UMEM Educational Pearls

• peak age of coin ingestion is 1-3 years, 60% being males
• CXR is recommended, and if in esophagus the flat surface of coin is seen on the AP view with the edge seen on the lateral view
• if in the stomach, expectant observation (3-4 days) in the absence of abdominal pain and vomiting
• 20% of coins will lodge in the esoophagus at the level of the cricopharyngeus muscle, aortic arch, and lower esophageal sphincter
• the change in composition of pennies from cooper to zinc in recent years has increased the potential for mucosal corrosion
• all coins lodged in the proximal esophagus should be removed endoscoopically as soon as possible
• coins in the mid- to lower esophagus may be observed for 12-24 hours if asymptomatic, but should undergo endoscopy if the coin fails to pass in that time period

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To feed of off Dr. Liferidge's last pearl - a few more points relevant to your Emergency Department practice:

• Lidocaine toxicity ranges between 5-7mg/kg
• Typical vial used for suture repair is 10cc of 1% lidocaine. 
• 1% = (1g/100cc) thus 100mg lidocaine in one vial
• 70 kg x 5mg/kg = 350 mg typical adult toxic dose (3+vials)
• 10 kg x 5mg/kg = 50 mg peds toxic dose (<1vial)
• Case reports of viscous lidocaine (4%) causing seizures. Very classically in pediatric cases. Cause is from oral transmucosal absorption, bypassing the large first pass effect if absorbed from the stomach.
• Classic symptoms are termed "feeling drunk" progressing to seizure. Shortly after CNS effect can have suppression of intrinsic pacemaker leading to sinus arrest, AV block, hypotension and death

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• Lidocaine toxicity typically manifests as central nervous system symptoms such as tongue numbness, tinnitus, visual disturbances, seizure, and cardiovascular depression.

• The maximum dose of lidocaine without epinephrine is 5 mg/kg (4.5 mg/kg, to be exact) and 7 mg/kg for lidocaine with epinephrine.  The total maxiumum dose is 300 mg.

Internal Jugular CVC Placement and Posterior Wall Penetration

• For a variety of reasons, many critically ill ED patients require central venous access.
• Ultrasound guidance, especially with catheters placed in the internal jugular (IJ), has become standard practice in many EDs.
• Ultrasound guidance is associated with higher success rates, reduced insertion attempts, and reduced placement failures.
• Importantly, ultrasound allows you to visualize the carotid artery which often either partially overlies or even sits direclty under the IJ.
• Recent literature, however, suggests that posterior wall penetration of the IJ, even with ultrasound guidance, may be much more common than previously thought.
• Take Home Point: Even when using ultrasound, maintain strict visualization of the needle in the IJ lumen and recognize that posterior wall penetration (into the carotid) can easily occur.

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Aortoenteric Fistula (AEF)-Beware the Upper GI Bleed!

Important points about AEF:

• Most of the time this is a complication of AAA repair (secondary fistula)
• Fistula site normally in the duodenum (the graft erodes into the duodenum)
• "Herald bleed" seen in 20-80% of patients (bleeding stops spontaneously then stops prior to massive hemorrhage)
• Diagnostic studies frequently waste too much time. As a rule of thumb, any unstable patient with a history of AAA repair who presents with a massive GI bleed should probably be taken to the OR for emergent laparotomy. Stable patients may need to get a CT scan and/or EGD (although EGD misses many of these)
• Failure to consider the diagnosis (and act) may lead to bad patient outcomes
• Have a low threshold to call a gastroenterologist AND a surgeon when this diagnosis is being entertained. If you are wrong and it isn't an AEF, no big deal. But if you are correct, you may have saved a life!

Pearl: Suspect a aortoenteric fistula in any patient with a prior AAA repair who presents with an upper GI bleed (may also be lower GI bleed)

The elderly are at tremendous risk of death after MI, in no small part because we tend to undertreat them. The 30-day mortality rate after MI in patients < 65 is 3%.

In patients 65-74, the 30-day mortality is 10%.

In patients 75-84, the 30-day mortality is 20%.

In patients > 85, the 30-day mortality is 30%.

Be vigilant and be aggressive with elderly patients. Their early management has a tremendous bearing on their later outcomes.

Postpartum Headaches:

• Occurs in up to 40% of woman during the first week after delivery.
• Though thoughts of Sheehan's syndrome (pituitary infarction), and SAH might come to mind the most common causes are due to migranes and tension headcaches.
• About 5% are spinal  (postdural) headaches due to a persistant CSF leak from spinal anesthesia or a complication of their epidural catheters.
• Rare causes include embolic stroke, carotid and vertebral artery dissections, SAH, Central Venous Sinus Thrombosis and Sheehan syndrome.

