Pleuritis

 

Pleurisy is inflammation of the pleura.

Classification:

nDry pleurisy (pleuritis sicca)

nPleurisy with effusion (pleuritis exudativa)

 

The character of the inflammatory effusion may be different: serous, serofibrinous, purulent, and haemorrhagic.

Etiology and pathogenesis

—      Serous and serofibrinous pleurisy (tuberculosis in 70-90 per cent of cases, pneumonia, certain infections, and also rheumatism in 10-30 per cent of cases)

—      Purulent process (pneumococci, streptococci, staphylococci, and other microbes)

—      Haemorrhagic pleurisy (tuberculosis of the pleura, bronchogenic cancer of the lung with involvement of the pleura, and also in injuries to the chest)

 

DRY PLEURISY

Clinical picture

—     pain in the chest (a characteristic symptom )which becomes stronger during breathing and coughing.

—     cough (is usually dry)

—     general indisposition;

—     subfebrile temperature

—         Respiration is superficial (deep breathing intensifies friction of the pleural membranes to cause pain). Lying on the affected side lessens the pain. Inspection of the patient can reveal unilateral thoracic lagging during respiration. Percussion fails to detect any changes except decreased mobility of the lung border on the affected side. Auscultation determines pleural friction sound over the inflamed site.

 

—      Normal pleural fluid has the following characteristics: clear ultrafiltrate of plasma, pH 7.60-7.64, protein content less than 2% (1-2 g/dL), fewer than 1000 WBCs per cubic millimeter, glucose content similar to that of plasma, lactate dehydrogenase (LDH) level less than 50% of plasma and sodium, and potassium and calcium concentration similar to that of the interstitial fluid.

 

 

—     Transudative pleural effusion

—     Congestive heart failure (most common transudative effusion)
Hepatic cirrhosis with and without ascites
Nephrotic syndrome
Peritoneal dialysis/continuous ambulatory peritoneal
dialysis
Hypoproteinemia (eg, severe starvation)
Glomerulonephritis
Superior vena cava obstruction
Urinothorax

 

 

—        Exudative pleural effusion

—        Malignant disorders – Metastatic disease to the pleura or lungs, primary lung cancer, mesothelioma, Kaposi sarcoma, lymphoma, leukemia

—        Infectious diseases – Bacterial, fungal, parasitic, and viral infections; infection with atypical organisms such as Mycoplasma, Rickettsiae, Chlamydia, Legionella

—        GI diseases and conditions – Pancreatic disease (acute or chronic disease, pseudocyst, pancreatic abscess), Whipple disease, intraabdominal abscess (eg, subphrenic, intrasplenic, intrahepatic), esophageal perforation (spontaneous/iatrogenic), abdominal surgery, diaphragmatic hernia, endoscopic variceal sclerotherapy

—        Collagen vascular diseases – Rheumatoid arthritis, systemic lupus erythematosus, drug-induced lupus syndrome (procainamide, hydralazine, quinidine, isoniazid, phenytoin, tetracycline, penicillin, chlorpromazine), immunoblastic lymphadenopathy (angioimmunoblastic lymphadenopathy), Sjцgren syndrome, familial Mediterranean fever, Churg-Strauss syndrome, Wegener granulomatosis

 

—      Benign asbestos effusion

—      Meigs syndrome – Benign solid ovariaeoplasm associated with ascites and pleural effusion

—      Drug-induced primary pleural disease – Nitrofurantoin, dantrolene, methysergide, bromocriptine, amiodarone, procarbazine, methotrexate, ergonovine, ergotamine, oxprenolol, maleate, practolol, minoxidil, bleomycin, interleukin-2, propylthiouracil, isotretinoin, metronidazole, mitomycin

—      Injury after cardiac surgery (Dressler syndrome) – Injury reported after cardiac surgery, pacemaker implantation, myocardial infarction, blunt chest trauma, angioplasty

—      Uremic pleuritis

—      Yellow nail syndrome

—      Ruptured ectopic pregnancy

—      Electrical burns

Causes of transudtive and exudative effusions

 

Characteristics of transudate and exudate

 

 

 

 

PLEURISY WITH EFFUSION

 

Clinical picture

—      Complains: fever, pain or the feeling of heaviness in the side, dyspnea (which develops due to respiratory insufficiency caused by com­pression of the lung). Cough is usually mild (or absent in some cases).

—      Objective examination: The patient’s general condition is grave, especially in purulent pleurisy, which is attended by high temperature with pronounced circadian fluctuations, chills, and signs of general toxicosis. Inspection of the patient reveals asymmetry of the chest due to enlargement of the side where the effusion accumulated; the affected side of the chest usually lags behind respiratory movements. Vocal fremitus is not transmitted at the area fluid accumulation.

Cyanosis in pleurisy with effusion due to respiratory insufficiency  is caused by lung collapse and limitation of its respiratory surface

 

—      Percussion over the area of fluid accumulation produces dullness. The upper limit of dullness is usually the S-shaped curve (Damoiseau’s curve) whose upper point is in the posterior axillary line. The effusion thus occupies the area, which is a triangle both anteriorly am posteriorly. The Damoiseau curve is formed because exudate pleurisy with effusion more freely accumulates in the lateral portions of the pleural cavity, mostly in the costal-diaphragmatic sinus.

 

In addition  to the Damoiseau curve, two triangles can be determined by percussion in pleurisy with effusion. The Garland triangle is found on the affected side is characterized by a dulled tympanic sound. It corresponds to the lung pressed by the effusion, and is located between the spine and the Damoiseau curve. The Rauchfuss-Grocco triangle is found on the healthy and is a kind of extension of dullness determined on the affected side, sides of the triangle are formed by the diaphragm and the spine, while the continued Damoiseau curve is the hypotenuse.

 

Treatment

—Bed rest

—Treatment of underlying lung disease

—Pleuritic pain can be managed with NSAIDs (indomethacin 25mg orally 2-3 times daily) or oral opioids (codeine 30-60 mg orally every 8 hours)

—Thoracentesis to relieve breathlessness (750-1000 ml of fluid can be aspirated in one manipulation if necessary)

—      Antibiotics (eg, for parapneumonic effusions) and diuretics (eg, for effusions associated with CHF) are commonly used in the initial management of pleural effusions in the ED. The selection of drugs in each class depends on the cause of the effusion and its clinical presentation. Particular attention must be given to potential drug interactions, adverse effects, and preexisting conditions.

 

 Tuberculous  pleural  effusion

—    TB remains the most common cause of

    pleural effusion in young people

—    Etiology:  tubercle bacillus

—    Pathogenesis:  host hypersensitivity to

    tubercular protein in pleural tubercles

—    Delayed  hypersensitivity

Clinical Manifestations

—    Generalized symptoms of toxicity of TB: fever, sweats, fatigue, weight loss ss, etc.

—    Pleuritic pain, dyspnea, coughlea, etc.

—    Pleural fluid is  exudative and usually

   reveals  lymphocytosis

—    Rarely pleural fluid is blood stained

—    Tubercular tests usually positive

 

 

Empyema

—    Thick purulent fluid with more than 100,000

    cells  per  cubic  millimeter  or  fluid  with  PH

    values   less   than  or  equal  to  7. 20   should

    be  treated  as  a  presumptive  empyema

—    The general objectives of therapy of empyema

    are the elimination of both the systemic and

    local infection.

 

 

 Treatment of acute and chronic empyema

      1.    Control of infection

                        systemic and local

      2. Repeated  thoracentesis or drainage of the empyema

    

         3. Chronic  empyema  is  primarily treated operatively

                

       4. Operative therapy is also indicated in  the empyema  with   associated bronchopleural fistula or with the

               ipsilateral  ruined  lung

 

Malignant pleural effusion

If dyspnea caused by malignant pleural effusion is relieved by thoracentesis but fluid reaccumulates (with dyspnea), chronic (intermittent) drainage or pleurodesis is indicated. Pleurodesis is done by instilling a sclerosing agent into the pleural space to fuse the visceral and parietal pleura and eliminate the space. The most effective and commonly used sclerosing agents are talc, doxycycline, and bleomycin delivered via chest tube or thoracoscopy.

