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ANESTHETIC MANAGEMENT LAP CHOLECYSTECTOMY WITH COPD
- 1. ANESTHETIC MANAGEMENT FORLAPAROSCOPIC CHOLECYSTECTOMY IN PATIENT WITH COPD DR RAMKRISHNA BHUE 3RD YEAR PGT MKCG MCH BERHAMPUR
- 2. Summary of thecase • NAME : Mr. Natraj Bisoi • AGE/SEX : 56 YRS/ MALE • Address : kukudakhandi , Ganjam • Occupation : bus driver • Education :Studied upto Class X • DATE OF ADMISSION : 17/10/17
- 3. Chief complaints • Painabdomen off and on for last 3 months • Fever for last 5 days • 4 episodes of vomiting on the day of admission
- 4. Initial Management Initially Patientwas seen by local physician Diagnosed as a case of acute cholecystitis with cholelithiasis Patient received antibiotics (ciprofloxacin/metronidazole), analgesics (PCM, Drotaverine), Pantoprazole and Ondansetron Later patient was referred to MKCG MCH In Medical College, Patient was continued on the conservative management and planned for Laparoscopic cholecystectomy
- 5. Comorbidity • Cough andwheeze: off and on for last 5 years • Further questioning revealed: Smoker for last35 years 25/day, now reduced to ~10 Increased cough, expectoration from last week currently taking Salbutamol puffs, ipravent puffs and budenoside inhaler (local physician consultation) Can climb 2 flights with difficulty – gets breathless Clinically RS : barrel chest, wheeze and ronchi present CVS NAD on examination
- 6. • B.P :128/76mmHg • PULSE : 78/min, regular, (arterial wall palpable) • RESPIRATION : 22b/m • TEMPREATURE : 36.6 c • SpO2 : 93% (room air) • Body wt :50 kg
- 7. Investigations available atPAC visit: Blood: Hb – 14gm/dl TC: RBC- 5.8* 10^6/ul WBC- 16,000/ul DC – 42(N), 38(L), 11(M), 9(E) BILIRUBIN (TOTAL) 1.7 mg/ dL BILIRUBIN (DIRECT) 1.0 mg/ dL BILIRUBIN INDIRECT 0.7 mg/ dl SGPT- 97, SGOT – 102, Alk Phos – 205 FBS – 98 mg/dl USG – Calculus Cholecystitis ECG – NAD Sr, Na – 141 Sr K – 4.7 Sr urea – 38 Sr creat. – 1.2 CXR: • increased bronchovascular markings • flattened hemidiaphragms(bilat)
- 8. Plan of management: Patientof Acute Calculus Cholecystitis with Acute on Chronic COPD Posted for Laparoscopic Cholecystectomy
- 9. Discussion • Chronic ObstructivePulmonary Disease (COPD) is a common, preventable and treatable disease that is characterized by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases • Includes:- I. CHRONIC BRONCHITIS II. EMPHYSEMA III.SMALLAIRWAY DISEASE
- 10. Chronic Bronchitis: (ClinicalDefinition) 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 COPD
- 11. COPD: Risk factors Hostfactors: •Genetic factors: Eg. α1 Antitrypsin Deficiency •Gender : Prevalence more in males. ?Females more susceptible •Airway Hyperresponsiveness Exposures: •Smoking: Most Important Risk Factor •Passive/second hand ,smoking exposure • dust and smokes •Environmental pollution •Recurrent bronchopulmonary infections
- 12. PATHOGENESIS Tobacco smoke &other noxious gases Inflammatory response in airways Tissue Destruction Impaired defense against tissue destruction Impaired repair mechanisms Proteinase & Antiproteinase imbalance Oxidative Stress Alpha 1 antitrypsin def.
