Alcohol-related diseases

When should I consider steroids in my patient with alcoholic hepatitis?

FA Manian MD, MPH, , , , , , , , , , Leave a comment

The short answer is not very often! In the treatment of alcoholic hepatitis (AH), steroids are reserved for a narrow group of patients only, with a 2018 meta-analysis finding a reduction in short-term mortality (average 36%) at 28 days but not at 6 months.1

The most studied scoring system to help clinicians decide whether a patient should get steroids is the Maddrey’s Discriminant Function (MDF), which is based on the prothrombin and total bilirubin. A score of ≥32 indicates severe disease and potential response to steroids, while a score <32 indicates mild to moderate disease, for which the risk of steroids (e.g. infection, worsening ulcer disease/bleeding, and glucose intolerance) may outweigh any potential benefit.

However, even with a score ≥32, the likelihood of patient adherence to 28 days of steroid therapy, risk of infection and other steroid-related complications should be carefully considered in individual patients. It’s also important to note that a 2008 meta-analysis showed that patients with a very high MDF score of >54 actually had higher mortality rates with steroid therapy, possibly related to the lack of response in very advanced disease as well as high infection risk.2

Many clinicians also use the Lille’s score to help determine whether a patient is a responder after 7 days of initial therapy. A score >0.45 (calculated based on bilirubin levels at day 0 and 7 and other initial labs and age) indicates poor response and that steroids may be stopped due to its risks.3

Based on the result of a small retrospective study, Glasgow Alcoholic Hepatitis (GAH) score has also been suggested as a means of further defining patients with a MDF ≥32 who may potentially benefit from steroids (ie, score ≥9).4

Bonus pearl: Did you know that pentoxifylline, a tumor necrosis factor (TNF), has generally not been found to be effective in the treatment of AH?5,6

Contributed by Tom Wang, MD, Mass General Hospital, Boston, MA.

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References

  1. Louvet A, et al. “Corticosteroids reduce risk of death within 28 days for patients with severe alcoholic hepatitis, compared with pentoxifylline or Placebo—a meta-analysis of individual data from controlled trials.” Gastroenterology 2018; 155: 458-468. https://www.sciencedirect.com/science/article/abs/pii/S0016508518344950
  2. Rambaldi A, et al. “Systematic review: glucocorticosteroids for alcoholic hepatitis–a Cochrane Hepato‐Biliary Group systematic review with meta‐analyses and trial sequential analyses of randomized clinical trials.” Alimentary pharmacology & therapeutics 2008; 27: 1167-1178. https://onlinelibrary.wiley.com/doi/full/10.1111/j.1365-2036.2008.03685.x
  3. Louvet A, et al. “The Lille model: a new tool for therapeutic strategy in patients with severe alcoholic hepatitis treated with steroids.” Hepatology 2007; 45: 1348-1354. https://www.ncbi.nlm.nih.gov/pubmed/17518367
  4. Forrest EH, et al. “Analysis of factors predictive of mortality in alcoholic hepatitis and derivation and validation of the Glasgow alcoholic hepatitis score.” Gut 2005; 54: 1174-1179. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1774903/
  5. Thursz MR, et al. “Prednisolone or pentoxifylline for alcoholic hepatitis.” N Engl J Med 2015; 372: 1619-1628. https://www.nejm.org/doi/full/10.1056/NEJMoa1412278
  6. Parker R. “Systematic review: pentoxifylline for the treatment of severe alcoholic hepatitis.” Alimentary Pharm Therapeutics 2018; 37: 845-854. https://onlinelibrary.wiley.com/doi/10.1111/apt.12279

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

When should I consider steroids in my patient with alcoholic hepatitis?

Why can’t my patient with alcohol-related liver disease be placed on the liver transplant list for at least 6 months after his last drink?

