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Case Presentation: Pleural Effusion
Identification Data
Name: Mrs. Suman Devi
Age/Sex: 68 years/Female
Education: Primary school
Occupation: Homemaker
Address: Rural Rajasthan
Date of admission:
Date of examination:
Informant: Patient's son
Presenting Complaints
Progressive shortness of breath for 3 months
Dry cough for 2 months
Right-sided chest pain for 1 month
History of Present Illness Mrs. Suman Devi, a 68-year-old female, reports that her symptoms began insidiously about three months ago with progressive shortness of breath. Initially, it occurred on moderate exertion (e.g., walking up stairs) (grade 1 MMRC) but has gradually worsened to the point where she now feels breathless even at rest(MMRC grade 4) during exacerbations. She finds relief on lying on her right side. No history of any nocturnal awakening due to dyspnoea.
Approximately two months ago, she developed a dry, irritating cough, which is non-productive and tends to worsen at night. While she found some temporary relief with sips of water, the cough remained a persistent and bothersome symptom, contributing to her overall fatigue and impacting her quality of life. The cough was not associated with fever, chills, or any particular odor.
For the last one month, she has experienced a dull aching pain on the right side of her chest. The pain is constant, non-radiating, and is exacerbated by deep breathing and coughing. She denies any history of trauma to the chest.
She reports significant weight loss of approximately 5 kilograms over the last 3 months, along with generalized fatigue and anorexia. She denies any fever, night sweats, palpitations, orthopnea, or paroxysmal nocturnal dyspnea. There is no history of hemoptysis, swelling of legs, or symptoms suggestive of connective tissue disease.
Past History
Hypertension diagnosed 10 years ago, on irregular medication.
No history of diabetes mellitus, tuberculosis, or bronchial asthma.
No history of any major surgeries.
Family History
No known history of malignancy or similar illnesses in the family.
Personal History
Normal sleep and appetite (until recently).
Non-smoker, non-alcoholic.
Diet: Mixed diet.
No significant occupational exposures.
Socioeconomic History
Lives in a rural area, in a semi-pucca house with adequate ventilation.
Joint family of 8 members in 3 rooms.
Uses LPG for cooking.
Drinks water from a borewell with a filtration system.
General Examination Patient conscious, oriented, cooperative. Moderately built, undernourished (BMI 17.5 kg/m²). Pallor present. No cyanosis, icterus, clubbing, or lymphadenopathy. Vitals:
PR: 96/min, regular, normal volume and character.
BP: 130/80 mmHg in right upper limb in sitting position.
RR: 28/min, thoraco-abdominal.
Temp: 99.2°F (afebrile).
SpO₂: 94% (room air).
Upper Respiratory Examination Normal. No nasal polyps or sinus tenderness. Tonsils and posterior pharyngeal wall normal.
Respiratory System Examination Inspection
Shape of chest: Symmetrical.
Trachea appears to be shifted to the left (away from the side of effusion).
Apical impulse not visible.
Respiratory movements appear reduced on the right side of the chest.
No scars or visible accessory muscle use at rest.
Palpation
No rise in temperature or tenderness.
Trachea shifted to the left.
Apex beat impalpable.
Respiratory movements are reduced on the right hemithorax.
Chest expansion significantly reduced on the right lower zone.
Vocal fremitus diminished to absent over the right infrascapular, axillary and infra axillary regions.
Percussion
Supraclavicular: Resonant bilaterally.
Clavicular: Resonant bilaterally.
Infraclavicular: Resonant bilaterally.
Mammary: Dullness at right 4th ICS extending downwards.
Axillary: Stony dullness on the right side, extending up to the 3rd intercostal space.
Infra-axillary: Stony dullness on the right side.
Suprascapular: Resonant bilaterally.
Interscapular: Resonant bilaterally.
Infrascapular: Stony dullness on the right side with a curved upper border (Ellis-S-curve) and stony dullness in the right axillary region.
Auscultation
Supraclavicular: Normal vesicular breath sounds bilaterally.
Clavicular: Normal vesicular breath sounds bilaterally.
Infraclavicular: Normal vesicular breath sounds bilaterally.
Mammary: Diminished breath sounds on the right side.
