sjs sk 3 emergency

8/10/2019 SJS SK 3 Emergency

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1. SJS

a. DefinisiStevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN) is a rare (occurring in

approximately 2 to 3 people/million population/year in Europe and the US), life-threatening,

intolerance reaction of the skin. It is most often caused by drugs (most commonly

sulfonamides, nonsteroidal anti-inflammatory drugs, antimalarials, anticonvulsants, andallopurinol).

SJS/TEN is characterized by a macular exanthema (atypical targets) which focusses on the

face, neck, and the central trunk regions.

b. Etiologi

Causative Drugs

More than 100 drugs have been associated with the development of SJS/TEN in

single case reports or retrospective studies.[8,9,35] Such reports are not helpful,

though, in quantifying the relative risk associated with a specific drug.[36] Similarly,population based studies aimed at estimating the risk associated with drug by

correlating its usage in a certain population with the incidence of SJS/TEN do not

supply reliable data due to the rarity of SJS/TEN. To solve this problem, prospective

case control studies have been initiated which compare the drugs taken by index

patients to those taken by controls. Relative risks and the influ- ence of cofactors such

as age, gender, region, multiple drug intake, or underlying diseases can thus be

calculated by multivariate analysis. The results of the first of such studies have been

published (table II)[12]but more are to follow. Although the list of causative drugs

may vary from country to country and over time because of differences in drug use,

the following groups of drugs are most often associated with SJS/TEN: antibacterialsulfonamides [especially trimethoprim-sulfamethoxazole (cotrimoxazole)],

anticonvulsants [phenytoin, carbamazepine, phenobarbital (phe- nobarbitone),valproic acid (sodium valproate), and more recently lamotrigine], nonsteroidal anti-

inflammatory drugs (NSAIDs, especially oxicam derivatives), antimalarials and

allopurinol. Among nonsulfonamide antibacterials, significant relative risks have been

reported for cephalosporins, quinolones, tetracyclines, and aminopenicillins, as well as

imidazole antifungals.

The incubation time between (a single) drug intake and onset of SJS/TEN varies

from a few days to 2 to 3 weeks but may in exceptional cases be up to 1 month. If adrug is taken on an everyday basis, the risk for SJS/TEN is highest in the first weeks

of administration and is then greatly reduced, as documented in recent case control

studies.


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c. Patogenesis

The pathomechanisms of drug induced SJS/TEN are only partially understood.

Clinical observations (the lag period between exposure and the onset of the eruption,

shortening of the lag period and the increasing severity of SJS/TEN with repeated

exposures) as well as the presence of predominantly CD8+ T lymphocytes and

activated macrophages in the epidermis,[24-26] and additionally CD4+ T cells in the

dermis, indicate a cytotoxic cellular immune reaction directed at keratinocytes; thelatter, in turn, express adhesion molecules and MHC II. There is a drastic

overexpression of tissue necrosis factor- (TNF) in the epidermis,[27] derived from

macrophages as well as from keratinocytes, which is obviously linked to extensive

apoptosis. TNF may both directly induce apoptosis and attract more effector cells.

The pivotal role of TNF is underscored by the observation that TNF inducing

agents like ultrviolet B light[28] or x-rays[29] have a po- tentiating effect on SJS/TEN. It

has been recently shown that, in TEN, keratinocytes express lytic Fas ligand (FasL,

CD95L) and soluble FasL is present in high levels in the peripheral blood.[30] It

appears that FasL expression which triggers apoptosis by inter- action with Fas(CD95, a cell surface death receptor physiologi- cally expressed by keratinocytes) is


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the critical step in the genesis of SJS/TEN.

Causative drugs or their metabolites are thought to act as haptens and to render

keratinocytes antigenic by binding to their surfaces, being presented on both MHC I

and II molecules.[31] Propensity for drug eruptions, including SJS/TEN, has been

linked to defects of the detoxification systems of the keratinocytes:[32] their incidenceis increased in the slow acetylator phe- notype[33] and in HIV-infected patients who

are deficient in glu- tathione, an important scavenger of toxic compounds. Also, SJS/

TEN may arise in the context of the carbamazepine or hydantoin hypersensitivity

syndrome which is characterized by defective cytochrome P450 detoxification of

aromatic compounds.

d. Manifestasi Klinis

Gejala prodromal berkisar antara 1-14 hari berupa demam, lesu, batuk, pilekl, nyeri

menelan, nyeri dada, muntah, pegal otot dan atralgia yang sangat bervariasi dalamderajat berat dan kombinasi gejala tersebut.Setelah itu akan timbul lesi di:

1. Kulit; berupa eritema, papel, vesikel, atau bula secara simetris pada hampir

seluruh tubuh. Lesi yang spesifik berupa lesi target, bila bula kurang dari 10%

disebut Steven Johnson Syndrome, 10-30% disebut Steven Johnson Syndrome-

Toxic Epidermolysis Necroticans (SJS-TEN), lebih dari 30% Toxic Epidermolysis

Necroticans (TEN). Sekitar 80% penyebab TEN adalah obat.

2. Mukosa (mulut, tenggorokan dan genital); berupa vesikel, bula, erosi, ekskoriasi,

perdarahan dan krusta berwarna merah,

3. Mata; berupa konjungtivitis kataralis, blefarokonjungtivitis, iritis, iridosiklitis,

kelopak mata edema dan sulit dibuka, pada kasus berat terjadi erosi dan

perforasi kornea.

SJS/TEN often begins with nonspecific influenza-like prodromi like fever, myalgias

and arthralgias, malaise, headache, rhinitis, sore throat, cough, nausea, and/or diarrhea

that may last from 1 to 14 days. The rash sets on suddenly and symmetrically in the

facial, neck, chin, and central trunk areas and spreads within few days to the

extremities and the rest of the body (figure 1). The individual lesions are macular,

rather ill defined, roundish, pale livid (spots) and often exhibit dusky centers

reminiscent of target lesions (flat atypical targets). At times, the lesions may be

slightly raised (raised atypical targets) but typical targets (as defined by wheal-likeelevation and 3 concentric components) are very rare. The lesions tend to coalesce;

they are tender and exhibit a positive Nikolskys sign. The epidermis becomes

necrotic, loose, and easily detachable in large sheets, particularly at sites on lips,

buccal, and palatinal mucosa but may expand to the entire oral cavity, pharynx,

larynx, nasal cavity, and even esophagus or trachea in severe cases. Symptoms begin

with burning sensations, blisters arise and break, leading to severely painful erosions

covered by necrotic epithelium, fibrin and/or hemorrhagic crusts. Conjunctival

involvement begins with burning and injection, fol- lowed by an erosive

pseudomembranous conjunctivitis, at times with corneal erosions. In severe cases,

skin appendages such as hair (eyelashes) and nails may be shed.


