EUH Morning Report: What physical examination findings help diagnose or rule out cardiac tamponade, and what are the diagnostic test characteristics of those findings?

The Bottom Line: Diagnosis is usually based on the presence of symptoms and signs and confirmed by echocardiography. The urgency of echocardiograpm depends on the degree of suspicion, and presence versus absence of pulsus pardoxus on examination.

Typical presentation of cardiac tamponade include:

cardiac tamponade pic

References: DynaMed Plus [Internet]. Ipswich (MA): EBSCO Information Services. 1995 – . Record No. 114102, Pericardial effusion and tamponade; [updated 2017 Jun 15, cited 2018 Sep 17]; [about 13 screens]. Emory login required.

Simel DL, Roy CL, Minor MA, Brookhart M, Choudhry NK. Cardiac TamponadeIn: Simel DL, Rennie D. eds. The Rational Clinical Examination: Evidence-Based Clinical Diagnosis New York, NY: McGraw-Hill; 2009. Accessed September 17, 2018.


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.”

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: Review of Still’s Disease

The Bottom Line: Still’s disease, more specifically adult-onset Still’s disease (AOSD) is  a diagnosis of exclusion. Various infectious, neoplastic, and autoimmune diseases can mimic its clinical manifestations and need to be ruled out for diagnosis (DynaMed Plus, 2018). It is a rare systemic inflammatory disease with 1-34 cases per 1 million people. AOSD is equally distributed among men and women, with peak ages of onset of 15-25 and 36-46 years (Giacomelli et a, 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: George Still described 22 children with systemic onset juvenile idiopathic arthritis in 1897. In 1971, Eric Bywaters reported 14 adult patients with symptoms similar to pediatric Still’s disease, such as skin rash, fever, and polyarthritis. Thus, AOSD was defined. It remains a multisystemic disorder of unknown etiology and difficult diagnosis (Giacomelli et al, 2018).

Current AOSD treatment is aimed at targeting pro-inflammatory signs and symptoms, preventing organ damage and life-threatening complications, minimizing adverse effects. Giacomelli et al (2018) confess that recent evidence suggest new insights in AOSD pathogenesis and highlight new therapeutic targets, thus AOSD management may be improving “in the next future.”

EUH Krakow Conference: What is the best diagnostic test for coccidioidomycosis?

The Bottom Line: A definitive diagnosis can be made by the following tests:

  • Microscopic examination or fungal culture.
  • Antibody testing: Immunoglobulin (Ig)M antibodies may be present within 1-3 weeks of illness onset, and are indicative of recent infection.
    • IgG antibodies are present within 2-3 weeks of onset and may last for several months. Increasing titers or tier > 1:32 suggests increased infectious activity and dissemination.
  • Antigen detection: Antigen levels are highest early in the infection. Detection is useful for diagnosing immunocompromised patients that may not develop antibody response.

If evaluation is not clear, a tissue biopsy may be required. If extrapulmonary disease is suspected, imaging and lumbar puncture may be needed.

(DynaMed Plus, 2018)

Reference: DynaMed Plus [Internet]. Ipswich (MA): EBSCO Information Services. 1995 – . Record No. 116164, Coccidioidomycosis; [updated 2018 Aug 30, cited 2018 Sep 10]. Emory login required.

Summary: Suspect coccidioidomycosis in patients with clinical syndromes, exposure history, and risk factors listed below. Blood tests may show elevated erythrocyte sedimentation rate and eosinophilia.

  • acute pneumonia is the most common clinical presentation
  • less common manifestations include chronic pneumonia, skin nodules, bone and joint infections, and meningitis
  • residence in or travel to endemic regions such as the southwestern United States is the most common exposure
  • impaired cell mediated immunity such as HIV infection, solid organ transplantation, and pregnancy are risk factors for extrapulmonary and severe disease

(DynaMed Plus, 2018)


EUHM Report: What is the etiology of Streptococcus anginosus?

The S anginosus group, often referred to as Streptococcus milleri , are commensals of the oropharyngeal, GI, and genitourinary microflora that can cause invasive  pyogenic infections in various sites. While more commonly associated with CNS, abdominal, head and neck, bloodstream, and thoracic infections, the three species that make up S anginosus have been associated with differing clinical manifestations.

Sunwoo, Bernie Y, and Wallace T Miller. “Streptococcus Anginosus Infections: Crossing Tissue Planes.” Chest. 146, no. 4 (2014): E121-125.

While more commonly associated with CNS, abdominal, head and neck, bloodstream, and thoracic infections, the three species that make up S anginosus have been associated with differing clinical manifestation.  The S anginosus group of organisms is known to be highly virulent and rapidly progressive, and it is not surprising that they might cross tissue planes.  Given the potential utility of radiographic extension across tissue planes in raising the differential of S anginosus , further research on the radiographic presentations of thoracic S anginosus is needed.

Grady Morning Report: What are the most recent diagnostic criteria for MS?

The Bottom Line: Despite the incorporation of MRI and other paraclinical evidence into the diagnostic scheme, careful clinical evaluation and judgment, and the principle of “no better explanation” remain the most important aspects of MS diagnosis and should not be replaced by any diagnostic test.

Reference: Milo R, Miller A. Revised diagnostic criteria of multiple sclerosis. Autoimmun Rev. 2014 Apr-May;13(4-5):518-24. 

