All posts by cauriemma

Moffitt HemOnc Pearls 3/7/18 – Lung Cancer & TLS

Thank you to the great Sam Brondfield for joining us AND presenting a fascinating case! We discussed an older woman with metastatic lung adenocarcinoma on erlotinib transferred from OSH with shock with markedly elevated uric acid, LDH, and renal failure.

  1. Erlotinib is an EGFR inhibitor and used in the treatment of metastatic lung adenocarcinoma with positive EGFR mutations. In general, these medications are tolerated very well. The primary side effects experienced include folliculitis and diarrhea. See below for more details about specific lung cancer mutations.
  2. Not all cancers have equal bleeding risk. Guidelines suggest avoiding anticoagulation in patients with RCC, melanoma, choroid germ cell, and medullary thyroid cancer if they have brain metastases as they are at high risk for intracranial hemorrhage.
  3. Lung cancer is the only cancer for which guidelines recommend brain imaging as part of the initial screening (in patients with metastatic disease or any patient with small cell lung cancer).
  4. 5% of lung adenocarcinomas can transform into small cell lung cancer. Small cell cancers are a subset of neuroendocrine cancer, and can arise from multiple types of cells. We are most familiar with discussing small cell lung cancer, but this is also seen in the setting of prostate cancer.

Lung Cancer Targeted Treatment

There has been great progress over the years in treatment of lung cancer. We now routinely test for a variety of specific mutations in metastatic lung adenocarcinoma and in squamous cell carcinoma. See the pie chart below for a breakdown of the various known mutations. Many of these now have targeted therapies. This image comes from the Lung Cancer Initiative, a great resource that also outlines the various treatments to target distinct mutations.



Refresher on the Etiologies of Shock

  • Distributive
    • Sepsis
    • Anaphylactic
    • Vasoplegia
      • Adrenal insufficiency
      • Neurogenic
  • Hypovolemic/Hemorrhagic (crystalloid vs. blood)
  • Cardiogenic
  • Obstructive
    • PE
    • Tamponade
    • PTX
    • Abdominal compartment syndrome

Spontaneous Tumor Lysis Syndrome

Check out this case series and review of TLS in small cell lung cancer.  This is a rare, but highly morbid complication of small cell lung cancer. While TLS is more commonly seen in hematologic malignancies, namely Burkitt lymphoma, AML and ALL, there are reports in the literature of its association with various solid tumors.

Lung Cancer Evernote:



Moffitt Cardiology Report – 3.6.18 – Syncope

Thank you to Armond for presenting a case of a elderly man with AF and Parkinson disease presenting with exertional syncope found to have a depressed EF and cath showing 95% LAD occlusion.

Key Pearls

  1. When working up a patient who presents with syncope the history is the most important diagnostic tool.
  2. Concerning features suggestive of cardiac cause include syncope with exertion, lack of prodromal symptoms, and trauma.
  3. After syncope from ANY cause you may see myoclonic jerks 2/2 to global anoxia of the brain. See this video for an example of healthy medical students with induced syncope and subsequent myoclonic jerks.
  4. We define Ventricular Tachycardia as > or = 3 VPCs at rate of at least 100. Sustained VT is > 30 seconds or VT with hemodynamic compromise. Non-sustained VT is < 30 seconds.

General Approach to Syncope

  • Cardiac
    • Structural: chest pain, dyspnea, exertional, post-operative
    • Arrhythmia: sudden syncope, injury, palpitations
  • Reflex Mediated
    • Vasovagal: warmth, nausea, prodrome, tunnel vision
    • Situational: occurs after certain activity (micturition, cough)
    • Neurocardiogenic: Provocable stimulus
    • Carotid sinus hypersensitivity
  • Neurologic
    • Seizures
  • Orthostatic Hypotension
  • Medications
  • Unknown

Clinical Features Suggestive of VT

    • Age > 35 (positive predictive value of 85%)
    • Structural heart disease!!
    • Previous MI or hx of ischemic heart disease
    • Congestive heart failure
    • Cardiomyopathy
    • Family history of sudden cardiac death (suggesting conditions such as HOCM, congenital long QT syndrome, Brugada syndrome or arrhythmogenic right ventricular dysplasia that are associated with episodes of VT)
  • WHEN is doubt shock it out!!



