2. PATHO-PHYSIOLOGY
CO is endogenous by- product of heme degradation
Its normal level increases during pregnancy 20%_40%
About 30% to 40% of this increase due to increase of
RBC load, and 15% comes from the fetus .
Fetus CO-HB 20% more than the mother .
Cause of this increase related to increase progesterone level
which induce heme metabolism by hepatic enzyme .
3.
4. Exogenous CO comes from partial burn of carbon
CO poisoning comes from increase its level in the air in closed
space .
Factors affecting CO uptakes :
1)Partial pressure of CO/ O2
2)ventilator rate
3)Duration of exposure
Minutes ventilation increase during
pregnancy make mother and fetus in the
highest level of suitability .
5. BIOCHEMICAL ASPECT OF CO POISONING
In the lung CO binds more slowly to Hb than O2
but once it binds to Hb its becomes extremely slow to dissociate
There is two form of Hb:
1)De-oxy state ( T ) chain has high affinity to
O2
2)Oxy state (R) chain has high affinity to CO
At CO partial pressure of 0.16 mmHg 75%
of Hb combine with CO
Less than 0.1% of inspired air
6.
7. FETUS AND CO POISONING
Fetus has( Hb F) which has high affinity to O2
than (Hb A) of the mother .
(Hb F) shift O2_ Hb dissociation curve to the left (
decrease dissociation of O2 from Hb ).
CO level in the fetus is also higher and also makes
the curve shifts to the left.
8. Acute CO exposure: death due to anoxia before
COHb increases .
Chronic exposure: COHb increases +++
Critical level 60% not possible to measure in the fetus but you
evaluated in the mother
Elimination in mother need 2hr
Elimination in fetus needs 7Hr
9.
10. TERATOGENIC EFFECT OF CO POISONING
Depends on gestational age:
Embryonic stage : neurological skeletal effect
Cleft palate .
Fetal phase: anoxia encephalopathy, growth restriction .
3rd trimester: premature delivery, decrease immunity, Rt side
cardiomegaly, delay myelination .
11. CO NEUROTOXICITY
23% to 47% of patients with CO poisoning develop delayed
neurological injury (the most frequent CO morbidity) .
Patient develops within 6 days to 3 weeks despite appropriate
management:
Impairment concentration and, or learning,
dementia,
cogwheel rigidity,
amnesia,
depression
12. PATHOLOGY OF CO NEUROTOXICITY
NE and dopamine increase after CO poisoning .
Oxidative stress and inflammatory response leads to
demyelination of nerves decrease nerve conductivity.
CO increase NO level in the blood vessels lead to vasodilatation;
increase brain blood flow and
neutrophils; secrete inflammatory response cause perivasciular
cell injury .
In the brain tissue microglia attacks oligodendrocytes produce
demyelination effect
14. Skeletal muscle necrosis can happen due to ischemia
Rhabdomyelesis leads to acute renal failure
Can be prevented or managed by supportive care with good
hydration
15. MANAGEMENT OF CO POISONING
symptoms and signs are not specific mimic viral
infection and gastroenteritis .
Best way to diagnose is to consider it often in
D.D (differential diagnosis) .
One needs high degree of suspicious to discover
CO poisoning
16. First aid starts with removal from closed space to open .
Start with 15 L 100% hyperbaric( HBO) O2 with
non rebreathing mask
HBO reduces elimination time from 4hr on room air to
about 20 minutes .
17. Indication of HBO in pregnancy
COHb > 15-20%
Maternal neurological signs
Evidence of fetal compromise
100% O2 recommended 5 times period longer in
pregnant patient than slandered considering fetal
CO elimination delay
