Category Archives: General Internal Medicine

Moffitt Pearls 10.2.17 – Upper GI Bleed

Key Pearls for Upper GI Bleed Evaluation and Management

  • JAMA Rational Clinical Exam series: Does this patient have a severe upper GI bleed? A great resource for evaluation of a patient with suspected upper GI bleed attached below!
  • Bleeding sources proximal to the ligament of Treitz are considered Upper GI bleeds by definition

-> Top 3 causes include peptic ulcer bleed, gastritis and variceal bleed.

  • NG lavage with blood or coffee grounds has a positive LR of 9.6 for UGIB, but sensitivity is only 44%! If it’s there, you’re likely dealing with UGIB, but if it’s not, you still might be!
  • The other features that have solid likelihood ratios for UGIB are melena on exam (LR, 25) and BUN/Cr ratio >30 (LR, 7.5).
  • Blood clots in the stool make UGIB much less likely (LR 0.05).
  • The Blatchford prediction score efficiently identifies patients who do NOT need urgent scope. Score components are HR, BP, hgb, BUN, melena, syncope (as in our patient today), liver disease, and heart failure.
  • Remember: We usually use a transfusion threshold of hgb 7.0, but if someone is unstable and actively bleeding, transfuse regardless of hgb level!



Moffitt Pearls – Rheumatology Report – 8.21.2017 – Evan’s Syndrome and SLE

Thank you to Leah for presenting a very interesting case of a young man with history of lupus c/b APS and DVT presenting with thrombocytopenia+ hemolysis found to have Evan’s Syndrome (ITP + AIHA)!


Key Pearls

  1. Although the term is falling out of favor Evan’s syndrome describes the combo of ITP & AIHA.
  2. For unclear reasons, lupus flares are often accompanied by a dissociation between ESR (high) and CRP (nl or minimal elevation). Other findings of flare (vs. infection) include drop in complement, recued leukocyte count and + RBC casts and/or proteinuria.
  3. Direct oral anticoagulants have not been studied nor are they recommended as anticoagulants in patients with lupus and known DVT. Treat with warfarin or LMWH only!


More on Evan’s Syndrome

  • Combination of Coombs-positive warm AIHA and immune thrombocytopenia (ITP).
  • Antibodies that cause platelet destruction are unique from those that cause AIHA.
  • Differential Diagnosis:
    • Infectious (eg, HCV, HIV)
    • SLE
    • Lymphoproliferative disorders
    • Common Variable immunodeficiency
  • Treatment (similar to ITP, however azathioprine and cyclophosphamide are used)
    • First line therapy: Glucocorticoid @ 1-2 mg/kg +/- IVIG
    • Second line: Azathioprine or rituximab
    • Third line: Splenectomy
    • Under investigation: Eltrombopag –> a TPO receptor agonist stimulating platelet formation

American College of Rheumatology Classification of SLE

[Always verify all prior diagnoses of rheumatological conditions]

  • SLE Criteria > 3 of 11 ( Se & Sp > 95% and all DO NOT have to be at the same time)
    • Cutaneous Manifestations
      • Malar Rash
      • Photosensitivity
      • Discoid Rash
      • Oral ulcer
    • MSK
      • Nonerosive arthritis – oligioarticualr; symmetrical, migratory
    • Cardiopulmonary
      • Serositis – pleuritic or pericarditis
    • Renal
      • Proteinuria or cellular Casts – > 500 mg/dL on UA or 3+ on dip


    • Neurological
      • Seizures OR psychosis


    • Hematological
      • Hemolytic anemia or leukopenia, or lymphopenia or thrombocytopenia
    • Serologies
      • +ANA
      • +anti-dsDNA or antiphopholipid Abs


Review of Hemolytic Anemias based on Smear


Moffitt Pearls 8.15.17 – Anaphylaxis and Drug Reactions

Case Summary:

Thank you to Karen for presenting a mystery case of a young man with hx of asthma, seasonal allergies and eczema p/w perioral edema, itching and profound hypotension concerning for anaphylaxis! We discussed the importance of early therapy for anaphylaxis, drug reaction patterns and the possibility of serum sickness in the setting of Bactrim exposure and the atypical nature of her presentation.


Key Pearls

  1. Anaphylaxis is a Type 1 IgE mediated hypersensitivity reaction that usually occurs within in minutes of an allergen exposure.
    • Volume and IM epinephrine are mainstays of therapy and should NOT be delayed.
  2. Drug reactions are often delayed days to weeks from drug exposure (make sure to review a log) and are mediated by Type IV hypersensitivity.
  3. Angioedema may be manifested by IgE mediated (Type I Hypersensitivity) drug reaction
    • IgE-mediated reactions tend to become more severe & progress toward anaphylaxis (Bactrum as in our case) upon re-exposure to causative agent


Classification of Allergic Reactions

Type Description Mechanism Clinical Features
I Anaphylactic Usually IgE dependent release of vasoactive substances (histamine, prostaglandins and leukotrienes) Anaphylaxis (definition below), Angioedema, urticarial, GI Sx and bronchospasm
II Antibody (AB)-dependent cytotoxicity Antigen/Haptan associated with cell binds AB -> cell/tissue damage Hemolytic anemia, Interstitial nephritis
III Immune Complex Disease Formation of Antigen-Antibody (AB) Complexes Causes damage Serum Sickness
IV Cell-mediated or Delayed Hypersensitivity Antigen sensitizes T cells, then mediates tissue injury Delayed dermatitis or drug reaction

Drug Reaction Patterns Discussed

SJS (< 10 % body surface area)/TEN (>30% body surface area)

  • Mucosal involvement required, occurs usually within 8 weeks of drug exposure


  • Systemic involvement (fever, adenopathy elevated LFTs) driven by eosinophilia; Reaction begins 2-6 weeks after exposure to offending drug


  • Reaction often occurs 48-72 hours after drug exposure

Fixed Drug Eruption

  • Usually without mucosal involvement, occurs anytime – days to weeks after drug exposure


  • >90% of body surface area involved; ddx wide and includes drugs ~ 20% cases and malignancy (Cutaneous T-cell lymphoma)



Moffitt Pearls – 8.11.17 – Saddle Nose Deformity, Upper GI Bleeding &Munchausen Syndrome

Thank you to HH and Neil for both presenting today! HH first presented a mini case of a patient who came in for a gout flare that was found to have a saddle nose deformity.

Neil then presented the interesting case of a young woman with a hx of gastric ulcers presented with epigastric pain and hematemesis who after extensive work-up including CT and EGD was found to have Munchausen syndrome!************************************************************************************

Key Pearls

  1. The differential diagnosis for saddle nose deformity falls into the classic triad of infectious, inflammatory and malignancy per table below.
  2. 80% of upper GU bleeds are due to four causes: peptic ulcer disease (35%), esophagogastric varices (30%), esophagitis (10%) and Mallory-Weiss tears (~5%).
  3. The management strategy for a pt. w/ munchausen syndrome is VERY difficult, but should include a single provider (w/ help from psychiatry) and goal to limit interventions + discuss diagnosis with patient in a supportive manner.


Differential Diagnosis for Saddle Nose Deformities

Infectious Inflammatory Malignancy Other
Syphilis GCA (formerly Wegner’s) NK T-cell Lymphoma Trauma
Leprosy Sarcoidosis Locally invasive tumor (BCC) Cocaine
TB Relapsing polychondritis Lymphomatoid Granulomatosis Surgery
Cutaneous Leishmaniosis      
Septal abscess      

 Differential Diagnosis for Hematemesis AND Fever

  • Mallory-Weiss Tear
  • Peptic ulcer bleeds c/b perforation
  • Hemosuccus pancreaticus (pseudoaneurysm/aneurysm)
  • Upper GI Malignancy – hemobilia, widespread esophageal/gastric malignancy

Munchausen Syndrome or Factitious d/o Imposed on Self

  • Definition: Falsified general medical or psychiatric symptoms
  • Risk Factors: Females, Unmarried, Healthcare professional
  • Diagnostic Criteria (DSM-5):
  1. Falsification of physical or psychological signs or symptoms, or induction of injury or disease, associated with identified deception
  2. The individual presents himself or herself to others as ill, impaired, or injured
  3. The deceptive behavior is evident even in the absence of obvious external rewards
  4. The behavior is not better explained by another mental disorder, such as delusional disorder or another psychotic disorderPrognosis: Very poor even as multiple studies have shown limited benefit even with psychotherapy
  • Management: One provider should oversee pt with help of psychiatry w/ goal to limit interventions. One should be sure to exclude all possible medical conditions and then discuss diagnosis w/ pt in supportive manner


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)