Topic Speaker

Oxygen cascade and CO2 Homeostasis Ramkumar V

Myasthenia Gravis Lokesh Kashyap
Anaesthesia for Scoliosis Surgery - Case Anjan Trikha
Lung isolation techniques and One lung S Rajeshwari
ventilation
Difficult airway (TMJ ankylosis and burn Ramkumar V
contracture) - Case
Anaesthetic considerations for Cleft lip/ Asha Tyagi
palate - Case
Child with hydrocephalus for VP shunt – Gyanendra P Singh
Case
Regional Anaesthesia and anticoagulation – Maj General. Rashmi Dutta
current guidelines
Obstructive Jaundice for Whipple’s surgery - Aruna Jain
Case
Cirrhosis for non-transplant surgery – Case Lalit Sehgal
Perioperative management of paediatric Dilip Shende
ophthalmic surgeries (Open globe injury and
Strabismus surgery) - Cases
Management of Tracheostomy – Case Vandana Talwar
Morbid obesity for bariatric surgery Aruna Parameswari
Perioperative management of COPD and Pankaj Kundra
Bronchial Asthma for laparoscopic surgery –
Case
Child with congenital heart disease for Hernia Usha Saha
surgery (VSD and TOF) – Case
Peripheral vascular disease with limb ischemia Anoop R Gogia
– anaesthetic considerations
Coronary Artery Disease for Hemicolectomy Akhil K Singh
- Case
Patient with permanent pacemaker/AICD for Vimi Rewari
non cardiac surgery - Case
Management of a patient with Intercostal Kapil Dev Soni
Chest Drain – Case
Coronary artery bypass – On pump vs Off Poonam Malhotra Kapoor
pump

 10/26/18

Oxygen Cascade Introduction

and Carbon Dioxide All fluids (gases as well as liquids)
Homeostasis move along pressure or concentration
gradients

Ramkumar Venkateswaran, MD
Chief Medical Officer : Mission Smile
Former Professor & Head, Kasturba Medical College, Manipal

41

Dudhsagar Waterfalls - Goa Why do we breathe?

Oxygen sustains life
Carbon dioxide - the end-product of
cellular metabolism needs to be
eliminated

39

Oxygen cascade Oxygen cascade

Steps (pressure or Journey of oxygen molecules from the
tension gradients) atmosphere to the mitochondrial factories
down which oxygen
moves from one
phase to another

37

1
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Air contains 21% oxygen Oxygen Cascade

At sea level with an ambient pressure of
760 mm Hg, the partial pressure exerted
by oxygen in dry air is:
PO 2 insp air dry = PB x 0.21

= 760 x 0.21

= 159 mm Hg
36 35

Air gets warmed and humidified Oxygen Cascade

Water vapour at 37℃ exerts a partial
pressure of 47 mm Hg

PO 2 insp air humid & warm = (PB - 47) x 0.21

= 713 x 0.21

= 149 mm Hg
34 33

The ideal alveolus O 2=150; CO 2=0

Ventilation and perfusion well matched (V/Q=1)

O 2=100
CO 2=40

O 2=40; CO 2=45

Normal VA/Q
32 31

2
 10/26/18

V/Q ratios and gas exchange The ideal alveolus

Ventilation and perfusion well matched (V/Q=1)
Lung V/Q ratio Mean Mean
region PAO 2 PACO 2 What is the effect of V/Q mismatch?
(mm Hg) (mm Hg)
Apex
Middle 1.0 100 40
Base
30 29

Spectrum of VA/Q ratios

V/Q ratios and gas exchange
O 2=150; CO 2=0

Lung V/Q ratio Mean Mean

region PAO 2 PACO 2
O 2=40 O 2=100 O 2=150 (mm Hg) (mm Hg)
CO 2=45 CO 2=40 CO 2=0 Apex 3.3 132 32
Middle 1.0 100 40
O 2=40; CO 2=45 Base 0.66 89 42
0 Normal VA/Q 27
8

Physiological shunts Physiological shunts

Blood returning from non-ideal alveoli Blood returning from non-ideal alveoli
Bronchial veins Bronchial veins
Thebesian veins Thebesian veins

2% to 5% of cardiac output

26 25

3
 10/26/18

Alveolar-arterial PO2 difference Oxygen Cascade

Results in a PaO2 of 100 mm Hg
and a PaCO2 of 40 mm Hg

24 23

Blood exiting the left ventricle What happens at the tissues?

Near-fully oxygenated blood distributed through aorta An average of 40 mm Hg oxygen tension
and its branches to tissues Jog Falls, Karnataka
drives oxygen into the tissues
Individual regional perfusions
constitute a spectrum (very Pasteur point of around 1 to 4 mm Hg at
richly perfused to very poorly the level of mitochondria
perfused) causing multiple
cascades in the
oxygen “waterfall”

21

Oxygen Cascade
Carbon dioxide
homeostasis

20 19

4
 10/26/18

What are the numbers? What are the numbers?

Average 70 kg adult produces Average 70 kg adult produces
around 200 mL of CO2 per minute around 200 mL of CO2 per minute
Total body stores of CO2 ….. Total body stores of CO2 …..
equivalent to 120 litres

18 17

“The CO2 Cascade”

“The CO2 Cascade”
Mitochondria

Cytoplasm Cytoplasm

Extracellular fluid

Blood Blood

“The CO2 Cascade” Carbon dioxide is carried in 3 forms

Form in which carried Percentage
Blood
Carbonic acid 8
Alveoli Bicarbonate 80
Carbamino compound 12
Atmospheric air

Blood
13

5
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Carbon dioxide is carried in 3 forms

As carbonic acid
Form in which carried Percentage
CO2 + H2O = H2CO3 [1]
Carbonic acid 8
Bicarbonate 80 H2CO3 = CO2 + H2O [2]
Carbamino compound 12
Carbonic anhydrase enzyme acts as a
Total CO2 of 45 to 55 mL/dL catalyst both ways

12 11

Carbonic anhydrase As bicarbonate

16 isoenzymes of CA in mammals CO2 + H2O = H2CO3
CA II In RBCs H2CO3 = H+ + HCO3-
CA IV Membrane-bound on
pulmonary capillaries

10 9

Fate of carbon dioxide in the blood

As bicarbonate
CO2 + H2O = H2CO3
H2CO3 = H+ + HCO3- RBC
by
HCO3- exits from RBC into the plasma in
exchange for Cl-
“Ping-pong mechanism” (Band 3 protein) Plasma

“Hamburger phenomenon or Chloride shift”

8

6
 10/26/18

Plasma

by by

Red blood cell

Carbon dioxide homeostasis

As carbamino compound
COCO
2 production
production
CO 2 binds to amino group (R-NH2) on 2

proteins Central
chemoreceptors
Small fraction to plasma proteins
whereas bulk of carbamino complex
formed with alpha and beta chains of
haemoglobin
Alveolar
ventilation
4

Oxygen Cascade “CO2 Cascade”

Haldane effect
Reduced haemoglobin at peripheral
tissues has 3.5 times the ability to bind
CO 2 as compared to oxyhaemoglobin
Oxygenation of haemoglobin at lungs has
the opposite action, helping to unload
CO 2 in the pulmonary capillaries
Blood
2 In summary.…. Thank you

7
 10/26/18

Myasthenia gravis
• “Myasthenia gravis” – grave
muscle weakness
• Autoimmune disease disorder of
Myasthenia Gravis Neuromuscular junction
• ↓ Postsynaptic AChRs and
Dr Lokesh Kashyap Antibodies to Ach receptors
• Fluctuating muscle weakness that
Professor
worsens with exertion, and
Department Of Anaesthesiology, improves with rest
Pain Medicine and Critical Care
All India Institute Of Medical Sciences

Demographics of MG Symptoms
• Incidence/Prevalence in USA: 10-20 /100,000
• Snarl Face
• Predominant age:
• Fluctuating weakness
Ages 20-40.
with periods of
Peak incidence in females – 3 rd & males in 5 - 6 th decades
remission
• Sex : • Worsens with exertion
Adults – F > M (3:2)
Children - 3:2
• Ocular, bulbar and
Peripheral weakness
Children - myasthenia + associated disease
Enlarged Thymus (70%) or Thymoma (10%)

Diagnosis Neostigmine/ Tensilon test

Neostigmine0.02mg.kg or Edrophonium 2 mg bolus i.v.
• Suspect it: Clinical S/S
ü Neostigmine/ Tensilon
test Improvement No change
• Electrical : NCS i i
ü RNST, Positive additional i.v.
• SFEMG,
• Immunological:
ü ACHR’s AB
• AntimusK Ab.
ü CT Thorax

1
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Electrodiagnostictesting Management of MG
Repetitive nerve stimulation test Single fibre electromyography

Symptomatic Immune directed

– Rapid ↓ of 15% • Selective recording of action management treatment
amplitude CMAP. potentials from 2 adjacent
AchE inhibitors, Long term treatment
– Single dose muscle fibres in same motor
edrophonium prevent unit presynaptic agents • Immunosuppressive agents
corticosteroids,azathioprine,
decremental response • Sensitivity - 92-100% Pyridostigmine
mycophenolate, cyclophosphamide
– Sensitivity – 75% • Confirmatory but not • Thymectomy
specific
Short term treatment
To treat Myasthenic crisis
IV immunoglobulins
Plasmapharesis

Anticholinesterase medication Immunosuppression

• First-line treatment: • Indications:

– Significantly symptomatic on
Pyridostigmine pyridostigmine
• Muscarinic symptoms limit – Symptomatic after initial
max dose response to pyridostigmine

• Treatment plan:
– Starting drug:
glucocorticoids/cyclosporin/t
acrolimus
– Poor responders/ side effect
to steroid :
• Azathioprine / mycophenolate
• Cyclosporin/tacrolimus

Plasmapheresis
• Plasma in blood is removed and replaced with Clinical classification (Osserman) 1971
replacement fluids I Ocular myasthenia — ocular muscles only
• Continuous-flow machines IA Peripheral muscles positive electromyogram for MG
– Remove whole blood from one IV site
– Simultaneous and continuous return of II Generalized myasthenia
IIA Mild - No respiratory involvement, slow progression
reconstituted elements through another IV site IIB Moderate –more severe progression
• Exchange one plasma volume - 3 hours -No respiratory involvement
• 5 exchages (3-4 L/exchange) over 10-14 days
III Acute fulminating myasthenia -
• Indications Rapid onset. Involvement of muscles of respiration.
– Preoperative preparation Progression within 6 months
– Treatment of myasthenic crisis/ acute exacerbations
– Bridge therapy IV Late severe myasthenia - 2 years after onset
– Periodically to maintain remission

2
 10/26/18

MGFA classsification Diseases Typically Associated With MG

• Diabetes
• Rheumatoid Arthritis
• Lupus
• Thyroid diseases.
• Demyelination CNS Disease
• Other Auto immune diseases

MGFA- Myasthenis Gravis Foundation of America

Annals of Thoracic Surgery, vol. 70, no. 1, pp. 327–334, 2000.

Anaesthetic Challenges Response to drugs: Summary

Concerns Drug Interactions DRUGS INTERACTIONS
NONDEPOLARIZING NM BLOCKERS INCREASED SENSTIVITY
• Co morbid conditions.. • Antibiotics
SUCCINYLCHOLINE RESISTANCE TO BLOCKADE AND DELAYED
• NMB agents- sensitivity. – Aminoglycosides: ONSET
• Sugammadex-reversal. – Quinolones INHALATIONAL AGENTS REDUCE NEUROMUSCULAR
• Lung Isolation. – Macrolides TRANSMISSION
• Position. • Anticonvulsants. INTRAVEINOUS AGENTS NO EFFECT
• Awake extubation/ Recovery. • Steroids. LOCAL ANESTTHETICS PROLONGED ACTION AND INCREASED
TOXICITY OF ESTER LINKED AGENTS WITH
• Crisis- Myasthenic/ Cholinergic • Beta-blocking agents:. ANTICHOLINESTERASE THERAPY &
• Postop Ventilation and pain • Local anesthetics agents PLASMAPHERESIS
management. • Magnesium ANTIBIOTICS NEUROMUSCULAR BLOCKADE INCREASES
WITH AMINOGLYCOSIDES, ERYTHROMYCIN
etc.

Open-> VATS-> Robotic Thymectomy Induction

IV/ Inhalational

Patient breathes O 2 and N 2 O

Record baseline NM responses

Muscle relaxant No muscle relaxant

Atracurium 1/10 th – Deepen with volatile agents,

1/20 th of usual dose airway blocks/ 4ml of 4%
lignocaine spray

Intubate Intubate

3
 10/26/18

da Vinci Robot surgical system

a three arm da Vinci® robot
surgical system

Console

Video
monitor

3D video imaging + set of telemanipulated flexible effector instruments

Surgical Management- 1 Surgeon at 2 Surgeon at

Thymectomy Console table side

• Indicated
• Introduces trocars &
– Patients positive for anti-AChR Ab Console triggers highly connects it to rob otic
– Patients with thymoma sensitive motion sensors arms
that transfer the surgeon’s • Changes rob otic
• Not done in movement to the tip of instrumen ts t hrough t he
– Anti MuSK Ab the instruments other ports
– Ocular MG
– Late onset MG (> 60 yrs)
– Age less than 16 yrs
• Benefits evolve over several years: In about 80%
patients

Points to Consider While Robotic

Surgical System is in Use
• Multi-institutional series four Major European
Centres
• 134 patients of thymoma were operated
• No changes in patients position on OR table
• left-sided (38%), once the robot has been docked
• right-sided (59.8%) or Campos JH: Curr Opin Anaesthesiol 2010; 23:1.
• bilateral (2.2%) robotic approach. • Protection of pressure points arms and legs
• Avoidance of stretching the arms
Robotic thymectomy is a technically feasible and J Cardiothoracic Vasc Anesth 2009; 23: 584.
safe procedure • Attention to crushing injuries by robotic arms
• Low complication rates & short hospital stay Campos JH: Minerva Anestesiol 2013; 79:1
More cases are necessary in order to consider this
as a standard approach.
Ann Cardiothoras Surg 2016 Jan ; 5; 18

4
 10/26/18

Endo Wrists Surgical instruments VATS Thymectomy

• Safer and easier dissection of vascular and

nervous structures than VATS- remote, fixed
and • difficult to reach areas of neck &
Provide several deg rees of motion- exceeds
mediastinum.
capacity of a surgeon’s hand in open surgery
• Left-sided
• Two degrees approach preferred-perfect
of axial rotation to replicate
human wrist-like
visualization of the movements.
aortic window & less
phrenic nerve injury

Minimal Invasive surgery:

Contralateral Capnothorax
CO2 capnothorax-Better visualization
• Insufflation started at low pr 4-5 mmHg
• Intrathoracic pressures not exceed 10–15 mmHg.
– Pr >25 mmHg-compromise venous return and cardiac compliance; • Inadequate vent
– Injury to the contralateral pleura- elevated
intrathoracic pressure in the contralateral hemithorax
• Ventilation difficult.
• Cardiovascular collapse or tension pneumothorax
• Subcutaneous emphysema. • Increase in PaCO2
• Gas Embolization.
• Fall in SpO2

Advantages of Robotic Thoracic surgery Disadvantages of Robotic Thoracic surgery

• Increasing surgical times.
• Shorter hospital length of stay.
• Cost and outcomes.
• Less pain.
• Lack of tactile sense.
• Less blood loss & need for transfusion
• Potential- conversion to open procedure.
• Minimal scarring.
•Better vision.
• Teamwork – More OT personnel
Failure of equipment.
•Better maneuverability of the tips
• Faster recovery. needed
of the instruments. • Minimal net revenue.
• Faster return to normal activities. Campos J. In Slinger P. Principles and Practice of Thoracic anaesthesia. 2011; 445
Campos JH: Anaesthesia International 2011; 19-22

Campos J. In Slinger P. Principles and Practice of Thoracic anaesthesia. 2011; 445

5
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Anaesthesiologists concern Anaesthesia

• Use of lung isolation technique- DLT/ Bronchial • Induction- Propofol.
blockers. Left DLT preferred • Intubation DLT / Bronchial blocker.
– Greater margin of safety. • Ensure that ETT is well secured.
– Faster & more reliable lung collapse. • Note change in position of tube during
• Use of Fibreoptic bronchoscopes. positioning and malplacement.
• Use of CO 2 insufflation. • Use of NM blockers under NMJ monitoring.
• FiO 2 0.5-1. use air+ Opiod+ Inhalation agent.
• V/Q impairement- surgical manipulation
• Reversal- use of LMA till recovery.
• Positioning – tube migrations & complications

Double-Lumen Tube (DLT) Left vs. Right DLTs

• ETT with 2 lumens (and 2 cuffs)

to allow lung isolation — Right-sided DLTs have special cuff
• Colorless tracheal lumen with with side-hole allowing RUL
large colorless tracheal cuff ventilation/deflation
– Use 10cc syringe
• Blue bronchial lumen with small h ttp ://www.ai c.cu h k.ed u .h k/web 8 /ETT%2 0 p i ctu res.h tm

— Left-sided DLTs do not have this

blue bronchial cuff
requirement and thus are used in the
– Use 3cc syringe
majority of cases requiring a DLT
• Termed “left” and “right” based L R
on location of bronchial lumen
h ttp ://www.fazzi n i .i t/en gl i sh /sch ed a.asp ?co d i ce=1 3 .9 9 3 0

www.accessmed i ci n e.ca

Monitoring Ventilation
• Electrocardiogram
Invasive BP • PEEP 5 cm H 2O to the ventilated lung.
Comorbid conditions
• Hemodynamics- NIBP Inexperienced team or new robot • CPAP 5 cm H 2O/ O2 insufflation of non-ventilated lung .
• Oxygenation- SpO2 , ABG • Peak inspiratory pressure <30 cm H2O.
• PaCO2 45 mmHg.
• Capnometry
• Pressure controlled/ Volume Control Ventilation.
• Temperature • FiO2 0.6-1.
• Recruitment maneuver.
• Neuromuscular Junction
Monitoring

6
 10/26/18

Postoperative Analgesia- Multimodal Extubation

• Systemic Analgesia
– PCA: Morphine/ Fentanyl • Expect a delay in awakening- Myasthenia
– Paracetamol IV
• Elevate head end of bed.
– NSAIDS- Diclofenac, Ketorolac
• Local Anesthetics/Nerve Blocks
• Watch for surgical emphysema.
– Intercostal Nerve Blocks
– Local Infiltration • Ensure return of neuromuscular function.
ü Essential to use NMT monitor (TOF)
– Paravertebral Block • Monitor in HDU/ ICU, CPAP
ü Ensure full recovery (TOF ratio 0.9) before
– Epidural Analgesia • Crisis.
terminating anaesthetics

Myasthenia Crisis Cholinergic crisis

Prediction of postoperative ventilation
• Duration of disease ≥ 6yrs: 12
- • COPD : 10
Edrophonium. • S/S: Bronchospasm, cyanosis,
• Shortness of breath – Colic, confusion,
– Fasciculation, seizures, ataxia,
• Pyridostigmine dose ≥ 750mg/day: 8
• Extreme muscle weakness
• General fatigueablility
, • VC < 2.9 litres: 4
– Bradycardia, hypertension

• Respiratory muscle paralysis

• Most severe 2 hr after last dose < 10 : Extubate after surgery
of anticholinesterase
• Precipitated by a progression in
• Rare if pyridostigmine dose
>12 : Require post op ventilation
severity of disease due to
<120 mg every three hours
- Infection
• T/t:
- Recent surgery
- Interruption of immuno- – Atropine 0.4-2mg or üNot a good predictor for VATS
suppresants. glycopyrrolate 0.2 to 1mg Leventhal SR, Orkin FK, Hirsch RA. Prediction of the need for post op mechanical
– Respiratory support ventilation in myasthenia gravis.Anesthesiology 1980;53:26

Other predictors of post op ventilation

• Preoperative bulbar symptoms
• History of myasthenic crisis
• Intraoperative blood loss > 1litre
• Serum AChR antibody >100 nmol/ml Two groups: Standard GA Vs
• > 20% decremental response in RNS LMA spontaneously ventilate.
• Spontaneous breathing patients.
Watanabe A, Watanabe T, ObamT, et al.. J ThoracCardiovascSurg.
2004;127:868-76 Less Incidence
Gritti P, Sgarzi M, Carrara B, et al. Acta Anaesthesiol Scand. 2012;56:66-75 • Postoperative Myasth Crisis
• Mechanical ventilation and
• Shorter hospital stay
J ThoracCardiovascSurg. 2018;155:1882-9.

