Acute Flaccid Paralysis

Oleh: Mia Audina

Pembimbing: Dr. Liza Chairani, Sp.A, M.Kes
 PENDAHULUAN

• WHO: extremity
weakness of fast-
onset individuals,
DIAGNOSA
often including
weakness of
• WHO: 200 Diagnosis: • There are many
respiratory muscles
30% - 60% namely AFP
and swallowing,
GBS. complications
develops to
maximum severity in • Minister of Health RI: In such as: skeletal
1-10 days Indonesia 32 diagnoses: deformity to
Poliomyelitis, death due to
• Menkes RI : all Polioencephalitis,
children aged less respiratory
Guillan-Barre Syndrome,
than 15 years with
Transverse myelitis, muscle paralysis
paralysis that is Therefore write
Flaccid muscle paralysis,
flaccid (layuh), occur referrals
Transient paralysis of a
acutely (suddenly),
limb, and mononeuritis.
not caused by forced
ruda • number of cases of Non
Polio AFP Indonesia
2017: 1409, with the
definisi number of cases in
southern Sumatra: 51
LITERATURE REVIEW…
 Definition
 Acute flaccid paralysis (AFP) is defined as all children
younger than 15 years with flaccid (layuh) paralysis,
occurring acutely (suddenly), not caused by forced ruda.

acute
flaccid

rapid progressive
development between 1- limp paralysis, weakness
14 days from the onset of or stiffness is not stiff, or
initial symptoms (pain, a decrease in muscle
tingling, thickness / tone.
numbness) to maximal
paralysis
Symptoms
Weak
symmetrical
proximal
muscles
Muscle
Autonomic weakness
dysfunction due to
fatigue

Symmetrical
quadriparesis
flaccid
Ophthalmop Flaccid
legia paraparesis
accompanie with sensory
d by motor level
weakness disorders
Damage
that covers
the medulla
oblongata
Physical examination

Assess
distribution and Spinal
Reflexes.
degree of tenderness.
weakness.

Pain when the

Sensory General
limbs are lifted
disorders. description.
(radiculopathy).
Scale of muscle strength
Value interpretation
5/5 Able to move joints in full motion, able to resist gravitational
forces, able to fight with full prisoners.

4/5 Able to move joints with gravitational force, able to fight with
moderate prisoners

3/5 Only able to fight gravity.

2/5 Unable to resist gravity (passive movement).

1/5 Muscle contractions can be palpated without moving the

joints.
0/5 There is no muscle contraction
Causes of AFP(Kemenkes RI 2007)

 Poliomyelitis  Quadriplegia/Tetraplegia
 Polioencephalitis  Plegia-unspecified
 Guillan-Barre Syndrome  Plegia-other
 Transverse myelitis  Flaccid muscle paralysis
 Paraplegia  Transient paralysis of a limb
 Diplegia  Myelitis postvaccinal
 Monoplegia-upper  Mononeuritis upper-limb
 Monoplegia-lower  Mononeuritis lower-limb
 Peripheral
Acute Myelopathy
neuropathy (Cord compression , Demyelinating
(Anterior horn cell disease, Muscle diseases, Ischaemic cord damage)
disorders)

Disorders of
Systemic disease neuromuscular
(Acute porphyrias, Critical illness transmission
neuropathy, Acute myopathy in ICU (Myasthenia gravis, Botulism. Insecticide
patients) (organophosphate poisoning), Tick bite
paralysis, Snake bite)
Supporting investigation

lumbar
puncture

tensilon
test /
Blood test
prostigmin
test

neuroimaging

serum
electrophy
protein
siological
electropho
test
resis
paraneopla
stic
antibody
screening
Penatalaksanaan

airway breathing circulation

• Make sure • Ensure • Check

the airway adequate blood
is awake ventilation pressure /
pulse
frequency

Special management
according to the
disease diagnosed
 Report it
Supportive Symptomatic
immediately

examination
Education Physiotherapy of faecal
specimens
 Differential diagnosis
Poliomielitis Guillain-bare Myastenia Gravis

Onset gradually Quickly and suddenly Gradual and volatile

Simetris unilateral bilateral unilateral

Fever + + -

Autonomic nervus abnormal abnormal normal

System
Sensoric fx abnormal abnormal normal

Swallowing disorder + + +

N III,IV,VI Disorder - + +

Respiratory Disfungtion - + +

N VII disorder - - +

Physiologic reflx - - -

Prognosis Slow healing Slow healing Remition-Relaps

Therapy Salin hipertonik, aspirin, Physical therapy, Neostigmin, efedrin,

diazepam, physical plasmaferesis, steroid, timektomi
therapy, immunization IVIg, steroid
Poliomielytis
(synonim:Acute anterior poliomeilytis, infantile paralysis, penyakit
Heine dan meidin)

 paralysis or paralysis caused by a virus, namely

poliovirus (PV), enters the body through the mouth,
infects the intestinal tract. This virus can enter the
bloodstream and flow to the central nervous system
causing weakening of the muscles and sometimes
paralysis (paralysis).
Poliomielitis
Clinical manifestations

1. Abortive polyomyelitis: malaise, anorexia, nausea,

vomiting, headache, sore throat, constipation, and
abdominal pain.
2. Nonparalytic polyomyelitis: symptoms are like abortive
poliomyelitis except for more severe headache, nausea
and vomiting and there is pain and stiffness of the
posterior neck muscles, body and legs. Physical
examination shows signs of stiff neck.
3. Paralytic polyomeilitis: symptoms are like abortive
poliomyelitis, with pain, spasticity, neck stiffness and
spinal stiffness, and hypertension at the onset of the
disease. On physical examination the typical paralysis
distribution is sometimes not.
Poliomyelitis
Diagnosis

