Problem 10 Flashcards
What are some of the complications for thromboembolie veineuse
postthrombotic syndrome (chronic venous insufficency, damage to the valves -> swelling and aching) pulmonary hypertension
What is the pathophysiology
- inflammation and platelet activation: Virchow’s triad leads to recruitment of activated platelets, which release microparticles. These microparticles contain proinflammatory mediators that bind neutrophils, stimulating them to release their nuclear material and form web-like extracellular networks called neutrophil extracellular traps. These prothrombotic networks contain histones that stimulate platelet aggregation and promote platelet-dependent thrombin generation. Venous thrombi form and flourish in an environment of stasis, low oxygen tension, and upregulation of proinflammatory genes.
- prothrombotic states: mutations and other risk factors
- embolization: deep venous thrombi detach -> vena cava -> right atrium -> right ventricle -> the pulmonary arterial circulation, thereby causing acute PE. Paradoxically, these thrombi occasionally embolize to the arterial circulation through a patent foramen ovale or atrial septal defect. Many patients with PE have no evidence of DVT because the clot has already embolized to the lungs.
What is the Virchow triad
venous stasis, hypercoagulability, and endothelial injury
What are some of the genetic risk factors
The two most common autosomal dominant genetic mutations are factor V Leiden, activated protein C (which inactivates clotting factors V and VIII), and the prothrombin gene mutation, which increases the plasma prothrombin concentration. Antithrombin, protein C, and protein S are naturally occurring coagulation inhibitors. Deficiencies of these inhibitors are associated with VTE but are rare.
What are some of the auto-immune syndromes that are risk factors
Antiphospholipid antibody syndrome is the most common acquired cause of thrombophilia and is associated with venous or arterial thrombosis.
What are some of the risk factors
cancer, obesity, cigarette smoking, systemic arterial hypertension, chronic obstructive pulmonary disease, chronic kidney disease, blood transfusion, long-haul air travel, air pollution, estrogen-containing contraceptives, pregnancy, postmenopausal hormone replacement, surgery, and trauma. Inflammation predisposes to thrombosis, and conditions such as psoriasis and inflammatory bowel disease have become recognized risk factors of VTE. Sedentary lifestyle.
What happens when a blood clot is in the lungs
The most common gas exchange abnormalities are arterial hypoxemia and an increased alveolar-arterial O2 tension gradient, which represents the inefficiency of O2 transfer across the lungs. Anatomic dead space increases because breathed gas does not enter gas exchange units of the lung. Physiologic dead space increases because ventilation to gas exchange units exceeds venous blood flow through the pulmonary capillaries.
Other pathophysiologic abnormalities include:
- Increased pulmonary vascular resistance due to vascular obstruction or platelet secretion of vasoconstricting neurohumoral agents such as serotonin. Release of vasoactive mediators can produce ventilation-perfusion mismatching at sites remote from the embolus, thereby accounting for discordance between a small PE and a large alveolar-arterial O2 gradient.
- Impaired gas exchange due to increased alveolar dead space from vascular obstruction, hypoxemia from alveolar hypoventilation relative to perfusion in the non-obstructed lung, right-to-left shunting, or impaired carbon monoxide transfer due to loss of gas exchange surface.
- Alveolar hyperventilation due to reflex stimulation of irritant receptors.
- Increased airway resistance due to constriction of airways distal to the bronchi.
- Decreased pulmonary compliance due to lung edema, lung hemorrhage, or loss of surfactant.
What happens to the heart
Pulmonary artery obstruction and neurohumoral mediators cause a rise in pulmonary artery pressure and in pulmonary vascular resistance. When RV wall tension rises, RV dilation and dysfunction ensue, with release of the cardiac biomarker, brain natriuretic peptide. The interventricular septum bulges into and compresses an intrinsically normal left ventricle (LV). Diastolic LV dysfunction reduces LV distensibility and impairs LV filling. Increased RV wall tension also compresses the right coronary artery, limits myocardial oxygen supply, and precipitates right coronary artery ischemia and RV microinfarction, with release of cardiac biomarkers such as troponin. Underfilling of the LV may lead to a fall in LV cardiac output and systemic arterial pressure, with consequent circulatory collapse and death.
