UMEM Educational Pearls

Exertional Heat Stroke (EHS)

With football preseason starting across the country, it is important to review this topic

EHS is a medical emergency resulting from progressive failure of normal thermoregulation

EHS has a high mortality

               -2^nd most common cause of death in football players

History and Exam

Hyperthermia/Core temperature greater than 40°C (104°F)

Initial profuse sweating with eventual cessation of sweating with hot, dry skin

CNS dysfunction – disorientation, confusion, dizziness, inappropriate behavior, difficulties maintaining balance, seizures, coma

Other: Tachycardia/hyperventilation, fatigue, vomiting, headache

Multi-organ involvement: CNS, cardiac damage, renal failure, hepatic necrosis, muscle (rhabdomyolysis), GI (ischemic colitis), heme (DIC), ARDS

The single most important thing you can do on the field is recognize this entity. Early recognition leads to earlier initiation of treatment which is life saving.

Rapid cooling is key. This is often stated but what this means is whole body immersion in ice water. This should be available and ready for all summer practices.

The temperature needs to be lowered to below 39°C (102°F)

Also consider a cooling blanket, fanning, ice to body

DO NOT put them on ambo without initiating cooling!!!

Sustaining heat injury predisposes to subsequent heat related injury

• Anticoagulation is the mainstay for treatment of acute cerebral venous thrombosis (CVT) to prevent clot propagation, recanalize occluded veins and sinuses, and prevent new venous thrombosis.
• A recent meta-analysis of 4 RCTs compared the efficacy and safety of low molecular weight heparin (LMWH) vs. unfractionated heparin (UFH) for the treatment of CVT.
• All studies were small, with 20 to 66 patients each.
• Treatment with LMWH compared with UFH had similar mortality (OR 0.21; 95% CI 0.02-2.44; p=0.21) and disability (OR 0.5; 95% CI 0.11-2.23; p=0.36). 

Bottom Line: LMWH appear to be similar in efficacy and safety compared with UFH for the management of CVT.

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Respiratory alkalosis is the most common acid-base disturbance in acute severe asthma.

Lactic acidosis is also extremely common, developing in up to 40%. This may be related to:

- tissue hypoxia

- increased respiratory muscle usage related to work of breathing

- beta agonist therapy

The first report of beta agonist administration associated with hyperlactatemia was in 1981 in patients treated for preterm labor with terbutaline. Since then, numerous case reports and studies have linked IV and inhaled beta agonist administration with the development/worsening of lactic acidosis in severe asthmatics in the ICU and in the ED.

The exact mechanism is unclear, but is thought to be related to adrenergic stimulation leading to increased conversion of pyruvate to lactate.

In a study published in Chest in 2014, investigators evaluated plasma albuterol levels and serum lactate levels, as well as FEV1.

They found plasma albuterol levels correlated with lactate concentration and maintained significant association after adjusting for asthma severity (suggesting the association was independent of work of breathing/respiratory muscle usage).

Furthermore, several reports have suggested that dyspnea may improve in patients with elevated lactate and acidosis after beta agonists are withheld.

Take Home Points:

- Beta agonist therapy may contribute to lactic acidosis.

- Lactic acidosis may contribute to respiratory distress.

- In patients on prolonged, high-dose beta agonist therapy, consider checking a serum lactate periodically. If elevated, consider whether worsening lactic acidosis is contributing to respiratory distress and contemplate transitioning to less frequent treatments.

-Patients with severe asthma exacerbation and elevated serum lactate must have thorough evaluation for true tissue hypoxia/hypoperfusion. **Beta agonist associated hyperlactatemia should be a diagnosis of exclusion.**

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Is your older patient hard of hearing (HoH)? Instead of shouting, get a stethoscope. Put the ear buds in your patient's ears and talk into the bell. It is a hearing amplifier you carry with you.

Bonus pearl: If you use the disposable stethoscopes, then the patient can keep it in their room and use it whenever anyone wants to talk to them.

