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Anaesthesia for Patients with COPD

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1 Anaesthesia for Patients with COPD
Dr Sajith Damodaran University College of Medical Sciences & GTB Hospital, Delhi

2 COPD: Pathophysiology, Diagnosis, Treatment

3 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. In patients with COPD either of these conditions may be present but the relative contribution of each is different.

4 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. In patients with COPD either of these conditions may be present but the relative contribution of each is different.

5 COPD: Chronic Bronchitis Includes: Peripheral Airways disease
Emphysema Doesn’t include Asthma, Asthmatic Bronchitis Cystic Fibrosis Bronchiactesis Pulmonary fibrosis due to other causes

6 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

7 Comparative features of COPD
Chronic Bronchitis Empysema Mech of Airway Obstruction Decreased Lumen d/t mucus & inflammation Loss of elastic recoil Dysnoea Moderate Severe FEV1 Decreased PaO2 Marked Decrease (Blue Bloater) Modest Decrease (Pink Puffer) PaCO2 Increased Normal or Decreased Diffusing capacity Normal Hematocrit Cor Pulmonale Marked Mild Prognosis Poor Good

8 COPD: Risk factors Host 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

9 Natural History: It is increasingly apparent that COPD often has its roots decades before the onset of symptoms [14]. Impaired growth of lung function during childhood and adolescence, caused by recurrent infections or tobacco smoking, may lead to lower maximally attained lung function in early adulthood [16]. This abnormal growth will, often combined with a shortened plateau phase in teenage smokers, increase the risk of COPD. This is visualised in figure 1 [17]. Fig 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 (Kerstjens HAM, Rijcken B, Schouten JP, Postma DS. Decline of FEV1 by age and smoking status: facts, figures, and fallacies. Thorax 1997; 52: 820–827.)

10 Pathophysiology: Pathological changes are seen in 4 major compartments of lungs: central airways Peripheral airways lung parenchyma pulmonary vasculature.

11 Airflow limitation and hyperinflation
Pathophysiology: Excessive Mucus production Central Airways: (cartilaginous airways >2mm of internal diameter) Bronchial glands hypertrophy Goblet cell metaplasia Airway Wall Changes: Inflammatory Cells Loss of cilia and ciliary dysfunction Squamous metaplasia of the airway epithelium Increased 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 Airflow limitation and hyperinflation

12 Airflow limitation and hyperinflation
Pathophysiology: 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 Airflow limitation and hyperinflation Pulmonary HTN RV dysfunction (cor Pulmonale) 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

13 Pathogenesis: Tobacco smoke & other noxious gases
Alpha 1 antitrypsin def. Increased Neutrophils, Lymphocytes & Macrophages Proteinase & Antiproteinase imbalance Inflammatory response in airways Oxidative Stress Tissue Destruction Impaired defense against tissue destruction Impaired repair mechanisms

14 Physiological Effects:
Mucous hypersecretion and cilliary dysfunction Goblet cell hyperplasia & squamous metaplasia Airflow limitation and hyperinflation Airway remodelling Loss of eleastic 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 Vasoconstrictoin,Endothelial dysfunction Remodelling of arteries & capillary destruction Systemic effects

15 Diagnosis Clinical Features: Symptoms: Physical Examination:
Cough: Initially intermittent Present throughout the day Sputum: Tenacious & mucoid Purulent Infection Dyspnoea: Progressively worsens Persistant Physical Examination: Respiratory Signs Barrel Chest Pursed lip breathing Adventitious Ronchi/Wheeze Systemic Signs Cyanosis Neck vein enlargement Peripheral edema Liver enlargement Loss of muscle mass Exposure: Smoking, in pack years

16 Diagnosis Investigations: Spirometry
Assessment of severity Following progress Chest Radiograph: To exclude other diseases Emphysematous changes Bronchodilator Reversibility Exclude Bronchial Asthma <20% Alpha-1 Antitrypsin levels Young COPD with Family History

17 GOLD Classification Stage Characteristics I: Mild FEV1/FVC < 70%
FEV1 ≤ 80% predicted, with/without chronic symptoms II: Moderate 50% ≤ FEV1 ≤ 80% predicted, with/without chronic symptoms III: Severe 30% ≤ FEV1 ≤ 50% predicted, with/without chronic symptoms IV: Very severe FEV1 < 30% predicted or < 50% predicted plus chronic respiratory failure (PaO2 < 60mm Hg &/or PaCO2 > 50mm Hg)

18 Treatment Modifying natural history of Disease: Symptomatic:
Smoking cessation Long term oxygen therapy Symptomatic: Bronchodilators Antibiotics Others Pulmonary Rehabilitation Nutrition

19 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, Counselling & behavioural support Nicotine replacement Patches chewing gum Inhaler nasal spray lozenges Bupriopion It approximately doubles quit rates compared to placebo. • Treatment is usually initiated at 150 mg daily and increased to 150 mg twice daily after 3 days, if tolerated. • The quit day should be after 1 week of treatment. • Treatment is generally continued for 7–12 weeks. • Bupropion may be more effective than nicotine replacement therapy for individuals with a past history of depression. Contraindications include increased seizure risk, bulimia, concurrent use of monoamine oxidase inhibitors or a bupropion preparation for depression.

