VA AM report 9.19.17: DVT/PE version 3.0

Case summary: Thanks to Adam Tabbaa (double-double) for presenting a case of a 70M with PMH obesity presenting with LLE edema and dyspnea and found to have a PE that made our nerd-hearts sing!

Top pearls:

  1. Anti-coag clinic pearl: for patients with a positive LE ultrasound OR CTPE, getting that second confirmatory imaging study (e.g. either CTPE or LE ultrasound) can seem like overkill. However, for providers who follow patients longitudinally, this additional imaging is useful (e.g. for serial imaging comparison, to monitor clot burden when considering whether to come off of anticoagulation)
  2. The most recent CHEST VTE guidelines recommend DOACs (e.g. apixaban) as FIRST LINE for DVT/PE over vitamin K antagonists except patients with cancer-associated thrombosis (though clinical trials are underway to test DOACs in cancer).
  3. Per a recent NEJM study, there is little benefit to screening for malignancy in unprovoked PE.

Why get an ultrasound in addition to a CTPE? Can be helpful for providers who follow patients longitudinally!

  1. Serial imaging comparison
  2. Helps when trying to get patients OFF anticoagulation (can follow serial U/S)
  3. Helps if patient has subsegmental PE on CTPE (if have a DVT, this supports anticoagulation)

No benefit to screening for malignancy with CT abdomen/pelvis in unprovoked PE

  1. 854 patients randomized to limited cancer screening (basic blood testing, chest radiography, and screening for breast, cervical, and prostate cancer) versus limited + CT A/P. There was no significant difference between the two study groups in the mean time to a cancer diagnosis (4.2 months in the limited-screening group and 4.0 months in the limited-screening-plus-CT group, P=0.88) or in cancer-related mortality (1.4% and 0.9%, P=0.75).

http://www.nejm.org/doi/full/10.1056/NEJMoa1506623

 


DOACs are FIRST LINE for DVT/PE!

  1. In AT10, the first-line recommended anticoagulant therapy includes dabigatran, rivaroxaban, apixaban, or edoxaban over vitamin K antagonists (VKA) or low molecular weight heparin (LMWH).
  2. The one exception is in patients with cancer-associated thrombosis. In this subset, AT10 recommends LMWH over VKA or DOACs with extended therapy.

http://www.chestnet.org/News/Press-Releases/2016/01/AT10-VTE


PE Risk stratification

  1. Rely on vital signs, biochemical markers, TTE and imaging to risk stratify VTE patients.
  2. Note that degree of clot burden does not factor into risk stratification (as long as PE is segmental).
  3. Here is a nifty risk stratification algorithm.

JAC_Template

Management of PE: An Update. J Am Coll Cardiol 2016;67;976-990.


Filed under: Morning Report

ZSFG AM Report Pearls 9/19/2017: HIV-Associated Neurocognitive disorders

Thank you to Kendra Wulczyn and Cynthia, our Sub-I, for presenting a very interesting case of a patient with 4 months of weight loss, confusion who presented initially with hypotension and tachycardia, ultimately found to have a new diagnosis of HIV and HIV-Encephalopathy which is now responding well to ART. Special thanks to Susa Coffey, our HIV expert for dropping lots of knowledge!
Top Pearls:
  1. Indolent HIV-associated infections causing AMS to consider: TB, CNS lymphoma, endemic fungal infections, PML (related to JC virus)
  2. HIV-encephalopathy is part of a broader category of HIV-associated neurocognitive disorders that can range from asymptomatic changes is neurocognitive function to dementia
  3. HIV-Encephalopathy should be considered when infectious and malignancy-associated diagnoses have been ruled out and there are characteristic MRI findings (discussed below).

