Earliest Sign of Malignant Hyperthermia

[drlee]

There is some controversy apparently on what exactly is the first sign of malignant hyperthermia. Some references say unexplained tachycardia, whereas other mention increased in end-tidal carbon dioxide levels. If a board question asks this questions, what would be the correct one? 😕

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[pgg]

There is some controversy apparently on what exactly is the first sign of malignant hyperthermia. Some references say unexplained tachycardia, whereas other mention increased in end-tidal carbon dioxide levels. If a board question asks this questions, what would be the correct one? 😕

I'd answer ETCO2 if the question was ambiguous and both tachycardia and ETCO2 were options. Tachycardia is so nonspecific ... the classic scenario is rising ETCO2 that you can't keep up with despite large increases in minute ventilation.

 

[Planktonmd]

There is some controversy apparently on what exactly is the first sign of malignant hyperthermia. Some references say unexplained tachycardia, whereas other mention increased in end-tidal carbon dioxide levels. If a board question asks this questions, what would be the correct one? 😕

Masseter spasm.

 

[powermd]

I've beens studying Barash like crazy lately, and read about MH yesterday. According to the book, an unexpected rise in ETCO2 is the most sensitive and specific early sign. 25% of patients having masseter muscle rigidity will be susceptible to MH. If a patient develops masseter rigidity not bad enough to preclude laryngoscopy, you can proceed with the case if you are using an etco2 monitor, have means to cool the patient, dantrolene immediately available, and are confident you would be able to manage MH. Otherwise, cancel surgery, and monitor for 24 hrs. If the CK rises substantially, that may be grounds for a neuro consult to rule out myotonic syndrome and an MH contracture test.

The classic course of MH can be summarized: Tachypnea > tachycardia > hypertension > ventricular dysrhythmias > muscle rigidity > temp rise > muscle blockade break through > peripheral mottling > sweating, cyanosis > labs - resp/met acidosis normal oxygenation, hyper K, hyper Ca, lactacidemia, myoglobinuria, CK > 20K.

 

[coprolalia]

The classic course of MH can be summarized: Tachypnea > tachycardia > hypertension > ventricular dysrhythmias > muscle rigidity > temp rise > muscle blockade break through > peripheral mottling > sweating, cyanosis > labs - resp/met acidosis normal oxygenation, hyper K, hyper Ca, lactacidemia, myoglobinuria, CK > 20K....

... death.

-copro

 

[Planktonmd]

I've beens studying Barash like crazy lately, and read about MH yesterday. According to the book, an unexpected rise in ETCO2 is the most sensitive and specific early sign. 25% of patients having masseter muscle rigidity will be susceptible to MH. If a patient develops masseter rigidity not bad enough to preclude laryngoscopy, you can proceed with the case if you are using an etco2 monitor, have means to cool the patient, dantrolene immediately available, and are confident you would be able to manage MH. Otherwise, cancel surgery, and monitor for 24 hrs. If the CK rises substantially, that may be grounds for a neuro consult to rule out myotonic syndrome and an MH contracture test.

The classic course of MH can be summarized: Tachypnea > tachycardia > hypertension > ventricular dysrhythmias > muscle rigidity > temp rise > muscle blockade break through > peripheral mottling > sweating, cyanosis > labs - resp/met acidosis normal oxygenation, hyper K, hyper Ca, lactacidemia, myoglobinuria, CK > 20K.

If you are asking what is the earliest sign then it is masseter spasm, that does not mean it is sensitive or Specific it is just the earliest.
If you see it you'd better get ready and consider your options.