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Anaesthetic management for Laparoscopic Cholecystectomy in a patient with COPD
Dr. Pallab Kanti NathMD AnaesthesiaSenior Resident
Department of AnaesthesiologyMedical College, Kolkata
Summary of the caseNAME : Mr. Pulak Dutta
AGE/SEX : 62 YRS/ MALE
Address : LP. 64/2, Birati
Occupation : Carpenter
Education :Studied upto Class X
DATE OF ADMISSION : 25/11/15
Chief complaints
• Pain abdomen off and on for last 4 months
• Fever for last 3 days
• Three episodes of vomiting on the day of admission
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 Medical College, Kolkata for further management
In Medical College, Patient was continued on the conservative
management and planned for Laparoscopic cholecystectomy
Comorbidity Cough and wheeze: off and on for last 5 years
Further questioning revealed: Smoker for last45 years 20 /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
vitals
• B.P : 138/86mmHg• PULSE : 88/min, regular, (arterial wall palpable)• RESPIRATION : 20b/m• TEMPREATURE : 36.6 c• SpO2 : 92% (room air)• Body wt :65 kg
Investigations available at PAC visit:
Blood:Hb – 13gm/dlTC:
RBC- 5.8* 10^6/ulWBC- 16,000/ulDC – 42(N), 38(L), 11(M), 9(E)
BILIRUBIN (TOTAL) 1.7 mg/ dLBILIRUBIN (DIRECT) 1.0 mg/ dLBILIRUBIN INDIRECT 0.7 mg/ dl
SGPT- 97, SGOT – 102, Alk Phos – 205
Ur/Cr, Sodium/Potassium, Blood Glucose(F/PP)- NAD
USG – Calculus Cholecystitis
ECG - NAD
CXR:• increased bronchovascular markings
• flattened hemidiaphragms(bilat)
Plan of management:
Patient of Acute Calculus Cholecystitis
with Acute on Chronic COPD
Posted for Laparoscopic Cholecystectomy
Discussion
• COPD• Laparoscopic Surgery
Anaesthetic implications And management
COPD
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
Airspace collapse
Low V/Q
Hypoxia
Airway narrowingAlveolar hypoventilation
Hypoxia in COPD
AJRCCM 2001; 163: 283-91
Causes of Hypercapnia in COPD
Inspiratory muscle fatigue
V / QMismatch
Reduced ventilatory responseto CO2
Chronic hypoxia
Pulmonary vasoconstriction
MuscularizationIntimal hyperplasiaFibrosisObliteration
Pulmonary hypertension
Cor pulmonale
Death
Edema
Pulmonary Hypertension in COPD
Source: Peter J. Barnes, MD
Polar forms of COPD:CHRONIC BRONCHITIS
Chronic bronchitis is defined by a productive cough on most days for at least three months for at least two consecutive years and which cannot be attributed to other pulmonary or cardiac causes.
Polar forms of COPD: EMPHYSEMA
Emphysema is characterised by destruction of alveolar walls, resulting in abnormal enlargement of airspaces and loss of lung elasticity, with consequent obstruction of peripheral airways.
Lung Volumes in COPD
Differences Between COPD and AsthmaParameters 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.
Extrapulmonary comorbidities in COPD Commonly seen
Weight loss Nutritional abnormalities Skeletal muscle dysfunction
Increased risk of Myocardial infarction Angina Osteoporosis, bone fractures
Respiratory infection Depression Diabetes Sleep-disorders Anemia Glaucoma
Common consequences RVH Cor pulmonale
Laparoscopic Cholecystectomy
Advantages……. “minimally invasive” “ minimal access”
Reduced stress response
Reduced acute phase reactants; CRP, IL 6
Reduced metabolic response; N2 balance & immune function better preserved
Not much reduction in endocrine response; Plasma cortisol, catecholamines similar (pain, discomfort from peritoneal stretch, hemodynamic dist, vent changes)
Reduced pain and analgesic requirements
Less acute pain Shorter duration of pain Less analgesic consumption Smaller incision; less superficial trauma More of visceral pain, shoulder tip pain
Decreased postoperative respiratory dysfunction
Less pain Less atelactasis, less respiratory infection Diaphragmatic function impaired but less than after
laparotomy Pulm fn less impaired (30-38% less than lap)
Pneumoperitoneum
• Abdominal insufflation w/ CO2, helium, nitrous oxide, or oxygen to ~ 15 mmHg– Normal Intra-abdominal pressure (IAP) < 5 mmHg
• CO2 most commonly used gas. – Noncombustible = safe to use with electrosurgical devices– Solubility in blood and reactivity w/ soluble buffering systems minimize
the risk of gas emboli ( )
• Systemic absorption thought to be facilitated by CO2 specific widening of inter-cellular junctions in peritoneum buffering of CO2 as above Systemic Acidification
Pathophysiological effects of laparoscopy
Due to
- creation of a pneumoperitoneum
- positioning
Effects of Pneumoperitoneum...
