Emerggyency Medicine Attack of the Killer Migraine! Pearls

Emergency Medicine g yPearls

Attack of the Killer Migraine! gDroperidol to the Rescue!

Megan Musselman, PharmD, BCPSEmergency Medicine Clinical Pharmacist

The University of Kansas Hospital

Megan Musselman, PharmD, BCPSEmergency Medicine Clinical Pharmacist

The University of Kansas Hospital

Disclosure

Megan Musselman reports no relevant financial relationships.

Acute Migraine

- Headache lasting 4-72 hours with at least 2 characteristics:- Unilateral location - Photophobia

- Pulsating quality - Phonophobia

- Moderate-to-severe intensity - Nausea/Vomiting

- Aggravated by routine activityAggravated by routine activity

- Have experienced 5 attacks in lifetime without a known secondary cause

Kelley NE, et al. Headache. 2012;52:114‐28.

General Management in the ED

- Headaches are the 4th most common reason for emergency department visits- > 1.5 million visits/year

- Affecting women > men

- Approach to treatment:- Replace volume depletion

- Blood pressure management

- Serum magnesium replacement

- Assessment of preferential route of treatment

- Onset of action


Treatment Options in the EDDrug Class Agents Indication

Analgesics/Opioids/Non‐steroidal anti‐inflammatorydrugs

Acetaminophen/hydrocodone, morphine, meperidine/ibuprofen, naproxen sodium, ketorolac

‐ First line treatment option

‐ Caffeine as an adjunct

A i i M l id Fi li f iAnti‐emetics Metoclopramide,prochlorperazine, droperidol

‐ First line for patients experiencing nausea and vomiting

Non‐selective 5‐hydroxytryptamine receptor agonists

Ergotamine ‐ Second line treatment option

Selective 5‐hydroxytryptamine receptor agonists

Sumatriptan, Zolmitriptan ‐ Second line treatment option


Emergency Medicine Pearls 2012 2012 Midyear Clinical Meeting

© 2012 American Society of Health-System Pharmacists Page 1 of 32

Droperidol (Inapsine®)

Studied in the 1950’s as an alternative for morphine Class:

• Butyrophenone

Mechanism of action: • Potent dopamine2 receptor antagonist and alpha1 receptorPotent dopamine2 receptor antagonist and alpha1 receptor

antagonist

Onset of Action:• IM/IV- peak serum levels in 1 hour• Half-life: 2 hours

Adverse events:• QT prolongation, extrapyramidal side effects (drug-induced

parkinsonism), tachycardia, orthostatic hypotension

Richards JR, et al. J Emerg Med. 2003;24:441‐7.

Evidence

Study Comparison DroperidolResults

Side Effects

Silberstein, et al.

Droperidol (0.1‐8.25 mg) IM versus placebo

Greater pain relief at 2 hours; P < 0.01

‐ Sedation and anxiety

‐ 30% of patientsreceiving > 2 75 mgreceiving > 2.75 mg

Miner, et al. Droperidol 5 mg IM versus prochlorperazine10 mg IM/IV

Greater pain reduction at 1 hour; P < 0.001

‐ No difference‐ Most common

sedation

Weaver et al. Droperidol 2.5 mg IV versus prochlorperazine10 mg IV

Pain‐free at 30 minutes; P < 0.01

‐ No difference‐ Most common

akathisia

Richman, et al.

Droperidol 2.5 mg IM versus meperidine 1.5 mg/kg IM

Similar pain reduction; P=0.33

‐ Drop > akathisia‐ Meperidine >

sedation


Management of Side Effects

Torsades de pointes• 9 cases have been reported in the last 30 years

• Only occurred in patients receiving doses > 5 mg

Drug induced parkinsonism Drug-induced parkinsonism• Administration of concomitant anticholinergic medication

Orthostatic hypotension• Pretreat with a normal saline bolus


Take Home Points

Droperidol 0.625-2.5 mg IV/IM for acute migraine attacks is an efficacious option with minimal side effects

Only need to obtain a baseline QTc prior to administration• Routine cardiac monitoring not necessary

Most patients experience pain-relief in 2 hours or less

Short half-life allowing quick ED discharge

Pharmacists can play a role in reducing the occurrence of drug-related side effects• Home medication histories• Pre-medication agents

Silberstein SD, et al. Neuro. 2003;60:315‐21.

Pediatric Intranasal MidazolamPediatric Intranasal Midazolam

Kimberly Glasoe, PharmDEmergency Medicine Clinical Pharmacist

Mercy Hospital – Allina HealthCoon Rapids, MN

Kimberly Glasoe, PharmDEmergency Medicine Clinical Pharmacist

Mercy Hospital – Allina HealthCoon Rapids, MN

Disclosure

Kimberly Glasoe reports no relevant financial relationships.



Objective

Identify scenarios where intranasal midazolam would be appropriate for mild to moderate pediatric sedation

Nasal Atomizer and AdministrationMAD Nasal™ - Intranasal mucosal atomization device

Intranasal Midazolam Dosing

Midazolam 0.2-0.5 mg/kg

Lower end dose 0.2 mg/kg• Imaging studies

• Positioning

Hi h d d 0 5 /k Higher end dose 0.5 mg/kg• Laceration repair

• Ortho procedures

• IV line placement

Maximum 10 mg/dose or repeat administration

Pharmacokinetics

Onset~ 4 - 6 minutes

Peak~ 10 - 14 minutes

• 55% bioavailable compared to IV

0 utes

Duration~ 45 - 60 minutes

Additional Information

Midazolam concentration 5 mg/ml

Maximum volume per nare – 1 ml

Burning with administration – few/no patients reported memory of pain

Monotherapy – shows no significant respiratory depression

Others in literature – fentanyl, sufentanyl, naloxone, ketamine

Conclusion

Intranasal midazolam allows for a rapid, non-invasive & reliable method for mild to moderate pediatric sedation



References

Acworth, J.P., D. Purdie, and R.C. Clark, Intravenous ketamine plus midazolam is superior to intranasal midazolam for emergency paediatric procedural sedation. Emerg Med J. 2001;18(1):39-45.

Bates, B.A., S.A. Schutzman, and G.R. Fleisher, A comparison of intranasal sufentanil and midazolam to intramuscular meperidine, promethazine, and chlorpromazine for conscious sedation in children. Ann Emerg Med.1994;24(4):646-51.

Chiaretti, A., G. Barone, et al. Intranasal lidocaine and midazolam for procedural , , , psedation in children. Arch Dis Child. 2011 Feb;96(2):160-3.

Gilchrist, F., A.M. Cairns, and J.A. Leitch, The use of intranasal midazolam in the treatment of paediatric dental patients. Anaesthesia. 2007;62(12):1262-5.

Knoester, P.D, et al. Pharmacokinetics and pharmacodynamics of midazolam administered as a concentrated intranasal spray. A study in healthy volunteers.British Journal of Clinical Pharmacology. 2002;53(5):501-7.

Yealy, D.M., et al., Intranasal midazolam as a sedative for children during laceration repair. Am J Emerg Med. 1992;10(6):584-7.

Wermeling, D.P. et al., Bioavailability and pharmacokinetics of lorazepam after intranasal, intravenous, and intramuscular administration. J Clin Pharmacol.2001;41(11):1225-31.

[Don’t] Take My Breath Away: The Role of Glucagon in Acute AsthmaThe Role of Glucagon in Acute Asthma

ExacerbationNadia Awad, Pharm.D.

PGY‐2 Emergency Medicine Pharmacy Resident

Robert Wood Johnson University Hospital

New Brunswick, New Jersey

Nadia Awad, Pharm.D.


Robert Wood Johnson University Hospital

New Brunswick, New Jersey

Disclosure

Nadia Awad reports no relevant financial relationships

Learning Objective

Describe the various doses and routes of administration for glucagon in the management of acute asthma exacerbation

Clinical Vignette

SH is a 42‐year‐old female who presents to the emergency department with the following chief complaint:

“It’s happening again…I just need to be intubated.”

Clinical Vignette (cont’d.)