• Most headaches can be treated the same as any other person.
• Make sure you inquire about breast feeding and ensure the medications you are giving will not be excreted into the breast milk. 
• If your patient has signs of hypopituitarism an MRI scan will be needed to make the diagnosis of Sheehan syndrome.

• triad of chronic sinusitis, bronchiecctasis, and situs inversus
• recurrent acute otitis media and nasl polyps also common
• syndrome is due to an ultrastructural abnormality of the cilia in which dynein arms are absent resulting in ciliary dysfunction and mucus stasis and frequent sinopulmonary infections
• situs inversus is due to the absence of the influence of cilia function on viscera development
• diagnosed by bronchoscopy for cilia biopsy

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Ciguatera

• Heat resistant toxin found in fish, thus cooking doesn't protect you
• Found in over 400 species of fish but bioaccumulates in fish so predator tropical reef fish have higher concentration: grouper, barrucuda, snapper, parrotfish
• Found in tropical areas (See attached map for hot bed locations - in case you vacation there)
• Clinical Findings: Very neat hot-cold reversal where you place you hand in bucket of ice water and it feels like it is burning and visa versa, GI symptoms, paresthesias, ataxia and even hallucinations (very cool)
• Treatment: attempts with mannitol and gabapentin are reasonable and safe but completely unproven. Supportive care

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• During the emergency department management of all stroke patients, an NPO (nothing by mouth) status should be maintained until a formal swallow study can be performed to determine whether there is dysphagia.

• The best predictor of dysphagia (swallowing difficulty) in a stroke patient is the presence of dysarthria (motor speech abnormality).

• While the absence of a gag reflex, may suggest some degree of dysphagia, remember that about 10 to 15% of people lack a gag reflex.

Dexmedetomidine and the Critically Ill

• Dexmedetomidine is a newer sedative agent that is being used with increasing frequency in the critically ill
• A few pieces of information regarding dexmedetomidine:
  • highly selective alpha-2 agonist
  • produces dose-dependent sedation and anxiolysis while maintaining arousability at deep levels of sedation (hypercapnic arousal is preserved)
  • onset of action is approximately 15 minutes with peak concentration achieved in about 1 hour
  • metabolized via the liver
  • no known active or toxic metabolites
  • loading dose of 1 mcg/kg over 10 minutes followed by 0.2 - 0.7 mcg/kg/hr
• Primary side effect is bradycardia at excessive doses
• Cost is an issue when compared to propofol and midazolam

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Jones fracture

• Fracture of proximal metaphyseal 5th metatarsal
  • located w/in 1.5 cm distal to tuberosity of 5th metatarsal
• Prone to malunion
  • Watershed area (poor blood supply)
  • Under tension from multiple tendons
• Treatment
  • Immobilize with posterior-mold splint
  • Non-weight bearing - crutches
  • Prompt orthopedic evaluation
    • Some cases are managed with non-weight bearing casts
    • Others are repaired operatively.
    • Delayed jones fractures with malunion will require operative repair.
• Distinguish from pseudo-jones fracture (dancers fracture)
  • metatarsal styloid avulsion fracture, generally does not require operative repair
  • much more common than true Jones fracture.

Presented with persistant foot pain from
Jones fracture malunion.

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• results from failure of the upper femoral epiphysis, which allows displacement of the femoral head on the femoral neck
• onset may be sudden, but more often is gradual
• pain frequently is referred to the knee, but can also occur in the hip
• limp and out-toeing are common, with loss of medial hip rotation
• majority of patients are 7-15 years old, and are aboce the 95th percentile for weight
• AP or frog-leg lateral xrays of the hip are diagnostic

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• Dysarthria is a motor speech abnormality that commonly results from stroke and is related to focal muscular deficits in the face.

• One of the most challenging aspects of recognizing dysarthria relates to distinguishing it from apraxia. 

• Apraxia has nothing to do with a focal motor deficit, but rather a cortical deficit which results in an inability to optimally execute the function of the facial musculature.

• Isolated dysarthria without other neurologic deficit, termed pure dysarthria, is rare and thought to result from multiple lacunar infarcts causing hypoperfusion of the frontal cortex.

