Carbon monoxide intoxication

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Classification according to ICD-10
T58 Toxic effects of carbon monoxide
ICD-10 online (WHO version 2019)
U-tube manometer for monitoring the overpressure of a breathing air supply

The carbon monoxide poisoning or carbon monoxide poisoning (also carbon monoxide poisoning , carbon monoxide intoxication , CO poisoning , CO intoxication and carbonic oxide ) describes a disease induced by application or inhalation of gaseous poison carbon monoxide is caused (CO) to humans. It can lead to death within a short time.

frequency

Between 2000 and 2009 there was an average of 374 annual accidental deaths from carbon monoxide poisoning in Germany; in 2015 there were 648 patients (0.8 deaths / 100,000 inhabitants). The number of unreported cases is high because CO intoxication is unspecific Symptoms are often not recognized or misdiagnosed. While the number of fatal poisonings in Germany has increased in recent years, it has decreased in the USA. In 2014, 1,319 people died of carbon monoxide poisoning in the USA, which corresponds to an incidence comparable to that in Germany.

Sources of carbon monoxide

Carbon monoxide (CO) results from the incomplete combustion of carbonaceous materials at high temperatures and with a low supply of oxygen (see smoke gas poisoning ). Typical sources are fires, defective gas boilers, but also decorative and heating chimneys, which can release CO if there is insufficient air supply or exhaust gas discharge. Unchanged playing suicide attempts (→ charcoal-burning suicide ) a major role. Until the introduction of catalytic converter technology and the associated reduction in the CO concentration from approx. 10% to 0.3%, suicides with car exhaust fumes were at the top of the statistics, but now more often the burning of charcoal when grilling indoors leads to death. In adolescents, the use of water pipes occasionally results in clinically symptomatic carbon monoxide poisoning.

Symptoms

CO is an invisible and odorless gas that does not irritate the respiratory tract and therefore usually goes unnoticed. In English, carbon monoxide is called a silent killer .

Carbon monoxide poisoning is particularly treacherous because not only the gas cannot be perceived by humans, but the symptoms are so varied that the first signs are often not perceived as poisoning and the cause is therefore not initially eliminated. NDR, health guide:

“Symptoms of carbon monoxide poisoning include nausea, headache, racing heart, drowsiness, hallucinations, apathy, seizures and shortness of breath. If the poisoning occurs during sleep, the person becomes unconscious, breathing stops and death occurs.

If the CO concentration is high, there is only a short period of time between the first symptoms and loss of consciousness. Those affected often have no symptoms at first. Because the blood turns cherry red, they even have a healthy complexion. When you try to get up, all body functions suddenly fail and you can no longer leave the room. "

With increasing duration and concentration of the carbon monoxide level, the following symptoms and disease states occur:

  • Short duration and / or concentration
  • No complaints
  • Fatigue headache
  • malaise
  • psychological change
  • Anxiety or depression
  • nausea
  • Vomit
  • dizziness
  • confusion
  • Seizures
  • Ataxia
  • unconsciousness
  • stroke
  • Heart attack
  • death
  • High concentration and / or duration

Effect of carbon monoxide as a function of the ambient concentration in parts per million:

concentration Symptoms
35 ppm (0.0035%) Headache and dizziness within 6–8 hours
100 ppm (0.01%) Mild headache in 2-3 hours
200 ppm (0.02%) Mild headache within 2-3 hours, loss of judgment
400 ppm (0.04%) Severe headache within 1–2 hours
800 ppm (0.08%) Headache, dizziness, nausea and cramps within 45 minutes, unconsciousness within 2 hours
1,600 ppm (0.16%) Headache, increased heart rate , dizziness and nausea within 20 minutes, death in less than 2 hours
3,200 ppm (0.32%) Headache, dizziness, and nausea in 5–10 minutes. Death within 30 minutes.
6,400 ppm (0.64%) Headache and dizziness in 1–2 minutes. Seizures, respiratory failure, and death in less than 20 minutes.
12,800 ppm (1.28%) Loss of consciousness after 2–3 breaths. Death in less than 3 minutes.

Pathophysiology

Ball-and-stick model of a heme group with a carbonyl ligand as it occurs in carboxyhemoglobin ( Fe atom in orange)

Carbon monoxide is a strong complex compound with heme-containing enzymes such as hemoglobin and forms carboxyhemoglobin. It displaces the oxygen from its transport molecule in the blood (hemoglobin) with a 200 to 300-fold affinity in adults and 600-fold affinity in the fetus, thereby reducing the oxygen supply to the tissue. This triggers a series of secondary reactions, the most serious of which is tissue hypoxia up to and including myocardial infarction and cerebral infarction.

The musculature of the musculoskeletal system and the heart contain myoglobin for the intermediate storage of oxygen. Myoglobin also binds carbon monoxide very strongly and thereby loses the ability to store oxygen. This reduces the heart's pumping capacity. Muscle strength is limited, so that the poisoned often cannot escape from the danger area on their own.

Carbon monoxide also binds to cytochrome c oxidases and thus affects the respiratory chain of the mitochondria. In addition to the deterioration in the use of oxygen for energy generation, activation of HIF 1-α is triggered.

By binding carbon monoxide to a heme protein in platelets, increased nitric oxide synthesis is triggered. This activates massive vascular and inflammatory mechanisms, which make the situation even worse. There is a clumping of platelets and neutrophil granulocytes . The latter degranulate, releasing numerous proinflammatory cytokines.

As a clinical endpoint, the poisoning manifests itself in hypoxia of particularly sensitive tissues, the central nervous system and later, especially with a corresponding pre-existing disease, also of the heart muscle. After increasing clouding of consciousness up to a coma and complicating cardiac arrhythmias, death ultimately occurs due to brain swelling, respiratory and circulatory failure.

forecast

Acute carbon monoxide poisoning in the United States kills 1 to 3% of people treated. Carbon monoxide concentration and duration of exposure are the most important prognostic parameters. In addition to the concentration of carbon monoxide, the severity of the poisoning is determined by the general health of the person concerned: Elderly people, the sick, especially people with heart disease and unborn children are more sensitive to carbon monoxide than healthy adults. CO poisoning increases the risk of heart attacks and arrhythmias if the patient had pre-existing coronary artery disease.

Unborn children are at a particularly high risk because they are dependent on the mother's oxygen supply and the hemoglobin F in their blood has an even higher affinity for carbon monoxide than the hemoglobin in adults. Through the interposition of the maternal circulation, carbon monoxide floods the unborn child with a delay, but is also eliminated with a delay.

Long-term consequences of acute CO poisoning

If the poisoning survives, 10 to 40% of the victims show permanent damage to the heart and nervous system such as memory and concentration disorders, psychoses, movement disorders (Parkinsonoid), heart failure and cardiac arrhythmias.

treatment

There is always a need for treatment when people have stayed in rooms polluted with CO and show clinical signs of intoxication. The measured CO-HB value is not relevant for establishing the indication and thus for not treating it. The CO load in the blood can quickly decrease and the CO-HB value normalize. For the patient, the intracellular exposure (brain, heart muscle, etc.) is of decisive relevance, which cannot be recorded with the CO-HB measurement.

The therapy of CO intoxication is ultimately based on a reversal of the mechanisms by eliminating the carbon monoxide as quickly as possible and simultaneously eliminating the hypoxia.

This can be achieved by administering pure oxygen (15-25 l / min constant flow system with reservoir or demand system) under normal atmospheric pressure, which reduces the CO half-life (half-life) from 320 min to 97 min leads. As an acute therapy, this administration of oxygen should be carried out as soon as possible after rescue from the scene of the accident and continued until all symptoms have been eliminated.

The CO elimination - also intercellularly - is increased by means of hyperbaric oxygen therapy (HBO), in which medically pure oxygen is supplied under an increased ambient pressure in special overpressure chambers. The HBO can reduce the half-life of the carbon monoxide to 23 minutes. At the same time, the physically bound oxygen in the blood is increased many times over, which leads to a "luxury oxygenation" of the tissues that are primarily undersupplied by the poisoning: The amount of oxygen physically dissolved in the plasma is only 0.3 ml O 2 / dl blood when breathing in air and at normal ambient pressure . At 3 bar alveolar oxygen pressure this rises to 6.8 ml / dl, the oxygen partial pressure rises from about 100 mmHg to a pO 2 of 2200 mmHg. The vasoconstricting effect of hyperbaric oxygen therapy can also reduce the accompanying swelling of the brain.

The intracellular CO concentration can be reduced faster under HBO than with oxygen under normal pressure, because the concentration gradient for CO is increased from intracellular to extracellular and the overpressure of oxygen also has an intracellular effect and displaces CO from its bonds.

If neurological or cardiac symptoms are evident, patients should be given hyperbaric oxygen therapy (HBO) within 6 hours. This also applies to again symptom-free patients with a CO-HB of more than 20% and pregnant women. In pregnant women, the indication should be given particularly generously, as fetal hemoglobin is far more sensitive to CO and the extent of the child's poisoning cannot be assessed from the clinical condition of the mother.

The side effects of HBO are marginal and are essentially limited to patients who cannot equalize the pressure. In uncooperative, unconscious or unconscious patients, a bilateral paracentesis (eardrum rupture ) should always be performed to avoid a rupture of the eardrum.

Therapy is only prohibited in a few cases (absolute contraindication): These are prior chemotherapy with bleomycin and untreated pneumothorax.

Since a small pneumothorax can expand massively under decompression when "surfacing" and develop into a life-threatening picture of tension pneumothorax within a very short time, this must be excluded or treated before beginning (chest drainage). Patients with chronic obstructive pulmonary disease (COPD) and corresponding structural changes in the lungs are particularly at risk.

Chronic CO poisoning

Chronic carbon monoxide poisoning consists of the cumulative effects of the damage caused by several successive intoxications, which alone do not lead to death. (For example, after repeated inhalation of small amounts of CO by heaters, drivers and traffic police officers, significant amounts of gas are not stored in the blood or tissue.

Smoke

Only recently has the dangerousness of CO in tobacco smoke been explicitly pointed out, including through appropriate warnings on the carbon monoxide content in the smoke of cigarettes . Regular smoking leads to a slight, permanent but reversible intoxication of the body with carbon monoxide. This also has objectively measurable consequences. Water pipe smokers ingest large amounts of carbon monoxide. The CO comes from the burning of the water pipe charcoal (see also Shisha ).

Inquest

Occasionally, suspicion of carbon monoxide poisoning is raised only when a corpse is found. The coloring of the dead spots, which are not bluish-livid but bright red, is characteristic. It must be noted that bright red dead spots can appear very early post-mortem, even without carbon monoxide, or through exposure to cold due to diffusion reoxygenation. To distinguish one should look at the death spots in the area of ​​the nail bed. When it is cold, these are still blue-livid; when there is carbon monoxide intoxication, they are light red. The typical, cherry-red dead spots are only clearly noticeable at a CO-HB value of 30%.

Individual evidence

  1. ^ A b c Lars Eichhorn, Marcus Thudium, Björn Jüttner: The diagnosis and treatment of carbon monoxide poisoning . In: Deutsches Aerzteblatt Online . December 24, 2018, ISSN  1866-0452 , doi : 10.3238 / arztebl.2018.0863 ( aerzteblatt.de [accessed June 9, 2019]).
  2. ^ A b Jason J Rose, Ling Wang, Qinzi Xu, Charles F McTiernan, Sruti Shiva: Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy . In: American Journal of Respiratory and Critical Care Medicine . tape 195 , no. 5 , 2017, ISSN  1535-4970 , p. 596-606 , doi : 10.1164 / rccm.201606-1275CI , PMID 27753502 , PMC 5363978 (free full text).
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  5. ↑ Lars Eichhorn, Dirk Michaelis, Michael Kemmerer, Björn Jüttner, Kay Tetzlaff: Carbon monoxide poisoning from waterpipe smoking: a retrospective cohort study . In: Clinical Toxicology (Philadelphia, Pa.) . tape 56 , no. 4 , 2018, ISSN  1556-9519 , p. 264-272 , doi : 10.1080 / 15563650.2017.1375115 , PMID 28906147 .
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  7. ↑ Daniel Herder, André Zand-Vakili, Lars Hansen: You must know that about the gas accident in Harbug. Hamburger Abendblatt, quote: “At 10 pm, a 60-year-old complained of heart problems, at 2 am a 75-year-old reported after a fall, at 4 am a 21-year-old complained of nausea. 'The individual clinical pictures were too different for our people to assume that carbon monoxide poisoning was the cause,' says fire department spokesman Hendrik Frese. "
  8. ↑ Carbon monoxide: prevent poisoning. NDR - Counselor Health, as of February 7, 2017
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  16. Jump up ↑ Neil B Hampson, Susan L Dunn, UHMCS / CDC CO Poisoning Surveillance Group: Symptoms of carbon monoxide poisoning do not correlate with the initial carboxyhemoglobin level . In: Undersea & Hyperbaric Medicine: Journal of the Undersea and Hyperbaric Medical Society, Inc . tape 39 , no. 2 , 2012, ISSN  1066-2936 , p. 657-665 , PMID 22530449 .
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  31. ↑ umad.de
  32. Jump up ↑ Jens Schubert, Jürgen Hahn, Gerhard Dettbarn, Albrecht Seidel, Andreas Luch, Thomas G. Schulz: Mainstream Smoke of the Waterpipe: Does this Environmental Matrix Reveal as Significant Source of Toxic Compounds. In: Toxicology Letters . 205, 2011, pp. 279-284, doi: 10.1016 / j.toxlet.2011.06.017 .
  33. ^ Benno Schäffer, Oliver Peschel: The differential diagnosis of light-red livor mortis . In: Deutsches Aerzteblatt Online . September 3, 2018, ISSN  1866-0452 , doi : 10.3238 / arztebl.2018.0585 .