• Pediatric visits for behavioral and mental health issues is on the rise.
• From 2008 to 2015, rates of PED visits for suicidal thoughts/attempts doubled.
• Shortage of pediatric psychiatrists:  8,300 nationwide with a need for 30,000.
• Deinstitionalized Movement of 1980's, has worsened this ED crisis-based culture.
• 50% of all mental illness begins by age 14.
• 1 in 5 children experience a mental disorder in a given year.
• Aggressive or agitated behavior in pediatric patients is different from adults.
• Children are more amenable to environmental and behavioral techniques, especially verbal de-escalation, once a trigger is identified.
• If not successful, avoid physical restraints and consider medications instead.
• Review current or previously prescribed medications, and consider extra/early/higher dosing. If naive to medications:
• First line is Diphenhydramine.
• Followed by Chlorpromazine, Risperidone, and Olanzapine
• Thorazine should be avoided in children under 12 years due to extra-pyramidal effects.
• Lorazapam not recommneded in children under 12 years, as it can cause disinhibition and worsen behavior.
• Avoid sedating children with neurodevelopmental disorders as they can have paradoxical reactions to diphenhydramine and benzodiazepines, and antipsychotics sometimes are not as effective.
• Boarding is common due to lack of resources, so starting treatment in the ED is imperative. 

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Scromboid (histamine fish poisoning) can be easily misdiagnosed since its' clinical presentation can mimic that of allergy. Seen most frequently in the summer and occurring with Scombroideafish (tuna, mackerel, bonito, skipjack) but also with large dark meat fish (sardines and anchovies) and even more commonly with nonscromboid fish such as mahi mahi and amber jack. In warm conditions when fish is improperly refrigerated, bacterial histidine decarboxylase converts muscle histidine into histamine which quickly accumulates. Histamine is heat stable and not destroyed with cooking. 

• Clinical features: Intense flushing of face, neck, and upper torso, urticaria, abdominal cramps, headache, palpitations, diarrhea, nausea, vomiting, burning of the mouth and throat.
• Symptoms begin within minutes of ingestion and typically last several hours
• Self limiting condition. Mainstay of treatment is H1 blockers (antihistamines) and good supportive care. If bronchospam present steroids and inhaled B2 agonists should be administered.

Bottom Line:

Scromboid poisoning is due to histamine ingestion and is often misdiagnosed as allergic reaction. It is preventable with proper fish storage.

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When managing transplant patients it is important to keep in mind the anatomic and physiologic changes that occur with the complete extraction of one person's body part to replace another's. 

For cardiac transplant patients with symptomatic bradycardia:

• Remember that due to lack of autonomic/vagal innervation, resting HR should be around 90 bpm.
• HR will not respond to atropine. Use direct sympathomimetics like epinephrine instead.
• If medication is unsuccessful, proceed to transcutaneous or transvenous pacing.

For cardiac transplant patients with tachyarrythmias:

• They are particularly sensitive to adenosine; for SVT start with 1 to 3mg adenosine push (3mg is usually effective) to avoid sustained bradycardia or asystole.
• Digoxin is not effective as an antiarrhythmic.
• Diltiazem can decrease the metabolism of calcineurin inhibitor immunosuppressive agents (such as cyclosporine and tacrolimus), so while it can be used there may need to be dose adjustments to these medications. 

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Hyponatremia in the Brain Injured Patient

• Hyponatremia is the most common electrolyte disorder in neurocritical care and is associated with increased ICP.
• The two most common causes of hyponatremia in this patient population are cerebral salt wasting syndrome and SIADH.
• Symptomatic hyponatremia should be treated with hypertonic saline:
  • 30-45 ml of 10% NaCl or
  • 100-150 ml of 3% NaCl
• In order to prevent osmotic demyelination syndrome (ODM), sodium should not be corrected by more than 10 mmol/L/day.
• The risk of ODM is low when acute hyponatremia develops in less than 48 hours.

