The Diagnosis and Treatment of Carbon Monoxide Poisoning

Abstract

arbon monoxide (CO) at low concentrations is an odorless and colorless gas with a molecular weight that is similar to that of air. It develops in incomplete combustion processes of substances containing carbon (e1). In addition to fires, defect gas boilers, or wood pellet storage facilities, the risk of poisoning as a result of smoking hookah has become a focus in recent years (1, e2). Relevant alerting key words and the use of portable CO meters are intended to raise awareness in rescue personnel.In the USA, 20 000-50 000 cases of carbon monoxide poisoning occur every year (2). Treatment for accidental carbon monoxide poisoning costs the US healthcare system some $1.3 billion every year (e3). For Germany, the only available data are those from the German Federal Statistical Office, for inpatients and deaths with a diagnosis of CO intoxication (T58 in ICD-10) (e4). In the USA, the total number of deaths due to CO poisoning fell between 1999 and 2014 (from 1967 cases to 1319 cases) (e5), whereas in Germany, numbers have steadily risen in recent years. In 2015, 648 patients died as a result of CO poisoning (0.8 deaths/100 000 population) (eTable). Fatality depends on exposure times to CO and its concentrations and is crucially affected by the toxicity of further gases involved (comparative case series [3]). PathophysiologyCarbon monoxide diffuses rapidly through the alveolar membrane and binds with an affinity that is 230-300 times that of oxygen, preferably to the iron ion in heme. Conformation changes lead to a leftward shift in the position of the oxyhemoglobin dissociation curve, to reduced oxygen transport capacity, and to reduced oxygen release into the peripheral tissue (2). Within tissue, CO also binds to other heme-containing proteins, such as skeletal and myocardial myoglobin. Since elimination times in tissue and blood differ (e7), tissue injury can also develop with a delay.At the cellular level, carbon monoxide leads-among others-to an activation of neutrophils, to a proliferation of lymphocytes, to mitochondrial dysfunction, and to lipid peroxidation (2, 4). The development of oxygen radicals, oxidative stress, inflammation, and apoptosis is comparable to a reperfusion injury and constitutes a substantial damage mechanism (2, 5, 6).

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“…Every patient with clinical symptoms of CO intoxication should be treated with high oxygen partial pressure until the COHb concentration has dropped to 3% or clinical symptoms have resolved completely. Eichhorn, et al [1], Wolf, et al [13], Mathieu, et al [14] The level of carboxyhemoglobin values in all patients who received NBO therapy in our hospital was <25%, as confirmed by a pulse CO-oximeter in the prehospital setting, and no patients had any severe symptoms. Accordingly, SpCO monitoring may be useful for selecting the treatment and appropriate medical facility for conveyance in the management of patients with CO poisoning by the DH.…”

“…Given this situation, HBO therapy should be the method of choice in adult patients with neurological deficits, cardiac ischemia, loss of consciousness, metabolic acidosis, and carboxyhemoglobin values >25%. Eichhorn, et al [1], Wolf, et al [13], Mathieu, et al [14] However, regardless of these inclusion criteria, any decision to treat is always an individual decision. Every patient with clinical symptoms of CO intoxication should be treated with high oxygen partial pressure until the COHb concentration has dropped to 3% or clinical symptoms have resolved completely.…”

“…The indications of HBO for patients with CO poisoning have been described. Eichhorn, et al [1], Wolf, et al [13], Mathieu, et al [14] However, who should be transported by air or ground services remains a clinical question. Thus, future prospective studies involving a greater number of patients with a comparison with transportation by ground ambulance or only NBO therapy are needed.…”

“…The clinical symptoms of acute CO poisoning range from headache and dizziness to loss of orientation, symptoms of cardiac angina, loss of consciousness, and death, depending on the concentration and duration of exposure. Eichhorn, et al [1], Rose, et al [2], Wu and Juurlink [3] Administration of 100% oxygen (normobaric oxygen [NBO]) as early as possible is recommended for all patients with CO poisoning, although the higher the partial pressure of oxygen provided, the shorter the elimination period, so hyperbaric oxygen (HBO) therapy is recommend for patients with CO poisoning whenever possible. Weaver [4] However, medical facilities capable of providing HBO are limited, especially for severely ill patients who need intensive care.…”

Changes in the morphology of erythrocytes after <i>in vitro</i> exposure of blood to carbon monoxide

“…Подобные явления наблюдаются и при действии других физико-химических факторов на кровь [12,13]. Отравление СО диагностируют на основании клинической картины [14] и показателей СО в крови [15]. Изучение влияния СО на морфологию и агрегацию эритроцитов -весьма актуальная задача, так как ее решение позволит предположить клинические проявления симптомов отравления и, возможно, предоставить новые объективные методы исследования.…”