Cutaneous Vascular Diseases

Cutaneous Vascular Diseases
by:Rick Lin, DO MPH
KCOM Dermatology Residency Program

Raynaud’s Phenomenon
* Intermittent constriction of the small digital arteries and arterioles
* Persistently cyanotic and painful
* Aggrevated by cold weather
* Young middle aged women
* Assoc c scleroderma, dermatomyositis, LE, Mixed connective tissue diseases, Sjogren’s RA, and paroxysmal hemoglobinuria.
* Scleroderma is the underlying condition for more than half of the patients
* Maybe caused by medications, ie bleomycin

The LDI images below graphically illustrate the vasospasm of Raynaud’s phenomenon following a cold provocation.

Raynaud’s Disease
* Primary disorders
* Pallor, cyanosis, hyperemia, and numbness of the finger
* Precipitated by cold.
* Present for 2 years with out associated disease finding
* Good prognosis
* Multifactorial.
* Increase alpha-2 sympathetic receptor activity on vessels.
* Endothelia dysfunction
* Deficiency in calcitonin gene related protein
* Central thermoregulatory defects
* Treatment include avoidance of aggravating factor, ie cold.
* Vasodilating drugs, nifedipine, 10-20 mg tid; prazosin 1-3 mg tid
* Nitroglycerin 2% local application

Erythromelalgia
* Aka erythermalgia and acromelalgia
* May be secondary to myeloproliferative disease such as polycythemia vera, TTP
* Responds to treatment of primary disorders
* Cold water immersion

Livedo Reticularis
* Mottled or reticulated pink/reddish/blue discoloration
* Assoc c LE, DM, scleroderma, RA
* Side effect of amantadine

Necrotizing livedo reticularis
* Assoc c nodules and ulcerations
* Result from sever atherosclerotic disease
* Sneddon’s syndrome

Livedoid Vasculitis
* atrophie blanche
o White stellate scars of ulcers
* PURPLE (Painful purpuric ulcer with reticular pattern of the lower extremity)
* Histologically shows chronic perivascular hemorrhage.

Treatment
* Low Dosage of Aspirin 325mg qd
* Nifedipine 10mg TID
* Pentoxifylline 400mg BID-TID

Marshall-White Syndrome
* Bier’s Spot: White spot appear on hand with blood pressure cuff
* Consist of Bier’s spot and is associated with insomnia and tachycardia
* White middle age men

Purpura
* Multifocal extravasation of blood into the skin
* Petechiae <3mm
* Ecchymosis
* Vobices (vibex) – Linear
* Hematoma – pool-like collection
* Complete blood count
* PT and PTT

Thrombocytopenic Purpura
* Three Large Categories:
o Accelerated platelet destruction
o Deficient platelet production
o Unknown pathogenesis

Idiopathic Thrombocytopenic Purpura
* Aka autoimmune thrombocytopenic purpura
* Aka Werlhof’s disease
* Bleeding occurs when platelet count drops below 50,000
* Risk greatly increased for serious hemorrhage when count goes below 10,000
* Acute variety occurs in children following season viral illness in 50% of the patient.
* Lag between illness and onset of purpura is 2 weeks
* Resolve spontaneously with minimal therapy
* Chronic case may result in death.
* Chronic form most often occur in adult
* Evaluate patient with Tc99M radionuclide scan to look for accessory spleen
* Result of platelet injury by antibodies of IgG class
* Treatment include Splenectomy, systemic corticosteroid, IVIg

These are the kidneys from a case of idiopathic thrombocytopenic purpura. Petechiae are found throughout the renal parenchyma.

Drug-Induced Thrombocytopenia
* Drug induced antiplatelet antibodies
* May be caused by sulfonamides, digoxin, quinine, quinidine, PCN, furosemide, Lidocaine, methyldopa

Thrombotic Thrombocytopenic Purpura
* Aka Moschcowitz syndrome
* Pentad of thrombocytopenia, hemolytic anemia, renal abnormalities, fever, CNS disturbance.
* Delay in diagnosis may lead to a mortality rate as high as 90%
* Positive histologic diagnosis require gingival biopsies looking for subendothelial hyaline deposits
* Exchange plasmapheresis is required for treatment. 80% patient survive if treatment is instituted.

Dysproteinemic Purpura
* Aka Nonthrombocytopenic purpura
* Aka purpura cryoglobulinemica
* Aka cryofibrinogenemia
* Occur most frequently in multiple myeloma and macroglobulinemia of monoclonal IgM, IgG, or Bence Jones cryoglobulin.
* Tx with plasmaphoresis, systemic steroid, and immunosuppressors.