20 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 (Anthonisen NR et al,Lung Health Study Research Group. Smoking and lung function of Lung Health Study participants after 11 years. Am J Respir Crit Care Med 2002; 166: 675–679.

21 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.

22 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

23 Treatment: Symptomatic Measures
Bronchodilators: Anticholinergics Beta Agonists Methylxanthines Corticosteroids N-Acetyl Cysteine α1 Antitrypsin augmentation Vaccination Others: No proven effect Leukotriene receptor antagonists/cromones Maintenance antibiotic therapy Immunoregulators Vasodilators: NO, CCB

24 Surgical Treatment Bullectomy Lung Volume Reduction Surgery
short-term improvements in airflow obstruction lung volumes hypoxaemia and hypercapnia exercise capacity dyspnoea Lung Volume Reduction Surgery potentially long-term improvement in survival Spirometry exercise tolerance Lung Transplantation

25 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 Infectious process [7, 8]: viral (Rhinovirus spp., influenza); bacteria (Haemophilus influenzae, Streptococcus pneumoniae, Moraxella catarrhalis, Enterobacteriaceae spp., Pseudomonas spp.).

26 COPD: Exacerbations 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.

27 COPD: Exacerbations Indication for ICU admission:
Impending or actual respiratory failure Presence of other end-organ dysfunction shock renal failure liver failure neurological disturbance Haemodynamic instability

28 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 Ventillatory support: NIV, Invasive ventillation

29 In a nutshell Optimal disease management entails redesigning standard medical care to integrate rehabilitative elements into a system of patient self-management and regular exercise

30 ………. Preparation for Anaesthesia

31 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 Weak HPV, blunted Ventilatory responses to hypoxia and CO2 retention

32 Age Related Pulmonary Changes:
Pathological changes Effect Implications Decreased efficiency of lung parenchyma Decreased VC Increased RV Respiratory Failure Decreased Muscle strength Decreased Compliance, FEV1 Poor cough Infection Alveolar septal destruction Decreased alveolar area Decreased gas exchange Brohchiolar damage Increased closing volume Air trapping Decreased PaO2 Dilated upper airways Increased VD Decreased reactivity Decreased laryngeal reflexes Decreased vent response to hypoxia, hypercarbia Increased Aspiration Increased resp. failure

33 Anaesthetic Considerations in patients with COPD undergoing surgery:
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

34 Anaesthetic Considerations in patients with COPD undergoing surgery:
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

35 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

36 Pre-operative assessment: 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

37 Pre-operative assessment: Examination
Respiratory failure Hypercapnia Hypoxia Cyanosis Cor Pulmonale and Right heart failure Dependant edema tender enlarged liver Pulmonary hypertension Loud P2 Right Parasternal heave Tricuspid regurgitation Body Habitus Obesity/ Malnourished Active infection Sputum- change in quantity, nature Fever Crepitations

38 Preoperative Assessment: 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

39 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

40 Pulmonary Function Tests:
Measurement 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 PEF(L/sec) L/min Slope of FV curve MVV(L/min) L/min TLC 6000 ml RV 1500 mL RV/TLC(%) 0.25 N

41 Spirometric tracing in COPD patients
FEV1 FVC seconds 2 1 3 4 5 Litres COPD NORMAL 60% 3900 2350 80% 5200 4150 Normal FEV1/FVC

42 Maximum inspiratory and expiratory flow-volume curves (i. e
Maximum inspiratory and expiratory flow-volume curves (i.e., flow-volume loops) in four types of airway obstruction.

43 Preoperative Assessment: Investigations
ECG Signs of RVH: RAD p Pulmonale in Lead II Predominant R wave in V1-3 RS 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

44 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

45 Effects of smoking: Cardiac Effects: Respiratory 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

46 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 normalise Airway 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

47 Dilatation of Airways:
Bronchodilators: Only small increase in FEV1 Alleviate symptoms by decreasing hyperinflation & dyspnoea Improve exercise tolerance Anticholinergics Beta Agonists Methylxanthines

48 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 ml X 4 times daily Tiotropium - long lasting Side Effects: Dry Mouth, metallic taste Caution in Prostatism & Glaucoma Better in COPD then asthma S/E – Dryness of mouth, Scratching of trachea, Cough, nervousness

49 Beta Blockers: Act by increasing cAMP Specific β2 agonist –
Salbutamol : oral 2-4 mg/ – 0.5 mg i.m /s.c 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

50 Bronchodilators: 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.

51 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 Not bronchodilators. ↓ bronchial reactivity and edema ↓ inflammatory response

52 ………. AnaestheTIC Technique

53 Anaesthetic Technique
COPD is not a limitation on the choice of anaesthesia. Type of Anaesthesia doesn’t predictably influence Post op pulmonary complications.

