A 50-year-old male presented with palpitations, chest discomfort and dyspnea for 3 days following hip replacement surgery 15 days prior. Investigations revealed elevated D-dimer, signs of right heart strain on echocardiogram, and CT pulmonary angiogram showed bilateral saddle pulmonary embolism. He was treated with oxygen, low molecular weight heparin and rivaroxaban. Symptoms resolved and follow up echo showed improvement. He was discharged on long term anticoagulation for pulmonary embolism.

2. Pulmonary Embolism
A Case Report
Dr Badar Ahmad Jamal
PGR Cardiology
National Hospital & Medical Center

3. CASE SUMMARY
 50 years old male patient of average built, from upper middle class
socioeconomic background presented with c/o palpitation & apprehension,
with vague chest discomfort worsening for the past 2-3 days
 The said symptoms started about 3 days ago when he was otherwise well
but had restricted ambulation secondary to left sided total hip replacement
15 days prior to admission. No h/o SOB / orthopnea / pedal puffiness.
 Started suddenly, while he was at rest.
 Chest discomfort was centrally distributed, dull in character, non radiating
with no specific aggravating / relieving factors.
 Worsened over the course of preceding 3 days.

4. Cont..
 Past Medical history notable for Type II Diabetes &
Hypertension controlled on metformin/sitagliptin 50/1000
OD and amlodipine 5mg once daily.
 No Past h/o clinical ASCVD / PAD / VTE. No diagnosed pro-
coagulant state.
 Recent past surgical history of left sided total hip
replacement 15 days back followed by immobilization

5. Continued …
 BP 130/70, R.R 27/min
 Rapid Pulse Rate 150/min
 Peripheral O2 sat. 93% at room air
 S1+S2 with tachycardia, no appreciable murmur
 Chest b/l clear, shallow breathe, no added sounds
 No leg swelling / DVT clinical signs
 12 lead ECG as follows,
 CXR .. Follows…

6. Sinus tachycardia with rate ~ 150/min. Normal P wave duration (60msec.) , morphology and polarity.
Shortened PR segment, normal PR interval (~140msec.). Normal R wave upstroke and peak time
(~20msec)throughout. Pathological Q waves in lead III (S1Q3T3 constellation). Borderline prolonged
QRS ~120msec. RSR’ pattern in V1, dominant R waves in leads V1, V2 (RBBB morphology), deep S
waves in lead I, slurred S waves most prominent in V5-V6. J-point /st depression in lateral leads. T
wave inversion in lead III (S1Q3T3 constellation) and V1 (RBBB). QTc ~ Framingham 412 / Hodges
478msec. Electrical axis ~ 60degree.

7. CXR AP view. Trachea is central, normal b/l bronchovascular markings with
sharp angles. Pulmonary artery appears enlarged on rt side (Fleischner’s sign),
with apparent calcified right hilar lymph nodes.

8. Cont…
Misc. Lab. Profile
D Dimer 3733 ng/ml (<500ng/ml)
Arterial pCo2 27 mm of Hg, pH 7.50
Troponin I (ng/ml) 1) 0.54 2) 1.56
Unremarkable CBC, liver and renal profile, s. electrolytes
Unremarkable CUS b/l lower limbs
>>>PULMONARY EMBOLISM

9. Transthoracic Echo
 McConnels sign
 RV Base 44mm (<42mm)
 RVSTDI 9cm/sec (<9.5)
 TAPSE 13mm
 Abnormal Septal Motion
 PASP 30mmHg
 Normal LV systolic function / valves morphology