FA Manian MD, MPH, , , , , , , , Leave a comment

Although many centers impose a 6-month sobriety rule before patients can be listed for liver transplant, this rule has been increasingly challenged based on the results of more recent studies and ethical issues. 1-10

The argument for enforcing a 6-month sobriety rule is in part based on earlier studies (often small and/or single center) that reported an association between less than 6 months of sobriety before liver transplantation and relapse.5-6 Another frequently cited reason for postponing liver transplantation is to allow the liver enough time to recover from adverse effect of recent alcohol consumption before assessing the need for transplantation.6

Arguments against the 6-month sobriety rule include the very limited life-expectancy (often 3 months or less) of patients with severe alcohol-related liver disease who do not respond to medical therapy and increasing number of studies supporting earlier transplantation particularly in selected patients (eg, severe acute alcoholic hepatitis [SAAH], acute-on-chronic liver failure [ACLF]).1,7,9,10,

Further supporting a less stringent transplantation rule are a low rate (about 4%) of death or graft loss in alcohol-related liver disease patients who experience a relapse and lack of significant differences in survival between non-relapsers, occasional drinkers and problem drinkers.1 A 2019 multicenter, prospective study in the U.S. also found that early liver transplant for alcohol-related  liver disease was associated with comparable patient and graft survival as those without alcohol-related liver disease at 5 years post-transplant but increased risk of death at 10 years. 10

Bonus Pearl: Did you know that alcohol-related liver disease is now the most common diagnosis among patients undergoing liver transplantation in the U.S.? 10

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References

  1. Obed A, Stern S, Jarrad A, et al. Six month abstinence rule for liver transplantation in severe alcoholic liver disease patients. W J Gastroenterol 2015; 21:4423-26. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4394109/
  2. Bramstedt KA, Jabbour N. When alcohol abstinence criteria create ethical dilemmas for the liver transplant team. J Med Ethics 2006;32:263-65. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2579412/
  3. Kollmann D, Rashoul-Rockenschaub S, Steiner I, et al. Good outcome after liver transplantation for ALD without a 6 months abstinence rule prior to transplantation including post-tranplantation CDT monitoring for alcohol relapse assement— a retrospective study. Transplant International 2016;29:559-67. https://onlinelibrary.wiley.com/doi/epdf/10.1111/tri.12756
  4. Osorio RW, Ascher NL, Avery M, et al. Predicting recidivism after orthoptic liver transplantation for alcoholic liver disease. Hepatoloty 1994;20:105-110. https://aasldpubs.onlinelibrary.wiley.com/doi/epdf/10.1002/hep.1840200117
  5. Carbonneau M, Jensen LA, Bain VG. Alcohol use while on the liver transplant waiting list: a single-center experience. Liver Transplantation 2010;16:91-97. https://aasldpubs.onlinelibrary.wiley.com/doi/full/10.1002/lt.21957
  6. Harnanan A. Challenging the “six-month sober” rule for liver transplants in Canada. McGill Journal of Law and Health. Dec 12, 2019. https://mjlh.mcgill.ca/2019/12/12/challenging-the-six-month-sober-rule-for-liver-transplants-in-canada/
  7. Lee BP, Mehta N, Platt L, et al. Outcomes of early liver transplantation for patients with severe alcoholic hepatitis. Gastroenterology 2018;155:422-430.e1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6460480/
  8. Rice JP, Lee BP. Early liver transplantation for alcohol-associated liver disease: need for engagement and education of all stakeholders. Hepatol Communications 2019;3: 1019-21. https://aasldpubs.onlinelibrary.wiley.com/doi/pdf/10.1002/hep4.1385
  9. Lee BP, Vittinghoff E, Pletcher MJ, et al. Medicaid policy and liver transplant for alcohol-related liver disease. Hepatology; November 8, 2019 https://aasldpubs.onlinelibrary.wiley.com/doi/pdf/10.1002/hep.31027
  10. Lee BP, Vittinghoff E, Dodge JL, et al. National trends and long-term outcomes of liver transplant for alcohol-associated liver disease in the United States. JAMA Intern Med 2019;179:340-48. https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2720757?widget=personalizedcontent&previousarticle=2720750

Contributed in part by Nneka Ufere, MD, GI Division, Massachusetts General Hospital, Boston, MA

Why can’t my patient with alcohol-related liver disease be placed on the liver transplant list for at least 6 months after his last drink?

What’s causing an isolated GGT elevation in my patient with an abnormal alkaline phosphatase on her routine admission lab?

FA Manian MD, MPH, , , , , , , , , , , , , , , , , , , Leave a comment

Although serum gamma-glutamyl transpeptidase or GGT is a very sensitive test for liver disease, especially of biliary origin, it’s by no means a very specific test. Besides the liver, GGT is found in the kidneys, pancreas, prostate, heart, brain, and seminal vesicles but not in bone (1-4).

