Sei sulla pagina 1di 94

ANAESTHESIA AND LIVER

DISEASE
Dr.Pratheeba Durairaj ,M.D,D.A,

9.1.09

Liver Functions

The liver conjugates bilirubin, produced from the


degradation of the haemoglobin
- water-soluble form of bilirubin is then excreted
into the bile ducts
The bile salts produced by the liver are passed to the
gut - necessary for the absorption of the fat-soluble
vitamins A, D, E and K.
Synthesis of proteins - most clotting factors,
albumin.
Lipid metabolism - cholesterol and triglycerides
synthesised here.
Carbohydrate metabolism - synthesis and breakdown
of glycogen . It stores glycogen and releases glucose
into the blood when the blood glucose falls for any
reason.
Biotransformation of drugs either by oxidation or
conjugation - render them water-soluble - more
easily excreted.

Hati konjugasi bilirubin, dihasilkan dari degradasi hemoglobin


Bentuk yang larut dalam air bilirubin kemudian dibuang ke
dalam saluran empedu
Garam empedu yang diproduksi oleh hati dilewatkan ke usus yang diperlukan untuk penyerapan vitamin larut lemak A, D, E
dan K.
Sintesis protein - faktor yang paling pembekuan, albumin.
Metabolisme lipid - kolesterol dan trigliserida disintesis di sini.
Metabolisme karbohidrat - sintesis dan pemecahan glikogen.
Yang menyimpan glikogen dan melepaskan glukosa ke dalam
darah ketika glukosa darah turun untuk alasan apapun.
Biotransformasi obat baik oleh oksidasi atau konjugasi membuat mereka larut dalam air - lebih mudah dikeluarkan.

Impaired liver function

Direct effects

Hypoglycemia, Lactic acidosis , Hyper metabolism,


Azotemia and Impaired urea synthesis.
Jaundice appears when serum bilirubin exceeds 35
mol/l
Defects in cholesterol metabolism together with intrahepatic cholestasis may lead to production of poor
quality bile and malabsorbtion of fat and fat-soluble
vitamins.
Reduced synthesis of proteins such as albumin, clotting
factors, thyroid binding globulin and pseudocholinesterase.
Impaired hormone biotransformation, reduced
production of modulator proteins and reduced protein
binding lead to increased circulating levels of hormones
such as insulin, thyroxine, T3, aldosterone and oestrogen

Ggn fungsi hati


efek langsung
Hipoglikemia, asidosis laktat, metabolisme Hyper, azotemia dan
sintesis urea Gangguan.
Penyakit kuning muncul ketika bilirubin serum melebihi 35
umol / l
Cacat dalam metabolisme kolesterol bersama dengan intra-hati
kolestasis dapat menyebabkan produksi kualitas empedu miskin
dan malabsorbtion vitamin lemak dan larut dalam lemak.
Mengurangi sintesis protein seperti albumin, faktor pembekuan,
tiroid binding globulin dan pseudo-cholinesterase.
Gangguan biotransformasi hormon, mengurangi produksi
protein modulator dan mengurangi protein yang mengikat
menyebabkan peningkatan tingkat sirkulasi hormon seperti
insulin, tiroksin, T3, aldosteron dan estrogen

Indirect effects

Cardiovascular changes
Vasodilatation and vascular shunting are
almost invariable in ESLD.
Low systemic vascular resistance (SVR)
results in high cardiac output and high
mixed venous oxygen saturations
Intrapulmonary & arteriovenous shunting
Pulmonary hypertension may develop
Tachycardia, bounding pulse ,Ejection
systolic murmur

Efek tidak langsung


perubahan kardiovaskular
Vasodilatasi dan shunting pembuluh darah
hampir tidak berubah-ubah di ESLD.
Hasil resistensi vaskuler sistemik rendah
(SVR) curah jantung yang tinggi dan dicampur
vena saturasi oksigen yang tinggi
Intrapulmonary & arteriovenous shunting
Hipertensi pulmonal dapat mengembangkan
Takikardia, melompat-lompat pulsa, Ejection
murmur sistolik

Pulmonary changes
Pulmonary problems are both vascular and mechanical.
Hepato-Pulmonary syndrome triad of end
stage liver disease, A-a gradient >2 kPa ,
intrapulmonary vascular dilation
Impaired pulmonary function in absence of
cardiopulmonary disease
Impaired hypoxic vaso-constriction and ventilation
perfusion mismatch lead to arterial desaturation and
clubbing if chronic.
Cyanosis ,dyspnoea , platypnea, orthodeoxia
[desaturation pronounced in upright position relieved
by recumbency ]
Pleural effusions together with ascites can cause
considerable mechanical embarrassment of respiration
and a reduction in functional residual lung capacity.

Perubahan paru
Masalah paru-paru keduanya vaskular dan mekanik.
Sindrom hepato-paru - triad penyakit hati stadium akhir, Aa
gradien> 2 kPa, pelebaran pembuluh darah intrapulmonary
Gangguan fungsi paru dalam ketiadaan penyakit
cardiopulmonary
Gangguan hipoksia vaso-konstriksi dan ventilasi perfusi
mismatch menyebabkan desaturasi arteri dan clubbing jika
kronis.
Sianosis, dyspnoea, platypnea, orthodeoxia [desaturasi
diucapkan dalam posisi tegak lega dengan penyerahan diri]
Efusi pleura bersama dengan ascites dapat menimbulkan
rasa malu mekanik cukup respirasi dan penurunan
kapasitas paru residual fungsional.