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Lorazepam Infusions

• There is some literature that propofol may be better for sedation in the mechanically ventilated patient, yet many emergency physicians still do not have access to the medication
• Lorazepam infusions are frequently used in many EDs for sedation of the mechanically ventilated patient
• Patients receiving continuous infusions of lorazepam are at risk for propylene glycol toxicity
• Propylene glycol toxicity primarily causes a metabolic acidosis and acute tubular necrosis
• Critically ill patients with renal or hepatic dysfunction are at increased risk of toxicity
• Monitoring propylene glycol levels are impractical
• Rather, check the osmol gap: a gap > 10 - 15 reflects significany propylene glycol accumulation
• Hemodialysis effectively removes propylene glycol

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Great case of bradycardia today in the ED-requiring transvenous pacemaker....cause?? K 7.6

Some bradycardia pearls:

• The dose of atropine is 0.5 mg IV. Can be repeated.
• Heart transplant patients will not respond to atropine as the transplant is denervated. Go right to pacing.
• Consider glucagon if suspected beta blocker toxicity....and be prepared...most patients vomit!
• DON"T FORGET THE K! A frequent cause of weird and insuspected bradycardia. I have had at least 3 cases of bradycardia (two requiring TV pacemaker insertion in the ED) due to hyperK in the last 3-4 weeks.
• Capture of the ventricle occurs when the complexes on the monitor become wide (assuming they weren't already wide)
• Search for the cause (MI, tox, metabolic, etc.)

A recent study from Mayo evaluated 238 patients with acute pericarditis and found that the "classic" features of acute pericarditis that we learned about are actually not as common as we think:

1. Only 50% of patients reported that their pain was positional and 70% reported that their pain was pleuritic. On the other hand, 12% reported pain that was typical anginal in nature.

2. Only 35-45% of patients reported a recent history of a viral illness.

3. Only 15-25% of patients had a friction rub.

4. Further complicating matters was the presence of positive troponin levels in 13% of the patients.

In this study, 17% of patients were sent for PCI because the treating physicians diagnosed the patients as having an acute MI. This study highlights the importance of maintaining pericarditis in the DDx of any patients with chest pain, even when it "sounds like an MI," and also maintaining vigilance for atypical features of pericarditis.

NG Tubes and Foleys:

Dovetailing off Dr. Hayes Lidocaine pearl on Thursday I thought we could provide an additional pearl on how to decrease pain with the insertion of Foleys and NG tubes.

Most providers use regular surgilube and coat the tip of the NG  tube and foley with it prior to inserting it.  Unfortunately this tends to only lubricate the first several centimeters of the passage you are trying to transverse, making the rest of the way a little uncomfortable.

Using a Uroget of viscious lidocaine allows you to actually inject the lubricant into the nares or urethral meatus.  This will provide better lubrication of the entire passage and also provide some anesthesia.

Even if you do not want to use lidocaine most foley kits come with a syringe full of surgilube that can be injected into the urethral meatus helping to lubricate the passage.

One of the options in our armamentarium prior to inserting an NG tube or performing a non-emergent nasotracheal intubation is nebulized lidocaine. However, the total dose is always a concern with this anesthetic agent before we have to worry about toxicity such as lightheadedness, tremors, hallucinations, seizures, and cardiac arrest. Here are some points to remember:

• Maximum IV dose is 3 mg/kg when used as an antiarryhthmic in ACLS.
• Maximum subcutaneous/intradermal dose is 4.5 mg/kg. When used in combination with epinephrine, this value is increased to 7 mg/kg.
• One study evaluated lidocaine plasma levels after nebulized administration and found that a dose of 400 mg (5.7 mg/kg in a 70 kg patient) produced a peak of 1.1 mcg/ml, far below the 5 mcg/ml level associated with toxicity.
• Application to real-life: Using 4% topical lidocaine in a 5-mL nebulizer will give a total dose of 200 mg. This is within the range of safe, studied doses, and will provide the anesthetic effect you (and the patient) desires.

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• While most typically only test and document that "cranial nerves II - XII are intact" when examining a patient, I would argue that cranial nerve I should also be tested in all head injury cases wherein there was significant facial/nasal trauma
• Direct blows to the face, by way of airbag deployment, dash board trauma, or assault, for example, can easily cause the ethmoid bone (see image below) to fracture leaving the olfactory nerve exposed to potential trauma as it crosses the cribiform plate.
• Shearing of this nerve can cause irreversible anosmia or hyposmia (inability or decreased ability to smell, respectively).
• The easiest, most effective way to test cranial nerve I is one nostril at a time (occlude the one not being tested), using items such as coffee, peppermint oil, or cloves.  More annoying smells like that of an alcohol prep or benzoin, can also be used and would likely be more readily accessible in an emergency department.