Rocuronium is fast becoming the agent of choice for RSI in the Emergency Department. Here is a head to head comparison of the two drugs to understand why:
| Rocuronium | Succinycholine | |
| Dose | 1-1.2mg/kg | 1mg/kg |
| Onset | 1-1.5min | 1min |
| Duration | 7-12min | 30-40min |
| Histamine Release | No | Minimal Yes |
| CVS Effect | Tachycardia rare | Severe Brady rare |
| Other Adverse Effect | No fasciculations, No ICP effect, No Rhabdo | Fasciculations, increase ICP, rhabdo, movement of displaced Fxs |
You have a 44 y/o female patient with an arterial line monitoring her blood pressure which is reading 302/156 mm Hg. Her heart rate is 140 bpm. Her history reveals she is taking a monoamine oxidase inhibitor (MAOI) and has inadvertantly ingested tyramine at her friend's cheese/wine party. What do you do?
Rodenticides have taken many forms. The following is a list of some of the more interesting ones either due to the mechanism of toxicity or how it is lethal. All of these are also toxic to people.
1) Strychnine - Glycine Antagonist at the post-synaptic spinal cord neurons - patient or rat will have convulsion of the extremeties but will be awake, alert and in extreme pain. Essentially look like generalized seizure except awake. Treatment: Benzodiazepines, Analgesia, Supportive
2) Brodifacoum - Long Acting Coumarin - rat eats, later develops elevated INR then tries to run through thin cracks in the wall or takes a little too high of a jump, then boom - subdural or some other internal hemorrhage. In human, they can stay anticoagulated for weeks after an overdose. Treatment: Vitamin K and large padded room
3) Cholecalciferol - Vitamin D precursor - there are big blocks of this drug in the NY and other subway systems. Rat nibbles, gets hypercalcemic, then gets thirsty because of this. Rat runs out into middle of subway to drink out of puddle then - splatt - the M train to Brooklyn comes along. Treatment: IVF, Loop Diuretics, Bisphosphonates
Octreotide
Tetrodotoxin - Sodium Channel blocker - Extremely toxic causes paresthesias, dysrhythmias and paralysis - Found in the sushi called Fugu (From the Pufferfish) - Eating the sushi is considered a delicacy and goal is to get just enough of the toxin to get perioral paresthesias after eating. - Also found in the blue-ringed octopus, angelfish and parrot fish. Enjoy your seafood and take a look at the attached pic of actual fugu.
A few previous pearls have touched on identifying drugs that cause QT prolongation. In our patient population, methadone is one of the more common causes of drug-induced prolonged QT syndrome. Of 692 physicians surveyed (35% family practitioners, 25% internests, 22% psychiatrists, and 8% self-identified addiction specialists) only 41% were aware of methadone's QT-prolonging properties and just 24% were aware of methadone's association with torsade de pointes.
Now that you know, what do you do when a patient on methadone presents with a QTC of 580 msec and intermittent runs of vtach and torsade de pointes?
The answer is... the exact same thing you would do with any other patient who presents this way, regardless of the cause.
Buprenorphine, an alternative to methadone, is not associated with prolonged QT syndrome.
Although we tend to think of ACS with cocaine use, there are many other serious complications, including:
Watch out for tradename and generic name's of medications.
They can get the patient and yourself into trouble:
Classic example is my own case: Insert a central line in a patient - subclavian - and shortly after completion am alerted the patient's INR is 25. No adverse outcome but when I reviewed the med list, I did not see coumadin or warfarin and assumed I was in the clear. Patient was on jantoven.
Happy Holidays
A search of the toxicology literature will reveal that naloxone has been tried in many different overdose situations. It is thought that the endogenous opioid system mediates several physiologic and pharmacologic pathways.
Bottom line: In none of these instances was improvement as dramatic or consistent as in the reversal of the toxic effects of an opioid. Naloxone can certainly be tried in non-opioid overdoses but should not be considered a first-line antidote. The most benefit appears to be with clonidine.
