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Street Drugs

In those patients who abuse drugs - especially the amphetamines - who develop mania, about 50% of them will have psychotic symptoms along with their mania. If you compare that versus what we see in manic-depressive illness, 15% of manic-depressive patients will also be psychotic. Substances frequently cause mania with psychosis. And itís particularly difficult to treat. We also see depression, especially with the central nervous system depressants like the barbiturates, the benzodiazepines and alcohol, as you know, we can see with all of them or any of them delirium or confusion states where we have inattentiveness, fluctuating sleep arousal, disturbance in the sleep/wake cycle, those criteria for delirium. We can also see agitation and aggression, so as we go through these drugs weíll also talk hopefully about not only the pharmacologic management, but also maybe some kind of

Suspicion of drug use usually is entertained because of physiological parameters - like hypertension, tachycardia - or oftentimes itís because of mental status changes; confusion, psychosis, belligerence, agitation. We frequently get urine drug screens, although - as I hope weíll be able to point out today - my hope is that we can identify or some close to identifying the offending substance based on physical examination history. A lot of - like us, for example - we may do a urine drug screen or a serum drug screen and we may or may not get that information back quickly enough to help us make a decision in the clinical setting. So my hope is that we can use some of the symptoms we know to kind of predict what we think is on board. I donít know about you, but for us the rule is usually polysubstance abuse. Is it for you too? When youíve seen intoxication usually itís not just a single drug thatís on board. So hopefully we will be able to kind of predict what we see based on the pharmacological and neurochemical aspects of these substances. When we do do drug screen, we try to use them whenever possible. We can talk about the ethical aspect of that, but in the emergency room setting - if thereís an issue of dangerousness - we usually waive certain confidentiality issues because itís necessary for medical treatment. Blood tests, which would include serum level for other medications that they may be on that may masquerade as mental status change. For example, a classic offender for confusion and intoxication would be tricyclic antidepressants that are taken in overdose. It can psychotic, it can be delirious. Usually you are going to get an anticholinergic intoxication but they can look like a patient who is on

As you know, most of the patients who we see who are active substance abusers, they are not the worlds greatest or honest historians. So I think when we see a confused and/or obtunded patient, itís really a case where we need to get as much collateral information from family, friends or whoever brought the patient in. Even from the

We saw a patient in the hospital - this is several years ago - we were asked to see the patient for confusion. The patient was confused, tachycardic, hypertensive and had a real fine tremor. You could

Now specifically we will break these drugs up into their different kind of areas, if you will. But when you look at the amphetamine class, or they sympathomimetics, thereís really two basic types. One is the classic cocaine prototype and the other kind of cousin or whatever you would like to call it would be - what we have seen a lot of - would be the methamphetamine or the crank. Both of these have similar autonomic pictures but they have two different mechanisms of action. Cocaine works like an antidepressant. It is actually a re-uptake blocker of both norepinephrine and dopamine. So it acts like an antidepressant. In fact itís a very effective antidepressant, but itís half life is

As you know, multiple ways of taking these drugs. Popularity-wise, most people - at least in our area - are smoking it. Some people are injecting it, but the bioavailability of smoking it is almost instantaneous. Itís also cheaper and cleaner. So we see a lot more smoke-able forms of crack cocaine and methamphetamine. But it can be used intravenously. It can be snorted and it can be mucosally absorbed. But it has 

I was told a couple of weeks ago by a patient, who does a lot of speaking with me who is a recovering cocaine patient who does a lot of speaking, and he was telling me that one of the hot, popular combos on the street now is using an amphetamine plus Prozac. Have you heard that at all? The theory makes some sense because basically Prozac will tend to intensify the effects of other drugs that we use and it has a very long half life. From what the patient tells me, thereís a more intensified high. Because Prozac, as you know, is broken down into an active metabolite that will last in your system for seven days, so they can take Ö heíll do a once a week, 40 mg bolus of 

The next class would be the CNS depressants. You could also put in here the barbiturates, the benzodiazepines. You could also put in alcohol. Iím not going to talk about those but I will say like the Quaaludes, the methaqualone or barbiturate they share kind of similar neurophysiology and as you remember, they - most of them - are GABA agonists. They are agonists to the GABA receptor, or benzodiazepine receptor site and they are oftentimes cross-tolerant for one another. So barbiturates are cross-tolerant with benzodiazepines or

The barbiturate prototypes, their effects are GABA agonists so they cause drowsiness. You can see delirium or confusion. Usually itís a sweating patient. There are cerebellar effects so thereís ataxia. Usually the pupils are smaller but not the pinpoint pupils that you see with narcotic overdose. Usually the patient is hypotensive and bradycardic. So itís a hypotensive, bradycardic, usually cool temperature patient with small pupils. It used to be that in an intoxication state thereís not really an antidote, although there are some studies, there are some places that do use the - in withdrawal cases - will use some pathomimetics to