7
10/26/18

8
 10/26/18

Thoracic anesthesia: Managing

surgery and anesthesia
Lung Isolation Techniques
and q Protection of the un-involved, healthy lung
One-lung Ventilation q Improving surgical access in open
Anesthetic management:
procedures:
Adequate depth, oxygenation, ventilation
q Esophagus
Rajeshwari Subramaniam Post-operative
q Sympathetic chain analgesia
All India Institute of Medical Sciences q Thoracic aorta
q Improving surgical access in minimally
invasive surgery:
AIIMS Anaesthesia Post Graduate q Lung isolation imperative
Assembly, Oct 18-21s t, 2018

What is ‘lung isolation?’

• Both lungs although morphologically
Selection and
insertion different function as one unit
Indications • Their anatomic delineation is helpful in
separating from one another if needed
• May be necessary when surgical position
endangers safety of the healthy lung, or
Types of tubes for other reasons
Management of OLV

Adult Pediatric

RATS
Indications: Absolute
ü Broncho-pleural fistula
• Prevention of
uPulmonary
ü Large unilateral lung cyst
contamination of ü Major bronchial injury
hemorrhage
healthy lung ü Severe lung contusion
uLung abscess
• Differential ventilation ü Post transplanted lung
uInfected lung cyst
ü Lung lavage
• Surgical VATS Collapsed lung
procedures § Video-assisted thoracoscopic
surgery (VATS)
§ Robotic-assisted thoracoscopic
surgery (RATS)
§ Robotic-assisted Cardiac surgery

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Options available for lung

Indications: Relative isolation
Bronchial • Gordon-
blockers • Arndt Green
• Cohen • Vellacott
High-priority Low-priority
Single-lumen • Fogarty • Fuji WRETT
q Upper lobectomy via Endobronchial tubes • EZ Mallinckrodt
thoracotomy
² Esophagectomy • Uniblocker Sheridan
q Pneumonectomy
² Middle and lower Double-lumen Rusch
q Thoracic aortic tubes(DLTs)
aneurysm repair
lobectomies Silbronco
² Thymectomy
q Lung volume • Sturtzbecher
reduction surgery
² Thoracic sympathectomy Tube with blocker
² Spine surgery • Univent
q Minimally invasive
cardiac surgery Pediatric tubes Marraro bilumen

Structure of a DLT
• Two lumina fused
together
• One ends as tracheal
lumen
Double-Lumen Tubes (DLTs) • Other continues as
bronchial lumen
• Tube has two curves
• Machine end : two
discrete lumina for
independent lung
ventilation

Types of DLTs Carlen’s tube

q Originally for bronchospirometry
• Historical: • Modern:
• Mallinckrodt q 7mm ID for male and 6 mm ID
• Carlens for females
• Bryce-Smith • Rusch
q Increased airway resistance
• Robertshaw • Portex
• Sheridan q Carinal hook
• All had Right and
Left prototypes • All are basic q Automatically enters L bronchus White
• All placed Robertshaw in
q Oval in cross section in
design horizontal plane
blind/rigid
R cuff slotted
bronchoscope

2
 10/26/18

Antero-posterior
Bryce-Smith tube lumina Robertshaw Tube (L and R)
²Lumina placed
antero-posteriorly

²No carinal hook

²Right-sided version:

²‘Bryce-Smith and Salt’

²D shaped lumina
R cuff slotted Lumina side-to-side, D shaped

Modern Robertshaw prototypes

Selecting the correct DLT

Rusch
Sheridan

Mallinckrodt Portex
Side Size

Why is a left-sided DLT better?

Tracheobronchial anatomy

• Improved ‘Margin of Safety’: A-B

3
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Use of L DLT for both R and L

surgery Sleeve resection of left bronchus

Indications of right DLT

• Distorted anatomy of entrance of LMB:
• Intra-bronchial lesion
• Descending thoracic aortic aneurysm
• Left lung transplantation Mallinckrodt

• Left sleeve resection

• Left pneumonectomy: ±

Sheridan

L bronchogenic ca
Modified R cuffs

4
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Selection of DLT size Sizes available

Right-sided DLT
(French)

T Diameter
Tracheal diameter (TD) for DLT
Cl-carina • TD measured at level of the clavicle on the
preoperative P-A chest radiograph
• Leads to use of a larger left-sided LDT

Height and DLT size: Brodsky Clavicle-carina distance

For each 10 cm é or ê in height,
depth of insertion é or ê by 1 cm. 0.75 × Cl to Car (cm)10 +0.112 × ht (cm) +6

• For a 170 cm man with clavicle-carina

distance of 8 cm:
• 1.75 x 8 +0.112 x 170 + 6= 39.04 cm

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Optimal size of DLT Checklist prior to DLT insertion

• A DLT:
• Airway assessment to
• that passes through the
glottis easily rule out difficulty
• navigates trachea • Fiberoptic system to
without resistance check position
• fits the bronchus with • Alternative technique
only a small air leak to visualize larynx
when its bronchial cuff
is deflated

Contraindications Techniques of insertion

• Difficult airway
• Small patient (child) Technique

• Airway lesion/tumor
• Critically ill patient
Under
on ventilator ‘Blind’ Vision
• RSI
• Post operative
ventilation
Macintosh C-MAC FOB
• Obese adults

DLT insertion using C-MAC Insertion with FOB

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Auscultation
Checking DLT position

Troubleshooting during Fiberoptic check

auscultation, (L) DLT

Maneuver Finding Interpretation

Clamping bronchial No air entry on R Tracheal lumen

lumen side also in L bronchus
Clamping bronchial Air entry on both Tube too much out
lumen sides
Clamping tracheal Air entry on both Bronchial cuff too
(R) lumen sides loose/tube out

Luminal diameters and FOB Troubleshooting with FOB

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Newer DLTs: The ‘Viva-sight’ Silbroncho DLT

• Made of silicone
• Retains shape,
softens
• Opaque walls
make FOB difficult
• Sizes: 33F, 35F,
37F and 39F
• Outer diameter of
bronchial lumen
larger

Silbroncho DLT
Tubes with bronchial blockers

q Easier to place
q Can achieve lobar blockade

Especially suitable for acutely angled left

bronchi

The Univent Tube

Stuertzbecher Tube and Blocker

Tracheal cuff

Blocker (7/9 cm)

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The Univent tube

• Sizes:
• 3.5, 4.5, 6, 6.5, 7, 7.5, 8,
8.5, 9
• 3.5 mm: 7.5-8.0 mm ED
• 4.5 mm: 8.5-9.0mm ED
• Cost!!!!! > $350 per tube

Indications for bronchial

blockers

• MMP III/IV
• Unexpected
1. Difficult Airway • Restricted
lung separation neck
mobility
• Segmental
• Morbid obesity
Bronchial blockers blockade
• Distorted
• Lung isolation
2. Intra operative in tracheobronchial
intubated
• Lung cyst
anatomy
• ICU
CCAMpatient
3. Pediatric lung • Thoracoscopic
isolation procedures

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Bronchial blockers Types

Advantages • Fogarty embolectomy catheter
Disadvantages
• Easy recognition of • Arndt blocker
anatomy
• Ventilation not possible for • Cohen Flexi-tip blocker
• Best device for difficult
collapsed lung
airways, children • Uni blocker
• Small channel for
• No damage to cuff suctioning
• Tube need not be
• EZ blocker
• High incidence of
changed for post
dislodgement
operative ventilation
• Conversion fro OLVà
• Lobar blockade possible DLVà OLV difficult

Bronchial blockers
Size
Age(years)
0-1 3
The Fogarty Catheter 1-2 3
2-4 3
4-6 4/5
6-8 4/5
8-10 4/5
10-12 5/6
>12 6
Fogarty Cohen Uni blocker Arndt
5 Fr catheter(1.6 mm)+2.2 mm FOB will fit in ETT 4.5

Fogarty placement Fogarty placement in children

• Can be internal or external to the tube
• Except 2 &3 Fr, all have a guidewire to 6 mo-2 yrs
provide desired angulation
• Positioning facilitated with FOB
• After inflation should be secured to ETT
• No channel for suction/CPAP/deflation
• Deflation is slow

2-8 yrs ODB + OD BB/ IDTT<.9

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 10/26/18

Adult Fogarty

• 7Fr (65cm)
• 9Fr (78 cm)
• Can be used for lung collapse/CPAP
application

Torque-control blocker Univent Torque control blocker Univent

• Wire mesh coated with polyurethane offers
torque control
• Shaft pre-designed as ‘hockey stick’ shape
• Central lumen has removable metallic
stylet
• High volume balloon accepts 8 ml air,
pressure < 30 mm Hg
• Caution while stapling

Arndt Wire-guided
Endobronchial Blocker (WEB) Arndt blocker: Technique

• 5, 7, 9 Fr independent blocker
• Has spherical/elliptical balloon cuffs
• Spherical (R) and elliptical (L)
• Inner lumen has nylon wire projecting as
loop
• For right side can be introduced free of
wire loop

11
 10/26/18

Advantages of the Arndt blocker Cohen Flexi-tip blocker

• Turning wheel allows
deployment of pre-angled
• Critically ill intubated patients who require tip
OLV • High volume low pressure
cuff
• Selective lobar blockade • Useful for selective
• Difficult airways and OLV (oral/ nasal) bronchial blockade

• Tracheostomised patients
• Robotic surgery
• CPAP may be applied

EZ Blocker Double lumen tubes

• End split into a ‘Y’ Advantages Disadvantages
• Limbs 4 cm long
• Color coded cuffs • Difficulty in
• Large lumen
• Shafts and ends have a selecting size
facilitates
hollow channel • More difficult to
suctioning
• Stable-useful in prone place
• Best device to
position • Potential damage
protect from soiling
• Tip of ETT should be at to tracheal cuff
• Conversion fro 2-1
least 4 cm above carina • Rare major
lung and back
• Rapid intubation tracheobronchial
easy, reliable
injuries

Bronchial blockers Comparison of blockers

Advantages Disadvantages
• Recognition of
bronchial anatomy • Dislodgement
• Selective blockade • Seal not fail-safe
feasible • Suction/CPAP
• Best for difficult difficult
airway • Conversion from
• Does not need to 2-1 and 1-2
be changed difficult
• Cuff damage rare

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Steps
• Choose appropriate technique of lung
isolation, confirm with FOB
Managing one-lung ventilation • Ventilate operated lung with 100% O2
• Easier collapse due to absorption atelectasis
(OLV)
• Arterial line for intermittent ABG
• Dedicated suction catheters for each tube
lumen
• Provision for extra oxygen flowmeter
• Start OLV 5-15 minutes before thoracotomy*

Factors related to é or ê
Problems with OLV hypoxemia during OLV
• Hypoxemia • é Hypoxemia • ê Hypoxemia
• Incidence ≈ 5-10% ² Supine position Ø Lateral/prone position
• Few case series: 1% ² Volume-controlled Ø Pressure-controlled
• VATS/ mediastinal procedures: 8% ventilation ventilation
• Electronic charting reveals éé incidence ² R lung surgery Ø L lung surgery
² Normal FEV 1 Ø ê FEV 1 **
• Non/ partial collapse of operated lung ² Normal PaO2 with TLV Ø êPaO2 with TLV
• High airway pressures ² Peripheral lesions Ø Large, more central lesions
² éé PEEP to dependent needing
• Air trapping
lung lobectomy/pneumonectomy
• Acute lung injury ² Large difference between Ø Capnometry minimally
TLV and OLV and different
capnometry

Effect of position on oxygenation Effect of location of lesion

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Reducing intra operative Managing OLV

hypoxemia
• Optimize lung function pre operatively
• Ensure patient not anemic
• Select correct technique of lung isolation
• Will patient tolerate whole lung isolation?
• Pre operative PFT
• Location of lesion
• Will lobar blockade be sufficient?
• Epidural dexmedetomidine
• TIVA

Ventilation strategy for

dependent lung
² Propensity for hypoxemia
- Compromised from all sides
- Atelectasis, alveolar collapseà HPV
- Diversion of blood to collapsed lung
- Strategy to maintain lung volume
² Aim for moderate é in lung volume
- High volumeà shunting of blood
- Lowà atelectasis
² Avoidance of lung injury by poor
strategy
Suggested strategy
• Tidal volume:
• Large volumes injurious, do not é oxygenation
• Small volumes (6-8ml/kg)à hypoxemia
• Must be augmented with PEEP 4-6 cm H2O
Low TV
• Caution with(6-8 ml/kg) with moderate (4-6
PEEP:
cm H2O) PEEP
• If auto-PEEP being generated, will not help
• Useful only if atelectasis is the cause
• Patients with high/ normal FEV1 likely to benefit

Recognize air-
trapping Changes in PIP and EtCO2
‘Stacking’à Intrinsic
PEEPà Shunt

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Intra-operative hypoxemia Strategy

• Notify surgeon
• é FiO2
• If no effect, temporarily switch to two-lung
ventilation
u Dependent lung: u Non ventilated lung:
• Assess tube position with FOB
u Divert perfusion u Minimize perfusion
• Suction out ventilated lung u Maximize u CPAP
• Rule out bronchospasm in ventilated lung ventilationàPEEP

Intra operative hypoxemia:

dependent lung Approach to non-dependent lung
• CPAP
• Airway recruitment maneuvers:
• 3-5 cm H2 O
• Barotrauma • Can be provided at 200-
• Cytokine release and lung injury 500 ml O2 flow through
auxiliary flowmeter with a
• Hemodynamic effects catheter, till lung just
inflates
• PEEP 4-6 cm • However may still bother
the surgeon
• ê PVR in dependent lung • IV Almitrine ê
• NO (5-10 ppm) perfusion(pulmonary
vasoconstrictor)
• Epoprostanol
• TIVA

Modifications of CPAP Lobar insufflation of oxygen

• Selective lobar insufflation

• Intermittent small-volume oxygen
insufflation
• Compression of non-operated lung
• THRIVE

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Algorithm for hypoxemia

Intermittent insufflation

Take-home points
• One-lung ventilation is a planned
procedure
• Choice of correct tube important
• Patient contra indications to be kept in Thank you!!!
mind
• Airway should not be jeopardized
• Hypoxemia can occur in 5-10% of patients

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Temporomandibular Points for discussion

joint ankylosis ❈ What are the important clinical findings?

Ramkumar Venkateswaran, Manipal

TMJ ankylosis TMJ ankylosis

TMJ ankylosis Points for discussion

❈ What are the important clinical findings?
❈ What are the anaesthetic concerns specific to age?
❈ What airway options are available?
❈ Outline an anaesthetic plan
❈ Do we need an extubation strategy?

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 10/26/18

Any other questions related to Burns contracture

TMJ ankylosis?

Ramkumar Venkateswaran, Manipal

Points for discussion Burns contracture

❈ What is the extent of burns?
❈ Has it compromised the airway?
❈ Evaluate the AP and lateral profiles of the face

Burns contracture Burns contracture

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Points for discussion Any other questions related to burns

❈ What is the extent of burns? related to burns contracture?
❈ Has it compromised the airway?
❈ Evaluate the AP and lateral profiles of the face
❈ Describe anaesthetic options available
❈ Are there any concerns of blood loss?

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 10/26/18

Child with Hydrocephalus for Ventriculo-Peritoneal Shunt

Child with Hydrocephalus for üChild

VentriculoPeritoneal Shunt üHydrocephalus Anaesthesia

üVentriculo-Peritoneal (VP) Shunt
Dr G P Singh
Associate Professor
Department of Neuroanaesthesiology & Critical Care
Neurosciences Centre
All India Institute of Medical Sciences, New Delhi

Anaesthetic Management of Child posted for

Hydrocephalus
VP Shunt surgery
Condition in which there is an accumulation of CSF within the brain
• Preoperative Assessment
Incidence: 0.3 – 1.5 / 100 live births in USA
• Preparation – Equipment and Monitoring Occurs in all age groups

• Intraoperative- Induction, Maintenance and Recovery Causes: Congenital (aqueductal stenosis, neural defects, arachnoid cysts, Dandy-

Walker syndrome, Arnold-Chiari malformation etc)

• Post Operative care including Pain management Acquired (CNS infections, meningitis, brain tumours, head trauma,
intracranial haemorrhage etc)

Hydrocephalus Hydrocephalus
• Mechanism: ↑Secretion
Types: Non-communicating or Obstructive HCP (most common)

Obstruction to flow Communicating or Non obstructive HCP

↓Absorption
Normal Pressure HCP (intermittent ↑ ICP)
Hydrocephalus Rise in ICP Hydrocephalus ex vacuo also refers to enlargement of cerebral
ventricles and sub-arachnoid spaces (no ↑ ICP)
Normal ICP range: Term Infants 1.5-6 mmHg eg: Post traumatic, schizophrenia
Children 3-7 mmHg (Compensatory enlargement of the CSF-spaces in response to brain parenchyma loss)
Adults 7-15 mmHg

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Hydrocephalus
Investigations: CT Scan/ MRI
Diagnosis
• Symptoms and Signs: Infants/children may present with vague symptoms/signs
üHeadache
üNausea/Vomiting
üIrritability Dilated Ventricles
üPoor feeding
üLethargy
üIncreased head circumference
üExpanding sutures or bulging fontanelles
üSunset sign (“sundowning” of the eyes)
üLower motor deficit
üSigns of ↑ ICP : Cushing’s response (bradycardia, hypertension)
Papilloedema, Pupillary changes

Mickey Mouse sign Hydrocephalus

Monro-Kellie Doctrine
Brain matter + Blood + CSF = Volume Constant

INITIALLY ↑ in vol of one will be compensated by ↓ of other

Later ↑ ICP

CPP = MAP – ICP

↑ ICP ↓ CPP ↓ Oxygenation Ischemia

Hydrocephalus Hydrocephalus
Treatment: Shunting of CSF
• Endoscopic Third Ventriculostomy

• Shunt surgery: Proximal end in the ventricle of Brain & Distal end at site where CSF is absorbed

Types- Ventriculo-peritoneal (VP Shunt)

Ventriculo- atrial
Ventriculo-pleural

• Shunts Classification: . Low pressure shunt (0-5, 8-12)

• Medium pressure (5-10, 12-16)

• High pressure (> 10, 16-20)

• Programmable shunts (adjustable pressure)

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Anaesthesia for VP Shunt

VP shunt surgery
• Pre-operative assessment:
• Routine PAC
•Elective - Chronically raised ICP Current and Past medical history, Allergies
Previous H/O anaesthesia exposure & problems if any
•Emergency – Acute rise in ICP Current medications (anticonvulsants, diuretics, acetazolamide)
Co-morbities: High possibility of congenital CVS
(coning, coma, respiratory arrest, death) Respiratory system , recurrent resp. Infection
Neurological dysfunction
Through examination: Airway, CVS, Resp, Neurological (consciousness)
Volume status (Vomiting/ dehydration)
Last oral intake

Anaesthesia for VP Shunt Anaesthesia for VP Shunt

Investigation: • Intraoperative Monitoring:
• Hb and Clotting parameters
ØStandard Monitoring
• Urea & Electrolytes (vomiting, dehydration)
ECG, SpO2, NIBP
• ABG, X-ray chest (pulmonary pathology)
EtCO2, EtAA, FiO2
• Others as per the co-morbidities & condition of patient
Urine Output, Temp.
Ø Others (If co-morbidities)
Premedication: Avoid sedatives if features of raised ICP
Anxiety- Midazolam (under observation only)
Resp depression, hypoventilation, ↑ CO2 ↑ ICP

Anaesthesia for VP Shunt

Anaesthesia for VP Shunt
• Induction of Anaesthesia:
Goal: Avoid acute Rise in ICP and Fall in CPP • Analgesic: Short acting opioids (fentanyl, remifentanil)
ü Prevent hypercarbia • Muscle relaxants: NDMRs preferable
ü Prevent Hypotension
Emergency RSI: Sch can be used

Airway: Secured with ETT (proper fixation)

Anaesthetic Agents: Intravenous (except Ketamine)
Inhalational (Migration of tube is a concerns in children/infant)
(IV agents better than IH in raised ICP features) Eyes: Closed and taped

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Anaesthesia for VP Shunt

Anaesthesia for VP Shunt
• Airway difficult (large head size)

