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ABCs of poisoning care

Kent R. Olson, MD

The first priority in the poisoned patient is to assure a patent airway and adequate breathing. Respiratory arrest and pulmonary aspiration are two common complications of depressed mental status that can lead to serious morbidity or death.


The airway may be obstructed by a floppy tongue or by secretions or vomitus. Position the patient to enhance patency by slightly tilting the head backward (extension of the neck) while lifting the head forward relative to the chest (the “sniffing position”). Or, lift the chin forward by placing your fingers behind the angle of the jaw on each side --- this lifts the tongue forward, relieving obstruction, and it often provides an uncomfortable stimulus that may awaken the mildly intoxicated patient.

Fig 1 & 2 - Airway obstruction in supine positing, and Head tilt.
[[image:space/showimage/Head_tilt1.jpg]] [[image:space/showimage/Head_tilt2.jpg width="211" height="225"]]

Fig 3 - Jaw thrust
  • In patients with mild airway depression who are not going to be intubated, it is prudent to place them in the left lateral decubitus position to allow the tongue to fall sideways and to make it less likely that the person will aspirate gastric secretions if they vomit. In the patient with deep coma, an artificial airway can be placed in the nasopharynx or oropharynx to make bag-valve mask ventilation easier while preparing for endotracheal intubation.
  • Since pulmonary aspiration of gastric contents is a serious complication of coma or seizures, it is important to asses the ability of the patient to protect the airway. Normally, the cough reflex is activated when foreign substances enter the upper trachea. However, with CNS depression these protective reflexes are often dulled and pulmonary aspiration may occur. Various methods have been employed to asses the competency of the airway reflexes, such as determining the gag response, but they are only indirect estimates of the actual airway responsiveness. And, making the patient gag might result in vomiting which increases the risk of aspiration. Other indirect methods of assessing the airway reflex include the eyelash (“blink”) response, nasopharyngeal irritant response (e.g., ammonia capsule or stimulating the nasal passage with a q-tip), or the corneal reflex. None is foolproof but they help to determine if the patient is unable to protect their airway.

Endotracheal intubation: If it is obvious that the airway reflexes are impaired (deep coma, no gag or cough reflex) then the patient will need to be intubated endotracheally. This is usually performed via the orotracheal route, although if the patient is breathing spontaneously the nasotracheal route can be used. Rapid sequence intubation (RSI) is a standardized procedure that includes pre-oxygenation, administration of sedative-hypnotic drugs (e.g., midazolam, etomidate) and muscle relaxants (e.g., succinylcholine, rocuronium) in conjunction with orotracheal intubation. After intubation, a rapid assessment is needed to assure that the endotracheal tube is in the trachea and not the esophagus. This is done by listening over the lungs and stomach, watching for chest rise with ventilation, and use of a carbon dioxide detector on the end of the ET tube. Looking for condensation in the ET tube is also helpful.


If the patient is breathing spontaneously and appears to have satisfactory airway protective reflexes, determine the adequacy of minute ventilation. This can be done by direct observation of the rise and fall of the chest, the measured rate of breathing, and noting a pink color to the mucous membranes indicating oxygenation. Arterial blood gases are definitive but not always readily available and frequently not needed. Pulse oximetry gives an estimate of oxygenation which can be reassuring in the patient who also appears to be ventilating adequately by visual inspection.
  • Pitfalls in assessment include failure to adequately estimate the rate and depth of breathing, and over-reliance on the pulse oximeter. The pulse oximetry device does not measure ventilation, and therefore cannot predict a rising pCO2. In addition, the device is unable to distinguish oxygenated hemoglobin from blood that is poisoned by carbon monoxide, because the carboxyhemoglobin complex has a pink color that is read falsely as oxyhemoglobin by the device.
  • Even a simple arterial blood gas measurement of the pO2 is insufficient to diagnose CO poisoning because the pO2 measures only that oxygen which is dissolved in plasma, not that which is attached to hemoglobin; in a patient with severe CO poisoning and a carboxyhemoglobin of 55%, for example, the pO2 will be normal. A special blood gas machine (a “co-oximeter”) is needed to measure the carboxyhemoglobin level.
  • A similar problem occurs in patients with methemoglobinemia. In this case the hemoglobin is oxidized and unable to carry oxygen, yet the pO2 will be normal because, as in patients with CO poisoning, the absorption of oxygen across the alveoli is not impaired. With methemoglobinemia the pulse oximeter will give an abnormal reading, but it is not proportional to the percentage of hemoglobin that is oxidized; for example, a patient with 25% or 55% methemoglobinemia will read about 88-90% on the pulse oximeter.

Most patients with acute poisoning causing CNS depression can be satisfactorily managed with good supportive care, including airway positioning and assisted ventilation. Some patients will also have depression of their cardiovascular tone, and may need IV fluids or vasopressors.


Start at least one intravenous line, and draw some blood for routine testing (e.g., complete blood count, electrolytes, BUN and creatinine, glucose, liver enzymes, and acetaminophen level). Place the patient on a cardiac monitor, if available, and determinethe rate and rhythm of cardiac activity. Measure the blood pressure.