Case Report:

Massive Left-Sided Pleural Effusion and Normocytic Normochromic Anemia

A. Medical Data A 37 year lady was admitted to Ulin Hospital on March 4, 2013. She presented with shortness of breath and left chest pain. The complain reduced by a change of position; into left side and sitting position. The onset was a week before hospitalized, and it increased day to day. The breath did not correlate with activity and time (i.e. at night). The chest pain did not spread to any location. She denied palpitation, vomit, and epigastric pain. She never had the same complain before. She had dull chest trauma history 6 months before hospitalized because of traffic accidents. Therefore, she had hematoma on her chest and it disappeared 2 month after. The past history reported no dyspepsia syndrome, heart attack, or bronchial asthma. The family history never had the same complain. She also presented dry nonproductive cough for 2 days. The onset was acute. She denied blood cough or reddish sputum. She had no contact to cough sufferers. She denied history of fever, snoring, wheeze or weight loss. She denied sweating at night. She was not a cigarette smoker, but had contacted to pesticide for many years. She presented bleeding gum since 3 days before hospitalized. The blood covered sterile cotton for 1 hour. Bleeding stopped by deep pressure. The source of bleeding was from teeth leave at molar I. She was intense weakness since 3 days ago. She sometimes felt dizziness. She had not loss of appetite. Her nutrition was good. She denied epistaxis, bleeding vomit, defecation and urination. She did not take any 1

supplement, medication and alcohol. At that time, she was not menstruating. She got normally menstrual cycle; it was 7 days a month. She had no contraceptives. She was not known diabetic or hypertensive. In past history, she never got the same symptom. She denied prolong bleeding before. From family history, the same symptom, history of blood disorder was not reported. On physical examination, generally she was looked like moderate weakness. Her nutrition was normally. She was compos mentis. Blood pressure 130/90 mm of Hg, pulse rate 93/min, respiratory rate 36/min, temperature 36.6oC General survey revealed pale; skin was pale and cold, the conjunctiva and lip were pale. No bleeding nose. The bleeding gum was found at molar I. No jugular venous distention and peripheral lymphadenopathy. Respiratory system findings were consistent with left sided massive pleural effusion; reduced tactile fremitus, dullness on percussion and reduced breath sounds. Examination of heart was regular rhythm, no pathologic sign, no murmurs. The abdomen, extremity, and nervous system was unremarkable. Other systems were essentially normal. Routine blood examination showed Hb 8.6g%, WBC 6,900/ul, Erythrocytes 3.12 million/ul, platelet 248,000/ul, Ht 26.8 vol%, MCV 86.1 fl, MCHC 32.0%. Routine blood biochemistry revealed random blood glucose 129 mg/dl, urea 18 mg/dl, creatinine 0.7 mg/dl, SGOT 11 IU/l, SGPT 9 IU/l. X-ray chest PA view showed homogenous opacity appearance on left hemithorax with mediastinal shift towards opposite side. Cardiac, left costofrenicus angle, and cardiofrenicus angle appearance were not visible. It revealed left sided massive pleural effusion.

Picture 1. Pleural effusion appearance from AP CXR

From emergency unit, the pharmacology treatment was given. She got intravenous Ringer Lactate (RL), tranexamic acid injection 2x500 mg, Novalgin injection 3x1 ampul, and Gastrofer injection 2x1 ampul. She was hospitalized to recovery her condition. On March 6, 2013 (2 day care) she got packed red cells (PRC) transfusion about 2 kolf. After that, the hemoglobin level was increased. Hb 10.6 g/%, WBC 6,700/ul, Erythrocytes 40.8 milion/ul, Ht 33.5 vol%, platelet 254,000/ul, MCV 82.1, MCH 25.7, MCHC 31.3.. Generally, her condition was better. Tumor marker was checked. LDH 405, CEA 0.75. On March 8, 2013 (4 day care), based on the chest radiograph, an intercostal tube was inserted in left 5th intercostal space in the mid axillary line. Hemorrhagic pleural fluid was aspirated. It was about 2750 ml. The patient felt better than before insertion of intercostals tube. From cytology examination, 3

pleural fluid showed presence of nonspecific massive inflammatory. Pleural fluid did not show presence of malignant cells.

Picture 2. Massive Hemorrhagic Pleural Fluid The intercostals tube was inserted for a week. On March 14, 2013 (8 day care), the chest radiograph showed decreasing of pleural effusion.

Picture 3. Decreasing of pleural effusion

On March 22, 2013, the chest radiograph showed recurrent massive pleural effusion.