Purpura Hyperglobulinemica
* Aka Waldenstrom’s hyperglobulinemic purpura
* Consist of episodic showers of petechiae occuring on all parts of body
* Diffuse peppery distribution, resembling Schamberg’s
* Most useful labtest is protein electrophoresis
* Hyperglobulinemic purpura occurs most commonly in women.
* Frequently seen with Hepatitis C and Sjogren’s syndrome, keratoconjunctivitis sicca, RA
* Histologically: derma vessels with perivascular infiltrate of mononuclear cells.
* Benign and chronic course. Assoc c various of connective tissue diseases.

Waldenstrom’s Macroglobulinemia
* Bleeding from mucous membrane of the mouth and nose, lymphadenopathy, hepatomegaly, retina hemorrhage, and RARELY the purpura
* Perivasular infiltrate containing lymphocytes and neutrophils and eosinophils
* Plasmaphoresis until adequate dose of chlorambucil is administered. Cyclophosphamide and corticosteriods are treatment options as well

A Skull X Ray showed a single, small, left-sided lytic Defect.
Drug- and Food Induced Purpura
* Drug induced purpura may occurs without platelet destruction.
* Cocaine induced thrombosis with infarct skin assoc c skin popping.
* Rumpel-Leede sign: distal shower of petechiae that occurs immediately after the release of pressure from a tourniqut release. Associated with capillary fragility.
* Topical EMLA can induce purpura in 30m.
Solar Purpura
* Large, sharply outlined 1-5 cm dark purplish red ecchymoses on dormsum of the forearm
* Less frequently, back of the hand

Purpura Fulminans
* Aka purpura gangrenosa
* Severe, rapidly fatal reaction occurring most commonly in children after infectious illness
* May follows scarlet fever, strep pharyngitis, and meningococcal meningitis.
* Assoc c Protein C or S deficiency in Neonates
* Management is supportive
* Protein C replacement if protein C deficiency is present
* Fresh frozen plasma maybe useful

Disseminated Intravascular Coagulation
* Up to 2/3 of DIC patients have skin lesions
* Minute, widspread petechiae, ecchymoses, ischemic necrosis of the skin and hemorrhage bullae.
* Elevated PT and PTT, fibrin degradation products
* Decrease platelets, decreased fibrinogen

Disseminated Intravascular Coagulation
* All patient needs to receive vitamin K replacement to exclude vitamin K deficiency.

Fibrinolysis Syndrome
* An acute hemorrhagic state brought by inability of the blood to clot
* Massive hemorrhages into the skin produce blackish, purplish swelling.
* Can be a complication of pregnancy in cases of placental previa, eclampsia, and fatal death
* Excessive fibrinolysis

Blue Muffin Baby
* Purpuric lesions observed in newborns with congenital rubella
* Assoc c disease that produce extramedullary erythropoesis
* Generalized dark blue to magenta nonblanchable, indurated, round, oval hemispheric papules 1-7mm
* Evaluation c biopsy, TORCH serology, CBC, viral culture.
Itching Purpura

* Aka diseminated pruriginous angiodermatitis
* Orange-purpleish-red petechiae evolve completely and may become confluent in 2 weeks
* Runs its course in 3-6 months. May become chronic
* Unknown etiology

Deep Vein Thrombosis
* Almost always affect femoral vein
* Leads to Reversible ischemia or frank gangrene
* Significant superficial vein thrombosis is a risk factor for DVT
* Pulmonary Embolism is a major concern
* Malignant Neoplasms are the most common underlying condition
* Pulmonary Embolism has 40% mortality
* DVT is assoc c 35% of cancer associated causes as the first sign
* Patient younger than 40 with DVT prompt for search for cancer

Superficial Thrombophlebitis
* Painful induration with erythema
* Linear or branching configuration forming cords
* Assoc c hypercoagulable state
* Need to be evaluated for possibility of deep veous disease

Mondor’s Disease
* 3:1 = women:men
* Age range 30-60
* Sudden appearance of a cord like thrombosed vein along the anterior-lateral chest wall
* First red and tender and subsequently change into a painless tough, fibrous band.
* No systemic symptom associated
* Treatment of the symptom: hot moist dressing with NSAID
* Runs its course for 3-6 months.

