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.
Notes to myself:
- The show notes are perfect. There really is nothing in the notes that isn’t important. So just review the notes.
- Be sure and review the podcast and show notes for Emergency Medicine Cases’ Ep 149 Liver Emergencies: Thrombosis and Bleeding, Portal Vein Thrombosis, SBP, Paracentesis Tips and Tricks, November 2020, Helman, A. Himmel, W, Steinhart, B.
- The above resource is outstanding and contains information not available in other resources on serious liver disease.
Here are excerpts that I do just to reinforce my learning.
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.
