Anaesthetic management of obstructive jaundice - PowerPoint Presentation

Slide1

Anaesthetic management of obstructive jaundice

Dr.S.Parthasarathy

MD DA

DNB

PhD FICA IDRA

Slide2

Anatomy

Slide3

Functions of liver

The liver is vital for

protein synthesis

glucose homeostasis

bilirubin

excretion

toxin removal

the liver has a substantial functional reserve because of its dual blood supply: portal-venous (75%) and hepatic-arterial (25%).

 

Slide4

The liver conjugates

bilirubin

,

produced from the degradation of the haemoglobin of red cells that are at the end of their normal life span.

This now water-soluble form of

bilirubin

is then excreted into the bile ducts and thence into the small intestine

Slide5

Physiology

Bile acids

are derivatives of cholesterol synthesized in the

hepatocyte

.

Cholesterol, ingested as part of the diet or derived from hepatic synthesis is converted into the bile, which are then

conjugated

to an amino acid (

glycine

or

taurine

) to yield the conjugated form that is

actively secreted into

cannaliculi

.

Slide6

Pathophysiology of obstruction

As conjugated

bilirubin

is water-soluble it will be excreted in the urine which becomes dark.

Stools are pale as a result of poor lipid absorption.

the absorption of vitamin K is dependent on the excretion of bile salts into the small intestine.

Slide7

Obstructive Jaundice – causes

extrahepatic

cholestasis

choledocholithiasis

,

tumors

of the bile ducts and pancreas, postoperative strictures,

primary

sclerosing

cholangitis

,

acute or chronic pancreatitis

Slide8

Obstructive Jaundice – causes

intrahepatic

cholestasis

carcinomas of the

intrahepatic

ducts,

primary

sclerosing

hepatitis

bacterial

cholangitis

,

hepatic metastases,

Slide9

Bile salts increase

so what ??

Bile salts cause

prolong steroid NMB

ARF by ATN

Cardiac arrhythmias

Slide10

bilirubin increase

causes

↓ SVR

Resistance to

vasopressors

↑ incidence of

periop

renal failure

Slide11

What for - it comes to us ?

Surgery in these cases is to remove or bypass the obstruction or to drain infected obstructed bile.

i.e

.

CBD exploration

T tube insertion

Resection tumour

Choledocho

jejunostomy

and bypass

Slide12

Surgery??

CTP class C,

high MELD score,

ASA class V,

acute hepatitis,

severe

coagulopathy

,

severe

extrahepatic

manifestations of liver disease (

eg

, acute renal failure, hypoxia,

cardiomyopathy

).

Slide13

Bad cases

ERCP.

Percutaneous

drainage

Come down on

bilirubin

, sepsis,

And try for major procedure

Slide14

Obs. Jaundice different!!

Obstructive jaundice and

hepatocellular

disease may not go together

Only common thing

hyperbilirubinemia

Slide15

Preop assessment

Routine assessment

Secretory

function

Serum

bilirubin

1.25 mg = 20 µmol.

Jaundice

can be

prehepatic

(haemolytic), hepatic (

hepatocellular

) or

posthepatic

(obstructive) in origin.

Conj or

unconj

.

Slide16

Synthetic function

Synthesis of many proteins takes place in the liver including most clotting factors and many carrier proteins, such as albumin, which to a varying degree bind drugs used during anaesthesia. How to assess??

Serum albumin

Prothrombin

time and INR

Slide17

Metabolic function

Alanine

Transaminase

(ALT) and

Aspartate

Transaminase

(AST)-raised

menas

hepatocellular

damage

Alkaline

Phosphatase

(ALP)

Gammaglutamyl

Transferase

Signifies obstruction

Abnormal liver enzyme results -- 4% of normal individuals and up to 36% of psychiatric patients

Slide18

coagulation

Prothrombin

time and INR

Inj.

Vit

K as

vit

. K1 10-20 mg, 6-8hrly, 3 days

or FFP

Correct

coagulopathy

with vitamin K and FFP to achieve

prothrombin

time within 3 seconds of normal.

Sometimes DDAVP helpful

Slide19

Decreased synthetic function

evidence of decreased protein synthesis, with oedema and

ascites

,

signs of delayed clotting only partly reversed by vitamin K administration,

and even encephalopathy

Alkalosis, hepatic encephalopathy more concerned in liver diseases

Slide20

Child-Pugh score

Measure

1

point

2

points

3

points

Total

bilirubin

,

(mg/dl) (<2) (2-3) (>3)

Serum alb

>35 28-35 <28

INR

<1.7 1.71-2.20 > 2.20

Ascites

None Mild Severe

Hepatic

encep.

None

Grade I-II Grade III-IV

Slide21

Ascites

;

paracentesis

, diuretics

Minimize

ascites

why?

decrease risk of abdominal-wall

herniation

,

wound dehiscence, problems with ventilation.

Encephalopathy

–

lactulose

,

Avoid –

azotemia

, GI bleed, constipation, alkalosis , sedatives

Slide22

Model For End-Stage Liver Disease

MELD = 3.8[

Ln

serum

bilirubin

(mg/

dL

)] + 11.2[

Ln

INR] + 9.6[

Ln

serum

creatinine

(mg/

dL

)] + 6.4

where

Ln

is the natural logarithm

MELD score > 14 – high risk

Slide23

Pre op investigations & assessment

Hb

%

Edema,

ascites

.

