MSC - F. Surgery Answers 2025
.pdf
Pulmonary hemorrhage
Bronchiectasis
Respiratory failure
Amyloidosis
Extension to adjacent structures (mediastinitis, chest wall abscess)
Causes of Progression to Chronic Lung Abscess
Inadequate drainage of pus due to bronchial obstruction or complex fistulas
Pleural adhesions limiting lung collapse
Presence of sequestra (dead lung tissue)
Poor or inappropriate antibiotic therapy
Pneumosclerosis (lung fibrosis)
Large (>6 cm) or multiple abscess cavities
Clinic of Chronic Lung Abscess
Alternating exacerbations and remissions
Symptoms: weakness, chest pain, dyspnea, cough with purulent sputum
Physical signs: clubbing, "watch-glass" nails, amphoric breath sounds over cavity
Systemic signs of chronic infection and respiratory insufficiency
Diagnosis
Prolonged symptoms (>2 months)
Chest X-ray/CT showing thick-walled cavity with air-fluid level and dense capsule
Sputum analysis to exclude TB and malignancy
Bronchoscopy and biopsy if needed for differential diagnosis
Treatment
Conservative: improve drainage (postural drainage, inhalations), targeted antibiotics, detoxification, immune support
Surgical: lobectomy, bilobectomy, or pneumonectomy in refractory or complicated cases
Surgery carries significant risk; mortality 7–12%.
3.Pyopneumothorax, causes, clinic, diagnosis, treatment.
Pyopneumothorax is a severe complication of purulent-destructive lung diseases where pus and air accumulate simultaneously in the pleural cavity, typically due to rupture of a lung abscess or empyema.
Causes (Etiology & Pathogenesis)
Rupture of acute lung abscess, gangrene, or suppurated pulmonary cyst into the pleural space.
Rupture of pleural empyema into bronchus creating a bronchopleural fistula.
Infection of traumatic or spontaneous pneumothorax.
Disintegrating tumors of lungs, pleura, or esophagus.
Pathophysiology includes necrosis of the abscess wall and visceral pleura, allowing pus and air into pleural cavity, causing lung collapse and severe inflammation.
Classification
Simple vs. Tense pyopneumothorax (degree of lung collapse and mediastinal shift)
Clinical course types (Spasokukotsky classification):
o Acute (violent)
o Soft
o Erased (subclinical/latent)
Clinical Presentation
Sudden sharp pleuritic chest pain ("dagger stab")
Severe dyspnea, cyanosis, and respiratory failure
Signs of systemic toxicity: fever, chills, leukocytosis, increased ESR
Physical exam: decreased chest movement on affected side, dullness at base with shifting, tympanitis above dullness, diminished breath sounds and vocal fremitus, mediastinal shift to opposite side.
Possible signs of bronchopleural or pleurocutaneous fistula (if pus drains externally).
Diagnosis
Chest X-ray: air-fluid level in pleural cavity, lung collapse, mediastinal shift.
CT scan: precise localization and extent of lung and pleural pathology.
Pleural fluid aspiration: pus mixed with air confirms diagnosis; fluid sent for bacteriology and sensitivity testing.
Pleurography if needed for chronic empyema to assess cavity size and adhesions.
Bronchoscopy for assessment and potential bronchial occlusion.
Treatment
Goals:
Evacuate pus and air from pleural cavity.
Restore lung expansion.
Control infection in pleural space and lungs.
Close bronchopleural communication.
Steps:
1.Emergency thoracentesis and drainage with continuous active aspiration via chest tubes and vacuum systems.
2.Bronchial management: temporary bronchial occlusion (valvular bronchoblockage) during bronchoscopy if drainage is ineffective.
3.Antibiotic therapy tailored to cultures.
4.Supportive care: nutrition, protein supplementation, correction of hypoproteinemia, and volemic status.
5.Surgical intervention (lobectomy or pneumonectomy) reserved for lifethreatening complications (e.g., massive hemorrhage, failure of conservative therapy).
