Clinical Presentation

CO poisoning is still poorly understood as far as its presentation (30 % of mistakes in diagnosis37) and long-term consequences are concerned.

The usual clinical presentation begins with minor signs (generalised weakness, headache, nausea, vertigo), later followed by muscular weakness, collapse and loss of consciousness; eventually hypertonic coma with exaggerated tendon reflexes supervene with signs of pyramidal irritation. Death eventually occurs due to cardiorespiratory failure38.

The clinical presentation may mimic a number of other common conditions which may take the precedence in the differential diagnosis (e.g., influenza; alcohol intoxication; migraine; angina; etc.) which delays appropriate treatment or, worse, results in the patient being sent home to rest in the contaminated environment that originally caused the problem. Thus, the diagnosis relies on a high index of suspicion, confirmation of exposure to

CO by COHb determination, followed by a concerted effort in determining the source of CO exposure and eliminating it.

Table 2.2.3-2. Clinical picture of CO poisoning in relation with levels of carboxyhaemoglobin

Although there are former studies relating clinical severity to COHb levels (Table 2.2.3-2), it is very important to emphasise that this is at odds with clinical experience. The level of CO measured in the hospital setting is preceded by a variable delay, frequently also affected by the administration of oxygen, making the level highly variable and correlating poorly with the original exposure levels39.

COHb levels can be measured in venous or capillary blood - arterial blood gas is not required unless required by the medical condition of the patient.

Measuring COHb is usually carried out by CO-oximetry using spectrophotometry. There is a physiological COHb level between 0.3 and 0.5%, and a 1 to 2% variation due to urban pollution. The main variable is exposure to tobacco with heavy smokers reaching levels of up to 10%. Hence CO poisoning can be presumed whenever the COHb level is above 10% in non-smokers or 15% in smokers40. Lower COHb levels do not exclude the possibility of CO poisoning but require consideration of smoking habits and any delays or oxygen administration between the CO poisoning and blood sampling. Importantly, it must be noted that current pulse oximetry equipment is unable to distinguish between HbO2 and COHb. They are not useful for diagnosis and - more dangerously - they overestimated blood oxygen content.

In appropriate circumstances (mass casualties or doubtful CO poisoning) with conscious subjects able to control their breathing) exhaled CO may be measured in lieu of COHb. The former does not require venipuncture and the results are rapid. A level of 50 parts per million (ppm) or 0.005% CO in expired air is the equivalent of about 6% COHb while 80 ppm level or 0.0085 equates to about 10%41,42.

Measuring CO concentration in the atmosphere may also be helpful. Normal levels for CO are under 10 ppm. A level of 50 ppm is abnormal, even though it would take some time for toxicity to develop depending on

Symptoms

Asymptomatic

Weakness, headache

Severe headaches, nausea, vertigo

Nausea, vomiting, blurred vision, muscle weakness

Loss of consciousness, tachypnoea, tachycardia

Coma, convulsions

Cardiovascular collapse, respiratory distress_

0 - 10 10 - 20 20 - 30 30 - 40 40 - 50 50 - 60 > 60

the patient's level of activity and breathing rate. Exposure to 1000 ppm or higher can be rapidly incapacitating or fatal - as may be observed in rescue teams.

Severe complications in the acute phase of CO poisoning, largely affect the cardiovascular system with, collapse, arrythmias, coronary ischemia ; and acute pulmonary oedema. Rhabdomyolysis may also occur with a risk of subsequent acute renal failure (Table 2.2.3-3).

Short term mortality is not the biggest area of concern. It is the long-term complications that vex clinician and prompt the controversies regarding optimal treatment. These include (1) persistent neurological deficits, such as persistent coma or cerebral dysfunction and (2) persistent neurological manifestations (PNM) which may appear up to a month after the exposure -frequently following apparent recovery. They may include Parkinsonism, confusion, dementia and memory disorders.

Table 2.2.3-3. Immediate complications with relation to severity of CO poisoning

Group

0 I

II

III

IV

Total

Number of patients

96 273

213

169

23

774

Cardiovascular

0 5 (2 %)

15 (7 %)

22 (13 %)

12 (52 %)

54 (7 %)

complications including

• Collapse

-

-

3

3

6

• Coronary

3

6

7

3

19

ischemia

2

7

4

5

18

• Arrhythmia

Respiratory complications • Pulmonary oedema

1 (0.4 %)

%)

9 (39 %)

39 (5 %)

• Bronchial-super-

2

2

11

infection

-

7

6

21

• Bronchospasm

1

1

15 4

1

9

Other complications

0 0

1 (0.5 %)

1 (0.6 %)

1 (0.4 %)

3 (0.4 %)

Group 0 : Normal consciousness, no loss of consciousness, no neurological signs

Group I : Normal consciousness, no loss of consciousness, objectives sign(s) on neurological examination

Group II : Normal consciousness, initial loss of consciousness Group III : Stage I or II coma Group IV : Stage III or IV coma

A significant difference (p<0.01) was observed between groups 0 and I vs., groups II, III and IV, as far as immediate complications are concerned. Similarly, there was a great difference between group II and groups III and IV. Thus loss of consciousness or altered consciousness is associated with more immediate complications; coma even more frequently so.

Group 0 : Normal consciousness, no loss of consciousness, no neurological signs

Group I : Normal consciousness, no loss of consciousness, objectives sign(s) on neurological examination

Group II : Normal consciousness, initial loss of consciousness Group III : Stage I or II coma Group IV : Stage III or IV coma

A significant difference (p<0.01) was observed between groups 0 and I vs., groups II, III and IV, as far as immediate complications are concerned. Similarly, there was a great difference between group II and groups III and IV. Thus loss of consciousness or altered consciousness is associated with more immediate complications; coma even more frequently so.

In the early 1970's, Smith et Brandon43 reported a follow-up study showing that after CO poisoning, after excluding those patients with immediate neurological involvement, 33% of the remaining patients suffered behavioural disorders and 43% suffered memory impairment despite an apparent recovery. In a review of literature at the time, Ginsberg & Romano44 determined PNM to occur in 15 to 40% of seemingly recovered patients. These occurred within 3 to 240 days after CO poisoning. PNM has been investigated by medical imaging and several characteristic patterns of injury have been reported using CT, MRI and PET scanning. The most commonly affected areas are the globus pallidus and the white matter38.

Unfortunately there are no clinical or biological markers for PNM. However, age (> 60 years) and loss or altered consciousness seem to be risk factors45,46. Psychometric tests may be more sensitive in detecting early neurological involvement and prompt more aggressive treatment regimens47.

Fortunately PNM improve or disappear in 50 to 75% of cases within 1 year of the event. Many uncontrolled clinical studies have reported that HBO in the acute phase appears to decrease the frequency of PNM39,48-50 when compared to historic or normobaric oxygen (NBO) controls45,51.

The pathophysiological mechanisms for these lesions still remain to be clarified, but hypoxia alone cannot account for them. The appearance of ischemia-reperfusion injury with delayed neuronal apoptosis offers a more attractive alternative hypothesis at present.

0 0

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