All posts by cssoran

VA Ambulatory Report 4.4.18 – New Atrial flutter

Thanks Anne for presenting your patient from clinic last week.  The patient is a 60 yo F with a pmhx of HTN and DCIS who presented to clinic with dyspnea on exertion found to have atrial flutter with rates in the 130-150s.

Sam Brondfield joined us and dropped some knowledge bombs about DOACs

DOAC MOA Reversal agent? Things to consider
Dabigitran Thrombin inhibitor idraucizumab -Common SE: dyspepsia
Rivaroxaban Xa inhibitor -Once daily dosing
-Least amount of data in elderly patients
Apixaban Xa inhibitor -Lowest bleeding risk
-Least dependent on creatinine clearance, safest in renal disease
Other considerations: insurance coverage, drug interactions


How is Aflutter different from Afib?

  • Background
    • Afib – associated with some underlying heart disease causing large atrium, increased atrial pressures or inflammation
    • Typical Aflutter – reentrant circuit involves the cavo-tricuspid isthmus
      • sawtooth negative flutter waves in the leads II, III, and aVF
    • Atypical flutter – not involving the cavo-triscupid isthmus
  • Work-up of new onset of atrial flutter is the same as afib
    • Any disorder that causes Afib can also cause Aflutter
      • Also commonly occurs after treating Afib with an antiarrythmic or ablation
      • It is an uncommon complication of acute MI in the absence of other symptoms
    • Assess for hyperthyroidism, heart failure, pulmonary disease
    • Tests to order
      • Echo: Looking at size of artia and ventricles, ventricular function, and valves and TEE if plan for cardioversion without optimal anticoagulation
  •  Management
    • Rate Control: Same general approach as Afib, but harder to achieve
      • Use non-dihydropyridine CCB or BB
      • Consider dig or amio if decompensated HF
    • Rhythm control
      • Cardioversion should be urgently in patients with rates >150 or in those who have hemodynamic compromise or who have WPW
      • Ablation is the treatment of choice given the high rate of recurrence of aflutter and the high success rate of the procedure
    • Stroke prevention
      • Limited data to suggest the optimal approach to anticoagulation in atrial flutter given rarity of persistent A flutter and the frequency of co-existence with Afib
      • Thromboembolic risk may be lower than in Afib, but most recommend approaching anticoagulation the same as they would in a patient with Afib as these patients may also be having episodes of Afib

Ambulatory Report 3.20.18 – EBV and Elk

Thanks Dan for presenting your patient a young male with 1 month of fever and cough after hunting deer in New Mexico ultimately diagnosed with EBV.

Jin reminded of us one way to approach a problem is to use a Venn Diagram of symptoms, in this case cough and fever, to help us focus our differential on the diagnoses that fall in the overlap region.  Check out a recent Clinical Reasoning publication (with Goop as senior author!)  describing a slightly different way of using venn diagrams called the Pivot and Cluster.  This approach focuses on a common diagnosis as the pivot around which you can group a cluster of alternative diagnoses.

EBV Serologies

  • Presentation
    • Typical presentation of infectious mononucleosis: fever, pharyngitis, adenopathy, fatigue, and atypical lymphocytosis
      • Typically cervical posterior chain lymphadenopathy, the the lymphadenopathy can be more generalized as well
    • Variants
      • Mild disease: mild pharyngitis or tonsilitis
      • “Typhoidal form” fever and lymphadenopathy without the pharyngitis
      • Very young or very old often present less typically
  • EBV diagnostic tests
    • Monospot – rapid heterophile antibody test
      • If patient has consistent symptoms and positive monospot, there is no need for further testing.
      • However the sensitivity is ~85% and therefore there is the possibility of false negative.
    • EBV-specific antibodies
      • IgM Viral Capsid Antibody is present at the time of infection remains positive for ~ 3 months
        • Other herpesviruses (eg, CMV) can induce IgM antibodies to cell lines that express EBV antigens
      • IgG Viral Capsid Antibody becomes positive at the time of infection whereas IgG nuclear antigen takes 6-12 weeks to be present


