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CA LM SNG NHC C
PGS.TSCao Phi Phong
Ngy 14/10/2013
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Bnh s
- Bnh nhn nam, 36 tui, Bnh Dng.
- Ngh nghip: ti x
- Nhp vin: 14 gi 50 pht ngy 07 05 2013
- L do nhp vin: Sp mi, yu c t chi
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- Bnh khi pht 01 thng trc nhp vin bnh nhn sp mi mt (T), nhn i. 02 tun sau bnh nhn yu tay (T), mi c, yu tay (P).
- 01 tun trc nhp vin bnh nhn cm thy yu c ton thn: yu c 02 chi di, c nhai, tnh trng yu c thay i trongngy, tng khi lm vic, thnh thong kh th.
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Bnh nhn n khm trung tm chn on Y
Khoa Ha Ho pht hin u tuyn c, chuyn n
bnh vin Phm Ngc Thch, chuyn n bnh
vin Ch Ry.
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- Bnh nhn khng nhc u, khng st, n ung khng sc, ging ni khng thay i.
- Khng c yu t thun li nh nhim trng, stress hay dng thuc trc .
- Hin ti tnh, tip xc tt, nhn m, sp mi mt (T) > (P), mi c t chi, c vng c, c nhai, tai
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Tin cn
1. Bn thn
- Chn thng u cch 10 nm ( vng vo u)
- Khng ht thuc l.
- Thnh thong c ung ru.
- Cha pht hin bnh l khc nh bnh phi, bnh gan, thn, d ng.
2. Gia nh
- Khng ai trong gia nh mc bnh tng t.
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Khm bnh
+ M 72 ln/pht, nhit 37oC, HA 120/70 mmHg, nhp th 20 ln/1 pht u.
Khm thn kinh
- Tnh, tip xc tt
- ng t: 2,5 mm, trn u 2 bn, phn x nh sng bnh thng. Sp mi mt (T) > (P),yu c nng mi.
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- Yu c vng mi.
- Vn ng mt (T) gii hn nhn sang (T).
- Mt (T) nhm khng kn > (P): h khe mi.
- Bnh nhn tai (T), khng gim thnh lc.
- Dy XI : C c n chm 2 bn cn i, yu c thang. Sc c nng vai 4/5.
- Sc c t chi: 5/5, yu kn o gc chi >
ngn chi.
- Cc phn khc bnh thng
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Tm tt
Bnh nhn nam, 36 tui, nhp vin v sp mi,
yu c t chi.
- Bnh 01 tun, din tin t t khong 01 thng trc vi cc triu chng: sp mi, nhn i, yu c ton thn.
- Sp mi, nhn i (khng cn), nhn m.
- Yu c vng mi, t chi yu kn o gc chi > ngn chi, c vng c cng b nh hng
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Bin lun:
-Da vo bnh s v lm sng bnh nhn c biu hin u
tin cc c mt: sp mi, nhn i v c nhai. Sau yu
c t chi, ton thn, yu c dao ng v d mt mi. Ph
hp bnh nhc c.
-Nhc c mt, nhc c ton thn nh, tin trin t t,
khng c cn nhc c, phn mc II A.
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TNG QUAN V NHC C
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Chn on
- Chn on v tr
- Chn on phn bit
Cn lm sng
iu tr
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Gii phu
Neuromuscular Junction (NMJ) Cc thnh phn: Presynaptic membrane Postsynaptic membrane Synaptic cleft
Presynaptic membrane : cha bcc Acetylcholine (ACh) which are v phng thch vo khe xi-nap (synaptic cleft ) l thuc vocalcium
ACh tc ng trn ACh receptors (AChR) trn postsynaptic membrane
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Ri lon dn tuyn thn kinh- c
Bnh sinh chia 2 nhm :
(1) Hi chng nhc c bm sinh
(sai st di truyn tip hp thn kinh-c )
(2) Hi chng nhc c mc phi
(ri lon t min v c cht)
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(1) Hi chng nhc c bm sinh do cc sai st di truyn tip hp thn kinh-c bao gm:
Th th acetylcholine(AChR),
Th th kt tp protein xi-nap(Rapsyn),
Choline acetyl transferase(ChaT),
Acetylcholinesterase(AChE),
Dok-7 (downstream of tyrosine kinase 7 )
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(2) hi chng nhc c mcphi do ri lon t min vc cht
Th th acetylcholine(AChR),
Men c chuyn bit (muscle-specific kinase: MuSK),
Knh calcium.
Knh sodium.
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Ri lon tip hp thn kinh c mc phi
Myasthenia Gravis
Lambert Eaton)-Myasthenic Syndrome (LEMS)
Toxic or Metabolic Botulism Hypermagnesemia
Drugs (D-Penicillamine)
Organophosphate toxicity
Snake, spider, scorpion bites
T
MiN
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Ca lm sang
BN nam,60 tui co tin cn hut thuc l nhiu nm
Nhp vin yu c gc chi, chi di nhiu hn chi trn, kho khn ng ln khi ngi trn gh, au c gc chi khi chm vao, triu chng tin trin m i, st cn, mt moi.
Khm sc c gc gim, c bit sau hot ng sc c co ci thin sau o gim li. Pxgx gim, tng khi co c chu ng.
Bnh nhn than kh ming sinh ly gim sut, bon, hay chong mt t th.
Chn on ?
Cc xet nghim cn lam?
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Lambert-Eaton Myasthenic Syndrome
2/3 ca l tin ung th (paraneoplastic) nam
1/3 ca l t min (autoimmune) n
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Triu chng lm sng Lambert-Eaton Myasthenic Syndrome?
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+++
+++
Ach
Ach
Ach
Ca++
Ca++
Ca++
NMJ
m = n X pm: number of quanta releasedp: probability of releasen: the number of quanta in axon
In LEMS: p
Parasympathetic
Sympathetic
Enteric neurons
are all affected.
This post exercise facilitation seems likely to be
due to the temporary build up of Ca++ in the
nerve terminal which results in a striking
potentiation of release, temporarily increasing the
safety factor.
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Lm sng LEMS
Yu c v d mt (Weakness and fatigability)
- Muscles in proximal leg and the pelvic girdle are most severely affected
- Mild bulbar muscle weakness and ptosis may also occur.
Gim phn x: hyporeflexia, but muscle wasting is infrequent
Ri lon thn kinh thc vt: Autonomic dysfunction (e.g., dry mouth, loss of pupillaryreflex, decreased sweating, erectile dysfunction)
An increase in DTRs after contraction is a
hallmark of LEMS.
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Repetitive nerve stimulation (RNS):
confirm the diagnosis
Compound muscle action potentials (CMAPs):
small, often less than 10% of normal, and fall
during 1- to 5-Hz RNS (slow RNS).
Cn lm sng
-
p ng vi RNS: thay v gim p ng
bin (amplitude) vn ng, ghi nhn
gia tng bin vi kch thch lp li(kch
thch 10 Hz hay cao hn)
Lambert Eaton syndrome
Increased strength with sustained contraction; Evidence of lung carcinoma; EMG findings similar to botulism
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Rapid RNS
Facilitation > 100% in most muscles tested or > 400% in any muscle, the patient almost certainlyhas LEMS.
If facilitation is less than 50% in all muscles tested the patient still may have LEMS, especially if weakness has been present for only a short time or the patient has been partially treated.
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Rapid RNS
During stimulation at 20-50 Hz, the CMAP increases in size (ie, facilitation) and characteristically becomes at least twice (200%)the size of the initial response.
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- A similar increase in CMAP size is seen
immediately after the patient voluntarily contracts
the muscle maximally for several seconds.
- In LEMS, the CMAP amplitude is low in most
muscles tested.
- This finding is also non-specific and is
commonly observed in other neuromuscular
diseases.
-
iu tr
Identify and treat underlying malignancy; may lead to partial remission if treated.
Medications- 3,4-Diaminopyridine is the drug of choice; it increases
calcium influx.
- Cholinesterase inhibitors have a weak effect; they are usually used as adjunctive therapy.
- Immunotherapy (e.g., corticosteroids or azathioprine)
Plasmapheresis
Intravenous immunoglobulin therapy
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Bnh nhn n 45 tui nhp vin v nhn i, sp mi, ni kh v yu t chi, tay chn nhiu sang thngnhim trng ngoi da.
Tin s chch heroin
Khm thn kinh
- Sc c 4/5(chi trn yu hn chi di)
- Phn x gn c (+)
- Phn x bnh l ()
- Cm gic nng su bnh thng
Ca lm sng
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VS: 37.1, 125/90 (93/70 ng), 105, 18, sat 98%
Tnh to
Hp tc khi khm
Tim phi, bng bnh thng,
ng t 7mm, sp mi(ptosis)
Chn on v tr tn thng?
