All posts by gsmith003

ZSFG AM Report Pearls 10/11/17: Perioperative Management of Anticoagulation

Thank you to Dr. Dan Reiss for presenting the case of a patient on anticoagulation for atrial flutter and a left atrial thrombus who was scheduled to undergo a planned surgical procedure. We discussed perioperative anticoagulation guidelines and considerations.

Peri-Operative Management of Anticoagulation:
Broad Framework:
  • Assess bleeding risk
  • Assess thrombotic risk
  • Consider:
    • Patient Factors
    • Procedure Factors
  • Use a resource of Guidelines to help make your decision (as there are lots of caveats and factors to remember)
Assessing Thrombotic Risk
  • High Risk
    • CHADS2 5-6
    • TIA/CVA < 3 months
    • Afib w/ stoke/TIA w/in 12 months
    • Acute VTE or arterial embolism within 3 months
    • Mechanical aortic valve prosthesis and history of CVA/TIA/AFIB/low EF
    • Mechanical mitral valve prosthesis or 2 or more prosthetic heart valves
    • Caged ball or tilting disk aortic valve prosthesis
    • Rheumatic mitral valve disease
    • History of recurrent VTE while on anticoagulation or during brief interruption
    • Severe thrombophilia (deficiency of protein C, protein S or antithrombin, antiphospholipid antibodies, or multiple thrombophilic abnormalities)
    • VTE within 6 months in setting of cancer with a very high thrombotic risk
  • Moderate Risk
    • CHADS2 3-4
    • Non-valvular atrial fibrillation with history of stroke/TIA > 12 months prior
    • Unprovoked VTE within the past 3 to 12 months
    • Cancer-associated VTE within 6 months (if cancer is high TE risk, may consider bridge)*
    • Mechanical aortic valve prosthesis with one or more of the following: hypertension, diabetes, age >75 yr
    • Non-severe thrombophilia (heterozygous factor V Leiden, PT20210 mutation)
  • Low Risk
    • CHADS2 0-2, no prior TIA/CVA
    • Non-valvular atrial fibrillation without history of stroke/TIA  VTE occurring >12 months ago
    • Mechanical aortic valve prosthesis without atrial fibrillation (AFIB) or other major risk factors for stroke (low EF, hypercoag state)
CHEST Guidelines for Thrombotic Risk
Assessing Risk of Bleeding
  • History of bleeding
  • Talk to surgeon to assess risk of procedure, surgeon’s comfort
Peri-Operative Management of Anti-Platelets:
Single Agent Antiplatelet (i.e. Aspirin only for primary or secondary prevention)
  • Almost always OK to stop if asked by surgeon
  • Many surgeons and surgical procedures are probably OK to complete while on ASA
 
Dual Antiplatelet Therapy
  • Typically should NOT be interrupted for 6 months if taking for a coronary stent
    • i.e. should delay surgery if cannot be done on dual antiplatelet
    • Less data available able recommendation if on dual antiplatelet for other reasons
  • Talk with surgeon about bleeding risks

Resources:

Evernote:

  • Anticoag in Peri-Operative: https://www.evernote.com/shard/s509/sh/5ebffea1-5109-4c43-8a1d-cdfa489acd4c/9b9148b43647e57d3ba0f9cd1f0ab8e0
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ZSFG AM Report Pearls 10/10/17: HIV Hx Taking and PCP PPx Pearls

Thank you to Maxime for presenting an interesting case of a patient with poorly-controlled HIV with a low CD4 count who presented with SOB and AMS of 2 days duration. We discussed the challenges of framing severely immunosuppressed patients who may have multiple issues. We also captured a few pearls from Susa Coffey about HIV care.

Key Components of an HIV-History:

  • **Last CD4 & Viral Load – helpful esp within the last 6 months
    • Consider new CD4 count if >6 months since last, recognizing CD4 altered in acute illness
  • **Use of ARVs – especially noting ability to adhere to regimen
  • Hx of Opportunistic Infections – may raise your suspicion for particular etiologies
  • CD4 Nadir – gives you  sense of where their CD4 may be if they have not been able to adhere to an ARV regimen and may help raise suspicion for OIs

 

PCP/PJP Pneumocystis Prophylaxis:

Indications:
  • CD4 <200
  • Consider in CD4% <14%
  • Consider in CD4 200-250 if ARVs are going to be delayed
  • NOTE: Not needed if already on PPx or Toxoplasmosis with pyrimethamine-sulfadiazine
Prophylaxis Regimens:
  • TMP-SMX (Bactrim) 1 DS tablet daily (although 1 single-strength also effective)
    • Note: should re-challenge with Bactrim even if they have a mild reaction (as long as not life threatening reaction)
    • Only consider alternative therapy if life-threatening reaction like Stevens-Johnson Syndrome pr TEN
  • Dapsone
  • Dapsone + Pyrimethamine plus leucovorin (especially if need toxoplasmosis ppx needed)

