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Identification Name Age Marital status Occupation Address : Mr. Yz : 45 years old : Married : Farmer : Desa Tampang tuah Kecamatan Pematang Sawah, Agung, Tanggamus. Sex Tribe Religion Education Height Weight : Male : Java : Islam : High school : 160 cm : 42 kg Kota


Taken from : Autoanamnesis Date Time : August 28th, 2013 : 12.00 WIB

Main symptomp Additional symptomps

: Hard to breathe : Cough, fever, night-sweat, limp, lack of appetite

I. History of Current Disease Patient came with hard to breathe complaint since 3 moths ago. He felt burndened so he could not do usual activities. Patient also complained of coughing since 3 months ago with thick sputum without blood. Patient also got fever with increased

temperature at night time combined with cold sweat. Patient lose appetite and felt weak. History of smoking detected. In a day the patients could spend up to 1 pack of cigarettes. No family members had experience the same disease. History of hypertension and diabetic is denied.

II. History of previous disease -

III. History of family disease -

B. Physical Check Up I. General Check Up Blood tension Pulse RR T Sense Nutrition Cyanosis General Edema Habitus Way patient walks Mobility : 110/70 mmHg : 94 x/minute : 38 x/minute : 36,2 Celcius degree : Compos mentis : Lack of nutrition :: Low extrimity (+/+) :: Normal : Passive

II. Psychological aspects Behaviour Natural feeling : Normal : Normal

Thought proccess : Normal

III. Generalist status Skin Lymph Head Eyes Ear Mouth Neck Chest : brown, normal temperature, dry, ikterus (-), edema of extrimity (+) : no enlargement : normal expression, facial symmetry, facial edema (-), lip cyanosis : ananemic conjuctiva, anikterik sclera, palpebra edema (-) : deafness (-), wax (-), blockage (-) : normal lips, normal tounge, normal teeth, smell breath (-) : JVP5+0 cmH20, normal thyroid gland, normal lymph gland : Normal form

Lungs Inspection front : left : normal

right: more lagged Rear : left : normal

Right : more lagged


front :


: normal tactile fremitus

right: weaken tactile fremitus rear : left : normal tactile fremitus

right: weaken tactile fremitus

Percussion front :


: resonant

right: resonant and dim in ICS IV rear : left : resonant

right: resonant and dim di ICS IV


front : left

: vescular +, rhonki -, wheezing -

right: vesicular weaken, rhonki +, wheezing -

Rear :


: vesicular +, rhonki -, wheezing -

right: vesicular weaken, rhonki +, wheezing -

Heart Inspection : Iktus cordis is not visible Palpation : Iktus cordis (+), thrill (-)

Percussion : Heart is not dilated Auscultation : HS I-II regular, murmur (-), gallop (-)

Abdomen Inspection : looks flat, symmetrical Palpation : Abdominal wall Liver Splen Kidney Percussion : timpany Auscultation : normal bowel sound : no pain when pushed : not palpable : not palpable : ballotement (-), pain when pushed (-)

Limbs Arm Right Muscle Tonus Mass Joint Movement Strength Eutrofi Normotonus Normal Normal Active 5 Left Eutrofi normotonus Normal Normal Active 5

Feet Right Muscle Joint Movement Strength Edema Wound Varices Normal Normal Active 5 + Normal Left Normal Normal Active 5 + Normal -

Reflex Right Tendon reflex Biceps Triceps Patella Achilles Cremasteric Phatologic reflex (-) Normal Normal Normal Normal Normal Normal (-) Left Normal Normal Normal Normal Normal Normal

C. Additional check up 1. Laboratory Date: 27th August, 2013

Hematology Hb ESR Leucocyte : 8,3 gr/dl : 35 mm/hour : 4900/ul (12-16 gr/dl) (0-20 mm/hour) (4500 10.700/ul)

Type calculation Basophil : 0 % Eosinophil : 1 % Rod Segment Limphocyte Monocyte : 4 % :0% : 82 % (increased) : 13 %

Blood chemistry SGOT SGPT Ureum Creatinin Gula darah sewaktu Date: August 28th, 2013 : 35 U/L : 25 U/L : 30 mg/dl : 0,7 mg/dl : 85 mg/dl (6-30 U/L) (6-45 U/L) (10-40 mg/dl) (0,7-1,3 mg/dl) (70-200 mg/dl)

Blood chemistry Protein total Albumin Globulin : 5,5 g/dl : 1,7 g/dl : 3,8 g/dl (3,5-5 g/dl) (2,3-3,5 g/dl) (2,5-1,2 g/d)

BTA Timed Morning Timed :+ :+ :+

Pleura fluid check up Macroscopic Color Clarity Microscopic Number of cells Glucosa Protein Chlorida : >1000 sel/ul : 1 mg/dl : 2 gr/ul :(720-750 mg CI/dl) (0-5 cell/ul) (50-80 mg/dl) : Brown : Feculent

PMN MN Rivalta test Ph

: 67 % : 33 % : - (negative) : 8,0

Thorax X-ray Fluid on pulmo dextra and pulmonary infiltrate

D. Work diagnostic and basic diagnostic


Work diagnostic Empiema e.c TB Paru


Basic diagnostic From anamnesis obtained, there is complaint of hard-breathe, cough, fever, and limp body. From physical lung check up, the right lung is slightly lagging, in fremitus tactile palpation, right lung is weaken. From percussion check up, there are differences in the sound from resonant to dim in ICS IV in the right lung. From auscultation,the right lung weaken. From additional check up, there is

brown feculent liquid when pleura function is done. From BTA check up +. From X ray check up, there is infiltrate and fluid in the right lung. Differential diagnosis : Pleural effusion

Recommended check up - Cytology check up

Management plan - Infusion of RL XX gtt/mnt - Infusion of plasbumin 20% 100cc - 2 RHZE / 4 HR : Rifampisin tab 450 mg (1x1 tab)

Isoniazid tab 300 mg Pirazinamid tab 500 mg Etambutol tab 500 mg - Metronidazole inf 3x1 fls - Ceftriaxone 2x1 gr

(1x1 tab) (1x2 tab) (1x2 tab)

- Salbutamol 0,5 mg / GG 1 tab / Interhistin tab / Metil prednisolon 2mg 2x1 - Paracetamol (if fever exists) - Antacid 3x1 - B complex 3x1 - Dexamethason 3x1



A. Definition TB is an airborne disease caused by the bacterium Mycobacterium tuberculosis (M. tuberculosis). M. tuberculosis and seven very closely related mycobacterial species (M. bovis, M. africanum, M. microti, M. caprae, M. pinnipedii, M. canetti and M. mungi) together comprise what is known as the M. tuberculosis complex. Most, but not all, of these species have been found to cause disease in humans. In the United States, the majority of TB cases are caused by M. tuberculosis. M. tuberculosis organisms are also called tubercle bacilli.

B. Pathophysiology Once inhaled, the infectious droplets settle throughout the airways. The majority of the bacilli are trapped in the upper parts of the airways where the mucus-secreting goblet cells exist. The mucus produced catches foreign substances, and the cilia on the surface of the cells constantly beat the mucus and its entrapped particles upward fo removal. This system provides the body with an initial physical defense that prevents infection in most persons exposed to tuberculosis. Bacteria in droplets that bypass the mucociliary system and reach the alveoli are quickly surrounded and engulfed by alveolar macrophages, the most abundant immune effector cells present in alveolar spaces. These macrophages, the next line of host defense, are part of the innate immune system and provide an opportunity for the body to destroy the invading mycobacteria and prevent infection. Macrophages are readily


available phagocytic cells that combat many pathogens without requiring previous exposure to the pathogens. Several mechanisms and macrophage receptors are involved in uptake of the mycobacteria. The mycobacterial lipoarabinomannan is a key ligand for a macrophage receptor. The

complement system also plays a role in the phagocytosis of the bacteria. The complement protein C3 binds to the cell wall and enhances recognition of the mycobacteria by macrophages. Opsonization by C3 is rapid, even in the air spaces of a host with no previous exposure to M tuberculosis. The subsequent phagocytosis by macrophages initiates a cascade of events that results in either successful control of the infection, followed by latent tuberculosis, or progression to active disease, called primary progressive tuberculosis. The outcome is essentially determined by the quality of the host defenses and the balance that occurs between host defenses and the invading mycobacteria. After being ingested by macrophages, the mycobacteria continue to multiply slowly, with bacterial cell division occurring every 25 to 32 hours. Regardless of whether the infection becomes controlled or progresses, initial development involves production of proteolytic enzymes and cytokines by macrophages in an attempt to degrade the bacteria. Released cytokines attract T lymphocytes to the site, the cells that constitute cell-mediated immunity. Macrophages then present myco - bacterial antigens on their surface to the T cells. This initial immune process continues for 2 to 12 weeks; the microorganisms continue to grow until they reach sufficient numbers to fully elicit the cell-mediated immune response, which can be detected by a skin test. For persons with intact cellmediated immunity, the next defensive step is formation of granulomas around the M tuberculosis organisms16 (Figure 1).


These nodular-type lesions form from an accumulation of activated T lymphocytes and macrophages, which creates a microenvironment that limits replication and the spread of the mycobacteria. This environment destroys macro phages and produces early solid necrosis at the center of the lesion; however, the bacilli are able to adapt to survive. In fact, M tuberculosis organisms can change their phenotypi expression, such as protein regulation, to enhance survival. By 2 or 3 weeks, the necrotic environment resembles soft cheese, often referred to caseous necrosis, and is characterized by low oxygen levels, low pH, and limited nutrients. This condition restricts further growth and establishes latency. Lesions in persons with an adequate immune system generally undergo fibrosis and calcification, successfully controlling the


infection so that the bacilli are contained in the dormant, healed lesions. Lesions in persons with less effective immune systems progress to primary progressive tuberculosis. For less immunocompetent persons, granuloma formation is initiated yet ultimately is unsuccessful in containing the bacilli. The necrotic tissue undergoes liquefaction, and the fibrous wall loses structural integrity. The semiliquid necrotic material can then drain into a bronchus or nearby blood vessel, leaving an air-filled cavity at the original site. In patients infected with M tuberculosis, droplets can be coughed up from the bronchus and infect other persons. If discharge into a vessel occurs, occurrence of extrapulmonary tuberculosis is likely. Bacilli can also drain into the lymphatic system and collect in the tracheobronchial lymph nodes of the affected lung, where the organisms can form new caseous granulomas.

C. Clinical Manifestations As the cellular processes occur, tuberculosis may develop differently in each patient, accordi status of the patients immune system. Stages include latency, primary disease, primary progressive disease, and extrapulmonary disease. Each stage has differen clinical manifestations (Table 1).

Primary Disease


Primary pulmonary tuberculosis is often asymptomatic, so that the results of diagnostic tests (Table 2) are the only evidence of the disease. Although primary disease essentially exists subclinically, some self-limiting findings might be noticed in an assessment. Associated paratracheal lymphadenopathy may occur because the bacilli spread from the lungs through the lymphatic system. If the primary lesion enlarges, pleural effusion is a distinguishing finding. This effusion develops because the bacilli infiltrate the pleural space from an adjacent area. The effusion may remain small and resolve spontaneously, or it may become large enough to induce symptoms such as fever, pleuritic chest pain, and dyspnea. Dyspnea is due to poor gas exchange in the areas of affected lung tissue. Dullness to percussion and a lack of breath sounds are physical findings indicative of pleural effusion because excess fluid has entered the pleural space.

Primary Progressive Tuberculosis Active tuberculosis develops in only 5% to 10% of persons exposed to M tuberculosis. When a patient progresses to active tuberculosis, early signs and symptoms are often nonspecific. Manifestations often include progressive fatigue, malaise, weight loss, and a low-grade fever accompanied by chills and night sweats. Wasting, a classic feature


of tuberculosis, is due to the lack of appetite and the altered metabolism associated with the inflammatory and immune responses. Wasting involves the loss of both fat and lean tissue; the decreased muscle mass contributes to the fatigue. Finger clubbing, a late sign of poor oxygenation, may occur; however, it does not indicate the extent o disease. A cough eventually develops in most patients. Although the cough may initially be nonproductive, it advances to a productive cough of purulent sputum. The sputum may also be streaked with blood. Hemopty sis can be due to destruction of apatent vessel located in the wall of the cavity, the rupture of a dilated vessel in a cavity, or the formation of an aspergilloma in an old cavity. The inflamed parenchyma may cause pleuritic chest pain. Extensive disease may lead to dyspnea or orthopnea because the increased interstitial volume leads to a decrease in lung diffusion capacity. Although many patients with active disease have few physical findings, rales may be detected over involved areas during inspiration, particularly after a cough. Hematologic studies might reveal anemia, which is the cause of the weakness and fatigue. Leukocytosis may also occur because of the large increase in the number of leukocytes, or white blood cells, in response to the infection.

D. Laboratory and Diagnostic Studies Active tuberculosis may be considered as a possible diagnosis when findings on a chest radiograph of a patient being evaluated for respiratory symptoms are abnormal, as occurs in most patients with pulmonary tuberculosis. The radiographs may show the characteristic findings of infiltrates with cavitation in the upper and middle lobes of the lungs (Figure 2).


However, specific groups of patients, such as the elderly and patients with advanced infection by human immunodeficiency virus, may not have these typical findings. Compared with other patients, both groups have the classic cavitation less often and may have lower-lobe infiltrates as a prominent finding. Although abnormal findings on a chest radiograph may suggest tuberculosis, they are not diagnostic for the disease.

Traditionally, the first laboratory test used to detect active tuberculosis in a patient with abnormal findings on chest radiographs is examination of a sputum smear for the presence of acid-fast bacilli (Table 2). Also, because the bacilli have entered the sputum, the patient is infectious to others. According to the Centers for Disease Control and Prevention,17 3 sputum specimens should be used for detection of pulmonary tuberculosis, with specimens collected in the morning on consecutive days. However, recently, investigators have questioned the need for 3 specimens. Leonard et al concluded that examination of 2 specimens is just as sensitive. For the test, sputum is smeared on a slide, stained, dried, and then treated with alcohol.


Any bacilli that are present will remain red because they will not destain. The test is not specific for tuberculosis, because other mycobacteria give the same results, but it does provide a quick method to determine if respiratory precautions should be maintained while more definitive testing is performed. Results of sputum smears should be available within 24 hours of the specimen collection.17

E. Diagnosis The Standard Definitive diagnosis of tuberculosis requires the identification of M tuberculosis in a culture of a diagnostic specimen. The most frequent sample used from a patient with a persistent and productive cough is sputum. Because most mycobacteria grow slowly, 3 to 6 weeks may be required for detectable growth on solid media. However, a newer, alternative method in which highperformance liquid chromatography is used to isolate and differentiate cell wall mycolic acids provides confirmation of the disease in 4 to 14 days. Conventionally, 3 sputum samples were also used for culture diagnosis, but the use of 2 specimens, as mentioned earlier for smears, also applies for cultures. After medications are started, the effectiveness of the therapy is assessed by obtaining sputum samples for smears. Once again, the traditional requirement of 3 sputum smears negative for M tuberculosis may be unnecessary when determining if respiratory isolation can be discontinued.26 A patient is considered to have achieved culture conversion when a culture is negative for the mycobacteria after a succession of cultures have been positive; culture conversion is the most important objective evaluation of response to treatment.

Alternatives Unfortunately, not all patients with tuberculosis can be detected by culture of sputum specimens, a situation that can lead to delayed or missed diagnosis.