HEPATORENAL SYNDROME

Low GFR
Low renal blood flow
No other cause for renal failure
Functional renal failure
Symptoms water retention,
Azotemia, hyponatremia, & oliguria

Rendah GFR
Rendah aliran darah ginjal
Tidak ada penyebab lain gagal ginjal
"gagal ginjal Fungsional"
Gejala - retensi air, azotemia,
hiponatremia, & oliguria

Hepatorenal failure

Causes may be
Pre and peroperative dehydration
Hypovolaemia
Falls in renal blood flow during surgery,
Direct effect of the excess conjugated
bilirubin on the renal tubules or possibly an
increased absorption of endotoxin from the
gut.
Not a major risk in patients with Prehepatic
jaundice.

Penyebab mungkin
Pra dan peroperative dehidrasi
hipovolemia
Falls di aliran darah ginjal selama operasi,
Efek langsung dari kelebihan bilirubin
terkonjugasi pada tubulus ginjal atau mungkin
penyerapan peningkatan endotoksin dari usus.
Bukan risiko utama pada pasien dengan Prehepatic
ikterus.

Management
of Hepato renal syndrome

Avoid it developing by ensuring adequate hydration


and a urine flow of at least 50mls/hr in the average
adult patient.
In moderately elevated bilirubin - simple fluid loading
for 12 hours before surgery using 0.9% NaCl and
during the operation.
If the urine output is not maintained - Mannitol
10%
Bilirubin greatly elevated (>140 micromols/litre), intravenous fluids during the 24 hours before surgery
and for 36 hours postoperatively.
Mannitol 10% 0.5-1g/kg - prior to surgery
without making the patient dehydrated as a result of
an over-zealous diuresis.

Menghindari berkembang dengan memastikan hidrasi yang


memadai dan aliran urin minimal 50mls/hr pada pasien
dewasa rata-rata.
Dalam cukup tinggi bilirubin - pemuatan cairan sederhana
selama 12 jam sebelum operasi menggunakan NaCl 0,9%
dan selama operasi.
Jika output urin tidak dipertahankan - Manitol 10%
Bilirubin sangat ditinggikan (> 140 micromols / liter), cairan infus selama 24 jam sebelum operasi dan selama 36
jam pasca operasi.
Manitol 10% 0.5-1g/kg - sebelum operasi tanpa
membuat pasien dehidrasi sebagai akibat dari diuresis
terlalu bersemangat.

Neurological problems

Mechanisms leading to deepening


encephalopathy -incompletely understood.
Due to accumulation of neurotoxic
compounds penetrating an impaired bloodbrain barrier.
Symptoms can occur in chronic as well as in
acute disease, may be rapid in onset
Precipitated by a gastrointestinal bleed,
dietary protein overload or sepsis.
Somnolence can be exacerbated by sedative
drugs and narcotics.
Rapid correction of hyponatraemia can lead
to osmotic demyelination and central pontine
myelinolysis and should be avoided

HAEMATOLOGICAL PROBLEMS

Anaemia may be the result of nutritional


deficiency, toxic bone marrow depression or
gastrointestinal bleeding from varices or
erosions.
Coagulation defects arise from
thrombocytopenia, platelet dysfunction and
decreased levels of circulating clotting factors.
Clotting factor levels fall because of impaired
synthesis, vitamin K malabsorbtion and
intravascular consumption.
The short half-life of clotting factors means that
INR or Prothrombin Ratio (PTR) can reliably be
used to evaluate residual hepatic function.
Treatment Vit K ,FFP

MASALAH hematologis
Anemia mungkin merupakan hasil dari kekurangan gizi,
beracun depresi sumsum tulang atau perdarahan
gastrointestinal dari varises atau erosi.
Koagulasi cacat timbul dari trombositopenia, disfungsi
trombosit dan penurunan tingkat sirkulasi faktor
pembekuan.
Tingkat faktor pembekuan jatuh karena gangguan sintesis,
vitamin K malabsorbtion dan konsumsi intravaskular.
Paruh pendek faktor pembekuan berarti INR atau
Prothrombin Ratio (PTR) dipercaya dapat digunakan untuk
mengevaluasi fungsi hati residual.
Pengobatan-Vit K, FFP

GASTROINTESTINAL SYSTEM
Rupture of oesophageal

varices
Vassopressin & octreotide reduce portal
hypertension
Susceptibility to infection - increased
Drug disposition
Cholestasis will reduce absorption of fatsoluble drugs after oral administration.
Compartment changes and altered protein
binding will affect volume of distribution,
clearance and re-distribution.
Patients with liver dysfunction may be
particularly sensitive to opiates and
benzodiazepines due to altered end-organ
sensitivity

SISTEM SALURAN CERNA


Pecahnya varises esofagus
Vassopressin & octreotide-mengurangi hipertensi portal
Kerentanan terhadap infeksi - meningkat
disposisi obat
Kolestasis akan mengurangi penyerapan obat yang larut
dalam lemak setelah pemberian oral.
Perubahan Kompartemen dan mengikat protein diubah
akan mempengaruhi volume distribusi, bea dan re-distribusi.
Pasien dengan disfungsi hati mungkin sangat sensitif
terhadap opiat dan benzodiazepin karena mengubah
sensitivitas organ akhir

Effect of hepatic dysfunction on


anaesthetics
Albumin -increased free fraction
Altered volume of distribution [Ascites & increased
total body water compartment],
Reduced metabolism alters drug pharmacodynamics
Opiods Morphine ,pethidine - respiratory depression &
sedation
Sedative /hypnotic drugs
Benzodiazepines prolonged
NDMR
Prolonged action for vecuronium and pancuronium
DMR
Decreased serum cholinesterase activity

