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ANAESTHESIA FOR PATIENTS WITH COPD
Dr
Aftab Hussain
COPD: PATHOPHYSIOLOGY, DIAGNOSIS, TREATMENT
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
Definition:
Disease state characterised by airflow limitation that is not fully reversible
The airflow limitation is usually progressive and is associated with an abnormal inflammatory response of the lungs to noxious particles or gases, primarily caused by cigarette smoking.
airflow limitation
not fully reversible
progressive
inflammatory response
COPD:
Includes:
•Chronic Bronchitis
•Emphysema
•Peripheral Airways
diseaseDoesn’t include
•Asthma, Asthmatic Bronchitis
•Cystic Fibrosis•Bronchiactesis
•Pulmonary fibrosis due to other
causes
COPD
Chronic Bronchitis: (Clinical Definition) Chronic productive cough for 3 months in each of 2
successive years in a patient in whom other causes of productive chronic cough have been excluded.
Emphysema: (Pathological Definition) The presence of permanent enlargement of the airspaces
distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis
COMPARATIVE FEATURES OF COPDFeature Chronic
BronchitisEmphysema
Mech of Airway Obstruction
Decreased Lumen d/t mucus & inflammation
Loss of elastic recoil
Dyspnoea Moderate Severe
FEV1 Decreased Decreased
PaO2 Marked Decrease (Blue Bloater)
Modest Decrease (Pink Puffer)
PaCO2 Increased Normal or Decreased
Diffusing capacity Normal Decreased
Hematocrit Increased Normal
Cor Pulmonale Marked Mild
Prognosis Poor Good
COPD: RISK FACTORSHost factos:•Genetic factors: Eg. α1 Antitrypsin Deficiency•Sex : Prevalence more in males.
?Females more susceptible•Airway hyperactivity, Immunoglobulin E and asthma
Exposures:•Smoking: Most Important Risk Factor•Socioeconomic status•Occupation•Environmental pollution•Perinatal events and childhood illness•Recurrent bronchopulmonary infections•Diet
PATHOPHYSIOLOGY:
Pathological changes are seen in 4 major compartments of lungs:
central airways Peripheral airways lung parenchyma pulmonary vasculature.
PATHOPHYSIOLOGY CONTD.:Central Airways: (cartilaginous airways >2mm of internal diameter)•Bronchial glands hypertrophy•Goblet cell metaplasia
•Airway Wall Changes:
•Inflammatory Cells
Squamous metaplasia of the airway epitheliumIncreased smooth muscle and connective tissue
Peripheral airways (noncartilaginous airways<2mm internal diameter)•Bronchiolitis•Pathological extension of goblet cells and squamous metaplasia•Inflammatory cells•Fibrosis and increased deposition of collagen in the airway walls
Excessive Mucus production
Loss of cilia and ciliary dysfunction
Airflow limitation
and hyperinflatio
n
PATHOPHYSIOLOGY CONTD.:Lung parenchyma (respiratory bronchioles, alveoli and capillaries)
•Emphysema (abnormal englagement of air spaces distal to terminal bronchioles) occurs in the parenchyma:
2 Types: Centrilobular and Panlobular• Early microscopic lesion progress to Bullae over time.• Results in significant loss of alveolar attachments, which contributes
to peripheral airway collapse•Inflammatory cells
Pulmonary Vasculature:•Thickening of the vessel wall and endothelial dysfunction•Increased vascular smooth muscle & inflammatory infiltration of the vessel wall•Collagen deposition and emphysematous destruction of the capillary bed
Airflow limitation and hyperinflation
•Pulmonary HTN•RV dysfunction (cor Pulmonale)
Increased Neutrophils, Lymphocytes &
Macrophages
PATHOGENESIS:Tobacco smoke &
other noxious gases
Inflammatory response in
airways
Tissue DestructionImpaired defense against tissue destructionImpaired repair mechanisms
Proteinase & Antiproteinase
imbalance
Oxidative Stress
Alpha 1 antitrypsin
def.
