory. Such patients pose a great
challenge to surgery, anaesthesia, obstetrics, trauma and in the ICU.
Acid
Base Disturbances of OSA
Respiratory acidosis is limited to sleep, in the
beginning. Longer the problem, alterations occur in breathing patterns,
desensitization of respiratory center to hypercapnia leads to typeII
respiratory failure. This leads to increased dependence on hypoxic drive
for ventilation. Pickwickian syndrome is characterized by obesity,
hypersomnolence, hypoxia, hypercapnia, right ventricular failure and
polycythemia.
Airway
Perfect airway particularly upper is essential before
any anaesthetic management. Difficulties are encountered for mask
ventilation. Tracheal intubations may be difficult. The percentage of
difficult intubation is quoted to be 13%. Excessive fat at upper airway,
short neck, high anteriorly placed larynx, restricted cervical spine
movements are a few problems.
Obesity and Lung Volume
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Increased mass of abdominal and thoracic contents
alters the lung volumes. Decrease in functional residual capacity (FRC)
is seen exponentially with increasing BMI. Expiratory reserve volume and
total lung capacity are decreased. FRC may be reduced in upright
position to the extent that it falls within the range of closing
capacity with subsequent small airway closure, ventilation perfusion
mismatch, right to left shunting and arterial hypoxemia. The reduction
of FRC impairs the capacity of obese patients to tolerate apnoea. They
desaturate rapidly after induction of anaesthesia despite preoxygenation
due to smaller O2 reservoir and increase in oxygen consumption. Residual
volume remains normal or slightly increased due to increased gas
trapping and coexisting obstructive airway disease.
O2 Consumption and CO2 Production
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Both are increased in obese patients as a result of
metabolic activity of excess fat and increased workload on supportive
tissues. In exercise O2 consumption rises more sharply than in the non
obese.
Gas
Exchange
Only modest defect in gas exchange is noted in the
obese patients with a reduction in PaO2, increase in AaO2 gradient with
increase in shunt fraction. This is increased markedly with induction of
anaesthesia, PEEP improves the PaO2, but at the expense of cardiac
output and O2 delivery.
Compliance
and Resistance
Increased BMI exponentially decreases compliance. As
fat content increases, compliance decreases. This is due to increase in
pulmonary blood volume, increased total respiratory resistance and
shallow rapid breathing, which can limit maximum ventilatory capacity.
These are more markedly observed in supine position.
Work
of Breathing
30% increase is observed in work of breathing. If
hypoventilation occurs in daytime the work of breathing may approach
four times than predicted.
Cardiovascular System
Higher incidence of cardiovascular morbidity is
associated with obesity. Mild to moderate hypertension is found in
60-70% and severe in 5-10%, with 3-4mmHg increase in systolic and 2mmHg
increase in diastolic pressure for every 10kg increase of weight is
noted. It is the commonest problem followed by ischaemic heart disease.
An expansion of extracellular volume resulting in hypervolaemia and
increase in cardiac output is characteristic of obesity-induced
hypertension. Exact mechanism is not known but interplay of genetic,
hormonal, renal and haemodynamic factors are implicated.
Hyperinsulinaemia activating sympathetic nervous system, causing sodium
retention, increase in pressor norepinephrine and angiotensin II
activity. Concentric hypertrophy of left ventricle leads to cardiac
failure. Obesity is independent risk factors for Ischaemic Heart Disease
(IHD) and is more common in individuals with central obesity. Blood
volume is increased, most extra volume being distributed to fat organ.
Splanchnic blood flow is increased by 20%, renal and cerebral blood
flows are normal. Cardiac arrhythmias can be precipitated in obese by
any number of factors, viz. hypoxia, hypercapnia, electrolyte imbalance,
diuretic therapy, fatty infiltration of conducting tissue.
Cardiac
Function
Obese are at risk of specific form of obesity induced
cardiac dysfunction. Left ventricular systolic and diastolic functions
are affected. Obesity induced cardiomyopathy is well-documented.
Blood volume is increased and cardiac output increase by 20-30ml/kg of
excess body fat. They tolerate exercise poorly. Any increase in cardiac
output is by increase in heart rate.
Obesity
and Diabetes
Obesity is an independent risk factor for Type
II Diabetes. More than 10% of incidences of abnormal glucose tolerance
are seen in patients undergoing bariatric surgery.
Thromboembolic Disease
Deep vein thrombosis appears twice as common in obese
patients. It is the commonest complication of bariatric surgery with an
incidence of 2.4% - 4.5% and is due to prolonged immobilization, leading
to venous stasis, polycythemia, and increased abdominal pressure with
increased pressure on deep vein. Decreased fibrinolytic activity with
increased fibrinogen concentration could also be responsible.
Obesity and GI Disorders
Obesity is associated with increase in intra
abdominal pressure, high volume and low pH of gastric contents, delayed
gastric emptying, and increased incidence of gastro esophageal reflux.
There is a high risk for aspiration of gastric content followed by
pneumonia. Gastric volume is 75% higher than the normal individuals.
