Tag: Malignant Hyperthermia

Clinical Topic: Malignant Hyperthermia Review

Highlights of Malignant Hyperthermia

Early in our Anesthesia training, we were all taught about the dreaded Malignant Hyperthermia.  As we settle into clinical practice, we all remember that MH is a potential risk but give it very little thought.   SRNA Ola Akigbogun, from the Mercer University School of Medicine Nurse Anesthesia Program has offered the following review for procrna.com readers. The bullet format allows us to quickly review the highlights of treating MH.   Ola will graduate in the fall of 2012.  Read his profile and contact him if you are looking for a new graduate who is a motivated and committed to excellence.

Definition

  • Malignant Hyperthermia is characterized by an acute metabolic state in muscle tissue following induction of general anesthesia and in the post operative phase of anesthesia.
  • Malignant Hyperthermia is rare 1:15000 in pediatrics and 1:40000 in the adult population.
  •   Most common in pediatric cases.
  • Patients with mild to moderate MMR, King Denborough syndrome, Duchenne’s muscular dystrophy, Central core disease and Osteogenesis imperfecta are usually susceptible to Malignant Hyperthermia.

History

  • First formal description in 1960 by Denborough and Lovell
  • The first case report allowed for a very solid understanding of the pathophysiology of Malignant Hyperthermia. The patient was a young man who stated that his relatives died without any apparent cause during anesthesia.
  • This patient was anesthetized with halothane and developed tachycardia, hot sweaty skin, and cyanosis. The early recognition of this symptom saved him and lead to the further research and developments of Malignant Hyperthermia
  • In 1970 many of the clinical symptoms of MH were reported
  • In 1970 Kalow et al suggested the development of an in vitro diagnostic test which involved the exposure of biopsied muscle to caffeine and Halothane.
  • In 1975 Harrison reported that dantrolene was successful in the treatment of MH.
  • MH registry in the United States in the late 1980’s
  • In 1985, Lopez and His colleagues demonstrated that intracellular calcium concentration was increased during an episode and that dantrolene was successful in its reversal.
  • In 1990’s molecular biological techniques where applied to identify genes that are susceptible to MH.

Pathophysiology

  • Triggered by Succinylcholine and halogenated agents in greater than 80% of reported cases.
  • Why malignant hyperthermia does not occur after every exposure to halogenated agents is not fully understood.
  • Malignant Hyperthermia is believed to occur due to an uncontrollable increase in the intracellular calcium in skeletal muscle. The sudden release of intracellular calcium removes the inhibitory properties of troponin which results in intense muscle contraction.
  • Increased adenosine triphophatase activity results in an uncontrollable increase in aerobic and anaerobic metabolism. The severe hypermetabolic state created is responsible for increase oxygen consumption and CO2 production leading to severe lactic acidosis and hyperthermia.
  • It was first believed that the abnormal  ryanodine Ryr1 receptor in patients with MH was responsible, but further studies have shown that MH pts may have a normal ryanodine receptors and that abnormalities in secondary messengers such as fatty acids may be the problem. An abnormal sodium channel may also be responsible for malignant hyperthermia.

 

Triggering Factors

  • Halothane
  • Enflurane
  • Isoflurane
  • Desflurane
  • Sevoflurane
  • Succinylcholine

Signs of malignant Hyperthermia

  • The earliest sign and symptom that will present is an increase in ETCO2.  ETCO2 can occur due to other reasons, but when other problems are ruled out treatment of MH should begin.
  • Other additional early signs include tachycardia, tachypnea, and rigidity of the masseter muscle called trismus. However, trismus often occurs with pediatric patients, in particular when intubating, so this sign must be taken into consideration with all other signs and symptoms.

Late Signs

  • Unstable blood pressure, cyanosis and/or mottling of the skin, diaphoresis, cardiac dysrhythmia
  • Hyperthermia. The patient’s temperature may elevate as much as 1-2°C every five minutes.
  • Hyperkalemia, Hypernatremia, Metabolic acidosis, Hyperphosphatemia, elevated CK levels.
  • Dark red blood in the surgical field
  • Myoglobinuria

Malignant Hyperthermia Protocol

1. Immediately discontinue anesthesia, including Succinylcholine. Life-threatening surgery will be continued, but with the use of a different anesthetic agent and machine to prevent residual inhalation agent from triggering a second episode.

2. Hyperventilate 100% oxygen at a high flow rate of 10L/min. to treat effects of hypercapnia, metabolic acidosis, and increased oxygen consumption

3. Dantrolene 2.5mg/kg IV as soon as possible; given every five minutes until symptoms subside.

4. Change ventilator tubing and soda lime canister. Some anesthesia providers may still perform this action, but research has shown that it is not necessary to change the breathing circuit and anesthesia machine since the oxygen delivery rapidly clears the machine of the anesthetic gases.

5. Sodium bicarbonate 1-2 mEq/kg IV to combat metabolic acidosis due to increase of lactate in the circulatory system.

6. Ice packs Apply to groin area, axillary regions, and sides of neck – where major arteries are located.

7. Iced lavage the stomach and rectum with cold fluids to lower temperature. It is recommended not to lavage the bladder since the fluids can alter the true amount of urine being excreted by the patient and alters measurement of output.

8. Mannitol or furosemide Muscle cells are destroyed during an MH crisis and the myoglobin that is released accumulates in the kidneys, obstructing urinary flow, referred to as myoglobinuria. Diuretics are given IV to promote and maintain urinary flow in order prevent renal damage. Mannitol 0.25g/kg IV; furosemide 1mg/kg IV; up to four doses each. Urinary output of 2ml/kg/hr or higher must be maintained to prevent renal failure.**skip this step if dantrium IV is used because it contains 3g of mannitol.

9. lidocaine to treat arrhythmias secondary to electrolyte imbalances. Procainamide removed due to practitioners not beeen familiar with the drug.

10. Dextrose and insulin Treat hyperkalemia due to the release of potassium into the circulatory system as muscle cells are destroyed. Dextrose 25-50g IV; regular insulin 10 units in 50ml of 50% dextrose in water given IV.

11. Monitor urine output Insert Foley catheter if one is not in place

12. Monitor electrolyte levels Blood samples taken every 10 minutes to measure sodium, potassium, chlorides,calcium, phosphate, and magnesium levels.

13. Perform clotting studies

14. ABG Every 5 to 10 minutes

15. Arterial blood pressure Insert line if one is not in place

16. Central venous pressure Insert line if one is not in place.

17. Pt should be monitored in PACU for at least 4 hours then transferred to ICU for 24-72 hrs monitoring.

 

Dantrolene

  • Hydantoin derivative which intereferes with muscle contraction by binding to the RYr1 receptor and inhibiting calcium ion release from the SR.
  • 2.5mg/kg IV every 5 mins until episode is terminated. Upper dosage is 10mg/kg
  • Dantrolene is packages in 20mg vials and it is to be reconstituted with 60ml of sterile water. The reconstitution can be very time consuming
  • Half life is about 6 hrs.
  • Recent studies show that prophylactic use of dantrolene can increase muscle weakness and is not indicated. The anesthesia provider should proceed with the use of non triggering agents
  • 36 vials of dantrolene should be made available upon diagnosis of MH

 

References