DR. FAISAL AL-SAWAFIEMERGENCY MEDICINE

R1

OBJECTIVESOBJECTIVES

SKIN FUNCTIONAPPROACH TO PATIENT WITH RASHACUTE SKIN FAILURECOMMON CHALLENGING RASHESALGORITHM FOR DIAGNOSING PATIENT

WITH RASHSUMMARY

Skin functionsThe integument system of the human occupy 16% of total body WT.

Protection: an anatomical barrier

Sensation

Heat regulation

Control of evaporation

Storage and synthesis: lipids and water

HISTORYHISTORY The following key questions should be a part of every patient history: 1. When did the rash appear, and how quickly did it progress? The most lethal rashes often progress rapidly. Acute

urticaria with anaphylaxis 2. Did the rash change over time? ANTRAX: PUPURA THEN ULCERATE THEN BLACK SCAR TSS. SSSS, TEN : ERYTHEMATOUS RASH THEN

DESUQUMATION

3. What was the progression of the rash? Where did the rash start?

Vasculitic rashes generally spread in a peripheral-to-central pattern,

*viral rashes (e.g., varicella) start centrally and spread peripherally.

4. Is the lesion pruritic? Itching is, mediated by histamine released by mast cells. *Diffuse pruritus without a rash can be seen in biliary cirrhosis or certain cancers, especially lymphomas. *Pruritus with a diffuse rash may be from an acute allergic reaction or , dermatitis, scabies

5. Has there been any recent travel? * a petechial rash in someone who has

been to a wooded area may be Rocky Mountain spotted fever,

* typhus if travel to the southwestern United States, and a maculopapular rash that spreads from the trunk to the

extremities.

6. What medications is the patient taking? Cutaneous drug reactions occur in about 2%-3%

of hospitalized patients and 1% of OPD CASES7. What is the patient’s past medical history ?**patients with an artificial heart valve, cardiac

valvular lesions, or IV drug use may have endocarditis.

**herpes zoster associated with HIV**erythema multiforme following herpes simplex

or mycoplasma infections.

EXAMINATIONEXAMINATION

GENERAL APPEARNCE VITALS HEAD TO EXAMINATIONDESCRIPTION OF THE RASH

MACULAR : DRUG ERUPTION, VIRAL EXANTHEMA, TOXIC OR

INFECTIOUS ERYTHEMA, VITILIGO, TINEA VERSICOLOR, CELLUL.

PAPULE:ACNE, BCC, MELANOMA, ATOPIC DEMATITIS,

URTICARIA, ECZEMA, ….PLAQUE:ECZEMA, PITYARSIS ROSEA, PSOIASISWHEEL:URTICARIA, ANGIOEDEMA

PUSTULE:ACNE, FOLLECULITIS, GONOCOCCEMIA,

HYDRADENITIS SUPPURATIVA, HERPETIC INFECTION…..

VESICLE:HERPETIC INFECTION, IMPETIGO…

Acute skin failure(ASF) is

A state of total dysfunction of the skin resulting from different dermatological conditions.

It constitutes a dermatological emergency and requires a multi-disciplinary, intensive care approach.

SO

HEAT REGULATOR: loss of normal temperature control

failure to prevent percutaneous loss of fluid, electrolytes and protein, with resulting

imbalance ,

failure of the mechanical barrier to prevent penetration of foreign materials

case

50 year old male diagnosed recently as brain tumor starting 5 days back anticonvulsant medication,

also diagnosed recently as gout and start

medication for thatPresnting to LHC with rashes all over body

o/e :Vitals stableMaculopapular rash

over trunks and upper limbs

Topical steroids and antibiotics

Then after 2 days present to A&E with

A 2007 multinational study from Europe and indicated that allopurinol was the most common cause of SJS and TEN in these areas .

STEVEN-JOHNSON SYNDROMESTEVEN-JOHNSON SYNDROME

It is characterized by a prodrome of malaise and

fever, followed by the rapid onset of

erythematous or purpuric macules and plaques .

The skin lesions (<10%) progress to epidermal

necrosis and sloughing .