• Roll below the shoulders

• Head beyond the edge of table
supported be assistant

• Intubation in Lateral

Anaesthesia for VP Shunt Anaesthesia for VP Shunt

• Positioning: Maintenance of Anaesthesia: (Balanced anaesthesia technique)
- Supine Goal – Avoid fall in BP & CPP and rise in ICP
- Neck turned to opposite side • Inhalational agents not more than 1.5 MAC (Iso/Sevo/Des)
(can increase ICP)
- Roll below the shoulder to or IV agents (propofol)

facilitate tunnelling of the shunt (N2O increase CBF and thus CBV- Not recommended)
• Short acting Opioids (fentanyl/ ramifentanil)
Always check ETT, after positioning • NDMRs (vec/ roc/ atra/ cis-atra)
Cover the patient as much as possible

Anaesthesia for VP Shunt Anaesthesia for VP Shunt

Tunnelling of Shunt catheter: Increase HR & ICP • Fluid Management: Goal- Maintain CPP
• Increase Depth of Anaesthesia or (Iso-volemia, iso-osmolarity, iso-oncotic)
Normal saline commonly used
• Additional doses of Opioids
Dextrose containing fluids avoided

• Premature infants: Avoid hypo/hyper glycaemia

Temperature: Large area exposed hypothermia
Monitor glucose (dextrose if indicated)
(warm fluids, covers as much possible, warming devices)

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Anaesthesia for VP Shunt Anaesthesia for VP Shunt

• Extubation: Preoperative status Postoperative Care:
Intraoperative course
Post Operative Pain- Local infiltration + Paracetamol (IV or PR)
Uneventful surgery Reversal and Extubation Opioids (under observation only)
Post operative Monitoring-
Goal : Rapid recovery and Early Neurological examination Close monitoring for hemodynamics and other vitals
Some preterm infants- apnoea (respiratory support)

Take Home Message Take Home Message

• Proper Pre-op assessment
• Prevent hypothermia
Anticipation of problems and preparedness to handle
• Maintain volume, electrolytes and glucose levels
Identify signs of raised ICP
Difficult airway • Early recovery and extubation (if possible)

Associated Co-morbidites • Monitor Vitals and Pain control in postoperative period

• Avoid sedation if possible or give under observation only • Neurological examination (close observation)
• Goal: Maintain CPP (avoid rise in ICP or fall in MAP), avoid hypercarbia, hypoxia
• Intraoperative: Skin incision/ Tunnelling - Attenuation of symp. response

Thank You

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 10/26/18

Maj Gen (Prof ) Rashmi Datta, VSM

MD (Anaes), DNB (Gen. Med), DNB (Aviation Med), FICA
Consultant, Anaesthesia & Critical Care

Director & Commandant

Command Hospital, Chandimandir

Types of Antithrombotic Drugs Types of Antithrombotic Drugs …

— Both prevent clots from forming and growing: — Anticoagulants -
— Anticoagulants – — Oral:
— Inhibit the initiation & progress of coagulation — Vitamin K antagonists – Warfarin , Phenprocoumon
— Inhibits fibrin-clot formation & propagation & Dicumarol
— Non-vitamin K antagonist oral anticoagulants

— Antiplatelet agents – — Direct thrombin inhibitor - Dabigatran

— Direct factor Xa inhibitors

— Prevent platelet adhesion, activation, & aggregation
— Rivaroxaban, Apixaban, Edoxaban, Betrixaban

— Parentral:
— Unfractionated heparin & LMWH

— Direct factor Xa inhibitors

— Fondaparinux

— Direct thrombin inhibitors

Types of Antithrombotic Drugs

— Antiplatelet agents - prevent platelets adhesion,
activation & aggregation
— Aspirin
— NSAIDS The major complication related to
— COX-2 Inhibitors
anticoagulation is bleeding
— Thienopyridine Derivatives
— Platelet GP IIb/IIIa inhibitors

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Factors that increase risk of a major

Major Bleeding Sites bleed

— Intraspinal — Intensity of anticoagulant effect

— Intracranial — Increased age
— Intraocular — Female gender
— Retroperitoneal — Use of aspirin
— Mediastinal — History of Gastrointestional bleed
— Duration of treatment

Epidural Hematoma
Formation Epidural Space vs Intrathecal Space
— Epidural space is richly supplied with a venous
plexus
— Due to spontaneous bleed
— Due to trauma induced by a needle — Area around the spinal cord is
fixed. Bleeding results in
compression, ischemia, nerve
trauma, and paralysis

— Bleeding into intrathecal space

is diluted by the CSF(usually less
devastating)

Incidence of Epidural Hematoma Risk Factors for the Development of

Formation Epidural Hematoma
— Epidural anesthesia: 1:150,000 to 1:190,000 — Anatomic abnormalities of the SC or vertebral
column

— Spinal anesthesia: 1:220,000

— Epidural anesthesia & anticoagulants
administered during surgery: 33:100,000
— Spinal anesthesia & anticoagulants
administered during surgery: 1:100,000
— Vascular abnormalities
— Pathologic/medicati on induced alterations in
homeostasis
— Alcohol abuse
— Chronic renal insufficiency
— Difficult and/or traumatic needle placement
— Epidural catheter removal

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Signs and Symptoms of an Epidural

Hematoma Diagnostic Testing
— Low back pain (sharp and irradiating) — MRI (preferred)
— Sensory and motor loss (numbness and — CT scan (may miss small hematomas)
tingling/motor weakness long after block should — Myelogram
have abated)
— Bowel and/or bladder dysfunction
— Paraplegia

Treatment and Outcome Factors Affecting Recovery

— Must be treated within 8-12 h of onset of — Size and location of the hematoma
symptoms
— Speed of hematoma development
— Emergency decompressive laminectomy with
hematoma evacuation — Severity and nature of pre-existing neurological
problems
— Outcome is generally poor

Warfarin
— Actions:
— Inhibits Vit K epoxide reductase
— Interfers with carboxylation of Vit K–dependent
clotting factors (VII, IX, X, and thrombin)
— Inhibits anticoagulant proteins C & S
— Metabolized by C-P450 enzymes à interaction with a
broad range of foods and drugs

3
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Warfarin Warfarin…
— Effect last for several days: — Half-life:
— Complicates exact dosing
— F- VII 6–8 h
— Regular monitoring necessary PT/INR — Anticoagulant protein C 6–7 h
— F- II 50 h
— F- X 4–5 days
PTT

Raised PTT + Normal INR — INR is unpredictable during initial stages as

H/O Bleeding prolongation is due to:
— Reduced F- VII & Protein C
Yes No
— Washout of existing clotting factors
F VIII F-XII
F IX Prekalikrein
F XI High-mol-wt kininogen

Warfarin… Warfarin…ASRA Recommendations

— Full effect of Warfarin — INR value of <1.4 acceptable for the performance of
— 2-5 mg PO qDay – 4-5 days NAB
— 10 mg PO - 4-5 days — Excellent perioperative hemostasis when the INR
value was ≤1.5
— 15 mg warfarin x 2–3 days -48–72 h
— Reversal: — At INR values of 1.5–2.0:
— Conc of F-II 74%–82% of baseline
— FFP + Vit K
— Conc of F-VII levels 27%–54% of baseline
— Emergency - 3-factor or 4-factor Plasma Complex
Concentrates
— Activities of 40% are considered adequate for
— On discontinuation: normal hemostasis in major surgery

— 4–6 days – synthesis of new biologically active Vit

K factors

Warfarin…ASRA Recommendations
Warfarin…ASRA
Chronic Oral Warfarin Therapy Recommendations
— Stop if — Pts neurologic status should be checked routinely
— Mean daily dose > 5 mg od — During epidural analgesic infusion
— INR >3 — 24 h after catheter has been removed
— Dose reduced for pts likely to have an enhanced
response to the drug, esp the elderly — Dilute concentrations of LA should be utilized to
— Concurrent use of other medications increases the minimize the degree of sensory and motor blockade.
risk of bleeding complications without affecting the
INR An INR of 1.4, in the absence of easy bruisability & normal liver
— Aspirin function is acceptable before injection in pts planned for NAB

— NSAIDs INR should be checked if the pt took warfarin >24 h earlier

— Heparins
INR should be normal 5 days after warfarin is stopped before a NAB

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Dabigatran Dabigatran…
— Onset of anti-coag effect:
— Selective & Direct thrombin inhibitor — 1.5-3 h
— Half-life:
— 14–17 h
— ESRD – 14-28 h
Direct thrombin — Reversal:
inhibitor
— Activated charcoal –within 2 h of ingestion
— Dialysis - speeds drug elimination
— Plasma Complex Concentrates
— 3 (F- II, IX, & X) clotting factors
— 4 (F- II, VII, IX, & X) clotting factors
— Idarucizumab, binds with free & thrombin-boun d
dabigatran, recently approved by the FDA

Rivaroxaban & Apixaban

Dabigatran…
— Monitoring: — Selective & Direct F-Xa inhibitor
— Ecarin clotting time - directly measures thrombin
generation
— Dilute Thrombin time/thrombin clotting time
— aPTT - but the relationship is linear Direct F-Xa
— PT is the least sensitive test inhibition

Dabigatran is primarily dependent on the kidneys for elimination, & half-life

is doubled in patients with kidney disease

A longer interval between stoppage of the drug and neuraxial procedure,

probably 6 days, is recommended in these patients

Rivaroxaban
Apixaban
— Onset of anti-coag effect: — Onset of anti-coag effect:
— 2.5-4 h — 1-2 h

— Half-life: — Half-life:
— 11-13 h
— 6-9 h
— ESRD – 11-13 h
— ESRD – 11-13 h — Monitoring:
— Monitoring: — PT not sensitive
— PT but specifically calibrated for rivaroxaban — Anti-Xa assay

— Anti-Xa assay
— Reversal:
— Andexanet - recombinant modified human F- Xa
— Reversal: decoy protein that binds & sequesters F- Xa
— Activated charcoal - given within 8 h after intake inhibitors
— 4-factor PCC — Not yet clinically available in USA

5
 10/26/18

Newer ACs…ASRA
Recommendations ASRA Recommendations…
Recommended time intervals beforeor after neuraxial procedure &
— 8 h – Time for the clot to stabilize - time to peak epidural catheter for the new AC
onset of the drug European
Scandinavian
Drug ½ Life Guidelines 5 ½ lives
— 4–6 half- lives between stoppage of the drug & NA Guidelines
injection is recommended until there is more 12-17h Contraindic 85h (4d)
experience with these agents Dabigatran
ated per Data not
28 hours (renal manufactur available 6d (renal
— 6-8h - time to peak effect of drug is recommended disease) er patients)
before drug is resumed after catheter removal 9-13h
Rivaroxaban 22-26h 18h 65h (3d)
— 24-h interval probably safest
15.2 +/-8.5h Data not
Apixaban 26-30h 75h (3-4d)
Drug EuropeanGuidelines Scandinavian available
Guidelines
At 5 half-lives, 96.8% of the drug is eliminated. The upper limit of
Rivaroxaban 4-6h 6h
the half-life was used to calculate the 5 half-lives of the drug
Dabigatran 6h 6h
Apixaban 4-6h 6h The European and Scandinavian guidelines used a 2 half-life
interval when data is available.

Heparin

Binds with
antithrombinà
accelerates its ability
to inactivate thrombin
factors Xaand IXa

PF-4

vWF

Heparin… Heparin…
— Onset of anti-coag effect: — Neutralized by:
— S/C -1–2 h — Protamine
— IV – PTT inc 2–4 x base- line level 5 min after IV injection
— Assoc with :
of 10,000 units of heparin
— Immunologic thrombocytopenia
— Half-life:
— Immune-mediate d thrombosis.
— 1.5–2 h
— Lasts for 4-6 h
— Monitoring:
— aPTT >1.5-2 x N
— Whole blood CT elevated ~ 2.5 -3 x N
— Heparin level of 0.2–0.4 U/mL
— Not monitored if SC

6
 10/26/18

LMWH Enoxaparin (Lovenox)

Dalteparin (Fragmin)
LMWH…
Tinzaparin (Innohep) — Onset of anti-coag effect:
— S/C -3–6 h
— IV – 2-4 h
Binds with — Half-life:
antithrombinà
accelerates its ability — 2-4 x Heparin
to inactivate thrombin
factors Xaand IXa
— Monitoring:
— Not req
— Except in
— Pts with renal insufficiency
— < 50 kg or >80 kg

Heparin &
LMWH… LMWH…Recommendations
— Adv of LMWH over UFH: — NA procedures avoided in patients with known
— Higher and more predictable bioavailability& coagulopathy
anticoagulant effect after SC adm
— Longer biological half-life — Surgery delayed 24 h in patients with a
— resistance to inhibition by activated platelets traumatic tap
— Monitoring of response is not required
— Dose adjustment for wt not necessary
— Time from NA procedure to systemic
— Dose-dependen t antithrombotic effect can be heparinization should be > 1 h
accurately assessed by anti-Xa activity levels
— Lower incidence of HIT
— Heparinization & reversal should be monitored &
controlled tightly.

Heparin & LMWH…

ASRA Recommendations
Recommendations Prior to Catheter After Catheter
Drug Half-life Remarks
Placement removal
— Epidural catheter should be removed when Catheter
normal coagulation is restored & pt monitored PTT < 40 can be safely
closely for signs of spinal hematoma Heparin IV Usual hold time 2-4 h 1-2 h removed if
is 4 h last dose
given >6 h
— NA procedures can be performed in pts on If given upto
twice-daily SC heparin LMWH 4 days prior
4 h do platelet
SC
count
— Due to lack of adequate data, NA procedures If prophylactic
dose of LMWH, If therapeutic
not be performed in patients on thrice-daily SC 12-h interval dose of LMWH,
heparin recommended a 24-h interval
before NA appropriate
procedure

7
 10/26/18

Fondaparinux Fondaparinux…
— Adv of fondaparinux over
— LMWH or UFH
— selective for factor Xa
Binds with — Risk of HIT is lower as no effect on PF4
antithrombinà — Caution in pts with renal dysfunction
accelerates its ability
to inactivate thrombin — Direct factor Xa inhibitors
factors Xa — Effects mediated indirectly through antithrombin III

ASRA Recommendations
Prior to After
Drug Catheter Catheter Half-life Remarks
Placement removal
Fondaparinux 72 h 12 h 17-21 h -

Thrombin Inhibitors Thrombin Inhibitors

— Recombinant hirudin derivatives inhibit both free &
clot-bound thrombin ASRA Recommendations
Prior to After
— Desirudin
Drug Catheter Catheter Half-life Remarks
— Lepirudin Placement removal
— Bivalirudin Longer in
pts with
— Argatroban, an l-arginine derivative, has a similar Argatroban
Wait till
2 h 40-50 min renal
mechanism of action aPTT <40
impairmen
— Reversal: ts
No statement regarding risk assessment and
— Nil
Lepirudin patient management made

Role of Platelets
— Platelets form the clot:
— Activation – Thrombinà ADP
— Adhesion - Deposition of platelets on
subendothelial matrix
— Aggregation - Cohesion of platelets
— Secretion -Release of platelet granule proteins
— Procoagulant activity -Enhancement of thrombin
generation

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 10/26/18

Platelet Activation …Stimuli Platelet Activation…

— Thrombin cleaves the external domain of G protein-
Weak Strong coupled Protease-Activated Receptors esp PAR-1 &
PAR-4 to initiate trans-membrane signaling
— ADP — Thrombin
— Epinephrine — Collagen

— Specific receptors also

for
— Epinephrine
— Thromboxane A2
— Collagen

— ADP Receptor P2Y1 : G q-coupled receptor signals

— P2Y1 : G q-coupled receptor signals through
through PL Cβ & PK C à platelet shape change &
phospholipase Cβ & protein kinase C à platelet shape
transient aggregation
change & transient aggregation
— ADP Receptor P2Y12 : G i-coupled receptor signals by
— P2Y12 : G i-coupled receptor signals by inhibiting
inhibiting membrane-boun d AC à
membrane-boun d AC à
— Decrease intracellular cAMP levels,
— Decrease intracellular cAMP levels,
— Activating phosphoinositide 3-kinase
— Activating phosphoinositide 3-kinase

Platelet Activation…Adhesion Platelet Activation…Aggregation

— Mediated — Involves binding of
by binding of fibrinogen to GPIIb-IIIa
platelet surface complex
receptor GP — Only stimulated
— GP Ib-IX-V platelets as GP Iib-IIIa
complex to the undergoes a
adhesive conformational change
protein (vWF)
— Converted from a low-
in
subendothelial affinity fibrinogen
matrix receptor to a high-
— GP Ic-IIa to affinity receptor in a
collagen fibrils process termed inside- — Fibrinogen serves to
in the matrix out signaling bridge activated
platelets

9
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Platelet Activation…Secretion AntiPlatelet Drugs

— From platelet granules — COX Inhibitors
— ADP and serotonin — Acetylsalicylic acid (aspirin)
— Stimulation & recruitment of additional — COX-2 Inhibitors
platelets — Phosphodiesterase Inhibitors
— Adhesive proteins fibronectin & thrombospondin — Dipyridamole

— Reinforcement & stabilization of platelet — ADP / P2Y12 receptor antagonists

aggregates — Clopidogrel
— Factor V — Prasugrel
— Ticagrelor
— Thromboxane
— Cangrelor - recently been licensed
— Vasoconstriction
— Glycoprotein IIb/IIIa inhibitors
— Growth factors (PDGF) à
— Abciximab
— Proliferation of smooth muscle cells
— Triofiban
— Tissue repair — Eptifibatide

Ticlodipine
Clopidogril
Pasugrel; Elinogrel
Tigagrelor; Cangrelor

Aspirin

Abciximab
Eptifibatide
Tirofiban

Guidelines…Aspirin and NSAIDS Guidelines…COX 2 Inhibitors

— Either medication alone does not increase risk
— Compared with aspirin or NSAIDs, the effect of COX-
— Need to scrutinize dosages, duration of therapy &
2 inhibitors on platelet aggregation & bleeding times
concomitant medications that may affect
coagulation are not different from placebo
— Look for:
— History of easy bruisability — Platelet properties of these drugs make them ideal
— History of excessive bleeding for perioperative use when NA blocks are planned :
— Female gender — Rofecoxib & valdecoxib withdrawn from market –
CVS effects
— Increased age
— No wholly accepted laboratory tests — Celecoxib dosages lower than previously
recommended
— Normal BT does not indicate normal homeostasis
— Abnormal BT does not necessarily indicate abnormal
homeostasis

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Guidelines…ADP Antagonists Guidelines…ADP Antagonists

— Clopidogrel:
— Stop prior to a neuraxial block
— Restart 6–24 h after NA procedure or catheter
— Ticlopidine for 14 days.
removal
— Clopidogrel for 7 days
— Scandinavian guidelines: Restart drugs at the
— Prasugrel for 7 days
time of catheter removal
— Ticagrelor for 5 days
— Prasugrel & Ticagrelor:
— European Society of Anaesthesiology guidelines:
— If a spinal / epidural must be performed, a test
6 h between removal of epidural catheter &
of platelet function is recommended to ensure
resumption
that the residual platelet inhibition is gone or
negligible. — Other reviews: Caution in restarting
— Rapid effect
— There is no accepted laboratory tests for these — Potent anti-platelet inhibition
medications. — 24-h interval more appropriate

Guidelines… GP IIb/IIIa inhibitors

— Ivy bleeding time was considered to be a reliable predictor of abnormal
— No NAB should be undertaken until platelet function bleeding in patients receiving antiplatelet drugs.
— post-aspirin bleeding time is not a reliable indicator of platelet function
is normal
— Special platelet function assays are now available to monitor platelet
aggregation and degranulation. The platelet function analyzer (PFA) is a test of
in vitro platelet function. It is a good screening test for von Willebrand disease
and monitors the effect of desmopressin administration. The PFA is prolonged
— GP IIb/IIIa inhibitors are contraindicated within 4 after antiplatelet therapy. 68 Unfortunately, the PFA-100 is not a sensitive test for
monitoring the antiplatelet function of the P2Y12 inhibitors clopidogrel,
weeks of surgery prasugrel, and ticagrelor. How- ever, the PFA-200, a recent updateof the PFA-
100, 69 appears to be sensitive to the effects of the P2Y12 inhibitors. However,
point-of-care studies on this new PFA test are still lacking.
— Newer tests that monitor P2Y12 receptor activity include the vasodilator-
— If one is received postoperatively, after a neuraxial stimulated phosphoprotein (VASP) assay, 70,71 the VerifyNow assay,72 the
multiple-platelet aggregometry test (Multiplate), 73 and the platelet mapping
block, there should be careful monitoring of the component of the Thromboelastograph (TEG). 74 The VerifyNow assay can
monitor the antiplatelet effects of aspirin and the P2Y12 inhibitors. 75 The
neurological status platelet mapping component of the TEG is commonly used in surgery and
anesthesiology, whereas Veri- fyNow is the predominant assay in clinical
cardiology. A review on the monitoring of platelet function has been discussed
by several reviews and is beyond the scope of this chapter. 48,76

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Case History
OBSTRUCTIVE JAUNDICE • 62yr male
anaesthesia for whipple’s procedure - c/o gradual yellowish discolouration of eyes & skin-1 mth
- Passing urine dark colour, clay coloured stools-1 mth

DR. ARUNA JAIN - Associated heaviness in rt upper and mid abdomen

- Itching all over body-20 days
DIRECTOR-PROFESSOR - Nausea(no vomit)- 5 days
DEPARTMENT OF ANAESTHESIOLOGY - Significant weight loss-6 months
PAST AND FAMILY HISTORY: not significant
LADY HARDINGE MEDICAL COLLEGE
PERSONAL HISTORY: tobacco chewing-10 yr,
NEW DELHI occasional alcoholic

Case History-contd. Important Negative History

• PHYSICAL EXAMINATION:
- Weight: 50kg, BMI: 18, sclera : yellow • No prodromal symptoms suggestive of Hepatitis
-Pulse: 76/min regular, B.P: 106/68mmhg
-scratch marks present over arms and abdomen (Fever, rigor, arthralgia)
-Airway normal.
• Drug/alcohol abuse/injection/blood transfusion
-Respiratory system, CVS,CNS normal.
-Abdomen: scratch marks present, no obvious abnormality • GI bleed/ascites
no lump(hepatosplenomegaly),no fluid thrill
• Past history of contact with hepatitis patient,
recent surgery or anaesthesia exposure

What is jaundice ? Sites of examination.

• How will you confirm diagnosis?

• Symptom complex- Yellowish discoloration of sclera,

• What are the various problems/anaesthetic
mucus membrane and body tissue(Bil > 2mg%). considerations?

• Sites- Sclera(increased affinity to elastin),undersurface • How will you do preoperative preparation and
assessment?
of tongue, palms, soles, skin surfaces.
• Anaesthetic management?

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OBJECTIVE Microstructure and Histology

• To Know Anatomy and Physiology
(Liver and biliary system)

• To understand the spectrum of liver disease

(Parenchymal/Obstructive)

• To understand the pathophysiological consequences of

Obstructive Jaundice

• Perioperative management of Patient with Obstructive

Jaundice

Blood Supply of Liver

Control of Liver Blood Flow
A. INTRINSIC
Ø AUTOREGULATION
- Hepatic artery-80 mmHg
- Portal vein- flow from spleen, intestine
-resistance to vascular bed
CCF ?
Ø ARTERIOVENOUS RECIPROCITY (HABR)
Portal hypertension?

• Unique- 25% of c.o.p (1100-1800ml/min ) Ø HUMORAL FACTORS-angiotensinII, catecholamines,

vasopressin, glucagon
• Portal vein- valveless, resistance to flow 6-10% of hep a.
- pressure depends on pr within hep v.

Control of Liver Blood Flow(contd.)

EXTRINSIC:
INCREASE HBF:
• Feeding(hyperosmolarit y)
• Supine posture
• Glucagon
• Drugs: Beta agonist
DECREASE HBF:
• Hepatic cirrhosis
• Upright posture
• Hypercapnia
• Hypocapnia/IPPV/PEEP
• Drugs: vasopressor
beta blocker
alpha agonist
Anesthetic agent:
inhalational
intravenous,opioid,
Surgery ,haemorrhage
Physiologic Functions of Liver
I. CARBOHYDRATE METABOLISM
• Storage of Glycogen
II. FAT METABOLISM
• Synthesis and Catabolism
II. PROTEIN METABOLISM
• All proteins except γ globulin & factor III, IV & VIII
• Importance – binding of drugs
- oncotic pressure
- coagulation
- hydrolysis (Pseudocholinesterse)
(L.A.,suxa/mivacurium,esmolol,trimetaphan)

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Physiologic Functions of Liver (cont.) Physiologic Functions of Liver

IV. REGULATION OF BLOOD COAGULATION – (contd.)
Synthesis of Coagulant, anticoagulants and fibrinolytics IX. Other functions -

V. DRUG METABOLISM (xenobiotics) –

• Bile secretion- 600-1200 ml/ day
Lipophilic →water soluble, less active alkaline- bile acids/bile salts, bilirubin, cholesterol,
VI. ENDOCRINE FUNCTIONS- phospholipids, protein, electrolytes & water
Synthesis- IGF1,angiotensinogen, thrombopoetin
Inactivate- cortisol, aldosterone, glucagon, thyroxin & testosterone. • BILIRUBIN METABOLISM
VII. ANTIBACTERIAL actions

VIII. Site of formation & destruction of RBC’s

Spectrum of Liver Disease

• Parenchymal- Acute & Chronic Hepatitis
-Hepatic Cirrhosis (+ portal Hypertention )

• Cholestatic -Intrahepatic – viral hepatitis

– drug induced
-Extrahepatic (Obstructive jaundice)
– Calculi, stricture, growth.
parenchymal disease: cholestasis + hepatic dysfunction.
obstructive jaundice: hepatic function preserved till late.

Clinical features-Slight malaise (mild hepatitis)

- Coma (advanced liver damage)
Obst- Dyspepsia ,dull pain –abdomen, yellowish discoloration.

Obstructive Jaundice Pathophysiological Consequences

• Primary mechanism- Obst. Of E.H. bile duct. - Liveruptake normal, canalicular secretion block
-Sinusoidal endothelium-Highly permeable

• Bile duct pressure- Normal – 10-15 cm H2O

> 15 cm → bile flow decreases Obstructive
> 30 cm → bile flow stops jaundice

• Obstruction to bile flow – content escape into sinusoidal

blood-to the circulation. BILE ABSENCE OF RETENTION OF
CONSTITUENTS BILE IN BILE SOLUTES IN
IN SERUM INTESTINE LIVER

3

Pathophysiological Consequences
a) BILE CONSTITUENTS IN SERUM
- Increase Conj. Bil. - Jaundice(Bil > 2 mg%),
- NO CNS toxicity.
- >20mg%: critical (renal toxicity)
- Serum bile acids - Pruritus
- Haemolysis of RBC
- Bile Salts - Hypotension, Bradycardia
- Dysfn of kuffers cell-Endotoxemia
- Hypercholestremia -Atheromatosis
-Xanthomas
Systemic Alterations
a) Haemodynamic –Hyperkinetic circulation( ↓ PVR- ↑ C.O)
Bile SALTS - Impaired myocardial contractility
- bradycardia,vasodilatation- collapse
- Decreased sensitivity to vasopressor
(immediate volume replacement)
b)Renal alterations : (High bilirubin load)
- mild renal vasoconstriction
- renal hypoperfusion
- refractoriness of tubules to ADH
(Hypovolemia)
- nephrotoxicity -bile salts,endotoxins,
inflammatory mediator
-Prevent Hypovolemia & maintain urine output
- I/V Fluid
- Dopamine 2 µg/kg/min
- Mannitol 10% 1 gm/kg/hr
Surgical Procedures
• Ca gall bladder – radical cholecystectomy+ wedge
resection +CBD exploration
• Choledocholithiasis – ERCP removal or CBD
exploration/bilioenteric anastomosis
• Cholangiocarcinoma – liver resection &/or Local excision
of lesion or Whipple’s procedure
• Biliary stricture – hepaticojejunostomy/liver resection
• Periampullary Carcinoma – Whipple’s
• Chr. Pancreatitis with Ca head pancreas –
• Whipple’s +bilioenteric anastomosis.
10/26/18
Pathophysiological Consequences
b) ABSENCE OF BILE IN INTESTINE
- Bile acid/salt –Malabsorption steatorrhoea
Malabsorption vit. A, D, E, K
Escape of Endotoxin in Portal Blood.
-Bilirubin – Acholic stool.
c) RETENTION OF BILE SOLUTES IN LIVER
- Liver transport process-initialy normal
- Bile acid in hepatocyte → dysfn cytochrome P450
- Protein synthesis – ¯Albumin & clotting factor
Obstruction >1 yr –I/Hepatic bil .fibrosis –H/cell. damage
-
c) Sepsis:
-associated cholangitis and bactebilia
- ¯Phagocytic activity of kupffer’s cell (bile acid)
- Endotoxin
d) Co-agulopathy (low grade DIC)
-vit K malabsorption(II,VII,IX,X)- ↑ PT
Increase Endotoxins
- -Long lasting obstruction- ↓ coagulation factors-FFP
e) Bone disease
-Vit. D def. and hypocalcemia→ osteoporosis
f) Vit. deficiency Vit. A, D, E, K (earliest)
(night blindness,osteoporosis& muscle weakness,
leg cramps and easy bruising)
g) Haemorrhagic gastritis and stress ulcer
h) Impaired wound healing
Preoperative Assessment
OBJECTIVES
1.To know pattern and degree of liver dysfunction.
2. Assess effect on other system.
3. To ensure – post operative facilities (High risk patient).
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Preoperative Investigations B. INDICES OF BILE OBSTRUCTION:

To know the pattern of disease :
S. Bilirubin : Conjugated/unconjugated - ALP(35-100 IU/L): bile duct cells.
bone, intestine, liver, placenta.
A. INDICES OF HEPATOCELLULAR DAMAGE:
AST(SGOT):less specific(heart,sk.msl,kid,brain) - 5-Nucleotidase : Specific

- ALT(SGPT): more specific(mainly liver) - Gamma Glutamyl Transferase: Poor specificity

(Massive parenchymal damage- may be low)

- Glutathione S transferase :An. Agents/ischemic liver injury.

ALT/AST ALK PO4 HEPATOCELLULAR OBSTRUCTIVE
- Gamma Glutamyl transpeptidase – alcohol / hep. Metastasis
>6 <2.5 90% 10%
Biliary obstruction.
<6 >2.5 10% 80%

B) To judge the synthetic ability of liver

Serum albumin – < 2·5 gm% - severe damage

• Albumin/globulin ratio – reversed.
• Prothrombin time –> 1·5 sec. Over control
Risk Assessment ?
– INR - > 1.3
(D/D – Parentral Vit. K – Obst. Jaundice)

C) To assess other organ involvement

Hb, TLC, DLC,
Platelet count, clotting abnormality- PT,PTTK,INR
Serum - Proteins, albumin, sugar
KFT – Urea ,creatinine
CXR,ECG,ABG

Risk Factors Obstructive Disease Perioperative Management

PITT et al (1983) DIXON et al(1983)
• Principles- essentially same (compensated or
decompensated- lower margin of safety)
Increased creatinine Hct < 30%
Hypoalbuminemia Malignant Obst. Lesion • Obstructive Jaundice
Bil > 150 mmol/ L Bil > 180mmol/L(>11mg%) -Fairly intact hepatocyte function
Alk. PO4 > 100IU Alk. PO4 > 100 IU -Problem of RAAS/drug pharmacokinetic
Age > 60 yrs. - do not apply
FRIEDMAN et al(1999)
-azotemia • Still High Risk- Renal Failure (preventive measures)
-hypoalbuminemia - Infection- (AB, Bile Salts)
-cholangitis. - Bleeding- (PT-correctable)

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Anaesthetic Goals Maintaining Hepatic Blood Flow

AVOID :
• Sympathetic stimulation
• Hypotension (decreased venous return / cardiac ou tput)
caused by :
Maintain ü Haemorrhage
ü Cardiac depressant drugs
• Hepatic oxygen supply – demand relationship
ü Regional anaesthesia e.g.; thoracic epidural analgesia
(Hepatic blood flow ,oxygenation) • Hypocapnia, Hypoxemia
• Pressure effects caused by
• Prophylaxis – preserve Renal function ü Surgical retraction
ü Tumors
ü Ascites / Laparoscopy
• Hepatic venous congestion caused by
ü Head down position, IPPV, Rt. side heart failure

Maintaining Renal function Pre Operative Preparation

Preoperatively
• Avoid NSAIDs & nephrotoxic antibiotics e.g.;
(aminoglycosides)
• Oral bile salts to normalize gut flora
• Prophylactic antibiotics to prevent sepsis
• Drainage stent - ↓ Hyperbilirubinaemia
• -Acute cholangitis
• - Obst jaundice- renal dysfn.
• - Co-morbidities delaying surgery.
Intraoperatively
• Avoid hypotension & hypoxaemia
• Avoid dehydration
• Renal dose dopamine? / mannitol / furosemide
1) Coagulation
- Inj. Vit K 10 mg i.m. OD for 3 days at least 48 – 72 hrs
before surgery
- FFP – if PT > 2.5 secs of control value
- cryoprecipitate – if fibrinogen level is decreased
2) Anxiolytic – short acting benzodiazipines
3) Oral H 2 antagonist
4) Biliary drainage
5) Hydration + urine out put (mannitol ???)

Anaesthesia Technique
Intra Operative Monitoring Regional anaesthesia
Routine Longer & extensive surgeries
Supplement to GA for intra & post operative analgesia.
• ECG, NIBP • Intra arterial and CVP
Concerns - coagulopathy
- hypotension
• SpO2, EtCO2
• Biochemical: B.Sugar, ABG, Choice of anaesthetic agent:
• Urine output -No drug contraindicated.
Electrolytes
Consider
• Temperature :Effect on hepatic blood flow
• Hematology: Hb, PT, PTTK, TEG Renal dysfunction
• NMJ monitoring
Co existing hepatocellular disorder
Hepatotoxic & cholestatic drugs
Drug metabolism

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General Anaesthesia
1) Inductionagent –
Thiopentone / propofol
Slow titrated doses - avoid hypotension
Gentle intubation - avoid sympathetic stimulation

2) Muscle relaxants
Suxamethonium - RSI
Atracurium (drug of choice) o– Hoffman’s elimination
Vecuronium – can be used
Rocuronium -Avoid(biliary excretion)

3) Opioids
Fentanyl ( drug of choice) – maintain hepatic oxygen
supply and demand
Spasm of sphincter of oddi (<3%)
Fentanyl > Morphine > Pethidine > Butorphenol
Treatment – nalaxone, glucagon, atropine,NTG
4) Volatile agents
Isoflurane – maintains HBF and oxygen supply
Sevoflurane better than Isoflurane.
Postoperative Management
1) Minor Surgery
N/ms block reversed →O2 enrich air.
2) Major surgery
- Continue IPPV in Postop. period
- Fluid & Electrolyte imbalance
- CVS stability achieved.
- Hypothermia corrected.
- Urine Output 1 ml/kg/hr.
3) Antibiotics + H2 receptor antagonist

4) Adequate analgesia (Small doses/Epidural)

5) Blood / blood product replaced.

Believe in yourself
but don’t be overconfident;
Be satisfied
but know that you can always
improve!

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Case 1
• 59-year-old male c/o Ca buccal mucosa posted for commando procedure
and ALT free flap.
• Preoperative
• History – tobacco chewer, DM
Cirrhosis For Non-transplant • Investigations – HCV+ve, SGPT 82, PT/ INR 18secs/1.4
• Undergoes surgery (approx. - 12 Hours) àintraoperative blood loss 250 ml,
Surgery however, there was hemodynamic instability requiring vasopressors.
• Postoperative:
Dr Lalit Sehgal, MD, DNB, MBA, PGCC • Elective ventilation support (long procedure, plastic surgery request and
hemodynamic instability).
Senior Consultant & Head
• PRVC mode; iv fluids, antimicrobials & vasopressors continued; sedation –
Surgical ICU & Liver Transplant Anesthesia midazolam & fentanyl; Hb – 11 g%.
Rajiv Gandhi Cancer Institute & Research Centre
New Delhi

Case 1
POD1
• Sedation stopped, still requiring minimal dose of vasopressors.
• However, patient is agitated, disoriented, confused, throwing his arms and trying
to pull off tubes & lines.
• INR -1.8 What went wrong??
POD3
• INR 2.4, agitation continues, patient develops abdominal distension & pain
àUSG abdomen – large ascites +, liver – small & irregular, coarse echotexture,
raised portal pressure à Ascites tapping done.
Later course
• Waxing & waning, in-between weaning from ventilator, however, is not sustained
à tracheostomy is performed àpatient develops sepsis àdies on POD29.

Outline Anatomy
• Clinical Anatomy & Functions Of Liver • Largest organ in human body after
skin
• Spectrum & Epidemiology of CLD
• Weight: 1.4-1.7 kg
• Complications of CLD
• Receives 25% of cardiac output ~1.5
• Perioperative Risk Assessment Liter/min
• Preoperative Evaluation & Optimization • Unique dual blood supply
• Intraoperative Management • Hepatic arterial buffer response:
• Changes in portal venous flow cause
• Take Home reciprocal change in hepatic arterial flow.
• Semi-reciprocal system.

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Functions Functions
BIOSYNTHETIC DRUG AND TOXIN METABOLISM
• Amino acid synthesis, gluconeogenesis, glycogenolysis, glycogenesis • PHASE –I: oxidation/reduction/hydrolysis, p450 based drug detoxification

• Protein metabolism, lipid metabolism, lipogenesis and lipoprotein synthesis • PHASE –II: conjugation, gluconeogenesis, beta oxidation of fatty acids and
cholesterol synthesis
• Coagulation factors production (fibrinogen, prothrombin, V, VI, IX, X, XI,
protein C, protein S)
• Bile production and excretion
STORAGE
• Glycogen, Vit A, D, B12, iron and copper.
• Albumin, hormone synthesis

Spectrum of Liver Disease Epidemiology

PARENCHYMAL • Prevalence of liver disease is increasing
• Acute - infectious or non infectious • HCV, HBV, Alcoholic and Non Alcoholic fatty liver disease (NAFLD)
• Chronic Hepatitis – alcohol, autoimmune, drugs, inherited (Wilson, alpha 1
antitrypsin), NASH, viral • 23rd leading cause of disease burden.
• Hepatic Cirrhosis (+portal hypertension) • 13th most common cause of mortality worldwide.
CHOLESTATIC
• In a study, 70% of patients reported not being aware of their cirrhosis
• Intrahepatic
à a huge number of underdiagnosed patients.
• Viral hepatitis • Up to 10% patient of CLD undergo surgery in last 2 years of life.
• Drug induced
• Extrahepatic (Obstructive jaundice) • Mortality rate in patient with cirrhosis undergoing surgical procedures
• Calculi, stricture, growth varies from 8.3-25% (1.1% in non cirrhotic patient).

Chronic Liver Disease (CLD)

• Cirrhosis - various causes
2 distinct phases: compensated and decompensated. Perioperative Care Of Patients With
• Compensated CLD – median survival 12 years. Liver Disease
• Decompensated cirrhosis - median survival of less than 2 years.

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Goals of Management
The optimal management of such patients requires:
• Determine the effect of liver disease in perioperative outcome.
• Estimation of functional hepatic reserve. Complications of CLD
• To understand various risk scoring system and there prognostic
significance.
• Assessment and stratification of the risk of surgery.
• Correction of underlying conditions, if feasible.
• To plan optimal anesthesia strategy.
• Early recognition and treatment of complications.

Complications of liver diseases Impaired liver function – Direct Effects

• Direct and Systemic • Hypoglycemia, Lactic acidosis, Hyper metabolism, Azotemia and Impaired
• Refractory ascites urea synthesis.
• Spontaneous bacterial peritonitis (SBP) • Jaundice when serum bilirubin > 2mg/dl (35 µmol/l)
• Fluid and electrolyte disturbances • Defects in cholesterol metabolism together with intra-hepatic cholestasis
• Hepatorenal syndrome (HRS) à production of poor quality bile and malabsorption of fat and fat-soluble
• Portal hypertensive bleedings vitamins.
• Hepatic encephalopathy (HE) • Reduced synthesis of proteins such as albumin, clotting factors, thyroid
• Hepatocellular carcinoma (HCC) binding globulin and pseudo-cholinesterase.
• Malnutrition • Impaired hormone biotransformation, reduced production of modulator
• Progress of other medical diseases proteins and reduced protein binding lead to increased circulating levels of
hormones such as insulin, thyroxine, T3, aldosterone and estrogen.

