MH and Awareness

• Succ and inhaled volatile anesthetics
• Don’t give Succto any child unless it is an emergency, Black box in children incidence is much higher is children and adolescents for MH, generally adult is considered 18, not size related

• It is more frequently seen in young men with an average age of 15 and those of
• Caucasian northern European dissent. Highest incidence in the United States is
• in the Midwest.  Furthermore, MH is
• extremely dangerous in younger athletic males with large amounts of muscle mass
• due to the ability of the muscles to increase body temperature to even greater
• levels

• The incidence in North American and Europe are 1 in 15,000 for adolescents
• 1 in 50,000- 150,000 for adults.
• Overall incidence during anesthesia is approx 1 in 10,000 general anesthetics in the general population

• FALSE! Neither family history nor  previous exposure to
• anesthesia can accurately predict its occurrence.
• 2/3 of susceptible MH
• patients manifest the syndrome during their first general anesthetic. 
• The other 1/3 manifest during subsequent
• administration of anesthetics.

Dantrolene

• A sustained, significant hypermetabolic state and  an abnormality in skeletal muscle
• biochemistry that results in muscle destruction or rhabdomyolysis).
• The disorder results in hyperthermia, tachycardia, high end-tidal CO2, skeletal
• muscle rigidity, and acidosis. Doesn’t always manifest on the first anesthetic

• Autosomal dominent inherited disorder with a defect on the ryanodine receptor RYR1.
• skeletal muscle calcium-releasing channel found on chromosome 19.  Genes on chromosomes 1, 3, 7, and 17 have also been linked with MH in different families RYR1 is in a more open resting state than normal that results in an intracellular calcium release rate that is
• three times that in people without MH.

• 1. halogenated agents and/or succinylcholine results in the uncontrolled release of free calcium from the sarcoplasmic reticulum in muscle tissue in MH patients 
• 2. increase in calcium there is an increase in action between the actin and myosin leading to sustained muscle contractures
• 3. excessive breakdown of adenosine triophosphate or ATP due to this hypermetabolic state
• 4. generalized skeletal muscle rigidity, destruction, and rhabdomyolysis 
• 5. excessive metabolic stimulation leads to increased CO2 production and the formation of lactic acidosis and respiratory acidosis
• 6. generalized skeletal muscle rigidity due to the ATP being exhausted
• 7. Depletion of ATP there is a disruption of the skeletal muscle cell membrane that allows potassium, calcium, creatine kinase, and myoglobin to leak into the extracellular fluid. Loss of potassium from the muscle cells result in hyperkalemia, metabolic acidosis and cardiac arrhythmias
• 8. Released myoglobin causes myoglobinuria, disseminated intravascular coagulation, and renal failure. Renal tubules get clogged by myoglobin.

trauma, exercise, heat, stress, and infection

Muscle contraction, metabolic stimulation, increase lactic acid, increased CO2, increased temp, increased HR, Increased BP

• 1. Doubling or tripling of ETCO1
• 2. Arrhythmia's such as VFIB, occurring within minutes is MOST COMMON CAUSE OF DEATH
• 3. Fever is inconsistent, often a late sign
• 4. ARF and DIC can rapidly develop
• 5. Later complications include: skeletal muscle swelling, cerebral edema, hepatic failure, left heart failure

TRUE!

• 1. Increasing ETCO2, over min to hours, requiring increasing MV to maintain normal EtCO2
• 2. Masseter Muscle Rigidity
• 3. Tachycardia

• It is jaw muscle tightness with limb muscle flaccidity after admin of succhinylcholine. Keeping in mind that incomplete relaxation or a tight jaw is different from MMR often described as Jaws of Steel. Additionally myotonia can cause MMR. However the safest thing to do if MMR presents is to wake the pt up, as intubation will be unlikely as well.
• MMR is preductive of MH in up to 25% of cases, and is associated with myoglobinuria.
• After an episode of MMR, the patient should be observed carefully for a period of 12-24 hours.

