Category Archives: Morning Report

Moffitt Morning Report: Low flow, low gradient severe aortic stenosis!

Happy Tues, Moffitt!

Thanks to Lily for presenting a very interesting case of a middle-aged woman with CAD, HFrEF, PAH, low-flow, low-gradient severe AS, mod MR/TR, and ESRD who was transferred from an OSH with cardiogenic shock. We talked about how to diagnose severe AS and also got an opportunity to learn about low-flow, low-gradient severe AS. See pearls below and awesome review article that Lily provided attached!

 TLC (Tim and Laura, your Chiefs)


Diagnostic criteria for degree of aortic stenosis

As we reviewed this morning, there are several diagnostic criteria for how to categorize aortic stenosis based on the flow gradient across the valve and the measured valve area on echo. I made a table to summarize our discussion:

  Mild AS Moderate AS Severe AS
Peak aortic velosity (m/s) 2.0-2.9 3.0-3.9 >4.0
Mean gradient (mmHg) <25 25-40 >40
Aortic valve area (cm2) >1.5 1.0-1.5 <1.0


  • KEY POINT: Severe AS = mean gradient >40mmHg and aortic valve area <1cm2.
  • Triad of symptoms of AS: Syncope, heart failure, angina
  • Significant risk factors for AS: Bicuspid aortic valve, rheumatic heart disease


What is low-flow, low-gradient  severe AS?

  • However, given that the gradients are a squared function of flow, even a modest decrease in flow may lead to an important reduction in gradient. These patients can have severe AS by valve area but may have normal gradients and normal AS as occurred in our patient this morning (remember her valve area was <1cm2 but her mean gradient was 25mmHg which falls into the moderate category above. In the literature, they call these patients “Low-flow, low-gradient (LF-LG) severe AS”).
  • Why does this happen? Typically, these patients have a dilated LV with markedly decreased LV systolic function, most often due to ischemic heart disease and/or to afterload mismatch
  • Sometimes for these patients it can be useful to re-calculate valve area and pressure gradients during exercise or during dobutamine stress test to see how valve areas and cardiac outputs change
  • Prognosis is usually poor (survival rate <50% at 3yr follow-up) if treated medically, but operative risk is high (6-33%) if treated surgically

Source: Pibarot, Philippe, and Jean G. Dumesnil. “Low-flow, low-gradient aortic stenosis with normal and depressed left ventricular ejection fraction.” Journal of the American College of Cardiology 60.19 (2012): 1845-1853.


Mt. Zion report 9/18/18: Erythema nodosum!?

Thanks Anne for presenting a middle aged lady with hypothyroidism and obesity presenting with tender subacute subcutaneous bilateral anterior shin nodules, possibly concerning for erythema nodosum!

Differential diagnosis for lower extremity skin nodules:

  • Panniculitis
    • Erythema nodosum = most common type of panniculitis!
  • Stasis dermatitis
  • Nodular pretibial myxedema
  • Varicose veins
  • Superficial thrombophlebitis
  • Dermatofibromas
  • Infectious etiologies – bacterial, fungal, mycobacterial
    • Most often ulcerate!
  • Malignancy – BCC, SCC, melanoma, metastatic disease, cutaneous lymphomas
    • Suspect cutaneous T cell lymphomas if no other identifiable cause, lesions persist for several months, lack of spontaneous involution, and lesions continue to progress
  • Vasculitis – cutaneous polyarteritis nodosa (usually accompanied by livedo & systemic symptoms), nodular vasculitis (seen with TB)
  • Lipodermatosclerosis (usually presents as skin induration but initial phase can have subcutaneous nodules)

Erythema Nodosum

  • Appearance:  erythematous painful lumps usually 1-6 cm in diameter
    • Almost ALWAYS on anterior shins but can spread to thighs
    • RARELY ulcerate or necrose
    • USUALLY resolve spontaneously within 2-8 weeks (can sometimes have “bruising” around the areas during healing process)erythema nodosum etiologies
  • Usually clinical diagnosis
    • Do good medication history
    • Consider CBC with diff, throat culture with ASO titer, CXR (for LAD concerning for sarcoid, lymphoma; signs of TB), PPD, ESR/CRP, +/- infectious workup depending on history and epidemiology, malignancy review to make sure up to date on age appropriate screening
  • If any doubts about diagnosis OR symptoms persistent OR lesions worsening, NEED biopsy with dermatology!



