Postoperative jaundice is defined as elevated bilirubin levels occurring after surgery, which can have many causes. It is estimated that around 1 in 80 patients undergoing surgery, especially cardiac surgery, may experience significant postoperative liver dysfunction unrelated to the surgery or anesthesia. Possible causes of postoperative jaundice include hemolysis, acute or chronic liver disease, inherited liver disorders, medications, infections, and decreased hepatic blood flow during or after surgery. Evaluation involves distinguishing between pre-hepatic, hepatic, or post-hepatic causes through history, examination, and liver function tests. Identifying and addressing reversible causes is important.
2. Definition-
Postoperative jaundice is defined as the elevation of
bilirubin that occurs after the completion of surgery and
has many possible causes, associated laboratory
findings, and implications.
It can, but not always, be associated with icterus.
3. Jaundice Factfile-
Approximately 1 out of 80 healthy patients who
undergo surgery under anaesthesia (mostly cardiac
surgery) may have clinically significant post
operative liver dysfunction that is totally unrelated
to surgery or anaesthesia
7. Hemolytic Jaundice results in unconjugated
hyperbilirubinemia.
10% of transfused RBCs hemolyse within the first 24
hours following transfusion. Each unit of blood
provides a bilirubin load of 250 mgs/100 cc of
blood.
Prosthetic cardiac valves known to cause the same.
Diagnosed by Biochemical tests
Elevated LDH
Ser. Unconjugated Bilirubin
Reticulocyte count
Urinary Haptoglobulin
9. Warrants assessment of the patient’s
condition and sequential biochemical
profiles.
Coagulopathy corrected with Vit K.
Usually subside within 3-4 weeks.
Failure of Vit K to correct a prolonged PT
typically indicates the presence of hepatic
parenchymal dysfunction
10. Primary biliary tract problem
Significant liver disease
Severe sepsis
11. Early - Increased splanchnic blood flow as
a consequence of increased hepatic oxygen
extraction to support phagocytosis of
sudden overload of bacterial endotoxins.
Late - Constricted splanchnic
vasculature due to septic shock.
Dysregulation of physiologic hepatic
arterial buffer response.
12. Passive hepatic congestion due to CCF
causes little if any damage to liver.
Prognosis depends on the severity of
underlying cardiac illness.
Reversible after the cardiac function is
improved
13. There are essentially 3 types of
hepatobiliary disorders associated with
parenteral nutrition (PN) therapy: steatosis,
cholestasis, and gallbladder sludge/stones.
Etiologic factors specifically related to the
PN formulation or nutrient intake have also
been evaluated, including excessive calorie
intake, dextrose-to-lipid ratio, amino acid
dose, taurine deficiency, IV fat emulsion
(IVFE) dose, carnitine deficiency, choline
deficiency, and continuous vs cyclic
infusion.
14. Minor increases in serum aminotransferase
concentrations are relatively common in
patients receiving PN therapy and generally
require no intervention.
The primary indicator of cholestasis is a
serum conjugated bilirubin >2 mg/dL.
When a patient receiving PN develops liver
complications, it is necessary to rule out all
treatable causes and minimize other risk
factors.
All potential hepatotoxic medications and
herbal supplements should be eliminated.
15. Modifications to the PN regimen that may
be helpful include reduction of calories,
reduction of IVFE dose to <1 g/kg/d,
supplementation of taurine in the infant,
and use of cyclic infusion. Initiation of even
small amounts of enteral nutrition and use
of ursodiol may be beneficial in stimulating
bile flow.
In the long-term PN patient with severe and
progressive liver disease, intestinal or liver
transplantation may be the only remaining
treatment option.
16. N20 – Higher prevalence of jaundice in
personnel chronically exposed to N2O.
Propofol, midazolam, fentanyl have not
been shown to significantly alter hepatic
function.
Very large doses (>750 mgs) of
thiopentone may cause hepatic
dysfunction.
17. Incidence 1:7000-30,000
It is even rarer in paediatric patients and with
the newer volatile agents.
The risk is thought to be higher in
- women,
- middle aged,
- obese,
- repeated exposure within 4 weeks
18. Possible immunological mechanism..
Hepatic blood flow is decreased by
halothane in parallel with an overall
decrease in cardiac output.
Avoid repeat exposure within 3 months.
History of unexplained jaundice following
Halothane use is an absolute contraindication for
its further usage
21. Obtain following History
H/O Blood transfusion
H/O IV drug abuse
Alcohol
Hepatotoxic drugs, toxins,infections
Family History
Past Medical History
Any Surgery
26. Distinguish whether jaundice is prehepatic, hepatic or
post hepatic.
Identify reversible causes.
Patients with active liver disease, such as hepatitis, are
at high risk of deterioration during surgery and this
should be avoided or delayed where possible.
Hypoperfusion, haemodilution and other factors that
reduce the delivery of oxygen to the liver or increase
the bilirubin load are thought to cause postoperative
hyperbilirubinaemia and should be avoided.
Longer the operative time and the larger the volume of
blood transfused, the higher the incidence of
postoperative hyperbilirubinaemia