Malignant hyperthermia

The article "Malignant hyperthermia" is the basis for this AORN Journal independent study. The behavioral objectives and examination for this program were prepared by Janet S. West, RN, BSN, CNOR, clinical editor, with consultation from Patricia A. Beachy, RN, MS, professional education specialist, Center for Perioperative Education.

A minimum score of 70% on the multiple-choice examination is necessary to earn four contact hours for this independent study. Participants receive feedback on incorrect answers. Each applicant who successfully completes this study will receive a certificate of completion. The deadline for submitting this study is Sept 30, 1997.

Send the completed application form, multiple-choice examination, learner evaluation, and appropriate fee to

* direct peritoneal or thoracic ravage (if these cavities are open),

* indirect abdominal ravage through a nasal gastric tube,

* extracorporeal perfusion if the patient's core body temperature exceeds 40 [degrees] C (104 [degrees] F), and

* external cooling measures (eg, packing bags of ice around the patient's axillae, groin, neck, and head; placing temperature regulating blankets under and over the patient).(18)

The patient's bladder is not ravaged because the anesthesia care provider needs to monitor the patient's urine output. If the patient does not have a Foley catheter, the circulating nurse inserts an appropriate-sized Foley catheter into the patient's bladder and attaches it to a metered collection bag to allow the anesthesia care provider to monitor the patient's urine output and myoglobinuria levels. All cooling agents and equipment are discontinued after the patient's core body temperature decreases to 38.0 [degrees] C (100.4 [degrees] F) to avoid inadvertent patient hypothermia.(19) The anesthesia care provider uses a temperature probe (eg, tympanic, nasopharyngeal, esophageal, rectal, pulmonary) to monitor the patient's core body temperature.

As dantrolene sodium is difficult to reconstitute, two RNs are needed to mix and administer the medication IV push (ie, preferably into a central venous line). The anesthesia care provider draws arterial blood gas (ABG) specimens and blood samples for electrolytes; clotting studies (eg, prothrombin time, partial thromboplastin, fibrinogen); and CPK, lactate dehydrogenase, serum myoglobin, and blood urea nitrogen levels.(20) The MHAUS' recommendations for treatment of an MH crisis during the acute and postacute phases of patient care are shown in Table 5.

Dantrolene sodium is supplied in 70-mL vials that contain 20 mg of dantrolene sodium, 3 g of 20% mannitol, and sufficient sodium hydroxide to yield a pH of approximately 9.5 when reconstituted with 60 mL of sterile water for injection without a bacteriostatic agent. The mixed solution should be clear yellow to yellow/orange after two to three minutes of vigorous shaking. It is administered IV push beginning with an initial bolus of 2 to 3 mg/kg and then titrated to approximately 1 mg/kg every four hours to a maximum cumulative dose of 10 mg/kg or until the MH signs and symptoms are reversed.(22) The patient continues to take dantrolene sodium for 48 to 72 hours after the initial diagnosis of an MH episode,(23) and the patient can be discharged on oral dantrolene sodium. Dantrolene sodium has a few possible side effects, which include

* nausea,

* diarrhea,

* temporary muscle weakness (eg, decreased handgrip, lower extremity muscle weakness),

* double vision, and

* dizziness.(24)

Possible adverse reactions to dantrolene sodium may include pulmonary edema, thrombophlebitis, urticaria, erythema, and anaphylaxis. It should be used with caution in patients with muscle weakness or muscle diseases because it exacerbates muscle weakness.(25) The MHAUS recommends that 36 vials of dantrolene sodium (ie, the minimum amount needed to treat a 70-kg [154-lb] patient) be kept in health care facilities at all times.(26)

Other medications. The anesthesia care provider may direct perioperative nurses to administer

* 50% IV dextrose solution with insulin (ie, 10 U regular insulin in 50 mL of 50% dextrose solution) to treat hyperkalemia by promoting the reuptake of potassium into the intracellular fluid space,

* 10% IV calcium chloride (ie, 2 to 5 mg/kg) for emergency treatment of cardiac toxicity that can be associated with hyperkalemia,

* an IV osmotic diuretic (eg, 20% mannitol) or a loop diuretic (eg, furosemide) to maintain urinary output and prevent acute renal failure,

* 8.4% IV sodium bicarbonate (ie, 1 to 2 mEq/kg) to correct metabolic acidosis,

* IV heparin sodium (1,000 U/mL concentration) to treat DIC, and

* IV procainamide hydrochloride (ie, 15 mg/kg) to treat arrhythmias (eg, ventricular fibrillation).(27)

If lactated Ringer's IV solution is infusing into the patient, it should be discontinued immediately because it could contribute to the patient's acidosis. Calcium channel blockers (eg, IV verapamil hydrochloride) should be avoided because they may cause hyperkalemia and cardiovascular collapse. In addition, IV procainamide hydrochloride should be administered for premature ventricular contractions (PVCs) because it decreases calcium ion levels in the bloodstream and increases cardiac and skeletal muscle rigor.(28) Dysrhythmias in adults that persist after they are treated for metabolic acidosis and hyperkalemia may be treated with a 100 mg IV bolus of 2% IV lidocaine hydrochloride, followed by an IV lidocaine drip of 1 mg/kg.(29)

Postacute treatment phase. After the MH crisis, the PACU nurses, and later the intensive care unit (ICU) nurses, monitor and document the patient's

* vital signs (ie, BP, heart rate [HR], respiration [R], temperature [T]),

* electrocardiogram (ECG) readings,

* pulse oximetry [O.sub.2] levels,

* [ETCO.sub.2] levels,

* urinary output,

* level of consciousness,

* myoglobinuria levels, and

* skin appearance.

Blood specimens are obtained for serum myoglobin, CPK, and electrolyte levels; clotting studies; and ABGs. The patient is monitored in the ICU for 24 to 48 hours because MH can recur up to 48 hours after a patient has been normalized (de, recrudescence occurs in about 25% of all MHS patients).(30)

Muscle breakdown continues 24 hours after an MH episode; therefore, the patient may experience a temporary decrease in handgrip strength and weaknesses in his or her lower extremity muscles, especially when walking downstairs. As these symptoms may persist for up to 48 hours after an MH episode, nurses instruct the patient not to operate a motor vehicle or engage in hazardous activities after discharge. The patient also may experience dizziness, double vision, difficulty swallowing, and choking.(31)

After the patient is alert, the ICU nurses begin discharge planning to prevent future problems. The nurses explain what happened to the patient while he or she was under general anesthesia, and they answer the patient's questions about the nature of MH and the causes of MH susceptibility. Discharge teaching includes a patient referral to MHAUS to learn more about regional MH centers where patients and family members can be tested for MH susceptibility.

In addition, the nurses encourage the patient to wear a medical identification bracelet and carry a card in his or her wallet that indicates a predisposition to MH. The surgeon also notifies the patient's family physician about the patient's MH susceptibility. The MHAUS advises patients who experience muscle rigidity under general anesthesia and their family members to be registered and categorized as MHS patients for future surgical procedures.(32) Table 7 lists some of the critical pathways used in the surgical services' collaborative action plan for MH at Wayne (NJ) General Hospital, an affiliate of the St Barnabas Health Care System.

* two RNs to reconstitute and administer the IV dantrolene sodium;

* the mobile MH supply cart, portable MH medication box, and defibrillator;

* a person to go to the cafeteria for bags of ice; and

* a pharmacist to send 18 additional vials of IV dantrolene sodium to the OR (ie, total of 36 vials).

The circulating nurse told the audience that she would insert a Foley catheter with a metered collection bag and that she would document all medications used during the MH crisis, including doses, times, routes, and patient responses. The circulating nurse asked the two RNs who had just arrived to mix and IV push the dantrolene sodium under the direction of the anesthesia care provider. She asked other OR personnel to bring in IV bags of cooled normal saline and cooled bottles of normal saline for irrigation. The circulating nurse told the audience she would contact the nurses in the PACU about the MH crisis and that they would set up a ventilator in the PACU. She told the PACU nurses that she would call with the ventilator settings before Mary was transferred to the PACU.

The anesthesia care provider ventilated Mary with 100% [O.sub.2] at 10L/min while the OR nurses administered the dantrolene sodium IV push. Mary's core body temperature continued to rise and at 10:44 AM (de, 21 minutes after general anesthesia began), it was 40 [degrees] C (104 [degrees] F). The anesthesia care provider inserted a 14-gauge IV line in Mary's femoral artery and used this access as a central line. He asked the circulating nurse to assist him in obtaining blood specimens from the central line for ABGs, electrolytes, and clotting studies.

The anesthesia care provider told the audience that Mary's ECG readings indicated PVCs, the capnograph showed an [ETCO.sub.2] level of 72 mm Hg, and the esophageal temperature probe registered a core body temperature of 42.0 [degrees] C (107.6 [degrees] F). He stated he would perform a gastric ravage with cooled normal saline through the patient's nasogastric tube and would administer IV procainamide hydrochloride to treat the patient's PVCs.