 
Obesity, alcohol consumption and drugs are common causes of GGT elevation (2). As early as 1960s, elevated GGT was reported in such seemingly disparate conditions as diabetes mellitus, congestive heart failure, myocardial infarction, nephrotic syndrome and renal neoplasm (3). Nonalcoholic steatohepatitis, viral hepatitis, biliary obstruction, COPD, liver metastasis, drug-induced liver injury can all cause GGT elevation (1-4).

 
An isolated GGT does not necessarily indicate serious or progressive liver disease. That’s one reason it’s often not included in routine “liver panel” lab tests (1).

What to do when GGT is high but other liver panel tests such as ALT, AST, albumin, and bilirubin are normal? If your patient is at risk of acquired liver disease, then further workup may be necessary (eg, hepatitis B and C screening tests). Alcohol consumption should be queried. Don’t forget conditions associated with iron overload. If your patient is obese, diabetic or has elevated both lipids, an ultrasound of the liver to look for fatty liver should be considered. In the absence of risk factors, symptoms, or physical exam suggestive of liver disease, isolated GGT elevation should not require further investigation (1).

 
One good thing that may come out of finding an isolated elevated GGT is to encourage your patient to curb alcohol consumption or lose weight when indicated. But don’t rely on a normal GGT to rule out heavy alcohol consumption as it may miss 70% to 80% of cases (6)! 

 
Bonus Pearl: Did you know that GGT activity is thought to increase in alcohol use due to its role in maintaining intracellular glutathione, an anti-oxidant, at adequate levels to protect cells from oxidative stress caused by alcohol?

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References

1. Carey WD. How should a patient with an isolated GGT elevation be evaluated? Clev Clin J Med 2000;67:315-16. https://www.ncbi.nlm.nih.gov/pubmed/10832186
2. Newsome PN, Cramb R, Davison SM, et al. Guidelines on the management of abnormal liver blood tests. Gut 2018;67:6-19. https://gut.bmj.com/content/gutjnl/67/1/6.full.pdf
3. Whitfield JB, Pounder RE, Neale G, et al. Serum gamma-glutamyl transpeptidase activity in liver disease. Gut 1972;13:702-8. https://www.ncbi.nlm.nih.gov/pubmed/4404786
4. Tekin O, Uraldi C, Isik B, et al. Clinical importance of gamma glutamyltransferase in the Ankara-Pursaklar region of Turkey. Medscape General Medicine 2004;6(1):e16. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1140713/
5. Van Beek JHDA, de Moor MHM, Geels LM, et al. The association of alcohol intake with gamma-glutamyl transferase (GGT) levels:evidence for correlated genetic effects. Drug Alcohol Depend 2014;134:99-105. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3909645/

6. Bertholet N, Winter MR, Cheng DM, et al. How accurate are blood (or breath) tests for identifying self-reported heavy drinking among people with alcohol dependence? Alcohol and Alcoholism 2014;49:423-29. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4060735/pdf/agu016.pdf

What’s causing an isolated GGT elevation in my patient with an abnormal alkaline phosphatase on her routine admission lab?

I am admitting a patient with diabetes mellitus (DM) due to chronic pancreatitis. Should I manage her diabetes any differently than my other patients with DM?

FA Manian MD, MPH, , , , , , , , Leave a comment

You may have to!  That’s because patients with DM due to pancreatic disease (also known as “pancreatogenic [Type 3C] diabetes”) tend to have more labile blood glucoses with particular predisposition to severe hypoglycemic episodes due to the impairment of glucagon production by pancreatic alpha-cells. 1-3

This observation dates back to a 1977 study where a high rate of hypoglycemic episodes was found among 59 patients with chronic pancreatitis (most with insulin-dependent DM), including 3 deaths and 2 suffering from severe brain damage following hypoglycemic coma. Interestingly, low basal glucagon levels were found in the latter patients, supporting impairment in glucagon synthesis. Of note, while hypoglycemia is a serious problem in these patients, they are not spared from complications of chronic hyperglycemia, including retinopathy and kidney disease.2

As for the blood glucose management in type 3C DM, since the principle endocrine defect is insulin deficiency, insulin therapy is preferred for most patients, particularly those who are acutely ill or are hospitalized. For otherwise more stable patients with mild hyperglycemia, metformin is an ideal agent as it enhances hepatic insulin sensitivity without the risk of hypoglycemia. As a bonus, metformin may also decrease the risk of pancreatic cancer in chronic pancreatitis, based on observational studies. 4

Also, don’t forget that concurrent pancreatic exocrine insufficiency is common in patients with type 3C DM and requires oral pancreatic enzyme requirement with meals.

