yogabook / pathologie / raynaud syndrome

Raynaud’s syndrome (vasospastic syndrome)

Definition of

Paroxysmal ischemia of the arteries/arterioles caused by vasoconstriction (vasospasms, hence the term vasospastic syndrome), usually of fingers 2-5. forms:

1. Primary: without known underlying disease, but with genetic disposition, involvement of hormonal factors with constitutional-hereditary lability (W:M 4:1). Triggered by endo- and exogenous noxae as well as psychological stress (stress causes peripheral vasoconstriction). The disease usually first appears in adolescence or young adulthood and can regress; women are more frequently affected. Hypoxia-induced tissue damage does not occur here.
   or mainly due to local cold stimuli.
2. Secondary: sometimes without organic vascular disease(Sudeck’sdystrophy, root compression, spinal affections, ergotism, sympathetic irritation), but usually with organic vascular disease (especially arteritis from the collagenosis group, particularly in scleroderma). However, the vasospastic component can also be largely absent in organic circulatory disorders, although there is naturally sensitivity to cold due to reduced blood flow (e.g. in arteriosclerosis, endarteritis obliterans, thromboembolism). e.g. in thrombangitis obliterans, progressive scleroderma, arteriosclerosis, cervical rib and scalenusanterior syndrome, cryoglobulinemia, cold agglutinin disease, after various traumas (e.g. pneumatic hammer work) and intoxications (e.g. vinyl chloride, heavy metals), phaeochromocytoma, dermatomyositis. In contrast to the primary form, the secondary form can cause hypoxia-induced vascular damage.

Primary Raunaud’s syndrome affects 60-90% of women between the ages of 15 and 40. There are several diseases that can adversely affect an existing Raynaud’s syndrome: Carpal tunnel syndrome, PAVK,

ICD I73

Cause

Causes of the primary form:

1. unknown/genetic disposition (hyperactive a-2A-adrenergic receptor for adrenaline, ADRA2A; transcription factor IRX1: increased IRX1 production), plus factors that increase sympathetic tone

Causes of the secondary form:

1. Collagenoses such as SLR or systemic scleroderma,
2. RA,
3. Arteriosclerosis,
4. Vasculitides,
5. Cryoglobulinemia,
6. Polimyositis,
7. Hypothyroidism,
8. traumatic,
9. Vibration damage,
10. Thomocytosis,
11. Cryoglobulinemia,
12. Medication (beta blockers, decongestant nasal sprays, clonidine, migraine painkillers: ergotamine, methysergide),
13. recreational drugs such as nicotine, cocaine, amphetamines

Predisposing

primary form: Smoking, prolonged vibration such as when working on machines

Diagnosis

1. The diagnosis is usually made clinically/anamnestically.
2. Blood laboratory, urine
3. Test for reaction to dilators: if there is no improvement, there is another disorder such as arteriosclerotic plaques.
4. Nail bed microscopy to clarify changes typical of SLE and scleroderma
5. Raynaud’s Condition Score for the assessment of subjective impairment

Symptoms

The primary form is usually seizure-like, the seizures usually last about half an hour and consist of three phases in the full picture (tricolor phenomenon):

1. Phase 1: initially ischemia with pallor (fingers or, more rarely, toes), followed later by stabbing or tingling pain
2. Phase 2: Cyanosis, venous drainage disorder and livid coloration (blue coloration) of the fingers with increasing heat, this phase can also be painful
3. Phase 3: when the arteries become wider again: painful reactive hyperemia with redness

As a rule, fingers 2-5 of both hands are equally affected, the thumbs are not. Further symptoms may occur: Numbness, discomfort and rarely pain, especially in the secondary form:

1. trophic changes with growth disorders of the nails, point necrosis of the fingertips, nail fold necrosis and larger acral necrosis („rat bite necrosis“, after healing „rat bite scars“), wound healing disorders, ulcers

Complications

1. Tissue damage due to trophic disorders in the secondary form

Therapy

1. The frequency of seizures can be reduced by calcium antagonists or nitro preparations (locally as an ointment or orally). Prognosis: The long-term prognosis does not depend on the vasospasticity, but on the underlying disease
2. Cold and dampness must be avoided, especially in the cold-irritable form, and this applies to the whole body. Cold and dampness must be avoided, especially in the cold-induced form, which applies to the whole body.
3. Avoid factors that trigger vasoconstriction: Inhalation smoking: Active and passive smoking are contraindicated. The influence of coffee has not been sufficiently clarified and must be observed by the patient. Stress is also a possible triggering or favoring factor due to the hyperadrenergic state.
4. If necessary, calcium channel blockers with delayed action, used gradually. In severe cases, calcium channel blockers with an immediate effect to counteract the risk of hypoxia damage. Nitroglycerin ointment, mixed with Vaseline, which leads less frequently to side effects such as headaches than other applications of nitroglycerin.
5. Iloprost or bosentan for ulcer formation, also being tested: angiotensin receptor blockers, phosphodiesterase 5 inhibitors, antidepressants such as fluoxetine.
6. Positive effects are generally observed with acupuncture, Botox injections, low-level laser therapy, biofeedback, spinal cord stimulation, local heat application such as heated gloves.
7. If Raynaud’s syndrome occurs in the context of an anxiety disorder: Behavioral therapy
8. In very severe cases, denervation.