* Mucosal membranes are affected (ocular, oral,

and genital) .

Toxic epidermal necrolysisToxic epidermal necrolysis involves sloughing of greater than 30

percent of the body surface area .also begins with a prodrome of fever and

malaise, . temperatures are typically higher than those seen with SJS, often exceeding 39 degrees Celsius.

Mucous membranes are involved in SKIN DESUQEMQTION.

WHY A CHALLENGE RASHWHY A CHALLENGE RASH??

SEPTIC SHOCKHYPOVOLEMIC SHOCKELECTROLYTES IMBALANCEMULTIORGAN DYSFUNCTION

Ophthalmologic - Conjunctival lesions ,Excessive tearing sometimes occurs from obstruction of the tear punctae .

Urogenital - Urethritis ,dysuria or even urinary retention .

Pulmonary - dyspnea, hypoxia, bronchial hypersecretion, tracheobronchitis, pulmonary edema, bacterial pneumonitis, and bronchiolitis obliterans .

Erythema multiforme (EM)

Is an acute, self-limiting, mucocutaneous reaction pattern to many viral, bacterial, protozoal and fungal infections, tumors, drugs, autoimmune states and miscellaneous conditions.

The most frequent cause is HSV infection followed by mycoplasma pneumoniae.

Clinical spectrum of EM ranges from mild (erythema multiforme minor) to severe form (Steven-Johnson’s syndrome-TEN complex and TEN)

Variable prodromal symptoms and a symmetrically distributedpolymorphic rash classically with iris or target lesions seen on hands with a central vesicle, or erythema surrounded by a pale and then a red ring.

The eruption in SJS(Severe EM) occurs preferentially periorificially or on mucocutaneous locations as painful erosions with thick adherent crusts.

Cutaneous lesions frequently begin on the extensor extremities, and may spread centripetally to other areas.

Lesions are usually asymptomatic, although some patients may note pruritus or a burning sensation.

EM may also involve mucosal surfaces, presenting as painful erythematous patches, erosions, or bullae.

The diagnosis of acute erythema multiforme typically is

based upon the patient's history and clinical findings.

When the diagnosis is uncertain, skin biopsies are useful for establishing the diagnosis.

Hemorrhagic erosions of the lips in EM ,

Severe eye-involvement in EM ,

managment

ABCICU

** The management of patients requires well-synchronized teamwork.

** In addition to experienced dermatologists, internists & well-trained, devoted nursing staff are needed for continuous monitoring of patients.

The pillars in the management of such patients are **nursing care ;

**monitoring hemodynamic changes ;**fluid, electrolyte balance and nutrition ;**prevention of complication (e.g. sepsis);

**prompt identification of risk factors; &**topical therapy.

Nursing care and general measures

** Patients can be managed in burn units or in a specialized ward .

** The environmental temperature should be maintained at 30°-32°C;alternatively, an infrared lamp can be used to reduce shivering & the associated energy loss.

** Use of air-fluidized beds & a burn-cage ensures patient comfort & easy handling.

Regular cleaning & removal of crusts from the oral & nasal cavities, & care of eyes, genitalia & perianal region has to be ensured.

* bathing in lukewarm water (35°-38°C) is recommended

* Introduction of an I.V line & urinary catheter or condom drainage are mandatory .

* A nasogastric tube should be considered in the presence of severe mucosal involvement restricting oral intake or in severely ill patients .

It helps in feeding, and assessing the gastric emptying.

*An hourly record of the PR, RR , BP, & urine volume & osmolality is essential .

*The body temp & gastric emptying should be recorded every 3 to 4 hours .

* An accurate daily intake-output chart should be maintained .

Monitoring hemodynamic changes

A urine output of 50-100 ml/hour and an osmolality lower than 1020 are indicative of adequate tissue perfusion.

**However, while assessing the adequacy of urine output in these patients, hyperglycemia has to be ruled out as it is commonly associated.

** TEN is often compared with burn injury, the fluid requirement is 2/3rd to 3/4th of that of patients with burns covering the same area.

