Category Archives: Morning Report

ZSFG Morning Report 11/27/18: Mycobacterium haemophilum

Thanks to Akemi for presenting a fascinating case of a middle-aged man with type 2 diabetes and AIDS presenting with scattered ulcers and an axillary abscess growing Mycobacterium haemophilum presenting with worsening ulcers and pustules several months after restarting antiretrovirals. We discussed nontuberculous mycobacterium in general and their ability to cause skin and soft tissue infections, particularly in the setting of immunocompromise. We also discussed the possibility of paradoxical immune reconstitution syndrome in the setting of antiretroviral resumption.

For more reading, check out this article on M haemophilum dactylitis and tenosynovitis from last year by some of the ID folks here at San Francisco General:


Moffitt GI Report 11/14/18: HSV Hepatitis

Thanks to Megan for presenting an amazing case of a young immunosuppressed woman with UC who presented with fevers and vague complaints, found to have very elevated LFTs and ultimately diagnosed with HSV hepatitis. Kudos to the medicine team for thinking about this early and treating her empirically. Thanks to Dr. Ostroff for many of the pearls.

TLC (Tim and Laura, your Chiefs)

Top Pearls:

  • In UC and Crohn’s disease, begin screening colonoscopy’s eight years after disease or symptom onset. Repeat every 1-3 years.
    • Lifetime risk of colon cancer is approximately 1% per year after 10 years of having the disease (in other words, if you were diagnosed with UC 25 years ago, you have a 25% lifetime risk of CRC in the absence of colectomy)
  • Use the IBD orderset at Moffitt for patients who you think may have an IBD flare. This will guide you through some diagnostics, and most importantly, steer you toward non-opioid pain management.
  • ALT elevation is the best laboratory predictor of biliary pancreatitis, so always consider this when ALT is elevated in the s/o abd pain.

Framework for ALT/AST elevations (blast from the past!)

ALT, AST < 5 x ULN Intermediate ALT, AST > 15 x ULN
ALT-predominant Chronic HCV

Chronic HBV

Acute viral hepatitis (A-E, EBV, CMV)




Autoimmune hepatitis

Alpha-antitrypsin deficiency

Wilson’s disease

Celiac disease

Overlap of mild and severe causes Acute viral hepatitis (A-E, HSV)


Ischemic hepatitis

Autoimmune hepatitis

Wilson’s disease

Acute bile duct obstruction

Acute Budd-Chiari syndrome

Hepatic artery ligation

AST-predominant EtOH related



Nonhepatic Hemolysis


Thyroid disease

Strenuous exercise



HSV Hepatitis Key points:

  • Rare cause of liver failure, accounting for 1% of all ALF
  • BUT it is extremely severe, with mortality rates of around 75%
  • HSV sepsis can also manifest as encephalitis, pneumonia, esophagitis. May see local infection as well (dermal lesions)
  • At risk populations: patients on immunosuppressive meds (TNF-inhibitors, chemo, post-transplant), HIV, pregnancy esp in 3rd trimester
  • Whenever you have ALF of unknown etiology, especially in the at risk populations above, start empiric acyclovir!

Check out this review article to learn more!




Moffitt Morning Report Pearls: HIV + abd pain, diffuse lymphadenopathy, and MAC IRIS!

Happy Tuesday, Moffitt!

Thanks to Lev for presenting the case of a young man with HIV who presented with abdominal pain and night sweats, who was found to have diffuse lymphadenopathy on CT abd/pelvis and ultimately diagnosed with MAC IRIS. Tons of great pearls, thanks to Jen Babik for being our discussant!

TLC (Tim and Laura, your Chiefs)


Top Pearls:

  • You may see patients on these single pill integrase-inhibitor regimens:
    • Bictarvy (bictegravir-emtricitabine-tenofovir alafenamide): single pill integrase-inhibitor regimen (new)
    • Trimeq (Dolutegravir, abacavir, and lamivudine): Need to first check HLA-B*5701 first.
  • Two types of IRIS:
    • Unmasking IRIS: Had a previous infection (like MAC, TB), and once you have immune reconstitution, you start to have symptoms
    • Paradoxical IRIS: Begin to get better after starting ARVs, then get worse again
  • Think about sending these five things when you get a biopsy:
    • Path (+/- flow cytometry)
    • Bacterial cx
    • Fungal cx
    • AFB cx
    • Hold sample for PCR (decide if this is needed once path comes back, but make sure to hold it in case!)


