Peripheral Vascular Diseases Flashcards

1
Q
A

Reynaud

Description: Idiopathic intermittent episodes of vasoconstriction of digital arteries, precapillary arterioles, and cutaneous arteriovenous shunts in response to cold, emotional stress, or blunt trauma

Pt Common presentation: A triphasic color change of the fingers (occasionally the toes, rarely nipples) is the principal physical manifestation.

The initial color is white from extreme pallor, then blue from cyanosis, and finally, with warming/vasodilatation, the skin appears red. Thumbs are rarely involved.

Associated symptoms: Swelling, throbbing, and paresthesias are associated symptoms.

What defines Primary Reynauds?

Episodes are bilateral and nonprogressive. not associated with a connective tissue disorder

What defines Secondary Reynauds

Progressive and asymmetric. Typically associated with an underlying connective tissue disorder

Epidemiology: W:M 4:1; 75% before 40

Etiology and Pathophysiology?

Unknown.

Risk Factors

  • Existing autoimmune or connective tissue disorder
  • End-stage renal disease with hemodialysis may increase risk if a steal phenomenon develops in association with the arterial-venous shunt.
  • Primary and secondary disease associated with elevated homocysteine levels
  • Smoking is not associated with increased risk of Raynaud phenomenon but may worsen symptoms.

General Prevention

  • Avoid cold exposure.
  • Tobacco cessation
  • No relationship has been established between Raynaud phenomenon and vibratory tool use.

Common associated conditions w/ secondary raynaud

  • Scleroderma; SLE; polymyositis
  • Sjögren syndrome; occlusive vascular disease

Primary S/Sx

  • Symmetric attacks involving fingers
  • Family history of connective tissue disorder
  • Absence of tissue necrosis, ulceration, or gangrene
  • If after ≥2 years of symptoms, no abnormal clinical or laboratory signs have developed, secondary disease is unlikely.

Secondary S/Sx

  • Onset typically after 40 years of age
  • Asymmetric episodes more intense and painful
  • Arthritis, myalgias, fever, dry eyes and/or mouth, rash, or cardiopulmonary symptoms
  • History of medication and/or recreational drug use
  • Exposure to toxic agents
  • Repetitive trauma

Physical Exam

Pallor (whiteness) of fingertips with cold exposure, then cyanosis (blue) and then redness and pain with warming

Ischemic attacks evidenced by demarcated or cyanotic skin limited to digits; usually starts on one digit and spreads symmetrically to remaining fingers of both hands. The thumb is typically spared.

Rarely involves other tissues

Beau lines: transverse linear depressions in nail plate on most or all fingernails that occurs after exposure to cold or any insult that disrupts normal nail growth

Livedo reticularis: mottling of the skin of the arms and legs; benign and reverses with warming

Primary

Normal physical exam

Nail bed capillaries have normal appearance: Place 1 drop of grade B immersion oil on skin at base of the fingernail and view capillaries with handheld ophthalmoscope at 10 to 40 diopters.

Secondary PE

  • Skin changes, arthritis, and abnormal lung findings suggest connective tissue disease.
  • Ischemic skin lesions: ulceration of finger pads (autoamputation in severe, prolonged cases)
  • Nail bed capillary distortion including giant loops, avascular areas, and increased tortuosity
  • Abnormal Allen test (Have patient open and close hand several times and then tightly into a fist. Sequentially occlude the ulnar and radial arteries while the patient opens hand to reveal the return of color as a measure of circulation.)

Primary labs?

Antinuclear antibody: negative

ESR: normal

Secondary labs:

  • Tests for secondary causes (e.g., CBC, ESR)
  • Positive autoantibody has low positive predictive value for connective tissue disease (30%).
  • Antibodies to specific autoantigens (e.g., scleroderma with anticentromere or anti-topoisomerase antibodies)
  • Videocapillaroscopy is gold standard (200 times magnification).

What is the treatment?

  • Dress warmly, wear gloves, avoid cold temperatures.
  • During attacks, rotate the arms in a windmill pattern or place the hands under warm water or in a warm body fold to alleviate symptoms.
  • Tobacco cessation
  • Avoid β-blockers, amphetamines, ergot alkaloids, and sumatriptan.
  • Finger guards to protect ulcerated fingertips

Medication

First Line
Calcium channel blockers (CCBs). Nifedipine is the best studied and most frequently used.

Contraindications pregnancy, CHF

Precautions: may cause headache, dizziness, lightheadedness, edema, or hypotension Increases serum level of digoxin

Second Line

Amlodipine and nicardipine are effective and may have fewer adverse effects.

