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What’s the problem with carbon monoxide? Well, it binds to hemoglobin very very avidly. If it is bound to hemoglobin, oxygen can’t bind to hemoglobin. So you get hemoglobin that’s all bound up and the only oxygen that you have left is that that’s dissolved in the plasma, which is very little oxygen. It also shifts the oxygen-hemoglobin curve to the left, and it, in and of itself, is a direct poison to the cytochrome oxidase system, so even if you did have oxygen around, your body couldn’t utilize it and you would be stuck with anaerobic metabolism.

So how do you diagnose this? Well, a history of exposure is helpful. If somebody is in a fire, it’s pretty straightforward and is something you would screen for. The problem is, oftentimes there is uncertain exposure. It’s in the home environment and there has been a dysfunction of a combustion device in the home. It may be in the middle of winter. Someone who doesn’t have a heating system and they are burning charcoal in a relatively enclosed space, which will release carbon monoxide and poison everyone.
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The symptomatology is dyspnea, headache from the lack of oxygen. They will start getting irritable as they get progressively hypoxemic, nausea, vomiting, dizziness, very confused, oftentimes very combative, leading to lack of consciousness, coma, and death. How do you diagnose this? A couple of things to be aware of. Your blood gas measures partial pressure of oxygen, so it measures your PO2. It doesn’t directly measure oxygen saturation. Your PO2 in your blood stream will be fine. The problem is that your hemoglobin has no oxygen bound to it. So your blood gas, as far as your PO2, will look fine, the calculated saturation that shows up on your blood gas will also be fine. How about pulse oximetry? Well, unfortunately carboxyhemoglobin absorbs light energy very similar to hemoglobin. So a pulse oximetry will mislead you into thinking your hemoglobin is fully saturated with oxygen. It’s fully saturated. The problem is that it’s with carbon monoxide. So neither a blood gas or pulse oximetry are helpful and they may be very falsely misleading. What you need to do is send arterial blood for what’s called “co-oximetry” where they will measure saturation, oxygen/hemoglobin saturations directly in the laboratory.
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Therapy; obviously you want to remove them from the environment in which they have been poisoned. You want to give them 100% oxygen. The half-life of carboxyhemoglobin is dependent on the PO2 in the blood stream. You are at room air, the half-life of carboxyhemoglobin is hours, like five to six hours. If you get somebody on 100% oxygen, you take it down to 90 minutes, and if you have a hyperbaric chamber that’s just sitting there waiting for a patient, you apply 2 ½ times atmospheric pressure and 100% oxygen; you get the half-life of carboxyhemoglobin down to 30 minutes. The other care is really supportive. Support the organ dysfunction, the neurologic sequelae, the pulmonary dysfunction that you may see secondary to the carbon monoxide poisoning.
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Heat stroke is a medical emergency. These patients need very aggressive cooling. This may involve packing them in ice externally. It may involve administering cool fluids to every orifice and IV site to bring down their body temperature rapidly. They need to be fluid resuscitated, they are essentially all dehydrated and vasodilated, and they need ongoing supportive care.
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Now there is a specific syndrome in young children that has been reported, of hemorrhagic shock and encephalopathy syndrome. Which is basically unexplained severe hyperthermia in young children without an infectious etiology defined, which is associated with a very significant encephalopathy. These patients develop shock, DIC and actually have a high mortality rate. In the initial series, 100% mortality rate was reported. Now survivors have been reported, but it still does have a high mortality rate. It is uncommon but has been the source of questions in the past.
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Smoke inhalation; another environmental disaster. If you happen to be in a fire you get asphyxiated. Fire consumes oxygen, it leaves what you are breathing to be relatively oxygen-free, and although you are having air exchange you are not getting oxygen to your tissues. You may have a thermal injury, although this is a much less common cause of death, where you actually have flame injury to the tissues. A thermal injury with super-heated environments, gases especially if there is steam involved, you may get airway injury from the high temperatures. This is typically supraglottic. By the time it gets down to your lungs the gases have usually cooled enough that you don’t have burning all the way down your lungs. You may begin to develop airway edema. If you have a child who has stridor following a burn injury, they have soot in their oropharynx, you want to establish an airway quickly before it swells shut. So burns to the lip or nose, soot in the mouth, singed nasal hair, stridor, hoarseness or respiratory distress, are all indications for intubation. Don’t wait and hope that they are going to get better. They are going to get worse before they get better and they need an airway.
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Carbon monoxide; combustion releases carbon monoxide. When it’s in a fire it will be associated with soot and other things. You can get carbon monoxide poisoning in other environments. Exhaust systems of furnaces may dysfunction and everyone in the home may in fact have carbon monoxide poisoning. It’s a colorless, odorless gas so they won’t know it until they are losing consciousness or having changes. We are going to talk a little about the pathophysiology, the diagnosis and the therapy. Again, it’s colorless, odorless, non-irritating gas. Sounds like a pretty good way to kill somebody, to me.

