Malignant hyperthermia :

advances in clinical
management and diagnosis
Nurliyana binti Ramli
11-2014-192

Malignant hyperthermia
1960 severe reaction under GA
Malignant caused fatality
Hyperthermia high body
temperature
(late feature, therefore early
intervention is important)
Earliest clinical feature : end tidal
[Co2] and tachycardia

Preoperative diagnosis
CAUSES.
Exposure of susceptible individual to
triggering drugs
Family history
- Abnormal musculoskeletal associated
with MH
Eg. Scoliosis , hernias , strabismus

Pt. with history of :

1. Exertional heat stroke
2. Exercise induced rhabdomyolisis
. More than 1 episode investigated
for MH
- routine Preoperative biochemical
screen
= serum C-kinase

Causes of increased serum [c-kinase]

Identifiable

hypothyroid (commonest)
, myopathies , exercise ,
denervation syndrome, MCI ,
rhabdomyolisis (trauma, drugs)

Idiopathic

MH susceptibility , Duschenne
dystrophy carriers, hemolytic sy.
Previous neuroleptic malignant sy.

When common and uncommon causes from the

table above excluded thus indicative of MH

Presentation during anesthesia

No spesific clinical feature.

It changes according to their timing of onset reaction

Timing

Clinical signs

Changes in
monitors

Biochemical
changes

Early

Masseter spasm after

succinylcholine
Tachypnoe
Rapid exhaustion of soda
lime
Hot soda lime canister
Irregular pulse

ventilation/min

PaCO2

Succeeding
Patient hot to touch
Cyanosis
Dark blood in wound
Irregular pulse
Late

Generalized muscle rigidity

Prolonged bleeding
Dark urine
Oliguria
(irregular pulse)

end tidal CO2

Tachycardia
Perked T waves on
Ecg
Rising body temp
SPo2

pH
Pao2
[K+]

Peaked T waves on
BCG

c-kinase
myoglobinuria
[K+]

Soda lime
CO2 absorber.

Postoperative presentation
Onset MH varies in speed
CASES : After potent inhalant administration metabolic
stimulation, clinical feature in 10 minutes or several
hours
Speed of onset depends on types of drug used
Speed onset >> intracellular [Ca2+] >> stimulates
sarcoplasmic reticulum Ca2+ activate mx. Ca inducedCa released sustain MH rx. so, even triggered already
eliminated (initial intervention) clinical sign reappear.

Pharmalogical triggers of
MH
Potent inhalational anaesthethic drug
-

Halothane ,
Isoflurane
Sevoflurane
Desflurane

Neuromuscular blocking drugs

- Succinylcholine cause increase intracellular
[Ca2+]
- Most affect masseter muscle because , masseter m.
contains proportion of type I fibres
- Myofilament type I fibres : more sensitive to Ca2+
compared to type II fibres.

 Phenothiazine
- Anticholinergic actions antidiaphoresis
(mostly children) > heat loss , so
high body temperature
- MH rx. If consumed before general
anesthesia.
Other drugs
- Anticholinergic drugs , exacerbate
pyrexia because anti-diaphoresis rx.

Laboratory diagnosis of MH
IVCT ( in vitro contracture test)
- Living skeletal muscle , expose to
halothane and caffeine
Ryanodine contracture test
distinguish MH-susceptible from
normal patients.
Chlorocresol

Molecular genetics of MH
Studies : Chr 19q12.1-13.2 locus of
RYR1 (ryanodine receptor gene),
the gene encoding
Skeletal muscle sarcoplasmic reticulum
ca2+ release channel.

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