……. created by intraperitoneal insufflation of CO2 at 1-6 lpm - Respiratory - CVS - regional blood flow - dysrhythmias - GIT - hypothermia
Respiratory Effects
1. Changes in ventilation2. Increase in PaCO23. Endobronchial intubation 4. CO2 subcutaneous emphysema5. Pneumothorax6. Gas embolism
Changes in Ventilation
compliance (30-50% ) thoracopulmonary
in FRC (elevation of diaphragm)
airway pressure changes in distribution of
ventilation & perfusion
*IAP 15 mmHg exerts pressure 50 kg on diaphragm
Increase in PaCO2
s to reach plateau in 15-30 mins depends on IAP EtCO2 plateaus after 25-30 mins
Any rise after that – search for cause !
Causes for PaCO2
1. Absorption from peritoneal cavity- diffusibility, area, perfusion2. V/Q mismatch; abdominal distention, patient position, mechanical ventilation, CO3. Depression of ventilation by anaesthetics if spontaneously breathing4. metabolism ( light anaesthesia, MH)5. Complications; CO2 emphysema, capnothorax, CO2 embolism, endobronchial intubation
10-25% in alveolar ventilation for normocapnia
Remains unchanged if under LA ( MV s)
EtCO2 is an imperfect index of PaCO2 if dead space ventilation ( PaCO2 may be high despite normalization of EtCO2 by increasing MV)
In ASA class II/III pts - poor correlation b/w PaCO2 & EtCO2
Other Respiratory Effects
Endobronchial Intubation Due to cephalad displacement of diaphragm cephalad
displacement of carina Paw, SpO2 4. S/c Emphysema5. Pneumothorax6. Gas embolism
Cardiovascular Effects
Peritoneal insufflation to IAP > 10 mmHg (in normal pts) for significant alterations in hemodynamics
Biphasic effect on Cardiac Output Initial transient due to splanchnic compression (IAP<15) Then CO (10-30%)
Due to - venous return
To attenuate- Fluid loading pre &
intraoperatively- Head low before insuffln- Pneumatic compression- Elastic bandage legs
SVR Due to; - direct compression abdominal aorta & abdominal
organs - Reflex symp response to CO - Release of neurohumoral factors vasopressin,
catechols, renin-angiotensin PVR HR slight , unchanged arterial BP despite CO
IntraAbdominal Pressure
Pooling of 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
Cardiac arrhythmias
Reflex ’s in vagal tone sudden peritoneal stretch bradycardia, arrhythmias, asystole
- Stop insuffln, atropine, deepen anaesthesia PaCO2 ? May not correlate Use of halothane Pts with cardiac disease Gas embolism hypoxia
GIT Effects
Due to intra abdominal pressure ?? ? risk of aspiration BUT Changes in LES tone maintenance of pressure gradient
across GE junction risk of regurgitation
Head down position prevents regurgitated material from entering the airway
Hypothermia
Significant heat loss may occur
Due to – insufflation of cold gases
Temperature of gases
Rate of gas flow
Leakage through the ports etc
Positions in laparoscopic surgeries
Trendelenburg / head down; pelvic, inframesocolic surgery Reverse Trendelenburg / head up; supramesocolic surgery Lateral
Lithotomy
Effects of Positioning……
Crdiovascular
Respiratory
Nerve and other injuries
Care of eyes, iv lines, ETT etc
HEAD DOWN
CVS effects; - CVP - CO - Systemic vasodilation & bradycardia due to baroreceptor reflex to hydrostatic pr. - transmural pressure in pelvic viscera blood loss, gas embolism
Respiratory effects; - Atelactasis - FRC, TLC - pulmonary compliance Cerebral circuln - CBF ICP ( low compliance) IOP -
HEAD UP
CVS effects; - venous return - CVP - CO - MAP Resp ; less significant changes Venous stasis ; aggravated if lithotomy
compound hemodynamic changes due to pneumoperitoneum
Nerve injury
Potential hazard
Avoid overextension arms, use shoulder braces with caution, no impingement on brachial plexus
Lower limb palsies especially peroneal neuropathy, meralgia paraesthetica, femoral neuropathy
Common peroneal n. - lithotomy
Preoperative Evaluation
Absolute C/I rare, include; - ICP ( tumor, hydrocephalus, head injury) - hypovolaemia - VP shunt - peritoneo-jugular shunt - ? Glaucoma - ? Severe CHF, severe VHD
Anaesthetic management
Calculus cholecystitis COPD
Posted for Laparoscopic Cholecystectomy
Preoperative workup
Complete hemogram Serum electrolytes Urine analysis Electrocardiogram Chest x-ray PFT including ABG ECHO
Indications for PFT:
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
Assessment of Severity (Spirometry)
Mild Moderate 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
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
Preoperative Preparation
Stop smoking 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 Diuretics, digitalis
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
Perioperative steroids? Which patients?What are equivalent doses of steroids?