Thank you to Michelle Mourad for this educational slide from last week’s awesome M@M.

Syncope Evernote:

Moffitt Pearls 3/5/18 – Splenomegaly, Pigmented gallstones, and the Monospot test

Thank you Ashley and Dave for presenting a case of a young woman with a week of abdominal pain and jaundice following an upper respiratory infection found to have laboratory evidence of hemolysis and a pigmented gallstone via ERCP.

Key Pearls:

  1. Causes of splenomegaly can be broken down in the following way:
    • Increased WORK of the spleen:
      1. immune response hypertrophy (as seen in infections like EBV)
      2. RBC destruction hypertrophy (as in hereditary spherocytosis or thalassemia)
    • Less blood coming out of the spleen:
      1. congestion (as in portal hypertension or splenic vein thrombosis)
    • Stuff in the spleen that shouldn’t be there:
      1. myeloproliferative disorders (like CML)
      2. infiltrative diseases (sarcoid)
      3. malignancy (especially lymphoma and CLL)
  2. Pigmented gallstones are rare – less than 1% of stones according to our GI colleagues!
    • In general, when we describe pigmented stones, we mean either black or brown colored stones.
    • Black stones are formed in the gallbladder in sterile bile and are associated with advanced age, chronic hemolysis, alcoholism, cirrhosis, pancreatitis, and total parenteral nutrition. This is often due to elevated levels of circulating bilirubin.
    • Brown stones form not only within the GB, but also within the intra and extrahepatic ducts; they are uniformly infected with enteric bacteria and are usually associated with ascending cholangitis.
    • For more reading, here’s a review about gallstone disease.
  3. The test characteristics of the heterophile antibody (AKA the monospot test) are not perfect and can lead to both false positive and false negative results. As a result, the CDC no longer recommends using this assay and instead using EBV serologies. Here are some slides that break it down from a prior M&M:



Splenomegaly Evernote:


Moffitt Pearls 3/2/18 – MSSA bacteremia and Sepsis 3

Thank you to Alex for presenting the case of a middle aged transgender female p/w a week of abdominal/flank pain found to have a psoas abscess and 3/3 blood cultures + for MSSA. Interestingly, this patient had presented 3 days prior reporting dysuria to an OSH ED and a urine culture showed 5000CFUs of staph at that time.

Key Pearls

  1. Staph aureus in the urine, even with low CFUs, should always make you pause and consider the possibility of hematogenous infection. See this prior UCSF blog post from the amazing Grant Smith for more on Staph Aureus bacteremia.
  2. There have been 3 interventions shown to reduce mortality in Staph Aureus Bacteremia (SAB):
    • ID Consult
    • Order a echocardiogram
    • choose the appropriate antibiotics based on sensitivities

**See this journal watch article for more information about the practices that reduce mortality in patients with SAB **

    • Risk-adjusted OR: 0.61 for ID consultation, 0.73 for echocardiography, and 0.74 for suitable antibiotics.
    • Risk-adjusted SAB-related mortality declined from 23.5% in 2003 to 18.2% in 2014.
    • The researchers estimated that about 57% of this decrease could be ascribed to increased use of the three evidence-based metrics.
  1. Sepsis definitions have changed. Check out below for lots of references and comparisons of early warning systems.

Sepsis 3

The third international consensus definitions for sepsis and septic shock were published in Jama in 2016 amid some controversy. Let’s review the definitions and some key take-aways.

Sepsis: “life-threatening organ dysfunction due to dysregulated host response to infection”.

KEY POINT: Sepsis DOES NOT = Infection alone. Sepsis = Infection+ Dysregulation

Sepsis is actually a minority of patients with infections (see the figure below from this commentary in Critical Care).


Clinical criteria for sepsis 3 is met with organ dysfunction as defined by an increase of 2 points or more in the Sequential Organ Failure Assessment (SOFA) score

    • for patients with infections, an increase of 2 SOFA points gives an overall mortality rate of 10%

The SOFA score is a 7-item score made of clinical and laboratory findings – using the worst values in the first 24 hours of care.