Calciphylaxis
* End-stage renal disease patients with metastatic calcification are most exclusively affected by this disease.
* Reticulated violaceous, mottled patches
* Progress into ecchymosis, central necrosis, and ulceration
* 50%+ morbidity and mortality
* Death is usually caused by staphylococcal sepsis after infection
* Hyperbaric oxygen has used with some success

* On low magnification, basophilic alteration of a fibrous septum can be seen Fibrin thrombi are also present within many of the blood vessels of the subcutaneous adipose tissue (Figure 3). Higher magnification identifies calcium deposition within the fibrous septum, primarily on elastic fibers (Figure 4, Figure 5). Higher magnification of the same area with Verhoeff-van Gieson stain confirms the presence of fragmented elastic fibers (Figure 6). Special stain for calcium (von-Kossa) identifies calcium deposition both within the septum of the fat lobule (Figure 7) and within the walls of blood vessels (Figure 8).
Fibrin thrombi are also present within many of the blood vessels of the subcutaneous adipose tissue

Higher magnification of the same area with Verhoeff-van Gieson stain confirms the presence of fragmented elastic fibers

Special stain for calcium (von-Kossa) identifies calcium deposition both within the septum of the fat lobule

Scorbutic Purpura
* Bleeding gums
* Deficiency in Vitamin C
Achenbach’s Syndrome
* Aka Paroxysmal Hand Hematoma
* Spontaneous focal hemrhage into palm or volar suface
* Transitory localized pain followed by rapid swelling and bluish discoloration
* Acute nature with rapid resolution

Painful Bruising Syndrome
* Aka Autoerythrocyte Sensitization
* Aka Gardner-Diamond Syndrome
* Distinctive localized purpuric reaction
* Young and middle-aged women with some emotional disturbance
* Emotional upset is the precipitating factor
* Intracutaneous injections of erythrocytes stroma evoke lesions
* Some believe the symptome to be artifactual.

Psychogenic Purpura
* Similar purpura as Painful bruising syndrome
* Absence of erythrocytes sensitivity
* Secretan’s syndrome: factitial lymphedema of the hand
* L’oedeme bleu: factitial lymphadema of the arm

Pigmentary Purpuric Eruption
* Pigmented purpuric eruptions of the lower extremities
* Similar histologic finding
* Shamberg’s
* Majocci’s
* Gougerot-Blum

Shamberg Diseases
* Aka progressive pigmentary dermatosis
* Grains of cayenne pepper
* Lesions seldom itch
* Favors lower shins and ankles

Majocchi’s Disease
* Aka purpura annularis telangiectodes
* Bluish annular macules 1-3cm in diameter with telangiectatic puncta
* Begins symmetrically at lower extremities
* Involution requires as long as a year, and may prolong indefinitely
* Asymptomatic.
Gougerot-Blum
* Pigmented purpuric lichenoid dermatitis
* Minute, rust-colored lichenoid papules that fuse into plaques of various hues
* Legs, thighs, and lower trunk
* Differentiate from Schamberg based on distribution and lichenoid lesions.
* Lichen Aureus

Ducas Kapetanakis pigmented purpura
* Histologically present with distinguished from others by presence of spongiosis
* Must be distinguished from mycosis fungoides
Histology

* Purupra Majocchi-Schamberg is characterized by slight alteration of superficial capillaries with hemorrhage and perivascular lymphocytic infiltrate.

Cutaneous Vascular Diseases Part-1.ppt
Cutaneous Vascular Diseases Part-2.ppt

Read more...

Syphilis

Syphilis
by: Erik Austin, D.O., M.P.H.

Syphilis
* AKA lues
* Contagious, sexually transmitted disease caused by the
* Spirochete: Treponema pallidum
* Enters through skin or mucous membrane where primary manifestations are seen

Treponema pallidum
* Spiral spirochete that is mobile
* # of spirals varies from 4 to 14
* Length is 5 to 20 microns
* Can be seen on fresh primary or secondary lesions by darkfield microscopy or fluorescent antibody techniques

Syphilis epidemiology
* Major health problem throughout world
* 2.6 cases per 100,000 in 1999 in the US
* Lowest level ever recorded
* Concentrated in 28 counties in the SE U.S.
* Mainly gay men and crack cocaine users
* Enhances risk of transmission of HIV
* HIV testing recommended in all patients with syphilis
* Reportable disease

Serologic Tests
* Testing reveals patients immune status not whether they are currently infected
* Non-treponemal antigen test uses lipoidal antigens rather than T. pallidum or components of it
* RPR = rapid plasma reagin
* VDRL = Venereal Disease Research Laboratory
* Positive within 5 to 6 weeks after infection
* Strongly positive in secondary phase
* Strength of reaction is stated in dilutions
* May become negative with treatment or over decades
* MHA-TP: microhemagglutination assay for T. pallidum
* FTA-ABS: fluorescent treponemal antibody absorption test
* All positive nontreponemal test results should be confirmed with a specific treponemal test
* Treponemal tests become positive early, useful in confirming primary syphilis
* Remain positive for life, useful in diagnosing late disease
* Treatment results in loss of positivity in 13-24% of patients