Has she been here before?• SH has been in the ER more than a dozen times in the past 3 months

• Previous visits related to acute exacerbations of• Previous visits related to acute exacerbations of asthma secondary to ethanol abuse

• Non‐compliant with medications

• Has been intubated several times and required admission to the intensive care unit



Clinical Vignette (cont’d.)

SH presents with tachypnea and acute shortness of breath with audible wheezing

Physical exam:

• HR 115 bpm; RR 43 bpm with signs of accessoryHR 115 bpm; RR 43 bpm with signs of accessory muscle use; 88% O2 saturation on room air

• Decreased breath sounds bilaterally with inspiratory and expiratory wheezing

Readings from peak flow meter are consistently in the red zone between 150 and 160 L/min

“Run of the Mill”

Oxygen therapy

Nebulized solution of albuterol 2.5 mg and ipratropium 0.5 mg q20 minutes x 3 doses

Methylprednisolone 125 mg IV x 1Methylprednisolone 125 mg IV x 1

SH is not showing any signs of improvement

• Treatment with continuous nebulized albuterol is started at a rate of 10 mg/hr

“Kitchen Sink”

Terbutaline 0.25 mg SQ x 1 dose

Magnesium sulfate 2 g IV x 1 dose

Still no improvement

• Loading dose of aminophylline 400 mg IV is ordered• Loading dose of aminophylline 400 mg IV is ordered

The ED attending physician asks:

“Can we try glucagon in this patient?”

Rationale

Glucagon is a 29‐amino acid polypeptide hormone

• Produced and secreted by the α‐cells of the islets of Langerhans in the pancreasof Langerhans in the pancreas

Mechanism of action:

• Causes relaxation of the bronchial smooth muscles

• Stimulates adenyl cyclase to activate the synthesis of cyclic adenosine monophosphate (cAMP)

Give Me Proof

Study Design Population Intervention Results

(1) Open‐label,non‐blinded, non‐controlled study

n = 14

• ED adult patients • Mild to moderately

severe asthma exacerbation

Glucagon 1 mg IV over 1 minute

8/14 (57%) achieved a mean increase in PEFR of ≥ 60 mL/min after

10 minutes

( ) d d l(2) Randomized,double‐blind, placebo‐

controlled study

n = 46

• Adult ED patients• Asthma exacerbation• Peak expiratory flow

rate (PEFR) < 350 mL/min at presentation

Glucagon 0.03 mg/kg IV over 2

minutes

Placebo: equivalentvolume of normal saline solution

Improvement in PEFR of ≥ 60 mL/min after

10 minutes:

Glucagon: 2/21 (9.5%)Placebo: 3/25 (12%)

1Wilson et al. J Emerg Med 1990; 8:127‐130.2Wilber et al. Ann Emerg Med 2000; 36:427‐431.

Switching It Up

Nebulized Glucagon for Bronchospasm in Asthmatic Patients

Study Design Randomized, double‐blind, placebo‐controlled, crossover study in pulmonary function lab

Populationand Methods

• History of chronic stable asthma (n = 10)• Methacholine challenge administered to the point at which baseline forced expiratory volume in one second (FEV1) decreased by at least 20%

Intervention • Glucagon 2 mg administered via nebulization and effects on FEV1 were compared to nebulized normal saline

• Nebulized albuterol 2.5 mg given after administration of either treatment • Patients returned one week later to receive alternative solution (nebulized glucagon or normal saline)

Results Improvement in FEV1 after 15 minutes:• Nebulized glucagon: 58% ± 15% • Nebulized normal saline: 36% ± 7%

Melanson et al. Am J Emerg Med 1998; 16:272‐275.

p < 0.05



Take Home Message

Effects of glucagon in treating bronchospasm associated with acute asthma exacerbation has mixed results

Anecdotally, intravenous glucagon at a dose of 2 mg has been administered at RWJUH to select patients with bronchospasm with positive results

Can be considered as a last‐line option if patients with acute asthma exacerbation do not show improvement with standard therapy

The Use of Richmond Agitation Sedation Scale (RASS) for Alcohol Withdrawal in the(RASS) for Alcohol Withdrawal in the

Emergency Department

Lauren King, PharmD


The Johns Hopkins Hospital

Lauren King, PharmD


The Johns Hopkins Hospital

Disclosure

Lauren King reports no relevant financial relationships.

Objective

Describe the benefits of using RASS for the assessment of acute alcohol withdrawal in an adult emergency department

Acute Withdrawal Disorder

Pathophysiology

• Reduced transmission of GABAA pathway

• Enhanced neurotransmission in glutamate pathway

Symptoms y p

• May occur within hours of the last drink• Typically do not develop until 48 – 72 hours after last drink

• Agitation

• Tachycardia

• Fever

• Diaphoresis

• Hypertension

Arch Intern Med. 2004;164:1405‐12.

How do healthcare professionalstitrate therapy?py



Scales Used to Titrate Therapy

Clinical Institute Withdrawal Assessment of Alcohol Scale, Revised (CIWA‐Ar)

Alcohol Withdrawal Syndrome (AWS) Type Indicator

Minnesota Detoxification Scale (MINDS)

Subjective Clinical Assessment

Scale name Description Advantages Disadvantages

CIWA – Ar • 10 symptoms categories including nausea and vomiting,tactile, auditory, and visual disturbances, tremor, paroxysmal sweats, anxiety, headache, agitation, orientation and clouding of sensorium

• Considers variety of symptoms

• Simple scoring system

• Vital signs not accounted for in scoring

• Specific verbiage necessary for accurate assessment

• Time to perform assessment

AWS Type Indicator • 3 categories of symptoms including CNS excitation

• Considers variety of symptoms and

• Complex assessment and documentationincluding CNS excitation,

adrenergic hyperactivity and delirium

• Treatment dictated by symptoms present

symptoms and treatment directed to specific symptomatology

• Simple scoring system• Accounts for vital signs

and documentation• Time to perform

assessment

MINDS • 9 symptom categories including pulse, diastolic blood pressure, tremor, sweat, hallucinations, agitation, orientation, delusions, seizures

• Considers variety of symptoms

• Accounts for vital signs

• Complex scoring system

• Time to performassessment

• Not validated

The Addition Research Foundation Clinical Institute Withdrawal Assessment for Alcohol, revised ScalePharmacotherapy. 2005;25(8):1073‐83.Pharmacotherapy. 2007;27(4):510 – 8.

Institution Guidelines

Provider orders nurse‐driven alcohol withdrawal protocol and assesses patient’s baseline RASS

Nurse titrates medication administration to a goal RASS of ‐1 b d id li th t d li ht lbased upon guidelines that recommend light somnolence as the recommended therapeutic endpoint

Arch Intern Med. 2004;164:1405‐12.

AWS Guidelines compared to RASS

Light somnolence

• State in which patient is awake but tends to fall asleep unless stimulated or is sleeping but easily aroused

RASS of ‐1

• Patient responds to verbal stimuli by opening his/her eyes and maintain eye contact for >10 seconds

Arch Intern Med. 2004;164:1405‐12.

Richmond Agitation‐Sedation Score (RASS)Score Term Description

+4 Combative Overly combative, violent, immediate danger to staff

+3 Very agitated Pulls or removes tubes or catheters; aggressive

+2 Agitated Frequent non‐purposeful movement, fights ventilator

+1 Restless Anxious, but movements are not aggressive or vigorous

0 Alert and calm

‐1 Drowsy Not fully alert, but has sustained awakening (eye opening and eye contact) to voice (greater than or equal to 10 seconds)

Verbal stimulation

‐2 Light sedation Briefly awakens with eye contact to voice (<10 seconds)

Verbal stimulation

‐3 Moderate sedation Movement or eye opening to voice (but no eye contact)

Verbal stimulation

‐4 Deep sedation No response to voice, but has movement or eye opening to physical stimulation

Physical stimulation

‐5 Unarousable No response to voice or physical stimulation Physical stimulation

RASS Procedure

Observe the patient. Is patient alert and calm? (score 0)

Does the patient have behavior that is consistent with restlessness or agitation • Score +1 to +4 using the criteria



RASS Procedure (cont’d)

If the patient is not alert, in a loud speaking voice state patient’s name and direct patient to open eyes and look at speaker. Repeat if necessary. Can prompt patient to continue looking at speaker.