Additionally, many critically ill patients have trouble producing the necessary material from the lungs and instead produce saliva or nasopharyngeal discharge. For patients who have difficulty generating sputum, inhalation of an aerosol of normal saline can be used to induce sputum for collection. However, if sputum specimens are still inadequate, or the index of suspicion for tuberculosis is still high despite cultures negative for M tuberculosis, alternative approaches are available. Bronchoscopy with bronchial washings or bronchoalveolar lavage can provide sputum for diagnosis. In bronchial washing, a fiberoptic bronchoscope is inserted into the lungs, and fluid is squirted in and then collected, essentially washing out a sample of cells and secretions from the alveolar and bronchial airspaces. Aliquots obtained from subsequent lavages constitute bronchoalveolar lavage specimens. In patients with involvement of intrathoracic lymph nodes, as indicated by adenopathy suggestive of tuberculosis, who have sputum smears negative for M tuberculosis, culture of specimens collected by transbronchial needle aspiration can be used to accurately and immediately diagnose the disease. With this technique, specimens are collected by inserting a 19-gauge flexible histology needle through a bronchoscopy tube; patients are sedated but conscious, and computed tomography scans are used for guidance. Technological Advancements Newer diagnostic techniques for faster detection of M tuberculosis include nucleic acid amplification tests. In these tests, molecular biology methods are used to amplify DNA and RNA, facilitating rapid detection of

microorganisms; the tests have been approved by the Food and Drug Administration.30 One method is the polymerase chain reaction assay, which can be used to differentiate M tuberculosis from other mycobacteria on the basis of genetic information and provides results within hours. Although the test can provide rapid confirmation of M tuberculosis in sputum specimens positive for acidfast bacilli, it has limitations, including high cost, low sensitivity, and low availability. A polymerase chain reaction assay positive


for M tuberculosis in conjunction with a sputum smear positive for the organism indicates true tuberculosis, but in a patient with a sputum smear negative for the organism, the positive polymerase chain reaction assay should be considered carefully along with clinical indicators. The results of these assays can not be relied on as the sole guide for isolation or therapy.

F. Diagnosing Latency Once patients recover from a primary M tuberculosis infection and the infection becomes latent, sputum specimens are negative for the organisms, and findings on chest radiographs are typically normal. These patients also do not have signs or symptoms of infection, and they are not infectious to others. Tuberculin skin testing is the most common method used to screen for latent M tuberculosis.1 The 1234tuberculin skin test is performed by intradermally injecting 0.1 mL of intermediate-strength purified protein derivative (PPD) that contains 5 tuberculin units. After 48 to 72 hours, the injection site is examined for induration but not redness (Figure 3, Table 3).

Although the test is useful because the PPD elicits a skin reaction via cellmediated immunity when injected in patients previously infected with mycobacteria, it is limited because it is not specific for the species of mycobacteria. Many proteins in the PPD product are highly conserved in various species of mycobacteria. Also, the test is of limited value in patients


with active tuberculosis because of its low sensitivity and specificity. Falsenegatives can occur in patients who are immunocompromised or malnourished, because these patients cannot mount an immune response to the injection, and in 20% to 25% of patients who have active tuberculosis, because there is a time lag of 2 to 10 weeks between infection and the Tlymphocyte response required for a positive skin reaction. Falsepositives can occur in patients who have infections caused by mycobacteria other than M tuberculosis or who have been given BCG vaccine.33 The tuberculin skin test was the only test available to detect latent tuberculosis until an interferonrelease assay, called QuantiFERON-TB test, was approved by the Food and Drug Administration in 2001. Then, in 2005, a new interferonassay, called QuantiFERON-TB Gold was approved and is intended to replace the QuantiFERON-TB test, which is no longer commercially available. In both tests, the cell-mediated reactivity to M tuberculosis is determined by incubating whole blood with an antigen and then using an enzymelinked immunosorbent assay to measure the amount of interferon- released from white blood cells. In the QuantiFERON-TB Gold test, 2 synthetic antigenic proteins specific in PPD are used rather than a PPD admixture, making this test more sensitive than its predecessor. QuantiFERON-TB Gold provides results in less than 24 hours and can be used to detect both active and latent tuberculosis. The results of the QuantiFERON-TB Gold test are similar to those of the tuberculin skin test, and the Centers for Disease Control and Prevention now recommend that the QuantiFERON-TB Gold test be used in all instances in which the tuberculin skin test formerly would have been used.

Management Physical measures (if possible or practical) include the following:

Isolate patients with possible TB in a private room with negative pressure Have medical staff wear high-efficiency disposable masks sufficient to filter the bacillus


Continue isolation until sputum smears are negative for 3 consecutive determinations (usually after approximately 2-4 weeks of treatment)

Initial empiric pharmacologic therapy consists of the following 4-drug regimens:

Isoniazid Rifampin Pyrazinamide Either ethambutol or streptomycin

Special considerations for drug therapy in pregnant women include the following:

In the United States, pyrazinamide is reserved for women with suspected MDR-TB

Streptomycin should not be used Preventive treatment is recommended during pregnancy Pregnant women are at increased risk for isoniazid-induced hepatotoxicity Breastfeeding can be continued during preventive therapy

Special considerations for drug therapy in children include the following:

Most children with TB can be treated with isoniazid and rifampin for 6 months, along with pyrazinamide for the first 2 months if the culture from the source case is fully susceptible.

For postnatal TB, the treatment duration may be increased to 9 or 12 months

Ethambutol is often avoided in young children

Special considerations for drug therapy in HIV-infected patients include the following:

Dose adjustments may be necessar


Rifampin must be avoided in patients receiving protease inhibitors; rifabutin may be substituted

Considerations in patients receiving antiretroviral therapy include the following:

Patients with HIV and TB may develop a paradoxical response when starting antiretroviral therapy

Starting antiretroviral therapy early (eg, < 4 weeks after the start of TB treatment) may reduce progression to AIDS and death

In patients with higher CD4+ T-cell counts, it may be reasonable to defer antiretroviral therapy until the continuation phase of TB treatment

Multidrug-resistant TB When MDR-TB is suspected, start treatment empirically before culture results become available, then modify the regimen as necessary. Never add a single new drug to a failing regimen. Administer at least 3 (preferably 4-5) of the following medications, according to drug susceptibilities:

An aminoglycoside: Streptomycin, amikacin, capreomycin, kanamycin A fluoroquinolone: Levofloxacin (best suited over the long term), ciprofloxacin, ofloxacin

A thioamide: Ethionamide, prothionamide Pyrazinamide Ethambutol Cycloserine Terizidone Para-aminosalicylic acid Rifabutin as a substitute for rifampin

Surgical resection is recommended for patients with MDR-TB whose prognosis with medical treatment is poor. Procedures include the following:

Segmentectomy (rarely used)


Lobectomy Pneumonectomy Pleurectomy for thick pleural peel (rarely indicated)


A. Overview Empyema is a collection of pus (dead cells and infected fluid) inside a body cavity. Usually, this term refers to pus inside pleural cavity, or pleural space. The pleural cavity is the thin space between the surface of lungs and the inner lining of chest wall. A cavity is a hollow space. Lungs sit inside chest cavity, just as brain rests inside skull cavity. Any fluid inside the chest cavity decreases the amount of space that lungs have to expand. In order to fill with air when breathe in, lungs must be able to fully expand. When breathe, lungs should expand smoothly and painlessly within the pleural cavity inside chest. When lungs cant expand properly, have trouble getting the oxygen you need. This causes short of breath and it may even hurt for to breathe. Because empyema is pus, and pus is caused by an infection, empyema can lead to life-threatening problems such as sepsis (bacteria in the blood) and shock. According to the American College of Chest Physicians, empyema is a potentially life-threatening medical emergency.

Description Empyema may have a number of causes but is most frequently a complication of pneumonia. Its development can be divided into three phases: an acute phase in which the body cavity fills with a thin fluid containing some pus; a second stage in which the fluid thickens and a fibrous, coagulation protein (fibrin) begins to accumulate within the cavity; and a third or chronic stage in


which the lung or other organ is encased within a thick covering of fibrous material.

B. Etiology Empyema thoracis can be caused by a number of different organisms, including bacteria, fungi, and amebas, in connection with pneumonia, chest wounds, chest surgery, lung abscesses, or a ruptured esophagus. The infective organism can get into the pleural cavity either through the bloodstream or other circulatory system, in secretions from lung tissue, or on the surfaces of surgical instruments or objects that cause open chest wounds. The most common organisms that cause empyema are the following influenzae,

bacteria Streptococcus



and Staphylococcus aureus. S. aureus is the most common cause in all age groups, accounting for 90% of cases of empyema in infants and children. Pelvic empyema in women is most often caused by Bacteroides strains or Pseudomonas aeruginosa. In elderly, chronically ill, or alcoholic patients, empyema is often caused by Klebsiella pneumoniae species of bacteria. When the disease organisms arrive in the cavity surrounding the lungs, they infect the tissues that cover the lungs and line the chest wall. As the body attempts to fight off the infection, the cavity fills up with tissue fluid, pus, and dead tissue cells. Empyema of the gall bladder or pelvis results from similar reactions to infection in those parts of the body. According to the British Medical Journal, the greatest risk factors for empyema are: pneumonia, risk factors for pneumonia, and medical procedures that invo lve the lung and its surrounding structures. Chest trauma and pre-existing lung diseases, such as COPD and lung cancer, also create an increased risk for empyema. According to Chest, people who have pre-existing lung diseases who develop empyema are more likely to die than those who do not.


Pneumonia & the Presence of Risk Factors for Pneumonia Seventy percent of empyema cases occur as a result of pneumonia. People who have difficulty swallowing, those who are immunocompromised, and those who use drugs or abuse alcohol have an increased risk for pneumonia. If you have been treated for pneumonia but didnt get better, you might have empyema.

Risk From Medical Procedures Twenty percent of empyema cases are related to medical procedures such as chest surgery and thoracentesis. Thoracentesis is a procedure that involves using needles and tubes to drain fluid from the pleural space. Medical instruments can transfer bacteria into pleural cavity.

C. Classification According to the medical journal Chest, there are two classes of empyema: simple and complex.

1. Simple Empyema Simple empyema is seen early in the course of the illness. In simple empyema, pus is present, but it is free flowing. Treatment at the simple stage is best, because the pleural cavity can easily be drained.

2. Complex Empyema In complex empyema, the inflammation is more severe. The longer have empyema that is left untreated, the greater the chance that you will develop complex empyema. In cases of severe inflammation, your body forms lots of scar tissue in the pleural space. Formation of scar tissue causes the cavity to become divided into multiple, smaller cavities. This is called loculation.


Loculation creates complications, because infected areas that have been walled off can be difficult to drain. Complete drainage of pus from the pleural cavity is essential for treatment.

D. Symptoms The signs and symptoms of empyema vary somewhat according to the location of the infection and its severity. In empyema thoracis, patients usually exhibit symptoms of pneumonia, including fever, cough, fatigue, shortness of breath, and chest pain. They may prefer to lie on the side of the body affected by the empyema. Family members may notice bad breath. In severe cases, the patient may become dehydrated, cough up blood or greenishbrown sputum, run a fever as high as 105F (40.6C), or fall into a coma. Patients with thoracic empyema may develop potentially life-threatening complications if the condition is not treated. The infected tissues may develop large collections of pus (abscesses) that can rupture into the patient's airway, or the infection may spread to the tissues surrounding the heart. In extreme cases the empyema may spread to the brain by means of bacteria carried in the bloodstream. In pelvic empyema, the infection produces large amounts of thick, foulsmelling pus that is rapidly replaced even after drainage. Empyema of the gallbladder is marked by intense pain on the upper right side of the abdomen, high fever, and rigidity of the muscles over the infected area.