- 13. PATHOLOGY Pathological changes occurin 4 major areas of lungs:- Large airways Small airways Lung parenchyma Pulmonary vasculature
- 14. Large Airways: (cartilaginousairways >2mm of internal diameter) •Bronchial glands hypertrophy •Goblet cell metaplasia •Airway Wall Changes: •Inflammatory Cells Squamous metaplasia of the airway epithelium Increased smooth muscle and connective tissue Small 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 hyperinflation
- 15. Lung parenchyma (respiratorybronchioles, alveoli and capillaries) •Emphysema (abnormal enlargement 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)
- 16. Pathophysiology of COPD •Increased mucus production and reduced mucociliary clearance - cough production • Loss of elastic recoil - airway collapse • Increase smooth muscle tone • Pulmonary hyperinflation • Gas exchange abnormalities - hypoxemia and/or hypercapnia
- 17. Airspace collapse Low V/Q Hypoxia Airwaynarrowing Alveolar hypoventilation Hypoxia in COPD AJRCCM 2001; 163: 283-91
- 18. Chronic hypoxia Pulmonary vasoconstriction Muscularization Intimal hyperplasia Fibrosis Obliteration Pulmonaryhypertension Cor pulmonale Death Edema Pulmonary Hypertension in COPD Source: Peter J. Barnes, MD
- 19. PINK PUFFER BLUEBLOATER
- 20. emphysema underlyingpathology. destruction of the airways distal to the terminal bronchiole - destruction of the pulmonary capillary bed & decrease ability to oxygenate the blood. lesser surface area for gas exchange, also lesser vascular bed but ventilation-perfusion mismatch lower than blue bloaters. PINK PUFFER
- 21. compensate byhyperventilation (the "puffer" part) so relatively normal ABGs. Eventually, low cardiac output, people develop muscle wasting and weight loss. They actually have less hypoxemia and appear to have a "pink" complexion and hence "pink puffer"
- 22. primary lungpathology is chronic bronchitis. excessive mucus production with airway obstruction - hyperplasia of mucus-producing glands, goblet cell metaplasia, and chronic inflammation around bronchi. BLUE BLOATER
- 23. increased obstructionleads decrease in ventilation and increasing cardiac output causing perfusion mismatch leading to hypoxemia, hypercapnia and polycythemia. Because of increasing obstruction, their residual lung volume gradually increases (the "bloating" part). They are hypoxemic/cyanotic because they actually have worse hypoxemia than pink puffers and this manifests as bluish lips and faces.
- 24.
- 25. Differences Between COPDand Asthma Parameters COPD Asthma Onset Mid-life Early in life (often childhood) Symptoms Slowly progressive Vary from day to day and peak in the night/early morning History Long smoking history or exposure to smoking and bio-mass fuel History of allergy, rhinitis and/or eczema. Inflammatory cells Neutrophils Eosinophils Airway hyperresponsiveness Absent Present Airflow limitation Largely irreversible usually < 15% or 200 ml change Largely reversible usually > 15% or 200 ml change.
