Clinical analysis of patient with Chronic Cor Pulmonale. Clinical analysis of patient with Pleuritis.
CHRONIC COR PULMONALE
Picture 10. Patients with Cor Pulmonale
Background: Cor pulmonale is defined as an alteration in the structure and function of the right ventricle caused by a primary disorder of the respiratory system. Pulmonary hypertension is the common link between lung dysfunction and the heart in cor pulmonale. Right-sided ventricular disease caused by a primary abnormality of the left side of the heart or congenital heart disease is not considered cor pulmonale, but cor pulmonale can develop secondary to a wide variety of cardiopulmonary disease processes. Although cor pulmonale commonly has a chronic and slowly progressive course, acute onset or worsening cor pulmonale with life-threatening complications can occur.
Pathophysiology: Several different pathophysiologic mechanisms can lead to pulmonary hypertension and, subsequently, to cor pulmonale. These pathogenetic mechanisms include (1) pulmonary vasoconstriction due to alveolar hypoxia or blood acidemia; (2) anatomic compromise of the pulmonary vascular bed secondary to lung disorders, eg, emphysema, pulmonary thromboembolism, interstitial lung disease; (3) increased blood viscosity secondary to blood disorders, eg, polycythemia vera, sickle cell disease, macroglobulinemia; and (4) idiopathic primary pulmonary hypertension. The result is increased pulmonary arterial pressure.
The right ventricle (RV) is a thin-walled chamber that is more a volume pump than a pressure pump. It adapts better to changing preloads than afterloads. With an increase in afterload, the RV increases systolic pressure to keep the gradient. At a point, further increase in the degree of pulmonary arterial pressure brings significant RV dilation, an increase in RV end-diastolic pressure, and circulatory collapse. A decrease in RV output with a decrease in diastolic left ventricle (
Right ventricular overload is associated with septal displacement toward the left ventricle. Septal displacement, which is seen in echocardiography, can be another factor that decreases
Cor pulmonale usually presents chronically, but 2 main conditions can cause acute cor pulmonale: massive pulmonary embolism (more common) and acute respiratory distress syndrome (ARDS). The underlying pathophysiology in massive pulmonary embolism causing cor pulmonale is the sudden increase in pulmonary resistance. In ARDS, 2 factors cause RV overload: the pathologic features of the syndrome itself and mechanical ventilation. Mechanical ventilation, especially higher tidal volume, requires a higher transpulmonary pressure. In chronic cor pulmonale, right ventricular hypertrophy (RVH) generally predominates. In acute cor pulmonale, right ventricular dilatation mainly occurs (picture 11).
History: Clinical manifestations of cor pulmonale generally are nonspecific. The symptoms may be subtle, especially in early stages of the disease, and mistakenly may be attributed to the underlying pulmonary pathology.
- The patient may complain of fatigue, tachypnea, exertional dyspnea, and cough.
- Anginal chest pain also can occur and may be due to right ventricular ischemia (it usually does not respond to nitrates) or pulmonary artery stretching.
- Hemoptysis may occur because of rupture of a dilated or atherosclerotic pulmonary artery. Other conditions, such as tumors, bronchiectasis, and pulmonary infarction, should be excluded before attributing hemoptysis to pulmonary hypertension. Rarely, the patient may complain of hoarseness due to compression of the left recurrent laryngeal nerve by a dilated pulmonary artery.
- Variety of neurologic symptoms may be seen due to decreased cardiac output and hypoxemia.
- In advanced stages, passive hepatic congestion secondary to severe right ventricular failure may lead to anorexia, right upper quadrant abdominal discomfort, and jaundice.
- Syncope with exertion, which may be seen in severe disease, reflects a relative inability to increase cardiac output during exercise with a subsequent drop in the systemic arterial pressure.
- Elevated pulmonary artery pressure can lead to elevated right atrial pressure, peripheral venous pressure, and then capillary pressure and by increasing the hydrostatic gradient, it leads to transudation of fluid, which appears as peripheral edema. Although this is the simplest explanation for peripheral edema in cor pulmonale, other hypotheses explain this symptom, especially in a fraction of patients with COPD who do not show increase in right atrial pressure. A decrease in glomerular filtration rate (GFR) and filtration of sodium and stimulation of arginine vasopressin (which decreases free water excretion) due to hypoxemia play important pathophysiologic roles in this setting and may even have a role for peripheral edema in patients with cor pulmonale who have elevated right atrial pressure.
