ASSISTANT PROFESSOR

CASE PRESENTATION

Date of Admission Time of Admission

27 may 2011 , friday :6.00 pm

PERSONAL IDENTIFICATION Name Age Address shahida bibi 67 years old MPS (VILLAGE) Farmer

Occupation

CHIEF COMPLAINT
o Fever cough and lethargy
HISTORY OF PRESENTING ILLNESS

Previously patient is well until fever is started 5days ago, which was low grade,on and off. It was associated with chills and rigorsand usually worsen at night. Patient took Paracetamol tablet but fever temporarily resolved. Patient also developed cough during fever. It was non productive cough (dry cough). She had no vomiting and did not coughing out blood.

. She also had occasional shortness of breath and pleuritic pain when coughing. The pleuritic pain is dull in nature. She prefers to lie down as it can relieve the pain. otherwise, no orthopnea, no wheezing and no night sweats. She also had poor appetite but she can tolerating well. On day 5 of her illness, patient's condition became worse and she also complained of lethargy. Patient went to emergency department yesterday and temperature was documented at 37.5 C. Patient was then warded to ward 1.

PAST MEDICAL HISTORY

This is the patient's 3rd admission. First admission was due to tonsil operation when she was 16 years old. Second was due to eye procedure 10 years ago. Patient is a known case of hypertension (HPT) , diagnosed for more than 10 years. She is now under treatment and follow up at MMCH .She is compliance to her medication. She has no previous history of IHD or CVA. No history of Diabetes Mellitus or asthma. Allergies : The patient has no allergy to any food or drugs.

FAMILY HISTORY
The patient is the 2nd child out of 7 siblings. The parents and her 3rd and youngest brother died of nature causes. There are no history of atopy, asthma and TB in the family.

SOCIAL HISTORY
She is married with 3 children. Her husband just passed away and currently she is staying home alone. She is a non- smoker, non alcoholic drinker She has cats in her house

1. GENERAL EXAMINATION:
The patient is alert and conscious, well oriented to time, place and people. She is lying comfortably in supine position. She is not in pain and respiratory distress.She is mildly dehydrated. Blood pressure: 128/ 70 mmHg Pulse rate: 90 beats/minute. Good volume and regular rhythm

Respiratory rate: 22 breaths /minute Temperature: 37.0C Sp02: 97 % .Pallor : no conjunctival pallor noted Cyanosis : no peripheral or central cyanosis Jaundice : no jaundice noted Clubbing : no clubbing noted Oedema : no pitting oedema Head / neck : normocephalic Neck : The jugular venous pressure is not raised and no lymph nodes enlargement detected. No neck stiffness

Eyes : not sunken, arcus angle Oral cavity : Oral hygiene is poor Ears : no discharge, normal shape Throats : not injected, tonsil bilaterally not enlarged Abdomen : no scar, abdomen is soft and non tender Hands: There are no muscle wasting and no gross deformity.(-) clubbing ,no palmar erythema, not pallor CVS : Ejection systolc murmur,grade 3/6 and radiates to right aortic on auscultation.

Inspection Symmetrical & abdomino thoracal respiratory

Palpation Percusion Auscultation

Symmetrical Increased at lower zone of right side Dullness at lower lobe of right lung Bronchial breathing on both side Fine crepitations > right side, no ronchi Not done

SUMMARY
SHAHIDA

BIBI, 67 years old,came with chieft complaint of fever for 5 days, cough and lethargy. She is known case pf HPT for more than 10 years. No family hx of asthma and Tb. On chest examination revealed increase of vocal fremitus, dullnes on percussion and fine crepitation on auscultation on lower lobe of right lung.

