Tag Archives: Moffitt

Cardiology Report 5/31: Polymorphic VT and ECMO

Polymorphic VT (from this handy reference: PMID 24139193, http://www.sciencedirect.com/science/article/pii/S0146280613001138 )

  • Structural heart disease
    • Ischemia
    • Other non-ischemic causes
  • No structural heart disease
    • Channelopathies: long QT, short QT, Brugada and some other complicated EP diagnoses
    • Acquired
      • Electrolytes
      • Drugs (QT prolonging agents or dig)
      • Intracranial process
 

AM renal report pearls 5/27: renal disease and sarcoidosis!

Renal disease and sarcoidosis – a short list of ddx

  • Hypercalcemia-related are the most common! (remember, for sarcoid, the mechanism of hypercalcemia is from granulomas and elevated 1,25-OH vitamin D. Patients can get hypercalciuria without hypercalcemia!)
    • Nephrolithiasis
    • DI
  • Interstitial nephritis (note that chronic interstitial nephritis can have a bland UA! Need renal biopsy to diagnose!)
  • Glomerular disease
  • Isolated renal vasculitis
  • Nephrocalcinosis

 

Here is a nice paper on renal manifestations of sarcoid:  http://www.kidneyatlas.org/book4/adk4-08.pdf

renal sarcoid

Evernote: https://www.evernote.com/shard/s34/sh/8883f23e-0d68-43ae-891e-a9054122844f/9ba77dbf63da2f3173bd75ab5137e2db

Moffitt Oncology Report Pearls 5/25: Waldenstrom Macroglobulinemia

What is it? IgM monoclonal gammopathy and is categorized as a lymphoplasmacytic lymphoma (not quite like multiple myeloma that has clear plasmytic differentiation!)

 

Clinical features:

  • Cytopenias
  • Lymphadenopathy
  • Cryoglobulinemia
  • Hyperviscosity syndrome
  • End-organ dysfunction from tissue deposition (hepatosplenomegaly)

 

Diagnosis

  • IgM monoclonal gammopathy
  • >= 10% small lymphocytes with plasmacytoid differentiation
  • Immunophenotype (cell surface markers like CD138+ and others)
  • Can be hard to distinguish with other malignancies
    • Waldenstrom vs CLL: CD5 negative if Waldenstrom
    • Waldenstrom vs MM: CD56 negative if Waldenstrom

 

Treatment: the threshold to begin treatment is driven by symptoms and the exact regimen is patient specific based on tolerability considerations (drug side effects) and symptom profile: Bleeding concerns? How sick? Neuropathy?

  • If hyperviscosity syndrome, must start plasmapheresis!!
    • Rituximab can cause an IgM flare in 40-60% of patients and paradoxically worsen hyperviscosity initially!
    • Serum viscosity test >4-6 (normal range 1.4-1.8) is when you can expect hyperviscosity symptoms

AM cardiology report pearls 5/24: TAVR complications and digoxin toxicity

Indications for TAVR: severe AS and inoperable or high risk for operation. 30% of patients with severe AS meet indications for TAVR. (note, bicuspid valve is currently an indication)

 

Two types of TAVR valves:

  • Balloon expandable (Edwards valve) – the current generation of Edwards valves have a sleeve. This decreases the risk of aortic insufficiency but increases the risk of conduction abnormalities (10% of patients need a PPM!)
  • Self-expanding (Core valve)

 

Complications of TAVR: YY’s approach is to break this down into acute vs chronic complications, and under each category, think about complications of the access site vs the valve itself. The three main numbers to know are: <1% mortality, 2.5% risk of stroke, and 10% risk of heart block requiring PPM

  • Acute complications:
    • Access site
      • Bleeding
      • Perforation
    • Valve
      • Aortic root rupture
      • Valve embolization (LV, aorta)
      • Stroke (2.5% risk!)
      • Aortic insufficiency
      • Mitral stenosis
      • Ventricular perforation (1%)
    • Chronic complications
      • Access site
        • Infection
        • Bleeding
      • Valve
        • Heart block (10%)
        • LV dysfunction
        • Pericardial effusion
        • Infection

 

Digoxin toxicity:

  • Acutely, patients commonly p/w AMS, GI symptoms
  • Arrhythmias are the most dangerous toxicity – and patients can have virtually any type of arrhythmia! A few we discussed at report:
    • Regularized afib
    • Junctional rhythms
    • Alternating BBB
    • VT/VF
  • Digoxin levels NOT meaningful!
  • Give digibind if there are unstable/life-threatening arrhythmias

 

Evernote: https://www.evernote.com/shard/s34/sh/e49b8469-fa38-489d-a5ba-1720b65a8388/9f51cc630f6f9e8c0db445e40a3d4274

Moffitt Report 5/23: Chylothorax and Mucocutaneous Lupus

Two great cases today: one about chylothorax and one about mucocutaneous lupus which got us thinking about abdominal manifestations of lupus!

Chylothorax (TG >110mg/dL, usually exudative, can become lymphopenic and malnourished!)

  • Trauma
    • Surgical and procedural (including central lines)
    • Nonsurgical: penetrating or non-penetrating trauma to the neck/thorax/upper abdomen, but can even happen with vomiting, coughing
  • Non-traumatic: think about obstruction
    • Malignant neoplasm (most common!): lymphoma mostly, also primary lung, mediastinal tumors
    • Non-malignant: long list involving thing’s that can cause obstruction of the normal lymphatic flow (LAM, granulomatous infections, subclavian thrombus, SVC syndrome)

 

Abdominal manifestations of lupus

  • Intestinal pseudo-obstruction
  • Autoimmune hepatitis
  • Acute pancreatitis
  • Mesenteric vasculitis
  • Peritonitis (less common than pleural or pericardial involvement)
  • Protein losing enteropathy

Moffitt Report Pearls 5/18: Thalamic stroke and Hypothermia

Thalamic strokes (check out this paper that Leslie found)

  • 2.4% of ischemic strokes
  • Etiology: small artery disease with HTN as the main risk factor
  • Clinic signs/symptoms: many potential manifestations as the thalamus has many different functions. Exact presentation depends on what part of the thalamus is affected
    • sensorimotor deficits (weakness and numbness) without cortical signs (aphasia, agnosia, neglect, apraxis or hemianopsia)
      • g. hemisensory loss
    • gaze palsy
    • memory impairment/neuropsych
    • frontal-like syndrome
    • confusion/coma
  • Quick pearl anatomy pearl: this patient had bilateral thalamic strokes and there is a anatomic variant called the Artery of Percheron which results in a single dominant perforating artery to the thalamus

 

Hypothermia framework from Harry and UpToDate

  • Increased heat loss
    • Environmental exposure
    • Vasodilation: drugs, toxins, cirrhosis, sepsis
    • Skin disorders: burns, psoriasis
    • Iatrogenic (CRRT, cardiopulmonary bypass)
  • Decreased heat production
    • Endocrine: adrenal insufficiency, hypopit, hypothyroid
    • Neuromuscular inefficiency (e.g. impaired shivering)
    • Insufficient fuel: malnutrition, hypoglycemia
  • Impaired regulation (central): stroke, SAH, hypothalamic dysfunction, drugs

Cardiology Report 5/17: DAPT and Ventricular Tachycardia

Update 5/18: thanks to Tom Cascino for giving us another tip on localizing VT!

Take-home point: dual anti-platelet ACC/AHA guidelines changed as of 3/2016. The key points are:

  • Dual anti-platelet therapy is needed post-DES for a minimum for 6 months (used to be 12 months)
    • After this point, must individualize therapy based on risk of ischemia vs risk of bleeding. If the patient has high bleeding risk based on history, can stop at 6 months. If the patient had a high risk lesion and is at risk of cardiac ischemia, can extend therapy to 12 months
  • Elective non-cardiac surgery should be postponed post-DES for 6 months (used to be 12 months)

 

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 (thanks to UCSF med graduate Tom Cascino, a cardiology fellow at Michigan for pointing this one out!)

 

For more on the management of VT, check out Lekshmi’s old blog post for excellent info.