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Laboratory testing for Spinal Epidural Abscess

CBC

The CBC is poorly sensitive/specific

The WBC count may be nml or elevated

Left shift and bandemia may or may not be present

ESR and CRP

Sensitive but not specific

Elevated in >80% with vertebral osteomyelitis.

• Sensitive for spinal infection, but not extremely specific.

• ESR
  • ESR was elevated in 94-100% of patients with SEA vs. only 33% of non-SEA patients
• CRP
  • Less useful for acute diagnosis since CRP levels rise faster and return to baseline faster than ESR
    • Elevated CRP seen in 87% of patients with SEA as well as in 50% of patients with spine pain not due to a SEA
  • Better used as a marker of response to treatment.

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• Misdiagnosis of neurologic emergencies can result in serious neurologic dysfunction or death.
• A recent retrospective analysis using AHRQ databases looked at >3 million adults discharged from the ED with diagnoses of atraumatic headache or back pain.
• A serious neurologic condition or death occurred within 30 days after ED discharge in:
  • 0.5% of patients with nonspecific diagnosis of headache
  • 0.2% of patients with nonspecific diagnosis of back pain
• The frequency of adverse outcome was highest between days 1 and 3 after ED discharge.
• The most frequent adverse outcome was ischemic stroke (18.1%) for headache and intraspinal abscess (44%) for back pain.
• Age ≥ 85, male sex, non-Hispanic white, comorbidities such as neurologic disorders, HIV/AIDS, and malignancy were associated with higher incidence of adverse outcome.

Bottom Line: The rate of serious neurologic conditions missed at an initial ED visit is low.  However, the potential harm of misdiagnosis can be substantial.

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Kratom (Mitragyna speciosa) has been used for centuries in Southeast Asia to manage pain and opium withdrawal. It is increasingly being used in the U.S. for similar purpose. The U.S. DEA lists Kratom as a “drug of concern”.

Effects of Kratom leaves

• 1 – 5 gm: mild stimulatory effects
• 5 – 15 gm: opioid-like effects
• >15 gm: sedative effects

A study reviewed National Poison Data System (2011 to 2017) to evaluate the clinical effects/outcomes of Kratom exposure.

Finding: (N=1807; single-substance: 1174; multiple-substance: 633])

• 2/3 of all exposure occurred in 2016 – 2017 via oral route (83.0%)
• 88.9% were adults (> 20 years old) 
• 86.1% of the exposures occurred in private residence
• Fatality: 11 (2 deaths occurred after an isolated exposure to Kratom)

Common symptoms

• Agitation: 22.9%
• Tachycardia: 21.4%
• Drowsiness/lethargy: 14.3%
• Nausea/vomiting: 13.2% - 14.6%
• Confusion: 10.6%
• Hypertension: 10.1%
• Seizure (single/multiple): 9.6%
• Respiratory depression: 3.6%

Disposition

• Admitted to a health care facility: 31.8% (n=498)
  • Critical care unit: 14.0%
  • Non-critical care: 13.1%
  • Psychiatric facility: 4.7%

Bottom line:

• Kratom use is associated with a wide spectrum of clinical signs/symptoms.
• Death from isolated exposure to Kratom is rare. 

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The PROTRACH study recently compared preoxygenation with standard bag valve mask (BVM) at 15 lpm to preoxygenation + apneic oxygenation with high flow nasal cannula 60 lpm/100% FiO2 in patients undergoing rapid sequence intubation.

• There was no significant difference in the primary outcome of median lowest SpO2 during intubation. 
• There were more intubation complications in the BVM group compared to the HFNC group:
  • Severe complications: SpO2 <80%, severe hypotension (SBP < 80mmHg or vasopressor initiation/increase by 30%), and cardiac arrest (6% HFNC vs 16% BVM, RR 0.38, 95% CI 0.15-0.95, p=0.03). 
  • Moderate complications: aspiration, cardiac arrhythmia, agitation, and esophageal intubation (0% HFNC vs 7% BVM, p= 0.01). 
• There was no difference in ventilator days, ICU length of stay, or mortality.

