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ER28 Emergency Medicine Toronto Notes 2023

•general examination

• mental status

• sexual maturity

patient should remove clothes and place in paper bag

• document abrasions, bruises,lacerations,torn frenulum/broken teeth (indicates oral penetration)

•pelvic exam and specimen collection

ideally before urination or defecation

examine for seminalstains, hymen,signs of trauma

• collect moistened swabs of dried seminal stains

• pubic hair combings and cuttings

speculum exam

lubricate with water only

vaginal lacerations,foreign bodies

Pap smear,oral/cervical/rectal culture for gonorrhea and chlamydia

posterior fornix secretions if present or aspiration of saline irrigation

immediate wet smear for motile sperm

air-dried slides for immotile sperm, acid phosphatase, ABO group

•fingernail scrapings and saliva sample from victim

Investigations

•Venereal Disease Research Lab (VDRL): repeat in 3 mo if negative

•serum p-hCCi

•blood for ABO group, Rh type, baseline serology (e.g. hepatitis, HIV)

Management

•involve local/regional sexual assault team (sexual assault forensic examiner orsexual assault nurse

examiner)

•medical

• suture lacerations, tetanus prophylaxis

gynecology consult for foreign body, complex lacerations

assume positive for gonorrhea and chlamydia

management:azithromycin 1 g PO x 1 dose (alt:doxycycline 100 mg PO BID x 10 d) and

ceftriaxone 250 mg IM x 1 dose

may start post-exposure prophylaxis for hepatitis B,syphilis, HIV

pre and post counselling for HIV testing

pregnancy prophylaxis offered

levonorgestrel 1.5 g PO ST'

AT (Plan B*)

•psychological

high incidence of psychologicalsequelae

have victim change and shower after exam completed

Disposition

•discharge if injuries/social situation permit

•follow-up with physician in rape crisis center within 24 h for repeat pregnancy and S'

l

'

l testing

•best if patient does not leave ED alone

INTIMATE PARTNER VIOLENCE

•women are usually the victims, but male victimization also occurs

•identify the problem (need high index of suspicion)

suggestive injuries(bruises,sprains, abrasions, occasionally fractures, burns,or other injuries;

often inconsistent with history'provided)

somatic symptoms(chronic and vague complaints)

• psychosocial symptoms

• clinician impression (your '

gut feeling’ e.g. overbearing partner that won’t leave patient’sside)

•if disclosed, be supportive and assess danger

•patient must consent to follow-up investigation/reporting (unless patient is <16 y/o)

Management

•treat injuries and document findings

•ask about sexual assault and children at home (encourage notification of police)

•safety plan with good follow- up with family physician/social worker

r i

L J

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ER29 Emergency Medicine Toronto Notes 2023

Medical Emergencies

Most Common Triggersfor Anaphylaxis

. Foods (nuts,shellfish, etc.)

• Stings

. Drugs(penicillin. NSAIDs. ACEl)

• Radiographic contrast media

• Blood products

• Latex

Anaphylaxis and Allergic Reactions

Etiology

• anaphylaxis is an exaggerated immune-mediated hypersensitivity reaction that leadsto systemic

histamine and vasoactive mediator release leading to increased vascular permeability and

vasodilation

• regardless ofthe etiology, the presentation and management of anaphylactic reactions are the same

• epinephrine ( 1 :1000) 0.3-0.5 mg (1M in anterolateral thigh)

• allergic (e.g. re-exposure to allergen)

• non-allergic (e.g. exercise-induced)

Diagnostic Criteria

• diagnosis of anaphylaxis is highly likely with any of the following:

1.acute onset of an illness (min to h) with involvement of the skin, mucosal tissue, and at least one of

respiratory compromise (e.g. dyspnea, wheeze, stridor, hypoxemia)

hypotension/end-organ dysfunction (e.g. hypotonia, collapse, syncope, incontinence)

2. two or more of the following after exposure to a LI KLLV allergen for that patient (min to h)

involvement of the skin-mucosal tissue

respiratory compromise

hypotension or associated symptoms

persistent gastrointestinal symptoms (e.g. crampy abdominal pain, vomiting)

3.hypotension after exposure to a KNOWN allergen for that patient (min to h)

management is also appropriate in cases which do not fulfill criteria, but who have had

previous episodes of anaphylaxis

life-threatening differentials for anaphylaxis include asthma and septic shock

angioedema may mimic anaphylaxis but tends not to improve with standard anaphylaxis

treatment

Management

• moderate reaction: generalized urticaria, angioedema,wheezing, tachycardia

• epinephrine (1 :1000) 0.3-0.5 mg (1M in anterolateral thigh)

