Fm 7 Flashcards
Differential of Unilateral Lower Extremity Edema 5
Most Likely Diagnoses
Lymphedema
Lymphedema is generally painless, but patients may experience a chronic dull, heavy sensation in the leg. In the early stages of lymphedema, the edema is soft and pits easily with pressure. In the chronic stages, the limb has a woody texture and the tissues become indurated and fibrotic.
Lymphedema initially involves the foot and gradually progresses up the leg so that the entire limb becomes edematous.
Cellulitis
Cellulitis is an acute inflammatory condition of the skin characterized by localized pain erythema, swelling, and heat.
Small breaks of skin are associated with streptococcal infection, whereas staphylococcal cellulitis is commonly associated with larger wounds, ulcers, or abscesses.
Patients with diabetes are more susceptible to infections like cellulitis. Diabetic neuropathy causes an unawareness of abnormal pressure distribution, ill-fitting shoes, and cuts or punctures which then develop ulcers.
Vascular disease with diminished blood supply contributes to the development of the lesion, and infection is common.
DVT
Classic symptoms of DVT include swelling, pain, and discoloration in the affected extremity.
Physical examination may reveal the palpable cord of a thrombosed vein, unilateral edema, warmth, and superficial venous dilation.
Classic signs of DVT, including Homan’s sign (pain on passive dorsiflexion of the foot), edema, tenderness, and warmth, are difficult to ignore, but they are of low predictive value and can occur in other conditions such as musculoskeletal injury, cellulitis, and venous insufficiency.
Chronic venous insufficiency may result from DVT and/or valvular incompetence. Following DVT, the valve leaflets become thickened and contracted so that they are incapable of preventing retrograde flow of blood; the vein becomes rigid and thick-walled. Although most veins recanalize after an episode of thrombosis, some may remain occluded. Secondary incompetence develops in distal valves because high pressures distend the vein and separate the leaflets.
Primary deep venous thrombosis can also occur without previous thrombosis. Patients with venous thrombosis often complain of a dull ache in the leg that worsens with prolonged standing and resolves with leg elevation. Examination reveals increased leg circumference, edema, and superficial varicose veins.
The presence of a thrombus in a vein may be accompanied by an inflammatory response in the vessel which may be minimal or may be characterized by granulocyte infiltration, loss of endothelium, and edema. This inflammatory process may also result in a low grade fever.
Smoking and obesity, are the most robust risk factors in the development of DVT and are independent of other risk factors. Diabetes, sedentary lifestyle, hypertension, hyperlipidemia, increasing age, prolonged immobility, surgery, trauma, malignancy, pregnancy, estrogenic medications (e.g., oral contraceptive pills, hormone therapy, tamoxifen (Nolvadex)), congestive heart failure, hyperhomocystinemia, diseases that alter blood viscosity (e.g., polycythemia, sickle cell disease, multiple myeloma), and inherited thrombophilias are other potential risk factors in the development of DVT.
Venous insufficiency
The edema of venous insufficiency can be differentiated from chronic lymphedema as venous insufficiency edema is softer, and there is often erythema, dermatitis, and hyperpigmentation along the distal aspect of the leg, and skin ulceration may occur near the medial and lateral malleoli.
Obesity is commonly associated with venous insufficiency.
Peripheral arterial disease
Peripheral arterial disease (PAD) is the presence of systemic atherosclerosis in arteries distal to the arch of the aorta. As a result of the atherosclerotic process, patients with PAD develop narrowing of these arteries.
Patients with PAD have a history of claudication, which manifests as cramp-like muscle pain occurring with exercise and subsiding rapidly with rest. In addition, later in the course of the disease, patients may present with night pain, nonhealing ulcers, and skin color changes.
An ankle-brachial index (ABI) can be done to determine the presence of PVD. An ABI of <0.9 is consistent with the disease.
Classic risk factors for PAD are smoking, diabetes mellitus, hypertension, and hyperlipidemia. Obesity (body mass index (BMI) >30) increases risk for PAD as well. Recent trials have added chronic renal insufficiency, elevated C-reactive protein levels, and hyperhomocysteinemia to the list of risk factors.