The results of Mary's initial ABG analysis (de, pH = 7.28 [normal range = 7.35 to 7.45], serum bicarbonate level = 20 mEq/L [normal range = 24 to 26 mEq/L]) indicated that she was in metabolic acidosis, and her electrolyte test results showed a potassium level of 7.2 mEq/L (normal range = 3.5 to 5.5 mEq/L). The anesthesia care provider told the audience that he would administer 50 mL of 50% IV dextrose solution mixed with 10 U of regular insulin IV push to promote potassium reuptake. As Mary's urinary output was only 20 mL/hr, he planned to administer furosemide IV push. The anesthesia care provider also told the audience that Mary's pH was 7.16, so he would administer 50 mEq of sodium bicarbonate IV push.

At 11:02 AM (de, 41 minutes after general anesthesia began), Mary's [ETCO.sub.2] level was 55 mm Hg, and her core body temperature decreased to 40 [degrees] C (104 [degrees] F). Mary's HR was 138 bpm, and she had less masseter muscle rigidity. Twelve vials of IV dantrolene sodium were used in the OR to resolve the MH crisis. The circulating nurse told the audience that the patient was ready to be transported to the PACU, and she called the PACU nurses with the ventilator settings requested by the anesthesia care provider.

Postacute phase treatment. After the OR mock demonstration, the PACU nurse addressed the audience. She outlined what would happen during Mary's stay in the PACU (de, the minimum stay is four hours after an MH crisis). The PACU nurses would maintain the femoral artery line for drawing blood samples, and the anesthesia care provider would insert a triple lumen catheter for central venous pressure monitoring of possible fluid shifts. The PACU nurse also explained to the audience that the anesthesia care provider would insert a pulmonary artery catheter if Mary became hemodynamically unstable.

The PACU nurses would irrigate Mary's nasogastric tube and suction her endotracheal tube PRN. They also would monitor Mary's vital signs, [ETCO.sub.2] levels, ventilator alarms, urine output, pupil size and reactivity, and skin for mottling and cyanosis in the extremities. The nurses would administer IV dantrolene sodium 1 mg/kg every six hours for 24 to 48 hours as ordered, and the anesthesia care provider would titrate Mary's dose. Blood samples for laboratory tests would be drawn as ordered, and Mary would be kept in a quiet environment for recuperation. The PACU nurses would monitor Mary for possible complications, including possible renal failure (ie, increased myoglobinuria, hypotension), DIC, heart failure, pulmonary edema, and brain function deterioration.

A question and answer period followed the mock MH crisis demonstration. The feedback from the participants' evaluation forms showed that the mock MH crisis demonstration was a very effective tool for reinforcing the inservice program on MH. The inservice program also served as the impetus for the development of our facility's MH protocol and collaborative action plan mentioned previously.

FUTURE RESEARCH

The goal of MHAUS is to eliminate the mortality associated with MH and to relieve MH symptoms. Although funding for MH research is limited, the MHAUS believes further research is necessary to

* develop a simple, inexpensive diagnostic test for MH susceptibility;

* clarify the accuracy of the muscle biopsy diagnostic test;

* identify the actual epidemiology of MH;

* note the direct and indirect causes of MH by studying the molecular biology of the syndrome;

* determine if previously unidentified medications might be harmful to MHS patients; and

* enhance medical professionals' knowledge of MH.(38)

CONCLUSION

Although MH crises are rare, perioperative staff members need to be prepared to deal with these events. Nurse managers and educators can prepare staff members through literature distribution, inservice programs, and mock MH crisis demonstrations. Successful resolutions of MH crises depend on staff members' thorough knowledge of MH and early recognition of the signs and symptoms of impending MH crises. Perioperative staff members also should understand their roles during MH crises and be knowledgeable about MH supplies and medications. Adequate preparation is the hallmark of positive patient outcomes in MH crises.

NOTES

(1.) V L Struebing, "Differential diagnosis of malignant hyperthermia: A case report," AANA Journal 63 (October 1995) 455-460.

(2.) Ibid, 455.

(3.) A J Donnelly, "Malignant hyperthermia: Epidemiology, pathophysiology, treatment," AORN Journal 59 (February 1994) 393-405.

(4.) S Curtis, "AANA Journal Course: Update for nurse anesthetists--Genetic testing for malignant hyperthermia," AANA Journal 64 (December 1996) 557-562.

(5.) Donnelly, "Malignant hyperthermia: Epidemiology, pathophysiology, treatment," 395.

(6.) Curtis, "AANA Journal Course: Update for nurse anesthetists--Genetic testing for malignant hyperthermia," 558.

(7.) Struebing, "Differential diagnosis of malignant hyperthermia: A case report," 455.

(8.) Malignant Hyperthermia Association of the United States, Malignant Hyperthermia: Knowing Your Role (Sherburne, NY: Malignant Hyperthermia Association of the United States, 1994) 3; Malignant Hyperthermia Association of the United States, Understanding Malignant Hyperthermia (Sherburne, NY: Malignant Hyperthermia Association of the United States, 1996) 16.

(9.) Malignant Hyperthermia Association of the United States, Malignant Hyperthermia: Knowing Your Role, 3-4.

(10.) Ibid.

(11.) Malignant Hyperthermia Association of the United States, What is Malignant Hyperthermia? (Sherburne, NY: Malignant Hyperthermia Association of the United States, 1996) 1-2.

(12.) P H Rivera, C Worley, "This looks like malignant hyperthermia!" Journal of Post Anesthesia Nursing 10 (October 1995) 265-276.

(13.) Malignant Hyperthermia Association of the United States, Clinical Update 199511996: Managing Malignant Hyperthermia (Sherburne, NY: Malignant Hyperthermia Association of the United States, 1995) 1-2.

(14.) Rivera, Worley, "This looks like malignant hyperthermia!" 265.

(15.) Struebing, "Differential diagnosis of malignant hyperthermia: A case report," 457-459.

(16.) Donnelly, "Malignant hyperthermia: Epidemiology, pathophysiology, treatment," 400.

(17.) Malignant Hyperthermia Association of the United States, Emergency Therapy for Malignant Hyperthermia (Sherburne, NY: Malignant Hyperthermia Association of the United States, 1995) poster.

(18.) C F Beck, "Malignant hyperthermia: Are you prepared?" AORN Journal 59 (February 1994) 367-390.

(19.) Ibid, 376.

(20.) Malignant Hyperthermia Association of the United States, Malignant Hyperthermia: Knowing Your Role, 11, 15-17; Malignant Hyperthermia Association of the United States, Emergency Therapy for Malignant Hyperthermia, poster.

(21.) Physicians' Desk Reference, 50th ed (Montvale, NJ: Medical Economics Co, 1996) 1983-1984.

(22.) Ibid.

(23.) Malignant Hyperthermia Association of the United States, Preventing Malignant Hyperthermia: An Anesthesia Protocol (Sherbume, NY: Malignant Hyperthermia Association of the United States, 1996) 6.

(24.) Physicians' Desk Reference, 50th ed, 1984.

(25.) Malignant Hyperthermia Association of the United States, Managing Malignant Hyperthermia: Drugs, Equipment, and the Antidote, Dantrolene Sodium (Sherbume, NY: Malignant Hyperthermia Association of the United States, 1996) 1-2.

(26.) Malignant Hyperthermia Association of the United States, Dantrolene sodium--The Specific Treatment for Malignant Hyperthermia (Sherbume, NY: Malignant Hyperthermia Association of the United States, 1994) 2-3.

(27.) Malignant Hyperthermia Association of the United States, Emergency Therapy for Malignant Hyperthermia, poster, Donnelly,"Malignant hyperthermia: Epidemiology, pathophysiology, treatment," 400.

(28.) Donnelly, "Malignant hyperthermia: Epidemiology, pathophysiology, treatment," 400.

(29.) Beck, "Malignant hyperthermia: Are you prepared?" 377.

(30.) Malignant Hyperthermia Association of the United States, Clinical Update 1995/1996: Managing Malignant Hyperthermia (Sherbume, NY: Malignant Hyperthermia Association of the United States, 1996) 6.

(31.) Physicians' Desk Reference, 50th ed, 1984.

(32.) Malignant Hyperthermia Association of the United States, Understanding Malignant Hyperthermia 17.

(33.) Malignant Hyperthermia Association of the United States, Testing for Susceptibility to Malignant Hyperthermia (Sherbume, NY: Malignant Hyperthermia Association of the United States, 1994) 1.

(34.) Struebing, "Differential diagnosis of malignant hyperthermia: A case report," 460.

(35.) Malignant Hyperthermia Association of the United States, Testing for Susceptibility to Malignant Hyperthermia, 2.

(36.) Physicians' Desk Reference, 50th ed, 1984.

(37.) T J J Blanck et al, Malignant Hyperthermia: The Clinical Syndrome (Cincinnati: Proctor & Gamble Pharmaceuticals, 1980) Videotape.

(38.) Malignant Hyperthermia Association of the United States, Understanding Malignant Hyperthermia, 20-21.

SUGGESTED READING

Grillo, P P. "Malignant hyperthermia crisis: Planning a mock demonstration." AORN Journal 52 (September 1990) 585-591.

Stein, R H. "The perioperative nurse's role in anesthesia management." AORN Journal 62 (November 1995) 794-804.

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Debra Dunn, RN, MBA, CNOR, is an OR staffnurse, Wayne (NJ) General Hospital, an affiliate of the St Barnabas Health Care System.

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