Diseases, Disorders information » Shock

Smoke inhalation

Disorders — Mon, 08 Dec 2008 15:14:01 +0000

Smoke inhalation; fires tend to release very noxious substances. If you are burning plastics or some other substances you may have very toxic smoke. Early that is going to cause bronchospasm, some lung consolidation. As you go from a day or two, you are going to start getting pulmonary edema from capillary leak in your lungs, and as you get a little bit further out you are going to tend to get bronchopneumonia.

The therapy for this is entirely supportive. If they need airway management and ventilatory support, that’s what they get. Steroids have been advocated in the past, but in controlled trials they seem to be of no benefit and may increase the risk of infection. So steroids are no longer advocated.

The problem with carbon monoxide

Disorders — Wed, 03 Dec 2008 16:44:33 +0000

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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Prognosis. Shock

Disorders — Mon, 01 Dec 2008 19:29:44 +0000

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.

Acute hypoxemia

Disorders — Fri, 28 Nov 2008 17:02:24 +0000

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.

Radiologic studies

Disorders — Thu, 27 Nov 2008 15:27:33 +0000

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

Disorders — Wed, 26 Nov 2008 14:21:59 +0000

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.

Trauma

Disorders — Tue, 25 Nov 2008 22:46:52 +0000

Trauma; the scenario I’m going to present to you is kind of an abbreviated advanced trauma/life support scenario. What you want to do is pick up injuries that are likely to be life threatening or cause long term morbidity quickly and treat them effectively and resuscitate each problem as you discover it. After the patient has been stabilized, you are going to go back and do a little more thorough exam with a secondary survey, and then begin definitive therapy.
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The primary survey; it’s very easy to get distracted by the fractured femur sticking out of the thigh, the foot that’s twisted on backwards. Other than blood loss, that’s not going to kill them. What’s going to kill them is the fact that while you are looking at their ankle they quit breathing. So be very systematic in your assessment; airway, breathing, maintain cervical spine precautions with the airway. Cervical spine injuries in children with survivable injuries are relatively uncommon. That doesn’t mean you should ignore them. I would not let someone asphyxiate because you are concerned about intubating them. Breathing; listen to the lungs for asymmetry. Think about pneumothorax, hemothorax. Circulation; IV access and fluid resuscitation. Remember you can put interosseus needles in, using bone marrow needles, up to the age of six and maybe even a little bit beyond. It may be very effective in initial fluid resuscitation. If somebody has a crushing chest injury, be suspicious of pericardial effusions and the need for pericardial centesis. In keeping with the ABC’s, we end up with D which stands for disability, which really reflects the neurologic status. Advanced trauma life support talks about the AVPU system of assessing the level of consciousness. A, being alert, V means that they respond to verbal commands, P to painful, and U means they are unresponsive.
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Pupillary response and lateralizing weakness; you are looking for very gross neurologic changes. You are not writing letters in the palm of their hand and asking them what they are. This is a very quick neurologic survey to make sure that they don’t have any potentially life threatening or long term morbidity-threatening problems.

The therapy for your shock state

Disorders — Tue, 25 Nov 2008 15:36:00 +0000

So overall, what is going to be the therapy for your shock state? You are going to treat the underlying cause. If you are suspicious that somebody has septic shock, some antibiotics might be a good thing to do. You are going to stabilize their airway and breathing, that is, if they have quit breathing you are going to breathe for them, and you are going to administer fluids. And this is where you are going to want to pay attention to the underlying etiology of the shock. For all of the forms that we talked about, other than cardiogenic shock, fluids are going to be your mainstay of therapy and may require very large volumes of fluid. Usually given in 20 ml/kg aliquots and they may end up getting 100 ml/kg over a couple of hours. Now if you are concerned that someone is in cardiogenic shock, that is not going to help them out. You are going to make their cardiogenic shock worse. So I think that certainly if they don’t respond to an initial fluid resuscitation you are going to want to reassess all of the suggestive findings of cardiogenic shock; liver size, pulmonary findings, jugular venous distention.
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If the fluid is not being effective, regardless of the form of shock, or if you are dealing with cardiogenic shock you are going to want to move on to inotropic agents and vasoactive agents. Some of them that are utilized include epinephrine, which affects all of your receptors – alpha, beta receptors – and maybe your first drug of choice in septic shock because of it’s nice effects on the vasculature. Norepinephrine is a potent vasoconstrictor and something you may lean towards with a severe distributive shock. Dopamine has multiple effects which may be beneficial. If you are dealing with a specific cardiogenic shock, you are looking for something with good inotropic support – that is, increase the contractility of the heart. Dobutamine and milrinone are likely to be the drugs that you are going to utilize. Oftentimes combination drugs are used, either similar classes or different classes. It would not be unusual to combine milrinone and dobutamine, or milrinone and another inotropic agent, or the combination of vasoactive agents, vasoconstrictors such as epinephrine and norepinephrine plus a little dopamine to hopefully help renal perfusion.
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Remember one member of distributive shock, that is spinal cord injury, should get high doses of steroids given early as it has been shown to improve long term spinal cord function.
Trauma is the leading cause of death in children more than one year of age. Under a year of age it’s kind of a whole hodgepodge of congenital difficulties. Once you get to a year of age, if you’ve made it that far, you are most likely to die of trauma than anything else. The key to trauma is to prevent it. Anticipatory guidance, seat-belts, don’t have open windows on third stories where children are likely to plummet to their death.