- 26. Extrapulmonary comorbidities inCOPD • Commonly seen ▫ Weight loss ▫ Skeletal muscle wasting • Increased risk of ▫ Myocardial infarction ▫ Angina ▫ Osteoporosis, bone fractures • Respiratory infection • Depression • Diabetes • Sleep-disorders • Anemia • Glaucoma Common consequences RVH Cor pulmonale
- 27. Laparoscopic Cholecystectomy • Reducedstress response • Early recovery and return of GI function • Reduced post op. analgesia • Decreased wound infection • Improved cosmetic • Better post op respiratory functions
- 28. Pneumoperitoneum • Abdominal insufflationw/ CO2, helium, nitrous oxide, 12 – 16 mmHg – Normal Intra-abdominal pressure (IAP) < 5 mmHg • CO2 most commonly used gas. – Noncombustible = safe to use with electrosurgical devices – Solubility in blood
- 29. Respiratory Effects Pneumoperitoneum 1. Changesin ventilation 2. Increase in PaCO2 3. Endobronchial intubation 4. CO2 subcutaneous emphysema 5. Pneumothorax 6. Gas embolism
- 30. Changes in Ventilation • thoracopulmonary compliance (30-50% ) • in FRC (elevation of diaphragm) • airway pressure • changes in distribution of ventilation & perfusion *IAP 15 mmHg exerts pressure 50 kg on diaphragm
- 31. Causes for PaCO2 1. Absorption from peritoneal cavity 2. V/Q mismatch -abdominal distention, patient position, mechanical ventilation, CO 3. Depression of ventilation by anaesthetics if spontaneously breathing 4. metabolism ( light anaesthesia, MH)
- 32. Other Respiratory Effects EndobronchialIntubation Due to cephalad displacement of diaphragm cephalad displacement of carina Paw, SpO2 4. S/c Emphysema 5. Pneumothorax 6. Gas embolism
- 33. Cardiovascular Effects • Peritonealinsufflations Biphasic effect on Cardiac Output Initial transient CO due to splanchnic compression (IAP<15) Then CO (10-30%) Due to - venous return
- 34. • SVR -direct compression abdominal aorta & abdominal organs - Reflex symp response to CO - Release of neurohumoral factors vasopressin, catechols, renin-angiotensin activation • PVR • HR , unchanged • arterial BP despite CO
- 35. IntraAbdominal Pressure Poolingof blood legs caval comp Vn Res I/thoracic pr peritoneal recs stimn? vasc res aorta & abdal organs Neurohumoral factors Venous return inotropism? SystemicVasc Res Cardiac Output Arterial pressure
- 36. Cardiac arrhythmias • Reflex’s in vagal tone sudden peritoneal stretch bradycardia, arrhythmias, asystole - Stop insuffln, atropine, deepen anaesthesia • PaCO2 • Use of halothane • Pts with cardiac disease • Gas embolism • hypoxia
- 37. GIT Effects • Dueto intra abdominal pressure risk of aspiration • Head down position prevents regurgitated material from entering the airway
- 38. Hypothermia • Due to– insufflation of cold gases • Temperature of gases • cold fluid used for toileting • Leakage through the ports etc
- 39. Trenderdelberg position • CVSeffects; - CVP - CO - Systemic vasodilation & bradycardia due to baroreceptor reflex to hydrostatic pr. • Respiratory effects; - Atelactasis - FRC, TLC - pulmonary compliance • Cerebral circuln - CBF ICP ( low compliance) • IOP -
- 40. Reverse Trendelenburg • CVSeffects; - venous return - CVP - CO - MAP • Improve respiratory function
- 41. Nerve injury • dueoverextension arms, ulnar nerve and brachial plexus injuries • Lower limb palsies especially peroneal neuropathy, meralgia paraesthetica, femoral neuropathy • Common peroneal n. - lithotomy
- 42. Anaesthetic management • Calculus cholecystitis •COPD Posted for Laparoscopic Cholecystectomy
- 43. Preoperative workup • Complete hemogram •Serum electrolytes • Urine analysis • ECG • Chest x-ray • PFT including ABG • ECHO