10. CTPA
B/l extensive saddle pulmonary embolism.

11. CASE MANAGEMENT / COURSE,, TO FOLLOW …

12. LITERATURE
REVIEW

13. Overview
 Annual incidence rates for PE range from 39–115 per 100 000 population
 Embolic partial / complete obstruction of pulmonary artery or its lobar
/segmental / sub-segmental branches
 Results in gross V/Q mismatch and chaos in pulmonary hemodynamics,
leads to hypoxemia, Rt sided heart failure, shock. May end up with fatality
 Classified majorly as massive / sub-massive
 Early diagnosis and prompt treatment is the key to better outcome
 3rd most common cause of cardiovascular death globally
 Mortality Rate is 30% if left untreated and 8% with Rx

14. Pathophysiology
VTE > Embolization to pulmonary vasculature.
V/Q mismatch in lungs.
Increased PVR / Acutely increased RV pressure overload
Overwhelmed compensatory mechanisms
Subsequent hypoxemia, RV dysfunction and dilatation with
compromised RV output
Reduced filling of LA / preload with subsequent hemodynamic collapse
Gives the typical constellation of hypoxemic respiratory and circulatory
failure.

15. Mechanism of Shock
Low CO
Vasomotor Reflex
Leading to decreased Systemic Arterial
Resistance

17. Classification
In order to risk stratify / predict outcome / devise appropriate
treatment strategy
 MASSIVE
Sustained hypotension (systolic BP <90 mm Hg for 15 min or requiring
ionotropic support) or pulselessness or sustained heart rate < 40 BPM with
signs/symptoms of shock (AHA)
 SUB-MASSIVE
Systolic BP > 90 mm Hg > not fulfilling MASSIVE criteria

18. ESC Def. Acute High Risk PE

19. PE Risk Factors

20. Clinical Manifestations
 Dyspnea
 Chest pain (sub-sternal /pleuritic)
 Cough
 Hemoptysis
 Calf/leg pain in case of DVT
 Tachypnea, Tachycardia, RV S3 Gallop, PSM (TR), hypoxemia,
hypocapnea, pulsatile liver, JVD
 Fever
 Hypotension

21. Whom to suspect?
 PE stands as a likely differential dx
 Clinical signs of DVT
 Tachycardia H.R > 100/min
 Immobilization of atleast 3 days / surgery in past 4 weeks
 Previously, h/o objectively diagnosed VTE
 Hemoptysis
 Malignancy under Rx/Palliation in the last 6 months
Unexplained SOB with normal / near normal lung auscultation and
CXR, with hypoxemia and hypocapnea

22. Pretest Probability Scoring
 Clinical signs of DVT ..... 3
 PE stands as a likely differential …. 3
 H.R > 100/min …. 1.5
 Immobilization of >3 days /surgery in past 4 weeks …. 1.5
 Previously, h/o objectively diagnosed VTE …. 1.5
 Hemoptysis …. 1
 Malignancy under Rx/Palliation in the last 6 months …. 1
<2 = Low Risk 2-6=Moderate Risk >6=High Risk
Incidence 1.3% Incidence 16.2% Incidence 37.5%
WELLS SCORE

23. Cont…
GENEVA SCORE

24. Investigations
 CTPA – gold standard (Filling Defects ) Sensitivity 86%, specificity 93%
V/Q SPECT / PLANAR VQ / Pulmonary Angiography
 D-Dimers (age adjusted) sensitivity 95%, specificity unreliable
 ECG, CXR
 Echocardiography (TTE) – Adjunct. NPV 40-50% only
 CUS lower limb deep veins sensitivity >90%, specificity of ∼95% for proximal
symptomatic DVT
 Supportive

25. ECG changes
 Sinus Tachycardia
 RBBB
 RV Strain
 S1Q3T3
 Precordial ST elevation
 Isolated Right Axis Deviation

26. CXR Findings
 Fleischner sign: enlarged pulmonary artery (20%)
 Hampton hump: peripheral wedge of airspace opacity and implies lung
infarction (20%) PPV: ~29%, NPV: ~76%
 Westermark sign: regional oligemia, highest positive predictive value PPV:
~38%, NPV: ~76%
 pleural effusion (35%) - PPV: ~28%, NPV ~76%
 Palla sign : enlarged right descending pulmonary artery
 Chang sign : dilated right descending pulmonary artery with sudden cut-off

