UMEM Educational Pearls

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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• Ischemic cerebellar strokes are often associated with posterior inferior cerebellar artery (PICA) insufficiencies.   
• Unlike vertebrobasilar strokes which typically present with vertigo accompanied by evidence of of brainstem ischemia like diplopia, dysarthria, dysphagia, and numbness, cerebellar strokes may present with isolated vertigo, making the diagnosis elusive given the challenging task of differentiating a central from peripheral process.  
• Central vertigo, particularly when due to cerebellar infarct, tends to be associated with severe gait instability, such that the patient often falls while walking, nystagmus which may be multi-directional or purely vertical, and deafness or tinnitus tend to be absent.
• Given that edema formation and mass effect are more likely to result from cerebellar infarcts as compared to other types of strokes, these patients are often best served in an intensive care setting for at least the first 24 hours following onset. 

• Necrotizing enterocolitis with predilection for cecum.
• Occurs in the immunosuppressed, especially when neutropenic (<500 PMNs)
• Typically a polymicrobial infection; gram positive cocci, gram negative rods, anaerobes, and/or fungal. 
• Classically, right lower quadrant pain but can present with diffuse abdominal pain and peritoneal signs.
• CT scan with IV and PO contrast is diagnostic (see below)
• Treatment:
  • Culture and begin broad spectrum antibiotics (cover anaerobes) and antifungals (if suspected) 
  • Aggressive resuscitation
  • Surgical consult for GI perforation or clinical deterioration
• High mortality (40-50%)

TIP: Suspect when abdominal pain presents 10-14 after chemotherapy (when PMNs are lowest).

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Question

50 yo female s/p motor vehicle crash. Diagnosis?

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Iliopsoas tendonitis and Iliopsoas Syndrome

• Iliopsoas tendonitis is inflammation of the iliopsoas muscle which can also affect the bursa lying under the iliopsoas muscle tendon.  
• Iliopsoas syndrome is a stretch, tear or complete rupture of the iliopsoas muscle and/or iliopsoas tendon.
• The iliopsoas muscle and tendon are commonly injured from acute trauma and/or overuse resulting from repetitive hip flexion.
• The pain may radiate down the anterior thigh to the knee.
• One variant is the internal snapping hip syndrome which results in an audible snap or click in the hip or groin with hip flexion.
• Treatment consists of rest, stretching exercises, physical therapy and NSAIDs.

The following list of medications have been associated with the development of Lupus Anticoagulants. Though it sounds like they should anticoagulate, they interfere with the Protein C system which means that they could induce a pro-thrombotic state - good short list to know:

Chlorpromazine (Thorazine

Procainamide (sorry Amal, I know you love that drug)

Hydralazine

Quinidine

Phenytoin

• Treating stroke patients older than age 80 with intravenous tissue plasminogen activator (IV-tPA) continues to be a controversial topic, primarily due to its perceived association with increased rates of intracranial hemorrhage (ICH).

• Reliable analysis of robust datasets from the Safe Implementation of Treatment in Stroke-International Stroke Thrombolysis Register (SITS-ISTR) has shown that, in fact, IV-tPA patients older than age 80:

             (1) do not have increased risk for clinically significant ICH,

             (2) have early clinical improvement similar to younger patients, and

             (3) have poor outcomes related to increased mortality (odds ratio 30% versus 12%), rather than

                   to higher rates of functional dependence (i.e. Modified Rankin Score 3 to 5). 

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Acute Liver Failure (ALF)

• ALF is defined as sudden and severe liver failure in a patient without preexisting liver disease.
• The clinical presentation can include altered mental status, coagulopathy, MODS, & cerebral edema.
• In the US, the most common cause of ALF is drug-induced (e.g. acetaminophen).
• Important components of the ED management of patients with ALF include:
  • Monitoring and correcting hypoglycemia (may need infusion of D20)
  • Monitoring and maintaining a normal sodium concentration
  • Volume resuscitation with isotonic crystalloids or colloids
  • Prophylactic administration of broad spectrum antibiotics (given high incidence of sepsis)
  • Consideration for continuous veno-venous hemodiafiltration (CVVHD) for severe elevations in ammonia and acidosis (even if renal function is normal)
  • Transfer to center capable of liver transplantation

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