INFLAMMATORY CASCADE IN COPD AND ASTHMA
PHYSIOLOGICAL EFFECTS: Mucous hypersecretion and cilliary dysfunction
Goblet cell hyperplasia & squamous metaplasia Airflow limitation and hyperinflation
Airway remodelling Loss of elastic recoil Destruction of alveolar supports Accumulation of mucus, inflammatory cells & exudate
Gas exchange abnormalities: (Hypoxemia +/- Hypercapnia) Abnormal V/Q ratios Abnormal DLCO
Pulmonary hypertension Hypoxic Vasoconstriction,Endothelial dysfunction Remodelling of arteries & capillary destruction
Systemic effects
DIAGNOSIS
Clinical Features:Symptoms:Cough: Initially intermittent
Present throughout the daySputum:Tenacious & mucoid
Purulent InfectionDyspnoea: Progressively worsens, Persistant
Exposure: Smoking, in pack years
Physical Examination:Respiratory Signs
• Barrel Chest• Pursed lip breathing• Adventitious
Ronchi/WheezeSystemic Signs
• Cyanosis• Neck vein enlargement• Peripheral edema• Liver enlargement• Loss of muscle mass
Investigations:Spirometry
• Diagnosis• Assessment of severity• Following progress
Chest Radiograph: To exclude other diseases
• Emphysematous changesBronchodilator Reversibility
• Exclude Bronchial Asthma• <20%
Alpha-1 Antitrypsin levels• Young COPD with Family History
Diagnosis contd.:
GOLD CLASSIFICATION
Stage Characteristics
I: Mild FEV1/FVC < 70%FEV1 ≤ 80% predicted, with/without chronic symptoms
II: Moderate FEV1/FVC < 70%50% ≤ FEV1 ≤ 80% predicted, with/without chronic symptoms
III: Severe FEV1/FVC < 70%30% ≤ FEV1 ≤ 50% predicted, with/without chronic symptoms
IV: Very severe
FEV1/FVC < 70%FEV1 < 30% predicted or < 50% predicted plus chronic respiratory failure (PaO2 < 60mm Hg &/or PaCO2 > 50mm Hg)
TREATMENT
Modifying natural history of Disease: Smoking cessation Long term oxygen therapy
Symptomatic: Bronchodilators Antibiotics Others
Pulmonary Rehabilitation Nutrition
MANAGEMENT OF COPD STAGE I: MILD COPD
Characteristics Recom. Treatment
• FEV1/FVC < 70 %
• FEV1 > 80 % predicted• With or without chronic symptoms
• Short-acting bronchodilator as
needed
MANAGEMENT OF COPD CONTD.
STAGE II: MODERATE COPD
Characteristics Recom. Treatment
• FEV1/FVC < 70%
• 50% < FEV1< 80% predicted• With or without chronic
symptoms
• Short-acting broncho-dilator as needed• Regular treatment with one or more long-acting bronchodilators• Rehabilitation
MANAGEMENT OF COPD CONTD. STAGE III: SEVERE COPD
Characteristics Recom. Treatment
• FEV1/FVC < 70%
• 30% < FEV1 < 50% predicted• With or without chronic
symptoms
• Short-acting bronchodilator as needed• Regular treatment
with one or more long-acting
bronchodilators• Inhaled glucocortico
steroids if repeated exacerbations
• Rehabilitation
MANAGEMENT OF COPD CONTD.
STAGE IV: VERY SEVERE COPD
Characteristics Recom. Treatment
• FEV1/FVC < 70%
• FEV1 < 30% predicted or FEV1 < 50% predicted plus chronic respiratory failure
• Short-acting bronchodilator as needed • Regular treatment with one or more long-acting bronchodilators• Inhaled glucocorticosteroids if repeated exacerbations• Treat complications• Rehabilitation• Long-term oxygen therapy if respiratory failure• Consider surgical options
TREATMENT: OXYGEN THERAPY
Long Term Oxygen Therapy(LTOT):
Improves survival, exercise, sleep and cognitive performance.
Oxygen delivery methods include nasal continuous flow, reservoir cannulas and transtracheal catheter.
Physiological indications for oxygen include an arterial oxygen tension (PaO2) <7.3 kPa (55 mmHg). The therapeutic goal is to maintain SpO2 >90% during rest, sleep and exertion.
