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Case Report:

Massive Left-Sided Pleural Effusion and NormocyticNormochromic Anemia

A. Medical DataA 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


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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 36.6 oC

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.


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Picture 1. Pleural effusion appearance from AP CXR

From emergency unit, the pharmacology treatment was given. She got

intravenousRinger 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,


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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


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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.


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B. Base Data ResumeA 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 36.6oC , 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,


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


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showed presence of nonspecific massive inflammatory. Pleural fluid did not

show presence of malignant cells.

C. Problem ListBased on the data above, in this case we find two problems. They are:

1) Massive Left-Sided Pleural Effusion2) Normocytic normochromic anemia et causa blood loss

D. Primary Planning

No Problem Planning

Diagnosis

Planning

Treatment

Planning

monitor

Planning

Education

1. MassiveLeft-sided

Pleural

Effusion

a. CT ScanThoracic

b.USGgynecologic

c. Pleural fluidanalysis

1) O2 nasal 2-4lpm

2) Thoracocentesis

3) Pleuorodesis

i. Sign andsymptom

of pleural

effusion

ii. CXR

2 NormocyticNormochro

mic Anemia

a. Reticulocytcount

b. PeriferBlood

Slide

1) PRCtransfusion 2

kolf

2) InjectionTranexamic

acid 3x500

mg

i.Sign andsymptom of

anemia

ii.Routine

Blood

Examination

Nutritionintake


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E. DiscussionBased 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 EffusionIn 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
http://emedicine.medscape.com/article/1003121-overviewhttp://emedicine.medscape.com/article/1003121-overview


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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.6

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


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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 datasuggest that an elevation in capillary wedge pressure is the most important

determinant in the development of pleural effusion in congestive heart failure.


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b) Decreased oncotic pressure in the microvascular circulation due tohypoalbuminemia, which increases the tendency to form pleural interstitial

fluid.

c) Increased negative pressure in the pleural space, also increasing the tendencyfor pleural fluid formation; this can happen with a large atelectasis.

d) Separation of the pleural surfaces, which could decrease the movement offluid inthe pleural space and inhibit pleural lymphatic drainage; this can

happen with a trapped lung.

e) Increased permeability of the microvascular circulation due to inflammatorymediators, 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 bytumor or fibrosis.

g) Movement of ascitic fluid from the peritoneal space through eitherdiaphragmatic 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


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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

patients4

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
http://emedicine.medscape.com/article/300157-overviewhttp://emedicine.medscape.com/article/300157-overview


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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


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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 AnemiaAnemia 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


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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.

2The 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 lysine-

binding 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. SummaryA 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,


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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