Fascinating Pearl: Did you know that in patients with type 3C DM, hyperglycemia is mediated not only by decreased production of insulin, but also by decreased synthesis of pancreatic polypeptide, a peptide that mediates hepatic insulin sensitivity and glucose production? 5

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References

  1. Linde, J, Nilsson LH, Barany FR. Diabetes and hypoglycemia in chronic pancreatitis. Scand J Gastroenterol. 2012;12, 369–373. https://www.ncbi.nlm.nih.gov/pubmed/867001
  2. Andersen D. The practical importance of recognizing pancreatogenic or type 3c diabetes. Diabetes Metab Res Rev. 2012;28:326-328. https://onlinelibrary.wiley.com/doi/abs/10.1002/dmrr.2285
  3. Cui YF, Andersen DK. Pancreatogenic diabetes: Special considerations for management. Pancreatology. 2011;11(3):279-294. doi:10.1159/000329188. https://jhu.pure.elsevier.com/en/publications/pancreatogenic-diabetes-special-considerations-for-management-4
  4. Evans J, Donnelly L, Emsley-Smith A. Metformin and reduced risk of cancer in diabetic patients. Br Med J. 2005;330:1304-1305. https://www.researchgate.net/publication/7888859_Metformin_and_reduced_risk_of_cancer_in_diabetic_patients
  5. Rabiee A. Gafiatsatos P, Salas-Carnillo R. Pancreatic polypeptide administration enhances insulin sensitivity and reduces the insulin requirement of patents on insulin pump therapy. J Diabetes Sci Technol 2011;5:1521-28.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3262724/

Contributed by Hugo Torres, MD, MPH, Hospital Medicine Unit, Mass General Hospital, Boston, Massachusetts

I am admitting a patient with diabetes mellitus (DM) due to chronic pancreatitis. Should I manage her diabetes any differently than my other patients with DM?

Why does my patient with alcoholic cirrhosis have macrocytic anemia?

FA Manian MD, MPH, , , , , , , , , , , 1 Comment

Macrocytic anemia is commonly due to folate or vitamin B12 (cobalamin) deficiency.1 Deficiency in these vitamins can be related broadly to poor intake, poor absorption, or drug interference. In patients with chronic excess alcohol consumption, both intake and/or absorption of these vitamins may be affected.

Although folate deficiency is increasingly rare in many developed countries due to mandatory folate fortification of flour and uncooked-grain, alcohol use can be associated with malnourishment severe enough to causes folate deficiency. In addition, alcohol itself can alter folate metabolism and absorption.  More specifically, chronic alcohol consumption has been shown to be associated with decreased folate absorption by the small intestine, altered intrahepatic processing and distribution between the systemic and enterohepatic folate circulations as well as increased folate urinary excretion. 2 Though uncommon,3 alcohol can also be associated with a food B12 malabsorption process, whereby despite adequate intake, B12 is not released or absorbed from food. 4

But what if serum folate and B12 levels return as normal in our patient with macrocytosis? It turns out that alcohol consumption, independent of folate or B12 deficiency, may also cause macrocytosis. 5 Though the exact mechanism is unknown, it may be related to alcohol’s direct toxicity or that of its metabolites; alcohol is oxidized to acetaldehyde, which affects membranes of red blood cells (RBCs) and their precursors by forming adducts with erythroid proteins,6 and interfering with cell division.7 Interestingly, alcohol-related macrocytosis may appear before anemia is detected and can resolve within 2-4 months of abstinence.

In addition to alcohol, cirrhosis itself may be associated with macrocytic anemia caused by lipid deposition on RBC membranes.1