Long-term steroids >10 mgs prednisolone daily Pts on steroids >10 mgs daily, in last 3 months. Pts on high dose inhalation steroids Prednisolone 5 mgs is equivalent to
Betamethasone 750 microgms Cortisone acetate 25 mgs Dexamethasone 6 mgs Hydrocortisone 20 mgs Methylprednisolone 4 mgs
Recommendations for perioperative steroids
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.
Monitoring HR, continuous ECG Intermittent BP EtCO2 SpO2 Temp Intra abdominal pressure Airway pressure, Expired tidal and minute volume IBP, ? CVP,? PCWP – patients with heart disease TEE - pts with more severe heart disease ABG- as Δa-EtCO2 - pts with severe heart disease Hourly urine output
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
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 Minimise tilt < 20°; slow
Ctd……..
Check ETT after positioning
Adjust ventilation to maintain EtCO2 about 35 mm Hg by MV by 15-25%
Adequate anaesthesia depth
Omission of N2O may improve surgical condns
Consider use of vasodilators like nicardipine, 2 agonists, remifentanil
Regional anaesthesia Avoids risk 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 be worse than light GA
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 Better performance of respiratory therapy manoeuvres May reduce postoperative pulmonary complications May reduce risk of DVT
Premedication Steroid hydrocortisone 100mg 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
Small dose of benzodiazepine acceptable Avoid H2 receptor antagonists
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 But watch for hemodynamic compromise Agent of choice in stable patient
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 – Laparoscopy)
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 Morphine, pethidine may cause histamine release
End of Anaesthesia
Any problems anticipated during reversal? Neostigmine may provoke bronchospasm
Atropine 1.2-1.8mg or glycopyrrolate 0.6mg before neostigmine
Extubation : deep or late, awake? Deep extubation may reduce chance of bronchospasm But in this case delayed extubation may be preferred May require a period of postoperative ventilation Awake, obeying commands Sustained head lift Adequate gas exchange
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)
Postoperative problems common with Laparoscopy Pain
PONV(40-75%)
Lung fns-diaph dysfn (residual pneumoperitoneum, phrenic n neuropraxia)
Oxygen therapy
Pain relief
More visceral than somatic pain
Higher IAP –more pain
LA infiltration- intraperitoneal, port site
Shoulder pain - careful evacuation of residual CO2
Preoperative NSAIDs
Intra & post operative opioids
Use multimodal analgesia
Postoperative pulmonary complications
Decreased FRC Large incision Postoperative pain Splinting of the diaphragm Decreased sputum clearance Atelectasis, Pneumonia Mechanical ventilation, prolonged ICU / hospital stay Delayed ambulation DVT, PE Cor pulmonale
Complications of laparoscopy
PONV Shoulder pain Surgical instrumentation - misplacement Verress
needle, concealed hge, stomach & bladder injury CVS; collapse, vasovagal, dysrhythmias, mc dysfn, gas
embolism Pulmonary; hypoxia, hypercapnia, endobronchial
intubation, pneumothorax, pneumonia, pneumomediastinum, s/c emphysema
Nerve injuries – improper positioning ICP ; IOP DVT
Subcutaneous emphysema; extraperitoneal insufflation – accidental/ intentional
Pneumomediastinum, pneumopericardium; Pneumothorax ; Capnothorax -Embryonic channels/ peritoneopleural ducts right side - Defects in diaphragm,weak points in oesophageal & aortic
hiatus - Pleural tears at level of GE junction left side - Rupture of emphysematous bullae Pneumothorax
Thank You