Purpura is a group of
diseases characterized by skin petechiae and may be associated with other
local or systemic manifestations.
Petechiae are small,
purpuric lesions up to 2 mm across while ecchymoses or bruises are larger
extravasations of blood.
Purpura is normally
distinguished from erythema when pressure is applied by finger or by
pressure of a slide on the erythematous patch (diascopy )fails to blanch
the lesion.
The characteristic color
changes in purpuric lesions vary from purple, orange, brown and even blue
and green. Discoloration of the skin or mucous membrane is due to
extravasations of blood.
Types
of Purpura
Classification of purpura
is usually unsatisfactory. There are different classifications in the
different textbooks depending either on the morphological or etiological
characters of these diseases.
-
Thrombocytopenic purpura
This type of purpura is
related to platelet abnormality either due to reduced formation or their
destruction by different factors . Purpura due to platelet deficiency
usually occurs with a platelet count below 10000 /mm3 and is seldom
observed with a count abov50000/mm3.
Platelet plug is formed
as a result of injury or disease of the vascular wall releasing serotenin
and thromboxane A2 causing vasoconstriction and increase adhesion and
aggregation of the platelets forming a platelet plug.
Developing platelet plugs
are reinforced by fibrin strands formed as a result of activation of the
plasma clotting system by platelet factor3 when this is exposed by
alterations in the surface characteristics of the aggregated platelets.
Etiology
Thrombocytopenia purpura
may be primary (idiopathic ) due to unknown causative factors or secondary
to different agents.
-
Idiopathic thrombocytopenia purpura.
This disorder
results from immune destruction of platelets. Viral antigen-antibody
reactions may be demonstrated in acute forms of the disease, whilst most
chronic cases are associated with antiplatelet autoantibodies. The
platelets fall below 50 000/mm3 and may even be absent.
-
Secondary thrombocytopenia purpura.
Different external and
internal factors may cause thrombocytopenia purpura
-
Drugs:
The most common drugs that
can cause purpura are:
Antibiotics: different
antibiotics may cause purpura such as:
Ampicillin,penicillin,Chloramphenicol, Rifampicines, Sulfonamides and
Trimethoprine.
Analgesics:
acetylsalicylic acid , phenylbutazone .
Other drugs: quinine ,
quinidine , sedormid and thiazides .
-
Chemicals: benzol, and snake
venom.
-
Infections: septicemia,
typhoid, typhus, smallpox, chickenpox, vaccinia, scarlet fever,
influenza, and subacute bacterial endocarditis.
-
Bone marrow diseases: leukemia,
aplastic anemia and pernicious anemia are the commonest causes of
thrombocytopenia.
-
Splenomegaly: may be associated
with purpura .
-
Haemangioma:thrombocytopenia
may be associated with haemangiomas.
-
Wiskott-Aldrich syndrome:
(thrombocytopenia, eczema and infections).
-
Uraemia: that is rare in
children in whom thrombocytopenic purpura and bleeding are associated
with fever, hemolytic anemia , renal and neurological symptoms.
-
Physical factors: such as sun
stoke .
Clinical
Manifestations
Thrombocytopenic purpura
may occur at any age, but in two-thirds of cases it occurs in young age .
Females are more commonly affected than males.
The onset may be gradual
or, acute especially in children. There is an appreciable mortality,
especially in the acute form, mainly from cerebrovascular accidents.
Bleeding occurs into the
skin with areas of petechiae or larger hemorrhages and may occur in
internal organs.
Joint involvement is
unusual.
The spleen may be
slightly enlarged .
Spontaneous remission
occurs in a proportion of acute cases, but is rare in chronic cases of
more than 3 months‘ duration in which a continuous or fluctuating course
may occur.
Diagnosis
Clinical picture.
Blood picture: low
platelet count , Megakaryocytes are present in normal or increased numbers
in the bone marrow.
Negative bone-marrow
findings.
Differential
Diagnosis
Systemic lupus
Drug-induced purpura
Disseminated
intravascular coagulation
Renal failure.
Treatment
-
Treatment of the
cause.
-
Corticosteroids .
-
Immunoglobulins .
-
Splenectomy is of
real help in most chronic cases and in acute cases not responding to
corticosteroids . After Splenectomy the platelet count tends to remain
low but the purpura tends to improve.
