Diagnosis

Signs and symptoms of CO injury correlate reasonably well with on-the-scene co-oximetry determination of HbCO. However, by the time the patient gets to the ED after breathing air and with prehospital oxygen administration, the positive predictive value (PPV) of HbCO levels falls considerably. A very careful history, coupled with a careful screening neurologic examination that includes a CO neuropsychometric screening battery (CONSB), is a sensitive but not specific assay for CO intoxication. The CONSB has a good PPV for discerning neurologic dysfunction or injury from CO intoxication. 1 l4 The CONSB should be done with the patient breathing room air to be most sensitive.

Patients with CO exposure and only mild symptoms (no loss of consciousness, no cardiopulmonary symptoms, awake and cooperative) require minimal ancillary testing: a measure of HbCO and possibly an electrocardiogram (ECG) to detect silent myocardial ischemia. Patients with moderate to severe exposures should have additional studies done to assess the extent of ischemic injury.

1. Co-oximetry determination of HbCO measures actual levels. Pulse oximetry confuses HbCO for oxyhemoglobin and gives spuriously high values for percent of oxygen saturation.15

2. The extent of metabolic acidosis—as measured by the serum pH, serum bicarbonate level, or serum lactate level—is a measure of the ischemic damage. CO, by blocking the cytochrome chain, reduces pyruvate utilization by the Krebs cycle, and the excess pyruvate is metabolized to lactate ( Fig 198-3). The arterial blood gases (ABG), serum electrolytes, and serum lactate are used to detect metabolic acidosis.

FIG. 198-3. In mitochondria, the cytochrome aa3 CO ligand brings to a halt the orderly flow of electrons from food sources to oxygen. As a result, pyruvate stops its entry into the Krebs cycle and redirects its metabolic route to formation of lactate.

3. A complete blood count (CBC) will help in evaluating hemoglobin level to estimate arterial oxygen content (Ca o2).

4. The ECG is indicated if the patient has chest pain, palpitations, or dysrhythmia on the monitoring lead. The ECG should also be used in older patients who may have silent myocardial ischemia.

5. The extent of myocardial injury can be measured by serum CK isoenzyme (CK-MB) and troponin levels.

6. The extent of skeletal muscle injury (e.g., rhabdomyolysis) can be measured by serum CK, serum myoglobin, and urine myoglobin.

7. For patients short of breath, with abnormal ausculatory findings, or with multiple trauma, the chest radiograph is indicated.

8. Urine toxicologic screens can be useful when concurrent drug ingestion is suspected.

9. Computed tomography (CT) and magnetic resonance imaging (MRI) of the brain are modestly sensitive but nonspecific in documenting CNS ischemic injury 6 h after CO exposure.16 Diffusion-weighted MRI brain scanning is being investigated for its utility in defining brain injury from CO intoxication.

10. Single-photon-emission computed tomography (SPECT) with radiolabeled hexamethylpropylene amine oxime (HMPAO-technetium 99m) is immediately sensitive but not specific for acute ischemic CNS injury in CO poisoning.17 The brain HMPAO/SPECT scan has the advantage that the radionuclide may be initially injected as the patient arrives in the emergency department without interrupting the resuscitation effort. The patient can be scanned later after stabilization, with a lasting "snapshot" of pre-resuscitation brain metabolism and perfusion. The bulk of HMPAO is taken up by the brain on first pass as it crosses the blood-brain barrier. Accordingly, the HMPAO "locks" into CNS tissue without much redistribution during the successive half-lives of the HMPAO radionuclide. The positron emission tomography (PET) brain scan may be helpful in illustrating CNS ischemic injury, but the scanner is rarely available and hard to have on-line for critically injured patients.

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