Biologic False-Positive Test Results
* Positive test with no history or clinical evidence of syphilis
* Acute BFP: those that revert to negative in less than 6 months
* Chronic BFP: those that persist > 6 months

BFP Test Results in Syphilis
* Acute BFP
* Vaccinations
* Infections
* pregnancy
* Chronic BFP
* Connective tissue disease (SLE)
* Liver disease
* Blood transfusions
* IVDA

Cutaneous Syphilis
* Chancre is usually the first cutaneous lesion
* 18 to 21 days after infection
* Round indurated papule with an eroded surface that exudes a serous fluid
* Usually painless and heals without scarring

Chancre
* Inguinal adenopathy 1-2 weeks after chancre
* Generally occur singly, but may be multiple
* Diameter mm to cm

Chancres
* In women, the genital chancre is less often observed due to location within the vagina and cervix
* Edema of labia may occur
* Untreated, the chancre heals spontaneously in 1 to 4 months
* Constitutional symptoms begin just as chancres disappear
* Extragenital chancre: may be larger, frequently on lips, rarely tongue, tonsil, breast, finger, anus.

Chancre Histology
* Ulcer covered by neutrophils and fibrin
* Dense infiltrate of lymphocytes and and plasma cells
* Spirochetes seen with with silver stains; Warthin-Starry
* Direct fluorescent antibody tissue test (DFAT-TP) = serous exudate collected on a slide sent for exam

Serology
* Nontreponemal tests positive 50%
* Treponemal tests positive 90%
* Positivity depends upon duration of infection, if chancre has been present for several weeks, test is usually positive

Chancre vs. Chancroid
* Incubation 3 weeks
* Painless
* Hard
* Lymphadenopathy may be bilateral, nontender, nonsuppurative
* Incubation 4-7 days
* Painful
* Soft
* Lymphadenopathy unilateral, tender, suppurative

DDx in Syphilis
* Chancroid - multiple lesions, may coexist with chancre, must r/o syphilis
* Granuloma Inguinale - indurated nodule that erodes, soft red granulation tissue, Donovan bodies in macrophages with Wright or Giemsa stain
* Lymphogranuloma Venereum - small, painless, superficial non indurated ulcer, primary lesions followed in 7 to 30 days by adenopathy
* HSV - grouped vesicles, burning pain

Secondary Syphilis
* Skin manifestations in 80% called syphilids
* Symmetric, generalized, superficial, macular - later papular, pustular
* May affect face, shoulders, flanks, palms and soles, anal or genital areas

Secondary Syphilis Macular Eruptions
* Exanthematic erythema 6-8 weeks after chancre - may last hours to months
* Round, slightly scaly ham-colored macules
* Pain and pruritus may be present
* Generalized adenopathy

Secondary Syphilis Papular Eruptions
* Occurs on face and flexures of arms, legs, and trunk
* Yellowish-red spots may appear on palmar and plantar surfaces
* Ollendorf’s sign = tender papule
* May produce a psoriasiform eruption
* May appear as minute scale-capped papules
* Tend to be disseminated, but may be localized, asymmetrical, configurate, hypertrophic or confluent.
* Annular syphilid - mimics sarcoidosis and is more common in blacks
* Pustular syphilid – rare - face, trunk, extremities red small crust-covered ulceration
* Rupial syphilid - superficial ulceration is covered with a pile of terraced crusts resembling an oyster shell.
* Lues Maligna - rare, severe ulcerations, pustules, or rupioid lesions, accompanied by severe constitutional symptoms.
* Condylomata lata - papular mass, weeping, gray 1-3cm, groin, anus (not vegetative like condylomata acuminata)
* Syphilitic alopecia - irregular, scalp has a moth-eaten appearance 5% of pts

Secondary Syphilis Mucous Membrane
* Present in 1/3 of secondary syphilis
* Most common is “syphilitic sore throat”
* Diffuse pharyngitis, hoarseness
* Tongue may show patches of desquamation of papillae
* Ulcerations of tongue and lips in late stages
* Mucous patches are the most characteristic mucous membrane lesions; macerated, flat. Grayish, rounded erosions covered by a delicate, soggy membrane.

