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) b) c) d) A mono spot test Nasal pharyngeal swab for influenza test COHb level 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 patients problem is TRUE?
a) A special antidote kit is required b) Carboxyhemoglobin level is not helpful in this case c) Treatment must continue longer in patients with this exposure than from other sources d) The patients oxygenhemoglobin dissociation curve is shifted to the right e) 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 Monoxide Automotive exhaust Motorboat exhaust Propane-fueled heaters Wood- or coal-burning stoves or heaters Structure fires Gasoline-powered generators or motors Natural gaspowered heaters/furnaces/generators Methylene chloride Forklifts

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 ischemiareperfusion 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 patients 2. patients with mental status changes 3. 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 findingsranges from normal to injury pattern Bilateral 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;65:245247

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 halflife 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 Treatment Syncope Confusion/altered mental status Seizure Coma Focal neurologic deficit Pregnancy 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 Considerations
Symptom Severity
Minimal or no symptoms Headache Vomiting Elevated CO level Ataxia, seizure, syncope, chest pain, focal neurologic deficit, dyspnea, ECG changes

Disposition
Home Home after symptom resolution Hospitalize Consult with hyperbaric specialist

Comments
Assess safety issues Administer 100% O2 in ED Observe 4 h Assess safety issues Administer 100% O2 in ED CO level, comorbid conditionsincluding pregnancyand 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) b) c) d) A mono spot test Nasal pharyngeal swab for influenza test COHb level 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 patients problem is TRUE?
a) A special antidote kit is required b) Carboxyhemoglobin level is not helpful in this case c) Treatment must continue longer in patients with this exposure than from other sources d) The patients oxygenhemoglobin dissociation curve is shifted to the right e) Severe metabolic acidosis may be present