PHYSIOLOGICAL INDICATIONS FOR LONG-TERM OXYGEN THERAPY (LTOT)
PaO2 mmHg SaO2 % LTOT indication Qualifying condition
≤55 ≤88 Absolute None
55–59 89 Relative with qualifier “P” Pulmonale, polycythemia >55%
History of edema
≥60 ≥90 None except with qualifier Exercise desaturation
Sleep desaturation not corrected by CPAP
Lung disease with severe dyspnea
responding to O2
SURGICAL TREATMENT
Bullectomy short-term improvements in
airflow obstruction lung volumes hypoxaemia and hypercapnia exercise capacity dyspnoea
Lung Volume Reduction Surgery potentially long-term improvement in survival short-term improvements in
Spirometry lung volumes exercise tolerance dyspnoea
Lung Transplantation
COPD: EXACERBATIONS
Definition: An exacerbation of COPD is an event in
the natural course of the disease characterised by a change in the patient’s baseline dyspnoea, cough and/or sputum beyond day-to-day variability sufficient to warrant a change in management.
Precipitating Causes: Infections: Bacterial, Viral Air pollution exposure Non compliance with LTOT
COPD: EXACERBATIONS CONTD.:
Indication for Hospitalisation: The presence of high-risk comorbid conditions
pneumonia, cardiac arrhythmia, congestive heart failure, diabetes mellitus, renal or liver failure
Inadequate response to outpatient management
Marked increase in dyspnoea, orthopnoea Worsening hypoxaemia & hypercapnia Changes in mental status Uncertain diagnosis.
COPD: EXACERBATIONS CONTD.:
Indication for ICU admission: Impending or actual respiratory failure Presence of other end-organ
dysfunction shock renal failure liver failure neurological disturbance
Haemodynamic instability
TREATMENT Supplemental Oxygen (if SPO2 < 90%)
Bronchodilators: Nebulised Beta Agonists, Ipratropium with spacer/MDI
Corticosteroids Inhaled, Oral
Antibiotics: If change in sputum characteristics Based on local antibiotic resistance Amoxycillin/Clavulamate, Respiratory Flouroquinolones
Ventilatory support: NIV, Invasive ventilation
………. PREPARATION FOR ANAESTHESIA
ANAESTHETIC CONSIDERATIONS IN PATIENTS WITH COPD UNDERGOING SURGERY:Patient Factors: Advanced age Poor general condition, nutritional status Co morbid conditions
HTN Diabetes Heart Disease Obesity Sleep Apnea
Blunted Ventilatory responses to hypoxia and CO2 retention
AGE RELATED PULMONARY CHANGES:Pathological changes
Effect Implications
Decreased efficiency of lung parenchyma
Decreased VCIncreased RV
Respiratory Failure
Decreased Muscle strength
Decreased Compliance, FEV1
Poor coughInfection
Alveolar septal destruction
Decreased alveolar area
Decreased gas exchange
Brohchiolar damage Increased closing volume
Air trappingDecreased PaO2
Dilated upper airways
Increased VD Decreased gas exchange
Decreased reactivity Decreased laryngeal reflexesDecreased vent response to hypoxia, hypercarbia
Increased AspirationIncreased resp. failure
ANAESTHETIC CONSIDERATIONS IN PATIENTS WITH COPD UNDERGOING SURGERY CONTD.:
Problems due to Disease Exacerbation of Bronchial inflammation
d/t Airway instrumentation preoperative airway infection surgery induced immunosuppression increased WOB Increased post operative pulmonary
complications
ANAESTHETIC CONSIDERATIONS IN PATIENTS WITH COPD UNDERGOING SURGERY CONTD.: Problems due to Anaesthesia:
GA decreases lung volumes, promotes V/Q mismatch FRC reduced during anaesthesia, CC parallels FRC Anaesthetic drugs blunt Ventilatory responses to hypoxia &
CO2 Postoperative Atelectasis & hypoxemia Postoperative pain limits coughing & lung expansion
Problems due to Surgery: Site : most important predictor of Post op complications Duration: > 3 hours Position
PRE-OPERATIVE ASSESSMENT:History:
Smoking Cough: Type, Progression, Recent RTI Sputum: Quantity, color, blood Dyspnea Exercise intolerance Occupation, Allergies Symptoms of cardiac or respiratory failure
PRE-OPERATIVE ASSESSMENT CONTD.: EXAMINATION
Physical Examination: Better at assessing chance of post op complications
Airway obstruction hyperinflation of chest, Barrel chest Decreased breath sounds Expiratory ronchi Prolonged expiration: Watch & Stethoscope test, >4 sec