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Definition:
HIV-Associated Neurocognitive disorders include a broad-spectrum of disease
  • Asymptomatic neurocognitive impairment
  • Mild neurocognitive impairment
  • HIV dementia
Pathophysiology:
  • HIV is neuroinvasive – HIV invades mononuclear cells in the CNS
    • Infected cells -> microglial activation -> diffuse myelin loss -> neuronal death -> astroglial proliferation
  • ARVs can have low penetrance through the blood-brain barrier
  • Remember that the pathophysiology of HIV-related neurocognitive disorders coincides with normal aging and now there are many more older people with HIV
Clinical Presentation:
The clinical syndrome of HAD comprises of a combination of cognitive, behavioral and motor dysfunction like gait disturbance and tremors . While there is some individual variation, frequent manifestations include: inattention and reduced concentration, apathy and dulling of personality, psychomotor slowing, marked motor slowing and ataxia.
Often presents after years of untreated HIV and with low CD4 counts.
Diagnosis:
MRI Findings:
  • Rule out infectious etiologies and PML (JC virus)
  • Brain parenchymal loss – increased CSF fluid, decrease in striatal gray matter volume, decrease in cerebral white matter volume
  • Patchy areas of high signal intensity on T2-weighted and fluid-attenuated inversion recovery sequences with relative sparing of the subcortical white matter and posterior fossa structures.
Treatment:
-HAART treatment – although variable in the degree to which this reverses the cognitive impairment
Sources:
  • Mateen FJ & Mills EJ. (2012). Aging and HIV-related cognitive loss. JAMA 308(4):349-350.
  • Silva MTT, Wagner S, Grinsztejn B. (2009). Human immunodeficiency virus encephalopathy: Cognitive and radiographic improvement after antiretroviral therapy. Arch Neurol. 66(8):1040-1041.
  • https://radiopaedia.org/articles/hiv-associated-dementia
Evernote:
  • HIV Encephalopathy: https://www.evernote.com/shard/s509/sh/ac41a753-0706-4fe7-899f-45e4160734b3/de194e1409950b0c41954c964057e749

 


Filed under: Morning Report

Cardiology Report – Septemeber 19th

Cardiology Report Pearls 9/19/17 – Syncope & Aortic Stenosis

Thank you, Kelly, for presenting a case of an older male who presented with exertional syncope found to have severe, progressive aortic stenosis.

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Key Pearls:

  1. Aortic stenosis with a tricuspid aortic valve is generally a disease of octogenarians. If presenting earlier, consider monocuspid (20-30s) or bicuspid valves (40s-60s).
  2. Remember that bicuspid aortic valves are also associated with aortic root dilatation – which increases the risk of both aortic insufficiency and aortic dissection.
  1. Severity of aortic stenosis is determined by valve area (< 1.1 cm), peak velocity (> across the valve, and gradient across the valve. These metrics have some caveats (e.g low EF and cirrhosis c/b portal HTN) and are very operator dependent.

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Approach to Sudden Collapse:

Cardiac

  • Abnormal structural
    • HCM (35%) -> also remember ARVC or LV non-compaction
    • Anomalous origin of a coronary artery (17%)
    • Myocarditis (6%)
    • Valvular – mitral valve prolapse or aortic stenosis (~2%)
  • Structural normal
    • Long QtC
    • Channel defects such as Brugada syndrome
    • Catecholaminergic polymorphic VT
    • Electrolytes – Potassium, Magnesium, Calcium
    • Trauma – commotio cordis

Non-cardiac

  1. Heat Stroke
  2. Seizure or neurological – bleeds
  3. Dehydration
  4. Toxicology – supplements in athletes

Flashback to this previous post on syncope.

Schematic of the Continuity Equation to Calculate Velocity:

AS1.png

 

Survival in Aortic Stenosis

as2.png

as3

Remember the big 3 symptoms that portend significantly increased mortality in aortic stenosis: syncope, angina, and heart failure. Mortality remains low while patients are asymptomatic. After angina, syncope, or dyspnea related to heart failure develops, the prognosis worsens dramatically if severe aortic stenosis is left untreated. The epidemiology of untreated and treated aortic stenosis was first described in the 1960s by Ross and Braunwald.

Simplified Approach to Management of Aortic Stenosis:

as4

References:

  1. http://ccn.aacnjournals.org/cgi/content-nw/full/28/3/40/F2
  2. https://www.escardio.org/static_file/Escardio/Subspecialty/EACVI/position-papers/EAE-recommendations-valve-stenosis.pdf
  3. http://circ.ahajournals.org/content/126/1/118

 


Filed under: Morning Report