Blood Coagulation Case Study

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Case Study #37 M.M., a 76-year-old retired schoolteacher, underwent open reduction and internal fixation for a fracture of his right femur. His preoperative control prothrombin time was 11sec/1.0 and his aPTT was 35 seconds. He has been on bed rest for the first 2 days postoperatively. At 0600, his vital signs were 132/84, 80 with regular rhythm, 18 unlabored, and 99 F (37.2 C). He is awake, alert, and oriented with no adventitious heart sounds. Breath sounds are clear but diminished in the bases bilaterally. Bowel sounds are present, and he is taking sips of clear liquids. An IV of D5 ½ NS is infusing 75 mL/hr in his left hand and orders are to change it to a saline lock in the morning if he is able to maintain adequate PO fluid intake.…show more content…
The physician will gain information from each of these tests to diagnose M.M. Blood coagulation studies screen for PE and also test to detect a prothrombotic state. ABG’s on room air will determine oxygenation of the tissues and pulmonary function. Continuous pulse oximetry is to ensure that he is profusing oxygen effectively and receiving as much oxygen as he needs. Chest x-ray will directly image blood clots causing blockages in the pulmonary arteries. 12-lead ECG will monitor heart rhythm and detect heart dysrhythmias. (Goldhaber & Morrison, 2010). The physician orders ABGs on room air instead of with supplemental O2 in order to get a more accurate lab result of the patient’s condition without supplemental oxygen. Case Study Progress. The room air ABG results are reviewed. According to the results M.M. is in respiratory acidosis. Because of M.M.’s increased Kussmaul respirations he is unable to fully express carbon dioxide from his lungs causing the carbon dioxide concentration of the blood to increase and the pH to decrease causing acidosis. The physician will likely order a ventilation/perfusion (V/Q) lung scan and a continuous heparin…show more content…
They are most commonly caused by blood clots that travel to the lungs from the legs or rarely from other parts of the body (Harms, 2014). M.M.’s pulmonary embolism is most likely from blood clots that formed in his legs because of bed rest. There are two forms of embolus: fat and blood clot embolus in the lungs. Altered mental status is a characteristic of a fat embolus. Decreased SaO2 is a characteristic of a fat embolus. Petechiae is a characteristic of a fat embolus. Chest is characteristic of both a fat embolus and a blood clot embolus of the lungs. Crackles are characteristic of a fat embolism. Increased respirations and pulse are characteristic of a blood clot embolus of the lung. It is important to know where the embolus is coming from to better treat M.M. Before the latest PTT/INR results are back, the physician orders a heparin bolus of 5000 units IV followed by an infusion of 1200 units/hr. The lab calls with a critical value—the aPTT is 120 seconds. Based on these results, the physician is called and asked to change the heparin order to a slower rate because if the aPTT is between 100-120 seconds, heparin needs to be decreased by 100

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