J
J receptors, see Juxtapulmonary capillary receptors
J wave, see Hypothermia
Jackson, Charles T (1805–1880). US chemist, present at Wells’ unsuccessful demonstration of N2O in 1846; suggested diethyl ether to Morton for dental topical anaesthesia instead. Applied for the patent rights to ether jointly with Morton, the latter subsequently taking over 90% of Jackson’s share. Jackson later claimed sole credit for the discovery of anaesthesia.
Jackson, Chevalier (1865–1958). Renowned US laryngologist. Perfected a direct-vision laryngoscope in the early 1900s, and wrote extensively on laryngoscopy and tracheal insufflation.
• Normal formation and metabolism of bilirubin:
haemoglobin is broken down to amino acids and haem in the reticuloendothelial system. Haem is further metabolised to lipid-soluble unconjugated bilirubin that is transported (bound to albumin) to the liver.
in the liver, unconjugated bilirubin is conjugated with glucuronic acid, rendering it water-soluble.
increased bilirubin production, e.g. haemolysis. Usually mild. Unconjugated and conjugated bilirubin levels are raised, with increased urinary urobilinogen.
impaired conjugation of bilirubin, e.g. hepatitis, cirrhosis, drug-induced (e.g. α-methyldopa, paracetamol), hepatic failure. Unconjugated bilirubin is raised; urinary urobilinogen may be raised because the liver is unable to re-excrete it.
congenital abnormalities of bilirubin transport are rare, except for Gilbert’s syndrome (hepatic glucuronyltransferase deficiency causing mild unconjugated bilirubinaemia with otherwise normal liver function tests and no urinary bilirubin).
obstruction of bile drainage, e.g. gallstones, pancreatic carcinoma, cholangitis, cholecystitis (extrahepatic), primary biliary cirrhosis, drug-induced, e.g. contraceptives. Conjugated bilirubin is raised, often markedly, and is excreted in the urine, which is dark (but with reduced urobilinogen). Faeces are pale and fatty. Itching is common.
The latter two types are frequently mixed and difficult to distinguish.
Jaundice in ICU patients is often part of the presenting problem (e.g. in hepatic failure, biliary obstruction, sepsis) or may result from drug therapy, the development of acalculous cholecystitis, haemolysis of intra-abdominal haematoma, ischaemic hepatitis (in shocked patients) or the administration of TPN. It may also be part of multiple organ dysfunction syndrome.
support of other organs, e.g. circulation, respiration.
treatment of associated clotting abnormalities, e.g. with clotting factors, vitamin K.
preoperative assessment as above, and for hepatic failure, depending on severity and cause.
risk of perioperative acute kidney injury due to acute tubular necrosis or hepatorenal syndrome:
– especially common with obstructive jaundice, since bilirubin levels are often highest.
– more likely if dehydration or biliary sepsis is present.
– plasma urea/creatinine is monitored preoperatively.
– preoperative iv hydration is instituted to maintain urine flow above 1 ml/kg/h.
– mannitol may be given if bilirubin is very high or urine output inadequate despite hydration. Furosemide has also been used.
anaesthetic drugs and techniques as for hepatic failure.
• Postoperative jaundice may be due to:
underlying medical/surgical conditions.
