A patient of Rtiad traffic accident undergoes emergency open reduction and internal fixation for a pelvic fracture. He recovers well during the postoperative period. However on 3rd postoperative day, he develops chest pain and collapses. Examination reveals fine petechial rash over the trunk, tachycardia, tachypnea and hypotension. Chest xray shows dilatation of right sided heart and diffuse lung infiltrates. What could have caused this condition?
Correct Answer: Long bone fracture
Description: Ref: Harrison's Principles of Internal Medicine, 18th edition, pg 2170Explanation:The scenario described is a classical ease of 'Fat embolism'A fat embolism is a type of embolism that is often caused by physical trauma such as fracture of long bones, soft tissue trauma and burns.Fat EmbolismIt is a type of embolism that is often caused by physical trauma such as fracture of long bones, soft tissue trauma and burns.Unlike emboli that arise from thrombi (blood clots), fat emboli are small and multiple, and thus have widespread effects.Symptoms usually occur 1-3 days after a traumatic injuryPulmonary (shortness of breath, hypoxemia) Neurological (agitation, delirium, or coma).Dermatological (petechial rash )Haematological (anaemia, low platelets)More frequently in closed fractures of the pelvis or long bones.The petechial rash, which usually resolves in 5-7 days, (Pathognomonic): occurs in 20-509)Hypoxemia due to ventilation-perfusion inequality and intrapulmonary shunting.Acute cor pulmonale is manifested by respiratory distress, hypoxemia, hypotension and elevated central venous pressure.The chest X-ray may show evenly distributed, fleck-like pulmonary shadows {Snow Storm appearance), increased pulmonary markings and dilated right side of the heart.Pulmonary embolismPredisposing factors for pulmonary embolism are:Prothrombotic states: Mutant factor V Leiden, deficiency of antithrombin, protein C & S, hyperhomocysteinemia, APLA, OC pills, pregnancy, cancer, surgery, trauma, bed-ridden patient, long-air travel, COPDPathophysiology:Hypoxemia, increased alveolar-arterial gradient, increased pulmonary vascular & airway resistanceImpaired gas exchange, alveolar hyperventilation, decreased pulmonary complianceSymptoms - massive VTE- sudden hypotension, moderate: RV hypokinesia on ECHOPleuritic chest pain- small, peripheral infarction,Unexplained breathlessness- MC symptom, tachypnea -MC signNon thrombotic PE- fat, air, amniotic fluid.cement, hair, talc, cottonTests-D-Dimer assay- sensitive 'rule out' testFalse positive inMI, pneumonia, sepsis, cancer, pregnancy, post-op stateABG- low pO2 & pCO2, high A-a gradientS.troponin, heart- type fatty acid binding protein, BNP. NT-pro BNP} due to RV microinfarctionECG-Sinus tachycardiaAcute right axis deviationRBBBSIQ3TS signT-wave inversion in VI-V4CXR-Hampton's sign-peripheral wedge shaped density above diaphragm,Westermark's sign - focal oligemia,Palla's sign- enlarged right pulmonary arteryECHO- Mc-Connel's sign- Hypokinesia of RV free wall, normal RV apexMu11idetector-rov. spiral CT- Very sensitive, non invasive testPulmonary angiography -- Cold standardTest (Most specificTreatment:UFH/ LMWH/Fondapari nux/ Warfari nNovel anticoagulants- DTI-Argatroban, lepirudin. bivalirudin; Factor Xa inhibilor- RivaroxabanFibrinolysis with t-PA dissolves thrombus, prevents serotonin release, prevents recurrence of PE by lysing source of thrombusEmbolectomyPrevention:High risk surgery, total hip replacement, medical illness, long-term bed ridden patientMini-UFH/LMWH/fondaprinux/IPC/ rivaroxaban/dalteparinFor 4-5 wksI VC filters
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