Management protocol of carbon Monoxide poisoning

1. BY
KEROLUS EKRAM GAD SHEHATA
• P G Y - I I I I M R E S I D E N T , A I N S H A M S U N I V E R S I T Y
• E C F M G C E R T I F I E D
Management protocol for
Carbon Monoxide Intoxication

2. General hints
 CO is a SILENT KILLER
 Odorless, Colorless, Tasteless
 Needs a high index of suspicion for early
diagnosis.
 Wide scope of symptoms and presentations that
can be misdiagnosed as something else.
 May lead to delayed and even permanent
sequalae.

3. Presentation
 Careful and detailed history taking can be the
only clue to diagnose CO poisoning.
 Mainly in winter months.
 Mostly group of poisoned people.
 Circumstances may include: Showering using
gas heaters, fires in a closed space, running
vehicles in a closed garage, setting fire to warm
up, using coal grills at homes in a closed space.

4. Clinical Manifestations
CNS: dizziness, confusion, HEADACHE
(frontal), ataxia, tinnitus, loss of
consciousness or seizures
GIT: Nausea, vomiting, abdominal pain.
Respiratory: Shortness of breath, chest
pain
Signs: Tachycardia, Tachypnea, DCL

5. Take Care!!
 Diagnosis can be challenging to the inexperienced ER
physician as it can be mistaken for:
1. Food poisoning … HEADACHE is not the patient’s
main concern.
2. Other causes of disturbed conscious level:
Medical or Toxicological.
So, a high index of suspicion is needed for a prompt
diagnosis and management of this toxicologic emergency.

6. How to proceed..?
 Vitals are VITAL.
 General assessment of the patient’s condition should
be done in a focused, wise manner aiming for knowing:
1. The circumstances of the event
2. Duration of exposure
3. Premorbid conditions
4. GCS +/- any signs of lateralization
Exclude other causes of DCL e.g. hypoglycemia, hepatic,
renal, CNS trauma, drugs…etc.

7. How to proceed..? Cont’d
 Start High flow Oxygen as soon as possible using
a nonrebreathable mask (60 % at a flow > 10 L/min).
 N.B. 100% Oxygen can be delivered only via ETT & HBO.
 If there is severe headache or non improving DCL, we can
use measures to decrease the ICT e.g.
1. Mannitol (1-2 gm/kg): provided that there is no
hypotension or disturbed kidney functions.
2. Corticosteroids e.g. prednisone or hydrocortisone.
Supportive treatment e.g. Crystalloids for hypotension

8. Take care!!
 PaO2 & SaO2 NORMAL
 Extremes of age are more liable for severe toxicity.
 Fetuses of pregnant females may suffer a wide variety
of neurologic deficits even at low levels of COHB.
 When to intubate:
1. Non-improving DCL.
2. GCS < 8 from the start.
 Aim of Intubation
1. Deliver 100% oxygen
2. Protection against aspiration

9. Investigations
 Routine investigations: Glucose, Na, K
 ABG: Metabolic acidosis .. Correlate with the degree of
tissue hypoxia
N.B. Never to be corrected with NaHCO3… Further
shift of O2-dissociation curve to the Left… Further tissue
hypoxia.
 COHB level: there could be a mismatch with the
presenting symptoms if there is long delay of the patient
or in the presence of comorbid conditions. It also can’t
predict the patient's prognosis or the development of
delayed sequalae.

10. Investigations, Cont’d
 ECG: to detect early signs of ischaemic heart diseases
especially in cardiac patients and in the elderly
 Cardiac biomarkers: To confirm ischaemic heart disease.
N.B. Treatment of CO-induced cardiac ischaemia is
OXYGEN/HBO.
 Renal Function tests: especially in the elderly patients or
in those who will be given Mannitol.
 Chest X-ray: To detect ARDS (with prolonged oxygen
therapy) or ventilator-acquired pneumonia

11. Investigations, Cont’d
 CT brain: To exclude intracranial causes of DCL e.g. Hge.
Especially if there is a history of falling on the head (take
care in these patients NOT to give too many crystalloids
as they worsens the cerebral edema)
 MRI brain: done for those who don’t regain
consciousness for a long time e.g. days to detect any
other causes of DCL or to detect demyelination of CNS
areas causing the delayed neuro-psychiatric sequalae.
 CPK: if you suspect rhabdomyolysis (rare) esp. for long
bed-ridden patients.

12. How to manage?
 Aim: to regain and maintain tissue oxygenation till the
end of T1/2 of COHB.
 Methods:
1. Nasal prongs: least effective.
2. Nonrebreathable masks
3. ETT: only way to deliver 100% O2. Patient is put on the
ventilator for 6 hours then reasess to wean.

13. How to manage?...Cont’d
 Hypotension…cautious use of crystalloids so as
not to increase the cerebral edema.
 For patients with severe headache and those
presenting with DCL from the start… Mannitol
+/- Corticosteroids to decrease the ICT.
 Reassessment of the patient’s response to
treatment

14. When to admit?
1. Unstable vital data even with initial ER management
2. Non improving DCL, GCS <8
3. Presence of premorbid cardiac condition in an elderly
patient.
4. Severe non improving metabolic acidosis.
5. Ischaemic changes in the ECG
6. Patients presenting with Pulmonary edema (can be
cardiogenic or non-cardiogenic)
7. COHB > 40 % .. controversial

15. Hyperbaric oxygen
 100 % Oxygen provided under pressures > 1 atm.
 Aim: Decrease T1/2 of COHB to 20 minutes, protect
against CO-induced post ischaemic reperfusion injury
and may protect against the delayed neuropsychiatric
sequalae (Not an evidence-based fact).
 Needs transportation, so the patient should be
vitally stable prior to the transport.
 Not available in all places all the time.

16. Who will benefit from HBO?
1. History of loss of consciousness or DCL.
2. Cerebellar findings e.g. ataxia, vertigo
3. CVS depression +/- IHD.
4. Extremes of age
5. Pregnant females.
6. Non improving metabolic acidosis
7. COHB > 40 % on presentation…controversial.
8. Delayed neuro-psychiatric sequalae

17. Neuro-Psychiatric sequalae
 Wide scope
 Can’t be predicted but one study showed that patients presenting
with cerebellar signs may have increased risk.
 Its prognosis can’t be determined
 Needs both short and long term follow up
 The role of HBO in its prevention and treatment is still controversial
1. 3D: Dementia, Depression, Disorientation
2. 4P + 1B: Psychosis, Personality changes, Parkinsonian features,
Paralysis + Blindness
3. Children: decrease in their cognitive functions

18. Questions & Comments