 

Lung abscess

Essentials of Diagnosis

• Development of pulmonary symptoms about 1-2 weeks after possible aspiration, bronchial obstruction, or previous pneumonia.

• Septic fever and sweats, and periodic sudden ex­pectoration of large amounts of purulent, foul-smelling, or “musty” sputum. Hemoptysis may occur.

• X-ray density with central radiolucency and fluid level.

 

General Considerations

Lung abscess develops wheecrosis and liquefaction occur in an area where necrotizing pneumonia is present (picture 1-3). Symptoms and signs occur 1-2 weeks after the following events:

(1) massive-aspira­tion of upper respiratory tract secretions and microbial flora, especially during profound suppression of cough reflex (eg, with alcohol, drugs, unconsciousness, anesthesia, brain trauma);

(2) bronchial obstruction (eg, by atelectasis, foreign body, neoplasm);

(3) pres­ence of pneumonias, especially those caused by gram-negative bacteria or staphylococci;

(4) forma­tion of septic emboli from other foci of infection, or, during bacteremia, with pulmonary infarcts.

Abscess is more commonly in the lower dependent portions of the lung.

Differential Diagnosis

Differentiate from other causes of pulmonary cavitation: tuberculosis, bronchogenic carcinoma, mycotic infections, and staphylococcal or gram-nega­tive bacterial pneumonia.

Treatment

Postural drainage and bronchoscopy are impor­tant to promote drainage of secretions.

A. Acute Abscess: Intensive antibacterial ther­apy is necessary to prevent further destruction of lung tissue. While cultures and sensitivity tests are pending, treatment should be started with penicillin G, 2-6 million units daily. In penicillin hypersensitivity clindamycin and chloramphenicol are alternatives. If the patient improves on antimicrobial drugs (and postural drainage), the drugs should be continued for 4—8 weeks. If the patient fails to respond significantly to the initial treatment, laboratory results may suggest other antimicrobials, eg, nafcillin for staphylococci, cefotaxime for Klebsiella, cefoxitin or metronidazole for mixed anaerobes. Postural drainage is important adjunctive treatment. Percutaneous catheter drainage has been used successfully in selected cases. Surgical therapy is indicated mainly for severe hemoptysis and for me infrequent abscesses that fail to respond to antimicrobial management. Failure of fever to subside after 2 weeks of therapy, abscess diameter of more than 6 cm, and very thick cavity waits are all factors that lessen the likelihood of success with nonsurgical treatment alone.

B. Chronic Abscess: After acute systemic man­ifestations have subsided, the abscess may persist. Although many patients with chronic lung abscess can be cured with  long-term treatment with antibacterial agents, surgery may occasionally be required.

Complications

Rupture of pus into the pleural space (empyema) causes severe symptoms: increase in fever, marked pleural pain, and sweating; the patient becomes “tox­ic” in appearance. Adequate drainage of empyema is mandatory. In chronic abscess, severe and even fatal hemorrhage may occur. Metastatic brain abscess is a well-recognized complication, and the infection may seed other organ sites. Bronchiectasis may occur as a sequela to lung abscess even when the abscess itself is cured.

Prognosis   

The prognosis in acute abscess is excellent with prompt and intensive antibiotic therapy. About 80% of patients are healed within 7-8 weeks. The incidenee of chronic abscess is consequently low; In chronic cases, surgery is curative.

 

Bronchiectasis

Essentials of Diagnosis:

• Chronic cough with expectoration of large amounts of purulent sputum; hemoptysis.

• Rales and rhonchi over lower lobes.

• X-ray of chest reveals little; bronchograms show characteristic dilatations.