Axillary: Absent breath sounds on the right side.
Infra-axillary: Absent breath sounds on the right side.
Suprascapular: Normal vesicular breath sounds bilaterally.
Interscapular: Normal vesicular breath sounds bilaterally.
Infrascapular: Absent breath sounds on the right side with egophony and bronchial breath sounds just above the level of dullness (Ewart's sign in some cases).
Vocal resonance: Diminished to absent over the area of dullness.
Summary Mrs. Suman Devi, a 68-year-old female with a history of hypertension, presents with a 3-month history of progressive dyspnea, a 2-month history of dry cough, and 1 month of right-sided pleuritic chest pain, along with significant weight loss and fatigue. General examination reveals pallor and undernutrition. Respiratory system examination shows tracheal shift to the left, reduced movements and vocal fremitus on the right, stony dullness on percussion over the right hemithorax (classic Ellis-S-curve), and absent breath sounds on the right side with egophony and bronchial breath sounds at the upper border of dullness.
The clinical picture is highly suggestive of a significant right-sided pleural effusion. Given her age, constitutional symptoms, and the insidious onset, malignancy, tuberculosis, or cardiac causes should be considered in the differential diagnosis. Further evaluation with chest X-ray (PA and lateral views), pleural fluid analysis (biochemistry, cytology, microbiology, ADA), sputum for AFB, and potentially CT chest and pleural biopsy, is warranted to determine the etiology and guide management.
Viva Questions & Answers on Pleural Effusion
1. Empyema
Q1: Define empyema.
A1: Empyema is the presence of frank pus in the pleural cavity. It is a severe form of parapneumonic effusion, characterized by gross pus or positive Gram stain/culture of pleural fluid.
Q2: What are the common causes of empyema?
A2: The most common cause is bacterial pneumonia, leading to a complicated parapneumonic effusion. Other causes include thoracic surgery, chest trauma, ruptured lung abscess, esophageal perforation, and subdiaphragmatic abscess.
Q3: How do you differentiate a complicated parapneumonic effusion from empyema based on pleural fluid analysis?
A3: While both are exudative, empyema specifically shows frank pus, a positive Gram stain or culture, and often a very low pH (<7.0) and very low glucose (<40 mg/dL). A complicated parapneumonic effusion might have similar biochemical parameters (low pH/glucose) but typically not frank pus or a positive Gram stain/culture initially.
2. Pleural Fibrosis
Q1: What is pleural fibrosis?
A1: Pleural fibrosis is the thickening and scarring of the pleura, which can restrict lung expansion. It occurs as a result of chronic inflammation or repeated injury to the pleura.
Q2: Name some causes of significant pleural fibrosis.
A2: Common causes include chronic pleural effusions (e.g., tuberculous pleurisy, empyema), asbestos exposure (leading to diffuse pleural thickening), hemothorax, radiation therapy to the chest, and rheumatoid pleurisy.
Q3: How does pleural fibrosis manifest clinically?
A3: Clinically, it can cause restrictive lung disease, leading to progressive dyspnea on exertion. On examination, there may be reduced chest expansion, dullness on percussion, and diminished breath sounds over the affected area.
3. Hydropneumothorax
Q1: Define hydropneumothorax.
A1: Hydropneumothorax is the presence of both fluid (hydro-) and air (-pneumothorax) in the pleural cavity.
Q2: What are the common causes of hydropneumothorax?
A2: It often results from a spontaneous pneumothorax complicated by an exudative effusion, or from trauma (e.g., penetrating chest injury), iatrogenic causes (e.g., during thoracentesis), or a ruptured lung abscess or empyema eroding into the bronchus.
Q3: How is hydropneumothorax diagnosed clinically and radiologically?
A3: Clinically, there will be signs of both fluid (dullness, absent breath sounds) and air (hyper-resonance/tympanitic note). A characteristic finding is a "splashing" sound on succussion. Radiologically, a chest X-ray will show a horizontal air-fluid level within the pleural space.
4. D'Espine Sign
Q1: What is D'Espine sign?
A1: D'Espine sign refers to the presence of egophony or bronchial breath sounds heard over the spinous processes below the level of the bifurcation of the trachea (T3-T4 downwards).
Q2: What is its significance?
A2: It traditionally suggests enlarged mediastinal lymph nodes, particularly those due to tuberculosis, which transmit sounds more clearly to the vertebral column. It is less commonly used as a primary diagnostic sign in modern practice.
5. Light's Criteria
Q1: State Light's Criteria for exudative pleural effusion.
A1: An effusion is considered exudative if at least one of the following three criteria is met:
Pleural fluid protein / Serum protein ratio > 0.5
Pleural fluid LDH / Serum LDH ratio > 0.6
Pleural fluid LDH > 2/3rds the upper limit of normal for serum LDH.
Q2: Why are Light's Criteria important in the evaluation of pleural effusion?
A2: They help differentiate between transudative and exudative effusions. Transudative effusions are typically due to systemic factors (e.g., heart failure, liver cirrhosis), while exudative effusions are due to local pleural disease (e.g., infection, malignancy, inflammation). This distinction guides further investigation and management.
Q3: Can Light's Criteria misclassify an effusion? Give an example.
A3: Yes, Light's Criteria can misclassify some transudative effusions as exudative, particularly in patients who have been on diuretics for heart failure. Diuretics can concentrate the pleural fluid protein and LDH, causing it to meet exudative criteria even if the underlying cause is transudative.
6. Causes of Predominant Unilateral Pleural Effusion
Q1: List common causes of predominant left-sided pleural effusion.
A1: Pancreatitis, esophageal rupture, Dressler's syndrome (post-MI pericarditis), splenic infarction, subphrenic abscess on the left, and cardiac causes (though often bilateral, left-sided predominance can occur).
Q2: List common causes of predominant right-sided pleural effusion.
A2: Liver cirrhosis with ascites (hepatic hydrothorax), Meigs' syndrome (ovarian fibroma with ascites), subphrenic abscess on the right, amoebic liver abscess rupturing into the pleural space, and cardiac causes.
Q3: What are the common causes of recurrent pleural effusion?
A3: Malignancy (most common cause of recurrent exudative effusion), heart failure (recurrent transudative effusion if not adequately managed), tuberculosis, recurrent pulmonary embolism, connective tissue diseases (e.g., SLE, rheumatoid arthritis), and chronic kidney disease.
7. Lymphatic Drainage of Pleura
Q1: Describe the lymphatic drainage of the pleura.
A1: Lymphatics of the parietal pleura drain into the intercostal, internal mammary, parasternal, and diaphragmatic lymph nodes. Lymphatics of the visceral pleura drain into the bronchopulmonary lymph nodes (hilar lymph nodes). Pleural fluid is primarily reabsorbed via the parietal pleural lymphatics.
8. Succession Splash
Q1: What is "succession splash" and what does it indicate?
A1: Succession splash is a distinct splashing sound heard on auscultation over the chest when the patient is shaken. It indicates the presence of both fluid and air in a body cavity, specifically within the pleural space (hydropneumothorax) or a distended stomach.
Q2: How do you elicit a succession splash?
A2: The patient is instructed to hold their breath, and the examiner shakes the patient's torso vigorously while listening over the chest with a stethoscope.
9. Characteristics of Normal Pleural Fluid
Q1: Describe the normal characteristics of pleural fluid.
A1: Normal pleural fluid is a small amount (typically 5-15 mL), clear, pale yellow, and acellular or has very few cells (<1000 cells/µL, predominantly mesothelial cells and macrophages). It has a low protein content (<1.5 g/dL) and low LDH, reflecting its formation as an ultrafiltrate of plasma.
10. Encysted Pleural Effusion
Q1: What is an encysted (loculated) pleural effusion?
A1: An encysted or loculated pleural effusion is a collection of pleural fluid that is trapped or walled off by fibrous adhesions within the pleural space, preventing it from moving freely with changes in patient position.
Q2: How does an encysted effusion differ from a free-flowing effusion on imaging?
A2: On chest X-ray or CT scan, a free-flowing effusion will typically layer out and obliterate the costophrenic angle or form a meniscus. An encysted effusion, however, will maintain its shape and position regardless of patient positioning and may have an atypical shape.
Q3: Why is it important to identify an encysted effusion?