See also a related pearl at  www.Pearls4Peers.com

References

  1. Hoffbrand V, Provan D. ABC of clinical haematology: macrocytic anaemias. BMJ 2011;314(7078):430–430. https://www.ncbi.nlm.nih.gov/pubmed/9040391
  2. Medici V, Halsted CH. Folate, alcohol, and liver disease. Mol Nutr Food Res 2013;57(4):596–606. https://www.ncbi.nlm.nih.gov/pubmed/23136133
  3. Bode C, Bode CJ. Effect of alcohol consumption on the gut. Best Pract Res Clin Gastroenterol [Internet] 2003;17(4):575–92. https://www.sciencedirect.com/science/article/pii/S1521691803000349
  4. Dali-Youcef N, Andrès E. An update on cobalamin deficiency in adults. QJM 2009;102(1):17–28. https://academic.oup.com/qjmed/article/102/1/17/1502492
  5. Savage DG, Ogundipe A, Allen RH, Stabler SP, Lindenbaum J. Etiology and diagnostic Evaluation of macrocytosis. Am J Med Sci [Internet] 2000;319(6):343–52. http://dx.doi.org/10.1016/S0002-9629(15)40772-4 https://www.ncbi.nlm.nih.gov/pubmed/10875288
  6. Latvala J, Parkkila S, Melkko J, Niemelä O. Acetaldehyde adducts in blood and bone marrow of patients with ethanol-induced erythrocyte abnormalities. Mol Med 2001;7(6):401–5. https://www.ncbi.nlm.nih.gov/pubmed/11474133
  7. Wickramasinghe SN, Malik F. Acetaldehyde causes a prolongation of the doubling time and an increase in the modal volume of cells in culture. Alcohol Clin Exp Res 1986;10(3):350–4. https://www.ncbi.nlm.nih.gov/pubmed/3526962

 

Contributed by Kim Schaefer, Harvard medical student, Boston, MA

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Why does my patient with alcoholic cirrhosis have macrocytic anemia?

My hospitalized patient with sepsis has persistently elevated lactic acid despite volume resuscitation, source control, and adequate oxygenation. What could I be missing?

FA Manian MD, MPH, , , , , , , , , , , , , , , Leave a comment

Although the causes of lactic acidosis are legion (eg, sepsis, tissue hypoperfusion, ischemic bowel, malignancy, medications, liver dysfunction), thiamine deficiency (TD) is an often-overlooked cause of persistently elevated serum lactic acid (LA) in critically ill hospitalized patients,1 reported in 20-70% of septic patients.2  Septic shock patients may be particularly at risk of TD because of increased mitochondrial oxidative stress, decreased nutritional intake and presence of comorbid conditions (eg,  alcoholism, persistent vomiting).3

Early recognition of TD in hospitalized patients may be particularly difficult because of the frequent absence of the “classic” signs and symptoms of Wernicke’s encephalopathy (eg, ataxia, cranial nerve palsies and confusion) and lack of readily available confirmatory laboratory tests.4

TD-related lactic acidosis should be suspected when an elevated LA persists despite adequate treatment of its putative cause(s) (4,5). Administration of IV thiamine in this setting may result in rapid clearance of LA.3-5

TD causes lactic acidosis type B which is due to the generation of excess LA, not impairment in tissue oxygenation, as is the case for lactic acidosis type A. Thiamine is an essential co-factor in aerobic metabolism, facilitating the conversion of pyruvate to acetyl-CoA which enters the citric acid (Krebs) cycle within the mitochondria. In TD, pyruvate does not undergo aerobic metabolism and is converted to LA instead, leading to lactic acidosis.

Bonus pearl: Did you know that because of its limited tissue storage, thiamine stores may be depleted within only 3 weeks of reduced oral intake!

References

  1. O’Donnell K. Lactic acidosis: a lesser known side effect of thiamine deficiency. Practical Gastroenterol March 2017:24.   https://www.practicalgastro.com/article/176921/Lactic-Acidosis-Lesser-Known-Side-Effect-of-Thiamine-Deficiency
  2. Marik PE. Thiamine: an essential component of the metabolic resuscitation protocol. Crit Care Med 2018;46:1869-70. https://journals.lww.com/ccmjournal/Fulltext/2018/11000/Thiamine___An_Essential_Component_of_the_Metabolic.23.aspx
  3. Woolum JA, Abner EL, Kelly A, et al. Effect of thiamine administration on lactate clearance and mortality in patients with septic shock. Crit Care Med 2018;46:1747-52. https://journals.lww.com/ccmjournal/Fulltext/2018/11000/Effect_of_Thiamine_Administration_on_Lactate.5.aspx
  4. Kourouni I, Pirrotta S, Mathew J, et al. Thiamine: an underutilized agent in refractory lactic acidosis. Chest 2016; 150:247A. https://journal.chestnet.org/article/S0012-3692(16)56459-9/pdf
  5. Shah S, Wald E. Type B lactic acidosis secondary to thiamine deficiency in a child with malignancy. Pediatrics 2015; 135:e221-e224. http://pediatrics.aappublications.org/content/135/1/e221

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My hospitalized patient with sepsis has persistently elevated lactic acid despite volume resuscitation, source control, and adequate oxygenation. What could I be missing?