• Score 1 to 3 using criteria• Score ‐1 to ‐3 using criteria

If patient does not response to voice, physically stimulate patient by shaking shoulder then perform sternal rub if necessary.• Score ‐4 to ‐5 using criteria

Advantages to RASS

Validated tool for sedation

Less symptoms to assess compared to other tools for alcohol withdrawal leading to quick nursing assessment

Well known to health care professionals

Disadvantages to RASS

Potential for inter‐rater variability

Not specific to alcohol withdrawal

Summary

Goal of managing alcohol withdrawal in the emergency department is rapid titration of benzodiazepines in short

frequency to gain adequate symptom controlHeart to Heart: Recognizing Undiagnosed

Congenital Heart Disease in the EDCongenital Heart Disease in the ED

Leah Hatfield, PharmD, BCPSClinical Pharmacist Specialist, UNC Healthcare

Assistant Clinical Professor, UNC Eshelman School of [email protected]

Leah Hatfield, PharmD, BCPSClinical Pharmacist Specialist, UNC Healthcare

Assistant Clinical Professor, UNC Eshelman School of [email protected]

Disclosure

Leah Hatfield reports no relevant financial relationships

It’s NOT Just Another Sick Baby!



Presentation to the ED

A 3 week old infant presents to the ED and the parents note the following complaints:• Poor sleep• Poor feeding toleranceg• Persistent fussiness and irritability

DON’T always assume the obvious:• Normal newborn• Neonatal sepsis or infection• Colic or GERD

Symptoms of CHD at Presentation

Easy to Recognize

Congestive heart failure

Cyanosis

Shock

A Little More Tricky

Feeding difficulty

Tachypnea

Fussiness or agitation Shock

Diaphoresis

Murmur

Abnormal heart rate

Fussiness or agitation

Coughing and wheezing

Lethargy

Poor weight gain

Asymptomatic

Types of Lesions: Ductal Dependent

Left Sided

HLHS

Aortic stenosis

Coarctation of the aorta

Right Sided

Tetralogy of Fallot

Pulmonary atresia

Coarctation of the aorta

Interrupted aortic arch

Types of Lesions: Non-Ductal Dependent

Atrial septal defect

Ventricular septal defect

ALCAPA

Congenital cardiomyopathy

The Ductus Arteriosus

PDA

Definitive Diagnosis

Assess BP and pulses in all four extremities

Pulse oximetry

Chest radiography

Hyperoxia test Hyperoxia test

Echocardiogram



Acute Management

ABC’s, not as easy as 1-2-3• Oxygen may help or harm

• Fluid should be used judiciously to improve perfusionp

Access• Upper extremity or scalp IV

• Avoid IO in patients with poor peripheral pulse or perfusion

Acute Management: Alprostadil

Initiate immediately for suspected ductal dependent lesion• Rule out sepsis prior to initiation

• 0.05-0.1mcg/kg/min, titrate to clinical effect

• Decrease dose once ductus reopens

Monitor for expected adverse effects• Apnea

• Nonpathologic hyperthermia

• Decreased SVR

Thank You Think, Pair, Share!

From the Pearls you just heard, discuss with someone near you…

What is something you can apply in your setting?

What are challenges you would encounter?

Alternative Dosing of Adenosine:Does Size Really Matter?Does Size Really Matter?

Daniel Jarrell, PharmDPGY2 Emergency Medicine Resident

University of Arizona

Daniel Jarrell, PharmDPGY2 Emergency Medicine Resident

University of Arizona

Disclosure

Daniel Jarrell reports no relevant financial relationships.



What should you do?

60 year old male with heart palpitations• EKG reveals supraventricular tachycardia

• Heart rate – 165 beats per minute

• Past medical history• Appendectomy 2 months agoAppendectomy 2 months ago

• Access – intraosseous

• Weight – 85kg

Attending physician would like to chemically cardiovertwith adenosine

Objective

At the end of this pearl, the listener will be able to…• Choose appropriate dosing of adenosine for alternative vascular

access

Adenosine

Depress sinus node rate and transient atrioventricular (AV) nodal block

Diagnostic and therapeutic use

Extremely short duration of action

Rankin et al. Am Heart J. 1990.DiMarco et al. J Am Coll Cardiol. 1985.

2010 ACLS Guidelines

Recommend initial dose of 6mg given peripherally• May repeat with 12mg if ineffective

• 0.1mg/kg – 0.3mg/kg for pediatrics

Reduce initial dose to 3mg Reduce initial dose to 3mg…• Post-cardiac transplant patients

• Concomitant use of dipyridamole or carbamazepine

• Administration through a central vein

Increased dose may be necessary when…• Significant blood concentrations of theophylline or caffeine

presentNeumar et al. ACLS Guidelines. Circulation. 2010.

Central vs Peripheral

Route of administration influenced efficacy

Mean effective dose (p < 0.005)• Central (femoral vein): 3.8mg

P i h l ( t bit l f i ) 8 4• Peripheral (antecubital fossa vein): 8.4mg

Rankin et al. Am Heart J. 1990.

Central vs Peripheral

Mean dose required (p < 0.0001)• Central: 3.8 1.6mg

• Peripheral: 6.3 3.3mg

Time from dose to termination of SVT (p < 0.0001)• Central: 12 7 5 1 seconds• Central: 12.7 5.1 seconds

• Peripheral: 19.2 7.9 seconds

No difference in total frequency of adverse effects

Lower doses of adenosine more effective after central vs peripheral administration• Initial dose via central vascular access should be 3mg

McIntosh‐Yellin et al. J Am Coll Cardiol. 1993.



Intraosseous

Animal model to determine effective dose via peripheral, central, and intraosseous routes• Central: 0.087mg/kg

• Peripheral: 0.159mg/kg

• Intraosseous: 0 127mg/kgIntraosseous: 0.127mg/kg• p = 0.006 (central vs peripheral)

• p < 0.03 (central vs peripheral vs IO)

• p = non-signficant (central vs IO or peripheral vs IO)

Conclude intraosseous route effective for adenosine administration• Effective dose between peripheral and central dosing

Getschman et al. Arch Pediatr Adolesc Med. 1994.

Intraosseous

Case report demonstrating successful intraosseous administration of adenosine to terminate SVT

11-day-old female presented to ED with SVT• History of SVT on day of birth converted with IV adenosine

• IV access difficult to obtain IO access initiated• IV access difficult to obtain, IO access initiated

• 0.1mg/kg adenosine via IO converted to NSR• Reverted to SVT but converted with additional 0.1mg/kg dose

Friedman. Ann Emerg Med. 1996.

Intraosseous

Case reports of unreliable termination of SVT 2 month old with previous cases of SVT responsive to IV

adenosine• 0.05mg/kg, 0.15mg/kg, 0.25mg/kg all via IO with no resolution

• No transient asystole

• 0.1mg/kg given through peripheral IV terminated SVT

4 month old with previous case of SVT responsive to IV adenosine• 0.1mg/kg, 0.2mg/kg both IO with no resolution

• No transient asystole

• 0.1mg/kg, 0.2mg/kg central (femoral) IV caused transient asystole, conversion to NSR, then return to SVT

Goodman et al. Pediatr Emer Care. 2012.

What should you do?

60-year-old male with heart palpitations• EKG reveals supraventricular tachycardia

• Heart rate – 165 beats per minute

• Past medical history• Appendectomy 2 months agoppe decto y o t s ago

• Access – intraosseous

• Weight – 85kg

Attending physician would like to chemically cardiovertwith adenosine

4-5mg initial dose followed by 8-10mg if necessary

References

Babuty D, Aupart M, Cosnay P et al. Electrocardiographic and Electrophysiologic Properties of Cardiac Allografts. J Cardiovasc Electrophysiol. 1994;5:1053-63.