Cardiovascular Changes Pulmonary Complications

• Hepatic hydrothorax
• Hyperdynamic state with high CO
• Ascites à elevation of the diaphragm
• Tachycardia, bounding pulse, ejection systolic murmur • Reduced FRC
• Predisposed to atelectasis
• Reduced SVR with hypotension.
• Restrictive ventilation HYPOXIA
• Intrapulmonary and arteriovenous shunting • Increase WOB
• Risk of aspiration
• Pulmonary hypertension may develop
• Cirrhotic cardiomyopathy • Preoperative thoracocentesis not recommended, if hypoxemia not severe
• Heart failure (late stage). • Incentive spirometer perioperatively-prevent atelectasis

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Portopulmonary Hypertension (PPHTN) Hepatopulmonary syndrome

• Progressive dyspnea on exertion. • Triad of the following:
• Hypoxemia & later Right heart failure. • Chronic liver disease.
• Hypoxemia (PaO2 <80 mmHg or alveolar to arterial oxygen gradient >20 mm Hg).
• Definition: • Intrapulmonary arteriovenous dilatation or shunts as detected by bubble-contrast
Mean pulmonary artery pressure (mPAP) >25 mm Hg, pulmonary artery occlusion pressure (PAOP)
15< mm Hg, pulmonary vascular resistance (PVR) >240 dyne/s/cm−5 . echocardiography, lung perfusion scanning, or pulmonary angiography.
• Echocardiography – screening method of choice. • Orthodeoxia.
• RVsys >50 mm Hg
• Right heart catheterization to characterize pulmonary hemodynamics. • SpO2 in sitting position < 95% àABG (PaO2 <80mmHg) àBubble contrast
• Increases the perioperative and long-term risks. Echo.
• Optimize mPAP- • No effective treatment.
• Endothelin receptor anatagonists(Busentan, Ambrisentan) • Higher perioperative mortality.
• PDE5 Inhibitors (Sildenafil, Tadafil)
• i.v. Epoprostenol, PGI2 • Liver transplant is the treatment of choice.

Gastrointestinal disorder Esophageal varices

1. Portal hypertension • Variceal banding
• Portal pressure >10mmHg • Prophylactic beta blockers
• Collateral venous circulation, ascites, splenomegaly • TIPS
• UGI bleed secondary to bleeding oesophageal/ gastric varices and peptic ulcer
• Ascites –Increased risk of abdominal wound dehiscence, abdominal wall herniation,
respiratory compromise, SBP.
• Splenomegaly – sequestration of platelets à thrombocytopenia.
2. Delayed gastric emptying – acid aspiration syndrome.
3. Vomiting and diarrhea with dehydration.

Ascites Ascites – Management

• Grades of ascites: • Fluid restriction is not necessary in most patients.
• Grade 1: ascites only detected by • Low sodium diet.
ultrasound • Diuretics (Furosemide + spironolactone)
• Grade 2: moderate with • Monitoring – patient weight, s. creatinine & electrolytes.
symmetrical distention of the
abdomen • Paracentesis with albumin replacement
• Grade 3: large or tense with • For large volume paracentesis - albumin infusion of 8-10 g/L of fluid
marked abdominal distension removed
• Replacement with albumin 8g/L of fluid removed.
• TIPSS
• Peritoneovenous shunt: for historical interest only

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Spontaneous Bacterial Peritonitis Hyponatremia

• Definition: infection of the ascitic fluid in the absence of any known intra- • Definition: Serum sodium <130 mmol/L.
abdominal source.
• Ascites with abdominal pain • Cause: impaired free water clearance by the kidneys due to non-osmotic
• Diagnosis: positive ascites culture and/or polymorphonuclear cell count ≥250 hypersecretion of ADH.
cells/mm3.
• Diagnostic paracentesis • A late event and is considered as ominous sign.
• Hospital admission • Can lead to severe ascites, HE, renal impairment, and increased hospital
• Norfloxacin (400 mg/day) significantly reduces the probability of SBP. stay.
• Secondary long-term prophylaxis is recommended for all patients with a history
of SBP. • MELD Na proposed.
• Antibiotic prophylaxis in patients with an upper GI bleed irrespective of the
presence or absence of ascites.

Hyponatremia Coagulation Abnormalities

Management:
Antihemostatic Prohemostatic
• Serum Na >125 mmol/L - no specific measures are required.
• Serum Na level is <125 mmol/L: Thrombocytopenia ­­FvW and FVIII
• Stop diuretics. Alteration of platelet functions
• Fluid Restriction <1000ml/day.
• Correction of hypokalemia. ¯¯Factors II, V, VII, IX, X, XI ¯¯Protein C, protein S, protein Z,
• Infusion of albumin (100 g/24 h). Abnormalities of fibrinogen AT(III), heparin-CoFII, a2-
macroglobulin
• Rapid correction with hypertonic saline can lead to more complications.
• Judicious use in symptomatic patients.
• V-2 receptor antagonists (aquaretics, vaptans)- tolvaptan, lixivaptan, satavaptan?? ¯¯a2-anti-plasmine, TAFI ¯¯plasminogen
• Increase the risk of variceal bleed – contraindicated. ­t-PA ­PAI-1

T. Lisman et al. J Hepatol 2002;37:280-7

Coagulopathy Thromboelastograph
• PT – 35.3 s, INR – 3.97, aPTT – 47 s, Platelet Count – 49000/mm 3
• Multifactorial
• Poor absorption of vitamin K
• Due to cholestasis or impaired synthesis of coagulation factors.
• Parenteral vitamin K and transfusions of fresh frozen plasma.
• Cryoprecipitate if s/s of fluid overload.
• Intravenous recombinant factor VIIa.
• For patients with thrombocytopenia, platelet transfusion.
• Prolonged bleeding time can be corrected by desmopressin acetate.
• Potential risk of fluid overload, pulmonary congestion and ↑ portal • Reduces the procedure-related unnecessary transfusions and its related
venous pressures. complications without increasing bleeding complications.

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Renal Dysfunction – Hepato-Renal Syndrome HRS/ Renal Dysfunction – Prevention &

(HRS) Management
• Functional renal defect • Nephrotoxic drugs (e.g. Radio contrast dye, aminoglycoside) should be used with
• Intense vasoconstriction of afferent renal arteriole 2° to hypovolemia or hypotension caution, best avoided.
reducing GFR and renal perfusion.
• Avoid NSAIDS.
• Risk to develop renal failure (RF) - spontaneously (hepatorenal syndrome
[HRS]) or iatrogenically (diuretics, nephrotoxic drugs). • Avoid large volume paracentesis without albumin replacement.
• HRS – A diagnosis of exclusion (obstruction, volume depletion, ATN, and • All diuretics should be stopped. Stop diuretics if serum creatinine is >1.7 mg/dL.
drug-induced nephrotoxicity). • Fluid challenge with 1.5 L of isotonic saline.
• Preoperative renal function significantly affects postoperative survival. • Combination of
• Types of HRS • Vasoconstrictor drugs, such as vasopressin analogues, noradrenalin, and the combination of
• Type I HRS: rapidly progressive renal failure with an increase in the serum creatinine midodrine and octreotide together,
to more than 2.5 mg/dL within 14 days and marked oliguria. • Plasma volume expansion with 20% albumin (1 g/kg intravenously on day 1, 20-40g daily
• Type II HRS: stable or slowly progressive impairment in renal function in patients thereafter).
with refractory ascites.
• HD or CVVHD as a bridge to liver transplant.

Hepatic Encephalopathy (HE) HE

• Mechanism incompletely understood à Due to accumulation of Precipitating factors:
neurotoxic compounds penetrating an impaired blood-brain barrier. • Renal and electrolyte abnormalities
• GI bleeding
• Diagnosis of exclusion. • Infection
• Exclude other etiologies: space-occupying lesions, vascular events, metabolic • Constipation
disorders, and infectious diseases. • Benzodiazepines, narcotics, or other
aasedatives
• Symptoms can occur in chronic as well as in acute disease, may be
• Excessive dietary protein intake
rapid in onset.
• Worsening liver function, e.g., portal vein
aathrombosis
• Noncompliance with medications,
aaespecially lactulose

HE – Grading HE – Treatment
West Haven classification system: • Correcting the precipitating event. • Neomycin 3-6 g/day in divided doses
• Grade 0 - Minimal hepatic encephalopathy; minimal changes in memory, concentration, might be added. Alternatively,
intellectual function, and coordination; lack of detectable changes in personality or behavior; • Intubation to be considered.
asterixis is absent. metronidazole, Rifaxamin.
• Placement of nasogastric tube. • Reduce gluconeogenesis
• Grade 1 - Trivial lack of awareness; shortened attention span; impaired addition or subtraction;
hypersomnia, insomnia, or inversion of sleep pattern; euphoria, depression, or irritability; mild • Nonabsorbable disaccharides such as • Significant source of production of
confusion; slowing of ability to perform mental tasks lactulose: endogenous ammonia.
• Grade 2 - Lethargy or apathy; disorientation; inappropriate behavior; slurred speech; obvious • Starting dose - 20 mL, 3-4 times daily, • At least of 400 calories daily in the form
asterixis; drowsiness, lethargy, gross deficits in ability to perform mental tasks, obvious of IV glucose.
personality changes, inappropriate behavior, and intermittent disorientation, usually regarding • 2-4 soft bowel movements per day.
time • Ammonia level is a poor predictor of
• Grade 3 - Somnolent but can be aroused; unable to perform mental tasks; disorientation about
• Low-protein diet (minimum 30 g/day).
the degree of encephalopathy in CLD.
time and place; marked confusion; amnesia; occasional fits of rage; present but incomprehensible • Zinc replacement.
speech • Improvement in mental status is the
• Grade 4 - Coma with or without response to painful stimuli therapeutic end point.

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Malnutrition Infections
• Common and is a risk factor for mortality. • Impaired immunity à Prone to infections
• Accurate assessment of nutrition is challenging. • Higher incidence of MDROs.
• Total amount of calories - at least 30-35 kcal/kg/day.
• Prophylactic antibiotics are recommended:
• Adults - daily 1-2 g protein/kg of dry body weight. • Low-protein ascites (<1.5 g/dL) (primary prophylaxis)
• Nutritional supplement – Enteral and Parenteral • Prior history of SBP (secondary prophylaxis)
• Daily multivitamin and other supplements as needed. • GI hemorrhage.
• Untreated infections have increased morbidity and mortality.
• High dose vitamin B1 (Thiamine) in Alcoholics.
• Specific fat-soluble vitamin supplements, if a deficiency is present.
• Perioperative nutritional supplementation reduces short term mortality but impact on
long term mortality unclear.

Psychosocial Stress
• Extremely stress à increase the risk of depression and/or anxiety
• Declining health.
• Uncertainty about the results. Perioperative Risk Assessment
• Inability to continue working and participating in daily activities.

• Patients with chronic HCV have a greater incidence of depression and

anxiety. Patients who experience significant psychological distress have
increased complications.

Severity and nature of the underlying liver

Assessment of the risk factors
disease
• Severity and nature of the underlying liver disease. • Degree of hepatic dysfunction, portal hypertension, and its
• Type of surgery. complications as ascites, intra-abdominal varices, renal impairment,
and portopulmonary hypertension.
• Preoperative risk stratification of patients with liver cirrhosis is
challenging. • Child-Turcotte-Pugh Score
• MELD score

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CTP Score

Child-Turcotte-Pugh Score
• Originally developed by Child and Turcotte in 1964 to predict the
mortality during surgery.
• Modified by Pugh in 1973

CTP Score CTP score and Mortality Risk

• Patients with class A may have ascites, hyperbilirubinemia, and portal Author(s ) Journal & year Child A Child B Child C
hypertension. G arris on et al Ann Surg. 1984 10% 31% 76%
Mans our et al Surgery. 1997 10% 30% 82%
• The variables, ascites and hepatic encephalopathy, are graded subjectively,
are operator dependent - problem with its reproducibility. Talem et al Clin G as troenterol 2% 12% 12%
Hepatol. 2010
• Arbitrary selection of cutoff values for its parameters, such as albumin,
bilirubin, and prothrombin time (PT).
• Equal weightage to all variables. Elective surgery is well tolerated in patients with Child class A,
• It is unable to stratify patients with severely decompensated liver disease. permitted with careful preoperative preparation in patients with Child
class B, and contraindicated in patients with Child class C.
• It has never been prospectively validated.

Model for end-stage liver disease (MELD)

MELD
score
0.957 ×loge(creatinine [mg/dL]) + 0.378 ×loge(bilirubin [mg/dL]) + • To predict perioperative mortality.
1.120 ×loge(INR) + 0.643 • Objective.
• Created to predict mortality after TIPS • Does not rely on cut-off values.
• To stratify the risks in patients awaiting liver transplant • MELD less than 10—consider low risk
• Any value less than 1 is given a value of 1. • MELD 10 to 15—intermediate risk, should be managed with caution.
• if the dialysis occurred twice in the last 1 week, the factor for serum • MELD greater than 15—high risk
creatinine value is 4.0. • MELD score above 15 – Avoid elective surgery, consider for liver
• 6-40 transplantation.
• Validated and is used extensively.

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MELD Score and Risk of Mortality CTP v/s MELD

• Higher postoperative morbidity with MELD score >8. • MELD scores of <10 – CTP A
• Higher postoperative morbidity and mortality with MELD score >14. • MELD scores 10-14 – CTP B
• A 1% increase in mortality for each MELD point until 20 and a 2% • MELD scores of 14 – CTP C
increase in mortality with each MELD point after 20. • The MELD score was found to be superior to CTP class in predicting the
• A MELD score of 5-15 had mortality of 5% to 11%, outcomes of intra-abdominal surgery.
• Mortality of 26%, 50%, and 67% - MELD value of 25, 35, and 45. • CTP better in quantifying the risk in compensated CLD, whereas MELD is
better predictor in decompensated.
• Both scoring systems are comparable in predicting the short-term
outcomes.

MELD & CTP scores do not account for:

• Presence of Hepato-pulmonary syndrome.
• Presence of porto-pulmonary hypertension
• h/o variceal bleed There is no such thing called –
• h/o SBP “A good cirrhotic patient!”

Type of surgery
High-risk surgery in patients with liver disease:
• Emergency surgery (Any type).
• Abdominal surgery – cholecystectomy, gastric bypass, biliary procedures, peptic
ulcers, and colon resection.
• Biliary tract surgery: Patients with cirrhosis are at increased risk of gallstones and
their complications.
• Child class C patients, cholecystostomy, rather than cholecystectomy, is considered.
• Cardiac Surgery: Procedures that require cardiopulmonary bypass.
• Hepatic Resection: Hepatectomies in cirrhotic patients are associated with
increased risks.
• The extent of hepatectomy is a predictor of mortality.
• Surgery with high anticipated blood loss.

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Other Determinants of Adverse Outcome

• ASA Physical status
• Predicts early postoperative outcome.
• Advanced age
• Concomitant cardiovascular disease.

Contraindications To Elective Surgery Contraindications To Elective Surgery

• In patients with abnormal liver tests. • Severe extrahepatic complications
• Acute hepatitis: Patients with acute hepatitis of any cause. • Hypoxemia
• Alcoholic hepatitis: Alcoholic hepatitis greatly increases perioperative • Cardiomyopathy, Heart failure
mortality. • Acute renal failure
• Acute liver failure: (Development of jaundice, coagulopathy, and
hepatic encephalopathy within 2-6 weeks without preexisting liver
disease).
• All surgery other than liver transplantation is contraindicated.
• Decompensated cirrhosis. CTP C/ MELD >15
• Should be considered for surgery only in life-threatening situations, such as
an incarcerated hernia, gangrenous cholecystitis, or bowel infarction.

Decision Making

Preoperative Evaluation

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Preoperative Evaluation Preoperative Evaluation

• History • History of risk factors for liver disease - chronic alcohol use, blood
• Detailed Physical Examination transfusion, substance use, tattooing, or family history of liver disease
à Evaluate for CLD.
• focus on the clinical signs of chronic liver disease and features of
• Suspect for CLD à
portal hypertension.
• Obese
• Laboratory tests – CBC, LFT, PT, aPTT, INR, KFT
• Patient clinical features of cirrhosis
Palmer erythema, s pider nevi, as cites , s plenomegaly, leg edema, gynecomas tia, tes ticular atrophy,
temporal was ting, parotid gland enlargement, or jaundice.

• Routine evaluation of liver function tests prior to surgery, in patients

without known liver disease, is not recommended.

Preoperative Evaluation Cardiac Condition

Incidental finding of ↓ platelets, ↑ PT, • DSE-For screening CAD (predictive value variable in advanced
Positive viral marker for HBV/ HCV cirrhosis)
↑ bilirubin, ↓ albumin, or ↑ liver enzymes
• Beta blockers
• Strongly indicated if no contraindication
Suggest presence of CLD • Reduces perioperative myocardial ischemia
• Decreases portal pressure
Thorough assessment is required to evaluate presence
& severity of liver disease prior to elective surgery.

Tests To Assess The Complications Of Liver

Disease
• Liver imaging and AFP, CA19-9 to exclude neoplasms.
• Doppler ultrasound: to exclude portal vein thrombosis.
• Upper GI endoscopy: to assess portal hypertension.
Preoperative optimization
• Bone densitometry: in selected patients.
• Neuropsychologic testing: selected patients.
• ABG: to exclude hepatopulmonary syndrome.

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Preoperative Optimization
• Particular attention needs to be paid to the management of common
complications of advanced liver disease.

Miscellaneous
• Glucose intolerance –insulin infusion caution: risk of hypoglycemia.
• Osteomalacia – dietary supplement with Vit D and Calcitriol.
• Peptic Ulcer Disease-PPI Therapy.
Intraoperative Management
• Alcohol abuse – abstinence to avoid withdrawal symptoms; increased
risk of paracetamol induced hepatotoxicity.

Perioperative Pathophysiology Management Goals

Hemodynamic changes during surgery • Careful monitoring of hemodynamic parameters and titration of
• Reflex systemic hypotension d/t traction of abdominal viscera anaesthetic agents.
• Hemorrhage • Maintain hemodynamic stability and organ perfusion with fluids, blood
• Vasodilatation products and vasopressors.
• Reduced blood supply to the liver (Anesthesia/ retractors)
• Maintain Oxygen demand supply ratio in liver.
• Optimize renal perfusion.
Ischemic injury to remaining functioning hepatocytes

Increased chances of acute decompensation.

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Intravenous Anaesthetic Agents Inhalational agents

• Induction agent - titration of dose to avoid hypotension more important than the • Decrease Liver blood flow.
particular drug. • Biggest reduction with halothane and enflurane.
• Isoflurane is considered safe as long as the systemic blood pressure is not
• Increased sensitivity to benzodiazepines à should be avoided.
reduced by 30%..
• Thiopental- dose should be reduce d/t reduce plasma proteins – increase unbound
• Little change with sevoflurane and desflurane.
protein & prolong duration of action.
• Desflurane is considered the safest anesthetic agent;
• Propofol – No significant change in elimination half life. • Ability to preserve the hepatic blood flow
• However, increase sensitivity to cardiorespiratory depressant effects. • Cardiac output
• Minimal hepatic metabolism
• Etomidate – may be used safely but little advantage over thiopentone.
• Rapidly excretion

Neuromuscular Blocking Agents Opioids

• Scoline –higher dose required due to increase in volume of distribution, • Morphine – delayed elimination d/t reduced hepatic blood flow &
prolong action d/t decrease pseudocholinesterase concentration. extraction ratio.
• Steroid base NMBs (vecuronium & rocuronium) –prolong elimination. • May precipitate hepatic encephalopathy in pts with decompensated
liver failure.
• Atracurium & cistracurium – suitable NMBs.
• Fentanyl – titrate dose (no active metabolites & renally excreted).
• Doxacurium preferred muscle relaxant in longer procedure as it is
metabolized by kidney.
• Alfentanil – elimination reduced.
• Remifentanil – ideally suitable intraoperatively.
• Metabolize by tissue & plasma esterase

Regional Anaesthesia Inotropes/vasopressors

• Spinal/ Epidural à may reduce BP.
• Noradrenaline or Phenylephrine
• May be contraindicated - Coagulopathy &/ or thrombocytopenia.
• Vasopressin/ Terlipressin

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Postoperative monitoring Postoperative Pain Relief

• For signs of hepatic decompensation – Ascites; worsening jaundice, • Reduce dose and frequency of opioids
HE, coagulopathy, and renal impairment. • IV fentanyl PCA
• Prothrombin time • Tramadol - said to be safe with mild hepatic impairment
• Serum bilirubin • Epidural/ TAP/ wound catheter infusions – amides will have delayed
• Serum creatinine elimination and accumulate.
• Blood glucose levels • Paracetamol – 2-3 g/day
• ABG – pH, Lactate, HCO3 • if severe liver failure – avoid
• The maximum decompensation on POD2-3. • Avoid NSAIDs (Nephrotoxicity, GI bleed, platelet dysfunction)
• The risk of decompensation after surgery is not reduced even if local • Associated with liver dysfunction
or spinal anesthesia is used. Valproate, amitryptiline, carbamazepine

Case 1 Take Home

• 59-year-old male c/o Ca buccal mucosa posted for commando procedure • Patients with liver disease who undergo surgery have an increased risk of
and ALT free flap. morbidity and mortality.
• Preoperative
• History – tobacco chewer, DM • Elective surgery should be postponed in patients with abnormal liver tests.
• Investigations – HCV+ve, SGPT 82, PT/ INR 18secs/1.4 • In patients with acute liver disease, elective surgery should be postponed
• Undergoes surgery (approx. - 12 Hours) àintraoperative blood loss 250 ml, until symptoms resolve.
however, there was hemodynamic instability requiring vasopressors.
• Postoperative: • In cases of chronic liver diseases, it is mandatory to assess the severity of
• Elective ventilation support (long procedure, plastic surgery request and underlying disease before deciding whether to proceed with surgery.
hemodynamic instability).
• PRVC mode; iv fluids, antimicrobials & vasopressors continued; sedation –
midazolam & fentanyl; Hb – 11 g%.