• 1. acidosis
• 2. hypoxia
• 3. hypercarbia
• 4. elevated CK
• 5. Hyperkalemia
• 6. hypercalcemia
• 7.hyperphosphatemia

• 1. A: Ask about personal and family past history of Malignant Hyperthermia, Adverse Anesthesia
• reactions (unexplained fever or death during   
• anesthesia). Aware of clinical signs of MH.
• 2. B : Body temperature monitoring for all patients undergoing general anesthesia for other than brief procedures.
• 3. C:  Capnographic monitoring for all patients undergoing general anesthesia. 
• 4. D  Dantrolene: have dantrolene available wherever MH trigger anesthetics are used.

Emergency Treatment:

• 1. A:  Ask for Help
• Ask for the MH cart and for dantrolene. Agents/Anesthesia: Stop anesthesia triggering agents and the surgery.
• 2. B: Breathing: hyperventilate with 100% oxygen.
• 3. C: Cooling,if the patient is hot (aggressively down to 380C):insert large bore IV catheters. 
• Cold intravenous fluids (NS) 15 cc/ kg IV
• 3 times.  Irrigate the wound and stomach  with cold saline. Call MH Hotline: 1-800-644-9737 or 1-315-464-7079 1-800 MH HYPER
• 4. D:  DANTROLENE: give dantrolene IV, 2-2.5 mg/kg, and repeat the dose until the signs are controlled.
• 5. E:  Check Electrolytes, especially potassium.

• Secondary Steps
• 1. A: Acidosis? Assess initial and subsequent arterial or venous blood gases. Is there mixed metabolic and respiratory
• acidosis?
• 2.B: Bicarbonate? 1-2 mEq/kgguided by pH and base deficit.
• 3. C:  Circulation/monitoring:consider arterial line, central venous catheter,laboratories: arterial/venous blood gases,
• myoglobin levels.CBC,Coagulation tests CK,
• 4. D:  Dysrhythmias: generally subside with resolution of the hypermetabolicphase of MH.  Arrhythmias can be treated with amiodarone, lidocaine, procainamide, adenosine, or other drugs indicated according to the ACLS protocol. Remember impact of hyperkalemia.Diuresis: assure diuresis greater than 1 ml/kg/h.
• 5. E:  Electrolytes: if hyperkalemic, treat with bicarbonate, glucose/insulin, calcium.
• 6.F:  Follow up: A: Arterial and venous blood gases. B: Body temperature (core) avoid hyper/hypothermia. C: end-tidal CO2, CK, Coagulation tests. D: Diuresis (urine output and color). E: Electrolytes.

• Dysrhythmias
• – Calcium channel blockers should NOT be used – Verapamil can interact with Dantrolene to produce hyperkalemia (already a problem) and myocardial depression

Direct acting skeletal muscle relaxant

Acts to dissociate intracellular excitation contraction coupling by binding to RYR1 Ca++ channel receptor interfering with the release of Ca++ from the SR

Decrease temp in Thyroid Storm and Neuroleptic Malignant Syndrome

• 20mg with 3 gm of Mannitol
• 6 hours

Mannitol causes osmotic diuresis, as well as excretion of K+, Ca++, phosphorous, chloride,Mg++, Urea & uric acid, so ensure foley cath in place

• Dose: 2-2.5mg/kg Q 5 min.
• Continue: 1mg/kg Q 6hrs x 24-48 hrs.
• T1/2 = 6 hrs.
• More than 10 mg/kg may be given as dictated by clinical circumstances

TRUE! smallest dose of dantrolene needed is recommended and following LFT's

The caffeine halothane contracture test, It is a biopsy and test that is performed in a diagnostic center. Genetic testing can supplement caffein halothane contracture test.

• 1. thiopental
• 2. propofol
• 3. midazolam
• 4. diazepam
• 5. opioids
• 6. cisatracurium/atracurium
• 7. rocuronium, vecuronium, pancuronium
• 8. Neostigmine and glyco

blood relative with an MH reaction or positive muscle biopsy

• 1. scheduled as first case of the day
• 2. Oral sedation with misaz
• 3. an anesthesia machine that does not have exposure to volatile anesthetics or a machine that has been flushed to reduce anesthetic concentration
• 4. if an anesthetic machine is flushed, new equipment should be used and FGF should not be reduced below 10Lmin if a charcoal filter is not used
• 5. Essential monitors include EtCO2, temperature

• Occurs when a patient becomes conscious during a procedure performed under general anesthesia and subsequently has recall of these events” (ASA Task Force, 2006) 
• Is caused by administration of GA inadequate to maintain unsonsciousness and to prevent recall during surgical stimulation.
• Does not include dreaming Does not include implicit memory

Ability of the patient to retrieve stored memories

Ability of the patient to recall specific events, noises, sensations, that occur during GA

Subconscious changes in behavior or performance with the ability to recall specific events during GA

• 1. A higher incidence is reported in obstetric general anesthesia – 0.4%  Emergent c-section where worry of baby sometimes presides
• 2.  The incidence in cardiac surgery ranges from 1.1% to 1.5%. CABG off pump especially with rapid changes in hemodynamics
• 3. Major trauma rates of awareness are 11% to 43% but have decreased with better resuscitation of patients

• 1. history of substance abuse (BENZO, OPIOID COCAINE)
• 2. difficult intubation
• 3. chronic pain patient on increased doses of opioids
• 4. limited hemodynamic reserve ASA III-V
• 5. History of awareness

• 1. muscle relaxants
• 2. TIVA
• 3. N2O opioid anesthesia
• 4. Surgery performed at night – awareness attributed to fatigue of provider,most cases of anesthesia awareness are attributed to human error, wrong drug administration, failure of equipment
• 5.In 44% of events awareness was felt to be due to low inspired volatile agent concentrations or inadequate hypnosis In 40% of events awareness was atributed to drug error with the inadvertant paralysis of an awake patient In 16% of cases causation could not be identified

• 1. acute trauma with hypovolemia
• 2. ASA III-V
• 3. Cardiac surgery off pump
• 4. impaired CV status
• 5. Csection under GA
• 6. Severe end stage lung disease
• 7. bronch, laryngoscopy or both
• 8. history of awareness
• 9. Expected hypotension with treatment
• 10. Chronic use of opiois or benzos
• 11. heavy ETOH
• 12. Anticipated difficult intubation

• 1. asses the risk of awareness and incorporate the possibility of awareness as part of the informed consent for high risk patients
• 2. check all anesthesia equipment
• 3. consider pre-medication with amnestic agents
• 4. clearly label all drug syringes when they are drawn up

• 1. Consider use of brain function monitor in high risk scenarios
• 2. provide additional doses of hypnotic or initiate volatile agent administration for repeated intubation attempts
• 3. use EtCO2 monitor with the low alarm set for sufficient volatile concentration to prevent awareness
• 4. when using TIVA, ensure patent intravenous line and periodically check the function of the syringe pump
• 5. avoid excessive muscle paralysis unless required for surgical indications, routinely use a peripheral nerve stimulator to assess degree of paralysis
• 6. perform postoperative assessment and refer to appropriate psychosocial support

• 1.Interview the patient after the procedure and take a detailed account of his or her experience, include this in the patients chart
• 2.Apologize and assure the patient of
• credibility of his/her account….sympathize  
• 3.Explain possible reasons for occurrence (light anesthesia 2/2 cardiac instability etc.)
• 4.Offer the patient psychological or psychiatric support, referral of patient to specialist
• 5.Notify surgical team members of event

TRUE!

FALSE!

• 1. auditory perceptions and being unable to move or breath
• 2. anxiety, stress, pain, and sensation of ETT

1-2 out of 1000 cases

• 1. large anesthetic requirements
• 2. equipment misuse or failure
• 3. smaller doses of anesthetic
• 4. ASA status of III-V