Why is my hospitalized patient with alcohol withdrawal syndrome so thrombocytopenic?

FA Manian MD, MPH, , , , , , , , , , , , , , Leave a comment

Although thrombocytopenia associated with chronic alcoholism may be related to complications of cirrhosis (eg, platelet sequestration in spleen due to portal hypertension, poor platelet production, and increased platelet destruction) (1), it may also occur in the absence of cirrhosis due to the direct toxic effect of alcohol on platelet production and survival (2).

 
In a prospective study of patients ingesting the equivalent of a fifth or more daily of 86 proof whiskey admitted for treatment of alcohol withdrawal—without evidence of severe liver disease, infection or sepsis— 81% had initial platelet counts below 150,000/µl, with about one-third having platelet counts below 100,000 µl (as low as 24,000/ul) (3).

 
In most patients, 2-3 days elapsed before the platelet count began to rise significantly, peaking 5-18 days after admission. Others have also reported that platelet counts rise within 5-7 days and normalize in a few weeks after alcohol withdrawal (1); bleeding complications have been uncommon in this setting.

 
Perhaps even more intriguing is the report of the association between thrombocytopenia in early alcohol withdrawal and the development of delirium tremens or seizures (sensitivity and specificity ~ 70%, positive predictive value less than 10% but with a negative predictive value of 99%) (4)! In fact, the authors suggested that, if their findings are corroborated, a normal platelet count could potentially be used to identify patients at low risk of alcohol withdrawal syndrome and therefore outpatient therapy. 

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References
1. Mitchell O, Feldman D, Diakow M, et al. The pathophysiology of thrombocytopenia in chronic liver disease. Hepatic Medicine: Evidence and Research 2016;8 39-50. https://www.dovepress.com/the-pathophysiology-of-thrombocytopenia-in-chronic-liver-disease-peer-reviewed-article-HMER

2. Cowan DH. Effect of alcoholism on hemostasis. Semin Hematol 1980;17:137-47. https://www.ncbi.nlm.nih.gov/pubmed/6990498

3. Cowan DH, Hines JD. Thrombocytopenia of severe alcoholism. Ann Intern Med 1971;74:37-43. http://annals.org/aim/article-abstract/685069/thrombocytopenia-severe-alcoholism.

4. Berggren U, Falke C, Berglund KJ, et al. Thrombocytopenia in early alcohol withdrawal is associated with development of delirium tremens or seizures. Alcohol & Alcoholism 2009;44:382-86. https://www.ncbi.nlm.nih.gov/pubmed/19293148

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

Why is my hospitalized patient with alcohol withdrawal syndrome so thrombocytopenic?

My 35 year old patient with chronic alcoholism blames benign prostatic hypertrophy for his difficulty voiding. Could his bladder dysfunction be related to his alcoholism?

FA Manian MD, MPH, , , Leave a comment

Several case reports in the literature have stressed the association of bladder dysfunction (BD) with chronic alcohol abuse1,2.  Although some cases may be associated with concurrent thiamine deficiency (with its attendant neuropathy), other cases of BD do not appear to be. The mechanism of BD in this setting may be related to the toxic effect of alcohol on peripheral, autonomic and/or central nervous systems2,3.

Binge drinking may also be associated with urinary retention, with spontaneous atraumatic urinary bladder rupture having been reported on several occasions4. Lastly, alcohol withdrawal alone may precipitate urinary retention5.  

Unfortunately, many cases of abdominal pain due to urinary retention in the setting of alcohol abuse or withdrawal may be mistakenly attributed to ascites or other causes5.  High index of suspicion for BD is essential to minimize its complications.

In our patient, given the low prevalence of benign prostatic hypertrophy in men less than 40 years of age, urinary retention due to alcohol-related BD is more likely.

