cola 2017 (or 14)1/11/2018 9 acute pericarditis - treatment • nsaids • ibuprofen, indomethacin,...

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1/11/2018 1 COLA 2017 (or 14) Omar Francis, DO Jennifer Stevenson, DO, FACEP Henry Ford Health System MCEP Winter Symposium January 26, 2018 Immune Thrombocytopenic Purpura (ITP) Medscape. Craig M Kessler, MD. Updated December 2, 2016

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Page 1: COLA 2017 (or 14)1/11/2018 9 Acute Pericarditis - Treatment • NSAIDS • Ibuprofen, indomethacin, aspirin • Aspirin is the preferred post MI • Colchicine • European Society

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1

COLA 2017 (or 14)

Omar Francis, DO

Jennifer Stevenson, DO, FACEP

Henry Ford Health System

MCEP Winter Symposium

January 26, 2018

Immune Thrombocytopenic Purpura (ITP)

• Medscape. Craig M Kessler, MD. Updated December 2, 2016

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Pathophysiology

epidemiology

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Signs and symptoms

NOT ITP ITP

Diagnosis

• Isolated thrombocytopenia

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Management

Morbidity/Mortality

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Prognosis

Acute Pericarditis

New England Journal of Medicine : 371;25 - December 2014

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Acute Pericarditis – Case

A previously healthy 25-year-old man presents with pleuritic pain in the left side of the chest of 3 hours’ duration, radiating to the left trapezius ridge and relieved by sitting forward. On physical examination, he appears anxious. His pulse is 104 beats per minute and regular, his blood pressure is 125/80 mm Hg without a paradoxical pulse, and his temperature is 37.8°C. A three-component friction rub is auscultated along the left sternal border. An electrocardiogram (ECG) reveals ST-segment elevations in multiple leads, which are consistent with acute pericarditis. How should this case be managed?

Acute Pericarditis - Introduction

• 80 – 90% of cases idiopathic • assumed viral

• 10 – 20% of cases• post-cardiac syndromes

• connective tissue diseases (SLE)

• genetic auto-inflammatory diseases• TRAPS and familial Mediterranean fever

• Incidence : 5% of ED patients with non-ischemic CP

• 2:1 Male to Female ratio

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Acute Pericarditis – Introduction

• 1/3 of idiopathic pericarditis is associated with myocarditis

• *Mortality is low and prognosis is excellent

• Left-ventricular dysfunction is uncommon

• Pericardial effusions are present in 2/3 of patients

• *Sequela include Beck’s Triade & cardiac tamponade

• Most patients have one or two recurrences

Acute Pericarditis – Clinical Features

• Pleuritic chest pain

• Viral illness

• Sinus tachycardia and low-grade fever

• Pericardial friction rub

• ECG changes – diffuse ST elevation

• Pericardial effusion

• Diagnosis – 2 of the following :

• chest pain consistent with pericarditis, pericardial friction rub, typical ECG changes, or a pericardial effusion

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Acute Pericarditis - Diagnostics

• CBC, CRP, troponin I, Cr, LFTs

• WBC count modestly elevated.

• WBC > 13,000 suggests specific cause

• Anemia suggests underlying disorder

• CRP elevated in 75% of cases

• CXR usually normal

• Echocardiogram routinely indicated

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Acute Pericarditis - Treatment

• NSAIDS

• Ibuprofen, indomethacin, aspirin

• Aspirin is the preferred post MI

• Colchicine

• European Society of Cardiology 2004 guidelines

• recommended NSAIDs + colchicine

• ICAP trial 2013

• Glucocorticoids • immune-mediated disorders

• Pericardiocentesis - cardiac tamponade

• consider in patients with large effusions without tamponade

Acute Pericarditis – Treatment

• Disposition• Low-risk patients maybe discharged (Imazzio et al)

• NONE of the following:

• fever, immunosuppression, trauma, myopericarditis, a large pericardial effusion, cardiac tamponade & not on anticoagulant

