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Would you recognize this ‘invisible’ encephalopathy?
Mr. Z, an obese adult with a history of portal hypertension and cirrhosis from alcoholism, visits your clinic because he is having difficulty sleeping and concentrating at work. He recently reduced his alcohol use and has improved support from his spouse. He walks into your office with an unremarkable gait before stopping to jot down a note in crisp, neat handwriting. He sits facing you, making good eye contact and exhibiting no involuntary movements. As has been the case at previous visits, Mr. Z is fully oriented to person, place, and time. You can follow one another’s train of thought and collaborate on treatment decisions. You’ve ruled out hepatic encephalopathy. Could you be missing something?
Hepatic encephalopathy is a neuropsychiatric condition caused by metabolic changes secondary to liver dysfunction and/or by blood flow bypassing the portal venous system. Signs and symptoms of hepatic encephalopathy range from subtle changes in cognition and affect to coma.Pathophysiologic mechanisms involved in hepatic encephalopathy include inflammation, neurotoxins, oxidative stress, permeability changes in the blood-brain barrier, and impaired brain energy metabolism.1
Patients with poor liver function commonly have psychometrically detectable cognitive and psychomotor deficits that can substantially affect their lives. When such deficits are undetectable by
Approximately 22% to 74% of patients with liver dysfunction develop MHE.2 Prevalence estimates vary widely because of the poor standardization of diagnostic criteria and potential underdiagnosis due to a lack of obvious symptoms.2
How is MHE diagnosed?
The most commonly administered psychometric test to assess for MHE is the Psychometric Hepatic Encephalopathy Score, a written test that measures motor speed and accuracy, concentration, attention, visual perception, visual-spatial orientation, visual construction, and memory.3,4 Other methods for evaluating MHE, including EEG, MRI, single-photon emission CT, positron emission tomography, and determining a patient’s frequency threshold of perceiving a flickering light, have predictive power, but they do not have a well-defined, standardized role in the diagnosis of MHE.2 Although ammonia levels can correlate with severity of impairment in episodic hepatic encephalopathy, they are not well correlated with the deficits in MHE, and often it is not feasible to properly measure ammonia concentrations in outpatient settings.2
Limited treatment options
Few studies have investigated interventions specifically for MHE. The beststudied treatments are lactulose5 and rifaximin.6 Lactulose reduces the formation of ammonia and the absorption of both ammonia and glutamine in the colonic lumen.5 In addition to improving MHE, lactulose helps prevent the recurrence of episodic overt hepatic encephalopathy.5 The antibiotic rifaximin kills ammonia-producing gut bacteria because it is minimally absorbed in the digestive system. No studies investigating rifaximin have observed antibiotic resistance, even with prolonged use. Rifaximin improves cognitive ability, driving ability, and quality of life in patients with MHE. Adding rifaximin to a treatment regimen that includes lactulose also can reduce the recurrence of overt hepatic encephalopathy.6 Branched chain amino acids, L-carnitine, L-ornithine aspartate, treating a comorbid zinc deficiency, probiotics, and increasing vegetable protein intake relative to animal protein intake may also have roles in treating MHE.2
1. Hadjihambi A, Arias N, Sheikh M, et al. Hepatic encephalopathy: a critical current review. Hepatol Int. 2018;12(suppl 1):S135-S147.
2. Zhan T, Stremmel W. The diagnosis and treatment of minimal hepatic encephalopathy. Dtsch Arztebl Int. 2012;109(10):180-1877.
3. Weissenborn K, Ennen JC, Schomerus H, et al. Neuropsychological characterization of hepatic encephalopathy. J Hepatol. 2001;34(5):768-773.
4. Nabi E, Bajaj J. Useful tests for hepatic encephalopathy in clinical practice. Curr Gastroenterol Rep. 2014;16(1):362.
5. Sharma BC, Sharma P, Agrawal A, et al. Secondary prophylaxis of hepatic encephalopathy: an open-label randomized controlled trial of lactulose versus placebo. Gastroenterology. 2009;137(3):885-891.
6. Bass NM, Mullen KD, Sanyal A et al. Rifaximin treatment in hepatic encephalopathy. N Engl J Med. 2010;362:1071-1081.
Mr. Z, an obese adult with a history of portal hypertension and cirrhosis from alcoholism, visits your clinic because he is having difficulty sleeping and concentrating at work. He recently reduced his alcohol use and has improved support from his spouse. He walks into your office with an unremarkable gait before stopping to jot down a note in crisp, neat handwriting. He sits facing you, making good eye contact and exhibiting no involuntary movements. As has been the case at previous visits, Mr. Z is fully oriented to person, place, and time. You can follow one another’s train of thought and collaborate on treatment decisions. You’ve ruled out hepatic encephalopathy. Could you be missing something?