Pengaruh disfungsi hati


pada anestesi
Albumin-peningkatan fraksi gratis
Volume Diubah distribusi [Ascites & kompartemen air total
tubuh meningkat],
Mengurangi metabolisme obat-mengubah farmakodinamik
opiods Morfin, petidin - depresi pernapasan & sedasi
Obat penenang / hipnotik
Benzodiazepin - berkepanjangan
NDMR
Tindakan berkepanjangan selama vecuronium dan pancuronium
DMR
Aktivitas kolinesterase serum menurun

The Effect of Anaesthetics on Liver


Function
VOLATILE AGENTS
Halothane - HABF/PBF, disturb HABR [hepatic
arterial buffer response]
Sevoflurane ,isoflurane maintain HABR
SEVO > ISO > DES > HALO
IV ANAESTHETICS
Thiopentone /etomidate -THBF
Propofol - THBF splanchnic vasodilator
Ketamine no effects
REGIONAL ANAESTHESIA
High epidural may reduce THBF

Pengaruh Anastetik pada


Fungsi Hati
AGEN VOLATILE
Halotan - HABF / PBF, mengganggu HABR [hati
respon penyangga arteri]
Sevoflurane, isoflurane mempertahankan HABR
Sevo> ISO> DES> HALO
IV Anastetik
Thiopentone / etomidate - THBF
Propofol - vasodilator THBF-splanikus
Ketamine - tidak ada efek
DAERAH ANESTESI
Tinggi epidural dapat mengurangi THBF

Effect of General Anaesthesia on liver


functions in patients with preexisting
liver diseases

Indian Journal of Anaesthesia. 1989 Apr; 37(2): 61-6


ABSTRACT: Effects of anaesthetics on liver
functions were studies in 13 patients having no liver
disease (group I) and 11 patients having liver
disease (group II).
Serum cholinesterase increased significantly in both
the group. Rise in SGOT levels was significant only
in group I, who had greater surgical trauma and not
in the other group of patients (group II).
Significant decrease in total serum proteins was
seen on different postoperative days in group I but
only on 5th postoperative day in group II.
It was concluded that presence of liver disease does
not increase the adverse effect of anaesthesia on
liver function and that surgical trauma is more
important than anaesthesia in producing liver
dysfunction.

Pengaruh Anestesi Umum pada fungsi hati


pada pasien dengan penyakit hati yang sudah
ada sebelumnya
Indian Journal of Anaesthesia. 1989 April, 37 (2): 61-6
Abstraksi: Pengaruh anestesi pada fungsi hati adalah studi pada 13
pasien tidak memiliki penyakit hati (kelompok I) dan 11 pasien
memiliki penyakit hati (kelompok II).
Cholinesterase serum meningkat secara signifikan pada kedua
kelompok. Kenaikan tingkat SGOT hanya signifikan pada kelompok
I, yang memiliki trauma bedah yang lebih besar dan tidak pada
kelompok lain pasien (kelompok II).
Penurunan signifikan dalam total protein serum terlihat pada harihari pasca operasi yang berbeda pada kelompok I tetapi hanya
pada 5 hari pasca operasi pada kelompok II.
Disimpulkan bahwa kehadiran penyakit hati tidak meningkatkan
efek merugikan dari anestesi pada fungsi hati dan trauma bedah
lebih penting daripada anestesi dalam memproduksi disfungsi hati.

Signs of Liver Disease

Jaundice
Hepatomegaly
Spider Naevi
Splenomegaly
Scratch Marks
Ascites
Palmer Erythema

Dilated Abdominal
Veins
Peripheral Oedema
Finger Clubbing
Testicular Atrophy
Bruising
Gynaecomastia
Confusion/Coma

penyakit kuning
hepatomegali
Spider nevi
splenomegali
Marks Scratch
asites
palmer Eritema

Vena perut
membesar
peripheral Edema
Finger Clubbing
Atrofi testis
memar
ginekomastia
Kebingungan /
Coma

Jaundice
Prehepatic jaundice [haemolysis]
Massive intravascular haemolysis - as in
some forms of malaria or in sickle cell
anemia
Hepatocellular function is normal but
overwhelmed - increased unconjugated
bilirubin

Intact Protein and carbohydrate metabolism

No reduction in the absorption of Vitamin K


or production of clotting factors.
Hepatocellular jaundice

Hepatitis or Cirrhosis
decreased protein synthesis, signs of
delayed clotting, and even encephalopathy.

Pykt kuning
Prehepatic ikterus [hemolisis]
Besar intravaskular hemolisis - seperti dalam beberapa
bentuk malaria atau pada anemia sel sabit
Fungsi Hepatocellular normal tapi kewalahan meningkat unconjugated bilirubin
Protein utuh dan metabolisme karbohidrat
Tidak ada pengurangan penyerapan vitamin K atau
produksi faktor pembekuan.
hepatocellular penyakit kuning
Hepatitis atau Sirosis
sintesis protein menurun, tanda-tanda tertunda
pembekuan, dan bahkan ensefalopati.

CONTD
Obstructive Jaundice
Biliary obstruction - from a stone in the common
bile duct, pancreatic tumour or ascending
cholangitis
Hepatocellular function is normal
Excess plasma bilirubin is chiefly conjugated excreted in the urine which becomes dark.
Stools are pale as a result of poor lipid
absorption.
Protein synthesis is normal
Vitamin K dependant clotting factors reduced
as the absorption of vitamin K is
dependent on the excretion of bile salts into the
small intestine clotting time prolonged
parenteral vitamin K.

obstruktif Kuning
Obstruksi bilier - dari batu di saluran empedu, tumor
pankreas atau naik cholangitis
Fungsi Hepatocellular normal
Kelebihan bilirubin plasma terutama terkonjugasi diekskresikan dalam urin yang menjadi gelap.
Kotoran yang pucat akibat penyerapan lipid miskin.
Sintesis protein normal
Vitamin K tergantung faktor pembekuan dikurangi
sebagai penyerapan vitamin K tergantung
pada ekskresi garam empedu ke dalam usus kecil
pembekuan waktu lama parenteral vitamin K.