  • Blake et al. Erythema Nodosum: A review of an uncommon panniculitis. Dermatology Online Journal 2014; 20(4).
  • Chowaniec et al 2016. Erythema Nodosum – review of literature. Rheumatologica 2016; 54, 2: 79–82.



Mt. Zion Report 9/17: LBP in young person!

Happy Monday, y’all!

Today we talked about a young female with recent nephrolithiasis, severe depression and recent hospitalization, and family history of sarcoidosis presenting with progressive inflammatory lower back pain, ultimately found to have spondyloarthropathy. We discussed the features of inflammatory back pain, reviewed some exam maneuvers, and talked about ideal imaging modality for sacroilitis!

First off, check out this great diagram made by last year’s Ambulatory Chief extraordinaire Christy Soran:

Lower back pain

Remember the features of inflammatory back pain:

  1. Age of onset <40 years
  2. Gradual onset
  3. Improvement with exercise/activity
  4. No/minimal improvement with rest
  5. Pain at night
  6. Morning stiffness

Tips to distinguish SI joint pain from other areas of back pain?

  • Buttock pain (classically alternating between two sides but can be unilateral as well)
  • FABER maneuver: Flexion, ABduction, External Rotation (remember the “Figure 4”)
    • If pain: indicates SI joint disease
    • If limited ROM: indicates hip or iliopsoas disease
    • How good is this test? sensitivity=0.60-0.77, specificity=0.16-0.75
      • Can also be positive in labral tears!



Key locations of pain on exam:

location of pain

Extra-skeletal manifestations of spondyloarthropathy (AKA your ROS for every patient with inflammatory LBP!)

  • Anterior Uveitis (always ask about eye pain, photophobia, change in vision)
  • IBD (50% of patients with AS can have asymptomatic mucosal ulcerations; ask about diarrhea, weight changes, abdominal pain/cramping)
  • Psoriasis (ask about rash, nail changes, other joint involvement)
  • Recent infections (GI/GU infections)
  • Dactylitis/enthesitis (ask about other joint or tissue swelling)

Which imaging modality is best for spondyloarthropathy?

AP pelvis plain film is first line imaging – cost effective, sufficient for sacroilitis, and easy to order for comparison for disease progression!

What about SI joint xrays? NOT preferred as AP pelvis gives more information related to hip disease, pelvis enthesopathy and the pubic symphasis. In addition, AP pelvis is LESS radiation exposure than SI joint 3 view xrays.

Who needs MRI or HLAB27?

  • Consider MRI sacrum and HLAB27 if plain films negative but history/exam highly suspicious
  • Diagnosis of Ankylosing Spondylitis can be made from the following:
    • Sacroilitis on imaging + > 1 sign of spondyloarthropathy
    • HLAB27 antigen present + > 2 signs of spondyloarthropathy
(from UptoDate)

Complications of AS?

  • Osteopenia, osteoporosis
  • Cervical spine fracture/injury or spontaneous subluxation of the atlantoaxial joint (C1-C2) (similar to RA)
  • Cardiovascular disease
  • Pulmonary disease (restrictive lung disease)
  • Increased risk of nephrolithiasis (due to disordered calcium/vitamin D metabolism, also higher risk if history of IBD)

Other final pearls:

  • 30% of patients can have normal inflammatory markers (usually a better prognosis!)
  • Patients with nephrolithiasis and spondyloarthropathy should be evaluated for IBD
  • NSAIDs are mainstay of treatment (help with pain relief, maintain mobility, and can halt radiographic progression) – first line, can be used during flares or continuously.  TNFa inhibitors currently only used if symptomatic despite NSAID compliance or if NSAIDs contraindicated!

Evernote: Evernote for LBP & AS


Moffitt Morning Report: EBV-associated HLH!

Happy Monday, Moffitt!

Thank you to Dan Minter for presenting an awesome case of an elderly man who presented with weight loss and fevers, and was found to have liver injury in a cholestatic pattern, AKI, and pancytopenia. He was diagnosed with EBV, HLH (meeting all 8 criteria, see criteria below!), and ultimately thought to have NK cell leukemia. See the case report that Dan wrote up about this case here:! So many teaching points and thanks for the awesome participation from all!