Secondary Syphilis Systemic Involvement
* Lymphadenopathy common.
* Acute glomerulonephritis, gastritis, proctitis, hepatitis, meningitis, iritis, uveitis, optic neuritis, Bell’s palsy, pulmonary nodular infiltrates, osteomyelitis, polyarthritis.

Secondary Syphilis Diagnosis
* Nontreponemal serologic tests for syphilis are strongly reactive (seronegativity rarely in AIDS)
* Spirochetes on darkfield exam

Secondary Syphilis DDx “Great Imitator”
* Pityriasis rosea
* Drug eruptions (pruritic)
* Lichen planus; Wickham’s striae, Koebner’s, pruritic
* Psoriasis; no adenopathy
* Sarcoidosis; need serology and silver staining of biopsy
* Infectious mononucleosis, false pos RPR
* Geographic tongue
* Aphthous stomatitis

Latent Syphilis
* After the lesions of secondary syphilis have involuted, a latent period occurs where the patient has no clinical signs, but positive serological tests
* May last a few months or a lifetime
* 60-70% of pts that are untreated remain asymptomatic for life
* Women may infect unborn child for 2 years
Late Syphilis
* Defined by CDC as infection of greater than 1 years duration
* Tertiary Cutaneous Syphilis
* Late Osseous Syphilis
* Neurosyphilis
* Late Cardiovascular Syphilis

Tertiary Cutaneous Syphilis
* Tertiary syphilids usually occur 3-5 years after infection
* 16% of untreated pts will develop lesions of skin, mucous membrane, bone or joints
* Skin lesions are localized, destructive, heal with scarring

Tertiary Syphilids
* Two main types; Nodular syphilid and the Gumma
* Nodular - reddish brown firm papules or nodules 2mm or larger, scales.
* Gumma - larger

Nodular Tertiary Syphilid
* Lesions tend to form rings and undergo involution as new lesions develop
* Characteristic circular or serpiginous pattern
* “kidney-shaped” lesion occurs on the extensor surfaces of the arms and on back
* Patches have scars and fresh ulcerated lesions
* Process may last for years, slowly marching across large areas of skin

Gumma
* May occur as unilateral, isolated, single or disseminated lesions, or serpiginous
* May be restricted to the skin, or originate in deeper tissues, and break down the skin
* Lesions begin as small nodules, enlarge to several centimeters
* Central necrosis, deep ulcer with a gummy base, most frequent site is lower legs

Diagnosis of Tertiary Syphilis
* Histopathology - tuberculoid granules with multinucleated giant cells
* Nontreponemal tests (VDRL, RPR) positive in 75%
* Treponemal tests (FTA-ABS, MHA-TP, TPI) positive in nearly 100%
* Darkfield negative, PCR may be positive

DDx Tertiary Syphilis
* R/O tumors; SCCA tongue, leukemic infiltrates, sarcoidosis
* Ulcerated syphilids resemble scrofula, atypical mycobacterium, sporotrichosis, blastomycosis
* Mycosis fungoides (CTCL) has eczema and pruritus
* Perforation of hard palate and septum

Late Osseous Syphilis
* Gummatous lesions can involve the periosteum and bone
* Head, face, tibia
* Periostitis, osteomyelitis, osteitis, gummatous osteoarthritis
* “Osteocope” - bone pain often at night
* Charcot joint - loss of contours of joint, hypermobility, painless
* Associated with tabes dorsalis

Neurosyphilis
* CNS involvement with syphilis can occur at any stage
* Most are asymptomatic; CSF shows pleocytosis
* 4-10% of untreated pts will develop neurosyphilis

Early Neurosyphilis
* First year of infection - meningeal
* Headache, stiff neck, cranial nerve disorders, seizures, delirium, increased ICP

Meningovascular Neurosyphilis
* 4-7 years after infection
* Thrombosis of vessels in the CNS
* Hemiplegia, aphasia, hemianopsia, transverse myelitis, progressive muscular atrophy
* CN palsies; CN IIX, III, IV, VI
* “Argyll Robertson Pupil” accommodates, but doesn’t react

Late Neurosyphilis
* Parenchymatous neurosyphilis occurs more than 10 years after infection
* Two classical patterns; Tabes Dorsalis, and General Paresis

Tabes Dorsalis
* Degeneration of the dorsal roots of the spinal nerves and posterior columns of the the spinal cord
* Gastric crisis with severe pain and vomiting is most common
* Pain, urination problems, paresthesias, ataxia, diplopia, vertigo, deafness
* Signs: Argyll Robertson pupil, reduced lower cord reflexes, Romberg sign, sensory loss, atonic bladder, Charcot’s joints, optic atrophy
* Personality changes, memory loss, apathy, megalomania, delusions, dementia

