There has been some controversy regarding the actual clinical benefit of non-invasive ventilation (NIV) for patients with cardiogenic pulmonary edema in recent years. However a recent Cochrane review has confirmed the benefit of NIV for these patients. Early (ED) use of NIV is associated with a decrease in both intubation rates and mortality. The NNT to prevent one intubation is 8, and the NNT to prevent one hospital mortality is 13. To put this in perspective, the NNT for NIV to prevent death in patients with cardiogenic pulmonary edema is lower than the NNT for thrombolytics to prevent death in acute MI.

One key point to remember is that it MUST be used early! If you wait until your patient is decompensating, it is often too late. Start the NIV as soon as possible in these patients.

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Emergency physicians are often called upon to provide event coverage for marathons.

Prolonged endurance racing is safe for the majority of participants.

Hyponatremia (8.2% - 13.5%)  - finishing times of greater than 4 hours is an independent risk factor

Hypokalemia – uncommon

Renal function – BUN > 30 or Cr > 1.4 mg/dL (23.6%). There is no data that this is of any clinical significance.

Cardiac Troponin - (11%) had significant increases (troponin T > or = 0.075 ng/mL or  troponin I > or = 0.5 ng/mL). Elevations were more commonly seen with weight loss and increased Cr levels and may be associated with running inexperience (< 5 previous marathons) and young age (< 30 years) though interestingly not with race duration or traditional cardiac risk factors.

Findings are similar for men and women

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• occurs when the small opening in the abdominal muscles which allows passage of umbilical cord does not completley close after birth
• allowing intestinal loops to pass through the opening
• 10% of all children are affected
• more common in blacks, girls, and premature infants
• most resolve by age 1year, but consider outpatient referral if becoming larger or still present after 2-3 years of age
• emergent consultation if not reducible, but rarely as most are harmless

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• Transient Ischemic Attacks (TIA's) are warning signs of something worse to come and must not be ignored.
• Within 90 days of a TIA, about 10.5% of patients go on to have a full blown stroke, half of which occur within 1 to 2 days of their emergency department visit.
• Have an extremely low threshold to admit TIA patients in order that a work-up to determine the source and risk factors can be completed promptly.
• The typical TIA work-up consists of a brain CT, brain MRI, an electrocardiograph and cardiac monitoring (to evaluate for arrhythmia such as atrial fibrillation), echocardiogram (to evaluate heart function, check for a patent foramen ovale and clots), and carotid doppler ultrasound (to evaluate for atherosclerotic disease).

Amiodarone is a class III anti-arrhythmic for tachyarrhythmias

Although most patients remain euthyroid on amiodarone, 4-18% develop thyroid disease months to years after exposure.

Amiodarone-induced thyroid disease occurs because amiodarone is structurally similar to triiodothyronine and thyroxine and each 200mg tablet contains 75 mg of iodine.

Two types of amiodarone-induced thyroid disease:

• Amiodarone-induced hypothyroidism (AIH)
• Amiodarone-induced thyrotoxicosis (AIT)

Amiodarone-induced hypothyroidism (AIH)

• Presents with subtle to overt hypothyroidism 
• Treat by discontinuing amiodarone; thyroid recovers within 3 months
• If amiodarone cannot be discontinued, start levothyroxine

Amiodarone-induced thyrotoxicosis (AIT)

• Sudden symptom onset months to years following exposure; mean 2-47 months post-exposure
• Can be a life-threatening presentation (similar to thyroid storm) with severe cardiac manifestations and hemodynamic instability
• Treatment (treat like thyroid storm, if severe)
  • Discontinue drug, if possible
  • Thionamides (inhibit enzyme producing thyroid hormones)
  • Methimazole or propylthiouracil
  • Beta-blockers
  • Steroids
  • Airway and hemodynamic support

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DDx for JVD + hypotension + clear lungs:
     RV infarction
     massive PE
     tension PTX (clear lung)
     pericardial tamponade

Assuming your physical exam diagnoses tension PTX, you only need two simple tests to make the diagnosis amongst the other possibilities:
    1.  EKG: RV infarction will almost always show a concurrent inferior MI;
    2.  bedside U/S: tamponade patients have effusion, PE patients have RV distension

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Patients requiring anticoagulation for HIT or with a history of HIT may be initiated on argatroban.  We have recently been seeing increased utilization.  Here are some important points to remember.

