Critical Post-Arrest Interventions
Is there an association between pulmonary aspiration, vomiting or any serious adverse event and the preprocedural fasting time?
The odds ratio of any adverse event did not increase significantly with each additional hour of fasting duration for both solids and liquids.
The guidelines set by the American Society of Anesthesiology for fasting include a minimum of 2 hours for clear liquids, 4 hours for breast milk, 6 hours for formula and light meals and 8 hours for solid meals containing fatty foods or meat.
This was a secondary analysis of a multicenter prospective cohort study of children 0-18 years who received procedural sedation in 6 Canadian pediatric emergency departments from 2010-2015. 6183 children were included with 99.7% meeting ASA 1 or 2 categories. 2974 patients did not meet the American Society of Anesthesiology fasting guidelines for solids and 510 patients did not meet the fasting guidelines for liquids. The overall incidence of adverse events was 11.6%. There were no cases of pulmonary aspiration. There was a total of 717 adverse events. 315 events were vomiting. Oxygen and vomiting were the most common adverse events.
The highly-awaited PARAMEDIC2 trial results are in:
Interestingly, the authors also queried the public as to what mattered to them most:
Bottom Line:
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
-2nd 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
Bottom Line: LMWH appear to be similar in efficacy and safety compared with UFH for the management of CVT.
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.**
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.
| Clinical Definition | Treatment | |
| Initial episode, non-severe | WBC ≤ 15,000 AND SCr <1.5 |
If above agents unavailable, metronidazole PO 500mg 3x daily
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| Initial episode, severe | WBC ≥ 15,000 OR SCr >1.5 |
|
| Initial episode, fulminant | Hypotension, shock, ileus, megacolon |
|
| First Recurrence |
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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
Results
AST/ALT ratio
CK/AST ratio
CK/ALT ratio
Conclusion
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
Improving Analgesia in Mechanically Ventilated ED Patients
Bottom Line:
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
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:
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.
Independent studies have demonstrated:
Bottom Line:
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 2nd stinger in that season, do NOT return to play in the same game
-if 3rd 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.
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
57 of 125 patients received physostigmine per treating team.
Of the remaining patients,
Delirium control
Adverse events (physostigmine group vs. non-physo group) - no statistically significant difference.
Conclusion:
Physostigmine can safely control antimuscarinic/anticholinergic-induced delirium.