Drugs,
Pharmcodynamics and Kinetics
Obesity leads to alteration in distribution, binding
and elimination of many drugs. For drugs with narrow therapeutic indices
like aminoglycosides and digoxin, toxic reactions can occur if patients
are dosed according to actual body weight. Drug dose should be reduced
keeping the ideal body weight in view; absorption of drugs given orally
remains unchanged in obese patient.
Volume
of Distribution (VD)
Apparent volume distribution of a drug in obese
patient, depends on number of factors, which include the size of fat
organ, increase in lean body mass, increase in blood volume, and cardiac
output, reduced total body water, alterations in plasma protein binding
and lipophilicity of drug. High lipophilic drugs have increased volume
distribution (Thiopentone). Increase in the volume distribution will
reduce the elimination half-life unless the clearance is increased.
Thiopentone, Benzodiazepines, and potent inhalation agents, may persist
for longer time after discontinuation. Regarding protein binding,
alteration may occur due to high levels of cholesterol, which inhibits
protein binding, therefore more free drug is available. In contrast
increased concentrations of a acid glycoprotein may increase the degree
of protein binding of other drugs (e.g. local anaesthetics) so reducing
the free plasma fraction.
Elimination
Clearance is mostly reduced in obese patients.
Cardiac failure and decrease in liver blood flow may slow elimination of
midazolam and lignocaine. Renal clearance increased is obesity because
of the increased renal blood flow and GFR. If renal impairment is
present elimination takes longer time. Hepatic metabolism is altered in
obese patients for volatile agents. Reductive metabolism of halothane is
more in obese patients. This may be important factor in liver injury.
Nephrotoxicity can occur due to high fluoride concentrations with
halothane and enflurane. Sevoflurane has 5% biotransformation but does
not show adverse effects. Isoflurane does not increase fluoride
concentration, and remains the agent of choice in obese.
ANAESTHETIC
IMPLICATIONS
Preoperative: It is important to have a thorough
clinical examination with excellent and relevant history looking for
hypertension with appropriate sized cuff, signs of cardiac failure, viz.
increase in jugular pulse, added heart sounds, pulmonary crackles,
hepato jugular reflex and peripheral edema. These signs may be difficult
to elicit in the morbidly obese. A thorough assessment of respiratory
system for OSA is very essential.
Investigations
Besides routine investigations, ECG is mandatory,
tachy arrythmias are common. Echo may be difficult but will provide
valuable information regarding eccentric left ventricular hypertrophy.
TEE may provide more insight. Cardiological evaluation is beneficial for
further investigation. Optimization of blood pressure, treatment of
cardiac failure, or if necessary, coronary angioplasty may be suggested.
X-ray chest, lung functions, baseline arterial blood gases may be useful
in morbidly obese. A thorough history regarding respiratory function,
sleep apnoea are a must. Signs of right ventricular failure must be
looked for. 0:P>
Airway
assessment
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To plan the type of airway management is mandatory. A
through examination can prevent the catastrophes, as it will enable to
select the best technique for the patient. Preoperative evaluation of
airway must include
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Assessment of head and neck, flexion and
extension and lateral rotation.
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Assessment of jaw mobility and mouth opening.
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Inspection of oropharynx.
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Check the patency of nostrils
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Inspection of previous anesthetic charts. If
potential airway obstruction is suspected direct or indirect
laryngoscopy, CT scan of soft tissues would be helpful.
Assessment
of veins
Assessment of veins for placing infusion must be done
in the pre operative visit. Examination of feet and back for any ulcers
or sore is mandatory. Examination of calf muscles for any redness or
tenderness gives a fairly good idea regarding deep vein thrombosis.
Preoperative
medication
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Avoid narcotics and sedatives. Avoid intramuscular
and subcutaneous injections. If fibre optic intubation is planned,
include an antisailagogue like glycopyrrolate. All morbidly obese must
have acid prophylaxis. A combination of H2 blocker, e.g. ranitidine
150mg and prokinetic e.g. metaclopromide 10mg given orally 12 hrs
and 2hrs before surgery will reduce risk of aspiration. Some
anaesthetists prefer to give 30ml 0.3 M citrate before induction.
Continue the normal medications on day of surgery. Stop ACE inhibitors
the day before surgery. Dextrose-Insulin regimen should be followed in
all diabetics, unless it is a very short surgical procedure. Insulin
requirements may increase in postoperative period. Prophylactic
antibiotics are given as per the hospital protocols, should have
discussion with surgeon and microbiologist.
Position
and transfer
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Extra care is required in transferring the obese
patient and special tables having adequate padding of pressure areas are
used. Appropriate manpower to shift is mandatory. Compression of
inferior vena cava is avoided by lateral tilt or a wedge. Transfer of
obese patients is done in their own bed.
Intravenous
lines
Peripheral lines may be difficult. Establish central
line in the beginning to avoid calamities. Even these are difficult in
morbidly obese. Doppler or ultrasound guided placements could reduce
complications.
Monitoring
Intraarterial blood pressure measurement is advocated
for all but most minor procedures, ECG, Pulse oximetry, Capnography,
neuromuscular monitors are essential. Central catheters are essential
and PA Catheter where indicated.
Regional
anaesthesia
Where ever it is possible and feasible, regional
anaesthesia should be administered. The advantages are that one can
reduce the use of opioids, inhalational agents, reduce postoperative
complications, and prevent loss of airway and prevention of aspiration.
Excellent postoperative analgesia can be given by placing a epidural
catheters in sitting position, using ultrasound for identification of
the space is helpful. Local anaesthetic requirements are reduced in
morbidly obese. Higher blocks are common. Blocks extending above T5 can
cause cardiorespiratory collapse. All resuscitation equipment should be
handy.
Systemic
opioids
These are hazardous in obese patients, and intra
muscular route is not recommended. If intravenous route is preferred,
patient controlled analgesia should be the best option. Oral analgesics
like paracetamol and cox2 inhibitors may be appropriate. Postoperative
analgesia with local anaesthetics and opioids via the epidural catheter
will provide ideal pain relief with minimal complications.
Obstetrics
and morbidly obese
All attending complications are compounded. Regional
anaesthesia is a better choice; avoid general anaesthesia as far as
possible. Sitting an epidural catheter during labor is a better option.
Local anesthetic requirement may be reduced by up to 25% in obese
pregnant state.
The
ideal anesthetic agents, which can be used in an obese individual, can
be summarized as propofol for induction, atracurium for relaxation,
remifentanyl for opioids and iso or sevoflurane as inhalation agents.
All ideal drugs may not be available or may not be cost effective.
Therefore the anaesthesiologists should, with their understanding of
pathophysiology, use the drugs and techniques to the best of their
ability to cause least morbidity.
Obesity
and Trauma
The out come in obese patients with trauma is poor.
The obese patients have more blunt trauma, chest trauma is more when
compared to head injury. Investigations are more difficult to handle and
interpret. They may require earlier respiratory support and higher
oxygen concentration.
Obese
patient in ICU
It is generally believed that the outcome of obese
patients is poor. Postoperative pulmonary events are more in obese
patients. Morbidly obese may present in emergency room and intensive
care staff with formidable challenges. Better understanding of the
pathophysiology and complications may improve the outcome.
Anaesthesiologist has a major role to play as the perioperative
physician at every level.
BARIATRIC
SURGERY
(weight reductive surgery)
The
indications for bariatric are as follows
BMI
>40kg/m2
BMI
>35kg/m2 with co morbidities
Should
show that dietary attempts have been ineffective
It
addresses both perioperative care and long-term management. The patients
must have a clear understanding of risk, benefit, and complications, and
may require life long management strategies. Bariatric surgery comprises
two types namely Restrictive and Malabsorptive. The common operations
include Rouxen Y grade bypass, vertical banded gastroplasty,
pancreaticobiliary diversion and its variations, various gastric banding
procedures, gastric bypass procedures and laproscopic procedures of the
above-mentioned operations. The preoperative evaluation consists of
obesity evaluation, behavioural evaluation, medical evaluation, surgical
evaluation, which includes education & potential risk, and
anaesthetic evaluation.
Complications
The complications
associated with bariatric surgery are : nutritional deficiencies,
cardiovascular disease and sudden death, pulmonary embolism, which is
the leading cause of death, bleeding and spleenic injury,
gastrointestinal leaks - leading to sepsis, wound infections 1-3%, wound
dehiscence, vomiting and diarrhea and stomal dilatation. The morbidity
and mortality has come down for these procedures ranging from 10% and
less than 19%.
As
we enter the new millennium severe obesity remains an incurable disease.
The consequences and cost to society are significant. Though etiology is
becoming more clear, non-surgical treatments are still inadequate for
achieving sustained and significant weight loss. Surgical procedures
have evolved into safe and effective options. Newer technologies such as
laparoscopy should add further advances to the field. For appropriately
selected patients, surgery can achieve weight loss necessary to prevent
the development of significant medical conditions and improve the
quality of life. Unfortunately dietary indiscrimination and
malabsorptive eating behaviour can result in weight loss failure despite
an excellent surgical result. Therefore preoperative evaluation and
education is a corner stone for long-term success.
CONCLUSIONS
Morbidly
obese patients are encountered commonly. With changing lifestyles, high
incidence of diabetes and coronary disease in the younger individuals,
one may encounter them in the practice of anaesthesia for different
types of surgical procedures, bariatric surgeries, investigations,
trauma and in ICU setup. They do pose tremendous challenges.
Understanding the pathophysiology, anticipating the problem and
preventing calamities by a systematic approach will certainly bring down
the complications rate.
References:
1. J.P.Adams and P.G.Murphy. Obesity in anaesthesia
and intensive care. BJA 2000; 85 (1):91-108.
2. Anthony P.Adams, Jereney N Cashnar. Recent
Advances in Anaesthesia and Analgesia. Churchill Livingston 2000;
Chapter II, Vol 21.
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