Tag Archives: id

Vertebral Osteomyelitis/Discitis

23 Dec

submitted by Amit Kumar, M.D.


3 main mechanisms of infection:

  • Hematogenous spread
  • direct inoculation (trauma, spinal surgeries/procedures)
  • contiguous spread from adjacent tissues



  • Staph aureus (>50%)
  • enteric gram-neg bacilli (following GU procedures)
  • psuedomonas/candida (often due to IV sepsis or IVDU)
  • group B strep (esp. in diabetics)

Signs & symptoms:

  • Localized spinal pain
  • leukocytosis
  • elevated ESR/CRP
  • fever
  • new radicular symptoms

Diagnostic strategies: Blood culture, MRI (most sensitive radiologic technique), biopsy (open/CT guided)

Differentials: Spinal epidural abscess, psoas abscess, herniated disc, spinal metastasis, vertebral compression fracture

Treatment: Pain control, ANTIBIOTICS (empiric followed by pathogen-directed. Routinely for minimum of 6 weeks), surgery (indications: neuro deficits, abscess needing drainage, cord compression)


  • Posterior extension leading to epidural/subdural abscess or meningitis.
  • Anterolateral extension leading to paravertebral/psoas abscess.

***Picture: High signal is T2-weighted MRI at the disc and adjacent vertebral body compatible with diagnosis





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.



  1. http://www.uptodate.com/contents/septic-arthritis-inadults?source=search_result&search=septic+joint&selectedTitle=1~150
  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.
  1. http://www.wheelessonline.com/ortho/septic_arthritis
  2. picture 1, picture 2

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


Useful Tool: Necrotizing fasciitis score

6 Jul

the LRINEC = laboratory risk indicator for necrotizing fasciitis


-the score is based off of a retrospective observational study comparing laboratory results of patients with confirmed necrotizing fasciitis and those with severe cellulitis or abscess


-six criteria: CRP, WBC, hemoglobin, sodium, creatinine, glucose


-each of the criteria are weighted with a point value


-values totaling a LRINEC score >6 had a sensitivity of 90% and specificity of 95%; PPV 92% and NPV 95%


-useful tool? Sure. But also keep in mind this cut-off still missed 10% of patients with necrotizing fasciitis


-Summary: a LRINEC score > 6 could be used as a potential tool to rule in necrotizing fasciitis, but a score <6 should not be used to rule out the diagnosis



Wong CH, Khin LW, Heng KS, Tan KC, Low CO. The LRINEC (laboratory risk indicator for necrotizing fasciitis) score: a tool for distinguishing necrotizing fasciitis from other soft tissue infections. Crit Care Med. 2004 Jul; 32 (7):1535-41. PubMed PMID: 15241098.; MDCalc site; picture


Submitted by K Estes



visual aid: soft-tissue ultrasound

7 May

(apologies for the layoff between posts; busy time lately, but should be back into a rhythm)

some nice images via this April E-Med Journal article (for when you next need to determine if there’s something there to I & D):

Arrows (top to bottom) indicate: epidermis, subcutaneous tissue, muscle, bone


to help differentiate the sometimes difficult to distinguish (left to right): cellulitis, abscess, lymph node


References: emed journal article + pictures

strength in numbers: meningitis

7 Apr

just to keep you honest (highlights via this EMdocs article)

“classic triad” (fever, altered mental status, stiff neck)

  • 95% had fever,
  • 88% had neck stiffness,
  • 78% had altered mental status.
  • only 44% of patients with meningitis had all three 


Neck pain: 28% sensitivity

headache: 50% sensitivity


avoid minimizing afebrile patients, especially in the elderly population: as many as 18% of these patients with meningeal infection may be afebrile

Kernig and Brudzinski signs

  • 95% specificity
  • sensitivity is as low as 5%.


“jolt test” (headache accentuated by horizontal rotation of the head at a frequency of two to three times per second)

  •  sensitivities ranging from 97% to 21%


opening pressure: as many as 9% are less than 14 cm/H20


their conclusion: “Ultimately, outside of a positive CSF culture, no one test or exam should rule in or out the diagnosis of meningitis
References: emdocs article; picture

Kanavel signs for flexor tenosynovitis

12 Mar

(some via an old post, but came up recently, and was the most basic evidence found on a pubmed biopsy.  if anyone knows of any larger data/studies, please share in the comments section)

Kanavel signs for flexor tenosynovitis

  • pain on passive extension (early finding)
  • finger held in flexion
  • uniform swelling of finger
  • tenderness to percussion along flexor tendon sheath (late finding)

incidence of H&P findings in 75 patients with flexor tenosynovitis

  • fusiform swelling (97%)
  • pain on passive extension (72%)
  • semiflexed posture (69%)
  • subcutaneous purulence (68%)
  • tenderness along flexor sheath (64%)
  • elevated WBC (59%)
  • diabetes mellitus (35%)
  • skin necrosis (23%)
  • fever (17%)


overall, the 4 signs aren’t perfect, but are there individually in at least 2/3rds of patients

one study of 41 patients with flexor tenosynovitis:

  • all patients had tenderness along the flexor tendon sheath and pain with passive extension.
  • only 22/41 patients (54%) had all four Kanavel signs


IV antibiotics: staph and strep coverage, think pasturella for bite-associated infections

–surgery: consult your hand surgeon ASAP

Kanavel signs for flexor tenosynovitis (REVISITED)

  • pain on passive extension (early finding)
  • finger held in flexion
  • uniform swelling of finger
  • tenderness to percussion along flexor tendon sheath (late finding)

Reference(s): uptodate.com: infectious tenosynovitis; study; picture.; article