Cardiogenic shock

Disorders — Mon, 24 Nov 2008 17:21:41 +0000

Cardiogenic shock; typically, although not always, there is a suggestive medical history. When you look at the patient you may in fact see a big scar running down the middle of their sternum. Always a warning sign that something has happened to their heart. So get a medical history. Tachycardia will essentially always be present unless the cause of their shock is that they are having a bradydysrhythmia. You can obviously be in shock because you have a heart rate of 30 and you are not tachycardic. You will have poor perfusion, again, the compensatory mechanism of vasoconstriction. Some clinical clues that in fact you are dealing with cardiogenic shock, rather than hypovolemic shock, will be pulmonary exam; you may hear rales throughout the lung fields, you may hear the heart shifted over and enlarged. You may have a gallop rhythm. Your heart may be large by chest x-ray. The liver might be quite large, and although we don’t typically look for jugular venous distention on children, you can certainly observe it. So look for it, you may find it. These are all things that would suggest a cardiac function problem rather than hypovolemia or other etiologies of shock.
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Septic shock; again, history may be very helpful. Certainly if somebody is very febrile it’s one of the things you will entertain. The findings will be similar in that you will be tachycardic. The thing that will be different oftentimes about septic shock, especially early on, is that you will have systemic vasodilation which will make your skin look very well perfused. So if someone shows up hypotensive, with instantaneous capillary refill, don’t be reassured by the capillary refill. It’s because they are inappropriately vasodilated and they are undoubtedly septic. Again, your heart and liver will be small early on. On laboratory examination you may see either a high white count or a low white count. Septic shock is really a combination of distributive shock where you have misdistribution of your fluids, cardiogenic shock where your heart doesn’t work so well, and hypovolemia where you likely have had volume loss.

A pure distributive shock will be a shock state where your blood flow is not appropriate for your body. You may have a history – if someone has a knife wound to their spinal cord, you might suspect that they’ve lost all their sympathetic enervation to the lower half of their body. They vasodilated and they are not distributing their blood flow appropriately. Anaphylactic shock where you have vasodilation is a form of distributive shock. Again, tachycardia. Very sensitive finding. You will be hypotensive and much like septic shock, you will be warm and well perfused, at least until your blood pressure begins to fall significantly.

Shock

Disorders — Mon, 24 Nov 2008 15:47:40 +0000

Shock can be seen at three different phases. Compensated shock; which just maintains that the patient, through compensatory mechanisms, is able to maintain a blood pressure. It doesn’t mean that they are able to maintain perfusion to the tissues. It just means that they are not yet hypotensive. A de-compensated shock means that they are no longer able to maintain a blood pressure and at some phase your patient is going to enter irreversible shock, which – no matter what you do at that point – your patient is destined to die. Obviously you would like to see patients in the early phases of shock and not in the later phases. There is an easy way to remember normal blood pressures, which is in your handout. Systolic pressure should be greater than 60 mmHg up to a month, 70 from a month to a year, and 70+ the quantity two times the age, if you are above a year of age. Obviously if you are 60-year-old your normal blood pressure should not be 190. These are minimal blood pressures, these are not normal blood pressures. They are good estimates of 5th percentile. So if you are below these you are hypotensive.

What are the shock patterns that you can see in patients? We are going to talk about these a little bit, each individually; hypovolemic shock, cardiogenic shock, septic shock and distributive shock. Hypovolemic shock; you would like to have some sort of a history suggesting that your patient is hypovolemic. Lack of intake, vomiting, diarrhea, something that would decrease their volume status. Tachycardia is very sensitive for hypovolemia. That is, if you are hypovolemic you will undoubtedly be tachycardic. Some children will get tachycardic just seeing your approach. So it’s not a very specific indicator, but it is sensitive. Poor perfusion, the body’s compensation to hypovolemia, is to vasoconstrict peripheral tissue beds so you will see cold, cool extremities with delayed capillary refill. And since your intravascular volume is small, your heart size will be small and your liver will be small, which may be discernible on physical examination.