The progression of the condition can be monitored by marking the boundaries with a special pencil for marking on skin.Since treatment usually involves dealing with the underlying condition, cases of spontaneous subcutaneous emphysema may require nothing more than bed rest, medication to control pain, and perhaps supplemental oxygen. Breathing oxygen may help the body to absorb the subcutaneous air more quickly. Prognosis
Air in subcutaneous tissue does not usually pose a lethal threat; small amounts of air are reabsorbed by the body. Once the pneumothorax or pneumomediastinum that causes the subcutaneous emphysema is resolved, with or without medical intervention, the subcutaneous emphysema will usually clear. However, spontaneous subcutaneous emphysema can, in rare cases, progress to a life-threatening condition, and subcutaneous emphysema due to mechanical ventilation may induce ventilatory failure. History
The first report of subcutaneous emphysema resulting from air in the mediastinum was made in 1850 in a patient who had been coughing violently. In 1900, the first recorded case of spontaneous subcutaneous emphysema was reported in a bugler for the Royal Marines who had had a tooth extracted: playing the instrument had forced air through the hole where the tooth had been and into the tissues of his face. Since then, another case of spontaneous subcutaneous emphysema was reported in a submariner for the US Navy who had had a root canal in the past; the increased pressure in the submarine forced air through it and into his face.
The reason for the delay in therapeutic effect is not fully understood, but it is believed to be due to many factors, including achieving steady-state levels of MAO inhibition and the resulting adaptations in mean neurotransmitter levels, the possibility of necessary desensitization of autoreceptors which normally inhibit the release of neurotransmitters like serotonin and dopamine, and also the upregulation of enzymes such as serotonin N-acetyltransferase. Typically, a therapeutic response to MAOIs is associated with an inhibition of at least 80-85% of monoamine oxidase activity. Pharmacokinetics
Phenelzine is administered orally in the form of phenelzine sulfate and is rapidly absorbed from the gastrointestinal tract. Time to peak plasma concentration is 43 minutes and half-life is 11.6 hours. Unlike most other drugs, phenelzine irreversibly disables MAO, and as a result, it does not necessarily need to be present in the blood at all times for its effects to be sustained. Because of this, upon phenelzine treatment being ceased, its effects typically do not actually wear off until the body replenishes its enzyme stores, a process which can take as long as 2–3 weeks. Phenelzine is metabolized primarily in the liver and its metabolites are excreted in the urine. Oxidation is the primary routine of metabolism, and the major metabolites are phenylacetic acid and parahydroxyphenylacetic acid, recovered as about 73% of the excreted dose of phenelzine in the urine over the course of 96 hours after single doses. Acetylation to N2-acetylphenelzine is a minor pathway.