CASE PRESENTATIONCASE PRESENTATION

Idan Khan

CaseCase

71 y/o male brought in by EMS71 y/o male brought in by EMS

–Very healthy 71 y/oVery healthy 71 y/o

–Skiing all day no problems Skiing all day no problems

–c/o pain / tingling/ weakness to right c/o pain / tingling/ weakness to right arm, SOB arm, SOB

CaseCase

Where and what to do??Where and what to do??

CaseCase

HistoryHistory

–Skiing all morningSkiing all morning

–Afternoon at home acute onset SOB (5-10 min)Afternoon at home acute onset SOB (5-10 min)

–ResolvedResolved

–Acute onset pain weakness and discoloration to Acute onset pain weakness and discoloration to right arm (unable to move arm)right arm (unable to move arm)

–Called EMSCalled EMS

CaseCase

Past HxPast Hx

–HealthyHealthy

–Ex-smoker 15 pack yrsEx-smoker 15 pack yrs

–High cholesterol on zocorHigh cholesterol on zocor

CaseCase

EMSEMS

–Same hx as previousSame hx as previous

–O2 sat 80 % RA increased to 92% on NRBO2 sat 80 % RA increased to 92% on NRB

–BP 168/98, HR 115, RR 20BP 168/98, HR 115, RR 20

–Arm : white / purpleArm : white / purple

CaseCase

ED EvaluationED Evaluation

–Vitals: 159/99, HR 122, RR 20Vitals: 159/99, HR 122, RR 20

–O2 sat 83% RA, increased to 96% NRBO2 sat 83% RA, increased to 96% NRB

–Fit looking 71 y/oFit looking 71 y/o

CaseCasePEPE

– A+O x3, speaking in full sentences, didn’t look labored but was A+O x3, speaking in full sentences, didn’t look labored but was tachypnictachypnic

– H+N: normalH+N: normal

– Chest: clear, no rubChest: clear, no rub

– CV: CV:

• active precordiumactive precordium

• S1, S2 no S3 or S4, no murmursS1, S2 no S3 or S4, no murmurs

• ? JVD? JVD

– Abdo: normalAbdo: normal

CasePE (con’t)

– Right arm• Purple in colour (from mid upper arm)• Cool to touch• Decreased cap refill• No radial pulse• Motor 4 -/ 5 (left 5/5)

Case Investigations?

– ECG– CXR– ABG????– Blood work

• CBC, LYTES, PT, INR, CK

ECG

X-Ray

CaseCBC:

– WBC 11– Hb 160– Plt 147

Lytes– Na 143, Cl 105, K 4.5, CO2 18– INR 1.0, CK 93

CaseABG

7.41 / 34 / 217 / 21

A-a gradient: (Alveolar – arterial)

Alveolar: FIO2 x (BP – PP H2O) – (1.25 x PCO2)

1 x (665 – 47) – ( 1.25 x 21) = 618 – 26 = 592

Arterial : 217

A-a gradient : 592 – 217 = 375 (extremely elevated)

Normal : (5-10) or ( age/4) + 4

- 71/4 + 4 = 22 mmHg

CaseDDX ?

What is your most likely diagnosis??

Case

What to do next?– Pt started on heparin (earlier)– ICU and vascular consulted

Any further investigations/treatment??

PE : Epidemiology

What about PE?– Epidemiology

• MC preventable hospital death• MC undiagnosed hospital death• True incidence unknown

– 650,000 cases / yr US– 200,000 deaths

PE : Epidemiology

Epidemiology– 1980

• 21% of all ED pts with pleuritic CP had a PE– Mortality

• Usually within the first hour• But large # die with subsequent emboli• Acute mortality correlates with RV function• Long term mortality correlates with comorbid illness• Age <40 mortality : 2.5%• Age >40 mortality : 18% (some studies geriatrics 39% even when

treated• Overall untreated : 30% mortality• Treated: 5% mortality

PE: Causes

Cause– 90% from lower extremities

• Catheter related upper ext PE : up to 15%

– PIOPED• 50% immobilization within 3 months of PE• 40% trauma or surgery

– Neoplasm• Responsible for 4% of thromboembolic disease• Several studies: idiopathic PE (neoplasm eventually in ~ 9%)

PE: Clinical Features

Clinical Features– Younger pts:

• 30% no risk factors• 60% normal vitals

– 97% have some combination of :• Dyspnea, tachypnea, or pleuritic CP

– Up to 10% will have syncope

PE: Physical Exam

Physical Exam– HR is normal in 70% pts– RR < 20 in 30% pts– Homans sign : flip a coin

PE: ECG

ECG– 20 - 30% normal ECG– 50% NSSTTW changes– RBBB, right axis deviation, ST depression,

rarely S1, Q3, T3– A-fib !

PE: CXR

CXR– 84% pts will have an abn CXR– MS findings”

• Atelectasis, blunting of CP angle (effusion),elevated hemidiaphragm

– Other signs:• Hamptons Hump• Westermark sign• Fleischner sign

PE: A-a Gradient

A – a Gradient– >1/4 of all pts with PE will have P02 >80– Some pts can have sat 100% RA– PIOPED

• 8-10% pts had normal A-a gradient• A-a gradient nonspecific• Not required in the work-up of PE !!!

CaseWhat next?

– Echo• Moderate TR• Pulmonary artery pressures 90-100!• Hypokinetic RV• Normal LV function• Positive bubble study !

