ZSFG AM Report Pearls 3/1/18: Ain’t No Platelet High Enough: Thrombocytosis DDx, Complications, and Treatment

Thank you to the ZSFG team for presenting a great case of a patient with a gluteal abscess who presented with a significant neutrophilic leukocytosis and extreme thrombocytosis. We reviewed the differential, complications, and treatment of thrombocytosis.


Pearls on Etiology:
  • Degree of elevation does not help distinguish reactive (aka seconday) thrombocytosis from primary thrombocytosis
    • One study demonstrated that 82% of pts with plts >1 million were reactive
  • There are presently no diagnostic findings that can definitively distinguish between clonal and secondary (reactive) thrombocytosis.
Differential Diagnosis for Thrombocytosis:
  • Reactive Thrombocytosis (Secondary)
    • Most common
    • Secondary process from surgery, infection, cancer, chronic inflammation
    • Note that occult malignancy could cause this and is difficult to diagnose
  • Familial Thrombocytosis (Familial/Congenital)
    • Rare cases of autosomal dominant disorder, gain of function mutations in thrombopoietin gene
    • However, now recognized as a genetically heterogeneous disorder
  • Clonal Thrombocytosis (Primary)
    • Chronic myeloproliferative disorder
      • Essential thrombocytosis
      • Polycythemia vera
      • May occur in other myeloproliferative disorder but ET and PV are most common (for example, prefibrotic myelofibrosis which can evolve into overt myelofibrosis)
Clinical Complications from Thrombocytosis:
Clonal Thrombocytosis
Secondary (Reactive) Thrombocytosis
Underlying systemic disease
Often clinically apparent
Digital or cerebrovascular ischemia
Large vessel arterial or venous thrombosis
Increased risk
Bleeding complications
Increased risk
Yes, in about 40% of pts
Peripheral blood smear
Giant platelets
Normal platelets
Platelet function
May be abnormal
Bone marrow megakarylocytes (Number)
Morphologic Features
Giant, dysplastic forms w/ increased ploidy, assoc w/ large masses of platelet debrid
Treatment Algorithm:



Source: Schafer, AI. (2004). Thrombocytosis. NEJM. 350:1211-9.

Evernote: https://www.evernote.com/shard/s509/sh/5fd9cf19-9708-443f-b65c-fc0400c5c298/683c51013b18898fc7554eb5694aca17

ZSFG AM Report Pearls 2/27/2018: I Don’t Know Much About Algebra, But I Know 1 + 1 = 2: Adding Rifampin to Vancomycin in MRSA Infections

Thank you to our Jackie, Laura, and Lisa for presenting a case of a patient with septic arhthritis and endocarditis. In addition to reviewing a checklist for Staph aureus bacteremia, we dove into the indications for adding Rifampin to Vancomycin for MRSA infections.


Staph Aureus Bacteremia

~50-60% of staph aureus = MRSA
-Blood cultures
-If positive, repeat, if positive, repeat, if positive repeat
-No need to repeat if cultures are still cooking
-Assess lines/hardware other access sites
Obligatory Studies:
1) TTE
2) If LBP, must get MRI (abcess)
-Vancomycin 15mg/kg q12 hours if renal function (call pharmacy for help)
    -Goal trough ~15
-Follow-up on sensitivities and narrow if MSSA
-Follow-up on troughs and make sure your dosing is appropriate
Duration of Tx:
-14 days no matter what (well, negative ECHO, quickly clear cultures)
-4 weeks (if longer time to clear, i.e. >1st f/u set)
-6 weeks (endocarditis, osteomyelitis)
When to Use Vancomycin + Rifampin in MRSA Infections:
  1. Hardware infection
  2. Spinal infection/Osteomyelitis (B-III Recommendation)
  3. Prosthetic valve
  4. MRSA Meningitis
  5. Extensive or ongoing metastatic disease


Evernote: https://www.evernote.com/shard/s509/sh/56aee00b-3055-42ff-8db1-a703483ef41b/d63ff43b419a88961caeb2d326d63a64

Source: Liu C et al. (2011). Clinical practice guidelines by the infectious diseases society of America for the treatment of methicillin-resistant Staphylococcus aureus infections in adults and children. Clinical Infectious Diseases. 52:e18-55.

ZSFG AM Report Pearls 2/15/2018: Rock You Like A Hurricane – “Secondary Gout” from Lymphoma

Thank to Harry Han for presenting a really interesting case in AM report of a young man with a history of gout who developed pancreatitis and was then found to have a small bowel lymphoma. This case raised many questions but one interesting question was whether the gout in a young man was a canary in the coal mine for the lymphoma….?


Secondary Gout Associated with Myeloproliferative Disorders


  • Gout is caused by hyperuricemia
  • Myeloproliferative disorders can lead to an overproduction of urate from an excessive cell turnover
  • Has been described in polycythemia vera and other myeloproliferative disorders


  • Often the serum urate level is higher than primary gout
  • Multiple joints tend to be involved in secondary compared to primary
  • Possibly more likely to have more extensive tophi and nephrolithiasis compared to primary gout (based on small case series)Secondary Gout


  • Treatment of underlying myeloproliferative disorder
  • Urate lowering therapies just like primary gout!



  • Emmerson, BT. (1996). The management of gout. NEJM. 334:445-451
  • Yu, T. (2005). Secondary gout associated with myeloproliferative diseases. Arthritis & Rheumatism. 8(4):765-771.

Evernote: https://www.evernote.com/shard/s509/sh/11eaa988-d88a-4fb4-a4fb-64e639c13140/5b2b6003ddf15ad597a92bccea1107de