Topical management

** An oozy denuded skin should be managed conservatively .

** In patients with TEN, the detachable epidermis is preferably left in place.

** Topical agents (0.5% silver nitrate) **Non-physiologic lipids (petrolatum jelly, lanolin) in

vapor-permeable dressings (gauze) can be used as barrier repair agents.

**Use of physiologic lipids (component mixture of cholesterol, ceramide and free fatty acids in an optimized ratio of 3:1:1), accelerates the barrier repair.

** Moreover, use of these emollients prevents the skin surface from sticking to the bed or the apparel .

Other measuresOther measures

**** Individual cases should be considered for sedatives like sedatives like diazepam or morphine to reduce anxiety and diazepam or morphine to reduce anxiety and

apprehension, and H2-blockers to prevent stress ulcersapprehension, and H2-blockers to prevent stress ulcers .

**** In the presence of significant hyperglycemia, insulinhyperglycemia, insulin should be added as per medical advice.

**** Ophthalmic careOphthalmic care should be provided in the form of protective ocular pads, periodic instillation of normal saline or artificial tears, and preventive measures for synechiae formation.

***The poor prognostic factors in ASF are

**older age**larger body surface area involvement

**presence of severe neutropenia**early thrombocytopenia

**high blood urea nitrogen level**a causative drug with long half life in drug-

induced cases.

GLUCOCORTICOIDSGLUCOCORTICOIDS

studies result in avoiding GLUCOCORTICOIDS in children with SJS, as this therapy can cause significant side effects and the overall prognosis is good with supportive care alone.

Studies result in favor of administration of glucocorticoids to adult patients in whom SJS has been diagnosed within 24 to 48 hours, while recognizing that the evidence of clear benefit is inadequate. We suggest administering prednisone, 2 mg/kg daily (or an equivalent amount of prednisolone or methylprednisolone), 5-7 days .

do not give glucocorticoids to treat adults with TEN because of concern for increased risk of sepsis, although the evidence of harm is not conclusive.

Intravenous ImmunoglobulinIntravenous Immunoglobulin  

2010 Oct 15.High-dose intravenous

immunoglobulins in the treatment of Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis in Chinese patients: a retrospective study of 82 cases.

24 CORTICOIDS AND IVIG58 GLUCOCORTICOIDS

IVIG and corticosteroids shortened the duration of

hospitalization from 26.4 ± 9.5 d to 18.1 ± 5.3 d (P <

0.05). No significant difference was observed in the

incidence of complications between the two groups

(54.2% vs 39.7%, P > 0.05). The actual mortalities

were 12.5% in the IVIG group and 3.4% in

corticosteroid group respectively,

Intravenous ImmunoglobulinIntravenous Immunoglobulin  

(with doses ranging from 0.65 to 5.8 grams/kg divided over one to five days).

PlasmapheresisPlasmapheresis,,

have been reported to be beneficial in several studies of patients with TEN

Bullous diseases

Immunobullous diseases like pemphigus, pemphigoid, and hereditarymechanobullous disorders like epidermolysis bullosa can be disabling and even life-threatening in some cases

Pemphigus vulgaris

There are three main types of pemphigus- P foliaceous, (the blister is in the superficial granular layers), P vulgaris, (the blisters form just above the basal layer) and paraneoplastic pemphigus that occurs in association with malignancy

Flaccid blisters are the primary lesions associated with painful erosions and Oral mucosal involvement .

Large erosive areas in a patient with pemphigus vulgaris

Generalized pustular psoriasisGeneralized pustular psoriasis

Is a rare but serious and even life-threatening form of psoriasis. Is a rare but serious and even life-threatening form of psoriasis. Sheets of small, sterile yellowish pustules develop on an erythematous Sheets of small, sterile yellowish pustules develop on an erythematous background and may rapidly spread . The onset is often acute. background and may rapidly spread . The onset is often acute. The patient is unwell, with fever and malaise, and requires hospital admissionThe patient is unwell, with fever and malaise, and requires hospital admission