• antihistamine: cetirizine 10 mg PO/1V

salbutamol ( Ventolin*) 1 cc via MD1

• severe reaction/evolution:severe wheezing, laryngeal/pulmonary edema, shock

• ABCs, may need definitive airway (e.g. ETT) due to airway ede

• epinephrine ( 1 :1000) 1 -10 pg/min IV (or via ETT if no IV access) titrated to desired effect

antihistamine: diphenhydramine (Benadryl*) 50 mg IV (~ 1 mg/kg) or cetirizine (Reactine* ) 10

mg IV

• glucocorticoids: methylprednisolone 125-250 mg IV or prednisone/prcdnisolone 40-60 mg PO

large volumes of crystalloid may lie required

• patients on (5-blockers may not respond to epinephrine in an anaphylactic reaction and may benefit

from glucagon for reversal

Disposition

• monitor for 4-8 h in ED (minimum) and arrange follow-up with family physician in 24-48 h

• can have second phase (biphasic) reaction up to 72 h later, patient may need to be supervised

• educate patient on avoidance of allergens

• instructions to seek immediate medical attention in ED during any future anaphylaxis reaction, even

when self-treatment has been self-initiated

• medications

• epinephrine auto-injector

• HI antagonist (cetirizine 10 mg PO once daily or Benadryl’ 50 mg PO q4-6 h x3 d)

Second-generation H 1 antagonists (e.g. cetirizine) are less sedating than first-generation H1

antagonists (e.g. Benadryl*)

• glucocorticoids not recommended if good response to epinephrine and absence of asthma; if

indicated, methylprednisolone 1-2 mg/kg/d for 2 d issufficient

Anaphylaxis should be suspected

if airway, breathing,or especially

circulation compromise is present after

exposure to a known allergen

Hypotension is defined assBP >30%

decrease from baseline or

• >11 yr:<90 mmHg

• 1-10 yr:<70 mmHg + (2 x age)

• 1mo-1yr: <70 mmHg

Early

o

epinephrine is lifesaving and there

are no absolute contraindications

n

Paediatric Dosing

Epinephrine:001 mg/kg IM up to 0.5

mg q5-10 min

Initial crystalloid bolus:20-30 mL/kg.

reassess

Epinephrine infusion:0.1-1.5 pg/kg/min

Diphenhydramine:1mg/kg PO/IV

q4-6 h

Methylprednisolone:1-2 mgikg IV

Beware

o

of the silent chest in asthma

exacerbations.This is a medical

emergency and requires aggressive

treatment.Intubation of patients with

severe asthma is extremely high risk and

maximum medical therapy should be

used to avoid it if possible

Asthma

•see Respirologv, R7 and Paediatrics. P91

•chronic inflammatory airway disease with episodes of bronchospasm and inflammation resulting in

reversible airflow obstruction r -t

L

History and Physical

•find cause(s) of asthma exacerbation (e.g. viral, environmental, etc,)

•history of asthma control;severity of exacerbations (e.g. 1CU, intubation history)

•signs of respiratory distress (e.g. accessory muscle use)

•vitals,specifically 0 2 saturation

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ER30 Emergency Medicine Toronto Notes 2023

Investigations

• peak flow meter

• ± ABCi if in severe respiratory distress

CXR if diagnosis is uncertain to rule out pneumonia, pneumothorax, etc.

Elements of Well-Controlled Asthma

Can Respir J 2010:17(1):15-24

• Daytime symptoms <4x2wk

• Nocturnal symptoms <1x/wk

• No limitation in activity

• No absence from work/school

• Rescue inhaler use <4x2wk

• FEVi <90% personal best

• PEF <10-15% diurnal variation

. Mild infrequent exacerbations

Table 19. Asthma Assessment and Management

Classifications History and Physical Exam Management

Exhausted,confused, diaphoretic, cyanotic

Silent chest,ineffective respiratory effort

Decreased NR.respiratory rale (RR ) >30. pCO 2

»45 mmHg

02 sat <90% despite supplemental 02

Anticipate need for intubation

100% 02. cardiac monitor. IV access

Inlubale (consider induction with ketamine)

Short acting 3-agonist [Ventolin!

