MALIGNANT

HYPERTHERMIA
Dr. Shailendra.V.L.
Specialist in Anesthesia,
Al Bukariya general hospital
 CASE HISTORY
A 5 year old boy for tonsillectomy &
adenoidectomy was induced with
halothane by mask. Three minutes
later, succinylcholine is given. Mild
muscle rigidity of the jaw is noted, but
intubation is accomplished. The child
is noted to develop a bradycardiac
cardiac arrest. ( asystole )
 CASE HISTORY
A 9 year old girl develops masseter
muscle rigidity after propofol
induction and succinylcholine
administration. Rigidity of the
arms is also noted. But end - tidal
CO2 is normal
 CASE HISTORY
A 16 year old patient was maintained on
isoflurane and vecuronium. At the end of
the surgery, she is breathing 20 times per
minute and her end-tidal CO2 is 65mm
Hg. She suddenly develops ventricular
premature contractions. Her forehead
skin temperature is 99 F.
DEFINITION OF M H
It is charecterised by hyper
metabolic response to potent inhalation
agents and succinylcholine resulting in
increased CO2 production, oxygen
consumption, fever, tachycardia,
tachypnoea, acidosis, hyperkalemia,
myoglobinuria, increased CPK,
cyanosis & death
 HISTORY OF M H
 1960: Critical worldwide insight into MH
began when Denborough & Lovell described
a 21 year Australian, with an open leg # who
was more anxious about anaesthesia, because
10 of his relatives had died during anaesthesia.
 1966: Hall reported on MH induced by
halothane & succinylcholine in swines. The
human & porcine forms are virtually identical.
 1975: Harrison described efficacy of
Dantrolene in preventing & treating porcine
MH, which was confirmed in humans.
INCIDENCE OF M H
 1 in 12,000 pediatric anesthetics
 1 in 40,000 adult anesthetics
 Incidence has an apparent geographic
variation – more prevalent in US
 2/3 of susceptible patients manifest
this syndrome during their first
anesthetic
GENETICS OF M H
 Three modes of inheritance:
• Autosomal dominant
• Autosomal recessive
• Unclassified
 The Gene for MH is located
on Chromosome 19, which is also
the genetic coding site for Ryanodine
receptors ( Calcium release channel)
of skeletal muscle sarcoplasmic reticulum
PATHOPHYSIOLOGY OF MH
 Defect in excitation—contraction coupling of
calcium in the sarcolemma in the muscle
 The basic defect lies in the muscle fiber
involving cellular membrane permeability of
the sarcoplasmic reticulum, which results in an
inability to control calcium concentrations
within the fiber.
 The resultant events are heat production &
muscle contracture secondary to enhanced
glycolysis, uncoupling of oxidative
phosphorylation, & activation of actin-myosin
filaments.
TRIGERING AGENTS FOR MH
IN ORDER OR THEIR TRIGERRING POTENTIAL:

 Halothane
 Enflurane
 Isoflurane
 Desflurane
 Sevoflorane
 Ether
 Chloroform
 Suxamethonium
 SIGNS OF M H
 Tachycardia
 Tachypnoea
 Arterial hypoxemia
 Hypercarbia
 Metabolic & Respiratory acidosis
 Hyperkalemia
 Cardiac arrhythmias
 Hypotension
 Skeletal muscle rigidity ( masseter spasm )
 Increased body temperature
 Increased CPK levels – 20,000 I.U.
EARLY DIAGNOSTIC
SIGNS OF MH
 Rising end-tidal CO2 concentration
 Inappropriate tachycardia
 Hypertension, hypoxemia & acidosis
INVESTIGATIONS
 Capnograph:
• Rising EtCO2
 Pulse oximeter:
• Falling saturation
 ECG monitor:
• Tachycardia
• Arrythmias
- Ventricular bigemeny
- Multifocal premature beats