-
Immunosuppressive
therapy: is indicated in cases, which fail to respond to splenectomy and
steroids or where splenectomy is contra-indicated .
-
Danazol may be of
help in some cases.
Fig. 345. Purpura
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Fig.346
Purpura (Vasculitis)
|
Fig.347. Vasculitis |
Fig. 348. Purpura
|
Fig. 349. Purpura
|
-
Non
Thrombocytopenic Purpura
Vascular
purpura
Non-thrombocytopenic
purpura comprises the vast majority of cases of purpura.
Blood may leak as a
result of:
Damage to small blood
vessels.
Increase in the
intraluminar pressure.
Deficient vascular
support.
Bleeding may arise from a
disturbance of one or more of the following mechanisms:
-
Contraction of the
vessel wall.
-
Plugging of small
vessels by platelets.
-
Coagulation of blood.
Often all these factors
operate together and the exact role and importance of each in the
pathogenesis of the purpuric reaction varies.
Other factors leading to
these disturbances are multiple and obscure.
Etiology
of Vascular Purpura.
-
Damage to the blood
vessels.
Capillary fragility
depends upon numerous factors, including the integrity of the capillary
endothelium itself and also the ability of platelets to fill any gaps,
which may arise in it .
The capillary resistance
can be determined by a simple test called Hess test. This can be achieved
by inflating a sphygmomanometer cuff around the upper arm to a constant
pressure of 80 mm of mercury (or less if this approaches the systolic
blood pressure) for 5 min.
Petechiae may develop in
the presence of abnormalities of the vascular wall, thrombocytopenia or
platelet dysfunction, and can be counted after releasing the pressure. Up
to five in a measured area 5 cm across just below the ante cubital fossa
may be considered normal. Raised intravascular pressure may cause purpura
in the absence of any other disease.
Simple petechial lesions
may develop after prolonged coughing, vomiting or by pressure on localized
area of the skin .
Direct damage due to a
trauma or secondary to different factors as immunological factors in
Schwartzmann phenomenon that is due to antigen-antibody reaction causing
hemorrhagic necrosis of arterioles and venules.
-
Raised
intravascular pressure.
Etiology
-
Hypertension.
-
Gravity and venous
stasis are most important causes of purpura.
-
Suction of a certain
part of the skin may cause localized purpura such as in self-inflicted
lesion , in dermatitis artefacta.
-
Different physical
factors as cold , pressure , trauma or change in gravity.
-
Infections.
-
Additives to food and
beverages due to tartrazine and other food additives.
-
Drugs
Different drugs and
toxins may cause purpura which are mainly the following:
Arsenic, atropine,
bismuth, barbiturates, carbromal, chloramphenicol, chlorothiazide,
chlorpromazine, di-ethyl stilboestrol, gold, hair dye, isoniazid, iodides,
menthol, meprobamate, paraaminosalicylic acid, piperazine, quinidine,
quinine, reserpine, snake venoms, sodium salicylate, sulphonamides, ,
thiouracil, tolbutamide and glyceryl trinitrate.
Corticosteroids Purpura
This type of purpura is
due to lack of support of the blood vessels. Strong potent topical
steroids as Colbetasol used for a long time can cause local dermal
collagen atrophy, telengectasia where the blood vessels looses their
support, become fragile and rupture causing local purpuric rash.
-
Solar Radiation
Prolonged exposure to sun
will also lead to collagen atrophy leading to loss of support to the
dermal arterioles and venules.
This type of purpura
occurs mainly on sun-exposed parts of the hands and forearms or on the
legs. Lesions appear after minor trauma or apparently spontaneously.
-
Scurvy purpura
The support for the blood
vessels is abnormal in scurvy. Either small or large bruises may appear on
the limbs with mild trauma. Petechial hemorrhages may also occur,
especially on the legs and from the gums.
-
Toxic purpura
Capillary damage may be
direct due to certain toxins that cause toxic effect to the vascular wall
or due to an allergic reaction without any change in the platelet count or
morphology .
Drugs such as certain
antibiotics (chloramphenicol, sulphonamides) quinine, carbromal and
barbiturate may cause capillary damage.
-
Contact purpura
Certain substances may
cause contact purpura such as azodyes, rubber additives, certain clothing
(khaki cloth) used by the army.
