Category Archives: Morning Report

MOFFITT MORNING REPORT PEARLS 3/21/17: Our Anaerobic Friend Bacteroides!

Good morning everyone! Thanks to Dan for presenting the case of a young woman with alcohol withdrawal who was found to have colitis and bacteremia with possible colonic perforation. Pearls below on our old anaerobic friend, Bacteroides!


Top Pearls:

  1. Bacteroides is the major anaerobic pathogen causing intraabdominal infection and bacteremia.
  2. Metronidazole is the narrowest drug of choice against Bacteroides.
  3. Clindamycin and fluoroquinolones do not have reliable activity against Bacteroides.


For those who want more info:

The “B. fragilis group” (which includes various Bacteroides strains as well as Parabacteroides) are the major anaerobic pathogens causing intraabdominal/pelvic sepsis and bacteremia. Bacteroides do not typically cause anaerobic infections above the diaphragm, where the major anaerobic pathogens are Fusobacterium, Prevotella, and peptostreptococci. These orodental and pulmonary infections usually have mixed flora which are often resistant to metronidazole.

Resistance rates among anaerobic bacteria are increasing. A significant number of Bacteroides strains are now resistant to clindamycin (44%), moxifloxacin (38%), and cefoxitin (10%).

Antibiotics predictably active against Bacteroides (resistance rate): Metronidazole (<1%), Zosyn (0.5%), Unasyn (3%), tigecycline (4%), carbapenems (<1%, up to 5% in one study).

Two cases of MDR B. fragilis have been reported in the U.S. Eek!!

The conclusion here is that metronidazole, carbapenems, and zosyn/unasyn are predictably active against Bacteroides. Clindamycin and fluoroquinolones do not have reliable activity.

*Pearl: Use Clinda above the diaphragm and Flagyl below the diaphragm.

In one study (Redondo MC Clin Infect Dis 1995), patients with B. fragilis group bacteremia had 28% mortality, and 20% increased mortality compared to matched control patients with the same principal diagnosis but without bacteremia.

*Pearl: “Diarrhea” is derived from the Greek “to flow through.” Eww.





Cardiac sarcoid

Cardiac sarcoid workupToday we discussed a fantastic case with Izzy about a woman presenting with acute on chronic HF symptoms and chest tightness who is c/f a presentation of cardiac sarcoid!

Cardiac sarcoid: Cardiac sarcoid is a rare event occurring in 5% of patients with systemic sarcoid. Clinical manifestations include conduction abnormalities (BBB, AVB), tachyarrhythmia, cardiomyopathy, CHF, valvular dysfunction, and sudden cardiac death. Pericardial disease is rare. Cor pulmonale can occur with advanced lung disease.

Sarcoid can actually infiltrate the coronary arteries leading to spasm or vasculitis and can thus cause anginal symptoms!

The cardiac manifestations can precede, follow, or occur during involvement of the lungs or other organs.

Attached is a helpful algorithm for making the dx.

Utility of imaging in cardiac sarcoid:

Much of the discussion today was also about the imaging findings that may lead you to suspect a dx of cardiac sarcoid. Below are the findings based on various imaging modalities that may lead you to suspect cardiac sarcoid:

ECHO: 1st line imaging. LV dilatation, septal thinning, segmental or global hypokinesia of the LV or RV, aneurism formation, valvular regurgitation, simulated LV hypertrophy from infiltration into the myocardium.

Cardiac MRI: Technique of choice for the dx of cardiac sarcoid w/ the highest sensitivity and specificity. Late gadolinium enhancement (LGE) may have prognostic value in evaluating chronic sarcoid as you have scar formation and increased risk of death presumably from arrhythmia.

Cardiac PET: Excellent imaging modality for active sarcoid, but less specific as can have false positives with other inflammatory myocardial diseases.

Hypoglycemia redux

Thank you to Katie Sullivan for presenting a case last Thursday of a patient with hypoglycemia and eosinophilia who was found to have pan hypo pit.
In these pearls: We talked about organizing the hypoglycemia ddx by organ system and a good first pass workup. This time, we organized it differently – insulin-mediated vs insulin-independent. See below.
Insulin mediated
  • Exogenous
    • insulin
    • sulfonylureas (either due to excess intake or decreased clearance)
  • Endogenous
    • islet cell hyperplasia
    • insulinoma
    • Adrenal insufficiency
non-Insulin mediated
  • glucose consumption doesn’t meet demand
    • poor access to food
    • giant, rapidly divided tumors that consume all glucose
  • malabsorption of glucose (for example after gastric surgery)
  • decreased glycogen stores or poor gluconeogenesis
    • malnutrition
    • liver failure
    • ESRD
    • adrenal insufficiency
  • decreased glucagon
    • Lisa Murphy pearl! In any pancreatic failure state (chronic pancreatitis, post pancreatectomy), the patient loses both their alpha and beta cells. So not only do they develop diabetes, they have hard to manage hypoglycemia because they don’t make glucagon.
Bonus Lisa Murphy Pearls
  • Growth hormone is an under appreciated player in the hypoglycemia orchestra. It’s one of the counter-regulatory hormones, along with cortisol and glucagon. Growth hormone stimulates hepatic gluconeogenesis and reduces glucose utilization in the peripheral tissues.
    • While attempting to figure out the mechanism here, I found this only mildly relevant NEJM article from 1962 that provides some early experimental evidence about what growth hormone does.  It uses unfortunate terminology like “panhypopituitary dwarfs”. A good reminder that medical literature has come a long way in describing patients respectfully.
  • Hormone loss in pan hypo pit
    • When the pituitary is compressed or lost slowly over time, the hormone production disappears in a very evolutionarily rational way. The reproduction and growth-related hormones go first, while the necessary for life hormone (cortisol) goes last.
      • In other words, hormones are usually lost in this order:  Growth hormone -> gonadotropins-> thyroid hormones -> cortisol
  • Hypoglycemia in ESRD – pro tips
    • two mechanisms
      • gluconeogenesis – 20% in the kidneys, 80% in the liver
      • uremia impairs hepatic glycogen uptake
    • We talk often about ESRD as a risk factor for hypoglycemia. Lisa explained that ESRD-induced hypoglycemia is rare in isolation.  Along with ESRD, a patient needs a second hit to the counter-regulatory cascade – food insecurity, liver failure, adrenal insufficiency – to have clinically detectible hypoglycemia from ESRD.


We had a terrific inaugural rheumatology report this morning with Sarah Goglin. Thanks to Max and Beth for presenting the case of an elderly woman with positive P-ANCA diagnosed with AIN on renal biopsy, likely NSAID-associated! Some highlights below:


Top Pearls:

  1. ANCA positivity is not specific for vasculitis!
  2. When complement levels are low, there are immune complexes forming from somewhere!
  3. Complement levels are usually normal in ANCA-associated vasculitis (aka pauci-immune).


For those who want more info:

See these prior Moffitt pearls on ANCA-associated vasculitides:

Vasculitis isn’t the only cause of ANCA positivity! We expanded our differential for P-ANCA (MPO) positivity to include:

  • MPA
  • EGPA
  • Sometimes GPA! (usually C-ANCA but can be P-ANCA too)
  • SLE
  • RA
  • IBD
  • Malignancy
  • Chronic infection
  • Drugs (particularly PTU, sulfa, and hydralazine)
  • ILD (UIP and NSIP)! Thanks Sarah for sharing this recently described association.

See this recent article about ANCA and ILD:


We also discussed our differential for low vs normal complement levels.

If C3 and C4 levels are low, the cause is immune complexes. Think SLE, Sjogren, MCTD, post-streptococcal GN, chronic infection (SBE, osteo), or cryoglobulinemic vasculitis (typically very low C4 level in this last one).

If C3 and C4 levels are normal and vasculitis is a concern, think ANCA-associated, drug-induced, malignancy, or IGA vasculitis (formerly HSP).

What about low C4 with normal C3? Think about disorders causing angioedema, either hereditary angioedema or acquired C1 inhibitor deficiency. Other causes include SLE, cryoglobulinemia, and membranoproliferative GN.

What about low C3 with normal C4? Uncommon in clinical medicine, indicates activation of alternative complement pathway. Occasionally happens in SLE, atypical HUS, contrast dye reactions, and transiently at onset of dialysis or ECMO. Most common in pediatric renal disease.

What about CH50? Measures total complement function and is more of a screening tool to detect a classical pathway deficiency. Here, we usually just send C3 and C4 and skip the CH50.

See these ZSFG pearls for a cool diagram at the end showing us how to think about small vessel vasculitis causes broken down by complement levels. Diagram copied below:





Have a great day everyone!




Acute Lymphoblastic Leukemia and TLS

Congratulations and Happy Match Day!!! Thank you to Dan Reiss, for presenting a case of a middle-aged woman with systemic symptoms and pancytopenia, who was diagnosed with new acute lymphoblastic leukemia. We discussed ALL as an entity and also discussed tumor lysis syndrome!

SamMy (Sam & Myung)



  • ALL is a rare disease in adults. Prognosis in adult-onset ALL is poor, with long-term survival of only about 40% with treatment.
  • A positive Philadelphia chromosome confers a poorer prognosis.
  • Tumor lysis syndrome is an oncologic emergency and requires urgent treatment: hydration, hypouricemic agents (allopurinol, rasburicase), management of severe electrolyte abnormalities (hyperK tx, phos binders, calcium repletion), and possible dialysis


Acute Lymphoblastic Leukemia

  • We all recall from our med school years, that ALL is the most common form of cancer in children (~30% of all childhood malignancies).
  • ALL in adults is a rare disease. However, there is a bimodal peak in incidence of ALL, so late-onset ALL can occur.
  • In general, prognosis in poorer in ALL of adults compared to that in children.  Long-term survival of older adults with ALL who are intensively treated is only 40%.


  • ALL can be subdivided into B cell ALL vs T cell ALL
  • Prognostic Factors
    • Certain cytogenetic findings are associated with poor prognosis– Philadelphia chromosome positivity, t(4;11), complex abnormalities (more than 5 chromosomal changes)
    • B-cell disease is associated with higher treatment failure rates


  • Treatment
    • Induction chemotherapy à consolidation à maintenance
    • CD20/CD 22 antibodies as adjuncts to chemotherapy in B-cell ALL are being tested in RCTs.
    • Tyrosine kinase inhibitors for Philadelphia + ALL
    • Bone Marrow Transplantation


Tumor Lysis Syndrome (Blast from the Past)

Tumor lysis is an oncologic emergency caused by massive tumor cell lysis and release of potassium, phosphate, and uric acid. Uric acid or calcium phosphate crystal deposition can cause acute kidney injury.

2 or more of these values (or 25% change from baseline values) are necessary for “laboratory TLS”:

  • Uric acid >8 mg/dL
  • Potassium >6 mEq/L
  • Phosphorus >4.5 mg/dL
  • Calcium <7 mg/dL

Risk factors include high tumor cell proliferation rate, large tumor burden, kidney disease, dehydration, and chemosensitive tumors. TLS occurs much more frequently in hematologic malignancy compared to solid tumors.

TLS typically occurs after chemotherapy (usually within a week), and more cases are being seen with targeted therapies.

Prevention and treatment are determined by risk stratification but can include hydration, hypouricemic agents (allopurinol, rasburicase), management of severe electrolyte abnormalities (hyperK tx, phos binders, calcium repletion), and possible dialysis

“Clinical TLS” = Laboratory TLS + AKI, cardiac arrhythmia, or seizure.

Evernote Link:

VA Intern Report 3.16.17- Multiple Myeloma pearly pearls

#What is it: A plasma cell neoplasm that produces a specific type of immunoglobulin

#How does it present: No shame in forgetting your CRAB mnemonic: Hypercalcemia, renal insufficiency, anemia, and bone pain caused by lytic lesions as a result of plasma cell proliferation!

*Brad Lewis pearl/warning: Unexplained anemia and slightly worsened renal function can go unnoticed/unworked up for years, which is not good. When you see an unexplained anemia and/or renal insufficiency, train your brain to consider multiple myeloma and look for it.

#Epi: 1% of all cancers, 10% of heme malignancies, for whatever reason increased risk in African-Americans, usually in the 7th+ decade of life, more commen in men.