 

References

  1. Yuan R, Carcciolo VJ, Kulaga M. Chronic abdominal distension secondary to urinary retention in a patient with alcoholism. JAMA 2002;287;318-19.
  2. Sheremata WA, Sherwin I. Alcoholic myelopathy with spastic urinary bladder. Dis Nerv Syst 1972;33:136-139.
  3. Mellion M, Gilchrist JM, De La Monte S. Alcohol-related peripheral neuropathy: nutritional, toxic or both? Muscle Nerve 2011;43:309-16.
  4. Muneer M, Abdelrahman H, El-Menyar A, et al. Spontaneous atraumatic urinary bladder rupture secondary to alcohol intoxication: a case report and review of literature. Am J Case Rep 2015;16:778-81.
  5. Iga J-I, Taniguchi T, Ohmori T. Acute abdominal distension secondary to urinary retention in a patient after alcohol withdrawal. Alcohol Alcoholism 2005;40:86-87.
My 35 year old patient with chronic alcoholism blames benign prostatic hypertrophy for his difficulty voiding. Could his bladder dysfunction be related to his alcoholism?

When should I seriously consider active tuberculosis (TB) in my newly-admitted HIV-negative patient with a cough?

FA Manian MD, MPH, , , , , , , Leave a comment

Active TB should be suspected based on a combination of epidemiological (eg, exposure, travel to, or residence in a high prevalence area, history of prior TB), clinical (eg, cough lasting 2-3 weeks or longer, fever, night sweats, weight loss, fatigue, less commonly, chest pain, dyspnea, and hemoptysis), chest radiograph abnormalities (eg, infiltrates, fibrosis, cavitation), and histopathologic (eg, caseating granuloma)1.

Among HIV-negative patients, the highest prevalence of TB is found those who have been incarcerated, use intravenous drugs, have alcohol use disorder, or are immunocompromised (including diabetes mellitus)2,3. 

Patients suspected of TB based on clinical criteria should undergo chest radiography.  Reactivation pulmonary TB (~90% of TB in adults) classically presents with upper lobe and/or the superior segment of the lower lobe disease.  Remember that up to 5% of patients with active pulmonary TB have normal chest radiograph, however4.  

All hospitalized patients suspected of having active TB should be placed on appropriate isolation precautions until TB is excluded.

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References

  1. Sia IG, Wieland ML. Current concepts in the management of tuberculosis. Mayo Clin Proc. 2011;86:348-361. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3068897/
  2. Center for Disease Control. Tuberculosis: Data and Statistics. https://www.cdc.gov/tb/statistics/default.htm. Accessed October 3, 2016.
  3. World Health Organization. Tuberculosis. http://www.who.int/mediacentre/ factsheets/fs104/en/. Accessed October 3, 2016.
  4. Marciniuk, D, McNab, BD, Martin WT, Hoeppner, VH. Detection of pulmonary tuberculosis in patients with a normal chest radiograph. Chest 1999;115:445-452. https://journal.chestnet.org/article/S0012-3692(15)50590-4/abstract

 

 

Contributed by Charles C. Jain MD, Medical Resident, Massachusetts General Hospital

 

When should I seriously consider active tuberculosis (TB) in my newly-admitted HIV-negative patient with a cough?

My patient with chronic alcoholism is showing signs of alcohol withdrawal even though his blood alcohol level (BAL) is still elevated. Is this possible?

FA Manian MD, MPH, , , , , , Leave a comment

Absolutely! For patients with chronic alcohol dependence, any acute decline in their BAL may precipitate withdrawal (1).

For example, if a patient typically drinks enough alcohol on a daily basis to sustain a BAL of 350 mg/dl, any significant drop in BAL (e.g. down to 125 mg/dl) may be associated with early signs of withdrawal such as nervousness, tachycardia and elevated blood pressure.

Another scenario that could lead to withdrawal symptoms despite an elevated BAL involves patients who use both alcohol and benzodiazepines chronically. In such patients— because the 2 substances have cross-reactive effects on the brain— a significant reduction in the dose or frequency of benzodiazepines may also lead to withdrawal despite an elevated BAL.  Also remember that symptoms of benzodiazepine withdrawal may begin within 24 h or up to 2 weeks following its cessation (2).

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Reference

  1. Roffman JL, Stern TA.  Alcohol withdrawal in the setting of elevated blood alcohol levels. Prim Care Companion J Clin Psychiatry. 2006; 8(3):170-173 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1540391/
  2. Greenberg MI. Benzodiazepine withdrawal: potentially fatal, commonly missed, Emergency Medicine News 2001;23:18. https://journals.lww.com/em-news/pages/articleviewer.aspx?year=2001&issue=12000&article=00013&type=Fulltext

 

Contributed by Stephanie Meller, MD, Boston, MA

 

 

My patient with chronic alcoholism is showing signs of alcohol withdrawal even though his blood alcohol level (BAL) is still elevated. Is this possible?