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Malignant Hyperthermia

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Malignant Hyperthermia Malignant Hyperthermia Presentation Transcript

  • 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.
  • "Thank you"