Food Poisoning Associated Acquired Methemoglobinemia: A Case Report

Introduction

Availability of sufficient amounts of safe and nutritious food is vital to sustaining life and promoting good health. Unsafe food containing harmful bacteria, viruses, parasites or chemical substances, causes more than 200 diseases – ranging from diarrhoea to cancers. Approximately 600 million people suffer from illness after eating contaminated food and 420 000 die annually. Among them, 40% are children under 5 years of age.1Food contamination is a serious concern across the globe especially in low-income-countries. High concentration of chemicals used as food preservatives can lead to serious illness.² We present a three-year-old girl with food poisoning associated acquired methemoglobinemia.

Case Report

A three-year-old girl was admitted to Parami General Hospital with a sudden episode of cyanosis. Five hours before admission, she ate four roasted chicken sausages brought from a shop at a street market nearby her home. Two hours later, she vomited twice which contained old food. Her mother noticed that her daughter was drowsy and she looked blue. Parents brought her to a general practitioner. The general practitioner found that she had profound peripheral and central cyanosis. Her SpO₂ was 62% on room air. Therefore, she was referred to Parami General Hospital.

She was a previously healthy girl. She had neither cyanotic congenital heart disease nor chronic respiratory problems. She had no history of taking any medicine, including traditional ones. Her immunization status was up-to-date as per Myanmar EPI schedule. Her mother, who ate the same type of one roasted chicken sausage, also vomited once but she did not have any cyanosis. Her father and her older siblings are healthy. No known history of congenital methemoglobinemia among family members.

On examination, she was quite drowsy. She had marked peripheral and central cyanosis. However, she was not dyspneic and did not have any respiratory distress. She did not have pallor or finger clubbing. She had tachycardia (heart rate 165 per minute). Her blood pressure was normal (100/70 mmHg) and SpO2 was 82% with 10 L of oxygen with a non-rebreather mask. Her respiratory rate was 32 per minute. Her heart sounds were normal and she had no added sound. Respiratory examination was also normal. Apart from drowsiness, nervous system examination was also normal.

Fig.1.Marked central cyanosis

In view of a sudden episode of profound peripheral and central cyanosis without any cardiopulmonary problem, acquired methemoglobinemia was suspected and treatment was started immediately after taking blood samples for investigations.

Full blood count was normal (Hb 10.5 g%, WBC 13.59 x 109/L, Platelet count 345 x 109/L). Liver function test (ALT 16.8 U/L, AST 27 U/L, ALP 166 U/L, Bilirubin 3.9 umol/L), urea,electrolytes, creatinine (Urea 3.9 mmol/L, Na+ 137.5 mmol/L, K+3.99 mmol/L, chloride 106 mmol/L, creatinine 35.2umol/L), random blood sugar (5.5 mmol/L), G6PD level (7.6 IU/g Hb) were also normal. She had mild metabolic acidosis with bicarbonate 18 mmol/L. Her blood methemoglobin level was high (MetHb 50%).

She was finally diagnosed as having acquired methemoglobinemia.

Oxygen 10L with a non-rebreather mask was given. However, she was not responding to oxygen therapy at all initially. Intravenous ascorbic acid (vitamin C) 1 gram was given over 8 hours. Intravenous dextrose saline (5% dextrose and 0.9% sodium chloride) 3ml per kg per hour was given for 24 hours. Her peripheral and central cyanosis disappeared after 6 hours. Her oxygen saturation went up gradually and reached over 95% without oxygen after 12 hours. Her heart rate dropped to normal after 12 hours. Then, she tolerated oral feeding well. Her condition improved significantly and was discharged from hospital 36 hours later. Oral ascorbic acid 500 mg twice a day was given for one week. One week later, she was reviewed at an outpatient clinic and found to be completely well.

Discussion

Methemoglobinemia (MetHb) is a rare cause of cyanosis in the pediatric population that can cause significant morbidity and mortality. MetHb occurs when the iron atom in hemoglobin loses one electronto an oxidant, and the Fe II istransformed into Fe III. Because Fe III iron is unableto bind oxygen, and the oxygen affinity of any remaining Fe II in the hemoglobin is increased, a left shift occurs inthe oxygen dissociation curve, resulting in functional anemia and impaired oxygen delivery to the tissues.3 There are two forms of methemoglobinemia, congenital and acquired forms. Acquired methemoglobinemia is usually caused by ingestion of drugs or exposure to toxic substances that cause acceleration of Hb oxidization from the ferrous to the ferric state. The drugs that cause methemoglobinemia are numerous, including sulfonamides, lidocaine and otheraniline derivatives, and nitrites. Nitrates used as preservatives in foods can also be trigger agents. The clinical presentation is widely variable and it depends on levels of MetHb.⁴ The main features are cyanosis, pallor, fatigue, weakness, headache, drowsiness, metabolic acidosis, seizures, dysrhythmias, coma, and death.⁵ In this patient, she presented with a sudden episode of profound peripheral and central cyanosis after having roasted chicken sausages which was bought from a shop at a street market. The sausages might contain a high level of nitrates or other harmful chemicals which are commonly used as food preservatives. The drug of choice for treatment of acquired methemoglobinemia is intravenous methylene blue (MB). However, intravenous form of MB is not available in Myanmar. In addition, MB is contraindicated in people with G6PD deficiency as it is not only effective but also causes severe hemolysis. Ascorbic acid is the drug of choice in G6PD deficient patients.6 In our patient, she responded to intravenous ascorbic acid beautifully.

Conclusion

Food safety is a matter of grave concern in Myanmar. Acquired methemoglobinemia should be considered in healthy children who present with a sudden episode of profound peripheral and central cyanosis without abnormal cardiopulmonary findings. Ascorbic acid is also very effective in the treatment of acquired methemoglobinemia.

References

1. World Health Organization.Food safety. [cited March 23, 2022]Available from:https://www.who.int/news-room/fact-sheets/detail/food-safety.
2. Rather IA, Koh WY, Paek WK andLim J (2017) The Sources of ChemicalContaminants in Food and Their Health Implication. Front. Pharmacol. 8:830.
3. Prchal J. Methemoglobinemia and other Dyshemoglobinemias. 10th ed. McGraw Hill; 2021.
4. Wright RO, Lewander WJ, Woolf AD. Methemoglobinemia: etiology, pharmacology, and clinical management. Ann Emerg Med. 1999;34(5):646-656.
5. Skold A, Cosco DL, Klein R. Methemoglobinemia: pathogenesis, diagnosis, and management. South Med J. 2011;104(11):757-761.
6. Rehman A, Shehadeh M, Khirfan D, Jones A. Severe acute haemolytic anaemia associated with severe methaemoglobinaemia in a G6PD-deficient man. BMJ Case Rep. 2018; 2018:223369.

Author Information

Aung Khin Thein¹, Phooe Thit Shein², Cho Thair², Swe Zin Hlaing², May Thu Thu Aung², Kaung Sett Win², Thet Naing Soe²

1. Associate Professor/ Consultant Paediatrician, Yankin Children Hospital
2. Medical officers, Parami General Hospital