Archive | October, 2015

WBC – too high or too low?

23 Oct
WBC TOO HIGH (Hyperleukocytosis):
  • WBC > 50k (often >100k)
  • usually with AML or CML with blast crisis
  • symptoms usually pulm or neuro – due to white cells plugging microvasculature and/or tissue hypoxemia with cytokine damage
  • call oncology (need chemo or leukopheresis)
  • IV fluids
  • antibiotics
  • only chemo improves mortality
WBC TOO LOW (neutropenia):
  • fever is sometimes the earliest/only symptoms (due to muted inflamm response)
  • neutropenia = ANC < 1500 cells/uL
  • severe neutropenia = ANC < 500
ANC = WBC count X (%PMNs + %Bands)
  • IV antibiotics
  • IV Fluids
  • pan infectious workup (blood cx’s, urine, etc)


SLIGHT TANGENT, since we’re talking about low immune response…
10 second version:
absolute lymphocyte count = ALC 
ALC < 2500 (95% sensitive for CD4 <200)
ALC < 800 (91% specific for CD4 <200)
 There you go.  

4 T’s of life threatening post-partum hemorrhage

20 Oct
via the crashingpatient’s compilaton on some critical L&D emergencies:
Differential — 4 T’s:
TONE – uterine atony
TRAUMA – genital tract trauma
TISSUE – retained placental tissue
THROMBIN – coagulopathies
Treatment Options:
  • Empty the uterus: deliver fetus/placenta/retained products
  • Oxytocin / ergometrine / prostaglandin
  • Massage & bimanual compression of uterus
  • Repair genital tract injury
  • Uterine packing, blakemore or Rusch balloon
  • Compression of aorta
  • Surgical or IR: internal iliac or uterine artery ligation, hysterectomy, arterial embolisation

Lemierre’s Syndrome

15 Oct

What is it?  Lemierre’s Syndrome also known as postanginal septicemia refers to thrombophlebitis of the internal jugular vein.  See figure 1 below.


Figure 1:  Red arrow indicating infected thrombus of internal jugular vein.


Signs and Symptoms:  Lemierre’s Syndrome usually develops as a complication of a bacterial pharyngitis in young, healthy adults. Patients usually start with a sore throat, fever, and general body weakness. These are followed by swollen cervical lymph nodes, a tender or painful neck, with continued fevers. Sepsis and even septic shock can ensue. Karkos et. al did systematic review in 2009 looking at 84 studies/114 patients who had Lemierre’s syndrome . Table 1 shows the sources of infections.


Pathophysiology: Lemierre’s syndrome occurs most often when a bacterial throat infection, usually Fusobacterium necrophorum) progresses to the formation of a peritonsillar abscess. When the abscess wall ruptures internally, the drainage carrying bacteria seeps through the soft tissue and infects the nearby structures. Spread of infection to the nearby jugular vein leads to  inflammation surrounding the vein and compression of the vein may lead to clot formation.


Why is it so dangerous?  The infected thrombus of the internal jugular vein is a perfect gateway for the spread of bacteria through the bloodstream. Besides causing sepsis and septic shock, pieces of the infected clot break off leading to septic emboli of the pulmonary vasculature, where abscesses, nodules, cavitary lesions and pleural effusions develop.  Emboli can also affect the joints, muscles and soft tissues, liver, spleen, kidneys and brain.


Treatment:  Fusobacterium necrophorum is generally highly susceptible to beta-lactams, metronidazole, clindamycin and third generation cephalosporins. Additionally, a co-infection by another bacterium may co-exist. For these reasons is often advised not to use monotherapy in treating Lemierre’s syndrome.  The role of anticoagulation in treating Lemierre’s syndrome remains controversial.  Karkos et al. showed overall mortality to be 5%.


Submitted by Joran Sequeira, M.D.



  • Karkos et al. Lemierre’s Syndrome: a systematic review. August 2009. Laryngoscope, 119 (8): 1552-1559.
  • Syed et al. Lemierre syndrome: two cases and a review. September 2007. The Laryngoscope(The American Laryngological, Rhinological & Otological Society; Lippincott Williams & Wilkins). 117 (9): 1605–1610


concussion precautions: what do you tell your patients?

6 Oct


Some rapid-fire pearls to help you discuss the next steps with your concussion patients:


On the day of:

NO RETURN TO PLAY (or activities with the potential for contact/re-injury)


Next few days: 

  • limit activity and cognitive load (e.g. no video games, limit workload for students, etc)
  • limit meds (acetaminophen is ok), if possible


Overall graduated return to protocol recommendations (usually 24-hrs between stages):


  1. no activity
  2. light exercise (<70% maximal HR)
  3. sport-specific exercise (e.g. running/skating)
  4. non-contact training (e.g. passing drills)
  5. full-contact practice
  6. return to play


What it means:

  1. recovery time
  2. increasing HR
  3. adding movement
  4. coordination & cognitive load
  5. restore confidence and assess functional skills
  6. normal game play


If symptomatic at any stage, go back to the previous level, then try again in 24 hrs. 


References: emdocs article; Mccrory P, et al. “Consensus Statement on Concussion in Sport—the 4th International Conference on Concussion in Sport Held in Zurich, November 2012.” Clinical Journal of Sport Medicine 23.2 (2013): 89-117.; NATA position statement; picture