PULMONARY EMBOLISM

JO-ANN VOSLOO

DEPARTMENT CRITICAL CARE

SBAH

Embolism

1. Thrombo-embolism DVT: legs/iliac veins/IVC**

2. Septic emboli infective endocarditis

3. Tumor e.g. choriocarcinoma

4. Fat embolism

5. Air

6. Amniotic fluid

7. Placenta

**VTE = venous thromboembolism

(PE plus DVT)

5% of in-hospital deaths

PE rare from below knee DVT

Venous thrombo-embolism(VTE)

Clinical presentation

Depends on : number, size and distribution of emboli

: underlying cardiovascular reserve

• Acutely breathless

• Hypoxia(mismatch ventilation/perfusion)

• Sudden collapse

• Unilateral pleuritic chest pain

• Uni- or bilateral changes on CXR

• Hemoptysis

• Tachicardia / fever

Diagnosis is difficult in critically ill patient

40% of pt with DVT will develop PE

5% of pt with VTE develop chronic pulm hypertension

Recurrent VTE due to activated Prot C resistance mediated by factor V Leiden mutation

Pathophysiology (VTE)

• Pulmonary arterial obstruction and release of vasoactive agents from platelets/hypoxia

pulmonary vascular resistance and pulmonary hypertension

RV preload increases /Decreased Rt heart perfusion(Rt coronary

artery)

Paradoxial interventricular shift/RV dilatation and dysfunction

(opening of foramen ovale with Rt to Lt shunt and paradoxical arterial

embolisation)

OR

• Massive pulmonary embolism

Sudden collapse due to acute low cardiac output (shock)

Investigations:VTE

• CXR:

Most useful to exclude pneumonia, pneumothorax (diff. diagnosis)

• ECG

Exclude MI

Sinus tachicardia, ant. T-wave inversion, S1 Q3 T3 Rt heart strain, ST-segment

changes, Rt bundle branch block.

• ABG: Low PaO2

N – low PaCO2 /widening end tidal to PaCO2 gradient

Increased A-a gradient

Metabolic acidosis (massive pulm emb with CVS collapse)

• D-Dimer/Trop I/Pro-BNP

D-Dimer: Negative predictive value -- limited value in ICU setting

Investigations: VTE

• CT pulmonary angiogram: 1st line diagnostic test

Visualize distribution and extend of PE/Identify alternative diagnosis: pneumonia, pneumothorax,

aorta dissection.

• Echocardiography

RV dilatation, interventricular septal shift, RV dysfunction, Thrombus in RV or PA

• Ventilation – perfusion scan

For pt with normal CXR and cardiopulmonary disease

Diagnosis in ICU

• Despite presence of risk factors still relatively uncommon in critically ill pt

• However the diagnosis is frequently overlooked should it occur

• Clinical prediction systems:

Wells score

Geneva score

Management VTE

• General:

Recognize the problem

Oxygen

IV fluids for circulating shock

Opiates for pain

• Anticoagulation:

Start immediately if high probability of PE

UFH or LMWH

Overlap LMWH and Warfarin. Stop LMWH when INR =2

• Thrombolytic therapy:

Pt with massive PE and CVS collapse

Useful up to 14 days post Non-massive PE

Administration must be followed by heparin treatment

Complications: Major bleedings in 10% of pt. (treatment: FFP and antifibrinolytic agent

Aprotinin)

Exclude contra-indication e.g. intracranial hemorrhage

VTE

• Management cont. Surgical embolectomy

When thrombolytic therapy is contra-indicated or fails

Free floating thrombus

• Combine surgical embolectomy and thrombolytic therapy

• Percutaneous embolectomy

Can combine extraction with embolus fragmentation or catheter directed

thrombolysis

• Caval filters

When thrombolytic/anticoagulation therapy is contra-indicated

Recurrent PE on anticoagulation treatment

Following surgical embolectomy

RVCPP < 30mmHg RV failure and shock

RVCPP = MAP – [CVP + 1/3(PAPs - CVP)]

(right ventricular coronary perfusion pressure)

Therefore increase MAP and lower PAP vasopressor NA to increase MAP, (preferred to phenylephrine

due to added β-adrenoceptor effect). Alternative = adrenalin,

dopamine and vasopressin

judicious fluids

systemic vasodilators can be harmful (no dobutamine,

nitroglycerine and nitroprusside, milrinone)

IABalloon pump counterpulsation / ECMO can be beneficial

Inhaled NO selective pulmonary vasodilatation

AMNIOTIC FLUID EMBOLISM

(AFE) • Unpredictable, unpreventable, uncertain pathophysiology

• Incidence; 1 in 40 000 deliveries

• 5 – 10% of maternal deaths

• 20-50% of proven AFE die within 1st hour

• Neonatal mortality: 40%. High incidence of neurological deficits in survivors

• Maternal mortality: 40 - 86%. Survivors may have neurological sequelae.

