1.

SJS

a. Definisi
Stevens-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, and
allopurinol).
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 develop- ment of SJS/TEN in
single case reports or retrospective stud- ies.[8,9,35] Such reports are not helpful,
though, in quantifying the relative risk associated with a specific drug.[36] Similarly,
popu- lation 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 stud- ies 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 in- take, or underlying diseases can thus be
calculated by multivariate analysis. The results of the first of such studies have been
pub- lished (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: antibacterial
sulfonamides
[especially
trimethoprim-sulfamethoxazole
(cotrimoxazole)],
anticonvulsants [phenytoin, carbamazepine, phenobarbital (phe- nobarbitone),
valproic acid (sodium valproate), and more recen- tly lamotrigine], nonsteroidal antiinflammatory 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 a
drug 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.

c. Patogenesis

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

Clinical observations (the lag period be- tween 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; the
latter, in turn, express adhesion molecules and MHC II. There is a drastic
overexpression of tissue necrosis factor-(TNF) in the epider- mis,[27] derived from
macrophages as well as from keratinocytes, which is obviously linked to extensive
apoptosis. TNFmay both directly induce apoptosis and attract more effector cells.
The piv- otal role of TNFis underscored by the observation that TNFinducing
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

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 keratino- cytes:[32] their incidence
is 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 dalam
derajat 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 SyndromeToxic 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 prod- romi 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 tar- get lesions (flat atypical targets). At times, the lesions may be
slightly raised (raised atypical targets) but typical targets (as defined by wheal-like
elevation 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
cov- ered 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.

Systemic Signs and Internal Organ Involvement

Constitutional signs include fever, arthralgias, and weakness.[4] Internal organs are
more often involved in patients with wide- spread 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- chial
casts, bronchopneumonia and, at its most severe, acute re- spiratory distress
syndrome.[13,14] Less common are symptoms of the gastrointestinal tract such as
diarrhea, abdominal pain, gas- trointestinal 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 typical
histopathologic 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 infiltrating
lymphocyte 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 infections
and 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.

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 involve- ment 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 progres- sion 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 in- farction 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 le- sions, 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 but
char- acteristic further sequelae are tracheal, esophageal or anal stric- tures, 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.

Histopathology
Histopathology is characterized by prominent epidermal ne- crosis 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 the
epidermis (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 characterized 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 exan- thema with little tendency for confluence and its
acral distribution pattern. Other important differences are: low incidence of anogenital (but not oral!) mucosal involvement, history of prior episodes, association
with relapsing herpes simplex, and a prom- inent 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 distinc- tion 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 membrane
involvement and the paucity of constitutional symp- toms. Histopathology is similar
to SJS/TEN with the exception of more pronounced inflammation and a marked
edema of the papillary dermis. Often, history reveals prior episodes of milder
Fig. 4. Histopathology

of Stevens-Johnson syndrome/toxic epidermal necrolysis: full thickness

necrosis and detachment of the epidermis, a sparse inflammatory infiltrate of the dermis ( 25
magnification).

expression following intake of the culprit drugs. Generalized FDE takes a much
milder course than SJS/TEN.
5.4 Physical and Chemical Injury

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 mu- cous membrane involvement and absence of an antecedent macular rash. If necroses arise, they tend to involve deeper layers including, at times, the
skin 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- ylococcal
exotoxin exfoliatin, which elicits subcorneal acantho- lysis 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 the
absence of an antecedent macular rash (in- frequently there is a scarlatiniform
eruption), 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 diberikan
antibiotika 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, menghentikan
progresifitas penyakit dan mencegah kekambuhan. Beberapa literatur

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 tanda
awal 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 manage- ment of SJS/TEN and in general skin
care, that is, to a dermatol- ogy 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

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: with- drawal of the offending
drug, 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 lifethreatening 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 con- troversy as to whether systemic
corticosteroids 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 and
is 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, infec- tions 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.

8.2 Active Suppression of Disease Progression

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

been proposed to have beneficial ef- fects 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 (and
usually heterogeneous) patients series re- ported in the literature. Thus, at present,
there is no consensus as to which, if any, therapeutic measure will shorten the natural
course of the disease. Furthermore, many of the treatment modal- ities 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 dis- ease, 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 treat- ment 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 be- cause corticosteroids, if given for
longer than the phase of pro- gression, 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 the
principles 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 by
additional observations: mortality rates for SJS/TEN do not differ significantly
between countries where cor- ticosteroids 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 an
immune 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 measures
are procured (see sections 8.3 and 8.4), and if the phys- ical 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 and
less hazardous strategies before the issue is settled by appropriate controlled studies.

8.2.2 Immunoglobulins
Recently, intravenous administration of pooled human im- munoglobulins (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 dosages
ranging from 0.2 to 0.75 g/kg body weight/day for 4 consecutive days. In all patients,
rapid halting of disease pro- gression 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 caus- ative drug, its
metabolites 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
strate- gies 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 cyclospor- ine in SJS/TEN.[57-61]
It should not be considered a first line treat- ment option, however, for the same
reasons as cyclophosph- amide; also, its mechanisms of action in SJS/TEN are far
from clear, and a rapid effect (as necessary for the brief phase of pro- gression) 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

study had to be discontinued.[65] It remains unclear whether this outcome was due to
paradoxical enhancement of TNF production 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 pa- tients 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 later
onset than in burns. Hemodynamic shock is a possibility, but it is rare and occurs
mainly in unsatisfactory clinical settings and in patients with cardiovascular or
metabolic 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 rec- ommended. Central venous lines (as well as urinary
catheters) 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 infec- tion 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 should
be 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 treat- ment (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 <10% in our institution throughout
the past 2 decades.
8.5 Supportive Treatment
8.5.1 Skin

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-epitheliza- tion. Erosions
should be covered with gauze or hydrocolloid dressings. Sulfonamide containing
topical treatments should be
avoided. When using topical antibacterials or antiseptics, the pos- sibility 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 because unlike in burns the dermis is
largely uninvolved and re-epithelization is not a prob- lem.
8.5.2 Eyes
In the acute phase of conjunctival involvement, lubricants, corticosteroid and
antibacterial 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 and
increased 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 (<1%) for SJS and ranges from 5 to 50% in TEN. There is no
evidence from the literature that prognosis is better in an intensive care unit or a burn

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 proses
peradangannya 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

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 pengecilan
sedikit 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

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

normal. Jika disertai infeksi sekunder, leukosit dapat

meningkat.
c. Pada pemeriksaan laringoskopi indirek akan ditemukan
mukosa laring yang sangat sembab, hiperemis dan
tanpa 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 gejala pain killer dapat diberikan obat anti nyeri /
analgetik, hidung tersumbat dapat diberikan dekongestan nasal seperti
fenilpropanolamin (PP A), efedrin, pseudoefedrin, napasolin dapat
diberikan dalam bentuk oral ataupun spray.Pemberian antibiotika yang

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.

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

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 dan

pemulihannya 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.
j.

Komplikasi
Pencegahan

Pencegahan : Jangan merokok, hindari asap rokok karena

rokok 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

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.