Picture 4. Recurrent massive pleural effusion The physician planned her to take thoracic CT scan and gynecology USG for searching source of malignancy. But, unfortunately, the tools were failed and cant use at the time. Follow up studies were performed to determine the etiology of pleural effusion. At least, in this case we didnt find it.

B. Base Data Resume A 37 year lady presented with shortness of breath and left chest pain. It reduced by a change of position; into left side and sitting position. She also presented acute onset of dry nonproductive cough, and bleeding gum with intense weakness since 3 days ago. She denied history of fever, wheeze or weight loss. She had dull chest trauma history 6 months before. She was not known diabetic or hypertensive. She was not a cigarette smoker, but had contacted to pesticide for many years. On physical examination, general survey revealed mild pale, conjunctiva and lip were pale, blood pressure 130/90 mm of Hg, pulse rate 93/min, respiratory rate 36/min, temperature 36.6 oC , bleeding gum at molar I, no jugular venous distention, peripheral lymphadenopathy. Respiratory system findings were consistent with reduced tactile fremitus, dullness on percussion and reduced breath sounds. Examination of heart, chest, abdomen, nervous system, and other systems were unremarkable. Other systems were essentially normal. Routine blood examination showed Hb 8.6 g%, WBC 6,900/ul, Erythrocytes 3.12 million/ul, platelet 248,000/ul, Ht 26.8 vol%, MCV 86.1 fl, MCHC 32.0%. Routine blood biochemistry revealed random blood glucose-129 mg/dl, urea-18 mg/dl, creatinine-0.7 mg/dl, SGOT-11 IU/l, SGPT-9 IU/l. X-ray chest AP view showed left sided massive pleural effusion with mediastinal shift towards opposite side. an intercostal tube was inserted in left 5th intercostal space in the mid axillary line. Hemorrhagic pleural fluid was aspirated. It was about 2750 ml. From cytology examination, pleural fluid 6

showed presence of nonspecific massive inflammatory. Pleural fluid did not show presence of malignant cells.

C. Problem List Based on the data above, in this case we find two problems. They are: 1) Massive Left-Sided Pleural Effusion 2) Normocytic normochromic anemia et causa blood loss

D. Primary Planning

No 1.

Problem Massive Left-sided Pleural Effusion

Planning Diagnosis

Planning Treatment i.

Planning monitor Sign and symptom of pleural effusion CXR

Planning Education

a. CT Scan 1) O2 nasal 2-4 Thoracic lpm b. USG gynecologic 2) Thoracocent esis

ii. c. Pleural fluid 3) Pleuorodesis analysis 2 Normocytic Normochro mic Anemia a. Reticulocyt 1) PRC count transfusion 2 kolf b. Perifer Blood 2) Injection Slide Tranexamic acid 3x500 mg

i.Sign and Nutrition symptom of intake anemia ii.Routine Blood Examination

E. Discussion Based on the data, a diagnosis of massive left-sided pleural effusion and normocytic normochromic anemia were made. A pleural effusion is an abnormal collection of fluid in the pleural space resulting from excess fluid production or decreased absorption.1 Anemia is strictly defined as a decrease in red blood cell (RBC) mass. The function of the RBC is to deliver oxygen from the lungs to the tissues and carbon dioxide from the tissues to the lungs.2 In a normochromic normocytic anemia, the red cells are of normal size and contain the normal amount of hemoglobin but there is a reduction in number.3 1. Pleural Effusion In this case, the patient complained shortness of breath or dyspnea. The pathogenesis of dyspnea caused by a large pleural effusion has not been clearly elucidated, but several factors may be involved, including a decrease in the compliance of the chest wall, contralateral shifting of the mediastinum, a decrease in the ipsilateral lung volume, and reflex stimulation from the lungs and chest wall. 4 The patient also presented cough and left chest pain. Patients with pleural effusions usually have dyspnea, cough, and occasional sharp non radiating chest pain that is often pleuritic.5 The patient also presented cough and left chest pain. Patients with pleural effusions usually have dyspnea, cough, and occasional sharp non radiating chest pain that is often pleuritic.5 The symptoms depend on the amount of fluid and the underlying cause. Many patients have no symptoms at the time a pleural effusion 8