• Duration

• NSAIDs 1 – 2 weeks

• Poor response – consider work up

• Colchicine 3 months

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Acute Pericarditis – Recurrence

• Recurrent pericarditis • Women at higher risk

• Treatment with steroids

• Reinstitute NSAIDs and add colchicine

• Serious late complications (constrictive pericarditis) is rare

Acute Pericarditis – Future Study

• Future study• RCTs to guide choice and duration of anti-inflammatory agent

• Role of CRP level

• Role of novel immunomodulators

• immune globulins, anti–tumor necrosis factor α antibody, azathioprine, or interleukin-1β antagonists

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Acute Pericarditis – Case

A previously healthy 25-year-old man presents with pleuritic pain in the left side of the chest of 3 hours’ duration, radiating to the left trapezius ridge and relieved by sitting forward. On physical examination, he appears anxious. His pulse is 104 beats per minute and regular, his blood pressure is 125/80 mm Hg without a paradoxical pulse, and his temperature is 37.8°C. A three-component friction rub is auscultated along the left sternal border. An electrocardiogram (ECG) reveals ST-segment elevations in multiple leads, which are consistent with acute pericarditis. How should this case be managed?

Acute Pericarditis – Case

• Author recommends treatment with :

• *NSAID — (600 to 800 mg of ibuprofen every 6 to 8 h) for 10 to 14 days, with tapering based on clinical response —

• *and

• *Colchicine for 3 months

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Executive Summary: Heart Disease and Stroke Statistics - 2015 Update

• Circulation. 2015;131(4):434-441. American Heart Association 2015

Cardiovascular Health in the US

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Health Behaviors

Heath Factors

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Cardiovascular conditionsCardiovascular disease accounts for 1 in 3 deaths

That’s 1 death every 40 seconds!

That’s 900 people dead over one 10 hour shift!!!

On average, every 40 seconds someone has a stroke

Approximately every 34 seconds someone has an acute coronary event

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Pediatric ECMO

Journal of Emergency Medicine : 49;4 – February 2015

Pediatric ECMO

• Extracorporeal Membrane Oxygenation

• Standard of care in NICU

• Survival rates > 85% in neonates as a final rescue therapy

• severe and refractory hypoxemia secondary to meconium aspiration, respiratory distress syndrome, and primary pulmonary hypertension

• Option for EM patients?

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Pediatric ECMO

• Vascular access

• Peripheral – neck or femoral vessels

• Central – right atrium or aorta

• Seldinger, open surgical, direct central canalization via sternotomy or thoracotomy

• Adolescents – femoral vessels

Pediatric ECMO

• History

• 1936 – John Gibbon invented the bypass machine.

• 1950s – Silicone membrane enables prolonged use.

• 1971 – ECMO for ARDS in a adult with chest trauma.

• Late 1970s – RCTs on neonates yield survival of 56%

• 1980s – Technology adapted from neonates to peds.

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Pediatric ECMO

Pediatric ECMO

*Hemoglobin is saturated with oxygen as blood passed through the membrane oxygenator

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Pediatric ECMO

• VA ECMO : primary cardiac dysfunction

• VV ECMO : *reversible severe acute respiratory failure

Pediatric ECMO

• Selection

• ECMO considered a last option

• Highly invasive, life-threatening complications

• Guidelines vary by institution, no specific indications

• Goal is tissue perfusion and oxygenation, allowing for pulmonary and cardiac rest

• Neonates / infants : sepsis, bronchiolitis, CHDs

• Peds / Adolescents: *status asthmaticus, pneumonia, ARDS, near drowning, acute chest syndrome, post-traumatic lung injury, myocarditis, intractable dysrhythmia, βB / Ca-Channel blocker overdose

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Pediatric ECMO

• Inclusion• 1. PaO2/FiO2 <100 mm Hg

• 2. Respiratory acidosis due to severe hypercapnia

• 3. Pulmonary compliance < 30 mm Hg

• 4. Any child who does not meet the exclusion criteria and is in severe distress and near cardiac arrest