Physical: Physical findings may reflect the underlying lung disease or pulmonary hypertension, RVH, and RV failure.
- On inspection, an increase in chest diameter, labored respiratory efforts with retractions of chest wall, distended neck veins with prominent a or v waves, and cyanosis may be seen.
- On auscultation of the lungs, wheezes and crackles may be heard as signs of underlying lung disease. Turbulent flow through recanalized vessels in chronic thromboembolic pulmonary hypertension may be heard as systolic bruits in the lungs. Splitting of the second heart sound with accentuation of the pulmonic component can be heard in early stages. A systolic ejection murmur with sharp ejection click over the region of the pulmonary artery may be heard in advanced disease, along with a diastolic pulmonary regurgitation murmur.
- RVH is characterized by a left parasternal or subxiphoid heave. Hepatojugular reflex and pulsatile liver are signs of RV failure with systemic venous congestion.
- On percussion, hyperresonance of the lungs may be a sign of underlying COPD; ascites can be seen in severe disease.
Causes:
- Disorders with primary involvement of pulmonary vasculature and circulation
- Repeated pulmonary emboli
- Pulmonary vasculitis
- Pulmonary veno-occlusive disease
- Congenital heart disease with left-to-right shunting
- Sickle cell disease
- High altitude disease with pulmonary vasoconstriction
- Primary pulmonary hypertension
- Disorders with secondary involvement of pulmonary vasculature and circulation
- Parenchymal lung diseases (interstitial lung diseases, chronic obstructive lung diseases)
- Neuromuscular disorders (eg, myasthenia gravis, poliomyelitis, amyotrophic lateral sclerosis)
- Obstructive and central sleep apnea
- Thoracic deformities (eg, kyphoscoliosis)
Other Problems to be Considered:
Congestive (biventricular) heart failure
Primary pulmonic stenosis
Primary pulmonary hypertension
Right-sided heart failure due to congenital heart diseases
Right heart failure due to right ventricular infarction
- A general approach to diagnose cor pulmonale and to investigate its etiology starts with routine laboratory tests, chest radiography, and electrocardiography. Echocardiography gives valuable information about the disease and its etiology. Pulmonary function tests may become necessary to confirm the underlying lung disease. Ventilation/perfusion (V/Q) scan or chest CT scan may be performed if history and physical examination suggest pulmonary thromboembolism as the cause or if other diagnostic tests do not suggest other etiologies. Right heart catheterization is the most accurate but invasive test to confirm the diagnosis of cor pulmonale and gives important information regarding the underlying diseases. Any abnormal result in each of these tests may need further diagnostic evaluation in that specific direction.
- Laboratory investigations are directed toward defining the potential underlying etiologies as well as evaluating complications of cor pulmonale. In specific instances, appropriate lab studies may include the following: hematocrit for polycythemia (which can be a consequence of underlying lung disease but can also increase pulmonary arterial pressure by increasing viscosity), serum alpha1-antitrypsin if deficiency is suspected, and antinuclear antibody level for collagen vascular disease such as scleroderma. Hypercoagulability states can be evaluated by serum levels of proteins S and C, antithrombin III, factor V Leyden, anticardiolipin antibodies, and homocysteine.
- Arterial blood gas tests may provide important information about the level of oxygenation and type of acid-base disorder.
- Elevated braiatriuretic peptide (BNP) level alone is not adequate to establish presence of cor pulmonale, but it helps to diagnose cor pulmonale in conjunction with other noninvasive tests and in appropriate clinical settings. An elevated BNP level may actually be a natural mechanism to compensate for elevated pulmonary hypertension and right heart failure by promoting diuresis and natriuresis, vasodilating systemic and pulmonary vessels, and reducing circulating levels of endothelin and aldosterone.
Imaging Studies:
- Imaging studies may show evidence of underlying cardiopulmonary diseases, pulmonary hypertension, or its consequence, right ventricular enlargement.