Prognosis
Early and adequate drainage and infection control improve outcomes.
Untreated or poorly managed cases may progress to chronic empyema, bronchopleural fistula, mediastinitis, pulmonary hemorrhage, or death.
4.Complications of surgical interventions on the chest organs, causes, prevention, treatment.
1.Respiratory:
Atelectasis (poor ventilation) — prevent with deep breathing, treat with physiotherapy.
Pneumothorax (lung/pleura injury) — prevent with careful surgery, treat with chest tube.
Infection (pneumonia, empyema) — prevent with hygiene and antibiotics, treat with antibiotics and drainage.
2.Bleeding:
Causes: vessel injury, coagulopathy.
Prevent: meticulous technique, correct clotting.
Treat: surgical control, transfusion.
3.Bronchopleural Fistula:
Cause: poor stump closure, infection.
Prevent: proper closure, infection control.
Treat: drainage, possible surgery.
4.Empyema:
Cause: infected pleural space.
Prevent: asepsis, early drainage.
Treat: drainage, antibiotics.
5.Air Leak:
Cause: incomplete lung sealing.
Prevent: intraoperative leak test.
Treat: chest tube, surgery if persistent.
6.Cardiac:
Arrhythmias — prevent electrolyte imbalance, treat with meds.
Tamponade — prevent bleeding, treat with drainage.
7.Wound:
Infection, dehiscence — prevent asepsis, treat with antibiotics and care.
8.Thromboembolism:
Cause: immobility.
Prevent: mobilize early, anticoagulate.
Treat: anticoagulation.
5. Lung gangrene, etiology, clinic, diagnosis, principles of treatment. Differential diagnosis with lung abscess
Lung gangrene is a severe, necrotizing form of pulmonary infection, often considered a complication of untreated or inadequately treated lung abscess. It is characterized by widespread necrosis of lung parenchyma with insufficient demarcation, often involving multiple lobes and rapid tissue breakdown.
Etiology:
Progression of lung abscess or severe necrotizing pneumonia.
Often polymicrobial (aerobes + anaerobes), including Klebsiella, Staph aureus, Pseudomonas, anaerobic streptococci.
Predisposing factors: aspiration, bronchial obstruction (tumor, foreign body), immunosuppression.
Clinical Presentation:
Acute onset: high fever, rigors, chest pain, foul-smelling, copious, dirty gray/brown sputum.
Classic three-layered sputum: foamy top, serous middle, necrotic bottom.
No clinical improvement despite expectoration.
Chronic cases: slower onset in immunocompromised.
Severe intoxication, weight loss, gastroenteritis (from swallowed pus).
Tachycardia, hypotension, pleural rub, bronchial breathing.
Diagnosis:
Chest X-ray: heterogeneous infiltrate, multiple cavitations, sequestra, pleural effusion.
CT scan: better delineation of cavities and necrosis.
Lab: leukocytosis with left shift → leukopenia, anemia, aneosinophilia.
Microbiology: sputum culture, blood cultures.
Bronchoscopy: for diagnosis and drainage.
Complications:
Massive hemoptysis.
Pyopneumothorax, empyema.
Sepsis, contralateral spread.
Respiratory failure, multiorgan dysfunction.
Treatment Principles:
1.Hospitalization – thoracic surgery unit.
2.Isolation + supportive care – oxygen, high-calorie, high-protein diet.
3.Airway clearance:
o Postural drainage, mucolytics (bromhexine, ambroxol, NAC).
o Bronchodilators, proteolytic enzymes.
oSanitation bronchoscopy: rigid or fiberoptic.
4.Antibiotics – broad-spectrum, anaerobic + aerobic coverage (e.g., carbapenem + clindamycin).
5.Detox & immune support – IV fluids, correction of metabolic imbalances.
6.Surgery – indicated for failure of conservative therapy, hemorrhage, massive necrosis (lobectomy or pneumonectomy).
Prognosis:
Poor without aggressive treatment.
