strength in numbers: Pyelonephritis

3 Feb

some interesting stats, via a recent emdocs overview of pyelonephritis:


  • fever – present in up to 77% of patients
  • flank pain or CVA tenderness – 86%
  • elderly patients with NO fever – up to 33% (just to make our jobs difficult)



  • needs 10,000 colony forming units (CFU) per mm3 to confirm diagnosis
  • leukocyte esterase (LE):
    • sensitivity: 72% to 97%
    • specificity: 41% to 86%
  • nitrites:
    • sensitivity: 19% to 48%
    • specificity: 92% to 100%
  • Urine cultures positive in 90%


Patient with symptoms, but negative dipstick: what now?

“urine dipstick showed sensitivities as low as 75%, which is not acceptable if the patient has symptoms.”

also beware of pyelo mimics (e.g. pneumonia, PE, AAA, chronic pyelonephritis, PID, pelvic pain syndrome, prostatitis, diverticulitis, appendicitis, ovarian/testicular torsion, HZV, epidural abscess, and ectopic pregnancy)


Food for thought.


References: emdocs article; picture

Spinal Fractures in AS vs. DISH

14 Jan

submitted by Matthew Kongkatong, M.D.


Ankylosing spondylitis:

-Chronic inflammation of the spine causes progressive ossification of the paraspinous ligaments

-Prevalence 0.1%-1.4%



AS: “bamboo spine”, ossification of disc spaces


Diffuse Idiopathic Skeletal Hyperostosis (DISH):

-Non-inflammatory process of known etiology causes progressive ossification of paraspinous ligaments.

-Prevalence varies 2.9%-25%

-Associated with obesity, advanced age, and diabetes mellitus


DISH: “flowing candle wax”, preserved disc spaces


Spine fractures in DISH and AS

-Review article of 93 papers including 345 AS patients and 66 DISH patients

65% of AS and 69% of DISH patients sustained fractures via low energy mechanisms life falling from sitting or standing

Most (80% in AS and 60% in DISH) fractures were in the cervical spine and most were hyperextension type injuries.

-67% of AS and 40% of DISH patients had a neurologic deficit on presentation and 13% of AS and 15% of DISH patients had neurologic deterioration <3 months from presentation (compared to 0.08% in other population studies).

Most spine fractures are considered unstable because they extend into calcified ligaments and surrounding soft tissue, including into the intervertebral discs.

Calcified ligaments can transmit force and cause fractures in areas remote from the area of trauma.

References: Westerveld LA, Verlaan JJ, Oner FC: Spinal fractures in patients with ankylosing spinal disorders: a systematic review of the literature on treatment, neurological status and complications. Eur Spine J 2009, 18:145-156.;

orthostatics: useless?

8 Jan

came across this great video via LITFL: a quick talk 2410395945_a7240381d1by Anand Swaminathan, which looks at the (limited) evidence for orthostatics in the ED.

here’s the link (only 7-ish minutes, worth the watch):



orthostatics (change in vital signs with positional change) is different from symptomatic orthostasis (stand up, feel lightheaded)  –[personally, I care about the latter, not so much the former]

a large number of asymptomatic patients have orthostatics by numbers (~50%)

orthostatics in moderate blood/fluid loss ~25%-range sensitivities (pulse change)



orthostatic vital signs not particularly helpful

There you go.


References: LITFL post; picture



Lithium Toxicity

5 Jan

Submitted by Christina Brown, M.D.

QUICK PEARLS:lithium-300x225

Use – Mood stabilizing drug for bipolar disorder and depression.

Epidemiology – In 2010, there were 6307 cases of lithium intoxication reported to the American Association of Poison Control Centers [2,3].  A large proportion of patients on chronic lithium therapy experience at least one episode of toxicity during treatment [4].  

Pharmacodynamics – narrow therapeutic index. 

GI absorption: 

Therapeutic –

  • immediate release – Peaks at 1 to 2 hours s/p ingestion.
  • Sustained release – 2 to 4 hours s/p ingestion. 

