CRACKCast E216 – Jaundice

In CRACKCast, Podcast by Dillan RadomskeLeave a Comment

This episode of CRACKCast focuses on a slightly more uncommon ED presentation – jaundice. Grab a coffee and sit back as the CRACKCast crew (featuring Dr. Sey Shwetz, Saskatoon PGY-5 Emerg Resident/PEM fellow extraordinaire) go through the approach to your jaundiced patient.

Shownotes – PDF Here

Rosen’s in Perspective

Jaundice is one of those ED complaints that is a bit more rare than some of the standard cases we see every shift. However, there is a wide range of causes for jaundice, and an understanding of pathophysiology is key. We have got you covered here at CRACKCast – the next time you walk into a room and your patient is as yellow as Homer Simpson, you will know exactly what to do! 

A few points to highlight from those first few Rosen’s paragraphs. Jaundice is clinically evident at 2.5mg/dl or about 43µmol/L, first seen in tissues with relatively high concentrations of albumin (eyes and skin). Remember that there are 3 categories of bilirubin problems – increased production due to hemolysis, hepatocellular dysfunction causing impaired uptake and conjugation, and obstruction pathologies that prevent bilirubin excretion. When it comes to neurotoxicity, unconjugated bili is the one we worry about – this is not bound to albumin, and can cause encephalopathy and kernicterus.

[1] Explain broad causes of elevated bilirubin (obstructive, hepatocellular, and hemolysis) and the significance of direct vs. indirect hyperbilirubinemia (Fig 25.1)

Bilirubin is a byproduct of heme breakdown. 

This is released into its unconjugated form into the circulation and bound to albumin. It is then taken up into the hepatocytes where it is conjugated. Conjugated bilirubin is taken up and stored in the hepatocytes, and then subsequently excreted into the intestine. 

Direct hyperbilirubinemia = conjugated bilirubin 

  • Obstructive causes to consider: 
    • Choledocolithiasis 
    • Intrinsic bile duct disease (cholangitis, stricture, neoplasm, extrinsic compression) 
    • Extrinsic compression 
  • Hepatocellular causes
    • Viral hepatitis 
    • Hepatic failure 
    • Alcoholic hepatitis 
    • Ischemia 
    • Toxins 
    • Autoimmune hepatitis
    • HELLP syndrome 

Indirect hyperbilirubinemia = unconjugated bilirubin 

  • Hematologic causes 
    • Hemolysis 
    • Hematoma resorption 
    • Ineffective erythropoiesis 
    • Gilbert’s syndrome 

See figure 25.1 for more details. 

[2] Explain your approach to the history and physical exam in patients with jaundice (Fig 25.2) 

Figure 25.2: Pivotal points in the assessment of the jaundiced patient. 

History

  • Viral prodrome 
  • Liver disease 
  • Alcohol/IVDU 
  • Biliary surgery 
  • Fever/abdo pain 
  • Pregnancy 
  • Toxic ingestion 
  • Cancer history 
  • History of blood products 
  • Occupational exposure 
  • CV disease 
  • Trauma 
  • Travel history 

Exam: 

  • Mental status 
  • Abdominal tenderness/HSM 
  • Skin findings – petechiae/purpura, caput medusae, spider angiomata 
  • Ascites 
  • Pulsatile mass 

[3] List 10 causes of jaundice (Table 25.2) 

See Table 25.2 for the full list.

  • Fulminant Hepatic Failure
  • Toxin (acetaminophen)
  • Viral hepatitis
  • Alcohol
  • Ischemic insult
  • Reye’s syndrome
  • Cholangitis
  • Sepsis
  • Heatstroke
  • Obstructing AAA
  • Budd-Chiari syndrome
  • severe CHF
  • Transfusion reaction
  • Preeclampsia/HELLP
  • Acute fatty liver of pregnancy

[4] Explain your approach to ancillary testing in patients with jaundice. 

Lab considerations: 

Bilirubin

Conjugated – think hepatic causes 

Unconjugated – think hemolytic causes (LDH, haptoglobin, reticulocyte count, peripheral smear, Coombs test) 

Liver enzymes: 

  • AST (intracellular, liver, heart, muscle, kidneys, brain, pancreas, lungs, RBC, LBC) 
  • ALT (specific to Liver
  • ALP (liver, bone, placenta, gut) 
  • GGT – specific to liver, can help confirm that ALP elevation caused by liver 

Cholestatic vs. Hepatocellular pattern: 

Cholestatic enzymes = ALP/GGT/Bili 

Hepatocellular enzymes = AST/ALT 

Liver function tests: 

Albumin 

INR 

Imaging – in general, ultrasound is best place to start assessing for liver/gallbladder/CBD pathology (can assess for cirrhosis, portal HTN, and ascites as well). 

Acute abdomen/undifferentiated sick patient: CT abdo/pelvis is never a bad idea.

Wisecracks

[1] What are the stages of hepatic encephalopathy?  

Table 25.1 (Rosen’s 9th Edition)

CLINICAL STAGEINTELLECTUAL FUNCTIONNEUROMUSCULAR FUNCTION
SubclinicalNormal examination findings, but work or driving may be impairedSubtle changes in psychometric testing
Stage 1Impaired attention, irritability, depression, or personality changesTremor, incoordination, apraxia
Stage 2Drowsiness, behavioral changes, poor memory, disturbed sleepAsterixis, slowed or slurred speech, ataxia
Stage 3Confusion, disorientation, somnolence, amnesiaHypoactive reflexes, nystagmus, clonus, muscular rigidity
Stage 4Stupor and comaDilated pupils and decerebrate posturing; oculocephalic reflex

[2] What is the triad of acute hepatic failure?

 Jaundice, encephalopathy, coagulopathy (INR > 1.5)

These can be some of the sickest patients in the hospital. When managing acute hepatic failure, think of the the complications of liver failure and go from there: 

SCREAM 

  • Sepsis – fluids/antibiotics/source control. Increased susceptibility to bacterial and fungal infections  
  • Coagulopathy – vitamin K, FFP/Platelets if actively bleeding or invasive procedures required. GI bleeds can occur if pt has varices. 
  • Renal Failure – Dialysis if indicated. 
    • Hepatorenal syndrome and severe peripheral edema can occur
  • Encephalopathy – acute setting – ICP management, lactulose/limited protein intake in hospital. Consider intubating and initiating ICP care for grade ¾ encephalopathy 
  • Ascites (keep SBP on ddx) 
  • Metabolic (hypoglycemia, electrolyte imbalance, acidosis) 
    • Hypoglycemia – D10 infusion
    • Acidosis – Bicarb infusion 
    • Electrolytes – (hyponatremia, hypokalemia,  hypophosphatemia) 
  • Detoxification with NAC if due to acetaminophen ingestion 

[3] What is Charcot’s triad and Reynold’s pentad? 

These triads describe the spectrum of disease seen in ascending cholangitis. 

Charcot’s Triad

  1. Fever 
  2. RUQ pain 
  3. Jaundice 

Reynold’s Pentad 

  1. Charcot’s Triad plus 
  2. Shock 
  3. Altered mental status 

[4] What is the “1000s Club” and how do you become a member? 

There are a few things that will put your ALT/AST in the thousands:

  1.  Viral hepatitis 
  2. Ischemic liver (hypotension, hypoxia, sepsis) 
  3. Drugs/Tox (acetaminophen) 
  4. Autoimmune hepatitis 
  5. Gallstone disease (acute bile duct obstruction) 
  6. Budd Chiari Syndrome (hepatic venous outflow obstruction) 
  7. Hepatic artery ligation/celiac artery ligation 

This is a good list to know. It’s not a club you ever want to join. 

Thank you again to Dr. Shwetz for joining us!

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Dillan Radomske

Dillan Radomske

Dillan Radomske is an Emergency Medicine resident at the University of Saskatchewan. He is passionate about technology-enhanced medical education, podcast creation and production, and Indigenous advocacy. He is one of the new CRACKCast hosts, and aspires to continue to contribute to the field of FOAMed in the future.
Dillan Radomske
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Owen Scheirer

Owen Scheirer

Owen is a resident in the FRCPC Emergency Medicine program at the University of Saskatchewan. When he's not running around the emergency department, he's hanging out with his wife, new baby girl, and dog. Spare time = climbing and cycling!
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