Reactions to Cold

8/6/2019 Reactions to Cold

1/52

Cutaneous reactions to cold

Dr geetika paul


2/52

Physiological reactions to cold

Cutaneous changes depend upon:

Actual temperature achieved

Duration of chilling Rate of chilling

Rate of rewarming


3/52

Effect on vascular system

Constriction of arterioles and veins

Increase viscosity of blood

Changes in platelet adhesiveness Decrease conduction velocity in cutaneous

nerves


4/52

Direct effect of cold : veins> arteries

Rewarming and local metabolites

Greater dilator effect on arteries

Resumption of arterial flow

Oedema


5/52


6/52


7/52

Physiological reactions to cold

Diseases of cold exposure

Frostbite

Trench foot

Diseases of abnormal sensitivity to cold

Perniosis

Acrocyanosis

Livedo reticularis Raynauds phenomenon

Cryoglobulinaemia


8/52

Diseases of cold exposure

Frost bite

Trench foot


9/52

Frost bite

Etiology

Acute freezing of tissues onexposure to extreme degrees ofcold

Exposure of only a few seconds

duration may be sufficient tocause it

GREATER SEVERITY OF INJURY

Factors which increase rate ofloss ofheat ie contact with a

cold metal Wind chills

Prior cold injury


10/52

PATHOLOGY

Duration

Severity

Mild perivascular inflammatory change

Severe bulla formation & tissue necrosis


11/52

CLINICAL FEATURES

SITES

Toes, feet, fingers, ears, nose,

cheeks

Initial pain or feeling ofburning

Waxy and white affected skin

Muscles and nerves may bedamaged ; severe cases

arteries , bone and

subcutaneous tissue affected


12/52

Extent & severity of tissue damagebecomes apparent on rewarming Mild : Erythema, mild pain,

soreness

Severe: Blistering and destruction ofepidermis, dermis and deepertissues gangrene

Nerves & blood vessels persistentparaesthesia, abnormal sensitivityto cold, compromised nutrition to

tissue Muscles, subcutaneous tissue or

even bone may be injured


13/52

TREATMENT

Rapid rewarming : Water at 40- 42 C for 20 mins

Early administration of Heparin and LMW dextran

Vasodilator and thrombolytic agents

Surgical removal of gangrenous tissue


14/52

Trench foot

FACTORS

Prolonged exposure to cold

Damp and windy conditions Prolonged immobility

Dependency of the limbs

Vascular disease and smoking


15/52

PATHOLOGY

Dependent oedema and stasis

Perivascular inflammation

Actual occlusion of vessels with ischaemic necrosis Both myelinated and demyelinated nerve fibres

are damaged


16/52

CLINICAL FEATURES:

Cold anaesthetic limb

On rewarming Oedema

Hyperaemia

Painful paraesthesias

Cold sensitivity, vasomotorinstability, hyperhidrosis may persist


17/52

TREATMENT

Analgesics

Antibiotics Bed rest

Adjuvant vasodilator therapy


18/52

Diseases of abnormal sensitivity to

cold

Perniosis/ chill blains

Acrocyanosis

Livedo reticularis

Raynauds phenomenon

Cryoglobulinaemia

Cold urticaria


19/52

Perniosis/ chill blains

Localized, usually tender,inflammatory, erythematous, oftenitchy lesions which may blister orulcerate

ETIOLOGY

Genetic factors

Nutrition

Focal sepsis

Systemic diseases

Dysproteinemias

Myelodysplastic disease

Anorexia


20/52

PATHOLOGY

Idiopathic perniosis is primarily a disease of the

microvasculature

Persistent cold induced constriction of large

cutaneous arterioles

Persistent dilatation of the smaller, more

superficial vessels


21/52

HISTOPATHOLOGY

SUPERFICIAL/ ACRAL Epidermis: Necrotic keratinocytes , Spongiosis

Dermis : Intense oedema of papillary dermis

Marked perivascular mononuclear

cell infilterate of upper dermis

Fluffy oedema of blood vessel wall

DEEP/ THIGH:

Intense mononuclear infilterate throughout the dermis

and subcutaneous fat

Fluffy oedema of blood vessel wall


22/52

CLINICAL FEATURES ONSET

Early winters when humidity is

increased

Lesions are tender, pruritic, red orpurple lesions which may blister or

ulcerate

Sites

Fingers, toes, heels, lower legs,thighs, nose, ears

Individual lesions usually run a self

limiting course over about 3 weeks


23/52

TREATMENT

Prophylactic wearing of warm clothing

Calcium channel inhibitors

Nicotinic acid derivatives

Minoxidil application topically

Phototherapy


24/52

Acrocyanosis

Persistent cyanotic orerythrocyanoticdiscoloration of skin usuallywith a mottled pattern

Chiefly affects the hands

Peripheral arterioles are saidto react unduly to cold

Smaller vessels, especiallythose of the subpapillaryvenous plexus, are dilated

No neuronal deficit seen


25/52

ETIOLOGY

1. Idiopathic

2.