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Systemic Signs and Internal Organ Involvement

Constitutional signs include fever, arthralgias, and weakness.[4] Internal organs are

more often involved in patients with widespread and severe skin disease

(TEN>SJS).[4] The respiratory tract is most commonly affected by sloughing of

tracheal and bronchial mucosa leading to obstruction, expectoration of bron- chialcasts, bronchopneumonia and, at its most severe, acute respiratory distress

syndrome.[13,14] Less common are symptoms of the gastrointestinal tract such as

diarrhea, abdominal pain, gastrointestinal bleeding and colonic perforation, etc.[15]

Toxicity, dehydration, and water and electrolyte imbalances may proceed to

hemodynamic shock, coma, and seizures. Renal complications are rare[16] and occur

as a consequence of septicemia and shock.

e. Diagnosis

Minimal dermal inflammatory cell infiltrate and full-thickness necrosis of the epidermis are typicalhistopathologic findings in patients with Stevens-Johnson syndrome. Histopathologic examination of the skin

can also reveal the following:

Changes in the epidermal-dermal junction ranging from vacuolar alteration to subepidermal blisters

Dermal infiltrate: Superficial and mostly perivascular

Apoptosis of keratinocytes

CD4+ T lymphocytes predominating in the dermis; CD8+ T lymphocytes predominating in the

epidermis; the dermoepidermal junction and epidermis is infiltrated mostly by CD8+ T lymphocytes

Ocular examination can demonstrate the following:

Conjunctival biopsies from patients with active ocular disease show subepithelial plasma cells and

lymphocyte infiltration; lymphocytes also are present around vessel walls; the predominant infiltratinglymphocyte is the helper T cell

Immunohistology of the conjunctiva reveals numerous HLA-DRpositive cells in the substantia

propria, vessel walls, and epithelium

There are no specific laboratory studies (other than biopsy) that can definitively establish the diagnosis of

Stevens-Johnson syndrome.

Serum levels of the following are typically elevated in patients with Stevens-Johnson syndrome:

Tumor necrosis factor (TNF)-alpha Soluble interleukin 2-receptor

Interleukin 6

C-reactive protein

However, none of these serologic tests is used routinely in diagnosing and managing Stevens-Johnson

syndrome.

A complete blood count (CBC) may reveal a normal white blood cell (WBC) count or a nonspecific

leukocytosis. A severely elevated WBC count indicates the possibility of a superimposed bacterial infection.

Electrolytes and other chemistries may be needed to help manage related problems.

Skin and blood cultures have been advocated because the incidence of serious bacterial bloodstream infectionsand sepsis contribute to morbidity and mortality.

[32]In addition, cultures of urine and wounds are indicated when

an infection is clinically suspected. Determine renal function and evaluate urine for blood.


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Skin biopsy specimens demonstrate that the bullae are subepidermal. However, skin biopsy is not an emergency

department (ED) procedure. Epidermal cell necrosis may be noted. Perivascular areas are infiltrated with

lymphocytes.

Bronchoscopy, esophagogastroduodenoscopy (EGD), and colonoscopy may be indicated. Chest radiography

may indicate the existence of a pneumonitis when clinically suspected. Otherwise, routine plain films are not

indicated.

Grading

The severity of SJS/TEN varies within wide limits with re- spect to rapidity of

evolvement, degree of confluence, percentage of BSA affected, mucous membrane

and internal organ involvement as well as constitutional symptoms. It has thus

become cus- tomary to grade SJS/TEN according to the percentage of BSA involved:

SJS less than 10%, TEN more than 30%. For patients with more than 10% but less

than 30% BSA involvement, the term SJS/TEN-overlap has been suggested.[1]

However, it has to be noted that this grading system, although of prognostic relevance,

does not take account of the evolution of the rash in the early phase.

Course

Following the outbreak, SJS/TEN enters a phase of progression which usually lasts 4 to 5

days but can be considerably more protracted if the half-life of the offending drug is long

(e.g. long acting sulfonamides). Progression may halt at any extent from 10 to close to 100%

of the BSA being affected, and the patient enters the acme phase which again may take from

a few days up to 2 weeks, depending on the severity of SJS/TEN and the physical

constitution of the patient. It is the acme phase where the hazard of complications is highest:hemodynamic shock, myocardial infarction and, above all, septicemia. The phase of

regression is her- alded by lightening of the erythema, lessening of oozing and skin

tenderness, and transformation of the detached epidermis into dry blackish parchment-like

squames. Re-epithelization may take 1 to 2 weeks to be completed. Figure 3 shows the

typical course of SJS/TEN.

Skin erosions tend to heal without or with little scarring but may leave hypo- or

hyperpigmentation. Scarring alopecia and permanent nail loss has been reported. Scarring of

mucosal lesions, however, is seen in up to 30% of patients with TEN, leading

predominantly to ophthalmologic sequelae: synechiae, sym- blepharon, en- or ectropion and

trichiasis. Pannus formation and corneal opacities may at times lead to blindness. Rare butchar- acteristic further sequelae are tracheal, esophageal or anal strictures, phimosis, vaginal

or urethral strictures, and vaginal adeno- sis.[17,18] Damage to lacrimal and salivary glands

may provoke a Sjgren-like syndrome.

Laboratory Findings

SJS/TEN is accompanied by nonspecific findings such as elevated blood sedimentation rate,

mild to moderate elevation of liver enzyme levels and/or blood urea nitrogen, fluid and

electrolyte imbalances, leukocytosis and, not infrequently, eosinophilia, and

microalbuminuria.[4] Serum protein levels and/or peripheral CD4+ T lymphocyte levels may

be reduced. Neutropenia may occur and is regarded as a sign of poor prognosis.


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Histopathology

Histopathology is characterized by prominent epidermal necrosis contrasting with a

surprisingly sparse dermal inflammatory infiltrate (silent dermis).[4] In early stages,

satellite cell necrosis of the epidermis is seen, which proceeds to vacuolization necrosis of the

basal layer and full thickness epidermal necrosis in later stages, with sloughing of theepidermis (figure 4).

f. Diagnosis Banding

SJS/TEN is usually a straightforward diagnosis. Difficulties may arise in 2 situations:

viral or drug-induced macular eruptions on the one hand, which require the prediction

if they proceed to SJS/TEN or not; and on the other hand, other eruptions charac-

terized by widespread erythema and detachment of the skin.

5.1 Macular Eruptions

These may be morphologically indistinguishable from initial SJS/TEN but they do not

exhibit a positive Nikolskys sign and do not reveal prominent involvement of mucous

membranes.

