Bradycardia & MILLER FISHER Syndrome: Dr. Sri Murdiati, SP - JP (K), FIHA

bradycardia & MILLER FISHER
SYNDROME
Ferina MEGA SILVIA
1707101030131
Dr. Sri Murdiati, Sp.JP (K), FIHA
Cardiology and Vascular Medicine Department of Syiah Kuala University

Dr.Zainoel Abidin Hospital, Banda Aceh
PRELIMINARY
“
Miller Fisher syndrome (MFS) is named by Dr. C. Miller Fisher described in
1956 as a limited variant of ascending paralysis, Guillain-Barr syndromee
(GBS), accounts for approximately 5% of acute inflammatory
polyneuropathy.
symptom MFS is the main of ophthalmoplegia and ataxia with peripheral

neuropathy that only there symptom very mild clinical. This is in contrast
with GBS, in which weakness and sensory loss usuallyinto symptom main,
2
“
GBS in all world is around 1
to 2 from 100,000, Where
on variants MFS there on
partially small case (1 to 2
from 1,000,000).
Case this more many

MFS happen more often happen on man from on
on Asian, estimated woman with estimate ratio
between 15% to 25% type sex 2: 1 with age
Where if compared with average 43.6 year on early
In Indonesia own not
population west around appearance disease..
yet there is data
5% certainly about
pervalensi GBS and
MFS.2
3
CASE
REPORT
Identitas
pasien
Nama “
: Ny. I Q
Jenis Kelamin : Wanita
Usia : 32 Tahun
Alamat : Banda
‐ Aceh
Agama : Islam
Tanggal Masuk : 20/06/2019
Dikonsulkan : 24/06/2019
Rekam Medis : 1-18-60-03
5
“
Patient women 32 year consulted to part Cardiology from part neurology with
complaint chest flutter-debar and weak on all body that be perceived since
morning day, Patient already diagnosed with Millier Fisher syndrome,
initially patient come to IGD RSUDZA with complaint weak on second foot,
weak initially begins from sheath eye that difficult open so that patient appear
sleepy, then weaknesses happen on all body especially on hand and leg that
be accompanied with crowded breath, Patient too complain view hazy and
appear double. Fever, cold and painful head too already experienced patient
since some day before symptom appear,
6
hospital sheet ago
In October 2018 the patient do a
general checkup at a hospital in
Malaysia and was diagnosed with
GBS
On month February 2019 patient entry

RSUDZA with complaint weakness member
On month October 2018 : patient movement under and twitch recur on side face
in hospitalization in hospital in next left be accompanied with painful head,
Jakarta with complaint weakness Patient get therapy methylprednisolone with
member movement under and in tappering off. Patient return with complaint
improve and therapy oral
diagnosis syndrome Miller Fisher metylprednisolon.pasien routine control in
variant of GBS and get therapy Polyclinic with therapy methylprednisolone
intravenous Imunnoglobulin with dose maintanance,
Post treatment patient could do

activity light, but still difficulty do
movement from squat to position
7
stand up
anamnesis
Riwayat Riwayat Riwayat

Riwayat
Penyakit Penyakit Kebiasaan
Pengobatan
Dahulu Keluarga Sosial
Tidak ada anggota

keluarga dengan
keluhan yang sama
Riw.hipertensi (-),
Patient not ever
Metilprednisolon
riwayat DM (-), riwayat consumption
penyakit jantung (-) Lansoprazole
alcohol and not
Riw.hipertensi (-), smoke,
riwayat DM (-), riwayat
penyakit jantung (-)
8
VITAL SIGNS
Compos 49x/Menit
Mentis /
110/60 (regular, isi 20 x/ 36,8°C
mmHg cukup, kuat menit (Aksila)
GCS 15 angkat)
Physical examination
Mata Telinga (-/-)

Kepala Konjungtiva anemis (-/-), sklera Hidung : Deviasi septum -/-,
Normosefali, rambut hitam tidak mudah ikterik (-/-), Ptosis perdarahan -/-
dicabut (-/-), pupil bulat, isokor, Ø Mulut : Bibir deviasi ke kiri, bibir
3mm/3mm, RCL (+/+), RCTL (+ /+) sianosis (-)
Ekstremitas
Leher Superior :Akral hangat (+/+),
Bentuk simetris, trakea lurus di Jantung edema (-/-), sianosis (-/-)
tengah, BJ I >BJ II, bising jantung (-) Inferior : Akral hangat (+/+), edema
Pembesaran KGB dan tiroid (-/-),sianosis (-/-)
10
Pemeriksaan FIsik
Paru Abdomen
• Inspeksi : Pergerakan dada • Inspeksi : Datar, simetris

