The wounded lungs Shahil & Jesin Department of Pulmonary Medicine Karuna Medical College
HISTORY 23 year old female H/O RTA on while travelling on a scooter. Collision with a bike Difficulty in movement of left lower limb. No h/o LOC, vomiting or ENT bleed. Past H – H/O jaw surgery for micrognathism
EXAMINATION Pale Puncture wound and swelling on the left leg. Resp System – B/L breath sounds were present SpO 2 -96% in room air Open fracture left leg
Desaturated after the procedure. Requiring oxygen support during support in the post op period D-dimer was sent which was positive and she was subsequently started on anticoagulants. Condition deteriorated Pulmonology opinion obtained
PULMONARY EVALUATION Dyspnoeic and in respiratory distress. Pulse rate – 102/min SpO 2 -94% (8 litres O 2 ) O/E - Bilateral breath sounds were present with crepitation. CXR was repeated. ABG advised.
Progressive fall in Hb DATE HEMOGLOBIN 13 th March 9.5 14 th March 10.5 16 th March 9.7 17 th March 7.7 18 th March 7.6
ABG pH – 7.542 p CO2 – 29.1 pO2 – 39.9 HCO3 – 24.4 A-a gradient - 61
DIAGNOSIS Bilateral lung contusion ARDS
FURTHER COURSE PRBC transfusion. Anticoagulants stopped. Started in parenteral antibiotics. Corticosteroids. NIV supports. Gradually improved
DISCUSSION
INTRODUCTION Direct or indirect damage of the parenchyma of the lung that leads to oedema or alveolar hematoma and loss of the physiological structure and function of the lung. Results in:- Reduced gas exchange Increased pulmonary vascular resistance Decreased pulmonary compliance
HISTORY First described by Morgagani. Increased in number of cases due to wars. First WW – widespread use of explosives. Second WW – air raids Vietnam war – widespread use of X-rays.
PATHOPHYSIOLOGY Damage to compressed lung tissue. Shearing force of alveolar structures. Tear in lung tissue. Increase in airway pressure → gas within tissues expands → micro explosions within aerated tissue
Alveoli and capillary injury ↓ Hematoma followed by oedema formation ↓ Inflammatory response ↓ Alveolar collapse due to decreased surfactant ↓ ARDS
CLINICAL FEATURES Mild contusion asymptomatic. Dyspnoea, tachypnoea, tachycardia. Reduced breath sounds above area affected. Excessive bronchorrhea and haemoptysis – severe contusion
TIME COURSE Severe injury – manifests within hours and may even lead to death Milder injuries – gradual deterioration. Clinical features appear 24-48 hours after sustaining the injury.
RADIOLOGY X-ray – patchy consolidation Edges of the contused area are usually not well defined. CT scan – better Markedly detectable radiological abnormality within the first 24 hours indicate poor prognosis.
CUT PUMPKIN SIGN Dense non-segmental sub-pleural crescentic opacity on the side of impact and the lesion becoming less dense and non-homogenous (ground glass opacity) towards the deeper parenchyma. Characteristic of pulmonary contusion. The density and depth of the sub-pleural lesion is decided by the force of impact.
CONTRECOUP INJURY Dense opacity on the opposite side of the impact. Sparing of the outer 1-2mm rim of subpleural portion of the lung.
TREATMENT
PREVENTION
TREATMENT Avoid respiratory failure – clearing airways Ensure adequate tissue oxygenation – O 2 supplementation and PPV. No treatment currently available that could facilitate recovery.
PROGNOSIS Mild cases – spontaneous resolution within 3-7 days. Severe cases – fatal.
TAKE HOME MESSAGE Lung contusion can have a varied presentation. Should be suspected in patients with chest trauma even without obvious rib fractures. Cut pumpkin sign is characteristic. Treatment is mainly supportive. Can cause ARDS and be fatal.