Malignant hyperthermia is a rare, potentially life-threatening condition triggered by certain anesthetic agents. It causes a hypermetabolic response in skeletal muscle that can rapidly increase body temperature, heart rate, and carbon dioxide levels. Left untreated, it can lead to muscle breakdown, acidosis, and death. The document discusses the definition, causes, signs and symptoms, diagnosis through muscle biopsy testing, genetic basis involving mutations of the ryanodine receptor gene, and treatment of malignant hyperthermia.

1. Malignant
Hyperthermia
DR. RAVINDRA JHA
PGT 1st YEAR
KISHANGUNJ

2. MALIGNANT HYPERTHERMIA
 Defnition : An uncommon pharmacogenetic
disorder of skeletal muscle characterised by
marked skeletal muscle hypermetabolism in
response to some anaesthetic triggers
 First clinical case published in 1960 in LANCET, by
Denborough and Lovell.
 Association with porcine stress syndrome and
malignant hyperthermia described in early 1970
 2001: Punj et al (IRCH): Ist case of MH in India
 Autosomal dominant inheritance

3. EPIDEMIOLOGY
 Incidence : 1:50,000 in adults , 1:15,000 in children . It varies with
triggering agent . More prevalent in certain areas of a North
America.
 Common in young children, but may occur in all age
groups from infants to 70 yrs of age.
 Male > female.
 More common in pts with large ms bulk and general
anaesthesia after recent exercise.
 More frequent after ENT squint or dental operation due
to related short anaesthetic procedures
 Susceptible persons may have history of previous
uneventful anaesthesia even with triggering agent

4. Introduction
 Malignant Hyperthermia
 Pharmaco-genetic disorder
 In Genetically Susceptible.
 On exposure
 Volatile inhalational agents & Sch.
 Abnormal ↑↑ intracellular Ca²⁺
 Rapid ↑
 Body Temperature: Hyperthermia
 Skeletal muscle activity
 Rhabdomyolysis and metabolic acidosis
→ Death
Malignant

5. Clinical picture
 Clinical presentation is highly variable and it depends
on species, breed, genetic make up, and triggering
agents
 Time of onset : unpredictable, varying from within
minutes to several hours of induction; it may even
occur in post operative period in the recovery room
 The most potent triggering agent appear to be
induction of anaesthesia with halothane followed by
administration of succnylcholine. The symptoms
appear almost immediately
 Presentation is gradual and delayed in onset after
the induction with new halogenated anaesthetic
agents

7. Signs and symptoms
 Tachycardia : one of the earliest but a non specific
sign
 Tachypnea : in spontaneously ventilating patients.
 Increased sweating
 Increased body temperature : late and serious
sign of MH and may not be present at the time of
the diagnosis..
 During fulminant acute MH, body temperature
may increase at a rate of 1.8–3.6°F (1–2°C)
every 5 minutes
 Cyanosis, flushing or blanching of skin. Cola
coloured urine
 masseter spasm or generalised muscle rigidity
or both

8. Signs and symptoms
 Capnogram
Gradually increasing EtCO2 not related to other
possible causes.
 The earliest , the most sensitive and specific sign of
M.H
 Excessive heating and rapid exhaustion of CO2
absorber.
 Other possible causes:
 Hypoventilation
 Other causes of Hyper metabolism
Partial airway obstruction Absorption of
CO2 from exogenous source
 equipment malfunction.

9. Biochemical parameters..
– Respiratory with or without metabolic acidosis.
– Hypercarbia
– Hyperkalemia
– Hypercalcemia
– Hyperphosphatemia.
– Lacticacidemia.
– Myoglobinuria.
– Increase in creatinine kinase: neither a constant
feature nor signifies increase muscle metabolism
in intra operative period
– Abnormal coagulation tests

10. CLINICAL FEATURES
1.Inappropriate
tachycardia
2.Cardiac
arrhythmias
(Ventricularectopics
&Bigemini).
3.Unstabele arterial
Pressure.
1.Masster Spasm
with Sch.
2.Generalized
Musclerigidity
METABOLIC
1. Inappropriately
elevated CO2
production
(↑EtCO2, ↑RR).
2. ↑O2 Consumption
3. Mixed Metabolic
and Respiratory
acidosis
4. Profuse Sweating.
5. Mottling of skin.
CARDIOVASCULAR MUSCLE

13. NORMAL PHYSIOLOGY
STORE OPERATED CALCIUM ENTRY
1.Motor
neuron
releases
Ach
2.Ach binds to
Ach receptors -
opens Na⁺
channels &
generates APs
3. AP
reaches T
tubule
4. Voltage
Sensor
DHPR
receptor
s
activated
5.Ca²⁺ is released
from SER via
Ryanodine receptor.
(3isoforms: Cardiac,
Skeletal, Brain).
Biphasic response to
6. Ca²⁺ binds
to Troponin
and
promotes
actin-
7. SERCA pumps propel
Ca²⁺ back to the SR &
cause relaxation when
Ca²⁺ is <10 -7 M and
require ATP

14. EXCITATION CONTRACTION COUPLING…. Physiological basis
Depolarisation of sarcoplasma membrane spreads
along T tubule
Structural change of voltage gated DHPR receptor in T
tubule system which acts as voltage sensor
Coupling with RYR 1 (Ca release channel) in T tubule
Release of calcium from terminal cisternae
Binding of calcium with troponin followed by actin
myosin cross linkage resulting in ms contraction

15. When depolarisation is complete,
calcium is actively taken back in
sarcoplasmic reticulum via ATP-
dependent calcium pump (SERCA,
sarcoplasmic endoplasmic reticulum
calcium- ATPase ) in sarcoplasmic
reticulum

18. PATHOPHYSIOLOGY..
 In MH susceptible pts the anaesthetic triggering agents
cause prolonged opening of RYR1 channel ( calcium
release channel in muscle), overwhelming the reuptake
process, resulting in excess accumulation of calcium
intra cellularly.
 The sustained calcium overload stimulates several
metabolic pathways.
 Excess demand of ATP
 A hyper metabolic state
 It should be remembered that ms mass constitute 30-
40 % of body wt. so this hyper metabolic state leads to
excess generation of heat.

19. PATHOPHYSIOLOGY..
 The sustained increase in [Ca2+]i leads to muscle
contraction without relaxation, i.e. spasm, which, if
prolonged, develops into severe contracture.
 The muscle contracture greatly increases the extra
vascular resistance to muscle perfusion resulting in
ischemia initially locally and eventually systemically
 The excess oxygen need due to demand for
production of extra ATP relative to diminished
perfusion due to ischemia lead to metabolic
exhaustion, muscle oedema and ultimately result in
muscle breakdown.

21. PATHOPHYSIOLOGY
• Calcium releasing Unit (CRU)
– Key unit of Excitation
Contraction Coupling
– Includes Ryanodine
• Central component of CRU
• Interacts with Ca²⁺ V1.1 and
other proteins
• Homer 1, calstabin, triadin,
junctin, junctophilin etc.
– Predominantly affected by MH
mutations

22. EVALUATION

23. • Indications
– Individuals with “MH susceptible” contracture test
• Identify the mutation involved
– Can be offered as first line test if “hyperthermic
reaction under anesthesia”
– Ist degree relatives of an index case
• Risk of transmission: 50%
– Family member of a person +ve mutation test
– Contracture test
• Not available
• Refusal by patient
GENETICS AND DNA TESTING

24. Counselling of the Patients
• Should be directed to an MH testing centre for a
consultation to determine the need for muscle
biopsy or genetic testing.
• Should be counselled about their disorder and
the need to inform anaesthesiologists in the
future.
• Should be cautioned regarding the remote but
conceivable possibility of developing heat stroke in
extremely hot and humid environmental
conditions.

26. GENETIC BASIS
• Any mutation that results in altered regulation of
calcium in skeletal muscle can be associated with
the clinical syndrome of MH.
• Over 40 such distinct mutation sites have been
found, the most common being in genes that code
for the RYR1 (chromosome 19) and DHP
(chromosome 7) receptor.
• The pattern of inheritance is usually autosomal
dominant; however, de novo mutations have been
reported.
• A negative screen of the RyR1 gene does not rule
out MH susceptibility

27. Gene mutations associated with MHS have been
assigned a numbering sequence identifier
 MHS1 is associated with mutations in the gene
RYR1 encoding ryanodine receptor type 1
(chromosome 19q13.1).Mutations in RYR1 account
for about 50% to 70% of all cases of MHS. These
mutations are located in specific exons of the gene
and are termed MH "hot spots.“. More than 100
mutations have been reported in the RYR1gene.
 MHS2 has been linked to chromosomal locus
17q11.2-q24, which is associated with the voltage-
dependent sodium channel of the skeletal muscle
membrane.

28. Gene mutations associated with MHS have been
assigned a numbering sequence identifier
 MHS3 has been linked to chromosomal locus 7q21-
q22, the site of coding for DHP, the T-tubule bound
voltage sensor for RYR1.
 MHS4 has been linked to chromosomal locus 3q13.
 MHS5 is associated with mutations in the gene
encoding the α1 subunit of the dihydropyridine receptor
(CACNA1S) at chromosomal locus 1q32. Mutations in the
CACNA1S gene account for 1% of all cases of MHS.
 MHS6 has been linked to chromosomal locus 5p.

29. Indications for Muscle Biopsy Testing for
MH
 Definite Indications:
• Suspicious clinical history for MH
• First degree relative of a index case with a clinical
history of MH if the index case cannot be tested
(e.g, too young, too old, MH death, not willing to
undergo the muscle biopsy, no test centre
available)
• Family history of MH where genetic testing is
negative for mutation.
• Severe masseter muscle rigidity after
succinylcholine administration that is associated
with myoglobinuria and/or marked CK elevation

30. Possible Indications
• Unexplained rhabdomyolysis during or after surgery (may
present as sudden cardiac arrest due to hyperkalemia)
• Moderate to mild masseter muscle rigidity with
evidence of rhabdomyolysis
• Exercise-induced rhabdomyolysis
 Probably Not Indicated
 Sudden, unexpected cardiac arrest during anesthesia or
early postoperative period not associated with
rhabdomyolysis
 Age less than 5 years or weight less than 40 pounds
(insufficient muscle mass)
 Neuroleptic malignant syndrome

31. Muscle biopsy tests.. Protocols…
 Three major protocols…1)North American
2) European, 3) Japanese
 North American protocol (Caffeine Halothane
contracture test) utilizes exposure to 3% halothane
on 3 muscle bundles
 Sensitivity of 100% & specificity of 78%
 The European protocol (in vitro contracture test)
utilizes incremental exposure to halothane on 2
muscle bundles.
 Sensitivity: 97% specificity : 93%
 The Japanese protocol utilizes chemically skinned
muscle fibres

32. CONTRACTURE TEST
• Gold standard
– Sensitivity & Specificity
• >90%
– Detects abnormal muscle response to Halothane
and caffeine.
– Requires
• Muscle Harvesting: Quadriceps(MC),Rectus abdominus.
– Specimen Length: 15-25 mm, Thickness: 2-3 mm and Weight
100-150 mg (max 2-4gm).
– Local infiltration or femoral and lat. Femoral cut. nerve block.
– Weight>30 Kg and age > 4 years
It is 99 % sensitive and specific.
BUT
1. Inter laboratory variability.
2. Averages are recorded
3. Accuracy of caffeine and
halothane concentrations.

34. CONTRACTURE TEST
IVCT
• Used in Europe
• Both Incremental Halothane
(0.5-3%) and Incremental
caffeine 0.5 -32 m mol/l are
used (2X increments).
•
CHCT
• Used In USA
• Halothane is used at fixed 3
% and incremental caffeine
in 2X increments.
MH equivocal → MHs/MHc • MH susceptibleIF RESULT IS POSITIVE FOR EITHER CAFFEINE OR HALOTHANE

35. CONTRACTURE TEST
MH Susceptible
Positive response
to both halothane
and caffeine
MH Equivocal
Positive response
to either Caffeine
or halothane
MH Normal
Contracture less than 2 g
at Caffeine >3mmol/L or
Halothane>2%.
MH Susceptible
Positive response to both halothane
and caffeine
MHc: Positive response to Caffeine
MHH:Positive response to halothane.
MH Normal
Contracture less than 2 g
at Caffeine >3mmol/L or
Halothane>2%.

36. CHCT
• Also positive in..
central core disease
and
hypokalemic periodic paralysis

40. COMING BACK TO ELEPHANT IN THE
ROOM

43. DIFFRENTIAL DIAGNOSIS
 Pheochromocytoma
 Thyroid crisis
 Insufficient anesthesia or
analgesia
 Insufficient ventilation
 Anaphylactic reaction
 BRAINSTEM
HYPOTHALMIC INURY
 Neuromuscular disorders
 Malignant neuroleptic
syndrome
 Cerebral ischemia
 Procedural causes
 SEROTONIN
SYNDROME
 TRANSFUSION
REACTION

44. A VERY MUCH RELATED CONDITION
Masseter Muscle Rigidity
• Defined as jaw ms rigidity along with limb ms
flaccidity after administration of sch impeding
intubation and persisting for > 2 mins.
• MMR may be the first sign of MH, or it can develop
during an MH episode. However, it may also occur as
an exaggerated response to succinylcholine in normal
individuals.
• Slow tonic fiber of masseter and lateral pterygoid
ms responds to depolarising ms relaxant with
contracture, the reason of development of MMS.
• May occur even after pre treatment of
defasciculating dose of NDMR

45. GRADING
 The most common response to succinylcholine is “jaw
stiffness” that is subclinical and can only be detected using
special measuring devices. This is a normal response to
succinylcholine and is considered to be of no prognostic
significance with respect to MH.
 A greater increase in masseter spasm is called “jaw
tightness that interferes with intubation.” This group may
be quite large (1–2%) in children who are administered
halothane and succinylcholine. A small but unknown
number of these patients are at risk for MH.
 The most severe form of masseter muscle spasm has been
characterized as “the mouth could not be opened” or “jaws
of steel.” This group is documented to have an increased
incidence of fulminant MH and increased mortality if the
triggering agents are continued

46. MMS may occur in normal persons..
• 30% of patients with MMS prove to be MH
susceptible.
• Additional signs increase likelihood of MH
 50 – 60% if metabolic signs present, 70 – 80% if
muscle signs present,
• May be the first indication of previously
unsuspected muscle ds. Particularly myotonic
conditions..

47. TREATMENT FOR MMS
• If possible abandon surgery…
• Otherwise choose to MH safe technique..
• Allow 15 min to get the pt stabilised..monitor
ETCO2, temperature, and consider arterial line.
• Inv: blood for CK within 24 hr period, and first
voided urine for myoglobin

48. Differential Diagnosis
MH THYROTOXICOSIS PHEOCHROMOCYTOMA
ETCO 2
+++ ++ ++
 HR
+++ +++ +++
 BP
+ ++ +++
RIGIDITY
++ +/- -
ACIDOSIS
+++ - +

49.  MALIGNANT
HYPERTHERMIA
 Triggering agent: sch
and volatile
anaesthetics.
 An acute presentation
 • Pathophysiology:
altered ca
 release mechanism in
 skeletal ms.
 • Autosomal dominant
 •Tt : dantrolene iv
 NEUROLEPTIC MALIGNANT
SYNDROME
 Triggering agents :
antipsycotics,
 Occurs after long term drug
exposure.
 Pathophysiology: inhibition
of central dopaminergic
receptors in hypothalamus.
 Not familial not a inherited
disorder.
 Treatment:
 benzodiazepines,
 bromocriptine, dantrolene

50. Awake triggering…..
• Few cases of exercise induced rhabdomyolysis
have found to have MHS mutation
• There are some anecdotal reports that relate
heat stroke to awake MH episodes.
• But this areas are still controversial and needs
further documentation and evidence.

51. Outcome..
 Mortality un acceptably high.
 Mostly due to failure to recognize the syndrome
in the early phase.
 Earlier death rates were 80%
 Now come down to < 5% after introduction of
dantolene sodium.
 There is 25% recrudescence rate in 1st 24- 36 hrs.
 Even after successful treatment there may be
prolonged muscle pain and weakness (chronic slowly
progressive myopathy) for which physical
rehabilitation may be necessary.

52. TREATMENT
IMMEDIATELY
Declare emergency and call for Help.
Inform surgeons
Termination of Surgery
 Stop all Inhalational agents
Switch to Non Trigger anesthesia
Hyperventilation with flow 10 L
100% O2
Disconnect circuit.
Inform1800-MHHYPER Monitoring
•ECG, NIBP, EtCO2
•Wide bore IV
•Consider CVP, Arterial early
• Investigation
K+, CPK, ABG, Myoglobin,
Blood sugar

53. Death results from….
➢ Dysarrythmia from marked sympathetic stimulation and
Hyperkalemia
➢ Severe spasm making intubation and ventilation
impossible
➢ Myoglobinuric renal failure (acute tubular necrosis).
➢ Disseminated intravascular coagulation.
➢ Neurological damage.
➢ Multi organ failure when core temperature is elevated
beyond critical temperature ( >43 deg c).

54. TREATMENT
• Dantrolene
• Hydantoin derivative
– 2.5 mg/kg – Max 10 mg/Kg
– 20 mg/ ampoule
• 16-20 ampoules
– Mixed with sterile water.
• Takes 1.5 minutes to dissolve
• Others solun. → precipitation.
– t1/2: 10 -15 hours
– S/E: Respiratory muscle weakness, Cholestasis
synergistic toxicity with DILTIAZEM

55. About Dantrolene..
 Dantrolene sodium was first introduced in 1979 as an
injectable antidote for acute MH. Prior to that time, the drug
was available in an oral formulation for use as an adjunct in
the treatment of muscle spasticity associated with spinal
cord injury or cerebral palsy
 Dantrolene sodium inhibits the release of calcium from the SR by
binding to RYR1 and reverses the effects of MH i.e uncouples
depolarisation with contraction
Fast contracting twitch ms are affected more than slow
contracting antigravity ms.
 To continue upto 24- 48 hrs to prevent recrudescence and
worsening of rhabdomyolysis.

56. About Dantrolene..
• Generally safe in clinically recommended dose
• Has no effect on cardiac or smooth muscle.
• Side effects include nausea, malaise, light
headedness, muscle weakness, and irritation and
phlebitis at the intravenous site due to the high
pH of the drug. Hepatotoxicity after long term oral
use of the drug.
 Respiratory muscle weakness may occur when
large doses are used or when administered to
patients with an neuromuscular disorder

58. Immediate management:
 Call for help. Start dissolving the dantrolene in sterile water(not
saline).
 Termination of use of volatile anaesthetics and
succinylcholine.
 Removal the vaporizer and use of new circuit.
 Flushing the anaesthesia machine with high-flow oxygen (at
least 10 L/minute) for 20 minutes,
 Hyperventilation with 100% oxygen.
 Administration of 2-3 mg/kg dantrolene intravenously. Repeat
every 5 - 10 min upto 10 mg/ kg , till metabolic symptoms are
controlled.
 Monitor core temperature, electrocardiogram, arterial
blood pressure, and urine output.
 Active surface cooling , naso gastric and rectal lavage with cold
saline but avoid overcooling to body temp < 38 deg. c

59. Immediate management contd…
 Adequate Hydration with saline preferably cold.
 Management of acidosis with i.v bicarbonate 1-2 meq/kg iv
if not rapidly improved with dantrolene.
 Maintenance of urine output with mannitol (0.25 gm/kg iv )
and loop diuretics ( frusemide 1 mg/kg iv).
 Forced alkaline diuresis..
 Correction of Hyperkalemia with glucose-insulin, and
calcium.
 Cardiac dysarrhythmia usually responds to correction of
Hyperkalemia and acidosis.
 Persistent arrhythmias may be treated with standard anti
Arrhythmic like procainamide or lidocaine.
 CCB s should not be preferably used.

60. After initial stabilization……..
 Continue intravenous dantrolene for at least 24 h
after control of initial episode (approximately 1 mg/kg
q 6 h).
 Watch for recrudescence by monitoring in an
intensive care unit (ICU) for 36 h. Recrudescence
occurs in about 25% of MH cases.
 Avoid parenteral potassium.
 Ensure adequate urine output by alkaline diuresis
because myoglobinuria is common.

61. After initial stabilization……..
 Follow coagulation profile watching for the
occurrence of disseminated intravascular
coagulation (DIC).
 Measure creatine kinase (CK) every 6 h until
falling then at least daily until normal. CK may
remain elevated for 2weeks.To be kept in mind
that baseline CK may be elevated in some
patients post operatively.
 Counsel patients and families regarding
testing and future anaesthetics.

62. AAGBI TEMPLATE MH

64. The following are the supplies, equipment and drugs that
should be stocked in a MH cart
A.Supplies and equipment:
 IV solutions;
 Bucket for ice;
 Urine meter x 1;
 Foley catheter tray;
 60 mL syringes x 5;
 Urinalysis test strips;
 NG tubes, various sizes;
 CVP kits of various sizes;
 22G IV catheter, 1 inch x 4;
 24G IV catheter, ¾ inch x 4;
 Small and large plastic bags for ice;
 Blood administration sets and pumps;
 bladder, rectal temperature probes;