Hepatic encephalopathy is a neuropsychiatric condition caused by metabolic changes secondary to liver dysfunction and/or by blood flow bypassing the portal venous system. Signs and symptoms of hepatic encephalopathy range from subtle changes in cognition and affect to coma.Pathophysiologic mechanisms involved in hepatic encephalopathy include inflammation, neurotoxins, oxidative stress, permeability changes in the blood-brain barrier, and impaired brain energy metabolism.1
Patients with poor liver function commonly have psychometrically detectable cognitive and psychomotor deficits that can substantially affect their lives. When such deficits are undetectable by
Approximately 22% to 74% of patients with liver dysfunction develop MHE.2 Prevalence estimates vary widely because of the poor standardization of diagnostic criteria and potential underdiagnosis due to a lack of obvious symptoms.2
How is MHE diagnosed?
The most commonly administered psychometric test to assess for MHE is the Psychometric Hepatic Encephalopathy Score, a written test that measures motor speed and accuracy, concentration, attention, visual perception, visual-spatial orientation, visual construction, and memory.3,4 Other methods for evaluating MHE, including EEG, MRI, single-photon emission CT, positron emission tomography, and determining a patient’s frequency threshold of perceiving a flickering light, have predictive power, but they do not have a well-defined, standardized role in the diagnosis of MHE.2 Although ammonia levels can correlate with severity of impairment in episodic hepatic encephalopathy, they are not well correlated with the deficits in MHE, and often it is not feasible to properly measure ammonia concentrations in outpatient settings.2
Limited treatment options
Few studies have investigated interventions specifically for MHE. The beststudied treatments are lactulose5 and rifaximin.6 Lactulose reduces the formation of ammonia and the absorption of both ammonia and glutamine in the colonic lumen.5 In addition to improving MHE, lactulose helps prevent the recurrence of episodic overt hepatic encephalopathy.5 The antibiotic rifaximin kills ammonia-producing gut bacteria because it is minimally absorbed in the digestive system. No studies investigating rifaximin have observed antibiotic resistance, even with prolonged use. Rifaximin improves cognitive ability, driving ability, and quality of life in patients with MHE. Adding rifaximin to a treatment regimen that includes lactulose also can reduce the recurrence of overt hepatic encephalopathy.6 Branched chain amino acids, L-carnitine, L-ornithine aspartate, treating a comorbid zinc deficiency, probiotics, and increasing vegetable protein intake relative to animal protein intake may also have roles in treating MHE.2
Mr. Z, an obese adult with a history of portal hypertension and cirrhosis from alcoholism, visits your clinic because he is having difficulty sleeping and concentrating at work. He recently reduced his alcohol use and has improved support from his spouse. He walks into your office with an unremarkable gait before stopping to jot down a note in crisp, neat handwriting. He sits facing you, making good eye contact and exhibiting no involuntary movements. As has been the case at previous visits, Mr. Z is fully oriented to person, place, and time. You can follow one another’s train of thought and collaborate on treatment decisions. You’ve ruled out hepatic encephalopathy. Could you be missing something?
Hepatic encephalopathy is a neuropsychiatric condition caused by metabolic changes secondary to liver dysfunction and/or by blood flow bypassing the portal venous system. Signs and symptoms of hepatic encephalopathy range from subtle changes in cognition and affect to coma.Pathophysiologic mechanisms involved in hepatic encephalopathy include inflammation, neurotoxins, oxidative stress, permeability changes in the blood-brain barrier, and impaired brain energy metabolism.1
Patients with poor liver function commonly have psychometrically detectable cognitive and psychomotor deficits that can substantially affect their lives. When such deficits are undetectable by
Approximately 22% to 74% of patients with liver dysfunction develop MHE.2 Prevalence estimates vary widely because of the poor standardization of diagnostic criteria and potential underdiagnosis due to a lack of obvious symptoms.2
How is MHE diagnosed?
