ANALISIS CAIRAN SEREBROSPINAL UNTUK MENINGITIS TB

PENDAHULUAN

PEMERIKSAAN MAKROSKOPIS
Warna
Warna bisa jernih atau xantokrom

Kekeruhan
Tidak keruh, karena meskipun terjadi pleiositosis, peningkatan sel tidak lebih dari
200 ul, sehingga belum mengeruhkan cairan serebrospinal

Sedimen

Bekuan

PEMERIKSAAN MIKROSKOPIS
Hitung jumlah sel <500/mm3

Hitung jenis sel

Predominan of lymphosite

Bakterioskopis ????

PEMERIKSAAN KIMIA
Protein 50-500mg/dl (moderate to marked increase)
Kenaikan sedang kadar protein disebabkan karena proses peradangan oleh bakteri
mycobacterium tuberculosa yang membebaskan beberapa protein ataupun karena
peningkatan jumlah leukosit dengan predominan sel mononuklear.

Glukosa <40mg/dl (low)

Penurunan jumlah glukosa disebabkan oleh mycobacterium tuberculosa yang
menggunakannya sebagai bahan makanannya untuk membentuk energi

Chlorida <600mg/dl (low)

Kadar chlorida yang turun disesbkan oleh peningkatan protein

Pemeriksaan khusus (TBC)

a. Tes levinson
Pada tes ini akan menunjukkan kenaikan sedimen

b. Tes triptofan
 GBS

DIAGNOSA DAN DD
DIAGNOSA

Diagnosa ditegakkan berdasarkan temuan pada pemeriksaan neurologis

termasuk berkurang atau hilangnya refleks deep-tendon.

Pemeriksaan pendukung : fungsi lumbal, tes darah lengkap

fIGURE 1.

Algorithm for evaluation of a patient with a peripheral neuropathy. (ECG =

electrocardiogram; EMG/NCS = electron microscopy/nerve conduction studies;
AIDS = acquired immunodeficiency syndrome; FVC = forced vital capacity)
TABLE 1

Neuropathies by Pattern of Involvement

Focal
Entrapment
Common sites of compression
Myxedema
Rheumatoid arthritis
Amyloidosis
Acromegaly
Compressive neuropathies
Trauma
Ischemic lesions
Diabetes mellitus
Vasculitis
Leprosy
Sarcoidosis
Neoplastic infiltration or compression
Multifocal
Diabetes mellitus
Vasculitis
Polyarteritis nodosa
Systemic lupus erythematosus
Sjögren's syndrome
Sarcoidosis
Leprosy
HIV/AIDS
Multifocal variant of CIDP
Hereditary predisposition to pressure palsies

HIV = human immunodeficiency virus; AIDS = acquired immunodeficiency syndrome; CIDP =

chronic inflammatory demyelinating polyradiculoneuropathy.
TABLE 2

Distal Symmetric Sensorimotor Polyneuropathies

Endocrine diseases
Diabetes mellitus
Hypothyroidism
Acromegaly
Nutritional diseases
Alcoholism
Vitamin B12 deficiency
Folate deficiency
Whipple's disease
Postgastrectomy syndrome
Gastric restriction surgery for obesity
Thiamine deficiency
Hypophosphatemia
Critical illness polyneuropathy
Connective tissue diseases
Rheumatoid arthritis
Polyarteritis nodosa
Systemic lupus erythematosus
Churg-Strauss vasculitis
Cryoglobulinemia
Amyloidosis
Gouty neuropathy
Carcinomatous axonal sensorimotor polyneuropathy
Lymphomatous axonal sensorimotor polyneuropathy
Infectious diseases
Acquired immunodeficiency syndrome
Lyme disease
Sarcoidosis
Toxic neuropathy
Acrylamide
Carbon disulfide
Dichlorophenoxyacetic acid
Ethylene oxide
Hexacarbons
Carbon monoxide
Organophosphorus esters
Glue sniffing
Metal neuropathy
Chronic arsenic intoxication
Mercury
Gold
Thallium
Medications (see Table 8)
TABLE 3
Proximal Symmetric Motor Polyneuropathies

Guillain-Barré syndrome
Chronic inflammatory demyelinating polyradiculoneuropathy
Diabetes mellitus
Porphyria
Osteosclerotic myeloma
Waldenstrom's macroglobulinemia
Monoclonal gammopathy of undetermined significance
Acute arsenic polyneuropathy
Lymphoma
Diphtheria
HIV/AIDS
Lyme disease
Hypothyroidism
Vincristine (Oncovin, Vincosar PFS) toxicity

HIV = human immunodeficiency virus; AIDS = acquired immunodeficiency

syndrome.

TABLE 4
Neuropathies with Less Common Patterns of Involvement

Neuropathies with cranial nerve involvement

Diabetes mellitus
Guillain-Barré syndrome
HIV/AIDS
Lyme disease
Sarcoidosis
Neoplastic invasion of skull base or meninges
Diphtheria
Neuropathies predominant in upper limbs
Guillain-Barré syndrome
Diabetes mellitus
Porphyria
Hereditary motor sensory neuropathy
Vitamin B12 deficiency
Hereditary amyloid neuropathy type II*
Lead neuropathy
HIV = human immunodeficiency virus; AIDS = acquired immunodeficiency
syndrome.
*—Carpal tunnel syndrome resulting from amyloid deposits in the flexor
retinaculum.
TABLE 5

Comparative Patterns of Neuropathies and Neuronopathies by Fiber Type

Pure sensory neuropathies and neuronopathies

Paraneoplastic
Medications (see Table 8)
Carcinomatous sensory neuronopathy
Lymphomatous sensory neuronopathy
Sjögren's syndrome
Paraproteinemias
Nonsystemic vasculitic neuropathy
Idiopathic sensory neuronopathy
Styrene-induced peripheral neuropathy
Primary biliary cirrhosis
Crohn's disease
Chronic gluten enteropathy
Vitamin E deficiency
Hereditary sensory neuropathy types I and IV
Friedreich's ataxia
Small-fiber neuropathies
Leprosy
Diabetes mellitus
Alcoholic neuropathy
Amyloidosis
AIDS
Hereditary
Neuropathies with autonomic involvement
Diabetic neuropathy
Amyloidosis
Porphyria
Paraneoplastic neuropathy
Lymphoma
Thallium, arsenic, mercury toxicity
Thiamine deficiency
Vincristine (Oncovin, Vincosar PFS) toxicity
Guillain-Barré syndrome
Alcoholic neuropathy
Acute pandysautonomia
HIV/AIDS

AIDS = acquired immunodeficiency syndrome; HIV = human

immunodeficiency virus.
TABLE 6
Neuropathies with Abrupt/Rapid Onset

Ischemic neuropathies
Polyarteritis nodosa
Rheumatoid arthritis
Diabetes mellitus
Cranial neuropathies
Diabetic amyotrophy
Nerve compression
Hemorrhage
Swelling within a restricted anatomic
compartment (e.g., anterior tibial
syndrome)
Direct external compression
Penetrating wounds
Thermal injury
Iatrogenic (e.g.,
injection into nerves)
TABLE 8
Drugs Causing Neuropathies
Axonal
Vincristine (Oncovin, Vincosar PFS)
Paclitaxel (Taxol)
Nitrous oxide
Colchicine (Probenecid, Col-Probenecid)
Isoniazid (Laniazid)
Hydralazine (Apresoline)
Metronidazole (Flagyl)
Pyridoxine (Nestrex, Beesix)
Didanosine (Videx)
Lithium
Alfa interferon (Roferon-A, Intron A, Alferon N)
Dapsone
Phenytoin (Dilantin)
Cimetidine (Tagamet)
Disulfiram (Antabuse)
Chloroquine (Aralen)
Ethambutol (Myambutol)
Amitriptyline (Elavil, Endep)
Demyelinating
Amiodarone (Cordarone)
Chloroquine
Suramin (Fourneau 309, Bayer 205, Germanin)
Gold
Neuronopathy
Thalidomide (Synovir)
Cisplatin (Platinol)
Pyridoxine
TABLE 7

Differential Diagnosis of Neuropathies by Clinical Course

Chronic Relapsing/Re
Acute Onset Subacute Onset
Course/Insidious mitting
(Within Days) (Weeks To Months)
Onset Course
Maintained Hereditary
Guillain-
Guillain- exposure to motor
Barré
Barré toxic sensory
syndrom
syndrome agents/medicati neuropathie
e
ons s
Dominantly
Acute Persisting
inherited
intermittent nutritional CIDP
sensory
porphyria deficiency
neuropathy
Critical
illness Abnormal HIV/AID
CIDP
polyneurop metabolic state S
athy
Diphtheric Paraneoplastic
Toxic
neuropathy syndrome
Thallium Porphyri
CIDP
toxicity a

CIDP = chronic inflammatory demyelinating polyradiculoneuropathy; HIV =

human immunodeficiency virus; AIDS = acquired immunodeficiency
syndrome.
1st investigations to ordershow all

Test Result

nerve slowing of nerve conduction velocities

conduction
studies

LP elevated CSF protein, normal/slightly high lymphocytes (<50

cells/mm^3)

LFT elevated AST and ALT as high as 500 U/L; bilirubin may be
transiently elevated but rarely high enough to cause jaundice

spirometry may show reduced vital capacity, maximal inspiratory

pressure, or maximal expiratory pressure

antiganglioside Acute motor-sensory axonal neuropathy (AMSAN): GM1,

antibody GM1b, GD1a; acute motor axonal neuropathy (AMAN):
GM1, GM1a, GD1a, GalNac-GD1a; Miller-Fisher syndrome:
GQ1b, GT1a GQ1b; Miller-Fisher syndrome/GBS overlap
syndrome: GQ1b, GM1, GM1a, GD1a, GalNac-GD1a; acute
inflammatory demyelinating polyradiculoneuropathy (AIDP):
antibodies unknown; Miller-Fisher syndrome/GBS overlap
syndrome: GQ1*, GM1, GM1a, GD1a, GalNac-GD1a
DD
Condition Differentiating signs/symptoms
Transverse  Spinal cord disorders
myelitis including transverse myelitis
present with asymmetrical
motor or sensory loss
usually involving lower
extremities, early bowel or
bladder dysfunction with
persistent incontinence, and
segmental radicular pain.
 Physical examination
demonstrates upper motor
neuron signs (hyperreflexia,
positive Babinski's response)
and a sensory level.
Myasthenia  Early involvement of muscle
gravis groups including extra-
ocular, levator, pharyngeal
jaw, neck, and respiratory
muscles. Sometimes
presents without limb
weakness.
 Excessive fatigability and
variation of symptoms and
signs through the day is
common.
 Reflexes are preserved, and
sensory features,
dysautonomia, and bladder
Differentiating
investigations
 CSF analysis:
pleocytosis with
modest number of
lymphocytes and
increase in total
protein.
 MRI shows focal
demyelination with
possible enhancement
at the appropriate
level. [62]
 Electrophysiological
study shows normal
nerve conduction and
presence of
decremental response
to repetitive nerve
stimulation.
 EMG shows abnormal
jitter and blocking.
 Edrophonium test is
normally
positive. [121]However
, many centres do not
routinely perform this
 Differentiating
Condition Differentiating signs/symptoms investigations

dysfunction are absent. test because of

potential side effects.

Lambert-  Can be difficult to  Electrophysiological

Eaton differentiate because of study: hallmark is a low
myasthenic similar clinical amplitude compound
syndrome characteristics. However, muscle action potential
(LEMS) some characteristics are (CMAP) after single
more typical for LEMS. nerve stimulus,
These include slower increase in CMAP
development of clinical amplitude after
symptoms, dry mouth, lack voluntary contraction,
of objective sensory loss, or repetitive stimulation
rare involvement of at high
respiratory muscle group, frequencies. [121]
and potentiation of reflexes
after exercise or
contraction. [121]

Botulism  History of ingesting food  Electrophysiological

tainted with botulinum toxin. study: reduced
 Descending paralysis begins amplitude of evoked
in the bulbar muscles then muscle potentials,
the limbs, face, neck, and increase in amplitude
respiratory muscles. with repetitive nerve
 Respiratory muscles are stimulation, and
involved with mild limb increased number of
weakness, and reflexes are myopathic units, which
usually preserved. is atypical for
 Ptosis, dilated non-reactive GBS. [121]
pupils are present. Dilated

Condition Differentiating signs/symptoms
non-reactive pupils are
uncommon in GBS, but more
common in botulism.
 Constipation is also a
characteristic feature of
botulism. [121]
Polymyositis  Presence of pain and muscle
tenderness usually in the
shoulder and upper arm,
involvement of flexor neck
muscle disproportionate to
limb weakness, absence of
sensory symptoms,
preservation of reflexes,
absence of dysautonomia,
and presence of skin lesions,
which are uncommon
presentation for GBS. [121]
Vasculitic  Common features include
neuropathy painful asymmetrical
presentation of muscle
weakness, uncommon
involvement of cranial
nerves, respiratory paralysis,
and sphincter dysfunction.
 Usually patients complain of
fever, fatigue, weakness,
and arthralgia. [121]
Differentiating
investigations
 Elevated ESR and CK,
normal nerve
conduction study, and
myopathic changes
with fibrillation on
EMG.
 Muscle biopsy shows
muscle fibre
destruction and
regeneration, and
lymphocyte
infiltrates. [121]
 May have elevated
ESR.
 CSF does not show
albuminocytological
dissociation.
 Electrophysiological
study shows evidence
of denervation.
 Nerve biopsy shows
signs of inflammation
and scarring. [121]
http://www.who.int/mediacentre/factsheets/guillain-barre-syndrome/en/

Guillain–Barré syndrome
Fact sheet
Updated October 2016

TATALAKSANA
Berikut ini adalah rekomendasi untuk pengobatan dan perawatan orang
dengan sindrom Guillain-Barré:

Sindrom Guillain-Barré berpotensi mengancam nyawa. pasien GBS harus

dirawat di rumah sakit sehingga mereka dapat diawasi secara ketat.

Perawatan suportif meliputi pemantauan pernapasan, detak jantung dan

tekanan darah. Dalam kasus di mana kemampuan pasien untuk bernapas
terganggu, ia biasanya memakai ventilator. Semua pasien GBS harus dimonitor
untuk komplikasi, yang dapat mencakup detak normal jantung, infeksi,
pembekuan darah, dan tekanan darah tinggi atau rendah.

Tidak ada obat dikenal untuk GBS. Tetapi perawatan dapat membantu
meringankan dan memperpendek durasi dari gejala

Karena gbs adalah penyakit autoimunt, fase akut biasanya diobati dengan
imunoterapi, seperti plasma exchange untuk menghilangkan antibodi dari
darah atau imunoglobulin intravena. Hal ini paling sering menguntungkan bila
dimulai 7 sampai 14 hari setelah gejala muncul.

Dalam kasus di mana kelemahan otot berlanjut setelah fase akut penyakit,
pasien mungkin memerlukan pelayanan rehabilitasi untuk memperkuat otot-
otot mereka dan mengembalikan gerakan.

PROGNOSIS
Prognosis GBS umumnya menguntungkan, tetapi adalah sebuah penyakit
serius dengan angka kematian sekitar 10% dan sekitar 20% pasien dengan
cacat beratnyyu
 Drugs. 2004;64(6):597-610.

Guillain-Barré syndrome: epidemiology, pathophysiology

and management.
Kuwabara S1.
Author information

 1Department of Neurology, Chiba University School of Medicine, Chiba, Japan.

kuwabara-s@faculty.chiba-u.jp

https://www.ncbi.nlm.nih.gov/pubmed/15018590

KOMPLIKASI

Complicationshow all Timeframe Likelihood

respiratory failure short term medium

bladder areflexia short term medium

adynamic ileus short term medium

paralysis short term medium

fatigue long term high

immobilisation hypercalcaemia long term low

DVT variable medium