Septic Arthritis (quick review)

24 Nov

Risk Factors:

  • Age >80 years
  • Diabetes mellitus
  • Presence of prosthetic joint
  • Skin infection
  • Rheumatoid arthritis
  • Recent joint surgery
  • Intravenous drug abuse, alcoholism
  • Corticosteroid injection


Bacteremia is more likely to localize in a joint with preexisting arthritis, particularly if associated with synovitis.  Patients with RA may have additional predisposing factors, such as prior intraarticular steroid injections, maintenance immunosuppressive medications, and anti-tumor necrosis factor (TNF) therapy [1]. 


Mechanism:  Hematogenous spread to the joint.   Bacterial arthritis can also arise as a result of a bite or other trauma, direct inoculation of bacteria during joint surgery. 

Because synovial tissue has no limiting basement plate, bacterial organisms can quickly gain access to the synovial fluid, creating acute-onset joint inflammation with purulence. Following onset of infection, there is marked hyperplasia of the lining cells in the synovial membrane within seven days (1).


Differential Diagnosis

Reiter’s syndrome, pseudogout, GC arthritis, Lyme disease, RA, osteoarthritis, reactive arthritis


Clinical Manifestations:

A majority of patients with bacterial arthritis are febrile.  Older adult patients with septic arthritis are less likely to present with fever.  


Joint Aspiration:   Since this condition represents a closed abscess collection, the joint space should be drained. After initiation of treatment, serial synovial fluid analyses should reveal decrease inflammatory burden.


Synovial Fluid Profile

Greater > 2000 leukocytes/ml (5):

  • Traumatic Arthritis – < 5,000  (w/ RBCs) (5)
  • Reactive Arthritis – Recent genitourinary or gastrointestinal signs or symptoms, conjunctivitis, or skin or mucus membrane lesions (1).
  • Rheumatoid Arthritis – 10,000- 15,000 and 50 % polymorphs. Sterile incr protein, & decreased viscosity & decreased complement (5).
  • Toxic Synovitis – 15,000 and less than < 25 % polymorphs (5)

Greater > 50,000 leukocytes/ml (5):

  • Gout/Psuedogout – Synovial fluid analysis to r/in crystals (5).
  • Septic Arthritis – 80,000-200,000 and > 75% polymorphs (5).


ManagementOrthopaedics C/S and antimicrobial therapy

Antibiotic Therapy based on Synovial Fluid Analysis

If (+) GPC, treat w/ Vancomycin 30mg/kg q daily.

If (+) GNR, treat w/ Ceftriaxone 2g IV q daily. Duration of therapy:  Recommend IV x 14 days and transition to PO.

Complications – Cartilage degradation and inhibition of cartilage synthesis. Pressure necrosis from large synovial effusions may result in further cartilage and bone loss (1).


PrognosisInflammation and joint destruction may continue even in the setting of a sterile joint, despite effective antimicrobial therapy [1].


Submitted by Christina Brown, M.D.



  2. Mor A, Mitnick HJ, Greene JB, et al. Relapsing oligoarticular septic arthritis during etanercept treatment of rheumatoid arthritis. J Clin Rheumatol 2006; 12:87.
  1. Margaretten ME, Kohlwes J, Moore D, Bent S. Does this adult patient have septic arthritis? JAMA 2007; 297:1478.
  2. Goldenberg DL. Septic arthritis. Lancet 1998; 351:197.
  2. picture 1, picture 2

Spinal Shock

17 Nov

Definition – Spinal cord injury (SCI) that leads to loss of sympathetic tone below level of the injury.  Hypotension, bradycardia are key clinical signs s/p recent trauma.



  • Fracture of spinal element
  • Dislocation
  • Ligamentous Rupture
  • Disc herniation
  • GSW indirectly (Kinetic energy)


Clinical Signs/Symptoms

  • Paralysis
  • Anesthesia
  • Hypotension
  • Bradycardia (Unopposed Vagal activity).
  • Absent bowel and bladder control


Phases of spinal shock

Phase Time Physical exam finding Underlying physiological event
1 0–1d Areflexia/Hyporeflexia Loss of descending facilitation
2 1–3d Initial reflex return Denervation supersensitivity
3 1–4w Hyperreflexia (initial) Axon-supported synapse growth
4 1–12m Hyperreflexia, Spasticity Soma-supported synapse growth