↑WOB ↑ RR, ↑HR Accessory muscles used Tracheal tug Intercostal indrawing Tripod sitting posture
Body Habitus
Obesity/ Malnourished
Active infection Sputum- change in quantity,
nature Fever Crepitations
Respiratory failureHypercapniaHypoxiaCyanosis
Cor Pulmonale and Right heart failure
Dependant edema
tender enlarged liver
Pulmonary hypertensionLoud P2
Right Parasternal heaveTricuspid regurgitation
Pre-operative assessment: Examination contd.:
PREOPERATIVE ASSESSMENT CONTD. : INVESTIGATIONS
Complete Blood count Serum Electrolytes Blood Sugar Urinalysis ECG Arterial Blood Gases Diagnostic Radiology
Chest X Ray Spiral CT
Preoperative Pulmonary Function Tests Tool for optimisation of pre-op lung function Not to assess risk of post op pulmonary complications
INVESTIGATIONS: CHEST X-RAY Overinflation Depression or flattening of
diaphragm Increase in length of lung ↑ size of retrosternal
airspace ↑ lung markings- dirty lung Bullae +/- Vertical Cardiac silhouette ↑ transverse diameter of
chest, ribs horizontal, square chest
Enlarged pulmonary artery with rapid tapering in MZ
PULMONARY FUNCTION TESTS:
Measure Normal Obstructive Restrictive
FVC (L)
80% of TLC (4800)
FEV1 (L)
80% of FVC
FEV1/FVC(%)
75- 85% N to N to
FEV25%-75%(L/sec)
4-5 L/ sec N to
PEF(L/sec) 450- 700 L/min N to
Slope of FV curve
MVV(L/min) 160-180 L/min N to
TLC 6000 ml N to
RV 1500 mL
RV/TLC(%) 0.25 N
INDICATIONS FOR PFT(AMERICAN COLLEGE OF PHYSICIANS CONSENSUS
STATEMENT)
Cardiac, thoracic or upper abdominal surgery with a history of dyspnea, smoking
Lower abdominal surgery with a history of dyspnea, smoking and anticipated prolonged surgery
All patients undergoing lung resection Morbid obesity Any pulmonary disease Age > 70 years
FEV1
FEV1
FVC
seconds21 3 4 5
0
1
2
3
4
Litr
es
5
COPD
NORMAL
60%39002350COPD
80%52004150Normal
FEV1/FVCFVCFEV1
FVC
SPIROMETRIC TRACING IN COPD PATIENTS
MAXIMUM INSPIRATORY AND EXPIRATORY FLOW-VOLUME CURVES (I.E., FLOW-VOLUME LOOPS) IN FOUR TYPES OF AIRWAY OBSTRUCTION.
PREOPERATIVE ASSESSMENT: INVESTIGATIONS CONTD.
ECG Signs of RVH:
RAD p Pulmonale in Lead II Predominant R wave in V1-3 RSR1 pattern in precordial leads
Arterial Blood Gases: In moderate-severe disease Nocturnal sample in cor Pulmonale
Increased PaCO2 is prognostic marker Strong predictor of potential intra op respiratory failure & post op
Ventilatory failure Also, increased d/t post op pain, shivering, fever,respiratory depressants
Exercise testing:-expensive, cumbersome-Not validated in nonthoracic surgery-Parameter with greatest utility is decreased maximum O2 consumption
α1 Antitrypsin levels:-Non smokers-Premature or basilar emphysema-COPD with bronchiectasis-family history of α1AT deficiency
PRE-OPERATIVE PREPARATION Cessation of smoking Dilation of airways Loosening & Removal of secretions Eradication of infection Recognition of Cor Pulmonale and treatment Improve strength of skeletal muscles – nutrition,
exercise Correct electrolyte imbalance Familiarization with respiratory therapy, education,
motivation & facilitation of patient care
EFFECTS OF SMOKING: Cardiac Effects:
Risk factor for development of cardiovascular disease CO decreases Oxygen delivery & increases myocardial work Catecholamine release, coronary vasoconstriction Decreased exercise capacity
Respiratory Effects: Major risk factor for COPD Decreased Mucociliary activity Hyperreactive airways Decreased Pulmonary immune function
Other Systems Impairs wound healing
Smoking cessation and time course of beneficial Effects
Time after smoking Physiological Effects
12-24 Hrs Fall in CO & Nicotine levels
48-72 Hrs COHb levels normaliseAirway function improves
1-2 Weeks Decreased sputum production
4-6 Weeks PFTs improve
6-8 Weeks Normalisation of Immune function
8-12 Weeks Decreased overall post operative morbidity
NATURAL HISTORY:
Fig. 1. - The normal course of forced expiratory volume in one second (FEV1) over time (–––)is compared with the result of impaired growth of lung function (––– ) an accelerated decline(–––) and a shortened plateau phase (–––). All three abnormalities can be combined.. Decline of FEV1 by age and smoking . Thorax 1997; 52: 820–827.)
