Category Archives: General Internal Medicine

ZSFG ID Report Pearls: Epididymitis, GU TB, and Crypto meningitis in HIV-neg

We’ve had really exciting cases at ID report this month! Will highlight a few points about Cryptococcal meningitis in non-HIV patients and the infamous entity of epididymitis, with which our story begins…

Acute epididymitis:

Hx: <6 wks of (unilateral) pain, swelling, and inflammation of the epididymis (most patients won’t say that their epididymis hurts, but scrotal/testicular pain may be mentioned).

  • Occasionally involving the testis (epididymo-orchitis, like in 12% of patients w/ Behcets dz) or accompanied by urethritis which is usually asymptomatic

Frequent offenders:

  • Among sexually active men aged <35 years, C. trachomatis or N. gonorrhoeae.
  • If pt is insertive partner in anal sex, consider sexually transmitted enteric organisms (e.g., Escherichia coli and Pseudomonas spp.)
  • If >35 years of age, don’t forget CT/GC though bacteriuria is usually 2/2 obstructive urinary disease, urinary tract instrumentation or surgery, systemic disease, and immunosuppression.

Ddx: R/o STI, torsion, abscess, hydrocele, hernia, testicular cancer, drug reaction (AMIODARONE-induced epididymitis, self-limited situation w/ onset 4-71 months after introduction of amio, whoknew?!)



  • Suspect epididymitis by physical exam, tenderness around posterior testicle/epididymis
  • Diagnostics:
    • Use (urine) NAATs for the detection of N. gonorrhoeae and C. trachomatis
    • Gram stain & culture of urethral secretions
      • ≥5 WBC/oil immersion field is highly sensitive & specific urethritis; can see intracellular Gram-negative diplococci on Gram stain to dx gonococcal infxn


    • Positive leukocyte esterase test on first-void urine or urine w/ ≥10 WBC/hpf
    • Other STI’s: RPR, HIV
    • Sono—do this to r/o torsion as the ultrasound findings in epididymitis are of minimal utility in dx/tx and include epididymal hyperemia and swelling

Tx: CTX 250mg IM x1 + Doxy 100mg BID x10d OR if considering enteric organisms, Levofloxacin 500mg daily x10d.

  • For sexual partners: refer all sexual partners (within 60d prior to sx onset) for eval and tx; avoid sex until pt and all sexual partners have completed tx
  • Adjunct therapy:
    • Bed rest, ice, scrotal elevation (scrotal sling, perhaps)
    • Re-examine in 72hr to reassess dx and abx selection. FAILURE TO IMPROVE WARRANTS RE-EVAL OF DX/TX
    • If swelling and pain persists (like in the patient presented this morning), do a comprehensive eval for tumor, abscess, TB**, infarction, fungal infxn


Chronic epididymitis:

Dx by hx: ≥6 wks of discomfort and/or pain in the scrotum, testicle, or epididymis. The CDC recommends we divide this entity into inflammatory chronic epididymitis, obstructive chronic epididymitis, and chronic epididymalgia, but let’s not get crazy.

Frequent offenders:

  • Consider entities w/ granulomatous reaction, specifically Mycobacterium tuberculosis (TB) is the most common granulomatous disease affecting the epididymis

The case today ended up being GU TB, which brings up that in culture negative recurrent epididymitis (or really culture-negative anything), consider TB!

  • Up to 25% of patients w/ TB epididymitis have bilateral disease
  • Ultrasound shows enlarged hyperemic epididymis with multiple cysts and calcifications
  • Consider **Tuberculous epididymitis in pt’s w/ exposure to (this pt lived in India for 30yrs, left 5yrs ago) or h/o TB infxn or in pt’s who worsen clinically despite approp abx


At a separate, equally exciting ID report, we discussed the (Short) Ddx for high protein level in CSF:
-Epidural abscess
We also spent some time discussing Cryptococcal Meningitis in non-HIV patients:

-The patient presented had a negative serum CrAg, though a positive CSF CrAg. This is a rare, but observed entity…

-There is a group of patients who are non-HIV, non-transplant who get cryptococcal infections. Usually, they are more likely to get pulmonary crypto as the sole manifestation, though meningoencephalitis is also common. A few diagnostic pearls in this scenario:

  • Serum CrAg titers in immunocompromised hosts tend to be higher than titers in immunocompetent patients
  • Immunocompetent patients have higher mean CSF leukocyte counts, higher CSF protein, and lower CSF glucose
  • Immunocompetent patients are less likely to be India ink-positive
  • Higher 90-day and 1-year mortality for immunocompromised patients
  • CrAg test characteristics are pretty great (see table below) in HIV-patients, and there’ve been recent studies suggesting the sensitivity of the lateral flow assay (LFA) is just as good in non-HIV patients (PMCID: PMC4733170)


The false negative serum CrAg pearls below come from our 2003 UCSF Chief foremothers and forefathers!

