EUH Morning Report: How should we reduce the risk of Clostridium difficile-associated diarrhea (CDAD) in hospitalized patients who require antibiotics?

The Bottom Line: Moderate-quality evidence supports a significant protective effect of probiotics against CDAD, and higher-risk patients (e.g. patients with prior history of CDAD) stand to benefit more from prevention. Probiotics should not be given to patients who are immunocompromised, are pregnant, are in intensive care, or have prosthetic heart valves or certain preexisting gastrointestinal disorders (e.g., inflammatory bowel disease, ostomy). For most other hospitalized patients who receive antibiotics during hospitalization, prescribing 20 to 50 billion colony forming units of probiotics daily (starting within 24–48 hours of antibiotic initiation) can prevent CDAD (Dressler, 2017).

References: Dressler DD. Do probiotics prevent C. difficile-associated diarrhea in patients receiving antibiotics? NEJM Journal Watch. 2018 Mar 13.

Goldenberg JZ, Yap C, Lytvyn L, Lo CK, et al. Probiotics for the prevention of Clostridium difficile-associated diarrhea in adults and children. Cochrane Datbase Syst Rev. 2017 Dec 19;12:CD006095.

Summary: In summarizing their systematic review, Goldenberg et al (2017) state:

“This review includes 39 randomized trials with a total of 9955 participants. Thirty-one studies (8672 participants) assessed the effectiveness of probiotics for preventing CDAD among those taking antibiotics. Our results suggest that when probiotics are given with antibiotics the risk of developing CDAD is reduced by 60% on average. Among trials enrolling participants at high risk of developing CDAD (>5%), the potential benefit of probiotics is more pronounced with a 70% risk reduction on average. Side effects were assessed in 32 studies (8305 participants) and our results suggest that taking probiotics does not increase the risk of developing side effects. The most common side effects reported in these studies include abdominal cramping, nausea, fever, soft stools, flatulence, and taste disturbance.”

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EUH Morning Report: Do specific blood pressure medications lead to higher prevalence of Orthostatic Hypotension syncope or recurring syncope in older adults with dementia?

The Bottom Line: In older adults with dementia, nitrates and alpha-blockers alone and the combinations of ACE-Is and diuretics, alpha-blockers and diuretics, and ACE-Is and nitrates are more frequent in patients with syncope due to OH than in those without (Testa et al, 2018).

References: Testa G, Ceccofiglio A, Mussi C, Bellelli G, et al. Hypotenstive drugs and syncope due to orthostatic hypotension in older adults with dementia (syncope and dementia study). J Am Geriatr Soc. 2018 Aug;66(8):1532-1537. Doi:10/1111/jgs.15421.

Ungar A, Mussi C, Nicosia F, et al. Etiology of syncope and unexplained falls in elderly adults with dementia: Syncope and Dementia (SYD) Study. J Am Geriatr Soc. 2016 Aug;64(8):1567-1573. Doi:10.1111/jgs.14225.

Summary: The recent Syncope and Dementia (SYD) Study found that syncope due to OH was the most common type (50%) of syncope in a population of older adults with dementia and recurrent syncope. Additionally, in nearly half of the study’s participants, dementia was vascular in origin (Unger et al, 2016). Aggressive blood pressure treatment has been related to OH, although the role of specific drugs and combinations is unclear (Testa et al, 2018).

Testa et al (2018) found that the number of drugs administered and particular hypotensive drugs, specifically nitrates alone and combinations of ACE-Is and diuretics and of ACE-Is and nitrates, significantly increase the risk of syncope due to OH. Testa et al (2018) recommend using extreme caution when using these drugs in older adults with dementia.

EUH Morning Report: What is the sensitivity/specificity of the diagnostic criteria for Still’s disease?

The Bottom Line: The Yamaguchi’s criteria are the most sensitive (93.5%), followed by Cush’s (80.6%) and Calabro’s (80.6%). Fautrel’s criteria are 80.6% sensitivity and 98.5% specificity (Giacomelli et al, 2018).

References: DynaMed Plus [Internet]. Ipswich (MA): EBSCO Information Services. 1995 – . Record No. 114565, Adult-onset Still disease; [updated 2018 Aug 24, cited 2018 Sep 5]; [about 13 screens]. Emory login required.

Giacomelli R, Ruscitti P, Shoenfeld Y. A comprehensive review on adult onset Still’s disease. J Autoimmun. 2018 Sep;93:24-36. Doi:10.1016/j.jaut.2018.07.018.

