01
Overview
Carbon monoxide poisoning is very common in winter, especially in the cold north, and there are different degrees of sequelae due to carbon monoxide poisoning every year.
02
Concept
Carbon monoxide poisoning: refers to acute carbon monoxide poisoning caused by inhaling high concentrations of carbon monoxide in a short period of time or inhaling low concentrations for a long time. It is mostly caused by sudden exposure to turbid and poisonous gas. The onset of this disease is acute and sinister, and if not treated in time, it can be life-threatening.
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03
Physicochemical properties of carbon monoxide
Carbon monoxide poisoning usually refers to gas poisoning, which can produce carbon monoxide when carbon-containing substances are not completely burned in the production and living environment. It is a colorless, tasteless, odorless, non-irritating gas, insoluble in water, and can cause poisoning if inhaled through the respiratory tract. Compared with oxygen, carbon monoxide has a higher affinity for hemoglobin, so when carbon monoxide is inhaled by the body, hemoglobin loses its ability to carry oxygen, resulting in cell death and even life-threatening. COHb levels are a measure of disease severity.
04
Common clinical causes
1. In the past, it was mostly caused by the failure to pay attention to indoor ventilation when using vegetable fuel or briquette stove for cooking or heating indoors;
2. If the gas stove is aging, the connecting hose is aging or falling off, and the gas stove switch is forgotten or not turned off tightly, or the gas stove flame is blown out and the switch is not turned off in time, it will lead to carbon monoxide poisoning;
3. Improper installation of household gas water heater, the water heater needs to consume a lot of oxygen in the process of combustion, and carbon monoxide is retained indoors.
4. Staying in an unventilated and air-conditioned car for a long time in summer is also easy to cause carbon monoxide poisoning.
5. In the production process, the heat dissipation system of the coal-fired boiler fails, resulting in the leakage of the equipment for producing and transferring gas, and the air in the workplace is not circulated, which will lead to carbon monoxide poisoning.
6. In the closed plastic greenhouse where vegetables are planted in winter, coal stoves are used for heating and there are no perfect smoke exhaust facilities, which will also cause carbon monoxide poisoning due to poor air circulation.
05
Mechanism of intoxication
In 1857, physiologist Claude Bernard discovered that carbon monoxide competitively binds hemoglobin to form carboxyhemoglobin (COHb), which in turn reduces hemoglobin's oxygen-carrying capacity and tissue oxygen partial pressure (PaO2), resulting in tissue hypoxia. Therefore, COHb formation and tissue hypoxia have long been thought to be the main mechanisms of carbon monoxide toxicity.
Other mechanisms of carbon monoxide toxicity include:
(1) Carbon monoxide inhibits mitochondrial function, causing neuroexcitability, acidosis, ion imbalance and depolarization, oxidative stress and apoptosis, resulting in ischemic-hypoxic brain injury;
(2) Excessive carbon monoxide activates platelets, promotes neutrophil activation, adhesion and degranulation, and induces the body to produce immune and inflammatory responses;
(3) After ACOP, a complex was formed between myelin-related proteins and malondialdehyde, which induced an autoimmune cascade and destroyed the myelin sheath, resulting in delayed encephalopathy or residual neurological sequelae of carbon monoxide poisoning in the later stage;
(4) Carbon monoxide binds to myoglobin in the heart and skeletal muscle, causing direct damage.
Expert consensus: (1) The classical hypoxia mechanism centered on the COHb theory is an important mechanism of ACOP and the rational basis for the implementation of oxygen therapy;(2) The classical hypoxia theory of COHb cannot fully explain the mechanism of carbon monoxide poisoning, and the direct toxic effect of carbon monoxide on mitochondria is not mentioned in the classical hypoxia mechanism.
06
Clinical manifestations of carbon monoxide poisoning
1. Synergistic factors of poisoning degree: The degree of poisoning is affected by the following factors: (1) The greater the CO concentration, the longer the c0 exposure time, and the more severe the poisoning. (2) Accompanied by other toxic gases (such as sulfur dioxide, dichloromethane, etc.) will enhance toxicity. (3) Patients in high temperature environment, anemia, myocardial ischemia, cerebral insufficiency, fever, diabetes and hypoxemia caused by various reasons are seriously ill.
2. Nervous system:
(l) Toxic encephalopathy: diffuse functional and organic damage to the brain caused by acute carbon monoxide poisoning. (1) Whole brain symptoms: different degrees of consciousness disorders, psychiatric symptoms, convulsions and epilepsy. (2) Focal manifestations: such as hemiplegia, monoplegia, tremor, etc.
(2) Cerebral edema: impaired consciousness, vomiting, neck resistance, papilledema can be seen on fundus examination.
(3) Brain herniation: deepening coma, irregular breathing, unequal circle pupils, and loss of light response.
(4) Cortical blindness: caused by infarction, ischemia and poisoning of bilateral occipital lobes. Manifestations: (1) decreased visual acuity or blackness in both eyes, (2) pupillary light reflex, (3) good mental state.
(5) Peripheral nerve damage: Some moderate and severe patients find peripheral nerve damage after they are conscious, such as facial nerve paralysis and recurrent laryngeal nerve injury, and rarely long nerve injury.
(6) Cutaneous autonomic dystrophy: a small number of severe patients have red, swollen or blisters of different sizes on the limbs and trunk and can be connected into patches.
3. Respiratory system:
(1) Acute pulmonary edema: shortness of breath, white or pink foam from the mouth and nose, and large vesicle sounds in both lungs.
(2) Acute respiratory distress syndrome (ARDS) :(1) shortness of breath, cyanosis, irritability, anxiety, and sweating after ACOP. (2) respiratory distress, (3) hypoxemia, (4) lung x-ray showing increased lung markings, blurred margins, and patchy shadows, (5) pulmonary artery wedge pressure (PAWP) <18 mm Hg or clinical exclusion of left heart failure.
4. Circulatory system: a small number of cases can occur shock and arrhythmia, and the incidence of acute left heart failure is very low.
5. Urinary system:
(1) Prerenal azotemia: mostly caused by vomiting, insufficient intake, dehydration, decreased urine output and low blood pressure, blood urea nitrogen (BUN) and creatinine (Scr) increase, and urine output decreases. Prerenal azotemia can progress to acute ischemic tubular necrosis.
(2) Acute renal failure: Acute renal failure can be caused by the continuous action of prerenal factors such as renal volume depletion leading to long-term ischemia and hypoxia of the kidney, or the damage to the kidney caused by rhabdomyolysis syndrome resulting in hemorrhinoglobinuria.
6. Shock: manifested as low blood pressure, narrowing of pulse pressure difference, thin pulse, clammy and cold extremities, pale skin, prolonged capillary filling time, oliguria or anuria, etc. The main complications are:
(l) Rhabdomyolysis syndrome: During coma, the limbs or trunk are compressed by themselves for a long time, resulting in ischemia, edema, and necrosis of the trunk musculature of the compressed limbs. Necrotic muscle tissue releases a large amount of myoglobin and potassium into the blood, which can cause acute renal failure when excreted through the kidneys. Paresthesias, severe pain, numbness, decreased or absent sensation in the affected limb. The compressed limb is swollen, the skin is magnetic white or dark purple, and the peripheral arterial pulses are diminished or absent. There may even be myoglobinuria, oliguria, and progressive increases in blood urea nitrogen, creatinine, and potassium.
(2) Cerebral infarction: patients with moderate to severe ACOP. It is more common in patients with hypertension, diabetes, hyperlipidemia, with hemiplegia, hemiplegia or monoplegia, motor aphasia, hemianopia, etc.
(3) Intracerebral hemorrhage: patients with moderate to severe ACOP combined with intracerebral hemorrhage. Brain CT can confirm the diagnosis.
(4) Epileptic seizures or epilepsy: A small number of severe patients have seizures in the acute stage, and most of the seizures are relieved as the condition improves, and some patients are left with generalized seizures or partial seizures.
07
Grading of intoxication
After carbon monoxide poisoning, people generally feel headache, nausea, and weakness, which is mainly related to the concentration of carboxyhemoglobin (COHb) in the blood.
1. Mild poisoning: blood COHb concentration of 10%~20%. Symptoms include dizziness, headache, nausea, vomiting, and general weakness.
2. Moderate poisoning: blood COHb concentration of 30%~40%. The patient's lips are "cherry red" and the above symptoms are exacerbated by excitability, impaired judgment, motor disorders, hallucinations, vision loss, confusion, or shallow coma.
3. Severe poisoning: blood COHb concentration of 30%~50%. It is manifested as convulsions, deep coma, hypotension, arrhythmia and respiratory failure, some patients have aspiration pneumonia due to aspiration, stress ulcers, local damage to the brain, redness, swelling and blisters similar to burns on the skin at the pressure site, compressive muscle necrosis can occur in the compressed muscles, and myosin can be released to lead to acute renal failure.
08
INVESTIGATIONS
1. Determination of blood HbCO:
The qualitative test for normal carboxyhemoglobin is negative, and the normal value is between 0 and 2.3% for non-smokers and between 2.4% and 4.2% for smokers. Carboxyhemoglobin is mainly composed of carbon monoxide and hemoglobin, if its value is elevated mainly due to carbon monoxide poisoning, the patient's body carboxyhemoglobin concentration of more than 2% will appear nervous system reaction, when the value exceeds 5%, there will be a significant increase in coronary blood flow, when the value exceeds 10%, the patient will have myocardial hypoxia and injury and other symptoms, and in severe cases, death.
2. Serum enzymatic examination:
When the patient's CO environment is unclear and differential diagnosis is difficult, abnormal serum enzyme abnormalities are useful for diagnosing acute carbon monoxide poisoning (ACOP).
(1) Serum enzyme determination: phosphocreatine kinase (CPK), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), alanine aminotransferase (ALT) are more abundant in heart, lung, kidney, brain, skeletal muscle, gastrointestinal tract and other tissues, and can reach 10-1000 times of the normal value at ACOP. Enzymatic studies are important in the differential diagnosis and are elevated to a much greater extent than in acute myocardial infarction.
(2) Recommendation: Abnormal increase in serum enzymes is meaningful for the diagnosis of ACOP. When the c0 environment of coma patients is not clear and differential diagnosis is difficult, the combination of abnormal serum enzyme and blood gas analysis is an important laboratory index for the diagnosis of ACOP.
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3. Arterial blood gas analysis:
(1) Hypoxemia: The blood Pa02 of untreated poisoned patients is significantly reduced. The blood PaO2 of untreated poisoned patients was significantly reduced, and the lowest could be about 20~30 mm Hg.
(2) Acid-base imbalance: hypoxemia stimulates the carotid body and aortic body chemoreceptors, causing compensatory pulmonary hyperventilation, resulting in hypocapnia and respiratory alkalosis. The patient's prolonged hypoxemia reduces aerobic oxidation in tissues, enhances anaerobic digestion, produces a large number of organic acids, and metabolic acidosis occurs. As a result of changes in the condition, a variety of acid-base imbalances may occur, such as respiratory depression, pulmonary interstitial edema, and alveolar edema with respiratory acidosis and metabolic acidosis.
4. Renal function test: due to dehydration, shock, etc., severe ACOP can cause prerenal azotemia due to reduced renal blood flow and glomerular filtration rate. Acute renal failure occurs when renal ischemia is too prolonged or when it is not a traumatic rhabdomyolysis sign, and blood BUN and Scr are significantly increased. Recommendation: Severe patients should be routinely tested.
5. Electroencephalogram examination:
There are no specific changes, and mild ACOP is predominantly localized (frontal) theta and δ slow-wave increases, and moderate and severe slow-wave increases diffusely and extensively moderate or severe abnormalities in moderate and severe patients, and the correlation between the degree of EEG abnormalities and the disease has not been reported.
6. Cranial CT examination: Brain CT examination in patients with mild and moderate ACOP may or may not have abnormal changes. Patients with severe ACOP present with cerebral edema with or without lesions in the early stages. CT shows diffuse hypodensity of bilateral white matter, unclear gray-white matter demarcation, bilateral globus pallidus symmetrical hypodensity, and narrowing of the ventricles or sulci cisterns. After the cerebral edema disappeared, pallidus globus and white matter hypodense images were still visible, which were globus pallidus malapacia and demyelination of white matter nerve fibers, which could be accompanied by cerebral atrophy and, rarely, cerebral infarction. There are no convincing studies on the association between brain CT changes and the severity of the disease and the development of late-onset encephalopathy.
7. Brain magnetic resonance (MRI) examination: early bilateral globus pallidus length Tl, T2, bilateral cerebral hemisphere white matter equal T1, slightly longer T2, DWI and FLAIR are slightly hyperintense or hyperintense. Occasionally, abnormal signals of the internal capsule, brain and feet, substantia nigra, and hippocampus are observed. Signs of late hemioval center and lateral ventricular T1 and T2, FIAIR hyperintensity, ventricular enlargement, sulci widening, and cerebral atrophy.
8. Electrocardiogram:
Some patients present abnormally, but the changes are nonspecific for the diagnosis of ACOP. It is not distinguishable from the patient's underlying medical condition.
09
First aid measures
1. Turn off the open flame as soon as possible
After smelling the smell of gas, do not turn on the lights, do not touch the doorbell, and do not light an open flame to prevent an explosion. Ambulance personnel should ensure safety (cover their mouth and nose with a wet towel), turn off the gas, etc.
2. Get out of the poisoning environment
Open the doors and windows of the closed room to allow the patient to breathe fresh air immediately;
3. Suitable lying position
(1) Immediately place it in the lateral decubitus position, and loosen the patient's collar to ensure that the respiratory tract is unobstructed and prevent suffocation; closely observe the patient's consciousness, breathing and pulse, etc., if the patient's breathing and heartbeat stop, and there is no assistance from others, the rescuer needs to call the emergency number in time while doing cardiopulmonary resuscitation, and send the poisoned person to the hospital with hyperbaric oxygen chamber for rescue;
(2) For unconscious patients, their heads can be tilted to one side to prevent suffocation caused by vomiting and vomiting aspiration into the lungs;
4. Oxygen therapy
Oxygen therapy is the most effective treatment for carbon monoxide poisoning, and oxygen administration accelerates the dissociation of COHb and the excretion of carbon monoxide from the blood. Patients with mild toxicity may be given a nasal cannula to inhale high-concentration oxygen, and if the poisoning is moderate to severe, hyperbaric oxygen therapy is required.
10
Hyperbaric oxygen chamber treatment population
Hyperbaric oxygen is the most effective and convenient treatment for carbon monoxide toxicity, and specific treatment indications include:
(1) Patients with acute poisoning, severe carbon monoxide poisoning, coma, cardiopulmonary insufficiency;
(2) Patients who have been in a coma for carbon monoxide poisoning within 4 hours, or within 8 hours of being in a carbon monoxide environment, and who have relapsed after being awakened;
(3) Patients who are in a coma with carbon monoxide poisoning and still have poor reactions to the outside world after being treated and awakened, and have dizziness, headache, arrhythmia, convulsions and other cardiovascular and cerebral hypoxia;
(4) Patients with poor recovery effect of carbon monoxide poisoning after treatment and neuropsychiatric symptoms;
(5) Patients with delayed encephalopathy after carbon monoxide poisoning, with a duration of 6 months to 1 year;
(6) Patients who have regained consciousness but have elevated carboxyhemoglobin values;
(7) Patients with carbon monoxide poisoning, mild persistent dizziness, headache, or those over 40 years of age and severe mental exertion;
(8) Patients with abnormal EEG and CT examinations.
11
Mechanism of hyperbaric oxygen chamber therapy
1. Hyperbaric oxygen can quickly dissociate carbon monoxide and hemoglobin, play a positive role in promoting the elimination of carbon monoxide, and restore the oxygen-carrying function of hemoglobin; the higher the partial pressure of oxygen, the more obvious the dissociation of carbon monoxide and hemoglobin and the elimination of carbon monoxide, and gradually shorten the removal time of carbon monoxide with the increase of oxygen partial pressure.
2. Hyperbaric oxygen can increase the partial pressure of blood oxygen, thereby increasing the blood oxygen content, so that all tissues in the body can get sufficient dissolved oxygen, so that the body can reduce the dependence on hemoglobin oxygen transport, so that hypoxemia can be quickly corrected.
3. Hyperbaric oxygen can constrict intracranial blood vessels without affecting the content of blood oxygen, which is conducive to reducing intracranial pressure and quickly interrupting the vicious cycle of cerebral hypoxia and cerebral edema.
4. Hyperbaric oxygen can increase blood oxygen content and blood oxygen tension, so that the oxygen storage of human tissues and the diffusion radius of blood oxygen will also increase accordingly. Therefore, the hypoxic state of tissue cells can be significantly improved, which is conducive to relieving the inhibitory effect of carbon monoxide on cytochrome oxidase.
5. Hyperbaric oxygen can better prevent and treat various complications caused by acute carbon monoxide poisoning, including heart, lung, kidney, liver damage, shock, acid toxicity and other complications.
6. Hyperbaric oxygen has significant therapeutic effects on the sequelae of carbon monoxide poisoning and delayed encephalopathy, and its mechanism may be related to the following factors. First, the increase in the partial pressure of hyperbaric oxygen causes the brain tissue to obtain sufficient oxygen supply, which alleviates the cell breathing disorder and is conducive to the recovery of the cell structure and function of the central nervous system. Second, it promotes the establishment of cerebral blood vessel collateral circulation and reduces hypoxic damage to brain tissues. Third, high-pressure oxygen activates the biochemical processes of the central nervous system and enhances the electrophysiological effects of the brain.
12
Other treatments
1. Treatment of late-onset encephalopathy
Oxygen therapy: The current method is high-flow 100% hyperbaric oxygen or atmospheric oxygen, for hyperbaric oxygen treatment that cannot be given, atmospheric oxygen therapy should be given immediately, the general oxygen flow rate is 8~10L/min, until the patient's symptoms recover and COHb ≤3% (generally 6h).
Neuroprotective drugs
Neuroprotective drugs mainly include: brain metabolism and brain cell enablers, free radical scavengers, neurotrophic drugs, antioxidants and mitochondrial protective agents.
2. Mechanical ventilation
Patients with coma, asphyxia, and respiratory arrest should be given prompt endotracheal intubation, and mechanical ventilation should be considered.
3. Hypothermia treatment:
The concept of "selective brain hypothermia", that is, selective cooling of the brain through cranial cooling, so that the brain temperature drops rapidly and is maintained at a hypothermia level (33 -35°C), and the anal temperature is around 37.5°C. The protective effect of hypothermia on brain tissue damage is manifested in the following aspects: reducing cerebral oxygen consumption, reducing cerebral blood flow, delaying the occurrence of energy exhaustion, inhibiting inflammatory response, reducing cerebral edema, and reducing intracranial pressure. Studies have suggested that hypothermia therapy is beneficial in reducing brain damage in patients, and that hypothermia should not be treated for too short a short time.
Hypothermia therapy can be applied early to comatose patients, and hypothermia lasts for 3-5 days in comatose and unawake patients. Special attention should be paid to the rewarming process, and the rewarming should not be too fast.
4. Treatment of cerebral edema: after severe CO poisoning, cerebral edema reaches a peak in 24~48 hours. The following measures should be aggressively taken to reduce intracranial and restore brain function.
(1) Dehydration treatment: (1) 50ml intravenous infusion bolus of 50% glucose solution; (2) 20% mannitol 1~2g/kg intravenous infusion (10ml/in), once every 6~8 hours, reduce the dose after symptom relief; (3) furosemide 20~40mg intravenous injection, 8~12 hours/time.
(2) Glucocorticoid therapy: dexamethasone 10~20mg/d, course of treatment 3~5 days.
(3) Convulsive treatment: diazepam 10~20mg intravenous injection, phenytoin 0.5~1.0g intravenous infusion after convulsions stopped, repeated application according to the condition ~ 6 hours.
(4) Promote the recovery of brain cell function: commonly used intravenous drugs include adenosine triphosphate, coenzyme A, cytochrome C and high-dose vitamin C.
13
Poisoning precautions
1. Try not to burn coal indoors, including burning coal stoves for heating, as well as cooking hot pot with charcoal, using charcoal for barbecue, etc., which must be fueled with charcoal, and must be placed in a place where ventilation can be made, and the door cannot be closed for fear of cold wind from the outside entering the room. When heating, it is necessary to keep a certain distance between people and braziers, which can not only keep warm, but also do not directly inhale a large amount of carbon monoxide.
2. Households that use coal for heating should install chimneys in the living room, and the structure of the chimney should be tight, and the smoke exhaust should be good; Special attention should be paid to the weather with high air humidity and low air pressure, and indoor doors and windows should not be closed too tightly.
3. When using pipeline gas, it is necessary to prevent the pipeline from aging, running out of gas, and leakage, and prevent the flame from being extinguished during cooking, resulting in gas overflow.
4. Do not use obsolete water heaters, such as in-line water heaters and flue water heaters; do not use water heaters that exceed the time limit, the installation of water heaters is best to be installed by professionals, and it is not allowed to install, remove, or modify the gas appliances by yourself; do not close the bathroom doors and windows when bathing in winter, and do not take a bath for too long.
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5. When using a gas water heater, it is forbidden to install the gas water heater in the bathing room, and it should be installed outside the bathing room near the window or outdoors.
6. When driving, do not let the engine idle for a long time, when the car is stopped, do not turn on the air conditioning for too long, even if it is driving, you should often open the window, so that the air inside and outside the car produces convection;
7. Where possible, install carbon monoxide alarms in areas where carbon monoxide may be generated.