Take Home
• Patients with compensated cirrhosis and normal synthetic function have a
low risk.
• MELD and CTP scores can be used to stratify the risks of surgery for
patients with chronic liver disease. THANKS!
• Optimal preoperative management can reduce the risk of postoperative
morbidity and mortality.
• Meticulous perioperative management is required; including hemodynamic
stability; broadspectrum antibiotics; correction of coagulopathy;
improvement of nutritional status; avoidance of nephrotoxins and
sedatives that could precipitate hepatic encephalopathy; and intensive care
unit admission if needed.

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Management of
Tracheostomy
Dr Vandana Talwar
Professor and Consultant
Department of Anaesthesia and Intensive Care
VMMC and Safdarjung Hospital

Case
q 42 year old male, H/O RTA
q Intubated in the ER for unresponsiveness/airway protection
q B/L chest tubes for haemothorax
q Decompressive hemicraniotomy in the OR
q 14 days in ICU, intubated, GCS 10
q Failed multiple SBT, unable to wean ventilator settings to minimal
FiO2 and PEEP

Indications for Tracheostomy Indications for Tracheostomy

q Ventilation q Airway protection - Inefficient swallow / cough
q Prolonged weaning (> 7 days after 1s t SBT) q High SC injury, CVA, TBI
q Long-term MV due to chronic RF q NM diseases

q Airway obstruction q Secretions

Tumors, Trauma, Burns
Generalized weakness, altered mental status, excess secretions
q
q

q FB, Congenital anomalies, Paralyzed VC

q Infections, Postoperative

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Advantages Disadvantages
q Avoids direct laryngeal injury q Complications
q More secure airway q Bacterial airway colonization
q Improved patient comfort q Cost
q Reduced sedation requirement q Surgical scar
q Facilitates oral hygiene, nursing care, suctioning q Tracheal and stomal stenosis
q Improves patient mobility, speech & eating
q Decreased risk of nosocomial pneumonia
q Easier weaning from MV
q Earlier transition from ICU

Timing of Tracheostomy Contraindications to Tracheostomy in ICU

q An individualized patient approach is recommended q Hemodynamic instability
q Early tracheostomy not associated with ↓ in mortality, length of MV q Intracranial hypertension (ICP > 15mmHg)
& ICU stay or VAP q Severe hypoxemia: PaO2/FiO2< 100 mmHg, with PEEP > 10 cmH2O
q Early tracheostomy in specific instances: q Uncorrected bleeding disorders (platelets < 50 000/ mm3 and/or
q Blunt, multiple-organ trauma INR > 1.5 and/or PTT > 2 normal)
q Head trauma and poor GCS

q Acute spine trauma

q Refusal by the patient and/or family
q Thermal injury q Patient is dying or active treatment is being withdrawn
q Facial injuries - to facilitate facial fracture surgery, fixation and immobilization

Percutaneous Tracheostomy
Standard of care in ICU
q Intubated patients – FOB to guide and confirm placement
q Safely performed in refractory coagulopathy from liver disease & TBI
q Contraindications
q Difficulty anatomy (obesity, short neck, thyroid hypertrophy)
q Unstable cervical spine
q Anterior cervical infection
q Surgery or radiotherapy to the neck

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Percutaneous Tracheostomy Percutaneous Tracheostomy

Advantages of PCT

q Shorter operative time

q Decreased incidence of surgical complications (stoma infection and bleeding)
q Done bedside: transporting patient to OT avoided

q Expense of OT resources avoided

q Improved cosmetic result

Emergency Tracheostomy Parts of a

Tracheostomy Tube
q Requires skill, experience, adequate assistance, time, lighting and
proper equipment and instrumentation q Flange - secured with trach ties, stabilizes the
trach
q Complications 2 - 5 times higher q Outer Cannula - tube connected to
q Indications flange
q Transected trachea q Inner Cannula - removable for cleaning
q Anterior neck trauma with crushed larynx q Obturator - plastic guide with a smooth
q Severe facial trauma
rounded tip to guide outer cannula
during insertion
q Acute laryngeal obstruction or near-impending obstruction
q Cuff - Soft balloon around the end of the
q Pediatric patients
trach

Types of tracheostomy tubes Cleaning and Replacing the Inner Cannula

q PVC, silicone, metal q Allows maintenance of tube patency
q Single-lumen (no removable inner cannula) or dual-lumen (removable inner q Changing or cleaning the inner cannula helps to clear secretions
cannula) q Disposable or non-disposable
q With or without cuffs
q Inspected 3 / day, depending on the secretions
q Fenestrated tubes are used for speech in patients who are off MV

Openings on the superior aspect. When the inner cannula is removed,

cuff deflated, and external orifice occluded
(e.g., with a Passey-Muir type valve),
air can pass the VC allowing phonation

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Cleansing the Stoma Mobilization of Secretions

q Inspection of stoma 3 times / day – infection/ excoriation q Adequate hydration
q Wound clean and free of blood and secretions q HME, T piece, tracheostomy mask
q Physical mobility
q Dried secretions loosened with diluted hydrogen peroxide and q progressive mobility, exercises esp of UL
rinsed with physiological saline q siting in a chair - diaphragm is used more
q Dressing changes 2/ day and when dressing is soiled effectively, allowing an effective cough
q Removal of secretions
q suctioning and allowing the patient to cough
q When cough strength is less than 15 mL/kg,
or the cough reflex is diminished,
more frequent suctioning may be required

Cuff Pressure Replacing the

q Allows effective ventilation and/or airway protection Tracheostomy Ties
q 20 to 25 cm H2O (not > 30) Replaced as needed
q Monitoring important
q Underinflation → leakage of secretions around the cuff → VAP Skin underneath the ties should be
assessed
q Overinflation → tracheal stenosis
tracheomalacia, trachea innominate Trach ties should be secure, only 1 F
should fit between the tie and the neck
artery fistula, tracheal ulcerations,
fibrosis and TOF

Indications of changing a TT Tracheostomy Emergencies

q Not until 7 to 10 days after initial placement, to allow the tracheal stoma Hemorrhage
and tract to mature q Major bleeding – 5%
q In case it needs to be changed within 7 days, replaced over a guide, such
q Isthmus of thyroid gland, loss of a ligature or injury to a vein
as a suction catheter or tube changer
q Tracheoinnominate Artery Fistula – Rare, mortality is almost 100%
q Tracheotomy tube change must be guided by clinical considerations
q After 3 to 4 wks
q Indications of changing TT
q Functional problem - air leak in the balloon
q Management - oxygenation, cuff overinflation to tamponade the bleeding,
q Narrow lumen due to the buildup of dried secretions and translaryngeal intubation with direct digital compression followed by
q Switching to a new type of tube immediate surgery for repair
q Downsizing the tube prior to decannulation
q Endovascular embolization

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Tracheostomy Emergencies Tracheostomy Emergencies

Tube dislodgement and loss of airway Decannulation
q Tube is partially displaced q Tube is completely displaced from the stoma

q Dislodgement during the 1st postop week is a medical emergency q Immature stoma (<1 week old) –closes quickly. Immediate treatment

q Tube security is a priority is mask ventilation and orotracheal intubation

q Tracheostomy ties secure and snug (no more than a I F under the ties) q Mature stoma (>1 week old) - closes 50% in 12 hrs, 90% in 24 hrs &
q Removing wt and traction from ventilator circuit
q TT in a midline and neutral position
complete closure in 2 wks
q Minimize transport of the patient q Important to keep TT of same and 1 size smaller at bedside

q Tube security checked frequently

Tracheostomy Tracheostomy Complications

Emergencies -
Stomal Infection
Tube
q

Obstruction q Natural functions of warming, filtering and humidifying airway lost

q Measures to prevent VAP

Tracheostomy Complications Tracheostomy Complications

Bleeding
q Most common complication
q Normally - small amount, self-limited
q Frequent suctioning, switch to red rubber suction catheters
q Postoperative coughing and straining → venous bleeding (dislodging
a clot or ligature)
q If more than minimal / continues - explored and vessel ligated
q Minor bleeding - Elevating the head of the bed, packing the wound,
and/or using homeostatic materials
q Subcutaneous emphysema
q When dissection is extensive and/or the wound is closed tightly
q Resolves in 48 hrs
q If wound is closed tightly and patient is coughing or on IPPV -
pneumomediastinum, pneumopericardium, and/or tension pneumothorax
q Pneumothorax
q Cupola of the pleura extends into the neck esp in emphysema, children
q Postoperative Xray chest

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Tracheostomy Complications Tracheostomy Complications

Tracheal stenosis Tracheomalacia
q 3% to 12% require intervention q Sustained overinflation → Ischemic injury → Flaccid airway → air
q Stoma or just above the stoma, distal to VC trapping and retention of airway secretions → failure to wean
q Cause: bacterial infection or chondritis of the anterior and lateral
q Diagnosed by bronchoscopy
tracheal walls
q Prevention – TT in neutral position, limit traction & avoid overinflation
q Incidence may decrease
q Proper sized TT q Short-term treatment – longer TT to bypass the affected area
q Inflating cuffs only when indicated q Long-term treatment - stenting, tracheal resection or tracheoplasty
q Maintaining intracuff pressures
q PCT

Tracheostomy Complications Tracheostomy weaning

Tracheo esophageal fistula Good cough, manages own secretions, minimal suctioning reqt
q Incidence < than 1% q Cuff deflation

q Caused by injury to the posterior tracheal wall and cervical esophagus q Restitution of supraglottic airway through a 1-way valve and/or cap
q More common in pediatric age group q Cap - occludes the tracheostomy and restores normal airflow
q Early TEF is due to iatrogenic injury. Minimized by entering the trachea q One-way valve opens during inspiration to allow inhalation of air via TT &
closes during expiration to allow air to be shunted supraglottically. Enables
with a horizontal incision between 2 tracheal rings patients to achieve supraglottic expiratory airflow and improved subglottic
q Late TEF due to tracheal necrosis caused by tube movement or angulation pressure when coughing
(neck hyperflexion) or excessive cuff pressure
q Surgical repair

Tracheostomy weaning Tracheostomy weaning

q Reduced supraglottic airflow on placement of a one-way valve or cap
should trigger ENT referral for endoscopy & prompt consideration of
downsizing of the TT to allow more space for supraglottic air flow
q Decannulation – When?
q Tolerates a cap for a set period of time
q Sufficient bulbar function to swallow saliva
q Cough strength is sufficient to expectorate and/or swallow secretions
q Successful breathing with a capped and deflated No.7 tube in place
suggests that a patient will tolerate decannulation
q Patients discharged to the ward with a tracheostomy in place had
almost 3 times the mortality of those who were decannulated prior
to shifting

q No planned surgical interventions

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Patient and Caregiver Education

q Basic care of the tracheostomy
q Changing the tracheotomy tube as scheduled
q Cleaning or replacing the inner cannula
q Cleansing the stoma
q Replacing the tracheostomy holder or ties
q Suctioning
q How to use home equipment
q Indications of respiratory distress, infection and skin breakdown

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PERIPHERAL VASCULAR
DISEASE WITH LIMB ISCHEMIA- TYPES OF PVD
ANAESTHETIC
CONSIDERATIONS (A) CONNECTIVE TISSUE DISORDERS
DR. A. R. GOGIA E.g. : SCLERODERMA, SLE,
PROFESSOR & CONSULTANT, RHEUMATOID ARTHRITIS,
VARDHMAN MAHAVIR MEDICAL DERMATOMYOSITIS.
COLLEGE (B) ARTERIAL OCCLUSIVE DISEASES –
AND ATHEROSCLEROSIS, BUERGERS
SAFDARJANG HOSPITAL DISEASE , THORACIC OUTLET
NEW DELHI SYNDROME, CERVICAL RIB.
Cont……….

TYPES OF PVD TYPES OF PVD

(E) TRAUMA
- VIBRATION INJURY
(C) NEUROLOGIC SYNDROMES- - FROST BITE
- CARPAL TUNNEL SYNDROME - ELECTRIC SHOCK
- TYPING, PIANO
- REFLEX SYMPATHETIC DYSTROPHY (F) DRUGS
- SYRINGO MYELIA - ERGOT DERIVATIVES
(D) BLOOD DYSCRASIAS - B - BLOCKERS
- METHYSERGIDE
- MYELO & PROLIFERATIVE DISORDERS - ANTI CANCER AGENT e.g.
- BLEOMYCIN, CISPLATIN
- CRYOGLOBINEMIA. - TRICYCLIC ANTI
Cont……….. DEPRESSANTS

BUERGER’S DISEASE BUERGER’S DISEASE

HISTORY EXAMINATION

Ò 52Kg ,168Cm TALL MALE OF AVERAGE

Ò KISHORE 34Yrs. OLD, MANUAL LABOURER
Ò PAIN IN THE LIMBS ON WALKING - 3
MONTHS
Ò TINGLING SENSATION IN FINGERS & TOES -
2 MONTHS
Ò PAINFUL ULCER IN (RT) BIG TOE - 2
MONTHS
Ò BLUISH DISCOLARATION OF THE SKIN - ON
EXPOSURE TO COLD.
Ò CHRONIC BIDI SMOKER FOR LAST- 20 Yrs.
BUILT
Ò PULSE RATE 76/Min, BP 130/70MmHg
Ò (RT.) DORSALIS PEDIS A.. NOT
PALPABLE
Ò HAIR LOSS ON (RT) FOOT
Ò COLD TO TOUCH
Ò ULCER ON (RT) BIG TOE 2x2 Cm,
HARD CRENATED MARGINS,COVERED
WITH WHITISH DISCHARGE,VERY
TENDER
Ò CNS,CVS ARE UNREMARKABLE

1
 10/26/18

BUERGER’S DISEASE BUERGER’S DISEASE

WHAT IS
BUERGERS BUERGER’S DISEASE IS NON
DISEASE? ATHEROSCLEROTIC, SEGMENTAL,
WHO DESCRIBED INFLAMMATORY, VASO OCCLUSIVE DISEASE
IT FIRST? THAT AFFECTS THE SMALL SIZED ARTERIES
AND VEINS OF THE UPPER & LOWER
EXTREMITIES. IT IS ALSO KNOWN AS
THROMBO ANGIITIS OBLITERANS.LEO
BUERGER DESCRIBED THIS DISEASE IN
1908.HE CALLED IT SPONTANEOUS
GANGRENE.

BUERGER’S DISEASE BUERGER’S DISEASE

BESIDES SMALL & MEDIUM SIZED

WHAT ARE THE OTHER VESSELS
WHICH MAY GET INVOLVED IN
BUERGER’S DISEASE ?
ARTERIES AND VEINS OF THE
EXTREMITIES OTHER VESSELS LIKE
AORTA, CEREBRAL VESSELS,
CORONARIES, ILIAC, MESENTERIC,
PULMONARY & RENAL VESSELS CAN BE
INVOLVED.

BUERGER’S DISEASE CLINICAL FEATURES

Ò Thromboangitis Ò Classification Systems
obliterans É Major Criteria
Ò Relatively Ð Onset of distal extremity ischemic symptoms prior to
uncommon aqe 45
occlusive disease Ð Tobacco abuse
limited to the Ð Undiseased arteries proximal to brachial & popliteal
medium and small Ð Objective documentation of distal occlusive disease
arteries and veins by plethysmography
Ò Distal upper and Ð Exclusion of proximal embolic source, trauma,
autoimmune disease, hypercoagulable state,
lower limbs are the atherosclerosis
most frequently É Minor Criteria
affected
Ð Migratory superficial phlebitis
Ò Typically identified Ð Raynaud’s syndrome
in young adult men Ð Upper extremity involvement
who smoke Ð Instep claudication
Ò No typical lab abnormalities

2
 10/26/18

BUERGER’S DISEASE ANKLE-BRACHIAL INDEX

Ò Comparison of ankle
WHAT INVESTIGATIONS CAN HELP pressure to brachial SBP
measured by Doppler USG
CONFIRM THE DIAGNOSIS OF
Ò Reproducible, useful for
BUERGER’S DISEASE ? long term surveillance
Ò Normal 0.85-1.2
Ò Claudicants 0.5-0.7
Ò Critical ischemia < 0.4
Ò May be falsely elevated in
calcified vessels (DM)

BUERGER’S DISEASE BUERGER’S DISEASE

(A) ANGIOGRAPHY
NON ATHEROSCLEROTIC, OCCLUSIVE
LESIONS OF SMALL & MEDIUM SIZED
VESSELS WITH FORMATION OF DISTINCTIVE
SMALL VESSEL COLLATERALS KNOWN AS “
CORKSCREW COLLATERALS”.

Cont………..

BUERGER’S DISEASE BUERGER’S DISEASE

(B) EXCISIONAL BIOPSY & HISTO-PATHOLOGY
WHAT ARE THE AVAILABLE MODALITIES
ACUTE PHASE - INFLAMMATORY, SEGEMENTAL, OCCLUSIVE
THROMBI IN WALLS OF AFFECTED VESSELS. OF TREATMENT FOR PATIENTS OF
SUBACUTE PHASE - INTRALUMINAL THROMBUS IN PROCESS OF BUERGER’S DISEASE ?
ORGANISATION.
END STAGE PHASE - MATURE THROMBUS WITH VASCULAR
FIBROSIS.

Ò INTEGRITY OF INTERNAL ELASTIC LAMINA IS MAINTAINED IN ALL

STAGES.

3
 10/26/18

BUERGER’S DISEASE
CONSERVATIVE BUERGER’S DISEASE
Ò COMPLETE ABSTINENCE FROM TOBACCO SURGICAL TREATMENT
Ò AVOID EXPOSURE TO COLD Ò LOCAL DEBRIDEMENT
Ò USE OF WELL FITTING PROTECTIVE FOOT WEAR Ò AMPUTATION OF AFFECTED PARTS
Ò ARTERIAL BYE PASS OF LARGE VESSELS
Ò AVOIDENCE OF DRUGS THAT LEAD TO VASO CONSTRICTION
Ò SYMPATHECTOMY-SEGMEN TAL SUPPLY T10-L2
Ò USE OF VASO DILATORS & CORTICOSTEROIDS, PLATELET Ò P.G .FIBRES LEAVE SYM. CHAIN AT OR BELOW L2
INHIBITORS, ANTI COAGULANTS, THROMBO LYTICS IS NOT
Ò OMENTO PAXY FOR REVASCULARISATION
ESTABLISHED.
Ò ILOPROST-PROSTAGLANDIN I ,ANTI PLATELET WITH Ò ILIZAROV PROCEDURE ON TIBIA
VASODILATOR ACTIVITY,MORE EFFECTIVE BY INTRA ARTERIAL Ò SPINAL CORD STIMULATION FOR VASCULAR
Ò ROUTE
NEOGENESIS
Ò ENDOTHELIN ANTAGONIST BOSENTAN IS USED ORALLY AND
IT HELPS IN HEALING OF ULCERS
Ò AND DECREASING PAIN
Ò ACUPUNCTURE - VERY BENEFICIAL IN INITIAL
I/M VEGF GENE TRANSFER HAS SHOWN GOOD RESULTS STAGES.