History and physical fecal examination

examination

Blood test Viral breeding

Poliomielitis
Treatment

There is no causal
treatment, but
poliomyelitis can be
prevented through
vaccination.
Poliomielitis
complication

• Progressive • paralysis of • Permanent

muscle the chest paralysis
weakness muscles
Sindrom Guillain-Barre

comprehensive polioneuritis,
can be acute or subacute, may
occur spontaneously or after
an infection, and on
pathological examination:
there is no sign of
inflammation
Sindrom Guillain-Barre
Clinical Manifestations

 It is usually preceded by fever or upper respiratory tract

disease
 Asending paralysis is paralysis
 Flaccid type paralysis
 Paralysis can be preceded by hypesthesia, painful
anesthesia or paresthesia
 the affected muscles are symmetrical.
Sindrom Guillain-Barre
Diagnosis

 History and physical examination

 Cerebrospinal fluid examination:
- CSS protein increases to> 2x normal
- Found less than 10 white blood cells / mm3
- The results of negative bacterial cultures and viral
cultures rarely isolate certain viruses
Sindrom Guillain-Barre
Therapy

supportive action and physiotherapy:

 - If you need to do a tracheostomy, breathing apparatus if
the vital capacity drops below 50%
 - if there is bulbar paralysis or dysphagia, nasogastric or
gastrostomy is needed for feeding
 - Provision of corticosteroids: reduce pain
 - plasapheresis
Sindrom Guillain-Barre
Prognosis

 Good especially in children. Usually the repair is seen

within 7-10 days and perfect healing without sequelae
but sometimes healing lasts a long time.
 Death is caused by paralysis of the respiratory muscles
Neuritis traumatika

 Can be caused by trauma,

- directly for example due to injection (butt injection
dropfoot and deltoid drophand injection)
- indirectly can be an injury or nerve pressure.
 APF can occur within a few hours to several days after
trauma.
 Symmetrical, lasid, and areflexia.
Myastenia gravis

an autoimmune disorder (at

the neuromuscular junction)
that is characterized by an
abnormal and progressive
weakness in the skeletal
muscle that is used
continuously and is
accompanied by fatigue when
on the move.
Myastenia gravis
Diagnosis

Vocal cord Wartenberg

test test
Patients are The patient is
assigned to assigned to
count in a loud blink his eyes
voice continuously

Over time it will

be heard that Over time
his voice is ptosis will arise
getting weaker
Myastenia gravis
Diagnosis

• injected 2 mg of • injected 3 cc or 1.5 • 3 tablets of quinine

tensilon IV  If mg prostigmin were given for each
weak muscles merhylsulfate IM  200 mg3 hours
experience symptoms of then 3 tablets were
improvement  weakness given againif the
positive tests disappear symptoms gained
positive weightpositively
Tensilon Test Prostigmin
(edrophonium Test Kinin Test
chloride) (neostigmin)
Miastenia Gravis
management

 Get it with drugs or thymomectomy.

 Short-term therapy: plasma exchange (PE)2 or with
Intravenous Immunoglobulin (IVIG)2
 Long-term therapy: immunomodulating and
immunosuppressive with drugs such as corticosteroids,
azathioprine, cyclosporin and cyclophospamide
Myelitis transversa (TM)

neurological disorders caused

by the inflammatory process of
the white and gray matter of
the spinal cord, and can cause
axonal demyelination.
Myelitis transversa
symptoms

 weakness and numbness in both legs

 sensory and sphincter deficits
 Low back pain can occur in some patients
 Onset occurs suddenly and develops quickly in a few
hours and several days
Myelitis transversa
Cause

 TM can arise in isolation or with other diseases.

 When TM arises without visible comorbidities, it is
assumed to be idiopathic (abnormal imune system
against spinal cord)
 TM often occurs together with bacterial and viral
infections. 1/3 of patients with TM report flu-like illness
with fever.
Myelitis transversa
Therapy

 Therapy is usually only symptomatic, corticosteroids are

used as a therapy for inflammation of the spinal cord
 Plasma exchange or radical immunosupressant therapy
that can be used more if the steroid does not work
 Patients should follow a rehabilitation regimen for spinal
damage
 SIMPULAN

Acute flaccid paralysis Acute: rapid progressive Case of AFP: Poliomyelitis,

(AFP): all children aged less
than 15 years with flaccid
(layuh) paralysis, occur
acutely (suddenly), not
caused by forced ruda.
between 1-14 days
Flaccid: limp paralysis,
weakness or stiffness not stiff,
or a decrease in muscle tone
Polioencephalitis, Guillan-
Barre Syndrome, Transverse
myelitis, Flaccid muscle
paralysis, Transient paralysis
of a limb, dan mononeuritis.

Supporting Investigation:
neuroimaging, lumbar
puncture for, blood tests,
serum protein electrophoresis,
paraneoplastic antibody
screening, electrophysiological
tests, tensilon / prostigmin tar
tests.
AFP management is to
immediately report to the
Dinkes, supportive therapy,
symptomatic therapy for fecal
specimens, physiotherapy and
education.
 BIBLIOGRAPHY
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