-
Purpura associated
with infections
Purpura may be associated
with infection such as septicemia, meningococcal, rickettesial, viral
infections and subacute bacterial endocarditis. The purpura may also
appear in the prodromal period of many infections such as measles, where
this is often a sign of a severe infection.
Purpuric eruptions may
also be found in the course of candidal infections.
-
Purpura associated
with systemic diseases
Non-thrombocytopenic
purpura may be caused by a variety of systemic diseases. The mechanism of
capillary damage is unknown.
The common systemic
diseases associated with purpura are:
Uraemia
Liver diseases
Diabetes
Hemochromatosis and
carcinomas.
Amyloidosis due to
infiltration of the capillaries with amyloid.
Malnutrition: It seems
probable that changes in coagulation, platelets and capillaries all play
their part.
Fat embolism:Petechiae,
which may be few or very numerous, are an important sign . They occur
particularly on the upper part of the body 2-3 days after a major injury.
Minute fat emboli have been found within the vessels at the sites of the
petechiae.
Endocrine abnormalities:
such as in Cushing‘s disease.
DYSPROTEINAEMIC
PURPURA
Purpura may be the
presenting and sometimes the only symptom of disturbances in plasma
proteins.
It may occur with
cryoproteinaemia. This type appears most commonly on the unprotected parts
after exposure to cold.
Hyper globulinaemia due
to different causes such as idiopathic (Waldenstrom‘s) sarcoid, lupus
erythematosus, Sjogren‘s syndrome, myeloma, may give rise to purpura.
The clinical features of dysproteinaemic purpura are erythematous papules
that occur mainly on the legs and rapidly progress to form punctate
purpuric lesions
In mild cases the
eruption disappears within few days, but in more severe cases the purpura
becomes confluent and permanent.
A similar pattern has
been reported in association with cystic fibrosis, whether or not
associated with cryoglobulinaemia.
HENOCH-SCHOENLEINE
PURPURA
(Anaphlactoid
purpura)
This type affects
children and young adults . Urticaria and purpura with multisystmes
involvement of kidneys, bowel and joints characterize this type of
purpura.
Etiology
Damage to the walls of
small blood vessels due to deposition of immune-complex substances.
Cryoglobulins have been
found rather than the immune complexes.
An antigen associated
with upper respiratory tract infection is suspected to be part of the
usual cause of the immune response.
Clinical
Manifestations
General
manifestations:
The manifestations
usually begin with mild fever, sore throat, and upper respiratory tract
infections which may precede the skin rash.
Skin
manifestations:
Macular rash appears
first on the extensor surfaces of the limbs and buttocks, which becomes
rapidly, urticarial and purpuric with central necrosis of the lesions.
Systemic
manifestations
Renal involvement, which
is focal nephritis. This is a serious manifestation of the disease.
Bowel involvement leads
to abdominal colic and hemorrhage.
Polyarthritis and pain in
the joints are another manifestation.
The course of the disease
is chronic . It may take weeks for regression of the skin lesions, but
usually there is recurrence.
Renal and bowel
manifestations may improve or may cause serious complications.
CAPILLARITIS
OF UNKNOWN CAUSE
These are vascular
diseases of undetermined cause with different manifestations and share the
same histopathological features.
These include different
diseases mainly:
Schamberger‘s
Disease
This is a progressive
pigmented purpuric dermatosis of unknown etiology, affecting male children
and other age groups that may show familial incidence.
Clinical
Manifestations
The skin lesion is
irregular brown plaques that may present with different pigmentations due
to hemosidrin deposits. ‘Cayenne pepper‘ spots characterize the
lesions.
The condition is usually
asymptomatic , although there may be some slight itching. The eruption is
characteristically very chronic and may persist for many years. The
pattern of the eruption changes where these may show slow extension with
some clearing of the original lesions. Spontaneous cure may occur
eventually.
Differential
Diagnosis
Drug eruption: different
types of drugs particularly carbromal and other drugs may cause similar
types of purpuric skin lesions.
Food allergy and food
additives.
Clothing dermatitis.
Hyperglobulinaemic
purpura.
Early mycosis fungoides .
ITCHING
PURPURATOUS
(Eczematide-like
purpura )
Itching purpura is an
eczema like purpura, which begins usually as an eczematous purpuric
reaction around the ankles and spreads peripherally.
