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Raynauds Phenomenon-Dignosis & Evaluation
Raynaud's phenomenon is characterized by episodic vasospasm and ischemia of the extremities in response to cold or stress. Attacks typically involve color changes from white to blue to red. Primary Raynaud's has no known cause, while secondary Raynaud's is associated with underlying conditions like scleroderma. Nifedipine is currently the only drug approved for treatment, though research continues on therapies like topical nitroglycerin and rho kinase inhibitors to promote vasodilation.
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Raynauds Phenomenon-Dignosis & Evaluation
- 1. DR.W.A.P.S.R.WEERARATHNA REGISTRAR –WARD 10/02
- 2. What isRaynaud’s phenomenon Classificatin/types Raynaud’s phenomenon vs Acral cyanosis Pathogenesis of Raynaud’s phenomenon Clinical presentation Diagnostic work-up/evaluation of a patient Treatment/management Summary Refferences
- 4. Episodic digital ischemiamanifested clinically by the sequential development of digital blanching ,cyanosis, and rubor of the fingers/toes after cold exposure & subsequent rewarming.
- 5. Primary Raynaud’s/ Raynaud’s disease the causes is not known.(idiopathic) Secondary Raynaud’s / Raynaud’s phenomenon where the causes are known.
- 6. Expose to cold/ triggering factor Digital arteries at fingers and toes vasospasm Become pale, less blood flow and low O2 supply Capillaries/venules dialate Cyanosis due to deoxygenate blood Rewarming- (arteries dilate) Blood flow increase, high O2 supply Reactive hyperemia- Color change to bright red Affected area is warm and throbbing pain
- 10. Acrocyansis- Persistent, painless, symmetric cyanosis of the hands, feet, or face caused by vasospasm of the small vessels of the skin in response to cold. The digits and hands or feet are persistently cold and bluish, sweat profusely, and may swell. Unlike Raynaud syndrome, cyanosis persists and is not easily reversed, trophic changes and ulcers do not occur, and pain is absent. Pulses are normal.
- 11. 1.Primary or idiopathicRaynaud’s phenomenon : Raynaud’s disease 2. secondary Raynaud’s phenomenon : 1. Collagen vascular disease- Scleroderma SLE RA DM PM
- 12. 2. Arterialocclusive disease ATH of the extremities Thromboangitis obliterans Acute arterial occlusion Thorasic outlet syndrome 3. Pulmonary hypertension 4. Neurologic disorders Intervertebral disc disease Syringomyelia Spinal cord tumour Stroke PM CTS
- 13. 5. Blood dyscrasias Cold agglutinins Cryoglobulinemias Cryofibrogenemias Myeloproliferative disorders Waldenstrom’s macroglobulinemia
- 14. 6. Trauma Vibration injury Hammer hand syndrome Electric shock Cold injury Typing 7. Drugs Ergot derivatives Methyl sergide BB Bleomycin Vinblastin Cisplatin
- 15. Over 50% ofpatients with Raynaud’s phenomeneon Male:female = 1:5 Age- between 20 & 40 years Figers > Toes One or 2 finger tipsentire fingerall fingers in subsequent attacks Rarely ear lobes/tip of the nose/penis!
- 16. Occurs in frequentlywith migrain headaches & varient angina vasospstic disorders! Physical exam- entirely normal Fingers & toes may be cool between attacks May perspire excessively Sclerodactyly in about 10% Angiography of digits not indicated Milder phenomenon-<1% loose a part of a digit Spontaneous improvement in 15% Progressive disease in 30%
- 17. Ssc- about 80-90%have the disease presenting symptom in 30% Ischaemic fingertipulcersgangreneautoamputation SLE- 20% have the disease DM/PM- 30% of patients RA- frequently occurs Arteriosclerosis of the extremities-men >50 years Burger’s disease-uncommon,young,smoking men
- 18. Large/medium sized arterialocclusion due to thrombus Thorasic outlet syndrome- diminished intravascular pressure/ sympathetic stimulation in brachial plexus PHT-neurohormonal abnormalities in both pulmonary & digital arteries Blood dyscrasias-precipitation of plasma proteins/huperviscosity/RBS & PLT aggregation
- 19. Raynaud phenomenon canbe diagnosed on clinical grounds. Imaging studies, including thermography, isotope studies, and arteriography, have all been used, but none has proven superior to clinical assessment. However, patients with a fixed, nonreversible, cyanotic lesion require further evaluation of the vasculature.
