Professional Documents
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DISEASE
Dr.Pratheeba Durairaj ,M.D,D.A,
9.1.09
Liver Functions
Direct effects
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
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
Neurological problems
HAEMATOLOGICAL PROBLEMS
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
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
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
Contd
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
POINTS
1
SCORE
D
2
>35
28-35
<28
<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
[Mg /dl]
INR >2.3
Preoperative assessment
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
Anaesthetic Technique
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]
NEUROMUSCULAR BLOCKING
AGENTS
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
? Regional Anaesthesia
Contd
Postoperative
management
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
Per-operative considerations
CONTD
Bleeding oesophageal
varices
Intoxicated Alcoholic
Patients
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
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
Halothane Hepatitis
DIAGNOSIS
Contd
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.
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
IChP contd
Implications on Anaesthesia
Implications on anaesthesia
HELLP syndrome
CONTD
OCUPATIONAL HAZARD