Renal impairment in
Jaundice

Release of endotoxins into systemic


circulation
following biliary obstruction renal
failure
Prevention
- in high sr.bilirubin levels
percutaneous drainage of biliary tree
under antibiotic cover
- pre op oral bile salts - post op RF

Ggn ginjal di ikterus


Pelepasan endotoksin dalam sirkulasi
sistemik
setelah obstruksi bilier - gagal ginjal
pencegahan
- Tingkat sr.bilirubin tinggi perkutan drainase bilier bawah penutup
antibiotik
- Pre op garam empedu lisan -
pasca op RF

Liver Function Tests

Indication of severity, help to differentiate


between prehepatic, hepatocellular and
obstructive jaundice.
Jaundice - sign of an elevation of serum
bilirubin.
Protein and albumin levels are normal in
prehepatic or obstructive jaundice, low
values indicate hepatocellular damage.
clotting - Prothrombin Time
An elevated INR may indicate impaired
synthesis of clotting factors due to
hepatocellular damage or malabsorption
of vitamin K due to biliary obstruction.

Tes fungsi hati


Indikasi keparahan, membantu untuk membedakan
antara prehepatic, hepatoseluler dan ikterus
obstruktif.
Penyakit kuning - tanda ketinggian bilirubin serum.
Protein dan albumin tingkat normal dalam prehepatic
atau ikterus obstruktif, nilai rendah mengindikasikan
kerusakan hepatoseluler.
Waktu protrombin - pembekuan
Sebuah INR tinggi dapat mengindikasikan gangguan
sintesis faktor pembekuan akibat kerusakan
hepatoseluler atau malabsorpsi vitamin K karena
obstruksi bilier.

Contd

Prothrombin time[ half life - 6 -12 hrs ] best


indicator than Albumin [ half life 24 -48
days]
Alanine Transaminase (ALT) and Aspartate
Transaminase (AST) are enzymes that are released
into the circulation by damaged hepatocytes.
Raised levels indicate hepatocellular damage.
AST can also be elevated in other circumstances
such as myocardial infarction
Alkaline Phosphatase (ALP) is an enzyme localized
near the bile cannaliculi and is elevated in biliary
obstruction. Not specific to hepatobiliary disease,
[ raised in malignant bone disease].
An accompanying rise in Gamma glutamyl
Transferase (Gamma GT) suggests that the ALP is
from the liver.

Waktu protrombin [paruh - 6 -12 jam] - indikator


terbaik dari Albumin [paruh - 24 -48 hari]
Alanin Transaminase (ALT) dan aspartat Transaminase
(AST) adalah enzim yang dilepaskan ke dalam sirkulasi
oleh hepatosit yang rusak. Dibesarkan tingkat
mengindikasikan kerusakan hepatoseluler.
AST juga dapat meningkat pada keadaan lain seperti
infark miokard
Alkaline Phosphatase (ALP) adalah enzim lokal dekat
cannaliculi empedu dan meningkat pada obstruksi
bilier. Tidak spesifik untuk penyakit hepatobilier,
[dibesarkan di penyakit tulang ganas].
Kenaikan atas Gamma glutamyl transferase (Gamma
GT) menunjukkan bahwa ALP adalah dari hati.

Lanjutan..

Glutathione S transferase to
assess damage
due to anaesthetics
ALP Early in biliary obstruction
- Glutamyl trans peptidase rises
after alcohol & drug induced liver
damage
Plasma glucose should be measured

Lanjutan..
Glutathione - S - transferase-untuk
menilai kerusakan
karena anestesi
ALP-awal obstruksi bilier
- glutamil trans peptidase meningkat setelah alkohol &
kerusakan hati akibat obat
Plasma glukosa harus diukur

Risk and severity scoring

In 1964, Child and Turcotte classified risk for


patients with liver cirrhosis undergoing portocaval anastomosis for management of portal
hypertension.
Pugh et al at King's College Hospital
published a severity scoring system for
patients undergoing oesophageal transection
for bleeding oesophageal varices.
The two systems have been amalgamated and
provide a disease severity assessment based
on two clinical and three laboratory variables

Risiko dan keparahan


scoring
Pada tahun 1964, Anak dan risiko diklasifikasikan
Turcotte untuk pasien dengan sirosis hati
menjalani anastomosis porto-kava untuk
pengelolaan hipertensi portal.
Pugh et al di Rumah Sakit King College
menerbitkan sistem penilaian keparahan untuk
pasien yang menjalani transeksi esofagus untuk
perdarahan varises esofagus.
Kedua sistem telah digabung dan memberikan
penilaian keparahan penyakit berdasarkan dua
variabel laboratorium klinis dan tiga

PUGHS MODIFICATION OF CHILD GRADING


Clinical & Biochemical
variables

POINTS
1

SCORE
D
2

Serum albumin (g/L)

>35

28-35

<28

Serum bilirubin (mol/L)

<35
<2

35-60
2 -3

>60
>3

PT (seconds) prolonged
from control

1-4
INR [ <
1 .7]

4-10
INR [1.7
-2.3]

10

Ascites

None

Mild

Moderate

Encephalopathy

Absent

Grade I Grade III


II
IV

[Mg /dl]

POINTS : 5- 6 class A [5% Mortality] , 7 -9 Class B [10%


mortality], 10 -15 Class C [50% mortality]