is discovered. Possible symptoms include pleuritic chest pain, dyspnea, and dry nonproductive cough.6 The clinical history and physical examination can be quite helpful in indicating appropriate investigation. A history of cardiac, renal, or liver impairment can suggest a transudative effusion. A history of cancer can be suggestive of a malignant pleural effusion. Recent leg swelling or deep-vein thrombosis may result in an effusion related to pulmonary embolism. A history of recent or current pneumonia suggests a para pneumonic effusion, either complicated (empyema) or uncomplicated. Previous trauma may result in hemothorax or chylothorax.
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From anamnesis, patient had history of dull chest

trauma 6 months ago. But many data we found didnt support to conclude trauma was the etiology of pleural effusion because the accident had been 6 months before. Exactly, it should be acute pleural effusion if trauma result hemothorax. Patient was contacted to pesticide for many years. Previous exposure to asbestos is common in patients who have a benign effusion related to the exposure or have mesothelioma. Recent esophageal dilatation or endoscopy can result in esophageal rupture. Certain medications, including amiodarone, methotrexate, phenytoin, and nitrofurantoin, can cause pleural effusions. Rheumatoid arthritis and other autoimmune conditions can also result in effusions.5 In this case, we didnt know content of pesticide. Physical findings are reduced tactile fremitus, dullness on percussion, and diminished or absent breath sounds. A pleural rub may also be heard during late inspiration when the roughened pleural surfaces come together.6 9

Accumulation of pleural fluid produces a restrictive ventilator defect and decreases total lung capacity, functional capacity, and forced vital capacity. It may cause ventilation-perfusion mismatches due to partially atelectatic lungs in dependent areas and, if large enough, may compromise cardiac output by causing ventricular diastolic collapse.6 From CXR, we found massive left-sided pleural effusion. Accumulation of effusion volume can give clinical symptoms and they were detected from clinical examination and radiological. A number of the volume can make clinical pattern. Based on the volume effusion from PA chest radiograph pleural effusion was divided into light effusion, moderate effusion, larger or massive effusion (one sided hemithorax).7 Although the classification was based on chest X-ray can be not correlate to the severity of clinical especially if the effusion volume >500 ml. It was simply done by classifying the pleural effusion into two groups: non-larger groups (Slight and moderate) if the effusion volume is less than two-thirds hemithorax and large groups (larger and massive) if more than two-thirds the volume of hemithorax effusion and more frequently mentioned by term massive pleural effusion.7 Standard posteroanterior and lateral chest radiography remains the most important technique for the initial diagnosis of pleural effusion. Free pleural fluid flows to the most dependent part of the pleural space.6

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Lateral decubitus radiography is extremely valuable in the evaluation of a subpulmonic effusion. It is very sensitive, detecting effusions as small as 5 ml in experimental studies, and should be a routine test.6 On supine chest radiography, commonly used in intensive care, moderate to large pleural effusions may escape detection because the pleural fluid settles to the back, and no change in the diaphragm or lateral pleural edges may be noted. In these cases, a pleural effusion must be suspected when there is increased opacity of the hemithorax without obscuring of the vascular markings. If an effusion is suspected, lateral decubitus radiography or ultrasonography should be ordered, since both are more reliable for detecting small.6 Chest radiographs can also provide important clues to the cause of an effusion. Bilateral effusions accompanied by cardiomegaly are usually caused by congestive heart failure. Large unilateral effusions without contralateral mediastinal shift suggest a large atelectasis, infiltration of the lung with tumor, a mesothelioma, or a fixed mediastinum due to tumor or fibrosis.6 For a unilateral pleural effusion evident on chest radiographs, the differential diagnosis is extensive. The differential diagnosis for bilateral pleural effusions is narrower and includes causes of transudative effusions, such as cardiac, hepatic, and renal failure and hypoalbuminemia, and in rare cases, malignant neoplasm, pulmonary embolism, and rheumatoid arthritis.6

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Table 1. Caused of Transudation and Exudation Unilateral Pleural Effusion