Better outcomes with early diagnosis, effective drainage, and antibiotics.
Often leaves residual fibrosis or cavity; some cases progress to chronic suppuration.
Differential Diagnosis:
Lung cancer (esp. necrotizing central), TB, infected cysts, echinococcosis.
Requires imaging, cytology, sputum culture, bronchoscopy, and sometimes biopsy.
6. Bronchiectatic disease. Classification, stages of development, clinic, diagnosis, complications, indications for surgical treatment.
Definition
Bronchiectasis is a permanent, pathological dilation of bronchi caused by an inflammatory-destructive process involving the entire bronchial wall and adjacent tissues.
Epidemiology
Prevalence is approximately 0.5% of the population.
Etiopathogenesis
Congenital factors: Poor bronchial wall elasticity, bronchial lumen narrowing, structural lung tissue abnormalities.
Acquired factors: Recurrent or chronic lung infections (bronchitis, pneumonia), impaired ventilation, impaired blood and lymph circulation.
Pathophysiology:
o Atelectasis causes impaired bronchial drainage.
oBronchial lumens become occluded with mucus, leading to inflammation.
oVascular wall edema reduces circulation, causing tissue atrophy and bronchial wall sclerosis.
oConnective tissue overgrowth and mucosal degeneration cause irreversible loss of drainage and bronchial dilation.
Morphological types: Cylindrical, saccular, and mixed.
Clinical Stages and Manifestations
Stage I (Initial): Mild symptoms, persistent cough with small mucopurulent sputum, minimal systemic effects.
Stage II (Suppuration): Increased sputum (200+ ml/day), purulent sputum, cough intensifies, dyspnea, signs of systemic purulent intoxication, hemoptysis (30% cases), hemorrhage (10%).
Stage III (Destruction): Severe symptoms, sputum up to 600-700 ml/day, worsening systemic intoxication, cardiovascular complications in advanced stage.
Diagnosis
History and clinical exam (chest deformities, lag in chest expansion, auscultation revealing crackles).
Imaging:
o Chest X-ray/fluoroscopy shows indirect signs.
oBronchography (contrast introduced into bronchi) provides detailed anatomical information.
oCT scan is sensitive for extent and type of bronchial damage.
Bronchoscopy: Essential for mucosal assessment and therapeutic interventions.
Pulmonary function tests (spirometry), angiopulmonography, and circulatory evaluation assist in assessment.
Differential diagnosis includes tuberculosis, chronic bronchitis, asthma, pneumosclerosis.
Treatment
Conservative (early stages):
1.Restore bronchial patency.
2.Facilitate sputum clearance (physiotherapy, postural drainage).
3.Control infection and inflammation (antibiotics, anti-inflammatory agents).
4.Immunomodulation as needed. Success rate: 58-80% in early disease.
Surgical (advanced stages II and III):
oIndicated for uncontrolled infection, massive hemoptysis, or risk of gangrene/abscess.
oPreoperative optimization is crucial (inflammation control, organ function correction).
oSurgical extent varies from segmentectomy to pneumonectomy depending on disease extent.
7.Research methods for diseases of the lungs and pleura
I. Patient Complaints (Subjective Data)
Key symptoms of lung and pleural disease:
Dyspnea (shortness of breath):
o Can be inspiratory, expiratory, or mixed.
oSeen in airway obstruction, asthma, emphysema, pneumonia, pleurisy, etc.
Suffocation (asthma):
oIntense shortness of breath; may lead to asphyxia.
Cough:
oCan be dry or productive; continuous or periodic.
oTiming (morning, evening, night) helps identify cause (e.g., COPD, asthma, CHF).
Sputum:
oVaries in amount, color, odor, and viscosity.
oTypes: mucous, mucopurulent, purulent, putrid, or bloodstreaked.
Hemoptysis:
oBlood in sputum due to infections, cancer, infarction, or cardiac causes.
Chest pain:
oUsually pleural in origin—sharp, worsens with breathing or coughing.