rehabilitation of patient with pleural effusion
TRANSCRIPT
PHYSIOTHERAPY MANAGEMENT OF PATIENT WITH PLEURAL EFFUSION
SECONDARY TO PULMONARY EMBOLISM
Adeyemo Ademola BMR(PT) M.Sc PT
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
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.
PULMONARY EMBOLISM
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
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
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
Predisposing Factors
PRIMARY RISK FACTORS MINOR RISK FACTORS
Surgery Obesity
Major trauma Bed rest
Cancer Estrogens therapy
Congestive heart failure
Myocardial infarction
Immobilization
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
Abnormalities on Chest Radiography
Normal
Atelectasis or parenchyma density
Pleural Effusion
Pleural based opacity
Elevated diaphragm
Prominent central pulmonary artery
Cardiomegally
Pulmonary edema
Figure 1 Figure 2
Atelectasis
Atelectasis and parenchyma densities are quite common. Most of these densities are caused by pulmonary haemorrhage and edema
Pleural Effusion
Pleural effusions are common and most often unilateral
occupying less than 15% of a hemithorax
Elevated diaphragm
A diaphragm may be elevated, reflecting
volume loss in the affected lung.
Cardiomegaly
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.
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.
Only low-molecular-weight heparin, intermittent pneumatic compression
devices and graded compression stockings have been shown to reduce
the incidence of pulmonary embolism.
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.
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
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.
TYPES OF FLUID
Serous fluid (hydrothorax)
Blood (heamothorax)
Chyle (chylothorax)
Pus (pyothorax or empyema)
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
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
Meniscus sign
A LARGE LEFT PLEURAL EFFUSION
A MASSIVE LEFT SIDED EFFUSION IN A PATIENT PRESENTING WITH LUNG CANCER
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
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.
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
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
Case study cont’d
CVS
-B.P – 124/76 mmHg
-pulse – 101/min
Abdomen
-obese
-moves with respiration
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
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
Case study cont’d
Plan of management
To improve cardiopulmonary function
To prevent further cardiopulmonary complications
Improve fatigability and cardiopulmonary endurance
Case study cont’d
Means
-Incentive spirometry
-Chest physiotherapy
-Brisk walking
-Marching on the spot
-Treadmill
-Bicycle ergometry
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
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)
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
Physiotherapy management
Brisk walking
Marching on the spot
Treadmill
Bicycle ergometry
Reduces fatigability and improves cardiopulmonary endurance
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
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
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
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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