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: 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)


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 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.

EUH Morning Report: What is the rational clinical exam for ascites?

The Bottom Line: The examiner should ask about recent ankle edema, weight gain, or change in abdominal girth. Other potentially important items are a history of liver disease or congestive heart failure. The focused physical exam includes: (1) inspection for bulging flanks, (2) percussion for flank dullness, (3) a test for shifting dullness, and (4) a test for a fluid wave (Williams and Simel, 1992).


References: DynaMed Plus [Internet]. Ipswich (MA): EBSCO Information Services. 1995 – . Record No. 116330, Ascites; [updated 2017 Jul 31, cited 2018 Jun 22]; [about 20 screens]. Emory login required.

Williams JW Jr, Simel DL. The rational clinical examination. Does this patient have ascites? How to divine fluid in the abdomen. JAMA. 1992 May 20;267(19):2645-8.

Summary: Ascites is a symptom that may have important diagnostic, prognostic, and therapeutic implications. When clinically detectable, ascites may indicate underlying heart failure, liver disease, nephrotic syndrome, or malignancy (Williams & Simel, 1992).

Skin: assess for signs of liver disease

  • Jaundice
  • Spider veins
  • Palmar erythema
  • Caput medusa (abdominal wall collateral veins)


  • Jugular venous distention may be present secondary to heart failure


  • Look for associated pleural effusions (dependent rales)


  • Abdominal distention
  • Fluid wave
  • Shifting dullness
  • Umbilicus eversion
  • Low umbilicus position (Tanyol sign)
  • Flank dullness
    • About 1,500 mL of fluid must be present to be detected
    • If no flank dullness, patient has < 10% chance of ascites


  • Look for associated peripheral edema
  • Leukonychia (white nails) may be seen in advanced liver disease


  • Penile or scrotal edema may be seen

(DyanMed Plus, 2018)

New Intern Orientation: Adjusted ASCVD Risk

The Bottom Line: Major guidelines recommend that decisions about aspirin, blood pressure, and statin treatments be informed by 10-year CVD risk estimates from the PCEs, which were derived in 2013 using data from 5 cohort studies. These PCEs are controversial because of reports that they substantially misestimate risk. Two basic strategies to revise the PCEs could improve their accuracy: updating the data from which they are derived and changing the statistical methods used to derive them (Yadlowsky et al, 2018).

In his review of the recent study by Yadlowsky et al (2018), Dr. Dan Dressler provides the following example: Assume the patient is a 68-year-old white man with the following favorable risk profile: Total cholesterol, 160 mg/dL; HDL cholesterol, 55 mg/dL; blood pressure, 120/70 mm Hg; and no history of diabetes, hypertension, or smoking. His 10-year CVD risk is 12% on the ACC/AHA calculator, but only 6% on this new model’s calculator. The latter risk is below the threshold at which most clinicians would recommend statin therapy (Dressler, 2018).

References: Dressler DD. 10-year cardiovascular risk might be lower than we thought. NEJM Journal Watch. 2018 Jun 21.

Yadlowsky S, Hayward RA, Sussman JB, McClelland RL, et al. Clinical implications of revised pooled cohort equations for estimating atherosclerotic cardiovascular disease risk. Ann Intern Med. 2018 Jun 5. doi:10.7326/M17-3011

Summary: The clinical implications of the results suggest that the revised PCEs will reduce overestimation of risk in general and may prevent adverse events, health care costs, and inflated expectations of absolute risk and corresponding absolute therapeutic benefit. Additionally, use of the updated equations will correct erroneous, implausible risk estimates for many African American adults (Yadlowsky et al, 2018).

The study by Yadlowskey et al (2018) validates what some clinicians have observed in practice: Some patients are classified inaccurately as “high risk.” Although guidelines that depend on risk calculation would not necessarily need to change if risk calculators are updated, the number of patients who would be affected by guideline recommendations could be lowered dramatically (Dressler 2018).

EUH Krakow Conference: What are risk factors for cryptococcus gattii?

The Bottom Line:  The risk factors for acquiring cryptococcus gattii are:

  • Age > 50 years
  • History of smoking
  • Corticosteroid use
  • HIV infection
  • History of cancer
  • History of chronic lung disease


References: MacDougall L, Murray F, Romney M, Starr M, et al. Risk factors for Cryptococcus gattii infection, British Columbia, Canada. Emerg Infect Dis. 2011 Feb;17(2):193-199. Doi:10.3201/eid1702.101020

Bartlett KH, Cheng PY, Duncan C, Galanis E, et al. A decade of experience: Cryptococcus gattii in British Columbia. Mycopathologia. 2012 Jun;173(5-6):311-9. Doi:10.1007/s11046-011-9475-x.

Summary: Cryptococcus gattii is commonly believed to infect those with healthy immune systems, yet several immunosuppressive and pulmonary conditions seem to be risk factors (MacDougall et al, 2011).

EUH Hunt Conference: A review of Horner syndrome

The Bottom Line: Horner syndrome results from an interruption of sympathetic innervation to the eye. The classic triad is unilateral ptosis (slight narrowing of the ocular fissure), miosis (smaller pupil on the affected side), and anhidrosis (lack of perspiration on the forehead or face). Horner syndrome is not likely to cause any functional visual disturbance but is of great importance clinically as a “red flag” warning that the oculosympathetic pathway has been interrupted and thus there may be potentially life-threatening lesions in the head, neck, and chest.

Reference: Martin TJ. Horner syndrome: a clinical review. ACS Chem Neuroscience. 2018 Feb 21;9(2):177-186. Doi:10.1021/acschemneuro.7b00405

Summary: The first, and perhaps most important, aspect of evaluating suspected Horner syndrome is a careful history. The history often reveals an obvious cause, such as trauma or neck/chest surgery, or will show that the Horner syndrome had been present for many years and therefore may not require an extensive investigation. The history may also reveal other symptoms that would help localize the lesion causing the Horner syndrome. A careful examination is obviously also critical, as other causes of anisocoria or ptosis may need to be considered rather than Horner syndrome, and concomitant signs (for example, a sixth nerve paresis) may help localize a potential lesion. After this, pharmacologic testing can be helpful to confirm diagnosis. Many clinicians will elect not to evaluate Horner syndrome if it has been present for greater than two years.

Though often benign or idiopathic, the cause of Horner syndrome can be very threatening or even lethal, so understanding how to recognize, diagnose, and appropriately evaluate Horner syndrome is important to all clinicians.