Methaemoglobinemia - developinganaesthesia
METHEMOGLOBINEMIA
Introduction
Methemaglobinemia refers to hemoglobin, which contains its iron in the Fe+++ (ferric) form, as opposed to the normal Fe++ (ferrous) form.
Unlike the Fe++ form the Fe+++ form cannot carry oxygen.
Normal adults have levels of methemaglobin of up to 1%.
Levels that are greater than 1% are referred to as methemaglobinemia
A number of drugs and toxins can cause life-threatening methemaglobinemia. Treatment is with methylene blue.
Cyanosis not responding to oxygen therapy raises suspicion for the condition.
Diagnosis is by co-oximetry on arterial blood gases.
Normal Methemaglobin Metabolism
Fe+++ Hb
NADPH dependent NADH dependent
Met Hb reductase Met Hb reductase
(5%) (95%)
Fe++ Hb
Methylene Blue (acts as a co-factor for the minor pathway and therefore greatly enhances the activity of this pathway)
Causes of Methemaglobinemia
Congenital:
1. Hb M disease.
2. NADH dependent Met Hb reductase deficiency
Acquired:
Causes are drugs and toxins, which can act as oxidizing agents
The more common causative agents include:
1. Nitrites
2. Nitrates (much less so than the nitrites)
3. Aniline dyes:
● Inks, paints, varnish, shoe polish.
4. Some local anesthetic agents:
● Prilocaine, procaine.
5. Some antibiotics:
● Sulfonamides, dapsone.
6. Phenytoin
7 Quinones:
● Chloroquine, primaquine.
8. Toxins:
● Propanil (a commonly used herbicide)
Clinical Features
Cyanosis not responding to oxygen therapy.
The signs and symptoms are those of hypoxia.
| | |
|Level metHb |Clinical features |
| | |
|60% |Increasing signs of hypoxia, seizures, confusion, arrhythmias hypotension. |
| | |
|>70% |Can be lethal in otherwise healthy individuals. |
Investigations
Pulse oximetry:
Pulse oximeter reading will not be reliable.
● Methemaglobinemia interferes with normal oximetry.
● With increasing levels of methemoglobin, oximeter readings fall to about 85%, but then will stay around this level with further increases. Methemoglobin has a maximal light absorption at a wavelength similar to oxyhemaglobin (660 nm) and is therefore not readily differentiated from oxyhemoglobin.
ABGs:
For ABGs:
● The PaO2 will not be affected.
● Co-oximetry will give a direct met Hb level, the definitive diagnosis.
● A metabolic acidosis, reflecting tissue hypoxia.
Bedside absorbent filter paper test:
A crude bedside test is to drop some blood from the patient onto some filter paper, its color will appear typically chocolate brown, with levels above 20 %.
A more accurate approximation to the actual methemoglobin level can be achieved by use of a specifically designed color chart, (see Appendix 1 below).
Management
1. Immediate attention to the usual ABC issues of supportive care.
● IV access
● Establish ECG monitoring and pulse oximetry.
2. Consider charcoal if recent ingestion of causative agent and if airway is not (nor likely to be) compromised.
3. Methylene blue:
The specific antidote is methylene blue.
1 mg / Kg (= 0.1 ml / kg of the 1% solution) IV slowly over 5 minutes.
Up to 2 mg/kg (= 0.2 ml/ Kg of the 1% solution) IV slowly over 5 minutes may be given.1
This dose can be repeated in 30 minutes to one hour if necessary.
Follow each dose with a saline flush to reduce venous irritation.
Improvement should be seen within 30-60 minutes.
Therapeutic end points:
● Resolution of symptoms
● Falling methemoglobin levels.
If methylene blue fails to control methemaglobinemia consider exchange transfusion or hyperbaric oxygen therapy.
Failure of Methylene Blue Treatment for Methemaglobinemia:
The following will need to be considered:
● Wrong diagnosis:
♥ e.g. in sulfhemoglobinemia or CO poisoning methylene blue is not effective.
● The patient has NADPH met Hb reductase deficiency (very rare)
● The dose of methylene blue given has been excessive.
● The dose of methylene blue given has not been adequate.
● There is ongoing formation of methemaglobinemia, such as continual GIT absorption of a toxic agent.
Possible alternatives to methylene blue therapy include:
4. Hyperbaric oxygen therapy:
● The partial pressure of oxygen in plasma can be increased to such a degree as to ensure adequate oxygen transport in the absence of any functioning Hb.
5. Exchange transfusions:
● Exchange transfusions are an alternative for patients with G-6-P deficiency (methylene blue can cause massive hemolysis in these patients) or in patients who fail to respond to methylene blue therapy.
Appendix 1
References:
1. Methylene blue in L Murray et al. Toxicology Handbook 3rd 2015.
2. Zalstein S Methaemoglobinaemia case report in Emergency Medicine: 1993:5 p 71
3. Fathima Shihana et al. A Simple Quantitative Bedside Test to Determine Methemoglobin. Ann Emerg Med. 2010; 55: 184 - 189.
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