): nebulizer 5 mg conbnually

Short-acting anticholinergic (Alrovent:

):nebulizer 0.5 mg x 3

IV steroids:mcthylprednisolone 125 mg

Similar to above management

Magnesium sulphate 2 g IV

0J to achieve 02 sat >92%

Respiratory Arrest

Imminent

Severe Asthma Agitated, diaphoretic, laboured respirations

Speaking in words

No relief from 3-agonist

A sat <90%. FEVi < 50%

SOB atrest,cough, congestion, chest lightness

Speaking in phrases

Inadequate relief from 0-agonist

FEVi 50- 80%

Exertional SOB /cough with some nocturnal

symptoms

Difficulty Finishing sentences

FEVi >80%

Combined Inhaled 8-Agonist and Anticholinergic

Agents for Emergency Management In Adults

with Asthma

Cochrane 08Syst Rev 2017:C0001284

Purpose Oeteim.ne the effectiveness of combined

short-acting 8-agonist|SA8A) * short-acting

anticholinergic (SAAC) vs.SASAc me to reduce

hospita '

izahon in adult patients presenting to the EO

with an exacerbation of asthma.

Methods:Systematic review of RCIs.

Results: 23 trials.2224 patients.Combination

nhaled therapywas associated with reduced

Uellhood of hospitaliration (RR 072.95% Cl

0.59-0.82) for severe but not mild or moderate

asthma exacerbations.Combination therapy was also

associated with improved FEVI (MD 0.25L,95% Cl

0.02-0.48) and PEF (MO 24.88.95% Cl14.83-34.93)

and patients weie less likely to return to EO for

additional care|RR 0.80.95% Cl 0.66-0.98).In

contrast, patients receiving combination therapy

were more likely to experience adverse eventsthan

those treated with SABA alone (OR 2.03. 95% Cl

1.28-3.20).

Conclusions:Combination SAAC SABA therapy

reduces hospitalizations and improves pulmonary

luntlion in adults presenting tothe ED with acute

asthma.However, adults tecerring combination

therapy were more likely to experience adverse

events, such as tremor,agitation, and palpitations,

compared to patients receiving SABA alone.

02 to achieve 02 sat >92%

Short-acting 3-agonist ( Ventolin-

):MDI or nebulizer q5 min

Short-acting Anticholinergic (Alrovent '

):MD! or nebulizerx 3

Steroids:prednisone 40-60 mg P0

3-agonisl

Monitor FEVi

Consider steroids (MDI or P0)

Moderate Asthma

Mild Asthma

Disposition

• discharge is safe in patients with FEVI or peak expiratory flow ( PEE) >60% predicted, and maybe safe

if I FVI or PEE 40-60% predicted based on the patient’s risk factors for recurrence of severe attack

risk factorsfor recurrence:frequent FD visits, frequent hospitalizations, recent steroid use, recent

exacerbation, poor medication compliance, prolonged use of high dose (3-agonists

• p-agonist MDI with aerochamber 2-4 puffs q2-4 h until symptoms controlled, then PUN

• initiate inhaled corticosteroids with aerochamber if not already prescribed

if moderate to severe attack, administer prednisone 30-60 mg/d for 5-10 d with no taper

• counsel on medication adherence and educate on use of aerochamber

• follow up with primary care physician or asthma specialist

Cardiac Dysrhythmias

• see Cardiology and Cardiac Surgery.09

Bradydysrhythmias and AV Conduction Blocks

• AN' conduction blocks

• 1st degree: prolonged PR interval (>200 msec), no treatment required

2nd degree

Mohitz 1: gradual prolongation of PR interval then dropped QRS complex, usually benign

Mohitz 11: PR interval constant with dropped QRS complex, can progress to 3rd degree AV

block

• 3rd degree: P wave unrelated to QRS complex, PP and RR intervals constant

atropine and transcutaneous/transvenous pacing (atropine with caution)

if transcutaneous/transvenous pacing fails consider IV dopamine, epinephrine

• long-term treatment for Mobitz II and 3rd degree block -internal pacemaker

• sinus bradycardia (rate <60 bpm)

• can be normal (especially in athletes)

• causes: vagal stimulation, vomiting, Ml/ischemia, increased ICE,sinus node dysfunction,

hypothyroidism, drugs (e.g. (3-blockers, calcium channel blockers)

• treat if symptomatic (hypotension, chest pain)

acute: atropine ± transcutaneous/transvenous pacing

sick sinus: transcutaneous/transvenous pacing

drug induced: discontinue/reduce offending drug, consider antidotes

Adenosine vs. IntravenousCalcium Channel

Antagonistsfor Supraventricular Tachycardia

C ochrane OB Syst Rev 2012:00005154

Purpose Compare adenosine vs. calcium channel

antagonists in terminating supraventiicular

tachycardia.

