Links To And Excerpts From “Ep 148 Liver Emergencies: Acute Liver Failure, Hepatic Encephalopathy, Hepatorenal Syndrome, Liver Test Interpretation & Drugs to Avoid” From EMC

In this post I link to and excerpt from Emergency Medicine Cases latest podcast and show notes of Ep 148 Liver Emergencies: Acute Liver Failure, Hepatic Encephalopathy, Hepatorenal Syndrome, Liver Test Interpretation & Drugs to Avoid:*

*Helman, A. Himmel, W. Steinhart, B. Episode 148 Liver Emergencies: Acute Liver Failure, Hepatic Encephalopathy, Hepatorenal Syndrome, Liver Test Interpretation & Drugs to Avoid. Emergency Medicine Cases. November, 2020. https://emergencymedicinecases.com/liver-emergencies-acute-liver-failure-hepatic-encephalopathy-hepatorenal-syndrome-liver-test-interpretation. Accessed 11-11-2020.

Note to myself: The show notes are perfect. There really is nothing in the notes that isn’t important. So just review the notes.

Here are excerpts [I just included a couple of things because here, again, because I need to review all of the notes on EMC’s website.]:

Take home points for Liver Emergencies: Acute Liver Failure, Hepatic Encephalopathy, Hepatorenal Syndrome, Liver Test Interpretation & Drugs to Avoid

  • Have a low threshold to order acetaminophen levels in the sick liver patient
  • Sepsis is a common trigger of acute liver failure and may be subtle – when in doubt, treat on speculation
  • ED medications requiring dose adjustment or avoidance in the liver patient: NSAIDs, opioids, acetaminophen, benzodiazepines, antiepileptics (except levetiracetam), macrolides, B-blockers, amiodarone
  • Watch out for hypoglycemia in sick liver patients and start an infusion of D10W after you have corrected the hypoglycemia
  • Serum ammonia levels are unreliable and can be misleading; assume high ammonia levels in the patient suspected of hepatic encephalopathy and treat with lactulose and/or polyethylene glycol and rifaximin
  • IV albumin needs to be considered in the patient with acute liver failure, hepatorenal syndrome and hepatic encephalopathy
  • Have a low threshold to treat for hepatic encephalopathy and hepatorenal syndrome on speculation as they are both diagnoses of exclusion
  • Some patients with hepatic encephalopathy will develop cerebral edema and this may be subtle; keep the head of bed at 45 degrees and give hypertonic saline if there are any clinical signs of cerebral edema

Hepatic Encephalopathy: A Diagnosis of Exclusion

Step 1: Rule out other causes of altered level of awareness (LOA) including sepsis, renal failure, alcohol withdrawal and subdural hematoma.

Step 2: Assess for and address common precipitants of hepatic encephalopathy which include:

  • Medications – noncompliance/use of diuretics/benzodiazepines
  • GI bleeding
  • Hypokalemia
  • Alkalosis
  • Volume depletion
  • Sepsis

Step 3: Make the diagnosis

  • After excluding other causes of altered LOA look for asterixis (nonspecific – also seen in renal failure) and signs of cirrhosis
  • Diurnal sleep pattern reversal may help support a diagnosis of hepatic encephalopathy
  • In general, the more altered the patient is, the more severe the disease

Step 4: Correct presumed hyperammonemia (without the need for a serum ammonia level)

  • Lactulose 20 g (30mL) po, titrated to 3 to 4 soft stools per day (reduces mortality, serious complications)
  • If patient is NPO, Polyethylene glycol (PEG) via NG tube 4L over 4 hours (more rapid resolution of hepatic encephalopathy compared to lactulose in 2 small RCTs) or lactulose enema with 1–3 L of 20% solution

Step 5: Replace fluid and glucose deficits

  • NS is our experts’ crystalloid of choice for fluid replacement in hepatic encephalopathy
  • Consider albumin in patients with low serum albumin given some weak RCT evidence that it may improve outcomes in hepatic encephalopathy
  • One bolus of 50% dextrose may not be adequate therapy for hypoglycemia because of depleted glycogen stores; maintenance infusions of D10W or D25W should be administered after the D50W bolus

Step 6: Treat even the mildest hypokalemia

  • Hypokalemia contributes to hyperammonemia by decreasing ammonia excretion; correcting hypokalemia is thought to decrease ammonia levels in patients with hepatic encephalopathy

Step 7: Assess for and treat cerebral edema

  • Cerebral edema is the most common cause of death in patients with hepatic encephalopathy due to the rapid accumulation of ammonia
  • Cerebral edema may be clinically subtle; if suspected, keep the head of the bed elevated at 45 degrees and consider hypertonic saline (20 ml of 30% NaCl targeting a serum Na level between 145-150 mmol/L)

Step 8: Consider refaximin

  • Rifaximin 400-550 mg po daily – this antibiotic is not absorbed through the gut, eradicates E. Coli which produces ammonia, and is used for long term maintenance of patients with recurrent hepatic encephalopathy

Hepatorenal Syndrome: Another Diagnosis of Exclusion

Hepatorenal Syndrome carries a mortality rate of >50% in the absence of liver transplant. It is a diagnosis of exclusion.

 

 

 

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