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Diagnostic thoracentesis is required only if a patient has bilateral effusions that are unequal in size, has an effusion that does not respond to therapy, has pleuritic chest pain, or is febrile. The effusions usually improve quite quickly once diuretic therapy is started.5 Intrathoracic neoplasms, trauma, bleeding diathesis or tuberculosis may cause hemorrhagic pleural effusion as well. The postulated pathogenic mechanisms for hemorrhagic effusions include trans-diaphragmatic transfer of fluid via lymphatics, diaphragmatic perforation of pseudocyst and mediastinal extension.8 Hemorrhagic pleural fluid was aspirated. It was about 2750 ml. From cytology examination, pleural fluid showed presence of nonspecific massive inflammatory. Pleural fluid did not show presence of malignant cells. Fluid accumulation in the pleural space indicates disease. The accumulation is associated with many medical conditions that predispose to fluid accumulation via many different mechanisms, including increased pulmonary capillary pressure, decreased oncotic pressure, increased pleural membrane permeability, and obstruction of lymphatic flow.5 Pleural fluid is formed and removed slowly, at an equivalent rate, and has a lower protein concentration than lung and peripheral lymph. It can accumulate by one or more of the following mechanisms: 6 a) Increased hydrostatic pressure in the microvascular circulation: clinical data suggest that an elevation in capillary wedge pressure is the most important determinant in the development of pleural effusion in congestive heart failure. 13

b) Decreased oncotic pressure in the microvascular circulation due to hypoalbuminemia, which increases the tendency to form pleural interstitial fluid. c) Increased negative pressure in the pleural space, also increasing the tendency for pleural fluid formation; this can happen with a large atelectasis. d) Separation of the pleural surfaces, which could decrease the movement of fluid inthe pleural space and inhibit pleural lymphatic drainage; this can happen with a trapped lung. e) Increased permeability of the microvascular circulation due to inflammatory mediators, which would allow more fluid and protein to leak across the lung and visceral surface into pleural space; this has been documented with infections such as pneumonia. f) Impaired lymphatic drainage from the pleural surface due to blockage by tumor or fibrosis. g) Movement of ascitic fluid from the peritoneal space through either diaphragmatic lymphatics or diaphragmatic defects. A Variety of disease states are associated with the development of pleural effusions, which sometimes makes the differential diagnosis problematic. Pleural effusion can be classified into two categories, transudative and exudative, based on the characteristics of the pleural fluid. While transudative effusions are the result of changes in hydrostatic or oncotic pressure with no pathological change in the structure of the pleural membrane or condition of the vascular wall.

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Exudative effusions collect in the pleural cavity as a result of pathological changes or structural breakdown of the pleura.9

Table 2. Criteria for Classification of Exudates and Transudate 6

If a pleural effusion is likely to be a transudate, initial laboratory tests can be limited to levels of protein, cholesterol, and lactate dehydrogenase in the pleural fluid These tests could be an alternative to all the measurements required by Lights criteria. If the effusion is exudative, further studies should be undertaken to establish a diagnosis provides an initial diagnostic algorithm for pleural effusion.6

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Picture 5. Approach to Pleural Effusion 6

Picture 6. Definitive Diagnosis Based On Pleural Fluid Analysis6

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Cytology is positive in approximately 60 percent of malignant pleural effusions. Negative test results are related to factors such as the type of tumor (e.g., commonly negative with mesothelioma, sarcoma, and lymphoma); the tumor burden in the pleural space; and the expertise of the cytologist.1

If the aspirated pleural fluid during thoracentesis is bloody, especially in a large size effusion, this has led to the conventional knowledge that a hemorrhagic pleural effusion most commonly suggests one of the three following diagnoses: malignant disease, trauma or pulmonary embolization. Less frequent diagnoses for a hemorrhagic pleural effusion may include pneumonia, hematologic disorders or endomitriosis.10

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Therapeutic thoracentesis should be performed in virtuallyall dyspneic patients with malignant pleural effusions to determine its effect on breathlessness and rate and degree of recurrence. In some dyspneic patients with a large effusion and contralateral mediastinal shift, some clinicians may choose to proceed directly to chest tube drainage and chemical pleurodesis or thoracoscopy with talc poudrage. Rapid recurrence of the effusion dictates the need for immediate treatment; stability and absence of symptoms may warrant observation. If dyspnea is not relieved by thoracentesis, other causes should be investigated, such as lymphangitic carcinomatosis, atelectasis,

thromboembolism, and tumor embolism.4 Thoracentesis is urgent when it is suspected that blood (i.e., hemothorax) or pus (i.e. empyema) is in the pleural space, because immediate tube thoracostomy is indicated in these situations.1 Thoracentesis can be performed on almost any patient with a pleural effusion. There are no absolute contraindications. Relative contraindications include a bleeding diathesis, systemic anticoagulation, a small volume of pleural fluid, mechanical ventilation, inability of the patient to cooperate, and cutaneous disease such as herpes zoster infection at the needle entry site.11 The volume of fluid that can be safely removed from the pleural space during a therapeutic thoracocentesis is unknown. Ideally, monitoring of pleural fluid pressure during the procedure should determine that volume. If pleural fluid pressure does not decrease below 20 cm H2O, fluid removal usually can be continued safely. As most clinicians do not measure pleural pressure during 18