Late Cardiovascular Syphilis
* Occurs in 10% of untreated pts
* Aortitis, aortic insufficiency, coronary disease, aortic aneurysm

Congenital Syphilis
* Prenatal syphilis acquired in utero
* Infection through the placenta usually does not occur before the fourth month, so treatment of the mother before this time will almost always prevent infection in the fetus.
* If infection occurs after the fourth month 40% risk of fetal death

* 40% of pregnancies in women with untreated early syphilis will result in a syphilitic infant.
* Most neonates with congenital syphilis are normal at birth.
* Early congenital syphilis - lesions occurring within first two years of life
* Late congenital syphilis - lesion occur after two years

Early Congenital Syphilis
* Cutaneous manifestations appear most commonly during 3rd week
* Snuffles (a form of Rhinitis) is most frequent, bloody drainage, ulcers may develop, later septal perfs
* 30-60% of infants develop cutaneous lesions similar to secondary syphilis
* Red to copper maculopapular, become large, scaling, pustules, crusting
* Face, arms, buttocks, legs, palms and soles

Early Congenital Syphilis
* Face, perineum, and intertriginous areas, usually fissured lesions resembling mucous patches. Radial scarring results leading to Rhagades
* Bone lesions occur in 70-80% , epiphysitis is common and causes pain on motion, leading to infant refusing to move; Parrot’s pseudoparalysis.
* Radiologic features of the bone lesions in congenital syphilis during the first 6 months are characteristic.
* Bone lesions occur at the epiphyseal ends of long bones.
* Lymphadenopathy, hepatomegaly, nephrotic syndrome, meningitis, nerve palsies may all occur

Late Congenital Syphilis
* Lesions are two types - malformations of tissue affected at critical growth periods (Stigmata) and persistent inflammatory foci
* Inflammatory - lesions of the cornea, bones, and central nervous system, i.e., interstitial keratitis in 20-50%, perisynovitis of knees (Clutton’s joints), tabes dorsalis, seizures, and paresis

Late Congenital Syphilis
* Malformations (Stigmata) - destructive effects leave scars or developmental defects
* Hutchinson’s Triad - Changes in incisors, corneal scars, and eighth nerve deafness
* Also, saber shins, rhagades of the lips, saddle nose, mulberry molars

Hutchinson’s Teeth
* Malformation of the central upper incisors that appears in the second or permanent teeth. Teeth are cylindrical rather than flattened, cutting edge narrower than base, notch may develop
* Mulberry molar - first molar hyperplastic, flat occlusal surface covered with knobs representing abortive cusps

Treatment of Syphilis
* PCN is drug of choice for treatment of all stages of syphilis.
* HIV testing is recommended in all patients
* If less than one year; 2.4M U of Benzathine PCN G
* PCN-allergic; Tetracycline 500mg QID for 14 days

Jarisch- Herxheimer Reaction
* Febrile reaction occurs after the initial dose of antisyphilitic tx, 60-90% of pts
* 6-8 hours after dose - chills, fever, myalgia, increase in inflammation (neurosyphilis)

Treatment of Sex Partners
* Persons exposed to a patient with early syphilis within the previous 3 months should be treated, even if seronegative
* Single dose azithromycin effective in treating incubating syphilis

Serologic Testing after Tx
* VDRL or RPR repeated every 3 months in first year, every 6 months in second year, than annually
* A fourfold decrease in titer should be seen at 6 months, if not then 3 weekly PCN IM injections
* Response for latent syphilis is slower, 12-24 months
* If not responding; HIV and CSF testing repeated
* Pts with late syphilis may be “serofast”, and titers may not improve
* Neurosyphilis pts should have CSF every 6 months

Syphilis and HIV
* Most HIV pts exhibit the classic clinical manifestations and course, and respond similarly to tx
* More likely to present with secondary syphilis and have a persistent chancre

Yaws
* Treponema pallidum subsp. Pertenue
* Endemic in some tropical, rural regions
* Overcrowding, poor hygiene, transmitted by contact with infected lesions
* Children, disabling course, affects skin, bones, and joints

Early Yaws
* Primary papule or group of papules appear at site of inoculation after 3 week incubation period, initial lesion becomes larger and crusted (Mother Yaw, maman pian )
* Feet, legs, buttocks, face, not genitals
* Mother yaw disappears after a few months
* Secondary Yaws – appears weeks or months after mother yaw appears. May be smaller and appear around primary lesion; may be annular (ringworm yaws)
* Condylomata may develop around body orifices and creases
* Palms and soles may form hyperkeratotic plaques leading to a painful crab-like gait (crab yaws)

