Kocher Criteria for Septic Arthritis in Children:

Septic arthritis should be suspected in children that have a painful joint especially if they do not want to weight bear.  Orthopedics uses the Kocher Criteria to determine the probability of whether the joint is infected. 

Four elements make up the criteria:

• Erythrocyte Sedimentation Rate >40
• WBC > 12
• Non weight-bearing on the affected joint
• Fever.

If only one sign is present there is a 3% chance the child has a septic joint.

• 2/4 criteria = 40%
• 3/4 criteria = 93%
• 4/4 criteria = 99%

The true incidence of drug-induced seizure is very difficult to determine, however, a nice poison center study attempted to determine clinical factors associated with complications (potentially life-threatening) of drug-induced seizures. They found 3 predictors that demonstrated statistically significant associations:

1. Stimulant Exposure (i.e. cocaine, amphetamines etc)
2. Initial acidosis
3. Hyperglycemia (limitation they do not give incidence of DM)

They found a 60% complication rate in drug-induced seizures which is much higher than epileptic seizures. Makes sense since these patients are often sedated/altered or vomiting.

Stimulant Exposure is much more prominent in this population and has increased in mortality.

Interesting point with hyperglycemia, may be a novel marker for poor prognosis. Several studies have confirmed an association between hyperglycemia and increased neuronal injury and mortality in other settings like CVA and TBI.

Take home point - Drug-induced Seizure has a high complication rate in the ED. Watch for the 3 predictors as that may clue you in to the increased risk.

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• A persistent systolic blood pressure (BP) > 185 and/or a diastolic BP > 110, is a contraindication to thrombolytic therapy in acute ischemic stroke patients.

• In cases such as these, the following antihypertensive regimens may be used in order to attempt to proceed with administering thrombolytic therapy as soon as possible:

1. Nicardipine infusion 5 mg/hour; titrate up by 2.5 mg/h every 5 - 15 minutes as needed to a maximum of 15 mg/h; reduce to 3 mg/h once desired BP is reached,
2. Labetalol 10-20 mg IV over 1-2 minutes; may repeat once, OR
3. Other agents such as hydralazine or enalapril when appropriate.

• Note that these options are based on 2010 recommendations which no longer include the use of nitropaste, as was the case with the prior recommendations from 2007.

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AKI in the Critically Ill Cancer Patient

• Acute kidney injury (AKI) is common in the critically ill cancer patient and associated with worse outcomes.
• The incidence seems to be higher in patients with hematologic malignancies.
• Despite many different etiologies for AKI in cancer patients (tumor lysis syndrome, hypercalcemia, chemotherapeutic drugs, etc) the most common cause is sepsis, accounting for 58-65% of causes.
• Given the emphasis on early antibiotic administration in sepsis, be sure to double check the potential for nephrotoxicity of antibiotics for this patient population.  When possible, avoid nephrotoxic meds, such as aminoglycosides, that can worsen AKI.

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Question

13 y.o. with shoulder trauma (during basketball game). Arm held in adduction and exquisite scapular tenderness. Diagnosis?

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Proton pump inhibitors should be avoided in patients being treated with clopidogrel. PPIs appear to attenuate the effect of clopidogrel, and there's even some suggestion that the addition of PPIs to the medication regimen of patients taking clopidogrel may be associated with an increased risk of rehospitalization or death.

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Kienbock’s disease is a rare entity involving collapse of the lunate due to avascular necrosis and  vascular insufficiency.

Occurs most commonly in young adults aged 15 to 40 years.

Cause is unknown but believed to be due to remote trauma or repetitive microtrauma in at risk individuals.

Patients complain of wrist pain, stiffness and swelling

On exam, limited range of motion, decreased grip strength and passive dorsiflexion of the 3^rd digit produces pain.

Dx: plain film in the ED and with MRI as an outpatient.

Tx:  Wrist immobilization with splint and refer to orthopedics. Ultimate treatment is individualized and there is no clear consensus.

Lunate sclerosis seen on plain film

http://orthoinfo.aaos.org/figures/A00017F02.jpg

AVN of the lunate seen on MRI

http://www.assh.org/Public/HandConditions/PublishingImages/KeinbocksMRI_figure3.JPG

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If there is a single truth of pediatric emergency medicine, it is that kids love to stuff things into their noses.  A particular danger (aside from batteries, covered in a previous pearl) is the magnet.  

Specifically, two magnets (as seen with magnet ear and nose rings, frequently worn by children and teens whose pesky parents won't allow piercings), attracted across the nasal septum can cause necrosis and perforation within hours.

Here's how to save yourself (and some noses):

1.  Place a strong magnet such a mechanic's pocket magnet (<$10), or a pacer inhibition magnet within 1.5cm of the magnets.  Be careful not to apply pressure to the septum.
2. Watch for the opposite side magnet to fall out of the nose.
3. Easily remove the second magnet, which is no longer stuck to anything...you can use the strong magnet from step 1 at the nare opening to assist.
4. Though this method is generally non-traumatic, you should pre-treat the nares with 4% lidocaine and 1:1,000 epinephrine spray to minimize potential bleeding.

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Dehydration and subsequent prerenal acute kidney injury can result when temperatures begin to rise in the summer months.  As a result, medications with narrow therapeutic indices that are primarily renally excreted may accumulate.  Here are the specific ones to look out for:

• Digoxin
• Lithium
• Colchicine
• Phenobarbital and theophylline (partially eliminated unchanged by the kidneys)

• Visual fixation typically suppresses nystagmus caused by a peripheral lesion, but it does not usually suppress nystagmus from a central lesion. It may be therefore be helpful to manipulate a patient's visual fixation to determine whether their nystagmus is due to a central or peripheral lesion.
• Frenzel lenses (see attached picture) are large magnifiers that blur vision and inhibit visual fixation.  When a patient looks through this type of lens, one would expect peripheral nystagmus to increase, as visual fixation would be inhibited.
• If Frenzel lenses are not available, ask the patient to maintain their visual gaze on a single location to reproduce visual fixation.  Then note whether the nystagmus ceases (i.e. peripheral lesion) or continues (i.e. central lesion).

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• 1106081213_fresnel-lens.jpg (14 Kb)

Bleeding associated with uremia is a spectrum, from mild cases (e.g., bruising or prolonged bleeding from venipuncture) to life-threatening (e.g., GI or intracranial bleed). The exact pathologic mechanisms are not understood, but are likely multi-factorial (e.g., dysfunctional von Willebrand’s Factor (vWF) and factor VIII, increased NO, etc.)

Besides dialysis, treatments for uremic bleeding include:

1. DDAVP (fastest)
   1. 0.3-0.4 micrograms/kg IV or SC
   2. Increases vWF and factor VIII release
   3. Advantages: Begins < 1 hour
   4. Disadvantages: Tachyphylaxis; Stored factors deplete
2. Cryoprecipitate
   1. Replaces fibrinogen, vWF, and factor VIII
   2. Advantages: Works 1-4 hours
   3. Disadvantages: transfusion reactions, infections, pulmonary edema, etc.
3. Conjugated Estrogens
   1. Unclear mechanism; possibly increases ADP and thromboxane activity
   2. 0.6 mg/kg once daily x 5 days
   3. Advantages: Short and long-term effects
   4. Disadvantages: Hot flashes (males too!)
4. Recombinant Erythropoietin (slowest)
   1. 40-150 U/kg three times weekly
   2. Multiple mechanisms
   3. Advantages: Helps anemia (common in renal failure) as well as bleeding complications.
   4. Disadvantages: Up to 7 days to observe effects

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Question

A 20 year-old female presents with bilateral neck pain that occurred at rest. No other complaints. See if you can find the subtle clue on the x-ray...

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Prasugrel is a new thienopyridine alternative to clopidogrel and is now listed as an option in the 2011 ACC/AHA Non-STEMI ACS Guidelines. Studies comparing it versus clopidogrel show a slight benefit in terms of adverse cardiac events, but at the expense of a slight increase in bleeding complications. Though the guidelines state no preference between prasugrel vs. clopidogral for NSTEMI ACS patients, prasugrel is finding a role in patients who appear to have a genetic resistance to the effects of clopidogrel (unlikely you'll know this in the ED, but you'll start seeing more patients started on this medication in the outpatient setting).

