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Have you ever experienced body numbness? Pulmonary embolism could be the cause

Definition

Formation of a thrombi in the pulmonary vasculature

Pathogenesis

-More than 90% of pulmonary emboli arise from thrombi in the deep venous system of the lower extremities.

-Right cardiac chambers and the vena cava with its major branches account for the rest.

Factors promoting DVT are best defined by the Virchow’s triad i.e.

1. Stasis of blood

2. Vessel wall abnormality i.e. endothelial damage

3. Blood coagulation system alteration

1. Blood stasis causes include

-Bed ridden patients e.g. comatose or ICU patients

-Surgical procedures requiring 30 minutes or more under general anesthesia

-Post partum period / pregnancy

-Left and right ventricular failure

-Atrial fibrillation

2. Blood wall abnormalities include

-Vasculitis e.g. in rheumatoid arthritis, SLE, mixed connective tissue disorder, progressive systemic sclerosis.

-Antiphospholipid antibody

-Endocarditis

3. Blood coagulation system alteration 

-Deficiency of antithrombin III, protein C and S e.g. ephritic syndrome

--Carcinoma

Use of estrogen, tamoxifen (used in ca breast) 

4. Other factors promoting DVT and PTE

-Leg trauma

-Hip fracture

-Smoking

-Obesity

-Malignancy

-Myeloproliferative disorders (causes hyper viscosity)

-Sickle cell anemia

-Venous catheter

 Pathogenesis

Venous stasis is the most important feature predisposing to venous thrombosis. The venous sinuses are esp. vulnerable to stasis and thrombosis and platelets become adherent in these sites. A thrombus develops and enlarges by successive deposition of aggregated plateletss, leukocytes and fibrin. Propagation of the thrombus may then proceed upstream or retrograde.

Thrombus in the pulmonary artery forms in two ways:

The thrombus that arises from a systemic vein and is swept into the venous circulation through the heart and into the pulmonary artery

The thrombus that occurs insitu in the pul. artery distal to an occluding embolus following stagnant blood flow in the vessel.

Venous thrombi, usually from DVT, pass into the pulmonary circulation and block blood flow to the lungs. Thrombi originating from large veins of lower legs such as popliteal, femoral and iliac are the causes in 95% of pulmonary embolism.

Proximal embolic (from iliac, femoral and pelvic veins are the most common forming over 50% cases of PE. Upper limb emboli are possible especially following trauma, surgery or cannulations.

The effects of a thrombus/ emboli in the pulmonary tree include:-

Pulmonary effect – Alteration in ventilation perfusion ratio which leads to increase in the physiological dead space with resultant lung collapse and hypoxemia. Lung collapse is also due to reduced surfactant.

Haemodynamic changes – Back pressure in the pulmonary artery leads to infarction of lung tissue from inadequate blood supply, reduced cardiac output and a decrease in venous return. The cardiopulmonary effects that occur are largely due to mechanical factors resulting into a reflex effects that causes bronchoconstriction, tachypnea and pulmonary HTN. Lung collapse eventually results from pulmonary oedema.

The sudden increase in pulmonary vascular resistance leads to pushing of the septum to the left side with resultant myocardial ischaemia, hypotension and circulatory collapse.


Paradoxical emboli: – Emboli which that is carried from the venous side of the circulation to the arterial side or vice versa. Also called crossed embolus and is usually through an AV communication e.g. patent foramen ovale, septal defects and AV shunts 

Clinical presentation

These depend on the number, size and distribution of emboli. The acute physiologic response of apt who suffers a PE is dependent on the pts age, baseline physiology, cormobid dzs cardiopulmonary health.           

Always consider the risk factors involved and if patient has unexplained dyspnea, pleuritic chest pain and haemoptysis.

In small – medium PE – the symptoms include sudden pleuritic chest pain, breathlessness, cough and haemoptysis.

In massive PE – this is rare but can cause sudden collapse and death. The patients mostly present with the following:-

 Symptoms

Sudden severe central chest pain usually 2o MI.

Acute breathlessness

Air hunger

Haemoptysis

Dizziness

Syncope

Altered mentation.


Signs

Pyrexia or sweating

Pale

Dyspnoea

Cyanosis

Tachycardia

Hypotension

↑JVP with a prominent “a” wave

Right ventricular heave with gallop rhythm and a split 2nd heart sound ( Accentuated P2.) 

In multiple recurrent PE, the patient presents with breathlessness for a prolonged period of time, syncope, fatigue on exertion and pulmonary HTN.

O /E - Gen. exams – dyspnoic, resp. distress, sweating, diaphoretic, anxious and pale.

Vital signs - ↓BP, ↑PR, ↑RR, low grade fever.

R /S – tachypnoic, cyanosed, stone dullness, ↓air entry, pleural rub with crackles.

CVS - ↑PR, ↑JVP, ↓BP, neck veins distension, left parasternal heave, S4 gallop rhythm, murmur.

NB: Classically PE presents 10/7 post OP.

P/A – Tender pulsatile hepatomegaly

MSS – Lower limb swelling with calf muscle tenderness.

Well’s diagnostic criteria for suspected PE (risk stratification criteria)

Description 

Score

Patient with S+S of DVT

Calf pain

Calf swelling

Alt. diagnosis is less likely than PE

Tachycardia with HR ↑ 100

History of immobilization or surgery in the past 1 month

History of previous DVT or PE

History of haemoptysis

History of malignancy whether past or present

A high score of ≥6 points →PE is likely.

A score of 2-6 → mod. Risk of PE.

A score <2 → low chance of PE

NB: In the history taking – always consider 

S+S

Aetilogical / risk factor

DDX – Diagnosing of PE is difficult due to signs and symptoms similar to a number of other of other cardiopulmonary disorders.

DDX

Pneumonia 

Ischaemic heart disease

Pneumothorax

Asthma

COPD

Pericarditis

Fractures especially ribs

Anxiety disorder

Investigations

Plain CXR – mostly normal or may have 

 Blunting of costophrenic angle.

Wedge shaped peripheral density (embolus) just above the diaphragm 

(Hampton’s lump)

Dilatation of right pulmonary artery along the mediastinum (Palla’s sign)

Diminished distal vascular markings or focal hypovascularity (Westermark’s sign)

ECG – Usually normal in small PE. The most common findings on the ECG include Sinus tachycardia. Other features are atrial fibrillation, tall T- wave, and right atrial enlargement with features consistent of pulmonary HTN. 

The classic pattern of a deep S wave in lead I and a deep Q wave and T wave inversion in leads III (“S1- Q3- T3”) change is rare.  

Echocardiography: In massive PE – Right ventricular hypokinesis (Mc’Connel’s sign).

Blood tests:

FBC- ↑PMN,↑ESR especially in ischaemia

U/E

Coagulation screen – R/O coagulopathies

Enzymes - ↑lactate dehydrogenase.

Plasma D – dimers – this is the most important blood test because up to 95% of patients have ↑D – dimer (>500 namograms) a negative D – dimer test excludes a PE but a positive test does not prove a diagnosis of PE and imaging is required

NB: If D – dimer is low, it rules out PE

Arterial BGA – hyperventilation, type 1 respiratory failure.

 CT pulmonary angiography – shows cut off of the vessels and a filling defect. It also shows dilated right pulmonary trunk and its branches.

MRI – gives same changes like in CT scan. The advantage is that unlike CT scan, there is no radiation with MRI.

V/Q scan – radionucliotide substance in inj. into the vessels → shows areas of defect and aid in diagnosis.

Doppler U/S of lower limbs to R/O DVT- may be necessary.


