Ver el código de «Carbon monoxide toxicity»

==Background==
*Colorless, odorless gas 
*Most toxic component in [[smoke inhalation]] and major contributor to fire-related deaths 
**Can co-occur with [[Cyanide]] toxicity in industrial fires 
*Case fatality rate as high as 30%<ref>Nikkanen H, Skolnik A. Diagnosis and management of carbon monoxide poisoning in the emergency department. Emerg Med Practice 2011;13(2):1-14.</ref>
*Peak incidence in winter months for unintentional exposure

===Sources===
''Formed from incomplete combustion of hydrocarbons''
*Automotive exhaust 
*Propane-fueled heaters 
*Wood or coal-burning heaters 
*Structure fires 
*Gasoline-powered motors 
*Natural gas-powered heaters
*Waterpipe/Hookah <ref>Eichhorn, L., Michaelis, D., Kemmerer, M., Jüttner, B., & Tetzlaff, K. (2018). Carbon monoxide poisoning from waterpipe smoking: a retrospective cohort study. Clinical Toxicology , 56(4), 264–272.</ref>
*Methylene chloride (a degreasing solvent found in most paint strippers) fume inhalation
**Metabolized by the liver into carbon monoxide resulting in delayed toxicity (8 hours or longer)<ref>Hoffman RS, Nelson, LS, Goldfrank LR et al. Goldfrank's Toxicologic Emergencies, Eleventh Edition. McGraw-Hill Education / Medical; 2019.</ref>

===Pathophysiology===
*[[Hypoxia]]
**Binding affinity of hemoglobin for CO (carboxyhemoglobin) is 200x that of O2 
**Half-Life 
***Room air: ~5hrs 
***100% O2: ~1hr 
***HBO 2.5atm: 24min 
*[[Lactic acidosis]]
**CO inhibits oxidative phosphorylation 
*[[Hypotension]] 
**CO induces NO2 and guanylate cyclase release → vasodilation release
**CO binds to myoglobin and alters its function
*CO damage at cellular level due to reactive oxygen species, lipid peroxidation, and cellular apoptosis
**Occurs in CNS and leads to neurological sequela

==Clinical Features==
[[File:CO toxicity symptoms (en).jpg|thumb|Clinical features of CO toxicity]]
''May range from "flu-like" symptoms to coma''
*CNS 
**[[Headache]] 
**Visual disturbances 
**Confusion 
**[[Ataxia]]
**[[Seizure]]
**[[Syncope]]
**[[Retinal hemorrhage]] 
**Focal neurologic deficit 
**Coma
*GI 
**[[Vomiting]]
*Pulm 
**Dyspnea/tachypnea 
*Cardio 
**[[Chest pain]] 
**[[ECG]] changes/[[dysrhythmias]]
*Derm 
**[[Bullous skin lesions]] 
**Classic finding of cherry red oral mucosa is rarely seen in living patients
***More likely seen in > 25% COhemoglobin levels

===Expected CNS Function by COhemoglobin%===
{| {{table}}
| align="center" style="background:#f0f0f0;"|'''COhemoglobin'''
| align="center" style="background:#f0f0f0;"|'''Presentation'''
|-
| 10-20%||Confusion and agitation secondary to mild hypoxia
|-
| 20-30%||Progressive obtundation and nausea
|-
| >40%||Almost always unconscious
|-
| >60%||Survival is very rare
|}

===Symptoms By Frequency<ref>Lavonas EJ. Carbon monoxide poisoning. In: Shannon M, Borron S, Burns M, eds. Haddad and Winchester’s Clinical Management of Poisoning and Drug Overdose. Philadelphia, Pa: Elsevier; 2007:1297-1307.</ref>===
{| class="wikitable"
|-
! Symptom !! %
|-
| [[Headache]] || 85
|-
| [[Dizzy]] || 69
|-
| Fatigue || 67
|-
| [[Nausea]] or [[Vomiting]] || 52
|-
| Confusion || 37
|-
| LOC || 35
|-
| [[Dyspnea]] || 7
|}

===Delayed Neurological Sequela<ref>Nikkanen H, Skolnik A. Diagnosis and management of carbon monoxide poisoning in the emergency department. Emerg Med Practice 2011;13(2):1-14.</ref>===
*Can occur days to weeks after apparent resolution of acute symptoms in up to 46% of patients. The globus pallidus is the most commonly affected area.
*Persistent, disabling, or permanent 
*Cognitive sequelae lasting one month or more appear to occur in 25-50 percent of patients with loss of consciousness or CO levels > 25%. 
*Includes:
**Cognitive effects
**Motor disturbances
**Ataxia
**Neuropathies
**Psychosis
**Dementia

==Differential Diagnosis==
''A "great mimicker" due to the presentation of poisoning being diverse and nonspecific''
*[[Viral syndrome]]
*[[Depression]]
*Chronic fatigue syndrome
*[[Chest pain]]
*Other [[headache]]
*[[ARDS]]
*[[Acute mountain sickness]]
*[[Lactic acidosis]]
*[[Diabetic ketoacidosis]]
*[[Meningitis]]
*[[Methemoglobinemia]]
*[[Opioid toxicity|Opioid]] or [[Ethanol toxicity|toxic alcohol poisoning]]
*[[Inhalation exposure]]

===Further Considerations===
*[[Dichloromethane methylene chloride toxicity]]
**Consider when level not decreasing as expected, or is increasing due to prolonged absorption through skin/respiratory tract.

{{Toxic gas exposure DDX}}
{{Burn DDX}}

==Evaluation==
===Workup===
*[[VBG]] (ABGs are no longer considered necessary<ref>Lopez DM, et al. Relationship between arterial, mixed venous, and internal jugular carboxyhemoglobin concentrations at low, medium, and high concentrations in a piglet model of carbon monoxide toxicity. Crit Care Med. 2000; 28(6):1998-2001.</ref> as venous and arterial COHg levels will be within ±2%<ref>Touger M. et al. Relationship between venous and arterial carboxyhemoglobin levels in patients with suspected carbon monoxide poisoning. Ann Emerg Med 1995;33:105-109.</ref>)
**CO-oximetry analysis will provide carboxyhemoglobin level 
**pH will be low secondary to metabolic acidosis caused by anaerobic metabolism and elevated lactate levels
*Pulse CO-oximetry
**Special pulse CO-ox can accurately determine CO level<ref>Coulange M, et al. Reliability of new pulse CO-oximeter in victims of carbon monoxide poisoning. Undersea Hyperb Med. 2008; 35(2):107-111. </ref>
*Lactate (usually not significantly elevated, and if so should raise concern for cyanide toxicity) <ref> Wardi G, Brice J, Correia M, Liu D, Self M, Tainter C. Demystifying Lactate in the Emergency Department. Ann Emerg Med. 2020 Feb;75(2):287-298. doi: 10.1016/j.annemergmed.2019.06.027. Epub 2019 Aug 29. Erratum in: Ann Emerg Med. 2020 Apr;75(4):557. PMID: 31474479. </ref>
*Chemistry 
*[[Troponin]] 
*Total CK ([[rhabdomyolysis]]) 
*[[Beta-HCG]]
*[[ECG]] 
**May range from normal to STEMI (most common ST/T changes, then prolonged QT)
***Few of the patients with AMI from CO have occlusive lesions in their arteries 
*Head CT 
**Identified radiographically within 12 hours of exposure 
**Bilateral hypodense lesions in the basal ganglia: globus pallidus, putamen, and caudate nuclei<ref>Lee, DC: Hydrocarbons, in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 7. St. Louis, Mosby, Inc., 2010, (Ch) 156:p 2035-2038</ref>

===Diagnosis===
*Must have high clinical suspicion (esp in [[coma]], [[altered mental status]], or [[anion gap acidosis]]) 
**Comatose patients removed from fire should be assumed to have CO poisoning 
*Carboxyhemoglobin Level 
**Interpretation must take into account time since exposure and O2 treatment 
**Normal value in non-smokers is ~1%, normal value in smokers may be up to 10% 
**Symptoms and COhemoglobin levels do not always correlate well 
*Pulse oximetry is unreliable 
**COhemoglobin registers the same as O2hemoglobin so will have artificially high SpO2 
**O2 saturation gap reflects discordance of SpO2 by pulse oximeter vs by VBG

==Management==
===General Management===
*If smoke inhalation, good pulmonary toilet is very important
*'''NEVER''' use steroids in smoke inhalation injury; intubate early if concern for obstructing edema
*O2 100% by NRB or ETT 
**Provide O2 until COhemoglobin value <10% 
**Early PEEP prevents progressive atelectasis and improves O2 diffusion
**In general, COhemoglobin levels fall rapidly to < 10% within 30 min of 100% O2
**Maintain 100% O2 for additional 2-3 hrs after < 10%, since anaerobic COmetabolism is occuring due to cytochrome oxidase poisoning<ref>MetroHealth Medical Center Burn ICU Handbook (Not a policy manual), Cleveland, OH</ref>
***Anaerobic metabolism universally seen with COhemoglobin > 40%
***Monitor for return of aerobic metabolism with normal serum bicarbonate levels
*Consider other combustion products such as [[Cyanide]]

===[[Hyperbaric medicine|Hyperbaric Therapy (HBO)]]===
*Decision to initiate HBO should be made in consultation with a hyperbaric specialist 
*There is controversy regarding benefit<ref>http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1116883/pdf/1083.pdf</ref><ref>Juurlink, D. N., Isbister, G., Bennett, M. H. and Lavonas, E. J. (1996) ‘Hyperbaric oxygen for carbon monoxide poisoning’, Cochrane Database of Systematic Reviews</ref>
**Three HBO treatments within 24hrs shown to reduce risk of cognitive sequelae 6 weeks and 12 months after CO poisoning<ref>Weaver, L. et al. Hyperbaric Oxygen For Acute Carbon Monoxide Poisoning. NEJM. 2002:347(14):1057 http://emed.wustl.edu/Portals/2/Answer%20Key%20PDF/2012/January2012/SecondYear.pdf</ref>
**However, another study showed no benefit and suggested worse outcomes in HBO therapy<ref> Scheinkestel C. et al. Med J Aust 1999; 170 (5): 203-210. Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomized controlled clinical trial http://www.mja.com.au/journal/1999/170/5/hyperbaric-or-normobaric-oxygen-acute-carbon-monoxide-poisoning-randomised</ref>
*Patient must be stable prior to transport since response to acute medical conditions while undergoing hyperbaric therapy in a chamber is difficult.
*'''Indications (generally accepted guidelines):''' <ref>Practice Recommendations in the Diagnosis, Management and Prevention of Carbon Monoxide Poisoning. Hampson NB et al. Am J Respir Crit Care Med 2012 Oct 18</ref>
**[[Syncope]] 
**Confusion/[[altered mental status]] 
**[[Seizure]]
**[[Coma]]
**[[Focal neuro deficit]]
**[[Pregnancy]] with COhemoglobin level >15% 
***Fetal Hb tends to bind more CO
**Blood level >25% 
**[[Acute myocardial ischemia]]
**Prolonged CO exposure with minor clinical findings (“soaking”)<ref>Marx, John A., and Peter Rosen. Rosen's Emergency Medicine - Concepts and Clinical Practice E-Book: Edition 9. Philadelphia, PA: Elsevier/Saunders, 2017. Pg 2387</ref>

==Disposition==
===Minimal or no symptoms===
*Discharge
**If discharging patient, may need to alert local fire/police services to evaluate home/work before they return. Check with your local branch.
**Patient's should not be discharged to an environment where they will become toxic again

===Mildly symptomatic===
*[[Headache]], [[vomiting]], elevated COhemoglobin level 
*Discharge after 4hr obs and symptom resolution and assurance that the discharge environment is safe

===Severely symptomatic===
*[[Ataxia]], [[syncope]], [[chest pain]], [[focal neuro deficit]], [[dyspnea]], [[ECG]] changes, pregnant with COhemoglobin >15% 
*Admit; discuss with hyperbaric specialist

==See Also==
*[[Toxidromes]]
*[[Burns]]
*[[Cyanide]]
*[[Methemoglobinemia]]

==External Links==
[https://www.acep.org/patient-care/clinical-policies/carbon-monoxide-poisoning/ ACEP Clinical Policy Statement on Carbon Monoxide Poisoining]

==References==
<references/>

[[Category:Toxicology]]