Methods:Systematic lev lew of RCIsforany patient

presenting with supiaventiicutar tachycardia.

Results 2 RCIs.822 participants. Moderate quality

evidence shows no differences mthe number or

people revetting to sinusrhythm who were treated

with adenosire or calcium channel antagonist (89.7%

vs.92.9%. OR 1.51). low-quality evidence suggests no

differences in major adverse event rales.

Conclusions:Mnderate-quality evidence shows

no differences in effectsof adenosine andcakium

channel antagonists lor treatment of upravrntiicular

tachycardia on reverting tosinus ihythm.and

low-quality evidence suggests no differences in the

incidence of hypotension.

Supraventricular Tachydysrhythmias (narrow QRS)

sinus tachycardia (rate >100 bpm)

• causes: increased sympathetic tone, drugs, fever,shock, anemia, thyrotoxicosis, Ml, HF,

emotional, pain, etc.

• search for and treat underlying cause

• regular rhythm (i.e. not sinus tachycardia)

• vagal maneuvers (e.g. carotid massage, Valsalva), adenosine 6 mg IV push, if no conversion give

12 mg, can repeat 12 mg dose once, electrical cardioversion if vagal maneuvers and adenosine

unsuccessful

• rhythm converts: probable reentrant tachycardia (atrioventricular (AV) nodal reentrant

tachycardia (AVNRi) more common than AV reentrant tachycardia (AVRT)

monitor for recurrence

treat recurrence with adenosine or longer acting medications

+

If a patient with tachydysrhythmia

is unstable,perform immediate

synchronized cardioversion

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ER31 Emergency Medicine Toronto Notes 2023

rhythm does not convert:atrial flutter, ectopic atrial tachycardia, junctional tachycardia

rate control (diltiazem, p-blockers) or rhythm control with cardioversion

• consult cardiology if refractory

•irregular rhythm

probable AFib,atrial flutter, or multifocal atrial tachycardia

» rate control (e.g.diltiazem, p-blockers),or rhythm control if AFib/flutter and at least <48h from

onset

N patient has Wolff-Parklnson-White

and is in AFib,use amiodarone or

procainamide or cardiovert avoid AV

nodal blocking agents (adenosine,

digoxln, diltiazem. verapamil,

8-blockers),as these can increase

conduction through bypass tract,leading

to cardiac arrest

Atrial Fibrillation

•most common sustained dysrhythmia; no organized P waves (atrial rate >300/min), irregularly

irregular heart rate, narrow QRS (typically)

•etiology: HTN,CAD, thyrotoxicosis, FtOH (holiday heart), valvular disease, pericarditis,

cardiomyopathy,sinus node dysfunction

•treatment principles:stroke prevention, treatsymptoms, identifv/treat underlying cause

•decreases cardiac output by 20-30% (due to loss of organized atrial contractions)

•acute management

» if unstable; immediate synchronized cardioversion

hemodynamically stable patients with AFib <48 h:rhythm or rate control ± electrical or chemical

cardioversion

•electrical cardioversion; synchronized direct current (DC) cardioversion

•chemical cardioversion; procainamide, flecainide, propafenone

•long-term management:rate or rhythm control,consider anticoagulation (see Cardiology and Cardiac

Surgery.CHADS2 score, C23)

<§>

Causes of Atrial Fibrillation

C ("sea”) PIRATES

CHF,Cardiomyopathy

Pulmonary embolism

Ischaemic heart disease

Rheumatic or valvular disease

Anemia

Thyroid (hyperthyroidism)

EtOH. Elevated blood pressure

Sick Sinus. Stress - surgery, sepsis

Ventricular Tachydysrhythmias (wide QRS)

•VTach (rate usually 140-200 bpm)

definition:3or more consecutive ventricular beats at >100 bpm

etiology:CAD with Ml isthe most common cause

• treatment:sustained VTach (>30 s) is an emergency

hemodynamic compromise:synchronized DC cardioversion

no hemodynamic compromise:synchronized DC cardioversion, amiodarone, procainamide