Summary: Over the years, several sets of criteria have been proposed for the diagnosis of MS, based on the principles of dissemination in space (DIS) and dissemination in time (DIT) of CNS lesions, and the exclusion of other diseases with similar characteristics. With each revision, new diagnostic criteria modified disease definitions and diagnostic thresholds, while aiming at maintaining sensitivity and improving specificity. According to the older Schumacher and Poser criteria, MS can be diagnosed clinically by demonstrating 2 separate attacks (fulfilling DIT criteria) involving at least 2 different areas of the CNS (fulfilling DIS criteria). The 2001 McDonald criteria and their 2005 revision incorporated defined magnetic resonance imaging (MRI) criteria for DIS and DIT that provided guidance on how to diagnose MS after CIS. The most recent 2010 McDonald criteria simplify requirements for DIS and DIT and may allow for an earlier diagnosis of MS from a single baseline brain MRI if there are both silent gadolinium-enhancing and nonenhancing lesions.

EUH Morning Report: Should lasix (furosemide) be considered in the setting of hypercalcemia?

The Bottom Line: Avoid loop diuretics in the setting of acute hypercalcemia, except may be considered for patients with concomitant volume overload.

Loop Diuretic:

  • inhibits calcium resorption in distal renal tubule
  • may worsen volume depletion and electrolyte derangements and should be used with caution
  • no evidence to support use in acute hypercalcemia
    • may be used to control volume overload
    • associated with hypokalemia and possibly contributes to dehydration

(DynaMed Plus, 2016)

References: DynaMed Plus [Internet]. Ipswich (MA): EBSCO Information Services. 1995 – . Record No. 116018, Hypercalcemia; [updated 2016 Dec 27, cited 2018 Jul 19]; [about 10 screens]. Emory login required.

LeGrand SB, Leskuski D, Zama I. Narrative review: furosemide for hypercalcemia: an unproven yet common practice. Annals of Internal Medicine. 2008;149(4):259-263.

Saitz R. Furosemide for hypercalcemia: Neither proven nor recommended. NEJM Journal Watch. 2008 Sept 25.

Summary: In his review of LeGrand et al (2008), Dr. Richard Saitz provides the following summary and comment.

A literature review found little support for the use of the diuretic furosemide to treat hypercalcemia.

Many textbooks recommend saline and furosemide as first-line management for hypercalcemia. Investigators searched the literature since 1950 for studies of furosemide or bisphosphonate use for hypercalcemia in people.

They identified nine reports — the most recent from 1983 — involving 37 patients treated with furosemide for hypercalcemia; doses ranged from 240 mg to 2400 mg. Calcium normalized in 14 of 39 episodes, and within 12 hours in only two cases. Intensive monitoring was accompanied by replacement of fluid and electrolyte losses. Complications included hypernatremia, coma, metabolic acidosis, hypophosphatemia and hypomagnesemia, altered mental status, and tetany.

Investigators identified 56 clinical studies of bisphosphonates — 34 were randomized and included more than 1000 patients. In a systematic review of 26 studies of bisphosphonate use in hypercalcemia of cancer, calcium levels normalized in more than 70% of patients. The authors conclude that volume repletion and bisphosphonate therapy should be the standard management strategy for hypercalcemia, with furosemide used only for managing fluid overload.


Forced saline diuresis for hypercalcemia is a long-standing practice that persists, even in authoritative texts, despite the absence of evidence for its efficacy, the existence of known risks, and the availability of other proven treatments. Saline and bisphosphonates, with or without calcitonin, are the standard of care for hypercalcemia.

(Saitz, 2008)

EUH Hunt Conference: What diagnostic testing are available for Creutzfeldt-Jackob disease (CJD)?

The Bottom Line: CJD is a rare neurodegenerative condition with a rapid disease course and 100% mortality rate. The most challenging aspect of CJD is its diagnosis (Manix et al, 2015). According to DynaMed Plus (2015), the most reliable diagnostic testing are:

  • obtain blood tests to rule out other causes of progressive dementia
  • magnetic resonance imaging (MRI)findings may suggest Creutzfeldt-Jakob disease (CJD), or an alternate diagnosis
  • consider lumbar puncture for cerebrospinal fluid(CSF) studies
    • routine tests usually normal
    • American Academy of Neurology (AAN) recommends ordering CSF protein 14-3-3 assayto decrease uncertainty of diagnosis in patients with rapidly progressive dementia who are strongly suspected of having sporadic form of CJD and for whom diagnosis remains uncertain, but test is not as specific as S100b
  • electroencephalogram (EEG)associated with distinct pattern for sporadic, but not variant, CJD
  • brain biopsy
    • not recommended as procedure to confirm clinical diagnosis due to potential complications and need to destroy instruments used
    • brain biopsy only indicated if possibility remains of alternative diagnosis that is treatable

References:  DynaMed Plus [Internet]. Ipswich (MA): EBSCO Information Services. 1995 – . Record No. 114980, Creutzfeldt-Jakob disease; [updated 2015 May 01, cited 2018 Aug 13]; [about 17 screens]. Emory login required.

Manix M, Kalakoti P, Henry M, Thakur J, et al. Creutzfeldt-Jackob disease: updated diagnostic criteria, treatment algorithm, and the utility of brain biopsy. Neurosurg Focus. 2015 Nov;39(5):E2. Doi:10.3171/2015.8.FOCUS15328.