Consider five patients...
Patient One: You respond to a house to visit a 23-year-old male with a history of paranoid schizophrenia. His mother called 911 because he is agitated, similar to previous episodes of medication noncompliance. After introducing yourself to the patient, you find that “agitated” is a good adjective for him. He is pacing, restless, and emotionally distressed, with rapid speech. He denies drug or alcohol use but is anxious about the presence of police. You get him to calm down a little and agree to a more complete exam. His head-to-toe exam is atraumatic, but he is sweating and twitchy. His pupils are equal and reactive from 8 to 7 millimeters. He has a blood pressure of 190/100, a heart rate of 120, and a respiratory rate of 22. When you question him why his blood pressure and heart rate are so high, he insists it is due to anxiety over the police. He and police officers have “some history.” What do you think is going on? Is he just nervous about the police, mixed with a dusting of undermedicated paranoia and psychosis? Or is there something else?
Patient Two: You respond to a sixteen-year-old girl who took an unknown amount of an unknown medication with suicidal intent. The patient is awake but doesn’t respond to questions. It looks like she may be hallucinating, because she holds eye focus on nothing at all. She is writhing around with occasional myoclonic jerks. Her secondary exam is atraumatic, her pupils are dilated at 8 mm, and her skin is flushed, hot (feverish feeling, subjectively), and dry. Speaking of dry, her mucus membranes are dry to the point of visible cotton mouth. Her blood pressure is 100/70, her heart rate is 120 beats per minute, and she has a slow respiratory rate at about six or eight per minute with a room air saturation of 92%. Any idea of what she took? Is there an antidote you can give her?
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By Sam Metsfan (Apartment in New York) [Public domain], via Wikimedia Commons
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Patient Three: You respond to a large home in the suburbs for an unconscious party. The patient is a 43-year-old female, in bed, gently snoring. She is dressed for bed in a nightgown and her family says she never woke up this morning to make them breakfast. When they went to check on her, she wouldn’t wake up even when they shook her. The patient has a history of low-grade depression and hypertension for which she takes an antidepressant and hydrochloro-something. The patient’s head-to-toe exam is atraumatic and there is nothing out of the ordinary in the room. There is no response to voice or painful stimuli. Her blood pressure is 100/70 with a heart rate of 60 and weak snoring respirations at 4 per minute. She has a room air saturation of 82% and there is some subtle purple cyanosis in her fingernails. Her pupils are small (2mm) and her blood glucose is 88 mg/dL. A firefighter has a BVM in his hand and raises his eyebrows as if to ask if he should get to work with it. Should he start bagging her? What do you think is going on? Why is she unresponsive?
Patient Four: This call is a nightmare. You respond to the report of chest pain in a 65-year-old male. His wife states he was cleaning out the shed in the back. He walked out of the shed holding his chest with both hands, sweating profusely, puked, and fell to the ground. He may have had a seizure but his wife is too upset to be a good witness. You find the patient supine, snoring, and profoundly diaphoretic. The firefighters on scene are suctioning some vomit and foamy secretions out of his airway. Judging by the overwhelming smell, he lost control of his bowels. There are some minor muscle fasiculations in his facial muscles. The twitching may be seizure activity so you check his eyes. His pupils are approximately 4mm and slowly reactive, but there is no nystagmus and his limbs are flaccid so it doesn’t seem as though this is likely to be an active seizure. His blood pressure is 110/90, heart rate is 100 beats per minute, his respiratory rate is 28 gurgling breaths per minute, and his room air saturation is 88%. An ECG is attempted but unreadable because the electrodes won’t stick to his sweaty skin. What is happening here? What are you worried about on this scene?
Patient Five: You respond to a 35-year-old female pulled over for suspicion of driving while intoxicated. The police officer wants you to “clear the patient for jail” because she tells him she has medical conditions. She is obviously intoxicated, swaying in place with slurred speech. The patient doesn’t have any specific current complaints and gets too distracted to directly answer any questions about her medical conditions. She denies alcohol consumption and just wants to go home. Her secondary exam is atraumatic with midpoint pupils, no nystagmus, and no smell of alcohol. Her blood pressure is 100/70 with a heart rate of 62 and a respiratory rate of 12 per minute. Her blood glucose is 172 mg/dL. Her speech is slurred and her gait is slow and ataxic. She will fall asleep if you don’t interact with her, but points out that it is after midnight and she is tired. Is she drunk? Is she good to go to jail, or do you have a medical concern?