Late Yaws
* 10% progress to late stage where gummas occur
* Ulcer with clean edges that tend to fuse to form con figurate and serpiginous patterns similar to tertiary syphilis
* Bone, joint, saddle nose, saber shin, Gangosa (destruction of palate and nose)
* Diagnosis = Darkfield, VDRL or RPR

Endemic Syphilis (Bejel)
* Bejel is a Bedouin term for nonvenereal treponematosis, nomadic tribes of North Africa, Southwest Asia, Eastern Mediterranean
* T. pallidum subsp. Endemicum
* Usually occurs in childhood through skin contact
* May affect the skin, oral mucosa, and skeletal system

Bejel
* Primary lesions rare, probably go undetected in the oral mucosa
* Secondary oral lesions - shallow, painless ulcers, laryngitis
* Condyloma of axillae and groin, lymphadenopathy, osteoperiostitis causes night leg pain
* Untreated secondary bejel heals in 6-9 months
* Tertiary stage - gummatous ulcerations of the skin, nasopharynx, and bone.
* Neuro - uveitis, choritis, optic atrophy

Pinta
* T. carateum; nonvenereal, endemic
* Only skin lesions occur
* All ages, Brazilian rain forest
* Primary Stage - 7 to 60 days after inoculation. Lesion begins as a tiny red papules and become an elevated erythematous infiltrated plaque 10cm in diameter over 2-3 months. Legs -satellite lesions, no erosion or ulceration as in chancres.
* Secondary Stage - 5 months to 1 year
* Small, scaling papules that enlarge and coalesce – affects extremities and face
* Red to blue, black with postinflammatory hyperpigmentation
* Nontreponemal tests reactive in 60%
* Late Dyschromic Stage - young adults – may appear as hyperpigmented and depigmented macules resembling vitiligo
* Face, waist, wrist, trochanteric areas
* Histo - acanthosis, lichenoid, spirochetes in epidermis

Treatment of Yaws, Bejel, and Pinta
* Benzathine PCN G 1.2 to 2.4 M units IM
* Tetracycline 500mg QID for adults
* EES 10mg/kg children QID for 14 days
Nonvenereal Treponematoses
* Yaws
* Endemic Syphilis
* Pinta

Treatment
* Syphilis >1year; 2.4M PCN G weekly for 3 weeks Pcn-allergic; Tetra 500mg QID for 30 days
* Neurosyphilis; IV
* Infant 100,000 to 150,000 units/kg/day Procaine PCN BID for first seven days of life

Syphilis.ppt

Read more...

Common Foot & Ankle Problems

Common Foot & Ankle Problems

Hallux Valgus / Bunion Deformity
* A structural (bony) deformity where the metatarsal bones spread apart causing a prominent bone to protrude on the inside of the foot.
* A progressive deformity.
* May be treated conservatively, but usually requires surgical correction if pain persists.

Bunion prior to correction
Bunion after correction
Severe Hallux Valgus / Bunion Deformity
Cut in bone and fixation with screws

Tailor’s Bunion / Bunionette
* Bony deformity which is located on the outside part of the foot.
* The bump, bunionette or Tailor’s Bunion, can become very painful due to shoe irritation.
* Tailor’s bunions may be treated conservatively. Surgical correction may be necessary.

Note prominent 5th metatarsal head with swelling
Note Bowing of the Metatarsal
Note Straight Metatarsal
After Correction
Prior to Correction
Tailor’s Bunion / Bunionette
Hammertoe Deformity
* Contracted or abnormal position of the toes, which may be flexible or rigid in nature.
* Usually caused by weakened muscles of the foot.
* May cause pain due to irritation from other toes. The pain may be exasperated by tight fitting shoes.
* Hammertoes are often accompanied by a corn or callous.
Toe prior to surgery
Toe after surgery
Hammertoe Deformity
Hallux Rigidus
* Osteoarthritis of the big toe joint usually associated with pain and restricted motion.
* May be caused by injury or repetitive joint damage due to a biomechanical / structural problem of the foot.
* Chronic wear and tear causes a wearing out of the cartilage at the joint and bone spurs to form.
Hallux Rigidus of the Big Toe Joint
Note bone spur formation

