Rehabilitation of patient with pleural effusion

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PHYSIOTHERAPY MANAGEMENT OF PATIENT WITH PLEURAL EFFUSION SECONDARY TO PULMONARY EMBOLISM Adeyemo Ademola BMR(PT) M.Sc PT

Transcript of Rehabilitation of patient with pleural effusion

Page 1: Rehabilitation of patient with pleural effusion

PHYSIOTHERAPY MANAGEMENT OF PATIENT WITH PLEURAL EFFUSION

SECONDARY TO PULMONARY EMBOLISM

Adeyemo Ademola BMR(PT) M.Sc PT

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BACKGROUND

Pulmonary embolism(PE) is the third greatest causeof mortality from cardiovascular disease, aftermyocardial infarction and cerebrovascular stroke.

At least 600,000 persons have been estimated tohave a pulmonary embolic event each year in theUSA.

Because pleural effusions occur in about 30% ofpatients with pulmonary emboli, 180,000 cases ofpleural effusion from pulmonary emboli shouldoccur annually

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PULMONARY EMBOLISM(PE)

Pulmonary embolism is a clinically significant obstruction of part or all of the pulmonary vascular tree usually caused by thrombus from distant site.

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PULMONARY EMBOLISM

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PATHOPHYSIOLOGY OF PE

-The majority of clinically significant pulmonary embolibegin in the pelvic or lower extremity veins.

Initiated by

• Platelet aggregation around venous valvesinuses.

• Activation of the clotting cascade• Virchow's triad

venous stasis,injury to the vessel wall,and increased blood coaguability

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DIAGNOSIS OF PULMONARY EMBOLISM(PE)

Clinical picture. Signs and symptoms Risk or predisposing factors for DVT Ventilation-perfusion mismatch Diagnostic Tests for PE.

-A chest radiograph -ECG-Ventilation-perfusion scanning (V/Q scanning). -Angiography-Spiral CT-D-dimer

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Signs and Symptoms of PE

Dyspnoea

Pleuritic Pain

Cough

Leg Swelling

Leg Pain

Haemoptysis

Palpitations

Wheezing

Angina-Like pain

N.B. The signs and symptoms serve only to raise thesuspicion of pulmonary embolus

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Predisposing Factors

PRIMARY RISK FACTORS MINOR RISK FACTORS

Surgery Obesity

Major trauma Bed rest

Cancer Estrogens therapy

Congestive heart failure

Myocardial infarction

Immobilization

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Ventilation-perfusion Mismatch

By calculating A-a O2 gradient = PaO2 (alveolar) -PaO2 (arterial)

Normal A-a O2 gradient is 5-20 and increases with age.

-Elevated in 80% to 90% in PE

-Normal in 10% to 20% in PE

PAO2 (alveolar) = 150 - 1.2(PaCO2), assuming patient breathing room air

150 - 1.2 (40) = 102 150 –1.2 (35) = 108

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Abnormalities on Chest Radiography

Normal

Atelectasis or parenchyma density

Pleural Effusion

Pleural based opacity

Elevated diaphragm

Prominent central pulmonary artery

Cardiomegally

Pulmonary edema

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Figure 1 Figure 2

Atelectasis

Atelectasis and parenchyma densities are quite common. Most of these densities are caused by pulmonary haemorrhage and edema

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Pleural Effusion

Pleural effusions are common and most often unilateral

occupying less than 15% of a hemithorax

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Elevated diaphragm

A diaphragm may be elevated, reflecting

volume loss in the affected lung.

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Cardiomegaly

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Treatment of Pulmonary Embolism

Manage as for Respiratory Distress

- O2 monitoring,

- Fluid resuscitation for secondary right-sided heart failure,

- Inotropic Drugs.

Anticoagulant :Oral anticoagulant and LMWH.

Thrombolysis.

Caval Interruption.

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PREVENTION OF PE

Postoperative DVT Prophylaxis

If not given prophylaxis, 15% to 30% of patients with abdominal surgery will develop a DVT.

DVT prophylaxis after surgery is cost effective and reduces the incidence of DVT and PE.