5.2 Herpes-Simplex-Associated Erythema Multiforme

As mentioned above, HAEM is distinct from SJS/TEN by its primary lesion (typical

target lesion), its much sparser exanthema with little tendency for confluence and its

acral distribution pattern. Other important differences are: low incidence of an-

ogenital (but not oral!) mucosal involvement, history of prior episodes, association

with relapsing herpes simplex, and a prominent inflammatory infiltrate in

histopathology.[19]

5.3 Generalized Bullous Fixed Drug Eruption

Multilocular or generalized confluent bullous FDE is a clas- sical differential

diagnosis of SJS/TEN. Main points of distinction are its primary lesions, which are

large patches (faintly dis- cernible even after confluence), most often irregularly

distributed and of a characteristic purplish-livid color, the rarity of mucous membraneinvolvement and the paucity of constitutional symptoms. Histopathology is similar

to SJS/TEN with the exception of more pronounced inflammation and a markededema of the papillary dermis. Often, history reveals prior episodes of milder

Fig. 4. Histopathology of Stevens-Johnson syndrome/toxic epidermal necrolysis: full thicknessnecrosis and detachment of the epidermis, a sparse inflammatory infiltrate of the dermis ( 25magnification).

expression following intake of the culprit drugs. Generalized FDE takes a much

milder course than SJS/TEN.

5.4 Physical and Chemical Injury


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Diagnosis is straightforward if history is available but may be difficult in unconscious

patients. Injury by exogenous agents is characterized by an artificial distribution

pattern, rarity of mucous membrane involvement and absence of an antecedent mac-

ular rash. If necroses arise, they tend to involve deeper layers including, at times, theskin appendages, whereas they are purely epidermal in SJS/TEN.

5.5 Staphylococcal Scalded Skin Syndrome

Staphylococcal scalded skin syndrome (SSSS) is linked to a phage group 2

Staphylococcus aureus infection, most often of infants and children.[20] Frequent sites

of infection are the upper respiratory tract and the skin (bullous impetigo, omphalitis).

Skin symptoms are mediated by hematogenous dispersion of the staph- ylococcalexotoxin exfoliatin, which elicits subcorneal acantholysis and leads to extensive,

faint, and ill described erythemas and detachment of the horny layer in large sheets

resembling scalding. Sites most often involved are the face, axillary and inguinal folds

and sites of mechanical stress (neck, back). Distinction from SJS/ TEN is based on theabsence of an antecedent macular rash (infrequently there is a scarlatiniformeruption), absence of mucosal lesions and of internal organ involvement, and by

histology or exfoliative cytology (subcorneal acantholysis versus epidermal

g. Tatalaksana

Penatalaksanaan utama adalah menghentikan obat yang diduga sebagai

penyebab SSJ, sementara itu kemungkinan infeksi herpes simplex dan

Mycoplasma pneumoniae harus disingkirkan. Selanjutnya perawatan

lebih bersifat simtomatik.4.

Antihistamin dianjurkan untuk mengatasi gejala pruritus / gatal bisa dipakai

feniramin hidrogen maleat (Avil) dapat diberikan dengan dosis untuk usia 1-3

tahun 7,5 mg/dosis, untuk usia 3-12 tahun 15 mg/dosis, diberikan 3 kali/hari,

diphenhidramin hidrokloride (Benadril) 1mg/kg BB tiap kali sampai 3 kali per

hari. Sedangkan untuk setirizin dapat diberikan dosis untuk usia anak 25 tahun:2.5 mg/dosis,1 kali/hari; >6 tahun: 5-10 mg/dosis,1 kali/hari.

5. Blisterkulitbisadikompresbasahdenganlarutanlarutanburowi.

6. Papula dan makula pada kulit baik intak diberikan steroid topikal, kecuali kulit

yang terbuka.

Pengobatan infeksi kulit dengan antibiotika. Antibiotika yang paling beresiko tinggi

adalah -lactam dan sulfa jangan digunakan. Untuk terapi awal dapat diberikanantibiotika spektrum luas, selanjutnya berdasarkan hasil biakan dan uji resistensi

kuman dari sediaan lesi kulit dan darah. Terapi infeksi sekunder menggunakan

antibiotika yang jarang menimbulkan alergi, berspektrum luas, bersifat bakterisidal dan

tidak bersifat nefrotoksik, misalnya klindamisin 8-16 mg/kg/hari secara intravena,

diberikan 2 kali/hari.

7.Kotikosteroid: deksametason dosis awal 1mg/kg BB bolus intravena, kemudian

dilanjutkan 0,2-0,5 mg/kg BB intravena tiap 6 jam. Penggunaan steroid sistemik

masih kontroversi. Beberapa peneliti menyetujui pemberian kortikosteroid

sistemik beralasan bahwa kortikosteroid akan menurunkan beratnya penyakit,

mempercepat konvalesensi, mencegah komplikasi berat, menghentikanprogresifitas penyakit dan mencegah kekambuhan. Beberapa literatur


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menyatakan pemberian kortikosteroid sistemik dapat mengurangi inflamasi

dengan cara memperbaiki integritas kapiler, memacu sintesa lipokortin,

menekan ekspresi molekul adesi. Selain itu kortikosteroid dapat meregulasi

respons imun melalui down regulation ekspresi gen sitokin. Mereka yang tidak

setuju pemberian kortikosteroid berargumentasi bahwa kortikosteroid akan

menghambat penyembuhan luka, meningkatkan resiko infeksi, menutupi tandaawal sepsis, perdarahan gastro-intestinal dan meningkatkan mortalitas. Faktor

lain yang harus dipertimbangkan yaitu harus tappering off 1-3 minggu. Bila tidak

ada perbaikan dalam 3-5 hari, maka sebaiknya pemberian kortikosteroid

dihentikan. Lesi mulut diberi kenalog in orabase.

8.Intravena Imunoglobulin (IVIG). Dosis awal dengan 0.5 mg/kg BB pada hari 1, 2, 3, 4,

dan 6 masuk rumah sakit. Pemberian IVIG akan menghambat reseptor FAS

dalam proses kematian keratinosit yang dimediasi FAS.

Perawatan konservatif ditujukan untuk:

1. Perawatan lesi kulit yang terbuka, seperti perawatan luka bakar.

Koordinasi dengan unit luka bakar sangat diperlukan.2. Terapi cairan dan elektrolit.

Lesi kulit yang terbuka seringkali disertaipengeluaran cairan disertai elektrolit.

3. Alimentasi kalori dan protein secara parenteral. Lesi pada saluran cerna

menyebabkan kesulitan asupan makanan dan minuman.

