Question 10.2

The following arterial blood gas was obtained from a 19-year-old chemistry student who presents with dyspnoea, cyanosis and feeling unwell. He has been handling chemicals today and admits to recreational drug use but takes no prescribed medicines. His observations on 8 L/min oxygen via a Hudson mask are as follows:

Temperature:               37.2ºC

Heart rate:                                    130 beats/min sinus

Blood Pressure:                                    140/73 mmHg

Oxygen Saturation:                                    82%

His initial arterial blood gas analysis is given below:

Parameter Patient Value Adult Normal Range
FiO2 0.4  
pH 7.45 7.35 – 7.45
pO2 219 mmHg (29.2 kPa)  
pCO2 37.8 mmHg (5.04 kPa) 35.0 – 45.0 (4.60 – 6.00)
SpO2 98.1%  
Bicarbonate 26.6 mmol/L* 22.0 – 26.0
Base Excess 2.6 mmol/L* -2.0 – +2.0
Lactate 0.9 mmol/L 0.5 – 1.6
Sodium 139 mmol/L 135 – 145
Potassium 3.9 mmol/L 3.5 – 5.0
Chloride 107 mmol/L* 95 – 105
Ionised Calcium 1.18 mmol/L 1.15 – 1.29
Glucose 7.1 mmol/L* 3.5 – 6.0

a) What is the diagnosis? (10% marks)

b) Name two recreational drugs and two chemical compounds that can cause this condition other than prescribed medicines. (20% marks)

c) What emergency treatment would you give? (20% marks)

d) In what circumstance would your treatment of choice be contraindicated? (10% marks)

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College answer

Not available.


a) This is methaemoglobinaemia. The chemistry student is hopped up on nitrites. The specific clues to this diagnosis are

  • Cyanosis, which the college examiners kindly alerted us to
  • Periphaeral pulse oximeter sats of 82%
  • Arterial blood gas analyser oximeter sats of 98.1%

Thus, this is methaemoglobinaemia.

Now, one should point out that when you write "SpO2", the little "p" usually means "pulse", and so it is confusing and weird to see it in the ABG results. Usually the blood gas analyser will report an "SaO2", where the "a" stands for "arterial". It may seem pedantic to pick on these minor elements, but then some might say that ICU is all about being thorough and detailed. It is especially confusing to find this mistake in a question where specifically the difference between the pulse oximeter and the arterial oximeter is a critically important part of the diagnosis.

Anyway: methaemoglobinaemia.

b) Recreational drugs which cause methaemoglobinaemia are:

  • Amyl nitrite
  • Phenylamine (also known as aniline, a volatile solvent inhaled by reprobates for amusement)
  • Excipients cut into street cocaine (usually benzocaine, so you can't feel your face)

Non-recreational chemical compounds are numbered in the countless thousands; though the author confesses he has not personally audited this list to make sure none of these substances has any enjoyable effects. Briefly:

  • Sodium nitrite (used in making home-made sausage products)
  • Ammonium nitrite (a fertiliser)
  • Nitrobenzene (an industrial solvent)
  • 2-Chloro-m-toluidine 
  • Xylidene
  • Trinitrotoluene
  • p-Dinitrosobenzene

You could also have used use nitric oxide, so long as you mention that it is a part of internal combustion engine exhaust (even though it could theoretically also be used medically to treat pulmonary hypertension). In case it is necessary in some future version of this question, prescribed medicines which cause methaemoglobinaemia include:

  • Nitric oxide (pulmonary vasodilator)
  • Nitroprusside (systemic vasodilator)
  • Dapsone (a second line agent for PJP prophylaxis/treatment)

c) Emergency treatment of methaemoglobinaemia:

This is discussed in much more detail in Question 1 from the second paper of 2004, where it was a full 10-mark question. Here, for 20% of the mark, you would only have time to write this much:

  • Glucose infusion
  • Methylene blue 1-2mg/kg over 5 minutes
  • Ascorbic acid, 200mg/kg if the patient has G6PD deficiency.

d) "your treatment of choice be contraindicated" if the patient has G6PD deficiency. If your treatment of choice was ascobic acid, you would be just fine. 

  • G6PD provides the NADPH for methamoglobin reductase. If G6PD is deficient, haemolysis will occur after administration of methylene blue (Rosen et al, 1971)


Wright, Robert O., William J. Lewander, and Alan D. Woolf. "Methemoglobinemia: etiology, pharmacology, and clinical management."Annals of emergency medicine 34.5 (1999): 646-656.

ROSEN, PETER J., et al. "Failure of methylene blue treatment in toxic methemoglobinemiaAssociation with glucose-6-phosphate dehydrogenase deficiency." Annals of internal medicine 75.1 (1971): 83-86.