Prophylactic medications for HIV with low CD-4 count:

CD4 < 200

  • PCP:TMP/SMX DS 1 Tab daily

CD4 < 100…above plus…

  • Toxo (if seropositive): TMP/SMX DS 1 Tab Daily
  • Histo(if living in endemic area): Itraconazole 200mg Daily

CD4 < 50…above plus…

  • MAC:Azithromycin 1200mg weekly


HIV and GI symptoms:

  • Esophagitis: Candida, CMV, HSV
  • Infectious diarrhea: Cdiff, CMV, cryptosporidia, isosporidia
  • Lymphadenopathy: TB, MAC, histo (also see ddx for diffuse LAD below!)
  • Malignancy: KS, lymphoma
  • Structural/non-HIV related: appendicitis, diverticulitis, cholecystitis, etc


Differential for diffuse lymphadenopathy:

Think about four big categories of disease:

  1. Infectious:
    • Bacterial: Bartonella, Brucella, syphilis, TB, MAC
    • Viral: EBV, HIV, CMV
    • Fungal: Endemic fungi – histo most likely to cause diffuse LAD
    • Parasitic: Toxo
  2. Malignancy: Lymphoma, KS
  3. Rheumatologic/autoimmune: SLE, Still’s, sarcoid, IgG4 dx
  4. Drug: Serum sickness, DRESS


Mycobacterium Avium Complex infection in HIV

Clinical signs/symptoms

  • Disseminated disease: fever, night sweats, weight loss, abdominal pain, cough, diarrhea
  • Localized disease:
    • Lymphadenitis: fever, leukocytosis, inflammation of a lymph node. Mostly 2/2 IRIS
    • Atypical MAC: Mastitis, spinal MAC, osteomyelitis, bursitis, etc


  • Radiographic evidence of disseminated MAC: LAD on CT, particularly mesenteric/abdominal
  • Microbiology evidence: blood or LN biopsy


  • Macrolide + ethambutol
  • Add rifabutin in patients failure ART
  • Duration = 12 months
  • With IRIS, consider corticosteroids but depends on the severity of illness and other factors

POCUS, Eosinophilia, and DRESS!

Hi Moffitt,

This morning was Point of care ultrasound (POCUS) report! Thanks to Trevor for presenting a case of an elderly man who presented with AKI, volume overload, eosinophilia, and a rash. We talked about the utility of POCUS in conjunction with the physical exam to confirm that he was volume overloaded, which was attributed to him stopping his diuretics in the s/o an AKI. The rash and eosinophilia prompted a skin biopsy, and he was found to have DRESS. Some pearls on these topics below!

TLC (Tim and Laura, your Chiefs)


Key points about POCUS

  1. Think of POC ultrasound as a piece of the routine physical exam
  2. IVC ultrasound is most helpful on the far extremes of interpretation
  3. The most strongly supported uses of bedside cardiac ultrasound are for ruling out large pericardial effusions and noting qualitative LV systolic function

Steps to reading an ultrasound

First identify and confirm the following:

  • Probe
  • Orientation
  • Depth
  • Location of image (think about what you should be seeing in this part of the body)
  • Image quality
  • Identify structures and findings

POCUS IVC interpretation

  1. Confirm location: First, to know you’re looking at the IVC and in the right place, you need to see either the right atrium or the hepatic vein.
  2. What you’re looking for:
    1. Max diameter IVC size 2cm distal from the insertion of the hepatic vein: less than or greater than 2.2cm
    2. Collapsibility: less than or great than 50%
  3. Clinical meaning: Most useful in the extremes!
    1. IVC <2.2 and >50% collapsible = CVP <7
    2. IVC >2.2 and 50% collapsible or vice versa = CVP 8-12
    3. IVC >2.2 and <50% collapsible = CVP>13

POCUS Parasternal long axis

As a novice, focus on identifying the following:

  • Large pericardial effusion
  • Gross LV systolic function


Peripheral eosinophilia and hypereosinophilia syndromes


  • Eosinophilia: Absolute eosinophil count >500
  • Hypereosinophilia: Severe eosinophilia >1500, worry esp if >5000 since risk of end organ damage (check cardiac fxn!)