CASECASE

10 YEAR OLD BOY, HE GOT INJRY TO HIS UPPER LIMB (LENGTH 3CM , DEEP 1CM),

HE DID NOT SEEK ANY TREATMENT OR CLEAN HIS WOUND

WOUND BECOME INFLAMMED, THEN STARTED TO GET FEVER AND SKIN RASH

PARENTS GIVE HIM OMOL, BUT RASH BECAME MORE AGGRESSIVE (SKIN EASILY DETACH ON PALPATION)

o/eErythematous skin rashes over trunk and

limbs with some areas of peeling off skin

STAPH. TSS

DISEASE COURSEDISEASE COURSE

PHASE I: SUDDEN APPEARANCE OF TENDER ERYTHEMA WITH A SNANDPAPERLIKE TEXTURE

PHASE II: EXFOLIATIVE PHASE, SKIN WRINKLE AND PEEL OFF EVEN WITH PRESSURE (NIKOLSKY SIGN), BULLAE OR BLISTER MAY APPER

PHASE III: 3-5 DAYS SKIN DESQUMATES, NORMAL SKIN 10-14 DAYS

staph. TSSstaph. TSS

symptoms/examPresents as acute febrile illness with high

fever, myalgia, vomiting, headache, pharyngitis

Accompanied with diffuse, non pruritic , exanthema , starts on trunk then spread, subsequent desquamation occur.

Other manifestation: conjunctivitis, strawberry tongue, erythema hand& sole

Rapid progression to hypotension

AetiologyAetiology

Linked with extoxin producing staph aureus

Associated with TAMPONS USE, NASAL PACKS , surgical wounds

Why a challenge rashWhy a challenge rash??

profound shock, renal failure, sepsis, adult respiratory distress syndrome. The overall mortality is 30%, andcan reach 80% in the elderly.

TreatmentPatients with TSS and STSS require ABCD. Some will need vasopressors, inotropic

agents, and mechanical ventilation. In staph TSS, remove the source of staphylococcal

colonization, such as vaginal tampons, nasal packing, or breast implants

Antibiotic therapy with anti-staphylococcal coverage is recommended.:

Intravenous beta-lactamase-resistant antibiotics (oxacillin,nafcillin, cefoxitin, vancomycin, or clindamycin)

should be started as soon as the diagnosis is considered.

Strep. TSSStrep. TSSAffects mostly healthy people 20-50 yrsAffects multiple organ system with fever,

hypotension, skin findings of edema, erythema or bullae.

Aetiology:Invasive soft-tissue strep. Pyogenes (GAS)

infection, such as cellulitis or myositis

MANAGEMENTMANAGEMENT

  ABCSurgical involvementStart of antibioticsIVIG

Hemodynamic support — Massive amounts of intravenous fluids (10

to 20 L/day) are often necessary to maintain perfusion

vasopressors (eg, dopamine and/or norepinephrine) may also be required.

Surgical therapy — Prompt and aggressive exploration and

debridement of suspected deep-seated S. pyogenes infection is mandatory .

Antibiotic therapyAntibiotic therapy

Clindamycin —Should be a first choice and should be started

immediately A retrospective review of 56 children with

invasive GAS infections noted that a favorable outcome was more likely in patients who received a protein synthesis-inhibiting antibiotic (eg, clindamycin) compared to those who received only a cell wall-inhibiting antibiotic (eg, beta-lactams) (83 versus 14 percent with beta-lactams had a favorable outcome) .

IVIGIVIGincluding neutralization of streptococcal

toxins,inhibition of T-cell proliferation, neutralizing antibodies against several

streptococcal toxins such as the pyrogenic exotoxins , streptolysin O,

Staphylococcal Scalded Skin Syndrome A spectrum of superficial blistering skin disorders caused by the

exfoliative toxins of some strains of Staphylococcus aureus.

It is a syndrome of acute exfoliation of the skin typically following an erythematous cellulitis .

Severity of SSSS varies from a few blisters localized to the site of infection to a severe exfoliation affecting almost the entire body.

treatment

ABCICUSeptic precaution? antibiotic

CASE

15

Acute rheumatic fever

a nonsuppurative sequela of group A streptococcus pharyngitis that occurs two to four weeks following infection.