*Causes of a false negative serum cryptococcal antigen test*: tests for antigen against crypto surface polysaccharide

  • The serum CrAg is often negative in non-HIV patients
  • Low titers of cryptococcus
  • Early infection
  • Presence of immune complexes
  • Poorly encapsulated strains with low production of polysaccharide
  • Prozone phenomenon of high titers




Sadek I, Biron P, Kus T: Amiodarone-induced epididymitis: report of a new case and literature review of 12 cases. Can J Cardiol 9:833, 1993 [PMID:8281484]
Pappas PG. Cryptococcal Infections in Non-Hiv-Infected Patients. Transactions of the American Clinical and Climatological Association. 2013;124:61-79.
Jitmuang A, Panackal AA, Williamson PR, Bennett JE, Dekker JP, Zelazny AM. Performance of the Cryptococcal Antigen Lateral Flow Assay in Non-HIV-Related Cryptococcosis. Diekema DJ, ed. Journal of Clinical Microbiology. 2016;54(2):460-463. doi:10.1128/JCM.02223-15.

ZSFG Pearls: The Five E’s of Ultrasound and a touch of VT

In ZSFG intern report yesterday, there was a riveting discussion about a patient with extensive coronary history who presented with syncope and developed a mysterious and unstable tachyarrhythmia, ultimately diagnosed as (surprise!) VT.

First, we reviewed how bedside ultrasound can help us and what we can learn with it. From emergency medicine and point-of-care ultrasound literature, here are the…

Five E’s of Ultrasound:

Effusion: assess for a pericardial effusion         
Ejection: qualitative LVEF review
Equality: specifically ventricular equality, referring to the relative size of the RV to the LV Exit: from the heart or assessing the aortic root for aneurysm/dissection
Entrance: to the heart aka the IVC review with respiratory variation

In practice, the effusion and entrance assessment tend to be used the most (…and most reliably). More information on these E’s can be found through this extensive review from the Journal of the Society for Academic Emergency Medicine:

If, after this teaser, you are yearning for more training in ultrasound, ask your friendly critical care residents/fellows/attendings to go through how they use that Sonosite, ask Nima your burning questions during the June simulation intern half day, and sign up for ultrasound elective available on block months 2nd/3rd year for extra formal teaching!


Now, on to Ventricular Tachycardia…

Nora Goldbadger pearl: The patient in report had a somewhat irregular appearing rhythm on EKG. It was ultimately thought to be, and responded to treatment for, VT. When we asked Nora Goldschlager how this irregular character was possible, she said “I’m not making this up…but there are exit blocks that can cause up to 40ms of delay.” This apparently adds an illusion of irregularity to the VT rhythm strip. BOOM.
Also, if you didn’t click the Goldbadger above, will just leave this here for your viewing pleasure:

To diagnose VT, we like to use the ole Brugada criteria below. Generally, If any of the criteria is satisfied, VT is the Dx. If none are fulfilled, an SVT is the Dx (AVRT in WPW is an exception).


Here is a more attractive Ventricular Tachycardia stepwise approach. This comes to us from Lekshmi, former Moffitt chief, now pulm fellow.

  1. Stable or unstable? If unstable (hypotension, chest pain, or altered mental status), proceed with ACLS and assume it’s VT!
    1. In general, if patient is unstable, assume it’s VT, and if patient is stable, you have more time to figure it out & is more likely to be SVT BUT you can be fooled with slow VT!
  2. Any risk factors for VT? (e.g. Prior MI, prior cardiac surgery, known scars)? If so, assume it’s VT!
  3. Do they have a prior EKG with an old LBBB or old RBBB? If the patient is stable AND has an old bundle branch block, more likely to be SVT with aberrancy
  4. Check for capture or fusion beats: If these are present, it’s VT. these beats have the highest positive predictive value for VT.
  5. Check for A-V dissociation: A-V dissociation is not required for VT, but is strongly suggestive
  6. Check for concordance: Look for concordant morphology in leads V1-V6 (i.e. all negative or all positive)
  7. R wave in aVR present aka “Up in aVR”? This is the Vereckei criteria which is a quick tip for seeing if VT as well!