EFFECT OF SMOKING AND SMOKING CESSATION ON LUNG FUNCTION:
Loss of lung function over 11 yrs in the Lung Health Study for continuous smokers(–––), intermittent quitters (–––) and sustained quitters (–––). FEV1: forced expiratory volume in one second.Smoking and lung function of Lung Health Study participants after 11 years. Am J Respir CritCare Med 2002; 166: 675–679.
TREATMENT: SMOKING CESSATION Need:
Most important cause of COPD
Major risk factor for atherosclerotic vascular disease, cancer, peptic ulcer and osteoporosis.
Quitting smoking slows progressive loss of lung function & reduces symptoms
Motivation, Counseling & behavioural support
Nicotine replacementPatches chewing gumInhalernasal spraylozenges
Bupriopion
DILATATION OF AIRWAYS: Bronchodilators:
Only small increase in FEV1 Alleviate symptoms by decreasing hyperinflation &
dyspnoea Improve exercise tolerance
Anticholinergics Beta Agonists Methylxanthines
ANTICHOLINERGICS: Block muscarinic receptors Onset of action within 30 Min Ipratropium –
40-80 μg by inhalation 20 μg/ puff – 2 puffs X 3-4 times 250 μg / ml respirator soln. 0.4- 2 ml X 4 times daily
Tiotropium - long lasting Side Effects:
Dry Mouth, metallic taste Caution in Prostatism & Glaucoma
BETA BLOCKERS: Act by increasing cAMP Specific β2 agonist –
Salbutamol : oral 2-4 mg/ 0.25 – 0.5 mg i.m /s.c ,100-200 μg inhalation muscle tremors, palpitations, throat irritation
Terbutaline : oral 5 mg/ 0.25 mg s.c./ 250 μg inhalation
Salmeterol : Long acting (12 hrs) 50 μg BD- 200 μg BD
Formeterol, Bambuterol
METHYLXATHINES: Mode of Action
– inhibition of phospodiesterase,↑ cAMP, cGMP – Bronchodilatation
Adenosine receptor antagonism↑ Ca release from SR
Oral(Theophyllin) & Intravenous (Aminophylline, Theophyllin) loading – 5-6 mg/kg Previous use – 3 mg/kg Maintenace –
1.0mg/kg h for smokers 0.5mg/kg/h for nonsmokers 0.3 mg/kg/h for severely ill patients.
INHALED CORTICOSTEROIDS: Anti-inflammatory Restore responsiveness to β2 agonist Reduce severity and frequency of
exacerbations Do not alter rate of decline of FEV1
Beclomethasone, Budesonide, Fluticasone
Dose: 200 μg BD ↑ upto 400 μg QID > 1600 μg / day- suppression of HPA
axis
………. ANAESTHETIC TECHNIQUE
ANAESTHETIC TECHNIQUECOPD is not a limitation on the choice of
anaesthesia.Type of Anaesthesia doesn’t predictably
influence Post op pulmonary complications.
CONCERNS IN RANeuraxial Techniques:•No significant effect on Resp function: Level above T6 not recommended•No interference with airway Avoids bronchospasm•No swings in intrathoracic pressure•No danger of pneumothorax from N2O•Sedation reqd. May compromise expiratory fn.