CO is formed from the incomplete combustion of carbon materials, eg. fires, stoves, portable heaters CO reversibly binds hemoglobin, producing carboxyhemoglobin (HbCO). This causes oxygen to bind more tightly to hemoglobin, releasing less in the tissues. Because of this, it affects the organs with the highest oxygen requirements most profoundly (eg. brain and heart).
Symptoms are mainly neurological and cardiovascular, but may include a wide variety of non-specific symptoms. The initial symptoms of CO poisoning may include headache and flu-like illness progressing to confusion, agitation, lethargy, seizures and coma.
Place patients on 100% oxygen to decrease the half-life of HbCO. Though controversial, HBO therapy is thought to decrease the incidence of neurologic sequelae. HBO therapy should be considered for patients with a HbCO level above 20%, severely symptomatic patients with lower levels, and pregnant patients. Remember that pulse oximetry will not be accurate.
Tryptophan - a precursor to melatonin, it is often blamed for the post prandial coma that many go into after a big turkey dinner. Never mind the 5000 kcals that was consumed during the meal. The supplement really doesn't help with sleeping. Interestingly, turkey isn't even in the top 10 or 20 of foods that contain tryptophan. The top five are:
1) Game meat (Elk): 746 mg of tryptophan
2) Seaweed (Spirulina): 736 mg of tryptophan
3) Spinach: 690 mg of tryptophan
4) Egg White: 673 mg of tryptophan
5) Soy protein: 630 mg of tryptophan
Supplements of L-tryptophan have been contaminated with a compound that has been associated with eosinophilia myalgia syndrome.
How many times have you had a patient with an allergy to codeine described as stomach upset? Or how about a rash with morphine (probably secondary to histamine release)? True anaphylactic reactions to opioids are very rare (< 1%). But what happens when you have a patient with a true allergy, but still need to give an opioid? No problem, you just need to choose one that is structurally different.
All of the group 1 and 2 agents are structurally very similar to each other and should not be given if a true allergy exists to any other natural or semi-synthetic derivative. Group 3 agents have structures different enough that they can be given to a patient intolerant to the natural or semi-synthetics without fear of cross reactivity. They are also very different from others in this same group.
This is a psychoactive herb which can induce strong dissociative effects by stimulation of the kappa receptor. It has become increasingly well known and available in modern culture, and popularized by YouTube Salvia (also known as Sage, Diviner's Sage, Magic Mint, or Sally D) is usually smoked, but can be chewed or ingested.
The high it produces is very intense, but lasts only approximately 10 minutes. Currently many states have enacted legislation against it, including Fla, IL, KA, MI, MO, ND, OK and VA, but it is available over the internet.
The following video demonstrates clinical effects of drug.
Although it is amusing, this is not meant to condone use.
(if you can not view the embeded video here is the link)
http://www.youtube.com/watch?v=w6dgXX0ytSo
Methylenedioxymethamphetamine (MDMA) or "Ecstasy"
A designer club drug that has been classified as a "hallucinogenic" amphetamine though it does not cause visual hallucinations like are reported with LSD. It has many of the sympathomimetic effects like other amphetamines but its main mechanism of action which both causes the euphoria and toxicity is serotonin agonism. Since Anti-diuretic hormone is released by the hypothalamus under the direct regulation of serotonin, there is a transient but dangerous episode of Syndrome of Inappropriate ADH (SIADH). Combined with the club culture and fear of dehydration while taking MDMA, patients ingest MDMA concomitantly with free water through the night further exacerbating the hyponatremia. The time sequence of events for these patient is (women appear genetically predisposed to this phenomena):
Treatment: Fluid restriction - this is the one time that the 1L NS Bolus can kill a patient with cerebral edema. If you must give fluid give 3% NaCl if there is symptomatic hyponatremia. Remember the patient has dropped their sodium in about 24 hours so you can replenish in about the same time quite safely and even faster in severe cases. Treated correctly, patients improve rapidly - within 24-48 hours. Read a great case report in the reference below.
Olanzapine (Zyprexa)
This is an atypical antipsychotic that gained popularity because it caused less sedation and fewer extrapyramidal effects. However, there are many other adverse effects that need to be emphasized. Some of these may contribute to a patient's condition in the ED:
