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The first thing any of us think about when smoke inhalation is suspected is CO (carbon monoxide) poisoning. Likewise we are all trained to recognize and treat CO poisoning. All of our ambulances, and those apparatuses with BLS or ALS medical gear, have a pulse oximeter that can also measure CO saturation. This gives us a fairly reliable, quick and non-invasive way of making a definitive diagnose in the field.
But CO is not the only killer when it comes to smoke inhalation. In a French study, as many as 64% of patients treated for smoke inhalation also had life threatening levels of cyanide (CN) in their blood. We rarely think of CN poisoning, unless there is a hazmat sign outside the building. And these buildings are invariably industrial. But even in a normal house fire fatal levels of CN can occur. Wool, silk, cotton and paper give off CN when they burn. So do plastic and other polymers.
The problem is cyanide is a cellular poison. That's kind of the cruel irony here. If I recognize or if I think about someone being a potential cyanide poisoning victim, I can give them all the oxygen available, I can put them on continuous positive airway pressure (CPAP), I can put them on a nonrebreather mask, I can go ahead and intubate them, with 100% FIO2, but it's not going to work because the cells are still poisoned by the cyanide, and it's not going to help us. That's the cruel irony. I can oxygenate their blood, but the cells are still going to starve from lack of oxygen and ultimately die. So, what happens of course, the cells, because cyanide poisoning is a cytochrome oxidase in the mitochondria, can't utilize the oxygen no matter how much oxygen we're giving the patient. The cells shift over to an anaerobic metabolism, and you have a huge build up of lactic acidosis, and eventually the cells start to die. Not surprisingly, which organ systems are most sensitive to hypoxemia? The brain and the heart, so the signs and symptoms relate to hypoxemia of the brain.
Further complicating matters is the fact that CO and CN poisoning are indistinguishable. And in the field, or in smaller hospitals, we don’t have the opportunity to do ABG or VBG measurements.
So what treatments do we have?
The standard 3-part cyanide treatment kit is pretty useless in this case, because the side effects are hypotension and hypoxia. So you might end up with a patient who would have survived his condition, but was killed by the therapy. What we need is something that can be administered empirically in a pre-hospital setting.
Next on our list is the “Cyanokit”. This contains hydroxocobalamin. This is basically a B12 vitamin precursor that creates B12 when it binds with cyanide. I won’t go further into detail about its mechanism of action.
This is a very safe drug that has been used in pre-hospital treatment of smoke inhalation in France for 10 years. The only side effect is a very brief period of hypertension. This lets us administer it on suspicion of CN poisoning. It’s like giving Narcan for an unknown drug overdose: If it doesn’t help the patient, it doesn’t harm him either.
The Cyanokit is given just through a peripheral IV. It comes as a lyophilized freeze dried form. It looks orange to red because of the cobalt, which is the same thing that gives our hemoglobin in our blood a red color. Basically 250 cc of saline or Ringers Lactate is put into the box. It's shaken a little bit and just given as an IV infusion through any peripheral line. The recommended empiric dose for severe smoke inhalation is 5 g over 15 minutes. Once at the hospital, or in the field if it's a long transport time, an additional 5 g can be given as well. French studies have shown patients having gotten 15 g with no adverse effects.
So here is the suggestion for new standing orders/protocol for smoke inhalation:
Basically a patient who is suspected to have smoke inhalation, with soot around the nose and mouth, plus altered mental status, and/or any hemodynamic or respiratory compromise. That's your indication criteria. You would obviously remove the patient from the IDLH, or Immediate Danger to Life and Health. They're brought out away from the IDLH. Of course the prehospital providers are using the necessary protective personal equipment, or PPE. The initial ABCs are done. The patient is placed on 100% oxygen, but again 100% oxygen is not going to work because the cells are poisoned by the cyanide, and you go ahead and administer the 5-g dose of Cyanokit in the field. If the patient is still symptomatic or not markedly improved, and you're not at the hospital yet, you go ahead and give a second dose of 5 g in the field. The first 5 g is given through a regular peripheral IV over a 15-minute period of time.
If the patient is pregnant, contact medical control before administering.
Thoughts?
But CO is not the only killer when it comes to smoke inhalation. In a French study, as many as 64% of patients treated for smoke inhalation also had life threatening levels of cyanide (CN) in their blood. We rarely think of CN poisoning, unless there is a hazmat sign outside the building. And these buildings are invariably industrial. But even in a normal house fire fatal levels of CN can occur. Wool, silk, cotton and paper give off CN when they burn. So do plastic and other polymers.
The problem is cyanide is a cellular poison. That's kind of the cruel irony here. If I recognize or if I think about someone being a potential cyanide poisoning victim, I can give them all the oxygen available, I can put them on continuous positive airway pressure (CPAP), I can put them on a nonrebreather mask, I can go ahead and intubate them, with 100% FIO2, but it's not going to work because the cells are still poisoned by the cyanide, and it's not going to help us. That's the cruel irony. I can oxygenate their blood, but the cells are still going to starve from lack of oxygen and ultimately die. So, what happens of course, the cells, because cyanide poisoning is a cytochrome oxidase in the mitochondria, can't utilize the oxygen no matter how much oxygen we're giving the patient. The cells shift over to an anaerobic metabolism, and you have a huge build up of lactic acidosis, and eventually the cells start to die. Not surprisingly, which organ systems are most sensitive to hypoxemia? The brain and the heart, so the signs and symptoms relate to hypoxemia of the brain.
Further complicating matters is the fact that CO and CN poisoning are indistinguishable. And in the field, or in smaller hospitals, we don’t have the opportunity to do ABG or VBG measurements.
So what treatments do we have?
The standard 3-part cyanide treatment kit is pretty useless in this case, because the side effects are hypotension and hypoxia. So you might end up with a patient who would have survived his condition, but was killed by the therapy. What we need is something that can be administered empirically in a pre-hospital setting.
Next on our list is the “Cyanokit”. This contains hydroxocobalamin. This is basically a B12 vitamin precursor that creates B12 when it binds with cyanide. I won’t go further into detail about its mechanism of action.
This is a very safe drug that has been used in pre-hospital treatment of smoke inhalation in France for 10 years. The only side effect is a very brief period of hypertension. This lets us administer it on suspicion of CN poisoning. It’s like giving Narcan for an unknown drug overdose: If it doesn’t help the patient, it doesn’t harm him either.
The Cyanokit is given just through a peripheral IV. It comes as a lyophilized freeze dried form. It looks orange to red because of the cobalt, which is the same thing that gives our hemoglobin in our blood a red color. Basically 250 cc of saline or Ringers Lactate is put into the box. It's shaken a little bit and just given as an IV infusion through any peripheral line. The recommended empiric dose for severe smoke inhalation is 5 g over 15 minutes. Once at the hospital, or in the field if it's a long transport time, an additional 5 g can be given as well. French studies have shown patients having gotten 15 g with no adverse effects.
So here is the suggestion for new standing orders/protocol for smoke inhalation:
Basically a patient who is suspected to have smoke inhalation, with soot around the nose and mouth, plus altered mental status, and/or any hemodynamic or respiratory compromise. That's your indication criteria. You would obviously remove the patient from the IDLH, or Immediate Danger to Life and Health. They're brought out away from the IDLH. Of course the prehospital providers are using the necessary protective personal equipment, or PPE. The initial ABCs are done. The patient is placed on 100% oxygen, but again 100% oxygen is not going to work because the cells are poisoned by the cyanide, and you go ahead and administer the 5-g dose of Cyanokit in the field. If the patient is still symptomatic or not markedly improved, and you're not at the hospital yet, you go ahead and give a second dose of 5 g in the field. The first 5 g is given through a regular peripheral IV over a 15-minute period of time.
If the patient is pregnant, contact medical control before administering.
Thoughts?
I wrote one about twice as long, but figured that was a bit over the top.