What are the indicators of massive PE
Dyspnea, syncope, hypotension, and cyanosis
What are the characteristics of submassive PE
RV dysfunction despite normal systemic arterial pressure. The combination of right heart failure and release of cardiac biomarkers indicates a high risk of clinical deterioration.
Symptoms and signs of PE
dyspnee
Symptoms of TVP
cramps in the leg
Scors used to diagnose
geneva score
wells score
When do we use D-dimeres
if low or intermediate risk of PE
Diagnostics differentiels de TVP
Not all leg pain is due to DVT. Sudden, severe calf discomfort suggests a ruptured Baker’s cyst. Fever and chills usually herald cellulitis rather than DVT. Physical findings, if present, may consist only of mild palpation discomfort in the lower calf. However, massive DVT often presents with marked thigh swelling, tenderness, and erythema. Recurrent left thigh edema especially in young women raises the possibility of May-Thurner Syndrome, with right proximal iliac artery compression of the left proximal iliac vein. However, if a leg is diffusely edematous, DVT is unlikely. More probable is an acute exacerbation of venous insufficiency due to postthrombotic syndrome. Upper extremity venous thrombosis may present with asymmetry in the supraclavicular fossa or in the circumference of the upper arms.
Diagnostics differentiels d’une embolie pulmonaire
Pulmonary infarction usually indicates a small PE. This condition is exquisitely painful because the thrombus lodges peripherally, near the innervation of pleural nerves. Nonthrombotic PE etiologies include fat embolism after pelvic or long bone fracture, tumor embolism, bone marrow, and air embolism. Cement embolism and bony fragment embolism can occur after total hip or knee replacement. Intravenous drug users may inject themselves with a wide array of substances that can embolize, such as hair, talc, and cotton. Amniotic fluid embolism occurs when fetal membranes leak or tear at the placental margin.
Examens complementaires non-imaging
BLOOD TESTS
The quantitative plasma D-dimer ELISA rises in the presence of DVT or PE because of the breakdown of fibrin by plasmin. Elevation of D-dimer indicates endogenous although often clinically ineffective thrombolysis. A normal D-dimer is a useful “rule out” test.
ELEVATED CARDIAC BIOMARKERS
Serum troponin and plasma heart-type fatty acid–binding protein levels increase because of RV microinfarction. Myocardial stretch causes release of brain natriuretic peptide or NT-pro-brain natriuretic peptide.
ELECTROCARDIOGRAM
The most frequently cited abnormality, in addition to sinus tachycardia, is the S1Q3T3 sign: an S wave in lead I, a Q wave in lead III, and an inverted T wave in lead III. RV strain and ischemia cause the most common abnormality, T-wave inversion in leads V1 to V4.
What are some of the non invasive imaging
VENOUS ULTRASONOGRAPHY
Ultrasonography of the deep-venous system. With acute DVT, the vein loses its compressibility because of passive distention by acute thrombus. The diagnosis of acute DVT is even more secure when thrombus is directly visualized.
CHEST CT
CT of the chest with intravenous contrast is the principal imaging test for the diagnosis of PE. The CT scan also provides an excellent four-chamber view of the heart. RV enlargement on chest CT indicates an increased likelihood of death. pelvic and proximal leg DVT also can be diagnosed.
LUNG SCANNING
Lung scanning has become a second-line diagnostic test for PE, used mostly for patients who cannot tolerate intravenous contrast. Small particulate aggregates of albumin labeled with a gamma-emitting radionuclide are injected intravenously and are trapped in the pulmonary capillary bed. The perfusion scan defect indicates absent or decreased blood flow, possibly due to PE.
What is the treatment for TVP
PRIMARY THERAPY
consists of clot dissolution with pharmacomechanical therapy that usually includes low-dose catheter-directed thrombolysis. This approach is reserved for patients with extensive DVT.
SECONDARY PREVENTION
Anticoagulation or placement of an inferior vena cava filter. For patients with swelling of the legs when acute DVT is diagnosed, below-knee graduated compression stockings may be prescribed, usually 30–40 mmHg, to lessen patient discomfort. They should be replaced every 3 months because they lose their elasticity.