Up to 12 hours or longer may be required before peak levels are reached in acute overdose [5,6].

Lithium is a small molecule (74 Daltons) with no protein or tissue binding and is therefore amenable to hemodialysis.  Renal excretion. 

Risk factors – GI losses, acute decompensated heart failure, cirrhosis, diuretics, NSAIDs or ACE inhibitors [7-9].   Elderly patients have a lower glomerular filtration rate and a reduced volume of distribution (d/t to reductions in lean body mass and total body water). 


Clinical Presentation

Acute – Nausea, vomiting, and diarrhea; late neurologic sequelae

Chronic  – Neurologic findings; sluggishness, ataxia, confusion, agitation, and/or neuromuscular excitability (tremors, myoclonus)

Severe – Seizures, non-convulsive status epilepticus, or encephalopathy


Diagnostic Evaluation

Normal [Lithium] – 0.8-1.2 mEq/L.  Concentration may not correlate w/ severity.

Labs – BMP, CBC, Acetaminophen, Salicylate





Hemodialysis  – Indications:

Lithium > 4 mEq/L; regardless of clinical status

Lithium > 2.5mEq/L + signs of significant lithium toxicity (eg, seizures, depressed mental status), has renal insufficiency or other conditions that limit lithium excretion, or suffers from an illness that would be exacerbated by aggressive IV fluid hydration (eg, heart failure) [1].


  2. Pauzé DK, Brooks DE. Lithium toxicity from an Internet dietary supplement. J Med Toxicol 2007; 3:61.
  3. Bronstein AC, Spyker DA, Cantilena LR Jr, et al. 2010 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 28th Annual Report. Clin Toxicol (Phila) 2011; 49:910.
  4. Amdisen A. Clinical features and management of lithium poisoning. Med Toxicol Adverse Drug Exp 1988; 3:18.
  5. Ward ME, Musa MN, Bailey L. Clinical pharmacokinetics of lithium. J Clin Pharmacol 1994; 34:280.
  6. Dupuis RE, Cooper AA, Rosamond LJ, Campbell-Bright S. Multiple delayed peak lithium concentrations following acute intoxication with an extended-release product. Ann Pharmacother 1996; 30:356.
  7. Jefferson JW, Kalin NH. Serum lithium levels and long-term diuretic use. JAMA 1979; 241:1134.
  8. Phelan KM, Mosholder AD, Lu S. Lithium interaction with the cyclooxygenase 2 inhibitors rofecoxib and celecoxib and other nonsteroidal anti-inflammatory drugs. J Clin Psychiatry 2003; 64:1328.
  9. Timmer RT, Sands JM. Lithium intoxication. J Am Soc Nephrol 1999; 10:666.
  10. Boton R, Gaviria M, Batlle DC. Prevalence, pathogenesis, and treatment of renal dysfunction associated with chronic lithium therapy. Am J Kidney Dis 1987; 10:329.
  11. picture

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



picture of the day: orbital compartment syndrome

18 Dec

via this EM Ireland talk on eye injuries:

hopefully, you’ll be able to see some signs clinically (e.g. proptosis, pain with EOM) if you’re worried about retro-orbital hematoma causing orbital compartment syndrome, but if you’re on the fence, you might see this on CT:



signs of orbital compartment syndrome on CT:

  • loss of contour of globe
  • tenting of the globe
  • proptosis


References: EM Ireland post

the “JR knot” for securing central lines

14 Dec

via last month’s Procedural Pause from Dr. James Roberts:

traditionally we’re taught to thread a stitch through the central line base piece as we take the bite.


tie your knot first, then thread through the central line piece and tie it down.

Step 1: suture a knot on your patient

jr suture 1

Step 2: thread it through the central line anchor piece

jr suture 2

Step 3: tie another knot.  it all comes together.

jr suture 3

Simple enough, logical, easy to do.


Add it to the toolbox.


References: procedural pause video



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