• MOA: Direct thrombin inhibitor – reversibly binds to the active thrombin site of free and clot-associated thrombin
• Monitoring parameters:
  • aPTT prior to starting therapy (similar to heparin)
  • aPTT two hours after initiation of therapy or after dose change
  • Signs/symptoms of bleeding, LFTs, CBC, Hgb/Hct
• Dosing (general): 2 mcg/kg/min (actual body weight)
• Important notes:
  • Discontinue all heparin products including hep locks and coated catheters.  This includes all LMWH such as enoxaparin.
  • Causes false elevation of INR by cross-reacting with the INR assay

• radial head subluxation
• usually 1-3 years of age
• often after sudden longitudinal traction on extended arm with wrist in pronation
• tearing of annular ligament attachment to radial neck, with detatched portion trapped between subluxed raidal head and capitellum
• children refuse to use affected arm and hold in a flexed pronated position
• traditionally, reduce by supination of forearm with elbow in 90degrees of flexion
• newer reduction technique, hyperpronation with elbow flexion has better success rateand less pain

The mounting evidence on the use of 20% lipid emulsion or intrlipid has been growing for  any patient that is hemodynamically unstable due to a drug exposure. There is now a recent case report of a verapamil overdose patient that received intralipid and did well. They were able to measure verapamil levels before and after administration. They were able to remove the lipid from the serum to appropriately measure the level and found effective removal. This adds to the theory of the "lipid sink" where the lipid actually is binding/surrounding a lipophilic molecule effectively removing it from interaction.

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• Don't forget to give aspirin to patients presenting with acute ischemic stroke (AIS).

• Large trials such as the International Stroke Trial (IST)  and Chinese Acute Stroke Trial (CAST) have shown that starting 160 to 300 mg of aspirin within 48 hours of the presumed onset of ischemic stroke reduces the risk of early recurrent ischemic stroke, with no major increased risk of hemorrhagic conversion and with improved long-term outcome.

• Studies have also shown that high and low doses of aspirin (30 to 1200 mg per day) after AIS yield similar efficacy for preventing vascular events, but that higher doses are associated with a greater risk of gastrointestinal hemorrhage.

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Hepato-Renal Syndrome

• Hepato-renal syndrome (HRS) is the development of acute kidney injury (AKI) in patients with advanced cirrhosis.
• HRS is traditionally divided into two types based upon how quickly AKI develops:
  • Type I: a rapid decline in function in less than 2 weeks
  • Type II: a slow decline in function over weeks to months
• Type I is more likely to be seen in the ED and is often due to a precipitating event such as:
  • GI bleed
  • Spontaneous bacterial peritonitis (SBP)
  • Hypovolemia from aggressive diuresis
• In ED patients with advanced cirrhosis and new, or worsening, AKI think about HRS. 
• If suspected, look for precipitants (i.e. SBP), restore volume with IVFs, avoid nephrotoxins (IV contrast), and administer vasopressor therapy when indicated.

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Question

49 y.o. female on Trimethoprim/sulfamethoxazole presents with rash and oral mucus membrane lesions. Diagnosis?

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Paroxysmal supraventricular tachycardia (PSVT) is a common tachydysrhythmia encountered in ED practice. PSVT in itself has not been found to be an isolated manifestation of myocardial infarction or unstable angina (i.e. "isolated" = in the absence of other concerning symptoms, such as anginal-type pain, etc.).  Nevertheless, some physicians will routinely test cardiac troponin levels to evaluate for ACS in these patients. We should all remember, though, that tachydysrhythmias including PSVT are a potential cause of elevated troponin levels in the absence of coronary disease, and these elevations do NOT correlate with adverse outcomes unless other concerning symptoms/signs are present as well.

A recent study¹ corroborated this point: 11 out of 38 patients with PSVT had a positive troponin level. Only 2 of the 11 ruled in for ACS, and all of the patients were well at 30 days. Both patients presented with hypotension (SBP in the 70s) and also had other concerning symptoms, such as chest pain (both), dizziness (both), and dyspnea (one).

The takeaway point is simple: if you routinely send troponin levels on your patients for PSVT in the absence of other concerning symptoms/signs, you'll find yourself chasing a lot of false-positive levels.

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Pes Anserine Bursitis is an inflammatory condition of the medial knee

Occurs at the bursa of the pes anserinus which overlies the attachment of the 1) Sartorius 2) gracilis and 3) semitendinosis tendons

Note the location is 2-3 inches below the knee joint on the medial side

http://kneespecialistsurgeon.com/images/uploaded/Pes%20anserinus%20bursitis%20image.jpg

http://eso-cdn.bestpractice.bmj.com/best-practice/images/bp/en-gb/575-27_default.jpg

Patients complain of pain (especially with stair climbing)

PE: Tenderness to palpation of the bursa with mild swelling

DDx: MCL tear, medial meniscus injury, medial (knee) compartment arthritis

Treatment: Cessation/modification of offending activities, Icing and ice massage, NSAIDs, hamstring stretching and physical therapy. Failure of the above should prompt referral for bursal steroid injection.

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• 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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