The five major manifestations are migratory arthritis (predominantly involving the large joints), carditis and valvulitis (eg, pancarditis), central nervous system involvement (eg, Sydenham chorea), erythema marginatum, and subcutaneous nodules.

The four minor manifestations are arthralgia, fever, elevated acute phase reactants, and prolonged PR interval.

Arthritis usually is the earliest symptomatic manifestation of ARF. The natural history that the disease "migrates" from joint to joint. Joint pain usually is more prominent than objective signs of inflammation and is almost always transient.

Rheumatic fever causes a pancarditis,

CASECASE

23 YEAR OLD MALE , PRESENT TO A&E WITH HISTORY OF ITCHING RASH OVER HIS TRUNKS

STARTS AFTER EATING PEANUTSO/E:BP 80/50, PR 110CHEST: WHEEZE BILATERALLY

Severe and acute urticaria caused by penicillin allergy

ANAPHYLAXISANAPHYLAXIS

SEVERE SYSTEMIC HYPERSENSITIVITY REACTION CHARACTERISED BY MULTI SYSTEM INVOLVMENT, INCLUDE HYPOTENSION OR AIRWAY COMPROMISE

IgE DEPENDENT: RELEASE MEDIATORS FROM MAST CELLS

ANAPHYLACTOIDANAPHYLACTOID

RESPONSES THAT ARE CLINICALLY INDISTIGUSHBLE FROM ANAPHYLAXIS

NOT IgE DEPENDENTDON’T REQUIRE SENSITIZING EXPOSURE

WHY A CHALLENGE RASHWHY A CHALLENGE RASH??CAN LEAD TO AIRWAY , COMPROMISESHOCKDEATH

COMMON CAUSESCOMMON CAUSES

DRUGS: B-LACTAM, PENICILLIN, VANCOMYCIN, CONTRAST

FOODS: SHELLFISH, NUTS, WHEAT, MILK,EGGS, SEEDS

SIGNS AND SYMPTOMSSIGNS AND SYMPTOMSITCHING, ERYTHEMA, URTICARIA, EDEMAWHEEZE, LARYNGEAL OBSTRUCTION,

CYANOSISTACHYCARDIA, HYPOTENSION

Removal of the suspect inciting antigen (eg, stop infusion of a suspect medication)

Call for help (summon a resuscitation team in the hospital setting, call 911 or an equivalent service in the community setting)

Intramuscular injection of epinephrine Placement of the patient in the supine

position (if tolerated) Supplemental oxygen

Volume resussitation

Intramuscular injection —provides a more rapid increase in the plasma and

tissue concentrations of epinephrine . For adults, the recommended dose of epinephrine (1 mg per mL) is 0.3 to 0.5 mg per single dose, injected intramuscularly into the mid-anterolateral thigh (vastus lateralis muscle). This treatment may be repeated at 5 to 15 minute intervals,

For infants and children, the recommended dose of epinephrine (1 mg per mL) is 0.01 mg per kilogram (up to 0.5 mg per dose),

IV infusion; for patient who are not responding to treatment

Adult: 2-10 mic per minutes, titrated according to BP

Infants and child: 0.1-1 mg/kg/min.

CASECASE

25 YR OLD MALE WHO USE TO HAVE SEX WITH MULTIPLE PARTNER , STARTED TO GET PAINLES ULCER OVER HIS PENIS, WHICH HEALS SPONTANEOUSLY AFTER 2 WKS WITHOUT SEEKING TREATMENT

NOW, PRESENT WITH RASH OVER HIS TRUNK AND UPPER LIMBS

FLU LIKE SYMPTOMS, AND HAS INGUINAL LYMPHADENOPATHE (O/E)

syphilissyphilisThe spirochete: treponema pallidumPrimary syphilis: *painless genital ulcer * heals spontaneously 2-6 wkSecondary syphilis : (4-8 week after healing chancre) * rash , non pruruitic, maculopapular,

start on trunk then spread to extremeties *sore throat, flu-like symptoms *generalized lymphadenopathy

