Lactulose and Rifaximin…is there anything else I can do for HE?

There are several trials that explore additional options for the treatment of hepatic encephalopathy. Earlier this month, UT Southwestern researchers (including Dr. Amit Singal, Dr. Jennifer Cuthbert, and other former members of our division of Gastroenterology and Hepatology) published the results of The HELP Randomized Clinical Trial, which compared lactulose to polyethylene glycol (AKA miralax, or golytely!) for the treatment of HE. They concluded that “PEG led to more rapid HE resolution than standard therapy, suggesting that PEG may be superior to standard lactulose therapy in patients with cirrhosis hospitalized for acute HE.” Check out the article at JAMA Internal Medicine.


AMA Intern Med. 2014;174(11):1727-1733. doi:10.1001/jamainternmed.2014.4746.

A Current Review of the Diagnostic and Treatment Strategies of Hepatic Encephalopathy

From the International Journal of Hepatology, here is a more extensive review of the pathophysiology, diagnosis, and treatment of HE.

Z. Poh and P. E. J. Chang, “A Current Review of the Diagnostic and Treatment Strategies of Hepatic Encephalopathy,” International Journal of Hepatology, vol. 2012, Article ID 480309, 10 pages, 2012. doi:10.1155/2012/480309

I’m confused…

A Review of Hepatic Encephalopathy


  • Overt HE consists of neurological and psychiatric abnormalities that can be detected by
    bedside clinical tests, whereas minimal HE can only be distinguished by specific
    psychometric tests.
  • There are many grading scales available, including the long standing West Haven Criteria,
    which is the most commonly used system.

    • WestHaven Criteria
  • Diagnosis of overt HE requires the exclusion of alternate causes of altered mental status.
  • Serum ammonia levels should not be used as a diagnostic tool or as a means to monitor
    response to treatment.
  • Treatment of acute overt HE should include: 1) supportive care, 2) identifying and treating
    any precipitating factors, 3) reduction of nitrogenous load in the gut, and 4) assessment of
    need for long term therapy and liver transplant evaluation.
  • Lactulose can be used as initial drug therapy for the treatment of acute HE, even in the
    absence of high quality, placebo controlled trials, based on extensive clinical experience
    supporting efficacy. Rifaximin is a reasonable alternative in those who do not respond to
    lactulose alone.
  • Prevention of recurrent HE or treatment of persistent HE includes prevention or avoidance of
    precipitating factors and drug therapy (e.g. lactulose, rifaximin).
  • Protein restriction should be avoided as a general rule, as it can actually lead to worsening of
    HE. Cirrhotic patients are advised to consume 1.0 to 1.5 g/kg protein daily.
  • Liver transplant evaluation should be considered in appropriate candidates once a diagnosis
    of overt HE is made.

HE resistance

Continue reading I’m confused…

What’s that in your pleural space?

Parapneumonic Effusions

Parapneumonic effusions are effusions that occur in the pleural space adjacent to bacterial pneumonia.
  • Uncomplicated: exudative, normal pH/glucose and negative gram stain/culture
  • Complicated: exudative, low pH (<7.20), a low glucose and and often loculated
  • Empyema: pus and organism visible on gram stain, although cultures maybe negative
Indications for Thoracentesis
  • free flowing, layers > 25mm on a lateral decubitus film or CT
  • loculated
  • associated with thickened parietal pleura on CT scan, a finding suggestive of empyema
  • clearly delineated by US
Pleural Fluid Studies
  • See here for our previous review of pleural fluid studies
  • Large loculated or complicated parapneumonic effusion: chest tube
  • Empyema: chest tube and VATS with debridement +/- decortication
  • Same bugs that cause pneumonia: strep pneumo most common. Others include Strep milleri, Staph aureus and Enterobacteriaceae
  • Anaerobic bacteria have been cultured in 36 to 76% of empyema; Fusobacterium, Prevotella, Peptosteptococcus , Bacteroides.
  • Always cover for anaerobes (hard to culture so treat empirically)

The ferritin is that high? Really?

Today at Parkland Morning Report we discussed the appropriate work up of an elevated ferritin and potential etiologies. Below is a link to an article from The Journal of Hepatology by Dr. Adams and Dr. Barton, “A diagnostic approach to hyperferritinemia with a non-elevated transferrin saturation.”

Key Points:

  • Elevated ferritin is due to iron overload or a release of iron/ferritin due to inflammation.
  • Transferrin saturation is another important lab measurement in working up elevated ferritin levels. It can help distinguish an iron overload etiology versus inflammation.