Autoimmune Connective tissue disease

Antiphospholipid Ab syndrome

3. Neoplastic Paraproteinemias

Paraneoplastic syndrome

4. Cryoglobulinemia

5. Eating disorders Anorexia nervosa

Bulimia nervosa

6. Orthostatic disorders

7. Neurological disorders Brachial plexus neuropathy

8. Chronic arsenic poisoning

9. Drugs Butyl nitrate

INF alfa

10. Psychiatric Mental retardation

Schizophrenia

11. Essential thrombocythaemia


26/52

CLINICAL FEATURES

Often a familyhistory present ; genetic basis

Starts in adolescence and persists into adult life

Hands, face involved

Perniosis, erythrocyanosis, livedo reticularis may occur

simultaneously

DIAGNOSIS

Persistent cyanotic discoloration

Normal peripheral pulses

Absence of venous occlusion

TREATMENT

Vasodilators

Topical application: Nicotinic acid derivatives, minoxidil


27/52

Livedo reticularis

Mottled cyanoticdiscoloration of the skin witha characteristic network

pattern which is accentuatedby cold

Dark area of the networkcorresponds to the area ofanastomosis between 2cones, each supplied by anarteriole


28/52

CLINICAL FEATURES:

Mottled cyanotic discolorationoccurs commonly on legs, arms,trunk

Tingling and numbness of skin onexposure to cold

Mottling taking the form ofcomplete network or branchingconfiguration (LIVEDORACEMOSA)

Changes are initially reversible butafter a time vessels becomepermanently dilated andtelangiectatic


29/52

CLASSIFICATION

1. Physiological

Cutis marmorata

2. Idiopathic/ Primary

Congenital

Cutis marmorata telangiectatica congenita

Acquired Uncomplicated

With winter ulceration

With summer ulceration

With systemic vascular involvement

3. Secondary Intravascular obstruction

Vessel wall disease


30/52

Intravascular obstruction Stasis

Paralysis Cardiac failure

Occlusive disease Emboli

Compressed air

NSAIDs, minocycline

Thrombocythaemia

Cryoglobulins

Vessel wall disease Arteriosclerosis

Arteritis : PAN, SLE, RA, Dermatomyositis, lymphoma, pancreatitis

Infections TB, syphilis, hepatitis C, brucellosis, coxiella

Hyperparathyroidism and hypercalcemia


31/52

Treatment

Prophylactic

Cases with ulceration

Anticoagulants

Antithrombotic therapy

Prostacyclin

Treatment of underlying condition


32/52

Raynauds phenomenon

Raynauds phenomenon isdescribed as episodic digital

ischemic vasospasm

triggered by cold oremotional stress leading to a

pale and cyanotic skin with a

postischemic phase of

hyperemia; the typical

tricolore phenomenon


33/52

Characterized by sequentialcolour changes

Pallor cyanosis rubor

Pallor is essential for diagnosis

Causes of Raynaudsphenomenon

Primary Raynauds Phenomenon(Raynauds disease)

Secondary Raynauds phenomenon


34/52

Imbalance of vasoconstriction and vasodilation in Raynauds disease


35/52

Primary Raynauds Phenomenon

Primary Raynauds disease is common, with a

prevalence of 3% to 5% in the general population,

and remains uncomplicated without permanent

injury

Secondary Raynauds phenomenon

Occurs in patients with connective tissue disease,and might have a more severe progression with