Because even 7 items feels like too many to memorize, the qSOFA was developed to provide a more facile way to quickly get a sense of how sick a patient with a suspected infection may be. The quick SOFA, or qSOFA, can identify patients with suspected infection who are likely to have a prolonged ICU stay or to die in the hospital. A positive qSOFA is defined as meeting 2 or more HAT criteria:

  • Hypotension: SBP less than or equal to 100 mmHg
  • Altered mental status (any GCS less than 15)
  • Tachypnea: RR greater than or equal to 22

Septic shock: subset of sepsis in which underlying circulatory and cellular/metabolic abnormalities are profound enough to increase mortality.

  • Clinical criteria = Sepsis AND HoTN requiring pressors AND Lactate > 2 (despite adequate IVF)
  • With these criteria, hospital mortality is in excess of 40%


How do SOFA and qSOFA compare to SIRS?

  • While the FULL, 7-item SOFA score has a better AUROC than SIRS for predicting hospital mortality in ICU patients with suspected infection, the qSOFA does not.
  • The qSOFA does, however, have increased SPECIFICITY for identifying patients with sepsis.


  • For more reading, check out this fantastic PulmCrit post addressing the debate and summarizing the data from Churpek et al.’s study comparing the qSOFA to other commonly used early warning systems. Thanks to Colin for recommending!
  • The chart above and figure below,   showing comparisons of the various warning systems, both come from PulmCrit.Sepsis



Moffitt Morning Report 2/23/18

Thank you to Jesse for presenting an AWESOME case of an elderly woman with mechanical mitral and aortic valves due to rheumatic heart disease who presented with subacute shortness of breath found to have intravascular hemolysis and a leukocytosis ultimately diagnosed with staph endocarditis!

This case was so rich! Here are some focused pearls based on questions that came up:

Reticulocyte Review

When you order reticulocytes at Moffitt, the result in Apex is the Reticulocyte Count, i.e. the number of reticulocytes x10^9/L.

You can apply this number directly to the chart below to assess whether the reticulocyte response is appropriate for the degree of anemia based on the patient’s hemoglobin.


The blue line represents a Normal/Expected response in Absolute Retic Count based on varying Hemoglobins. If Hgb is normal at 14, then you shouldn’t have much of a reticulocyte count; conversely if your Hgb is low at 9, you should be mounting an absolute reticulocyte count in the 220s. Anything below the line represents an inappropriately low reticulocyte count.

For the patient we discussed today, the retic count in Apex was 204 and the hemoglobin was 9.3, putting the patient just about on the line for the expected reticulocyte count (red star).


If you prefer instead to calculate the reticulocyte index (aka reticulocyte production index), as you might using this MD Calc, you must first convert the reticulocyte count into a percentage of RBCs. Here is an example using the numbers from the case we discussed today:

Retic Count in Apex = # of retics x10^9/L = 204

RBC Count in Apex = # of RBCs x10^12/L = 3.69 ** notice the differences in exponents **

204 / 3690 = 5.5% = % of reticulocytes

Then you plug 5.5%, the patient’s hematocrit of 28.4% and a normal hematocrit of 42% into the MD Calc above, and arrive at an absolute reticulocyte count of 3.7 and a reticulocyte index of 2.5 – indicating an adequate reticulocyte response.

For those who want to know the math:

The Absolute Reticulocyte Count = % of retic * (Pts Hct / Normal Hct )

So for our patient: 5.5% * (28%/42%) = 3.7

Reticulocyte Index = Absolute Retic Ct / Maturation Factor

For our patient: 3.7 / 1.5 = 2.5

Maturation Factors:

  • Hct >35% : 1
  • 25-35% : 1.5
  • 20-25% : 2
  • Hct <20% : 2.5

A Retic Index > 2% suggests an adequate response, whereas <2% suggests hypoproliferation.


Treating Atrial Fibrillation in Sepsis

Here’s the observational study that I was alluding to in report that assessed practice patterns and outcomes associated with rate- and rhythm-targeted treatments for AF during sepsis.

The authors collected data on nearly 40,000 hospitalized patients who received IV therapy for atrial fibrillation during sepsis from hospitals across the United States. Striking findings from the study include the following:

  1. There was profound practice variation based on geographic location, hospital teaching status, physician specialty, and patient characteristics. A significant portion of the variation in choice of AF therapy (10%) was unexplained. Together, this suggests there is no “standard of care” for treatment of AF in sepsis.
  2. Among patients who received IV AF therapy, CCBs were the most frequently used initial medications, followed by BB, digoxin, and amiodarone.
  3. Using propensity score matching, the authors determined that hospital mortality was significantly lower for patients initially treated with BBs as compared to CCBs – there was no effect modification on this result by history of heart failure or presence of shock!