The eruption often has a
rather characteristic orange color.
Eczematous skin lesions
presenting as erythematous purpuric macules that may simulate shoe
dermatitis or drug reaction. The condition rarely becomes generalized,
affecting mainly exposed areas due to chaffing or friction.
Spontaneous improvement
is usual, but recurrences may occur.
Differential
Diagnosis
Drug reactions:Carbromal
sensitivity, Meprobamate and Carbamazepine.
Food allergy .
Clothing or rubber
contact dermatitis.
Schamberg‘s disease is
distinguished by its more persistent course and by the usual lack of
itching.
LICHEN
AUREUS
( Lichen
purpuricus)
This is a more localized,
more intensely purpuric eruption.
Clinical
Manifestations
Skin lesions begin as
rust-colored to purple non-itchy solitary macules, seldom truly golden,
which may resemble a bruise. Small vesicles may be seen in its course of
the disease, that may persist for few years.
Histopathological changes
are in the form of capillaritis, infiltration with lymphocytes and
histocytes.
Treatment
Topical steroids may be
helpful.
PURPURA
ANNULARIS TELENGECTODES
(
Majocchi's disease )
This type of capilliritis
may show familial tendency that affects mainly young adults of both sexes,
where any age is not immune.
Clinical
Manifestations
Lesions occur at any
site, often in the absence of venous stasis and may be few in number or
very numerous. Skin eruption presents with small annular plaques,
telangiectasia and haemosidrin deposits causing purple, yellow or brown
patches that may contain ‘cayenne pepper‘ spots.
Individual lesions
persist unchanged for many months or years, or there may be slow
centrifugal extension. Sometimes the lesions disappear and may recur with
the same eruption.
Treatment
The lesions are
asymptomatic and rarely treatment is needed .
COAGULATION
DEFECTS
These diseases are due to
defects in one or more of the numerous factors related to clotting with
abnormalities of the platelet functions .
NEONATAL
PURPURA
Vascular purpura is
uncommon in the neonatal period but may occur.
Hemorrhagic disease of
the newborn is due to an accentuation of the normal fall of prothrombin
within the first week of life.
Differential
Diagnosis
Purpura or bleeding
within the first month of life should be differentiated from different
types of purpuric skin diseases:
Deficiency of the
clotting factors .
Deficiency of the protein
S or protein C.
Hemophilia and other
bleeding diseases, which rarely cause bleeding at this age.
Thrombocytopenia may be
due to congenital failure of megakaryocytes.
Immunological mechanism
in a child whose mother has idiopathic thrombocytopenic purpura or
systemic lupus erythomatosus.
Neonatal rubella and
Wiskott-Aldrich syndrome.
Haemangiomas.
CUTANEOUS
SYSTEMIC ANGITIS
Cutaneous systemic
angitis is a complex and widespread necrosis of the small blood vessels.
Etiology
Different factors are
blamed to be the cause of systemic angitis.
These include:
Drugs: the
most common drugs which can cause systemic angitis are :sulfonamides, acetylsalicylic acid (Aspirin),
phenothiazines, barbiturates.
Infections:
Streptococcal infection , pyodermas , upper respiratory tract infection .
Insecticides and
weed killers.
Cutaneous systemic
angitis includes different diseases mainly :
NEONATAL
PURPURA FULMINANS
Purpura fulminans is a
serious disorder affects patients of different ages, but most commons in
children.
Clinical
Features
Lesions are characterized
by the development of more or less symmetrical and well-defined
“lakes“ of confluent ecchymosis without petechiae mainly on limbs,
trunk and face.
The onset is sudden, and
the lesions enlarge rapidly, with coalescence and often with the
development of hemorrhagic bullae and central necrosis. There is a
surrounding erythema and the lesions are tender. The patient is frequently
febrile. Vascular thrombosis is a particular feature of this disorder.
There is a substantial
danger of internal hemorrhage, shock and death.
Etiology
In older children, purpura fulminans may
have several causes. It is a highly characteristic feature of
meningococcal septicemia and may occur as a sequel to a number of other
infections, including common infections such as streptococcal infections,
varicella, and measles. In the neonate, however, its occurrence is very
suggestive of protein C deficiency .