E. Diagnosis A physician may consider the possibility of empyema thoracis in patients with pneumonia or other symptoms of lung infection. When listening to sounds within the patient's chest with a stethoscope, the sounds of breathing will be partly muffled and harder to hear in the patients with empyema. The area of the chest over the infection will sound dull when tapped or thumped (percussed). On an x ray, empyema thoracis will appear as a cloudy or opaque


area. The amount of fluid present in the pleural cavity can be estimated using an ultrasound imaging procedure. The diagnosis of empyema, however, has to be confirmed with laboratory tests because its symptoms can be caused by other disease conditions. The diagnosis of empyema is usually confirmed by analyzing a sample of fluid taken from the pleural cavity. The sample is obtained by a procedure called thoracentesis. In this procedure, the patient is given a local anesthetic, a needle is inserted into the pleural cavity through the back between the ribs on the infected side, and a sample of fluid is withdrawn. If the patient has empyema, there will be a very high level of one particular kind of immune cell (white blood cells), a high level of protein, and a very low level of blood sugar. The fluid can also be tested for the specific disease organism by staining or tissue cultures. In some cases, the color, smell, or consistency of the tissue fluid also helps to confirm the diagnosis.

Radiographic features Free-flowing pleural fluid collects in the dependent portion of the pleural space. On 2-view chest radiographs, pleural fluid obscures the costophrenic angle (as in the image below). Approximately 75 mL of fluid is required to blunt the posterior costophrenic angle on a lateral chest radiograph. Almost 200 mL of fluid is required to blunt the lateral costophrenic angles on frontal radiographs. If loculations have formed, fluid opacity may be seen in a nondependent area. The configuration of loculated fluid bulging out from the chest wall is a classically described but infrequently observed finding.


Posteroanterior (PA) chest radiograph of a man in his 50s who had a 2-week history of partially treated pneumonia. He presented with persistent fever and chest pain. The patchy bilateral lung parenchymal opacities indicate pneumonia. The obliterated left costophrenic angle suggests a left pleural effusion.

Although supine or semierect radiographs do not show pleural effusion as well as upright 2-view chest radiographs do, an ill patient is often unable to stand. A unilateral free-flowing effusion results in increased hazy opacity on the side of the affected hemithorax. If a pleural effusion is suspected, bilateral decubitus views are recommended. When an effusion is identified, the width of the layering fluid may be measured. If the width of the fluid is < 10 mm, the effusion may be managed medically and followed up with serial radiographs. However, if the effusion is wider than 10 mm, thoracentesis or catheter drainage should be performed, if clinically indicated. CT or ultrasonographic guidance is best for placing a pleural catheter for drainage

F. Treatment Empyema is treated using a combination of medications and surgical techniques. Treatment with medication involves intravenously administering a two-week course of antibiotics. It is important to give antibiotics as soon as


possible to prevent first-stage empyema from progressing to its later stages. The antibiotics most commonly used are penicillins with beta-lactamase (ampicillin/sulbactacm), cephalosporins (cefuroxime sodium), and flagyl (metronidazole). Clindamycin can be used for patients who are allergic to penicillin.

A chest tube is used to drain pus from the pleural space and allow the lungs to expand normally. Fluids lost, due to lack of appetite and fever, are replaced, and medications such as acetaminophen (Tylenol) can be used to bring down the fever and relieve discomfort. Patients experiencing difficulty breathing are also given oxygen therapy. Surgical treatment of empyema has two goals: drainage of the infected fluid and closing up of the space left in the pleural cavity. If the infection is still in its early stages, the fluid can be drained by thoracentesis. In second-stage empyema, the surgeon will insert a chest tube in the patient's rib cage or remove part of a rib (rib resection) in order to drain the fluid. In third-stage empyema, the surgeon may cut or peel away the thick fibrous layer coating the lung. This procedure is called decortication. When the fibrous covering is removed, the lung will expand to fill the space in the chest cavity. The doctor can use video-assisted thoracic surgery (VATS) techniques to position the chest tube or to perform a limited decortication. The VATS technique allows a physician to see within the body during certain surgical procedures. Empyema of the gallbladder is a serious condition that is treated with intravenous antibiotics and surgical removal of the gallbladder.

G. Prognosis The prognosis for recovery is generally good, except in those cases with complications, such as a brain abscess or bloodpoisoning, or cases caused by certain types of streptococci.



Broaddus VC, Light RW. Pleural effusion. In: Mason RJ, Broaddus VC, Martin TR, et al, eds. Murray and Nadel's Textbook of Respiratory Medicine. 5th ed. Philadelphia, PA: Elsevier Saunders; 2010:chap 68.

Calahan, F. J. (2008, Jan. 21). Acute empyema. Australian and New Zealand Journal of Surgery. Volume 10, Issue 4, pages 374379, April 1941. Retrieved May 7, 2012,

from http://onlinelibrary.wiley.com/doi/10.1111/j.14452197.1941.tb07153.x/abstract

Empyema, history and examination. (2011, Dec. 12). British Medical Journal Group. Retrieved May 7, 2012, from http://bestpractice.bmj.com/bestpractice/monograph/1008/diagnosis/history-and-examination.html

Empyema, treatment options. (2011, Dec. 12). British Medical Journal Group. Retrieved May 7, 2012, from http://bestpractice.bmj.com/bestpractice/monograph/1008/treatment/details.html

LeMense, G. P., Strange, C. and Sahn, S. A. (1995). Empyema thoracis: Therapeutic management and outcome. Chest. 107; 1532-1537. Retrieved May 7, 2012,

from http://chestjournal.chestpubs.org/content/107/6/1532.full.pdf

Light, R. W., (1995). A new classification of parapneumonic effusions and empyema. Chest. 108.2.299. Retrieved May 7, 2012, from


McCool FD. Diseases of the diaphragm, chest wall, pleura, and mediastinum. In: Goldman L, Schafer AI, eds.Goldman's Cecil Medicine. 24th ed. Philadelphia, PA: Elsevier Saunders; 2011:chap 99.