BUERGER’S DISEASE BUERGER’S DISEASE

WHAT ARE THE INVESTIGATIONS REQUIRED Ò COMPLETE HAEMOGRAM

FOR A PATIENT UNDERGOING LUMBAR Ò URINE - RE
SYMPATHECTOMY ON ONE SIDE ? - ME
Ò BLOOD UREA
Ò BLOOD SUGAR
Ò X-RAY CHEST- PA VIEW
Ò ECG

BUERGER’S DISEASE BUERGER’S DISEASE

CAN BE DONE UNDER REGIONAL OR GA
CONSIDERATION ARE :-
WHAT ANAESTHETIC TECHNIQUE YOU Ò POSITION OF PATIENT
WILL SELECT FOR PATIENT Ò PADDING PRESSURE POINTS
AMBIENT TEMP. OF O.T.
UNDERGOING LUMBAR
Ò

Ò USE OF WARM& HUMIDIFIED INSPIRED GASES

SYMPATHECTOMY ? Ò NON INVASIVE MONITORING OF SYSTEMIC PRESSURE
Ò POSSIBLE INTERACTION OF ANAESTHETIC DRUGS WITH
PERIPHERAL VASODILATORS
Ò NEED FOR SUPPLEMENTAL CORTICOSTEROIDS

4
 10/26/18

BUERGER’S DISEASE BUERGER’S DISEASE

Ò REGIONAL ANAESTHESIA -
ANKLE BLOCK
Ò OMIT VASO PRESSORS
WHAT ANAESTHESIA ONE CAN CHOOSE FROM LOCAL
FOR AMPUTATION OF BIG TOE ? ANAESTHETIC SOLUTION
Ò DEEP PERONEAL,
SUPERFICIAL PERONEAL,
TIBIAL NERVE TO BE
BLOCKED
Ò CAN BE DONE UNDER G.A.
OR REGIONAL BLOCK

THANK YOU

5
 10/26/18

Congenital Heart Disease Anesthetic Considerations I

TOF, VSD 1. Preop – Pt/Ds/Surg/Anesth
for related/El/Em

Inguinal Hernia Surgery 2. Intraop – Pt/Ds/Surg/Anesth

in a related/El/Em

Child 3. Postop – Pt/Ds/Surg/Anesth

Dr Usha Saha related/El/Em
LHMC, ND

Anesthetic Considerations II CHD - General

• Most common birth defect - 7-8% live births
1. Patient Related – GC, Age, Comorbidity,
• 30% undergo non cardiac surgeries in 1 st yr of life
psychological preparedness
• 85% survive to adulthood
2. Surgery Related – surgery & Technique
Open/Lap
3. Anesthesia Related – choice of anesthesia, Associated non-cardiac anomalies
CVS status, age, IV line in situ or not, • TEF
• Cleft lip/palate
4. Elective / Emergency
• Musculoskeletal / Neurological abnormalities
5. Disease Related – Diagnosed /not, corrected, • Genitourinary / Anorectal irregularities
optimized/associated /residual defects, • Genetic / Chromosomal aberrations / Syndromes – Downs
functional status, IE, drugs, inotropes, (Atlanto-Occipital Subluxation - airway problems), Turner,
complications (CCF, Arrhythmias, PHT) Marfans, Hurler, CATCH-22 syndrome (Cardiac, Abnormal
facies, Thymic hypoplasia, Cleft palate, Hypocalcemia)

CHD – Prevalence CHD – Surgical Risk

Indian Data
• 2005 - 2.5-5.2/1000 live births – VSD, PDA, TGA, PS
• 2011-14 – 19.4/1000 live births
• Under 5 yr age – VSD (33%), ASD (19%), TOF (16%)
Non-Cardiac Surgery - 2 -3 fold ↑ mortality
• Neonates / Infants /Premature/ Ex premature
• PHT
• Emergency Surgery
• Multiple co existing defects
Note -
• 75% CA < 2 yrs age – Anesthesia Related
• Incidence more in uncorrected CHD for Non
Cardiac Surgery

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 10/26/18

Closure of Structures
— Foramen Ovale - soon after birth
— Ductus Venosus- 7- 8 days
— Ductus Arteriosus- 10 – 21 days

—Persistence of Fetal Circulation (R→L):

- Preterm
- Acidosis
- Hypoxia
- Hypercarbia
- Severe Alkalosis

Cardiac Pressures mmHg NADA’S Criteria

At Birth Children Adults 2 major or 1 major + 2 minor – CHD
• RA 10 0-3 0-6
• LA 10 0-6 6-10 Major Minor
• RV 60/10 30/3 25/0-6
1. Systolic murmur >=Gr 3 1. Systolic murmur < Gr 3
• LV 60/10 100/60 120/0-10 2. Diastolic murmur 2. Abnormal 2 nd HS
• PA 60/40 30/10 25/10 3. Cyanosis 3. Abnormal ECG
4. CCF 4. Abnormal X-ray
• Aorta 60/40 100/60 120/80 5. Abnormal BP

SaO2 R = 75% L = 95%

Classification CHD - Diagnosis

• Echo – Anatomy, shunts, vent function, valve
ACYANOTIC (L → R) CYANOTIC (R → L) function
• Doppler & Color flow images – flow direction,
VSD (35%) TOF (5%) velocity, pressure gradient
ASD (9%) TGA (4%) • Cardiac Cath - Size, Location, Degree of Stenosis /
PDA (8%) EISENMENGER’S SYNDROME Shunt, P gradient, SO2
General Principle
PS (8%) EBSTEIN’S ANAMOLY
• Low LA & LV SaO2 – R→L shunt
AS (6%) TRUNCUS ARTERIOSUS • High RA & RV SaO2 – L → R shunt
COARCTATION OF AORTA (6%) TRICUSPID ATRESIA • Pulm BF : Systemic BF (Qp/Qs)
< 1 = R-L shunt
AORTO-PULMONARY TAPVD
FENESTRATIONS > 1 = L-R shunt

2
 10/26/18

TOF
Anomalies
1. RVOTO - Infundibular,
pulmonic, Supravalvular
2. VSD - subaortic
3. Overriding of Aorta
4. RVH

Pathophysiology
1. PVR > SVR
2. ↓Pulm bf
3. R→ L shunt

TOF Clinical Presentation TOF Coag & Rheology

s/s • Platelets - ↓ count & Function
• Infants - Cyanosis from birth, Tachypnea, Tachycardia
(>200/min), TET spells, Resp Distress at Feeding, Failure • Fibrinolysis - ↑d-Dimers & ↓ Fibrinogen
to thrive
• Children - Squatting Posture, Tachypnea, Palpitation, • ↓ F II, V, VIII, X, XI, XII
Dyspnea, Syncope, Chest pain, Clubbing, Hypertension,
Poor Functional Status
• Murmurs • Delayed hepatic maturation
• Low SO2 even with 100% FiO2
• ↑ PT, APTT
• Erthropoesis - ↑Hct – Hyperviscosity
• Endocarditis, Cbr abscess
• ↑WBC count & C-reactive protein (CRP) – Inf
Note - CCF – RARE (large VSD equilibrates Pressures)
• Hyperviscosity – Stasis, Thrombosis, Embolism

Natural Course CHD – Management

• Failure to thrive • Medical - Digoxin, Diuretics, β Blockers, ACEI,
PGEI, Vasodilators, Anticoag, Inotropes
• Cardiac Arrhythmias, Heart Block

• Hypertension (Systemic / Pulmonary) • Surgery - Palliative (PA banding) or Definitive

• TET Spells
Post Repair Complications –
• Thromboembolism
• Arrhythmias (SVT, conduction delay)
• Infections - Infective Endocarditis, Brain abscess • Valve incompetence
• Residual Defects
• Sudden Death

3
 10/26/18

TOF TET spells Categories of Patients

Hypercyanotic spells - cause For non Cardiac Surgery
• Cause - RV Infundibular spasm (inc R-L flow)
• Ppt factors - crying, feeding, stress, defecation
• Leading to - acidosis, hypoxia 1. Uncorrected TOF
• Symptoms - Acute cyanosis, Hyperventilation

Mgmt – (AIM – to dec R-L flow) 2. Previous Palliative / Corrective Surgery

1. Prevention - Avoid Ppt Factors
• Sedation, Correct Acidosis / Anemia, O2, Maintain SVR &
Preload, Avoid Dehydration, ß Blockers
3. Residual Defects / Post Surgical Complications
2. Mgmt Under Anaesthesia (above +
• IVF
• α agonist - Phenylephrine/ Ephedrine (↑SVR)
• β blocker – to ↓ Infundibular Spasm
4. Undiagnosed

CHD - Basic Principle Implications

Hagen Poiseuille Law of Laminar Flow Strength of anesth mgmt
Ω α 1/ r4
• Anticipate, Manipulate, Prevent - Dramatic /
(Ω is inversely proportional to 4 th power of radius)
Drastic HD changes
• If r ↓by 50% - Ω ↑es 16 folds • Able to alter SVR/PVR by drugs - Anesthetics,
• & ↓ Ω - ↑↑ blood flow (Q) Ionotropes, Vasodilators
• Hydration, IVF, preload/afterload relationship
Q = P / Ω
(bf is proportional to P & Inversely proportional to Ω) • Induction/ Maint Care
• Preserve Myoc function
(Q – bf,P – Pressure in Chamber/Vessel, Ω – Vascular Resistance. r - radius)

TOF – AIM - ↑ Pulm Output & ↓ Shunt TOF – AVOID - ↑ Systemic Output
1. ↓ PVR 2. ↑ SVR 1. ↑ PVR 2. ↓ SVR
• Hypoxia • Hyperthermia
• Hyperoxia, • Sympath + • Hypercapnia • Low Hct
• Hypocapnia • Vasoconstrictors • Hypothermia • Deep GA
• Low airway P, • Hypothermia • High Hct • Inhalational AA
• Low Hct
• Pulm Vasodilators – • Atelectasis • SAB, Epid
NO, volatile AAs, • IPPV / PEEP • Vasodilators,
vasopressin, PDEI • Acidosis Nitrites, PDEI
• Alkalosis • α agonists • β agonists

4
 10/26/18

TOF – Hernia Repair - PAE TOF – PAE - Gen Considerations

st
• 50% Rx by 1 wk of life, rest within 5 years
• Medical condition & drug history
• Functional status - activity, exercise tolerance, TET spells
precipitation
• Discuss with parents, pediatrician, cardiologist
• Review diagnostic/therapeutic interventions
• Formulate anesth plan
Chronic Hypoxemia - Polycythemia-Hyperviscosity
1. Hct > 65% - Tissue Hypoxia - ↑FiO2
2. Maintain IV Volume – avoid long periop NPO
3. Anemia (Fe Deficiency)
4. Hypoglycemia
5. Airway - Short trachea, Subglottic narrowing
(vascular malformations)
6. Pt on Diuretics – Hypochloremic Hypokalemic
Metab Alkaloisis

PAE Visits TOF – Hernia – Preop Investigations

• Simple/Moderately complex lesion + Well 1. CBC – Hb, Hct
Compensated - standard PAE visit
2. Coagulation profile

3. ABG, Oximetry
• Moderately complex lesions + Poor Reserve -
cardiologist evaluation, optimization 4. Blood Glucose - esp in NB & critically ill

5. Electrolytes

Clearance always by Anesthesiologist 6. ECG – Hypertrophy, Blocks, Arrhythmias, Strain

Cancellations - view Risk vs Benefit 7. ECHO, Cardiac Cath ???

TOF - Anesthetic Goals Preoperative Preparation

• ↑Pulm BF Optimize
• Adequate Anesthesia & Analgesia
• Prevent TET spells
• Avoid Hypovolemia / PEEP / High Airway P
• Care for Air /Paradoxical Embolism
1. Anemia
2. Respiratory inf - ↑es PVR & PHT
3. Poor Functional Status
4. Medication H/o - Aspirin, Diuretics, Digoxin,
Antiarrhythmics
5. Continue all Except Diuretics
6. Low-dose Aspirin – no risk for Hernia Surgery
7. NPO - Fasting time orders clearly written

5
 10/26/18

Premedication Endocarditis Prophylaxis AHA

Avoid a Crying child Routine Prophylaxis not needed if surgery
Route – Oral / IM / IV – Midaz, Keta, Glyco doesn’t warrant
• Under direct supervision, O2 , bag mask, SpO2
Oral
• Midaz (.5-1 mg/kg) / ketamine (2-4 mg/kg)
• Atropine 0.02 mg/kg Indications
IM • Prior H/o IE
• Midaz (.2mg/kg) / ketamine 1-2 mg/kg
• Repair within 6 mths/ Residual defects
• Glyco /atro .02 mg/kg
IV
• Midaz 0.02-.05 mg/kg titrated Hernia Repair – Children – No Need
• Glyco .02 mg/kg

TOF – Hernia - Anesthesia Technique TOF – GA - IV Induction

GA TOF (R- L shunt -↓Pulm bf)
RA
• Venous Return bypasses Lung - IV Drug reaches
Adv Adv Brain FASTER
• Commonly used induction AA • Minimal exposure to GA
- well tolerated • ↓ Arm Brain Circulation Time - Rapid IV Induction
• Minimal periop NPO
• Reliability
• Airway control Choice of IV Induction Agent
Disadv a. Ketamine - 2-5mg/kg – maintains PVR & SVR, sympathetic
Disadv
• Periop NPO effect, ↑secretions & catechol sec
• High failure rate in infants
• HD disturbance (SAB 5-30%) b. Etomidate – CVS stable, 0.3 mg/kg
• Pulm Complications • Limited duration c. Thio – 4–6 mg/kg – safe (↓ dose in compromised CHD)
• TET spells
d. Propofol – 1-1.5 mg/kg

TOF – GA - Inhalational Induction TOF – Choice of Inhalational AA

Halothane (Soluble AA) –
Prolonged Induction due to – • ↑Fi + Augmented Ventilation- rapid induction
• Myoc depression – ↓ SVR, HR, CO
• ↑Sensitivity to Catechol, Arrhythmias
• ↓ Pulm bf • ↓ Infundibular Spasm
• Pulm V blood – fully saturated with IAA IsoF
• Dilution of IAA in LV (VSD) - ↓ PP in LV, ↓SVR (risk of R-L shunting)
Aorta, Brain Sevo
• Mild ↓ SVR/ HR, more cardio-stable
• Insoluble (Iso, Sevo, DesF) – slow induction • May cause Diastolic Dysfunction
• Soluble (Halothane) – Rapid Induction DesF
• Pungent- not for induction (laryngospasm)
• ↑ HR & ↓SVR
• Less myoc depression than H

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 10/26/18

TOF - Intraop - MRs MONITORING

• ROUTINE – HR, ECG, NIBP, RR, SpO2, Temp
Any Relaxant can be used Others – for Hernia
• Precordial /Esophageal Steth
1. DMR - Scoline • Airway Manometery
• Urine Output ??
2. NDMR - Dtc, Pancuronium, Vecuronium, • TEE ??
Rocuronium, Atracurium Invasive vs Noninvasive
3. Secure the Airway - ET vs SGD Note
1. SpO2 Overestimates SaO2 as SaO2 ↓es
2. EtCO2 Underestimates PaCO2
Ventilation - Spontaneous vs IPPV – avoid
Apnea /Resp depression, PEEP, High Airway P 3. Discrepancy worsens with hypoxemia
4. When in doubt, obtain baseline ABG

Air bubble Precautions & N2 O Laparoscopic Surgery

• De air all IV lines Review
• Connect IV tubing while fluid is running • Can patient handle insults of Laparoscopy – CO2
• Remove all air from syringes loaded with drugs insufflation, PnP, Extreme Positions ??
• Inject with syringe held vertical, tap for bubbles to rise
• Avoid injection ports • IAP < 8-12 cmH 2O - well tolerated
• Never leave IV /central line open to air – Hernia ?? • IAP > 15-20 cmH 2O – Cardiopulmonary Compromise
• Use air filters

N2O -?? vs Air C/I – uncompensated CHD /Residual Defects / complex

• ↑ in size of air bubble - Micro bubbles become macro Defects
• FiN2O 50% – safe - no action on PVR & PAP in children
• Mild ↓ in CO at > 50%
Well-compensated CHD/Repair – Laparoscopy - SAFE
• Avoid in children with ↓Pulm bf, PHT, Poor Myoc Function

Regional Anaesthesia Pain Management

Sole Technique vs as Adjunct ?? • Pain effects - ↑catechols, TET spell
• Suitable following CHD Repair / Well Compensated
• Epidural Preferred
• RVOT Spasm – cyanosis, hypoxia, seizure,
• 1 st choice in older children acidosis, death
• Infants/ NB – along with Sedation/Light GA - 1 mg/kg
Tetracaine/Bupivacaine

• Awake SAB - well tolerated in older children (high risk • Intra & postop analgesia
CHD with PHT, CCF, multiple cardiac surgeries)
• ↓ in SVR - usually tolerated provided Adequate • Opioid infusion or PCA for major surgery
Preload & Gradual Onset of Block
• Care in patients with severe LV Outflow Obstruction
• C/I - anticoagulated patients, Severe Cyanosis • Oral PCM, Suppository, RA/ Caudal Epidural

7
 10/26/18

Opioid Analgesia Postop Care

a. Fentanyl - 1-2 mcg/kg
• HDU / ICU care
b. Sufenta - 0.2 – 0.5 mcg/kg
• Warm comfortable environment
c. Morphine – no CVS dep – for hernia?? • Continue O2, Maintain SaO2 (> 85%)
• Minimal opioids, Good analgesia
• NPO timing, Hydration
Adv of Narcotics
• Monitoring – ECG, HR, RR, BP, SpO2, Temp, UO
• Balanced anesthesia • Early Recognition of – Hypoventilation, Arrhythmias,
• ↓↓ need for IAA Ischemia, TET spells
• Appropriate Intervention & Management
• Maintain sympathetic tone, SVR, HR
• Quick recovery Note - ↑↑↑SaO2 –↓PVR- ↑Pulm BF -↓Systemic BF

Special Situation -1 Special Situation 2 -Post Palliative Repair

• Expected SaO2 - 75-85%
Uncompensated TOF
• Residual Defect
• Arrhythmias, Conduction Defects
• Maintain Ductal patency - PGE1 (0.03 -
0.1μ/kg/min) • Sensitivity to SVR / PVR changes

• S/e - Vasodilatation, Hypotension, Arrhythmias, If Severe Outflow Obstruction –POOR HD Reserve

Apnea, Seizures, Hyperthermia • IVAA - care with Thio/Propofol. Ketamine 1-2 mg/kg or
Etomidate 0.3 mg/kg - Preferred
• Will they present for Ing Hernia Surgery??? • Inhalational AA - in titrated dose maintaining HD stability

Special situation 3 - Pulmonary HT Special Situation 4

• Mean PAP > 25 mmHg at rest / > 35 mmHg at exercise Pacemaker/Automated Defibrillator
• Early stage – Responsive
• Late stage – Fixed – Unresponsive
• Note Underlying cardiac rhythm/ modes/
PHT Crisis - Keep all drugs ready – Be Prepared
settings
1. Prevention
• ↑ incidence among intubated patients
• Advocated - less-invasive airway management • Intraop troubleshooting - trained personnel
2. Mgmt (ACC/AHA Guidelines)
• Maintain CO & Pulm bf
• 100% O 2
• Inhaled NO, PDEI
• Inotropes

8
 10/26/18

VSD
• Most Common CHD 30% - Membranous 70%, Muscular
20%
• Spontaneous Closure – by 6 mths (30%), by 2- 5 yrs (40%)
• Isolated or with other defects (ASD, PDA, AV canal
defect)
Associated Common Anomalies - absent radius & ulna,
syndactyly, polydactyly, trisomy 13-15

s/s - Depend on Age, size of VSD, PVR:SVR

• Small VSD – minimal functional disturbance, asymptomatic -
Late diagnose, prone to IE
• Larger VSD – Large shunt, symptomatic – Early diagnosis

VSD VSD - Clinical Features

Pathophysiology • Symptomatic by 6 -10 weeks of age
L →R shunt - ↑Pulm bf & Pulmonary Congestion (PVR O/E
↓)
• Hyperkinetic precordium, systolic thrill
Consequences - PHT, RVH, CCF • Pan systolic murmur – L sternal border
• S1 & S2 masked, S2 widely split, loud P2
Mgmt • ECG - Normal, LVH, RVH, arrythmias
• For - Recurrent chest infections, Anemia, IE • X Ray Chest – N, LVH, Pulmonary Congestion
• To ↑PVR - Dobutamine, Milrinone • ECHO / Angio
• Baseline Investigations - CBC, electrolytes, Bld Sugar
• Surgical & Post Repair Complications
• Continue - Inotropes, Diuretics, Digoxin,
Antiarrhythmics

VSD for Herniorrhaphy VSD - Anesth Considerations

1. Unoperated VSD Goals Care at All Times
• Anaesthesia risk – Bronchospasm, CCF, PHT
crisis, Cardiac Arrest • Avoid changes in SVR /PVR
• Maintain HR, Rhythm
a. Premedication
• Consider all as with ↑↑ PVR • Avoid Myoc Depression
• Avoid ↑ Myoc Contractility – b. Induction
• Preop optimization ppt RV infundibular spasm & R-L
shunt
• Prevent Hypovolemia
c. MRs, IVF
2. Patients after VSD Repair – as N
• Avoid ↓ in Afterload (Prefer
• Conduction abnormalities in 10% Higher Preload) d. Reversal
• Residual Defects • Allow for slight L→R flow
• Always prevent ↑ R → L flow e. Postop
• Intracardiac air precaution • Overhydration – ppt CCF
• RV function ??