•V Fib:call a code blue,follow ACLS for pulseless arrest

•torsades de pointes

• looks like VTach but QRS ‘

rotates around baseline’ with changing axis and amplitude (twisted

ribbon)

• etiology: prolonged QT due to drugs(e.g. quinidine,TCAs, erythromycin,quinolones), electrolyte

imbalance (hypokalemia, hypomagnesemia), congenital

• treatment

IV Mg2

'

, temporary overdrive pacing,isoproterenol

correct cause of prolonged QT

Early or Delayed Cardioversion in hcnt

-Onset

Atrial Fibrillation

HUM 2019:310:1499 1308

Purpose: Patientswith recent-onset AFib commonly

undergo immediate restoration of sntrrs rhythm by

cardioversion.Whether this is necessary is not known,

since If rb often terminatesspontaneously.

Methods: Random ty assigned patients with stable,

recent-onset|<36 h ).symptomatic If bin the10 to

be treated with a wart-aod -see approach (delayed -

cardioversion group) or early cardioversion.Ihe

wait-and -see approach involved Initial Ueatment

with rate-control meditation only and delayed

cardioversion if the AFib did not resolve within 48 h.

Primaryendpoint:presence ofsinosrhythm at 4wk.

Results:Ihe presence of sinus rhythmat 4wk

occurred in 91% ol patients in the delayedcardioversion group and in 94% In the earlycardioversion grouj(M.005lor nnniiferiority).

Among the patients whn completed remote

monitoring during 4 wk olfollow-up.a recurrence ol

AFib occurred in 3t% ol the delayed-candioversion

group and In 29% ol the eariy-caidioitrsion group.

Conclusions:Wait-and-see appertain was noninferior to early cardioversion in stableAFib patients.

Acute Exacerbation of COPD

•see Respirologv. R8

•progressive development of irreversible airway obstruction, typically caused by smoking

History and Physical Exam

•cardinal symptoms of acute exacerbation of COPD (AECOPD):increased dyspnea, increased coughing

frequency or severity, increased sputum volume or purulence

•triggers:virus, pneumonia, PE,CHF, Ml, drugs

•characterize previous episodes and hospitalizations,smoking history

•vitalsigns, LOC,signs of respiratory distress, respiratory exam

Investigations

•CBC, electrolytes,CXR, ECG, consider ABG

•Pulmonary Function Tests are NOT useful in managing acute exacerbations

Management

•oxygen: keep O 1 saturation 88-92% (be aware of chronic hypercapnic/CO’

retainers but do not

withhold 01if hypoxic)

•bronchodilators:short-acting p-agonist (salbutamol 4-8 puffs via MDI with spacer ql5 min x3 PRN) ±

short

-acting anticholinergic (ipratropium 0.5 mg via MDI q30 min x3 PRN)

•steroids: prednisone 40-60 mg PO for 7-14 d, or methylprednisolone 1-2 mg/kg IV ifsevere

exacerbation,or unable to take PO

.antibiotics:trimethoprim/sulfamethoxazole, cephalosporins, respiratory quinolones(given if all 3

cardinal symptoms present or 2 cardinalsymptoms with increased sputum purulence or mechanical

ventilation); no antibiotics for mild exacerbation (only 1 of 3 cardinalsymptoms)

•ventilation:apply noninvasive positive-pressure ventilation (CPAP or Bi-PAP) ifsevere distress or

signs of fatigue, arterial pH <7.35, or hypercapnic

•if life-threatening,intubate in ED and refer to ICU admission for ventilation (chance of ventilation

dependency)

w

Physical Exam Findings In COPD

• Wheeze

• Maximum laryngeal height s4 cm

• Forced expiratory time 26 s

• Decreased breath sounds

• Decreased cardiac dullness

r ~\

LJ

Need to Rule Out with COPD

• Exacerbation

• Pneumothorax

• CHF exacerbation

. Acute Ml

• Pneumonia and other infectious

+

causes

. PE

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ER32 Emergency Medicine Toronto Notes 2023

•

Disposition

no guidelines for admission - based on clinical judgment, comorbidities, and presence/absence of m

ongoing symptoms

• lower threshold to admit if comorbid illness (e.g. diabetes, CHE, CAD, alcohol use disorder)

• if discharging, use antibiotics, taper steroids, up to 4-6 puffs QID of ipratropium and salbutamol, and

organize follow-up

Precipitant;of CHF Exacerbation

FAILURE

For got medication

Arrhythmia (Dysrhythmia)/Anemia

Ischaemia/Infarction/Infection

Lifestyle (e.g. high salt intake)