DIAGNOSIS
1. DIFFERRENTIAL DIAGNOSIS : - PNEUMONIA - BRONCHIECTASIS - TB 2. WORKING DIAGNOSIS : - Pneumonia

INVESTIGATIONS
BASIC :
Full Blood Count Blood Urea and Serum Electrolytes (BUSE) Creatinine Arterial BloodGases (ABG) Chest X-Ray

SPECIFIC :
Sputum FEME, C&S, AFB Blood C&S Pleural aspiration Bronchoscopy Serology (Mycoplasma, Chlamydia,Legionella) Immunoflourosence or Giemsa stain for PCP

PLAN
Monitor vital signs and SpO2 4 hourly Paracetamol tablet 1000 mg 8 hourly Tepid sponging prn Nasal Prong O2 3L prn Syrup Benadyl 15 ml TDS Septic management if fever more than 38C IV Augmetin 1.2 g TDS To review all investigations results

FOLLOW UP

INTERPRETATION
PA view, erect position Trachea :centrally located Clavicle :symmetrical in position , no fracture Bone :normal Homogenic opacity at right side of lung Honey-comb appearance on lower zone of right lung Diaphragm :dome shape Impression: pneumonia

2. FBC (Day1)
WBC 17000 NEUTROPHIL 85%

Impression of FBC result

Leukocytosis: WBC increased, neutrophil predominates suggestive of bacterial infection Plan: broad spectrum antibotics unitl blood C&S result came back

3. BUSE
Na 138 K 2.8 UREA 60 CREATININE 5

Impression of renal profile:

Hypokalemia: Potassium was 2.8 mmol Correction by adding 1g KCl IV High urea: Urea level was 60, correlates with mild dehydration Plan: IVD normal saline in 24 hours

Patient is 67 years old, woman came with chieft complaint of fever for 5 days, cough and lethargy. She On chest examination revealed increase of vocal fremitus, dullnes on percussion and fine crepitation on auscultation. Chest X-ray revealed the patchy infiltration at lower lobe of right lung. Patient is diagnosed to have Community-acquired pneumonia. Empirical antibiotic of IV amoxicillin with clavulanic acid ( beta-lactam antibiotic) is chose to treat the pneumonia

DISCUSSION

To exclude bronchiectasis because : no history of obstructive lung disease, along with bronchitis and cystic fibrosis. No history of frequent respiratory infections or chronic lung disease No CT scan was done to establish diagnosis and localize the bronchiectasis To exclude TB because: Negative AFB No history of weight loss No night sweats

PNEUMONIA

DEFINATION
Pneumonia is an inflammatory condition of the lung, especially of the alveoli (microscopic air sacs in the lungs) or when the lungs fill with fluid (called consolidation and exudation).

Pneumonia
Main Cause of 90% of Deaths From Respiratory Infection Worst M&M in Infants and Older People Predominantly Viral Etiology Highest Mortality by Bacterial Pathogens

ETIOLOGY
Infective causes: Bacterial: Gram +ve: Strep pneumoniae, Staph aureus Gram ve: H. influenzae, Klebsiella, Legionella Anaerobes Viral: Varicella virus, Influenza virus Fungal: Candida, Aspergillus Atypical: Mycoplasma, Chlamydia Helminths: Filariasis Non infective causes: Physical agents Allergic diseases Collagenic diseases

PATHOGENESIS
Main mechanisms by which bacteria reaches lung: Inhalation: organisms bypass normal respiratory defense mechanisms or patient inhales aerobic organisms that colonize the upper respiratory tract or respiratory support equipment Aspiration: occurs when patient aspirates colonized upper respiratory tract secretions Hematogenous: originate form a distant source and reach the lungs via blood stream

CLASSIFICATION
Site of infection: Lobar Bronchopneumonia Origin of infction: Community acquired pneumonia Nosocomial pneumonia ( hospital acqiures pneumonia): occur 48 hours after admission which was not incubating at the time of admission Aspiration pneumonia: occur when aspirate foreign matter into lungs Immunocompromised pneumonia

Based on etiology:
Bacterial Viral Fungal Atypical Aspiration

Respiratory symptoms:
Productive cough Sputum +/- hemoptysis Shortness of breath Pleuritic chest pain

Specific symptoms:
Abdominal pain

Advanced symptoms:
Cyanosis Alteration of mental status

Infection of the lung parenchyma in a person who is not hospitalized or living in a long-term care facility for 2 weeks 5.6 million cases annually in the U.S. Estimated total annual cost of health care = $8.4 billion Most common pathogen = S. pneumo (60-70% of CAP cases)

