Methylene blue and poison-induced hypotension
January 16, 2014, 5:53 pm
Refractory shock in drug overdose results mainly from myocardial depression and/or vasodilatation. Bedside echocardiography can be very helpful in sorting out these two mechanisms, each of which might require somewhat different therapy.
The best example of this is calcium channel blocker overdose. With myocardial depression, high-dose insulin/euglycemic therapy (HIT) should be considered early on. However, HIT would not be expected to produce significant vasoconstriction; therefore, with distributive shock, vasopressors (e.g., norepinephrine) may give better results.
There is evidence that methylene blue might have a role in reversing distributive shock from anaphylaxis, sepsis, and some poisonings. Methylene blue selectively inhibits the nitric oxide-cyclic guanosine monophosphate pathway that seems to be a key factor in distributive shock.
This interesting case report, from Melbourne Australia, describes a 41-year-old man who took a massive overdose of quetiapine (Seroquel). The serum quetiapine level was over 100 times therapeutic. In addition, he ingested much smaller amounts of carbamazepine, fluoxetine, valproate, and oxazepam.
On arrival at hospital, the patient had a systolic blood pressure of 90 mmHg. He was intubated and comatose, with a Glascow Coma Scale of 3. Over the next hours, despite receiving 4 L fluids and pressers (including norepinephrine and metaraminol) he became increasingly hypotensive (lowest systolic BP 50 mmHg.) A transthoracic echocardiogram showed a hyperdynamic left ventricle (ejection fraction = 70%) consistent with distributive shock.
Twelve hours post-ingestion the patient’s blood pressure was 88/40 mmHg. At that point, he was given an intravenous loading dose and infusion of methylene blue. Within one hour after receiving the loading dose, his hemodynamics markedly improved, vasopressors could be weaned, and his blood pressure rose to 90/40 mmHg.
Of course, a this case report does not prove that the methylene blue was responsible for the patient’s clinical improvement, and this treatment might not yet be ready for prime time. But it another small piece of evidence suggesting that in poisonings producing hypotension, vasodilatation and distributive shock, methylene blue may have role.
In their discussion, the authors note that adverse effects of methylene blue include nausea, vomiting, chest pain, confusion, sweating and hypertension. It is also an MAO inhibitor; despite this and the ingestion of fluoxetine (240 mg), there were no signs of serotonin syndrome.
NOTE: One other intervention that — although not yet proven — might have been reasonable to try would have intralipid emulsion therapy.