CA LM SNG NHC C

PGS.TSCao Phi Phong

Ngy 14/10/2013

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

- 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.

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.

- 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

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.

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.

- 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

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

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.

TNG QUAN V NHC C

Chn on

- Chn on v tr

- Chn on phn bit

Cn lm sng

iu tr

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

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)

(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 )

(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.

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

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?

Lambert-Eaton Myasthenic Syndrome

2/3 ca l tin ung th (paraneoplastic) nam

1/3 ca l t min (autoimmune) n

Triu chng lm sng Lambert-Eaton Myasthenic Syndrome?

+++

+++

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.

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.

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

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.

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.

- 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

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

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 ?

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

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.)

Lm sng Botulinum ?

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

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

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)

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

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

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

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

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

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

Cc ngh cn lm sng chn on?

Is it MG Crisis?

Edrophonium test

Tensilon test:

Sensitivity is 0.92 for ocular;

Sensitivity is 0.88 for generalized

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)

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

Ice test

2 min

ice

Ophthalmology 1999: 106:1282

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

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

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

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)

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

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

30 seconds post-ex Post-activation exhaustion

Normal MG

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.

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,

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

iu tr

a. Acetylcholinesterase inhibitors

(anticholinesterase drugs)

b. Immunosuppressive/immunomodulating agents

c. Plasma exchange (PE)

d. Thymectomy

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

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

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.

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)

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.

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)

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.

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