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Only low-molecular-weight heparin, intermittent pneumatic compression

devices and graded compression stockings have been shown to reduce

the incidence of pulmonary embolism.

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Pleural Effusionis the accumulation of abnormal volumes (>10-20ml) of fluid in the pleural space; the fluid-filled space that surrounds the lungs. Excess amounts of such fluid can

impair breathing by limiting the expansion of the lungs during respiration.

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PLEURAL EFFUSION DUE TO PULMONARYEMBOLISM

Pathophysiology

-The mechanism is usually increased interstitialfluid in the lungs as a result of ischemia or therelease of vasoactive cytokines or inflammatorymediators (e.g vascular endothelial growth factor) The excessive interstitial lung fluid traverses the visceral pleural

and accumulates into the pleural space

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PLEURAL EFFUSION DUE TO PULMONARY EMBOLISM

ON CHEST IMAGING Pleural effusions occur in 20–50% of patients with

pulmonary embolism Worsley and associates reviewed thechest radiographs of 383 patients in the ProspectiveInvestigation of Pulmonary Embolism Diagnosis (PIOPED I)study with angiographically proven pulmonary emboli andreported that 36% had a pleural effusion.

Two large multicenter studies comprising 2319 and 4033patients with pulmonary embolism reported that theincidence of pleural effusion was 23 and 21%, respectively,when assessed by chest radiograph.

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TYPES OF FLUID

Serous fluid (hydrothorax)

Blood (heamothorax)

Chyle (chylothorax)

Pus (pyothorax or empyema)

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PLEURAL EFFUSION cont’d

OTHER CAUSES Congestive heart failure

Pneumonia

Pulmonary embolism

Malignancy

A pleural effusion is not normal. It is not a disease but rathera complication of an underlying pathology

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PLEURAL EFFUSION cont’d

DIAGNOSIS Medical history

Physical exam

Chest x-ray

CLINICAL SIGNS Decreased chest movement

Stone dullness to percussion

Diminished breath sounds

Decreased focal resonance and fremitus

Pleural friction rub

Bronchial breathing and egophony

Trachea deviation

Meniscus sign

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Meniscus sign

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A LARGE LEFT PLEURAL EFFUSION

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A MASSIVE LEFT SIDED EFFUSION IN A PATIENT PRESENTING WITH LUNG CANCER

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PLEURAL EFFUSION cont’d

MEDICAL MANAGEMENT

ABCs of resuscitation

0xygen monitoring

Oxygen supplement

Treatment of underlying illness

Thoracentesis

Tube thoracostomy

COMPLICATION

Permanent decrease in lung function

Lung scarring

Empyema

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Case study

14/7/11

Pc-Cough × 5/7 -left sided pain chest pain × 2/7-Breathlessness × 1/7

PcHxA 39yrs old man who has been on admission 13/7 on account ofcough × 5/7 , chest pain(left sided) × 2/7 and breathlessness ×1/7 prior to admission. The cough reportedly contained bloodstained sputum and he was taken to a private hospital inOshogbo, Osun state from where he was referred to UCH. Patienthad since been managed as a case of left pulmonary infarctionwith pleural effusion secondary to pulmonary embolism.

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Case study cont’d

PmHx

- A known diabetes patient × 5years

- Known hypertensive (onset unknown)

FsHx

A trader who resides in osun state married in a mongamoussetting with six children. He does not smoke and reportedly quitalcohol 1 year ago.

o/e

A middle aged man met in long sitting bed propped to about90⁰, conscious, afebrile, acyanotic ,in obvious respiratorydistress and receiving oxygen supplement via intranasal catheter