• Exclusion

• 1. End-stage malignancies or advanced AIDS

• 2. Contraindications to the use of systemic anticoagulation

• 3. Cardiac arrest without neurologic function

• 4. *Traumatic cardiac arrest

• 5. Severe pulmonary disease ventilated aggressively for >10 d

Pediatric ECMO – Indications

• Respiratory failure • Pneumonia, asthma, ARDS, aspiration, burns

• Sepsis

• Cardiac arrest

• Hypothermic cardiac arrest

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Pediatric ECMO

• Complications • Blood clots in circuit (most common) in 19%

• Air embolism

• Blood loss

• Platelet consumption and DIC

• Intracranial hemorrhage – 7.4%

• CVA - 5.7%

• Myocardial stunning - 7%

• Hypertension – 13%

• Pneumothorax – 6%

Pediatric ECMO

• Management

• Standard resuscitation

• ECMO initiated in ED• *Blood products and heparin bedside

• Vent setting on ECMO

• Monitoring

• Circulation

• Sedation

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Pediatric ECMO

• Transport• Three centers have mobile ECMO

• Decision is difficult, early consultation important

• Emergency physicians have a unique opportunity to initiate treatment with ECMO

• Key is to have a transfer plan in place prior to presentation

Colorado Cannabis Legalization and its Effect on Emergency Care

• Annals of Emergency Medicine 2016

• Colorado legalized medical marijuana in 2000

• Stopped prosecution of growers and suppliers in 2009

• From 2009 to 2011 the number of medical marijuana licenses increased from 5,051 to 118,895

• Colorado legalized recreational marijuana in 2014

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It’s no big thing…

Marijuana Intoxication

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Marijuana Intoxication

Edibles

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Synthetics

Cannabinoid Hyperemesis Syndrome

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Pediatric Exposures

Therapeutic Benefits

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TXA for Traumatic Brain Injury

American Journal of Emergency Medicine : 32 – 2014

TXA for Traumatic Brain Injury

• In patients with or at risk of ICH

secondary to TBI, does TXA compared

to placebo improve outcomes?

• 1.4 million ER visits annually for TBI

• Secondary brain injury

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TXA for Traumatic Brain Injury

• Primary outcome measures• Death due to any cause after TBI assessed

• Neurologic outcomes

• Secondary outcome measures

• Hemorrhage progression, transfusion requirement,

neurosurgical intervention, & adverse effects

TXA for Traumatic Brain Injury

Two trials identified after search:

Study Patients Intervention Outcomes

CRASH-2 - 10 hospitals in India and

Colombia

- 270 adults

- Inclusion : trauma with or

at risk for significant

hemorrhage & TBI

TXA 1g IV over

10 min then 1 g

IV infusion over

8 hours

Primary – total hemorrhage growth from 1st to 2nd CT

at 24 – 48 h

Secondary – increase > 25% of total ICH, new ICH,

change in SAH grade, mass effect, new focal

ischemia, clinical outcomes

Yutthakase

-msunt et

al

- Single center in Thailand

- 240 adults

- Inclusion: non-

penetrating TBI

TXA 1g IV over

30 min then 1 g

IV infusion over

8 hours

Primary – progression of ICH by CT at 24 h, increase in

pressure effect

Secondary – in-hospital mortality, GCS at discharge,

transfusion requirement, neurosurgical intervention,

in-hospital thromboembolic events.

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TXA for Traumatic Brain Injury

TXA for Traumatic Brain Injury

• CRASH-2 & Yutthakasemsunt et al - Pooled data• In-hospital mortality relative risk of 0.64

• (95% CI, 0.41-1.02)

• Unfavorable functional status relative risk of 0.77

• (95% CI, 0.59-1.02)

• ICH progression, a relative risk of 0.76

• (95% CI, 0.58-0.98).