Peripheral Nerve Blocks:•Suitable for peripheral limb surgeries•Minimal respiratory effects•Supraclavicular techniques contraindicated in severe pulmonary disease
CONCERNS IN RA CONTD.:•Improved Surgical outcome:
Better pain controlAttenuation of neuroedocrine respones to
surgeryImprovement of tissue oxygenationMaintenance of immune functionFewer episodes of DVT, PE, stroke, blood
Tx•Technique of choice in perineal, pelvic extraperitoneal
& lower extremities•No benefit over GA in Intraperitoneal surgery,
or when high levels are needed
CONCERNS IN GA•Airway instrumentation & bronchospasm•Residual NMB•Nitrous Oxide•Attenuation of HPV•Respiratory depression with opioids, BZDs•Airway humidification
PREMEDICATION ↑ Sensitivity to the effect of respiratory
depressants Opioids & Benzodiazepines - ↓ response
to hypoxia, hypercarbia Bronchodilator puff / nebulisation,
inhaled steroids Atropine ?: Should be individualised
Decreases airway resistance Decreases secretion-induced airway
reactivityDecreases bronchospasm from reflex vagal
stimulationCause drying of secretions, mucus plugging
GENERAL ANAESTHESIA: INDUCTION Opioids:
Fentanyl(DoC) Morphine ,Pethidine Respiratory Depression, Histamine release,
Chest tightness
Propofol (DoC) Better suppression of laryngeal reflexes Hemodynamic compromise Agent of choice in stable patient
Ketamine Bronchodilator Catecholamine release, neural
inhibition Tachycardia and HT, may increase PVR
INTUBATION NMB :
Succinyl Choline (1-2mg/kg) Vecuronium(0.08-0.10 mg/kg) Rocuronium (0.6-1.2 mg/kg )
Attenuation of Intubation Response: IV lignocaine (1- 1.5 mg/kg) 90s prior to
laryngoscopy Fentanyl 1-5 microgram/Kg Esmolol 100-150mg bolus Adequate plane of anaesthesia prior to intubation
LMA Vs Endotracheal Tube Avoids tracheal stimulation P-LMA also allows for suctioning
MAINTENANCE
Muscle relaxant Prefer Vecuronium, Rocuronium, Cisatracurium Avoid Atracurium, Mivacurium, Doxacurium
( histamine release)
Volatile anaesthetic NO Caution in pulmonary bullae, dilution of
delivered O2
Inhalational agents attenuate HPV Sevoflurane: non pungent, bronchodilator Halothane: Non pungent, bronchodilator.
Slower onset & elimination, Sensitises to catecholamines
MAINTENANCEVentialatory Strategy: Aim: Maximise alveolar gas emptying
Minismise dynamic hyperinflation, iPEEP Settings:
Decrease minute vent Low frequency Adequate Exp time, Low I:E ratio, minimal exp
pause Reduce exp flow resistance Recruitment maneuvers Acceptance of mild hypercapnia & acidemia
Humidification of gases Pressure Cycled mode with decelerating flow.
MAINTENANCE Monitoring
ECG, NIBP Pulse Oximetry Capnography Neuromuscular Monitoring Depth of Anaesthesia
Intraoperative IV Fluids Excessive IV volume Water accumulation &
tissue edema Respiratory/heart failure Haemodynamic goal directed fluid loading Restrictive fluid administration
INTRAOPERATIVE INCREASED PIP Bronchospasm Light anaesthesia, coughing, bucking Obstruction in the circuit Blocked / kinked tube Endobronchial intubation Pneumothorax Pulmonary embolism Major Atelectasis Pulmonary edema Aspiration pneumonia Head down position, bowel packing
MANAGEMENT OF INTRAOPERATIVE BRONCHOSPASM Increase FiO2 Deepen anaesthesia
Commonest cause is surgical stimulation under light anaesthesia
Incremental dose of Ketamine or Propofol Relieve mechanical stimulation
endotracheal suction Stop surgery
β2 agonists – Nebulisation or MDI s/c Terbutaline, iv Adrenaline
intravenous Aminophyline Intravenous corticosteroid indicated if severe
bronchospasm
REVERSAL/ RECOVERY: Neostigmine - may provoke bronchospasm Atropine 1.2-1.8mg or Glycopyrrolate 0.6mg
before Neostigmine Tracheal toileting Extubation : deep or awake?