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Case study cont’d

Examinations

CNS

patient is conscious, alert and well oriented in TPP

Chest

Vesicular breath sounds

Reduced air entry in both lungs zones more pronounced in the left middle field

RR-20cpm

CTTD tube insitu draining serous fluid

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Case study cont’d

CVS

-B.P – 124/76 mmHg

-pulse – 101/min

Abdomen

-obese

-moves with respiration

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MSS- Gross muscle power is 4₊ in the upper limbs-Gross muscle power is 4₊ in the lower limbs-No bilateral pedal oedema-Swelling is observed in Rt calf muscles(not tender and

not pitting)-ROM is full in all joints and pain free in every

physiological movements Functional Assessment

-Talk test for dyspnoea :“PATIENT CAN ONLY RECITE UPTO 2ND LINE OF THE

PLEGDE-Patient is non ambulant

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Case study cont’d

InvestigationsX-RAY – Homogeneous opacity involving both lower and middlelung zones but more marked on the right with the trachea shiftto the rightECG – Sinus tachycardiaChest CT – Left pleural effusion and collapsed left lung withmediastinal shift to the rightDoppler – show no DVT in the Rt LL but plan for repeat

Analysis of findings↓ air entry in both lungs fieldLt pulmonary infarction and pleural effusionLt lung collapsed

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Case study cont’d

Plan of management

To improve cardiopulmonary function

To prevent further cardiopulmonary complications

Improve fatigability and cardiopulmonary endurance

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Case study cont’d

Means

-Incentive spirometry

-Chest physiotherapy

-Brisk walking

-Marching on the spot

-Treadmill

-Bicycle ergometry

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Physiotherapy management

Incentive spirometry

-Improves lung function

-Minimise fluid build-up in the lungs

-Improve air flow

Chest physiotherapy percussion

vibration

segmental deep breathing exercise

forced expiratory exercise

coughing techniques

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Physiotherapy management

Mechanism of CTTD drainage

Gravity as long as the chest drainage system is placed below the level

of the patient’s chest

Expiratory positive pressure from the patient push air and fluid out of the chest (e.g. incentive spirometer,

cough, Valsalva maneuver)

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Physiotherapy management

Care of CTTD

Ensure dependent drainage

Avoid kinks or obstruction

Avoid tube distraction or dislodgement

Observe volume and character of drainage during physiotherapy

Ambulation is advised when feasible

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Physiotherapy management

Brisk walking

Marching on the spot

Treadmill

Bicycle ergometry

Reduces fatigability and improves cardiopulmonary endurance

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PHYSIOTHERAPY INTERVENTION

It helps drain the excess fluid in the pleural space

Improves the lung function

Alleviate the breathlessness

Patient is ambulant with improve cardiopulmonary endurance and reduce fatigability

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Progression of management

TALK TEST is a method used for measuring exercise intensity. By judging your ability to talk during your work out at a low moderate pace(around a level 4-5 on the perceived exertion scale) if you are breathless, you are working out at a harder pace(around level 8-9)

AFTER 2WKS Patient was able to completely recite “the plegde” while

exercising at a low moderate pace AFTER 3WKSSerous fluid draining reduced in amountThe homogeneous opacity on x-ray also diminishing AFTER 4WKSPatient was able to workout at harder pace with less fatigue and

easily tiring out

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CONCLUSION

Pleural effusions secondary to pulmonary embolism are mostly small and unilateral, but may become loculated if diagnosis is delayed.

Physiotherapy management and intervention is key to restoring patient back to fitness and functional independence

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REFERENCES

Romero-Candeira S, Herna´ndez-Blasco L, Soler MJ, et al. Biochemical and cytologic characteristics of pleural effusion secondary to pulmonary embolism lism. Chest 2002; 121:465–469.

Porcel JM. The use of probrain natriuretic peptide in pleural fluid for the diagnosis of pleural effusions resulting from heartfailure.CurrOpinPulmMed 2005; 11:329–333.

LightRW.Pleuraldiseases.5thed.Philadelphia:LippincottWilliams&Wilkins;2007.

Jerjes-Sa´nchez C, Ramirez-Rivera A, Ibarra-Pe´rez C. TheDresslersyndrome after pulmonary embolism. Am J Cardiol 1996; 78:343–345.

Remy-JardinM, Pistolesi M, Goodman LR, et al. Management of suspectedacutepulmonaryembolismin the era of CT angiography: astatement fromthe 642.Fleischner Society. Radiology 2007; 245:315–329.

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