The greatest modifiable risk factor for the development and progression of peripheral arterial disease (PAD) is cigarette smoking. Cigarette smoking increases the odds for PAD by 1.4 for every ten cigarettes smoked per day.
Arterial insufficiency is four times more prevalent in patients with diabetes than in those without diabetes. Nearly half of patients who’ve had diabetes for 20 years or more have peripheral arterial disease (PAD), usually below the knees.
Dvt protocol
Wells score
Low probability 0 or less, do d dimer
High probability, do venous Doppler
Ulcer Classification: The Wagner Grading System 5
Management 3
The Wagner Grading System
Grade 1: Diabetic ulcer (superficial)
Grade 2: Ulcer extension (involving ligament, tendon, joint capsule or fascia)
Grade 3: Deep ulcer with abscess or osteomyelitis
Grade 4: Gangrene forefoot (partial)
Grade 5: Extensive gangrene of foot
Ulcer Management
Grade 1-2 ulcer management generally can be done as outpatient and should include extensive debridement, local wound care, and relief of pressure. If there is significant erythema and or purulent exudate, then treatment for infection is warranted.
Grade 3 lesions require evaluation for possible osteomyelitis as well as peripheral arterial disease. Both of these conditions may need to be addressed prior to resolution of the ulcer. Typically at least a brief hospitalization is required to address these issues.
Grade 5 lesions require emergent hospitalization and surgical consultation, often resulting in amputation.
Prevention of Embolism after discovering dvt
More than 95% of pulmonary emboli arise from thrombi in the deep venous system of the lower extremities. Ninety percent of deaths due to pulmonary embolism result within an hour or two – before diagnostic and therapeutic plans can be implemented. Therefore, prevention and prompt treatment of DVT is the most effective approach to prevention of, and death due to, embolism.
Dvt tx (outpatient and inpatient)
Most patients with DVT may be managed in the out-patient setting, though there are a few important exceptions (see below).
Two oral factor Xa inhibitors (rivaroxaban and apixaban) have been demonstrated to be safe as monotherapy for DVT (option B). These agents have been shown to have similar efficacy to warfarin in preventing PE, but have been demonstrated to cause fewer bleeding episodes than warfarin. Advantages include that they do not require any laboratory monitoring, so they are much easier for patients to take. Disadvantages include their cost (compared to warfarin, which is very inexpensive) and the unavailability of immediate reversal agents in the case of dangerous bleeding. The American College of Chest Physicians recently recommended the choice of factor Xa inhibitors or the direct thrombin inhibitor dabigatran (collectively referred to as non-vitamin K antagonist oral anticoagulants or NOACs) over warfarin for the management of DVT or PE.
The direct thrombin inhibitor dabigatran is another option for oral anticoagulation that has similar advantages to rivaroxaban and apixaban. It has not been studied as monotherapy however (option E), so it is recommended that patients be initiated on LMWH with five to 10 days of overlap.
Before the development of the novel oral anticoagulants (NOACs), warfarin was the mainstay of the management of DVT. It remains an acceptable option and remains commonly used in many settings. Warfarin is a better option for patients who can’t afford the cost of the NOACs and who are concerned about the lack of reversal agents. Warfarin takes several days to reach therapeutic efficacy, so simply starting it alone carries an unacceptable risk of PE (option A). Thus, patients must be started on either LMWH or unfractionated heparin while waiting for the patient’s INR to come into the therapeutic range (2-3). LMWH is the preferred anticoagulant to pair with warfarin in most settings, and may be administered in the outpatient setting (option D)
For many years, the standard of care for DVT was admission to the hospital and administration of unfractionated heparin overlapping with the initiation of warfarin (option C). Inpatient management remains the best option for patients who are hemodynamically unstable, who are at serious risk of acute bleeding with the initiation of anticoagulation (e.g. those with prior admission for gastrointestinal bleeding), or who have obstacles to outpatient management. Examples of this include the inability to afford NOACs and LMWH, or inability to get daily INRs checked during the initiation of warfarin therapy.