Upregulation of cardiac output

(e.g.pregnancy,hyperthyroidism)

Renal failure

Embolism (pulmonary)

Heart Failure

•see Cardiology and Cardiac Surgery, C40

Etiology

•causes of chronic heart failure: decreased myocardial contractility (ischaemia, infarction,

cardiomyopathy, myocarditis), pressure overload states ( H'

i

'

N, valve abnormalities, congenital heart

disease), restricted cardiac output (myocardial infiltrative disease, cardiac tamponade)

•precipitants of acute decompensated heart failure (ADHE)

cardiac (ischaemia, infarction, arrhythmia, e.g. AEib)

• medications (P-blockers, calcium channel blockers, NSAlDs, steroids, non-compliance)

• dietary (increased sodium and/or water intake)

• high output (anemia, infection, pregnancy, hyperthyroid)

• other (renal failure, hypertensive crisis, iatrogenic fluid overload - blood transfusions or IV fluids)

CHFonCXR

• Pulmonary vascular redistribution

. Perihilar infiltrates

• Interstitial edema.Kerley B lines

• Alveolar edema,bilateral infiltrates

• May see cardiomegaly. pleural

effusions

• Peribronchial cuffing

• Fissural thickening (fluid in fissure)

Presentation

•left-sided heart failure

• dyspnea, SOB on exertion, orthopnea, paroxysmal nocturnal dyspnea, nocturia, fatigue, altered

mental status, presyncope/syncope, angina, systemic hypotension

• hypoxia, decreased air entry to lungs, crackles, S3 or S4, pulmonary edema (on CXR), pleural

effusion (usually right-sided)

•right-sided heart failure

dependent bilateral pitting edema,|VP elevation and positive abdominojugular test, ascites,

hepatomegaly

•patients often present with a combination of right-sided and left-sided symptoms

Investigations

•blood work: CBC, electrolytes, AST,ALT, bilirubin, Cr, BUN, cardiac enzymes, brain natriuretic

peptide

•CXR: most useful test (see sidebar)

•EC(i: look for Ml. ischaemia (ST elevation/depression, T-wave inversion), LVH, atrial enlargement,

conduction abnormalities

•bedside ultrasound: B-lines, rule out cardiac tamponade

•echocardiogram:left ventricular function, structural heart disease

•rule out other serious diagnoses: PE, pneumothorax, pneumonia/empyema, AECOPD

Management

•ABCs, may require intubation if severe hypoxia

•sit upright, cardiac monitoring, and continuous pulse oximetry

•saline lock IV, l-

'

oley catheter only if patient cannot void in a commode at bedside

•100% 02 by mask

if poor response, may require Bi-PAP (preferred) or intubation

•medical

diuretic (if volume overloaded): furosemide 0.5- 1 mg/kg IV,titrate to response

vasodilators (ifsBP >100 mmHg): nitroglycerin 0.4 mg SL q5 min PRN ± topical Nitrodur* patch

(0.4-0.8 mg/h)

if patient not responding to treatment or showing signs of ischaemia (angina): nitroglycerine

5- 10 pg/min IV, titrate to response

Inotropes/vasopressors (if sBP <90 mmHg)

without signs of shock: dobutamine 2.5 pg/kg/min IV, titrate up to sBP >90 mmHg. always

have norepinephrine or epinephrine running alongside as dobutamine can cause reflex

tachycardia and hypotension

with signs ofshock: norepinephrine 8-12 pg/min IV, titrate up to sBP >90 mmHg

•treat precipitating factor - e.g. rate control ((1-blocker, calcium channel blockers) or rhythm-control

(electrical or chemical cardioversion) if new AEib

•cardiology or medicine consult

Acute Treatment of CHF

LMNOP

La six3 (furosemide)

Morphine

Nitroglycerin

Oxygen

Position (sit upright).Pressure (Bi-PAP)

Hospital Management Required if

• Acute Ml

• Pulmonary edema or severe

respiratory distress

• Severe complicating medical illness

(e.g. pneumonia)

. Anasarca

• Symptomatic hypotension or syncope

• Refractory to outpatient therapy

. Thromboembolic complications

requiring Interventions

• Clinically significant dysrhythmias

. Inadequate social support for safe

outpatient management

• Persistent hypoxia requiring

supplemental oxygen

DiagnosticAccuracy of FOCUS and CXR in Adults

With Symptoms Suggestive of ADHF

JAMA 2019;2:e190703

Purpose:lo compare the accuracy of Point-of -Care

lung Ultrasonography (lUS) unlit the accuracy ol CXR

in the diagnosis of cardiogenic pulmonary edema.