 

Sources:

  • CDC Guidelines for the Prevention and Treatment of Opportunistic Infections in HIV-Infected Adults and Adolescents: https://aidsinfo.nih.gov/guidelines/html/4/adult-and-adolescent-opportunistic-infection/321/pcp

Evernote:

  • PCP Prophylaxis: https://www.evernote.com/shard/s509/sh/a9ef840b-2b69-4c83-af7f-b39da84fa5ce/2c7cbba4a6c0e67f31a1c5f5b4202988

ZSFG AM Report Pearls 10/4/2017: Sarcoidosis

Thank you to our team at ZSFG for presenting the case of a patient with sarcoidosis who presented with a history of falls, weight loss, and shortness of breath that brought up some questions about the basics of sarcoidosis. Check out the post below about some basics on sarcoidosis.

SARCOIDOSIS:
Pathophysiology:
  • Fundamental abnormality is formation and accumulation of granulomas (compact, centrally organized collections of macrophages and epithelioid cells encircled by lymphocytes).
  • About 20-25% of patients will develop pulmonary fibrosis due to matrix metalloproteinases
Clinical Features:
  • Often first seen on CXR for another reason
  • Fatigue, night sweats, and weight loss are common
  • Lofgren’s Syndrome: arthritis, erythema nodosum, bilateral hilar adenopathy
  • 2/3 of patients have remission within a decade after diagnosis with few or no consequences
  • 1/3 of patients have unrelenting disease
Diagnosis:
  • Unless presenting with classic Lofgren’s syndrome, typically need to have a biopsy specimen demonstrating noncaseating epithelioid-cell granulomas in the absence of organisms or particles.
    • Should biopsy from easiest access point (skin, peripheral lymph nodes, lacrima glands)
    • Sometimes, you may still need a bronchoscopy to get lung tissues
  • Need to rule out other infections (i.e. TB, bacterial cultures)
  • There is no value to checking a serum ACE level:
Organ Involvement:
  • Pulmonary: can present with a restrictive spirometry pattern (underlying fibrosis), pulmonary HTN
  • Cutaneous: can be disfiguring can be macules, papules, plaques and erythema nodosum
  • Liver/Spleen: typically clinically silent liver problems, but can include liver failure
  • Neurologic: involved in 25% of patients on autopsy, 10% clinically. MRI with gadolinium is useful for detecting involvement. Complications common to uncommon:
    • Cranial-nerve palsies
    • Headache
    • Ataxia
    • Cognitive dysfunction
    • Weakness
    • Seizures
  • Optho: anterior uveitis most common manifestation
  • Cardiac: Typically cardiomyopathy, can also present with tachy- or brady-arrhythmias. Diagnosis helped with MRI with gad and PET scanning to aid in dx (biopsy is limited b/c of the patchy nature of disease).
  • Renal: Can have hypercaliuria and renal calculi
  • Bone: Bony lesions can be seen throughout the skeleton, often confused
Treatment:
Treatment for Sarcoid

Sources:

  • Iannuzzi MC et al. (2007). Medical progress – Sarcoidosis. NEJM 347:2153-2165.

Evernote:

  • Sarcoidosis: https://www.evernote.com/shard/s509/sh/ff61b59b-6f75-456d-b99d-972fa8a4c790/e83ad7376c5ec6e2f8d33d64c9528ddc

 

ZSFG AM Report Pearls 10/3/2017: Lymphogranuloma Venereum (LVG)

Thank you to Shirin Hemmat and Anne Rohlfing for presenting a really interesting case of lymphogranuloma venereum complicated by rectal abscess.

Lymphogranuloma Venereum (LVG)

Definition:
Genital ulcer disease caused by the L1, L2, and L3 serovars of Chlamydia trachomatis
 
Epidemiology:
Increasingly being reported in men who have sex with men (MSM)
Vast majority of cases are also in MSM who have HIV
Pathophysiology/Clinical Manifestations:
Predominantly disease of lymphatics
Can progress to cause lymphangitis, necrosis and eventually abscess formation
3 Stages of LGV:
  1. Primary Infection: genital ulcer or mucosal inflammatory reaction at site of inoculation. Incubation period 3-12 days.
  2. Secondary Infection: direct extension of the infection to regional lymph nodes. Typically 2-6 weeks after.
    1. Inguinal syndrome – buboe formation and can get “groove sign” which is groove between superficial and deep lymph nodes which are immensely swollen
    2. Anorectal syndrome – inflammatory mass may be present in rectum, can have proctocolitis with rectal discharge, anal pain, constipation, fever, tensemus. Also possible to have hemorrhagic proctocolitis.
  3. Late lymphogranuloma venereum: Fibrosis and strictures in the anogenital tract, can progress to elephantiasis, anal fistula, infertility
Diagnosis:
LGV Dx
Treatment:
  • Doxycycline 100mg BID x21 days
  • Alternatives: Erythromycin 400mg QID x21 days, Azithromycin 1gm orally weekly x3 weeks
  • Also consider co-treatment with Ceftriaxone 250mg IM X1
  • You should also discuss treating sexual partners and consider treating symptomatic and asymptomatic partners
 