Delacretaz E. Supraventricular Tachycardia. N Engl J Med. 2006;354:1039-51. DiMarco JP, Sellers TD, Lerman BB et al. Diagnostic and Therapeutic Use of Adenosine in Patients With Supraventricular

Tachyarrhythmias. J Am Coll Cardiol. 1985;6(2):417-25. Ellenbogen KA, Thames MD, DiMarco JP et al. Electrophysiological Effects of Adenosine in the Transplanted Human Heart:

Evidence of Supersensitivity. Circulation. 1990;81:821-8. Friedman FD. Intraosseous Adenosine for the Termination of Supraventricular Tachycardia in an Infant. Ann Emerg Med.

1996;28:356-8. Getschman SJ, Dietrich AM, Franklin WH et al. Intraosseous Adenosine: As Effective as Peripheral or Central Venous

Administration? Arch Pediatr Adolesc Med 1994;148:616 9Administration? Arch Pediatr Adolesc Med. 1994;148:616-9. Goodman IS, Lu CJ. Intraosseous Infusion is Unreliable for Adenosine Delivery in the Treatment of Supraventricular

Tachycardia. Pediatr Emer Care. 2012;28:47-8. Manole MD, Saladino RA. Emergency Department Management of the Pediatric Patient with Supraventricular Tachycardia.

Pediatric Emergency Care. 2007;23:176-89. McIntosh-Yellin NL, Drew BJ, Scheinman MM. Safety and Efficacy of Central Intravenous Bolus Administration of Adenosine

for Termination of Supraventricular Tachycardia. J Am Coll Cardiol. 1993;22:741-5. Neumar RW, Otto CW, Link MS et al. Part 8: Adult Advanced Cardiovascular Life Support: 2010 American Heart Association

Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122:S729-67. O’Nunain S, Jennison S, Bashir Y et al. Effects of Adenosine on Atrial Repolarization in the Transplanted Human Heart. Am

J Cardiol. 1993;71:248-51. Overholt ED, Rheuban KS, Gutgesell HP et al. Usefulness of Adenosine for Arrhythmias in Infants and Children. Am J

Cardiol. 1988;61:336-40. Rankin AC, Oldroyd KG, Chong E et al. Adenosine or Adenosine Triphosphate for Supraventricular Tachycardias?

Comparative Double-Blind Randomized Study in Patients with Spontaneous or Inducible Arrhythmias. American Heart Journal. 1990;119:316-23.

Propofol for Alcohol Withdrawal Syndrome:Imitation is the Sincerest Form of FlatteryImitation is the Sincerest Form of Flattery

Darrel W. Hughes, Pharm.D., BCPSClinical Specialist, Emergency Medicine

University Health SystemUniversity of Texas Health Science Center San Antonio

Darrel W. Hughes, Pharm.D., BCPSClinical Specialist, Emergency Medicine

University Health SystemUniversity of Texas Health Science Center San Antonio



Disclosure

Darrel W. Hughes reports no relevant financial relationships.

Why Should We Care?

Alcohol most widely abused drug in the world

8-31% of hospitalized patients develop alcohol withdrawal (AWD)withdrawal (AWD)

AWD may increase mortality 300%

Diagnostic Criteria

Cessation or reduction in heavy or prolonged alcohol use

Diagnostic Criteria

Two or more of the following developing hours to days after cessation or reduction• Autonomic hyperactivity

• Increased hand tremor

• Insomnia

• Nausea or vomiting

• Visual, tactile or auditory hallucinations or illusions

• Psychomotor agitation

• Anxiety

• Grand mal seizures

Diagnostic Criteria

Symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioningfunctioning

Diagnostic Criteria

Symptoms are not due to a general condition and are not better accounted for by another mental disorder



Neurophysiology

Chronic ingestion of alcohol• Decreases GABA-A1 receptor function

• Increases NMDA2 receptor function

D i ithd l f l h l During withdrawal of alcohol• NMDA overload

• Delirium, hallucinations and seizures

• Decreased GABA • Tremors, diaphoresis, tachycardia, anxiety and

seizures

1 Gamma‐amino‐butyric acid type A2 N‐methyl‐D‐aspartate

Benzodiazepine

Bind GABA-A receptors

Control agitation

Reduce• Mortality

• Duration of AWD symptoms

• Treatment complications

GABA receptor down regulation…• Saturation → refractoriness

Benzodiazepine Refractory Withdrawal

What to do?• More benzodiazepine…

• Waste of good benzodiazepine

• No added control of agitation• No added control of agitation

• q10 minute orders make nurses angry!!!

Give propofol a try!

Propofol for Alcohol Withdrawal

Dose dependent hypnotic effects (5-80 mcg/kg/min)

• Activates GABA-A receptors AND…

• Inhibits NMDA at glutamate receptor

Effective for benzodiazepine resistancep

Case series level of evidence• Clinical data soon???

Short t1/2 and predictable metabolism

SE: hypotension, hypertriglyceridemia and PRIS



Take Home Points

Alcohol withdrawal • Too much NDMA and not enough GABA

Benzodiazepine• Only affect GABA receptors

• Saturated GABA receptors → refractoriness

Propofol• Hits both GABA and NMDA receptors

• Imitates neuro-biochemistry of alcohol

Thank You!

“Everybody has to believe in something.....I believe I'll have another drink.”

-W. C. Fields

Ebbing the flow in trauma-induced gcoagulopathy

Brittany R. Traylor, PharmDUC Davis Medical Center

Sacramento, CA

Brittany R. Traylor, PharmDUC Davis Medical Center

Sacramento, CA

Disclosure

Brittany R. Traylor reports no relevant financial relationships.

Trauma-induced coagulopathy (TIC)

Exsanguination is the leading cause of preventable death among injured patients – up to 1/3 presenting with coagulopathy

TIC i t d ith 3 f ld i i t lit TIC associated with a 3-fold increase in mortality among injured patients

Coagulopathic patients with identical Injury Severity Scores (ISS) have doubled rates of mortality

Causes of Trauma-induced Coagulopathy

Loss coagulopathy

Dilutional coagulopathy

Consumption

Hyperfibrinolysis

Anemia

Hypothermia*

Acidosis*

Electrolyte disturbances



XIIaXIIa

XIaXIa

IXaIXa

VIIIaVIIIaVIIaVIIa

Va, VIIIa, Va, VIIIa,

Extrinsic Pathway – Activated by tissue factor in injured subendothelium. Measured by PT/INR

Intrinsic Pathway – Contact activated by platelets. Measured by aPTT

XaXa

Thrombin (IIa)

Thrombin (IIa)

Fibrin (Ia)Fibrin (Ia)

Degradation products

Degradation products

XaXa

Plasminogen Plasmin

XaXa

Fibrinogen (I)

Prothrombin (II)

Heparins/LMWHstPA

XIIIaXIIIa

University of Arizona Medical Center

Prothrombin Complex Concentrate (PCC) – replaces deficient clotting factors (II, IX, and X). These factors will still require activation in plasma

T i id (TXA) f ibl l Tranexamic acid (TXA) – forms a reversible complex that displaces plasminogen from fibrin resulting in inhibition of fibrinolysis

In vitro study

Results: • aPCC shortened clotting time from 11.8 to 7 minutes

• TXA increased clot lysis time from 6.0 to 16 or 37 minutes

• Combination shortened clotting time AND increased clot lysis time

The combination appears to improve clot stability

University of California, Davis Medical Center

Anti-inhibitor Coagulant Complex (FEIBA) – replaces deficient clotting factors in their active form (IIa, IXa, and Xa)

Recombinant Factor VIIa (rFVIIa) – replaces deficient ti t d l ti f t VIIactivated coagulation factor VII

Tranexamic acid (TXA) – inhibits fibrinolysis

Conclusion

May begin to see combinations of these products (PCC + TXA) being used

Some benefits over fresh frozen plasma (FFP)

More studies may help elucidate benefits and risks of these coagulation factor concentrates

Uncommon Pediatric Treatments in Traumas -Avoiding the "I wish I had known that" moment

Shannon Manzi, PharmD

Boston Children’s Hospital

Shannon Manzi, PharmD

Boston Children’s Hospital



Disclosure

Shannon Manzi reports no relevant financial relationships.

Objectives

Describe two situations more prevalent in pediatric trauma

Outline the use case for and against high dose steroids i di t i i l d tin pediatric spinal cord trauma

She swallowed what??!