simetris pada statis dan • Palpasi: Soepel, nyeri tekan
dinamis tidak ada, hepar dan lien
• Palpasi : Stem fremitus tidak teraba
kanan dan kiri sama • Perkusi : Timpani
• Perkusi : Sonor di seluruh • Auskultasi: Peristaltik (+)
lapang paru kesan normal
• Auskultasi : Vesikuler (+/+),
ronkhi (-/-), wheezing (-/-)
11
Examination Neurologi
‐ GCS: E4M6V5
‐ Sign Excitatory meningeal : Rigid nape (-)
‐ nerve cranial : Pupil: Round, Isokor,
Paresis (-)
‐ motor : 5555/5555
3333/3333
reflex Physiology reflex Pathology

biceps (+ 1 / + 1), triceps (+ 1 / + 1), Babinski (- / -), Chaddock (- / -),
patellar (+ 1 / + 1), Achilles (+ 1 / + 1) Schaeffer (- / -),
Oppenheim (- / -) , Gordon (- / -)
sensory : Glove and stocking hipoestesi

12
Function autonomous : in limit normal
1. Hemoglobin 12,5 g / dl
2. Hematokrit 36%
Supporting 3. erythrocytes 3.8 x10 /mm3
investigation 4. Trombosit 379 x10 /mm3
5. Leukocytes 13.4 x10 / mm
6. MCV 94 fL
Blood 7. MCH 33 pg
examination 8. MCHC 35%
Complete 9. RDW 11.9%
10. MPV 9,9 fL
(20 11. PDW 11,6 fL
/06/2019) 12. HitungJenis:
Eosinofil 0
Basophil 1
NetrofilBatang 0
NetrofilSegmen 74
Limfosit
13 20
Monosit 5
Na darah 142 mmol/ L
K darah 4, 2 mmol/L
Cl darah 109 mmol/ L
urea 16 mg /dL
creatinine 0.60 mg /dL
GDS 113 mg /dL
SGOT 18 U / L
SGPT 30 U / L
CT Scan Head in February 2019
Impression: Cerebral edema
15
16
EKG
ECG interpretation (24.06.2019 o'clock 10:37 pm)
calibration : 10 mm / mv QRS complex : 0.12 second

Speed : 25 mm / s Q pathological : There is no
rhythm: rhythm sine LVH : Not there is
Axis: normoaxis RVH : Not there is
QRS rate : 47 times / minute, regul ST segment : isoelectric
ar T wave : 0.08 second
P wave: Ada, 0.08 second Conclusion : Sinus bradycardia
PR interval : 0.12 second 17
EKG
ECG interpretation (24.06.2019 o'clock 10:37 pm)
calibration : 10 mm / mv QRS complex : 0.08 second

Speed : 25 mm / s Q pathological : There is no
Rhythm : rhythm sine LVH : Not there is
Axis : normoaxis RVH : Not there is
QRS rate : 62 times / minute, regul ST segment : isoelectric
ar T wave : 0.08 second
P wave : Ada, 0.08 second Conclusion : Sine rhtym, QRS rate 62x / i, normo
PR interval : 0.12 second axis
18
examination ekokordiografi
‐ Valve valve normal
‐ Dimension spaces heart normal
‐ Not there thrombus /vegetation intracardiac
‐ Function systolic normal LV
‐ Function systolic normal RV
‐ Function diastolic normal LV
‐ LVH (-)
‐ normal pericardium
‐ vessel blood big normal
‐ Conclusion:
‐ nomal ECHO
19
“
diagnosis
Diagnosa Tambahan:
Diagnosa Utama
Sinus Bradikardi
Sindrom Millier
Fisher Sindrom Cushing Syndrom
iatrogenik
20
Tatalaksana
Tatalaksana
Primary survey Airway : Tatalaksana kardiologi Tatalaksana Neurologi
Head Up300 Medikamentosa
Breathing : O2 Nasal Sulfas atrofin 1 amp/12jam iv. Methylprednisolon
kanul 2-4 L/menit Alprazolam 0,25 gr (k/p) 125mg/6 jam
Circulation : IVFD NaCl Ubi Q 1x 50mg Omeprazole 40 mg/
0,9% 20 gtt/menit Mydriatil (extra) 1gtt/hari 12jam
Sukralfat syr 15ml/8jam
21
follow Up
Daily
25/06/2019 26/06/2019 27/06/2019 28/06/2019
(H1) (H2) (H3) (H4)
Cardiology Cardiology Cardiology Cardiology
Seseak breath Weakness Member Weakness Member Weakness Member