If you’ve made it this far, patient is stable, and still not sure, now you can bust out Brugada criteria (see above)!

Lastly, want to know how to localize that VT focus. Kevin Duan, also a former Moffitt chief, dropped some knowledge on this before:

Localizing VT focus: some rules of thumb

  • Look at Lead I: if negative in lead I, the VT focus is coming from the lateral wall
  • Look at inferior leads: if negative, the VT focus is coming from the inferior wall
  • Look at aVR: if positive (NW axis), the VT focus is coming from the ventricles and heading towards the base (R shoulder)
  • Look at bundle branch pattern: if LBBB, then VT focus is in the RV; if RBBB, then VT focus in the LV
  • Look at V5,V6: if negative, the VT focus is coming from the apex


Previous Blog posts:
Hall et al. The “5Es” of Emergency Physician–performed Focused Cardiac Ultrasound: A Protocol for Rapid Identification of Effusion, Ejection, Equality, Exit, and Entrance. Journal of the Society of Academic Em Med. 2015: 22(5), 1553-2712.



Livedo reticularis and livedo racemosa

We’ve had a purple, net-like week here at ZSFG. At both M&M and intern report we talked about livedo rashes. After both conferences, I was still confused. So I looked it up in a dermatology textbook. Here’s what I learned.
Top pearls
  • Livedo reticularis can be primary and benign or secondary and very bad
  • Livedo racemosa is morphologically different and always bad
  • There’s a lot of conflicting information out there about the distinction between these two conditions!
Pathophysiology of livedo rashes
  • both racemosa and reticularis arise from deoxygenation or dilation of the venous plexus in the skin
  • veno-dilation can be benign (due to cold, called cutis marmorata) or from one of the following pathologic processes
    • small vessel sludging/clotting (due to coagulopathy)
    • vasospasm
    • vasculopathy
Livedo reticularis
  • the rash of classic Livedo reticularis  is “fishnet-like, red or purple mottling [that] surrounds a pallorous conical core.” The rings are closed/complete circles and relatively symmetric
  • Here’s a good picture from the mayo clinic. The circles can definitely bigger/more netlike.
Livedo racemosa
The rash of livedo racemosa is the same color, but tends to be more broken and asymmetric. It partially goes away with warming, but not completely.
Screen Shot 2017-02-17 at 10.59.24 AM.png
  • Livedo reticularis can be primary or secondary. 
    • primary is caused by cold or is idiopathic and requires no special management other than cold avoidance.
  • Livedo Racemosa is always secondary and bad.
    • Always, always test patients with racemosa for APLS.
  • The DDX for secondary reticularis and racemes is super broad, and can be categorized using the clotting, vasospasm, vasculopathy framework above. See a full differential below.
Let me know if you have a different framework for thinking about these! Every paper had a different definition and very strong opinions =)
Chadachan V, Dean SM, Eberhardt RT. Chapter 173. Cutaneous Changes in Peripheral Arterial Vascular Disease. In: Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ, Wolff K. eds. Fitzpatrick’s Dermatology in General Medicine, 8e New York, NY: McGraw-Hill; 2012. Accessed February 17, 2017.
Gunderson CG, Federman DG. Web of confusion Am J Med. 2011 Jun;124(6):501-4. (this is where the table comes from)

SFGH 5.31 pearls: metabolic alkalosis

  • Major causes metabolic alkalosis – Vomiting/NG suction, loop and thiazide diuretics, laxative abuse, mineralocorticoid excess, milk-alkali syndrome.
  • For those with profound alkalosis with hypovolemia, avoid resuscitation with plasmalyte, as it contains bicarb. Better to replete with NS w/K or just NS and replete K separately
  • Profound alkalemia also can cause a left shift of the oxygen dissociation curve, leading to impaired peripheral oxygen unloading and lactate elevation à give supplemental oxygen!
  • An elevated serum pH requires both an initial insult, (usually loss of hydrogen ions in the urine or GI tract) and a maintenance phase that prevents normalization of the pH. The maintenance phase causes include: volume contraction, renal impairment, decreased effective blood volume (CHF, cirrhosis) or a combination of these factors.
  • Remember that alkalemia drives phosphorus and potassium into cells, so labs will often show profound hypoK and hypo phos, but these numbers do not reflect total body stores
  • The lytes abnormalities associated with alkalemia can lead to muscle weakness, decreased cardiac contractility and increased risk for arrhythmia and should be corrected as soon as possible, keeping in mind that their extra-cellular levels will change as your correct the pH
  • Betahydroxy butyrate can be elevated in any ketotic state, not just DKA
  • Severe alkalemia can also cause seizure, agitation/disorientation, and coma due to decreased cerebral blood flow
  • Fun fact – the combination of 3 concomitant acid-base disorders is known as “the triple ripple”!