#Diagnosis: Anemia is the most common initial finding (~80% of cases), then bone pain (60%), renal disease (50%), hypercalcemia only in a quarter and portends a worse prognosis.

#LT Pearl! Myeloma doesn’t cause fevers by itself, look for infections!

Serum protein electrophoresis: picks up the monoclonal protein (M protein) secreted by the aberrant plasma cells, can also be done on urine. Adding the immunofixation confirms the type. In a small percentage (3% or so) of MM the plasma cells don’t secrete a detectable level of M protein (non-secretory MM) Usually it will be IgG but can also be IgA, or sometimes only pick up the light chain portion of the M protein (kappa or lambda) so also important to check serum free light chain levels up front. Also why the UPEP can still be useful as it will detect the light chains when serum doesn’t show up.

Shmear: Rouleaux are classic (more than 50%) can also see leukopenia and thrombocytopenia

BMBx: Gotta do it. Looking for 10% or more CLONAL plasma cells, or if other clinical criteria established can have less, can also biopsy other potential sites of involvement (plasmacytomas or isolated plasma cell tumors)

#Word about treatment: No clear benefit to treating MGUS or smoldering myeloma, usually wait until clinically apparent disease. BMT can be curative, treatment algorithms are complex, one question that came up was about lenalidomide (revlimid)

  • Thalidomide derivative so no go in pregnancy
  • increases risk of PE/DVT, as well as MI in patients w/ CAD
  • Also myelosuppressive (duh)
  • Works as an angiogenesis inhibiting agent

MOFFITT ENDOCRINE REPORT PEARLS 3/15/17: Papillary and Anaplastic Thyroid Cancer!

Thanks to Nick for presenting a case about metastatic thyroid cancer. We discussed the relationship between the papillary and anaplastic types of thyroid cancer with Mark Anderson, our endocrine report expert. Pearls below!


Top Pearls:

  1. The majority of patients with papillary thyroid cancer do not die of their disease.
  2. Most/all patients with papillary thyroid cancer need surgical resection and postoperative levothyroxine, but only higher risk patients need radioiodine therapy.
  3. Anaplastic thyroid cancer is usually a transformation from more differentiated thyroid cancer and is rapidly fatal.


For those who want more info:

Papillary Thyroid Cancer:

Risk Factors: Childhood radiation exposure (e.g. dental radiation before we had lead thyroid shields!) and family history of thyroid cancer.

Presentation: A thyroid nodule noted by the patient, physician, or incidental radiologic finding. Size of the tumor, older age at diagnosis, histological subtype, and presence of invasion or metastasis are the main features associated with worse morbidity and mortality. <10% of patients have metastases beyond the neck at the time of diagnosis (2/3 are pulmonary, 1/4 are skeletal).

Prognosis: Most patients with papillary thyroid cancer do not die of their disease (only ~5% cancer-related mortality over 15 years).

Treatment: All patients should have surgical resection including part or all of the thyroid gland, depending on extent of disease. Postoperatively, patients are stratified based on risk factors for persistent/recurrent disease. Most patients require postoperative levothyroxine (T4) to suppress TSH (TSH goal depends on risk stratification). Higher risk patients also receive postoperative radioiodine. Surveillance includes neck ultrasound, TSH, and serum thyroglobulin (Tg) levels to detect recurrent disease.


Anaplastic Thyroid Cancer:

Presentation: Rapidly enlarging neck mass. 20% have a history of differentiated thyroid cancer, which is often present concurrently!

Differential diagnosis: poorly differentiated thyroid cancer, lymphoma, melanoma, and sarcoma.

Prognosis: Nearly always rapidly fatal.

Treatment: Complete surgical resection with postoperative chemoradiation, or chemoradiation alone if disease is inoperable. Commonly used agents are doxorubicin, docetaxel, and cisplatin. Clinical trial enrollment and concurrent palliative care are recommended.

*Pearl: All anaplastic carcinomas are considered stage IV, regardless of the extent of disease!

Transformation: Anaplastic thyroid cancer usually arises from transformation of a differentiated thyroid cancer, though it can occur de novo. Transformation typically occurs in the thyroid or cervical lymph nodes, but may rarely occur at metastatic sites.




Have a great day everyone!