Each of those scenarios describes a patient who was poisoned by a specific toxin. Many substances cause consistent effects that can be grouped together and described as a toxidrome (toxic + syndrome = toxidrome). For example, the alcohol toxidrome would present with all the symptoms that come from alcohol consumption: the smell of alcohol on the patient’s breath, slurred speech, ataxia, nystagmus, nausea/vomiting, depressed or agitated behavior progressing to unconsciousness and even coma, and so on. There are probably dozens of toxidromes but five or six are well-known presentations that a good prehospital clinician should recognize.
Patient One is a sympathomimetic patient. Sympathomimetic agents mimic the sympathetic nervous system. The sympathetic nervous system is the fight or flight side of the autonomic system, so everything gets ramped up. Some examples of sympathomimetic agents include cocaine, methamphetamine, ephedrine, theophylline, and even caffeine. Patients are hyperalert, agitated, and paranoid. Sympathomimetic overdoses dilate pupils (mydriasis) and cause hyperthermia, tachycardia, hypertension, and tachypnea. Patients are often diaphoretic, tremulous, hyperreflexive, and can even have seizures. Treatments for sympathomimetic overdoses are to counteract the accelerated body responses with medications that slow everything down. Sedative-hypnotics like benzodiazepines are a great choice. Don't be silly and treat the hypertension and tachycardia directly with nitrates or antiarrhythmics. Treat the overdose, and that means benzos.
So why would someone believe that anxiety, agitation, and paranoia aren’t explained by schizophrenia? The patient is upset, so that could explain the hypertension and tachycardia, as well. The big sign for me are the patient’s pupils. Psychiatric issues don’t often cause mydriasis. Diaphoresis would be unusual, as well. Sweating outside of the gym is always a big deal. This patient eventually admitted to methamphetamine use.
Patient Two has symptoms that match up to a well-known mnemonic: “mad as a hatter, hot as hell, red as a beet, dry as a bone, full as a tick, and blind as a bat.” (I actually have a terrible time remembering this list. I think of this toxidrome as being like a dude in the desert.) Anticholinergic agents block the parasympathetic nervous system by blocking the action of acetylcholine. Think of the sympathetic-parasympathetic nervous systems like a teeter-totter. You can’t push both sides up at the same time. But you can get one side to elevate by pushing upwards, or you can have that side go up by pushing down on the opposite side. Anticholinergics lower the parasympathetic end of the teeter-totter, lessening the rest-and-digest actions and increasing the fight-or-flight side.
People experiencing anticholinergic overdose often have altered mentation that can present as agitation, hallucinations, delirium (mad as a hatter), and even coma. Mydriasis is common again (blind as a bat). Vital signs show hyperthermia (hot as hell), tachycardia and hypertension. Skin and mucus membranes are dry (dry as a bone) and the skin is often flushed (red as a beet) due to hyperthermia and the inability to sweat. Urinary retention and constipation (full as a tick) comes along with the package but are more difficult to recognize in the prehospital setting. Common examples of anticholinergic agents include antihistamines such as Benadryl, tricyclic antidepressants, and anti-Parkinson agents. Atropine is an anticholinergic that we carry on ambulances. Belladonna alkaloids such as Jimson weed have anticholinergic effects. Treatment revolves around supportive management until the effects wear off. If the patient is agitated, benzodiazepines are again a good choice to manage that. This patient took more than 1,000 milligrams of diphenhydramine.