therapeutic thoracentesis, we recommend removal of only 11.5 L of fluid at one sitting, as long as the patient does not develop dyspnea, chest pain, or severe cough.4 Pleurodesis is sticking process between visceral and parietal pleural chemically, by using mineral or mechanical, permanently to prevent the accumulation of fluid or the air in the cavity pleura. Chemical pleurodesis is accepted palliative therapy for patients with recurrent, symptomatic malignant pleural effusions. Various chemicals have been used in an attempt to produce pleurodesis. For many years, tetracycline was the sclerosing agent of choice. However, when it became commercially unavailable, alternative agents were investigated. Doxycycline, a tetracycline analog, has been recommended as a replacement for tetracycline. Although there are no direct studies comparing doxycycline with tetracycline, pleurodesis studies have demonstrated clinical success rates with doxycycline that are similar to those with tetracycline (historical data), with a success rate of up to 8085% in carefully selected patients 4 Because pleural effusion is a manifestation of underlying disease, its precise incidence is difficult to determine. However, the incidence in the United States is estimated to be at least 1.5 million cases annually. Congestive heart failure, bacterial pneumonia, malignancy, and pulmonary embolus are responsible for most of these cases.1 In additional, the incidence of pleural effusion at RS Persahabatan, Jakarta, Indonesia in 1994-1997 obtained 52.4% (120 of 229) of patients with malignancy pleural effusion.7 19

In Indonesia, the malignancy is the most cases for pleural effusions after lung tuberculosis. At RS Dr. Sutomo, Surabaya in 1999, malignancy pleural effusion recorded as much as 27.23%, only 25% of them showed positive cytology. The highest number of lung cancer cases is non-small cell lung cancer carcinoma type. It is approximately 75% of all lung cancer cases.5 This case, we suspect malignancy as etiology of pleural effusion. Malignant pleural effusions are a common clinical problem in patients with neo plastic disease.9 Malignancy should be considered and a diagnostic thoracentesis performed in any individual with a unilateral effusion or bilateral effusion and a normal heart size on chest radiograph. It is reasonable to order the following pleural fluid tests when considering malignancy: nucleated cell count and differential, total protein, lactate dehydrogenase (LDH), glucose, pH, amylase, and cytology.4 Although malignancy is a common cause of bloody effusions, at least half are not grossly hemorrhagic. The pleural fluid nucleated cell count typically shows a predominance of either lymphocytes or other mononuclear cells. The presence of 25% lymphocytes is unusual; pleural fluid eosinophilia does not exclude a malignant effusion.4 Approximately one-third of malignant effusions have a pleural fluid pH of less than 7.30 at presentation; this low pH is associated with glucose values of less than 60 mg /dl. The cause of these low-glucose, low-pH malignant effusions appears to be an increased tumor mass within the pleural space compared with 20

those with a higher pH effusion, resulting in decreased glucose transfer into the pleural space and decreased efflux of the acidic by-products of glucose metabolism, CO2, and lactic acid, due to an abnormal pleural membrane. Malignant effusions with a low pH and glucose concentration have been shown to have a higher initial diagnostic yield on cytologic examination, a worse survival, and a response to pleurodesis than those with normal pH and glucose.4 Tumor markers such as carcinoembryonic antigen (CEA), Leu-1, and mucin, may be helpful in establishing the diagnosis, as they are frequently positive in adenocarcinomas (5090%) but rarely seen with mesothelial cells or mesothelioma (010%).4 2. Normocytic Normochromic Anemia Anemia is a condition of lower than normal levels of healthy red blood cells circulating in the blood stream. The severity of anemia is measured by a persons hemoglobin level or hematocrit level.12 This patient presented bleeding gum with intense weakness since 3 days ago. On physical examination, general survey revealed mild pale, conjunctiva and lip were pale, bleeding gum at molar I. Routine blood examination showed Hb 8.6 g%, WBC 6,900/ul, Erythrocytes 3.12 million/ul, platelet 248,000/ul, Ht 26.8 vol%, MCV 86.1 fl, MCHC 32.0%. Base on the data, the diagnosis of normocytic normochromic anemia were made. In a normochromic normocytic anemia, the red cells are of normal size and contain the normal amount of hemoglobin but there is a reduction in number. This is seen in bone marrow failure syndromes, hemolysis, blood loss and 21

