• A 43 y/o woman presents with a 3-week history of intermittent headache, nausea, and fatigue. Her husband and children also have similar symptoms. They all were diagnosed with a viral syndrome by a private doctor. The symptoms began when it started to get cold. The symptoms are worse in the morning and improve while she is at work. Her V/S: 123/75, 83, 37.0, O2 98%. PE – unremarkable. What is the most appropriate next step to confirm your suspicion?a) A mono spot testb) Nasal pharyngeal swab for influenza testc) COHb leveld) Lead level

• A 35-year-old man presents complaining of headache, weakness, nausea, and vomiting after working with paint remover in an enclosed space. Which of the following statements regarding management of this patient’s problem is TRUE?a) A special antidote kit is requiredb) Carboxyhemoglobin level is not helpful in this casec) Treatment must continue longer in patients with this

exposure than from other sourcesd) The patient’s oxygen–hemoglobin dissociation curve is

shifted to the righte) Severe metabolic acidosis may be present

Carbon Monoxide

Carbon Monoxide (CO)

• an odorless, colorless, tasteless gas• produced by incomplete combustion of carbon

materials• normally present in air at < 10 parts per million (ppm)

or less; toxicity begins at 100 ppm• also an endogenous substance (normal breakdown of

heme)• 200-250 times greater affinity for hemoglobin than O2

• reversible binding at the iron-porphyrin center of hemoglobin, producing carboxyhemoglobin (COHb)

Sources of Carbon MonoxideAutomotive exhaustMotorboat exhaustPropane-fueled heatersWood- or coal-burning stoves or heatersStructure firesGasoline-powered generators or motorsNatural gas–powered heaters/furnaces/generatorsMethylene chlorideForklifts

Pathophysiology

• Half-lives of COHb– room air: 249 - 320 minutes– 100% oxygen: 74 - 80 minutes– methylene chloride exposure: up to 13 hours

• COHb level increase relative anemia & hypoxia

• There is a separate toxicity to carbon monoxide irrespective of the level of COHb.

Pathophysiology

• 10-15% of CO is dissolved unbound into plasma >>move>> intracellular

• CO inhibits cytochrome oxidase, interfering with cellular respiration and ATP generation a relative uncoupling of oxidative phosphorylation lactic acidosis

Pathophysiology

• Release of guanylate cyclase & nitric oxide endothelial dysfunction & vasodilatation hypotension

• Relative hypoxia + hypotension ischemia-reperfusion injury in cardiac myocytes, neuronal tissue

• Rhabdomyolysis, acute myocardial infarction, neuronal cell death

• Cells in the basal ganglia are particularly sensitive

Clinical Features

• Clinical presentation is highly variable• Clinical scenarios:

– unconscious patient pulled from a house fire, or from a running car in a closed garage

– the patient with "flu-like" symptoms– the elderly person presenting with syncope and

ischemic ECG changes

Shannon: Haddad and Winchester's Clinical Management of Poisoning and Drug Overdose, 4th ed.

Shannon: Haddad and Winchester's Clinical Management of Poisoning and Drug Overdose, 4th ed.

• CO poisoning should always be in the dDx for 1. comatose patients2. patients with mental status changes3. patients with an elevated anion gap

metabolic acidosis or otherwise unexplained lactic acidosis

• A comatose pt removed from a fire scene should be assumed to have CO poisoning until proven otherwise, even in the absence of cutaneous or airway burns.

Diagnosis

• blood COHb levels (using co-oximetry )• COHb serves as a marker of severity and helps

to stratify pts at risk for delayed sequelae• SaO2 appear artificially high in routine ABG• Correlation between arterial and venous

COHb levels is excellent VBG sample analyzed with co-oximetry is usually sufficient

Diagnostic Study Findings Associated with CO Poisoning↑ COHb level (normal 0-5%; not correlate well w/ symptoms)Artificially elevated oxyhemoglobin saturation using pulse oximetry (higher than the saturation on the ABG, pulse oximetry gap)↑ lactate↑ anion gap metabolic acidosis↑ CPK (rhabdomyolysis > cardiac source)↑ troponin (diffuse cardiac myonecrosis > focal CAD)Variable ECG findings—ranges from normal to injury patternBilateral globus pallidus lesions on MRI

Not recommend to rely solely on pulse co-oximeters to detect CO poisoning

Neuroimaging

• CT brain: change in 12 h of CO exposure + LOC• Symmetric low-density areas at globus

pallidus, putamen, caudate nuclei• CT changes in 24 h poor outcome• Not influence patient management• Reserved for patients who show poor

response or have an equivocal diagnosis• MRI appears to be superior

www.learningradiology.com

Bilateral hypodensity in the globus pallidus and hippocampal regions on admission CT.

Coric V et al. J Neurol Neurosurg Psychiatry 1998;65:245-247

©1998 by BMJ Publishing Group Ltd

Other Tests

• Neuron-specific enolase or S100B and CSF myelin basic protein are markers for CO neurotoxicity

• More useful to determine prognosis than diagnosis

Treatment

• Immediate removal from the contaminated environment

• Initial resuscitation steps• Supplemental oxygen (conc. ≈ FiO2 1.0)

immediately …and for at least 4 hours• Severely poisoned pts >> continuous cardiac

monitoring, an IV line established, and an ECG performed.

Hyperbaric Oxygen (HBO) Therapy

• Enhance elimination of COHb (reduces the half-life to ≈ 30 min)

• Increases amount of dissolved O2 in plasma• Reduces CO binding to other heme-containing

proteins• Questionable benefit over normobaric oxygen• May reduce incidence of neurologic sequelae• The question of who will benefit most, and when

to refer, remains controversial.

Commonly Utilized Indications for Referral for Hyperbaric Oxygen TreatmentSyncopeConfusion/altered mental statusSeizureComaFocal neurologic deficitPregnancy with COHb level >15%Blood level >25%Evidence of acute myocardial ischemia

Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 7th ed.

HBO Therapy

• The patient needs to be clinically stable (+ secure airway, stable hemodynamic) before referral or transport for HBO.

• Complications: – Pneumothorax– Barotrauma to the ears– Seizures from oxygen toxicity (usually with

prolonged or multiple treatments)– Gas embolism

Disposition ConsiderationsSymptom Severity Disposition Comments

Minimal or no symptoms

Home Assess safety issues

HeadacheVomitingElevated CO level

Home after symptom resolution

Administer 100% O2 in EDObserve 4 hAssess safety issues

Ataxia, seizure, syncope, chest pain, focal neurologic deficit, dyspnea, ECG changes

HospitalizeConsult with hyperbaric specialist

Administer 100% O2 in EDCO level, comorbid conditions—including pregnancy—and age; stability of the patient must be considered if considering transfer for hyperbaric oxygen

Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 7th ed.

Special Populations

• Children:– more susceptible (↑fetal hemoglobin,

↑metabolic rate)– HBO - good safety profile

• Elderly:– higher risk from poisoning (esp. serious comorbid)– CAD – low COHb (4-6%) can cause ECG changes &

myocardial ischemia

Special Populations

• Pregnant pts:– HBO therapy if they meet criteria or if there are

signs of fetal distress– Normobaric oxygen therapy should be prolonged

(slower elimination of CO from the fetus)

Thank You

• A 43 y/o woman presents with a 3-week history of intermittent headache, nausea, and fatigue. Her husband and children also have similar symptoms. They all were diagnosed with a viral syndrome by a private doctor. The symptoms began when it started to get cold. The symptoms are worse in the morning and improve while she is at work. Her V/S: 123/75, 83, 37.0, O2 98%. PE – unremarkable. What is the most appropriate next step to confirm your suspicion?a) A mono spot testb) Nasal pharyngeal swab for influenza testc) COHb leveld) Lead level

• A 35-year-old man presents complaining of headache, weakness, nausea, and vomiting after working with paint remover in an enclosed space. Which of the following statements regarding management of this patient’s problem is TRUE?a) A special antidote kit is requiredb) Carboxyhemoglobin level is not helpful in this casec) Treatment must continue longer in patients with this

exposure than from other sourcesd) The patient’s oxygen–hemoglobin dissociation curve is

shifted to the righte) Severe metabolic acidosis may be present