Button batteries and magnets

Serious ingestion, surgical intervention often necessary

Button batteries• Corrosion of the battery lodged in the esophagus can result in fistulas,

strictures, and erosions• Although some are made of mercury oxide, g y

mercury poisoning is unlikely due to poor GIabsorption

• One case report using PEG – not routinely recommended – removal must occur within 2 hours, required higher than usual volume

Magnets• Attract each other through intestinal wall, creating fistulas, erosions, acute

abdomen, etc

That must have hurt….

Methylene Blue for Joint Injuries Suspected open joint injuries – Extravasation is highly indicative of

open joint injury

1. 1% Lidocaine infiltration first (max 0.6 mL/kg). Additionally analgesia may be necessary.

2. 1 mL methylene blue in 500 mL NS instilled into the joint space. A large volume may be required.

Adverse effects• Injection of methylene blue into joint space has resulted in effusion in the treated

j i tjoint.

Contraindications:• Known hypersensitivity to the drug • Severe renal impairment • Glucose-6-phosphate dehydrogenase deficiency • Methemoglobinemia

Topical skin discoloration can be removed with a dilute solution of bleach if necessary.

Good reference with great pictures:• p://emedicine.medscape.com/article/114453-treatment



SCIWORA

SCIWORA – Spinal Cord Injury WithOut Radiographic Abnormality

Over 65% of cases occur in children < 8 years old Immediate transient deficits may be followed by severe deficits

hours later Some may resolve for 24 hours and return with severe deficits Some may resolve for 24 hours and return with severe deficits High dose methylprednisolone is NOT routinely recommended for

spinal cord injuries in children• NASCIS II trial – found benefit only in post hoc analysis, many questioned

methods, excluded kids < 12 years• NASCIS III trial – found benefit in 48 hr regimen, not 24 hr• Several others found no benefit, risks of severe GI bleed, infections

Fluid resuscitation and pressor therapy – alpha agonists such as norepinephrine or phenylephrine

Picture from /www.elearningdigital.com

Before you cut that…

Tissue entrapment by zipper

Before getting out the wire cutters – which freak out grown men let alone a 5 year old…

Try liberally applying mineral oil to the trapped area and iti 5 10 i t Oft th ti ill lid twaiting 5-10 minutes. Often the tissue will slide out

easily.

If not, a dose of intranasal midazolam before

using the wire cutters might be a good idea!

Not necessarily trauma, but good to know……

SVC syndrome

Superior Vena Cava (SVC) syndrome• Encircled by lymph nodes responsible for draining thoracic cavity

Most often seen in kids with Hodgkins or non-Hodgkinslymphoma• Massive adenopathy obstructs SVC, resulting in dilated chest and

neck veins, facial edema, drowsiness, stupor

All intravenous therapy must be via the lower extremities• SVC obstruction results in poor circulation in the upper extremities

and torso • Drug distribution is restricted and there is an increased risk of

thrombus formation.

When the Pain is Skin DeepTopical Analgesia in the EDTopical Analgesia in the ED

Courtney B. McKinney, PharmD, BCPSCritical Care Clinical Pharmacist

Intermountain Medical CenterSalt Lake City, Utah

Courtney B. McKinney, PharmD, BCPSCritical Care Clinical Pharmacist

Intermountain Medical CenterSalt Lake City, Utah



Disclosure

Courtney McKinney reports no relevant financial relationships.

Indications for Topical Analgesia

Things we DO in the ED

Venipuncture

Laceration or abrasion

Questions ASKED in the ED

Tattoos

Tattoo removaldebridement

First-degree burns Cosmetic procedures

Product Selection

Topical analgesia = topical anesthesia• Most commonly lidocaine based

Many available preparations/formulations• AerosolsAerosols

• Creams

• Gels

• Ointments

• Solutions for injection

• Compounded products

Product Selection

The product depends on the procedure

Key considerations in product selection• Is the skin broken or intact

• What is the surface area of the area involved

• What is your timeframe and setting

Three common products• Lidocaine 2.5%, Prilocaine 2.5% oil-in-water eutectic mixture

• Lidocaine 4% liposomal cream

• L.E.T solution or gel

Lidocaine/Prilocaine Eutectic Mixture

Dose: 1-2 gm/cm2 (max: 5 mg/kg lidocaine)

Application: intact skin only, occlusive dressing required, depth of penetration time dependent

Onset: 45-60 min

Duration: 2 hrs after removal

Pros: long lasting, ok to use on mucous membranes, studied in neonates

Cons: long onset, occlusive dressing required

Bottom line: consider for planned dermal procedures

EMLA®: package insert. APP Pharmaceuticals, 2008

Lidocaine 4% Liposomal Cream

Dose: 1-2 gm/cm2 (max: 5 mg/kg lidocaine)

Application: intact skin only, do not wash skin prior to application, occlusive dressing not required (recommended)

O t 30 i Onset: 30 min

Duration: 60 min

Pros: shorter onset, available OTC

Cons: No safety data in kids <2 yrs

Bottom line: good for minor burns or planned/non-emergent dermal procedures

LMX®: package insert. Ferndale Laboratories 2011



L.E.T Gel

Lidocaine 4%, epinephrine 0.05%, tetracaine 0.5% sterile compounded product

Dose: 1-3 ml (max: 5 mg/kg lidocaine)

Application: apply directly to open laceration/wound

Onset: 20 min

Duration: 45-60 min

Pros: ok to use on open skin, epinephrine may reduce systemic absorption and bleeding

Cons: epinephrine may cause vascular compromise

Bottom line: product of choice for open wounds

Schilling et al. Ann Emerg Med 1995;25:203‐8.

Large Surface Area Wounds

Otherwise known as “road rash”

Tends to cover more surface area than is practical or safe for the previously mentioned products

Make your own “Lido-Lube”Lid i 3 4 /k ( 1 2% l ti f i j ti )• Lidocaine 3-4 mg/kg (as 1 or 2% solution for injection)

• Large tube of sterile surgical lubricant

• Small emesis basin

• Mix in lubricant until the consistency is a thin gel

• Slather, wait 20 min, then scrub

Think, Pair, Share!




Wilderness Medicine:High Altitude Medicine ConcernsHigh Altitude Medicine Concerns

HAPE and HACE

Pam Walker, Pharm.D., BCPSClinical Coordinator- Emergency Medicine

Adjunct Clinical Assistant ProfessorUniversity of Michigan College of Pharmacy

University of Michigan Health Systems

Pam Walker, Pharm.D., BCPSClinical Coordinator- Emergency Medicine

Adjunct Clinical Assistant ProfessorUniversity of Michigan College of Pharmacy

University of Michigan Health Systems

Disclosure

Pamela Walker reports no relevant financial relationships.

Why High Altitude Sickness

Approximately 35 million people are travelling to altitudes greater than 3000 m• Nepal treks alone increased by 450% from 1994-2000

If not acclimated incidence of AMS is seen at altitudes of 2000 – 2500 m

Typical signs and symptoms include:• HA, nausea, vomiting, fatigue, insomnia, dizziness and anorexia

Pathophysiology not 100% understood• Current theory related to swelling of the brain

Generally self-limiting but can develop into high altitude pulmonary edema (HAPE) and/or cerebral edema (HACE)

Dumont L. et al. Travel Medicine and Infectious Disease (2005)3, 183‐188



Potential medical problems

Hypoxia High-altitude headache Acute Mountain sickness High-altitude cerebral

edema

High-altitude pulmonary edema (HAPE)

Organic brain syndrome Peripheral edema Retinopathyedema

Cerebrovascular syndromes

Retinopathy

Auerbach P. Wilderness Medicine 4th Ed

When is this a concern

Climbers/hikers that get to elevations > 2350 m (8000 ft.) are at risk for one of 3 forms of high altitude illness• Acute Mountain Sickness (AMS), HAPE and HACE

Best way to avoid is ensuring no overly rapid ascents• Published plans call for those > 2000 m to not increase their• Published plans call for those > 2000 m to not increase their

sleeping elevations by > 300 – 500 m and rest every 3rd to 4th

day

Definitions

High altitude = 1500 – 3500 m (4921- 11, 483 ft.)

Very high altitude = 3500 – 5500 m (11, 483 – 18, 045 ft.)