Hallux Rigidus of the Big Toe Joint
Note joint space narrowing and bone spur formation at the joint margins
Rheumatoid Arthritis
* An inherited arthritis which affects joints in the feet and hands.
* The joint destruction and deformities are progressive in nature.
* May predispose patients to bunion and hammertoe formation.
Bunion Deformity
Hammertoe Deformities
Rheumatoid Arthritis
Rheumatoid nodule
Plantar Wart
* Human papaloma virus infection in the feet.
* Warts are obtained by barefoot exposure to the virus.
* Warts are often spread in showers, gyms, or other areas where barefoot walking is common.
* May be treated with any number of methods but recurrence ranges between 18-22%.
Plantar Wart
Callous / Corn
* Thickened area of skin caused by chronic rubbing or irritation of a bony prominence by the ground or shoe gear.
* Very high areas of pressure within a callous can develop a painful central core.
* Lesions reoccur because the cause of the lesion is often from bone.
Callous / Corn
Athletes Foot
* A fungal infection typically caused by fungus found in soil (Dermatophyte).
* Picked up by contact with the fungus usually walking barefoot (Gym, hotel, pool, etc.).
* May occur anywhere on the foot and may burn and/or itch.
* The affected areas of skin will often peel or may have small blisters.
Ingrown Nails
* Toenail which grows into the skin. Most often caused by a wide toenail and an external pressure.
* The nail may cause pain or infection due the pressure of the nail border.
* May be treated with removal and/or antibiotics. May be permanently corrected with retaining a normal nail appearance.
Fungal Toenail
* A thickened nail caused by a fungus.
* Initially caused by an injury to the nail which allows the organism to enter the nail.
* Progressive in nature and slow growing.
* May spread to other nails or other people in close contact. Organism may also spread from nail to the skin (athletes foot).
* May be treated if pain or concerns arise.
Fungal Toenail
Fungal Infection which caused ingrown nail
Thickened curled nails caused by fungus
Nail Injury
* Chronic injury (i.e. athletic activities) causes injury to the nail root and results in nail horizontal layers.
* Isolated injury may also cause bleeding under the nail, leaving a dark spot which persists until the nail grows out.
Lines of injury
Dried blood under the nail plate from injury.
Eczema
Gout
Redness and swelling of the big toe joint
High Arched Feet / Pes Cavus
Pes Cavus / High Arch Feet
Flat Feet
Note low medial arch height
Pes Planus / Flat Feet
Note collapse of entire foot inward
Note low medial arch height
Plantar Fascitis / Heel Spur Syndrome
* Inflammation and partial tearing of a ligament band which attaches from the heel to the ball of the foot.
* Usually a result of poor arch support and overuse.
* May be accompanied by a calcified spur on the heel.
* Usually resolves with conservative treatments.
Ankle Sprain
* Tear or stretching of the ligaments of the ankle. Usually the ligaments on the outside of the ankle are involved.
* Caused by and twisting injury of the foot / ankle .
* Instability of the ankle can develop due to the ligament injury.
* Most often treated conservatively. Surgical repair can be performed to treat chronic ankle sprains.
Bruising after ankle sprain
Morton’s Neuroma
* Injured or compressed nerve most often between the 3rd and 4th toes.
* Burning / pain on the ball of the foot or toes.
* Patients may feel fullness or a mass in the area when they walk.
* Treatments may be conservative or surgical.
Haglund’s Deformity / Retrocalcaneal Exostosis
* Prominent bone on the back of the heel.
* Back of the heel is irritated by shoes and activity, which places pressure on the area.
* Can also be aggravated by a tight Achilles tendon over prominent heel bone.
* Treatments may be conservative or surgical.
Ulcerations
* Erosions of the skin caused by loss of sensation or poor circulation.
* Skin break down occurs which, places patients at risk for local or systemic infection.
Ischemic Ulceration(Ulcer due to poor circulation)
Diabetic Ulceration
Ganglion Cyst
* Benign soft tissue mass which arises from a weak area in a tendon lining or joint.
* Cyst is often filled with a gelatinous fluid.
* Cyst may change size depending on irritation.
Subungual Exostosis
* Bone and cartilage growth under the great toe nail.
* Pain may arise if pressure is placed over the area.
* May be treated with shoe style changes, nail removal or surgical removal.
Venous Stasis
* Discoloration of skin due to longstanding swelling of legs.
* Persistent swelling can lead to skin breakdown.
* Compression and elevation of the legs are essential to the prevention of complications.
Heel Fissuring / Cracking
Heel Fissuring with Hyperkeratosis
Fractured Proximal Phalanx (Toe)
Fractures
Hyperhydrosis
Achilles Tendonitis
Inflammation of tendon

Common Foot & Ankle Problems.ppt

Read more...