- Ventricular fibrillation
- Ventricular tachycardia
 INVESTIGATIONS
 ABG:
• Arterial hypoxemia
• Hypercarbia ( 100 to 200 mm of Hg )
• Respiratory & metabolic acidosis( Ph 7.15 to 6.8)
 Electrolytes:
• Hyperkalemia ( > than 6 mEq )
• Raised transaminase enzymes
• Markedly elevated CPK ( > 20,000 IU )
( peak levels after 12 to 24 hours of the episode )
 Plasma & urine myoglobin elevated
COMPLICATIONS OF M H
 DIC
 Pulmonary edema
 Acute renal failure
 CNS damage
• blindness, seizures, coma, paralysis
 CVS manifestations
• arrythmias
Differential diagnosis for MH
 Neuroleptic malignant syndrome
 Thyrotoxic crisis
 Cocaine toxicity
 Heat stroke
 Serotonin syndrome
 Status epilepticus
 Pheochromocytoma
TREATMENT OF M H
 Etiologic treatment:
• Dantrolene ( 2 – 3 mg/kg IV) as an
initial bolus, followed with repeat
doses every 5 – 10 minutes until
symptoms are controlled.
• Prevent recurrence (dantrolene 1 mg /
kg IV every 6 hours for 72 hours )
 TREATMENT OF M H
Symptomatic Treatment:
 Immediately terminate trigger drugs
& conclude surgery as soon as
possible
 Hyperventilate with 100 % oxygen
 Initiate active cooling
• Iced saline 15 ml / kg every 10 minutes
• Gatric lavage with iced saline
• Surface cooling
TREATMENT OF M H
Symptomatic treatment:
 Correct metabolic acidosis ( NaHCO3
1 – 2 m Eq/kg IV based on arterial ph
 Maintain urine output
 Hydration
 Mannitol ( 0.25 g/kg IV )
 Furosemide ( 1mg/ kg )
 Treatment of arrythmias
 Xylocaine infusion
 Monitor in ICU
 IDENTIFICATION OF
SUSECPTIBLE PATIENTS
 A detailed medical & family history
 Myopathic syndromes
• Duchenne muscular dystrophy
• Myotonia congenita
• Pectus carinatum
• Kyphoscoliosis
• Ostoegenis imperfecta
 IDENTIFICATION OF
SUSEPTIBLE PATIENTS
 Laboratory investigations:

• CPK levels ( 70% suseptibles have

elevated resting CPK levels )

• Electromyographic studies ( 50%

suseptibles show changes )
 IDENTIFICATION OF
SUSEPTIBLE PATIENTS
 Skeletal muscle biopsy:
• Taken from vastus muscle of thigh
under local anaesthesia.
• Muscle is subjected to isometric
contracture testing under influence of
caffeine or halothane or both. It
produces exaggerated contracture in
susceptible patients.
MANAGEMENT OFANAESTHESIA
“AVOID ALL TRIGGERING DRUGS ”
“ Regional blocks are preferred ”

 Premedication: barbiturates
or benzodiazepines can safely be
used

 Dantrolene prophylaxis adminstration

is controversial
MANAGEMENT OF ANAESTHESIA

 Pre-oxygenation for three minutes

 Induction: thiopentone / propofol
 Intubation : non depolarizing relaxants
 Maintainance: oxygen + nitrous oxide
 Reversal: neosigmine + atropine
 MANAGEMENT OF
ANAESTHESIA
 Anaesthesia machine without vaporisers
 New face mask and circle absorber

 New breathing circuit & reservoir bag

 Monitors:
• ECG monitor
• NIBP monitor
• Pulse oximeter
• End-tidal CO2 monitor
• Temperature
 NON-TRIGGERING AGENTS
FOR MH
 Barbiturates
 Opioids
 Propofol
 Benzodiazepines
 Nitrous oxide
 Anti-cholinergics
 Anti-cholinesterases
 Local anaesthetics
 Sympathominetics
 REFERENCES
 Anaesthesia & co-existing diseases –
Stoelting.
 Short practice of Anaesthesia – Churchill
Davidson
 Problem oriented Anaesthesia – Stoelting.
 American Society of Anaesthesia ( ASA )
Annual refresher lecture notes – 1998.
 Textbook of Anaesthesia – Ronald Miller.