• *No serious adverse effects associated with TXA group

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TXA for Traumatic Brain Injury

• Take home point:

• Hypothesis : administration of TXA to patients with TBI would reduce hematoma growth compared with placebo.

• This meta-analysis revealed a statistically significant reduction in hemorrhage progression in TBI patients receiving TXA.

• The pooled relative risks for in-hospital mortality and functional status were not statistically significant.

TXA for Traumatic Brain Injury

• TXA Mechanism of Action

• *Minimizing secondary injury

• Thromboplastin released in TBI - disturbs coagulation

• *TXA is a antifibrinolytic agent

• limits fibrinolysis & intracranial hemorrhage

TXA inhibits tissue

plasminogen activator

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TXA for Traumatic Brain Injury

• Limitations

• No studies found were adequately powered to detect any clinical outcomes

• CRASH-2 had extensive extracranial injuries

• Neither trial examined isolated TBIs

• Neither trial accounted for anticoagulants / antiplatlets

TXA for Traumatic Brain Injury

• Conclusions

• Pooled results from the 2 RCTs demonstrated statistically significant reduction in ICH progression with TXA.

• TXA has excellent safety profile.

• No statistical significant improvement in clinical outcome.

• Further evidence required – CRASH-3 trial ongoing.

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Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest

• New England Journal of Medicine 2016

• Randomized, double-blinded trial comparing amiodarone, lidocaine, and placebo use in shock refractory ventricular fibrillation and pulseless ventricular tachycardia

• Primary outcome was survival to hospital discharge

• Secondary outcome was favorable neurologic function at discharge

Survival to Discharge

24.4% 23.7% 21.0%

0.0%

25.0%

50.0%

75.0%

100.0%

Survival to Hosp. Discharge

Amio

Lido

Placebo

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Survival with Favorable Outcome

18.8% 17.5% 16.6%

0.0%

50.0%

100.0%

survical with favorable neurologic status

Amiodarone

Lidocaine

Placebo

Survival?

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Trial of Continuous or Interrupted Chest Compressions during CPR

Trial of Continuous or Interrupted Chest Compressions during CPR

• *Background

• 2015 AHA BLS guidelines : chest compressions is primary emphasis

• High quality CPR allow full chest recoil

• Recommended adult compression rate = 100-120 per minute

• Upper limit for compression depth in adult CPR is 2.4 inches

• Mechanical piston CPR devices no superiority over conventional CPR

• 25-33% of normal cardiac output with high quality CPR

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Trial of Continuous or Interrupted Chest Compressions during CPR

• Study design

• Intervention group - continuous chest compressions

• continuous chest compressions - 100 / min

• asynchronous positive-pressure ventilations – 10 / min

• Control group - Interrupted chest compressions

• Interrupted for ventilations at a ratio of 30 : 2

• positive pressure during a pause in compressions of less than 5 seconds

Trial of Continuous or Interrupted Chest Compressions during CPR

• Study design

• Resuscitation Outcomes Consortium (ROC)

• 114 EMS agencies

• Cluster randomizations

• Inclusions : adult nontraumatic cardiac arrest

• Exclusions : trauma, pregnancy, bystander CPR…

• Protocols monitored

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Trial of Continuous or Interrupted Chest Compressions during CPR

• Primary outcome • rate of survival to hospital discharge

• Secondary outcomes • neurologic function at discharge

• Rankin scale score ≤3 as favorable

Trial of Continuous or Interrupted Chest Compressions during CPR

• Primary outcome

• 12,613 patients in intervention group (continuous CPR)

• 9.0% survived to discharge

• 11,035 patients in control group (interrupted CPR)

• 9.7% survived to discharge

• *95% [CI], −1.5 to 0.1

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Trial of Continuous or Interrupted Chest Compressions during CPR