General Considerations

Bronchiectasis is a dilatation of small and medium-sized bronchi resulting from destruction of bronchial elastic and muscular elements. It may be, caused by pulmonary infections (eg, pneumonia, per­tussis, tuberculosis) or by a bronchial obstruction (eg, foreign bodies or extrinsic pressure). In many patients, a history of onset following one or more episodes of pulmonary infection, usually in early childhood, is obtained.

 

Clinical Findings

A.   Symptoms and Signs:

–         history of chronic cough with expectoration of large volumes of sputum, especially upon awakening. The sputum has a characteristic qual­ity of “layering out” into 3 layers upon standing, a frothy top layer, a middle clear layer, and a dense particulate bottom layer. It is usually purulent in ap­pearance and foul-smelling.

–         Intermittent hemoptysis, occasionally in dangerous proportions, is often combined with intercurrent respiratory infections. Symptoms occur most often in patients with idiopathic bronchiectasis. Idiopathic bronchiectasis occurs most fre­quently in the middle and lower lobes and posttuberculous bronchiectasis in the upper lobes. Hemoptysis is thought to result from erosion of bronchiolar mucosa with resultant destruction of un­derlying blood vessels.

–         Pulmonary insufficiency may result from progressive destruction of pulmonary tis­sue.

   Physical findings consist primarily of rales and rhonchi over the affected segments. If the condition is far-advanced, emaciation, cyanosis, and digital club­bing may appear.

 

B.   Laboratory Findings: There are no charac­teristic laboratory findings.

– If hypoxemia is chronic and severe, secondary polycythemia may develop.

– There may be either restrictive or obstructive pulmo­nary function defects associated with bronchiectasis.

– Hypoxemia and hypocapnia or hypercapnia may also be associated with the disease, depending on the se­verity of the underlying condition. .

  

C.X-Ray Findings: Plain films of the chest often show increased bronchopulmonary markings in af­fected segments; in severe cases there may be areas of radiodensities surrounding portions of radiolucency. Early in the course of bronchiectasis, however, the chest x-ray may be normal.

A bronchogram demonstrates saccular, cylindric, or fusiform dilatation of small and medium bronchi with consequent loss of the normal branching pattern.

Differential Diagnosis

The differential diagnosis includes other disorders that lead to chronic cough, sputum produc­tion, and hemoptysis, ie, chronic bronchitis, tuber­culosis, and bronchogenic carcinoma. The diagnosis of bronchiectasis is suggested by the patient’s history and can be confirmed only by bronchographic examination or histopathologic examination of surgically removed tissue.

Complications

Recurrent infection in poorly drained pulmonary segments leads to chronic suppuration and may cause pulmonary insufficiency. Complications include hemoptysis, respiratory failure, chronic cor pulmonale, and amyloidosis. There is also an increased incidence of brain abscess, which is thought to be secondary to abnormal anastomoses between bron­chial (systemic) and pulmonary venous circulation. These anastomoses produce right-to-left shunts and allow for the dissemination of septic emboli.

Treatment

A. General Measures and Medical Treatment:

1. Environmental changes– The patient should  avoid exposure to all common pulmonary irritants such as smoke, fumes, and dust and should stop smoking cigarettes.

2. Control of bronchial secretions (improved drainage)–

a. Postural drainage often gives effective relief of symptoms and should be utilized in every case. The patient should assume the position that gives maximum drainage, usually lying on a bed in the prone, supine, or right or left lateral decubitus position with the hips elevated on several pillows and no pillow under the head. Any effective position should be main­tained for 10 minutes, 2-4 times a day. The first drainage should be done upon awakening and tee last drainage at bedtime. Family members can be trained in the art of chest percussion to facilitate drainage of secretions.

b. Liquefaction of thick sputum may be pro­moted by inhaling warm mists and, in some cases, mucolytic agents such as acetylcysteine or 5% sodium bicarbonate given by aerosol may also be helpful.