- 44. Bed sides PFT •Cough test – cough after deep inspiration , recurrent cough – bronchitis • Wheeze test- 5 deep resps, ascultate btn shoulder blade for wheeze • Max Laryngeal Height – btn thyroid cartilage and suprasternal notch @ end of exp. <4 cm abnormal • Sabrasez breath holding test – deep breathe and hold. Asculatate @ trachea - >40s normal, 20-30s compromised, < 20s poor pulmonary reserve • Single breath count – count from 1 onwards after deep insp. , <15 – severe impairment of VC
- 45. • Forced ExpiratoryTime – ascultate @ trachea after deepest breathe & blow out as fast as possible- FET > 6s , severe exp. Flow obstuction • Sniders match test – ability to blow candle with open mouth @ 22cm – MBC >150l, @ 15cm MBC <100l, @ 7.5cm – MBC < 50 L •
- 46. Indications for PFT(Spirometry): •Patients in whom risk of surgery is high • Patients needing specialised postop respiratory care • Surgery should not be denied on the basis of abnormal PFT
- 47. Lung Volumes inCOPD
- 48. Assessment of Severity (Spirometry) MildModerate Severe Very severe FEV1/ FVC <70% FEV1 >80% FEV1/ FVC < 70% FEV1 50% - 80% FEV1/ FVC <70% FEV1 30% - 50% FEV1/ FVC <70% FEV1< 30% or chronic respiratory failure or right heart failure
- 49. PFT predictors ofincreased risk • FVC < 50% predicted • FEV1 < 50% predicted or < 2L • MVV < 50% predicted or < 50L/min • DLCO < 50% predicted • RV / TLC > 50% predicted Nunn and Milledge criteria: • FEV1 < 1L, PaO2 normal, PaCO2 Normal : Low Risk • FEV1 < 1L, PaO2 low, PaCO2 Normal : prolonged O2 • FEV1 < 1L, PaO2 low, PaCO2 High: Ventilation
- 51.
- 54. Preoperative Preparation • Stopsmoking ▫ Improves mucociliary function, decreases sputum production and airway reactivity : 2 months ▫ Reduce CO levels : 12 hours • Bronchodilators • Control of infection • Chest physiotherapy, hydration ▫ Familiarise patient with deep breathing exercises and respiratory therapy equipment that are likely to be used postop • Improve oxygenation • Steroids
- 55. Smoking cessation &time course Time course Beneficial effects 12 – 24 hours CO & nicotin levels 48 – 72 hours COHb levels normalise & airway function improve 1-2 weeks Sputum production 4 – 6 weeks PFTs improved 6 - 8 weeks Immune function & drug metabolism normalise 8 – 12 weeks Overall postop morbidity
- 56. Recommendations for perioperativesteroids Dose Surgery Recommended dose <10 mg/day Minor / Moderate / Major Additional steroid cover not required (assume normal HPA response) >10 mg/day Minor surgery 25 mg of hydrocort at induction & normal medications post-op >10 mg/day Moderate surgery Usual dose pre-op & 25 mg hydrocort IV at induction then 25 mg IV TDS for 1day then recommence pre-operative dosage >10 mg/day Major surgery Usual dose pre-op & 100 mg hydrocort at induction then 100 mg IV TDS for 2-3 days.
- 57. Monitoring • HR, continuousECG • Intermittent BP • EtCO2 • SpO2 • Temp • Intra abdominal pressure • Airway pressure, Expired tidal and minute volume • IBP, CVP,, TEE – patients with heart disease • ABG • Hourly urine output
- 58. Choice of Anaesthesia GeneralAnaesthesia • Allows control of ventilation, excellent muscle relaxation • Ensures oxygenation and CO2 elimination • IPPV overcomes decrease in lung compliance, increased resistance and decreased FRC • Comfort to patient, prolonged procedures
- 59. GA specifics forLaparoscopy • Preloading prior to pneumoperitoneum • Decompress stomach / bladder • Smooth induction and release of pneumoperitoneum • Keep IAP as low as possible; IAP < 12- 15 mmHg • Positioning; head low prior to insufflation Minimise tilt < 20°; slow
- 60. Ctd…….. • Check ETTafter positioning • Adjust ventilation to maintain EtCO2 about 35 mm Hg • Adequate anaesthesia depth • Omission of N2O may improve surgical condns • Consider use of vasodilators .