Patient Three is a common toxidrome, maybe the most common one that you will see in your career: opioid overdose. Opioids such as Vicodin, Percocet, Fentanyl, heroin, and morphine cause central nervous system depression that can present as an altered level of arousal and can easily progress to unresponsiveness and coma. The hallmark signs are pinpoint, constricted pupils (miosis) and ineffective respirations. The opioid intoxicated patient usually presents with bradypnea but apnea is common, as well. Pulmonary edema can be a consequence of ineffective breathing. Other vital signs can include bradycardia, hypotension, and hypothermia. Other clues of opioid overdose would be nearby equipment (syringes, spoons, and such), as well as needle marks on the body.
The treatment for opioid use is to provide supportive care. Make sure the patient’s airway is clear and support ventilations as needed. Naloxone isn’t the treatment for opioid overdose. Let me say that again: Narcan isn’t the treatment for opioid overdose. Narcan/naloxone is indicated to reverse ineffective breathing due to opioid overdose. There is a difference. As long as the patient is breathing well, I wouldn’t give Narcan even if I pulled a needle out of their unconscious arm. I have in the past, and got in fights for it. It isn’t so much that Narcan is likely to send the patient into unnecessary withdrawal, which is true, but rather that people sometimes take more than one drug. Sometimes the heroin is covering up the cocaine. When I removed the effects of heroin, all I was left with was full-on cocaine. And the fight started. So don’t ruin the high that people paid for. Give naloxone for respiratory depression, not opioid use. And remember that good BVM technique can solve ineffective respirations, even without Narcan.
Patient Four is a cholinergic overdose. Where anticholinergic overdoses (see above) are dry, everything that can secrete secretes in a cholinergic overdose. DUMBBBELS is a good mnemonic for cholinergic overdose signs and symptoms, if you’re into that kind of memory aid thing. Diarrhea, Urination, Miosis (pupil contraction), Bradycardia, Bronchorrhea (mucus), Bronchoconstriction, Emesis, Lacrimation, and Salivation. Patients can also present with confusion or even unconsciousness, muscular fasiculations, and seizures. The most common cholinergic agents are organophosphate pesticides that are common in a lot of garden chemicals. Carbamate insecticides, some nerve agents, nicotine, and physostigmine are also cholinergics. The good news from a treatment perspective is that cholinergic overdoses are treated with anticholinergic agents, and we have a good one – atropine. The bad news is that we don’t carry enough atropine to do much more than scratch the surface. Patients will need A LOT of atropine before they are better. Just keep giving all you have until the secretions dry up.
One of the bigger concerns with this scenario is scene safety. The organophosphate agent can attach to the patient’s clothing and pass to rescuers. In addition, continued poison absorption can still occur. Decontamination is necessary and provider safety should become paramount as soon as a cholinergic overdose is suspected. At least get dude’s clothes off and get any obvious contaminants off of him.
Finally, consider Patient Five. Is she intoxicated? She certainly acts like it on the surface. She is ataxic with slurred speech at a DUI stop. On the other hand, however, are the absence of the smell of alcohol on her breath and the absence of nystagmus. Honestly, I don’t look for nystagmus all that often. And my olfactory nerve is burnt out on alcohol. I can’t smell it anymore. I can certainly smell other odors, especially armpits, feet, ass, and despair. But not alcohol.
Sedative-hypnotic medications are central nervous system depressants that have similar presentations to alcohol intoxication. There can be CNS depression, confusion, and even unconsciousness. Pupillary signs are unhelpful here and vitals can often be normal. If vitals are altered, one would usually find signs of CNS depression again such as bradycardia, hypotension, and bradypnea. Common sedative-hypnotics include benzodiazepines, barbiturates, and alcohols like methanol. In this case, I think I would be uncomfortable in “clearing the patient for jail” unless I was absolutely comfortable with that outcome. I don’t feel like I should be comfortable here, in the absence of alcohol on the breath. What could be too many wine coolers could easily be too many Xanax. This lady took her evening Valium and then wound up behind the wheel for whatever reason. She wasn’t drunk.
Take the time to learn toxidromes. Medicine is funny. I mean, different patients can have the same problem and present differently. Two demographically similar patients can both be having an MI and be complaining about two completely different sets of symptoms. One can be hypertensive and the other hypotensive. That is what makes medicine interesting. But with toxic exposures and overdoses, many times the signs and symptoms are similar between patients. That is the power of the toxidrome.