Pathophysiology Heparin & Thrombocytopenia
QUESTION 1
A 22-year-old male is in the Surgical Intensive Care Unit (SICU) following a motor vehicle crash (MVC) where he sustained multiple life-threatening injuries including a torn aorta, ruptured spleen, and bilateral femur fractures. He has had difficulty maintaining his mean arterial pressure (MAP) and has required various vasopressors. He has a triple lumen central venous catheter (CVC) for monitoring his central venous pressure, administration of medications and blood products, as well as total parenteral nutrition. Per hospital protocol, he is receiving an unfractionated heparin 1:1000 flush after administration of each of the triple antibiotics that have been ordered to maintain patency of the lumens. Seven days post injury, the APRN in the SICU is reviewing the patient’s morning labs and notes that his platelet count has dropped precipitously to 50,000 /mm3 from 148,000/mm3 two days ago. The APRN suspects the patient is developing heparin induced thrombocytopenia (HIT).
Question 1 of 2:
What is underlying pathophysiology of heparin induced thrombocytopenia?
QUESTION 2
A 22-year-old male is in the Surgical Intensive Care Unit (SICU) following a motor vehicle crash (MVC) where he sustained multiple life-threatening injuries including a torn aorta, ruptured spleen, and bilateral femur fractures. He has had difficulty maintaining his mean arterial pressure (MAP) and has required various vasopressors. He has a triple lumen central venous catheter (CVC) for monitoring his central venous pressure, administration of medications and blood products, as well as total parenteral nutrition. Per hospital protocol, he is receiving an unfractionated heparin 1:1000 flush after administration of each of the triple antibiotics that have been ordered to maintain patency of the lumens. Seven days post injury, the APRN in the SICU is reviewing the patient’s morning labs and notes that his platelet count has dropped precipitously to 50,000 /mm3 from 148,000/mm3 two days ago. The APRN suspects the patient is developing heparin induced thrombocytopenia (HIT).
Question 2 of 2:
The APRN assesses the patient and notes there is a decreased right posterior tibial pulse with cyanosis of the entire foot. The APRN recognizes this probably represents arterial thrombus formation. How does someone who is receiving heparin develop arterial and venous thrombosis?
QUESTION 3
A 33-year-old female is brought to Urgent Care by her husband who states his wife has gotten suddenly confused and complains of a severe headache. He also noticed large bruises on her legs which were not there yesterday. Only significant past medical history is that the patient developed herpes zoster 2 weeks ago and was given acyclovir for treatment. Physical exam revealed well developed female who is only oriented to person. Large areas of ecchymosis noted on both arms and legs. Stat CBC revealed a platelet count of 18,000/mm3, hemoglobin of 8 g/dl and hematocrit of 24%. The patient was immediately transported to the Emergency Room by Emergency Medical Services (EMS) where further work up demonstrated idiopathic thrombotic thrombocytopenic purpura (TTP).
Question:
What is the pathophysiology of TTP?
QUESTION 4
A 64-year man is recovering from a transurethral resection of the prostate for treatment of benign prostate hyperplasia. The patient is receiving intravenous antibiotics for the urinary tract infection that was found on the preoperative urine culture and sensitivity (C & S). The post-operative course has been smooth and the APRN is removing the 3-way Foley catheter when there is a sudden release of bright red blood with many blood clots in the Foley bag. The patient becomes hypotensive, tachycardic and the APRN notes new ecchymoses on the patient’s arms and legs. The patient was immediately transferred to the surgical intensive care unit (SICU) and a stat hematology consult was conducted. Stat CBC, d-dimer, peripheral blood smear, partial thromboplastin time, Prothrombin time/international normalization ratio (INR), and fibrinogen labs were drawn. Results were:
CBC with markedly decreased platelet count, peripheral blood smear showed decreased number of platelets and presence of large platelets and fragmented red cells (schistocytes), prothrombin time prolonged as was the partial thromboplastin time. The d-dimer was markedly elevated, and fibrinogen level was low. The diagnosis of disseminated intravascular coagulation (DIC) was made based on clinical picture and laboratory data.
Question 1 of 2:
What is DIC and how does it develop?
QUESTION 5
A 64-year man is recovering from a transurethral resection of the prostate for treatment of benign prostate hyperplasia. The patient is receiving intravenous antibiotics for the urinary tract infection that was found on the preoperative urine culture and sensitivity (C & S). The post-operative course has been smooth and the APRN is removing the 3-way Foley catheter when there is a sudden release of bright red blood with many blood clots in the Foley bag. The patient becomes hypotensive, tachycardic and the APRN notes new ecchymoses on the patient’s arms and legs. The patient was immediately transferred to the surgical intensive care unit (SICU) and a stat hematology consult was conducted. Stat CBC, d-dimer, peripheral blood smear, partial thromboplastin time, Prothrombin time/international normalization ratio (INR), and fibrinogen labs were drawn. Results were:
CBC with markedly decreased platelet count, peripheral blood smear showed decreased number of platelets and presence of large platelets and fragmented red cells (schistocytes), prothrombin time prolonged as was the partial thromboplastin time. The d-dimer was markedly elevated, and fibrinogen level was low. The diagnosis of disseminated intravascular coagulation (DIC) was made based on clinical picture and laboratory data.
Question 2 of 2:
What factors contribute to the development of DIC?