RADANG II

DR. dr. Kiking Ritarwan SpS(K), MKT

Departemen Neurologi FK USU/ RSUP
Haji Adam Malik
Spektrum NeuroAIDS

Primary complication (non-

opportunistic disease)
HIV-Dementia
HIV-Sensory neuropathy
Secondary complication
(opportunistic disease)
Cerebral Toxoplasmosis
TB Meningitis / tuberculoma
Cryptococcal meningitis
Other opportunistic diseases....
 HIV Neuropathogenesis
Chronic CNS infection begins during primary
systemic infection and continues in nearly all
untreated seropositive individuals
progress to HIV-1 encephalitis (HIVE)
manifests as a clinical syndrome of cognitive,
motor, and behavioral dysfunction known as
the HIV-dementia
HIV Entry into CNS

Blood

Brain parechyma Scarano et al Nature Vol 5 Jan 2005

Blood BBB CNS Neuronal Cognitive

Infections damage Motor weakness
Encephalopathy
Komplikasi neurologi HIV
Brain Predominantly nonfocal
AIDS dementia complex
Acute HIV-related encephalitis
Cytomegalovirus encephalitis
Varicella-zoster virus encephalitis
Herpes simplex virus encephalitis
Metabolic encephalopathies
Predominantly focal
Cerebral toxoplasmosis
Primary CNS lymphoma
Progressive multifocal leukoencephalo-
pathy
Cryptococcoma
Brain abcess / tuberculoma
Neurosyphilis (meningovascular)
Vascular disorders
 Spinal cord
Vacuolar myelopathy
Herpes simplex or zoster myelitis
Meninges
Aseptic meningitis (HIV)
Cryptococcal meningitis
Tuberculous meningitis
Syphilitic meningitis
Metastatic lymphomatous meningitis
 Peripheral nerve and root and root
infectious
herpes zoster
cytomegalovirus lumbar polyradiculopathy
Virus or immune-related
acute and chronic inflammatory HIV poly-
neuritis
mononeuritis multiplex
sensorimotor demyelinating polyneuropathy
distal painful sensory polyneuritis
Muscle
polymyositis and other myopathies
Perjalanan penyakit infeksi HIV
Infeksi virus (2-3 minggu) sindroma retro-
viral akut (2-3 minggu) gejala menghilang +
serokonversi infeksi kronis HIV asimpto
matik (rata2 8 thn) infeksi HIV / AIDS
simptomatik (rata2 1,3 thn) kematian.
Window period masa dimana pemeriksa-
an test serologis utk antibodi HIV masih
negatif, tapi virus sdh ada dlm darah (sudah
mampu menularkan kpd orang lain)
 HIV dementia (AIDS Dementia Complex)

This progressive dementia occurs in AIDS,

owing to a direct primary HIV infection of
neurons or an indirect neurotoxicity induced
by presence of the virus in the brain
Pathology: the virus may be transported into
the brain by infected peripheral monocytes
(Trojan horse theory).
Manifestasi klinis demensia HIV:
Cognititive disorders
Gangguan kognitif, kesulitan konsentrasi, forgetfullness,
cognitive slowing. Kadang2 agitasi, mania.
Pd std awal sulit membedakan dgn keluhan psikiatri.
Motor abnormalities: ataksia, hiperreflels. Babinski refleks
srg muncul. Pada std lanjut : paraparese dgn
inkontinansia urin et alvii
Behavioural dysfunction : Apathy, altered personality,
disorientasi. Std akhir Mutism
 Anti Retroviral
ARV reduce the opportunistic infection

ARV can arrest HIV-dementia and reverse its

neurological disability.(Price J Infect Dis. 2008 May 15 )

Neurologist should have a competency in

prescribing ARV
 Anti Retroviral Treatment
HAART (highly active antiretroviral treatment )
Combination of three ARV
ARV indication
AIDS defining illness
CD4 < 350 cell/uL
Viral load > 50.000 copy/ml
When to start ? (first : treat opportunistic
infection, than start ARV)
 First Line ARV
(HAART : 3 drugs combination)
HAART : highly active antiretroviral therapy

Stavudine
Zidovudine

Lamivudine

Nevirapine Efavirenz
ARV Lini Satu
 First Line ARV (1)

Stavudine 2 X 1 . Neuropati, pankreatitis, atrofi otot

Lamivudin 2 X1
Efavirens 600 1 X 1, vivid dream, ngantuk, imbalance,
wanita hamil
 First Line ARV (2)

Stavudine sda
Lamivudin sda
Nevirapin 1 X 1 2 minggu pertama, selanjutnya 2 X 1
Alergi, fungsi hati
 First Line ARV (3)

Duviral : 2 X 1 (Zidovudin dan lamivudin)

Anemia, sakit kepala
Nevirapin sda
First Line ARV (4)
Second line ARV
ARV brain penetration
Low
Tenofovir
Didanosine
Ritonavir
Medium
Stavudine
Lamivudine
Efavirenz
Emtricitabine
High
Zidovudine
Nevirapine
 Initiation of ARV Therapy
Indication
AIDS defining illness
CD4 < 350 cell/uL
Viral load > 50.000 copy/ml
Patients preparation before starting ARV
Longlive treatment
Rule-out and treat opportunistic infection first
ARV adverse effect
Side effect
IRIS
Focal Brain Lesion (FBL)

HIV positif

Simptom intrakranial

Lesi fokal otak pd imaging ?

tidak

YA

Efek desak ruang ?

 CEREBRAL TOXOPLASMOSIS
Reactivation of latent infection
Toxo seroprevalence 12-46% (SA)
IgG indicates past infection (FN <3-6%)

CD4 > 200 virtually excludes Toxo

Over 80% have CD4 < 100

Typically multiple ring enhancing lesions on CT/MRI

27-43% have single lesions
Up to 10% may have diffuse encephalitis without any visible
focal lesions
The course of HIV/AIDS

Notes:
 PATOGENESIS
Transmission : via oral route & placenta.
Digestive enzym phagocytosis
Cyst Sporozoit

Trophozoite

Transported throughout the body via

lymphatic system & blood steam

Trophozoites proliferation

Cell
Skema-1. Algoritme Penatalaksanaan Keluhan Intraserebral bagi Penderita HIV-AIDS

Keluhan intrakranial

MRI

CT Scan

Atrofi Meningeal hidrosefalus SOL

normal
enhancement

Evaluasi LCS Shunt

(kalau perlu)

Positif Negatif
Lesi massa(-) Lesi massa (+)

Terapi sesuai Observasi

etiologi
Skema 2
Skema-2. Algoritme Penatalaksanaan Lesi massa Intrakranial pada penderita HIV-AIDS

Lesi massa intrakranial

Alert-lethargic Steroid ? Stupor-koma

stabil Perburukan cepat, massa besar
Dengan resiko herniasi

Lesi multipel Lesi tunggal

Serologi
toksoplasma

Positif Negatif

Obat antitoksoplasmosis Ancaman herniasi

Perbaikan

Ya Tidak Biopsi stereotaktik

Terapi toksoplasmosis Terapi sesuai Dekompresi dan

Seumur hidup etiologi biopsi terbuka
 Toxoplasmosis Clinical Features
Usually subacute over weeks
Headache 50%
Fever 45%
Behaviour changes 40%
Confusion 15-52%
Focal signs
Seizures 24-29%
 TREATMENT
Acute treatment : 3-6 weeks.
Induction : pyrimethamine 200 mg
First line :
Pyrimethamin 75-100 mg/day + sulfadiazine + folinic
acid or
Pyrimethamin + clindamycin + folinic acid.
Second line :
Azithromycin, clarithromycin, or atovaquone can
substitute for sulfadiazine.
Glucocorticoid life threatening condition.
 TREATMENT
Maintenance :
Until the immune system has sufficiently
reconstituted.
Pyrimethamine and sulfadiazine or
Pyrimethamine and clindamycin.
Stop :
Asymptomatik.
CD4+ > 200/cmm until 6 months.
 CT - Multiple ring enhancing lesions

Toxo more likely

Tuberculomas still
possible
 Differential Diagnosis
Toxoplasmosis P CNS L
Location Basal ganglia. Periventricular
Gray-white junction
Number of lesion Multiple Solitary>multiple
Enhancement pattern Ring Heterogeneous or
homogeneous.
Edema Moderate to marked Variable
T2-weighted image Hyperintense Isointense to
(lesion relative to hyperintense.
white matter)
Diffusion-weighted Usually hypointense Often hyperintense
image (positive)
 Differential Diagnosis
Toxoplasmosis P CNS L
MR perfusion Decreased Increased
MR spectroscopy Markedly elevated Markedly elevated
lactate. choline

SPECT thallium Cold-no thallium Hot-increased

(lesion relative to uptake thallium uptake.
white matter)
Other Toxoplasma IgG Ab EBV DNA amplified
(+) (90% of patients) by PCR in CSF
(most patients)
 Cytomegalovirus infections
Central or peripheral nervous system
In adults occur in immunocompromised individual
Etiology: CMV (DNA Virus) of the herpetic group
Clinical features:
-Encephalitis complication of organ
transplantation and AIDS. CD 4 < 50 cell/ mm3
- Symptoms enceph: headache, fever and
seizure
Treatment: antiviral agent (ganciclovir or foscarnet)
 Definisi Malaria Serebral (MS)
MS adalah malaria dengan penurunan kesadaran (
dewasa GCS < 9 dan anak
Blantyre coma score < 3) atau koma lebih dari 30
menit setelah serangan kejang yg tidak disebabkan
oleh penyakit lain.
MS komplikasi dari malaria falcifarum berat,
dijumpai st ensefalopati difus dengan penurunan
kesadaran dan berhubungan dengan sequestrasi
mikrovaskuler serebral.
 Blantyre coma scale(0-7)
Oculer response
- Follow mothers facial reaction 1
- non reaction 0
Verbal response
- Normal crying 2
- Whimpering 1
- no sound .. 0
Motoric response
- Localize pain 2
- rettraction of limb ..1
- non reaction 0
 Plasmodium falcifarum
morphology in stained preparation
Ring form: vary in
shape; double
chromatin, double
infection, accole

Trophozoit: rare in
peripheral blood
after half grown
Plasmodium falciparum
Morphology of all stadiums
 Patogenese
Ada 3 teori:
1. Teori mekanis :
tjdnya penyumbatan pemb drh otak akibat
tjdnya sitoadherens, sekuester, rosetting dan
faktor rheologi.
2. Teori Toksik menghasilkan TNF
3. Teori Permeabilitas: tjdnya adhesi parasit pd
endothel, vasculer serta banyak faktor toksik yg lepas
serta radikal bebas terutama Nitric oxide (NO).
 Diagnosa Malaria Serebral
Gjl Klinik : Trias malaria ( demam, menggigil, dan
berkeringat), Sakit kepala, ggn mental, nyeri tengkuk, kaku
otot dan kejang umum
Sering dijumpai splenomegali dan hepatomegali
Ggn kesadaran atau koma ( biasanya 24-72 jam)
Pemr darah (thin/thick smear) dijumpai bentuk aseksual P.
Falcifarum
Tidak ditemukan infeksi lain
Lain-lain:hipoglicaemia, hiponatremia, hipofosfatemia,
pleocytosis sampai 80 cel/ micron kubik, limfosit sampai 15
cel/ mikron kubik
CT/ MRI: edema serebri.
 Laboratorium
Pemeriksaan dengan mikroskop
- sediaan darah tebal dan tipis
Test diagnostik lain
- Metode immunokromatografi
- Analisa cairan Serebrospinal pd
Malaria serebral didapti peningkatan
limfosit > 15/ul.
- CT dan MRI: edema serebral
 Pengobatan Malaria Tanpa Komplikasi

Malaria Falsiparum

Lini pertama = Artesunat + Amodiakuin + Primakuin

Lini kedua = Kina + Doksisiklin atau Tetrasiklin + Primakuin

Pengobatan lini kedua diberikan jika pengobatan lini

pertama tidak efektif, dimana 28 hari setelah pemberian obat :

Gejala klinis memburuk dan parasit aseksual positif, atau

Gejala klinis tidak memburuk tetapi parasit aseksual tidak

berkurang (persisten) atau timbul kembali (rekurensi)

 Neurocisticercosis
Def: cysticercosis cellulosa is the larval stage of
development of the cestode Taenia solium
(pork tapeworm).
More than 60 million people are infected with
T. saginata world wide and about 4 million are
infected with T. solium
Life cycle
In Indonesia

North Sumatra West Kalimantan North Sulawesi

Irian Jaya

Lampung

Jakarta

Bali Flores

East Timor

Fig. I. Geographic distribution of in Indonesia until 1995. Areas endemic with taeniasis are indicated in colour.
( Modified from the unpublished report CDC & EH. Ministry of Health, Indonesia, 1983 1996 )
 Pathology :3 Form cysticercosis in CNS
1. A cystic form involving the ventricles and
brain parenchyma
2. A racemose form involving the meninges
3. A miliary form that is common in children
 PATOGENESIS
Human NCC : ingest food contaminated with
T.solium egg
Parasite survive over period of year
It secretes protease inhibitor, taeniastatin that
inhibit complement activation, neutrophyl,
lymphocyte and cytokine production.
Minimal inflammation around viable cyst
Inflammatory respons attacks the parasite,
leads to degeneration and calcification
RISK FACTOR
 CLINICAL MANIFESTATION

Number of the cysts

Location (parenchimal/spinal)
Parasite activity
Immune respons of the host
Map. Endemic Area of Taeniasis/ Cysticercosis in
North Sumatra

Samosir island
Samosir island
 Summarized Data of Taeniasis and Seroprevalence of
Cysticercosis in Samosir island, North Sumatra, 1972-2007
Taeniasis
District/island Prevalence (%) Reference
Samosir 9.5 (27/285) Kosin et al. (1972)
Samosir 1.9 (6/314) Cross et al. (1976)
Samosir 11.7 (11/94) Koesharjono et al. (1987)
Samosir 20.7 (28/135) Kosman et al. (1990)
Samosir 3.4 (2/58) Wandra et al. (2007)
Samosir 2.5 (6/240) Wandra et al. (2007)

Cysticercosis
District/island Seroprevalence Reference
(%)
Samosir 0.0 (0/58) Wandra et al. (2007)

Samosir 0.0 (0/105) Wandra et al. (2007)

 DIAGNOSIS NCC
Definitive
Present of the scolex on histologic examination or
on CT scan/MRI
Major criteria: CT scan cysticercus 0,5 2 cm;
EITB(enzym liked immuno transfer blot (+)
Minor criteria:Clinical symptom, Intracerebral
punctata< subcuatenous nodule
Diagnose : 2 major or 1 major criteria + 2 minor
criteria
 MRI
More sensitif for detect
parenchymal cyst, intraventricular
and subarachnoid cyst
 MANAGEMENT NCC

Anti parasitic drug

Symptomatic and anti-inflamatory
Surgery
 ANTI PARASITIC DRUG
Praziquantel :
50mg/kg/day, two weeks.
Albendazol :
15mg/kg/day, one month.
 SYMPTOMATIC/
ANTIINFLAMMATION
Corticosteroid :
Dexamethasone 4,5 12 mg/day, or
Prednisone 1mg/kg/day.
Decrease neurological symptoms due to
the death of the parasite.
Manitol 2g/kg/day, for acute intracranial
hypertension.
First line antiepileptic
 SURGERY
For excision of large cysts or cyst in the
ventricles
 Spinal Tuberculosis
(Potts Disease).
DR. dr. Kiking Ritarwan SpS(K), MKT
 Sinonim
Potts disease
Davids disease
Angular kyphosis
Kyposis secondary to tuberculosis
Tuberculosis of the spine
 35 % TB tulang
dan sendi 50%
tulang belakang
Penyebaran
hematogen dari
fokus esktraspinal

64
 The first found Pervicall Pott (England,1779),
triad of potts disease: abscess, gibuss,
paraplegia
Single or multiple vertebral involvement by
tuberculosis is frequently followed by spinal cord
compression due to development of cold abscess
in epidural space (Pott disease)
The most common site of infection is
thoracolumbar spine, rarely cervical spine.
 Tulang belakang :
50% dari seluruh kasus tuberkulosa tulang
15% dari kasus tuberkulosa ekstrapulmonal
3-5% dari seluruh kasus tuberkulosa
Area torako-lumbal terutama torakal bawah &
lumbal atas paling sering terlibat
Insidensi keterlibatan daerah servikal 2-3%

66
 Lokasi
1
Spondilitis TB
1
5
1.Paradiscal type >
2. Central type
2
3. Anterior type
4. Post Facet joint
3
4 5. Appendicial
Spondilitis Tuberkulosa
 Pathogenese
Begin from existence of primary focus outside vertebra [
extrapulmoner], later;then disseminate by hematogen to vertebra
and usually [regarding/ hit] part of corpus vertebrae anterior at
elbow intervertebralis discus.
Peaky earn happened just where as long as vertebra, but at most [at]
mid and under thoracalis vertebra and lumbal vertebra.
Can [regarding/ hit] one segment or some vertebra segment. [At] the
place can happened cheese that happened effect of forming [of]
granulasi network and destruction on corpus vertebra little by little
from anterior to posterior.
This Destruksi can generate anguler gibbus. Besides also earn also
happened " Cool abscess [ Cold Abcess]. Most [is] often met [by] cool
[by] abscess [at] thorakal vertebra 8 until lumbal 3.
70
Patofisiologi Spondilitis Tuberkulosa
Patofisiologi

Rute Penyebaran ke
Vertebra :
Arteri/hematogen
Vena (batson plexus)
Percontinuitatum
 Clinical manifestasion
Back Pain (79%)
Paraparese (66%)
Kyphosis (52%)
Fever (45%)
Sensory disturbances (34%)
Bowel and Bladder dysfunction (31%).
 Manifestasi Klinis
Keadaan Umum
Sakit kronis, demam, keringat
malam, anorexia, Penurunan
berat badan
Gejala Lokal
Nyeri lokal atau radikuler
Spasme otot punggung
night cries pada anak
Defisit neurologis
Deformitas
Manifestasi Klinis
Pemeriksaan Klinis
Deformitas, gibbus
Spasme otot
paravertebral
Defisit neurologis
 Diagnostic procedure
Pemeriksaan darah : LED meninggi> 100mm/jam
Tuberculin skin test (Purified Protein Derivative/ PPD) biasanya
positif
Biopsi kelenjar leher
Sputum utk BTA (+) dan kultur Mycobacterium tuberculosa
Radiologi
- proses spesifik di paru Thorax foto
- Vertebra : gibbus dan kyphosis
- CT Scan Vertebra : destruksi vertebra, soft tissue calcification, narrow
disc space, bone erosion (scalloping).
- MRI vertebra:
a. membedakan TB spondilitis atau pyogenic spondylitis,
b. melihat adanya kompresi saraf.
Foto Rontgen
CT Scan
MRI
ALGORITHME OF SPONDYLITIS TUBERCULOUS

81
 Treatment
1. Immobilisasi, best rest total, extrafeeding, brace, korset
2. Antituberculous drugs
Berdasarkan Pedoman Penatalaksanaan TB paru:
termasuk kategori I ( TB diluar paru):
# 2 bln pertama : Streptomycin, INH, Rif dan PZA
# Bulan 3-12 : INH dan Rifampin

3. Operative
- Indikasi operasi pada potts disease:
adanya defisit neurologis
adanya abses paravertebra [Cold Abses]
terapi konservatif gagal
severe kyposcoliosis
cord/ nerve compression
- Tindakan bedah yang dilakukan:
requires anterior abscess drainage
anterior spinal arthrodesis.
posterior spinal arthrodesis.
83
PROGNOSA
Dari 100 penderita ,yang mengalami disability
2 penderita mengalami reccurence paraplegia
setelah 3 tahun berobat, 1 penderita akibat
granuloma ekstramedularis dan 1 orang
dengan kifosis yang berat.
Angka mortalitas 20%.
 Tetanus
= Bacterial Toxins
Kiking Ritarwan

Localized or generalized muscle stiffness

Superimposed paroxysmal tonic spasm
(tetanospasmin)
Tetanospasmin blocks inhibitory interneurons
Autonomic instability
Normal mental status
Tetanus is a toxic infection caused by the anaerobe
Clostridium tetani.

Spores exist in the soil and faeces, portal of entry resulting in

human disease include traumatic and surgical wound,
injection side (parenteral drug abusers), skin ulcers, burn
and injected umbilical cords.

Producing exotoxins (tetanospasmin and tetanolysin).

Tetanospasmin is a very potent neurotoxin probably is

solely responsible for the disease.

Tetanolysin has no recognised pathogenic activity.

Tetanus germs are found everywhere, usually in soil,
dust, and manure.
Enter a wound produce a poison
spreads throughout the body.
The first signs :
Headache and spasms of the jaw muscles.
Irritable
Muscle spasms : neck, arms, legs, stomach.
Convulsions broken bones.
 Etiologi Clostridium tetani

Ada 2 bentuk :
1. Vegetatif : basil gram positif, obligat anaerob
ukuran :0,5-1,7 m x 2,1-18,1 m
motil, flagel
2. Spora : bentuk squash racket
tahan terhadap panas, resisten terhadap
berbagai desinfektan, dapat hidup bertahun
Spora tumbuh saat bersentuhan dengan luka (potensial
redox ) Eksotoksin :
Tetanospasmin (Tetanus toksin)
Tetanolysin
Clostridium tetani : bentuk spora dan vegetatif

An aerobic gram positive bacillus

Noncapsulated

Sporm forming

Found in soil, house dust, animal

Intestine and human feces
 Epidemiologi

Negara terbelakang, iklim tropis, lembab >>>

Seluruh usia neonatus, usia muda >>>
WHO, 1995 eradikasi : 800.000-1 juta/thn
kematian tetanus neonatal
Afrika, Asia Tenggara endemik

Insidens 18 per 100.000 populasi/ tahun

Cvjetanovic :
Afrika : 28/100.000
Asia : 15/100.000
Eropa : < 0,1/100.000
Amerika Utara : < 0,1/100.000
 Patofisiologi
C.tetani masuk ketubuh melalui LUKA

dalam kondisi anaerob spora berkembang

toksin diproduksi(TETANOSPASMIN)

Retrograde intraneuronal transport/ axon terminal

Motor neuron perifer/ med spinalis/ batang otak memblokade pelepasan inhibitory
neurotransmitter glycine and GABA di terminal presinaptik
akibatnya eksitasi firing rate motor neuron meningkat tanpa ada inhibisi sehingga
otot lebih meningkat tonus dan spasmenya

Jk blokade di MNJ maka toxin menginhibisi pelepasan Ach

presinaptik bisa menjadi PARALISIS
Tahapan tetanospasmin : berikatan, internalisasi dan aktifitas
 Focus of infection
Infected laceratioof puncture wound
Infected chronic wound and abscesses
Exposure via intravenous drug abuse
Neonates
No identifiable cause
Possible causes: otitis media, Burns, Intranasal
foreign bodies, corneal abrasion, dental or
surgical procedures.
 Gambaran Klinis

Masa inkubasi : jumlah toksin dan status imunisasi

MI biasanya 8 hari (3 21 hari)
semakin jauh tempat trauma dari SSP MI >>
Periode of onset : 1- 7 hari
MI dan periode of onset << keparahan >>

Klasifikasi tipe klinis (4) :

Generalized tetanus (Tetanus umum)
Localized tetanus (Tetanus lokal)
Cephalic tetanus (Tetanus sefalik)
Tetanus neonatorum
 Tetanus Umum

Paling umum : 80% dari kasus

Paling karakteristik : Lock jaw/ trismus
Dapat disertai : kaku kuduk, disfagia, rigiditas abdomen,
temperatur (2-40C)
Kasus berat risus sardonicus, opisthotonos
Karakteristik : spasme akut, paroksismal, nyeri, kejang
rangsang
Problem spasme obstruksi jalan nafas apneu
Masa inkubasi : 7-21 hari (tergantung jarak luka dengan CNS).
Pemulihan 4 minggu
 Tetanus Lokal

Bentuk paling ringan

Simptom awal : kaku, spt diikat, nyeri otot disekitar
luka,
twitching & spasme singkat
Sering luka di tangan atau lengan

Manufer diagnostik Recruitment spasm

mendahului onset Tetanus umum

Angka kematian 1%
Prognosa : Baik
 Tetanus Sefalik

Bentuk yang tidak lazim

Terjadi dgn Otitis media atau trauma kepala
Disfungsi saraf kranial N.VII >>>
Berkembang tetanus umum atau tetap lokal
Masa Inkubasi : 1 atau 2 hari
Otot yang terkena paralisa
Sering fatal prognosis buruk
 Tetanus Neonatorum

= tetanus umum akibat infeksi pada neonatus

Di negara miskin dari seluruh kematian neonatus
MI : 3 10 hari sesudah lahir

Disease of the seventh day

Terjadi karena imunitas maternal
Tanah, kotoran hewan tali pusat
tehnik aseptik yang kurang
Tanda-tanda : lemah, tidak mampu menghisap
spasme, rigiditas opisthotonos
Angka kematian : > 70%
 Tingkat keparahan

Table 1. Klasifikasi keparahan tetanus : Kriteria Patel-Joag

Kriteria 1 : Lockjaw, isolaterd spasm ,dysphasia, stiffness of muscle back
Kriteria 2 : Spasme, tanpa mempertimbangkan frekuensi atau keparahan
Kriteria 3 : Masa inkubasi tujuh hari (waktu diantara trauma dan tanda pertama)
Kriteria 4 : Periode of onset 48 jam (waktu antara tanda pertama(lockjaw) dan
kejang pertama)
Kriteria 5 : Peningkatan temperature : rectal 1000F, atau aksiler 990F

Grading :
Grade 1 : Kasus ringan : terdapat satu criteria, biasanya kriteria 1 atau 2 (tidak ada
kematian)
Grade 2 : Kasus sedang : terdapat 2 kriteria, biasanya kriteria 1 dan 2. Biasanya
masa inkubasi lebih dari 7 hari dan onset lebih dari 48 jam (kematian 10%)
Grade 3 : Kasus berat : terdapat 3 kriteria, biasanya masa inkubasi kurang dari 7
hari atau onset kurang dari 48 jam (kematian 32%)
Grade 4 : Kasus sangat berat : terdapat 4 kriteria (kematian 60%)
Grade 5 : Calculated mortality : kelima criteria, termasuk puerperal dan tetanus
neonatorum (kematian 84%)
 DIAGNOSA

Hanya secara klinis

Tes untuk konfirmasi (-)

Studi bakteriologi 1/3 pasien

Tetanus lokal mengenai Penyebab nerve

> 1saraf cranial palsy lain

TEST SPATULA
 Diagnosa Banding

1. Keracunan striknin
2. Reaksi Distonia
3. Meningitis
4. Penyakit temporomandibuler joint, proses inflamasi gigi,
mulut, tonsil dan faring
5. Rabies
6. Tetani
7. Stiff-man syndrome
8. Psychogenic disorders
Tabel 2. Diagnosa banding tetanus

Simptom Diagnosa banding

Trismus Alveolar/dental patologi
Temporo-mandibular disease
Kaku kuduk Muscle spasm
Meningitis
Disfagia Acute pharyngeal disease
Spasme Keracunan striknin
Lesi intrakranial
Drug-induced dystonic reactions
Neonatal tetanus Sepsis
Meningitis
Konvulsi
 PENATALAKSAAN

Rawat di ICU
Ruang rawat yang tenang stimulasi <<<
Prinsip manejemen :
eradikasi kuman
netralisit toksin diluar SSP
minimalisir efek toksin di SSP

Portal of entry
eksisi luka
gangren (+) amputasi
debridement spasme terkontrol
 Imunoterapi

pengobatan untuk menetralisir Tetanospasmin

imunisasi aktif

Human Tetanus Immunoglobulin (HTIG)

3.000 5.000 IU/ i.m.
Equine Antitetanus serum (ATS)
uji hipersensitifitas, desensitisasi
harga lebih murah
Sebaiknya 20.000 U diberikan IM sedgkan 10.000 U
diberikan IV sesudah 48 jam pemberian pertama
Intravenous Immune globulin (IVIG)
pemberian antitoksin sebelum debridement
 Kontrol Jalan nafas dan Ventilasi
spasme tetanik obstruksi jalan nafas
Endotracheal tube (ETT)
Trakeostomi moderate & severe

Antibiotika
mengurangi bentuk vegetatif
Sensitif Metronidazole, PNC, Sefalosporin,
Imipenem, makrolid, tetrasiklin
PNC central GABA antagonist => sdh ditinggalkan
Dosis : 100.000-200.000 IU/kg/hari
Metronidazole antibiotik pilihan
Dosis : 500 mg/ 8 jam/IV + dgn
clindamisin, erithromisin, tetrasiklin, vancomysin
 Kontrol Rigiditas & Spasme

Benzodiazepine : agonis GABA

dosis ~ 500 mg/ hari
tetanus neonatorum 15-40mg/kg/hr
Diazepam,Lorazepam, Midazolam
Diazepam 0,1 mg/kg IV/ 4 jam (dewasa 500
mg/ hr dan neonatus 15-40 mg/ hr), atau
midazolam 0,1 mg/ kgBB IV/ IM/ 4 jam, atau
midazolam 2- 10 mg/ jam IV, atau propanolol
infuse 1-10 mg / jam.
 Blokade NMJ

Obat GABAergik gagal blok NMJ

Vecuronium (0,1 mg/kg IV 6-8mg/jam)
Pancuronium : takikardi, hipertensi, CO
mengaburkan efek otonom

Terapi disfungsi otonom

sympathetic overactivity (SOA)

Labetolol, esmolol, clonidine, morfin sulfat

Magnesium sulfat
 Nutrisi
aktifitas otot & otonom kebutuhan nutrisi >>
ganggguan gastric emptying time nutrisi vena sentral

Komplikasi

komplikasi penyakit & komplikasi terapi

komplikasi pernafasan
komplikasi kardiovaskuler dan otonom
komplikasi sistemik lain
Tabel 3. Komplikasi tetanus
Sistim Komplikasi
Jalan nafas Aspirasi *
Laryngospasm/obstruction*
Sedative associated obstruction*

Respirasi Apnu*
Hipoksia*
Gagal nafas tipe I* (atelektasis, aspirasi,pneumonia)
Gagal nafas tipe II* (spasme laring, prolonged
truncal spasm, sedasi berlebihan)
ARDS*
Komplikasi ventilasi bantuan yang lama
(mis.pneumonia)
Komplikasi trakeostomi (mis.stenosis trakea)

Kardiovaskuler Takikardi* Hipertensi* Iskemia*

Hipotensi* Bradikardi*
Takiaritmia, bradiaritmia*
Asistole*
Gagal jantung*
Tabel 3. (lanjutan)

Ginjal High output renal failure*

Oliguric renal failure*
Urinary stasis and infection

Gastrointestinal Gastric stasis

Ileus
Diare
Pendarahan*

Lain-lain Berat badan menurun*

Tromboemboli*
Sepsis dan multiple organ failure*
Fraktur vertebra selama spasme
Avulsi tendon selama spasme
 Pencegahan

Imunisasi Aktif Profilaksis

Tetanus Toksoid imunitas 5 thn
Imunisasi ibu hamil mencegah tetanus
neonatorum
Imunitas ditransfer secara pasif : ibu fetus

Imunisasi paska trauma

Rekomendasi profilaksis : - kondisi luka
- riwayat imunisasi
Antitoksin : HTIG 250 unit
ATS 1500 unit
TABLE 12.1 Immunization against tetanus
----------------------------------------------------------------------------------------------------------------------------------------
Subject/vaccine and dose Age/interval
----------------------------------------------------------------------------------------------------------------------------------------
Children (age less than 7 years)*
1-DPT 6-8 weeks of age
2-DPT 4-8 weeks after previous dose
3-DPT 4-8 weeks after previous dose
4-DPT 1 year after previous dose
Booster DPT 4-6 years of age
Booster Td every 10 years after previous dose
Adults and children older than 7 years not previously immunized*
1-Td first encounter
2-Td 4-8 weeks after previous dose
3-Td 6 months1 year after previous dose
Booster-Td every 10 years after previous dose
Pregnant women*
Previously immunized :
Booster TT during first 6 months of pregnancy (optimal)
Or as late as 6 weeks before delivery
Previously unimmunized :
1-TT first encounter during pregnancy
2-TT 4 weeks after previous dose
----------------------------------------------------------------------------------------------------------------------------------------
* American Academy of Pediatrics (Peter et al. 1994); * World Health Organization, Expanded Programme on
Immunization (Whitman et al. 1992)
Abbreviations ; DPT, diphtheria and tetanus toxoids and pertussis vaccine adsorbed : Td, tetanus and reduced-
dose diphtheria toxoids adsorbed; TT, tetanus toxoid.
TABLE 12.2. Guidelines for tetanus prophylaxis in wound management
______________________________________________________________________
Vaccination status Clean, minor wounds Tetanus-prone wounds*
Td+ TIG Td+ TIG++
______________________________________________________________________

Unknown or <3 doses Yes No Yes No

3 doses
Last booster < 5 years No No No No
Last booster 5-10 years No No Yes No
Last booster > 10 years Yes No Yes Yes

Recommendations of the Advisory Committee on Immunization Practices-United States (CDC,

1992).

* Wounds contaminated with dirt, faeces, soil, saliva; puncture wounds; avulsions; and wounds
resulting from missiles, crushing, burns and frostbite. Wounds presenting after delay or
requiring debridementdue to the presence of necrotic tissue.

* Td : tetanus and reduced-dose diphthetia toxoids adsorbed; for children less than 7 years, DPT
(diphtheria and tetanus toxoids and pertussis vaccine adsorbed) is preffered.
++ 250-500 units human tetanus immune globulin; given intramuscularly in another area than the
Td.
 Prognostic Score for Tetanus of Gallais et al
Parameter Finding Score
incubation < 7 days 1
>= 7 days 0

extension < 2 days 1

>= 2 days 0

portal of entry intramuscular injections 2

umbilical uterine surgical burn compound fracture 1

all other portals or unknown 0

paroxysms >= 4 per hour 1

present but < 4 per hour 0

rectal temperature > 38.4 C 1

<= 38 C 0

pulse in beats per minute adults > 120 neonate > 150 1
adults <= 120 neonate <= 150 0
Score Mortality Rate
0 0%
1 4.22%
2 13.63%
3 30.43%
4 57.14%
5 70.73%
6 94.73%
7 100%
 POLIOMYELITIS
Sinonim : Acute Anterior Poliomyelitis,
Infantile Paralysis, Penyakit Heine Medin
Definition: Poliomyelitis is caused by
enterovirus that invades motor neurons in the
spinal cord and brain stem.
Polio virus menginfeksi melalui jalur fekal oral
(dari tangan ke mulut) tetapi dapat juga
melalui kontak langsung.
 Etiology and Pathology
Virus enterovirus (RNA virus)
Virus that invades motor neurons in the spinal
cord and brainstem
Neuronal death results in the atropy of muscles
fibers supplied by the affected motor unit, unless
there is a compensatory sprouting of new fibers
by surviving axons that contact and innervate
some of the newly denervates muscle fibers
effect is loss muscle fibres, muscle wasting and
weakness
 Clinical Features
Systemic features (rash, pharyngitis, diarrhea)
Muscle weakness
Muscle pain
Unaccustomed fatigue
Post polio syndrome occurs in approximately 30
% of patients who survive acute pomiomyelitis.
More common in women, 10% < 2 years, 70% <
10 years old.
Type of Infection: asymptomatic, abortif, aseptic
non paralytic, paralytic
 Asymptomatic poliomyelitis :
Infeksi polio paling banyak
Virus masuk ke sal pencernaan
keluar dlm feses
Tanpa tanda infeksi nyata
Hanya : panas, anoreksia, mencret,
batuk
 Abortive poliomyelitis :
Diagnosa ditegakkan bila ada wabah polio
Gejala :
Panas, malaise, anoreksia, nausea, muntah,
sakit kepala, konstipasi, sakit-perut,
faringitis, batuk, diare
Diagnosa pasti :
Isolasi virus polio
Selama wabah :
Anak tersangka : istirahat 1 mgg 1 bln
kmd evaluasi otot
 Non paralytic poliomyelitis :
Gejala: spt tipe abortive
Terutama :
Sakit kepala
Kekakuan otot :
Belakang leher
Badan
Tungkai
 Paralytic poliomyelitis
Poliomyelitis paralitic spinal: nyeri kepala,
demam, terjadi nyeri otot hebat. Dalam 1 2
hari, timbul paresis atau paralisis flaksid
simetris.
Poliomyelitis bulbar: disfungsi saraf cranial dan
medula spinalis. Ggn pernafasan + paralisis otot
ekstraokuler, wajah dan pengunyah.
Poliomyelitis bulbopsinal. Poliomyelitis bulbar+
paralitic
Polioensefalitis: Kejang, koma dan paralisis
spastik
 Diagnosis
Muscle biopsy
Pemeriksaan neurologis :
- Kelemahan otot (otot tubuh terserang paling
akhir, sensorik biasanya normal, Refleks
tendon menurun atau tidak sama sekali, atrofi
otot mulai terlihat 3-5 minggu setelah
paralisis, gangguan fungsi otonom, ganguan
saraf kranial.
 Pemeriksaan penunjang
Isolasi virus
Serologi
Cairan serebrospinal
 Treatment
There is no effective treatment
 RABIES
Is an acute, almost invariably fatal infectious
illness caused by a neurotrophic of the
rhabdovirus family
Bats, skunks, racoons and dog are implicated
human rabies
Occasionally rabies can be transmitted by other
means than an animal bite, including inhalation
of airbone virus in caves contaminated by bat
secretion
 Etiology and pathology
The rabies virus is a bullet shaped, enveloped
RNA containing virus that usually gains acces
to the body by a bite from a rabid animal.
The virus then replicated locally in muscle
cells, penetrates nerve ending, and travels in
retrograde fashion up the nerve axons to the
CNS.
 Clinical features
Incubation period 20 -90 days
Prodromal phase flu like symptoms, tingling,
burning, depression, bizzare behavior,
halucination, insomnia, hyperactivity
Excitation phase - muscle function, speech,
vision, anxiety, hydrophobia
Paralytic phase - muscles weaken,
consciousness fades, death
 Differential Diagnosis
Tetanus
Post vaccinal encephalomyelitis
 Treatment
Human diploid cell rabies vaccine (HDCV) or
rabies vaccine adsorbed (RVA)