Stauffer, John L. "Lung." In Current Medical Diagnosis and Treatment, 1998, edited by Stephen McPhee, et al., 37th ed. Stamford: Appleton & Lange, 1997.


Kurbatova EV, Cavanaugh JS, Dalton T, Click E, Cegielski JP. Epidemiology of pyrazinamide-resistant tuberculosis in the United States, 1999-2009. Clin Infect Dis. Jul 9 2013

Boggs W. Increasing Prevalence of Pyrazinamide-Resistant Tuberculosis. Medscape [serial online]. Available

at http://www.medscape.com/viewarticle/808192. Accessed July 29, 2013.

[Guideline] Treatment of tuberculosis. MMWR Recomm Rep. Jun 20 2003;52:1-77.

Swaminathan S, Narendran G, Venkatesan P, Iliayas S, Santhanakrishnan R, Menon PA, et al. Efficacy of a 6-month versus 9-month intermittent treatment regimen in HIV-infected patients with tuberculosis: a randomized clinical trial. Am J Respir Crit Care Med. Apr 1 2010;181(7):743-51.

Centers for Disease Control and Prevention. Managing Drug Interactions in the Treatment of HIV-Related Tuberculosis. CDC. Available

at http://www.cdc.gov/tb/TB_HIV_Drugs/default.htm. Accessed 08/20/2008.

[Best Evidence] Abdool Karim SS, Naidoo K, Grobler A, Padayatchi N, Baxter C, Gray A, et al. Timing of initiation of antiretroviral drugs during tuberculosis therapy. N Engl J Med. Feb 25 2010;362(8):697-706.[Medline].

Trk ME, Farrar JJ. When to start antiretroviral therapy in HIV-associated tuberculosis. N Engl J Med. Oct 20 2011;365(16):1538-40.

Targeted tuberculin testing and treatment of latent tuberculosis infection. American Thoracic Society.MMWR Recomm Rep. Jun 9 2000;49:1-51.

CDC. Recommendations for use of an isoniazid-rifapentine regimen with direct observation to treat latent Mycobacterium tuberculosis infection. MMWR. 2011;60:1650-1653.

Extensively Drug-Resistant Tuberculosis (XDR TB). Centers for Disease Control and Prevention. Available Accessed

at http://www.cdc.gov/tb/publications/factsheets/drtb/xdrtb.htm. November 7, 2012.


Asensio JA, Arbus A, Prez E, Gicquel B, Martin C. Live tuberculosis vaccines based on phoP mutants: a step towards clinical trials. Expert Opin Biol Ther. Feb 2008;8(2):201-11.

Wells CD, Cegielski JP, Nelson LJ, Laserson KF, Holtz TH, Finlay A, et al. HIV infection and multidrug-resistant tuberculosis: the perfect storm. J Infect Dis. Aug 15 2007;196 Suppl 1:S86-107.

[Best Evidence] Burman WJ, Goldberg S, Johnson JL, Muzanye G, Engle M, Mosher AW, et al. Moxifloxacin versus ethambutol in the first 2 months of treatment for pulmonary tuberculosis. Am J Respir Crit Care Med. Aug 1 2006;174(3):331-8.








Available Accessed

athttp://www.who.int/mediacentre/factsheets/fs104/en/index.html. October 13, 2010.








recommendations of the Federal Tuberculosis Task Force. MMWR Recomm Rep. Feb 13 2009;58:1-43.






Available Accessed

athttp://www.who.int/tb/challenges/mdr/tdrfaqs/en/index.html. November 26, 2012.

Mlambo CK, Warren RM, Poswa X, Victor TC, Duse AG, Marais E. Genotypic diversity of extensively drug-resistant tuberculosis (XDR-TB) in South Africa. Int J Tuberc Lung Dis. Jan 2008;12(1):99-104.

World Health Organization. Antituberculosis drug resistance in the world. The WHO/IUATLD global project on anti-tuberculosis drug resistance surveillance WHO. Geneva. 2008;1-120.









athttp://www.cdc.gov/mmwr/preview/mmwrhtml/mm6111a2.htm?s_cid=mm 6111a2_w.

Sokolove PE, Lee BS, Krawczyk JA, Banos PT, Gregson AL, Boyce DM, et al. Implementation of an emergency department triage procedure for the


detection and isolation of patients with active pulmonary tuberculosis. Ann Emerg Med. Apr 2000;35(4):327-36.

Moran GJ, McCabe F, Morgan MT, Talan DA. Delayed recognition and infection control for tuberculosis patients in the emergency department. Ann Emerg Med. Sep 1995;26(3):290-5.

Menzies D, Joshi R, Pai M. Risk of tuberculosis infection and disease associated with work in health care settings. Int J Tuberc Lung Dis. Jun 2007;11(6):593-605.