4. Pengendalian nyeri. Penggunaan NSAID beresiko paling tinggi sebaiknya tidak

digunakan untuk mengatasi nyeri.

Konsultasi

Konsultasi ke bagian oftalmologi untuk kelainan pada mata. Biasanya dokter mata

memberikan airmata artifisial, atau gentamisin tetes mata bila ada dugaan infeksi

sekunder. Secara rutin pasien juga kita konsulkan ke bagian kulit dan kelamin untuk

perawatan yang komprehensif. Konsultasi ke bagian bedah plastik sehubungan dengan

perawatan lesi kulit terbuka yang biasanya dirawat sebagaimana luka bakar.

Patient Management

The outcome of a patient with SJS/TEN depends on his/her rapid referral to a

specialized center experienced in the management of SJS/TEN and in general skin

care, that is, to a dermatology hospital. This does not apply, of course, to those

regions where dermatology is practiced as an outpatient specialty. Under no

circumstances may a patient with SJS/TEN be treated on an ambulatory basis because

supportive care and constant supervi- sion is no less important in his/her management

than are active therapeutic measures. This is important to note because many patients,in the initial stages of SJS/TEN, may feel fairly well or even euphoric and are

unwilling to be admitted to hospital. Al- though widely claimed, referral to an


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intensive care unit or to a burn center is not mandatory except when severe

complications are present; SJS/TEN is a skin disease which, if properly treated, is

linked to much less systemic symptoms than a second degree burn of the same BSA

extent.

The management of SJS/TEN rests on 3 cornerstones: withdrawal of the offendingdrug, active treatment, and supportive measures. Active therapeutic interventions

either attempt to curb the disease process in the phase of progression, to stabilize the

homeostasis of the patient and to fend off bacterial invasion in the progression or peak

phases, or to promote re-epithelization in the phase of regression. Currently, there are

no generally accepted regimens or treatment guidelines, and no controlled therapeutic

trials have ever been published. This is because SJS/TEN is an infrequent and life-threatening disease of high clinical variability which requires complex treatment and

care, adapted individually to each patient. Also, personal preference on the behalf of

the treating physician has often overruled the establishment of ratio- nal concepts.

This is particularly true for the long standing controversy as to whether systemiccorticosteroids should be given or not.

8.1 Withdrawal of the Suspected Offending Drugs

Obviously, the causative drug should rapidly be identified and withdrawn; [38] this

measure, however, does not immediately halt disease progression. It often turns out to

be a difficult task because no suitable laboratory tests are available at present, and the

detection of the most likely culprit is purely a matter of em- pirical calculation. The

latter is based on a careful history of drug intake with special focus on the past few

weeks, its relation to the

development of symptoms, and prior episodes of SJS/TEN. Retrospective analysis of

case series and prospective epidemio- logic studies provide data on the relative risk of

different drugs or drug families for causing SJS/TEN (table II). The most likely

offending drug is the one which has been newly administered in the past 4 weeks andis known as a risk drug for SJS/TEN.

Matters may be obscured by several factors: patients often take more than one drug,

and many patients will have just started to take drugs for the treatment of symptoms

which may in fact have been prodromi of a developing SJS/TEN (antimicrobials,

analgesics or NSAIDs). Furthermore, drug interactions, infections and diseases of

altered immune status may confound the situation and render it impossible to pinpoint

the most likely of- fender. From a practical point of view it is recommended in such

cases to discontinue all drugs that are not absolutely necessary.

Obviously, it would be most desirable to identify the culprit drug at least following

recovery in order to prevent re-exposure. Again, despite some reports to the contrary,

skin tests (patch, prick or intracutaneous) and lymphocyte transformation tests have

proved unreliable. Exposure tests are ethically unacceptable since they are likely to

induce severe relapses. In our institution, all suspected drugs are entered into the

patients file without test- ing, and the patient is strictly warned against reuse.


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8.2 Active Suppression of Disease Progression

A number of anti-inflammatory and/or immunosuppressive treatment modalities have

been proposed to have beneficial effects in SJS/TEN. The evidence is marred,however, by the lack of controlled trials and the fact that often no clear-cut distinction

between progression and peak phases is made in the single case reports and small (andusually heterogeneous) patients series reported in the literature. Thus, at present,

there is no consensus as to which, if any, therapeutic measure will shorten the naturalcourse of the disease. Furthermore, many of the treatment modalities have potential

harmful adverse effects which must be weighed against their benefits. As a

consequence, it has recently become the trend for many clinicians to abstain from the

use of modalities aimed at halting disease progression and to rely totally on supportive

measures. This pessimistic view, which is unique in the context of an acute immune

mediated life-threatening disease, must be attributed to a much too far-reaching and

unjustified equation of SJS/TEN with burn injuries.

8.2.1 Corticosteroids

Systemic corticosteroids have been the mainstay of the treatment of SJS/TEN for

long time but have come into disrepute in the past years. The scientific community

appears to be strangely divided over their use, fervent supporters[38-43]being fiercely

op posed by those who condemn corticosteroids and those who even consider them

detrimental.[10,44-47] The controversy arose because corticosteroids, if given for

longer than the phase of progression, clearly increase the risk of infection and thus

contribute considerably to mortality. This point was taken up by surgical intensive

care specialists who strived to shape the treatment of SJS/TEN according to theprinciples of the management of burns where systemic corticosteroids, are obviously

not indicated. This argument was expanded to the assumption that corticosteroids, in

principle, have no effect on disease progression. This idea was supported byadditional observations: mortality rates for SJS/TEN do not differ significantly

between countries where corticosteroids are commonly used (e.g. Germany, where

the usage is 80%) and those where physicians are reluctant to use them (e.g. France,

where the usage 20%), and that SJS/TEN may arise in patients who are receiving long

term corticosteroid treatment for other reasons.[48,49]

If corticosteroids do in fact curb disease progression, which may be expected in animmune mediated disease, they certainly do not shorten the duration of the peak and

the regression phases. Obviously corticosteroids are a double-edged sword in

SJS/TEN, because it is quite clear that they are not excessively efficacious and have to

be used with utmost caution. If given, relatively high initial doses are required (oral

methylprednisolone 1 to 2 mg/ kg/day), and rapid tapering is indicated as soon as

progression halts. They may be given only if all additional and supportive measuresare procured (see sections 8.3 and 8.4), and if the physical condition of the patient

permits. It is absolutely unacceptable to consider corticosteroids as the only and

sufficient therapeutic measure. It is to be expected that the controversy over the use of

corticosteroids will become irrelevant due to the availability of more efficacious andless hazardous strategies before the issue is settled by appropriate controlled studies.