Extreme altitude = > 5500 m (> 18, 045 ft.)


Oxygenation changes

High altitude = decrease PO2 in alveolus. Decreasing exercise performance with an increase in ventilation (decreased PCO2 arterial)


High Altitude Pulmonary Edema

Occurs worldwide with highest incidence in winter months• Ski tourism

Pulmonary vasoconstriction and pulmonary hypertension• Nitric oxide• Prostacyclins• Sildenafil• Inhaled β agonist• Dietary L-arginine• Gingko biloba

Treatment is supplemental O2 and decreasing altitude• With possible portable hyperbaric chamber

HAPE prophylaxis

Those that have had previous bouts of HAPE are susceptible, with unpredictable recurrence

Most studies is acetazolamide followed by dexamethasone• Acetazolamide can help by creating bicarbonate diuresis and• Acetazolamide can help by creating bicarbonate diuresis and

simulating respirations• Also aids with countering insomnia at lower doses

Current controversies over the actual prophylaxis dose• Acetazolamide typically dosed as 500 mg/d

• Recent meta-analysis claims NNT(3) with 750 mg/d is better

• Side effects big issue with dose; paresthias and polyuria

Luks AM. Wilderness & Environmental Medicine. 2010;21:146‐55.Dumont L. et al. Travel Medicine and Infectious Disease. 2005;3:183‐8.



HAPE prophylaxis

Paresthias with acetazolamide ~ 42.9% vs. 5.6% of control• Called jhum jhum in Nepali

Polyuria with acetazolamide ~ 33.3% vs. 10% of control

D th i f l f th ith t i di ti Dexamethasone is useful for those with contraindications to acetazolamide

Concerns with using dexamethasone as prophylaxis since it just masks signs/symptoms


HAPE prophylaxis

• Potentially dangerous since you may ascend too quickly since not feeling ill effects

• Recommendations to include are > 4000 m; since both we equally effective at higher doses• Dexamethasone 8 – 16 mg/d vs. acetazolamide 750 mg/d when

ascending > 500 m/dascending > 500 m/d

Dexamethasone is recommended in situations of contraindication with acetazolamide

Small trials also evaluated nifedipine 60 mg and spironolactone 75 mg and 100 mg


Other HAPE prophylaxis

Tadalafil was studied versus placebo in those that were susceptible to HAPE• Small numbers and limited clinical experience compare with

nifedipine

SildenafilSildenafil

Salmeterol also a single placebo controlled study found that it decreased HAPE by 50% in susceptible climbers• Not recommended as monotherapy

Luks AM. Wilderness & Environmental Medicine. 2010;21:146‐55.

HAPE treatment

Oxygen, but if oxygen not available then there are a few pharmaceutical choices• Nifepidine has been key agent based on a single non-

randomized unblinded study• Not to be used as sole agent unless decent is dangerous and no

supplemental )2

• Phospodiesterase-5 inhibitors

• Fewer sides effects then seen with nifedipine• Less hypotension and tachycardia

• Becoming the preferred choice

Luks AM. Wilderness & Environmental Medicine. 2010;21:146‐55.

High Altitude Cerebral Edema

Potentially fatal situation that arise quickly Brain swelling, clinically it is an encephalopathy Signs/symptoms include

• Confusion/changes in consciousness• AtaxiaAtaxia• Papilledema• Urinary retention/incontinence• Difficulty speaking• Lassitude progresses to not being able to care for themselves• Blindness• Seizures• Coma

Hacket PH, et al High Altitude Medicine and Biology. 2004;5(2):136‐46.Luks AM, et al. Wilderness & Environmental Medicine. 2010;21:146‐55.

HACE prophylaxis

Also includes acetazolamide and dexamethasone• Dexamethasone is probably utilized more frequently in those

that are having to ascend too quickly• Search and rescue workers, military personnel

• Duration should not be longer than 10 days• Prevent adrenal suppression




Treatment

Descend immediately any delay can be fatal• Concerns if this occurs while sleeping

• Keep descending until the last point the climber was “normal” or at least 500 m

• Stagger may linger for a few daysgg y g y

Treatment with dexamethasone

Oxygen therapy and Gamow or portable hyperbaric chamber


Thank you

Physostigmine: It’s BackPhysostigmine: It s Back

Nicole M. Acquisto, Pharm.D., BCPSEmergency Medicine Clinical Pharmacy Specialist,

Department of PharmacyAssistant Professor, Department of Emergency MedicineUniversity of Rochester Medical Center, Rochester, NY

[email protected]

Nicole M. Acquisto, Pharm.D., BCPSEmergency Medicine Clinical Pharmacy Specialist,

Department of PharmacyAssistant Professor, Department of Emergency MedicineUniversity of Rochester Medical Center, Rochester, NY

[email protected]

Disclosure

Nicole M. Acquisto reports no relevant financial relationships.

Anticholinergic Toxicity

Peripheral Dry skin Flushing Xerostomia

Central Confusion Disorientation Psychomotor agitation

Cessation of perspiration Hyperthermia Mydriasis Tachycardia Urinary retention Decreased bowel sounds

y g Delirium Visual or auditory

hallucinations Ataxia

Mechanism of Action

Choline

Acetyl‐CoA

+Nerve Terminal

Post‐synaptic membrane

ACh

Acetate

Choline

Acetylcholinesterase

AChReceptor

Physostigmine



A Little History…

Controversy is rooted in the publication of case reports documenting the development of seizures and asystole that occurred when it was administered in TCA overdose

Seizures tend to occur when physostigmine is administered t idl i th tti f l t i t ttoo rapidly or in the setting of a pro-convulsant co-ingestant

Bradycardia and asystole occur due to the potentiation of vagal effects on cardiac tissue

Asystole occurs more commonly in patients with underlying cardiac arrhythmias or conduction disorders

Pentel P, Peterson CD. Ann Emerg Med. 1980;9:588‐90.Frascogna N. Curr Opin Pediatr. 2007;19:201‐5.

The Come Back… Studies to support its use in anticholinergic toxicity related to:

• Pure anticholinergics, antihistamines, atypical antipsychotics, cyclic antidepressants

Physostigmine vs. benzodiazepines (n = 52 total)• Reversing agitation 96% vs. 24%

• Reversing delirium 87% vs. 0%g

• Shorter recovery time 12 vs. 24 hours

• No difference in the incidence of ADE and length of stay

8 years of physostigmine experience• Rate of ADE < 5 % - diaphoresis, nausea and vomiting

• Rate of seizures < 1 %

• No cardiac arrhythmias

Retrospective study (n = 39)• Brief seizure in one patient

Beaver KM, et al. Am J Emerg Med. 1998;16:505‐7.Padilla RB, et al. Am J Emerg Med. 2002;20:569‐70.WeizbergM, et al. Clin Toxicol. 2006;44:319‐25.Cole JB, et al. Am J Emerg Med. 2001.Suchard JR. J Emerg Med. 2003;25:185‐91.Burns MJ, et al. Ann Emerg Med. 2000;374‐81.Rasimas JJ, et al. Clin Toxicol. 2010;48:648.Schneir AB, et al. Ann Emerg Med. 2003;42:14‐9.

Physostigmine Indication

• To avoid a higher level of care, intubation, catheterization, chemical or physical restraints from an anticholinergic drug overdose

Adult dose• 0.5 – 2 mg IV undiluted push over 10 minutes, may repeat every

15 – 30 minutes as needed Pediatric dosePediatric dose

• 0.01 – 03 mg/kg/dose Onset

• 5 minutes Duration

• 30 minutes – 2 hours Monitor for cholinergic effects

• Atropine readily available

Contraindications

Cardiac conduction abnormalities • QRS prolongation (> 120 msec) or AV block

(Type II or III)

Bradycardia < 60 bpm

Gastrointestinal/urinary obstruction

ConclusionPhysostigminePhysostigmine

Can be safely used in patients with anticholinergic toxicity for the resolution of significant symptoms

Thank You!