PE: ECHO

ECHO– TTE: 85% sensitive for massive PE– TEE: 90% sen, up to 100% specific– Findings in PE

• Increased RV end diastolic pressures• Increased PA pressures• TR• Abn septal movement

PE: CT Scan

CT Scan– Sensitivity: 88-95%, Specificity: 92- 97%– Adv:

• Can detect other pathology– Disadv:

• Limits visualization to fourth gen pulm arteries• Hard to hold breath for scan!

Case

CT done– Bilateral filling defects (PE’s)– MASSIVE clot in the SVC/ and Right PA

Case

What would you do now?

– Pt taken to ICU and underwent thrombolysis

Thrombolysis and PE

Mechanism– Converts plasminogen to plasmin– Breaks down fibrin – Clot dissolution

Agents– tPA, Urokinase, SK– tPA targets clot specific plasminogen/fibrin– Urokinase – human urine or cultured human renal cells

Thrombolysis and PE

Evidence for TT and PE– Case reports and case series in early 1960’s

• Improved hemodynamics and perfusion– UPET (Urokinase Pulmonary Embolism Trial, 1970)

• 160 pts, heparin vs UK and heparin (12hr infusion)• Hemodynamics/ lung perfusion improved at 24 hrs • No mortality difference

Thrombolysis and PE

Evidence for TT and PE– Sharma et al (pts from UPET and USET)– Measured diffusion capacity and pulmonary

blood volume at 2 wks and 1 yr– Improved in the thrombolytic therapy gp– Concluded: TT more complete resolution of

clot beyond resolution of perfusion scan or angiography

Thrombolysis and PE

Evidence for TT and PE– Since UPET 8 smaller randomized trials– SK, UK, comparison etc.– All show variable benefit in either blood flow,

perfusion but no mortality benefit– PIOPED (13 pts rtPA or heparin)

• Pulm vascular resistance : Diff at 1 hr gone at 2 hrs

Thrombolysis and PE

Evidence for TT and PE– Goldhaber et al (1993)

• N=101, heparin vs rtPA and heparin• ECHO (3 and 24 hrs) and perfusion scans• rtPA improved RV function and lung perfusion• Trend to decreased recurrence of PE

Thrombolysis and PE

Evidence for TT and PE– Jerges et al 1995– Small study n=8, massive PE with shock– SK vs heparin– Heparin 4/4 died– rtPA 0/4 died– First evidence of mortality benefit???

Thrombolysis and PE

Evidence for TT and PE– PE registry (1993-1994) n=1001 pts– RV dysfunction/ pulm hypertension (no shock)– rtPA (n=169) vs heparin (n=719)– Mortality: 4.7 vs 11.1% (ARR 3.4%, RRR 31%)– Recurrent PE: 7.7 vs 18.7% (ARR 11%, RRR 59%)– Needs to be validated in a large PRCT

Thrombolysis and PE

Evidence for TT and PE– Long term benefit (Sharma et al)– Right heart cath 7 yrs after PE and either TT or

heparin– Heparin gp : higher PA pressures and higher

pulmonary vascular resistance– TT gp : values normal

Thrombolysis and PE

Conclusion– TT results in more rapid clot resolution,

perfusion and blood flow – No mortality difference in pts without shock

(but may be due to small studies)– Possible mortality benefit in pts with shock!

Thrombolysis and PE

Which agent to use??– SK for 24 hrs, UK for 12 hrs and rtPA for 2 hrs– Goldhaber et al

• rtPA 2 hr infusion, UK 24 hr infusion • Earlier clot resolution and improved hemodynamics

with rtPA at 2 hrs benefit gone at 24 hrs!• Mortality no diff• Increased hemorrhage in UK (double)

Thrombolysis and PE

Conclusion– All agents seem to be equal– rtPA has faster clot resolution but at 24 hrs no

benefit

Thrombolysis and PE

Other conclusions– Intra-arterial TT is no better than systemic

therapy (no increased risk of bleeding)– Time of administration: TT better if given early

but can have benefit out to 14 days

Thrombolysis and PE

Complications– Major hemorrhage (fatal hem, ICH, hem

requiring surgery or transfusion) : ~6% (heparin ~1.5%)

– ICH : ~1% (death in ~50% )• Decreased in SK

Thrombolysis and PE

Indication For Thrombolysis1) Hemodynamically unstable : shock or evidence

of hypoperfusion2) Hemodynamically stable: RV dysfunction? 3) ?? Large clot burden

Case

In ICU– Thrombolysis with improvement in RV function

(demonstrated by repeat echo)– U/S residual clot in superficial femoral and brachial

artery– IVC filter placed– Catheter placed tPA – no effect– Thrombectomy right arm– D/C to ward for monitoring– D/C home on lifelong anticoagulation

Case

Paradoxical embolus– Passage of venous embolus into the arterial circulation

typically across an intracardiac shunt– Dx can only be inferred– Dx usually made if:

• Documented venous thromboembolism• Acute arterial embolization• ECHO evidence of right to left shunt• Exclusion of a left sided source

Case

Paradoxical embolus– MC intra-cardiac defect – PFO

• Failed closure of the septum secundum– Frequency of PFO (autopsy)

• 29% (probe patent)• 6% (pencil patent)

What if????

What if pt with antithrombin III deficiency presents with sx compatible with PE

How do you treat this pt.????