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INTRODUCTION

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CASE HISTORY • Part 1

A 37-year-old man is admitted to the hospital intensive care unit for his third episode of acute pancreatitis. Other than a history of chronic alcoholism without evidence of cirrhosis, his past medical history is unremarkable. Examination reveals an anxious white male with a diffusely tender, somewhat rigid abdomen; few if any bowel sounds; and a positive Turner sign. Vital signs: BP - 110/60 mm Hg, P - 110 bpm, R - 16 bpm, temp - 38°C.

CBC: Hemoglobin/hematocrit - 11 g/dL/33%

MCV - 90 fL MCH - 30 pg MCHC - 33 g/dL

WBC count - 16,000/μL

Platelet count - 110,000/μL

Serum amylase and lipase - both elevated

Serum LDH - 1,000 IU/mL

Coagulation studies:

PT = 15.1 seconds (<14 seconds)

PTT = 42 seconds (22–35 seconds)

Questions
  • What abnormalities are apparent from the initial laboratory work?

  • In a patient with acute (hemorrhagic) pancreatitis, what additional coagulation studies are in order?

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Widespread activation of the coagulation pathways can occur as a part of a systemic illness. When severe, it presents as disseminated intravascular coagulation (DIC) with life-threatening intravascular clotting and fibrinolysis. This can result in sufficient platelet and coagulation factor depletion to cause severe bleeding. Other conditions are associated with lower-grade DIC or a process that is limited to platelet thrombus formation (so-called platelet DIC). In the latter case, organ damage can be the dominant abnormality. Therefore, it is important to be able to recognize the presence and nature of DIC because it will help to speed the diagnosis, prevent organ damage, and manage the patient's bleeding tendency.

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THROMBOSIS AND THROMBOLYSIS

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Thrombus formation is a highly controlled process, where platelet activation and aggregation, thrombin generation, and subsequent clot formation are under delicate control. Normal endothelial cells adjacent to a site of injury are responsible for limiting platelet activation and aggregation by releasing prostacyclin and nitric oxide and by degradation of adenosine 5′-diphosphate (ADP) by a membrane-associated ADPase (Figure 35-1). Tissue factor pathway inhibitor (TFPI) limits activation of factor X by binding to the TF-VIIa-Xa complex. At the same time, circulating thrombin is inactivated by antithrombin, a specific protease inhibitor. This reaction is facilitated by exogenous heparin and endogenous heparan sulfates, heparin-like molecules produced by endothelial cells. In addition, endothelial release of thrombomodulin after thrombin activation effectively downregulates thrombin activity by activating protein C, which then cleaves factors Va and VIIIa. Protein S is a cofactor in this latter reaction.

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FIGURE 35-1

Thrombosis and thrombolysis. The rush to fibrin clot formation in a consumptive coagulopathy is counteracted by several inhibitors. Endothelial cells release prostacyclin, nitric oxide, and ADPase to inhibit platelet activation and aggregation. Tissue factor pathway inhibitor (TFPI) inhibits factor X activation by binding to the TF-VIIa-Xa complex. In addition, thrombomodulin is induced by endothelial cells after activation by thrombin, and thrombomodulin catalyzes conversion of protein C to its activated form, which ...

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