TPA for the PE in PEATPA for the PE in PEA

Alison M. Jennett-Reznek, PharmD, BCPSClinical Pharmacist – Emergency Medicine

December 5, 2012

Alison M. Jennett-Reznek, PharmD, BCPSClinical Pharmacist – Emergency Medicine

December 5, 2012

Disclosure

Alison Jennett Reznek reports no relevant financial relationships.

Pulseless Electrical Activity

Electrical activity on the monitor

Pulses are absent

Pneumonic to remember causes:• 6 H’s and 6T’s

H’s T’s

HypovolemiaHypoxia

Hydrogen ionsHyper or Hypokalemia

HypoglycemiaHypothermia

Tablets or toxinsCardiac Tamponad

Tension pneumothoraxThrombosis (cardiac/pulmonary)

TachycardiaTrauma (hypovolemia)

Signs to suspect PE

Prior to onset of cardiac arrest:• Sudden onset of severe dyspnea

• Tachypnea

• Chest pain

• TachycardiaTachycardia

• Cough

• Hemoptysis

• Cyanosis

• Low oxygen saturation

Patient specific considerations• Risk factors for PE (i.e. cancer, recent travel, history of DVT)

Indication for use of TPA

Suspicion of PE is high• Potential for harm

Cardiac arrest within 15 minutes • Earlier use may result in more favorable outcome

• Use later in resuscitation efforts may be futile or even harmful• Use later in resuscitation efforts may be futile or even harmful

No contraindications• Hemorrhage or suspected bleeding

Dosing Recommendations

rt-PA • Most studied and utilized

• Bolus dosing recommended in cardiac arrest setting

• Shortened infusion time has been studied

• 50 mg50 mg

• 100 mg

Tenecteplase • Bolus dosing

• 30-50 mg (weight-based)



Time is Perfusion

Reconstitution• High-risk medications

• Follow package recommendations to avoid errors

• Do not shake

Individual variations Individual variations• rt-PA

• Transfer device creates large hole in protective stopper making removal difficult

• Tenecteplase• Device contains safety needle for protection

Additional Therapy

Dependent on ROSC

Considerations include:• Heparin bolus +/- infusion

• Repeat bolus of rt-PA

• Follow up infusion of rt PA• Follow-up infusion of rt-PA

Use of Intranasal Medications in the E D t tEmergency Department

Renee Petzel Gimbar, PharmDClinical Assistant Professor

Clinical Pharmacist, EM/Med ToxUniversity of Illinois at Chicago College of Pharmacy

University of Illinois Hospital and Health Sciences System

Renee Petzel Gimbar, PharmDClinical Assistant Professor

Clinical Pharmacist, EM/Med ToxUniversity of Illinois at Chicago College of Pharmacy

University of Illinois Hospital and Health Sciences System

Disclosure

Renee Petzel Gimbar reports no relevant financial relationships.

Intranasal (IN) Route New(er) route of medication delivery

Rapid administration and onset of effects• Faster ED door to med administration

Bypass GI tract, absorption into systemic circulation and CNS• Drug levels similar to IV

Use both pre-hospital (EMS) and in Emergency Department (ED)

MAD Medication Delivery

Mucosal Atomizer Device (MAD)• Delivery of medication via fine mist absorbed via the nasal

mucosa

Have necessary supplies to obtain IV/IO access prior to th d i i t ti f IN di ti ifthe administration of any IN medications if necessary.• If an appropriate therapeutic response is not achieved after 2 IN

doses, consider an alternate route of administration like IV/IO access.

The maximum volume administered in each nostril is 1 mL (or 2 mL total). • In smaller children, volume may be smaller. Use the highest

medication concentration available to limit the volume.



Seizures/Status Epilepticus

Studies comparing IN midazolam and rectal diazepam in both pre-hospital and ED setting in pediatric patients

IN midazolam found to be as effective, if not more effective in this setting

Pain

Use of IN fentanyl for acute pain in multiple practice settings including ED

Treatment of pain related to fractures, burns

Implementation of fentanyl for children in a mixed adult and pediatric ED reduces time

to analgesic administration4

Single-center study• Review of pediatric patients given either IV morphine or IN

fentanyl prior to and after initiation of IN fentanyl protocol

Excluded if hemodynamic instability altered level of Excluded if hemodynamic instability, altered level of consciousness, altered RR, known opioid rxn, epistaxis or bilateral occluded nasal passages

Medication administration at the discretion of physician

• Fentanyl dosed at 1.5mcg/kg for patients aged 1-15 years

Decreased time to administration in fentanyl group by at least half (00:59 min to 00:32 min)

Use of intranasal fentanyl for the relief of pediatric orthopedic trauma pain5

Prospective, non-blinded, interventional study

Clinically suspected fracture in ED triage

81 patients (age 3-18, mean age 8 years old)

Weighed in triage fentanyl 2 mcg/kg INWeighed in triage, fentanyl 2 mcg/kg IN • Max dose 100mcg

Measured pain scores at 10, 20 & 30 min • Rescue pain meds considered if no relief after 20 min

Use of intranasal fentanyl for the relief of pediatric orthopedic trauma pain5

72% of patients• Onset of analgesia w/in 10 min

• 70-78% of these patients with sustained decrease in pain relief over study period

9% of patients required rescue analgesia after 20 min• Half of these patients were aged 9-18

• No differences in types of fractures

No vomiting, hypoxia, hypotension

No nasal complaints after administration

ED IN Fentanyl Use

IN fentanyl: • Pain management

• Pediatric patients (age 12 months – 18 years old)• 1 – 2 mcg/kg up to a maximum dose of 100mcg (50mcg/mL), may cg/ g up to a a u dose o 00 cg (50 cg/ ), ay

repeat after 5 minutes if no effect, maximum 2 IN doses

• Adult patients• Initial IN midazolam can be dosed at 0.2mg/kg up to a maximum

single dose of 10mg (5mg/mL), may repeat after 5 minutes if no effect, maximum 2 IN doses



Moderate Sedation

Midazolam• Adults & pediatric patients (1 – 18 years old) for the treatment of

anxiolysis during moderate sedation

• Initial IN midazolam can be dosed at 0.3mg/kg up to a maximum single dose of 10mg (5mg/mL), may repeat after 5 minutes if no effect, maximum 2 IN doses

Fentanyl• Adults and pediatric patients (age 1-18 years) as part of

moderate sedation

• 1 – 2 mcg/kg up to a maximum dose of 100mcg (50mcg/mL), may repeat after 5 minutes if no effect, maximum 2 IN doses

Opioid Toxicity6

Previous use of naloxone by multiple routes for reversal of opioids

Use by paramedics in field

Retrospective review of 344 EMS patients who received doses of 0 4 2 mg naloxone IN vs control group whodoses of 0.4-2 mg naloxone IN vs control group who received IV

Use of IN naloxone as effective as IV naloxone in the field• Patients receiving IN naloxone received higher dose

ED IN Naloxone Use

If unable to obtain IV access:• IN naloxone

• Adult patients

• 0.4 - 2mg/dose every 1-2 minutes up to 10 mg

• Pediatric patients

• Less than 20kg : 0.1mg/kg up to 2 mg, may repeat every 1-2 minutes up to 10 mg

• Greater than 20kg: 0.4 - 2mg/dose every 1-2 minutes up to 10 mg

SHOULD OBTAIN IV ACCESS ASAP

Other medications

Limited data for use of ketamine and ketorolac

As more literature published may be able to expand the medications delivered by this route

References

1. Effects of intranasal midazolam and rectal diazepam on acute convulsions in children: prospective randomized study. J Child Neurol. 2002;17:123-6.

2. Intranasal midazolam vs rectal diazepam in acute childhood seizures. Pediatr Neurol. 2006;34:355-9.

3. Prehospital intranasal midazolam for the treatment of pediatric seizures. PediatrEmerg Care. 2007;23(3):148-53.

4 Holdgate A Cao A Lo KM The implementation of intranasal fentanyl for children in a4. Holdgate A, Cao A, Lo KM. The implementation of intranasal fentanyl for children in a mixed adult and pediatric emergency department reduces time to analgesic administration. Acad Emerg Med. 2010;17:214-7.

5. Saunders M, Adelgais K, Nelson D. Use of intranasal fentanyl for the relief of pediatric orthopedic trauma pain. Acad Emerg Med. 2010;17:1155-61.

