Carbon monoxide (CO) has the toxic effects of tissue hypoxia and produces various systemic and neurological complications. The main clinical manifestations of acute CO poisoning consist of symptoms caused by alterations of the cardiovascular system such as initial tachycardia and hypertension, and central nervous system symptoms such as headache, dizziness, paresis, convulsion and unconsciousness. CO poisoning also produces myocardial ischemia, atrial fibrillation, pneumonia, pulmonary edema, erythrocytosis, leucocytosis, hyperglycemia, muscle necrosis, acute renal failure, skin lesion, and changes in perception of the visual and auditory systems. Of considerable chinical interest, severe neurological manifestations may occur days or weekes after acute CO poisoning. Delayed sequelae of CO poisoning are not rare, usually occur in middle or older, and are clinically characterized by symptom triad of mental deterioration, urinary incontinence, and gait disturbance. Occasionally, movement disorders, particularly parkinsonism, are observed. In addition, peripheral neuropathy following CO poisoning usually occurs in young adults.
Animal ; Carbon Monoxide Poisoning/complications/*physiopathology ; Human

A 36-year-old man was brought unconscious to the emergency room; he suffered anoxic brain damage due to carbon monoxide (CO) intoxication, and had decerebrate rigidity clinically and died 1 month later after the acute insult. Computed tomography with contrast enhancement failed to show a brainstem lesion but the brainstem auditory evoked potential (BAEP) demonstrated the brainstem involvement. The BAEP can be used as an objective diagnostic aid for evaluating brainstem lesions in CO intoxication.
Adult ; Brain Stem/physiopathology* ; Carbon Monoxide Poisoning/physiopathology* ; Evoked Potentials, Auditory* ; Human ; Male

OBJECTIVETo investigate the startup detail of circulation dysfunction and its role in the progress of delayed neuropsychologic sequelae (DNS) after carbon monoxide (CO) poisoning with comparison with the model of ischemia-reperfusion.

METHODSThe ischemia-reperfusion rat model was established by Pulsinelli-Brierley method, and the CO poisoning rats model by i.p. injected with CO repeatedly respectively, and the rats were identified with DNS following the experiment of pathology and the ethnology.

RESULTSThe whole blood viscosity, plasma viscosity, hematocrit and fibrinogen increased significantly immediately after reperfusion, and recovered gradually with the ischemia-reperfusion rat model. The whole blood viscosity decreased significantly immediately after CO treated i.p. Especially at low shear rate, the hematocrit also declined remarkably in the early stage after CO treatment. But 1day later, these parameters turned to the trend of the ischemia-reperfusion rats. There was a prominent elevation of both indexes until the 14th day following CO injection i.p.

CONCLUSIONThere are significantly sustained hyper-coagulation and hyper-viscosity with circulation in rats after CO poisoning compared with ischemia-reperfusion model during the period of DNS, which might contribute to increase cerebral circulation resistance, blocked blood flow, and deteriorate hypoxemia in progression of DNS.

Animals ; Blood Circulation ; Carbon Monoxide Poisoning ; physiopathology ; Disease Models, Animal ; Hemorheology ; Male ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; physiopathology

Adult ; Carbon Monoxide Poisoning ; complications ; psychology ; Humans ; Male ; Middle Aged ; Nervous System Diseases ; chemically induced ; diagnosis ; physiopathology ; Suicide, Attempted ; psychology

Acute Disease ; Carbon Monoxide Poisoning ; enzymology ; physiopathology ; Creatine Kinase ; metabolism ; Creatine Kinase, MB Form ; Echocardiography ; Heart ; physiopathology ; Humans ; Hyperbaric Oxygenation ; Isoenzymes ; metabolism ; Myocardium ; enzymology

Of 32 cases suffering from acute carbon monoxide (CO) poisoning brainstem auditory evoked potential (BAEP) abnormalities were exhibited in 8 cases. the abnormalities of BAEPs could be divided into two patterns: a peripheral pattern (6 cases) of prolongation of latency to wave 1 without prolongation of interpeak latency, and a central pattern (2 cases) of prolongation of latencies to all waves and interpeak latencies. The indicence of BAEP abnormality tended to increase in accordance with an unconscious duration of more than 24 hours; during acute CO poisoning. A BAEP abnormality exhibiting a peripheral pattern usually returned to normal within one month after anoxia, but cases showing central pattern of BAEP abnormality died during acute anoxic insult due to the possible involvement of the brainstem. Thus, BAEPs can be used for evaluating the functional intergrity of the auditory pathways and for providing prognostic values in acute CO poisoning.
Acute Disease ; Adolescent ; Adult ; Aged ; Basal Ganglia/radiography ; Brain Stem/physiopathology* ; Carbon Monoxide Poisoning/physiopathology* ; Evoked Potentials, Auditory* ; Female ; Human ; Male ; Middle Age ; Tomography, X-Ray Computed

Acute Disease ; Adult ; Aged ; Blood-Brain Barrier ; physiopathology ; Brain Diseases ; blood ; chemically induced ; Carbon Monoxide Poisoning ; complications ; Female ; Humans ; Interleukin-6 ; blood ; Male ; Middle Aged

Carbon monoxide intoxication is the most prevalent cause of death from carbon monoxide poisoning. We herein report the case of a 56-year-old man who was found unconscious and smelled of smoke after exposure to carbon monoxide from a heater. He scored 5 on the Glasgow Coma Scale, and had respiratory insufficiency and elevated troponin I, creatine kinase-MB fraction and carboxyhaemoglobin levels. He was treated by mechanical ventilation. After regaining consciousness, brain magnetic resonance imaging showed diffusion restriction in the left occipital lobe; there was a loss of vision (right temporal hemianopsia), which improved by the follow-up session. Carbon monoxide intoxication may cause neurologic and cardiac sequelae, and the initial treatment includes oxygen therapy. Acute carbon monoxide poisoning can cause serious injury to the brain, heart and other organs; the most severe damages that could be inflicted to the brain include cerebral ischaemia and hypoxia, oedema, and neural cell degeneration and necrosis.
Brain ; physiopathology ; Brain Ischemia ; physiopathology ; Carbon Monoxide ; chemistry ; Carbon Monoxide Poisoning ; physiopathology ; Carboxyhemoglobin ; chemistry ; Creatine Kinase, MB Form ; blood ; Diffusion ; Glasgow Coma Scale ; Humans ; Hyperbaric Oxygenation ; Hypoxia ; Magnetic Resonance Imaging ; Male ; Middle Aged ; Myocardial Ischemia ; physiopathology ; Stroke ; physiopathology ; Troponin I ; blood

The regional cerebral blood flow of four patients with delayed carbon monoxide sequelae and four age matched controls was measured, using a xenon inhalation CT scan (GE 9800). Variable patterns of decreased cerebral blood perfusion according to the clinical state of the patient were noted among the patients. Follow up studies, 2 months later, indicated that there was a correlation between the fluctuation of symptoms and the changes in regional cerebral blood flow. It is suggested that the impairment of cerebral perfusion may play a critical role in delayed carbon monoxide sequelae.
Administration, Inhalation ; Aged ; Brain/*blood supply ; Brain Ischemia/chemically induced/physiopathology/*radiography ; Carbon Monoxide Poisoning/*complications ; Case Report ; Female ; Human ; Male ; Middle Age ; Regional Blood Flow/drug effects ; Support, Non-U.S. Gov't ; Time Factors ; Tomography, X-Ray Computed ; Xenon/administration and dosage/diagnostic use