- Chest roentgenography: In patients with chronic cor pulmonale, the chest radiograph may show enlargement of the central pulmonary arteries with oligemic peripheral lung fields. Pulmonary hypertension should be suspected when the right descending pulmonary artery is larger than 16 mm in diameter and the left pulmonary artery is larger than 18 mm in diameter. Right ventricular enlargement leads to an increase of the transverse diameter of the heart shadow to the right on the posteroanterior view and filling of the retrosternal air space on the lateral view. These findings have reduced sensitivity in the presence of kyphoscoliosis or hyperinflated lungs.
- Echocardiography (picture 12): Two-dimensional echocardiography usually demonstrates signs of chronic right ventricular pressure overload. As this overload progresses, increased thickness of the right ventricular wall with paradoxical motion of the interventricular septum during systole occurs. At an advanced stage, right ventricular dilatation occurs and the septum shows abnormal diastolic flattening. In extreme cases, the septum may actually bulge into the left ventricular cavity during diastole resulting in decreased diastolic volume of
LV and reduction ofLV
Doppler echocardiography is used now to estimate pulmonary arterial pressure, taking advantage of the functional tricuspid insufficiency that is usually present in pulmonary hypertension. Doppler echocardiography is considered the most reliable noninvasive technique to estimate pulmonary artery pressure. The efficacy of Doppler echocardiography may be limited by the ability to identify an adequate tricuspid regurgitant jet, which may be further enhanced by using saline contrast.
- thromboembolism as the underlying etiology of cor pulmonale. These tests may be performed early in the diagnostic workup if any evidence of pulmonary embolism appears in history and physical examination. The test may also be considered later in the workup if other tests are not suggestive of any other etiology. Pulmonary thromboembolism has a wide range of clinical presentations from massive embolism with acute and severe hemodynamic instability to multiple chronic peripheral embolisms that may present with cor pulmonale.
- Ultrafast,
ECG-gated CT
- Magnetic resonance imaging (MRI) of the heart is another modality that can provide valuable information about RV mass.
- Radionuclide ventriculography can determine RVEF noninvasively.
Other Tests:
- Electrocardiography (ECG): ECG abnormalities in cor pulmonale reflect the presence of RVH, RV strain, or underlying pulmonary disease. These electrocardiographic changes may include right axis deviation, R/S amplitude ratio in V1 greater than 1 (increase in anteriorly directed forces may be a sign of posterior infarct), R/S amplitude ratio in V6 less than 1, P-pulmonale pattern (an increase in P wave amplitude in leads 2, 3, and aVF), S1Q3T3 pattern and incomplete (or complete) right bundle branch block, especially if pulmonary embolism is the underlying etiology, low-voltage QRS because of underlying COPD with hyperinflation and increased AP diameter of the chest. Severe RVH may reflect as Q waves in the precordial leads that may be interpreted as anterior myocardial infarction by mistake (on the other hand, since electrical activity of the RV is significantly less than the LV, small changes in RV forces may be lost in ECG). See picture 13.
Picture 13. ECG of patient with Cor Pulmonale.
Criteria of Cor Pumonale
I. QRS morphology
- Limb leads
1. Right axis deviation
2. S > R in lead I
- Precordial leads
1. S > R in V5 – V6
2. S > R in V2
3. Lead V1 rs, Rs, or rS
- Orthogonal leads
1. S > R in lead X
2. Tall R wave in lead II
II. T wave variable
III. P wave
- Limb leads
1. Vertical axis
2. P > 3 mm in lead II or III
- Precordial leads
1. Negative P in lead V1
- In selected cases, pulmonary function testing may be indicated to determine underlying obstructive or interstitial lung disease.
Procedures:
- .
Cardiopulmonary support for patients experiencing acute cor pulmonale with resultant acute RV failure includes fluid loading and vasoconstrictor (eg, epinephrin) administration to maintain adequate blood pressure
Oxygen therapy, diuretics, vasodilators, digitalis, theophylline, and anticoagulation therapy are all different modalities used in the long-term management of chronic cor pulmonale.