What is the ttt for PE
ANTICOAGULATION
There are three major strategies: (1) the classical but waning strategy of parenteral anticoagulation with unfractionated heparin (UFH), low-molecular-weight heparin (LMWH), or fondaparinux “bridged” to warfarin, (2) parenteral therapy switched after 5 days to a novel oral anticoagulant such as dabigatran (a direct thrombin inhibitor) or edoxaban (an anti-Xa agent), or (3) oral anticoagulation monotherapy with rivaroxaban or apixaban (both are anti-Xa agents) with a 3-week or 1-week loading dose, respectively, followed by a maintenance dose without parenteral anticoagulation.
INFERIOR VENA CAVA FILTERS
The two principal indications for insertion of an IVC filter are (1) active bleeding that precludes anticoagulation and (2) recurrent venous thrombosis despite intensive anticoagulation. Prevention of recurrent PE in patients with right heart failure who are not candidates for fibrinolysis and prophylaxis of extremely high-risk patients are “softer” indications for filter placement. The filter itself may fail by permitting the passage of small- to medium-size clots. Large thrombi may embolize to the pulmonary arteries via collateral veins that develop.
Paradoxically, by providing a nidus for clot formation, filters increase the DVT rate, even though they usually prevent PE. Therefore, a common complication is recurrent DVT or caval thrombosis with marked leg swelling.
FIBRINOLYSIS
Successful fibrinolytic therapy rapidly reverses right heart failure and may result in a lower rate of death and recurrent PE by (1) dissolving much of the anatomically obstructing pulmonary arterial thrombus, (2) preventing the continued release of serotonin and other neurohumoral factors that exacerbate pulmonary hypertension, and (3) lysing much of the source of the thrombus in the pelvic or deep leg veins, thereby decreasing the likelihood of recurrent PE.
The preferred systemically administered fibrinolytic regimen is 100 mg of recombinant tissue plasminogen activator (tPA) prescribed as a continuous peripheral intravenous infusion over 2 h.
PULMONARY THROMBOENDARTERECTOMY
To treat chronic thromboembolic pulmonary hypertension.
How long should the patients be treated for
For DVT isolated to an upper extremity or calf that has been provoked by surgery, trauma, estrogen, or an indwelling central venous catheter or pacemaker, 3 months of anticoagulation usually suffice. For an initial episode of provoked proximal leg DVT or PE, 3–6 months of anticoagulation used to be the classic teaching. However, the EINSTEIN CHOICE study found that patients with provoked VTE derived as great a risk reduction in recurrent VTE with extended duration anticoagulation as patients with unprovoked VTE. For patients with cancer and VTE, prescribe LMWH as monotherapy without warfarin and continue anticoagulation indefinitely unless the patient is rendered cancer-free.
How to manage massive PE
For patients with massive PE and hypotension, replete volume with 500 mL of normal saline. Additional fluid should be infused with extreme caution because excessive fluid administration exacerbates RV wall stress, causes more profound RV ischemia, and worsens LV compliance and filling by causing further interventricular septal shift toward the LV. Dopamine and dobutamine are first-line inotropic agents for treatment of PE-related shock.
indication to fibrinolysis
De quoi depend le risque de MTEV/contraception
en fonction de la dose d’œstrogène, du type de CHC utilisé, de facteurs personnels (antécédents familiaux, obésité) et de sa durée d’utilisation
Quels types de CHC augmentent le plus le risque de MTEV
L’augmentation du risque de MTEV dépend de l’équilibre hormonal de la CHC. D’une manière générale, les formulations progestatives plus récentes (CHC de 3e génération (3G) et autres générations (contenant un progestatif tel que de l’acétate de cyprotérone ou de la drospirénone)) augmentent plus
le risque thrombotique veineux que des formulations plus anciennes, dites de 2e génération (2G) composées d’EE et de lévonorgestrel. En effet, comparés aux 2G, les CHC contenant du désogestrel ou du gestodène (3G) multiplient par environ 1,7 le risque de MTEV.
Un contraceptif récent combine le valérate d’estradiol au dienogest. Les données suggèrent, tant sur le plan biologique (marqueurs d’hémostase) que sur une étude épidémiologique isolée, qu’il confère un risque de MTEV proche de celui des 2G.