 3. Control of respiratory infection-Exposure to respiratory infections should be minimized and the patient should be vaccinated against influenza and pneumococcal pneumonia. Antibiotic therapy is indi­cated for acute exacerbations (ie, increased production of purulent sputum, hemoptysis, etc). Long-term or prophylactic antibiotic therapy is controversial, since it has not been conclusively shown to be of lasting benefit. Therefore, it seems rational to treat acute exacerbations in order to control infection but mini­mize  the emergence of resistant strains. Because the bacteria most commonly involved are H inftuenzae and S pneumoniae, the drug most commonly employed is ampicillin, 250-500 mg orally every 6 hours for 5 days. Alternative therapies for the penicillin-allergic patient are erythromycin, given in the same dosage schedule as ampicillin, or trimethoprim-sulfamethoxazole, 2 double-strength tablets twice a day for 5 days.

    B. Surgical Treatment: Surgical treatment is most often employed when hemoptysis with bron-chiectasis is recurrent and severe. Despite antibiotic therapy, localized bronchiectasis (eg, in a lower lobe or segment) with progressive uncontrolled infection and sputum production may be an indication for surgical removal of the affected segments.

 

Disorders causing chronic pulmonary insufficiency:

Pathogenetic classification

1.     Airways obstruction: Chronic bronchitis, Emphysema, Cystic fibrosis (mucoviscidosis), Bronchial asthma

2.     Abnormal Pulmonary Interstitium: Pulmonary Alveolitis, Interstitial Fibrosis, Sarcoidosis, Pneumoconiosis, Progressive systemic sclerosis, Rheumatoid lung, Disseminated carcinoma, Idiopathic fibrosis (Hamman-Rich syndrome), Drug sensitivity (hydralazine, busulfan, etc.), Hodgkin’s disease, Systemic lupus erythematosus, Radiation, Leukemia

3.     Alveolar Hypoventilation Without Primary Bronchopulmonary Disease. Functional: Sleep, chronic exposure to CO₂, metabolic alkalosis. Anatomic: abnormal respiratory center, abnormal chest cage (kyphoscoliosis, fibrothorax). Disordered neuromuscular function: Myasthenia gravis, infectious potyneuritis, muscular dystrophy, poliomyelitis, polymyositis. Obesity. Hypothyroidism.

Clinical classification of pulmonary insufficiency

Stage I– the breastlessness occurred in case of usual physical activity that previously didn’t course it (running, going upstears). Hemoglobin saturation by O₂ no less than 80%.

Stage II– the breastlessness occurred in case of low physical activity (walking on plain surface). Hemoglobin saturation by O₂ near about 60– 80%.

Stage III– the breastlessness occurred in rest. Hemoglobin saturation by O₂ less than 60%.

 

Main forms of respiratory insufficiency (according to B. E. Votchal)

1.     Central form – is the result of inhibition of respiratory center (narcosis, drugs, trauma, atherosclerosis, stroke etc.).

2.     Neuro–muscular form – is the result of disturbance of  conduction of signals from central nervous system to muscules (miastenia, poliemielitis etc.).

3.     Thoraco-diafragmal form – is the result of reduction of chest movements (chest degormation, kifoscoliosis etc.).

4.     Pulmonary form – is the result of pulmonary problems: decrease of pulmonary tissue (pneumonia, tumor), decrease of pulmonary tissue elasticity (fibrosis), narrowing of bronchial system (asthma, stenosis).

 

Clinical and instrumental characteristics of main types of ventilation insufficiency: obstructive, restrictive and mixed

1.     Obstructive type is caused by: a) spasm; b) mucous odema; c) hypersecretion; d) scar narrowing; e) endobronchial tumor; f) external pressuring of bronchus. Diagnostic criteria: dyspnoe after physical execiesing, dry cough, dry rales. Increasing of expiration period, on spirography– decrease of FEV_1.

2.     Restrictive  type is caused by: a) fibrosis; b) pleural disorders; c) pleural exudation; d) pneumoconiosis; e) tumors of lungs; f) pulmonectomia. Diagnostic crireria: on spirography– decrease of VC.

3.     Mixed type: both causes are aviable.

Diagnosis and treatment of pulmonary insufficiency depend on the certain disease (acute or chronic), that led to development of this syndrome (see the previous chapters in pulmonology).