Treatment
Treatment comprises rapid
transfusion of fresh frozen plasma.
INFANTILE
ACUTE HEMORRHAGIC EDEMA
It is a distinctive
disorder, comprising a combination of purpura, often in a cockade pattern,
and an inflammatory edema of the limbs and face, occurring almost
exclusively in children under the age of 2 years, with a tendency to
recurrence in the short term and subsequent spontaneous resolution .
The cause of infantile
hemorrhagic edema remains unknown, though it may represent an infantile
analogue of Henoch-Schonlein purpura.
DISSEMINATED
INTRAVASCULAR COAGULATION
(Purpura
Fulminans)
Disseminated
intravascular coagulation may produce a clinical picture varying from a
severe and rapidly fatal disorder to a relatively minor disorder.
Predisposing
Factors
This is due to congenital
or an acquired deficiency of the protein S and protein C components of the
anticoagulation system.
Etiology
The causes of
disseminated vascular coagulation are:
Extensive tissue damage .
Severe infections
(especially Gram negative septicemia).
Immune reactions.
Malignant disease.
Snake bites.
Giant haemangiomas.
The normal inhibitory
mechanisms of clotting are over-coming, so that there is intravenous
coagulation, followed by consumption and depletion of platelets and plasma
clotting factors.
Clinical
Manifestations
The manifestations
include bleeding, thrombo-embolism and hemolytic anemia.
The onset may be acute,
sub acute or chronic.
Mild
cases: show petechiae, purpuric
papules, hemorrhagic bullae and acral cyanosis. There is decreased
fibrinogen and increased fibrin degradation products. Skin biopsy may be
useful in showing intravascular thrombi.
Severe
cases: the onset is sudden, with
high fever and a very extensive, usually symmetrical, purpuric rash of the
extremities.
A fatal outcome may
follow within 2 or 3 days.
Treatment
Treatment of shock and
replacement therapy with platelets, fibrinogen, and fresh frozen plasma.
Symptomatic treatment.
Treatment of the cause.
The role of heparin is
still somewhat controversial.
MANIFESTATIONS
OF CUTANEOUS SYSTEMIC ANGITIS
Skin
manifestations
The lesion usually begins
in the lower legs, buttocks , hands and wrists. Mucous membrane lesions
are rare. Different skin lesions may appear either purpuric rash,
hemorrhagic vesicles and bullae may develop. Finally there are nodules and
ulceration, which persist for a long period .Usually one type of these
lesions, manifest either purpuic rash alone or vesicular type.
General
manifestations
Fever, malaise and
myalgia are frequent symptoms .
Burning sensation and
pain may be mild or sometimes severe depending on the site and extent of
the lesions.
Arthralgia and swollen
joints.
Kidney involvement :
leads to manifestations of glomerulonephritis.
Gastrointestinal
manifestations: haematemesis, melena, peptic ulceration, esophageal
ulceration. These usually manifest with nausea , vomiting , diarrhea and
anorexia .
Congestive heart failure
manifestations.
Lung involvement leads to
pneumonitis.
Eye changes: retinal
hemorrhage.
Neural manifestations:
peripheral neuritis , diplopia , dysphagia and hoarseness of the voice.
Diagnosis
Laboratory Tests:
ESR: is usually elevated
Hyperglobulinaemia.
IgG globulin and C3
complement appear in the areas of fibrinoid necrosis of the blood vessels
.
Treatment
Treatment of the cause.
Corticosteroids may help
some cases.
ALLERGIC
VASCULITIS
Cutaneous vasculitis is
characterized by purpuric or necrotic urticarial lesions and may be
associated with vasculitis of internal organs.
Histopathological changes
of cutaneous vasculitis are characteristic.
These include fibrinoid
changes in the small dermal blood vessels with polymorphonuclear and
‘nuclear dust infiltrate.
Blood
Picture.
The ESR may be normal,
but is usually raised. When ESR is much raised in urticarial vasculitis,
lupus erythematosus should be excluded.
Neutrophilia or
eosinophilia may occur.
Hypocomplementaemia is
usual.
Circulating immune
complexes are often demonstrated .
Differential
Diagnosis
Infection, drug intake,
internal neoplasia or collagen disease, where these may show cutaneous
vasculitis and should be excluded .
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