A3: Encysted effusions are more difficult to drain by simple thoracentesis and often require imaging guidance (ultrasound or CT) for aspiration or drainage, or even surgical intervention (e.g., VATS) for decortication. They are often associated with complicated parapneumonic effusions or empyema.
11. Management of Empyema
Q1: Outline the general principles of empyema management.
A1: Management involves:
Antibiotics: Broad-spectrum antibiotics covering likely pathogens, then tailored based on culture sensitivity.
Drainage: Prompt and complete drainage of pus. This can be achieved by:
Tube thoracostomy (chest drain): For initial drainage.
Intrapleural fibrinolytics: To break down septations and improve drainage, if loculations are present.
Video-assisted thoracoscopic surgery (VATS): For debridement and decortication in cases of loculated or persistent empyema.
Open thoracotomy and decortication: For chronic, organized empyema.
Nutritional support: Crucial for recovery.
Q2: When would you consider surgical intervention for empyema?
A2: Surgical intervention (VATS or thoracotomy with decortication) is considered if:
The empyema is loculated and not adequately drained by chest tube with or without fibrinolytics.
There is evidence of significant pleural peel preventing lung re-expansion.
Persistent sepsis despite adequate drainage and antibiotics.
Long-standing or chronic empyema.
12. Management of TB Pleural Effusion
Q1: How is tuberculous pleural effusion diagnosed?
A1: Diagnosis is based on clinical suspicion, exudative pleural fluid (high protein, high LDH, often lymphocytic predominance), elevated ADA (Adenosine Deaminase) level in pleural fluid (>40-60 U/L), positive pleural fluid culture for M. tuberculosis (though often low yield), pleural biopsy showing granulomas (gold standard), and sometimes interferon-gamma release assays (IGRAs).
Q2: What is the standard management for TB pleural effusion?
A2: The cornerstone of treatment is a full course of anti-tubercular therapy (ATT) similar to pulmonary tuberculosis (e.g., 2 months of HRZE followed by 4 months of HR). Therapeutic thoracentesis may be done for symptomatic relief from large effusions, but routine chest tube drainage is generally not recommended unless it's a very large, symptomatic effusion. Steroids may be considered in selected cases, especially with large effusions and severe symptoms, to reduce inflammation and subsequent pleural fibrosis, but their role is debated and not routinely used.
Q3: What is the role of steroids in TB pleural effusion?
A3: The role of corticosteroids is controversial. They might be considered in large, symptomatic effusions to reduce inflammation and potential for subsequent pleural thickening, but they do not shorten the course of ATT and may have side effects. They are generally not recommended routinely.
13. Management of Malignant Pleural Effusion
Q1: How is malignant pleural effusion diagnosed?
A1: Diagnosis is typically confirmed by pleural fluid cytology showing malignant cells (most common and specific method). If cytology is negative but suspicion remains high, thoracoscopy with pleural biopsy is the gold standard. Imaging (CT chest) may reveal the primary malignancy and associated pleural thickening or nodules.
Q2: What are the primary goals in managing malignant pleural effusion?
A2: The primary goals are symptomatic relief (dyspnea), prevention of recurrence, and improvement of quality of life, as it often signifies advanced disease.
Q3: Describe the various management options for recurrent symptomatic malignant pleural effusion.
A3:
Therapeutic Thoracentesis: For immediate symptomatic relief, but effusion typically recurs.
Tube Thoracostomy with Pleurodesis: Chemical pleurodesis (e.g., with talc, doxycycline, or bleomycin) involves instilling a sclerosing agent into the pleural space to induce inflammation and fibrosis, obliterating the pleural space and preventing fluid re-accumulation. This is done after complete drainage of the effusion via a chest tube.
Indwelling Pleural Catheter (IPC): A small, tunneled catheter inserted into the pleural space that allows the patient or caregiver to drain the fluid intermittently at home. This is an option for patients with limited life expectancy or those who fail pleurodesis.
Pleurectomy/Pleuroperitoneal shunt: Surgical options, less commonly performed but may be considered in selected patients.
Systemic anti-cancer therapy: Chemotherapy or targeted therapy may be used if the primary malignancy is chemosensitive and the patient's performance status allows. This may reduce fluid production.