Cost of beauty; prilocaine induced methemoglobinemia brain anoxia

Introduction

Hemoglobin (hb) is a molecule which carries oxygen from respiratory organs to the rest of the body. Hb binds to iron in a ferrous (fe 2+) oxidation state under normal conditions. However, the existence of oxidative stress is known to transform iron to ferric iron (fe 3+). Upon oxidation, hemoglobin or methemoglobin (methb) cannot bind to oxygen molecules. In methemoglobinemia, the hb is unable to release oxygen effectively to body tissues. While mild forms of methemoglobinemia can be asymptomatic, cyanosis, tachypnea, tachycardia, hypotension, confusion, and even death can be seen in the more severe cases. [1] there are three common causes of methemoglobinemia, including hemoglobinopathies, hereditary enzyme deficiencies (NADH methb reductase), and exposure to drugs.Brain anoxia


interestingly, hemoglobinopathies and hereditary enzyme deficiencies (NADH methb reductase) are the least common causes, whereas exposure to drugs is the most common. [2]

Many chemicals and drugs had been reported to cause toxic methemoglobinemia, including nitrite, nitrate, chlorate, quinine, aminobenzene, nitrobenzene, nitrotoluenes, phenacetin, chloroquine, dapson, phenytoin, sulphonamides, and local anesthetics. [3] methemoglobinemia, caused by prilocaine a local anesthesia is rare. [4] prilocaine, a derivative of toluidine, is an amide local anesthetic and has been shown to produce high methb levels. 2, 5 because of its rarity, our knowledge about treatment use is limited. In this paper, we discuss a treatment strategy using ascorbic acid for a patient diagnosed with methemoglobinemia by prilocaine.Brain anoxia research targets and strategies to understand best treatment strategies will be discussed.

Case report

A 30-year-old woman was admitted to emergency department (ED) with complaints of tachycardia, headache, dyspnea, and cyanosis. It was learned from her history that she was anesthetized with 2.5–3 vials (1000–1200 mg?) of prilocaine (citanest®) subcutaneously before a laser hair removal procedure. Although the severity of the symptoms decreased at the time of ED admission compared to the initial time point, her symptoms were still ongoing. The patient’s medical history was unremarkable. The tension arterial rate was 130/73 mmhg, pulse rate was 103/minute, body temperature was 37 °C, and respiratory rate was 20/minute.Brain anoxia the pulse oximeter measured O 2 saturation as 90%, and she had acral cyanosis. Electrocardiography revealed sinus tachycardia with a rate of 103/minute. Chest radiograph, complete blood counting, renal function tests and electrolytes were all in the normal range. Venous blood gas analyses revealed methb as 14.1%. Despite treatment with 4 L/minute O 2, her symptoms were still continual. She was admitted to the intensive care unit and 3 grams of ascorbic acid was given intravenously. Two hours after treatment, control methb was measured as 2.4%, and the patient was free of symptoms and with no complications. She was discharged as healthy upon a 48 hour of follow up period.

Discussion

Prilocaine at therapeutic doses (1–2 mg/kg) can cause limited methemoglobinemia without cyanosis. [6] the maximum safe dose of prilocaine is 8 mg/kg (maximum of 600 mg) as a single injection. [2] in this case, 1000–1200 mg of prilocaine was administered, in which the limits were highly exceeded.Brain anoxia the effects of local anesthetic induced methemoglobinemia are known and include seizures, respiratory compromise, myocardial infarction, shock state, coma, hypoxic encephalopathy, and death. In a retrospective study it was reported that most patients with a methemoglobin (≥8%) were symptomatic. [7]

In methemoglobinemia resulting from chemical substances, the first step of treatment is to avoid further exposure. If methemoglobinemia is under 20%, spontaneous recovery is usually observed after drug avoidance, but treatment may be necessary in newborns and infants. [8] methylene blue, ascorbic acid, and riboflavin have been suggested as treatment modalities. [9] methylene blue should be administered 1–2 mg/kg intravenously in five minutes, and repeated one hour later if adequate improvement is not observed. [10] it is contraindicated in patients with glucose 6 phosphate dehydrogenase deficiency because administration of methylene blue can cause aggravation of methemoglobinemia, chest pain, cyanosis and hemolytic anemia. [3] in such cases, ascorbic acid can be considered as an antidote. 11, 12 hyperbaric oxygen therapy and exchange transfusion is another option if methb level is over 70%.Brain anoxia

Ascorbic acid reduces methb by a non-enzymatic processes in animal and human erythrocytes in vitro, which makes ascorbic acid a candidate for treatment of methemoglobinemia. 13, 14 it is most commonly used orally in long term treatment of patients with hereditary methemoglobinemia. [1] although, methylene blue can be a first choice treatment of methemoglobinemia, if there is limited experience in the use of ascorbic acid in toxic methemoglobinemia. [15] although methb was measured relatively less (14.1%) in the present case, there was an indication of antidote therapy due to the patient being symptomatic. In addition, ascorbic acid was chosen because a limited supply of methylene blue in the hospital.Brain anoxia after administration of ascorbic acid, methb was measured as 2.4% and she was asymptomatic. Aydogan et al. Reported that two patients with methemoglobinemia recovered after ascorbic acid administration. [13] tekbas et al. Also reported an improvement in a patient with combined treatment of methylene blue and ascorbic acid caused by methemoglobinemia due to prilocaine given before intravascular laser therapy. [16]