5/19/16 Aeromonas SBP – morning report

Teaching Pearls

  • Aeromonas is a Gram Negative Rod and is the third leading cause of SBP in Korea
  • It causes a warm season diarrheal disease
  • Remember the three indications for SBP prophylaxis:
    • History of SBP, lifelong prophylaxis
    • Cirrhosis with GI Bleed, 7 days of prophylaxis
    • Ascitic protein < 1, prophylax while inpatient
  • Don’t forget to give Albumin 1.5grams/kg on Day 1 and 1.0gram/kg on Day 3 for patients with SBP
  • Remember to think about secondary bacterial peritonitis (from intestinal perforation, PUD) in the differential for SBP
  • Check out this review on AeromonasSBP!

Morning Report 12/30/15

  • Cryptococcosis is treated with Flucytosine, Ambisome for 2 weeks of Induction, and the Fluconazole for maintenance
  • Include Bacillary angiomatosis on the differential for Kaposi’s Sarcoma
  • Fungal infections can be due to Yeasts, Molds, or Dimorphic Fungi
    • Yeast: Think Single Celled Organisms, Candida and Cryptococcus
    • Mold: Think Filamentous with Hyphae. Aspergillus,  Mucor
    • Dimorphic Fungi: Can be both yeast or molds depending on the Temperature. Includes Histo, blasto, cocci
  • We didn’t get to this today, but here is a framework for organizing anti-fungal medications!

5/18/16 AM Report – Calciphylaxis

  • Think about calciphylaxis in your ESRD patients with non-healing ulcers in areas of adiposity (abdomen, buttocks, thighs, legs)
  • Biopsy shows arterial calcifications without vasculitis
  • Often associated with elevated PTH levels and elevated calcium-phosphorous product, hypoalbuminemia
  • Check out this UCSF resident hand-out on calciphylaxis!
  • We had a great review of features of chronic venous stasis including lipodermatosclerosis (inverted champagne bottle), atrophie blanche, telangiectasias, ulcerations on the medial ankles.
  • See the table below for comparison/contrast of arterial versus venous ulcers
Venous Arterial
Pathophysiology Reflux and Venous stasis, faulty valves Atherosclerosis, embolic
Skin Findings Lipodermatosclerosis (inverted champagne bottle)

Atrophie Blanche

Telangiectasias

Hyperpigmentation

Warm

Hairless

Pale, Shiny, Taut

Cold

Ulcers Shallow, superficial, irregular borders Punched out, deep, full thickness wounds
Pain Less painful usually, improves with leg elevation Severe pain, improves with lowering legs
Ulcer Location Medial and lateral malleolar Above bony prominences, pressure points, base of heel

5/17/16 AM Report: Exudative Pleural Effusions

Teaching Pearls

  • Think TB and malignancy in the differential for lymphocytic exudative pleural effusions
  • Right sided unilateral exudative effusion in a foreigner/traveler – consider entameoba histolytica, echinococcus, paragonimus
  • Pleural Color
    • Pale Yellow –> Transudate
    • Red/Bloody –> Malignancy
    • White –> chylothorax
    • Brown –> long standing bloody effusion, amoebic liver rupture “anchovy paste”
    • Black –> fungal infections
    • yellow-green –> Rheumatoid pleurisy
  • Rheumatoid pleurisy and complicated parapneumonic effusions cause the lowest pleural glucose
  • The yield of pleural fluid culture is low, pleural biopsy yield for TB is ~90%

Monday 5/16/16 Pauci-Immune GN

  • Diffuse Alveolar Hemorrhage is caused by disruption of the alveolar-capillary basement membrane
    • Diagnosed via progressively more hemorrhage after saline lavage on BAL (see image below!)
    • Chest Xray in DAH is non-specific, there can be new patchy/diffuse opacities
    • 33% DON’T have hemoptysis
    • Classically, DAH presents as acute onset cough, dyspnea, and hemoptysis
    • Causes
      • 1)  Vasculitis (MPA, GPA, Churg-Strauss)
      • 2) Pulmonary Renal Syndromes: Goodpastures, IgA Nephropathy
      • 3) Autoimmune: SLE, APLS
      • 4) Meds:  Amiodarone, cocaine, nitrofurantoin, anticoagulants
  • Nephritic Syndromes: Rapidly progressive GN occurs among the nephritic syndromes (not nephrotic syndromes). The nephritic syndromes can be divided per the image below.
    • c-anca more associated with Wegener, mpa and churg strauss more associated with p-anca, but significant overlap
    • Wegeners a/w sinusitis and Churg-strauss associated with eosinophilia and asthma
    • Pauci-Immune GN is called that because there are no immune deposits seen on immunofluoroscopyDAH
    • GN