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8.2.2 Immunoglobulins

Recently, intravenous administration of pooled human immunoglobulins (IVIG) has

emerged as a promising strategy for blocking disease progression, based on their

content of antibodies against FasL which are capable of preventing apoptotic cell

death in vitro.[30] In the original study, 10 patients were treated with IVIG dosagesranging from 0.2 to 0.75 g/kg body weight/day for 4 consecutive days. In all patients,

rapid halting of disease progression and recovery was observed. Similar favorable

results have been reported since in a number of individual cases. Still, pending

adequately sized controlled studies, this very expensive treatment should be reserved

for clinical trials. IVIG have a good safety profile, nephropathy being a rare but

dangerous adverse effect which may result in renal failure.

8.2.3 Plasmapheresis and Hemodialysis

Scattered reports[50-53] suggest that the removal of the causative drug, itsmetabolites or other toxic principles from the cir- culation may inhibit progression of

SJS/TEN. In the absence of formal proof and the stress linked to this treatment, these

strategies are not recommended at the present time.

8.2.4 Cyclophosphamide

Cyclophosphamide is an inhibitor of cell-mediated cytotox- icity. Although having

been successfully used in TEN according to a few reports,[54,55] it is a potent

immunosuppressive agent as well, and has itself been the causative drug in several

cases of SJS/TEN.[56]

8.2.5 Cyclosporine

Again, several case reports suggest the efficacy of cyclosporine in SJS/TEN.[57-61]

It should not be considered a first line treatment option, however, for the same

reasons as cyclophosphamide; also, its mechanisms of action in SJS/TEN are far

from clear, and a rapid effect (as necessary for the brief phase of progression) is

unlikely. It has been suggested that cyclosporine works by interacting with TNF

metabolism.[62]

8.2.6 Acetylcysteine

Acetylcysteine, with S-adenosyl-L-methionine, may act through replenishing cells

with antioxidant capacity and by in- hibiting cytokine-mediated immune reactions.

The evidence as to its use in SJS/TEN is sporadic.[63]

8.2.7 Thalidomide

The rationale for the experimental use of thalidomide, a known inhibitor of TNF,

was the understanding of the pivotal role of this cytokine in the genesis of

SJS/TEN.[64] Yet, in a ran- domized placebo controlled study, the thalidomide

recipients ex- hibited a significantly higher mortality than the control group, and the


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study had to be discontinued.[65] It remains unclear whether this outcome was due to

paradoxical enhancement of TNFproduction or effects, or to T cell stimulation

(mediated by interleukin-2).[66,67]

8.3 Maintenance of Hemodynamic Protein and Electrolyte Homeostasis

Despite its clinical resemblance, the pathomechanisms of SJS/TEN are totally

different from those of burn injuries, and the therapeutic principles of the latter,

therefore, do not apply to patients with SJS/TEN. The main difference is the virtual

absence of vascular damage in SJS/TEN; consequently, edema and loss of fluid into

the interstitial tissues is not a prominent feature. There is also much less loss of fluid

to the outside since tense and large blisters are only rarely formed. Water loss in

SJS/TEN mainly occurs by evaporation from erosions and is thus highest in the peak

phase. Metabolic acidosis is not a regular feature of SJS/TEN. Furthermore, second

degree burn injuries are even more painful than SJS/TEN. All of these factors

cooperate to render fluid and electrolyte imbalances much less drastic and of lateronset than in burns. Hemodynamic shock is a possibility, but it is rare and occurs

mainly in unsatisfactory clinical settings and in patients with cardiovascular ormetabolic compromise.

Blood pressure, hematocrit, blood gases, electrolytes, and serum proteins must be

monitored and adjusted appropriately.[68] Fluid replacement regimens as used for

burn injuries are not recommended. Central venous lines (as well as urinarycatheters) should not routinely be inserted.

8.4 Antibacterial Treatment

It is universally agreed that infections pose the most serious threat to patients with

SJS/TEN (especially when corticosteroids are given). Bacterial and fungal cultures

should therefore be taken at short intervals (2 to 3 time a week) from skin and

mucosal erosions, blood and sputum; oral and genital mucosae should be repeatedly

inspected for herpes simplex. In many patient series, antibacterials were only given

when clinical symptoms of infection were already present, and the causative

organism identified. This is probably due, on the one hand, to a reluctance of using

antibacterials prophylactically in surgical departments, and on the other hand, to the

fear of introducing a further drug in a patient with drug intolerance. This fear shouldbe weighed against the fact that antibacterials are only rarely the offending drug in

SJS/TEN, and that those with a known risk of severe cutaneous reactions like

sulfonamides, cephalosporins, aminopenicillins, macrolides or quinolones, can be

easily avoided. It has been the strategy of our group[4] to start prophylactic

antibacterial treatment (sodium penicillin, 10 million units twice daily right from the

beginning, and to adjust the antibacterial according to the cultured organism; pursuing

this strategy, the mortality rate of TEN was kept at


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Patients should be placed on an aluminum foil. Loose sheets of detached skin may

cautiously be removed, but early aggressive debridement as performed in burns is not

indicated because it is painful and increases the extent of the erosions; also, the

necroses are only superficial and represent no obstacle for re-epithelization. Erosionsshould be covered with gauze or hydrocolloid dressings. Sulfonamide containing

topical treatments should be

avoided. When using topical antibacterials or antiseptics, the possibility of systemic

absorption has to be considered. Fresh-frozen or cryopreserved cadaver allograft[69]

and porcine xenograft skin,[70] as well as biosynthetic dressings[71] have been

advocated, but their value is questionable becauseunlike in burnsthe dermis is

largely uninvolved and re-epithelization is not a problem.

8.5.2 Eyes

In the acute phase of conjunctival involvement, lubricants, corticosteroid andantibacterial collyria should be applied several times a day. Lid-globe adhesions

should be cautiously removed twice daily with a glass rod to avoid occlusion of the

fornices, taking care not to strip pseudomembranes which may lead to bleeding andincreased conjunctival scarring.[72,73]

8.5.3 Respiratory Tract

Supportive pulmonary care includes postural drainage and, if necessary, cautious

suctioning.

8.5.4 Alimentation

Patients are often unable to eat and drink due to their oral and/or esophageal mucosa

involvement, or to their poor general condition. Local anesthetics, in the form of a

mouth wash used before the meals, may be helpful. High calorie and high protein diet

or intravenous administration is recommended, taking into account the risk of

septicemia by intravenous lines.

h. Prognosis

Pada kasus yang tidak berat, prognosisnya baik, dan penyembuhan terjadi dalam waktu

2-3 minggu. Kematian berkisar antara 5-15% pada kasus berat dengan berbagai

komplikasi atau pengobatan terlambat dan tidak memadai. Prognosis lebih berat bila

terjadi purpura yang lebih luas. Kematian biasanya disebabkan oleh gangguan

keseimbangan cairan dan elektrolit, bronkopneumonia, serta sepsis.

Prognosis of SJS/TEN depends on its severity and the quality of medical care. [4,44]

Mortality is low (


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center. Mortality is most often due to septicemia (S. aureus, Pseudomo- nas spp.,

Candida spp., etc), pneumonia, myocardial infarction and cardiac insufficiency, rather

than to renal insufficiency and hemodynamic shock. Recovery is slow and may

require 3 to 6 weeks, and is often accompanied by scarring at mucosal sites.

i. Komplikasi

Sindroma Steven Johnson sering menimbulkan komplikasi pada mata berupa

simblefaron dan ulkus kornea. Komplikasi lain adalah timbulnya sembab, demam atau

malahan hipotermia, dan yang terberat adalah sepsis.

j. Pencegahan

2. LARINGITIS AKUT

a. Definisi

Laringitis akut merupakan penyakit yang umum pada anak-anak,

mempunyai onset yang cepat dan biasanya sembuh sendiri. Bila laringitis

berlangsung lebih dari 3 minggu maka disebut laringitis kronik. Laringitis

didefinisikan sebagai proses inflamasi yang melibatkan laring dan dapat

disebabkan oleh berbagai proses baik infeksi maupun non-infeksi.

Laringitis sering juga disebut juga dengan croup. Dalam prosesperadangannya laringitis sering melibatkan saluran pernafasan

dibawahnya yaitu trakea dan bronkus. Bila peradangan melibatkan laring

dan trakea maka diagnosis spesifiknya disebut laringotrakeitis, dan bila

peradangan sampai ke bronkus maka diagnosis spesifiknya disebut

laringotrakeobronkitis.

b.

Etiologi

Etiologi dari laringitis akut yaitu penggunaan suara berlebihan, gastro esophago reflux disease

(GERD), polusi lingkungan, terpapar dengan bahan berbahaya, atau bahan infeksius yang membawa kepada

infeksi saluran nafas atas. Bahan infeksius tersebut lebih sering virus tetapi dapat juga bakterial. Jarang

ditemukan radang dari laring disebabkan oleh kondisi autoimun seperti rematoid artritis, polikondritis berulang,

granulomatosis Wagener, atau sarkoidosis.

Virus yang sering menyebabkan laringitis akut antara lain virus parainfluenza tipe 1 sampai 3 (75%

dari kasus), virus influenza tipe A dan B, respiratory syncytial virus (RSV). Virus yang jarang menyebabkan

laringitis akut antara lain adenovirus, rhinovirus, coxsackievirus, coronavirus, enterovirus, virus herpes simplex,

reovirus, virus morbili (measles), virus mumps.

Bakteri walaupun jarang tetapi dapat juga menyebabkan laringitis akut, antara lain Haemophilus

influenzae type B, Staphylococcus aureus, Corynebacterium diphtheriae, Streptococcus group A, Moraxella

chatarralis, Escherichia coli, Klebsiella sp., Pseudomonas sp., Chlamydia trachomatis, Mycoplasma


15/21

pneumoniae, Bordatella pertussis, dan sangat jarang Coccidioides dan Cryptococcus. C. diphtheriae harus

dicurigai sebagai kuman penyebab terutama bila anak belum diimmunisasi, karena C. diphtheriae dapat

meyebabkan membranous obstructive laryngitis

Selain virus dan bakteri laringitis juga dapat disebabkan juga oleh jamur, antara

lain Candida albicans, Aspergilus sp., Histoplasmosis dan Blastomyces. Histoplasma dan

Blastomyces dapat menyebabkan laringitis sebagai komplikasi dari infeksi sistemik.

c. Patof

Laringitis akut merupakan inflamasi dari mukosa laring dan pita suara

yang berlangsung kurang dari 3 minggu. Parainfluenza virus, yang

merupakan penyebab terbanyak dari laringitis, masuk melalui inhalasi

dan menginfeksi sel dari epitelium saluran nafas lokal yang bersilia,

ditandai dengan edema dari lamina propria, submukosa, dan adventitia,

diikuti dengan infitrasi selular dengan histosit, limfosit, sel plasma dan

lekosit polimorfonuklear (PMN). Terjadi pembengkakan dan kemerahan

dari saluran nafas yang terlibat, kebanyakan ditemukan pada dinding

lateral dari trakea dibawah pita suara. Karena trakea subglotis dikelilingi

oleh kartilago krikoid, maka pembengkakan terjadi pada lumen saluran

nafas dalam, menjadikannya sempit, bahkan sampai hanya sebuah celah.

Daerah glotis dan subglotis pada bayi normalnya sempit, dan pengecilansedikit saja dari diameternya akan berakibat peningkatan hambatan

saluran nafas yang besar dan penurunan aliran udara. Seiring dengan

membesarnya diameter saluran nafas sesuai dengan pertumbuhan maka

akibat dari penyempitan saluran nafas akan berkurang. Sumbatan aliran

udara pada saluran nafas atas akan berakibat terjadinya stridor dan

kesulitan bernafas yang akan menuju pada hipoksia ketika sumbatan

yang terjadi berat. Hipoksia dengan sumbatan yang ringan menandakan

keterlibatan saluran nafas bawah dan ketidakseimbangan ventilasi dan

perfusi akibat sumbatan dari saluran nafas bawah atau infeksi parenkim

paru atau bahkan adanya cairan.

d. Manifest

Laringitis ditandai dengan suara yang serak, yang disertai dengan puncak suara (vocal pitch) yang

berkurang atau tidak ada suara (aphonia), batuk menggonggong, dan stridor inspirasi. Dapat terjadi juga demam

sampai 39-40, walaupun pada beberapa anak dapat tidak terjadi. Gejala tersebut ditandai khas dengan

perburukan pada malam hari, dan sering berulang dengan intensitas yang menurun untuk beberapa hari dan

sembuh sepenuhnya dalam seminggu. Gelisah dan menangis sangat memperburuk gejala-gejalanya. Anak

mungkin memilih untuk duduk atau dipegangi tegak. Pada anak yang lebih dewasa penyakitnya tidak begitu


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parah. Pada anggota keluarga lainnya mungkin didapatkan penyakit saluran pernafasan yang ringan.