Although it is not clear whether oxygen therapy has a mortality rate benefit in patients with cor pulmonale due to pulmonary disorders other than COPD, it may provide some degree of symptomatic relief and improvement in functional status. Therefore, oxygen therapy plays an important role in both the immediate setting and long-term management, especially in patients who are hypoxic and have COPD.
- Diuretics are used in the management of chronic cor pulmonale, particularly when the right ventricular filling volume is markedly elevated and in the management of associated peripheral edema.
- Vasodilator drugs have been advocated in the long-term management of chronic cor pulmonale with modest results. Calcium channel blockers, particularly oral sustained-release nifedipine and diltiazem, can lower pulmonary pressures, although they appear more effective in primary rather than secondary pulmonary hypertension.
- Beta-selective agonists epoprostenol, treprostinil, bosentan, and iloprost for treatment of primary pulmonary hypertension. Epoprostenol, treprostinil, and iloprost are prostacyclin PGI2 analogues and have potent vasodilatory properties.
- The use of cardiac glycosides, such as digitalis, in patients with cor pulmonale has been controversial, and the beneficial effect of these drugs is not as obvious as in the setting of left heart failure.
- In addition to bronchodilatory effect, theophylline has been reported to reduce pulmonary vascular resistance and pulmonary arterial pressures acutely in patients with chronic cor pulmonale secondary to COPD
- Anticoagulation with warfarin is recommended in patients at high risk for thromboembolism.
- Surgical Care:
- Phlebotomy is indicated in patients with chronic cor pulmonale and chronic hypoxia causing severe polycythemia, defined as hematocrit of 65 or more. Phlebotomy results in a decrease in mean pulmonary artery pressure, a decrease in mean pulmonary vascular resistance, and an improvement in exercise performance in such patients. There is, however, no evidence of improvement in survival. Generally, phlebotomy should be reserved as an adjunctive therapy for patients with acute decompensation of cor pulmonale and patients who remain significantly polycythemic despite appropriate long-term oxygen therapy. Replacement of the acute volume loss with a saline infusion may be necessary to avoid important decreases in systemic blood pressure.
|
Drug Name |
Furosemide (Lasix) — Example of diuretic agents used in the management of chronic cor pulmonale. Furosemide is a powerful loop diuretic that works on thick ascending limb of Henle loop, causing a reversible block in reabsorption of sodium, potassium, and chloride. |
|
Adult Dose |
20-80 mg/d PO/IV/IM; may titrate to maximum dose of 600 mg/d |
|
Pediatric Dose |
1-2 mg/kg/dose |
|
Contraindications |
Documented hypersensitivity; hepatic coma; anuria; concurrent severe electrolyte depletion |
|
Interactions |
Metformin decreases furosemide concentrations; furosemide interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle-relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides and furosemide; hearing loss of varying degrees may occur; anticoagulant activity of warfarin may be enhanced when taken concurrently with this medication; increased plasma lithium levels and toxicity are possible when taken concurrently with this medication |
|
Pregnancy |
C – Safety for use during pregnancy has not been established. |
|
Precautions |
Perform frequent serum electrolyte, carbon dioxide, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter |
Drug Category: Calcium channel blockers — These agents inhibit movement of calcium ions across the cell membrane, depressing both impulse formation (automaticity) and conduction velocity.
|
Drug Name |
Nifedipine (Procardia) — Especially in the sustained-release form, nifedipine is a calcium channel blocker that has proven to be fairly effective in the management of chronic cor pulmonale caused by primary pulmonary hypertension. Modifies the entry of calcium into the cells by blocking the slow or voltage-dependent calcium channels, resulting in vasodilation, which improves myocardial oxygen delivery. Sublingual administration generally is safe, despite theoretical concerns. |
|
Adult Dose |
10-30 mg SR cap PO tid; not to exceed 120-180 mg/d |
|
Pediatric Dose |
Not recommended |
|
Contraindications |
Documented hypersensitivity |
|
Interactions |
Monitor oral anticoagulants when used concomitantly; coadministration with any agent that can lower BP, including beta-blockers and opioids, can result in severe hypotension; H2 blockers (cimetidine) may increase toxicity |
|
Pregnancy |
C – Safety for use during pregnancy has not been established. |
|
Precautions |
Aortic stenosis; angina; congestive heart failure; pregnancy; nursing mothers; may cause lower extremity edema; allergic hepatitis has occurred but is rare |
Drug Category: Cardiac glycosides — These agents decrease AV nodal conduction primarily by increasing vagal tone.