 TLC (Tim and Laura, your Chiefs)


Cholestatic liver injury (elevated AlkP/GGT, Tbili)

Can break down into intrahepatic and extrahepatic causes


  • Primary sclerosing cholangitis (PSC)
  • Primary biliary cirrhosis (PBC)
  • Pregnancy: ICP
  • Medications (eg. antibiotics, contraceptives, TPN, anabolic steroids)
  • Infxn: Fungal, TB, echinococcocus


  • Gallstones
  • Malignancy
  • Primary Sclerosing cholangitis
  • Chronic pancreatitis
  • HIV cholangiopathy

To work up elevated LFTs in a cholestatic pattern:

  1. First check GGT to ensure biliary origin (elevated if biliary origin)
  2. Review medication list, stop possible offending meds
  3. Get a RUQ ultrasound
    1. If dilated ducts: Call hepatobiliary, consider MRCP/ERCP
    2. If normal ducts: Check anti-mitochondrial antibody (PBC) and consider liver biopsy to confirm dx if positive. Otherwise, consider broad work-up for other etiologies



  • In general, when all cell lines are down, the issue is likely in the bone marrow
  • Many causes, but one way to approach it is:
    • Aplastic (e.g. 2/2 viral infection, meds/toxins)
    • Infiltrative processes (e.g. infections, rheumatologic)
    • Fibrotic (e.g. myelofibrosis)


Short ddx for Ferritinemia

*of note, ferritin is an acute phase reactant so elevation is non-specific. But the higher it is (esp if >10K) the more you can think about this differential diagnosis).

  • Adult onset Still’s
  • HLH (hemophagocytic lymphohistiocytosis)
  • Disseminated histo
  • Lymphoma
  • Hemochromatosis


HLH (hemophagocytic lymphohistiocytosis) basics

  • Initial presentation: Often multiorgan involvement, cytopenias, hepatosplenomegaly with LFT abnormalities, neuro sxs
  • Pathophysiology: Disorder of excessive immune activation
  • Think about primary vs secondary HLH, and in adults always assume it’s secondary!
    • Primary HLH is often seen in kids and is related to an underlying genetic disorder
    • Secondary HLH: This is the case in almost all adult patients, so it is essential to look for the trigger! It is essentially an acquired disorder, with triggers including viral illness (esp EBV, CMV), lymphoma, as well as some rheumatologic disorders (most common association is juvenile idiopathic arthritis, but others as well). Always go hunting for the reason for HLH (eg. viral serologies, PET scan for lymphoma, BM biopsy) because affects treatment!
  • Diagnostic criteria (based on the HLH-2004 trial…): The patient must meet 5 of 8 of the below criteria!
  1. Fever >5
  2. Splenomegaly
  3. Cytopenias 9at least 2)
  4. Hypertriglyceridemia (fasting TG >265) and/or hypofibrinogenemia (<150)
  5. Hemophagocytosis in bone marrow, spleen, LN, o rliver
  6. Low or absent NK cell activity
  7. Ferritin >500 (though many people would say it needs to be higher)
    1. Elevated soluble CD25 (2 standard deviations above age-adjusted norm)
  • PEARL: As Rabih pointed out this morning, all relatively non-specific except very elevated ferritin, high TG, and low ESR can be helpful clues
  • Treatment:
    • High dose steroids + etoposide
      • PEARL: Typically as soon as you start steroids, fevers go away, as was the case here!
    • If EBV-induced, add rituximab. As Harry explained this morning, EBV assoc HLH can be particularly aggressive
    • If CMV-induced, add valgancyclovir
    • If +LP, add intrathecal treatment
  •  Prognosis:
    • Mortality is high without treatment
    • Poor prognostic signs: delayed diagnosis, neuro involvement, higher ferritin, slower rate of decline in ferritin, underlying malignancy

Moffitt Morning Report: Approach to headaches, prolactinoma!

Happy Friday, Moffitt!

Thank you to Max for presenting the case of a middle-aged man with headaches. MRI showed a pituitary adenomas. He was found to have a prolactinoma and started on cabergoline! We got a chance to review an approach to headaches, and then talked briefly about pituitary adenomas as well.