INR >2.3

Surgery in patients with liver


dysfunction

The Child-Pugh classification is a useful method of


staging the progress of liver decompensation.
Limited predictive value in anaesthesia and
surgery
Group A patients are lower risk and with
sufficient care can be considered as candidates for
most types of surgery.
Group B patients acceptable but correct
abnormalities
Group C patients present an extremely high
operative risk - surgical procedures in these
patients should be avoided if possible.- only
emergency or life-saving procedures should be
undertaken

Operasi pada pasien


dengan disfungsi hati
Klasifikasi Child-Pugh adalah metode yang berguna
untuk pementasan kemajuan dekompensasi hati.
Nilai prediktif terbatas di anestesi dan bedah
Kelompok pasien A adalah resiko yang lebih rendah
dan dengan hati yang cukup dapat dianggap sebagai
kandidat untuk sebagian besar jenis operasi.
Grup B pasien - diterima tetapi benar kelainan
Pasien Grup C menghadirkan risiko operasi yang
sangat tinggi - prosedur bedah pada pasien ini harus
dihindari jika mungkin -. Hanya darurat atau
prosedur yang menyelamatkan jiwa harus dilakukan

Preoperative assessment

Type and extent of liver disease


Extra hepatic effects
Risk assessment
Patients general condition- hydration ,nutrition
Associated co-morbid conditions
LFT
Consent
Premedication-short acting temazepam in absence
of neurological impairment orally avoid
intramuscular injections
H2 receptor antagonists
Preop Vit K ,optimal hydration

Penilaian perioperatif
Jenis dan tingkat penyakit hati
Efek hepatik Ekstra
penilaian risiko
Pasien umum kondisi-hidrasi, gizi
Terkait kondisi co-morbid
LFT
persetujuan
Premedikasi-short acting temazepam dalam ketiadaan
gangguan neurologis secara lisan-menghindari suntikan
intramuskular
Antagonis reseptor H2
Preop Vit K, hidrasi yang optimal

PREOP INVESTIGATIONS

Hematological Hb , Platelet
count,WBC Coagulation profile
Metabolic sr. glucose ,urea
,creatinine electrolytes
Cardio respiratory chest xray,ECG ,PFT, ABG
Liver function
sr.bilirubin,albumin,liver enzymes

Hematologi-Hb, hitung trombosit,


WBC profil Koagulasi
Metabolik - sr. glukosa, urea, kreatinin
elektrolit
Cardio pernafasan - x-ray dada, EKG,
PFT, ABG
Fungsi hati - sr.bilirubin, albumin,
enzim hati

Pre-op risk factors


associated with
postoperative mortality

Serum albumin <3g/L


Serum bilirubin >50 mol/L
PT >1.5 s over control
Presence of infection
WBC > 10,000
Treatment with more than two antibiotics
Presence of Ascites
Malnutrition
Emergency surgery

Faktor risiko pra-op


terkait dengan kematian
pasca
operasi
Albumin serum <3g / L
Bilirubin serum> 50 umol / L
PT> 1,5 s alih
Adanya infeksi
WBC> 10.000
Pengobatan dengan lebih dari dua antibiotik
Kehadiran Ascites
malnutrisi
operasi darurat

Anaesthetic Technique

Avoid hypotensive techniquesintra hepatic necrosis


High conc of oxygen -- - due to intrapulmonary shunts
Avoid hypotension & hypoxemia
Meticulous fluid balance
Ascites may lose a large amount of fluid rapidly
Concentrated albumin solutions to correct
hypoproteinemia
Fresh blood to prevent hypocalcemia due to
reduced metabolism of preservatives
FFP 12 - 15 ml/Kg Correct dilutional
coagulopathy
1 unit of FFP for every 1 unit of packed cells or 250
ml of 0.9% saline or colloid [500 ml of FFP -
Clotting factors by 20% ]
Maintenance of temperature

Hindari tekhnik hipotensi- nekrosis intra hepatik


Pekat tinggi oksigen --- karena pirau intrapulmonary
Hindari hipotensi & hipoksemia
Telisi Keseimbangan cairan Asites - mungkin kehilangan sejumlah besar cairan dengan
cepat
Solusi untuk albumin terkonsentrasi memperbaiki
hypoproteinemia
Segar darah untuk mencegah hipokalsemia karena
berkurangnya metabolisme pengawet
FFP 12 - 15 ml / Kg koagulopati dilusi-Benar
1 unit FFP untuk setiap 1 unit sel dikemas atau 250 ml salin 0,9%
atau koloid [500 ml FFP - faktor pembekuan sebesar 20%]
Pemeliharaan suhu

Monitoring

Monitoring of temperature
Coagulation status should be monitored platelet count ,fibrin
degradation products , prothrombin time , activated clotting
time, partial thromboplastin time
Thromboelastography has been used as a tool in liver
transplantation
Repeated BP cuff inflation may lead to bruising in patients
with altered haemostatic function
Insertion of Intra arterial line care to prevent haematoma
Jugular route is preferred in CVP monitoring
Oximetry
Urine output
Blood loss
Monitor ionized calcium

Pemantauan suhu
Status Koagulasi harus dipantau hitung-platelet, produk degradasi
fibrin, waktu protrombin, waktu pembekuan diaktifkan, waktu
tromboplastin parsial
Thromboelastography telah digunakan sebagai alat dalam
transplantasi hati
Berulang inflasi mungkin BP manset menyebabkan memar pada
pasien dengan fungsi hemostatik diubah
Penyisipan garis Intra arteri - hati untuk mencegah hematoma
Jugularis rute lebih disukai dalam pemantauan CVP
oksimetri
Output urine
kehilangan darah
Memantau kalsium terionisasi

DRUGS
Thiopentone intrinsic clearance delayed
but recovery not delayed because of
redistribution
Alcoholic cirrhosis larger dose of thio
cross tolerance
Halothane and enflurane reduce hepatic
arterial flow (vasodilatation, negative
inotropic effects)
Isoflurane increases hepatic blood flow
[preferred]