- 20. FBC withindices - To evaluate for polycythemic disorders, underlying malignancies, or autoimmune disorders RFT/BUN - To evaluate for possible renal impairment or dehydration S.Creatinine - To evaluate for possible renal impairment PT/INR - To observe for any evidence of hepatic dysfunction APTT - To observe for any evidence of antiphospholipid antibody disorder or hepatic dysfunction Serum glucose - To evaluate for diabetes TFT - To test for thyroid disorders
- 21. ANA -May be positive in autoimmune disorders and should be obtained in patients with features of these disorders Serum viscosity - Elevated in hyperviscosity syndromes such as paraproteinemias Serum CPK- Elevated in muscle damage such as PM/DM RF - May be elevated in RA, other autoimmune disorders, and some forms of cryoglobulinemia (monoclonal proteins in MM and Waldenström macroglobulinemia have an increased frequency of rheumatoid factor activity)
- 22. Hepatitis panel- Positive for HBV/HCV infection in many patients with cryoglobulinemia Cold agglutinins - Present in Mycoplasma infections and lymphomas Heavy metal screen - To asses for neuropathic pain due to poisoning Growth hormone - To evaluate for acromegaly Plasma metanephrine testing or 24-hour urinary collection for catecholamines and metanephrines - To evaluate for pheochromocytoma LAP score - To evaluate for leukemias in appropriate patients
- 23. Antiphospholipid antibodies studies- Including dilute Russell viper venom studies, anticardiolipin antibodies, and anti-beta-1-glycoprotein-2 antibodies Serum protein and urine electrophoresis - To evaluate for paraproteinemias Flow cytometry or acidified serum lysis (Ham) test - To evaluate for PNH
- 26. Nondrug therapymay be all that is required for mild cases of primary Raynaud phenomenon. With time, most patients learn to incorporate these therapies on their own. Avoiding inciting environmental factors, such as direct contact with frozen foods or cold drinks Insulation against cold and local warming, including gloves or heavy socks and electric and chemical warming devices Discontinuing drugs that may provoke vasospasm Avoiding smoking
- 27. Laser therapy mayresult in less frequent, less severe attacks. (This therapy needs more studies!) Studies of acupuncture have been limited, but have suggested some benefit. Biofeedback and relaxation have shown no difference in frequency or severity of attacks.
- 28. CCB’s- theclass of drugs most widely used for treatment of Raynaud syndrome— especially the dihydropyridines, the most potent vasodilators. Nifedipine is the customary first choice. The usual dosage is 30-120 mg of the extended-release formulation taken once daily. Start with the lowest dose and titrate up as tolerated. If adverse effects occur, decrease the dosage or use another agent, such as nicardipine, or a non-dihydropyridine calcium channel blocker such as such as amlodipine or diltiazem.
- 29. Patients should checktheir blood pressure regularly and may want to keep a log of the number and severity of attacks. This may help in evaluating the efficacy of therapeutic management. Other medications that have been studied in Raynaud phenomenon include the following:
- 30. Topical nitroglycerin (1%or 2%) Iloprost (prostaglandin analog) Selective serotonin reuptake inhibitors (SSRIs) Phosphodiesterase-5 enzyme inhibitors (sildenafil, tadalafil, vardenafil) Losartan Bosentan (endothelin receptor antagonist) – Orphan drug for treating new digital ulcers in patients with systemic sclerosis Botulinum toxin N-acetylcysteine – In patients with systemic sclerosis and digital ulcers
- 31. Therapy with antiplateletagents has been attempted but has not been proved effective. RCT by Gliddon et al showed no significant difference in attack frequency or severity between the ACEI quinapril and placebo. High-quality, well-designed, RCT’s are needed to study the effect of other pharmacotherapy. Anticoagulation is not indicated, except in rare cases of rapidly advancing digital ischemia.
- 32. Rho kinase inhibitors • Responsible for cold-induced expression of alpha- 2 adrenoceptors/vasodialators. Statins • In part due to Rho kinase inhibition Antiplatelet treatments? • Current trial at RNHRD (for primary and secondary Raynaud’s)
- 33. Raynaud’s phenomenonis caused by episodic vasospasm and ischaemia of the extremities, particularly the digits, in response to cold or emotional stimuli Attacks comprise a colour change in extremities from white (ischaemia), to blue (deoxygenation), and then to red (reperfusion) Primary Raynaud’s phenomenon is an exaggerated response to stimuli, with no known underlying cause Secondary Raynaud’s phenomenon is usually caused by connective tissue disease and patients are more likely to develop tissue damage Nifedipine is currently the only drug licensed for use in Raynaud’s phenomenon Key areas of ongoing research include a topical nitroglycerin and a rho kinase inhibitor (vasodilator)