 TLC (Tim and Laura, your Chiefs) + JV (Jess Valente)


Approach to Headache

Today we reviewed the types of headaches, separating primary vs. secondary headaches:

Primary Headache

1. Tension headache (70%)

  • Symptoms: Tight band around head. Worse throughout day.
  • Treatment: Acetaminophen, NSAIDs, ASA. Amitriptyline can be helpful for prevention

2. Migraine headache (15%)

  • Symptoms:
    • POUND: Pulsatile quality, One day duration, Unilateral, Nausea/vomiting, Debilitating (if score 4-5 likelihood ratio of 24 in multiple studies)
    • 25% patients experience aura. Does not need to precede headache. Increased stroke risk if aura so avoid OCPs
  • Treatment:
    • Acute: Cochrane review 2013- 400mg ibuprofen 57% effective; 1000mg acetaminophen 39% effective; Excedrin Migraine (acetaminophen 250mg, ASA 240mg, caffeine 65mg), sumatriptan 100mg (careful if on SSRI, CAD or stroke)
    • Prophylaxis: If 4-15x per month or HA >12hr, if failing acute tx. Effectiveness only apparent after taking the med for 1-3 months. Propranolol (or other beta blocker), valproic acid, topiramate
    • Refer to neurologist: Pregnancy, known structural brain anomalies, chronic daily headache >15x per month, failure of multiple medications, consideration for devices (TENS) or hospitalization (IV dihydroergotamine (DHE))

3. Cluster headache (0.1%)

  • Symptoms: Trigeneminal autonomic cephalgias- usually middle-aged men with severe unilateral pain behind eye at night, tearing… weeks of symptoms then remission for months-years. Assoc with structural brain lesions, esp pituitary tumors à Get MRI initially
  • Treatment: Acute– Sumatriptan, high flow oxygen. Prophylaxis– verapamil

4. Medication overuse headache (aka rebound headache)

  • Drugs that can cause rebound headaches: Fioricet (butalbital, apap, caffeine), 2. Acetaminophen 3. NSAIDs 4. Caffeine 5. Ergotamine 6. Opioids 7. Triptans
  • Treatment: Withdraw medication– try reducing 10% every 1-2wk, can give naproxen 500mg BID to relieve residual pain

Secondary Headache

  • Systemic infxn
  • Head injury
  • Vascular d/o- AVM, dissection, giant cell arteritis, SAH, reversible cerebral vasoconstriction syndrome (RCVS) (1%)
  • Posterior reversible encephalopathy syndrome (PRES)- 2/2 malignant HTN, pre-eclampsia, drugs. MRI with posterior white matter edema
  • Intracranial hypotension / low CSF volume: Positional- post-LP, POTS, spontaneous. Tx: Epidural blood patching if CSF leak
  • Increased CSF pressure: Idiopathic intracranial HTN (psudotumor cerebri)- obese women Tx: acetazolamide or topiramate
  • Don’t miss diagnosis: Tumor (0.1%- rare but don’t want to miss!) Red flags– get imaging: SNOOPSystemic symptoms, Neuro signs, Onset sudden particularly >40yr, Oof- Precipiated by cough/lifting/sex (signs of increased ICP), Previous headache has changed in quality


1. What’s the h/a phenotype?

  • PQRSTs – Provocation/Palliation, Quality/Quantity, Region/Radiaiton, Severity & associated Sx, Timing
    • Provocation – assoc w/ stress, foods, posture, menstruation, lack of sleep?
    • Palliation – what meds tried, how often meds taken, what was response to tx
    • Region – UNIlat vs. BIlat
    • Radiation – from neck or jaw
    • associated Sx – n/v, photo/phonophobia, lacrimation/rhinorrhea, aura
    • Timing – Frequency (including # of h/a per month), duration, onset (gradual or thunderclap)
  • Age at onset, FHx of migraine
  • Changes in vision
  • Recent Trauma
  • Relationship with food/alcohol
  • Recent changes in sleep, exercise, weight, diet, in work or lifestyle
  • Change in meds
  • Association with environmental factors
  • Effects on menstrual cycle & exogenous hormones, or change in birth control

2. Is it old or new?

  • Old and recurring without changes is generally more reassuring
  • New or changing/worsening are more concerning, esp in older or immunocompromised patients

3. Is it a Primary h/a or Secondary? Red flags?

  • Is this a Primary h/a disorder? (ie. Tension, Migraine, Cluster, Trigeminal autonomic cephalgias)
  • Is this a Secondary h/a disorder? (Some key questions: any systemic sx?  Neuro sx (weakness, numbness, focal neuro sx)?  Pulsatile tinnitus?  Positional? Etc)

Physical Exam

  • BP & HR
  • Listen for bruit at neck, eyes & head (and signs of AVMs)
  • Palpate head, neck, and shoulder
  • Check temporal & neck arteries
  • Examine spine & neck muscles
  • Neuro Exam: Mental status, CN exam, funduscopic exam (!), reflexes, coordination, gait

Do I need imaging?

  • Indications for imaging:
    • Focal neuro signs or sx
    • Onset of h/a with exertion, cough, etc
    • Orbital bruit
    • onset of h/a after age 50yr
    • Recent significant change in pattern, frequency, severity of h/a
    • Progressive worsening of h/a despite appropriate tx
  • MRI is preferred(better to detect metastases, edema, vascular lesions, other intracranial pathology)
  • Get CT quickly if concerning for a Thunderclap Headache(ie. Subarachnoid hemorrhage)

BONUS: Also, from the Chief Blog archive I found this awesome Approach to Headache in the Primary Care Setting Evernote from Chris Sha!


Pituitary Adenoma

This patient was found to have a pituitary adenoma, which may cause mass effect, hormonal hypersecretion, or hyposecretion. Here is a quick review

1. Mass effect: Headache, visual changes (bitemporal hemianopia bc compression of optic chiasm)- don’t forget to get the visual field testing

2. Hormonal Hypersecretion: Excess hormones secreted by pituitary.

  • Prolactin: Prolactinoma- Galactorrhea, amenorrhea/infertility, early menopause
    • Dx: Elevated prolactin. Differential diagnosis for elevated prolactin also includes other causes, such as consider pregnancy, hypothyroidism, psych meds, verapamil, opiates, cocaine. JV’s pearl today: If is only mildly elevating, ask the patient to do a fasting prolactin and make sure they’re resting 15min prior.
    • Tx: OCPs or dopamine agnoists (bromocriptine/cabergoline), NOT surgery.
  • GH: Acromegaly: large tongue/hands/feet, cardiomegaly, thyromegaly, DM
    • Dx: 1. IGF1 elevated 2. Oral glucose suppression test- can’t suppress GH 3. Pituitary MRI
    • Tx: Transsphenoidal tumor resection, octreotide suppresses GH
  • TSH: Very rare, usually co-secrete TSH and prolactin or GH, cause hyperthyroidism
  • ACTH: Cushing disease (vs. Cushing syndrome with from exogenous steroids) Dx: Dexamethasone suppression- can suppress if central but ectopic sources of ACTH cannot be suppressed. Also do biopsy. Tx: Resection

3. Hypopituitarism: Fewer hormones secreted. Tumor, XRT, Sheehan sydndrome (pregnancy), pituitary apoplexy (macroadenoma bleeds) infiltrative (sarcoid, hemochromatosis), head trauma, cavernous sinus thrombosis. Hormones typically lost in this order:

  • LH/FSH: Infertility, amenorrhea, impotence Tx: Depends on fertility goals
  • GH: Fatigue, fasting hypoglycemia. Isolated GH deficiency rare- only eval if other hormones missing too.
  • TSH: Hypothyroidism Tx: Levothyroxine
  • ACTH: Fatigue, but NO hyperpigmentation/skin bronzing, hypoK, eosinophilia. Dx: ACTH stimulation.
    • Tx: Replace missing hormones, esp steroids/T4. If pituitary apoplexy- emergency! Stress dose steroids
    • Pan-hypo pit: Hydrocortisone, desmopressin, testosterone, somatripin (GH replacement), levothyroxine all needed

Moffitt Ambulatory Report: Acute mitral regurgitation in clinic!

Hope everyone has had a great week – better late than never pearls 🙂 At our Moffitt ambulatory report, we discussed a middle-aged man with mitral valve prolapse who presented to clinic with worsening chronic chest pain, palpitations and shortness of breath and was found to have mitral valve rupture which was later complicated by candida esophagitis, H pylori PUD, and GIB.

