UMEM Educational Pearls - By Fermin Barrueto

You have a treat bag full of candy, which one can cause hypertension, hyopkalemia, metabolic alkalosis, rhabdomyolysis, low renin activity, thrombocytopenia and hypoaldosteronism. (scroll down for answer)

Licorice syrup or licorice extract contains glycyrrhizic acid which has a mineralcorticoid-like effect and can cause of all of the effects. Don't worry, Twizzlers and other usual licorice candies do not have true licorice extract in them. It is found in herbal remedies and some "natural" candies and licorice flavored cigars. Don't pick the licorice !

Yesterday's pearl generated several questions that I thought were worth answering briefly:

1) Why give it IM? Absorption rate is faster than SQ infiltration though theoretically could still cause necrosis

2) Is it only infilitration? Gangrene has occurred with inadvertent intra-arterial injection, SQ infiltration and even regular IV administration

3) Mechanism? Appears to be the drug and not diluent, diluting down the concentration as well as decreasing dose appears to help if you are going to give it IV

Here is a website if you wish to read more details:

https://www.ismp.org/newsletters/acutecare/articles/20060810.asp

If you are still using IV Phenergan, you need to be aware of the necrotic effect that occurs if it infiltrates. EDs have even removed it from their drug dispensing machines. It appears to be the drug and not the diluent. Mechanism is not completely understood. Below is a picture the plaintiff attorney will use about this well know adverse effect. If so many alternatives for IV antiemetic it is wise to reconsider IV phenergan.

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Drugs that cause hearing loss:

Reversible - Chloroquine, erythromycin, quinine, CO, loop diuretics, NSAIDS, ASA

Irreversible - aminoglycosides, bleomycin, vincristine, vinblastine, cisplatin, lead, mercury, arsenic

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There are Type 1C Anti-Dysrhythmics, like propafenone and flecainide, that are utilized to suppress atrial fibrillation. They are called Type 1C due to their sodium channel blocking effects. Flecainide has a potent effect on the ECG and has caused significant and resistant widening of the QRS complex. 

Typically, a sodium channel blocker like a TCA can be treated with hypertonic sodium bicarbonate but flecainide has been resistant to this at times and there is a reported overdose utilizing magnesium sulfate. (1) Keep that in mind if you were to see a widened QRS complex in the face of a flecainide ingestion.

There has been a Brugada ECG pattern also reported (I know Amal is smiling)  (2) ontop of the widened QRS, PR intervals though minimal effect on the QT.

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  1: Cabrera Ortega M, Gell Aboy J, Díaz Berto E, Monagas Docasal V. [Acute  flecainide overdose]. An Pediatr (Barc). 2011 Jan;74(1):56-8.       2: Martínez-Mateo V, Arias MA, Rodríguez-Padial L. [Brugada electrocardiographic  pattern elicited by flecainide overdose]. Med Clin (Barc). 2011 Mar  19;136(7):320. 

We will all see a patient that comes into the Emergency Department stating they have ingested some wild or self-picked mushrooms. Usually they will be actively vomiting and there will be no mushroom to identify. If there is, identification may still be difficult. There are no other clinical relevant symptoms that you can see until its too late. Amanita species is lethal and may require liver transplant. The most important question you can ask after trying to identify the mushroom is:

When did you eat the mushroom and how long after did the vomiting start?

As a general rule (with some exceptions), Amanita species cause vomiting and diarrhea in a delayed fashion 5-6 hours after ingestion. The other non hepatotoxic species usually cause vomiting within 1-3 hours.

Immediate vomiting <6 hrs from time of ingestion is good (usually).

The internet has become a wealth of information and some books have now gained internet noteriety. A chemist and author of the book - TIKHAL: Tryptamines I Have Known and Loved is an excellent example. 

Tryptamines include drugs like LSD and alpha-methyltryptamine (AMT). Vivid visual hallucinations and serotonin agonism, these drugs were glamorized by this author. He would synthesize a tryptamine and then "taste it". Take a look at the link below where he first describes the biochemical synthesis he performed then describes his dose response effect when he tried the drug.

