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Clinical manifestations of CO poisoning (1)


Acute poisoning




Acute carbon monoxide poisoning is the most common acute occupational poisoning in China. CO is also the cause of accidental living poisoning in many countries




Carbon monoxide is the leading cause of death from poisoning. The occurrence of acute CO poisoning is related to the concentration and time of CO exposure. The maximum allowable concentration of CO in workshop air in China is 30mg/m3. It has been proved that the CO concentration in the inhaled air is 240mg/m3 for 3 hours, and the COHB in HB can exceed 10%. When CO concentration reaches 292.5mg/m3, severe headache, dizziness and other symptoms can occur, and COHB can increase to 25%. When the CO concentration reaches 1170mg/m3, the coma can occur after inhalation for more than 60min, and the COHB is about 60% high. When the concentration of CO reaches 11700mg/m3, it can cause death in a few minutes, and the COHB can increase to 90%.




Clinically, the symptoms and signs of acute cerebral hypoxia are the main manifestations. If the symptoms such as headache, dizziness, palpitations and nausea appear after exposure to CO, the symptoms will disappear quickly after inhaling fresh air, it is a general contact reaction.




Mild victims experience severe headache, dizziness, heartbeat, dizziness, weakness in the limbs, nausea, vomiting, restlessness, unsteady gait, mild to moderate disturbance of consciousness (such as confusion, hazy state), but no coma. After leaving the poisoning site and inhaling fresh air or oxygen for several hours, the symptoms gradually recovered completely. In addition to the above symptoms, moderate users flushing face, sweating, pulse fast, consciousness disorders as shallow to moderate coma. After timely removal from the poisoning site and rescue, it can recover gradually, generally without obvious complications or sequelae.




Severe poisoning, consciousness disorder is serious, a deep coma or vegetative state. Common pupil is narrowed, normal to light reflection or slow, limb muscle tension heighten, closed teeth, or have parodic go cerebrum rigidity, tendon wall reflex and carry testes reflex disappear generally, tendon reflex exists or slow, and can appear incontinence of feces and urine. When cerebral edema continues to aggravate, performance continues deep coma, continuous cerebral ankylosis attack, pupil to light response and corneal reflex is slow, body temperature rises to 39 ~ 40℃, pulse is fast and weak, blood pressure drops, complexion is pale or cyanosis, limbs are cold, tidal breathing. In some patients, the fundus examination showed irregular retinal artery spasm, venous filling, or papillary edema, suggesting increased intracranial pressure and the possibility of cerebral herniation. However, in many patients, the fundus examination was negative, and even the cerebrospinal fluid examination pressure was normal, while the pathological anatomy still confirmed that there was serious brain edema.




Severe poisoning patients often appear restlessness, confusion of consciousness, loss of directional force, or loss of distant and near memory in the process of awakening from coma after treatment. After some patients regained their consciousness, cortical dysfunction could be found, such as apraxia, agnosia, agraphia, aphasia, cortical blindness or transient deafness. Can also appear to the mental symptoms of mental disorders. In addition, transient mild hemiplegia, Parkinson's disease, chorea, athetosis, or grand mal epilepsy have been reported. After active rescue treatment, most patients with severe poisoning can still recover completely. In a small number of patients with vegetative state, the symptoms are loss of consciousness, silence of opening eyes, decerebral rigidity and poor prognosis.




In addition to the expression of cerebral hypoxia mentioned above, hypoxic changes or complications of other organs may also occur in severely infected persons. Some patients have arrhythmia, severe myocardial damage or shock; Patients with pulmonary edema present with wet rales in the lungs and dyspnea. The liver is large in about one in five patients and usually shrinked after two weeks. Upper gastrointestinal bleeding may occur due to stress ulcer. The presence of myoglobinuria may lead to acute renal failure in patients with occasional complicated rhabdomyolysis and compartment syndrome. Some patients appear cutaneous autonomic nerve nutrition disorder, the performance is the extremities or cadre skin appears large, small blisters or similar scald skin lesions, or skin patches of red and swollen similar to erysipelas like changes, after symptomatic treatment is not difficult to heal. Hearing vestibular damage can be manifested as deafness, tinnitus and ocular concussion. There were still 2% ~ 3% of patients with nerve damage, the most commonly involved are the lateral femoral cutaneous nerve, ulnar nerve, median nerve, tibial nerve, peroneal nerve, etc., which may be related to local compression after coma.




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