DVT Therapy: Advantages of Low-Molecular Weight Heparin (LMWH) over Unfractionated Heparin 6
LMWH has several advantages over unfractionated heparin:
Longer biologic half-life so it can be administered subcutaneously once or twice daily
Laboratory monitoring is not required
Thrombocytopenia is less likely although periodic monitoring of platelets may be needed
Dosing is fixed
Bleeding complications are less common
LMWH may be used in the outpatient setting; whereas unfractionated heparin requires hospitalization as it is administered intravenously with the dosage based on body weight and titrated based on the activated partial thromboplastin time. One advantage to unfractionated heparin is that it can be immediately shut off and reversed in the case of bleeding due to its very short half-life. In a patient with a significant bleeding risk (e.g. recent admission for gastrointestinal bleeding), it is advisable to choose unfractionated heparin over low molecular weight heparin, which has a much longer half-life once injected.
DVT Treatment After Initial Stabilization 3
Warfarin
Prothrombopenic drugs like warfarin are not suitable for initial therapy in thromboembolism because their onset of action is too slow. Their only role is in maintaining anticoagulant protection for prolonged periods.
Monitor warfarin dose by measuring the INR and titrate the warfarin dose every three to seven days to an INR of 2.0-3.0. The advantages of warfarin include its minimal cost and familiarity among medical providers. Its disadvantages include its highly variable dosing range, its requirement of frequent laboratory monitoring, and its high rate of interactions with other medications.
Factor Xa inhibitors
This relatively new class of drugs has the advantage of not requiring weekly lab monitoring of INR and thus makes adherence an easier process. Fondaparinux is the parental form of the drug and could be used instead of LMWH. Rivaroxaban and apixaban are oral factor Xa inhibitors which may be used in place of warfarin. Although these drugs have been found to be as effective as and generally safer (i.e. fewer bleeding complications) than warfarin and LMWH, the negatives of this class of medications includes high cost and difficulty in reversing the anticoagulation in the face of a bleed.
Direct thrombin inhibitors
Dabigatran i s the only direct thrombin inhibitor available on the US market currently. Like the factor Xa inhibitors, dabigatran may be taken orally and does not require laboratory monitoring. It also has been demonstrated in meta-analyses to lead to fewer bleeding complications compared to warfarin. One potential advantage to dabigatran over the factor Xa inhibitors is that a reversal agent (idarucizumab) was recently approved by the FDA, which may be useful in the case of serious bleeding. Neither direct thrombin inhibitors or factor Xa inhibitors may be used in pregnant patients (unlike heparin, they cross the blood-placenta barrier) or in patient with significant renal disease.
How long to treat dvt 3
First proximal DVT or PE
Recommended duration of anticoagulation
Evidence
Provoked
From surgery or by a nonsurgical transient risk factor
Three months
1B
By a non-surgical risk factor and low or moderate bleeding risk
1B
3 months
Unprovoked If bleeding risk is low or moderate Three months. (May consider adding three more months after initial period) 1B If bleeding risk is high Three months 1B
Associated with active cancer
High or low bleeding risk
Extended treatment (i.e. no scheduled stop date)
1 or 2B
Patients with inherited coagulation disorders typically are anticoagulated indefinitely after an episode of thrombotic disease.
Criteria for Recommended Screening for Inherited Thrombophilia 4
Although there are no absolute indications for screening for inherited thrombophilias, expert opinion on which patients are likely to benefit from such investigations includes patients with one of the following:
Initial thrombosis occurring prior to age 50 without an immediately identified risk factor (e.g., idiopathic or unprovoked venous thrombosis).
A family history of venous thromboembolism.
Recurrent venous thrombosis.
Thrombosis occurring in unusual vascular beds such as portal, hepatic, mesenteric, or cerebral veins.
There is currently no evidence to support any change in outcome when using such a strategy.
Recommended Action When Goal INR is Overshot
If the goal INR is substantially overshot, it increases the risk of bleeding complications significantly.
Warfarin should be held, and an oral dose of Vitamin K should be given to reduce INR.
Omitting a dose of warfarin is an insufficient response to a potentially dangerous situation.
Probably the second best answer is to discontinue the warfarin and repeat the INR in 24 hours, and this would be appropriate if the INR was greater than five and less than nine.
It is inappropriate to continue warfarin at the current dose because of risk of bleeding.
Finally, discontinuing warfarin, giving 5 mg Vitamin K IV, and repeating until INR less than 4.0 is an overreaction to a supratherapeutic INR in a non-bleeding patient.