Community Acquired Pneumonia

Nosocomial Pneumonia
Hospital-acquired pneumonia (HAP) Occurs 48 hours or more after admission, which was not incubating at the time of admission Ventilator-associated pneumonia (VAP) Arises more than 48-72 hours after endotracheal intubation

Nosocomial Pneumonia
Healthcare-associated pneumonia (HCAP) Patients who were hospitalized in an acute care hospital for two or more days within 90 days of the infection; resided in a nursing home or LTC facility; received recent IV abx, chemotherapy, or wound care within the past 30 days of the current infection; or attended a hospital or hemodialysis clinic

Streptococcus pneumonia
Most common cause of CAP Gram positive diplococci Typical symptoms (e.g. malaise, shaking chills, fever, rusty sputum, pleuritic hest pain, cough) Lobar infiltrate on CXR Suppressed host

Atypical Pneumonia
#2 cause (especially in younger population) Commonly associated with milder Sxs: subacute onset, non-productive cough, no focal infiltrate on CXR Mycoplasma: younger Pts, extra-pulm Sxs (anemia, rashes), headache, sore throat Chlamydia: year round, URI Sx, sore throat Legionella: higher mortality rate, waterborne outbreaks, hyponatremia, diarrhea

Viral Pneumonia
More common cause in children RSV, influenza, parainfluenza Influenza most important viral cause in adults, especially during winter months Post-influenza pneumonia (secondary bacterial infection) S. pneumo, Staph aureus

DIAGNOSIS
History taking: suggestive signs and symptoms Physical examination Investigation Chest X-ray or other imaging techniques

S/S
General symptoms:
Fever - Malaise Chills and rigors - Nausea and vomiting Loss of appetite Myalgia

PHYSICAL EXAMINATION
Inspection: use of accessory muscles Palpation: decreased chest expansion, increased tactile fremitus Percussion: maybe dullness on affected lung, increased vocal resonance Auscultation: bronchial breathing, crepitations

Antigen Tests
Two commercially available tests detect pneumococcal and certain Legionella antigens in urine.

Polymerase Chain Reaction

Polymerase chain reaction (PCR) tests are available for a number of pathogens, including L. pneumophila and mycobacteria.

Serology
A fourfold rise in specific IgM antibody titer between acute- and convalescent-phase serum samples is generally considered diagnostic of infection with the pathogen in question. In the past, serologic tests were used to help identify atypical pathogens as well as some typical but relatively unusual organisms, such as Coxiella burnetii.

Differential Diagnosis
acute bronchitis acute exacerbations of chronic bronchitis heart failure pulmonary embolism radiation pneumonitis

Since the physician rarely knows the etiology of CAP at the outset of treatment, initial therapy is usually empirical and is designed to cover the most likely pathogens .In all cases, antibiotic treatment should be initiated as expeditiously as possible.

Management CAP

 Empirical Antibiotic Treatment of Community-Acquired Pneumonia Outpatients Previously healthy and no antibiotics in past 3 months A macrolide [clarithromycin (500 mg PO bid) or azithromycin (500 mg PO once, then 250 mg od)] or Doxycycline (100 mg PO bid) Comorbidities or antibiotics in past 3 months: select an alternative from a different class A respiratory fluoroquinolone [moxifloxacin (400 mg PO od), gemifloxacin (320 mg PO od), levofloxacin (750 mg PO od)] or A -lactam [preferred: high-dose amoxicillin (1 g tid) or amoxicillin/clavulanate (2 g bid); alternatives: ceftriaxone (12 g IV od), cefpodoxime (200 mg PO bid), cefuroxime (500 mg PO bid)] plus a macrolidea

In regions with a high rate of "high-level" pneumococcal macrolide resistance,b consider alternatives listed above for patients with comorbidities. Inpatients, non-ICU A respiratory fluoroquinolone [moxifloxacin (400 mg PO or IV od), gemifloxacin (320 mg PO od), levofloxacin (750 mg PO or IV od)] A -lactamc [cefotaxime (12 g IV q8h), ceftriaxone (12 g IV od), ampicillin (12 g IV q4 6h), ertapenem (1 g IV od in selected patients)] plus a macrolided [oral clarithromycin or azithromycin (as listed above for previously healthy patients) or IV azithromycin (1 g once, then 500 mg od)] Inpatients, ICU A -lactame [cefotaxime (12 g IV q8h), ceftriaxone (2 g IV od), ampicillin-sulbactam (2 g IV q8h)] plus Azithromycin or a fluoroquinolone (as listed above for inpatients, non-ICU)

Special concerns If Pseudomonas is a consideration An antipneumococcal, antipseudomonal -lactam [piperacillin/tazobactam (4.5 g IV q6h), cefepime (12 g IV q12h), imipenem (500 mg IV q6h), meropenem (1 g IV q8h)] plus either ciprofloxacin (400 mg IV q12h) or levofloxacin (750 mg IV od) The above -lactams plus an aminoglycoside [amikacin (15 mg/kg od) or tobramycin (1.7 mg/kg od) and azithromycin] The above -lactamsf plus an aminoglycoside plus an antipneumococcal fluoroquinolone

If CA-MRSA is a consideration

Add linezolid (600 mg IV q12h) or vancomycin (1 g IV q12h)

Failure to Improve
Patients who are slow to respond to therapy should be reevaluated at about day 3 (sooner if their condition is worsening rather than simply not improving), and a number of possible scenarios should be considered. (1)Is this a noninfectious condition? (2) If this is an infection, is the correct pathogen being targeted? (3) Is this a superinfection with a new nosocomial pathogen?

A number of noninfectious conditions can mimic pneumonia, including pulmonary edema, pulmonary embolism, lung carcinoma, radiation and hypersensitivity pneumonitis, and connective tissue disease involving the lungs. The pathogen may be resistant to the drug selected, or a sequestered focus (e.g., a lung abscess or empyema) may be blocking access of the antibiotic(s) to the pathogen.

It is also possible that CAP is the correct diagnosis but that a different pathogen (e.g., M. tuberculosis or a fungus) is the cause. In all cases of delayed response or deteriorating condition, the patient must be carefully reassessed and appropriate studies initiated.

Complications
respiratory failure Shock multiorgan failure bleeding diatheses exacerbation of comorbid illnesses. metastatic infection lung abscess complicated pleural effusion.

Follow-Up
Fever and leukocytosis usually resolve within 2 and 4 days, respectively, in otherwise healthy patients with CAP, but physical findings may persist longer. Chest radiographic abnormalities are slowest to resolve and may require 412 weeks to clear,

patient whose condition is improving and who (if hospitalized) has been discharged, a follow-up radiograph can be done ~46 weeks later. If relapse or recurrence is documented, particularly in the same lung segment, the possibility of an underlying neoplasm must be considered.

Prognosis
The prognosis of CAP depends on the patient's age, comorbidities, and site of treatment (inpatient or outpatient). Young patients without comorbidity do well and usually recover fully after ~2 weeks. Older patients and those with comorbid conditions can take several weeks longer to recover fully. The overall mortality rate for the outpatient group is <1%.

For patients requiring hospitalization, the overall mortality rate is estimated at 10%, with ~50% of the deaths directly attributable to pneumonia.

Prevention
Vaccination for influenza and pneumococcal

Bronchiectasis
Bronchiectasis is an abnormal and permanent dilatation of bronchi. It may be either focal, involving airways supplying a limited region of pulmonary parenchyma, or diffuse, involving airways in a more widespread distribution. Recent studies have estimated there to be about 110,000 patients with bronchiectasis in the United States. It is a disorder that typically affects older individuals; approximately two-thirds of patients are women.

Pathology
The bronchial dilatation of bronchiectasis is associated with destructive and inflammatory changes in the walls of medium-sized airways, Airway inflammation is primarily mediated by neutrophils and results in up-regulation of enzymes such as elastase and matrix metalloproteinases.

The normal structural components of the wall, including cartilage, muscle, and elastic tissue, are destroyed and may be replaced by fibrous tissue. The dilated airways frequently contain pools of thick, purulent material, while more peripheral airways are often occluded by secretions or obliterated and replaced by fibrous tissue. Three different patterns of bronchiectasis have been described. cylindrical bronchiectasis, varicose and saccular (cystic) bronchiectasis,

Etiology
Infectious Causes
Staphylococcus aureus Klebsiella Anaerobes Pseudomonas aeruginosa Haemophilus influenzaeAdenovirus and influenza virus Tuberculosis

Noninfectious Causes
inhalation of a toxic gas such as ammonia aspiration of acidic gastric contents 1-antitrypsin deficiency yellow nail syndrome Cystic fibrosis

Clinical Manifestations
persistent or recurrent cough and purulent sputum production. Repeated, purulent respiratory tract infections should raise clinical suspicion for bronchiectasis. Hemoptysis occurs in 5070% of cases and can be due to bleeding from friable, inflamed airway mucosa Dry" Bronchiectasis patients are either asymptomatic or have a nonproductive cough

Dyspnea or wheezing generally reflects either widespread bronchiectasis or underlying chronic obstructive pulmonary disease. With exacerbations of infection

Physical examination
Any combination of crackles, rhonchi, and wheezes may be heard, all of which reflect the damaged airways containing significant secretions.

clubbing may be present. Patients with severe diffuse disease, particularly those with chronic hypoxemia, may have associated cor pulmonale and right ventricular failure.

INVESTIGATION
Radiographic Findings
dilated airways with thickened walls, which result from peribronchial inflammation. These dilated airways are often crowded together in parallel. When seen longitudinally, the airways appear as "tram tracks"; when seen in crosssection, they produce "ring shadows." Because the dilated airways may be filled with secretions, the lumen may appear dense rather than radiolucent, producing an opaque tubular or branched tubular structure.

CT, especially with high-resolution images 1.01.5 mm thick, provides an excellent view of dilated airways. Consequently, it is now the standard technique for detecting or confirming the diagnosis of bronchiectasis.

sputum fiberoptic bronchoscopy

reveal an underlying endobronchial obstruction. In other cases, upper lobe involvement may be suggestive of either tuberculosis or ABPA.

measurement of sweat chloride levels for CF structural or functional assessment of nasal or bronchial cilia or sperm for primary ciliary dyskinesia quantitative assessment of immunoglobulins may explain recurrent airway infection.
Pulmonary function tests

Treatment
Therapy has several major goals (1)treatment of infection, particularly during acute exacerbations (2) improved clearance of tracheobronchial secretions (3) reduction of inflammation (4) treatment of an identifiable underlying problem.

Antibiotics are the cornerstone of bronchiectasis management. For patients with infrequent exacerbations characterized by an increase in quantity and purulence of the sputum, antibiotics are used only during acute episodes. Although choice of an antibiotic should be guided by Gram's stain and culture of sputum, empiric coverage (e.g., with amoxicillin, trimethoprimsulfamethoxazole, or levofloxacin) is often given initially.

Infection with P. aeruginosa is of particular concern, as it appears to be associated with greater rate of deterioration of lung function and worse quality of life. When Pseudomonas is present, oral therapy with a quinolone or parenteral therapy with an aminoglycoside, carbapenem, or third-generation cephalosporin is appropriate based on antibiotic sensitivity patterns. here are no firm guidelines for length of therapy, but a 1014 day course or longer is typically administered.

A variety of mechanical methods and devices accompanied by appropriate positioning can facilitate drainage in patients with copious secretions. Mucolytic agents to thin secretions and allow better clearance are controversial. Aerosolized recombinant DNase, which decreases viscosity of sputum by breaking down DNA released from neutrophils, has been shown to improve pulmonary function in CF but may be deleterious and should be avoided in bronchiectasis not associated with CF.

Bronchodilators to improve obstruction and aid clearance of secretions are particularly useful in patients with airway hyperreactivity and reversible airflow obstruction. when bronchiectasis is localized and the morbidity is substantial despite adequate medical therapy, surgical resection of the involved region of lung should be considered.