Summary: The Yamaguchi criteria is the most widely used diagnostic criteria for Still’s disease.still's criteria

(Giacomelli, et al, 2018)

EUH Morning Report: What is the criteria for liver transplantion in patients with hepatocellular carcinoma?

The Bottom Line: Liver transplant is recommended for patients with potentially resectable or transplantable disease according to performance status or lack of severe comorbidity, or in patients with unresectable disease who meet Milan or United Network for Organ Sharing (UNOS) criteria. Controversy exists over liver transplantation in patients with tumors marginally outside Milan or UNOS criteria, but some institutions may still consider it (DynaMed Plus, 2017).

  • Milan criteria for liver transplantation for hepatocellular carcinoma includes either of:
    • single lesion ≤ 5 cm in diameter
    • 2-3 lesions all ≤ 3 cm in diameter
  • UNOS criteria for liver transplantation for hepatocellular carcinoma includes both of:
    • Milan criteria
    • no evidence of macrovascular involvement or extrahepatic disease

Reference: DynaMed Plus [Internet]. Ipswich (MA): EBSCO Information Services. 1995 – . Record No. 909499, Management of early hepatocellular carcinoma / Liver Transplant; [updated 2017 May 31, cited 2018 June 28]; [about 24 screens]. Emory login required.

Summary: 

(DynaMed Plus, 2017)

Kokko Conference: Is Vitamin B12 deficiency one of the etiological causes of pancytopenia?

The Bottom Line: The etiological causes of pancytopenia vary depends on patients’ age, gender, country, and other conditions. Vitamin B12 deficiency is the most common treatable cause of pancytopenia.

Reference:

Yokuş O, Gedik H. Etiological causes of pancytopenia: A report of 137 cases. Avicenna J Med. 2016 Oct-Dec;6(4):109-112.

ARTICLE mentioned in Conference:

Stabler, SP. Clinical practice. Vitamin B12 deficiencyN Engl J Med. 2013 Jan 10;368(2):149-60. doi: 10.1056/NEJMcp1113996.

EUH Dressler Conference: What are standard treatments and NSAIDS for pericarditis?

The Bottom Line:  Aspirin or non-steroidal anti-inflammatory drugs are standard first-line therapy for acute pericarditis.

Acute pericarditis (for complete information, see DynaMed Plus):

  • ibuprofen 600 mg every 8 hours for 1-2 weeks, then taper by 200-440 mg every 1-2 weeks until resolution of symptoms and improvement of acute inflammatory markers
  • aspirin 750-1,000 mg orally every 8 hours for 1-2 weeks, then taper by 250-500 mg every 1-2 weeks until resolution of symptoms and improvement of acute inflammatory markers (preferred if other indication for antiplatelet therapy)
  • give colchicine as first-line therapy for acute pericarditis as adjunct to aspirin/NSAID (ESC Class I, Level A)
  • typical colchicine dosing for acute pericarditis
    • 0.5-0.6 mg once daily for 3 months for patients < 70 kg
    • 0.5-0.6 mg twice daily for 3 months for patients ≥ 70 kg
    • available tablets in United States (Colcrys) are 0.6 mg instead of 0.5 mg

Recurrent pericarditis (for complete information, see DynaMed Plus):

  • give aspirin or NSAIDs at full doses (if tolerated) until complete resolution of symptoms (ESC Class I, Level A)
  • if ischemic heart disease is a concern or antiplatelet therapy is required, aspirin should be considered at medium doses (1-2.4 g/day) (ESC Class IIa, Level C)
  • NSAIDs contraindicated in patients with pericarditis complicating acute myocardial infarction (aspirin preferred with addition of colchicine if unresponsive to high-dose aspirin)
  • aspirin 500-1,000 mg every 6-8 hours (range 1.5-4 g/day) for weeks-months, then taper by 250-500 mg every 1-2 weeks
  • ibuprofen 600 mg every 8 hours (range 1,200-2,400 mg/day) for weeks-months, then taper by 200-400 mg every 1-2 weeks
  • give colchicine 0.5 mg twice daily (or 0.5 mg daily for patients < 70 kg or intolerant to higher doses) for 6 months as adjunct to aspirin/NSAIDs
  • continuation of colchicine for > 6 months should be considered in select patients to improve response to medication and remission rates and prevent recurrences

References: Bach RG. ACP Journal Club. Colchicine reduced further recurrence after a first recurrence of pericarditis. Ann Intern Med. 2012 Feb 21;156(4):JC2-04. doi:10.7362/0003-4819-156-4-201202210-02004.