Prognosis; well, not surprisingly, the longer you have been under water and the longer you have been dead, the more likely you are to stay dead. So if you have been underwater for a long time you don’t do so well. If it’s taken resuscitation a long time to get your heart going, you don’t do so well. If you are still apneic by the time you get to the emergency department, you don’t do so well. If you are still pulseless, despite ACLS coming into the emergency department, you don’t do so well. People who are going to do well from near drowning typically have relatively rapid neurologic improvement. Even though they got CPR at the scene, you see them six or eight hours later and they are reaching for their endotracheal tubes and trying to pull it out. In the absence of neurologic improvement over the first day, their outcome is relatively dismal. The degree of metabolic acidosis, in some studies, has been shown to be a helpful predictor in outcome.
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Okay, moving on to environmental exposures. We see environmental exposures very rarely in the ICU. The Board questions almost always have one of these topics reflected; heat stroke, smoke inhalation, or carbon monoxide poisoning.
Heat stroke; heat stroke basically refers to a very high temperature, oftentimes as high as 106 or 107 degrees, where bad things begin to happen to the enzymes in your body. How does this happen? Well, you can have increased heat generation either from pyrogens generating a fever, exercise if you go out to run a marathon across Death Valley, not surprisingly your body temperature rises. Or if you have hypothalamic disregulation problems. Some children with severe neurologic injuries don’t have good hypothalamic regulation and they don’t regulate their temperature well. So they have increased generation of heat. Usually both problems of heat generation and heat dissipation are involved with the development of heat stroke. You can impair heat dissipation with bundling. Bundling decreases both convection and conductive losses of body temperature. If you are in a very hot environment, you have decreased radiation losses to the environment if it is very humid. So if it’s very hot and humid you have decreased evaporative heat losses to the environment, and if you have a congenital difficulty with sweating, you don’t want to go live in a hot environment and get overheated.
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What’s the pathophysiology of heat stroke? Usually you end up getting dehydrated. When you get dehydrated you have hemodynamic changes. Typically what the body would do with hypovolemia is vasoconstrict. Because your temperature is high, the body is trying to unload some of the heat, and what happens is that the body vasodilates. So you have low intravascular volume and you vasodilate. You can imagine that your hemodynamics don’t stay very good and you get very hypotensive. You may have tissue damage from the hypotension, and also directly. As your body starts hitting 42 degrees or above, 106 or 107, you start having enzymatic dysfunction, direct injury to the cells in your body, and a lot of secondary injury to the body. You’ll have altered mental status, you may develop ARDS from some of the pulmonary injuries, and some of the activation of some of the mediators within your body. Myocardial ischemia as you drop your blood pressure, you are tachycardic because you are very hot and your myocardial oxygen supply is very poor so you get myocardial ischemia. You get tissue breakdown of your muscles, with rhabdomyolysis, which gives you secondary renal failure. You develop DIC, hypoglycemia, hypocalcemia, and you end up dead.

Pulmonary; you have acute hypoxemia. You may develop a severe ARDS. The ARDS will actually end up being the cause of death in some patients with immersion events. The most common cause of death is the neurologic event.
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Cardiac; initially you get the sequelae of the anoxia and ischemia with asystole being by far the most common rhythm. You may transiently have some ventricular fibrillation or tachycardia and you are going to have poor cardiac function. Once you get someone resuscitated, if you are able to get their heart back beating again, the primary cardiac dysfunction is unlikely to be the cause of their demise.

Liver and kidney problems, although they may be transient, are rarely a major long term problem.
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Hypothermia; there is a difference between dying and getting cold and getting cold and dying. If they fish somebody out of a swimming pool who has been there overnight and they bring them into the emergency room, they are not surprisingly going to be cold. It doesn’t mean that they’ve had a cold water drowning and that they are going to be fine. When people talk about cold water drownings they refer to cold, cold water. Like falling through the ice. Southern California really doesn’t have anything approaching cold water drownings. You have to go up in the mountains and fall through some ice somewhere. So if your patient comes in cold from a swimming pool, it’s not a cold water drowning. It’s somebody who has been dead or dying for awhile.
Near drowning therapy is kind of boring to talk about. There is nothing magic about resuscitation a near drowning victim. Advanced cardiac life support; treat their dysrhythmias, treat their asystole. If they are cold you should warm them up. If they are 25 degrees because they have been dead over night, you are not going to be able to warm them up because they’ve been dead. So the old adage that you are not dead until you are warm and dead I think is a big misnomer. If they fall in through the ice and they have primary hypothermia it’s worth trying to warm them up with invasive warming techniques, maybe even cardiopulmonary bypass.
Supportive care. They should be observed, with a significant immersion event, at least eight hours. ICP monitoring has not been shown to alter outcome in anoxic ischemic events, such as near drowning, and is not advocated and not carried out at most institutions.