Sources:

 

Evernote:

Lymphogranuloma venereum: https://www.evernote.com/shard/s509/sh/a4f8985e-f9ff-46ec-9366-bcb2d838a584/0991bbdd56d80a72bf9a565d524b9407

 

ZSFG AM Report Pearls 9/25/2017: Syncope & Pulmonary Embolism and Post-Obstructive Pneumonia

 

Thank you to Jocelyn Ko for presenting an interesting case of a patient with multiple falls/syncope who was found to have a collapsed right middle lobe secondary to an obstructing mass in her bronchus. In our discussion we talked about recent studies finding pulmonary emboli in people presenting with syncope as well as postobstructive pneumonia. More details below, and thank you to Aartik Sarma, our pulm/crit care fellow for providing some great references.

 

Syncope and Pulmonary Embolism:

In a study of 560 patients in Italy admitted for a first episode of syncope in Italy, PE was ruled out by Wells score +/- D-Dimer in 330 (58.9%) of patients.

Of the remaining 230 patients,

Pulmonary Embolism was identified in 92 (42.2%)

-For those with an alternative reason for syncope, 12.7% had a PE

-For those without an alternative reason for syncope, 25.4% had a PE

Discussion: It remains unclear to what degree these pulmonary emboli contributed to the patient’s syncope, but this paper is one that is raising the discussion around the role of PE in syncope.

 

Mechanism of Syncope in PE:

-In massive PE, obstruction of blood flow in pulmonary artery resulting in reduced cardiac output

-Smaller PEs result in vagally mediated bradyarrhytmias (2/2 activation of pulmonary or ventricular stretch receptors)

 

Postobstructive Pneumonia:

In a single site study in Houston of 259 patients hospitalized with community-acquired pneumonia, researchers attempted to differentiate the clinical syndrome of post-obstructive community acquired pneumonia from bacterial community acquired pneumonia.

 

Those with post-obstructive community acquired pneumonia were significantly different in following ways:

  • -Have longer duration of symptoms (mean 14 days vs. 5 days, p=0.001)
  • -Have >5% weight loss (67.9% vs. 32.7%, p=0.003)
  • -Less likely to have sputum production (54.3% vs. 80.0%, p=0.009)
  • -Have hemoptysis (16.7% vs. 1.7%, p=0.029)
  • -Less likely to have fever (33.3% vs. 56.7%, p=0.037)
  • -Higher systolic blood pressure (130 vs. 117, p=0.016)
  • -Less likely to have WBC count >12K (33.3% vs 63.3%. p=0.007)
  • -Have higher platelet counts (323k vs 236k, p=0.022)
  • -Lower procalcitonin level (0.17 vs. 0.99, p-0.038)
  • -Have a cavity on radiology (16.7 vs 0.0, p=0.006)
  • -Less likely to have defervescence by 5 days of antibiotics (60% vs 94%, p=0.036)

 

Discussion: The authors argue that their results suggest that for many people with a post-obstructive do not have a clinical or lab evidence of a traditional bacterial infection. The authors note that it is very difficult to make this distinction upfront at the time of admission, but they suggest considering limiting antibiotic use, specifically they comment: “Our experience has been that when patients fail to respond to a first course of antibiotics, physicians repeat sputum cultures, which now are contaminated with newly acquired gram-negative colonizing organisms, and then give additional antibiotics to “cover” these newly recognized bacteria. The results of our study strongly oppose this kind of medical management. If a patient fails to defervesce with a first course of antibiotics, full attention should be focused on treating the obstructing lesion.”

 

Sources:

  • Prandoni P et al. (2016). Prevalence of pulmonary embolism among patients hospitalized for syncope. NEJM 375:1524-31.
  • Simpson RJ et al (1983). Vagal syncope during recurrent pulmonary embolism. JAMA 249(3):390-3.
  • Abers MS et al. (2016). Postobstructive pneumonia: An underdescribed syndrome. Clinical infectious diseases 62(8):957-961.