Elk Exposure

  • We started to think about how exposure to elk could contribute to the patient’s presentation.  Here are three infectious disease agents to know about when it come to elk
    • Brucella – can be contacted when butchering infected game animals including elk or from handling raw meat or eating undercooked meat from infected animals.
    • Echinococcus granulosus (Tapeworm) – primary infection often asymptomatic and then clinical manifestations depend on involved organ, most often affects lung or liver.  Primarily seen outside the US (Middle East, sub-saharan Africa, South America, China) but local transmission has been documented in part of the United States including the SW US.
    • Chronic Wasting Disease – bovine spongiform encephalopathy prion disease that has an increased incidence in the western united states elk population. The CDC states there is NO evidence it can be passed to humans

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VA Ambulatory Report 3.14.18 – The other FUO: Fistula of unknown origin

Okay, fistula of unknown origin is not a real phrase, but today’s case brought up a good discussion about fistulas. Bennett and Huat presented a case of a 50 yo male with air bubbles in his urine found to have a colovesicular fistula possibly due to diverticulitis.

Colovesicular fistula pearls

  • Most common presentation: pneumaturia or fecaluria.  Less common presentations: UTIs, urinary frequency, hematuria.
    • Pneumaturia is a rare manifestation of a UTI and should strongly raise your suspicion for a colovesicular fistula
  • Despite what we may expect, studies have shown urine culture more often grows one species (40-70% of cultures) instead of mixed flora.
  • Thanks Daniel for reminding us the benefit of oral contrast – Abdominal CT with oral or rectal contrast is the test of choice.  IV contrast is excreted renally and can cloud the picture.
  • Next step is identifying the cause of the fistula.  If no cause is identified on abdominal CT, next step is colonoscopy and/or cystoscopy to assess for malignancy given this will change your management.
  • Causes of bowel-vesicular fistulas
    • Diverticular disease: most common cause
    • Post-op
    • Spontaneous
    • IBD
    • Malignancy: Colon, bladder, cervix, prostate
    • Radiation
    • Other
  • Key Management Principles of Colovesicular Fistulas
    • Treat infection if present, but do not need suppressive antibiotics
    • Definitive treatment of fistula with surgery in majority of cases
      • If the cause is non-malignant, minimally symptomatic patient, and considered high surgical risk you can opt for watchful waiting

Check out this American Journal of Surgery article on Colovesicular fistulas.


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SFPC Ambulatory Report 3.8.18 – Buboes!

Thanks Soraya for presenting the case of a young male with HIV intermittently on ARVs with a painful groin mass likely a bubo due to LGV.

The following pearls are thanks to Soraya!

Differential for a bubo:
  • syphilis – painless ulcer, followed by LAN (usually b/l)
  • gonorrhea (proctitis)
  • HSV – painful vesicles, LAN (usually b/l)
  • chancroid – painful vesicles that become pustular and exudative  (tx: azithro 1g x1 or CTX 250 IM x1)
  • granuloma inguinale/donovanosis (Klebs granulomatosis) – painless, ulccerative lesions (friable, bleed); tx doxy x3 weeks (or azithro q week x3
  • cat scratch disease (bartonella henselae) – self limited LAN in kids x2-8 weeks; can tx azithromycin immunocompromised host or mod sxs
  • Tularemia – 1200 cases between 2000 and 2010, think ticks, outdoor activity, or with dead animals or skin, summer time, missouri/arkan/oklah. highly infectious (warn lab). tx streptomycin
  • bubonic plaque (y pestis) – fleas, few cases in US but reported. Southwest US. Tx doxy, FQ.
  • lymphoma
  • incarcerated inguinal hernia
  • TB or MAC
  • amebiasis (e. histolytica) – should see signs of invasive coliits wtih diarrhea, dysentery, heme-pos stools
Starts as ulceration (PAINLESS, usually not noticed) –> 2-6 weeks later you get regional tissue invasion & constitutional sxs. will penile, urethral, or vulvar inoculation –> inguinal LAN, whereas w/rectal disease, you get back pain or rectal pain from retroperitoneal LAN.  If you don’t treat the LGV, you get scarring and obstruction of lymphatics, which can cause regional lymphedema and genital elephantiasis (rectal diseaes –> strictures, anal fistulas).
Chlamydia and LGV (tips from Mark Jacobson): 
1.      All patients with clinical proctitis (e.g. tenesmus, rectal discharge) should have a standard rectal swab submitted for chlamydia nucleic acid testing (click on Chlamydial rectal TMA [PHL] when browsing in the Treatment/Labs section of eCW), AND a separate rectal swab in viral transport media (same tube and swab you use to submit a swab for herpes simplex) for LGV. For the latter, click on Chlamydial TMA Other (PHL) when browsing in the Treatment/Labs section of eCW and complete the PHL lab requisition attached to this memo with patient, clinician, and insurance info required, print, and give to our lab.
2.      LGV testing should only be ordered on a rectal swab obtained from a patient with clinical proctitis.  The LGV assay is not validated for other specimens, and asymptomatic LGV infection is not a clinically significant entity.
3.      Patients who have a positive rectal Chlamydia result can be treated with single dose azithromycin IF they have no symptoms or signs of proctitis.
4.      Patients who have a positive rectal Chlamydia result and signs or symptoms of proctititis should receive a one to three week course of doxycycline 100 mg bid, depending on the severity of symptoms.
5.      Patients have a positive rectal Chlamydia result, signs or symptoms of proctititis, and a positive LGV test result should receive a full three week course of doxycycline 100 mg bid.
6.      Note that the LGV assay will not be done if the simultaneously submitted standard rectal chlamydia assay result is negative.
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VA Ambulatory Report 3.7.18 – TB in clinic