Some of your radiologic studies may show something like this. This picture was actually very nice because it came with all these arrows on it. Although this one is not subtle, that’s a big epidural hematoma, a kind of lens-shaped. Not at all subtle. This also is not very subtle. You can see something that you may see on examination, which is a big overlying cephalhematoma, and then and intraparenchymal contusion and bleed.
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Okay, moving on in our dash through critical care. Near drowning; depending on what state you live in, it may in fact be the leading cause of death of young children. Certainly in California, Arizona, many of the southern states, near drowning, or drowning is the cause of death. If you’ve drowned you can’t near-drown, I guess. We are going to talk a little bit about the epidemiology, the pathophysiology, some of the clinical findings, your management and what is the prognosis of children who have immersion events.
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Near drowning again demonstrates that toddlers and adolescents share many things in common. Near drowning has two bi-modal peaks during those age ranges. Even in the young children, the 2-5-year-old there is a very impressive male to female predominance. Four times as many boys as little girls end up drowning. In the adolescents it’s very often high risk behavior that results in drownings. Alcohol is oftentimes involved, or other drugs. Oftentimes diving off of high cliffs or other places where there are associated traumatic injuries as well.
What’s the pathophysiology of near drowning? It’s really an anoxic ischemic injury that is preceded typically with anoxia being the primary event, as the patient is unable to ventilate. It’s hard to breathe when you are under water. If you are getting no oxygen, your heart and brain don’t do so well. You may have ischemic injury to all of the organs in the body, although most will recover and not be the cause of ongoing morbidity or mortality. Aspiration of water, 80-90% of patients have some aspiration of water, although it is typically relatively low volumes. All of the studies … many of the animal studies looking at things like near drowning do things like infuse 40 ml/kg in a dog’s tracheas. Drownings typically involve much much smaller volumes of water. And the differences that are pointed out in laboratory environments of fresh water versus salt water drownings, clinically you don’t see much difference. What you do see are some of the effects of anoxic ischemic injury to the brain. You have altered mental status, you oftentimes develop increased intracranial pressure a day or two following your anoxic ischemic event.

The Glasgow coma scale is used frequently to assess trauma victims in the field, through the EMS system, through the emergency department, oftentimes to the anesthetic suite if the patient is at all awake, and into the ICU. It is nice because it is relatively simple, it’s relatively consistent between observers and it provides a numerical scale that can be followed between multiple different people who are assuming and maybe passing on care to another team. If consists of three different systems; eye-opening, you get a total of four points, verbal you can get five points, and motor you can get six points, for a total of 15 points. In your handout they have the complete Glasgow coma score. Of some note is that if someone calls you to admit a patient to you or transport a patient, and they tell you that the Glasgow coma score is zero, they’ve told you two things. One is that the child is probably pretty sick, and two that they don’t know what the Glasgow coma scale is all about, because as you can see, dead people and inanimate objects have three points. The table in front of you gets a Glasgow coma score of three, so if someone gives one of your patients a lower score, you know they are in a heap of trouble.
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Okay, you’ve stabilized your patient, you’ve done your primary survey. As you’ve discovered problems, such as a pneumothorax, hemothorax, respiratory arrest, you’ve dealt with it, you’ve moved on. Now you are going to go back for a secondary survey and look for a little bit more subtle findings, generally in a head-to-toe approach. You are going to look at the head, palpate it, look for hematomas, other signs that may lead you to suspect emerging intracranial pathology. Cranial nerves. Repeat your primary survey, that is, make sure they are moving both sides of their body. Neck; you are going to look for tenderness. Consider the cervical spine unstable until it has been evaluated. Chest; look for subcutaneous emphysema as perhaps a more subtle sign of pneumothoraces underlying it. Abdomen; tenderness, presence of bowel sounds, distention. Perineum and rectum; looking for perhaps a spinal cord injury where you have lost all erectile tone. And certainly you are going to be looking at your musculoskeletal injuries that, until now, someone has been putting pressure on with the bone sticking out of the leg, and now you are going to be able to really take a better look at it.
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Trauma radiology; the C-spine and the spine itself are very controversial as to the best ways of evaluating them, and how extensive it needs to be. Some institutions relying only on an AP and a lateral x-ray of the cervical spine. Most centers require, especially in the unresponsive patient, further investigation which may be a CT of the spine, may go as far as a flexion/extension MRI in a patient who is not cooperative with examination. A head CT; indications, I think as head CT’s have become more prevalent with more rapid turnaround times, and there have been evidence of significant intracranial injuries with apparently more trivial injuries, the indications for head CT’s have diminished. That is, anybody who has any alteration in their Glasgow coma score, that is 14 out of 15, should be scanned. Anybody with a loss of consciousness of five minutes or greater should be scanned. And if the patient is going to be in an environment where they are going to lose your ability to examine them - like they are going in for an acute abdomen, traumatic, and they are going to disappear into anesthesia for awhile - you’d like to make sure there is not an evolving epidural hematoma that is going to be unrecognized under anesthesia. So if for some reason you are going to lose the ability to examine them, CT their head. Chest; at least an AP. Abdominal CTF is evidence of abdominal trauma and they are stable. If they are unstable with an enlarging abdomen and clinical intraabdominal catastrophe, they are in all likelihood going to go to the operating room straight-away rather than having an abdominal CT scan. If they are stabilized, you may want to give them an abdominal CT scan. The findings of pathology on the CT scan do not indicate the need for surgery. You can have significant splenic and hepatic lacerations, but if the patient stabilizes they will generally be managed non-operatively. Musculoskeletal; that bone sticking out of that leg, now you can get some pictures of it and see exactly what’s going on.