Kebanyakan pasien hanya bergejala stridor dan sesak nafas ringan sebelum mulai sembuh. Gejala tersebut

sering disertai dengan gejala-gejala seperti pilek, hidung tersumbat, batuk dan sakit menelan. Pada kebanyakan

pasien gejala tersebut timbul 1 sampai 3 hari sebelum gejala sumbatan jalan nafas terjadi.3,4,5,6

Pada pemeriksaan fisik, dapat ditemukan suara yang serak, coryza, faring yang meradang dan frekuensi

pernafasan dan denyut jantung yang meningkat, disertai pernafasan cuping hidung, retraksi suprasternal,

infrasternal dan intercostal serta stridor yang terus menerus, dan anak bisa sampai megap-megap (air hunger).

Bila terjadi sumbatan total jalan nafas maka akan didapatkan hipoksia dan saturasi oksigen yang rendah. Bila

hipoksia terjadi, anak akan menjadi gelisah dan tidak dapat beristirahat, atau dapat menjadi penurunan

kesadaran atau sianosis. Dan kegelisahan dan tangisan dari anak dapat memperburuk stridor akibat dari

penekanan dinamik dari saluran nafas yang tersumbat. Dari penelitian didapatkan bahwa frekuensi pernafasan

merupakan petunjuk yang paling baik untuk keadaan hipoksemia. Pada auskultasi suara pernafasan dapat

normal tanpa suara tambahan kecuali perambatan dari stridor. Kadang-kadang dapat ditemukan mengi yang

menandakan penyempitan yang parah, bronkitis, atau kemungkinan asma yang sudah ada sebelumnya.2,4,6

Dengan laringoskopi sering didapatkan kemerahan pada laring yang difus bersama dengan pelebaran

pembuluh darah dari pita suara. Pada literatur lain disebutkan gambaran laringoskopi yang pucat, disertai edema

yang berair dari jaringan subglotik. Kadang dapat ditemukan juga bercak-bercak dari sekresi. Dari pergerakan

pita suara dapat ditemukan asimetris dan tidak periodik. Sebetulnya pemeriksaan rontagen leher tidak berperan

dalam penentuan diagnosis, tetapi dapat ditemukan gambaran staplle sign (penyempitan dari supraglotis) pada

foto AP dan penyempitan subglotis pada foto lateral, walaupun kadang gambaran tersebut tidak didapatkan.

Pemeriksaan laboratorium tidak diperlukan, kecuali didapatkan eksudat maka dapat dilakukan pemeriksaan

gram dan kultur dengan tes sensitivitas. Tetapi kultur virus positif pada kebanyakan pasien. Dari darah

didapatkan lekositosis ringan dan limfositosis.

e. Diagnosis

a. Foto rontgen leher AP : bisa tampak pembengkakan

jaringan subglotis (Steeple sign). Tanda ini ditemukan

pada 50% kasus.

b.

Pemeriksaan laboratorium : gambaran darah dapat


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normal. Jika disertai infeksi sekunder, leukosit dapat

meningkat.

c. Pada pemeriksaan laringoskopi indirek akan ditemukan

mukosa laring yang sangat sembab, hiperemis dantanpa membran serta tampak pembengkakan subglotis

yaitu pembengkakan jaringan ikat pada konus elastikus

yang akan tampak dibawah pita suara.

f. Diagnosis banding

g. Tatalaksana

Umumnya penderita penyakit ini tidak perlu masuk rumah sakit, namun

ada indikasi masuk rumah sakit apabila :

Usia penderita dibawah 3 tahun

Tampak toksik, sianosis, dehidrasi atau axhausted

Diagnosis penderita masih belum jelas

Perawatan dirumah kurang memadai

9.Terapi :

Istirahat berbicara dan bersuara selama 2-3 hari

Jika pasien sesak dapat diberikan O2 2 l/ menit

Istirahat

Menghirup uap hangat dan dapat ditetesi minyak atsiri / minyak mint

bila ada muncul sumbatan dihidung atau penggunaan larutan garam

fisiologis (saline 0,9 %) yang dikemas dalam bentuk semprotan hidung

atau nasal spray

Medikamentosa : Parasetamol atau ibuprofen / antipiretik jika pasien

ada demam, bila ada gejalapain killer dapat diberikan obat anti nyeri /

analgetik, hidung tersumbat dapat diberikan dekongestan nasal seperti

fenilpropanolamin (PP A), efedrin, pseudoefedrin, napasolin dapatdiberikan dalam bentuk oral ataupun spray.Pemberian antibiotika yang


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adekuat yakni : ampisilin 100 mg/kgBB/hari, intravena, terbagi 4 dosis

atau kloramfenikol : 50 mg/kgBB/hari, intra vena, terbagi dalam 4 dosis

atau sefalosporin generasi 3 (cefotaksim atau ceftriakson) lalu dapat

diberikan kortikosteroid intravena berupa deksametason dengan dosis

0,5 mg/kgBB/hari terbagi dalam 3 dosis, diberikan selama 1-2 hari.

Pengisapan lendir dari tenggorok atau laring, bila penatalaksanaan ini

tidak berhasil maka dapat dilakukan endotrakeal atau trakeostomi bila

sudah terjadi obstruksi jalan nafas.

. Kebanyakan pasien mengalami hipoksemia, sehingga oksigenisasi harus dilakukan dan diberikan

oksigen yang dilembabkan. Oksigenisasi dapat dinilai pertama-tama dengan cara oximetry pulse noninvasif

untuk meminimalkan ketidaknyamanan dan memaksimalkan ketenangan pasien. Bila distres pernafasan parah

dan tidak responsif terhadap perawatan pertama makan harus diukur tekanan gas darah arteri untuk menilai

hiperkapnia dan asidosis respiratori. Tetapi harus diingat bahwa PaCO2 normal dapat tidak menggambarkan

keparahan penyakit karena sumbatan dapat terjadi tiba-tiba. Bila terjadi hiperkapnea maka kebanyakan pasien

membutuhkan jalan nafas buatan.5

Pemberian makan pada pasien harus mempertimbangkan keparahan pernyakitnya. Pada pasien yang

keadaannya gawat maka tidak boleh diberikan makan dan harus diberikan cairan intravena untuk

mempertahankan rehidrasi.5

Nebulisasi epinefrin rasemic sementara dapat memperbaiki distres pernafasan, dengan efek dalam

jam dari pemberian aerosol dan hilang efeknya setelah 2 jam. Namun tidak ada bukti bahwa penggunaan

epinefrin rasemic merubah dasar penyakit dari laringiti, tetapi penggunaannya telah memperkecil perlunya

saluran nafas buatan. Epinefrin rasemic dapat diberikan sering, sampai setiap setengah jam bila diperlukan

untuk melegakan distres pernafasan. Epinefrin resemic diberikan dalam dosis 0.25 ml dari larutan 2.25% untuk

setiap 5 kg Berat badan, sampai dosis maksimum 1.5 ml. Epinefrin rasemic ini harus diberikan dengan

nebulisasi dalam oksigen, karena dapat menyebabkan perburukan sementara dari ketidaksesuaian ventilasi dan

perfusi dalam paru-paru. Irama jantung dan nadi harus dimobitor dan obat harus dihentikan bila terjadi aritmia.