- 61. Regional anaesthesia • Avoidsrisk of bronchospasm due to intubation • Excellent intraoperative and postoperative analgesia • Problems ▫ Spontaneous ventilation may lead to hypoventilation ▫ Hypercarbia and acidosis can increase PVR ▫ Inadequate muscle relaxation, coughing / bucking ▫ High levels of spinal / epidural block Increase parasympathetic tone and cause bronchospasm Decrease ERV by ~50%, detrimental for active expiration Hypotension ▫ Prolonged procedure, patient discomfort, shivering ▫ Heavy sedation may required
- 62. My choice forthis case • GA combined with epidural analgesia ▫ All benefits of GA ▫ Excellent analgesia with epidural ▫ Reduced requirement of muscle relaxants ▫ Lower risk of hypotension ▫ Postoperative analgesia without excessive systemic narcotics ▫ May facilitate early ambulation ▫ May reduce postoperative pulmonary complications ▫ May reduce risk of DVT
- 63. Premedication • Steroid hydrocortisone100mg iv • Salbutamol 2 puffs, ipratropium 2 puffs, budenoside 2 puffs before sending to OT • Atropine ▫ Decreases airway resistance ▫ Decreases secretion-induced airway reactivity ▫ Decreases bronchospasm from reflex vagal stimulation ▫ But can cause drying of secretions, mucus plugging • Avoid H2 receptor antagonists
- 64. Induction • Avoid thiopentone ▫Thiobarbiturates may cause histamine release Prefer oxybarbiturates (methohexitone) ▫ Airway instrumentation or other stimulation under light thiopentone anaesthesia may provoke bronchospasm • Ketamine ▫ Tachycardia and HT, may increase PVR ▫ Agent of choice in unstable / wheezing patient • Propofol ▫ Offers marked protection from bronchospasm & PONV ▫ But watch for hemodynamic compromise ▫ Agent of choice in stable patient
- 65. Intubation • NDMR –vecuronium, rocuronium preferred • IV lignocaine prior to laryngoscopy and intubation • Narcotic • Deep plane of anaesthesia prior to intubation • LMA avoids tracheal stimulation (LMA Proseal – or Baska Mask)
- 66. Maintenance • IPPV • Musclerelaxant ▫ Avoid atracurium, mivacurium ▫ Prefer Vecuronium, pancuronioum, rocuronium • Inhaled agent ▫ Halothane most potent bronchodilator (< 1.7 MAC) ▫ Isoflurane comparable at higher MACs ▫ Irritant smell may provoke bronchospasm • Narcotic ▫ Fentanyl (choice) ▫ Morphine, pethidine may cause histamine release
- 67. End of Anaesthesia •Neostigmine may provoke bronchospasm ▫ Atropine 1.2-1.8mg or glyopyrrolate 10mcg/kg before neostigmine • Extubation : ▫ Deep extubation may reduce chance of bronchospasm ▫ May require a period of postoperative ventilation ▫ Awake, obeying commands ▫ Sustained head lift ▫ Adequate gas exchange
- 68. Postoperative management • Admitpatient into a ICU if ventilated ▫ HDU if not ventilated • Controlled Oxygen therapy • Provide good postoperative pain relief • Postoperative respiratory therapy ▫ Encourage lung inflation manoeuvres • Ambulate as early as possible to prevent pulmonary morbidity and other complications (such as DVT and PTE)
- 69. Pain relief • LAinfiltration- intraperitoneal, port site • Shoulder pain - careful evacuation of residual CO2 • Preoperative NSAIDs • Intra & post operative opioids • Use multimodal analgesia
- 70. LONG TERM OXYGENTHERAPY Long-term oxygen therapy(home oxygen therapy) is recommended if the Pao2 <55 mmHg, the hematocrit >55% or there is evidence of cor pulmonale The goal of supplemental oxygen administration is to achieve a Pao2 between 60 and 80 mmHg. This goal can usually be accomplished by delivering oxygen through a nasal cannula at 2L/min. The flow rate of oxygen is titrated as neeeded according to arterial blood gas or pulse oximetry measurements
- 72. Summary: Cigarette smokingis 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.
- 73.