Methods:Systematic renew with inclusion criteria

of patients presenting with dyspnea who underwent

both LUS and CXR on initial assessment.Imaging

resalts were compa red by > clinical expert after

either a medical record retie*

or a combination of

echocardiography findings andB-type natriuretic

peptide (BNP) criteria.Primary outcome

comparative accuracy of IUS a nd CXR in

AOHF as measured by the differences between the 2

modalities in pooled sensitivity and specificity.

Results:6studies met the iucl usion criteria:a total

of 1827 patients.Pooled estimateslor LUS were

Oitloi

estimate

wasthe

diagnosing

Venous Thromboembolism n

L J

sensitivity and 0.94 lot specificity. Pooled

isfor CAR weteO.23 for sensitrailyard 0.94

lorspecificity.Ihe relative sensitivity ratio of IUS.

compared with CXR,was12.No difference wasfound

in specificity between tests.

Conclusions:The findingssuggest that LUS is mure

sensitive than CXR in detecting pulmonary edema

n ADHF; LUS should be considered asan adjunct

(waging modality in the evaluation ol patientswith

dyspnea at nsktor AOHF.

• see Rcspiroloyv. RI 9

Risk Factors

• Virchow’

striad: alterations in blood flow (venous stasis), injury to endothelium (smoking, HTN,

surgery, catheter, trauma), hypercoagulable state (including pregnancy, use of oral contraceptive pills,

malignancy)

• clinical risk factors (see sidebar, Risk Factors for VIE, ER33)

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DEEP VEIN THROMBOSIS

Presentation (§)

• calf pain, unilateral leg swelling/erythema/edema, palpable cord along the deep venous system on

exam

• clinical signs/symptoms are unreliable for diagnosis and exclusion of DVT (may be asymptomatic;

bilateral leg presentation unlikely but does not rule out diagnosis; think inferior vena cava (IVC)

occlusion if bilateral DVT)

further investigation is often needed

Investigations

• use Wells’

criteria for DVT to guide investigations (see Figure 12, HR34 )

• D-dimer is only useful for ruling out DVT, and a D-dimer test result should only be considered in

cases where a low-moderate risk patient has a negative test (high sensitivity)

high-risk of false positivesin: elderly, infection, recent surgery', trauma, hemorrhage, late in

pregnancy,liver disease, cancer

• U/S has high sensitivity & specificity for proximal clot but only 73% sensitivity for calf DVT (may need

to repeat in 1 wk)

• if positive -treat for DVT unless anticoagulation is contraindicated

if negative and low-risk - rule out DVT

if negative and moderate to high-risk - repeat U/S in 5-7 d to rule out DVT

Management

• direct oral anticoagulants (DOAC) can be used in acute management ofsymptomatic DVT

• rivaroxaban: 15 mg PO BID for first 21 d; 20 mg PO once daily for remaining treatment (taken

with food at the same time each day)

apixaban: 10 mg PO BID for first 7 d; 5 mg PO BID for remaining treatment

• low molecular weight heparin (LM WH) unless patient also has renal failure

dalteparin 200 lU/kg SC q24 h or enoxaparin I mg/kg SC q24 h

• warfarin started at same time as LMWH (5 mg PO once daily initially followed by dosing based on

INK)

• LMWH discontinued when INR has been therapeutic (2-3) for 2 consecutive days

• consider thrombolysis if extensive DVT threatening limb compromise

• JVC filter or surgical thrombectomy considered if anticoagulation is contraindicated

• duration of anticoagulation: 3 mo if transient coagulopathy; 6 mo if unprovoked DVT; life-long if

ongoing coagulopathy

PULMONARY EMBOLISM

Presentation

• dyspnea, pleuritic chest pain, hemoptysis, tachypnea, cyanosis, hypoxia, fever

• clinical signs/symptoms are unreliable for diagnosis and exclusion of PE; investigation often needed

Investigations

• use Wells’

criteria for PE to guide investigations (see Figure 13, HR-16 )

• pulmonary embolism rule-out criteria (PERC) score (see EBM on sidebar, Kespirologv, R21) alone can

rule out PE in low-risk patients unless pregnant

• EC'