Thiopentone - izin intrinsik tertunda tapi


pemulihan tidak tertunda karena redistribusi
Beralkohol sirosis - dosis yang lebih besar
dari tio - cross toleransi
Halotan dan enfluran mengurangi aliran
arteri hepatik (vasodilatasi, efek inotropik
negatif)
Isoflurane meningkatkan aliran darah hati
[disukai]

NEUROMUSCULAR BLOCKING
AGENTS

Reduced plasma pseudo cholinesterase activity


Prolonged action- vecuronium ,
pancruonium[1.6 fold]
Decreased biliary excretion
Increased volume of distribution larger
initial doses
Recommended Atracurium metabolism
independent of liver and kidneys
For transplantation long acting agent such
as doxacurium

Mengurangi aktivitas cholinesterase semu plasma


Berkepanjangan tindakan-vecuronium,
pancruonium [1,6 kali lipat]
Penurunan ekskresi bilier
Peningkatan volume dosis awal distribusi
yang lebih besar
Rekomendasi Atracurium - metabolisme
independen hati dan ginjal
Untuk transplantasi - agen bertindak panjang
seperti doxacurium

OPIODS & SEDATIVES

Narcotics
Reduced metabolism of morphine and
pethidine
Prefer fentanyl
Remifentanyl - ideal
Benzodiazepines
Diazepam - prolonged half life
Oxazepam and lorazepam preferrred
metabolised by glucuronidation
without liver requirement

OPIODS & SEDATIVES


narkose
Mengurangi metabolisme morfin dan petidin
memilih fentanyl
Remifentanyl - ideal
Benzodiazepin
Diazepam - paruh berkepanjangan
oxazepam dan lorazepam lebih dipilihdimetabolisme oleh glucuronidation tanpa
membutuhkan hati untuk dimetabolisme

? Regional Anaesthesia

Contraindicated if PT >2.5 s above control,


platelet count < 50,000 /cu.mm, bleeding
time >12 mts
Spinal and epidural anaesthesia carries the
risk of epidural haematoma and paralysis if
there is abnormal clotting but there are
otherwise no special precautions.
The half-life of lignocaine is prolonged in
liver failure but this is not significant when
used in regional anaesthesia.
LA dose diminished in presence of Ascites

Kontraindikasi jika PT> 2,5 s atas kontrol, jumlah


trombosit <50.000 / cu.mm, waktu perdarahan>
12 mts
Spinal dan epidural anestesi membawa risiko
hematoma epidural dan kelumpuhan jika ada
pembekuan abnormal tetapi ada jika tidak ada
tindakan pencegahan khusus.
Waktu paruh dari lignocaine berkepanjangan
pada gagal hati tapi ini tidak signifikan bila
digunakan dalam anestesi regional.
LA dosis berkurang di hadapan Ascites

Canadian Journal of Anesthesia, Vol 45, 452459,


Obstetrical anaesthesia for a parturient with
preeclampsia, HELLP syndrome and acute cortical
blindness
A 39-yr-old woman, with three past
uncomplicated pregnancies presented at 33 wk
with acute cortical blindness.
Based on clinical and laboratory assessment, a
diagnosis of preeclampsia with HELLP
syndrome was made.
A CT scan of her head demonstrated ischaemic
lesions of her basal ganglia, extending
superiorly to involve both posterior parietal and
occipital regions.
Infusions of magnesium sulphate and
hydralazine were started and an urgent
Caesarean section was performed under
subarachnoid anaesthesia after insertion of an
arterial line and intravenous hydration.

Contd

The course of anaesthesia and surgery was uneventful


and she delivered a live 1540 g female infant.
By the following morning, she had recovered some
vision and visual recovery was complete by 72 hr
postpartum.
Her postoperative course was uneventful
CONCLUSION: Provided that it is not contraindicated
because of prohibitive risk to the mother, regional
anaesthesia has particular advantage in these
patients.
In particular, the use of spinal anaesthesia, which has
been discouraged by some for this patient population,
should be re-evaluated.

Postoperative
management

Oxygen enriched air


Major surgery elective post operative
ventilation
Replace blood loss
Maintain adequate urine output
Dopamine and inotropes should be
continued.
The principle complications are likely
to be continued bleeding, sepsis and
hepatic decompensation

Peri-operative considerations in ChildPugh A patients

Pre-operative
Aetiology of condition - virology,
Drug idiosyncrasy
Blood count and platelets
Clotting screen
Assess renal function
Previous anaesthetics
Per-operative
Consider drug bio-availability issues ?
Avoid drugs excreted via liver
Regional techniques acceptable if clotting
normal
Post-operative
Monitor for post-operative hepatic
decompensation
Possible prolonged duration of action in
opiates HDU / ITU care

Child-Pugh Group B/C patient


undergoing major surgery
Previous upper abdominal surgery, portal
hypertension and coagulopathy dramatically
increase the potential for per-operative blood loss
8-12 units of blood, together fresh frozen plasma
and platelets should be available.
Pre-medication
Sedative premedicants should be avoided in the
encephalopathic patient.
Other drugs may be needed pre-operatively and
include antibiotics and H2 receptor antagonists.
The oral or intravenous route used intramuscular injections should be avoided.
Coagulopathy may require correction with fresh
frozen plasma and platelets and renal replacement
therapy may need to be considered.

Per-operative considerations

Regional techniques -- considered carefully coagulopathy , epidural varices can pose an


additional risk.
Vascular access with a multi-lumen central
venous catheter together with at least one large
bore central line
Monitoring of arterial and central venous
pressures is mandatory.
Pulmonary artery, pulmonary capillary wedge
pressure and cardiac output measurements may
be necessary in the sick patient.
Trans-oesophageal echocardiography and
volumetric haemodynamic monitoring / pulse
contour analysis can provide significant
additional information for the strategic
management of these patients.

CONTD

Coagulation and fibrinolysis are major


concerns.
The potential for large volume blood replacement
means that temperature should be measured and
a fluid warmer and warming mattress used.
Regular per-operative estimation of INR/PTR may
be necessary - thromboelastography provides
useful intra-operative evaluation of coagulation.
Blood conservation - considered
Preservation of hepatic function - Nacetylcysteine (NAC) is a sulphur-containing
antioxidant - benefit patients with fulminant
hepatic failure.
NAC appears to improve oxygen delivery
and consumption, and reduce base deficit.
Renal Function - Dopamine may be useful

Bleeding oesophageal
varices

Bleeding oesophageal varices - lifethreatening complication of - often occur


against a background of abnormal clotting,
thrombocytopenia, encephalopathy and
Ascites.
Overall mortality is 30%.
The principles of anaesthetic management
Protect the airway.
Establish good vascular access.
Volume replacement - colloid, blood, fresh
frozen plasma and platelets. Avoid saline.
Check / correct clotting. Give Vitamin K,
correct fibrinolysis and review blood chemistry.

Intoxicated Alcoholic
Patients

Requires less anaesthetic additive depressant


effect of alcohol & anaesthetics
Ill - equipped to withstand stress & Acute blood
loss
Alcohol decrease the tolerance of brain to hypoxia
Risk of regurgitation & aspiration - alcohol
tone of lower oesophageal sphincter & slows
gastric emptying
Alcohol Interferes with platelet aggregation
Causes conc. of plasma catecholamines ?
Intraoperative dysarrhytmias

POSTOPERATIVE JAUNDICE
Mild 17%, marked - 4%

Patient factors
Congenital
hemolytic disorders
Acquired hemolytic
disorders
Pre existing liver
disease
Coagulopathy
Gilberts syndrome
Sepsis

Perioperative
factors
Anaesthetic induced
HBF
Bleeding
Hypotension
Blood transfusion
Biliary tree trauma
Viral hepatitis
Drugs
Halothane ,antibiotics
Nonsteroidal agents

POSTOPERATIVE JAUNDICE

Extravascular break down of haematoma [1 ltr]


-5000mg Bilirubin
500ml of blood transfusion contains 250 mg
bilirubin
Intravascular destruction of RBC can occur in
G6P-dehydrogenase defeciency,
cardiopulmonary bypass, Artificial valves,
sickle cell disease, multiple blood transfusions
Delayed transfusion reactions hemolysis
postop jaundice
Biliary obstruction due to surgery -bilirubin &
alkaline phosphatase within 3 days of surgery

Contd
Postop cholecystitis/pancreatitis may follow
non biliary surgery 3- 30 days post op
Post operative intrahepatic cholestasis
[benign] - associated with multiple blood
transfusions, hypoxia ,hypotension bilirubin & alkaline phosphatase within 27 days of surgery resolution in 3 weeks
Management
Prevention is the best treatment
Avoid precipitating factors

Halothane Hepatitis

The incidence is 1:7000-30,000 halothane


anaesthetics - higher in women, the middle
aged and the obese
Rarer in paediatric patients and with the
newer volatile agents.
Commonest iatrogenic cause of fulminant
hepatic failure
Unexplained liver damage within 28 days of
halothane exposure in previously normal
patient idiosyncratic reaction
Clinical features : malaise, anorexia,fever
within 7 days ,jaundice within days to 4 weeks

Halothane Hepatitis
DIAGNOSIS

Serum antibodies that react with specific liver


microsomal proteins that are altered by
trifluroacetyl chloride metabolite of halothane
Gross rise of Transaminases [500 -2000 u/l]
Risk factors
High - recent previous exposure [ 78 %]
previous adverse reaction
Uncertain - obesity
Female [1.6 :1 ]
Drug allergy [ 15 %]
Family history
Lymphocyte sensitivity to phenytoin

Contd

The cause not fully established - multifactorial - ?


possible immunological cause .
Immune sensitization to trifluoracetylated
proteins produced by Cyt P450 2E1 in genetically
predisposed subjects
Reduced hepatic blood flow and hypoxia are also
to blame
Related to the degree of metabolism of the volatile
agent, so toxic metabolites may be involved.
The onset time of the jaundice is shorter with
increasing numbers of exposures to halothane.
Nevertheless, enflurane and isoflurane are
associated with hepatic dysfunction, albeit
apparently at lower rates than halothane. WHO
database holds 225 and 159 reports respectively.

Halothane exposure
guidelines
Avoid Halothane if
Within at least 3 months of a previous
exposure
Previous adverse reactions -jaundice or
pyrexia
Family history of hepatic reactions to
halothane.
Pre - existing liver disease
Adverse reactions to Other volatile
anaesthetic agents.

