DISTURBANCES OF FLUIDS AND CIRCULATION

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Answers to Objectives and Practice Exercises

(pages 3-4 on handout)

  1. Self explanatory
  2. Read about thrombogenesis on pages 99 and following in Robbins. Know and understand the sequence of formation of the hemostatic plug (1) endothelial damage or denudation, (2) adhesion and aggregation of platelets, and (3) incorporation of fibrin into the hemostatic plug). Note that the vessel wall and the platelets and coagulation factors are 2 parts of Virchow's triad (vascular damage, abnormalities in flow, and hypercoagulability).

    The causes of bleeding are basically 3:

All types of bleeding can be defined in terms of abnormalities or one or more of these systems.

  1. Differences between arteries and veins include the velocity of flow and increased amounts of thrombolysins found in venous endothelium. Empirically, it is found that arteries tend to thrombose only after significant intimal damage and/or luminal stenosis, most commonly due to atherosclerosis. Veins, on the other hand, can thrombose with apparently minimal wall damage; in those cases, there is either sluggish blood flow, usually in the form of congestive heart failure, or a hypercoagulability state.
  2. Atherosclerosis is a disease of arteries causing intimal damage and luminal narrowing, providing 2 of the 3 factors in Virchow's triad, factors which promote thrombosis.
  3. Mural thrombi form on the walls of the left ventricle following large myocardial infarcts, due to both intimal damage secondary to the infarct and poor motion of the wall. Thrombi form in the left atrium and rheumatic heart disease because of sluggish flow due to mitral valve stenosis and atrial fibrillation, and also, some think, due to endocardial damage due to the acute rheumatic fever. More on this disease next fall. Mural thrombi form in an aortic aneurysm because of the wall damage and turbulent flow in the aneurysm.
  4. The patient's left leg is cool, pale and pulseless because of arterial atherosclerosis with subsequent decreased blood flow (hence less heat and color). The right leg has the venous thrombus, causing the leg to be congested and hyperemic (hence, warm and purple and swollen with increased blood). The pulse remains because the arterial system is intact in the right leg. The causes of arterial occlusion would include atherosclerosis with superimposed thrombus, but also could represent an embolus from some site proximal in the systemic circulation (usually the heart chambers or valves). The venous occlusion is most likely a thrombus but could also represent extrinsic compression by tumor, pregnancy, scarring from radiation or surgery. If the occlusion is thrombus, one or more of the following elements of Virchow's triad is at work: wall damage (trauma, surgical intervention, compression) changes in flow (congestive heart failure); or hypercoagulability state (due to surgery, trauma, congenital abnormalities of coagulation factors or platelets, etc).

  5. Finding a migratory thrombophlebitis combined with blue painful leg (phlegmasia cerulea dolens) indicates a high likelihood of a visceral cancer, probably a mucin secreting adenocarcinoma. The multiple thrombotic occlusions and emboli, on both venous and arterial sides, would support this contention. Adenocarcinoma of the pancreas is the tumor most commonly associated with this syndrome, although other mucin secreting adenocarcinomas and even other malignancies have been associated with it. Refer to the reading for other material.
  6. The patient has leg vein thrombi. We use the term thrombophlebitis to indicate a painful condition of the leg veins, and the term phlebothrombosis to indicate bland, asymptomatic vein thrombi. Either condition can give rise to pulmonary embolism, most frequently from the deep leg veins. Sometimes, these conditions appear to be idiopathic (no known cause) but in many, there are one or more elements of Virchow's triad at work. From what you know about Virchow's triad, you ought to be able to explain in medical terminology the pathogenesis and the evolution and fate of thrombi within veins. The words lysis, propagation, organization, calcification, and embolus should appear in your explanation. Remember that the unorganized "tail" of the venous thrombus is usually the portion that embolizes to the lungs. An adequate explanation to the family should consist of use of a drawing or diagram of the venous system, and simplified terminology, such as "solidification of the blood, pieces of which break off and travel in the bloodstream, pass through the heart, and lodge in the vessels in the lungs."
  7. Venous thrombi located in superficial veins rarely cause pulmonary embolism, and never of a size to be of clinical concern.
  8. Multiple pulmonary emboli, occurring over several days, weeks, or months, can lead to pulmonary infarcts, consequent loss of lung tissue, and hypoxia. In contrast, a massive pulmonary embolism, either following multiple small emboli or denovo, leads to sudden death by suddenly occluding the flow of blood from the right heart. Consequently, left heart output falls below the level necessary to sustain life and the patient dies suddenly, usually after a sudden loss of consciousness.
  9. These terms are in the glossary included in the handout on page 2.
  10. The inflammatory events at the border of most infarcts consist of reactive hyperemia (stasis) due to venous dilation, emigration of neutrophils due to chemotactic factors arising within the necrotic tissue (most likely arachidonic acid metabolites), and finally, ingrowth of capillaries and fibroblasts (granulation tissue) extending from the living tissue into the necrotic tissue. The healing begins at the border of the infarct, simply because that is where the living tissue is. There is no way for inflammatory cells or granulation tissue to reach the center of the infarct without traveling in from the border.
  11. The pathogenetic mechanisms for edema in the lungs and peripheral tissue are basically the same. Use the mnemonic S-I-L-K (which stands for Starling's forces, Inflammation, Lymphatic obstruction, and Kidney abnormalities. If you read about congestive heart failure and pulmonary edema (refer to your index), you will find that pulmonary edema is most commonly due to congestive heart failure, usually from abnormalities of the left ventricle or left sided cardiac valves. In those cases, the mechanism is increased hydrostatic pressure (due to abnormal Starling forces or sodium and water retention from kidney disease or kidney hypoperfusion). Pulmonary edema may also be due to endothelial damage from sepsis, lung damage from inhaled toxins or oxygen toxicity, or occasionally from chemotherapeutic agents. In these cases, the mechanism is usually that of inflammation. There are occasional cases of obstruction of lymphatics by tumor to explain pulmonary edema. The pulmonary edema can also be iatrogenic, caused by fluid overload from excess IV fluid. In the case of peripheral edema, the cause often is congestive heart failure, but also can be due to localized obstruction of veins by thrombus, extrinsic pressure due to pregnancy or tumor, or lymphatic obstruction. Inflammation, sepsis, trauma, lymphatic obstruction, and kidney disease can play a role in peripheral edema as well.
  12. The motor vehicle accident victim, despite his borderline low blood pressure and hematocrit, could have lost a considerable volume of blood from his lacerations, and is in danger of losing large volumes of fluid through the burns on his body surfaces. He may be using every compensatory mechanism he can to produce the low normal blood pressure and hematocrit. If he continues to lose fluid from his burns, as he most certainly will, he will go into shock from fluid loss. Decreased perfusion of organs can produce the following: in the brain, dizziness, abnormal mentation, and ultimately unconsciousness; in the heart, ischemia and ultimately subendocardial infarction; in the lungs, ARDS (adult respiratory distress syndrome); in the kidneys, oliguria and eventually acute tubular necrosis with renal shutdown; in the peripheral musculature, weakness; and in the GI tract, ileus with cessation of peristalsis, and eventually mucosal necrosis with hemorrhage, and sepsis due to admission of bacterial flora. The two major complications of burns are 1) fluid loss and 2) infection. The patient's hematocrit is nearly normal initially, because the remaining blood is not diluted by fluid; over the next 2 days the hematocrit falls due to fluid replacement administered by his caretakers. You should anticipate this and be ready to replace blood if necessary.


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