G and CXR are useful to rule out other causes (e.g. ACS, pneumonia, pericarditis) or to support

diagnosis of PE

EC(i changes in PE: sinus tachycardia, right ventricular strain (SIQ3T3, see Cardiology and

Cardiac Surgery, CIO ), T wave inversions in anterior and inferior leads, APib

CXR findings in PE: Hampton’

s hump (triangular density extending from pleura,sign of

pulmonary infarct) or Westermark'

ssign (dilatation of vessels proximal to an obstruction, with

collapse of vessels distal to obstruction, often with a sharp cutoff)

• D-dimer is only useful at ruling out a PE if it is negative in low-moderate risk patients (highly

sensitive)

• if positive D-dimer or high-probability patient, then pursue CT pulmonary angiography or V/Q

scan

• CT pulmonary angiography has high sensitivity and specificity for PE, may also indicate an

alternative diagnosis

• V/Q scan useful in pregnancy, when CT pulmonary angiography not available, or IV contrast

contraindicated

Risk Factors for VTE

THROMBOSIS

Trauma,travel

Hypercoagulable. hormone

replacement therapy (HRT)

Recreational drugs (IV drug use)

Old (age >60yr)

Malignancy

Birth control pill

Obesity,obstetrics

Surgery,smoking

Immobilization

Sickness (CHF. Ml. nephrotic syndrome,

vasculitis)

Wells’Criteria for DVT

Active cancer

Paralysis,paresis or recent

immobilization olleg

Recently bedridden x3 dot

major surgery within 4 wk

Local tenderness

Entire leg swollen

Calf swelling 3 cm

> asymptomatic leg

Unilateralpitting edema

Collateral superficial veins

Alternative 0« more likely •2

0:Low probability

1-2:Moderate probability

-3:High probabiriy

Wells’Criteria for PE

Previous Hx of DVT/PE 1.5

HR >100

Recent immobility or surgery *

1.5

Clinical signs of DVT

Alternate Dx less likely than PE *

3

Hemoptysis

1.5

3

+1

i

'

ll ter 1

-2:low probability

2-6:In

-6:High prtfcabMy

Signs of PE on CXR

Westermark's sign:abrupt tapering of

a vessel on chest film

Hampton's hump: a wedge-shaped

infiltrate that abuts the pleura

Effusion, atelectasis,or infiltrates 50%

normal

Both signs are specific but not sensitive

A normal CXR in the hypoxic patient

warrants a work-up for PE

Management

• treatment of PE with anticoagulation and duration of treatment is the same as for DVT (see above)

• thrombolysis indicated in massive PE, which is defined as acute PE with sustained hypotension (sBP

<90 mmHg for at least 15 min or requiring inotropic support, not due to a cause other than PE)

• catheter-directed thrombolysis or surgical thrombectomy may be considered in massive PE or if

anticoagulation is contraindicated

• often can be treated as an outpatient, may require analgesia for chest pain (narcotic or NSA1D)

• admit if hemodynamically unstable, require supplemental 02, major comorbidities, lack ofsufficient

social supports, unable to ambulate, need invasive therapy

referral to medicine for coagulopathy and malignancy workup

ri

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ER31EmergencyMedicine Toronto Notes 2023

Suspected (symptomatic ) acute DVT

I

PERC Score

• Age >S0 yr

• HR >100 bpm

• Oi saturation on room air <95%

. Prior Hx of DVT/PE

• Recent trauma orsurgery

• Hemoptysis

• Exogenous estrogen

• Clinical signssuggesting DVT

Compression U/S

1 i

Normal Inconclusive or inadequate study DVT present

i I I

Repeat U/S in 5 days Venography or MRI Treatment

4

DVT present DVT absent DVT present Negative for DVT Score1for each question:a score

0/8 means patient has <1.6% chance

of having a PE and avoids further

Investigation.Caution using the PERC

score in pregnant women asthe original

study excluded pregnant women

I

*

i 1

Treatment No treatment Treatment No treatment

Figure 11. Approach to suspected DVT

Determine need to investigate

via PERC score Positive >1/8 Negative 0/8

I D-dimer is only useful H it is negative:

Wells negative predictive value >99% '

Criteria PE excluded

Low Moderate/High 1

4

D-dimer assay

I 50% of patients with symptomatic

proximal DVT will develop PE. often

within daysto weeks of the event

4

^

CT pulmonary

angiogram ICT-PA)

<500 ng/mL >500 ng/ml