Cn nguyn ?
1. Sp mi
2. Dn ng t
3. Ni kh
4. Yu t chi
Presynaptic membrane ?
Postsynaptic membrane ?
Synaptic cleft ?
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Clostridium botulinum
Gram-positive obligate anaerobic bacillus
Spore-forming
Produces botulinum toxin
Heat sensitive as bacillus
Prefers low acid environment
Inglesby, T. The Washington Post
Wednesday, December 9, 1998; Page H01
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Botulism
Botulism is caused by Clostridium botulinum. There are three forms:
Food-borne botulism: from ingestion of contaminated food (e.g., tainted canned food)
Wound botulism: from a contaminated wound
Infantile botulism: from toxins produced by C. botulinum that colonize the intestine (e.g., history of honey ingestion or soil eating)
(There are eight types of C. botulinum with types A, B, and E being the most common types found in North America.)
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Lm sng Botulinum ?
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Pathogenesis
Wound Botulism from a heroin user.Jermann M, Hiersemenzel LP, Waespe W Drug-dependent patient with multiple
cutaneous abscesses and wound botulism
Schweiz Med Wochenschr 1999;129:1467
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Triu chng thn kinh
Diplopia / blurred vision
Ptosis
Slurred speech
Dysphagia / dry mouth
Muscle weakness
(Autonomic effects dry mouth, ileus, constipation,
urinary retention, dizziness, fatigue, dyspnea.)
Dysphagia, Diplopia, Dysarthria, Dry mouth the four
classic findings in botulism
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Chn on
Clinical diagnosis
Diagnostic tests help confirm
Toxin neutralization mouse bioassay
Serum, stool, or suspect foods
Infant botulism
C botulinum organism or toxin in feces
Electromyelography (EMG) demonstrates potentiation
Repetitive testing at 50 Hz should demonstrate potentiation from this supramaximal stimulation with jitter and blocking (bin ng v c ch)
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Chn on
Chn on xc nh Mt t 1-4 ngy
Kim nghim sinh hc trn chut (Mouse Bioassay) Type-specific antitoxin protects vs. toxin in sample
The assay can detect at minimal 0.03ng of toxin.
Cy (Culture) Fecal and gastric specimens cultured anaerobically
Results in 7 to 10 days
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Chn on
Lm g trc tin nu nghi ng
Immediately notify public health dept
Acquire therapeutic antitoxin
Send samples for diagnostic testing Serum, vomit, gastric aspirate, suspect food, stool
Collect serum before antitoxin given (ly huytthanh trc khi cho antitoxin)
If enema required, use sterile water(nu cn rarut, dng nc v trng)
Refrigerate samples and suspect foods
Get medication list to rule out anticholinesterases
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iu tr
Cholinesterase inhibitors are ineffective in botulism.
Treat with bivalent (A and B) or trivalent (A, B, and E) antitoxin, 20,000-40,000 units, 2-3 times per day.
For food-borne botulism, remove stomach and intestinal content, and administer antitoxin.
For wound botulism, administer antitoxin and penicillin
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PHN LOI
(Myasthenia Gravis Foundation of America clinical classification)
Class I: Any eye muscle weakness; possible ptosis; all other
muscle strength is normal
Class II: Mild weakness of other muscles; may have eye
muscle weakness of any severity
IIa: Predominantly limb or axial muscles or both
IIb: Predominantly oropharyngeal or respiratory muscles or
both
Nhm I
Nhm II
Nhm IIa
Nhm IIb
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PHN LOI
(Myasthenia Gravis Foundation of America clinical classification)
Class III: Moderate weakness of other muscles; may have
eye muscle weakness of any severity
IIIa: Predominantly limb or axial muscles or both
IIIb: Predominantly oropharyngeal or respiratory muscles or
both
Nhm III
Nhm IV
- Nhm IVa
- Nhm IVb
Nhm V
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PHN LOI
(Myasthenia Gravis Foundation of America clinical classification)
Class IV: Severe weakness of other muscles; may have
eye muscle weakness of any severity
IVa: Predominantly limb or axial muscles or both
IVb: Predominantly oropharyngeal or respiratory muscles
or both; use of feeding tube without intubation
Class V: Intubation needed to maintain airway.
Nhm III
Nhm IV
- Nhm IVa
- Nhm IVb
Nhm V
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Cc ngh cn lm sng chn on?
Is it MG Crisis?
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Edrophonium test
Tensilon test:
Sensitivity is 0.92 for ocular;
Sensitivity is 0.88 for generalized
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Edrophonium chloride
Inhibits acetylcholinesterase
Onset 30 seconds; duration 5-10 min
NEED A CLEAR OBJECTIVE ENDPOINT
Works best with complete ptosis
Compare to placebo (saline)
Prepare atropine
Give test dose 1-2 mg then up to 10 mg total
SFX:
salivation, sweating, nausea, abdo cramping, fasciculations; hypotension & bradycardia are rare (may be as low as 0.16%)
Sensitivity 71.5- 95%
Specificity: not clear but can be positive in many other conditions (even ALS or normal control)
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Ice pack test
If you have a droopy eyelid, your doctor may conduct an
ice pack test. In this test, a doctor places a bag filled
with ice on your eyelid. After two minutes, your doctor
removes the bag and analyzes your droopy eyelid for
signs of improvement. Doctors may conduct this test
instead of the edrophonium test.
Ice-pad test:
Best use for ocular MG
Sensitivity: 0.94 for ocular;
Sensitivity: 0.82 for generalized
Neuromuscular disorders 2006; 16: 459-67
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Ice test
2 min
ice
Ophthalmology 1999: 106:1282
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Blood analysis
1.Khng th khng AChR
2.Khng th khng MuSK
(1) 15% bnh nhn nhc c ton th khng pht hin khng th
khng AChR
(2) Khng th khng MuSK gp tr em, n gii tr tui, nhc c
ch yu c mt, hu hng, c v h hp
(3) C ch gy thiu st tip hp thn kinh c cha r
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AchR Abs trong nhc c?
Anti-AChR antibody bao nhiu phn trm trong nhc
c ton th v nhc c mt?
85-90% of generalized adult MG patients
50% of childhood MG
50-70% of Ocular MG
MUSK
>40% bnh nhn khng Ach Abs
Seronegative
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Muscle-specific receptor (MuSK)
Present in 50% of Ach-R Ab negative case
?Different pathogenesis with seropositive
Oculobulbar rather than pure ocular
Nil thymoma or even ?thymic atrophy
Respond less to cholinesterase inhibitor
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MuSK (muscle- specific kinase)
May be more difficult to treat and have permanent weaknessLess response to AchEIVery rare to have thymoma; effect of thymectomy =uncertainUsually NOT seen with pure ocular MG (1 case report)Usually NOT seen in patients with AChR positivity (1 case report)
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Cc khng th khc
1. Striational antibody (anti-striated muscle) Present in 30% of MG only, but 80% in those
thymoma-assocated MG
Useful marker of thymoma at age 20-50Semin Neurol 2004; 24:31
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in sinh l (Electrophysiological studies)
Repetitive nerve stimulation (RNS)
Motor nerve is stimulated 6-10 times under low
frequencies (2-3 Hz)
Positive result if decrement in compound
muscle action potential >10% within 4-5 stimuli
Post-activation exhaustion
Post-tetanus potentiation
Sensitivity: 50% if ocular
Sensitivity: 75% if generalized
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30 seconds post-ex Post-activation exhaustion
Normal MG
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Single-fiber electromyography (EMG)
Electromyography (EMG) measures the electrical
activity traveling between your brain and your muscle. It
involves inserting a fine wire electrode through your skin
and into a muscle.
In a single-fiber EMG, doctors test a single muscle fiber.
Most people find this test to be uncomfortable.
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Imaging scans
Bnh nhc c th mt
Khng th khng AChR thp v khng pht hin khong
50%, u tuyn hung rt t gp
Nhc c ton th vi khng th khng AChR(1) bnh nhc c khi pht sm thng gp n, lin
kt vi HLA-A1, B8, DR3. Tng sn tuyn c, khngth khng AChR cao, iu tr ct b tuyn c.
(2) Bnh nhc c khi pht tr, gia tng theo tui, yunhc c hu hng, chn on nhm x cng ct bn teoc, tai bin thn no, gp nam, tuyn c bnh thng.
(3) Bnh nhc c kt hp u tuyn c tui thng gp t30 n 60 tui,
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Cc thuc nh hng ln nhc c
Antibiotics: aminoglycosides; macrolides; fluoroquinolone; tetracyclines
Anesthetic: lidocaine; procaine; NMB
Cardiac: betablocker; CCB; procainamide
Steroids
Anticonvulsant: phenytoin; gabapentin
Others: Opiods; thyroxine; diuretics; anti-cholinergics; iodinated contrasts; URI
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iu tr
a. Acetylcholinesterase inhibitors
(anticholinesterase drugs)
b. Immunosuppressive/immunomodulating agents
c. Plasma exchange (PE)
d. Thymectomy
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1. Cholinesterase inhibitors as first-line therapy,
2. Thymectomy in patients with suspected thymoma
or those with moderate to severe weakness,
3. Immunosuppressive therapy.
(The patients limited response to cholinesterase inhibitors
and the severity of weakness with limitation of function led
to the performance of a thymectomy with histological
findings of thymic hyperplasia).
-
iu tr
4. Patients with ocular myasthenia only with Mestinon.
If patients are still symptomatic on Mestinon, treat with
prednisone in a slowly incrementing fashion
start-low, go-slow approach to prednisone treatment .
-
iu tr
3. Patients in myasthenic crisis (severe respiratory
distress or bulbar weakness) represent the opposite end of
the spectrum.
a. These patients should be admitted to an intensive care
unit (ICU) and followed closely, particularly for pulmonary
function.
b. When the forced vital capacity declines to less than 15
mL/kg or the negative inspiratory pressure is less than 30
cm H2O, consider elective intubation of the patient to
protect the airway, and begin mechanical ventilation.
Alternatively, bilevel positive airway pressure (BiPAP)
may be initiated and may alleviate the need for intubation
in patients who are not hypercapnic
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CHRONIC IMMUNOTHERAPIES
The second therapeutic modality in MG is the
administration of immunomodulating agents.
Glucocorticoids are widely used as well as other
agents, most commonly, azathioprine,
mycophenolate mofetil(cellcept), and cyclosporine.
The onset of action varies considerably, and this
plays a role in the choice of therapy
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CHRONIC IMMUNOTHERAPIES
The administration of moderate or high doses of
glucocorticoids leads to remission in about 30 percent of
patients and marked improvement in another 50 percent.
The onset of benefit generally begins within two to three
weeks.
However, a transient deterioration occurs in up to 50
percent of patients with MG when high-dose glucocorticoids
are started, usually occurring 5 to 10 days after the initiation
and lasting around five or six days.
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CHRONIC IMMUNOTHERAPIES
For this reason, glucocorticoids are most often started in
high doses only in hospitalized patients who are receiving
concurrent plasmapheresis or intravenous immune
globulin (IVIG) for myasthenic crisis (dng ng thi)
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Corticosteroids
Patients with moderate to severe generalized myasthenia
gravis receive prednisone. There are two treatment
strategies generally used when using prednisone in patients
with myasthenia gravis.
a) Aggressive high-dose daily steroids at the onset of
treatment.
b) A start-low and go-slow approach.
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Corticosteroids
c) The high-dose daily regimen leads to a much quicker
improvement of strength but there is about a 10% to 15%
chance of early worsening.
(This transient worsening is typically not seen in the start-low
and go slow approach, but it generally takes longer for patients
to improve)
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Corticosteroids:liu cao ngay t u
Ch nh: BN nhc c ton th t trung bnh n nng
Initiate treatment with prednisone 1.0 to 1.5 mg/kg/d
(up to 100 mg) for 2 weeks and then switch to alternate
day prednisone (e.g., 100 mg every other day) (iu tr
cch ngy).
If patients do not tolerate alternate day prednisone,
give them an equivalent dose of daily prednisone (e.g.,
50 mg daily).
-
Corticosteroids
Maintain the patients on this high dose of
prednisone until their strength has normalized or there
is a clear plateau in improvement.
Subsequently, slowly taper prednisone by 5 mg
every 2 to 3 weeks, down to 20 mg every other day.
At this point, taper even more slowly, by 2 mg every
4 weeks.
It is usually at these low doses that patients may
have a relapse.
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Corticosteroids
Most patients will require some amount of
immunosuppressive medication, to find the lowest
doses necessary to maintain their strength.
-
Corticosteroids: iu tr kt hp
The addition of other immunosuppressive agents (e.g.,
azathioprine) may have a prednisone-sparing effect.
Many authorities initiate treatment with one of these
agents at the same time that prednisone is started in the
hope that the prednisone may be tapered quickly and to a
lower dose than could be achieved by prednisone
monotherapy.
-
Corticosteroids: iu tr kt hp
Khi u iu tr thuc nhm 2 km prednisone
- postmenopausal women,
- patients with known osteoporosis,
- or those with increased risk of adverse reaction to
corticosteroids (e.g., patients with diabetes mellitus).
-
Corticosteroids
About 5% to 15% of patients experience a varying
degree of initial worsening after they are started on high
doses of steroids.
If patients have moderate weakness, it is reasonable
to hospitalize them for the first week after initiating
treatment with high-dose corticosteroids.
-
Corticosteroids: liu thptng dn
Do gia tng nguy c trm trng thm khi dng liu cao,
khuyn co khi u liu thp v tng dn
(start-low and go-slow).
Patients are started at a dose of 15 to 20 mg/d, and
the dose is slowly increased by 5 mg every 2 to 4 days
or so until definite improvement is noted.
Unfortunately, improvement takes much longer with
this approach and is thus not very useful in patients with
severe weakness.
-
Corticosteroids
Patients with mild generalized disease not controlled
with Mestinon or patients with ocular myasthenia.
However, recent mycophenolate mofetil studies
suggest that mild or moderate myasthenia in many
patients may be controlled by taking prednisone 20
mg daily (Muscle Study Group, 2008).
gradually switching over to this start-low, go-slow
approach in many myasthenic patients, except those
with more severe disease who need a quicker response.
-
Corticosteroids: bin chng
There are a multitude of potentially serious side
effects to the chronic administration of corticosteroids
(e.g., risk of infection, diabetes mellitus,
hypertension, glaucoma, osteoporosis, and aseptic
necrosis of the joints
-
Corticosteroids
Steroid myopathy versus relapse of myasthenia
gravis: High-dose, long-term steroids and lack of
physical activity can cause type 2 muscle fiber atrophy
with proximal muscle weakness.
This needs to be distinguished from weakness due
to relapse of the myasthenia.
-
Corticosteroids
Patients who become weaker during prednisone
tapering and have worsening of their decrement repetitive
stimulation(gim kch thch lp li) or increasing jitter and
blocking (chp chn hay nghn) on single-fiber EMG are
more likely experiencing a flare of the myasthenia( nhc
c bng ln)
In contrast, patients with continued high doses of
corticosteroids, normal repetitive stimulation and single-
fiber EMG results, and other evidence of steroid toxicity
(i.e., cushingoid appearance) may have type 2 muscle
fiber atrophy and could benefit from physical therapy and
reducing the dose of steroids..
Theo di in sinh l khi iu tr
-
iu tr min dch nhanh
(rapid immunotherapy)
Myasthenic crisis
Tin phu thymectomy hay phu thut khc
Khi bt cu tc dng chm hn iu tr min dch
Duy tr chu k thuyn gim bn nhc c khng
kim sot tt mc d dng thuc sa i min dch
ko di
iu tr trong cc tnh hung sau y:
-
iu tr bt cu (Bridge therapy)
Cho nhng bnh nhn c bit trnh dng
glucocorticoid (kim sot tiu ng km)
Thng dng hng thng IVIG cho n khi
iu tr min dch bt u c tc dng
-
iu tr bt cu (Bridge therapy)
Dng IVIG iu tr bt cu c th gip ch bnh nhn
nh v trung bnh, v lm tc dng nhanh hn cc
thuc sa i min dch lu di (chronic
immunomodulating) nh mycophenolate mofetil hay
cyclosporine
Kh khn hn trong iu tr bt cu vi
azathioprine bi v azathioprine c th tr hon bt
u tc dng di hn
-
iu tr bt cu (Bridge therapy)
Plasmapheresis thay phin hng thng, nhng
do tr ngi ng tnh mch khi dng thng
xuyn
Plasmapheresis trong thc hnh t dng iu
tr bt cu hn IVIG.
-
Khi no iu tr phu thut ?
-
Ch nh ct tuyn c (thymectomy)
Song song iu tr triu chng, iu tr c ch min dch
trong MG. Nghin cu iu tr phu thut do ch li lu di
Bnh nhn c thymoma r c ch nh phu thut. Tuy
nhin ch nh phu thut cho bnh nhn khng c u
(nonthymomatous tissue ) th t chc chn
-
Ch nh ct tuyn c (thymectomy)
Cho bnh nhn tin phu thut hnh ty hay c triu
chng h hp. Tr hon phu thut cho n khi kim sot
tt
iu tr IVIG hay thay huyt tng mt hay hai tun
trc phu thut
Nu c triu chng h hp hay hnh ty. Thi gian
phu thut hay k thut no thch hp vn cn bn ci
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