S and heart flutter- movement, Difficult movement, Difficult movement
debar. swallow, swallow
awareness: CM awareness: CM awareness: CM awareness: CM
O TD: 100 / 60mm TD: 100 / 70mmHg TD: 110 / 70mmHg TD: 110 / 70mmHg
Hg HR: 53 x / i HR: 58 x / i HR: 62 x / i
HR: 49 x / i RR: 20 x / i RR: 20 x / i RR: 20 x / i
RR: 20 x / i T: 36,7 0C T: 36,7 0 T: 36,7 0
T: 36,7 0C
• bradycardia • bradycardia • bradycardia bradycardia
A • Miller Fisher • Miller Fisher syndrome • Miller Fisher syndrome • Miller Fisher syndrome
syndrome
th/ th/ th/ th/
P 1 amp / 12 hours • sulfate atropine 1 amp • sulfate atropine 1 amp / • sulfate atropine 1 amp / 1
/ 12 hours 12 hours 2 hours
• Alprazolam 1x 0.25 mil • Alprazolam 1x 0.25 mill • Alprazolam 1x 0,25m
ligrams 23 igrams • tuber Q (Q Car 1x50mg)
• tuber Q (Q Car 1x50m • tuber Q (Q Car 1x50mg
29/06/2019 30/06/2019 1/07/2019 2/07/2019
(H5) (H6) (H7) (H8)
Weakness Member Weakness Member Weakness Member Weakness Member

S movement movement, movement movement

O TD: 100 / 60mmH TD: 100 / 70mmHg TD: 110 / 70mmHg TD: 110 / 70mmHg
g HR: 53 x / i HR: 58 x / i HR: 62 x / i
RR: 20 x / i T: 36,7 0C T: 36,7 0 T: 36,7 0
T: 36,7 0C
syndrome
th/ th/ th/ th/
P • sulfate atropine • sulfate atropine 1 amp • sulfate atropine 1 amp / • sulfate atropine 1 amp / 1
1 amp / 12 hour / 12 hours 12 hours 2 hours
s • Alprazolam 1x 0.25 mil • Alprazolam 1x 0.25 mill • Alprazolam 1x 0,25m
• Alprazolam 1x 0 ligrams igrams • tuber Q (Q Car 1x50mg)
24
.25 milligrams • tuber Q (Q Car 1x50m • tuber Q (Q Car 1x50mg
• tuber Q (Q Car g) )
3/07/2019 4/07/2019 5/07/2019 6/07/2019
(H5) (H6) (H7) (H8)


g HR: 83 x / i HR: 82 x / i HR: 84 x / i
RR: 20 x / i T: 36,7 0C T: 36,7 0 T: 36,7 0
T: 36,7 0C
syndrome
th/ th/ th/ th/
25
7/07/2019 8/07/2019 9/07/2019 10/07/2019
(H9) (H10) (H11) (H12)