Why a challeng rash ?Why a challeng rash ? Gastrointestinal abnormalities — The gastrointestinal

tract may become extensively infiltrated or ulcerated; Musculoskeletal abnormalities — Synovitis, osteitis,

and periostitis Renal abnormalities — immune-complex

glomerulonephritis or nephrotic syndrome Neurologic abnormalities — Invasion of the

cerebrospinal fluid (CSF) , MENINGITIS, DEMENTIA Ocular abnormalities — S anterior uveitis, posterior

uveitis, or panuveitis Cvs : arotitis

DIAGNOSISDIAGNOSISEarly stage:Dark fild microscopy (sensitivity 80%)Other stages: serological tests ( including

ESR)Consider LP if suspect meningitis

treatment guidelines 2006 issued by the CDC, as summarized below:

The following antibiotics have activity against syphilis: penicillin, doxycycline, azithromycin, and ceftriaxone.

benzathine penicillin G (a dose of 2.4 million units) should be administered as a single dose FOR primary or early latent syphilis and three doses for late latent syphilis.

Long-acting benzathine penicillin should only be given via the IM route; IV administration has been associated with cardiopulmonary arrest and death

In patients with severe penicillin allergy, alternative agents for the treatment of syphilis include doxycycline or azithromycin..

CASECASE33 YR OL FEMALE C/O SEVERAL DAYS OF

SEVERE HEADACHE WITH BRUISING TO HER EXTREMITIES

NO FEVER, NO VOMITING, NO NECK STIFFNESS, NO VISUAL CHANGE

NOT RELIEVED WITH PAIN KILLER, THEN SHE GOT ONE ATTACK OF TONIC- CLONIC SEIZURE

Causes — Most cases of TTP-HUS in adults are idiopathic .

DIAGNOSISDIAGNOSISMICROANGIOPATHIC HEMOLYTIC ANEMIA

WITH SCHISTOCYTES ON SMEARPLATELET COUNT 5000 TO 1x105/ULFEVERSEVERE HEADACHE

WHY IT IS A CHALLENGE RASH? WHY IT IS A CHALLENGE RASH?

RENAL ABNORMAL: RENAL INSUFFICINCY, PROTENUREA

NEUROLOGICAL ABNORMAL: HEADACHE, CONFUSION, SEIZURE OR COMA

TREATMENTTREATMENTEXCHANGE TRANSFUSION IS TREATMENT OF

CHOICEEXCHANGE PLASMAPHARESISAVOID PLATELET TRANSFUSIONPLASMA TRANSFUSION SHOULD NOT BE DONE AS

IT MAY CAUSE VOLUME OVERLOADBUT , RESERVED IN 2 SITUATION: 1) IF PLASMA EXCHANGE CAN NOT BE STARTED

PROMPTLY 2) IF Pt WITH SEVERE DISEASE BETWEEN

EXCHANGE SESSION

CASECASE

1 year old boy presented with history of fever for 1 day associated with poor feeding, vomiting , lethargic and spreading rash

O/E:febrile lethargic, purpuric rash over chest, upper and lower limb

Acute meningococcemia and meningococcal meningitis are caused by Neisseria meningitidis,

begin with colonization of the nasopharynx to systemic invasion, bacteremia, SEPSIS and/or CNS invasion.

Untreated meningococcemia is invariably fatal. Even with prompt treatment, the mortality rate is about 10%-

20%.

Common : * Children from 6 m to 1 yr of age * adult < 20 year * Persons with complement deficiencies, protein C&S

deficiency, or who are asplenic

The incubation period varies from 2- 10 days,

Symptoms: may begin with an upper respiratory infection. fever, chills, malaise, myalgias,headaches, nausea, and

vomiting. A rash is seen in more than 70% of people with

meningococcemia. Petechiae on the wrist and ankles, are the first sign of

impending septicemia. The petechiae spread to the rest of the body, becoming confluent and eventually developing into purpuric

Why it is a challenge rash ?Why it is a challenge rash ?Because if untreated early and

aggresively, it can lead to serious complication:

Cerebral: hearing loss, local vasculitis, local cerebral infarction, subdural effusion, hydrocephalus, cerebral abscess

INVESTIGATION

LP: CSF glucose concentration below 45 mg/dL (2.5 mmol/L), a protein concentration above 500 mg/dL, and a white cell count above 1000/microL.