28. Westermark Sign

29. Echocardiography
ECHOCARDIOGRAPHY SIGNS

31. Diagnostic Algorhithm (ESC)

32. Risk Stratification

33. PESI
Original Simplified

34. MANAGEMENT

35. Treatment Overview
 Supportive ABC / supplemental O2 (spo2 >90%) / cautious fluid Rx / basic
workup
 Anticoagulation is the mainstay. To be started in intermediate to high
pretest probability prior to confirmatory test results availability (ESC)
 Massive PE >> Thrombolysis ( SK / rtPA), systemic thrombolysis may be
considered in sub-massive high risk patients (ACC, ESC)
 Catheter directed therapy,, option in high bleed-risk cases with relative
contraindication to thrombolytics (ACC)
 Surgical Embolectomy in failed thrombolysis / absolute contraindication to
thrombolysis (ACC, ESC)
 Usual duration of anticoagulation is 3 months to 6 months for transient
risk factors. Exact duration varies from case to case
Targets : CLOT > HEMODYNAMICS >> OXYGEN LEVEL

36. Dosage of Anticoagulation
UFH
• 80 units/kg
loading dose
• 18unit/kg/hour
maintenance
with target
aPTT
1.5xControl
LMWH
• 1mg/kg SQ BD
Fondaparinux
(acc. to weight)
• <50kg=5mg,
• 50-100
Kg=7.5mg
• >100Kg=10mg
SC OD
NOAC
• Rivaroxaban:
15mg bd PO for
3 weeks
followed by
20mg OD
• Apixaban:
10mg BD PO
for 7 days,
followed by
5mg BD

38. Rx for Shock
 Cautious volume loading, saline, or Ringer's lactate, ≤500 mL over 15–30
min. Volume loading can over-distend the RV, worsen ventricular
interdependence, and reduce cardiac output
 Norepinephrine, 0.2–1.0 µg/kg/min. Excessive vasoconstriction may worsen
tissue perfusion
 Dobutamine, 2–20 µg/kg/min. May aggravate arterial hypotension if used
alone, without a vasopressor; may trigger or aggravate arrhythmias

39. MANAGEMENT
In the light of ESC Recommendations (COLOR CODED)

40. Initiation of Anticoag.
In case of VKA : overlap with parentral anticoag till INR is
2.5 (2.0-3.0)
Intermediate / High PreTest Probability : Start Anticoag. (without
delay) while diagnostic workup is in progress
Parentral Therapy : LWMH / Fondaparinux Prefered over
UFH (Intermediate Risk)
Oral Therapy : NOAC prefered over VKA if eligible
NOACs not recommended in severe renal impairment /
pregnancy / lactation / APLS

41. Reperfusion Therapy
Patients on Anticoag, developing hemodynamic deterioration
Surgical embolectomy / Catheter directed therapy as
alternatives to thrombolytic therapy
Rouine use of thrombolytic therapy in Intermediate / Low risk
PE is not recommended

42. Duration of Anticoag.
Therapeutic Anticoagulation duration > 3 months in all PE cases
Major Transient Risk Factor of VTE / PE – Discontinue anticoag.
after 3 months
Recurrent PE / VTE not secondary to Major Transient Risk factor
– INDEFINITE ANTICOAGULATION DURATION (lifelong)
Anticoag. With VKA for indefinite period (LifeLong)
First PE, No identifiable Risk factor / Persistent Risk Factor
(other than APLS) / MINOR Risk Factor –
Extended Anticog. for indefinite duration

43. Cont…
Extended Oral Anticoag (no malignancy), NOAC dose after 6
months of therapeutic dosage, should be reduced (Apixa
2.5mg BD, Rivarxaban 10mg OD)
Patients unable to tolerate / refuse to take oral anticoagulant -
ASPIRIN / SULODEXIDE may be considered for extended VTE
prophylaxis
Things to monitor in extended anticoagulation – Drug
Tolerance, adherence, bleeding risk, Hepatic and renal
functions at regular interval