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Cauda Equina Syndrome (CES)

A recent pearl discussed CES. This is a very challenging diagnosis to make, especially on initial presentation

The 5 “classic” characteristic features are

•  Bilateral radiculopathy
• Saddle anesthesia
• Altered bladder function
• Loss of anal tone
• Sexual dysfunction

Not all symptoms will be present in a given patient and there is no sign/symptom combination that either reliably diagnoses or excludes CES.

To illustrate how difficult this diagnosis is to make, a study looked at the predictive abilities of Neurosurgical residents.

Positive MRI for CES was accurately predicted by senior neurosurgical residents in approximately 50% of patients suspected of CES based on history and physical findings. As clinical certainty only becomes apparent with the classic symptoms (which are generally late findings) waiting to initiate MRI will delay decompressive surgery and can lead to worsened functional outcomes. This leads to increased MRI demand with more negative MRIs. Not surprisingly, only ~20% of MRI scans for suspected CES are positive.

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A True Tracheostomy Emergency

• Patients with a tracheostomy often present to the ED for evaluation of a potential complication.
• Consider a tracheoarterial fistula in any patient with a tracheostomy who presents with brisk bleeding.
• Most occur within 3 to 4 weeks following tracheostomy placement, and the most common location is the innominate artery.
• Up to 50% of patients will present with a sentinel bleed - an episode of brisk bleeding that has usually stopped at the time of presentation.
• For patients who present with active hemorrhage, overinflate the tracheostomy cuff in an attempt to tamponade the bleeding.
• If that does not stop the bleeding, remove the tracheostomy and compress the artery against the poterior sternum with your finger.

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Back pain with lower extremity symptoms can be concerning for cauda equina. Some pointers regarding the H&P:

• Symptoms develop within less than 24 hours in 90% of patients
• Urinary retention develops before incontinence, but up to 30% of patients will have neither.
• Saddle anesthesia or hypoesthesia is present in 81% of patients. Perineal numbness may be patchy, mild, and unilateral initially, making it difficult to elicit.

None of these symptoms independently predicts cauda equina syndrome with an accuracy greater than 65%.

Bottom Line: do not depend on any one finding to reliably exclude or confirm cauda equina.

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Despite ongoing research and efforts to improve our care of patients with ARDS, it remains an entity with high morbidity and mortality. Early recognition of the disease process and appropriate management by emergency physicians can have profound effects on the patient's course, especially in centers where ICU boarding continues to be an issue.

Recognition of ARDS (Berlin criteria)

• Acute in onset
• Bilateral infiltrates on chest imaging not due to cardiac failure/volume overload
• PaO2 : FiO2 < 300 despite PEEP of at least 5cmH2O 
• This is the standard ED patient who gets intubated with multifocal pneumonia and has continued hypoxemia

*An ABG should be obtained in the ED if physicians are unable to wean down FiO2 from high settings, if oxygenation by pulse ox is marginal, or if the patient is in a shock state.

Tenets of ARDS Management:

• Low tidal volume ventilation (6-8ml/kg ideal body weight*)
• Maintain plateau pressures (Pplat) < 30 cmH2O
• Driving pressure (Pplat – PEEP) < 15 cmH2O
• Goal PaO2 > 55-60 
• Permissive hypercapnia to pH >7.2

*IBW Males = 50 + 2.3 x [Height (in) - 60]   /  IBW Females = 45.5 + 2.3 x [Height (in) - 60]

Strategies for Refractory Hypoxemia in the ED:  You can't prone the patient, but what else can you do? 

1. Escalate PEEP in stepwise fashion

• ex: 2cmH20 every 10 minutes
• can use ARDSnet PEEP/FiO2 table as guide

2. Recruitment maneuvers

• "20 of PEEP for 20 seconds" or "30 for 30"
• if patient is "PEEP responsive," leave PEEP on a higher setting than when you started (ex: 10 instead of 5, 16 instead of 10)
• Risk of barotrauma with higher PEEPs and hypotension in underresuscitated or hemodynamically unstable patients due to decreased venous return

3. Appropriate sedation and neuromuscular blockade

• promotes patient synchrony with lung protective settings
• can result in improved oxygenation by itself

4. Inhaled pulmonary vasodilators (inhaled prostaglandins, nitric oxide) if known or suspected right heart failure or pulmonary hypertension

Bottom Line: Emergency physicians are the first line of defense against ARDS. Early recognition of the disease process and appropriate management is important to improve outcomes AND to help ICU physicians triage which patients need to be emergently proned or even who should potentially be referred for ECMO. 