Liver and Pregnancy

Normal in size
A decrease in total protein as well albumin.
An increase of the liver dependent clotting factors
such as fibrinogen.
An increase of alkaline phosphates 3-4 times
secondary to placental alkaline.
Sr.cholinesterase 30%
Normal transaminase [AST,ALT] levels and
bilirubin
Any increase in transaminase levels and bilirubin
good indicator of pregnancy induced liver
disease

Intrahepatic Cholestasis of
Pregnancy

Incidence 0.01%. Mainly in the third trimester


. Rare in black patients .
Strong family history .
High recurrence in subsequent pregnanacies
60-70%.
Pruritus alone - 80 percent ,
Jaundice develop in 20 percent
Infrequent, mild to moderate steatorrhea.
Bilirubin level less than 5 mg /dl , minimal or
no elevation in transaminases

IChP contd

Incidence of fetal distress and death high if early


delivery is not induced (deliver at week 38 if
pruritus , at week 36 in case of jaundice )
Parenteral vitamin K , Ursodeoxycholic acid , 15 mg
/kg , Cholestyramine binds bile acid salts ,
Dexamethasone
Pruritus resolve within two days of delivery but
bilurubin within 4-6 weeks

Implications on Anaesthesia

Check coagulation profile


Ask for vit K I.V
take care of high incidence of fetal distress ,
meconium-stained , prematurity ( neonatologist
must attend with incubator

Preeclampsia & Eclampsia

About 25% of patients with Severe pre-eclampsia


and 90% of those with eclampsia will have elevated
AST and ALT > 5 times and bilirubin < 5 mg/dl
If not associated with other criteria of HELLP
syndrome e.g. low platelets , haemolysis , we give
prophylactic dexamethasone 8mg/12hrs. beside
mg.sulphate , antihypertensive , albumin 20% /
50ml/day

Implications on anaesthesia

Painless labour with epidural to reduce stress


response which could continue to anaesthesia
provided INR <1.5
Difficult intubation because of edema - small cuffed
tube 6-7 mm
Adequate analgesia
Fluids restriction
Continue medications postoperative in ICU .

HELLP syndrome

Hemolysis , Elevated liver enzymes, Low


platelets
Peripartum multiorgan damage with preeclampsia result from very active platelets
aggregation everywhere with end organ ischemia
and congestion with deposition of fibrous network
and entraped haemolysed RBCs & platelets
necrosis & periportal haemorrhage
Nausea, vomiting , headache and upper right
abdominal pain ,hypotension /shock
Best markers are the maternal lactate
dehydrogenase level and the maternal platelet
count.

Congested liver of HELLP


syndrome

CONTD

Perinatal administration of dexamethasone in a


high dosage of 10 mg intravenously every 12 hours
has been shown to markedly improve the laboratory
abnormalities associated with HELLP syndrome.
Magnesium sulfate to prevent seizures.
Antihypertensive therapy if blood pressure is
greater than 160/110 mmHg despite the use of
magnesium sulfate.
Anesthesia like severe preclampsia
avoid trauma to liver
Vit. K if INR >1.5
FFP 4-6 if INR >2
Platelets 6-8 units if platelets <50.000.
Mortality maternal 50 - 60%,foetal -60%

ACUTE FATTY LIVER OF


PREGNANCY

Rare ,serious disorder ,unknown etiology


Symptoms in third trimester abdominal
pain ,nausea vomiting, anorexia,fatique ,
fever ,headache
Rapid progression bleeding, jaundice,
encephalopathy, renal failure, hepatic
failure, coagulopathy - PPH
Transaminases, hyperbilirubinemia,
prothrombin time --- DIC
Prompt delivery is advisable

Hepatic Rupture and


Infarction

Older multigravida mothers with preeclampsia (75 to


85 percent) are at higher risk.
Extremely rare, 1:40,000 to 1: 250,000 .
Patients with hepatic rupture typically present in
shock, with preceding right upper quadrant pain,
hypertension, elevated transaminase levels (greater
than 1,000 IU per L) and coagulopathy.
Therapy for hepatic rupture has included transfusion
of blood products and intravenous fluids, surgical
evacuation and arterial embolization with 75 percent
perinatal mortality rate have been noted in hepatic
rupture.
Hepatic infarction was typically present with fever
and marked elevations in transaminase levels. In
surviving patients, liver function and histopathology
are normal within six months of delivery

Anesthesia in pregnant women with


HELLP syndrome.

Retrospective study. For the period of 1 July


1996, through 30 June 2000
RESULTS: During the period of study 119 patients
had HELLP syndrome. Eighty-five patients had
cesarean delivery and 34 had vaginal delivery.
Seventy-one patients had diagnosed HELLP
syndrome previous to the anesthesia and 14
postcesarean delivery; the range platelet count
was 19000-143000/microl.
Of these 71, 58 had an epidural anesthesia, 9 had
general anesthesia and 4 had spinal anesthesia.
There were no neurologic complications or
bleeding in the epidural space.
CONCLUSION: We found no documentation of any
neurologic or hematologic complications of women
with HELLP syndrome and neuraxial anesthesia.

Subdural Hematoma following dural


puncture in a parturient with HELLP
syndrome

This complication occurred following


accidental dural puncture in a parturient
with thrombocytopenia (99,000L-1) who
subsequently developed the syndrome of
hemolysis, elevated liver enzymes and low
platelets.
On the first postoperative day, postdural
puncture headache (PDPH) developed.
An epidural blood patch (EBP) was deferred
to the third postoperative day because of a
platelet count of 21,000L-1.
Headache intensified from a typical PDPH
to one which was not posturally related.

A second EBP was abandoned after the


injection of 5 mL of blood because of
increasing headache during the procedure.
Magnetic resonance imaging revealed
bilateral temporal subdural hematomas.
The patient was managed conservatively and
discharged home without any sequelae.
Conclusion: It is conceivable that
thrombocytopenia together with possible
abnormal platelet function increased the risk
of subdural hematoma.
Alternative diagnoses to PDPH should be
considered whenever headache is not
posturally related.

OCUPATIONAL HAZARD

Risk of transmission of HBV following


inoculation is 5 -30%
May occur through needle prick/cuts/
sharp injuries/mucous membraneswaterproof dressing
Wear gloves while inserting a cannula
,airways, intubation & extubation
Sharps should not be handed directly to
others
See to the sterilisation of other
contaminated things