 

Evernote:

  • Syncope and PE: https://www.evernote.com/shard/s509/sh/a34c0b24-73c1-4f4b-9b11-f1016b4aab7e/61c3d3ef7263fb47dcd6ead014c7b7e7
  • Postobstructive Pneumonia: https://www.evernote.com/shard/s509/sh/de040661-f36d-42cf-9d68-cb02be115072/636ff8615e0a75bff308f50c42d3dee5

 

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

 

ZSFG AM Report Pearls 9/12/2017: Elevate CSF Protein and Parkinsonism-Hyperpyrexia Syndrome

Thank you to Mike Incze for presenting a SUPER interesting case of a patient with a history of Parkinson’s Disease who presented with fever, ridigity, tremor. CSF showed an elevated protein. In looking into this presentation, I learned about a clinical entity called Parkinsonism-Hyperpyrexia Syndrome (aka Akinetic Crisis). See below for more details

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CSF Fluid Analysis:

Diagnosis
Cells/mcL
Glucose
Protein
Opening Pressure
Normal
0-5, lymphocytes
45-85
15-45
70-180 mmH2O
Purulent meningitis (bacterial) community-acquired
200-200k, PMNs
Low (<45)
High (>50)
Markedly elevated
 Granulomatous meningitis (mycobacterial, fungal)
100-1000, mostly lymphocytes
Low (<45)
High (>50)
Moderately elevated
Spirochetal meningitis
100-1000, mostly lymphocytes
Normal
Moderately high (<50)
Normal to slightly elevated
Aseptic meningitis, viral or meningoencephalitis
25-2000, mostly lymphocytes
Normal or low
High (>50)
Slightly elevated
Neighborhood reaction – infection near CNS that spills cells, protein into CNS
Variably increased
Normal
Normal or high
Variable
Isolated Elevated Protein in CSF Fluid:
  • Immunoglobulins typically excluded by blood-brain barrier
  • Can occur either if disruption of blood-brain barrier or intrathecal production of IgG (multiple sclerosis)
    • Infections (Lyme disease)
    • Lymphoproliferative disease
    • Multiple sclerosis
    • Autoimmune diseases
    • Brain tumors
    • Neurosyphilis
    • TB meningitis
    • Subarachnoid hemorrhage
    • Leptomeningial disease

Parkinsonism-Hyperpyrexia Syndrome:
Case reports exist for patients who develop a clinical entity similar in nature to neuroleptic malignant syndrome (NMS) in the context of sudden withdrawal of medications or dose reductions of levodopa or dopamine agonists OR administration of typical and some atypical neuroleptics.
 
Pathophysiology (Similar to NMS):
-Blockage of dopamine receptors (or acute withdrawal of dopamine agonists) is the primary driver and effects correlate to different locations of dopamine receptors
  • Hypothalamus = Hyperthermia
  • Nigrostriatal pathways = Rigidity and Tremor
-Alternative hypothesis, rigidity and muscle damage effects the peripheral muscle system due to direct changes on the muscle mitochondrial function.
Clinical Presentation of Akinetic Crisis:
  • Altered mental status
  • Total Akinesia with dysphagia
  • Hyperthermia
  • Dysautonomia
  • Elevation of muscle enzymes
Management:
-Replace the anti-Parkinson medications at the dose that was used prior to the onset of symptoms
-Note: You can give meds orally via NG tube OR IV, there are also transdermal, IV and infusion agents
-Recommended to admit to the ICU for monitoring especially if significant hyperthermia and rigidity
-If not getting better after giving anti-Parkinson meds, consider dantrolene, bromocriptine, and/or amantadine (although there is not an evidence basis for these medications!)
Sources:
  • Onorfj M et al. (2009). Emergencies in parkinsonism: akinetic crisis, life-threatening dyskinesias and polyneuropathy during L-Dopa gel treatment. Parkinsonism and Related Disorders. 15S3: S233-S236
  • Thomas A et al. (2003). Acute akinesia or akinetic crisis in Parksinson’s Disease. Neurol Sci. 24:219-220.

Evernote:

  • CSF Fluid Analysis: https://www.evernote.com/shard/s509/sh/30cbf910-2a2e-4581-8a31-a23343e6fdf5/db7a8e1506919c51a0e35f517f0d9eb2
  • Parkinson’s Disease Overview: https://www.evernote.com/shard/s509/sh/a417cadc-e2df-480c-a4ca-aabfff701d6e/28fe44a36757ab53454d58a8656d3340
  • Parkinsonism-Hyperpyrexia Syndrome: https://www.evernote.com/shard/s509/sh/6e482206-fa77-4597-8d5a-0fcf43efb64c/b9f7eda61ac857337f3e6aae73d5e7bc