      Etiology: Lots of crazy mnemonics. One is NAACP

  • Neoplasms,
    • Monoclonal: Hyper-eosinophilic syndrome (can check for mutations like PGFRB, PDGFRA, FGGR-1, AEL, CEL, etc which cause a monoclonal eosinophil proliferation). If none of these mutations but it’s still a monoclonal population, it is sometimes called an idiopathic hypereosinophilic syndrome
    •  Polyclonal: T cell lymphoma, Hodgkins lymphoma, some solid-organ cancers cause reactive eosinophilia (eg cervical cancer, ovarian cancer, SCC, gastric and colon cancer, urothelial cancer of the bladder)
  • Allergies, which includes asthma and drug-induced eosinophilia (including DRESS!)
  • Adrenal insufficiency
  • Connective tissue diseases, like eosinophilic granulomatosis with polyangiitis (EGPA, formerly called Churg-Strauss) and RA
  • Parasites (lymphatic filiariasis, toxocara, trichinosis and strongyloides can all cause eos > 5,000! Note: only multicellular parasites cause eosinophilia). Besides parasites, other infections may also cause lower degrees of eosinophia (ABPA, cocci, HIV)
    • Bonus: P can also include Primary Eosinophilia syndromes (eg eosinophilic fasciitis, eosinophilic cellulitis, etc)


DRESS (Drug Reaction with Eosinophilia and Systemic Symptoms)

  • Basics:
    • DRESS = Drug-induced hypersensitivity reaction that includes skin eruption, hematologic abnormalities (eosinophilia, atypical lymphocytosis), lymphadenopathy, and internal organ involvement (liver, kidney, lung)
    • Most frequently reported drug culprits: antiepileptic medications, allopurinol, sulfonamides, dapsone, minocycline, vancomycin.
    • KEY timing: DRESS is characterized by a long latency (2-8 weeks) between drug exposure and disease onset. Course tends to be prolonged with frequent relapses DESPITE discontinuation of the culprit drug
  • Epidemiology
    • Frequency depends on the type of drug and immune status of the patient.
    • 1-5 per 10,000 patients exposed to anticonvulsants, carbamazepine and phenytoin
    • Higher incidence in patients taking lamotrigine (1 per 300).
  • Pathogenesis
    • Drug-specific immune activation + herpesvirus reactivation?!
    • HHV6 reactivation: reactivation of herpesvirus infection has been associated with DRESS. – Couple studies showed that an increase in antibody titer against HHV-6 was detected in approximately 60% of patients 2-4 weeks after onset of symptoms   (Tohyama et al., Br J Dermatol. 2007 Nov;157(5):934-40/ Picard et al., Sci Transl Med. 2010;2(46)ra62) – Disease relapses have been shown to be temporally related to detection of HHV-6 DNA in the peripheral blood
  • Clinical Presentation
    • Skin: morbilliform eruption, facial edema (1/2 of cases)
    • Systemic symptoms: fever, diffuse tender lymphadenopathy
    • Lab abnormalities: eosinophilia (50-90% of cases), atypical lymphocytosis, transaminitis
    • Organ involvement: Liver (cholestatic and hepatocellular injury), kidney (interstitial nephritis), pulmonary (interstitial pneumonitis), heart (eosinophilic myocarditis, pericarditis), muscle (myositis), peripheral nerves (polyneuritis), eye (uveitis)
  • Management
    • Withdrawal of med and supportive care

Mt. Zion AM report: The never-ending UTI…

Thanks to our attending presence and Dr. Mia Williams for presenting our Tuesday AM report case! We discussed a 65F with microhematuria and chronic lower back pain from Peru who presented to primary care with over three discrete episodes of recurrent dysuria, increased urinary frequency, and urinary hesitancy after self-treating with ciprofloxacin. Key learning points are below, with some TBD once urology sees the patient!

What are predisposing factors for UTIs?

  • Pregnancy
  • Diabetes
  • Immunocompromised state
  • Underlying urologic abnormalities (stones, surgeries causing abnormal anatomy, malignancy, organ prolapse, indwelling foley catheter, ureteral stents, polycystic kidney disease)
  • Urinary retention/neurogenic bladder
  • Fistulas, inflammatory bowel disease

If it’s not a UTI, what other condition could cause similar symptoms?

  • Other infections:
    • Urethritis / cervicitis
    • STIs (gonorrhea, chlamydia)
    • Tuberculosis – sterile pyuria!
    • Vaginitis – candida, bacterial vaginosis, trichomonas
  • Foreign body
  • Dermatologic conditions
    • Irritant dermatitis (think diarrhea, topicals)
    • Psoriasis
    • Lichen sclerosus
    • Atrophic vaginitis
  • Nephrolithiasis, urethral diverticula, vaginal/pelvic organ prolapse
  • Malignancy (usually with hematuria, other systemic symptoms) – bladder & renal cancers, lymphoma, metastatic disease, vulvar/vaginal cancers, prostate cancers in men
  • Interstitial cystitis (also called painful bladder syndrome) – often misdiagnosed as recurrent UTIs, key feature is increased urinary frequency and forced voiding to relieve dysuria. See table below from CCJM for other features!
    • IC


Who needs suppressive antibiotics for recurrent cystitis?

  • Defined as > 2 documented UTIs in 6 months or > 3 documented UTIs in 1 year
  • Helpful to determine re-infection versus relapse
    • Relapsing infection usually requires anatomic urologic evaluation and longer duration of abx therapy
  • First line therapies:
    • INCREASE fluid intake (2-3L of water per day recommended)
    • Avoid spermicides, irritants
    • Voiding after sex (not evidence based, but still recommended given no harm!)
  • Antibiotics (only start after documenting eradication of current UTI with negative cultures 1-2 weeks post-treatment!):
    • Intermittent self-treatment : Women with recurrent UTIs have > 85% accuracy in recognizing symptoms of subsequent UTI. Can safely offer self-treatment with antibiotics in women with clearly documented infections, self-motivated, compliant, and understanding of return precautions!
    • Postcoital prophylaxis – similar antibiotics as below but use only after sexual activity; choose in women who develop UTIs temporally after sex. Usually less antibiotic exposure overall depending on frequency of sexual activity.
    • Continuous prophylaxis – multiple regimens can be chosen – usually based on prior bugs, antibiotic allergies, resistance patterns
      • Bactrim daily or three times per week
      • Nitrofurantoin daily
      • Cephalexin daily
  • Topical estrogen in postmenopausal women with > 3 UTIs per year (helps re-establish normal vaginal flora and decrease overall risk of UTI)

What’s the recommended imaging modality to evaluate GU anatomy?

  • Who needs imaging?
    • UTIs with Proteus species (suggestive of stones)
    • Concern for nephrolithiasis
    • Relapsing infections with same organism despite adequate duration of treatment
    • Persistent hematuria despite treatment of infection
  • Simple recurrent UTIs – no imaging recommended
  • Any above risk factors or relapsing infection – ACR recommends starting with CT abdomen and pelvis without and with IV contrast (CT urogram preferred if persistent hematuria) to e/f diverticula or stones!
  • Renal ultrasound if concern for urinary retention to measure postvoid residual

ACR recurrent uti


Michels & Sands (2015). Dysuria: Evaluation and Differential Diagnosis in Adults. AAFP, 92(9): 779.

Rosenberg, Newman, & Page (2007). Interstitial cystitis/painful bladder syndrome: Symptom recognition is key to early identification, treatment. Cleveland Clinic Journal of Medicine, 74(3):Supplement S54.




Moffitt Cardiology Report: Wellens’, diffuse TWI, Takotsubos

Happy Election Day, Moffitt!

Don’t forget to vote today if you haven’t already! See Tim’s email from yesterday for ways to make it happen

Thanks to Megan M. for presenting an awesome case of a middle aged woman w/ h/o HFpEF who presented with SOB and diffuse, dynamic T-wave inversions, who was ultimately found to have stress cardiomyopathy. We covered a bunch of topics this morning including Wellens’ syndrome, ddx for diffuse TWI, and some basics about Takaksubo’s/stress cardiomyopathy.  See pearls below!

TLC (Tim and Laura, your Chiefs)
Wellens’ syndrome 

Wellens’ syndrome is a pattern of deeply inverted or biphasic T waves in V2-3, which is highly specific for a critical stenosis of the left anterior descending artery (LAD). It is due to a blockage and then unblockage of this region, with reversible ischemia in this region.   

There are two patterns of T-wave abnormality in Wellens’ syndrome: 

  • Type A = Biphasic, with initial positivity & terminal negativity (25% of cases)
  • Type B = Deeply and symmetrically inverted (75% of cases)

The T waves can evolve over time from a Type A to a Type B pattern (see an example of this here). 

Differential Diagnosis for Deep TWI 

If you have deep T wave inversions, consider this differential diagnosis: 

  • Digoxin toxicity
  • Intracranial hypertension
  • Wellens’ (ischemia)
  • Takotsubo
  • Electrolyte abnormalities (hypokalemia)

Takotsubo’s / Stress cardiomyopathy 

  • From the Japanese, “tako-tsubo” meaning “fishing pot for trapping octopus”,– (based on similarity to the shape of the LV in the typical form). Also known as broken heart syndrome : (, More common in elderly or postmenopausal women (80-100 percent of cases). Frequently with onset after acute emotional stress or an acute medical condition
  • Mimics acute MI with substernal chest pain, dyspnea, shock; Rule out pheochromocytoma, myocarditis, ACS
  • EKG: ST elevations in 30-50%, often troponin elevations
  • TTE: Apical ballooning in 50-66%, apical sparing in atypical cases
  • Cath: Clean coronaries
  • Complications: Heart failure, tachyarrhythmias, MR, shock
  • Treatment: No controlled data, reasonable to treat for LV dysfunction with ACE-I, beta blockers, and diuretics prn
  • Recovery often occurs in 1-4 weeks

Moffitt Pulmonary Report 11/5/18: Immunocompromised host PNA

Thanks to Elie and Jack for presenting the case of an elderly, immunosuppressed man who presented with fever and cough and was found to have diffuse consolidations and centrilobular nodules, ultimately diagnosed by sputum culture with staph aureus pneumonia. We had a great discussion of how to workup pulmonary infection in an immunocompromised host, and borrowed MANY pearls from the great Jen Babik. See below!

TLC (Tim and Laura, your Chiefs)


Assorted Pearls:

Non-HIV PCP Prophylaxis 2-2 rule: If on greater than or equal to 20mg prednisone for 2 weeks or more, give prophylaxis

Indications for steroids for PCP treatment:

  • PaO2 <70mmHg on room air and/or
  • A-A gradient of >35mmHg

Flu pearls:

  • In ICU-level patients with respiratory symptoms, treat empirically
  • Note that nasopharyngeal flu swabs may be falsely negative in critically ill patients who have had the flu for several days


Differential diagnosis of pulmonary infections based on pattern on chest imaging

Segmental/lobar Consolidation

  • Common bacterial pathogens (including Legionella)
  • Less common: TB, Nocardia, Fungal


  • Bacteria: septic emboli (especially if peripheral, cavitating)
  • Atypical bacteria: Mycobacteria, Nocardia
  • Fungal:
    • Yeasts: Cryptococcus
    • Dimorphics(endemics): Histoplasma, Coccidioides
    • Molds: Aspergillus, Zygomyces
  • Viral (small centrilobularnodules)
  • Malignancy

Diffuse Ground Glass Opacities

  • Atypicals (rarely Mycoplasma, Chlamydia, Q fever, leptospirosis)
  • PCP
  • Viral: Respiratory viruses (e.g., influenza, RSV, etc) or CMV
  • Toxoplasma
  • Strongyloides
  • Noninfectious: Drug-induced ALI, edema, DAH, ILD

Cavitary lesions

  • Infectious: Tb, bacterial (anaerobes 2/2 aspiration, staph/strep 2/2 septic emboli from endocarditis vs. primary pneumonia, klebsiella, actinomyces, rhodoccocus), fungal (histoplasmosis, blasto, cocci, crypto), molds (aspergillus))
  • Malignancy
  • Vasculitis: GPA
  • Aspiration of foreign body