g HR: 80 x / i HR: 80 x / i HR: 84 x / i
RR: 20 x / i T: 36,7 0C T: 36,7 0 T: 36,7 0
T: 36,7 0C
syndrome
th/ th/ th/ th/
26
review book
MILLER FISHER SYNDROME
28
DEFINITION
syndrome Miller Fisher is abnormality neurologic I that be marked with presence trias manifes
tation clinical that is presence ataxia (lack of balance) ophthalmoplegia (paralysis muscle eye
) and areflexia (disappearance reflex tendon)
syndrome Miller Fisher described first time on 1956 by a doctor nationality Canada named Charles
Miller Fisher. syndrome this constitute circumstances I, rarely found, and considered as something
variants from syndrome Guillain Barre, syndrome Guillain Barre constitute polyneuropathy I, is
symmetrical and ascending,
Difference SGB and syndrome Miller Fisher that is on group nerve that struck, and paralysis that happe
n begins from leg, then up to the top, While that on syndrome Miller Fisher paralysis starts from head he
ad (on muscle eye) and then neck and arm,
29
ETIOLOGY
microorganisms cause not yet ever found on patient and not constitute
disease that spread too not downgraded in hereditary, Disease this constitute process autoim
mune,
But around half from all case happen after disease infection virus or bacterium as below this
:
• Infection virus : Citomegalovirus (CMV), Ebstein Barr Virus (EBV), enterovirusHuman
Immunodefficiency Virus (HIV).
• Infection bacterium : Campilobacter jejuni, Mycoplasma Pneumonie,
• Pascah surgery and vaccinations,
30
Pathophysiology
Role antibody antigangliosida GQ1b on pathogenesis syndrome Miller Fisher known on early year
1990. Anti GQ1b known related with level severity from syndrome Miller Fisher. syndrome MF related
with presence anti GQ1b on more from 80% patient,
31
CLINICAL
Ophthalmoplegia
Ataksia
Neuropati peripheral
32
GOVERNANCE
Observation
plasmapheresis / plasma exchange
Injection immunoglobulins intravenous
Immunoadsorption
33
bradycardia
34
DEFINITION
bradycardia is beat heart that less from on 60 times /minute,
bradycardia relatively is beat heart more from 60 times /minute but still less from condition that should,
bradycardia will inflict problem when symptomatic or already inflict symptom result beat heart that too sl
ow
35
ETIOLOGY
1. disruption formation Impulse
 Sine bradycardia
Factor intrinsic Extrinsic factors
Degeneration idiopathic (process aging) Impaired autonomic syndrome
infarction / ischemia syncope Neurokardial
Disease infiltrative Carotid Sinus Hypersensitivity
sarcoidosis Situational disturbance
amyloidosis Cough
haemochromatosis defecation
Collagen-Vascular Diseases BAK
SLE Gag
rheumatoid Arthritis Drug
scleroderma beta Blocker
Myotonic muscular dystrophy Calcium-channel blockers
trauma Surgery clonidine
Valve replacement digoxin
Correction of congenital disease antiarrhythmic drugs
heart transplant Hipothyroid
Heredity disease hypothermia
Infectious diseases Neurological Disorders
Chagas' Disease electrolyte Disorders
endocarditis hypokalemia
36 hiperkalemi
 Sick Sinus Syndrome
(1) SInus bradycardia spontaneous that stay, which not caused by drug and not corresp
onding
with circumstances physiological;
(2) sinus arrest or exit block
(3) combination disruption conduction SA and AV
(4) bradycardia-tachycardia syndrome.
37
 Hypersensitive Carotid Sinus Syndrome
hypersensitivity branch afferent or efferen from reflex arch sine carotid cause Activation
vagal and or inhibition sympathetic, so that cause bradycardia and vasodilation,
38
2. disruption penghantaran Impulse
 AV Block level 1
 AV Block level 2
• Block level 2 Type I
39
• Block level 2 type II
• AV block level 3 ( Total AV block)
40
DISCUSSION
CASE DISCUSSION
Patient women 32 year consulted

to part Cardio from part neurology
“
Classification palpitations could
be divided into some that is
tachycardia (Tachycardia):
beat heart more from 100 times
per minute,
with complaint chest flutter-debar
and weak on all body that be bradycardia (bradycardia):
beat heart less from 60 times
perceived since 1 daySMRs.
per minute,
Fromexamination ECG available
Fibrillation: Heart rattle fast,
Heart rate 49x /minute,
contraction muscle heart that
not synchronous,
arrhythmias: tap heart not
regular
42
CASE DISCUSSION
initially patient come to IGD