• Secondary outcome – favorable neurologic function

• 883 of 12,560 patients (7.0%) in the intervention group

• 844 of 10,995 (7.7%) in the control group

• 95% CI, −1.4 to 0.1; P = 0.09

Trial of Continuous or Interrupted Chest Compressions during CPR

• Conclusion

• Continuous chest compressions with positive-pressure ventilation did not result in significantly higher rates of survival or favorable neurologic status than the rates with a strategy of chest compressions interrupted for ventilation

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Management of sickle cell disease summary of the 2014 evidence-based report by expert panel members

• JAMA 2014

Start the screening early

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Vaso-occlusive Crisis

Acute Chest Syndrome

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Acute Stroke

Other Acute Complications

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Chronic Complications

Hydroxyurea

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Blood Transfusion

Opiates and Sickle Cell Disease

• December 2017, Jeffery Glassberg, MD, MA ACEP Now

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Ischemic Limb Gangrene with Pulses

New England Journal of Medicine : 373;7 – August 2015

Ischemic Limb Gangrene with Pulses

• Two Distinct Syndromes

• Venous limb gangrene • *Acral necrosis in a limb with a DVT

• Cancer-Associated DIC• Heparin-Induced Thrombocytopenia

• Systemic peripheral gangrene • Acral necrosis in all limbs

• DIC• Pathologic thrombin generation • Impaired fibrinolysis & fibrin deposition

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Ischemic Limb Gangrene with Pulses

Ischemic Limb Gangrene with Pulses

• Venous Limb Gangrene - Cancer associated

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Ischemic Limb Gangrene with Pulses

• Venous Limb Gangrene - Heparin-Induced Thrombocytopenia

Ischemic Limb Gangrene with Pulses

• Venous Limb Gangrene

• Pathophysiology

• *Procoagulant factor VII and anticoagulant protein C have short half lives susceptible to depletion in consumptive coagulopathy

• Prothrombin has a much higher half life

• therefore….

• Despite high INR, microthrombosis persists

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Ischemic Limb Gangrene with Pulses

Ischemic Limb Gangrene with Pulses

• Prevention and Treatment

• Avoidance of warfarin in cancer associated DVT

• Avoidance of warfarin during the acute phase of HIT

• Vitamin K infusion for high INR

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Ischemic Limb Gangrene with Pulses

• Symmetric peripheral gangrene • Acral necrosis distal extremities

• Purpura fulminans • Multicentric, non-acral necrosis

• Septecemia associated DIC• Fever, hypotension, petechial rash confluent purpura

ischemia

Ischemic Limb Gangrene with Pulses

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Ischemic Limb Gangrene with Pulses

• Symmetric peripheral gangrene & Purpura Fulminans

Ischemic Limb Gangrene with Pulses

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Ischemic Limb Gangrene with Pulses

• Symmetric peripheral gangrene & Purpura Fulminans

• Microorganisms

• Neisseria meningitidis – children

• Streptococcus pneumoniae – adults

• Encapsulated bacteria – asplenic

• Group A strep, staphylococcus, gram-negatives

• Rickettsia, malaria, TB, rubeola, varicella

• Capnocytophagia from bites

Ischemic Limb Gangrene with Pulses

• Symmetric peripheral gangrene & Purpura Fulminans

• Acute ischemic hepatitis (shock liver)

• Can cause symmetric peripheral gangrene

• Limb necrosis 2 – 5 days after elevation of liver enzymes

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Ischemic Limb Gangrene with Pulses

• Treatment for venous limb gangrene and symmetric peripheral gangrene• Heparin

• Natural anticoagulant repletion (protein C)

• Maximize limb perfusion

• Surgical consideration and wound care

Ischemic Limb Gangrene with Pulses

• Summary • Venous limb gangrene and symmetric peripheral

gangrene are usually associated with microvascular thrombosis with underlying DIC.

• Prevention and treatment of venous gangrene requires correction of abnormalities associated with the use of vitamin K antagonists and aggressive anticoagulation

• Treatment of symmetric peripheral gangrene (with or without purpura fulminans) theoretically involves heparin-based anticoagulation and the substitution of natural anticoagulants.

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