|
Drug Name |
Digoxin (Lanoxin) — Has a positive inotropic effect on failing myocardium. Effect is achieved via inhibition of the Na+/K+-ATPase pump, leading to increase in intracellular sodium concentration along with concomitant increase in intracellular calcium concentration by means of calcium-sodium exchange mechanism. Net result is augmentation of myocardial contractility. |
|
Adult Dose |
0.125-0.375 mg |
|
Pediatric Dose |
8-10 mcg/kg/d PO/IV/IM; maximum dose 100-150 mcg/kg/d |
|
Contraindications |
Documented hypersensitivity; beriberi heart disease; idiopathic hypertrophic subaortic stenosis; constrictive pericarditis; carotid sinus syndrome |
|
Interactions |
Medications that may increase digoxin levels include alprazolam, benzodiazepines, bepridil, captopril, cyclosporine, propafenone, propantheline, quinidine, diltiazem, aminoglycosides, oral amiodarone, anticholinergics, diphenoxylate, erythromycin, felodipine, flecainide, hydroxychloroquine, itraconazole, nifedipine, omeprazole, quinine, ibuprofen, indomethacin, esmolol, tetracycline, tolbutamide, and verapamil; medications that may decrease serum digoxin levels include aminoglutethimide, antihistamines, cholestyramine, neomycin, penicillamine, aminoglycosides, oral colestipol, hydantoins, hypoglycemic agents, antineoplastic treatment combinations (eg, carmustine, bleomycin, methotrexate, cytarabine, doxorubicin, cyclophosphamide, vincristine, procarbazine), aluminum or magnesium antacids, rifampin, sucralfate, sulfasalazine, barbiturates, kaolin/pectin, and aminosalicylic acid |
|
Pregnancy |
C – Safety for use during pregnancy has not been established. |
|
Precautions |
Hypokalemia may reduce positive inotropic effect of digitalis; IV calcium may produce arrhythmias in digitalized patients; hypercalcemia predisposes patient to digitalis toxicity; hypocalcemia can make digoxin ineffective until serum calcium levels are normal; magnesium replacement therapy must be instituted in patients with hypomagnesemia to prevent digitalis toxicity; patients diagnosed with incomplete AV block may progress to complete block when treated with digoxin; exercise caution in hypothyroidism, hypoxia, and acute myocarditis |
Drug Category: Anticoagulants — These agents may reduce incidence of embolisms when used fast, effectively, and early.
|
Drug Name |
Warfarin (Coumadin) — Most commonly used oral anticoagulant. Interferes with hepatic synthesis of vitamin K-dependent coagulation factors. Used for prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders. |
|
Adult Dose |
2-10 mg/d PO/IV qd; adjust dose to an INR of 1.5:2 or higher depending on the condition requiring anticoagulation |
|
|
|
|
|
|
|
Interactions |
Griseofulvin, carbamazepine, glutethimide, estrogens, nafcillin, phenytoin, rifampin, barbiturates, cholestyramine, colestipol, vitamin K, spironolactone, oral contraceptives, and sucralfate may decrease anticoagulant effects; oral antibiotics, phenylbutazone, salicylates, sulfonamides, chloral hydrate, clofibrate, diazoxide, anabolic steroids, ketoconazole, ethacrynic acid, miconazole, nalidixic acid, sulfonylureas, allopurinol, chloramphenicol, cimetidine, disulfiram, metronidazole, phenylbutazone, phenytoin, propoxyphene, sulfonamides, gemfibrozil, acetaminophen, and sulindac may increase anticoagulant effects |
|
Pregnancy |
D – Unsafe in pregnancy |
|
Precautions |
Dose needs to be adjusted to INR; caution in bleeding tendency and hazardous active hemorrhagic conditions, malignant hypertension, patients at high risk of recurrent trauma, (eg, people with alcoholism or psychosis, unsupervised patients who are senile); warfarin anaphylaxis, hepatic, renal, thyroid, allergic, and hematologic hypocoagulable conditions and disorders; do not switch brands after achieving therapeutic response; caution in active tuberculosis or diabetes; patients with protein C or S deficiency are at risk of developing skiecrosis |
Drug Category: Methylxanthines — Potentiate exogenous catecholamines and stimulate endogenous catecholamine release and diaphragmatic muscular relaxation, which, in turn, stimulates bronchodilation.