RSUDZA with complaint limp on all
body, limp initially begins from
sheath eye that difficult open so
“
Patient diagnosed with Miller
Fisher syndrome variants from
Gullain barre syndrom that
constitute abnormality
that patient appear sleepy, old too neurologic I that be marked
long limp spread to all body with presence trias
especially on hand and leg that manifestation clinical that is
cause weakness on member presence ataxia (lack of
movement patient that be balance) ophthalmoplegia
accompanied with crowded breath, (paralysis muscle eye) and
Patient too complain view hazy and areflexia (disappearance reflex
appear double. tendon).
43
CASE
“
‐
There relationship Miller Fisher syndrome with sine bradycardia
44
‐ complication cardiovascular rarely reported on Miller Fisher
syndrome however cause constitute disruption nerve
autonomous,
‐ Kuzumoto et al showing presence relationship between test
abnormality nerve autonomous and antibody anti-GQ1b on
patient MFS. complication not only limited on disruption
Respiratory weight but too condition that more light Where patient
not need help Respiratory and can walk more from 5 meters.
‐ Level damage nerve motor not could predict occurrence
bradyarythmia that serious including stopping sine. appraisal
early on Event that threaten soul as that very important for action
prevention that right, as insertion tool spur heart, can immediately
taken,
neuropathy autonomous constitute complication important syndrome
Guillain-Barre, visible on around 60% case and rarely happen MFS.
Case this often happen on person adult young with case that more
weight for mortality, disruption autonomous heart on GBS including
hypertension unstable, hypotension orthostatic, and various type
arrhythmias heart including sine tachycardia, serious bradyarrhythmia
and asistole, Manifestation this happen result disruption from lane nerve
sympathetic and parasympathetic,
dysfunction autonomous general happen on GBS and manifest as activity
that excessive or not adequate from activity tap heart ,abnormality tap heart
varies cause hypotension postural, sweat excessive, and hypertension,
event heart arrhythmias general happen on GBS. greenland and Griggs
record at least there arrhythmias on 13 from 16 patient that be learned ,
and they too find correlation that significant between dysfunction nerve
autonomous and atrioventricular block, implantation tool spur heart while
could do on patient because stopping sine.
A episode bradycardia sine spontaneous usually happen on day fifth
after appearance symptom neurologic with period stopping sine and
asystole for 15 second and usually responds with fast on massages
heart that could restore rhythm sine without drug What even. After
that period bradycardia and asystole could observed in intermittent
for suction endotracheal, atropine intravenous, 1 mg, could increase
beat heart, usually into 80 to 90 per minute, and decrease frequency
and duration period asystolic, Next, could be given infusion
isoproterenol continue constantly for keep tap heart 80 to 90 per
minute,
Installation from pacemaker while initially considered but because
danger infection, management medical use atropine and
isoproterenol be used for avoid manipulation intracardiac
transvenous, If not there is improvement in status neurologic after 8
Sunday occurrence bradycardia and asystole, demand intracardiac
permanent alath spur heart could programmed, After mounted tool
spur heart should often controlled even to 6 month after
implantation,
neuropathy autonomous is picture general and important that appear on
cardiovascular, sudomotor, gastrointestinal and system more involve nerve
parasympathetic and sympathetic, in special, activity excessive vagal could
cause bradaritmia serious start from bradycardia to asystole and constitute
cause total Dead that significant, in general believed that bradyarrhythmia
this happen only on patient with disease weight, especially on patient that
need ventilation mechanical, however, there is some case that explain
bradiartimia without ventilation mechanical and even on patient that not too
severe, picture dysrhythmias that potential threaten soul this very important
for start therapy prevention that right as tool spur heart external or monitoring
on unit care intensive (ICU).
THANK YOU
53

Bradycardia & MILLER FISHER Syndrome: Dr. Sri Murdiati, SP - JP (K), FIHA

Diunggah oleh

Informasi Dokumen

Judul Asli

Hak Cipta

Format Tersedia

Bagikan dokumen Ini

Bagikan atau Tanam Dokumen

Opsi Berbagi

Apakah menurut Anda dokumen ini bermanfaat?

Apakah konten ini tidak pantas?

Hak Cipta:

Format Tersedia

Bradycardia & MILLER FISHER Syndrome: Dr. Sri Murdiati, SP - JP (K), FIHA

Diunggah oleh

Hak Cipta:

Format Tersedia

bradycardia & MILLER FISHER

Cardiology and Vascular Medicine Department of Syiah Kuala University

symptom MFS is the main of ophthalmoplegia and ataxia with peripheral

Case this more many

On month February 2019 patient entry

Post treatment patient could do

Riwayat Riwayat Riwayat

Tidak ada anggota

Mata Telinga (-/-)

• Inspeksi : Pergerakan dada • Inspeksi : Datar, simetris

reflex Physiology reflex Pathology

sensory : Glove and stocking hipoestesi

Cl darah 109 mmol/ L

Impression: Cerebral edema

calibration : 10 mm / mv QRS complex : 0.12 second

calibration : 10 mm / mv QRS complex : 0.08 second

Seseak breath Weakness Member Weakness Member Weakness Member

Weakness Member Weakness Member Weakness Member Weakness Member

awareness: CM awareness: CM awareness: CM awareness: CM

Weakness Member Weakness Member Weakness Member Weakness Member

awareness: CM awareness: CM awareness: CM awareness: CM

Weakness Member Weakness Member Weakness Member Weakness Member

awareness: CM awareness: CM awareness: CM awareness: CM

plasmapheresis / plasma exchange

Injection immunoglobulins intravenous

bradycardia is beat heart that less from on 60 times /minute,

• AV block level 3 ( Total AV block)

Patient women 32 year consulted

initially patient come to IGD

Anda mungkin juga menyukai