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In patients with lower back pain, there is good evidence that muscle relaxants reduce pain as compared to placebo and that different types are equally effective. However, the high incidence of significant side effects such as dizziness and sedation limits their use. Muscle relaxants may be beneficial in an every bedtime capacity thereby limiting side effects.

If cyclobenzaprine is used during daytime hours, a lower dose schedule may work as well as a higher dose with somewhat less somnolence (5 mg three times a day vs 10 mg three times a day. In general, muscle relaxants should only be used when patients cannot tolerate NSAIDs but can tolerate the side effect profile.

We commonly add muscle relaxants to NSAIDs hoping for a larger analgesic effect. However, combination therapy does not appear to be better than monotherapy. 

Adding cyclobenzaprine to high-dose ibuprofen does not seem to provide additional pain relief in the first 48 hours in ED patients with acute myofascial strain. Among an ED population with acute non radicular low back pain, a randomized trial found that adding cyclobenzaprine/other muscle relaxants to Naproxen did not improve functional outcomes or pain at one week or 3 months compared to naproxen alone.

Take home: Consider the limited usefulness use of muscle relaxants in ED patients with back pain

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The hyperoxia-hyperventilation test (aka 100% Oxygen Challenge test) is used to differentiate the cause of central cyanosis in the sick neonate. The majority of neonatal cyanosis is caused by either cardiac or respiratory pathology.

Classically the test is performed as follows:

1. An ABG is obtained with the neonate breathing room air

2. The patient is placed on 100% FiO2 for 10 minutes

3. A repeat ABG is performed looking for an increase in PaO2 to >150 mmHg

 -   If the hypoxia is secondary to a respiratory cause, the PaO2 should increase to >150 mmHg.

-    If the hypoxia is secondary to a congenital cardiac lesion (i.e. secondary to a right-to-left cardiac shunt) the PaO2 is not expected to rise significantly. 

In practice, many physicians instead use pulse oximetry and monitor the SpO2 pre and post administration of 10 minutes of 100% FiO2.

-          If after 10min of 100% FiO2, if SpO2 is not ? 95% (some resources use 85%) then the central cyanosis is likely secondary to intracardiac shunt.

-          When this occurs, presume the sick neonate is symptomatic from a congenital cardiac lesion and initiate prostaglandin E-1 (PGE1) at 0.05-0.01 mcg/kg/min. Use caution as PGE1 may cause apnea.

The primary tenet of poisoning treatment is to separate the patient from the poison. Gastric decontamination has been the cornerstone of poisoning treatment throughout history and methods include induced emesis, nasogastric suctioning, EGD or gastrostomy retrieval, activated charcoal, and whole bowel irrigation. Current guidelines for gastic decontamination are limited to few clinical situations. The detection of residual life threatening poisons in the stomach would be of value in predicting who might benefit from gastric decontamination in overdose.

Plain radiographs have variable sensitvity in detecting radioopaque pills. Computed tomography (CT) has been successful and gained wide acceptance in the detection of drug in body packers. In a recent study, authors studied the usefulness of non-contrast abdominal computed tomography for detection of residual drugs in the stomach in patients  presenting over 60 minutes from acute drug overdose:

• 140 patients were included in this study
• Median ingested drug amounts were 28 tablets or capsules
• Median time until CT scan was performed after drug ingestion was 4 hours
• Multiple types of drugs were ingested in 53.6%
• Sustained-release drugs  were ingested in 17.1 %
• Gastric lavage and WBI were performed on 32.9% patients
• Drugs were detected in 25.7% in the non-contrast CT scan performed over 60 min after ingestion.
• Total duration of hospital stay was significantly longer in the “presence of drugs” group

BOTTOM LINE:

Non-contrast CT may help to predict which patients would benefit from gastric decontamination in acute life-threatening drug poisonings.

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Does This Patient Have Pericardial Tamponade?

• Echocardiography is critical for the identification of a pericardial effusion and rapid diagnosis of pericardial tamponade.
• Common echocardiography findings that suggest tamponade include diastolic right ventricular collapse, systolic right atrial collapse, a plethoric IVC with minimal respiratory variation, and potentially exaggerated respiratory cycle changes in mitral and triscupid inflow velocities.
• Of these, systolic right atrial collapse is the earliest echocardiographic sign of tamponade, with a sensitivity ranging from 50% to 100%.
• Of the 4 standard echo views, systolic right atrial collapse can best be viewed in the apical 4-chamber and subxiphoid views.

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Hyponatremia is the most common electrolyte abnormality in hospitalized patients, affecting approximately 15-30% of patients.  Children have historically been given hypotonic maintenance IV fluids based off of theoretical calculations from the 1950s.  Multiple studies have shown complications related to iatrogenic hyponatremia, including increased length of hospital stay, seizures and death.

The American Academy of pediatrics completed a systematic review and developed an updated clinical practice guideline:

Patient's age 28 days to 18 years requiring maintenance IV fluids should receive isotonic solutions with the appropriate amount KCl and dextrose.

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Physostigmine is a cholinergic agent that can be administered to reverse delirium associated with anticholinergic toxicity. However, it is infrequenly used since the reports of cardiac arrest in patients with TCA overdose.

A recently published study reviewed 161 articles – involving 2299 patients – to determine the adverse effects and their frequency after the administration of physostigmine. 

Findings

Adverse effects were observed in 415 patients (18.1%)

• In patients with anticholinergic overdose: 7.7%
• In patients with non-anticholinergic agent overdose: 20.6%

Specific adverse effects

• Hypersalivation: 206 (9%) 
• Nausea/vomiting: 96 (4.2%)
• Seizure: 14 (0.61%)
• Symptomatic bradycardia: 8 (0.35%) – including 3 with bradyasystolic arrest
• Asymptomatic bradycardia: 4 (0.17%)
• Ventricular fibrillation: 1 (0.04%) patient had a history of coronary artery disease
• Cardiac arrest: 4 (0.17%)
• Death: 5 (0.22%)

Of 394 TCA overdose, adverse effects occurred in 14 patients (3.6%)

Conclusion

• Adverse effects from physostigmine occurs infrequently. 
• However, inappropriate dosing or use of physostigmine can result in cholinergic toxicity.
• For isolated anticholinergic toxicity (e.g. antihistamine overdose): physostigmine dosing: 0.5 mg (dilute in 5 – 10 mL normal saline) IV over 2 -5 minutes. May repeat every 5-10 minute to max dose total of 2 mg. (patient needs to be on cardiac monitor with atropine at bedside) 
• Therapeutic goal: reversal of delirium
• Avoid physostigmine in the presence of QRS widening (cardiac Na-channel blockade) and patients with history of underlying coronary artery disease.

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Neutropenic enterocolitis can occur in immunosuppressed patients, classically those being treated for malignancy (hematologic much more commonly than solid tumor). When involving the cecum specifically, it is known as "typhlitis."

It should be considered in any febrile neutropenic patients with abdominal pain or other symptoms of GI discomfort (diarrhea, vomiting, lower GI bleeding), and can be confirmed with CT imaging.

A recent study found that invasive fungal disease, most often candidemia, occurred in 20% of febrile neutropenic patients with CT-confirmed enteritis, a rate that increased to 30% if the patient was in septic shock.

Take Home: 

1. Have a lower threshold for abdominal CT imaging in your patients with febrile neutropenia and abdominal pain/GI symptoms, especially if they are critically ill.

2. Consider addition of IV antifungal therapy if they are hemodynamically unstable with enterocolitis on CT.

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