Nutrition

SPO2

Renal parameters.

Blood grouping typing

Slide24

Pre op

Systolic and diastolic BP

Widened PP suggests CLD

The goal platelet count is >50-100 × 103/L

Correct

preop

Hyponatremia

Hypokalemia

Hypomagnesemia

Hypoglycemia

More in liver disease

Slide25

Pre op asssesssment

CxR

ECG --CMP

USG, CT scan

Drug history

Alcoholism

HbsAg

Slide26

Infection more common

bacterial colonization of the

biliary

tree

impaired

Kupffer

cell function

defective

neutrophil

function

high rate of

endotoxemia

Pre op antibiotics

lactulose

+

Rifaximin

+ broad spectrum antibiotics.

Slide27

Perioperative mortality ranged from 8 to 28 percent

An

initial

hematocrit

value <30 percent

An initial serum

bilirubin

level >11 mg/

dL

(200 µmol/L)

A malignant cause of obstruction (

eg

, pancreatic carcinoma or

cholangiocarcinoma

)

Slide28

Respiratory system

Hepatopulmonary

syndrome

Pulmonary vascular dilatations, V

A

/Q mismatch

Reduced DLCO

Shift in

oxyhemoglobin

dissociation curve,

Portopulmonary

anastomoses

Pulmonary hypertension

Slide29

Respiratory system in obstruction alone ??

Restrictive lung pattern due to

ascites

Expiratory airflow obstruction

Chest wall

deformity,Pleural

effusions

Panacinar

emphysema

Pleuritis

, Bronchitis /

bronchiectasis

Hepatic hydrothorax

Impaired hypoxic vasoconstriction

Respiratory alkalosis

Slide30

Anaesthetics and liver disease

Nitrous oxide (N2O) produces decrease in portal blood flow, and mild vasoconstriction of the hepatic arterial system

But safe in the absence of hypoxemia

N2O - safe

Slide31

Volatile anaesthetics

All volatile

anesthetics

decrease hepatic blood flow

but

desflurane

and

sevoflurane

have the least significant effect on total hepatic blood flow and hepatic oxygen delivery,

halothane induces the most profound reductions in hepatic blood flow.

Isoflurane

ideal – in coagulation problems

Slide32

halothane

Do not use after prior history or family history of unexplained jaundice after halothane?

Do not use unless indicated?

Slide33

halothane

: "exercise care if obese, pre-existing liver disease, hypoxia likely“,

avoid if :

over 40 years old, long operation,

biliary

surgery, female patient, obese, allergic, sepsis, exposure less than 3 months previously

Slide34

Halothane and Jaundice

The incidence of this

halothane hepatitis

in adults is thought to be 1:7000-30,000 halothane anaesthetics.

rarer in paediatric patients and with the newer volatile agents.

The risk is higher in

women

, the middle aged and the

obese.

Slide35

IV anaesthetics

Slide36

IV drugs

propofol

,

etomidate

, and

midazolam

,- safe

Benzodiazepines in low doses acceptable

Thio

in high doses ??

Everything only in ??

Slide37

Relaxants

Atracurium

safe

Steroidal NMB s ??

Suxa

OK if renal parameters are normal

Slide38

Narcotics

All

opioids

increase tone of the common bile duct and the sphincter of

Oddi

But make patients pain free.

Use

remi

fentanyl

Can use

butrum

or

nalbuphine

if

perop

cholangiogram

is planned

Slide39

perop

cholangiogram

is planned

If narcotic induced spasm is problematic

Options are

Use NTG,

naloxone

Or

Inj

glucagon 2 mg IM

Slide40

Relaxants

Slide41

Factors decrease liver blood flow

IPPV + PEEP

Hypocapnia

& hypoxia

Upright Posture,

abd

. surgery

Cirrhosis, Alfa stimulants

Ganglion Blockers,H2 blockers

Vasopressin

Anaesthetics

– Volatile & intravenous

Important in liver diseases

Slide42

Monitoring

Simple

chole

or

whipple

s

If major ,

add

CVP, IBP,

temperature,NMJ,urine,ecg

Hyperbilirubinemic

Vent. Tachycardia

Difib

. Available

Slide43

Renal protection

adequate hydration and a urine flow of at least

50ml/hr

in the average adult patient.

If

bilirubin

20 mg%

IV fluids 24 hours before surgery and for 36 hours,

postop

.

IV

mannitol

10% 0.5-1g/kg

should be administered prior to surgery AND during surgery

Hydration and urine

Slide44

Renal protection

Pre op albumin infusion decreased

Post op renal failure

Slide45

Epidural and GA

If Coagulation parameters are ok

Post op and

intraop

analgesia

Epidural narcotics

Avoid hypoxemia, ETCO2

Maintain

hemodynamics

, urine output

Slide46

malignancy

Surgery – palliative or radical

Splanchnic

plexus block with alcohol

Possibility of thrombosis

Slide47

Post op

Pain

Hepatic flow , jaundice, encephalopathy

Renal protection

Oxygen and

hemodynamics

.

Slide48

Summary of

anaesthetic

management of obstructive jaundice ??

Slide49

Basically its - Child reading ABCD

Child – child

pugh

criteria

A –

a

ntibiotics

B –

b

lood,

biliary

spasm

(

nalbuphine

)

C –

c

oagulation-

vit

K

D –

d

iuretics

–(mannitol SOS)

Slide50