secondary anaemia. However, in secondary anemia after prolonged inflammation or infection, handling of iron can become impaired and a microcytic picture can appear as described above.3 A normocytic and normochromic anemia can be seen in anemia of chronic disease, blood loss, reduced bone marrow production of RBCs (such as marrow suppression caused by viral infection, toxin, drugs, immunologic diseases, marrow replacement by neoplastic infiltration, or myelodysplasia), or hemolysis (such as immune-mediated hemolytic anemia, microangiopathic hemolytic anemia, or mechanical damage by hypertension in patients with a prosthetic heart valve). In the absence of signs for bleeding, a normocytic anemia with increased polychromasia (reticulocytosis).13

Picture 7. Algorithm of Anemia13

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The purpose of establishing the etiology of an anemia is to permit selection of a specific and effective therapy. For example, corticosteroids are useful in the treatment of autoimmune hemolytic anemia.2 The purpose of establishing the etiology of an anemia is to permit selection of a specific and effective therapy. For example, corticosteroids are useful in the treatment of autoimmune hemolytic anemia.2 Treatments for anemia are also varied and which one is right for you depend on what is causing the anemia. In many cases of mild or moderate anemia, treating the underlying condition will be enough to get hemoglobin levels rising again. Patients with mild or moderate anemia may not have any anemia-related symptoms or only a few signs of tiredness. However, when anemia becomes severegenerally when hemoglobin drops to or below 7-8g/dl transfusions are often used to quickly raise hemoglobin levels to a normal range and reduce symptoms like significant fatigue and dizziness.2 The traditional practice of transfusing blood preoperatively when hemoglobin concentration is lower than 10 g/dl or hematocrit less than 30 percent can no longer be supported. An expert NIH panel has proposed a transfusion trigger of less than 7.0 g/dl with recommendations for more liberal transfusion criteria in patients at increased risk of suffering damage from decreased oxygen-carrying capacity. Indeed, in resting healthy subjects, isovolemic reductions of blood hemoglobin concentration to 5.0 g/dl produce no evidence of inadequate oxygen delivery because of effective compensation by a

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shift in the hemoglobin oxygen dissociation curve, a decrease in systemic vascular resistance, and increases in heart rate and stroke volume.14 In this case, the patient was given tranexamic acid 3x1 ampul. Tranexamic acid (TXA) is a synthetic analog of serin than reversibly inhibits fibrinolysis by blocking lysine union sites in the plasmin and plasminogen activator molecules. It has been used during more than 20 years in cardiac surgery, urology, ginecology, liver transplants, etc. 15 Despite intraoperative haemostasis, blood loss after TKA may be related to increased fibrinolytic activity, particularly during and immediately after operation. Tranexamic acid (TXA) inhibits fibrinolysis by blocking the lysinebinding sites of plasminogen to fibrin. The use of high doses of TXA during surgery has been recommended.16 An intravenous injection for patients undergoing TKA is the best method for rapidly raising and maintaining the therapeutic concentration of TNA into the synovial fluid and membrane. Pharmacokinetic studies indicated that a dose of 20 mg/kg of TNA is suitable for TKA since therapeutic levels can be maintained for approximately eight hours after operation, which covers the period of hyperfibrinolysis in cases of increased blood loss.16

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F. Summary A 37 year lady presented with shortness of breath and left chest pain. It reduced by a change of position; into left side and sitting position. She also presented acute onset of dry nonproductive cough, and bleeding gum with intense weakness since 3 days ago. From physical examination, general survey revealed mild pale, conjunctiva and lip were pale, gum was bleeding at molar I, blood pressure 130/90 mm of Hg, pulse rate 93/min, respiratory rate 36/min, temperature 36.6oC. Respiratory system findings were consistent with left sided massive pleural effusion; reduced tactile fremitus, dullness on percussion and reduced breath sounds. Examination of heart, chest, abdomen, nervous system, and other systems were essentially normal. Routine blood examination showed Hb 8.6 g%, WBC 6,900/ul, Erythrocytes 3.12 million/ul, platelet 248,000/ul, Ht 26.8 vol%, MCV 86.1 fl, MCHC 32.0%. X-ray chest PA view showed left sided massive pleural effusion without mediastinal shift towards opposite side. Hemorrhagic pleural fluid was aspirated. It was about 2750 ml. From cytology examination, pleural fluid showed presence of nonspecific massive inflammatory. At least, a diagnosis of massive left-sided pleural effusion and normocytic normochromic anemia were made.

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