DynaMed Plus [Internet]. Ipswich (MA): EBSCO Information Services. 1995 – . Record No. 115401, Acute and recurrent pericarditis/Treatment/Medications/Nonsteroidal anti-inflammatory drugs (NSAIDS); [updated 2017 Sep 26, cited 2017 Oct 12]; [about 19 screens]. University login required.

Imazio M, Brucato A, Cemin R, Ferrua S, et al. A randomized trial of colchicine for acute pericarditis. N Engl J Med. 2013 Oct 17;369(16):1522-8. doi:10.1056/NEJMoa1208536.

Summary: Because recurrence may imply a lack of sustained benefit from non-steroidal anti-inflammatory drugs, clinicians often prescribe corticosteroids, a common practice supported by limited observational data. Corticosteroid use in pericarditis, however, is associated with an increased risk for recurrence and side effects (Bach, 2012).

The CORP trial is the first multicenter, blinded, randomized, placebo-controlled trial to test the efficacy and safety of colchicine for recurrent pericarditis. Recurrence at 18 months and persistence of symptoms at 72 hours were reduced by > 50% compared with placebo. Notably, colchicine was well tolerated at the doses used, with no severe side effects, and drug withdrawal rates were similar to placebo.

In a separate randomized control trial, Imazio et al (2013) found that colchicine reduced the rate of symptom persistence at 72 hours (19.2% vs. 40.0%, P = 0.001), the number of recurrences per patient (0.21 vs. 0.52, P = 0.001), and the hospitalization rate (5.0% vs. 14.2%, P = 0.02). Colchicine also improved the remission rate at 1 week (85.0% vs. 58.3%, P<0.001).

Given the increased risk for recurrence and side effects with corticosteroids (2), colchicine should be strongly endorsed as first-line treatment for recurrent pericarditis (Bach, 2012).

EUH Morning Report: In patients with acute alcoholic hepatitis, does steroid therapy increase the risk of GI bleeding compared to no use of steroids?

The Bottom Line: For patients with acute alcoholic hepatitis, there isn’t literature to answer the question of whether steroid therapy increases risk of GI bleeding compared to no use of steroids. For patients with non-acute alcoholic liver disease who do not have concomitant GI bleeding., use of steroids does not appear to increase risk of GI bleeding when compared to placebo or no intervention.

References:

O’Shea RS, Dasarathy S, McCullough AJ, et al. Alcoholic liver disease. Hepatology. 2010 Jan;51(1):307-328. PMID: 20034030. doi: 10.1002/hep.23258

Comment on above article by O’Shea, Dasarathy, and McCullough: Singal AK. Comments on AASLD practice guidelines for alcoholic liver disease. Hepatology. 2010 May;51(5):1860-1861. PMID: 20432268. doi: 10.1002/hep.23605

Rambaldi A, Saconato HH, Christensen E, Thorlund K, Wetterslev J, Gluud C. Systematic review: glucocorticosteroids for alcoholic hepatitis — a Cochrane Hepato-Biliary Group systematic review with meta-analyses and trial sequential analyses of randomized clinical trials. Aliment Pharmacol Ther. 2008 Jun;27(12):1167-1178. PMID: 18363896. doi: 10.1111/j.1365-2036.2008.03685.x

References were found in DynaMed Plus. See DynaMed Plus → alcoholic liver disease → treatment → medications → medication to treat acute inflammation for patients with severe alcoholic hepatitis → steroids

Summary of evidence on whether steroid therapy increases the risk of GI bleeding compared to no use of steroids in patients with alcoholic hepatitis (not acute alcoholic hepatitis):

DynaMed Plus states, “efficacy of steroids has not been evaluated in patients with severe alcoholic hepatitis and concomitant…gastrointestinal bleeding,” an “exclusion criteria in many of the early studies of alcoholic hepatitis.”

Only one of the systematic reviews cited in DynaMed Plus on use of steroids versus placebo or no intervention mentioned bleeding as an outcome measure. It states, “Combining the results of four trials providing data demonstrated no significant effects of glucocorticosteroids on…variceal bleeding….Combining the results of the eight trials reporting adverse events demonstrated a significantly higher proportion of patients with adverse events in the glucocorticosteroid group (RR 3.63, 95% CI 1.95–6.76).” The glucocorticosteroids group of 239 patients had “one suspicious of gastrointestinal bleeding.”

EUH Morning Report: What is the ideal diuretic dosing strategy for diuretics in a patient admitted from home with acute decompensated HF and already on home diuretics?