|
Drug Name |
Theophylline (Aminophyllin, Theo-24, Theolair, Theo-Dur) — Mechanism of action is not well defined yet. Was formerly thought that this drug increases intracellular cyclic AMP by causing inhibition of phosphodiesterase; however, current data do not support that. |
|
Adult Dose |
Loading dose: 5.6 mg/kg IV over 20 min (based on aminophylline) |
|
Pediatric Dose |
6 weeks to 6 months: 0.5 mg/kg/h loading dose IV in first 12 h (based on aminophylline), followed by maintenance infusion of 12 mg/kg/d thereafter; may administer continuous infusion by dividing total daily dose by 24 h |
|
Contraindications |
Documented hypersensitivity; uncontrolled arrhythmias; peptic ulcers; hyperthyroidism; uncontrolled seizure disorders |
|
Interactions |
Effects may decrease with aminoglutethimide, barbiturates, carbamazepine, ketoconazole, loop diuretics, charcoal, hydantoins, phenobarbital, phenytoin, rifampin, isoniazid, and sympathomimetics; effects may increase with allopurinol, beta-blockers, ciprofloxacin, corticosteroids, disulfiram, quinolones, thyroid hormones, ephedrine, carbamazepine, cimetidine, erythromycin, macrolides, propranolol, and interferon |
|
Pregnancy |
C – Safety for use during pregnancy has not been established. |
|
Precautions |
Has low serum therapeutic-to-toxicity ratio, and, therefore, serum level monitoring is important; peptic ulcer; hypertension; tachyarrhythmias; hyperthyroidism; compromised cardiac function; do not inject IV solution faster than 25 mg/min; patients diagnosed with pulmonary edema or liver dysfunction are at greater risk of toxicity because of reduced drug clearance |
Drug Category: Endothelin receptor antagonists — Competitively bind to endothelin-1 (ET-1) receptors ETA and ETB causing reduction in pulmonary artery pressure (PAP), pulmonary vascular resistance (PVR), and mean right atrial pressure (RAP).
|
Drug Name |
Bosentan (Tracleer) — Endothelin receptor antagonist indicated for the treatment of pulmonary arterial hypertension in patients with WHO Class III or IV symptoms, to improve exercise ability and decrease rate of clinical worsening. Inhibits vessel constriction and elevation of blood pressure by competitively binding to endothelin-1 (ET-1) receptors ETA and ETB in endothelium and vascular smooth muscle. This leads to significant increase in cardiac index (CI) associated with significant reduction in pulmonary artery pressure (PAP), pulmonary vascular resistance (PVR), and mean right atrial pressure (RAP). Due to teratogenic potential, can only be prescribed through the Tracleer Access Program (1-866-228-3546). |
|
Adult Dose |
<40 kg: 62.5 mg PO bid; not to exceed 125 mg/d |
|
Pediatric Dose |
Not established; 62.5 mg |
|
Contraindications |
Documented hypersensitivity; coadministration with cyclosporine A or glyburide |
|
Interactions |
Toxicity may increase when administered concomitantly with inhibitors of isoenzymes CYP450 2C9 and CYP450 3A4 (eg, ketoconazole, erythromycin, fluoxetine, sertraline, amiodarone, and cyclosporine A); induces isoenzymes CYP450 2C9 and CYP450 3A4 causing decrease in plasma concentrations of drugs metabolized by these enzymes including glyburide as well as other hypoglycemics, cyclosporine A, hormonal contraceptives, simvastatin, and possibly other statins; hepatotoxicity increases with concomitant administration of glyburide |
|
Pregnancy |
X – Contraindicated in pregnancy |
|
Precautions |
Causes at least 3-fold elevation of liver aminotransferases (ie, ALT, AST) in about 11% of patients; may elevate bilirubin (serum aminotransferase levels must be measured prior to initiation of treatment and then monthly); caution in patients with mildly impaired liver function (avoid in patients with moderate or severe liver impairment); not recommended while breastfeeding; monitor hemoglobin levels after 1 and 3 mo of treatment and every 3 mo thereafter; exclude pregnancy before initiating treatment and prevent thereafter by use of reliable contraception; headache and nasopharyngitis may occur |
Pleurisy
Pleurisy – inflammation of pleura, usually producing an exudative pleural effusion and stabbing chest pain worsened by respiration and cough.