The polymerase chain reaction (PCR) is a sensitive and rapid tool for diagnosing meningococcal infection.

However, PCR has not replaced traditional culture methods because it cannot be used to determine antimicrobial susceptibility .

TREATMENTshould be admitted to an isolation room.

Supportive care involving IV fluids is crucial in the patient with overt or incipient shock.,ceftriaxone (2 g q12h) is the initial antibiotic

of choice to cover the most common bacterial causes of purpuric disease: N. meningitidis, H. influenzae, and S. pneumoniae.

OR CEFOTAXIMEDO NOT DELAY TREATMENT AFTER LP IF

SUSPECT

DEXAMETHASONE FOR BACTERIAL MENIGITIDIS

Abstract Four hundred twenty-nine patients with bacterial meningitis were assigned on a

nonselective alternating basis into one of two therapeutic regimens. Patients in Group I received dexamethasone in addition to standard antibacterial chemotherapy of ampicillin and chloramphenicol whereas those in Group II received antibacterial chemotherapy alone. Dexamethasone was given intramuscularly (8 mg to children younger than 12 years and 12 mg to adults every 12 hours for 3 days). Both treatment groups were comparable with regard to age, sex, duration of symptoms and state of consciousness at the time of hospitalization.

A significant reduction in the case fatality rate (P < 0.01) was observed in patients with p meningitis receiving dexamethasone; only 7 of 52 patients died compared with 22 of 54 patients not receiving dexamethasone. A reduction in the overall neurologic sequelae (hearing impairment and paresis) was observed in patients receiving dexamethasone. This reduction was significant only in patients with meningitis; none of the 45 surviving patients receiving steroids had hearing loss whereas 4 of 32 patients not receiving dexamethasone had severe hearing loss (P < 0.05). No significant difference was observed between the two groups with regard to time for patients to become afebrile or to regain consciousness or in the mean admission and 24- to 36-hour cerebrospinal fluid leukocyte count, glucose or protein content.

CASECASE

3 YEAR OLD BOY HAD DEVELOPED A HIGH GRADE FEVER OF 3 DAYS DURATION

O/E: RASH, MILD CONJUNCTIVITIS, AND CERVICAL LYMPHADENITIS, CRACKED LIPS

Ix: HIGH WBC , NEUT. , ESR

Kawasaki diseaseKawasaki diseaseAffect children from 6 month-4 yearCause : not known, bacterial toxin acting as

superantigenVasculitis affecting small & medium size

vesselsCF: fever more than 5 days, conjunctivitis,

mucous memebrane chang(pharymngeal injection, cracked lip,

strawberry tongue)Rash after 4 th day

Extremities: red and edematous palms and soles, peeling of fingers and toes

Ix: high wbc, neutophils and ESR,,

Why it is a challenging rash ?Why it is a challenging rash ?

Cause fetal complication if misdiagnosed.Aneurysms of coronary arteryMyocardial ischemia and sudden deathEchocardiogaphy=========================Rx: IV immunoglobulin within 10 daysAspirin :reduce risk of thrombosisAntiplatelet aggregation

Myocardial infarction in Kawasaki disease: Clinical analyses in 195 cases  .

 M.D.Hirohisa Katoa, b, , M.D.Eisei Ichinosea, b and M.D.Tomisaku a, b

aDepartment of Pediatrics, Division of Pediatric Cardiology, Kurume University School of Medicine, Japan

