Archive | January, 2016

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 ❤ 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.
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