Moffitt Report Pearls 5/16: Anti-cholinergic poisoning

Take-home from the case: make sure to ask about meds/herbals and ask your toxicologists for help!! This was the clincher in this case and avoided a lot of expensive testing!

Treatment of anti-cholinergic toxicity (handy overview table from UpToDate)

  • Decontamination: if an ingestion, consider charcoal if mental status in tact (otherwise avoid it due to aspiration risk)
  • Initial stabilization:
    1. If prolonged QRS or arrhythmia, use sodium bicarb
    2. If agitated or seizures, treat with benzos
    3. Try to cool patient’s if hyperthermic
  • Antidote
    1. Supportive care often enough
    2. If needs antidote (peripheral and CNS toxicity), treat with physostigmine. Physostigmine is a cholinesterase inhibitor so increases Ach concentrations
      1. Tertiary amine so can cross the BBB
      2. Be careful! Make sure to be prepared for cholinergic side effects when giving the antidote, so have the patient on tele and get atropine/pads at the bedside
  • Do this in consultation with a toxicologist


Anti-cholinergic side effects

  • Mad as a hatter (delirium and hallucinations)
  • Red as a beet (cutaneous vasodilation to compensate for loss of sweat production)
  • Blind as a bat (mydriasis and inability to accommodate so have blurry vision)
  • Dry as a bone (anhidrosis)
  • Hot as a hare (anhidrotic hyperthermia – can’t sweat and can get hyperthermic)
  • Full as a flask (urinary retention) – had not heard this one before


Check out this non-medical blog post about Datura Inoxia:

5.11.16 – VA Ambulatory Report Pearls – First time seizures: diagnosis/workup/management

First Time Seizures in Young Adults

Epidemiology: Many first seizures are unrecognized. The incidence of single seizures and recurrent epileptic seizures is estimated as 5-10% and the prevalence of epilepsy is 0.5-1% of the population. Epileptic seizures are responsible for 1% of hospital admissions and 3% of ED visits.

Recurrence and who may receive treatment after a first-time seizure:

  • Low risk patients with first seizures that have no neurological deficits, normal MRI, and EEG have a 35% risk of recurrence at five years. They are not usually offered treatment.
  • High risk patients with first seizures that have neurological deficits, MRI abnormalities, and/or EEG abnormalities have a 70% risk of recurrence at five years. They are typically offered treatment.

Per our neurology colleagues, the most common causes of a first time seizure in young adults are the following:

  • Idiopathic (can account for up to 50% of cases)
  • H/o trauma
    • Head injury accounts for a relatively small proportion of first time seizures. The risk to an individual who suffers head trauma can vary widely from minimal risk in people with a concussive head injury in which LOC or amnesia is < 30 minutes to a 12-fold increased risk over 10 years in people who suffer trauma-induced amnesia > 30 minutes, had a subdural hematoma at time of initial trauma, o a brain contusion.
  • H/o encephalitis
  • Viral encephalitis
  • Neurodevelopmental lesions* (e.g., cortical dysplasia in which there is a disruption in the proliferation of neuroblasts or abnormal migration of neurons to the developing cortex)
  • Genetic epilepsy syndromes*

The * indicates diagnoses that are less common after the age of 20 years old.

Attached: A nice review article in BMJ from 2014 on first time seizures in adults from the epidemiology –> differential –> workup and management.

VA Report Pearls: Microcytic Anemia!

Pearl 1: A good way to think (and teach) about microcytic anemia is to consider the ways in which microcytosis occurs. RBCs become microcytic due to a lack of hemoglobin, which can result from:

  • Lack of iron (iron deficiency, anemia of chronic inflammation)
  • Defects in heme synthesis (sideroblastic anemias)
  • Defects in the production of hemoglobin protein (thalassemias and hemoglobinopathies)

Pearl 2: Remember that in thalassemia (unlike iron deficiency and anemia of chronic inflammation), the RBC count may be normal or elevated, since the bone marrow is making large numbers of small cells. 

See the attached review article from the NEJM for more on microcytic anemia!

Microcytic Anemia_NEJM

Evernote Link