44. Anticoag in Malignancy
PE in Cancer : weight adjusted LWMH preferred over VKA for first
months
Rivaroxaban (IIA/LOE-C), Edoxaban (IIA/LOE-B) as alternative to
LMWH in patients without GI cancer
Extended anticoagulation (> 6 months) for indefinite period /
untill the cancer is cured
Incidental PE in cancer to be treated same as symptomatic PE in
case of (i) involvement of segmental/proximal branches (ii)
multiple segmental vessels (iii) single subsegmental vessel +
proven DVT

45. Risk of Recurrence

46. PE IN PREGNANCY

47.  a-If chest X-ray abnormal, consider also alternative cause of chest symptoms
 b-DVT in pelvic veins may not be ruled out by CUS. If the entire leg is swollen, or there is buttock pain or other
symptoms suggestive of pelvic thrombosis, consider magnetic resonance venography to rule out DVT. C
 c-CTPA technique must ensure very low foetal radiation exposure
 d-Perform full blood count (to measure haemoglobin and platelet count) and calculate creatinine clearance
before administration. Assess bleeding risk and ensure absence of contra-indications

48. Diagnosis

49. Treatment

51. FOLLOW UP

53. ..CONT..
 aAssess the persistence (or new onset) and severity of dyspnoea or functional
limitation, and also check for possible signs of VTE recurrence, cancer, or bleeding
complications of anticoagulation.
 bThe Medical Research Council scale can be used to standardize the evaluation of
dyspnoea; alternatively, the World Health Organization functional class can be
determined
 cAs defined by the ESC/ERS guidelines on the diagnosis and treatment of Pulmonary
Hypertension
 dRisk factors and predisposing conditions for CTEPH
 eCardiopulmonary exercise testing, if appropriate expertise and resources are available
on site; abnormal results include, among others, reduced maximal aerobic capacity
(peak oxygen consumption), increased ventilatory equivalent for carbon dioxide, and
reduced end-tidal carbon dioxide pressure.
 fConsider CPET in the diagnostic work-up.

55. Coming back to our case…
 Emergency Rx including oxygen supplementation,
 Admitted to HDU, supportive Rx rate, rhythm and vitals monitoring in critical
care unit
 Anticoag….. LWMH 60 SC BD
 Stable hemodynamics and spo2 throughout (on minimal o2)
 Interval Echo showed improvement, together with clinical parameters and
ECG.
 Switched to rivaroxaban 15mg BD and discharged home while maintaining
sat. at room air and symptoms completely resolved

56. Interval Investigation
 Repeat Echo, images …Resolution of McConnel sign
 Reversion of RVSTDI and TAPSE, RVBase 34, RVAct 110
 ECG Resolved S1Q3T3

57. ECHO 3rd Admission Day
ECHO on 25/10/23

58. CONT..
 Currently doing well on rivaroxaban and supportive Rx

59. Bibliography
 CURRENT Diagnosis & Treatment Cardiology 6th Ed.
 Marriot’s Practical Electrocardiography 12th Ed
 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism
developed in collaboration with the European Respiratory Society (ERS): The Task
Force for the diagnosis and management of acute pulmonary embolism of the European
Society of Cardiology (ESC).
https://academic.oup.com/eurheartj/article/41/4/543/5556136?login=false
 ACC/Management of PE (Online) https://www.acc.org/Latest-in-
Cardiology/Articles/2020/01/27/07/42/Management-of-PE
 Extended Anticoagulation After Pulmonary Embolism: A Multicenter Observational
Cohort Analysis (JAHA) https://www.ahajournals.org/doi/10.1161/JAHA.121.024425
 Misc. Online Sources