65. The following are the supplies, equipment and drugs that
should be stocked in a MH cart
 Irrigation tray with 60 mL irrigation syringe;
 16G, 18G, 20G IV catheters, 2-inch x 4 each;
 Transducer kits for arterial and CVP cannulation;
 3 mL syringes or ABG kit x 6 for blood gas analysis;
 10-12 bags of saline kept in a refrigerator for IV
cooling;
 Urine collection container to determine myoglobin
level;
 60 mL Toomey syringes x 2 with adaptor (used with
NG irrigation);
 Gastric lavage set with three-way indwelling catheter
for insertion into the rectum;
 Pulmonary artery, esophageal, nasopharyngeal,
tympanic membrane,bladder & rectal temp. probe

66. The following are the supplies, equipment and drugs that
should be stocked in a MH cart
B.Drugs:
 Three 1000-U vials of heparin;
 Two 10 mL vial calcium chloride;
 One 100-U vial of regular insulin;
 Ten 50 mL vials of 20% Mannitol;
 Thirty-six 20 mg vials of Dantrolene;
 Thirty-six 100 mL vials of sterile water;
 Two 50 mL vials of 50% dextrose in water;
 Five 50 mL vials sodium bicarbonate 8.4%;
 Four 2 mL pre-filled syringes of furosemide;
 Three pre-loaded syringes:
➢Lidocaine 2% for injection;
➢100mg/5mL or 100 mg/10mLAmiodarone can also be
used;
➢Lidocaine or procainamide should not be used if a
wide-QRS complex arrhythmia is caused by
hyperkalemia; it can cause asystole.

67. Anesthesia for the Patients Susceptible
to MH
• Patients susceptible to MH can be safely
anesthetized using non triggering agents
• primary regional anaesthetic technique is also
appropriate when feasible, all local anaesthetic are
considered safe.
• Core temperature and minute ventilation should be
monitored closely in all patients.
• To "clean" the anaesthesia machine and ensure
that the patient will not be exposed to trace
anaesthetic gases.
• To use fresh anaesthetic circuit..and use of
vaporizer free machine if possible..

68. Anesthesia for the Patients Susceptible
to MH contd…
• flushing the anaesthesia machine with high-flow
oxygen (at least 10 L/minute) for 20 minutes,
• placing tape over the vaporizer canisters to avoid
accidental administration
• The re breathing bag should be attached to the distal
end of the ventilator circuit with at least 5 ventilator
cycles per minute during the 20- minute flushing.
• The CO2absorber should be replaced with a fresh
absorber
• Dantrolene is not required prophylactically but should
be readily available.
• Postoperative observation for 4 hours is
recommended for patients

69. Safe anaesthetics
• Barbiturates
• Benzodiazepines
• Ketamine
• Opioids
• Proppofol
• NDMRs
• Local anaesthetics
• Droperidol

70. Drugs triggering MH
• Sch
• Volatile agents
– HAL>ISO>ENF>SEVO.
• ONDANSETRON
• *and these drug
should not be used
in MH susceptible

71. ANESTHESIA MH
SUSCEPTIBLITY
• Avoid trigger agents
• Flush the circuit with 10 L O2.
• Use Charcoal filter in anesthesia machine
• TIVA
• Regional anesthesia.
• Xenon (Case Report)

72. Management doesnot end insuccessful
treatment …
• Patients and his family members to be counseled
regarding the ds process and its future anaesthetic
implications.
• a muscle biopsy test is to be done to confirm the
diagnosis
• When ms biopsy is positive should go for genetic
mutation detection,
• Family members to be screened

73. Diseases associated with MHS
• Central core disease.
• Multicore myopathy or evan’s myopathy or MH
myopathy.
• King Denborough syndrome

74. Rhabdomyolysis, but NOT MH
 Brody’s disease
• Deficient calcium adenosine triphosphatase
 McArdle’s disease
• Myophosphorylase B deficiency
 Dystrophinopathies and other abnormalities of the
structural proteins in the muscle membrane
there is chronic elevation of CK indicating
chronic rhabdomyolysis
 Post operative myoglobinurea may be the only sign of M.H
without any other sign of increased muscle metabolism.
 But d/d of post operative myoglobinurea is large.

75. Lastly
• The anaesthetic protocol of different myopathy or
myotonic disorders and M.H are more or less
same
 But what
differs…. is that…
• The implications of a diagnosis of X-linked
myopathy, myotonia, or autosomal-dominant
ryanodine receptor mutation that are quite
different for the rest of their family.

76. THANKS FOR YOUR ATTENTION