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Lachgas: om te lachen?
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Nitrous oxide: no laughing matter In this case study, the authors discuss the dangers and medical relevance of the increasing recreational use of nitrous oxide. Nitrous oxide is a legal and readily available gas that has been gaining popularity as a drug in recent years, especially among young people. Unlike medicinal use where the nitrous oxide is mixed with oxygen, this is not the case when it comes to nitrous oxide used as a drug. For this reason, acute intoxication can cause temporary hypoxia resulting in coordination disorders, a slight loss of consciousness and a headache. Chronic intoxication causes myelo- and neuropathy due to a functional vitamin B12 deficiency. Clinically, motor weakness, gait ataxia and sensory abnormalities are mainly observed, in which the lower limbs are classically more affected than the upper limbs. The diagnosis is based on a combination of anamnestic and clinical findings, as well as typical findings on an MRI and electromyographic examination. The administration of vitamin B12 can be considered as part of the treatment. However, cessation of the nitrous oxide abuse itself is paramount for symptoms to disappear. In the event of a suspicious clinical presentation, care providers should therefore actively inquire about possible nitrous oxide use so that timely action can be taken.
Title: Lachgas: om te lachen?
Description:
Nitrous oxide: no laughing matter In this case study, the authors discuss the dangers and medical relevance of the increasing recreational use of nitrous oxide.
Nitrous oxide is a legal and readily available gas that has been gaining popularity as a drug in recent years, especially among young people.
Unlike medicinal use where the nitrous oxide is mixed with oxygen, this is not the case when it comes to nitrous oxide used as a drug.
For this reason, acute intoxication can cause temporary hypoxia resulting in coordination disorders, a slight loss of consciousness and a headache.
Chronic intoxication causes myelo- and neuropathy due to a functional vitamin B12 deficiency.
Clinically, motor weakness, gait ataxia and sensory abnormalities are mainly observed, in which the lower limbs are classically more affected than the upper limbs.
The diagnosis is based on a combination of anamnestic and clinical findings, as well as typical findings on an MRI and electromyographic examination.
The administration of vitamin B12 can be considered as part of the treatment.
However, cessation of the nitrous oxide abuse itself is paramount for symptoms to disappear.
In the event of a suspicious clinical presentation, care providers should therefore actively inquire about possible nitrous oxide use so that timely action can be taken.
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