NZMA Home

Table of contents
Current issue
Search journal
Archived issues
NZMJ Obituaries
Classifieds
Hotline (free ads)
How to subscribe
How to contribute
How to advertise
Contact Us
Copyright
Other journals
The New Zealand Medical Journal

 Journal of the New Zealand Medical Association, 04-August-2006, Vol 119 No 1239

Deadly meatballs—a near fatal case of methaemoglobinaemia
Ali Khan, Adrienne Adams, Greg Simmons, Timothy Sutton
A 47-year-old Māori male was found unresponsive and ‘blue’ by family members when they returned home at night. When last seen he had been playing cards with friends. He was brought in by ambulance.
At presentation, he was severely hypoxic and centrally cyanosed with SpO2 of 64% despite 100% oxygen. Temperature was 35.7°C, heart rate (HR) 126/minute, blood pressure (BP) 111/59 mmHg and Glasgow Coma Score (GCS) of 5/15 with urinary incontinence and tonic seizure-type movements.
Venesection yielded chocolate-brown coloured blood. Arterial blood gas analysis showed pH of 7.29, PO2 of 10.2 kPa, PCO2 of 4.7 kPa, HCO3 of 16 mmol/L, lactate of 9.2 mmol/L, and base excess of –9 mmol/L. Haematological and biochemical indices were normal.
A diagnosis of methaemoglobinaemia of uncertain trigger was made on clinical grounds. Treatment was then commenced with methylene blue (MB). His colour promptly returned to normal and cyanosis corrected. Arterial blood gas (ABG) analysis 2 hours after MB infusion (when he was feeling well), revealed a methaemoglobin (Met-Hb) level ~2.6%, still higher than normal (Due to a problem with the blood gas analyser, the Met-Hb level could not be measured earlier in the acute stage.) His rapid response to the MB infusion confirmed methaemoglobinaemia as the cause of the hypoxia. He made a full recovery and was discharged after 3 days.
Earlier on the evening of admission the patient had eaten microwave-heated meatballs. About an hour later he vomited then lost consciousness. The day after admission, the left-over meatballs were recovered by his daughter from the fridge and analysis in Environmental Science and Research (ESR) revealed the sodium nitrite level at 4.3% w/w (43000mg/kg), which exceeded the recommended nitrite level as meat preservative by 344-fold. The Auckland Regional Public Health Service was notified and an immediate inspection and product recall was initiated.
Seven trays totalling 56 meatballs were made at a local butchery 2 days before. The preparation involved mixing flavouring powder to minced meat. A bag of nitrite powder labelled ‘poison’ was kept alongside the bag of flavouring powder. A worker who knew very little English made the meatballs for the first time on that occasion, with verbal instruction from co-worker. He added 500 grams of nitrite to the minced meat instead of flavouring, not knowing the meaning of the word ‘poison’ written on the bag.
The patient had purchased one tray and two were purchased by another woman, who reported no ill effect from consumption; 32 meatballs remained unaccounted for. The majority of the customers were Pacific Islanders. Product recall notices were placed in local newspapers and aired over a local radio, but none were ever returned.
Meatballs are considered ‘cured meat’—and under the joint Australia New Zealand Food Standards Code, nitrite (as a meat preservative not exceeding 125 mg/kg) is permitted.1 Methemoglobinemia from consumption of cured meats is well recognised,2,3 but rarely are levels measured. One outbreak involving three cases implicated meat containing nitrite at 10,000–15,000 mg/kg, only one-third of the level in our case.
Methaemoglobinaemia is a potentially fatal condition. Ferrous iron in haemoglobin is oxidised to ferric form and resulting methaemoglobin is incapable of binding oxygen.4 This reduces the oxygen carrying capacity of blood and profound cyanosis ensues. Methemoglobinaemia can result from congenital deficiency,5 or acquired from excessive exposure to substances that oxidise haemoglobin including nitrite/nitrates, aniline derivatives, local anaesthetics, sulphonamides, dapsone, and quinones 6,7.
Nitrites/nitrate exposure is the commonest acquired cause which can result from inhalation of room odorisers,8 ingestion of contaminated water,9 or meat products where nitrite is used as preservative for its property of inhibiting growth of Clostridium botulinum.
Two enzyme systems in red blood cells (RBCs) reduce methaemoglobin (Met-Hb) to haemoglobin (Hb)—NADH cytochrome beta-5 reductase and reduced NADPH methaemoglobin reductase (for which methylene blue is a co-factor). Reduced methylene blue in turn reduces Met-Hb back to Hb, which is the basis of methylene blue therapy.10
This case highlights the need for care in the use of chemical food preservatives, and it emphasises the importance of staff training where potentially toxic food additives are used.
Author information: Ali Khan, Medical Registrar, Middlemore Hospital*; Adrienne Adams, Emergency Physician, Middlemore Hospital; Greg Simmons, Medical Officer, Auckland Regional Public Health Service; Timothy Sutton, Consultant Physician and Cardiologist, Middlemore Hospital; Auckland
(*Currently Cardiology Registrar at Auckland City Hospital)
Correspondence: Dr Ali Khan, Department of Cardiology, Level 3, Auckland City Hospital, Private Bag 92024, Grafton, Auckland. Fax: (09) 307 2899; Email address: ali.khan@adhb.govt.nz
References:
  1. The Australia New Zealand Food Standards Code. Canberra: Food Standards Australia New Zealand; 2001.
  2. Bakshi SP, Fahey JL, Pierce LE. Brief recording: sausage cyanosis--acquired methemoglobinemic nitrite poisoning. New Engl J Med. 1967;277:1072.
  3. Chan T. Food-borne nitrates and nitrites as a cause of methemoglobinaemia. Southeast Asian Journal of Tropical Medicine and Public Health. 1996;27:189–92.
  4. Conant JB. The oxidation of haemoglobin and other respiratory pigments. Harvey Lect. 1932-33;28,159–83.
  5. Gabel RA, Bunn HF. Hereditary methemoglobinemia as a source of cyanosis during anaesthesia. Anaesthesiology. 1974;40:516–18.
  6. Modarai B, Kapadia YK, Kerins M, Terris J. Methylene blue: a treatment for severe methaemoglobinaemia secondary to misuse of amyl nitrite. Emerg Med J. 2002;19:270–1.
  7. O'Donohue WJ, Moss LM, Angelillo VA. Acute methemoglobinemia by topical benzocaine and lignocaine. Arch Intern Med. 1980;140:1508–9.
  8. Shesser R, Mitchell J, Edelstein S. Methemoglobinemia from isobutyl nitrite preparations. Ann Emerg Med. 1981;10:262–4.
  9. MMWR: Morbidity and Mortality Weekly Report, 3 July 1997, Vol. 46; Issue 9, p202.
  10. Metz EN, Balcerzak SP, Sagon LR. Mechanism of methylene blue stimulation of the hexose monophosphate shunt in the erythrocyte. J Clin Invest. 1976;58:797–802.
     
Current issue | Search journal | Archived issues | Classifieds | Hotline (free ads)
Subscribe | Contribute | Advertise | Contact Us | Copyright | Other Journals