The most commonly administered psychometric test to assess for MHE is the Psychometric Hepatic Encephalopathy Score, a written test that measures motor speed and accuracy, concentration, attention, visual perception, visual-spatial orientation, visual construction, and memory.3,4 Other methods for evaluating MHE, including EEG, MRI, single-photon emission CT, positron emission tomography, and determining a patient’s frequency threshold of perceiving a flickering light, have predictive power, but they do not have a well-defined, standardized role in the diagnosis of MHE.2 Although ammonia levels can correlate with severity of impairment in episodic hepatic encephalopathy, they are not well correlated with the deficits in MHE, and often it is not feasible to properly measure ammonia concentrations in outpatient settings.2
Limited treatment options
Few studies have investigated interventions specifically for MHE. The beststudied treatments are lactulose5 and rifaximin.6 Lactulose reduces the formation of ammonia and the absorption of both ammonia and glutamine in the colonic lumen.5 In addition to improving MHE, lactulose helps prevent the recurrence of episodic overt hepatic encephalopathy.5 The antibiotic rifaximin kills ammonia-producing gut bacteria because it is minimally absorbed in the digestive system. No studies investigating rifaximin have observed antibiotic resistance, even with prolonged use. Rifaximin improves cognitive ability, driving ability, and quality of life in patients with MHE. Adding rifaximin to a treatment regimen that includes lactulose also can reduce the recurrence of overt hepatic encephalopathy.6 Branched chain amino acids, L-carnitine, L-ornithine aspartate, treating a comorbid zinc deficiency, probiotics, and increasing vegetable protein intake relative to animal protein intake may also have roles in treating MHE.2
1. Hadjihambi A, Arias N, Sheikh M, et al. Hepatic encephalopathy: a critical current review. Hepatol Int. 2018;12(suppl 1):S135-S147.
2. Zhan T, Stremmel W. The diagnosis and treatment of minimal hepatic encephalopathy. Dtsch Arztebl Int. 2012;109(10):180-1877.
3. Weissenborn K, Ennen JC, Schomerus H, et al. Neuropsychological characterization of hepatic encephalopathy. J Hepatol. 2001;34(5):768-773.
4. Nabi E, Bajaj J. Useful tests for hepatic encephalopathy in clinical practice. Curr Gastroenterol Rep. 2014;16(1):362.
5. Sharma BC, Sharma P, Agrawal A, et al. Secondary prophylaxis of hepatic encephalopathy: an open-label randomized controlled trial of lactulose versus placebo. Gastroenterology. 2009;137(3):885-891.
6. Bass NM, Mullen KD, Sanyal A et al. Rifaximin treatment in hepatic encephalopathy. N Engl J Med. 2010;362:1071-1081.
1. Hadjihambi A, Arias N, Sheikh M, et al. Hepatic encephalopathy: a critical current review. Hepatol Int. 2018;12(suppl 1):S135-S147.
2. Zhan T, Stremmel W. The diagnosis and treatment of minimal hepatic encephalopathy. Dtsch Arztebl Int. 2012;109(10):180-1877.
3. Weissenborn K, Ennen JC, Schomerus H, et al. Neuropsychological characterization of hepatic encephalopathy. J Hepatol. 2001;34(5):768-773.
4. Nabi E, Bajaj J. Useful tests for hepatic encephalopathy in clinical practice. Curr Gastroenterol Rep. 2014;16(1):362.
5. Sharma BC, Sharma P, Agrawal A, et al. Secondary prophylaxis of hepatic encephalopathy: an open-label randomized controlled trial of lactulose versus placebo. Gastroenterology. 2009;137(3):885-891.
6. Bass NM, Mullen KD, Sanyal A et al. Rifaximin treatment in hepatic encephalopathy. N Engl J Med. 2010;362:1071-1081.
5 Myths of tobacco cessation
Here are 5 commonly held beliefs about stopping tobacco use, and about your role in helping these patients, that go up in smoke on close inspection.
Treating nicotine use disorder isn’t really a psychiatrist’s job. False! Smoking is the leading preventable cause of death, causing 1 in every 5 deaths in the United States and as many as 1 of every 2 deaths among patients with depression, bipolar disorder, or schizophrenia.1,2 As psychiatrists, our experience with treating addiction positions us to address nicotine use disorder more effectively than deferring exclusively to primary care.
I can’t treat my patients’ nicotine dependence until they are ready to quit. Not so! Treatment with varenicline, bupropion, or nicotine replacement therapy is likely to decrease smoking even if the patient has not made a commitment to quit. A smoker treated with pharmacotherapy is more likely to try to quit than one who is not receiving medication.3,4
Motivational interviewing is an excellent intervention to facilitate readiness to quit smoking. Many smokers want to quit—but if they don’t believe that effective treatments exist or that psychiatrists provide such care, they won’t initiate that conversation with you.
