MALIGNANT HYPERTHERMIA Dr. Shailendra.V.L. Specialist in Anesthesia, Al Bukariya general hospital
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 )
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
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 :
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:
SIGNS OF M H
Metabolic & Respiratory acidosis
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
Hypertension, hypoxemia & acidosis
- Ventricular bigemeny
Multifocal premature beats
Hypercarbia ( 100 to 200 mm of Hg )
Respiratory & metabolic acidosis( Ph 7.15 to 6.8)
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
Acute renal failure
blindness, seizures, coma, paralysis
Differential diagnosis for MH
Neuroleptic malignant syndrome
TREATMENT OF M H
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
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
TREATMENT OF M H
Correct metabolic acidosis ( NaHCO3 1 – 2 m Eq/kg IV based on arterial ph