• IDSA/SHEA recently released a guideline update for the management of Clostridium difficle infections
• Discontinue inciting antibiotic therapy as soon as possible
• Metronidazole is no longer considered first line therapy for C. difficle infection
• Treatment course for 10 days unless initial fulminant or recurrence requiring vancomycin taper
• Remember: Vancomycin IV does not cross into the GI tract and cannot be used to treat C. difficile

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Delayed Onset Muscle Soreness (DOMS), aka “muscle fever”

Muscle pain and weakness following unfamiliar exercise

Occurs after high force, novel (unaccustomed) eccentric muscle contractions

               Occasionally isometric in an extended position

Eccentric exercise – controlled elongation

Slowly lowering yourself to start position doing pullups for example

Time of onset

Begins 6 to 12 Hours after exercise, Peaks 2-3days post and resolves in 5-7 days

               Speed of onset and severity are often related

How do you know if you have it?

Much like the flu, you know it when you have it. The simple act of getting out of a car, sitting down or walking down stairs is excruciatingly painful.

Cause:

Exact cause is unknown. Thought to be due to sarcolemma damage leading to intra cellular calcium release and activation of proteolytic enzymes. Creatine kinase leaks from muscle cells into plasma attracting inflammatory cells.

Treatment:

Best treatment is prevention: Repeated bout effect – a bout of eccentric or isometric exercise can prevent DOMS from the same exercise for 4-12 weeks.

               Stretching before exercise has not been shown to be effective prevention

Other modalities: rest, ice, heat, massage, electrical stimulation

Take home:

Eccentric exercises or novel activities should be introduced progressively over a period of 1 or 2 weeks at the beginning of the sporting season or the start of a new, novel exercise routine. For example, not starting the Insanity day one workout without “pretraining.” This will reduce the level of physical impairment and/or training disruption and lead to gains with much less pain.

Elevated transaminases are found in both rhabdomyolysis and delayed acetaminophen (APAP) toxicity. Establishing the cause of elevated transaminase can be difficult when there is unclear history of acetaminophen ingestion.

A retrospective study of patients with delayed acetaminophen toxicity or rhabdomyolysis from 2006 to 2011 was recently published.

The authors compared AST/ALT, CK/AST and CK/ALT ratio of 

• 160 in the rhabdomyolysis group
• 68 in the acetaminophen overdose (all)
• 29 in the delayed acetaminophen overdose group

Results

AST/ALT ratio

• Rhabdomyolysis group: 1.66
• APAP overdose (all): 1.38
• Delayed APAP overdose: 1.3

CK/AST ratio

• Rhabdomyolysis group: 21.3
• APAP overdose (all): 5.49
• Delayed APAP overdose: 3.8

CK/ALT ratio

• Rhabdomyolysis group: 37.1
• APAP overdose (all): 5.77
• Delayed APAP overdose: 5.03

Conclusion

• Significantly higher ratio of AST/ALT, CK/AST and CK/ALT were found in rhabdomyolysis patients than delayed APAP overdose patients.
• These finding are based on small study population and need further validation/research before clinical application.

An infarct of the spinal cord is technically considered a stroke

The most common risk factor is a recent aortic surgery. Can also occur with straining and lifting (rare)

Patients will present with symptoms of spinal cord involvement with a hyperacute onset (less than 4 hours)

Although the “classic” presentation is anterior cord syndrome (flaccid paralysis, dissociated sensory loss (pinprick and temperature), preserved dorsal column function), patients may present with loss of all functions below the level of infarct due to spinal shock, confusing the clinical picture.

The most common level is T10

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Improving Analgesia in Mechanically Ventilated ED Patients

• An analgosedation approach for mechanically ventilated patients has been shown to decrease the duration of mechanical ventilation and ICU LOS.
• The latest guidelines from the Society of Critical Care Medicine recommend an opioid as the initial agent, followed by a non-benzodiazepine sedative.
• Benzodiazepines have been shown to increase ICU delirium, increase the duration of mechanical ventilation, and increase ICU LOS.
• In a recent cohort study, ED physicians increased the use of opioid analgesics and markedly decreased the use of benzodiazepines in mechanically ventilated ED patients through an educational campaign and implementation of an electronic orderset.
• Take Home Point: An electronic health record orderset for mechanically ventilated ED patients can be helpful to guide clinicians and utilize an analgosedation approach.

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Question

Bottom Line:

1. The most often cited meta-analysis regarding route of PPI use in bleeding peptic ulcer disease evaluates rebleeding AFTER endoscopic treatment and only ulcers with high-risk features.  There is no good data on optimal pre-endoscopy dosing.
2. These studies appear to show non-inferiority of intermittent dosing with a trend towards superiority when compared with continuous dosing.
3. The proper dosing, frequency, and route of intermittent PPI use is widely variable without good data on an optimal regimen.
4. ED decision of intermittent vs continuous PPI should consider other patient factors including severity of illness, compatibility of IV lines (pantoprazole is often incompatible), and patient disposition.

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Question

Chest xrays (CXRs) may lead to longer length of stay, increased cost, unnecessary radiation exposure, and inappropriate antibiotic use.

CXR in asthma are indicated for:

-severe persistent respiratory distress, room air saturations <91%

- focal findings (localized rales, crackles, decreased breath sounds with or without a documented fever > 38.3) not improving on >11 hours of standard asthma therapy

- concern for pneumomediastinum or pneumothorax

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Sulfonylureas are commonly used oral hypoglycemic agents for type II diabetes. Agents on the market include glipizide (Glucotrol), glyburide (Micronase, Glynase, Dibeta) and glymepiride (Amaryl). These agents exert their effect by stimulation of insulin release from the pancreatic beta islet cells. Following overdose, hypoglycemia is usually seen within a few hours of ingestion and can be prolonged and profound. First line treatment for rapid correction of severe hypoglycemia is administration of an intravenous bolus of concentrated dextrose. However, use of dextrose infusion in attempt to maintain euglycemia is problematic as it can cause further release of insulin and rebound hypoglycemia. Octreotide ia a long acting synthetic somatostain analogue, blocks insulin secretion and has been shown to prevent recurrence of hypogylcemia better than placebo.

Bottom Line:

• Octreotide is the antidote of choice for sulfonylurea poisoning. Its use greatly simplifies management by avoiding the need for a central line, prolonged ICU admit, and frequent monitoring.
• Bolus 50 μg IV followed by an infusion of 25–50μg/h or give100 mcg subcutaneously with additional doses at 6-12 hour intervals for recurrent hypoglycemia. Octreotide has similar bioavailability by SC and IV route. It's duration of action can extend from 6 to 12 hours with SC use.
• After stopping Octreotide monitor for 12-24 hours for rebound hypoglycemia.

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When a do-not-intubate (DNI) hospice patient arrives in the ED with respiratory distress, consideration of non-invasive positive pressure ventilation (NIPPV) could invoke either a “What other option do I have?” or “Why torture the patient and prolong the dying process?” sentiment.

But what’s the data?

A recently-published meta-analysis¹ found that in DNI patients receiving NIPPV, there was a 56% survival rate to hospital discharge and 32% survival to 1-year.

• Higher survival was seen in patients with COPD and pulmonary edema as the cause of their respiratory failure, as opposed to pneumonia or malignancy.
• In surviving patients, there was no decrease in quality of life at 3 months; quality of life was not assessed in the time before death in nonsurvivors.
• In comfort-measures only (CMO) patients, patients receiving NIPPV had a mildly lower dyspnea score with less opiates required/administered.

Independent studies have demonstrated:

• Better survival with NIPPV for DNI COPD and CHF patients^2,3,4 who are awake and have a good cough.⁴
• No decrease in health-related quality of life or post-ICU psychological burden (symptoms of PTSD, anxiety, or depression) in DNI survivors receiving NIPPV.³
• 63% survival to hospital discharge & 49% survival to 90 days in DNI patients receiving NIVV, with no decrease in health-related quality of life in survivors. Survival was lower for CMO patients (14% and 0% at discharge and 90 days, respectively).⁵

Bottom Line:

1. NIPPV can benefit DNI patients -- most identifiably those with COPD or cardiogenic pulmonary edema as the etiology for their respiratory distress.
2. Mild benefits to dyspnea have been seen in CMO patients, without survival benefit. A trial of NIPPV therapy may be reasonable (especially in COPD or CHF) after frank discussion with the patient and his/her loved ones, with quick cessation if comfort is not achieved and/or more discomfort is caused.

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Stingers and Burners

Also known as transient brachial plexus neuropraxia, “dead arm syndrome,” or brachial plexopathy. Symptoms such as pain, burning, and/or paresthesias in a single upper limb, lasting seconds to minutes.

Usually involves more than one dermatome

May be associated with weakness.

               -Common in collision sports that involve tackling, such as football.

               -Most common C-spine injury in American Football.  

               -More than 50% of college football players sustain a stinger each year

-Having 1 stinger increases the risk of having another 3 fold

Mechansims: C5, C6 (deltoid,biceps) most commonly involved

-Traction injury due to forcible lateral neck flexion away with downward displacement of arm

-Nerve root compression during combined neck extension and lateral neck flexion

-Direct trauma to the brachial plexus in the supraclavicular fossa

Physical Exam:

-Examine muscle strength in the deltoid, biceps, and infraspinatus muscles

-Check sensation and reflexes in upper extremities

-Check C-spine range of motion and perform Spurling’s Test

Imaging:

Consider MRI for symptoms lasting more than 24 hours, bilateral symptoms or for recurrent stingers

Return to play guidelines vary:

-No neurologic symptoms

-Can return to play in same game if symptoms resolve within 15 minutes and no prior stingers that season.

-If 2^nd stinger in that season, do NOT return to play in the same game

-if 3^rd stinger in a season, consider imaging before return to play and consider sitting out the remainder of the season.

Abdominal pain in children can be just as frustrating as dizzy in the elderly. Your exam is targeted at quickly ruling out acute pathologies, but then what? The diagnosis is often  functional gastrointestinal disorders, like the ever exciting constipation. Abdominal migraine (AM) is an additional entity to consider during your emergency department evaluation.

The following factors are often associated with AM: 

- peak incidence at 7 years old

- paroxsymal, periumbilical abdominal pain lasting more than 1 hour

- family history of migraine

- episodes not otherwise explained by known pathology. 

AM can be associated with headache, pallor, anorexia, photophobia, and fatigue. There are multiple theories on the pathogenesis, which can be found in the article cited below. If there is a known history, and the patient is presenting with an exacerbation, the treatment protocols for migraine headache may be employed with good success. 

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Bottom Line:

AM is increasingly recognized as a source of recurrent abdominal pain in children. If other organic pathologies can be ruled out, this may be an important diagnosis to consider so your patient can get the appropriate follow up and outpatient management. 

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From 1960s to 1970s, physostigmine was routinely administered as part of the "coma cocktail." Since the publication of two cases by Pentel (1980) that resulted in asystole after administration of physostigmine in TCA poisoned patient, its use has declined significantly.

However, physostigmine still possess limited but clinically useful role in the management of patients with antimuscarinic/anticholinergic induced delirium.

Recently, a prospective observational study was performed in the use of physostigmine when recommended by a regional poison center.

In 1 year study period, physostigmine was recommended by a regional poison center in 125 of 154 patients with suspected antimuscarinic/anticholinergic toxicity. 

common exposures were

1. antihistamines (68%)
2. analgesics (19%)
3. antipsychotics (19%)

57 of 125 patients received physostigmine per treating team.

• median dose of physostigmine administered: 2 mg

Of the remaining patients,

• 35 patients did not receive any sedative agents
• 55 received benzodiazepines (56%)
• others received propofol (n=10), haloperidol (n=8), olanzapine (n=4), dexmedetomidine (n=3), etc.

Delirium control

• Physostigmine group 79% (45 of 57)
• No-physostigmine group: 36% (35 of 97)

Adverse events (physostigmine group vs. non-physo group) - no statistically significant difference.

• Intubation (n=7): 2 (3.5%) vs. 5 (5.2%)
• physical restraints (n=10): 3 (5.3%) vs. 7 (7.2%)
• vomiting (n=4): 3 (5.3%) vs. 1 (1.0%)

Conclusion:

Physostigmine can safely control antimuscarinic/anticholinergic-induced delirium.

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Legionella is an important cause of community-acquired pneumonia. It ranks among the three most common causes of severe CAP leading to ICU admission and carries a high mortality rate – up to 33%. Resulting from inhalation of aerosols containing Legionella species and subsequent lung infection, it is often associated with contaminated air conditioning systems, and other hot and cold water systems.

Recommended antibiotic regimens include a fluoroquinolone, either in monotherapy or combined with a macrolide (typically Levaquin +/- or Azithromycin).

A retrospective, observational study published in the Journal of Antimicrobial Chemotherapy in 2017 looked at 211 patients admitted to the ICU with confirmed severe legionella pneumonia treated with a fluoroquinolone vs a macrolide and monotherapy vs combination therapy. Combination therapy included fluoroquinolone + macrolide, fluoroquinolone + rifampicin, or macrolide + rifampicin.

Of these 211 cases, 146 (69%) developed ARDS and 54 (26%) died in the ICU. Mortality was lower in the fluoroquinolone-based group (21%) than in the non-fluoroquinolone based group (39%), and in the combination therapy group (20%) than in the monotherapy group (34%). In a multivariable analysis, fluoroquinolone-based therapy, but not combination therapy was associated with a reduced risk of mortality (HR 0.41).

Take Home Points:

-Remember, our usual blanket coverage with vanc + zosyn in the ED does not cover atypicals!

-Consider Levaquin instead of Azithro if there is clinical concern for Legionella PNA

           -hyponatremia, abnormal LFTs may be clues in the appropriate context

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Based in part upon Geriatric Emergency Department Guidelines, the American College of Emergency Physicians has initiated a Geriatric Emergency Department Accreditation Program. Emergency departments (EDs) can be accredited at one of three levels- Gold (Level 1), Silver (Level 2) and Bronze (Level 3). There are various aspects upon which and EDs’ level is determined, including nurse and physician staffing and education, appropriate policies and protocols, quality improvement activities, outcome measures, equipment and the physical environment.

• The rainy East coast spring has increased tick populations in endemic areas such as Maryland resulting in more tick bites.
• ED visits for known tick bites present acutely, often with parents bringing in the tick to be identified/tested.
• Routine serologic testing and antibiotic prophylaxis is not recommended after every tick bite.
• If an attached tick is engorged, identified as I. scapularis, and has been attached for >36 hours, then antibiotic prophylaxis for Lyme can be prescribed if started within 72 hours of tick removal in those patients > 8 years of age
• Prophylaxis: Single dose of doxycycline 4 mg/kg or 200mg max 
• If early Lyme Disese is present in the form of the classic rash of Erythema migrans, then treatment is doxycycline, 4 mg/kg or 100mg max BID for patients > 8 years of age or amoxicillin 50 mg/kg per day divided TID with 500 mg max TID in those < 8 years of age for 14 days 
• Serologic testing is false negative in the first month of testing, and unnecessary in the ED  for acute presentations.