Thanks Chris for presenting your patient who is an elderly man with a history of CAD and HTN who presented to clinic with history of tuberculosis and chest xray findings of apical scaring and pulmonary nodules.  We had a great discussion about the challenge of diagnosing TB and management strategies for active and latent TB in the outpatient setting.

TB Epidemiology

  • In countries with a low incidence of TB such as the US, the most common cause of active TB is reactivation of old disease.
  • In San Francisco the most common risk factor for TB is being foreign born in particular individuals from China, the Philippines, and Vietnam.
    • Check out this SFDPH Disease Control and Prevention Report for more epidemiology of TB in San Francisco.

Diagnosing TB 

  • Tuberculin skin testing (TST) vs. Interferon Gamma Release Assay (IGRA)
    • The decision to use TST vs. IGRA is based on patient characteristics, local resources, and cost.
    • The CDC recommends sending IGRA testing over TST in patients you have decided to test due to risk of exposure AND have a history of BCG vaccination or are unlikely to return for ppd read.
    • In other adult patients TST or IGRA are reasonable testing choices, although IGRA is slightly preferred due to better test characteristics (it is more specific)
    • A negative reaction in either test does NOT exclude TB
  • Sputum – AFB smear, culture, and gene expert
    • The policies at our hospitals have been updated and you only need 2 AFB smears and gene experts to decide about airborne isolation discontinuation for inpatients
  • Check out these clinical practice guidelines on the diagnosis of TB.

Management of TB

  • Is this active TB?
    • The diagnosis of active TB is based on symptoms, imaging, sputum AFB smear, culture, and gene expert
    • If a diagnosis of active TB is confirmed, most patients will be treated with directly observed therapy at TB clinicW
  • Which patients with LTBI should be treated?
    • There is a push these days to treat nearly all patients with confirmed LTBI if the patient agrees to be treated
    • There is a strong recommendation to treat patients who are at high risk of reactivation
      • Risk of activation in immunocompetent host is 5-15% over their lifetime
        • ~5% risk within the first 2 years of exposure and ~5% risk over the rest of the lifespan
      • Risk factors for reactivation TB or high incidence of TB: age (young children and elderly), HIV, meds that inhibit cellular immunity (TNF alpha inhibitors, steroids), history of head and neck or hematologic malignancies, organ transplant candidates/recipeints, ESRD, silicosis, low body weight, history of bypass surgery, prisoners, illicit drug use, smokers, homelessness, healthcare workers, foreign born, diabetes, or recent seroconversion.
    • Treatment regimens: Should be based on patient preference, comorbidities, side effects, and drug interactions
      • INH for 6-9 months
      • Rifampin for 3-4 months
      • INH + Rifampin for 3-4 months
      • Rifapentine + INH for 3 months

More TB related resources

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VA Ambulatory Report 2.28.18 – Don’t forget about the EAR! Barotrauma and Syphilis

We had two great mini cases both involving the ear!

Thank you Manoj for presenting your young patient who presented with 2 weeks of ear fullness that started immediately after skydiving and found to have hemotympanum.

Key learning points

  • Remember to ask your veteran patients about their service time and duties.  Vets that were part of airborne or parachute teams may have musculoskeletal problems (spine and heels in particular) from frequent forceful landings
  • Barotrauma
    • Remember the anatomy of the ear: the eustachian tubes allow pressure to differential on each side of the tympanic membrane to requilibrate by yawning, valsalva, or swallowing
    • Barotrauma to the middle ear can result when the pressure between the middle ear and outside of the tympanic membrane cannot equilibrate such as in air travel, scuba diving, or exposure to a blast
    • Extreme pressure differences can result in hemotympanium or ruptured TM
  • If you are worried about a basilar skull fracture, look for the following
    • Battle sign: Retroauricular or mastoid ecchymosis
    • Raccoon eyes: periorbital ecchymosis
    • Cranial Nerve VII paralysis
    • Clear rhinorrhea or otorrhea
    • Hemotympanum
  • In patients with hemotympanium without hearing loss or other concerning findings (vestibular findings, basilar skull fracture, facial weakness) can be observed.  If there is hearing loss or concerning findings, the patient should be evaluated urgently by ENT.
  • Check out this great review article of barotrauma after sky diving and scuba.


Next Santo presented the case of an elderly man who presented to primary care for chronic hearing loss and STI screening in the setting of high risk sexual behavior found to have otosyphilis.

  • We refreshed our memory of Weber and Rhine which are notoriously hard to inteprete!
    • In a patient with unilateral hearing loss, the weber and rhine can help distinguish between sensineural hearing loss (SNHL) and conductive hearing loss (CHL).  Air conduction measures CHL and bone conduction measures SNHL.
    • Weber: Remember this test is comparing both ears ability to hear with bone and air conduction.  Patients report which ear hears the sound louder
      • If there is conductive hearing loss on one side, the patient will only be getting input from bone conduction (without ambient noise) and therefore report a louder sound on the side with conductive loss.  CHL lateralizes to the bad side.
      • If there is SNHL on one side, the patient will not be getting bone input on the bad side and therefore will report that side is quieter.  SNHL lateralizes to the good side.
      • If there is normal hearing or symmetric hearing loss the sound in each ear will be equal
    • Rhine: This is only testing one ear and comparing bone vs. air conduction
      • If there is CHL –> Bone will be louder
      • If there is SNHL –> Air will be louder

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VA Ambulatory Report 2.21.18 – Sarcoid Diagnosis and Hematuria

We had two great case discussions today.

First Jeff presented an image of incidentally discovered pulmonary nodules and hilar lymphadenopathy.  The patient was diagnosed with sarcoid based on these imaging results alone.

Learning points:

  • How to diagnosis sarcoid:
    • If a patient is asymptomatic with characteristic radiographic findings – this is sufficient to make the diagnosis
    • For symptomatic patients, biopsy confirming noncaseating granulomas is required
  • For a new diagnosis of sarcoid monitor for complications and extrapulmonary involvement: EKG, eye symptoms, vitamin d levels, UA
  • In an asymptomatic patient with low grade radiologic changes, the management is observation only


Second, Akshai presented a patient seen in clinic the day prior with gross hematuria.

Learning points:

  • Gross hematuria should strongly increase your suspicion of malignancy. The incidence of malignancy in microscopic hematuria vs. gross hematuria  is ~2% vs. 20%.
  • Smokers are 4-7 times more likely to develop bladder cancer than non-smokers
  • CT Urography is the test of choice to evaluate for malignancy and nephrolithiasis.  CTU provides both functional and anatomic information about the kidney and ureter.  The pre-contrast phase evaluates for nephrolithiasis and hydronephrosis.  The post contrast phase evaluates renal and urothelial malignancies and can assess kidney function in the setting of obstruction.


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