A 64 year old hypertensive obese female was undergoing surgery for fracture femur under general anaesthesia. Intra-operatively her end tidal carbon dioxide decreased to 20 from 40 mm Hg, followed by hypotension and oxygen saturation of 85%. What would be the most probable cause:
Ans- B Fat Embolism Syndrome Fat embolism refers to the presence of fat globules in lung parenchyma and peripheral circulation after fracture of a long bone or other major trauma. And fat embolism syndrome reflects a serious systemic manifestation as a consequence to these emboli. Pathophysiology Fat embolism is a common phenomenon it is more commonly seen in patients with multiple fractures and in fractures (involving lower limbs especially femur) Fat originates from the site of trauma, particularly from the injured marrow of the fractured bones and the suggestion that the fat arises from the plasma as a result of agglutination of chylomicrons is not supported by in vivo experiments. Circulating fat globules>10 um in diameter occur in most adults after close fracture of long bones and histological traces of fat can be found in the lungs and other internal organs. Clinical Presentation The patient is usually young adult with a lower limb (esp. femur) fracture, most commonly after closed fractures of long bone (esp. shaft femur) and more so when fractures are multiple. It usually manifests itself with in 24-48 hoursQ, but occasionaly the onset may be delayed for several days. Early warning signs (with in 72 hours of injury) are a slight rise in temperature (pyrexia) and pulse rate (tachycardia)Q In more pronounced cases there is breathlessness, mild mental confusion or restlessness, pectechiae on chest, axillae, retina & conjuctival folds; progressing to marked respiratory distress & coma in severe cases. Pulmonary Manifestations Tachypnea (increased respiration rate) with cyanosis Dyspnea (breathlessness) Low oxygen content often with a normal CO2 reading indicating there is inadequate oxygenation PO2<60 mmHg Chest x-ray show snow storm appearance and mottling -a sign which rapidly disappears in a day or two. Cerebral Manifestation Headache Mild mental confusion or restlessness Irritability Delirium Stupor Convulsion Coma Cerebral signs may regress & recur, suggesting repeated flooding of the circulation with fresh emboli. Cutaneous Manifestation Diagnostic petechial rash seen on Supraclavicular Infraclavicular Shoulder Front & back of chest Axillae Retinae and Conjunctiva of lower lid Periumblical Laboratory Tests There is no characteristic laboratory test However suggestive findings are Thrombocytopenia (platelets <=1.5 lacks) P02 <60 mm Hg (8 kpa) Tachycardia Pyrexia Fall in hemoglobin value Microscopy of blood, sputum & urine for fat globules (gurd test) Fundoscopy of retina to see emboli, striate haemorrhages and fluffy exudates NCCT Head: shows characteristic focal emboli showers intracerebral region. Managment Prevention: Rough handling, inadequate immobilization and long journey to reach trauma centre are predisposing factors that must be avoided in long bone fractures. Fracture stabilization Removing fat emboli from circulation by Lipolytic agents as heparin (| serum lipase activity) Hypertonic glucose (decrease FFA production) Offset its effect by Vasodilation eg phenoxy benzamine Prompt correction of hypovolaemia Prophylactic use of O2 Dextran (expand plasma volume, reduce RBC aggregation and platelet adherence) Aprotinin (this protease inhibitor decrease platelet aggregation and serotonin release) Treatment of Established Case The aim of treatment is maintaining adequate oxygen level in the blood. If necessary by using intermittent positive pressure ventilation. Oxygen is the only therapeutic tool of proven use. It should be administered in sufficient amount to maintain arterial P02 >80 mm Hg O2 toxicity (pneumonitis) is avoided by using O2 conc. below 40% Steroids are given to avoid chemical pneumonitis resulting from break down of - pulmonary fat emboli into FFA.
Air embolism
Fat embolism
Pulmonary embolism
ARDS