Etiology
Pleurisy may result from an underlying lung process (eg, pneumonia, infarction, irritating substance into the pleural space (eg, with a ruptured esophagus, amebic empyema, or pancreatic pleurisy); transport of an infectious or noxious agent or neoplastic cells to the pleura via the bloodstream or lymphatics; parietal pleural injury (eg, trauma, especially rib fracture, or epidemic pleurodynia /due to coxsackievirus B/); asbestos-related pleural disease in which asbestos particles reach the pleura by traversing the conducting airways and respiratory tissues; or, rarely, pleural effusion related to drug ingestion.
Symptoms and Signs
Sudden pain is the dominant symptom of pleurisy. Typically, pleuritic pain is a stubbing sensation aggravated by breathing and coughing, but it can vary. It may only a vague discomfort, or it may occur only when the patient breathes deeply or coughs. The visceral pleura is insensitive; pain results from inflammation of parietal pleura, which is mainly innervated by intercostal nerves. Pain is usually felt over the pleuritic site but may be referred to distant regions. Irritation of posterior and peripheral portioms of the diaphragmatic pleura, which are supplied by the lower six intercostal nerves, may cause pain referred to the lower chest wall or abdomen and may simulate intra-abdominal disease. Irritation of the central portion of the diaphragmatic pleura, innervated by the phrenic nerves, causes pain referred to the neck and shoulder.
Respiration is usually rapid and shallow. Motion of the affected side may be limited. Breath sounds may be diminished. A pleural friction rub, although infrequent, is the characteristic physical sign.It may not be accompanied by pleuritic pain, but it usually is. The friction rub varies from a few intermittent sounds that may simulate crackles to a fully developed harsh grating, creaking, or leathery sound synchronous with respiration, heard on inspiration and expiration. Friction sounds due to pleuritis adjacent to the heart (pleuropericardial rub) may vary with the heart beat as well.
When pleural effusion develops, pleuritic pain usually subsides. Percussion dullness, absent tactile fremitus, decreased or absent breath sounds, and egophony at the upper border of the fluid are theoticeable. The larger the effusion, the more obvious the above signs. A large effusion may produce or contribute to dyspnea through diminished lung volume, especially if there is underlying pulmonary disease, mediastinal shift to the contralateral side, and diminished function and recruitment of inspiratory muscles due to an expanded thoracic cage.
Diagnosis
Pleurisy is readily diagnosed when characteristic pleuritic pain occurs. A pleural friction rub is pathognomonic. Pleurisy that produces referred abdominal pain is usually differentiated from acute inflammatory abdominal disease by x-ray and clinical evidence of a respiratory process; absence of nausea, vomiting, and disturbed bowel function; marked aggravation of pain by deep breathing or coughing; shallow rapid breathing; and a tendency toward relief of pain by pressure on the chest wall or abdomen. Intercostal neuritis may be confused with pleurisy, but the pain is rarely
Treatment
Treatment of the underlying disease is essential.
Chest pain may be relieved by wrapping the entire chest with two or three 6-in-wide nonadhesive elastic bandages, which must be reapplied once or twice daily. Acetaminophen 0.65 g qid or an NSAID is often effective. Oral narcotics may be necessary, but cough suppression may be not desired.
Adequate bronchial drainage must be provided to prevent pneumonia. A patient receiving narcotics should be urged to breathe deeply and cough when pain relief