  We analyzed clinical data from 195 patients (141 boys) with myocardial

infarction complicating Kawasaki disease, collected from 74 major hospitals in Japan. The myocardial infarction usually occurred within the first year of illness, but 27.2% of the patients had myocardial infarction more than 1 year later. The main symptoms of acute myocardial infarction were shock, unrest, vomiting, abdominal pain, and chest pain; chest pain was much more frequently recognized in the survivors and in older patients. The myocardial infarctions were asymptomatic in 37% of the patients. Twenty-two percent of the patients died during the first attack. Sixteen percent of the survivors of a first attack had a second attack. Forty-three percent of all survivors of the first or subsequent attack are doing well; however, others have some type of cardiac dysfunction, such as mitral regurgitation, decreased ejection fraction of the left ventricle, or left ventricular aneurysm. Coronary angiographic studies indicate that in most of the fatal cases there was obstruction either in the main left coronary artery or in both the main right coronary artery and the anterior descending artery. In survivors, one-vessel obstruction was frequently recognized, particularly in the right coronary artery.

Adult coronary artery disease probably due to childhood Kawasaki disease

H. Kato MD, Profa, , O. Inoue MDa, H. Toshima MDb, T. Kawasaki MDc, H. Fujiwara MDd an.

Abstract We have surveyed adult survivors of childhood Kawasaki disease

(KD) who had coronary artery disease that could be ascribed to KD. In response to questionnaires sent to cardiologists throughout Japan, 21 patients (17 men, 4 women, aged 20-63 years) with coronary lesions and a definite (2) or suspected (19) history of KD were reported. 5 patients had presented with acute myocardial infarction, 6 previous myocardial infarction, 9 angina pectoris, and 1 dilated cardiomyopathy. 16 patients had obstructions in two or more coronary arteries. 3 had died and 18 were alive with serious sequelae (mitral regurgitation, arrhythmias, congestive heart failure). Childhood KD should be included in the differential diagnosis of coronary artery disease in young adults

The Prevention of Coronary Artery Aneurysm in Kawasaki Disease: A Meta-analysis on the Efficacy of Aspirin and Immunoglobulin Treatment

Kritvikrom Durongpisitkul MD1, Vymutt J. Gururaj MD1, Joon M. Park MD1, ,

Conclusion. The incidence of CAA both at 30 and 60 days was significantly lower in low-IVIG than in ASA and in high-IVIG than in low-IVIG groups. Also, the incidence was lower in the single-IVIG than in the high-IVIG group, but this was noted at 30 days and not at 60 days. There was no statistically significant difference in the incidence of CAA both at 30 and 60 days between the high-IWIG-low-ASA

and high-IVIG-high-ASA groups.

CLINICAL EVALUATION OF SKIN RASH

POSSIBLE LIFE THREATINING

FLUID FILLEDSOLID

PUSTULARVESICOBULLOS

NONERYTHEMATOSERYTHEMATOS

NON ERYTHEMATOUS

VESICO-BULLOUS

PUSTULAR

*EM MAJOR*SJS, TEN

*PEMPHIGUSVULGARIS

*VARICELLA ZOOSTER

•2NDRY •SYPHILIS•ANTHRAX

*BACTERIAL FOLLICULITIS

*GONORRHEA

ERYTHEMATOUS

DIFFUSEERYTHEMAT

OUS

PETECHIALOR

PURPURIC

MACULO-PAPULAR

MACULOPAPULAR

PERIPHERALCENTRAL

SKIN CONTACT

YES NO

VIRAL EXANTHE

MA

*BCUTANEOUS DRUG

REACTION**LYME DISEASE

**PITYRIASISROSEA

*MENINGO-COCCAL

*HAND FOOTMOUTH

*RMSF*ERYTHEMA MULTIFORM

*2NDRY SYPHILIS

*ANTHRAX

+SC - SC

Evaluating The Petechial Rash Petechial rash➤ If the patient is ill-appearing, consider empiric treatment for meningococcemia and Rocky Mountain spotted fever➤ Does the patient have any sick contacts?

YES NO • Meningococcemia TRAVEL , INCIDENCE OF TICK BORN • Rubella YES NO • Epstein-Barr virus RMSV PALPABLE • Enterovirus DANGUE PURPURA FEVER YES NO • Gonococcemia VASCU- ITP LITIS TTP

DIFFUSE ERYTHEMATOUS

*TSS*SSSS

*KAWASAKI DISEASE