Smokeless tobacco isn’t so bad. Poppycock! Chewing and dipping tobacco contains many undesirable chemicals, including abrasives, salts, sweeteners, and carcinogens. Smokeless tobacco is a risk factor for cancer of the mouth and pancreas, as well as tooth decay, periodontal disease, hypertension, hyperlipidemia, myocardial infarction, and fatal stroke.5
Nicotine replacement products are as bad as smoking. Claptrap! You can reassure patients that nicotine is not a carcinogen. If your patients use the same amount of nicotine but replace tobacco in whole or in part with a patch, gum, or an inhaler, they will have better health even if they use nicotine replacement for the rest of their life. Nicotine replacement products are less addictive than cigarettes because they release nicotine more slowly. (Cigarettes bring peak levels of nicotine to the brain even faster than IV administration does.) Nicotine replacement is recommended for at least 3 months after quitting tobacco or for as long the patient needs it.3
Nicotine replacement products are dangerous for current smokers. Balderdash! Many patients are afraid of using nicotine from >1 source. A common myth is that using a nicotine patch while smoking increases the risk of heart attack, which discourages patients from trying a nicotine replacement product before they are sure they will stop smoking. Nicotine replacement is likely to reduce the frequency of their smoking and reduce harm, not add to it.3
1. Centers for Disease Control and Prevention. Smoking & tobacco use: tobacco-related mortality. http://www.cdc.gov/tobacco/ data_statistics/fact_sheets/ health_effects/tobacco_related_ mortality. Updated August 18, 2015. Accessed December 20, 2015.
2. Callaghan RC, Veldhuizen S, Jeysingh T, et al. Patterns of tobacco-related mortality among individuals diagnosed with schizophrenia, bipolar disorder, or depression. J Psychiatr Res. 2014;48(1):102-110.
3. Stead LF, Perera R, Bullen C, et al. Nicotine replacement therapy for smoking cessation. Cochrane Database Syst Rev. 2012;11:CD000146. doi: 10.1002/14651858.CD000146.pub4.
4. Ebbert JO, Hughes JR, West RJ, et al. Effect of varenicline on smoking cessation through smoking reduction: a randomized clinical trial. JAMA. 2015;313(7):678-694.
5. Piano MR, Benowitz NL, Fitzgerald GA, et al; American Heart Association Council on Cardiovascular Nursing. Impact of smokeless tobacco products on cardiovascular disease: implications for policy, prevention, and treatment: a policy statement from the American Heart Association. Circulation. 2010;122(15):1520-1544.
Here are 5 commonly held beliefs about stopping tobacco use, and about your role in helping these patients, that go up in smoke on close inspection.
Treating nicotine use disorder isn’t really a psychiatrist’s job. False! Smoking is the leading preventable cause of death, causing 1 in every 5 deaths in the United States and as many as 1 of every 2 deaths among patients with depression, bipolar disorder, or schizophrenia.1,2 As psychiatrists, our experience with treating addiction positions us to address nicotine use disorder more effectively than deferring exclusively to primary care.
I can’t treat my patients’ nicotine dependence until they are ready to quit. Not so! Treatment with varenicline, bupropion, or nicotine replacement therapy is likely to decrease smoking even if the patient has not made a commitment to quit. A smoker treated with pharmacotherapy is more likely to try to quit than one who is not receiving medication.3,4
Motivational interviewing is an excellent intervention to facilitate readiness to quit smoking. Many smokers want to quit—but if they don’t believe that effective treatments exist or that psychiatrists provide such care, they won’t initiate that conversation with you.
Smokeless tobacco isn’t so bad. Poppycock! Chewing and dipping tobacco contains many undesirable chemicals, including abrasives, salts, sweeteners, and carcinogens. Smokeless tobacco is a risk factor for cancer of the mouth and pancreas, as well as tooth decay, periodontal disease, hypertension, hyperlipidemia, myocardial infarction, and fatal stroke.5
Nicotine replacement products are as bad as smoking. Claptrap! You can reassure patients that nicotine is not a carcinogen. If your patients use the same amount of nicotine but replace tobacco in whole or in part with a patch, gum, or an inhaler, they will have better health even if they use nicotine replacement for the rest of their life. Nicotine replacement products are less addictive than cigarettes because they release nicotine more slowly. (Cigarettes bring peak levels of nicotine to the brain even faster than IV administration does.) Nicotine replacement is recommended for at least 3 months after quitting tobacco or for as long the patient needs it.3
Nicotine replacement products are dangerous for current smokers. Balderdash! Many patients are afraid of using nicotine from >1 source. A common myth is that using a nicotine patch while smoking increases the risk of heart attack, which discourages patients from trying a nicotine replacement product before they are sure they will stop smoking. Nicotine replacement is likely to reduce the frequency of their smoking and reduce harm, not add to it.3
Here are 5 commonly held beliefs about stopping tobacco use, and about your role in helping these patients, that go up in smoke on close inspection.