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Bila tidak terdapat epinefrin rasemic maka dapat digunakan epinefrin saja dengan dosis 5 ml larutan 1:1000

ternyata manjur setara 0,5 efinefrin rasemic 2.25% yang dilarutkan dengan 4.5 ml normal saline dalam

memperbaiki distres pernafasan pada laringitis. Efeknya juga hilang dalam 2 jam seperti resemic epinefrin.4,5,6

Pengguanaan kortikosteroid dalam terapi laringitis menimbulkan kontroversi. Pada awalnya penelitian

yang menilai kemanjuran steroid menggunakan metodologi yang salah dan menggunakan dosis yang kecil. Lalu

bukti-bukti mucul bahwa dosis steroid setara dengan 100 mg kortisol atau 0,3 mg/kg dexametason dapat jadi

efektif mengurangi keparahan laringitis dalam 12 dan 24 jam. Penelitian lebih lanjut menemukan bahwa

kemanjuran dari penggunaan dosis tunggal parenteral 0.6 mg/kg deksametason dalam mengurangi gejala dan

mempercepat kesembuhan, juga mengurangi kebutuhan perawatan intensif dan intubasi endotrakeal. Pada

pasien yang memerlukan intubasi, penggunaan prednisolon 2 mg/kg.hari telah menunjukan mempercepat

extubasi. Dalam sebuah penelitian pada 120 pasien dengan laringitis yang sedang, penggunaan dexamethasone

secara oral dengan dosis 0.15, 0.3 dan 0.6 mg/kg sama efektifnya untuk menghilangkan gejala dan kebutuhan

nebulisasi epinefrin. Malah, pertimbangan untuk menggunakan dexamethasone pada pasien dengan laringitis

yang parah sekarang direkomendasikan oleh Committee of Infectious Disease of the American Academy of

Paediatrics, The Infectious Diseases and Immunization Comittee of the Canadian Paediatric Society, dan the

Respiratory Committee of the Paediatric Societ of New Zealand. Penelitian terakhir lebih difokuskan kepada

pengguanaan steroid nebulisasi. Budesonide nebulisasi dengan dosis 2 mg telah menunjukkan kemanjuran

dalam memperbaiki stridor, batuk, dan berbagai kegawatan 2 jam setelah pengobatan. Onset yang cepat ini

menunjukkan efek steroid pada permeabilitas vaskular dibandingkan dengan efek anti inflamasi saja. Konsep ini

didukung oleh penelitian lebih baru yang menunjukkan nebulisasi 2 mg budesonide sama efektifnya dengan

nebulisasi 4 mg epinefrin dalam melegakan gejala. Lebih lanjut, nebulisasi 2 mg bunesonide secara statistik

sama manjurnya dengan 0.6 mg/kg dexamethasone per oral dalam mengurangi gejala, mengurangi kebutuhan

nebulisasi epinefrin dan mengurangi lama perawatan. Jadi dapat disimpulkan bahwa pada anak yang laringitis

harus menerima minimal 0.15 sampai 0.6 mg/kg deksametason dosis tunggal secara peroral, intramuscular,

maupun intravena. Dan bukti sekarang menunjukkan perlunya nebulisasi bunesonide, dengan dosis 2 mg

terutama pada keadaan darurat. Masih tidak diketahui apakah pemberian kortikosteroid berulang aman dan

menguntungkan. Efek samping yang dapat terjadi pada pemakaian kortikosteroid jangka lama antara lain

candidiasis.4,5,6


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Penggunaan helium-oksigen telah berhasil meningkatkan aliran udara pada pasien dengan obstruksi

saluran nafas atas. Kepadatan helium yang rendah mengurangi hambatan aliran udara yang turbulen.5,6

Selain pengobatan kadang pasien memerlukan juga intubasi endotrakeal. Intubasi harus dilakukan

dengan perhatian penuh, sehingga meminimalkan cedera dan inflamasi saluran nafas. Tube endotrkea harus

sampai 1 ukuran lebih kecil dari ukuran seharusnya berdasarkan usia pasien (atau seukuran dengan jari

kelingking pasien) dan tube dipotong untuk memperpendek panjangnya dan mengurangi resistensi aliran udara.

Setelah diintubasi pasien jarang memerlukan bantuan ventilator mekanik. Pasien harus diberi oksigen lembab

selama diintubasi. Penghisapan harus diminimalkan untuk mengurangi cedera saluran nafas. Anak dengan

laringitis memerlukan perawatan di rumah sakit untuk 24 jam sampai seminggu atau lebih, dan kriteria

pemulangan pasien harus terjadi perbaikan distres pernafasan dan tidak diperlukan terapi spesifik dalam 24

jam.5

Pemberian antibiotik tidak disarankan kecuali hasil kultur menunjukkan adanya streptococcus, dimana

penicillin adalah obat pilihannya.

h. Prognosis

Prognosis untuk penderita laringitis akut ini umumnya baik danpemulihannya selama satu minggu. Namun pada anak khususnya

pada usia 1-3 tahun penyakit ini dapat menyebabkan udem laring

dan udem subglotis sehingga dapat menimbulkan obstruksi jalan

nafas dan bila hal ini terjadi dapat dilakukan pemasangan

endotrakeal atau trakeostomi

i. Komplikasi

j. Pencegahan

Pencegahan : Jangan merokok, hindari asap rokok karenarokok akan membuat tenggorokan kering dan mengakibatkan

iritasi pada pita suara, minum banyak air karena cairan akan

membantu menjaga agar lendir yang terdapat pada

tenggorokan tidak terlalu banyak dan mudah untuk

dibersihkan, batasi penggunaan alkohol dan kafein untuk

mencegah tenggorokan kering. jangan berdehem untuk

membersihkan tenggorokan karena berdehem akan

menyebabkan terjadinya vibrasi abnormal pada pita suara,

meningkatkan pembengkakan dan berdehem juga akan


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menyebabkan tenggorokan memproduksi lebih banyak lendir.

DAFTAR PUSTAKA

Fritsch, P, & Sidoroff, A 2000, 'Drug-induced Stevens-Johnson syndrome/toxic

epidermal necrolysis',American Journal Of Clinical Dermatology, 1, 6, pp. 349-360,

MEDLINE Complete, EBSCOhost, viewed 22 September 2014.

sjs sk 3 emergency

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