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Pulmonary Embolism, Case Report of b/l PE & Literature Review

Pulmonary Embolism European Society of Cardiology (ESC), European Respiratory Society (ERS) Recommendations Pathophysiology Clinical Manifestations Diagnostic Algorithms Management Insight Anticoagulation guidelines Choice and duration of Anticoagulation Indications of Thrombolysis Follow up for CTEPH

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Pulmonary Embolism, Case Report of b/l PE & Literature Review
Pulmonary Embolism
A Case Report
Dr Badar Ahmad Jamal
PGR Cardiology
National Hospital & Medical Center
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.
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
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…
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.
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Pulmonary Embolism, Case Report of b/l PE & Literature Review

  • 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 …
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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