Prasugrel is contraindicated in patients with a history of TIA or stroke and it should not be given before cath is performed (in contrast, some protocols push for clopidogrel as early as possible, even before cath).

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Pathophysiology: Angiotensin converting enzyme (ACE) catalyzes the conversion of angiotensin I to angiotensin II.  It also degrades bradykinin.  Thus, ACE inhibitors have the effects of decreasing angiotensin II and increasing bradykinin.  In the presence of ACE inhibition, bradykinin can accumulate and interact with vascular bradykinin B2 receptors, causing vasodilation, increased vascular permeability, increased c-GMP, and release of nitric oxide.

Treatment: Even though we generally treat with standard allergic reaction medications, none counteract the mechanism causing the problem.  Steroids, H1-blockers, and H2-blockers should still be considered but may not alter the progression.  Airway monitoring and management is paramount.

Certain medications can cause a certain dermatologic pattern. Many fall into a generic waste basket of "contact dermatitis" but here are some more characteristic findings and the drugs that can cause them:

Alopecia - anticoagulants, chemo, phenytoin, retinoids, selenium, thallium

Erythema multiforme - allopurinol, barbiturates, carbamazepine, cimetidine, some antibiotics

Toxic Epidermal Necrolysis (TEN) - allopurinol, bactrim (sulfonamides), mithramycin, PCN, sulfasalazine, nitrofurantoin, phenytoin, prazocin

• Distinction between central and peripheral vertigo can be made clinically by way of close physical examination of nystagmus.  The chart below describes specific findings for each:

• 	PERIPHERAL	CENTRAL
  Nystagmus
  Direction	Fast phase away from lesion; never reverses direction	Sometimes reverses direction if looking in direction of slow phase
  Type	Horizontal with torsional component, never purely torsional or vertical	Can be in any direction
  Other neurologic signs	Absent	Often present
  Postural instability	Unidirectional instability, walking preserved
  Effect of visual fixation	Suppressed	Not Suppressed
  Deafness or tinnitus	May be present	Absent

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Cardiovascular Complication of ESLD

• Patients with end-stage liver disease (ESLD) can develop a number of complications that lead to, or complicate, critical illness.
• Regarding the cardiovascular system, ESLD patients can develop:
  • Hyperdynamic vasodilated cardiovasculature: low baseline blood pressure and high cardiac output
  • "Cirrhotic cardiomyopathy": impaired systolic response to stress or altered diastolic relaxation
  • Autonomic dysfunction: reduced responsiveness to vasoconstrictors
• ESLD patients also tend to have a normal or near-normal lactate at baseline, despite lactate being cleared more slowly.
• When managing the critically ill patient with ESLD, look for signs of heart failure, expect an abnormal response to vasopressors, think about steroids for persistent shock, and don't ascribe an elevated lactate simply to impaired hepatic clearance.

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Question

13 y.o. female with ankle pain following fall down escalator. What's the diagnosis? (Hint: Look very closely)

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Therapeutic hypothermia in post-cardiac arrest patients with return of spontaneous circulation + coma (GCS < 8) is now well-accepted, and the current recommendations are for continued sedation of these patients. Consider avoiding the use of midazolam for sedation in these patients. Midazolam is metabolized more slowly in hypothermic patients, resulting in accumulation and the potential for longer ventilation and ICU time.

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Transient brachial plexopathies aka Burners and Stingers

Brachial plexus injuries are the most common peripheral nerve injuries seen in athletes.

49-65% of all college football players have experienced at least one burner with a 87% recurrence rate.

Injuries most commonly occur at C5-C6 but may involve any root level.

3 Mechanisms: Commonly due to

1) Traction caused by lateral flexion of the neck away from the involved side

2) Compression of the upper plexus between shoulder pads and scapula

3) Nerve compression caused by neck hyperextension and ipsilateral rotation.

CC: Burning or numbness in the neck, shoulder and/or arm

Symptoms are UNILATERAL and tend to usually  last seconds to minutes

Symptoms are reproduced by the Spurling maneuver.

Function gradually returns from the proximal muscle groups to the distal muscle groups.

Because most burners are self-limited, the most important goal is to rule out an unstable cervical injury.

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