Emergency Management

  • A/B: patient with a high cervical cord injury may breathe poorly and may require airway suction or intubation.
  • C: Hypotension may occur due to blood loss from other injuries or due to blood pooling in the extremities lacking sympathetic tone because of the disruption of the autonomic nervous system (neurogenic shock).
    • Vasopressors are usually required. Levophed has been used widely amongst patient’s with TSCI with hypotension and bradycardia. Phenylephrine is theoretically taught as 1st line treatment but studies recommend goal of MAP > 85 – 90 (4,5). 
    • Elevation of the legs, the head-dependent position, blood replacement, and/or vasoactive agents may be required (1).
  • Secondary: check for bladder distension by palpation or ultrasound. A urinary catheter should be inserted as soon as possible.


Further Management

  • Cardiovascular complications— Neurogenic shock refers to hypotension, usually with bradycardia, attributed to interruption of autonomic pathways in the spinal cord causing decreased vascular resistance. Patients with TSCI may also suffer from hemodynamic shock related to blood loss and other complications.
    • An adequate blood pressure is believed to be critical in maintaining adequate perfusion to the injured spinal cord and thereby limiting secondary ischemic injury (goal MAP > 85 – 90 mmHg).
  • Respiratory complications – Weakness of the diaphragm and chest wall muscles leads to impaired clearance of secretions, ineffective cough, atelectasis, and hypoventilation.

Glucocorticoids — Methylprednisolone is the only treatment that has been suggested in clinical trials to improve neurologic outcomes — however, the evidence is limited, and its use is debated.  Methylprednisolone is contraindicated in patients with moderate to severe traumatic brain injury.

Surgery — Goals for surgical intervention in TSCI include stabilization of the spine, as well as reduction of dislocations and decompression of neural elements.


Submitted by Christina Brown.



  2. Jia X, Kowalski RG, Sciubba DM, Geocadin RG. Critical care of traumatic spinal cord injury. J Intensive Care Med 2013; 28:12.
  3. Vale FL, Burns J, Jackson AB, Hadley MN. Combined medical and surgical treatment after acute spinal cord injury: results of a prospective pilot study to assess the merits of aggressive medical resuscitation and blood pressure management. J Neurosurg 1997; 87:239.
  4. Blood pressure management after acute spinal cord injury. Neurosurgery 2002; 50:S58.
  5. Levi L, Wolf A, Belzberg H. Hemodynamic parameters in patients with acute cervical cord trauma: description, intervention, and prediction of outcome. Neurosurgery 1993; 33:1007.
  6. Stevens RD, Bhardwaj A, Kirsch JR, Mirski MA. Critical care and perioperative management in traumatic spinal cord injury. J Neurosurg Anesthesiol 2003; 15:215.
  7. Breslin K, Agrawal D. The use of methylprednisolone in acute spinal cord injury: a review of the evidence, controversies, and recommendations. Pediatr Emerg Care 2012; 28:1238.
  8. Breslin K, Agrawal D. The use of methylprednisolone in acute spinal cord injury: a review of the evidence, controversies, and recommendations. Pediatr Emerg Care 2012; 28:1238.
  9. TABLE:

septic arthritis vs. transient synovitis in kids

3 Nov

repost of an old entry, but came up again recently, worth a review:

–lots of overlap in signs/symptoms
–one article came up with a decent decision rule

J Bone Joint Surg Am. 1999 Dec;81(12):1662-70.
–looked at 282 cases, excluded 114 atypical patients (e.g. immunocompromised), leaving 168
–38 had “true” septic arthritis
septic arthritis defined by positive culture or joint WBC >= 50,000 cells/mm3

–four things they decided on that might differentiate:

  • history of fever
  • non-weight-bearing
  • erythrocyte sedimentation rate (ESR) >= 40 mm/hr
  • serum WBC > 12,000 cells/mm3

–predicted probability of septic arthritis using these four predictors:

  • < 0.2 percent for zero predictors
  • 3.0 percent for one predictor
  • 40.0 percent for two predictors
  • 93.1 percent for three predictors
  • 99.6 percent for four predictors

–septic arthritis is bad, transient synovitis not so bad
–hard to tell sometimes, signs/symptoms are often similar
–useful: history of fever, non-weight bearing, ESR>40, WBC>12k
–if none of the above: unlikely septic arthritis
–more of the above: worry a bit more

Reference(s): kocher article, picture

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


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