9
 10/26/18

VSD – Anesthetic Mgmt VSD – Special care

Pharmacokinetics of AA - not altered
VSD - L-R shunt - ↑Pulm bf All precautions for AIR Embolism & with N2O
• Slightly SLOWER Induction - Counter by ↑ Induction
dose
• IVAA - Delayed onset – Dilution in Pulm Circulation Hyperventilation with 100% O2 → ↓PVR → Pulm
• VSD + CCF + PHT + Outflow Obstruction – Opioid + Congestion → Hypoxemia – AVOID
Benzodiazepine induction
• Inhalational Induction - Pulmonary V blood not fully
saturated- Augmented pulm bf requires ↑↑ FiAA
• SevoF/ Etomidate & Fentanyl suitable NOTE - Gas exchange problems & deterioration
• IPPV well tolerated from pulmonary congestion - Any Time

VSD – Late Presentation Conclusion

Eisenmenger Complex - PHT with VSD
• Fixed Severe PHT - PVR > 800 dynes/cm5 Know your Patient
• Periop risks – Hypoxemia, Myoc disfunction, Arrhythmia, • Complexity of lesion
Cardiac arrest, PHT crisis, Thrombosis • Functional status
Anaesthetic Implications - as with TOF
• Duration of lesion - patient age
1. As for Hyperviscosity syndrome - Adequate IVF • Surgery planned
3. Avoid further Myoc Depression • Risk assessment
4. Keep SVR ↑ & ↓PVR • Optimization
5. Regional anaesthesia preferred • Goals, Planning & Preparation
6. Postoperative analgesia
7. ICU care
• Monitoring
• Complications – Prevention & Management
Eisenmenger Syndrome – CHD with Shunt Reversal • Postoperative care

Thank You

10
 10/26/18

Case Scenario
• A 26 year old male.
• Case of road traffic injury.
Management of Intercostal tube • Admitted with history of blunt trauma chest.
• On arrival to ED , he got intubated in view of
Dr.Kapil Dev Soni threatened airway .
Associate Prof .Critical Care • Intercostal chest tubes were inserted
JPN Apex Trauma Centre, AIIMS(ND) bilaterally due to diminished air entry and a
liter of crystalloid was infused .

Background
• Common ED/ICU procedure
• Essential for draining intrapleural collections.
• Used since long, yet no consensus on
management
• Great variability in practice
• Associated with complications in upto 30%

Issues Issues
• Site • Post- procedure care
• Size • Frequency of Chest x-ray
• Tunneling? • When to remove?
• Positioning the tube • How to remove?
• Use of suction • Advances in chest tube drainage systems.
• Role of prophylactic antibiotic

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Indications Indications
• Pneumothorax
• Hemothorax
• Pleural Effusion
• Recurrent symptomatic pleural effusions
• Empyema and parapneumonic effusions
• Chylothorax
• Postoperatively- thoracic and cardiac surgery
• Bronchopleural fistula

The objectives for Insertion- CECT Chest- Image

• To collapse any residual cavity.
• To ensure lung re-expansion.
• The achievement of these objectives depends on:
– Viscosity of the pleural fluid & debris
– Whether the fluid is uniloculated or multiloculated?
– Size of the underlying lung.
– Capability of the underlying lung to expand.
– Presence of air leaks

Size of the Chest Tube Size

• Selection depends upon : • A general understanding is
– Underlying indication – air or fluid – Large bore tubes are required to drain fluid
– Nature of fluid – blood or Pus or Serous – Small bore tubes are sufficient to drain air
– Rate of production – of fluid and Air • Larger chest tubes have been ascribed to
– Predicted course of the lung condition cause more pain
• Generated some interest in small bore tubes

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Steps of insertion Post procedure care-Principles

• Identify landmarks – 5th Intercostal
space midaxillary line • Individualized.
• Prepare the site ,infiltrate local
anesthesia ,position the patient. • Reason for chest tube placement
• Select appropriate size chest tube
,place the incision, separate
underlying tissue with blunt • Whether the patient is mechanically
dissection , enter pleural cavity with
chest tube . ventilated
• Ensure length of chest tube lies
within pleural cavity .
• Connect to pleural drainage unit
• Whether the patient had pulmonary resection
under water seal.
• Secure the placement with sutures
and place purse string as well .
• Order Chest Xray to confirm the
position

Post procedure care-Principles Physiology

• Water seal – most chest tubes are initially • Pleural space pressure is
subatmospheric to keep
placed under water seal to detect air leak in
lung expanded
initial 24 hours .
• Perfect sliding with low
• Suction – improves re exapansion of friction between visceral
underlying lung and help in drainage and parietal pleura.
• Rich in lymphatics.
• Pleural fluid is
hypooncotic-( 1 gm/dl
protein)

M at us chak, Geor ge M . , and Andr ew J . L echner . . "Pat hophys iology and Dis eas es of t he Pleur al Space. " Res pir at or y: An I nt egr at ed Appr oach t o Dis eas e Eds . Andr ew J . L echner , et al. New Yor k, NY: M cGr aw- Hil, 2012,

AIR or Fluid in Pleural Cavity? Pleural Drainage System

• 3 bottle system
• 2 bottle system
• 1 bottle system

• The goal is to provide provision of underwater

seal , collection chamber for fluid drainage
and application of suction ,preventing
backflow of air and fluid .
Zielins ka- Kr awcz yk, M . , Kr enke, R. , Gr abcz ak, E. M . , & Light , R. W . ( 2018) . Pleur al m anom et r y–his t or ic al backgr ound, r at ionale f or us e and m et hods of m eas ur em ent . Res pir at or y M edic ine, 136, 21–28.

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One and Two bottle systems Single bottle

• Just the underwater seal bottle
• Provides counterpressure to pleural pressure -
3cm
• Positive pleural pressure of > 3 cmH2O will force
air and fluid out
• Fluid collect will increase the fluid level
• As the fluid rises the pressure required to force
air and fluid out of chest will increase
• Single bottle becomes less efficient as time
passes

Three bottle systems Three Chamber Drain

• The depth of the vent tube determines the
negative pressure and amount of fluid
collection in the collection bottle does not.
• The pressure can be adjusted by adjusting the
depth of vent tube .
• Protects the pleural cavity from uncontrolled
wall suction
• No loss of efficiency with ongoing drainage
• Less chance of fluid reflux.

Dry Systems Suction -Controversy

• Should it applied or should not .

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Management of Chest tubes after

pulmonary resection
• Immediate air collection is frequent .
• Air collects retrosternal space and fluid in posterior space.
• Presence of smaller lung .
• The pressure require to inflate is considerable sub
atmospheric.
suction hastens the removal of air and fluid but does not offer improved • The remaining lung compliance is decreased.
clinical outcomes. However, the application of suction significantly reduced the • It gets over expanded and deformed.
occurrence of postoperative pneumothorax.
• Over expansion promotes persistent air leak and
pulmonary edema.
• Complications – ARDS,Atelactasis ,lung injury is frequent .

Filos s o PL, Sandr i A, Guer r er a F, et al. M anagem ent of Ches t Dr ains Af t er Thor acic Res ect ions . Thor ac Sur g Clin 2017; 27: 7- 11.

Lang P, M anic kavas agar M , Bur det t C, Tr eas ur e T, Fior ent ino F, Suct ion on ches t dr ains f ollowing lung r es ect ion: evidence and pr act ic e ar e not aligned. Eur J Car diot hor ac Sur g 2016; 49: 611–16.

Pulmonary resection … Thoracic Trauma

• Two chest tubes are commonly placed after major lung • Issues – massive bleeding and associated rib
resection .
fracture .
• Large bore tubes are preferred .
• Suction is routinely placed to favor air and fluid • Placement of chest tube is an intervention to
drainage. manage life threatening complications .
• Recently, several researcher are advocating placement
• Chest tube is used for pleural decompression
of a single chest tube
• Single chest tube is less painful.
from high pressures of accumulated blood.
• Allows patients to perform postoperative respiratory • The rapid collected blood may compress lung
physiotherapy leading to better lung expansion tissue and mediastinum
Filos s o PL, Sandr i A, Guer r er a F, et al. M anagem ent of Ches t Dr ains Af t er Thor acic Res ect ions . Thor ac Sur g Clin 2017; 27: 7- 11. M olnar TF. Thor acic Tr aum a: W hic h Ches t Tube W hen and W her e? Thor ac Sur g Clin 2017; 27: 13- 23.

Daily X-Ray Complications

• Common practice to have chest x-ray before • Displacement
rounds
• Obstruction
• Little evidence to show this is required
• May not be required • Pneumothorax
– If pleural apposition in post-op film • Equipment failure
• Patient asymptomatic Good clinical monitoring • Bleeding
• X-Ray needed • Lung parenchymal
– Shortness of breath injury
– Subcutaneous emphysema
• Infection
– Decreasing saturation

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When to remove? When to remove?

• When the tube has served its function • CT drainage less than 100 ml/day or < 2ml/kg/day
• Removed safely at end inspiration or end
expiration
• Decision to obtain Chest Xray following CT
removal depends upon patient clinical condition .
• Chest Xray is required in patients on mechanically
ventilation following CT removal .

How to remove? How to remove?

• End inspiration or end expiration: Equally divided • Since rate of recurrent PTX same- ??? Other
• Rate of recurrent pneumothorax- 2-24% factors
• Reinsertion rates: 1-6%
• Swift removal

• Immediate occlusion of the tube insertion site

• Removal by experienced person
• ? tunneling

Removal of Chest tube General Care

• Steps: • The tubes should not be unnecessarily long
– Ask the patient to take deep breath and hold . (No loops)
– Immediately close the gap by applying occlusive • Should not be clamped
dressing to prevent air going in. – Replacing fluid in container
– If two chest tube are in place,first remove – Planning to remove
posterior chest tube .
• Should be kept well below the level of patient
– Suction should be applied during removal
– Provocative chest tube clamping should be • Ensure adequate analgesia and mobilization
applied incase of prolonged air leak .
Venut a F, Dis o D, Anile M , Rendina EA, Onor at i I . Ches t t ubes : gener alit ies . Thor ac Sur g Clin 2017; 27: 1–5

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Take home
• 5 th ICS ant to mid axillary line. • Thanks
• 28-32F size tubes adequate.
• Suction only in case of large air leak.
• Careful monitoring and handling of tubes.
• If there is no blood/ pus/chyle, tubes may safely
be removed if draining <250 ml.
• Swift removal, immediate occlusion.
• Small air leaks may be managed by Heimlich
valve.

Questions

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CORONARY CIRCULATION
Coronary artery bypass Ø Heart is supplied by TWO CORONARY arteries:
Grafting 1- Right coronary artery---(RCA)
2- Left coronary artery---(LCA)
On Pump Vs Off Pump

Kulbhushan Saini Ø These coronary arteries arise at the root of the aorta.
Assistant Professor,
Anesthesia, Pain Medicine & Intensive Care,
AIIMS, New Delhi

Diagram of coronary circulation

Coronary artery & their branches
Ø LCA---- -Lt Anterior Descending (LAD)
-Circumflex Artery
Ø RCA ---- -Marginal Artery
-Posterior descending branch

* *

Left coronary artery (LCA) –Divides in

Anterior Descending (LAD) Right coronary artery(RCA) supplies:
Circumflex artery
q Right ventricle
Ø LAD--- Supplies anterior and apical parts of heart ,and Anterior 2/3rd of interventricular
septum.
q Part of interventricular septum (posterior 1/3rd)

Ø Circumflex branch-- supplies the lateral and posterior surface of heart. q Inferior part of left ventricle

q AV Node

* *

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Applied Aspect THE C A D

PCI Vs CABG

CABG
ØDisease of LM Coronary Artery
ØMultivessel disease( involving all 3
major epicardial vessels or the
proximal LAD plus a second artery
Ø associated EF<40% & DM
PCI
ØSVD in which lesion is anatomical
suitable
(Preferable in younger patients)

CORONARY ARTERY BYPASS SURGERY

Types of CABG

ON PUMP CABG OFF PUMP CABG

ØOn CPB with Cardioplegia ØOn Beating Heart without CPB

qApproach: Median sternotomy/ qSource of bypass grafts –IMA,

Left Anterolateral Thoracotomy saphenous v. and radial arteries

Basic circuit of cardiopulmonary

bypass

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On Pump CABG ØContact activation : Platelete dysfunction

ØHypothermia: platelete dysfunction, reversible coagulopathy,
ØMyocardial dysfunction- Cardiac Arrythmias, release of
Advantages Adverse Effects myocardial enzymes and compromised CO
ØThe surgeon is provided with the still ØInitiation of CPB associated with
heart marked increased in stress hormone ØNeurologic complications- Cognitive function changes to organic brain
damage and stroke. (emboli, atheromatous debris, fat or ischaemic events)
ØAbsence of blood in theanastomotic ØComplement and neutrophil
area activation- increase in capillary ØPost op lung dysfunction- pulmonary edema, ARDS, atelectasis, anoxia
ØEmpty flaccid heart can be permeability- increase risk of micro- ØGI dysfunction- splanchnic vasoconstriction leading to bowel ischaemia and
manipulated easily to expose all emboli bleeding
coronary branches ØHaemodilution
ØMetabolic, Electrolyte and acid base
disturbances

Off Pump CABG

Off Pump CABG
ØDevelopment of epicardial stabilizers has facilitated CABG withot the use of CPB,
also known as OPCAB
Subset: Contraindications:
ØLow morbidity with faster recovery and reduced procedural costs ØHigh risk of stroke ØHemodynamic Instability
ØFlexible stabilizer devices stabilize and verticalize the apex of heart ØHigh risk of renal dysfunction ØPoor quality target vessels
ØHigh risk of postoperative a) Intramyocardial
bleeding b) Diffusely diseased
ØSeverely atheromatous aorta or c) Calcified Coronaries
heavily calcified aorta
ØDec resp function

Monitoring: Changes during OPCAB:

ØEKG : II 3 3 %; V -75 %; II+V 8 0%; II+V2-5 10 0% sen sitiv ity fo r d etectin g ischemia
ØSp o 2 ,
ØCompression of RV freewall against septum – Diastolic dysfunction
ØIBP: Rig h t RA, Rig h t Femo ral A ØObstruction of RVOT
ØEtCO2 , PIP, Et Vo latile an co n c/MAC,
ØTemp eratu re,
ØVerticalization – normal blood from atria to ventricles decreased
ØCVP, ØDistortion of MV & TV
ØPA cath eter:
ØTEE: (Ab so lu te C/I: Oeso p hgeal strictu re, d iv erticu la, g ro wth , fresh su tu re lin es, eso ph ageal
ØIschemia
in terru p tio n . Relativ e: Sy mp tomatic h iatal h ern ia, co ag ulo path y, eso phg itis, eso ph ageal v arices, ØDecrease Coronary blood flow – 20-50%
u p p er GI bleed )
ØUrin e o u tp u t
ØABG/ BS
ØACT

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Conversion to On Pump: OPCAB

Goals: Steps:
ØHeart Rate – decrease ØInduction - Propofol ( THio –
ØRefractory hypotension ØPreload – Increased Inc HR, bronchospasm, airway
resistance)
ØAfterload – Maintain or
ØMalignant arrhythmias decrease ØAfter Induction : TEE & PA
catheter – CCO/ PA
ØMaintain- Contractility
ØNew RWMA ØInhalational anesthetics –
ØAvoid – tachycardia &
myocardial depression
ØComplete Cardiovascular collapse

OPCAB tissue stabilization and heart positioning devices.

OPCAB
G enzym e I m m obilizer
Steps : ut ilzes a st abilizat ion plat f or m and silast ic vessel loops

Ø Addnl drugs at Skin , Sternotomy and dis s ection around aorta

Ø M /W s evo 1 M AC + fent+ vec
Ø LIM A dis s ection
Ø Heparin
Ø Sequence of grafts : LAD ; PDA; OM t he M edt r onic O ct opus4 t issue st abilizer and St ar f ish2 hear t posit ioner
ut ilze vacuum suct ion t o st abilize and posit ion t he hear t .
Ø Octopus / Starfis h retractor
Ø Intracoronary s tents
Ø LAD : not much change
Ø PDA – verticalization : SV dec 45%; CO dec 35% and M AP & HR by 25%. New M R. EKG complexes s mall
in s ize
q Trendelenburg pos ition/ fluids /Phenylephrine 50-100mcg(M AP > 60mm Hg)
Cor o- Vasc Syst em ( Cor oNeo I nc)
Ø LCx – RVOT obs truction, dis tortion of M V & TV ilust r at es silast ic snar es t hat ar e looped ar ound t he t ar get cor onar y vessel
and t hen f ixed t o a sm all im m obile plat e, t hus dir ect ly im m obilizing t he t ar get vessel.
q Rotation of table to Right/ Rt Pleura opening/ trendelenburg pos ition/ fluids / Norad
Ø M onitor urine output

Ve rm a S e ta .l Circ ula tio n. 20 04 ;1 09 :12 06-1 21 1

Copyr ight © Am er ican Hear t Associat ion, I nc. All r ight s r eser ved.

CPB Management: CPB Management:

q While going on CPB : qDuring CPB:
ØDecrease BP < 9 0 mm Hg fo r can n u latio n .
ØAo rtic – Rep eated attemp ts, b lo o d lo ss, h aemato ma, d issectio n . ØPerfusion pressure
ØVen o u s : AFib ØHaematocrit
ØIn ad eq u ate an tico ag u latio n –
Ø Hep arin resistan ce
ØHemoglobinuria (high haematocrit, inadequate occlusion of pump
ØCan n u la malp o sitio n – Arterial lin e p ressu re h ig h , Ven o u s retu rn in ad eq u ate
head, mismatched blood transfusion, cold agglutinin antibodies,
ØEx treme h emo d ilu tio n excessive use of pump suckers)
ØLo w p erfu sio n p ressu re ØUrine output
ØHeart rh y th m
ØHyper/ hypokalemia
ØAwaren ess
ØBlo o d su g ar

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CPB Management: CPB Management:

qAt the time of cross clamp : qDuring Rewarming:
ØPlacement of cross clamp ØSlow rewarming. TCM temp < 37C, NPT 36 C and gradient between
ØArterial line pressure high TCM & perfusate of no more than 5-6C. (Excessive perfusate temp:
denaturation of proteins, cerebral hyperthermia, formation of bubbles).
ØImmediate arrest of heart after cardioplegia delivery
ØIncrease CPB flows: supports systemic BP, Increase O2 delivery as
O2 consumption increases.
ØInotropes
ØHyperglycemia
ØAwareness

CPB Management: CPB Management:

q At th e time o ff CPB :
qAt the time of cross clamp release:
ØAir in ch amb ers
ØTemperature ØHan d Ven tilatio n
ØDeairing : Ballotment of ventricles, Hand Ventilation, filling of heart ØRh y th m & o th er ECG ch an g es
ØRate – p acin g ?
ØRhythm? Xylocaine/ magnesium ØCo n tractility o f h eart – v isu al/ TEE
ØAcid o sis (isch emic my o card iu m p articu larly v u ln erab le to d etrimen tal effects o f acid o sis)
ØPo tassiu m lev els
ØHemo g lo b in
ØTemp eratu re
ØVo lu me to fill u p th e h eart
ØAwaren ess

Brief overview of CABG

Thank you for

your attention