• Amniotic fluid enters through uterine/cervical laceration/uterine veins at site of placental separation/placenta abruptio amnion fluid and fetal debris complement activation/physical blockage of pulmonary arteries/pulmonary vasoconstriction. Mediators in amniotic fluid can cause a picture equal to anaphylaxis.

• Clinical picture: severe dyspnoea, cyanosis, sudden CVS collapse, coma/convulsions. Can develop coagulopathy (DIC)

• Diagnosis: Clinical suspicion.

Confirmed by presence of fetal debri in pulmonary circulation(pulm aretery

catheter sample. (presence of squamous cells not diagnostic – also seen in non-pregnant patients and other

parturients)

AFE

• Treatment:

- Cardiopulmonary resuscitation, 100% O2

- Early pulmonary artery catheterisation (RV failure, Pulm Ht, later LV

failure)

- Urgent delivery of fetus (C-section)

- Supportive treatment

- Cryoprecipitate, r-Factor VIIa

• Survivors may have neurological sequelae.

PULMONARY TUMOR

EMBOLISM • Cancer patients have increased incidence of thrombo-embolism, as well as tumor

embolism. Therefore important to diagnose to avoid aggressive treatment in terminally ill patients. Often misdiagnosed as pulmonary thrombo-embolism.

• Incidence: 8,5% (all kinds of cancer)

26% for Ca of breast, stomach, liver, kidney and ChorioCa

• Can be: - Macro tumor embolus: blocking the bigger pulmonary arteries

- Micro-embolism: Clusters of tumor cells block septal or smaller arterioles.

- Lymphatic spread: Pulmonary lympangitic carcinomatosis. Tumor growth in interlobular

septal vessels and subpleural lymphatic vessels.

• Microemboli triggers fibrin deposition and neutrophil sequestration:

Increased permeability of endothelial cells

Intimal fibrosis, media hypertrophy endartiritis obliterance

PULMONARY TUMOR

EMBOLISM • Endartiritis obliterance, vasoconstriction pulmonary hypertension myocardial

hypertrophy/dilatation RV and RA.

• Diagnosis:

ABG: Resp alkalosis, increased A-a gradient, hypoxemia.

ECG: S1Q3pattern, sinus tachicardia, RV hypertrophy

CXR: Prominent pulm artery, RV enlargement, atelectesis, pleural effusion, features suggestive of pulm

TB(miliary TB picture)

Doppler echocardiography: Dilated Rt heart chambers

Lung biopsy: Gold standard for definitive diagnosis open lung biopsy or video-assisted thoracoscopic.

Pulmonary wedge aspiration cytology: if too hypoxic to undergo lung biopsy

Ventilation-perfusion radionuclide scanning: Segmental contour pattern numerous small defects that

outlines the pulmonary fissures and bronchopulmonary segments (non specific

finding also seen with vasculitis, fat embolism, septic emboli).

Pulmonary angiography/CT pulmonary angiogram

PACatheter: Pulmonary wedge aspiration cytology unfortunately not 100% sensitive

RV pressures increased (50-60mmHg)

PAPm increased (50-100mmHg)

PAWP = normal

Tumor associated monoclonal antibody imaging: Injection radiolabelled antibodies

PULMONARY TUMOR

EMBOLISM • Managemenrt:

- Distinguish from thrombo-embolism

- Complete resection of primary tumor

- Inferior vana cava filter for large emboli

- Chemotherapy (add hormonal therapy for breast, prostate and choriocarcinoma)

- Steroid therapy and anticoagulation therapy showed no benefit

- Palliative therapy: fluids, vasopressors, oxygen and control pleural effusion.

SEPTIC PULMONARY

EMBOLI(SPE) • Uncommon disorder

• Presents with: Incidious onset of fever

: Resp symptoms

: Lung infiltrates (non specific) poorly marginated lung nodules that

has tendency to cavitate

• Associated with: IV drug use

: Pelvic thrombophlebitis

: Suppurative process in head and neck region

: Indwelling catheters and devices(Lamierre Syndrome; anaerobic

thrombophlebitis internal jugular vein metastatic infection)

: Immunocompromised patients

• Infected embolic clot pulmonary artery branches infarction focal abscess

SPE

• CT scan:

*Lung abscesses, multiple nodules, cavitation, lung infiltrates

*Pleural effusion

*Empyema

*Pneumothorax

• Echocardiography/TEE

* In patients with suspected infective endocarditis

* Valvular vegetations, leaflet perforations, valvular insufficiency or dehiscence,

congestive heart failure, paravalvular abscesses.

• Blood cultures

TREATMENT:

• Early appropriate antibiotics

Control of infectious source

FAT EMBOLISM

• Incidence: 2-22%

• More commonly seen with:

- Femur, pelvis and tibia fractures

- Young males

- Closed long bone fractures

- Non – immobilized long bone fractures

- Placement of medullary nails (reaming)

• Occur 12-72h following injury

• Pathophysiology:

Fat droplets enter circulation occlusion of pulmonary vessels = EARLY PRESENTATION

hydrolysis of fat molecule forms FA stimulates

inflammatory response (lung) interstitial

hemorrhage, oedema, chemical pneumonitis) = LATE

PRESENTATION

FAT EMBOLISM

• Clinical picture:

- Tachicardia, hypotension, elevated CVP, low Hb

- Dyspnoea, hypoxemia

- Fever

- Thrombocytopenia Peticheal hemorrhages upper ant. chest/neck/face and

upper arms, oral mucosa and conjunctiva = PATHOGNOMONIC

- Confusion, agitation, lethargy, seizure, coma

• Diagnosis:

High index of suspicion

CXR: *snow storm appearance

* dilation of Rt side of heart

Laboratory tests: * Increase s-lipase (non specific)

* Fat lobules in blood, urine, sputum absence does not

exclude FES

FAT EMBOLISM

Treatment:

• Reduce and immobilize long bone fractures as soon as possible

• Prevent/treat hypovolemic shock

Suggest Albumin as resus fluid (binds fatty acids and may decrease extend

of disease.

• Mechanical ventilation (ARDS)

• High dose corticosteroids (controversial)

AIR EMBOLISM

• Venous air embolism (VEA)

• Associated with:

- Placement of central lines

- Penetrating or blunt trauma of chest/abdomen (4-14% incidence)

- High pressure mechanical ventilation (pneumothorax)

- Thoracocentesis

- Interventional radiology (0.3% incidence)

- Decompression sickness

- Cardiovascular, otolaryngiological and orthopaedic procedures

- Neurosurgical procedures

- Lumber puncture

- Ingestion of hydrogen peroxide

AIR EMBOLISM

Symptoms and signs:

• Symptoms are non-specific

• High index of suspicion

• Shock and cardiac arrest: need 5ml/kg air

• 2-3ml Air into cerebral circulation: can be fatal

• 0.5ml Air in LAD coronary artery VT

• Large AE in RV outflow obstruction systemic cardiovascular collapse

• Small multiple emboli into pulmonary arteries inflammatory changes V/Q mismatch resp. failure/pulmonary HT/enlarged Rt heart

• Via patent foramen ovale to cerebral circulation paradoxical arterial embolism stroke

• Hemoptysis

• Dysrythmia

• Agitation, confusion

• Substernal pain

AIR EMBOLISM

• Special investigations:

Transcranial doppler: cerebral micro-emboli

TEE/TTE: presence of air in RV outflow

CXR: Usually normal

Gas in PA

Pulm oedema

PA dilation

CT scan: AE can be identified

ECG: resembles that of PE

ETCO2: Non specific

Diff diagnosis: PE, massive blood loss, circulatory arrest, upper

airway obstruction, disconnection of CO2 monitor

ETN2 : non specific

AIR EMBOLISM

• Treatment:

- Place in left lateral decubitus position (Durant manuevre) and Trendellenburg

- Identify and prevent further entry of air

- Intubate + 100% O2

- Direct aspiration of air via central line success doubtfull

- CPR if indicated break large air bubbles into smaller ones Prevent air

lock.

- Supportive therapy for hypotension fluids +/- vasopressors

- HBOT (hyperbaric oxygen therapy): 1st choice

Treatment window: immediate to 6h after incident

Compression of existing bubbles creates a high diffusion gradient

resolution

Reference

• Cook RJ, Ashton RW, Augenbaugh GL, Ryu JH. Septic pulmonary embolism.

Presentinf features and clinical course of 14 patients. Chest 2005: 128; 162-

166.

• Qaseem A, Snow V, Barry P, et. al. Current diagnosis of venous

thromboembolism in primary care: A clinical practice guideline from the

American Academy of Family Physicians and the American College of

Physicians. Annuls of Internal Medicine 2007: 146; 454-458.

• Mehrishi S, Awan A, Mehrishi A, Fein A. Pulmonary tumor microembolism.

Hospital Physician 2004: 23-30.

• Davidsons Handbook: Principles and Practice of Medicine

• Oh’s Intensive Care Manual Sixth Edition