Mitral valve prolapse  

  • Types: Primary (sporadic, familial) versus Secondary (associated with connective tissue disorders like Marfans, Ehlers-Danlos)
  • Usually asymptomatic (discovered incidentally on clinical exam), but can present with symptoms of mitral regurgitation (complication of MVP) or MVP syndrome
    • Mitral valve prolapse syndrome: manifests with a variety of symptoms including palpitations, dyspnea, exercise tolerance, dizziness/syncope, anxiety, and chest pain.
    • Exam findings with MVP:  mid-systolic ejection click +/- murmur of mitral regurgitation
  • Monitoring:
    • Echocardiogram at diagnosis for further risk stratification
    • Interval echocardiogram depends on identification of mitral valve regurgitation (if none, can consider repeat TTE in 3-5 years or with change in symptoms)
  • Antibiotics before dental procedures NO LONGER recommended by ACC!

Mitral valve regurgitation

  • Monitoring:


TTE frequency

 *TTE should be performed with any change in symptom (dyspnea, reduced exercise tolerance, new onset atrial fibrillation!

Mild MR, no LV enlargement or dysfunction

Every 3-5 years

Moderate MR

Every 1-2 years

Severe MR

Every 6-12 months

  • Indications for surgery:
    • Symptoms!
    • Asymptomatic severe MR with reduced EF and/or enlarged LV size (LVESD ≥40 mm)
    • Undergoing cardiac surgery for other reasons
  • ACUTE mitral valve regurgitation/valve rupture:
    • Causes:
      • Mitral valve prolapse
      • Endocarditis
      • Rheumatic heart disease
      • Ischemia
      • Spontaneous leaflet rupture
    • Presentation:
      • Sudden onset respiratory distress 2/2 pulmonary edema (can be asymmetric!), hypotension, cardiogenic shock
      • Presentation is often LESS dramatic in patients with acute on chronic MR!!
        • Uptodate notes that these patients can present to clinic (like ours!) with increased SOB, fatigue, and weakness but not all the signs of heart failure!
        • Consider acute valve regurgitation in any patient with known valvular disease and pulmonary decompensation!
    • Management:

      • Tim reminded us of the exquisite sensitivity these patients have to high SVR –> our patient decompensated in the ambulance, likely due to elevated BPs from the stress of ambulance transfer!
      • Medical management involves respiratory stabilization with diuretics or intubation, improving cardiac output by decreasing severity of MR with IV nitroprusside.
      • Surgical management:
        • Nonischemic valve rupture –> mitral valve surgery
        • Acute MR from ischemia –> cardiac catheterization with cardiac support (intra-aortic balloon pumps can be used)
        • Ischemic papillary muscle rupture –> mitral valve surgery


  • It’s ok to send patients to the ED for high risk of clinical deterioration, need for expedited workup, and/or poor follow up/adherence to treatment plans
  • Take seriously when family members are worried about a patient. They often have a better sense of when the patient is really sick than anyone else!



Moffitt Pulm Report: Sweet Syndrome!

Thanks to Max for presenting a fascinating case of an elderly woman with a history of breast and bladder cancers and MDS who presented with cough, SOB and diffuse rash on the palms, chest, back and face, found on biopsy to have Sweet syndrome with an unknown cause of lung injury.

❤ TLC (Tim and Laura, your Chiefs)

Differential for diffuse GGO’s with consolidation:
• Bacterial (typical vs. atypical)
• Viral (would typically need to have bacterial superinfection to get dense consolidations)
• Fungal (would be atypical for endemic fungi to cause this – usually more nodular)
• Mycobacterial
• Strongyloides
• Pneumonitis
• Organizing pneumonia (paraneoplastic, autoimmune, drugs, inhalational, idiopathic)
• Malignancy
• Pulmonary edema
• Pulmonary hemorrhage (DAH)

  • Pearl: Do NOT need have hemoptysis. DAH is confirmed on BAL in patients with progressive anemia and lung infiltrates.

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. Some specific pearls:

  • Medication induced: Granulocyte-colony stimulating factor (G-CSF) is a common offender
  • Malignancy-associated: The malignancy most commonly seen is AML. In general, liquid onc > solid onc. Among solid tumors, GU, breast and GI are the most common.
    • In patients with previous histories of cancer, the development of Sweet syndrome may portend disease recurrence!

• Although extracutaneous manifestations of Sweet syndrome can happen (CNS, CV, liver), pulmonary Sweet syndrome is very rare. When it happens, it is usually in the form of neutrophilic alveolitis, pleural effusions or airway obstruction
Treatment of cutaneous Sweet Syndrome includes systemic and topical steroids and/or colchicine in addition to treatment of the underlying condition if one is found.