6. Merlin MA, Saybolt M, Kapitanyan R, Alter SM, et al.Intranasal naloxone delivery is an alternative to intravenous naloxone for opioid overdoses. Am J Emerg Med. 2010; 28:296-303.

7. UICHHSS Emergency Department Guideline for the use of Intranasal Medication

Nebulized Naloxone:A Kinder Gentler Awakening?A Kinder, Gentler Awakening?

Heather M. Schumann, PharmDAssociate Professor

California Northstate University College of Pharmacy

Heather M. Schumann, PharmDAssociate Professor

California Northstate University College of Pharmacy



Disclosure

Heather Schumann reports no relevant financial relationships.

The Situation

A 42 y/o male presents to the ED lethargic after overdosing on heroin.

BP 112/70 HR 84 RR 12 Temp AF O2 sat 70% 4L NC

PE: pinpoint pupils, shallow respirations, sclerosed veins

The MD orders naloxone, and nursing is attempting to start an IV

Would nebulized naloxone be appropriate for this patient?

Why the Need for Needleless Naloxone?

Rates of opioid abuse and overdoses are increasing

Prevention of occupational blood exposure in a high-risk patient population

Venous access not always readily obtainable

N Engl J Med. 2010;363:1981‐3.Prehospital Emergency Care 2012;16:289‐292.

Naloxone Opioid receptor antagonist indicated for reversal of

opioid induced respiratory depression

Various routes of administration• IV, IO, IM, SC, ET, IL, IN, nebulized

Onset of effect variable• Dependent on dose and route of administration

Duration of action variable• Dependent on dose of agonist and route of administration

Goldfrank’s toxicologic emergencies. New York, NY: McGraw Hill;2006:614‐7.Naloxone [package insert]. International Medication Systems, Limited, So. El Monte, CA; August 2001. http://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?id=614. Accessed September 24, 2012.

Nebulized Naloxone

Nebulized naloxone 2mg/3mL normal saline

Successfully reversed respiratory and CNS depression in a patient with methadone toxicity• O2 saturation 100% and normal mental status within 5 minutes

Repeat nebulized dose required ~ 1 hour later

Mild withdrawal symptoms noticed

Due to recurrence of symptoms continuous naloxone infusion initiated, resulting in severe opioid withdrawal requiring intubation

The Journal of Emergency Medicine. 2003;24:185‐187.

Nebulized Naloxone in the Prehospital Setting

105 patients received nebulized naloxone in the field for treatment of suspected opioid overdose, altered mental status or respiratory depression

22% had complete response

59% h d ti l 59% had partial response

19% had no response

Average dose 1.7-1.8mg for partial and complete responders

Patients with a complete response received naloxone earlier in their care

Prehospital Emergency Care 2012;16:289‐292.



Proposed Benefits of Nebulized Naloxone

Needless administration

Equipment already available in ED

Allows for dose titration• Patient can remove face mask if withdrawal beginning

• Nebulized dose can be repeated if symptoms recur

Severe withdrawal symptoms seem to be avoided

Questions Remaining

Is nebulized naloxone equivalent to intravenous naloxone? To intranasal therapy?

Which patients are most likely to benefit from nebulized naloxone?

Wh t th t i di ti t th ? What are the contraindications to therapy?

What is the minimal respiratory rate required for successful reversal with nebulized naloxone?

What is the optimal dose of nebulized naloxone?

At what point should rescue intravenous naloxone therapy be administered?

Prehospital Emergency Care 2012;16:289‐292.

Back to the Situation

A 42 y/o male presents to the ED lethargic after overdosing on heroin.

BP 112/70 HR 84 RR 12 Temp AF O2 sat 70% 4L NC

PE: pinpoint pupils, shallow respirations, sclerosed veins

The MD orders naloxone, and nursing is attempting to start an IV

Would nebulized naloxone be appropriate for this patient?

Pulling Bedside Tricks, Part II“Off Label” Medication UseOff Label Medication Use

Assisting with Patient Care in the Emergency Room

Joanne C. Witsil, PharmD, RN, BCPSClinical Pharmacist ‐ Emergency Medicine/Toxicology

Cook County Hospital (Stroger) Chicago, IL

Joanne C. Witsil, PharmD, RN, BCPSClinical Pharmacist ‐ Emergency Medicine/Toxicology

Cook County Hospital (Stroger) Chicago, IL

Disclosure

Joanne C. Witsil reports no relevant financial relationships.

Content Warning You are about to participate in an educational

session that may contain content of an adult nature. These slides are designed for ADULTS only and may include ideas that some viewers may find inappropriate since the information deviates from FDA approved use

If you are under the age of 18, if such material offends you or if it is illegal to view such material in your community, please EXIT NOW

If you stay, please ALWAYS put patient SAFETY FIRST • Consider all drug and patient factors prior to

using the following agents



Objective

Describe alternative uses for medications routinely used in the emergency department

Oh my, what is going on in your drawers!

Looking down the empty drawer in pyxis, drug shortages!• Treating Nausea and Vomiting

• No traditional agents such as; metoclopramide, prochlorperazine, ondansetron!

• Consider Haloperidol (Haldol®)• Dosing: 1- 5 mg IM/slow IVP

• Most respond to the 5 mg dose • Consider for postoperative

nausea/vomiting (PONV), cyclic vomiting syndrome, motion sickness/vertigo, migraine

Am Fam Physician. 2007;76:76-84.

Oh my, what is going on in your drawers!

Help me, I am in pain and all we have is normal saline flushes!

• Pain Control• Running out of traditional agents; no morphine,

hydromorphone fentanylhydromorphone, fentanyl

• Consider Low-dose Ketamine (LDK)

• Dosing: 0.25 – 0.5 mg/kg slow IVP over 1 minute

• Consider for acute causes of pain presented in the ED especially trauma cases to supplement opioids

Am J Emerg Med. 2010;28:820-27.Ann Emerg Med. 2012;59:497-503.

Rub this on to make it feel better!

Do not put my baby to sleep!• Avoiding procedural sedation in cutaneous

abscess drainage in children• Consider applying Lidocaine 4% topical cream

prior to incision and drainage (I&D) • Procedure

• Apply the topical anesthetic cream on the abscess area

• Cover with occlusive dressing for 30-40 minutes

• Results: 24% with topical anesthetic verses 41% without topical anesthetic needed procedural sedation

Cassidy-Smith T, et al. Amer J Emerg Med. 2010- in press. PMID:21129885

Rub this on to make it feel better!

Slippery when wet with blood!• Opening traumatic swollen eyelids for

examination• Consider applying benzoin swab stick along upper

and lower eyelids to increase traction when retracting eyelids

• Procedure• Clean and dry upper and lower eyelids to

remove all excess blood from lids• Apply thin layer of benzoin fluid to the

eyelids, taking care not to contact eye or eyelashes

• Allow benzoin to dry• Use fingers or Q-tips to gently retract the

lids http://academiclifeinem.blogspot.com/2011/03/trick-of-trade-benzoin-for-opening.html

What is going on down there!

Taken in CCH ED 08/09/12




Maggots (Myiasis)! Get them out of there!

• Taking care of a maggot infested wound• Depending on the type of infestation the following

techniques are considered;

• Surgical removal with local anesthesia

• Skin lesion is locally anesthetized

• Site excised surgically

• Primary wound closure once done

McIntosh, M, et al. Forensic Science International. 2011 Jul 210(1):12-5.http://emedicine.medscape.com/article/1491170-treatment.


• Occlusion/Suffocation

• Products include petroleum jelly, liquid paraffin, beeswax or heavy oil, lard or bacon strips over the central punctum

• Wait for larva to emerge and then pluck with ttweezers

• Wound cleansing until further intervention

• Diluted solutions such as Dakin’s, isopropyl alcohol, betadine, hydrogen peroxide

• Dakin’s>isopropyl alcohol>betadine> hydrogen peroxide (order of % kill)

• No statistically significant differenceshttp://emedicine.medscape.com/srticle/1491170-treatmentMcIntosh, M, et al. Forensic Science International. 2011 Jul 2010(1):12-5.

Thank you!Thank you!

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