Verhagen LM, van den Hof S, van Deutekom H, Hermans PW, Kremer K, Borgdorff MW, et al. Mycobacterial factors relevant for transmission of tuberculosis. J Infect Dis. May 2011;203(9):1249-55.

Leung CC, Lam TH, Chan WM, Yew WW, Ho KS, Leung G, et al. Lower risk of tuberculosis in obesity.Arch Intern Med. Jun 25 2007;167(12):1297304.

Slama K, Chiang CY, Enarson DA, Hassmiller K, Fanning A, Gupta P, et al. Tobacco and tuberculosis: a qualitative systematic review and metaanalysis. Int J Tuberc Lung Dis. Oct 2007;11(10):1049-61.

Keane J, Gershon S, Wise RP, Mirabile-Levens E, Kasznica J, Schwieterman WD, et al. Tuberculosis associated with infliximab, a tumor necrosis factor alpha-neutralizing agent. N Engl J Med. Oct 11 2001;345(15):1098-104.

Brassard P, Suissa S, Kezouh A, Ernst P. Inhaled Corticosteroids and Risk of Tuberculosis in Patients with Respiratory Diseases. Am J Respir Crit Care Med. Oct 1 2010

Bellamy R, Ruwende C, Corrah T, McAdam KP, Whittle HC, Hill AV. Variations in the NRAMP1 gene and susceptibility to tuberculosis in West Africans. N Engl J Med. Mar 5 1998;338(10):640-4.

Cervino AC, Lakiss S, Sow O, Hill AV. Allelic association between the NRAMP1 gene and susceptibility to tuberculosis in Guinea-Conakry. Ann Hum Genet. Nov 2000;64:507-12.


Searle S, Blackwell JM. Evidence for a functional repeat polymorphism in the promoter of the human NRAMP1 gene that correlates with autoimmune versus infectious disease susceptibility. J Med Genet. Apr 1999;36(4):295-9.

Tosh K, Campbell SJ, Fielding K, Sillah J, Bah B, Gustafson P, et al. Variants in the SP110 gene are associated with genetic susceptibility to tuberculosis in West Africa. Proc Natl Acad Sci U S A. Jul 5 2006;103(27):10364-8.

Khor CC, Vannberg FO, Chapman SJ, Guo H, Wong SH, Walley AJ, et al. CISH and susceptibility to infectious diseases. N Engl J Med. Jun 3 2010;362(22):2092-101.

Intemann CD, Thye T, Niemann S, Browne EN, et al. Autophagy gene variant IRGM -261T contributes to protection from tuberculosis caused by Mycobacterium tuberculosis but not by M. africanum strains. PLoS Pathog. Sep 2009;5(9):e1000577.

Rossouw M, Nel HJ, Cooke GS, van Helden PD, Hoal EG. Association between tuberculosis and a polymorphic NFkappaB binding site in the interferon gamma gene. Lancet. May 31 2003;361(9372):1871-2

Levin M, Newport MJ, D'Souza S, Kalabalikis P, Brown IN, Lenicker HM, et al. Familial disseminated atypical mycobacterial infection in childhood: a human mycobacterial susceptibility gene?. Lancet. Jan 14 1995;345(8942):7983.

Newport MJ, Huxley CM, Huston S, Hawrylowicz CM, Oostra BA, Williamson R, et al. A mutation in the interferon-gamma-receptor gene and susceptibility to mycobacterial infection. N Engl J Med. Dec 26 1996;335(26):1941-9.

Khor CC, Chapman SJ, Vannberg FO, Dunne A, Murphy C, Ling EY, et al. A Mal functional variant is associated with protection against invasive pneumococcal disease, bacteremia, malaria and tuberculosis.Nat Genet. Apr 2007;39(4):523-8.


Barreiro LB, Neyrolles O, Babb CL, Tailleux L, Quach H, McElreavey K, et al. Promoter variation in the DC-SIGN-encoding gene CD209 is associated with tuberculosis. PLoS Med. Feb 2006;3(2):e20.

CDC. Tuberculosis (TB). Data and Statistics. Available at http://www.cdc.gov/tb/statistics/default.htm. Accessed June 7, 2012.

WHO. Global tuberulosis control 2008: surveillance, planning, financing. World Health Organization. Available at http://www.who.int/topics/tuberculosis/en/. Accessed October 13, 2010.

Cox HS, Morrow M, Deutschmann PW. Long term efficacy of DOTS regimens for tuberculosis: systematic review. BMJ. Mar 1 2008;336(7642):484-7.

Jasmer RM, Bozeman L, Schwartzman K, Cave MD, Saukkonen JJ, Metchock B, et al. Recurrent tuberculosis in the United States and Canada: relapse or reinfection?. Am J Respir Crit Care Med. Dec 15 2004;170(12):1360-6.

van Rie A, Warren R, Richardson M, Victor TC, Gie RP, Enarson DA, et al. Exogenous reinfection as a cause of recurrent tuberculosis after curative treatment. N Engl J Med. Oct 14 1999;341(16):1174-9.

Waitt CJ, Peter K Banda N, White SA, Kampmann B, Kumwenda J, Heyderman RS, et al. Early deaths during tuberculosis treatment are associated with depressed innate responses, bacterial infection, and tuberculosis progression. J Infect Dis. Aug 2011;204(3):358-62.

Mazurek GH, Jereb J, Lobue P, Iademarco MF, Metchock B, Vernon A. Guidelines for using the QuantiFERON-TB Gold test for detecting Mycobacterium tuberculosis infection, United States. MMWR Recomm Rep. Dec 16 2005;54:49-55.