UMEM Educational Pearls

• second most common vasculitis of childhood
• leading cause of acquired heart disease in children
• usually in children <5years old
• year-round with clusters in spring and winter
• highest incidence in children of asian decent
• clinical diagnosis requires fever for at least 5 days and a minimum of 4 of the following:

1. bilateral conjunctival injection without exudate
2. rash (often macular, polymorphous with no vesicles, most prominent in perineum followed by desquamation
3. changes in the skin of the lips and oral cavity (red pharynx, dry fissured lips, strawberry tongue)
4. changes in the extremities (edema, redness of hands and feet followed by desquamation)
5. cervical lymphadenopathy

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• Idiopathic Intracranial Hypertension (IIH), previously known as Pseudotumor Cerebri, should be considered as a possible etiology of recurrent, often daily, headaches, particularly in obese, female patients.

• The pain is typically throbbing, sometimes unilateral, and severe.  In addition to headache, these patients often present with transient visual abnormality (72%), pulsatile tinnitus (60%), photopsia (seeing lights, flashes, colors) (54%), retrobulbar pain (44%), diplopia (38%), and sustained visual abnormality (26%).

• The most commonly encountered physical examination findings are (1) papilledema - the greater, the higher the risk for vision loss, (2) visual field loss (always check!), and (3) sixth cranial nerve palsy - due to increased pressure on this long-coursing intracranial nerve.

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Cancer patients admitted to ICUs with AKI or who develop AKI during their ICU stay have increased risk of morbidity and mortality. AKI in cancer patients is typically multi-factorial:

Causes indirectly related to malignancy

• Septic, cardiogenic, or hypovolemic shock (most common)

• Nephrotoxins:

  • Aminoglycosides

  • Contrast-induced nephropathy

  • Chemotherapy 

• Hemolytic-Uremic Syndrome

Causes directly related to malignancy

• Tumor-lysis syndrome

• Disseminated Intravascular Coagulation

• Obstruction of urinary tract by malignancy

• Multiple Myeloma of the kidney

• Hypercalcemia

Because AKI increases the already elevated morbidity and mortality in these patients, prevention (e.g., using low-osmolar IV contrast, avoiding nephrotoxins), early identification (e.g., strict attention to urine output and renal function), and aggressive treatment (e.g., early initiation of renal replacement therapy) is essential.

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There are several complications of acute aortic dissection that emergency physicians must be familiar with.

These include:

• Cardiac tamponade (most common cause of death)
• Acute aortic regurgitation
• Stroke
• Free intrathoracic rupture
• Malperfusion syndrome (kidney, spinal cord, bowel, extremity, etc.)

*Key Pearl: If a patient with suspected or confirmed acute aortic dissection suddenly arrests consider cardiac tamponade.

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Patients with Non-STE-ACS should not be given any NSAIDs aside from aspirin...that includes COX-2 agents. These medications in patients with acute or recent NSTE-ACS have been associated with an increased risk of hypertension, reinfarction, heart failure, myocardial rupture, and death.

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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).

Attachments

• 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