Home Page Flashcards MH & anesthesia for pt with neuromuscular disease - Flashcards

MH & anesthesia for pt with neuromuscular disease – Flashcards

Flashcard maker : Robert May

• Chronic disease of the neuromuscular junction
• Most prevalent neuromuscular disorder; Autoimmune disease

Myasthenia Gravis

Myasthenia has an abrupt or insidious onset

True

Affects Women: most often between 30-40 years of age
& Men: most often between 50-60 years of age

Myasthenia Gravis

Incidence: 3-30 people:1,000,000

postsynaptic Ach

Weakness is due to autoimmune destruction, blockage, or
inactivation of ________________ receptors at the NM junction,

postsynaptic

↓ed number of receptors & loss of folds on _________________membrane

Myasthenia Gravis is manifested by ↑ing skeletal muscle weakness, fatigability on effort, & at least partial restoration of function after rest

true

MG course includes fluctuating, periods of exacerbation & remission

true

↓ in the number of functional postsynaptic ACh receptors
• caused by immune-mediated destruction, blockage, or inactivation

Myasthenia Gravis

Mouth, eyes, pharynx, proximal limb, & shoulder muscles
most commonly affected with

Myasthenia Gravis

Myasthenis Gravis is associated with Extraocular muscle weakness ptosis & diplopia

true

Laryngeal & pharyngeal muscle weakness, dysarthria,
difficulty swallowing, problems clearing secretions, &
pulmonary aspiration are associated with

Myasthenia Gravis

Severe disease of myasthenia gravis has

respiratory muscle involvement

What accounts for much of the morbidity & mortality of myasthenia gravis

swallowing and respiratory dysfunction

With myasthenia gravis muscle strength deteriorate with rest, but improve with repeated effort

False

muscle strength improves with rest, but deteriorates rapidly with repeated effort in myasthenia gravis

true

enhanced and repetitive effort with mysathenia gravis will

enhance weakness

What is the treatment of Myasthenia Gravis

Anticholinesterase drugs (Pyridostigmine)
Corticosteroids or other immunosuppressants
Plasmapheresis – washes antibodies out of plasma
IV immunolgobulin (IVIg)
Thymectomy (remove the thymus gland)

How does Anticholinesterase drugs (Pyridostigmine) work

By inhibiting hydrolysis of Ach by acetylcholinesterase,
these drugs ↑ the amount of Ach at the NM junction

how does Corticosteroids or other immunosuppressants help myasthenia gravis

Corticosteroids- 80% remission rate
Azathioprine (Imuran) & cyclosporine works by suppressing immune system

what occurs with Under-dosing of an anticholinesterase

Myasthenic Crisis

Severe exacerbation of myasthenic lead to s/s

respiratory distress

Over-medicating of an anticholinesterase

Cholinergic Crisis

Produces a surplus of ACh at the NMJ, resulting in a depolarizing-like block & augmenting skeletal muscle weakness

Cholinergic Crisis

what are the Muscarinic side effects present in cholinergic crisis

Abdominal cramping, diarrhea, salivation, bradycardia, respiratory distress, miosis

what is Edrophonium Test used for?

To differentiate a myasthenic crisis from a cholinergic crisis

If you have increased strength after edrophonium test what does that diagnose?

myasthenic crisis

Increased weakness after edrophonium test mean patient is having a

cholinergic crisis

After up to 10mg IV edrophonium (Enlon, Tensilon) (a short-acting anticholinesterase)

How do you perform a enlon, tensilon, edrophonium test?

what is the Preferred anesthetic techniques for Myasthenia gravis?

Regional & Local

these patients are 2-3 times more resistant to succinylcholine

untreated myasthenia gravis patient

these patients exhibit normal or prolonged response to succinylcholine

treated myasthenia gravis patient

these patients are Extraordinarily sensitive to NDMR

myasthenia gravis

Overtreatment with NDMR reversal AChE inhibitors can cause cholinergic crisis & aggravate muscle weakness

true

Presence of cholinesterase inhibitors may potentiate vagal responses in these patients

mysathenia gravis

Respiratory depressant effects of sedatives, narcotics, & volatile agents may be exaggerated with these patients

myasthenia gravis

Relaxant effects of volatile agent may be sufficient for intubation in myasthenia gravis patient

true

why does a treated myasthenia gravis patient have a prolong duration of succinylcholine &
ester-type local anesthetics

because the anticholinesterase drugs these patients have been on for therapy also inhibit plasma cholinesterase

If you have a untreated myasthenia gravis patient for RSI, how will you dose the succinylcholine

increase succinylcholine dose to 1.5-2 mg/kg

Even a defasciculating dose can lead to nearly complete paralysis in these patients

myasthenia gravis

If NDMR needed for myasthenia gravis patient, you should use very small doses of short NDMR & monitor closely

true

why should reversal of NDMR with AChE inhibitor performed cautiously in myasthenia gravis patients

because overtreatment can lead to cholinergic crisis & aggravate muscle weakness

Should you avoid reversal by careful titration of NDMR to allow complete spontaneous recovery in myasthenia gravis patients

Yes

When should the patient with myasthenia gravis be extubated

when complete, sustained return of strength

Inform myasthenia gravis patient of risk of postop intubation & ventilation

Strength may appear to be adequate postop, but may deteriorate a few hours later

is a rare, autoimmune disease; mostly in men 50-70 years old; often seen in patients with small-cell lung Ca

Myasthenic Syndrome or Eaton-Lambert syndrome or Lambert-Eaton Myasthenic Syndrome (LEMS)

PRESYNAPTIC

LEMS is a disorder of neuromuscular transmission caused by antibodies that impair the _____________ release of ACh.

LEMS lambert-eaton myasthenic syndrome

The release of ACh is regulated by the influx of calcium through voltage-gated channels (VGCC) in nerve terminals. Pathogenic autoantibodies directed against these VGCC are thought to ↓ calcium influx & inhibit ACh release in this disease

Number & quality of postjunctional ACh receptors unaltered; end-plate sensitivity normal in this disease

LEMS

Characterized by muscle weakness, fatigue, hyporeflexia, & proximal limb muscle aches; diaphragm & other respiratory muscles involved

LEMS

There is Autonomic nervous system dysfunction with LEMS

True

What are the Autonomic nervous system dysfunction that occur with LEMS

Impaired gastric motility, orthostatic hypotension, urinary retention

weakness improves briefly with effort & is unaffected by
anticholinesterases

LEMS

What is the treatment for LEMS

No Cure; 3,4-Diaminopyridine (promotes presynaptic Ca++ influx &
↑s amount of ACh released; plasmapheresis; corticosteroids; IV immunoglobulin (IVIg); immunosuppressants

NDMR Reversal with anticholinesterase may be used with these patients

LEMS

Extremely sensitive to NDMR & succinylcholine

LEMS

Inhalation agents alone may be adequate for intubation in these patients

LEMS lambert eaton myasthenic and MG myasthenia gravis

Symptoms improve with repetitive movement

LEMS

Symptoms worsen with repetitive movements

These patients have decreased reflexes

LEMS

These patients have normal reflexes

LEMS is associated with thymoma

false; MG

MG is associated with oat cell lung cancer/small cell cancer

false

LEMS patients have ptosis and diplopia

false

LEMS usually no ptosis & usually no diplopia

true

has antibodies to POST synaptic acetylcholine receptors

myasthenia gravis

has antibodies to PRE synaptic acethylcholine receptors

LEMS

Chronic, progressive, inflammatory disease of the CNS

(MS) multiple sclerosis

The myelin sheath around the axon is damaged & destroyed with inflammation & scarring

Who does MS affect

• Affects: women 2x’s > men
• Women 20-40 yrs of age
• Rare in children or elderly

What are some causes of MS

Autoimmune – B & T lymphocytes & macrophages cells attack myelin
• ? – Viruses may play a role
• Not hereditary, but hereditary predisposition

Physical or mental stress is a risk factor for exacebation of MS

True

Physical or mental stress
• Hormonal disorders (e.g. during menopause)
• Infections (e.g. influenza)
• Desensitization in cases of allergy (e.g. hay fever)
• Immunostimulatory drugs

Risk factors responsible for acute attacks in MS patients

Acute exacerbations characterized by occurrence of new symptoms or recurrence of symptoms that had disappeared, persisting for > 24 hrs.

In many cases, symptoms develop for a few days & remain constant for 3-4 wks before declining slowly for 1 month.

There is a cure for MS

No cure; treatments to relieve symptoms, slow disease
progression, & prevent relapses

What are long term treatments of MS

Interferons: proteins synthesized by the body that are involved in
intercellular communication & play important role in immune system.
They have an anti-inflammatory activity, & are used to stabilize or
slow progression of the disease.
• Immunoglobulins (IVIg): proteins in blood, as antibodies involved in
immune reactions; effectiveness not yet established
• Glatiramer acetate: mostly in patients with mild symptoms
• Immunosuppressants

Acute exacerbation of MS is treated with Anti-inflammatory drugs (cortisone, glucocorticoids)

True

Stress of surgery will exacerbate symptoms of MS

False

The complications of surgery (infection & fever) does not exacerbate symptoms

False

Impact of surgery & anesthesia on MS related to severity of the disease process

True

Risk of elective surgery in presence of MS is same as in the general population for young & otherwise healthy adults, & in these patients, a diagnosis of MS is not an absolute contraindication for surgery.

True

MS is an absolute contraindication for elective surgery

False

Considerations for patients who are severely disabled or who have
respiratory problems as a result of MS

In patients with respiratory problems, the nature of the surgery, including the potential need for prolonged respiratory support & mechanical ventilation, should be considered. Patients should be informed in advance of these possibilities so they can decide whether to proceed with surgery.

An ↑ in body temperature of as little as 1°C can cause exacerbation of MS symptoms.

true

Increase of temperature in MS pt can lead to what?

↑s in temperature block the conduction of demyelinated nerves, leading to deterioration of nerve tissue at the sites of demyelination,& are more likely than the drugs used for anesthesia to cause postop exacerbation of symptoms of MS.

What is more likely than the drugs used for anesthesia to cause postop exacerbation of symptoms of MS.

An increase in temperature

GA & Regional have been used in MS pts

true

No unique interactions between MS & drugs used for GA, & no evidence supports recommendations for specific inhaled or IV anesthetic drugs

MS and anesthesia

There is a possibility of exaggerated K+ release after succinylcholine with who

Esp. in severely debilitated patients with neurological deficits & muscle atrophy

This drug may be safe in patients in remission or with mild symptoms of MS

succinylcholine

Possibility of prolonged responses & resistance to effects of NDMR in MS patients

True

Prolonged responses to NDMR consistent with existing degree of skeletal muscle weakness & ↓s in skeletal muscle mass in this disease

Why are MS patients resistant to effect of NDMR

Resistance to effects of NDMR also is possible & has been reported, possibly related to proliferation of extrajunctional cholinergic receptors in upper motor neuron lesions.

Duchenne’s Muscular Dystrophy develop proximal muscle weakness (pelvis & shoulders), manifested first as a gait disturbance

True

• Affects 1:3500 males; evident at 3-5 years

Duchenne’s Muscular Dystrophy

Most common & severe form of MD (inherited)

Duchenne’s Muscular Dystrophy

• Fibrous & fatty infiltration of muscles
• lead to progressive degeneration & necrosis of muscle fibers
• Affects skeletal, cardiac, & smooth muscle
• See enlargement of calf muscles

DMD

Duchenne’s Muscular Dystrophy affects skeletal, cardiac, & smooth muscle

True

You will see enlargement of calf muscles in LEMS

false, Duchenne’s Muscular Dystrophy

Progressive weakness & contractures lead to kyphoscoliosis in this disease

Duchenne’s Muscular Dystrophy

As Duchenne’s Muscular Dysrophy becomes severe,it leads to degeneration of

respiratory muscles
(ineffective cough, impaired swallowing,
inability to mobilize secretions),
cardiomyopathy (at 10-20 yrs), mitral
regurgitation, ventricular dysrhythmias

Duchenne’s Muscular Dystrophy is diagnosis is confirmed by muscle biopsy

true

By age 12, most confined to wheelchair

Duchenne’s Muscular Dystrophy

Death in early adulthood due to progressive
cardiomyopathy or pneumonia

These patients need Surgical steroid coverage (if on steroids)

Duchenne’s Muscular Dystrophy

Compromised cardiac & respiratory conditions may be masked by limited activity

Duchenne’s Muscular Dystrophy

Why do you omit/minimize preop sedation & use smallest possible amounts of anesthetics in DMD patients

Because these patients are VERY sensitive to respiratory depressant effects of opioids, sedatives, GA agents

Delayed pulmonary insufficiency, as late as 36 hours postop can occur in DMD patients

true

Since DMD patients are sensitive to myocardial depressant effects of inhalation agents, sedatives, &
narcotics what induction agent can be used successfully?

Ketamine

When you see sudden hypotension & tachycardia during GA in DMD patients, this can signal

heart failure

DMD patients are on aspiration prophylaxis measures d/t

Delayed gastric emptying + weak laryngeal reflexes

Judicious used of fluids with these patients

DMD, because when you see sudden hypotension & tachycardia during GA can signal heart failure in these patients

Succinylcholine is contraindicated in Duchenne’s Muscular Dystrophy

true

Why is Succinylcholine is contraindicated in Duchenne’s Muscular Dystrophy

because it would lead to profound hyperkalemia
(extensive trt: hyperventilation, CaCl, NaHCO3, glucose/insulin)
which would lead to ventricular fibrillation & intractable cardiac arrest

Local or Regional anesthesia preferred; if GA, use TIVA in DMD patients

true

DMD genetically associated with MH & ↑ed MH risk

False

Uncommon, life-threatening, hypermetabolic disorder of skeletal muscle (not cardiac or smooth muscle) triggered in susceptible individuals

Malignant Hyperthermia

MH is 2.5 to 4.5 times more common in males than females

True

Incidence: between 1:5,000 to 1:50,000 general anesthetics. Highest in young people (mean of 18.3 years)

Malignant Hyperthermia

Inherited, autosomal dominant; 1st formal case report in 1960’s

Malignant Hyperthermia

High-incidence US areas for MH

Wisconsin, Nebraska, West Virginia, Michigan

MH-susceptible patient may be anesthetized multiple times before an MH event

True

What is the mortality rate of MH

< 5%, depending on availability of Dantrolene & proper diagnosis & treatment

MH is a pharmacogenetic disease

true

What is a pharmacogenetic disease

Susceptible patients possess a genetic predisposition for the development of this disease, which is not manifested until they are exposed to triggering agents

Gene for MH is located on chromosome 19, which is also the genetic coding site for the Ca+ release channel of SKELETAL muscle sarcoplasmic reticulum______________________receptor

(ryanodine receptor, RYR1)

Some MH patients have a normal ryanodine receptor & abnormalities in 2nd messengers & modulators of calcium release, such as fatty acids & phosphatidylinositol, may be
present.

True

An abnormal sodium channel in skeletal muscle may also play a role

True

Abnormal cell permeability to Ca+ in SKELETAL muscle

leads to severe hypermetabolism in MH

(Ca+ “trapped” in intracellular space causes rigidity) (Ca+ is “stuck” inside cells)

What happens with Calcium in MH

Enhanced calcium release from sarcoplasmic reticulum leads to uncontrolled increase in extracellular calcium in skeletal muscle in MH

False, uncontrolled ↑ in INTRAcellular calcium in skeletal muscle

This sudden release of calcium from sarcoplasmic reticulum removes the inhibition of troponin in MH and causes

intense muscle contraction

In MH there is ↑ed muscle metabolism (by 2-3 times)

True, Energy-dependent re-uptake mechanisms attempt to remove excess calcium

In MH ↑ed O2 consumption, ↑ed CO2 production, ↑ed heat production, depletion of ATP stores, generation of lactic acid (anaerobic metabolism) are d/t

Accelerated cellular processes

Acidosis, hyperthermia, & ATP depletion lead to

sarcolemma/muscle membrane destruction

marked egress (exit) of potassium, myoglobin, & creatinine kinase from muscle cells to the extracellular fluid lead to

hyperkalemia, myoglobinuria, ↑ed CPK

Hypermetabolic state rapidly progresses and lead to

markedly ↑ing O2 consumption & CO2 production & producing severe lactic acidosis & hyperthermia

These may occur in as little as 15
minutes

• ↑ed sympathetic tone, acidosis, & hyperkalemia all predispose
patients to V-Fib & sudden death,

Family History of MH

MH; Unexplained anesthetic complications or mortality
• Muscle rigidity/stiffness or high fever under anesthesia
• High temperature or death during exercise

• Muscle rigidity/stiffness/cramping (unrelated to exercise)
• Dark or “coca-cola” colored urine after surgery or exercise
• Fevers of undetermined origin (esp. after surgery or other stressors)

Patient history could be susceptible to MH

These patient are a risk for MH

• Intolerance to caffeine (coffee, tea, sodas)
• Chronic subluxation of joints, hypermobility of joints
• Curvature of spinal column requiring treatment
• Strabismus
• Burkitt lymphoma
• Osteogenesis imperfecta
• Myelomeningocele

RECENT: NO RISK for MH over general population:

• Duchenne Muscular Dystrophy, Becker muscular dystrophy, neuroleptic malignant syndrome, myotonia congenita, myotonic dystrophy

These patient have STRONG clinical & /or genetic link to MH

1) Central core disease
2) King Denborough syndrome
3) Multiminicore disease

Amide local anesthetics are MH triggers

False

Phenothiazines/tricyclic antidepressants are MH trigger

false

Nitrous oxide IS NOT an MH trigger

True

Depolarizing muscle relaxants (succinylcholine) and ALL Volatile Inhaled Anesthetics are MH triggers

true

Heat stroke is an MH trigger

true

Strenuous exercise is not an MH trigger

False

Emotional stress, caffeine, infections are MH triggers

true

Onset of MH can occur in PACU, usually one hour after GA

true

MH can occur immediately after induction or several hours into surgery

true

Clinical features not uniform & time between initial signs & fulminant MH is variable

true

The average time between onset of 1st adverse sign & dantrolene administration is 35 minutes

true

The FIRST sign of MH is

• Hypercarbia – 1st sign (abrupt or gradual onset)
• ↑↑↑ ETCO2 (out of proportion to minute ventilation) (> 55 mmHg)

clinical manifestations of MH

• Hypercarbia
Unexplained tachycardia (Reflects release of epinephrine & norepinephrine)
• Rapid ventricular arrhythmias (bigeminy, multifocal PVCs, V-tach)
• ↓ed SaO2 (Cyanosis)
• Muscle rigidity (75% of cases) (Masseter muscles of jaw (& body)
• Labile BP (• Early – Hypertension • Late – Hypotension)
• Tachypnea (• Mixed acidosis (respiratory & metabolic)
• Skin signs vary (• Flushing due to vasodilation • Mottling/blanching due to vasoconstriction)

In MH muscle rigidity will be seen in

the masseter muscles of jaw & body

Muscle rigidity occurs in 75% of MH cases

true

Fever is a early sign of MH

false

Fever in MH

↑s 1-2 C every 5 minutes
• Reaches as high as 46 C (averages 39.3 C, or 102.7° F)

What will you see in arterial and central venous blood analysis in MH

Arterial hypoxemia
• Respiratory & Metabolic acidosis
• pH 60 mmHg)
• Base excess more negative than -8 mEq/L
• Marked central venous O2 desaturation

What happens to potassium levels with MH

Hyperkalemia – early (> 6 mEq/L) & Drops rapidly after normothermia returns

How do you treat hyperkalemia in MH

• Hyperventilation
• Insulin & glucose
• Diuresis (mannitol & lasix)

What are some clinical manifestations of MH that you will see in your breathing circuit

Rapid exhaustion of soda lime & heat
• Excessive breathing circuit heating

Transaminases & CPK will peak levels 12-24 hours after acute episode

true

Transaminases & CPK -plasma & urine myoglobin are markedly decreased in MH

False

what are the 12 TERMINAL signs of MH

• Cardiac arrest
• Myoglobinuric (acute) renal failure
• Consumptive coagulopathy (DIC)
• Hepatic dysfunction
• Pulmonary edema
• Cerebral edema
• Fixed pupils
• Areflexia
• Blindness, Seizures, Coma, Paralysis

DIFFERENTIAL DIAGNOSES of MH

• Insufficient anesthetic depth
• Hypoxia
• Neuroleptic malignant syndrome
• Propofol infusion syndrome
• Thyrotoxicosis (thyroid storm)
• Pheochromocytoma
• Sepsis

what 2 differential diagnosis of MH can also be treated with Dantrolene

neuroleptic malignant syndome & Thyrotoxicosis

How do you treat patient with positive family or personal history of MH

• Stress free atmosphere – preop med as needed
• AVOID volatile inhaled agents, DMR, Ca+, K+
• Prepare anesthesia machine
• Flush with O2 at 10 L/min x 20 min (old machines) up to 150 min (new machines)
• Change CO2 absorbent
• Remove vaporizers
• Disposable circuit
• MH cart; ice & 3000 mL cold IV solution readily available

What is a good technique to use in MH patients

Local
MAC
Regional when possible(no protection from stress MH)
GA- narcotics, barbs, NDMR, propofol,(TIVA)

Important monitoring

***Capnography***
• First line monitor; CO2 ↑s – 1st sign
•Pulse oximeter
•ECG – tachycardia, ventricular arrhythmias
•BP
• Core temp
• Last line monitor; Temp ↑s well into crisis

What is the treatment of MH CRISIS

• STOP anesthesia (volatile agent & succinylcholine) &
surgery immediately; Call for HELP
• HYPERVENTILATE with 100% O2 at high flows (10 L/min)
• DANTROLENE: • 2.5 mg/kg IV Q 5-10 minutes until symptoms abate • Typically use 2-5 mg/kg
• Rarely need > 10 mg/kg; if > 20 mg/kg given, re-evaluate diagnosis
• Titrate to: ↓ HR, muscle rigidity relaxation, ↓ in temperature
• Give in largest vein possible (phelbitis in small veins)
• Change breathing circuit & anesthesia machine
• CORRECTt severe metabolic ACIDosis with NaHCO3 1-2 mEq/kg IV, based on arterial pH & base deficit

list active cooling with cold solutions:

• NG lavage with iced saline
• Wound irrigation
• Foley catheter
• Cold IVF: NS; AVOID LR
• Surface cooling (hypothermia blanket, ice packs to groin, axilla, neck)

In MH crisis cooling measures are stopped when body temp ↓s to 38 C

true

what are the 3 treatments for hyperkalemia in MH crisis

• Hyperventilation
• Bicarbonate
• Insulin & glucose

Ventricular arrhythmias: Often respond to treatment of acidosis, but if not, give standard antiarrhythmics in MH crisis

true

You can give calcium channel blockers with dantrolene in MH crisis

false

How do you maintain UOP > 2 mL/kg/hr in MH crisis

• Hydration; Lasix (0.5-1.0 mg/kg); Mannitol (0.25 g/kg, as needed)

What labs are drawn during MH crisis

Electrolytes (serum K+, Ca+), ABGs, glucose Q 15 min. until stable
• CK, Coagulation profile, liver enzymes, blood & urine myoglobin

Dantrolene works at NMJ

false

Dantrolene works by

• Skeletal muscle relaxation/muscle weakness (does not work at NMJ) • ↓s amount of Ca+ released from sarcoplasmic reticulum
• Binds with ryanodine receptor & inhibits calcium release

Mix each vial of Dantrolene with 60 mL sterile water

true

Dantrolene should be protected from light

true

1 vial of dantrolene = 20mg

true

2.5 mg/kg IV every 5-10 minutes

Dantrolene dose

Dantrolene Dosing for a 70kg patient

175 mg IV every 5-10 minutes
• 9 vials every 5-10 minutes
• Repeat as needed until symptoms are controlled (rarely need > 10 mg/kg)
• Up to 700 mg (35 vials)
• Typically 2-5 mg/kg
• Typically use 140-350mg (7-17.5 vials)

Dantrolene cost

• Dantrolene shelf life: 30 months
• Cost: about $3,000 for 36 vial supply
• Should NOT be shared between facilities

What is the post op management if NO MH episode (in MH susceptible patient)

• Close PACU observation for at least 2.5 hours; then may D/C home

What is the post op management if MH episode (in MH susceptible patient)

• ICU x at least 36 hours
• 12-lead ECG for changes
• CPK, K+ (follow until normal)
• Temperature
• Instability may persist for days
• UOP > 1 mL/kg/hr
• Renal failure due to myoglobinuria
• Fluid redistribution (4mg/kg/24 hrs x 48 hrs)
• IV Dantrolene half-life: 6 hours
• Dantrolene 1mg/kg IV every 4-6 hrs x 24-48 hrs
• MH can recur within 24 hours (in 20-25% of cases)
• Mean time: 13 hours
• Most likely: muscular body type; > 150 minutes from induction to MH reaction
• Monitor liver function
• 0.1 – 0.2% incidence of hepatitis

what is the definitive diagnosis of MH

Biopsy of vastus muscle of thigh (MAC, SAB)

How is biopsy of vastus muscle performed

Skeletal muscle specimen subjected to isometric contracture
testing under the influence of caffeine or halothane, or both
(caffeine halothane contracture test, CHCT)
• Measure contractile response of muscle to caffeine, halothane, or both
• Caffeine & halothane produce exaggerated contracture of skeletal
muscle from a patient susceptible to MH
• Test is available at 4 medical centers in North America
• Patient must travel to testing site
• Patients who have survived an MH episode are considered MHS
• CHCT is for family members of MHS patient or for patients who have
had a suspicious but undiagnosed reaction to anesthesia

What other alternative testing for MH

• Alternative Testing: Genetic testing & DNA-based mutation
analysis
• Only about 25% of people at risk for MH are detected by genetic tests

MH & anesthesia for pt with neuromuscular disease – Flashcards

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