The risk here is that if you see a patient with a barbiturate overdose who then goes through withdrawal - which looks just like alcohol withdrawal, or benzodiazepine withdrawal - the patient who is on a barbiturate is about five times higher risk to have a withdrawal seizure than somebody on alcohol or somebody on benzodiazepines. So if we see withdrawal with a barbiturate patient, we will treat it very aggressively. Once again, as I say, I will tend to go with benzodiazepine because they are cross tolerant from one

The next class will be another class of CNS depressants and the old prototypes, heroin, morphine, but clinically my experience has been that although heroin is on the upswing here, the more common clinical scenario for me are people who use the prescription narcotic analgesics. The Percocetís the Percodanís, any of the codeine or opiate agonist mechanism of action are the opiate receptors, but also there is some cross reactivity with the GABA receptors too, like a benzodiazepine. What we see with the opiate 

Some of the dependency issues. These are the same patients who, some of them are on methadone treatment programs. This is, as you know, methadone is also an opiate so it also has a habit-forming potential but the studies still suggest that methadone maintenance is Ö if you can maintain patientís occupational and social function, they still do well and they tend to get into less antisocial activities and they tend to be more functional, even on the methadone. Trying to get patients off methadone has been, for me, very difficult. Very difficult. But some of the newer agents we are using with alcohol, because of that benzodiazepine-receptor kind of similarity, the naltrexone works both in alcohol abuse but also historically in narcotic abuse, 

Then we also have another classification which is called PCP. It kind of has itís own Ö similarly classified it as a amphetamine or sympathomimetic. Itís not really a hallucinogen. Itís really both. If you look at PCP itís probably the most psychogenic substance there is. In other words, I canít remember the last time I saw a PCP patient who was not psychotic. It makes some sense if you look at the pharmacology because PCP is a re-uptake blocker of serotonin, norepinephrine, dopamine and itís a blocker of acetylcholine. So itís anticholinergic, dopaminergic, norepinephrineergic and serotonergic. And thatís not a good combo. In fact, in intoxication this patient oftentimes looks exactly like a schizophrenic patient, paranoid type. Wide staring eye contact. The difference is they have all the autonomic arousal and schizophrenics usually donít have that hypertension, tachycardia. Usually they have nystagmus, their pupils are fixed - usually wide - you can see all kinds of mannerisms and 

So in this particular patient - because they are usually so agitated and psychotic - we will usually use a cocktail of benzodiazepine and a neuroleptic. So for us thatís usually Haldol. Our use of Haldol is mainly Ö all the antipsychotics will work but we tend to like Haldol because itís low dose, high potency, but it doesnít have a lot of anticholinergic side effects, which can sometimes worsen PCP intoxication and doesnít provide a lot of orthostasis like Thorazine or Mellaril can. Thorazine is a great sedating medicine but it has tremendous orthostasis, lots of anticholinergic side effects. So we tend to use Haldol because itís 

Another class of drugs of abuse would be inhalants. These would be the volatile hydrocarbons. These would be the glue-sniffing, benzene derivatives, gasoline sniffers. Some of the most amazing presentations Iíve ever seen, especially young kids who are glue sniffers, intoxicated who actually present high but stuporous, if that makes sense. Their subjective sense of mood is elevated but the present almost in a stuporous fashion sometimes, and oftentimes have very dramatic cognitive disturbances. So you can 

The question basically is with inhalants in the acute kind of setting, can you use certain nerve-sparing agents? Probably the one thatís been studied the most would be steroids as far as their antiinflammatory effect. The problem is that sometimes steroids in high dose can also exacerbate the psychosis and to my knowledge there hasnít been a real good controlled study that suggests thatís clearly prophylactic or helpful. The other thing about the inhalants is we are really not sure of what they do neurochemically. We know we see that neuronal degeneration, but we are not sure what neurophysiology is impaired. Whereas 

The last set would be the hallucinogens and that would include LSD, mushrooms, peyote and also one that we see here quite a bit, called ecstasy, which is methylene-dioxymethamphetamine. Itís an amphetamine name but it acts like a hallucinogen. The key component that separates these out as hallucinogens versus amphetamines is their mechanism of action. And these are all serotonergic. Whether or not they are serotonin agonists or re-uptake blockers of serotonin is relatively unknown. But these are 

Marijuana. I could but itís in kind of a separate category. I kind of Ö I didnít purposely not put that in, but to be honest with you, with marijuana you donít tend to see .. I put the things up here that we tend to see more in the hospital settings and emergency-type presentations. Very rarely do I see patients who are using marijuana who are intoxicated to the point where I see them in a medical hospital. What we do know about marijuana though, pharmacologically, is that it probably does elevate dopamine levels and itís probably true that it does seem to be a gateway-type of drug. Probably with its ability to increase dopamine, but itís far less potent in its ability to do that than the other substances of abuse that weíve talked about. Thereís also less autonomic effects with marijuana.