Treating nicotine use disorder isn’t really a psychiatrist’s job. False! Smoking is the leading preventable cause of death, causing 1 in every 5 deaths in the United States and as many as 1 of every 2 deaths among patients with depression, bipolar disorder, or schizophrenia.1,2 As psychiatrists, our experience with treating addiction positions us to address nicotine use disorder more effectively than deferring exclusively to primary care.
I can’t treat my patients’ nicotine dependence until they are ready to quit. Not so! Treatment with varenicline, bupropion, or nicotine replacement therapy is likely to decrease smoking even if the patient has not made a commitment to quit. A smoker treated with pharmacotherapy is more likely to try to quit than one who is not receiving medication.3,4
Motivational interviewing is an excellent intervention to facilitate readiness to quit smoking. Many smokers want to quit—but if they don’t believe that effective treatments exist or that psychiatrists provide such care, they won’t initiate that conversation with you.
Smokeless tobacco isn’t so bad. Poppycock! Chewing and dipping tobacco contains many undesirable chemicals, including abrasives, salts, sweeteners, and carcinogens. Smokeless tobacco is a risk factor for cancer of the mouth and pancreas, as well as tooth decay, periodontal disease, hypertension, hyperlipidemia, myocardial infarction, and fatal stroke.5
Nicotine replacement products are as bad as smoking. Claptrap! You can reassure patients that nicotine is not a carcinogen. If your patients use the same amount of nicotine but replace tobacco in whole or in part with a patch, gum, or an inhaler, they will have better health even if they use nicotine replacement for the rest of their life. Nicotine replacement products are less addictive than cigarettes because they release nicotine more slowly. (Cigarettes bring peak levels of nicotine to the brain even faster than IV administration does.) Nicotine replacement is recommended for at least 3 months after quitting tobacco or for as long the patient needs it.3
Nicotine replacement products are dangerous for current smokers. Balderdash! Many patients are afraid of using nicotine from >1 source. A common myth is that using a nicotine patch while smoking increases the risk of heart attack, which discourages patients from trying a nicotine replacement product before they are sure they will stop smoking. Nicotine replacement is likely to reduce the frequency of their smoking and reduce harm, not add to it.3
1. Centers for Disease Control and Prevention. Smoking & tobacco use: tobacco-related mortality. http://www.cdc.gov/tobacco/ data_statistics/fact_sheets/ health_effects/tobacco_related_ mortality. Updated August 18, 2015. Accessed December 20, 2015.
2. Callaghan RC, Veldhuizen S, Jeysingh T, et al. Patterns of tobacco-related mortality among individuals diagnosed with schizophrenia, bipolar disorder, or depression. J Psychiatr Res. 2014;48(1):102-110.
3. Stead LF, Perera R, Bullen C, et al. Nicotine replacement therapy for smoking cessation. Cochrane Database Syst Rev. 2012;11:CD000146. doi: 10.1002/14651858.CD000146.pub4.
4. Ebbert JO, Hughes JR, West RJ, et al. Effect of varenicline on smoking cessation through smoking reduction: a randomized clinical trial. JAMA. 2015;313(7):678-694.
5. Piano MR, Benowitz NL, Fitzgerald GA, et al; American Heart Association Council on Cardiovascular Nursing. Impact of smokeless tobacco products on cardiovascular disease: implications for policy, prevention, and treatment: a policy statement from the American Heart Association. Circulation. 2010;122(15):1520-1544.
1. Centers for Disease Control and Prevention. Smoking & tobacco use: tobacco-related mortality. http://www.cdc.gov/tobacco/ data_statistics/fact_sheets/ health_effects/tobacco_related_ mortality. Updated August 18, 2015. Accessed December 20, 2015.
2. Callaghan RC, Veldhuizen S, Jeysingh T, et al. Patterns of tobacco-related mortality among individuals diagnosed with schizophrenia, bipolar disorder, or depression. J Psychiatr Res. 2014;48(1):102-110.
3. Stead LF, Perera R, Bullen C, et al. Nicotine replacement therapy for smoking cessation. Cochrane Database Syst Rev. 2012;11:CD000146. doi: 10.1002/14651858.CD000146.pub4.
4. Ebbert JO, Hughes JR, West RJ, et al. Effect of varenicline on smoking cessation through smoking reduction: a randomized clinical trial. JAMA. 2015;313(7):678-694.
5. Piano MR, Benowitz NL, Fitzgerald GA, et al; American Heart Association Council on Cardiovascular Nursing. Impact of smokeless tobacco products on cardiovascular disease: implications for policy, prevention, and treatment: a policy statement from the American Heart Association. Circulation. 2010;122(15):1520-1544.