Deep extubation may reduce chance of bronchospasm
Deep
Difficult airway
Difficult intubation
Residual NMB
Full stomach
Good airway - accessible
Easy intubation
No Residual NMB
Normothermic
Not at increased risk of aspiration
NO YES
POST OPERATIVE CARE ↑ Risk of Post op pulmonary complications
Postoperative analgesia – • Parenteral NSAIDS• Neuraxial drugs • Nerve blocks • PCA
Postoperative respiratory therapy – • Chest physiotherapy & postural drainage • Voluntary Deep Breathing• Incentive Spirometry
POST OPERATIVE CARE Mechanical Ventilation:
Indications: Severe COPD undergoing major surgery FEV1/FVC<70% Preop. PaCO2 > 50mm Hg
FiO2 & Ventilator settings adjusted to maintain PaO2 60-100 mm Hg & PaCO2 in range that maintains pH at7.35-7.45
Continue Bronchodilators Oxygen therapy Lung Expansion maneuvers
POST OPERATIVE PULMONARY COMPLICATIONS: Incidence: 6.8% (Range 2-19%)
(Sementa et al, Annals of internal Medicine, 2006,144:581–95)
Include:AtelectasisBronchopneumoniaHypoxemiaRespiratory FailureBronchopleural fistulaPleural effusion
POST OPERATIVE PULMONARY COMPLICATIONS CONTD.:
Predictors of PPCs:
Patient Related:•Age > 70 yrs•ASA Class II or above•CHF•Pre-existing Pulmonary Disease•Functionally Dependent•Cigarette smoking•Hypoalbuminemia <3.5g/dLProcedure Related:•Emergency Surgery•Duration > 3 Hrs•GA•Abd, Thoracic, Head & Neck,Neuro, Vascular Surgery
POST OPERATIVE PULMONARY COMPLICATIONS CONTD.:Specific Risk Factors: COPD Bronchial Asthma GA OSA Advanced age Morbid Obesity(BMI > 40) Functional limitation Smoking > 20 Pack year Alcohol consumption (>60ml ethanol/day)
POST OPERATIVE PULMONARY COMPLICATIONS CONTD.:
Risk Reduction Strategies:Preoperative:•Smoking cessation•Bronchodilatation•Control infections•Patient Education
Intraoperative:•Minimally invasive surgery•Regional Anaesthesia•Duration < 3 Hrs
Post operative:•Lung Volume Expansion Maneuvers•Adequate Analgesia
POST OPERATIVE PULMONARY COMPLICATIONS CONTD.:
Post Operative Analgesia: Opioids Paravertebral/Intercostal N Blocks Epidural Analgesia
LA Opioids
NSAIDS Bronchospasm
POST OPERATIVE PULMONARY COMPLICATIONS CONTD.:
Lung Expansion maneuvers: Incentive spirometry Deep breathing exercises Chest Physiotherapy & postural drainage Intermittant Positive Pressure Ventilation CPAP, BiPAP Early Ambulation
SUMMARY: COPD is a progressive disease with increasing irreversible
airway obstruction. Cigarette smoking is the most important causative factor
for COPD Smoking cessation & LTOT are the only measures capable
of altering the natural history of COPD. COPD is not a contraindication for any particular
anaesthsia technique if patients have been appropriately stabilised.
COPD patients are prone to develop intraoperative and postoperative pulmonary complications.
Preoperative optimisation should include control of infection and wheezing.
Postoperative lung expansion maneuvers and adequate post op analgesia have been proven to decrease incidence of post op complications.
REFERENCES: Stoelting’s Anaesthesia & Coexisting Disease, 6th Ed. Standards for Diagnosis & Management of COPD Patients,
American Thoracic Society & European Respiratory Society Global Initiative for COPD Refresher course lectures, 57th National Conference of ISA COPD: Perioperative management, M.E.J. Anesth 2008 19(6) Periop Management of patients with COPD: Review, IJ COPD
2007:2(4) 493:515 Harrison’s Principles of Medicine, 17th Ed Principles of respiratory Care, Egan’s, 9th Ed Miller’s Anaesthsia, 7th Ed Irwin & Rippe’s Intensive care medicine, 6th Ed. Clinical Application of Mechanical Ventilation, David W
Chang, 3rd Ed COPD guidelines : American thoracic society
Thank you