54 Concerns in RA Neuraxial 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

55 Concerns in RA Improved Surgical outcome: Better pain control
Attenuation of neuroedocrine respones to surgery Improvement of tissue oxygenation Maintenance of immune function Fewer 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

56 Concerns in GA Airway instrumentation & bronchospasm Residual NMB
Nitrous Oxide Attenuation of HPV Respiratory depression with opioids, BZDs Airway humidification

57 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 reactivity Decreases bronchospasm from reflex vagal stimulation Cause drying of secretions, mucus plugging

58 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

59 Intubation NMB : Attenuation of Intubation Response:
Succinyl Choline (1-2mg/kg) Vecuronium( mg/kg) Rocuronium ( mg/kg ) Attenuation of Intubation Response: IV lignocaine ( mg/kg) 90s prior to laryngoscopy Fentanyl 1-5 microgram/Kg Esmolol mg bolus Adequate plane of anaesthesia prior to intubation LMA Vs Endotracheal Tube Avoids tracheal stimulation P-LMA also allows for suctioning

60 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

61 Maintenance Ventialatory 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. Reduce exp low res by bronchodilators, coriticosteroids, low res tubings, heliox The pressure ventilatory mode (PV) with a decelerating flow has the potential advantage of decreasing the peak airway pressure and providing more homogenous distribution of inspiratory airflow at a lower or similar mean distending pressure

62 Maintenance Monitoring Intraoperative IV Fluids 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

63 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

64 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

65 Reversal/ Recovery: Neostigmine - may provoke bronchospasm
Atropine mg or Glycopyrrolate 0.6mg before Neostigmine Tracheal toileting Extubation : deep or awake? Deep extubation may reduce chance of bronchospasm Deep NO YES Good airway - accessible Easy intubation No Residual NMB Normothermic Not at increased risk of aspiration Difficult airway Difficult intubation Residual NMB Full stomach

66 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

67 Post operative care Mechanical Ventilation: Continue Bronchodilators
Indications: Severe COPD undergoing major surgery FEV1/FVC<70% Preop PaCO2 > 50mm Hg FiO2 & Ventillator settings adjusted to maintain PaO mm Hg & PaCO2 in range that maintains pH at Continue Bronchodilators Oxygen therapy Lung Expansion maneuvers

68 Post Operative Pulmonary Complications:
Incidence: 6.8% (Range 2-19%) (Sementa et al, Annals of internal Medicine, 2006,144:581–95) Include: Atelectasis Bronchopneumonia Hypoxemia Respiratory Failure Bronchopleural fistula Pleural effusion Grade I complication entails any deviation from the normal postoperative course with no need for medical interventions, except antiemetics, antipyretics, analgesics, electrolytes, diuretics. Grades II and III involve complications requiring pharmacological treatment, blood transfusions or endoscopic, surgical or radiological interventions. Grade IV includes lifethreatening complications as well as single or multiple organ failure requiring ICU admission. Ultimately, perioperative death corresponds to a grade V.

69 Post Operative Pulmonary Complications:
Patient Related: Age > 70 yrs ASA Class II or above CHF Pre-existing Pulmonary Disease Functionally Dependent Cigarette smoking Hypoalbuimnemia , 3.5g/dL Predictors of PPCs: Procedure Related: Emergency Surgery Duration > 3 Hrs GA Abd, Thoracic, Head & Neck, Nuero, Vascular Surgery

70 Post Operative Pulmonary Complications:
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) he incidence of PPCs (except atelectasis) most often parallels the severity of respiratory impairment (moderate,if FEV1 50%–80%; severe, if FEV1 50%), particularly in patients with abnormal clinical findings (decreased breath sounds, wheezes, ronchi, prolonged expiration) and/or marked alterations of gas exchange (PaCO2 7 kPa, hypoxemia requiring supplemental oxygen). Br Asthma; Recent asthma symptoms, current use of anti-asthma drugs and history of tracheal intubation for asthma have all been associated with the development of PPCs.

71 Post Operative Pulmonary Complications:
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

72 Post Operative Pulmonary Complications:
Post Operative Analgesia: Opioids Paravertebral/Intercostal N Blocks Epidural Analgesia LA NSAIDS  Bronchospasm

73 Post Operative Pulmonary Complications:
Lung Expansion maneuvers: Incentive spirometry Deep breathing exercises Chest Physiotherapy & postural drainage Intermittant Positive Pressure Ventilation CPAP, BiPAP Early Ambulation Of proven benefit in decreasing PPCs. Decrease atelectasis by increasing lung volume All are equally efficacios Incentive spirometry: Simple. Inexpensive. Objective goal given to the patient provides sustained lung expansion & helps in opening closed alveoli. But needs patient coorperation. Positive pressure breathing tech not cost effective.

74 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.

75 References: Stoelting’s Anaesthesia & Coexisting Disease, 5th 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 (6) Post Operative Pulmonary Complications, IJA April 2006 Periop Management of patients with COPD: Review, IJ COPD 2007:2(4) 493:515 Harrison’s Principles of Medicine, 16th 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


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