The question is, in regard to some of the subcutaneous or even intramuscular misses if you will, of causing some localized vasoconstriction then eventually ischemia. Is there anything we can do about that? It may be possible to use some of the beta-blockers. Theyíve also experimented with vasodilators in those cases. Nothing in a controlled study that Iím aware of. Skin lesions with any of the street drugs? It depends on what kind of skin lesions you are talking about. The classic kind of skin-popper lesions would typically be seen with the narcotics and the opiates. Where thereís kind of pock-like marks on the 

In regard to screening parameters, my recommendation is do it as soon as you possible can. For example, you can turn a ... a lot of it depends on what kind of assays you use and what type of lab. A lot of it depends on the sophistication of the screen, but a classic screen will tend to be Ö I would say, itís more qualitative than quantitative. Certainly there is a level above which itís going to trip a positive test. For example, some of the athletes I work with, if you look at Olympic drug testing, they have very low ceilings so they have the ability to do both qualitative and quantitative screens. So not only can they tell if cocaine is in your system, but they can give you a nanogram measure of it. Most of the screens we use here are going to show us whether it trips

If you go with cocaine, short half life. You really got to get the drug screen within several hours of the use to be of benefit. If we go with the barbiturates, they are longer acting, so several days you may still tip something thatís positive. If itís the LPS you usually want to get it within the first 24-48 hours. If you go PCP - interestingly enough, about PCP - is both PCP and the hallucinogens tend to have high protein binding so sometimes both PCP and the hallucinogens will be fat stored. So sometimes you can trip off positive tests several days after, but you can also see tests in some patients that they are negative a day after. So itís very difficult. PCP is very unpredictable, whereas the inhalants - we donít even have a screen for inhalants because thatís mostly CNS toxicity and you may get some urinary findings. Then the hallucinogens, sometimes they will stay positive for several

Now weíll talk a little bit about some of the emergency presentations we see in medicine and psychiatry. What we are going to talk about is suicide today, but weíve talked, you can see anything from agitation to acute panic attacks. That can sometimes be an emergency presentation. Obviously manic episodes with psychosis - if we get time today weíll talk about some of the psychotropic medications. Delirium, weíve all seen. And what we just talked about were some of the intoxication states with

We look at those recent losses, presence or absence of depression and last, physical health. And in particular, loss of physical health or medical illness that has a pain component is a risk factor. So when I look at all these risk factors, the ones I look at are; which of these are not likely to change without treatment. Iím going to pay particular attention to the alcoholic. Iím going to try to stabilize the patient who has a history of violent behavior. Iím going to probably look at inpatient care if they are unwilling to

Then lethality and availability. We looked at resources that we talked before on the other risk factors; people who have poor cognitive abilities tend to be a little bit more at risk oftentimes because their problem solving abilities arenít as keen or arenít as sophisticated. Poor ability to establish relationships. In those people who are socially isolated and have a family that is relatively unresponsive, or they are distant, they are isolated, they are aloof. Those are patients who have high risk factor.

Itís interesting, as I talked before, it doesnít mean that if I see these low risk factors that Iím less concerned. All it is telling me is that maybe I could be less Ö what do I want to say? Less intensive, but it may require less of a level of treatment. Usually the 

Causes of encephalopathy. So for us the diagnostic issue in delirium is itís a medical illness causing encephalopathy. High mortality rate and the key is, the trick is, we must find whatís causing the encephalopathy. So that may be things like vascular disorders, tumors, postictal states. Includes hepatic encephalopathy, carbon monoxide poisoning, arrhythmias, hypotension, a number of electrolyte abnormalities, hypo and hyperthyroidism, toxic chemical exposures, all the particular drugs that can cause confusion with particular attention to anything that are anticholinergics. These are anti-memory. The antihypertensives can give you hypotension. Cimetidine can cause some problems, and so can the drugs of abuse. So, as my attending told me when I was a student, "Todd, you are never going to know every drug that there is. But the drugs you use, the medications you use, you should know everything about them." And that includes drug/drug interactions. For example, some of the newer information on the cytochrome P-450 system, in particular the enzymes that break down Prozac, also break down antiarrhythmics, codeine preps, Seldane and Hismanol. So some of the serotonin specific re-uptake inhibitors, like Prozac and Zoloft, can actually elevate drug levels of other medications that we use commonly. So just that we know drugs and what they do and that they can cause delirium, deficiency states - like Wernickeís encephalopathy - electrolyte imbalances. Neurons are particularly sensitive to hyponatremia. You see that commonly in confusion and delirium, with hyponatremic patients and any head trauma.