If you run into a drug or slang term in the ED you are not familiar with, the website www.erowid.org will likely have the translation. 

http://www.erowid.org/library/books_online/tihkal/tihkal48.shtml

When reviewing a patient's medication list, there are always some that should catch your eye. Digoxin is one since we can measure it, has a low therapeutic index and elimination is effected when renal function is diminished. Another drug that should catch your eye is SOTALOL. Renally cleared and affected by even a minimally lower than normal magnesium. The toxic effect even at therapeutic levels is torsades de pointes.

One study, in a 736 bed hospital, showed 89% of patients prescribed sotalol were on an inappropriate dose due to renal function and an odds ratio of 3.7 increased re-admission rate at 6 months for the patients on the inappropriate dose of sotalol.

We can catch this in the ED. Involve your pharmacist, ED pharmacist or local toxicologist for dosing calculations.

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Hyperglycemia in the setting of antipsychotic use has been reported mostly with olanzapine (Zyprexa) but does occur with other antipsychotics. A recent study from the NYC medical examiner's office details 17 deaths of DKA due to antipsychotics and found that (from highest to lowest incidence) quetiapine > olanzapine > risperidone were the atypical antipsychotics found with these deaths.

Remember hyperglycemia occurs with patients on antipsychotics and can lead to hyperglycemia hyperosmolar coma or DKA. Both can be lethal.

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Utilizing 20% lipid emulsion at a dose of 1.5 mL/kg (100 mL Bolus) IV with repeat in 15 minutes in no response is being recommended in patients hemodynamic instabiity due to poisoning.

Probably more effective in lipophilic drugs is a current theory for the mechanism of action - the "lipid sink". The idea is that the lipids envelope the drug pulling it off its receptors or sequestering it in the intravascular space. A recent paper has added another mechanism - direct inotropic and lusiptropic effects.(1)

Also, if you think the therapy is experimental, think again. Another recent paper surveyed Poison Control Centers and found 30/45 Poison Centers in the US have a defined protocol for utilization of lipid emulsion therapy. The PCCs are recommending it more.(2)

What was once considered just a purely experimental therapy only used at the very end of code is becoming more mainstream. Comfort with its safety profile and anectodotal effiicacy continues to mount.

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If you are working in a community hospital and have an acetaminophen overdose, one of the criteria to transfer the patient to a tertiary care center is presence of the King's College Criteria.

The below is taken from mdcalc.com -  http://www.mdcalc.com/kings-college-criteria-for-acetaminophen-toxicity/

Each one is assigned points and can be prognostic for severe toxicity and need for transplant. The lactate and phosphorus are new ones and have modified the criteria. Phosphorus is utilized to create glycogen. If the liver is injured and trying to heal, your phosphorus will be low (good). If the liver is injured and unable to repair itself the phosphorus will be high (bad). This single test has an excellent prognostic ability.

With recent events, a few notes about ricin seems appropriate:

1. Easy to make from castor bean though heat labile
2. No antidote, though Fab like digibind is in development
3. Granule size of the grain of sand can kill
4. Inhalation, IM, IV all effective
5. After immediate exposure likely no symptoms
6. Vomiting and diarrhea initially, acute lung injury and death in 3-5 days

CDC website: http://www.bt.cdc.gov/agent/ricin/

Cocaine toxicity is characterized by the sympathomimetic toxidrome: tachycardia, hypertension, hyperpyrexia, diaphoresis as well as sodium channel blocking effects that can cause local anesthesia topically, QRS widening and even seizure.

Usual treatment for a cocaine toxic patient is benzodiazepines and cooling. Be wary of end organ damage, trauma and seizures.

There was a recent study that looked at dexmedetomidine to treat the sympathomimetic effects. Placebo-controlled trial used cocaine-addicted volunteer and applied intranasal cocaine. Measuring skin sympathetic nerve activity and skin vascular resistance, this study, unfortunately, showed as the dose increased  MAP did not fall further and increased paradoxically in 4 of 12 subjects.

This highlights the incredible physiologic mechanism of catecholamine release from the CNS with cocaine. This mechanism overlaps some with the centrally acting alpha agonist - dexmedetomidine and was shown in the study by Kontak et al. 

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Question

A foley is inserted in a fire victim patient. Urine return is in picture. Describe the reason for this colored urine.

Special Thanks to Dr. Doug Sward for the urine picture 

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Typical opioid withdrawal include clinical symtpoms of piloerection, nausea, vomiting and diarrhea. If you were to see seizure, another etiology other than opioid withdrawal should be investigated. 

Except in the case of neonates borne to women who have been taking opioids chronically such as a methodone patient. Once the child is born, symptoms of withdrawal may take days to weeks to materialize though seizures typically occur <10 days. The child is at increased risk of SIDS as well.

There have been many attempts to reduce the incidence of contrast-induced nephropathy. Mechanism usually centers around antioxidant properties or free radical scavengers that prevent the acute kidney injury that may result after intravenous contrast. IV Fluid hydration, sodium bicarbonate and acetycysteine have been studied with only some evidence. There is also some controversial data that is beginning to surface regarding the use of atorvastatin with a recent article in Circulation 2012 that showed high dose atorvastatin (80mg) 24 hrs prior to angiography prevented contrast-induced acute kidney injury in patients with mild to medium risk. Link to article has been provided:

http://circ.ahajournals.org/content/126/25/3008

Cyclophosphamide-induced hemorrhagic cystitis is a well known to oncologists. This unique complication of this chemotherapeutic drug has a defined mechanism and could be seen in your Emergency Department.

- Hemorrhagic cystitis occurs in 46% of patients that receive cyclophosphamide

- Can occur even months after administration

- 5% can actually die from the hemorrhage

- Treatment: Bladder irrigation, hydration, supportive. Oral adminsitration of MESNA (2mercaptoethan sulfonate) and bladder irrigation with prostaglandins and even methylene blue have been attempted.

SSRIs and SNRIs like venlafaxine and sertraline are well known to cause hyponatremia. Usually considered safe, this adverse drug event can lead to weakness, confusion, seizure and even cerebral edema. Elderly are more susceptible to this adverse effect.

ADH is regulated by serotonin and thus the mechanism for the Hyponatremia is SIADH. 

Tolvaptan, a vasopressin receptor antagonist, has been a new treatment that has been used anecdotally in Europe. Waiting for the first US case report. 

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Despite a paucity of data, pain management clinics are administering topical gel mixtures that have included ketamine, tricyclics, calcium channel blockers and baclofen. Internet blogs have already identified this gel mixture as a way to "get high".  This is one of those google searches you have to do on your own.

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  1: Lynch ME, Clark AJ, Sawynok J, Sullivan MJ. Topical 2% amitriptyline and 1%  ketamine in neuropathic pain syndromes: a randomized, double-blind,  placebo-controlled trial. Anesthesiology. 2005 Jul;103(1):140-6.     2: Lynch ME, Clark AJ, Sawynok J. A pilot study examining topical amitriptyline, ketamine, and a combination of both in the treatment of neuropathic pain. Clin J Pain. 2003 Sep-Oct;19(5):323-8.    3: Uzaraga I, Gerbis B, Holwerda E, Gillis D, Wai E. Topical amitriptyline,  ketamine, and lidocaine in neuropathic pain caused by radiation skin reaction: a pilot study. Support Care Cancer. 2012 Jul;20(7):1515-24.   

Myth: The ornamental red plant - poinsettia - gained a reputation as a poisonous plant from a case report. In 1919, a 2-year-old child reportedly died from an ingestion and later an 8-month-old developed mucosal burns.  These anectdotal case reports perpetuated the myth that poinsettia plants are poisonous. In the modern literature there is one single case of anaphylaxis(1) due to poinsettia ingestion/exposure, an allergic dermatitis(2) and one case of dermatitis(4). 

Krenzelok et al.(3) showed there were 22,793 cases of poinsettia exposure and there were no fatalities reported to poison centers. 96.1% were kept at home without sequelae.

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  1: Kimata H. Anaphylaxis by poinsettia in infants with atopic eczema. Allergy.  2007 Jan;62(1):91-2.     2: Bala TM, Panda M. No poinsettia this Christmas. South Med J. 2006  Jul;99(7):772-3.    3: Krenzelok EP, Jacobsen TD, Aronis JM. Poinsettia exposures have good  outcomes...just as we thought. Am J Emerg Med. 1996 Nov;14(7):671-4.     4: Edwards N. Local toxicity from a poinsettia plant: a case report. J Pediatr.1983 Mar;102(3):404-5.