The Bottom Line: In managing patients admitted with heart failure exacerbation, the DOSE trial confirmed that furosemide (Lasix) intermittent bolus is equivalent to continuous drip, making continuous drip management unnecessary in nearly all situations. Furthermore, symptoms were similar in high dose bolus furosemide compared to low dose bolus furosemide, with only marginal differences in creatinine change in high-dose vs. low-dose furosemide boluses. However, the high-dose bolus patients had greater daily weight loss (more than 1kg additional fluid weight lost per day) compared to low dose patients.

Clinicians may consider up to 2.5 times the patient’s home daily furosemide dose, converted to IV in their diuretic bolus dosing for admitted patients with heart failure exacerbations.

Reference: Felker GM, Lee KL, Bull DA, Redfield MM, et al. Diuretic strategies in patients with acute decompensated heart failure. NEJM. 2011 Mar 3; 364(9):797-805.

Summary:  Although loop diuretics are an essential component of therapy for acute decompensated heart failure, there have been few prospective data to guide decision-making regarding the use of these agents. In the DOSE trial, no significant differences were found in either the patients’ global assessment of symptoms or the change in the creatinine level from baseline to 72 hours when diuretic therapy was administered by means of boluses as compared with continuous infusion or with a low-dose strategy as compared to a high-dose strategy (Felker et al, 2011).

Bolus vs. continuous infusion:

  • No difference in serious adverse events (44% in each group)
  • More cases of ventricular tachycardia with boluses than with continuous infusions (7 vs. 4)
  • More cases of renal failure with continuous infusion than with bolus (11 vs. 8)
  • More cases of myocardial infarction with boluses (4 vs. 1)

*These findings are not consistent with prior, smaller studies suggesting that continuous infusion, as compared with boluses, is associated with a lesser degree of renal dysfunction and greater diuresis.

High-dose vs. low-dose strategy:

  • Fewer in the high-dose group had serious adverse event than in the low-dose group (38% vs. 50%)
  • More cases of ventricular tachycardia with low-dose strategy than with high-dose strategy (7 vs. 4)
  • More cases of renal failure with low-dose strategy (12 vs. 7)
  • More cases of myocardial infarction with low-dose strategy (4 vs. 1)

*These findings suggest that prior observations linking high-dose diuretics with poor outcomes may reflect the severity of the illness rather than a harmful effect of high doses.

It must be noted that this study used a continuous placebo infusion in the patients assigned to boluses. The authors admit that this feature of the study design may have served to increase the time the patients were supine, a position that has been shown to enhance diuresis (Felker et al, 2011, p. 803). Also, the bolus group tended to receive a higher dose of the diuretic than did the continuous-infusion group.

EUH Resident Report: What are the guidelines for prophylaxis for dental procedures in patients with congenital heart disease?

The Bottom Line: Infective endocarditis (IE) prophylaxis for dental procedures should be recommended only for patients with underlying cardiac conditions associated with the highest risk of adverse outcome from IE. For patients with these underlying cardiac conditions, prophylaxis is recommended for all dental procedures that involve manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa. Prophylaxis is not recommended based solely on an increased lifetime risk of acquisition of IE (AHA, 2007).

References: American Heart Association. Prevention of infective endocarditis. Guidelines from the American Heart Association. Circulation. 2007.

European Society of Cardiology. Infective endocarditis (Guidelines on prevention, diagnosis, and treatment of): ESC clinical practice guidelines. 2015.

Summary: Recommendations for prophylaxis of IE in the highest-risk patients according to the type of at-risk procedure (Table 5, ESC, 2015).

m_ehv31921

 

TOE = transoesophageal echocardiography.

aClass of recommendation.

bLevel of evidence.

cFor management when infections are present, please refer to Section 3.5.3.

EUH Resident Report: What are indications for anticoagulants for primary prevention of left ventricular thrombosis?

Bottom line: Indications for anticoagulants for primary prevention of left ventricular thrombosis include patients with the following traits: large anterior infarctions (particularly in the anterior location), heart failure, and high embolic risk (including those with echocardiographic evidence of mobile and protruding thrombi, severe left ventricular dysfunction, or prior emboli).

Sources (two review articles):

Antithrombotic therapy in left ventricular thrombosis and systemic embolism. L L Cregler. The American heart journal, 1992, Vol.123(4 Pt 2), p.1110-1114.

Antithrombotic therapy in acute myocardial infarction: prevention of venous, left ventricular and coronary artery thromboembolism. B Stein, V Fuster. The American journal of cardiology, 1989, Vol.64(4), p.33B-40B.