 

PNH 5/9/16

  • Check out this excellent AAFP review of Hemolytic Anemia!
  • Hemolytic anemias can be framed as Congenital and Acquired
    • Congenital: Sickle Cell, Thalassemia, G6PD, Spherocytosis
    • Acquired: PNH, MAHA, Infections, Immune.  Further categorization of Immune HA:
      • Autoimmune: Warm (ie SLE) or Cold (ie Mycoplasma)
      • Alloimmune (ABO incompatibility)
      • Drug-Induced: Many drugs but classically 3/4th general cephalosporins
  • Hemolysis labs include Reticulocyte Count, Indirect bilirubin levels, Haptoglobin, LDH, hemoglobinurea, hemosiderinuria (elevated Hb on urine dipstick is an indicator of intravascular rather than extravascular hemolysis)
  •  PNH median age of onset is 30, life expectancy prior to Eculuzimab (see below) was about 10-15 years after diagnosis although this new drug may prolong life expectancy but it’s too early to know
  • Acute hemolytic events can occur after stress, infections, alcohol use
  • PNH is associated with venous and/or arterial thrombosis (venous more common) likely due to the hypercoagulable state from free hemoglobin in the bloodstream. The thrombi form in unusual areas – cerebral veins and abdominal veins.
  • Other clinical findings associated with PNH are cytopenias, smooth muscle dystonias (due to lack of NO, erectile dysfunction/dysphagia/abdominal pain)
  • Nocturnal hemolysis is thought to be due to intestinal absorption of LPS, a complement activator, at night
  • The pathophysiology of PNH is an acquired mutation causing lack of formation of phosphatidyllinositol (PGI) anchor on RBCS which present the CD59 and CD55 epitopes. Flow cytometry in PNH shows a lack of CD59 and CD55 cells. The lack of these markers causes the cells to be vulnerable to complement mediated lysis.
  • Eculuzimab blocks complement C5 thereby blocking destruction of RBCs. Patients on this medication are at risk for infections due to encapsulated organisms (ie Strep Pneumo, Neisseria meningitidis, Haemophilus influenza etc). Note this drug is 10,000 bucks a pop (infusion every 2 weeks)!

Morning Report CML 5/2/16

  • The natural history of Chronic Myeloid Leukemia is the chronic phase, accelerated phase, and the blast phase.
    • Chronic Phase: This is generally stable, chronic disease and patients can be asymptomatic. Often they are picked up on routine blood count showing leukocytosis. There is a 6% 5 year risk of progressing to blast phase when they are treated with Imatinib.
    • Accelerated Phase: This is when blasts are detected but they haven’t reached a high level of > 20%.
    • Blast Phase: This is conversion of CML to acute leukemia with > 20% blasts on peripheral smear or bone marrow. About 70% present with AML blast crisis and roughly 30% with ALL blast crisis. Treatment depends on whether flow cytometry/analysis shows AML or ALL.
  • Imatinib (Gleevec) is a first generation tyrosine kinase inhibitor. It is used for patients with chronic CML to help prevent progression to blast phase. Side effects include pulmonary edema, peripheral edema, muscle cramps, QTC prolongation, arrhythmias, among others.
  • Leukostasis which is defined as hyperleukocytosis (>50K WBC) with symptoms including CNS, respiratory, and cardiac. There are various thresholds for initiating leukapharesis depending on the type of leukemia, presence of symptoms, and level of WBC elevation. In general, AML is more likely than ALL to cause leukostasis. The acute leukemia’s are more likely to cause leukostasis than the chronic leukemias.
  • Leukopharesis can have serious side effects so only used when absolutely necessary.
  • Hydroxyurea blocks DNA synthesis and can be use in myeloproliferative disorders and CML. Of note also used in sickle cell disease as it increased Fetal Hemoglobin levels.
  • Clinical Pearl: ALL is more likely than AML to present with tumor lysis syndrome.