Morning Report 1/31/18 – Sinking Skull Flaps and Sweets!

Thank you, Chuka and Serge, for presenting mini-cases today! Chuka told us about an elderly woman admitted for a RLE DVT who had a recent subdural hematoma s/p craniotomy being treated with heparin bridge to warfarin who developed acute onset L sided weakness.

  • Sinking skull flap Syndrome AKA syndrome of the trephined is a rare complication after a large craniectomy, with a sunken skin above the bone defect with neurological symptoms such as severe headache, mental changes, focal deficits, or seizures. See more below.

Sinking Skull Flap Syndrome – Link to a clinical description with images in an article by Romero et al.

  • Principal symptoms: severe headache mental changes, focal deficits, or seizures
  • Treatment: primary goal is restoration of the pressure exerted by depression of craniectomy site
    • Cranioplasty is the principal surgical treatment that could improve the neurological deficits by decreasing local intracranial pressure and correcting abnormal CSF dynamics, but early restoration of the cranial flap is also associated with risk of infection
    • Conservative management with intrathecal saline infusion and Trendelenberg positioning is thought to be largely ineffective


Serge shared with us a case of a man with an acute onset of scattered, painful erythematous skin lesions found to have Sweet Syndrome.

  • Sweet syndrome is an acute febrile neutrophilic dermatosis. The clinical syndrome includes:
    • acute onset fever
    • leukocytosis
    • acute, tender, red plaques
    • papillary dermal infiltrate of neutrophils
  • Sweet Syndrome can occur as an idiopathic/primary condition or secondary to an underlying malignancy, infection, autoimmune disease, or medication effect. The malignancy most commonly seen is AML.
  • Treatment includes topical steroids and/or colchicine in addition to treatment of the underlying condition if one is found.

Sinking Skull Flap Syndrome Evernote:

Sweet Syndrome Evernote:

Morning Report 1/29/18 – Necrotizing Pneumonia

Thank you, Chuka, for presenting a case of a middle-aged man with sub-acute lightheadedness and dizziness found to be hypotensive with a significant leukocytosis and AKI found to have significant cavitary lung lesions, multiple PEs and moderate pneumothorax.

  1. Here’s a basic approach to cavitary lung lesions:

C = cancer – specifically bronchogenic carcinoma (most frequently SCC), cavitary pulmonary mets

A = autoimmune – granulomas – GPA, RA, sarcoid

V = vascular – both bland and septic pulmonary emboli with infarction

I = infection – primarily bacterial, fungal, pulmonary abscess, TB

necrotizing infxns: staph, anaerobic bacteria, mycobacteria, fungi (cocci, histo, blasto, aspergillus, crypto, mucor, PCP)

T = trauma – pneumatoceles

Y = youth – CPAM (congenital pulmonary airway malformation), pulmonary sequestration, bronchogenic cyst2

2.  Quick DDx for Shock:

Distributive: sepsis, anaphylaxis, vasopeglia (AI, neurogenic)

Cardiogenic: pump, rhythm, mechanical

Hypovolemic: hemorrhagic vs. volume depleted

Obstructive: PE, PTX, tamponade

3. Necrotizing pneumonia with pulmonary gangrene.

  • The options for treatment in patients with persistent sepsis and necrotizing pneumonia are limited. It’s important to ensure appropriate antimicrobial coverage (including assessing the MIC for any antibiotic you’re using!).
  • Chest tube drainage is often insufficient once a patient has progressed to pulmonary gangrene.
  • Unfortunately, there are no practice guidelines to direct the care of patients with necrotizing pneumonia, and determining if and when surgical intervention is needed is challenging.
  • Here is a case series of 5 patients with necrotizing pneumonia with pulmonary gangrene and here is a retrospective review of 35 patients who received pulmonary resection.

4.  Combined use of intrapleura tPT and DNase to improve fluid drainage in patients with pleural infections reduced the frequency of surgical referral and duration of hospital stay in the Mist 2 Trial.

Cavitary Lung Lesions Evernote: