CO/CYANIDE

Poisoning

Muath Alismail
Reviewed with Dr. Abrar
A 30 y/o man presents to the ED for SOB and Headache. The patient states he
brought his charcoal grill inside to cook.
Vital signs: BP 130/60, HR 110, RR 22, O2 96% on RA, and T 37.3
Labs: pH of 7.2 with a normal CO2 level.
Which of the following is the most likely explanation for these findings?

A. Carbon monoxide toxicity

B. Cocaine intoxication
C. Hypovolemic shock
D. Sepsis
A 30 y/o man presents to the ED for SOB and Headache. The patient states he
brought his charcoal grill inside to cook.
Vital signs: BP 130/60, HR 110, RR 22, O2 96% on RA, and T 37.3
Labs: pH of 7.2 with a normal CO2 level.
Which of the following is the most likely explanation for these findings?

A. Carbon monoxide toxicity

B. Cocaine intoxication
C. Hypovolemic shock
D. Sepsis
Introduction
Carbon monoxide (CO) is one of the most common toxic exposures that emergency
physicians will encounter.
It’s typically described as a colorless, odorless, tasteless gas cause of fatal poisoning,
either intentional (suicidal) or accidental,
Methylene chloride
● CO is also an endogenous substance, with production occurring in the body during
normal breakdown of heme.

● Normal physiologic CO levels (as carboxyhemoglobin) from this process are

approximately 1% in healthy nonsmokers and 4-10% in the active smoker.

● The most easily quantified physiologic effect is binding to hemoglobin to form

carboxyhemoglobin (COHb).

● The binding affinity of normal adult hemoglobin for carbon monoxide is over 200 times

that for oxygen

Clinical Features
bullous lesions cherry red oral mucosa or skin
Standard pulse oximetry is unreliable in the diagnosis of CO poisoning
 Standard pulse oximetry is unreliable in the diagnosis of CO poisoning

Co-oximetry measures total hemoglobin as well as

oxyhemoglobin, methemoglobin, and COHb saturation

There is excellent correlation between arterial and

venous COHb levels, so a VBG with co-oximetry is
sufficient in most cases.
Interpreting COHb Levels

The COHb level is not an absolute indicator of clinical severity, nor is rapid clearance of an
elevated level evidence of clinical improvement.
When interpreting COHb levels, consider time and duration of exposure, time from
exposure to presentation, treatment (such as high-flow oxygen) rendered in route, and
clinical symptoms.
In one series, 30% of 163 patients with CO poisoning had a normal COHb level at ED
presentation. Even in the absence of an elevated COHb level, the diagnosis is still made
by history of exposure and compatible symptoms or signs.
Therefore, The diagnosis of CO poisoning is clinical
Ancillary Tests

ABG and serum lactate levels. Elevated lactate from the interference in the
electron transport chain, an unexplained elevated anion gap metabolic
acidosis, elevated creatine phosphokinase, or elevated troponin may trigger
an investigation for CO poisoning. Consider concomitant cyanide poisoning. Also
consider additional toxicology testing for intentional CO poisoning.

ECG findings may range from entirely normal to ST-segment elevation myocardial
infarction. There does not appear to be any classic CO ECG pattern.
CO poisoning is associated with one
specific radiographic finding, globus pallidus
lesions Lesions are generally bilateral,
symmetric, and more common in severely
poisoned patients.

Globus Pallidus Lesions

Treatment
Remove the patient from CO source

Start 100% oxygen immediately.

Identify risks for possible referral for hyperbaric oxygen treatment

Elimination half-life of CO

● Room air: 4-5 hours

● 100% O2: 1-1.5 hour

● Hyperbaric O2: 20-30 minutes

Disposition

Low-risk features
mild symptoms such as headache, dizziness, or n/v, continue 100% oxygen until
symptoms have resolved and COHb is normal (<3%).

An ED observation period of 6 hours, with 100% oxygen, is recommended

*Methylene chloride exposure requires ≥8 hours

High-risk features
prior to referral or transport for hyperbaric oxygen, secure the airway, stabilize vital
signs, continue 100% oxygen, and identify and treat trauma or acute surgical or
Delayed neurologic sequelae

Reported neurologic effects include (eg, focal deficits and seizures) and those with
primarily psychiatric or cognitive findings (eg, apathy and memory deficits)

It can occur 4 days to 5 weeks after CO exposure. There are no widely

established diagnostic criteria for delayed injury, so the reported incidence varies
widely, from 3% to 40% of patients.

Risks include prolonged CO exposure (>6 hours), Glasgow Coma Scale score <9,
seizures at the time of initial presentation, and leukocytosis.
Cyanide Toxicity
 Introduction

Metabolic toxin that causes uncoupling of

the electron transport chain and,
as a result, anaerobic metabolism occurs.

This results in the clinical features seen on

presentation as well as a severe metabolic
acidosis and lactic acidosis
The decision to institute antidotal treatment of cyanide poisoning must be made
long before confirmatory laboratory studies can be obtained.

unexplainable lactic acidosis. Serum cyanide levels are not readily available.

Therefore, cyanide toxicity needs to be diagnosed clinically as delays in treatment

can result in significant comorbidities and death
Treatment

supportive care 100% oxygen along with

crystalloids and vasopressors for hypotension. Hydroxocobalamin (B12)
1st line

The two antidotes most commonly used are

cyanide antidote kit

(nitrites and thiosulfate)
Treatment

● Hydroxocobalamin is a metalloprotein that binds cyanide, removing it

from cytochrome oxidase and forming cyanocobalamin, which is then
eliminated via the kidneys.
● Dose of hydroxocobalamin in an adult patient is 5 grams IV over 15 min
● A second dose of 5 grams IV may be repeated once (for a total of 10 gm)
● The pediatric dose is 70 mg/kg (max dose of 5 grams) IV over 15 minutes.
Treatment

● Hydroxocobalamin has a low toxicity profile

side effects: transient hypertension, a

reddish discoloration of the skin, mucous
membranes and body fluid.

interference with chemistry and co-oximetry

tests has been reported; therefore,

Blood samples should be collected prior to administration

Treatment

the Cyanide Kit include:

● amyl nitrite for inhalation 10-mL vials

of 3%
● sodium nitrite (300 milligrams),
● sodium thiosulfate 50-mL vials of 25%
 Treatment

- In children, the sodium nitrite dose is adjusted

according to the hemoglobin level to keep the
methemoglobin level less than 30%

*If hemoglobin values are not available, the empiric dose of sodium nitrite for a
child less than 25 kg is based on the 10-gram hemoglobin concentration

- Nitrites side effects, including hypotension and the development of excessive

methemoglobinemia
Disposition

● Patients who receive cyanide antidotal therapy should be admitted for observation.

● Full recovery is anticipated in many cases of severe poisoning in which treatment is

initiated rapidly and cardiac arrest has not yet occurred.