Anaesthesia for COPD 15-09-14

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