When massive hemoptysis, often originating from the hypertrophied bronchial circulation, does not resolve with conservative therapy, including rest and antibiotics, therapeutic options are either surgical resection or bronchial arterial embolization . Although resection may be successful if disease is localized, embolization is preferable with widespread disease.

Pleural Effusion
The pleural space lies between the lung and chest wall and normally contains a very thin layer of fluid, which serves as a coupling system. A pleural effusion is present when there is an excess quantity of fluid in the pleural space

PATHOGENESIS
Pleural fluid accumulates when pleural fluid formation exceeds pleural fluid absorption. Normally, fluid enters the pleural space from the capillaries in the parietal pleura and is removed via the lymphatics situated in the parietal pleura. Fluid can also enter the pleural space from the interstitial spaces of the lung via the visceral pleura or from the peritoneal cavity via small holes in the diaphragm..

The lymphatics have the capacity to absorb 20 times more fluid than is normally formed. Accordingly, a pleural effusion may develop when there is excess pleural fluid formation (from the interstitial spaces of the lung, the parietal pleura, or the peritoneal cavity) or when there is decreased fluid removal by the lymphatics

Diagnostic Approach
When a patient is found to have a pleural effusion, an effort should be made to determine the. The first step is to determine whether the effusion is a transudate or an exudate. A transudative pleural effusion occurs when systemic factors that influence the formation and absorption of pleural fluid are altered. The leading causes of transudative pleural effusions are left ventricular failure and cirrhosis.

An exudative pleural effusion occurs when local factors that influence the formation and absorption of pleural fluid are altered. The leading causes of exudative pleural effusions are bacterial pneumonia, malignancy, viral infection, and pulmonary embolism. The primary reason to make this differentiation is that additional diagnostic procedures are indicated with exudative effusions to define the cause of the local disease.

Transudative and exudative pleural effusions are distinguished by measuring the lactate dehydrogenase (LDH) and protein levels in the pleural fluid. Exudative pleural effusions meet at least one of the following criteria, whereas transudative pleural effusions meet none: 1. pleural fluid protein/serum protein >0.5 2. pleural fluid LDH/serum LDH >0.6 3. pleural fluid LDH more than two-thirds normal upper limit for serum

The above criteria misidentify ~25% of transudates as exudates. If one or more of the exudative criteria are met and the patient is clinically thought to have a condition producing a transudative effusion, the difference between the protein levels in the serum and the pleural fluid should be measured. If this gradient is greater than 31 g/L (3.1 g/dL), the exudative categorization by the above criteria can be ignored because almost all such patients have a transudative pleural effusion.

If a patient has an exudative pleural effusion, the following tests on the pleural fluid should be obtained: description of the fluid, glucose level, differential cell count, microbiologic studies, and cytology.

Effusion Due to Heart Failure

The effusion occurs because the increased amounts of fluid in the lung interstitial spaces exit in part across the visceral pleura. If the effusion persists despite diuretic therapy, a diagnostic thoracentesis should be performed. A pleural fluid N-terminal pro-brain natriuretic peptide (NT-proBNP) >1500 pg/mL is virtually diagnostic of an effusion secondary to congestive heart failure.

Hepatic Hydrothorax Pleural effusions occur in ~5% of patients with cirrhosis and ascites. The predominant mechanism is the direct movement of peritoneal fluid through small openings in the diaphragm into the pleural space. The effusion is usually right-sided and frequently is large enough to produce severe dyspnea.

Parapneumonic Effusion Parapneumonic effusions are associated with bacterial pneumonia, lung abscess, or bronchiectasis and are probably the most common cause of exudative pleural effusion in the United States. Empyema refers to a grossly purulent effusion. Patients with aerobic bacterial pneumonia and pleural effusion present with an acute febrile illness consisting of chest pain, sputum production, and leukocytosis.

Patients with anaerobic infections present with a subacute illness with weight loss, a brisk leukocytosis, mild anemia, and a history of some factor that predisposes them to aspiration. The possibility of a parapneumonic effusion should be considered whenever a patient with a bacterial pneumonia is initially evaluated. The presence of free pleural fluid can be demonstrated with a lateral decubitus radiograph, computed tomography (CT) of the chest, or ultrasound.