No longer recommend ACEi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q
A

Etiology and Pathophysiology

  • Varicose veins are caused by venous insufficiency from faulty valves
  • Valvular dysfunction causing venous reflux and subsequently venous hypertension (HTN)
  • Failed valves allow blood to flow in the reverse direction (away from the heart), from deep to superficial and from proximal to distal veins.
  • Deep thrombophlebitis
  • Increased venous pressure from any cause
  • Congenital valvular incompetence
  • Trauma (consider arteriovenous fistula; listen for bruit)
  • Presumed to be due to a loss in vein wall elasticity with failure of the valve leaflets

Risk Factors

  • Increasing age
  • Pregnancy, especially multiple pregnancies
  • Prolonged standing
  • Obesity
  • History of phlebitis (postthrombotic syndrome)
  • Family history
  • Female sex
  • Increased height
  • Congenital valvular dysfunction

Commonly Associated Conditions

  • Stasis dermatitis
  • Large varicose veins may lead to skin changes and eventual stasis ulceration.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
A

Development of blood clot within the deep veins, usually accompanied by inflammation of the vessel wall

Major clinical consequences are embolization (usually to the lung), recurrent thrombosis, and postphlebitic syndrome.

Epidemiology

Age- and gender-adjusted incidence of venous thromboembolism (VTE) is 100 times higher in the hospital than in the community. Almost half of all VTEs occur either during or soon after discharge from a hospital stay or surgery.

Etiology and Pathophysiology

Factors involved may include venous stasis, endothelial injury, and hypercoagulability (Virchow triad).

What are the acquired Risk Factors

Acquired: previous DVT, cancer, immobilization, trauma, obesity, recent major surgery, medications (oral contraceptives, estrogens, tamoxifen), obesity, smoking, antiphospholipid syndrome, acute infectious process, thrombocytosis, pregnancy/puerperium, central venous catheters

What are the Hereditary risk factors?:

deficiencies of protein C, protein S, or antithrombin III; factor V Leiden R506Q, prothrombin G20210A mutation, dysfibrinogenemia, elevated factor VIII activity, hyperhomocysteinemia

History

Clinical assessment of bleeding risk (bleeding with previous history of anticoagulation, history of liver disease, recent surgeries, history of GI bleed) is important prior to initiating treatment.

Modified Wells criteria, a validated clinical prediction rule, is useful to determine pretest probability of having a DVT.

Physical Exam

Symptoms may present as pain, swelling, or discoloration but may be nonspecific or absent.

Resistance to dorsiflexion of the foot (Homan sign) is unreliable and nonspecific.

Edema, due to swelling of collateral veins, is the most specific symptom.

Uncommonly, patients may have phlegmasia alba dolens (“milk leg”) or phlegmasia cerulean dolens due to arterial occlusion secondary to extensive DVTs.

Diagnostic Tests & Interpretation
.

D-dimer (sensitive but not specific; has high negative predictive value [NPV]), indicated in patients with low pretest probability of DVT or PE but not indicated high pretest probability patients; false positives in liver disease, inflammation, malignancy, trauma, pregnancy, and recent surgery

Compression ultrasound (CUS): first-line imaging for DVT due to noninvasive nature and ease of use

In patients with suspected DVT, the diagnosis process should be guided by the assessment of the pretest probability.

Low pretest probability: high-sensitivity D-dimer assay sufficient to exclude DVT if negative. If positive, follow with CUS.

Moderate to high pretest probability: CUS initial test; if positive CUS, then treat DVT. If neg

Medication

Consider starting therapy even before diagnosis confirmation in patients with high pretest probability and acceptable risk of bleeding.

Anticoagulation is mainstay of therapy. Patients with PE or proximal DVT, long-term therapy (at least 3 months) is recommended. Duration of therapy after 3 months is case-by-case basis.

Direct oral anticoagulants (dabigatran, rivaroxaban, apixaban, or edoxaban) recommended instead of vitamin K antagonists for the first 3 months of treatment in patients with lower extremity DVT or PE and no cancer

Use and choice of anticoagulation should be considered based on patient’s history, bleeding risk, cost, and ease of compliance.

First Line

LMWH

Enoxaparin (Lovenox): 1 mg/kg/dose SC q12h or 1.5 mg/kg daily

Dalteparin (Fragmin): 200 U/kg SC q24h

Direct and indirect factor Xa inhibitors

Fondaparinux (Arixtra): 5 mg (body weight <50 kg), 7.5 mg (body weight = 50 to 100 kg), or 10 mg (body weight >100 kg) SC once daily

Rivaroxaban (Xarelto): 15 mg PO twice daily with food for the first 3 weeks then 20 mg PO every day

Apixaban (Eliquis): 10 mg PO twice daily for 1 week followed by 2.5 to 5.0 mg PO twice daily

Edoxaban (Savaysa): 60 mg PO daily (>60 kg), 30 mg PO daily (≤60 kg)

Thrombin inhibitors

Dabigatran (Pradaxa): 150 mg PO twice daily for creatinine clearance >30 mL/min

Vitamin K antagonists

Warfarin (Coumadin): Start with 2 to 5 mg/day. Adjust to a target INR of 2 to 3; overlap with parenteral anticoagulant for minimum of 5 days until therapeutic INR sustained ≥24 hours.

Adverse effects

All anticoagulants increase risk of bleeding.

Heparin and LMWH can also cause heparin-induced thrombocytopenia (HIT) (LMWH has lower risk) and injection site irritation.

Warfarin is teratogenic.

Dosage adjustments may be required for patients with decreased creatinine clearance.

Second Line
Heparin can be given by intermittent SC self-injection.

Pregnancy: LMWH; all others have pregnancy issues absolutely no warfarin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly