Vol. 112 No.

3 September 2011

MEDICAL MANAGEMENT AND PHARMACOLOGY UPDATE

Editors: F. John Firriolo and Nelson I. Rhodus

Malignant hyperthermia in the oral and maxillofacial surgery

patient: an update
Pavan Manohar Patil, BDS, MDS, DNB, FISCLP, Uttar Pradesh, India
SHARDA UNIVERSITY

Malignant hyperthermia (MH) is a pharmacogenetic disorder of skeletal muscle that presents as a

hypermetabolic response to potent volatile anesthetic gases, such as halothane, sevoflurane, desflurane, the
depolarizing muscle relaxant succinylcholine, and, rarely in humans, to stresses, such as vigorous exercise and heat.
The syndrome is likely to be fatal if untreated. Early recognition of the signs of MH provides the clinical diagnostic
clues. Diagnostic testing relies on assessing the in vitro contracture response of biopsied muscle to halothane, caffeine,
and other drugs. Dantrolene sodium is a specific antagonist of the pathophysiologic changes of MH and should be
available wherever general anesthesia is administered. The prevention and treatment of acute episodes of this disorder
is of paramount importance to the oral and maxillofacial surgeon. The management of such patients in the oral and
maxillofacial surgery setting and the recent advances in the field of MH are presented. (Oral Surg Oral Med Oral
Pathol Oral Radiol Endod 2011;112:e1-e7)

Malignant hyperthermia (MH) is a pharmacogenetic

disorder of skeletal muscle that presents as a hypermetabolic response to potent volatile anesthetic gases,
such as halothane, sevoflurane, desflurane, and the depolarizing muscle relaxant succinylcholine, and, rarely
in humans, to stresses, such as vigorous exercise and
heat.1 It was first described in 1960.2
The apparent features of the reactions were dominated by progressive hyperthermia and hence the name
MH.3 The malignant part of the name MH has been
useful in emphasizing the fatal nature of the condition.
Incidences of MH during routine dental and maxillofacial surgery have been reported,4 sometimes with fatal
consequences.5 At the dental office, an MH-susceptible
(MHS) patient exposed to excessive stresses (such as
pain, fear, or other triggering agents) may exhibit signs
and symptoms of MH.6 Oral and maxillofacial surgeons who use triggering agents like succinylcholine in
Reader, School of Dental Sciences, Sharda University, Uttar Pradesh,
India.
Received for publication Jan 20, 2011; returned for revision Apr 15,
2011; accepted for publication Apr 20, 2011.
1079-2104/$ - see front matter
2011 Mosby, Inc. All rights reserved.
doi:10.1016/j.tripleo.2011.04.034

their offices must be able to recognize and treat MH. As

routine oral and maxillofacial surgery procedures move
from the hospital to outpatient facilities where triggering agents are commonly used, the oral and maxillofacial surgeon must be aware of the signs, symptoms, and
management of MH to prepare for, and hopefully prevent, an MH episode. The purpose of this article is to
review the triggering agents; the incidence of occurrence; and the etiopathogenesis, diagnosis, prevention,
and management of an MH crisis.
EPIDEMIOLOGY
The incidence of MH episodes during anesthesia is
between 1:5000 and 1:50,000 to 100,000 anesthesias.7
Even though an MH crisis may develop at first exposure to anesthesia with those agents known to trigger an
MH episode, on average, patients require 3 anesthesias
before triggering. Reactions develop more frequently in
males than females (2:1).8 All ethnic groups are affected, in all parts of the world. The highest incidence
is in young people, with a mean age of all reactions of
18.3 years.8 It has been found that children younger
than 15 years comprised 52.1% of all reactions. Although described in the newborn, the earliest reaction
confirmed by testing is 6 months of age. The oldest is
78 years.9 MH crises develop not only in humans but in
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other species, particularly pigs, which have been a

valuable source for research. Reactions have also been
described in horses, dogs, and other animals.8 Genetically, MH is an autosomal dominant condition; the
estimated prevalence of the genetic abnormalities may
be as great as 1 in 3000 individuals (range 1:3000 to
1:8500).8 Most patients with central core disease
(CCD), an inherited myopathy characterized by muscle
weakness, are susceptible to MH. Multi-minicore disease also predisposes to episodes of MH.8
ETIOPATHOGENESIS
Numerous factors could be involved in triggering MH:
age, type of anesthetic, environmental temperature, mitigating drugs administered simultaneously, and degree of
stress. Symptoms are triggered by the nonhalogenated
anesthetic ether, by halogenated anesthetics (halothane,
isoflurane, enflurane, desflurane, sevoflurane), and by the
depolarizing muscle relaxant succinylcholine.10 Nitrous
oxide and amide local anesthetics also have been implicated in MH.11,12 The triggering agents cause an increase
in the concentration of free cytoplasmic calcium, which is
released from the sarcoplasmic reticulum stores via the
muscle ryanodine receptor.13 The ryanodine receptor
(RYR1) gene encodes the key channel that mediates the
calcium release in skeletal muscle during excitation-contraction coupling. Mutations in the ryanodine gene account for approximately 50% of the patients who are
susceptible to MH.4 This increase in cytoplasmic concentrations of calcium induces contracture of skeletal muscles
(often first noticed in the masseter muscle), activating
glycogenolysis and cell metabolism and thereby resulting
in heat and excess lactate production. Activation of the
oxidative cycle leads to high oxygen consumption and
carbon dioxide production, followed by muscular adenosine triphosphate depletion and systemic changes, such as
acidosis, hypercapnia, hypoxemia, tachycardia, and hyperthermia. During the course of the crisis, rhabdomyolysis occurs with subsequent creatinine kinase elevation,
hyperkalemia potentially leading to cardiac dysrhythmias
or even cardiac arrest, and myoglobinuria with the possibility of renal failure.13 Additional life-threatening complications include disseminated intravascular coagulation
(DIC), congestive heart failure, bowel ischemia, and compartment syndrome of the limbs secondary to profound
muscle swelling, and renal failure from rhabdomyolysis.
Indeed, when body temperature exceeds approximately
41C, DIC is the usual cause of death.
Differential diagnosis
A variety of unusual conditions may resemble MH
during anesthesia. These include sepsis, thyroid storm,
pheochromocytoma, and iatrogenic overheating. Outside the operating room, an MH-like syndrome may

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September 2011

occur following injection of ionic contrast media into

the cerebrospinal fluid, cocaine overdose, and the malignant neuroleptic syndrome.8
Laboratory diagnosis
The gold standard for diagnosis of MH is currently
the in vitro contracture test (IVCT), which is based on
contracture of muscle fibers in the presence of halothane or caffeine.8 A normal MH diagnosis (MHN) is
obtained when both tests are negative. A third diagnosis, MH equivocal (MHE), is obtained when only one
of the halothane or caffeine tests is positive. Recently,
the use of ryanodine14 (which binds selectively to the
calcium release channel) or 4-chloro-m-cresol15 as alternatives to halothane has shown promising results.
IVCT is expensive, confined to specialized testing centers, requires a surgical procedure, and can yield equivocal as well as false positive and negative results. DNA
analysis, however, offers an alternative to the IVCT,
requiring only a blood specimen, which can be sent to
an accredited diagnostic laboratory. DNA testing for
MH was first suggested in 1990, when a mutation
within the ryanodine receptor gene (RYR1) encoding
the skeletal muscle calcium release channel was identified.16 Since then, about 50% of MHs have been
linked to RYR1, with more than 100 mutations associated with MH identified within this gene.17 However,
because of the heterogeneity of the disorder, as well as
discordance within families, a negative DNA result
cannot be used to rule out MH susceptibility. A variety
of minimally invasive diagnostic tests are in development at present. One uses nuclear magnetic resonance
spectroscopy to evaluate ATP depletion during graded
exercise in vivo.18 MH patients have a greater breakdown of ATP and creatine phosphate, as well as an
increase in acid content compared with controls.
MANAGEMENT
Acute MH crisis
The following MH protocol sequence has been modified
from the recommendations of the Malignant Hyperthermia
Association of the United States [MHAUS]19 and would be
appropriate should an acute MH crisis occur in the ambulatory oral and maxillofacial surgery center (Table I).
Preventive measures
Preventive measures include a thorough anesthetic history to determine the possibility of the patient or a family
member having experienced an MH episode. When suspicion of MH exists, family members should not be given
trigger anesthetic agents, i.e., potent volatile anesthetic
agents, such as halothane, sevoflurane, desflurane, enflurane, isoflurane, or succinylcholine, and testing is recommended.8 Patients with any form of myotonia should not

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Table I. Management of an acute MH crisis in the ambulatory oral and maxillofacial center
1.
2.
3.
4.

First, recognize the signs of an MH episode (Table II).

Stop all triggering agents, call for assistance, and obtain dantrolene.
Hyperventilate with 100% oxygen at a flow of more than 10 L/min.
Halt the procedure as soon as possible; if emergent, continue with nontriggering anesthetic technique. If needed, deepen anesthesia with
opioids, benzodiazepines, barbiturates, or propofol. Do not waste time changing the circle system and CO2 absorbent.
5. Place an endotracheal tube (if one is not in place already) as soon as possible.
6. Give an initial dose of dantrolene 2.5 mg/kg intravenously through large bore cannula. Dantrolene 2.5 mg/kg is repeated every 5-10
minutes until there is a fall in heart rate, normal cardiac rhythm, reduction in muscle tone, and decline in body temperature. Sometimes,
more than 10 mg/kg (up to 30 mg/kg may be required).
7. Acidosis is treated with 1-2 mEq/kg of sodium bicarbonate in the absence of blood gas analysis.
8. Monitor temperature and cool the patient with core body temperature 39C with blankets, ice packs on the axilla, chest, back, and
groin. Lavage open body cavities like stomach, bladder, or rectum, if possible. Infuse cold saline intravenously and stop cooling if
temperature 38C.
9. Dysrhythmias usually respond to treatment of acidosis and hyperkalemia. Use standard drug therapy (beta blocker, esmolol 0.25 mg/kg
IV, or lidocaine 1 mg/kg IV) except calcium channel blockers, which may cause hyperkalemia or cardiac arrest in the presence of
dantrolene.
10. HyperkalemiaTreat with hyperventilation, bicarbonate 1-2 mEq/kg IV. For pediatric, 0.1 U insulin/kg and 1 mL/kg 50% glucose; for
adult, 10 units regulator insulin IV and 50 mL 50% glucose and calcium chloride 10 mg/kg or calcium gluconate 10-50 mg/kg for lifethreatening hyperkalemia. Check glucose levels hourly.
11. Transport to the emergency department for admission to intensive care unit. Follow ETCO2, electrolytes, blood gases, CK, core
temperature, urine output and color, coagulation studies. If CK and/or K rise more than transiently or urine output falls to less than 0.5
mL/kg/h, induce diuresis to 1 mL/kg/h and give bicarbonate to alkalinize urine to prevent myoglobinuria-induced renal failure. Venous
blood gas (e.g., femoral vein) values may document hypermetabolism better than arterial values. Central venous or PA monitoring as
needed and record minute ventilation. Place Foley catheter and monitor urine output.
The postacute phase treatment of an MH crisis should include the following:
1. Observation in an intensive care unit for at least 24 h because of the risk of recrudescence.
2. Dantrolene 1 mg/kg every 4-6 h or 0.25 mg/kg/h infusion for 24 h. Further doses if needed.
3. Frequent checks on vitals and laboratory values, especially arterial blood gases. CK every 8-12 h, less often as values trend downward.
4. Follow urinary myoglobin and institute therapy to prevent myoglobin precipitation in renal tubules and the subsequent development of
acute renal failure. CK levels above 10,000 IU/L are a presumptive sign of rhabdomyolysis and myoglobinuria. Follow standard intensive
care therapy for acute rhabdomyolysis and myoglobinuria (urine output 2 mL/kg/h by hydration and diuretics along with alkalinization of
urine with Na-bicarbonate infusion with careful attention to both urine and serum pH values).
5. Counsel the patient and family regarding MH and further precautions; refer them to MHAUS. Fill out and send in the AMRA form (http://
www.mhreg.org) and send a letter to the patient and her/his physician. Refer patient to the nearest biopsy center for follow-up.
AMRA, Adverse Metabolic or Muscular Reaction to Anesthesia; CK, creatine kinase; IV, intravenous; MH, malignant hyperthermia; MHAUS,
Malignant Hyperthermia Association of the United States.

Table II. Signs of malignant hyperthermia

Increasing ETCO2
Trunk or total body rigidity
Masseter spasm or trismus
Tachycardia/tachypnea
Mixed respiratory and metabolic acidosis
Increased temperature (may be late sign)
Myoglobinuria

receive succinylcholine. Patients with hypokalemic periodic paralysis, CCD, Duchenne or Becker muscular dystrophy, paramyotonia, or myotonia fluctuans should not
receive trigger agents.8 All patients receiving more than a
brief general anesthetic should have their core temperature
monitored. Young patients (younger than 12 approximately) should not receive succinylcholine for elective
procedures, so as to avoid the possibility of hyperkalemia
response in a patient with undiagnosed muscular dystrophy. Patients who are MH susceptible should be cautioned

regarding the remote, but conceivable possibility of heat

stroke in environments in which exposure to high heat and
humidity is possible.8
Management of the MH-susceptible patient for
anesthesia
The MHAUS recommendation20 states that intravenous conscious sedation with local anesthesia may be
safely administered to the MHS patient in the office
setting for such procedures as the surgical removal of
impacted third molars. Deep sedation or general anesthesia may also be used (obviously so long as no
triggering agents are administered) (Table III). Because
laryngospasm may occur in the unconscious patient,
and succinylcholine is contraindicated in MHS patients,
a nondepolarizing muscle relaxant must be available.
More rigorous standards are recommended if intubation
anesthesia or a prolonged procedure under general anesthesia is anticipated20 (Table IV). Once the patient
has undergone such an anesthetic without incident, he

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Table III. The safety of selected drugs in patients

susceptible to malignant hyperthermia
Do not use (trigger agents)
Cyclopropane
Depolarizing muscle relaxants (e.g., succinylcholine)
d-Tubocurarine
Ether
Methoxyflurane
Rapid intravenous potassium
Volatile inhalational anesthetics (desflurane, enflurane, halothane,
isoflurane, sevoflurane)
Use cautiously
Catecholamines
Haloperidol
Phenothiazines (chlorpromazine, prochlorperazine)
Safe to use
Anticholinergics
Anticholinesterases
Barbiturates
Benzodiazepines
Calcium
Droperidol
Etomidate
Ketamine
Local anesthetics
Narcotics
Nitrous oxide
Nondepolarizing muscle relaxants
Nonsteroidal anti-inflammatory drugs
Propofol
Adapted from Wappler F. Malignant hyperthermia. Eur J Anaesthesiol 2001;18:632.

Table IV. Management of an MH-susceptible patient

for surgery under intubation/general anesthesia
1. Avoid the use of MH-triggering drugs. The anesthesia machine
should be prepared by flowing 100% oxygen through the
machine at 10 L/min for at least 20 minutes. The ventilator
should also be included in purging the machine by cycling the
ventilator at the time of the oxygen flow. Vaporizers should be
disabled, drained, or removed if possible.
2. Continuously monitor the patients exhaled CO2 concentration.
3. Use a continuous temperature monitor (e.g., in the nasopharynx,
axilla, esophagus, or rectum).
4. Have an MH cart in the operating room, stocked with adequate
supplies of dantrolene sodium.
MH, malignant hyperthermia.

or she may be treated similar to any other patients.

Pretreatment with dantrolene is not necessary.
DISCUSSION
Even with proper management of MH, mortality is
reported at 5% to 10%.10 If MH triggers could be removed
from the office, patients would not be at risk of developing
MH. Barbiturates, benzodiazepines, narcotics, nitrous ox-

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ide, propofol, and local anesthetics can be used instead of

the inhalation anesthetics that trigger MH. Triggering anesthetics can be eliminated from the oral and maxillofacial
surgeons office. However, succinylcholine remains the
best drug for emergency management of laryngospasm
and rapid-sequence endotracheal intubation.21 Because
succinylcholine can trigger an MH crisis, dantrolene
should be available for acute management of MH. Dantrolene is a hydantoin derivative that inhibits calcium
release from the sarcoplasmic reticulum without influencing its reuptake. Reconstituting dantrolene is time-consuming and cumbersome, and calling for help immediately is crucial. Dantrolene is stored in 20-mg lyophilized
aliquots with 3 g of mannitol and must be reconstituted
with 60 mL of sterile water (without a bacteriostatic
agent) per vial. Warming the diluent speeds dissolving the
dantrolene. Dantrolene cannot be mixed with normal saline or lactated Ringers, as it precipitates in these solutions. The recommended dose is 2 to 3 mg/kg every 5
minutes, up to a total dose of 10 mg/kg if needed. Therefore, every operatory where general anesthesia is being
used must stock at least 36 vials of dantrolene sodium,
which is roughly equivalent to 10 mg/kg in an adult
patient.20 The reconstituted drug must be used in 6 hours.
Although dantrolene has been life saving, it is not a
perfect drug. Drawbacks include phlebitis, respiratory
muscle weakness with difficulty weaning from a ventilator, difficulty with solvation, and others. Given the timeconsuming process of mixing the initial dose of 9 vials of
dantrolene, each with 60 mL of sterile water (total of 540
mL), for a 70-kg patient, it may be a good idea to stock the
initial intravenous bolus dose (9-12 vials) in the office and
identifying a hospital with an emergency department that
has dantrolene available. It is unlikely that the oral and
maxillofacial surgeon managing an MH crisis will have
sufficient time to administer more than the first dose of
dantrolene while managing the acidosis, hypercarbia, hyperkalemia, dysrhythmias, and so on. After calling for
medical assistance and initiating the treatment of MH, it
would be best to transport the patient to an emergency
department that has dantrolene available and can obtain
blood gases, electrolytes, and laboratory studies needed to
guide management of the crisis. The patient with a severe
MH crisis will need to be admitted to the intensive care
unit for monitoring and continued administration of dantrolene. If the outpatient office is located in a remote area
or an emergency department with dantrolene is not near
the office, it will be necessary to stock the entire 36 vials.
Azumolene, a 30-fold more water-soluble analogue
of dantrolene, also works to decrease the release of
intracellular calcium by its action on the ryanodine
receptor.21 In MHS swine, azumolene was found to be
as potent as dantrolene.22 It has yet to be studied in vivo

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in humans, but may present a suitable alternative to

dantrolene in the treatment of MH.
Until a nondepolarizing muscle relaxant with properties similar to succinylcholine is available, it is difficult to justify the use of nondepolarizing agents for
emergency situations. Further studies are needed to
determine if low nonparalyzing doses of nondepolarizing muscle relaxants like rocuronium can be used to
reverse laryngospasm. Until all triggering agents can be
removed from the outpatient surgical facility, it is recommended that the oral and maxillofacial surgeon identify an emergency room that has dantrolene available
and have a minimum of 10 to 12 vials of dantrolene at
the outpatient facility.21
Increase in masticatory muscle tension following
succinylcholine administration may provide the first
sign that an individual may be susceptible to MH in the
absence of a positive family history.23 Doubts were
raised as to the validity of masseter muscle spasm as a
reliable indicator of MH susceptibility24; however, this
doubt was based on a false premise.25 Further illustration of the need to consider a patient developing masseter muscle spasm following succinylcholine as susceptible to MH was presented by Ramirez et al.,26
where they reported masticatory muscle rigidity in a
trauma patient leading to difficulty in tracheal intubation following succinylcholine use. Subsequently, the
patient developed metabolic features of MH when isoflurane was used for fixation of a humerus fracture.26
Severe or untreated cases of acute rhabdomyolysis may
result in life-threatening hyperkalemia, myoglobinuria, renal failure, and multiorgan system failure.27 Schenk et
al.28 consider early continuous venovenous hemofiltration
[CVVH] as a valuable therapeutic option in the management of severe rhabdomyolysis. However, the potential
benefits of early CVVH on outcome of acute myoglobinuric renal failure remain to be established.
A review of the literature reveals several cases of
MH related to dental treatment.4,5,29,30 Nitrous oxide
was implicated as the triggering agent in a 1985 report.12 Although some believe nitrous oxide to be a
trigger of MH, its frequent use as an anesthetic agent
with susceptible patients would seem to discount this
theory.13 The MHAUS considers its use safe in MHS
patients (Table III). Contraindication for the use of
amide local anesthetics is based on in vitro muscle
contracture studies.11 Amide anesthetics have been
demonstrated to cause muscle contraction, whereas ester anesthetics caused relaxation of muscle tissue,
which inhibits contracture.11 Reviews of the literature
have not demonstrated a clear link between amide
anesthetics and MH and it generally is accepted that
amide anesthetics are safe for MHS patients.11,31,32

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Choung33 described a postoperative variant of MH,

termed human stress syndrome, in a 17-year-old boy with
no significant history who underwent orthognathic surgery. Characterized by more subtle manifestations of MH
without any extreme elevation in body temperature, human stress syndrome can result from exposure to physical
or emotional stress outside a medical setting.33
Molecular genetic diagnostics hold great promise for a
noninvasive diagnostic test that is highly reproducible and
requires minimal biological material. As mutations in the
gene encoding the calcium-release gene in skeletal muscle
have been described as causal for MH, guidelines have
been developed for clinical molecular testing.1
In vitro contracture testing to diagnose MH susceptibility requires a muscle biopsy, which may be associated
with severe side effects for the patient. The caffeinehalothane contracture test requires a fresh muscle sample
that must be obtained immediately before testing and
therefore in close proximity to the biopsy center. The
North American protocol34 has sensitivity and a specificity of 97% to 98% and 78% to 80%, respectively (although specific values will vary from laboratory to laboratory). Thus, there is a 2% chance that contracture testing
will incorrectly mislabel an MHS individual as normal,
whereas there is a 20% chance that a person without the
disease will be labeled as susceptible.
There have been several attempts at developing a less
invasive test. Schuster et al.35 investigated a metabolic test
that involves intramuscular injection of caffeine and halothane, and subsequent measurement of interstitial lactate
by microdialysis to differentiate between MHS and MH
non-susceptible (MHN) individuals. In contrast to genetic
analysis, because of its functional characteristics, the test
is independent of the locus of an MH-causative mutation.
With genetic analysis, more than 150 MH-associated mutations were described and 28 MH-causative mutations
cover 30% to 50% of MH families.36 For epidemiologic
and economic reasons, primary genetic screening in any
MH suspect seems likely to be impossible. McKinney et
al.37 indicated the feasibility of using calcium release as an
assay for RyR1 function in human and porcine B-lymphocytes. Bina et al.38 successfully investigated a blood
test approach for malignant hyperthermia testing in a
swine model by demonstrating that 4-chloro-m-cresol
stimulation of porcine lymphocytes induced increased
adenosine formation in MHS cells relative to those from
normal swine. However, evaluation of adenosine formation in response to RyR1 agonists in human lymphocytes
is needed. Wehner et al.39 observed that in myotubes
derived from MH patients with identified mutations in
RyR1, calcium release induced by 4-CmC or caffeine was
increased compared with controls. The increased calcium
response in myoblasts segregated well with the MH phenotype. However, this assay, although promising, still

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requires surgical biopsy and myotube culture and thus is

not a significant improvement over the current Caffeine
Halothane Contracture Test.
Although research has focused on the ryanodine receptor, other defects have been described. For example, the
CACNL1A3 gene that encodes the -1 subunit of the
skeletal muscle dihydropyridine receptor has been implicated to play a causative role.40 In addition, calsequestrin-1 is a calcium-binding protein in skeletal muscle that,
when absent, leads to MH-like episodes in mice.41
Whether this defect is present in humans remains to be
determined, but such a defect could explain susceptibility
to MH in patients who do not have abnormal ryanodine
receptors. Interestingly, Capacchione et al.42 reported a
patient with exertional rhabdomyolysis and malignant hyperthermia in a rare patient with ryanodine receptor type 1
gene, L-type calcium channel -1 subunit gene, and calsequestrin-1 gene polymorphisms.
Whenever possible, nontriggering agents should be
considered for outpatient procedures to help avoid or
minimize MH cases. For instance, one study43 used only
the nontriggering agents propofol and vecuronium (nondepolarizing muscle relaxant), and reported no malignant
hyperthermia in 23,000 office-based plastic surgery procedures performed under general anesthesia. In addition,
multiple studies have demonstrated the safety of intravenous conscious sedation. A balanced anesthetic technique
using thiopental, nitrous oxide, and an opioid supplemented by a nondepolarizing muscle relaxant is typically
suggested for the MH-susceptible patient. However, malignant hyperthermia can also be triggered by nontriggering agents in fewer than 1% of susceptible patients.44
Therefore, continued and reasonable use of general anesthesia, especially with triggering agents, in office settings
and ambulatory surgical centers mandates active malignant hyperthermia protocols.
In wake of the possibility of an MH attack, temperature monitoring is currently considered a standard for
patients undergoing general anesthesia, although very
brief procedures (e.g., 15 minutes) may be an exception.45 Disposable thermocouple and thermistor probes
are available for monitoring core temperature. Preferred sites include tympanic membrane, esophagus,
nasopharynx, and rectum. These sites constitute anatomical areas of highly perfused tissues, the temperature of which is uniform and high in comparison with
the rest of the body.45,46 Skin surface monitoring is not
considered accurate or reliable because greater fluctuations occur and it is less reflective of core temperature.
The MHAUS and the Ambulatory Surgery Foundation (ASF) of the United States have jointly issued
guidelines47 for the transfer of care with regard to the
development of MH in suspected MH patients from
ambulatory centers to a hospital with all the necessary

equipment and expertise to treat such an emergency.

The patient must be shifted with a report data indicating
the cardiovascular signs, temperature and site, minute
ventilation with end-tidal CO2, electrolytes (if available), intravenous site, amount of dantrolene administered and response, presence of muscular rigidity, presence of urinary catheter, and color of urine. The
recommendations suggest that the patient be shifted
when thought to be stable, which can be recognized by
decreasing ETCO2, decreasing or stable heart rate, declining temperature, dantrolene administration has begun, and generalized muscle rigidity if present is declining. The anesthetist or surgeon transferring care of
the patient must have direct telephonic conversation
with the physician/anesthetist accepting care of the
patient at the receiving health care facility.
CONCLUSIONS
Unless procedures involve the use of topical or local
anesthetics, MHS individuals are not candidates for
office-based surgery at the average oral and maxillofacial clinic. Anyone identified for susceptibility to triggering agents should be referred to an accredited ambulatory surgical center or hospital for surgery. Even
without a positive history of MH, any surgical facility
using potent inhalation anesthetics or succinylcholine
must be prepared to treat MH.
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Reprint requests:
Pavan Manohar Patil, BDS, MDS, DNB, FISCLP
School of Dental Sciences
Plot 32 and 34
Sharda University
Greater Noida
Uttar Pradesh-201308, India
pavanpatil2000@yahoo.co.uk