digital necrosis and ulceration leading to disability


36/52


37/52

Secondary Raynauds Phenomenon

Causes1. Trauma or vibration

2. Connective tissue diseaseand vasculitis

SS, SLE, RA, Sjogrenssyndrome,MCTD,Dermatomyositis

3. Obstructive arterialdisease

Arteriosclerosis

Buergers disease

4. Neurologicaldisease Thoracic outlet syndrome

Carpel tunnel syndrome

5. Haematological disease Cryoglobulinemia

Paroxysmal hemoglobinuria

Waldenstromsmacroglobulinaemia

6. Drugs and toxins Ergot

Imipramine

blockers

Bromocriptine

Heavy metals OCPs

Clonidine

Bleomycin

Cyclosporin

Amphetamines

7. Miscellaneous Paraneoplastic syndrome

CRF

Hypothyroidism

Anorexia nervosa


38/52

CRITERIA FOR THE DIAGNOSIS OF PRIMARY

RAYNAUDS PHE

NOME

NON1. Intermittent attacks of discoloration of extremeties

2. Absence of evidence of organic peripheral arterial

occlusion

3. Symmetrical or bilateral distribution4. Exclusion of any disease, occupation, trauma or drug

ingestion

5. Absence of immunological abnormality

6. Female sex, age < 25 years

7. H/O cold intolerance since childhood

8. Normal nail fold capillaries


39/52

Secondary Raynaud's Syndrome

Periodic vasospastic attacks of pallor and

cyanosis Abnormal nailfold capillary pattern

Positive antinuclear antibody test

Abnormal erythrocyte sedimentation rate Presence of pitting scars or ulcers of the skin,

or gangrene in the fingers or toes


40/52

CLINICAL FEATURES:

Typical attack: Sudden pallor of1 or more digits cyanosis and erythema

Precipitated by cold, pressure or psychological stimuli

Raynauds disease:

F:M = 5:1

Age of onset < 40 years

Condition is usually symmetrical and affects several digits

Severe cases:

Telangiectasia of the nail fold Thinning and ridging of the nail

Atrophy or sclerosis of fingers (sclerodactyly)

Gangrene rarely


41/52

TREATMENT


42/52

Cryoglobulinaemia

Cryoglobulins are globulins precipitated from

plasma/ serum on cooling

Cryoglobulinemia is characterized by thepresence of cryoglobulins in the serum.

This may result in a clinical syndrome of systemic

inflammation (most commonly affecting thekidneys and skin) caused by cryoglobulin-

containing immune complexes.


43/52

Causes1. Infections

Glandular fever

Hepatitis B/ C Syphilis

Borreliosis

SABE

Leprosy

Kala azar

HIV

2. Autoimmune diseases SLE

RA

Sjogrens syndrome

Vasculitis

3. Lymphoproliferative disease Myeloma

Lymphoma

4. Liver disease

5. Sarcoidosis


44/52

Clinical features:

Intravascular precipitation of cryoglobulins occur

Purpura on exposed parts after cooling

Patchy livedo reticularis

Cold urticaria

Raynauds phenomenon

Atypical ulceration of legs Haemorrhages

Ischemic necrosis

Acrocyanosis

Nailfold capillary abnormalities

Treatment Anticoagulants

Corticosteroids

Plasmapharesis


45/52

Cold urticarias

Cold urticaria is a relatively uncommon

physical urticaria

There are two forms of cold urticaria, a rare

familial (hereditary) form and a more common

acquired form.

With both forms an urticarial rash develops

after being exposed to cold, cold water, and

cold objects.


46/52

Clinical features

The onset of rash after exposure to cold differsbetween the acquired and hereditary forms.

In the acquiredform, symptoms become

obvious in 2-5 minutes after exposure and lastfor 1-2 hours.

In the hereditary form, symptoms may not

become obvious until 9 to 48hours afterexposure and may last for up to 24-48hours


47/52

Signs and symptoms of cold urticaria include:

Itchy weals and angioedema that may belocalised (affecting certain parts of thebody) or generalised (rash over the wholebody).

In some cases systemic symptoms may

develop Shortness of breath, wheezing

Abdominal pain, gastrointestinalulcers

Rapid and irregular heartbeat

In very severe cases hypotension, shock,collapse and even death may occur


48/52

How is the diagnosis made?

Ice-cube test


49/52

Treatment

Patients with cold urticaria should learn to protect themselvesfrom a rapid drop in body temperature.

Any aquatic activities (e.

g.

swimming, surfing) should be doneunder supervision at all times.

Regular doses of antihistamines have generally proven to beineffective, but high doses may be helpful (e.g., four times theusual dose).

Some related medications that have been found to be usefulinclude cyproheptadine and doxepin

There have been reports of successful treatment withleucotriene antagonists, ciclosporin , systemic corticosteroidsand oral antibiotics


50/52

Departmental Studies


51/52

Role ofPentoxifylline in various Dermatoses

with special reference to Leg ulcersDr Shikha Sood -1994

Role ofPentoxifylline in treatment of chronic leg

ulcers of various etiologies was evaluated

Pentoxifylline in a dose of 400 mg tds was given to a

group of18 patients with chronic leg ulcers with

Raynauds phenomenon

88.

8% patients had moderate to markedimprovement after 6 weeks of therapy in the form of

decrease in the frequency and duration of attacks ,

decrease in the associated dysaesthesia and with

faster healing of ulcers


52/52

Thank you

Documents

Reactions to Cold