ISSN: 2373-6372GHOA

Gastroenterology & Hepatology: Open Access
Case report
Volume 2 Issue 4 - 2015
Case Report: Methemoglobinemia Caused by Benzocain Spray – A Warning for Surgeons
Jacob Eisdorfer1, Jalil Anwar2 and David Rivadeneira*1
1Department of Colon and Rectal Surgery, Hofstra North Shore LIJ School of Medicine, USA
2Department of Medicine, Huntington Hospital, USA
Received: July 8, 2015| Published: August 07, 2015
*Corresponding author: David Rivadeneira, MD, MBA, FACS, FASCRS, Department of Colon and Rectal Surgery, Hofstra North Shore LIJ School of Medicine, USA, 321-B Crossways Park Drive, Woodbury, NY 11797, USA, Tel: 631-470-1450; Fax: 631-470-1451; Email:
Citation: Eisdorfer J, Anwar J, Rivadeneira D (2015) Case Report: Methemoglobinemia Caused by Benzocain Spray – A Warning for Surgeons.Gastroenterol Hepatol Open Access 2(4):00048. DOI: 10.15406/ghoa.2015.02.00048

Abstract

Methemoglobinemia due to topical Benzocaine spray is an entity that has been well described in the literature, however it is quite uncommon. Many physicians use benzocain spray for patient comfort during and after several procedures, the most common being Transesophageal Echocardiography, Upper Endoscopy, Bronchoscopy, and Nasogastric Tube Placement. This condition is a potentially catastrophic one, especially if not considered, and diagnosed late. Methemoglobinemia should be considered in any patient who has oxygen resistant cyanosis, or an oxygen “saturation gap” between pulse oximetry and arterial blood gas, particularly if they are known to have had exposure to one of the substances that cause the condition. Herein we present a case of acquired methemoglobinemia, and a discussion of the pathophysiology, diagnosis and treatment.

Keywords: Methemoglobinemia; Surgery; Benzocaine; Topical anesthetic

Introduction

Methemoglobinemia is a condition whereby there is an increase in the fraction of methemoglobin in the red blood cells. The normal state of hemoglobin contains the iron molecule in the divalent ferrous state. Methemoglobin results from the oxidation of ferrous iron to a trivalent ferric iron. Methemoglobin cannot bind and carry oxygen. The outcome of this is a functional hypoxia due to the decreased oxygen carrying capacity of the red blood cells. Also, the remaining heme groups, which do not have the oxidized iron have an increased binding affinity for oxygen [1,2]. Therefore they do not release oxygen as easily at the tissue level and cause tissue hypoxia. As red blood cells are constantly exposed to oxidizing agents methemoglobin is formed at a rate of about three percent per day. Several physiologic mechanisms reduce it to deoxyhemoglobin. These pathways include the cytochrome b5, nicotinamide adenine dinucleotide (NADH), ascorbic acid, glucose-6-phosphate dehydrogenase (G6PD), and glutathione reduction enzyme systems. Under normal physiologic circumstances these mechanisms maintain equilibrium where the methemoglobin level is less than one percent [2].

Acquired Methemoglobinemia can be caused by a host of substances. Most commonly it is reported after the use of oropharyngeal topical anesthetic sprays such as Benzocaine, Lidocaine, and Prilocaine; Benzocaine is by far the most common. This results in elevated methemoglobin by direct or indirect oxidation of the hemoglobin [3]. Patients with methemoglobinemia may present with headaches, lack of energy, increased heart rate, shortness of breath, or light headedness. Signs that are present include cyanosis, dark brown discoloration of the blood, and low pulse oximetry in the presence of normal arterial blood gas readings [2,4]. Symptomatology has been correlated with methemoglobin levels. Levels in the ten percent to twenty-five percent range show cyanosis. Levels from thirty-five percent to forty percent cause headache, fatigue, dizziness and dyspnea. Levels of sixty percent can lead to arrhythmias, seizures, lethargy, and stupor. Levels greater than seventy percent have been associated with vascular collapse and death [5].

Treatment is generally begins with discontinuation of the offending agent. Not all acquired methemoglobinemia requires additional treatment. Usually if the methemoglobin level is lest then twenty percent and the patient is asymptomatic, no treatment is required. Generally if the methemoglobin level is greater than thirty percent, or there is cyanosis or respiratory or cardiac distress, the patient should be treated [5,6]. In the most severe cases, exchange transfusion or hyperbaric oxygen has been used with anecdotal success [6]. The treatment of choice for most cases is Methylene Blue, it provides an artificial electron transporter to aid in the reduction of methemoglobin. It is given in a dose of 1-2 mg/kg IV over five minutes [1]. Risks associated with Methylene Blue are as follows: Overdoses occur with doses larger than seven mg/kg, which can be cumulative from multiple administrations. Overdose can lead to dyspnea, chest pain, and hemolysis in certain individuals [7,8]. In patients with G6PD deficiency, Methylene Blue will likely be ineffective, and may lead to hemolysis [9].

Case Presentation

Our patient is an eighty-one year old female who presented with an adhesive small bowel obstruction. She was admitted to the hospital and had a short course of non-operative management. She continued to be obstipated and the decision was made to proceed to surgery. She underwent an abdominal exploration, and lysis of adhesions. Post operatively she had a nasogastric tube in place; she was given Benzocaine 20% spray topically for discomfort from the tube. After two applications she began to exhibit signs of cyanosis and her pulse oximetry reading fell to eighty-two percent, she had no respiratory difficulties. An arterial blood gas was obtained and the saturation was ninety-seven percent, at this time a methemoglobin level was obtained and it was 22%. The patient received 1mg/kg of Methylene Blue IV, six hours after this her cyanosis was gone, her saturation was 94% and her methemoglobin level was 8%, an additional methemoglobin level was obtained six hours later and it was three percent (Table 1).

Methemoglobin Level (%)

Pulse Oximetry (%)

Arterial Blood Gas O2 Saturation (%)

Cyanosis

Methylene Blue given

22

82

97

Yes

1mg/kg

8

94

98

No

None given

3

96

97

No

None given

Table 1: Patient response to treatment.

Discussion

Methemoglobinemia is a potentially fatal condition that is acquired due to an adverse reaction to a medication. Prior to this event our group used topical benzocaine spray as needed for anyone with any oriopharyngeal discomfort, and routinely for anyone with a nasogastric tube. Methemoglobinemia is extremely rare and the vast majority of patients who receive benzocaine spray will not develop this condition, however one must have a high index of suspicion in order to avoid delay in treatment and possibly a devastating outcome.

References

  1. Kane GC, Hoen SM, Beherenbeck TR, Mulvagh SL (2007) Benzocaine-induced methemoglobinemia based on the Mayo Clinic experience from 28478 transesophageal echocardiograms: incidence, outcomes, and predisposing factors. Arch Intern Med 167(18): 1977-1982.
  2. Chowdhary S, Bukoye B, Bhansali AM, Carbo AR, Adra M, et al. (2013) Risk of topical anesthetic-induced methemoglobinemia: a 10-year retrospective case-control study. JAMA Intern Med 173(9): 771-776.
  3. Taleb M, Ashraf Z, Valavoor S, Tinkel J (2013) Evaluation and management of acquired methemoglobinemia associated with topical benzocaine use. Am J Cardiovasc Drugs 13(5): 325-330.
  4. Skold A, Cosco DL, Klein R (2011) Methemoglobinemia: pathogenesis, diagnosis and management. South Med J 104(11): 757-761.
  5. El-Husseini A, Azarov N (2010) Is threshold for treatment of methemoglobinemia the same for all? A case report and literature review. Am J Emerg Med 28(6): e5-748.
  6. Goldstein GM, Doull J (1971) Treatment of Nitrite-Induced Methemoglobinemia with Hyperbaric Oxygen. Proc Soc Exp Biol Med 138(1): 137-139.
  7. Goluboff N, Wheaton R (1961) Methylene blue induced cyanosis and acute hemolytic anemia complicating the treatment of methemoglobinemia. J Pediatr 58: 86-89.
  8. Harvey JW, Keitt AS (1983) Studies of the efficacy and potential hazards of methylene blue therapy in aniline-induced methaemoglobinaemia. Br J Haematol 54(1): 29-41.
  9. Rosen PJ, Johnson C, McGehee WG, Beutler E (1971) Failure of methylene blue treatment in toxic methemoglobinemia. Association with glucose-6-phosphate dehydrogenase deficiency. Ann Intern Med 75(1): 83-86.
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