ARDS AND FAT EMBOLISM POST TOTAL HIP REPLACEMENT

post inter trochanteric fracture

1. ORTHO-RADIO MEET

2. ARDS ARDS – Acute respiratory distress syndrome is a acute onset, progressive , hypoxia condition with radiographic B/L lung infiltrates which develops after several diseases or injuries and is not derived from hydrostatic pulmonary oedema.

3. ARDS (BERLIN CRITERIA) 1 Acute onset( occurring within 1 week of an insult or after the onset of symptoms). 2 B/L opacities on chest radiograph not fully explained by collapse, effusions or nodules. 3 Exclusion of cardiac failure as the cause of symptoms. 4 Reduced oxygenation.

4. PULMONARY EXTRA-PULMONARY PNEUMONIA SEPSIS ASPIARTION OF GASTRIC CONTENTS SEVERE TARUMA WITH SHOCK AND MULTIPLE TRANSFUSIONS TRAUMA, BURNS ACUTE PANCREATITIS FAT/ AMNIOYIC FLUID EMBOLISM DIC NEAR DROWNING TRANSFUSION OF BLOOD CONTENTS SMOKE INHALATION DRUG OVERDOSE HEMORRHAGIC SHOCK OR REPERFUSION HIGH ALTITUDE PULMONARY OEDEMA NEUROGENIC OEDEMA CAUSES OF ARDS

5. PATHOPHYSIOLOGY

6. TYPICAL (CLASSICAL) CT FINDINGS- Bilateral roughly symmetrical consolidation and ground glass opacities with antero-posterior gradient of increasing density. ATYPICAL CT FINDINGS- Heterogenous/ non-symmetrical & non-dependent consolidation and ground glass opacities.

7. PHASES OF ARDS 1 EXUDATIVE PHASE- ( 1-7 days) Latency phase(12-24 hrs)- Chest x-ray is usually normal.

8. 2 . PROLIFERATIVE PHASE( 8-14 DAYS) During this phase, the rapid changes observed in exudative phase stabilizes.

9. 3. FIBROTIC PHASE(>15 days)

10. DIFFUSE SHADOWING IN THE LUNGS PNEUMONIA ARDS CARDIOGENIC PULMONARY EDEMA Patchy areas of consolidation with sparing at some places. Associated pleural effusion is common. Initially- predominantly interstitial shadowing with rapid evolution into a diffuse alveolar pattern. Opacities are widespread, symmetric involve the lungs peripherally as well as around the hila. All the lung zones are involved-both centrally and peripherally. Proximal pulmonary vessels remain well defined. CXR changes may persist 12 or more hours after the onset of symptoms. CXR appearances persist with minimal change on serial radiographs even when there is clinical improvement. Pleural effusions are rare. Cardiac enlargement. Lung shadows and the onset of symptoms at the same time. Changes predominantly at the lung base. Blurred margins of hilar vessels. CXR clears rapidly in response to treatment. Pleural effusion is common.

11. ARDS VS CARDIOGENIC PULMONARY EDEMA

12. CARDIOGENIC PULMONARY EDEMA

13. PULMONARY FAT EMBOLISM Occurs in patients with long bone fractures particularly femur and tibia and may occur in patients with severe trauma. Other causes includes soft tissue trauma, major burns, hemoglobinopat hy, overwhelming infection, tumours , blood transfusion, liposuction. Imaging findings become evident at 24-28 hrs of traumatic insult.

14. CT FEATURES OF PULMONARY FAT EMBOLISM Filling defects with fat embolism. Centrilobular nodules can be seen (particularly B/L upper lobes). GGO and consolidations with areas of lobular sparing (geographic pattern).Patchy and asymmetrical. Septal lines. No peri-bronchial cuffing.

15. FAT EMBOLISM SYNDROME It occurs as the result of innumerable small fat emboli leading to a multisystem dysfunction, characterized by the triad of: respiratory distress- dyspnea , hypoxia. cerebral abnormalities- drowsiness, confusion, convulsions, coma. petechial rash- particularly in chest, axilla, eyes. d isappears within a week.

16. Radiographic features vary whether cerebral fat embolism is due to microembolism or macroembolism . ON CT M icroembolism CT of the brain is normal in most cases  There may be evidence of diffuse edema with scattered low-attenuating areas and hemorrhage in some situations Macroembolism Hypodense vessel sign may be present 

17. STARFIELD APPEARANCE

18. WALNUT KERNEL MICROBLEED PATTERN

19. THANKS