Management of PE

Current emphasis on the management of PE centers on

Identification of people at risk

Appropriate prophylaxis

Definitive diagnosis and treatment

 Level of Rx:

Acute management

Prevention of further thrombus formation

Dissolution of embolus

Surgery


Acute management of PE

Quick assessment of patient

ABC

Airway – pulse oximetry

Breathing – RR, use of accessory muscles; give O2 by mask or mechanical ventilation (high flow O2 at 60-100%)

Circulation – central canular, wide bore canula for IV access. Manage ↓BP (hypotension) with judicious use of fluids (colloid infusion)

If BP <90mmHg systolic, give inotropic agent e.g. epinephrine or dobutamine.

Organize for ICU management.

Morphine for allaying anxiety and pain. Give with an anti-emetic.


Prevention of further thrombus formation:-

Start on anti coagulants

Heparin LMWH is more preferred; it can be given S/C, is given BD and has less risk of bleeding CMX, no need to monitor.

Dose 1mg/kg SC twice a day; need for monitoring is necessary in 

Patients who are obese

Patients with renal insufficiency.

Pregnant women.

Fondaparinax – an anti FXa. This requires less monitoring than LMWH because its dose is fixed.


Always start LMWH together with warfarin (PO) 5mg OD and titrate. Warfarin takes 36-72 hours to be effective. Warfarin inhibits vit. K- dependent factors, protein C and S which are pro-thrombotic. Ensure you achieve INR at between 2-3 and check every 3 days, then every week for a month, then once per month.

 

NB: Stop heparin when IRN >2.0; usually between 3-5 days.


Fractionated heparin – given IV, is short acting, most available in the district hospital.

There is need to thrombolyze patient.

Safe even in patients with severe renal failure

Dose IV 80 IU/kg as bolus then 18 IU/kg in infusion

S/C dose 17,500 IU BD

Monitor APTT- aim to achieve twice the normal range (every 2-3 days).

NB: LMWH- Enoxaparin or fondaparinax

A pentasacccharide factor Xa inhibitor. Is a once daily dose, is given S/C

     CI – Renal failure, Pregnancy

S/E

Heparin

Bleeding 

Heparin included thrombocytopemia


Warfarin

Bleeding (educate patient on bleeding) from mucous membranes.

If patient bleeds – stop Rx. The patient should immediately come to hospital; where vitamin K inj. or FFP is given.

Duration of anticoagulant therapy

If there is a reversible risk factor, the duration of treatment is 3/12 (three months), then stop Rx.

For idiopathic risk factors – Give Rx for indefinite duration.

For recurrent DVT as in HIV etc., give Rx indefinitely (for life)


In massive pulmonary thromboembolism

Give a thrombolytic agent or tissue plasminogen activators (tPA) agents. Streptokinase 250,000 units over 30 minutes, then decrease dose to 100,000 units after every hour for 12-72 hours.

tPA is given at 100mg IVI over 20 minutes.


NB: Thrombolytic agents lyse or dissolve the clot unlikely anticoagulants (heparin and warfarin) which stabilizes the clot

If the thrombolytic agents fail, then removal of the clot (embolectomy) or through use of catheters or surgery may be useful for those with bleeding disorders:-

Inferior vena cava filter can be used. 

Indications:-

Patient who is bleeding or has a bleeding tendency.

Patients with CI to anticoagulants.

Patients with recurrent PE.

The problem with filters is that small clots can pass and cause embolism.


Prevention of PE

Stop smoking

Exercise and early mobilization after surgery.

Elevation of lower extremities for gravity drainage of venous return.

Advice on weight reduction

Encourage use of graded compression stockings.

Sequential compression of legs by pneumatic boots.

Use of prophylactic anticoagulants incase of major surgery, major trauma and all immobile patients.

Stop hormonal replacement therapy (HRT) and the pill pre- OP. (2-4 weeks before surgery)


Complications of PE

Pulmonary infarction

Pulmonary h’ge

Pulmonary HTN

Pulmonary arteriosclerosis

Acute cor-pulmonale

Results in sudden death. 

Content created and supplied by: Pauline123 (via Opera News )

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