anaesthesia management of copd in laparoscopic pdf

Laparoscopic cholecystectomy

1. ANESTHETIC MANAGEMENT FOR LAPAROSCOPIC
CHOLECYSTECTOMY IN PATIENT WITH COPD
DR RAMKRISHNA BHUE
3
RD
YEAR PGT
MKCG MCH BERHAMPUR

2. Summary of the case
•NAME :Mr.NatrajBisoi
•AGE/SEX :56YRS/MALE
•Address :kukudakhandi ,Ganjam
•Occupation :busdriver
•Education :StudieduptoClassX
•DATEOFADMISSION :17/10/17

3. Chief complaints
•Pain abdomen 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 Patient was 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 and wheeze: 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 at PAC 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
SrK –4.7
Srurea –38
Srcreat. –1.2
CXR:
•increasedbronchovascular markings
•flattened hemidiaphragms(bilat)

8. Plan of management:
Patient of Acute Calculus Cholecystitis
with Acute on Chronic COPD
Posted for Laparoscopic Cholecystectomy

9. Discussion
•Chronic Obstructive Pulmonary 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.SMALL AIRWAY DISEASE

10. 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
COPD

11. COPD: Risk factors
Host factors:
•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 bronchopulmonaryinfections

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 occur in 4 major areas of
lungs:-
Large airways
Small airways
Lung parenchyma
Pulmonary vasculature

14. Large Airways: (cartilaginous airways >2mm of internal diameter)
•Bronchial glands hypertrophy
•Goblet cell metaplasia
•Airway Wall Changes:
•Inflammatory Cells
Squamousmetaplasiaof the airway epithelium
Increased smooth muscle and connective tissue
Small airways (noncartilaginousairways<2mm internal diameter)
•Bronchiolitis
•Pathological extension of goblet cells and squamousmetaplasia
•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 (respiratory bronchioles, alveoli and capillaries)
•Emphysema (abnormal enlargement of air spaces distal to terminal
bronchioles)
occurs in the parenchyma:
2 Types: Centrilobularand 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
(corPulmonale)

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
Airway narrowing
Alveolar hypoventilation
Hypoxia in
COPD
AJRCCM 2001; 163: 283-91

18. Chronic hypoxia
Pulmonary vasoconstriction
Muscularization
Intimal
hyperplasia
Fibrosis
Obliteration
Pulmonary hypertension
Cor pulmonale
Death
Edema
Pulmonary Hypertension in COPD
Source: Peter J. Barnes, MD

19. PINK PUFFER BLUE BLOATER

20. emphysema underlying pathology.
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 by hyperventilation (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 lung pathology 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 obstruction leads decrease in ventilation and
increasing cardiac output causing perfusion mismatch
leading to hypoxemia, hypercapniaand 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. Comparative features of COPD

25. Differences Between COPD and 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. Extrapulmonarycomorbiditiesin COPD
•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
•Reduced stress 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.Changes in ventilation
2.Increase in PaCO2
3.Endobronchialintubation
4.CO2 subcutaneous emphysema
5.Pneumothorax
6.Gas embolism

30. Changes in Ventilation
•thoracopulmonarycompliance(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 ventilationby anaestheticsif
spontaneously breathing
4. metabolism( light anaesthesia, MH)

32. Other Respiratory Effects
Endobronchial Intubation
Due to cephalad displacement of diaphragm 
cephalad displacement of carina Paw, 
SpO2
4.S/c Emphysema
5.Pneumothorax
6.Gas embolism

33. Cardiovascular Effects
•Peritoneal insufflations
Biphasic effect on Cardiac Output
Initial transient CO due to splanchniccompression
(IAP<15)
Then CO (10-30%)Due to
-venous return

34. •SVR
-direct compression abdominal aorta &
abdominal organs
-Reflex sympresponse to CO
-Release of neurohumoral factors vasopressin,
catechols, renin-angiotensinactivation
•PVR
•HR, unchanged
•arterial BPdespite CO

35. IntraAbdominal Pressure
Pooling of
blood legs
caval
comp
Vn
Res
I/thoracic prperitoneal
recs stimn?
vasc res
aorta &
abdal
organs
Neurohumoral factors
Venous
return
inotropism?
SystemicVasc Res
Cardiac Output
Arterial pressure

36. Cardiac arrhythmias
•Reflex ’s in vagaltonesudden peritoneal
stretch bradycardia, arrhythmias, asystole
-Stop insuffln, atropine, deepen anaesthesia
•PaCO2
•Use of halothane
•Pts with cardiac disease
•Gas embolism
•hypoxia

37. GIT Effects
•Due to intra abdominal pressure risk
of aspiration
•Head down position prevents regurgitated
material from entering the airway

38. Hypothermia
•Due to –insufflationof cold gases
•Temperature of gases
•cold fluid used for toileting
•Leakage through the ports etc

39. Trenderdelbergposition
•CVS effects;
-CVP
-CO
-Systemic vasodilation& bradycardiadue
to baroreceptorreflex to hydrostatic pr.
•Respiratory effects;
-Atelactasis
-FRC, TLC
-pulmonary compliance
•Cerebral circuln
-CBF ICP( low compliance)
•IOP -

40. Reverse Trendelenburg
•CVS effects;
-venous return
-CVP
-CO
-MAP
•Improve respiratory function

41. Nerve injury
•due overextension arms, ulnarnerve and
brachial plexus injuries
•Lower limb palsies especially peroneal
neuropathy, meralgiaparaesthetica, femoral
neuropathy
•Common peronealn. -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, ascultatebtnshoulder
blade for wheeze
•Max Laryngeal Height –btnthyroid cartilage and
suprasternalnotch @ end of exp. <4 cm abnormal
•Sabrasezbreath 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 Expiratory Time –ascultate@ trachea
after deepest breathe & blow out as fast as
possible-FET > 6s , severe exp. Flow obstuction
•Snidersmatch 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 in COPD

48. Assessment of Severity
(Spirometry)
Mild ModerateSevere Very severe
FEV
1/ FVC
<70%
FEV
1
>80%
FEV
1/ FVC
< 70%
FEV
1
50% -80%
FEV
1/ FVC
<70%
FEV
1
30% -50%
FEV
1/ FVC
<70%
FEV
1< 30%
or chronic
respiratory
failure or right
heart failure

49. PFT predictors of increased 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. ABCD Assessment tool

54. Preoperative Preparation
•Stop smoking
▫Improves mucociliaryfunction, 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 & nicotinlevels
48 –72 hours COHblevels 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 postopmorbidity

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 hydrocortat
induction then 100 mg IV TDS for 2-3 days.

57. Monitoring
•HR, continuous ECG
•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
General Anaesthesia
•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 for Laparoscopy
•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
Minimisetilt < 20°; slow

60. Ctd……..
•Check ETT after positioning
•Adjust ventilation to maintain EtCO2 about 35 mm Hg
•Adequate anaesthesiadepth
•Omission of N2O may improve surgical condns
•Consider use of vasodilators .

61. Regional anaesthesia
•Avoids risk of bronchospasmdue to intubation
•Excellent intraoperative and postoperative analgesia
•Problems
▫Spontaneous ventilation may lead to hypoventilation
▫Hypercarbiaand 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 for this 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 hydrocortisone 100mg iv
•Salbutamol 2 puffs, ipratropium 2 puffs,
budenoside2 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
▫Thiobarbituratesmay cause histamine release
Prefer oxybarbiturates(methohexitone)
▫Airway instrumentation or other stimulation under light
thiopentoneanaesthesiamay 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 anaesthesiaprior to intubation
•LMA avoids tracheal stimulation (LMA Proseal–
or Baska Mask)

66. Maintenance
•IPPV
•Muscle relaxant
▫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, pethidinemay cause histamine release

67. End of Anaesthesia
•Neostigmine may provoke bronchospasm
▫Atropine 1.2-1.8mg or glyopyrrolate10mcg/kg before
neostigmine
•Extubation:
▫Deep extubationmay reduce chance of bronchospasm
▫May require a period of postoperative ventilation
▫Awake, obeying commands
▫Sustained head lift
▫Adequate gas exchange

68. Postoperative management
•Admit patient 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
•LA infiltration-intraperitoneal, port site
•Shoulder pain -careful evacuation of residual CO2
•Preoperative NSAIDs
•Intra & post operative opioids
•Use multimodal analgesia

70. LONG TERM OXYGEN THERAPY
Long-term oxygen therapy(home oxygen therapy) is
recommended if the Pao2 <55 mmHg, the hematocrit >55% or
there is evidence of corpulmonale
The goal of supplemental oxygen administration is to achieve a
Pao2 between 60 and 80 mmHg. Thisgoal can usually be
accomplished by delivering oxygen through a nasal cannula at
2L/min. The flow rate of oxygen is titrated as neeededaccording
to arterial blood gas or pulse oximetrymeasurements

72. Summary:
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 anaesthsiatechnique if
patients have been appropriately stabilised.
COPD patients are prone to develop intraoperative and postoperative
pulmonary complications.
Preoperative optimisationshould 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. Thank You