If the free fluid separates the lung from the chest wall by >10 mm, a therapeutic thoracentesis should be performed. Factors indicating the likely need for a procedure more invasive than a thoracentesis (in increasing order of importance) include: 1:loculated pleural fluid 2:pleural fluid pH < 7.20 3:pleural fluid glucose < 3.3 mmol/L (<60 mg/dL) 4:positive Gram stain or culture of the pleural fluid 5:the presence of gross pus in the pleural space

If the fluid recurs after the initial therapeutic thoracentesis, and if any of the above characteristics are present, a repeat thoracentesis should be performed. If the fluid cannot be completely removed with the therapeutic thoracentesis, consideration should be given to inserting a chest tube and instilling a fibrinolytic (e.g., streptokinase, 250,000 units) or performing thoracoscopy with the breakdown of adhesions. Decortication should be considered when the above are ineffective.

Effusion Secondary to Malignancy The three tumors that cause ~75% of all malignant pleural effusions are lung carcinoma, breast carcinoma, and lymphoma. Most patients complain of dyspnea, which is frequently out of proportion to the size of the effusion. The pleural fluid is an exudate, and its glucose level may be reduced if the tumor burden in the pleural space is high.

The diagnosis is usually made via cytology of the pleural fluid. If the initial cytologic examination is negative, then thoracoscopy is the best next procedure if malignancy is strongly suspected. At the time of thoracoscopy, a procedure such as pleural abrasion should be performed to effect a pleurodesis. If thoracoscopy is unavailable, then needle biopsy of the pleura should be performed

Patients with a malignant pleural effusion are treated symptomatically for the most part, since the presence of the effusion indicates disseminated disease and most malignancies associated with pleural effusion are not curable with chemotherapy. The only symptom that can be attributed to the effusion itself is dyspnea. If the patient's lifestyle is compromised by dyspnea, and if the dyspnea is relieved with a therapeutic thoracentesis,

then one of the following procedures should be considered: (1)insertion of a small indwelling catheter; or (2) tube thoracostomy with the instillation of a sclerosing agent such as doxycycline, 500 mg.

Tuberculous Pleuritis Tuberculous pleural effusions are usually associated with primary TB and are thought to be due primarily to a hypersensitivity reaction to tuberculous protein in the pleural space. Patients with tuberculous pleuritis present with fever, weight loss, dyspnea, and/or pleuritic chest pain. The pleural fluid is an exudate with predominantly small lymphocytes.

The diagnosis is established by demonstrating high levels of TB markers in the pleural fluid (adenosine deaminase > 40 IU/L, interferon > 140 pg/mL, or positive polymerase chain reaction (PCR) for tuberculous DNA). Alternatively, the diagnosis can be established by culture of the pleural fluid, needle biopsy of the pleura, or thoracoscopy.

Effusion Secondary to Viral Infection Viral infections are probably responsible for a sizable percentage of undiagnosed exudative pleural effusions. In many series, no diagnosis is established for ~20% of exudative effusions, and these effusions resolve spontaneously with no long-term residua. The importance of these effusions is that one should not be too aggressive in trying to establish a diagnosis for the undiagnosed effusion, particularly if the patient is improving clinically.

Chylothorax A chylothorax occurs when the thoracic duct is disrupted and chyle accumulates in the pleural space. The most common cause of chylothorax is trauma, but it also may result from tumors in the mediastinum. Patients with chylothorax present with dyspnea, and a large pleural effusion is present on the chest radiograph. Thoracentesis reveals milky fluid, and biochemical analysis reveals a triglyceride level that exceeds 1.2 mmol/L (110 mg/dL).

Patients with chylothorax and no obvious trauma should have a lymphangiogram and a mediastinal CT scan to assess the mediastinum for lymph nodes. The treatment of choice for most chylothoraces is insertion of a chest tube plus the administration of octreotide. If these modalities fail, a pleuroperitoneal shunt should be placed unless the patient has chylous ascites. Patients with chylothoraces should not undergo prolonged tube thoracostomy with chest tube drainage because this will lead to malnutrition and immunologic incompetence.