Chronic Carbon Monoxide Poisoning

It has been well established in the scientific literature that there are numerous long-term complications from carbon monoxide poisoning. Again, these primarily affect the neurologic and the cardiovascular systems because these systems are most oxygen dependent.

Because the signs and symptoms of CO poisoning are so vague and nonspecific, CO exposure and poisoning are easy to miss. Failing to detect and diagnose CO poisoning can result in the patient being allowed to return to the contaminated environment with devastating outcomes. Missed CO-poisonings are a particular area of legal liability for fire and emergency personnel. Because of the associated risk, and insidious nature of CO poisoning, pulse CO-oximetry should be considered for all firefighter and EMS operations.

Neurological Complications of Chronic CO Poisoning:

One of the well-documented long-term effects of chronic CO poisoning is delayed neurologic
syndrome (DNS). As stated previously, the actual incidence of DNS is somewhat uncertain. It is clear that DNS is more common in patients who are symptomatic initially following CO exposure. This is particularly true for patients who suffer loss of consciousness during the initial CO exposure. The development of DNS is somewhat enigmatic. Generally, recovery from the initial CO poisoning is essentially normal. However, between 2 and 40 days later, the patient begins to develop behavioral and neurological deterioration. The most common signs and symptoms of DNS include: memory loss, confusion, ataxia, seizures, urinary incontinence, fecal incontinence, emotional lability, disorientation, hallucinations, Parkinsonism, mutism, cortical blindness, psychosis, gait disturbances, and other motor disturbances.

METHYLENE CHLORIDE

Methylene chloride is widely used in industry as a paint and adhesive remover (see
Figure 18•). Repetitive and prolonged exposure to methylene chloride can result in the
development of CO in the patient. Following exposure, methylene chloride is slowly metabolized
to CO in the liver. Victims of methylene chloride exposure do not pose a particular
contamination risk to rescuers. However, contaminated clothing and skin can
secondarily contaminate rescuers. In addition, vomitus from the exposed patient can offgas
methylene chloride, possibly exposing rescuers to the gas.
As one would expect, the effects of methylene chloride parallel those of CO. They include
central nervous system depression, respiratory depression, cardiac dysrhythmias,
respiratory tract irritation (at high levels), and non-cardiogenic pulmonary edema (at
high levels).
The treatment of methylene chloride poisoning is primarily symptomatic. No antidote
is available. It is important to support cardiac and respiratory functions. Also, as
with CO, high concentrations of oxygen should be administered. In addition to fully
saturating available hemoglobin, high concentration oxygen serves as an antagonist of
the metabolically-released CO.