M2E Too! Mellick's Multimedia EduBlog
E Too! Blog by Larry Mellick, MD, presents important clinical pearls using multimedia. Dr. Mellick is the former chairman of emergency medicine at Georgia Health Sciences Health System and a professor of emergency medicine and pediatrics at Georgia Health Sciences University in Augusta.
By its name, M2E Too! acknowledges that it is one of many emergency medicine blogs, but we hope this will serve as a creative commons for emergency physicians.
Tuesday, December 03, 2013
Thankfully, cannabinoid hyperemesis syndrome isn’t a life- or limb-threatening condition. Malpractice attorneys would be having a field day if it were. I have been attuned to this condition only for the past several years, but it’s apparent that this condition remains diagnostically elusive.
Every new case I pick up has presented previously to my or another community emergency department multiple times without anyone making the diagnosis. And the patient almost always has a trail of CT scans, abdominal ultrasounds, and other imaging studies as well as hundreds of dollars in laboratory testing. It’s known that this condition is commonly not recognized by health care providers, and patients often go years with this recurrent or cyclical condition before a diagnosis is eventually made. (Mayo Clin Proc 2009;84:76.)
This condition has only recently been described. Allen et al from South Australia initially recognized it in 2001 and first published a small case series in 2004. (Gut 2004;53:1566.) A number of small case series and case reports were subsequently published. A 2012 article by Simonetto et al from the Mayo Clinic is one of the largest case series published. These authors (Mayo Clin Proc 2012;87:114) reviewed 98 patients presenting with the syndrome, and proposed diagnostic criteria:
• Long-term cannabis use
• Severe cyclic nausea and vomiting
• Resolution with cannabis cessation
• Relief of symptoms with hot showers or baths
• Epigastric or periumbilical abdominal pain
• Weekly use of marijuana
Ironically, cannabis is well known for its antiemetic effects.
Supportive features include:
• Age under 50 years
• Weight loss of more than 5 kg
• Symptoms predominantly in the morning
• Normal bowel habits
• Negative laboratory, radiographic, and endoscopic test results
The historical clue that essentially nails the diagnosis is the patient report of temporary symptom relief from hot showers and baths. Generally, this bathing is described as compulsive. (Mayo Clin Proc 2009;84:76; Gut 2004;53:1566; Mayo Clin Proc 2012;87:114; Can J Gastroenterol 2010;24:284.) Patients with this syndrome will take multiple hot showers throughout the day. One author even used the term hydrophilia for this symptom. (Int J Gen Med 2013 Aug 19;6:685.)
These patients with nausea, vomiting, and abdominal pain are also fairly resistant to mainstream therapies like promethazine, odansetron (Zofran), dicyclomine, and morphine. We have had good therapeutic success with intravenous haloperidol when standard interventions fail or only partially relieve symptoms. At least one other author has had the same therapeutic experience, and reported the therapeutic benefit of 5 mg IV haloperidol. (Am J Emerg Med 2013;31:1003.e5-6.)
Cannabis is the world's most widely cultivated and consumed illicit drug, and the chances of your seeing this condition are excellent. (Bull Narc 2006;58[1-2]:1.) The chances of missing the diagnosis are equally good if you are not familiar with or aware of the condition.
Other causes of cyclical vomiting in adults and children should not be missed. This syndrome needs to be added to the list of those esoteric conditions causing cyclical vomiting. (Gut 2004;53:1566; J Gen Intern Med 2010;25:88.) Cannabinoid hyperemesis syndrome will always be at the top of my differential diagnosis list, however, because of the population seen in our emergency department.
The pathophysiology of this condition is not yet understood, but the central effects of long-term cannabis use on the hypothalamic-pituitary-adrenal axis is proposed as playing a major role in developing cannabinoid hyperemesis syndrome. (Mayo Clin Proc 2012;87:114.) Other effects attributed to marijuana include adverse effects on the respiratory and cardiovascular systems, impaired educational attainment, reduced workplace productivity, a role in motor vehicle crashes, and increased risk of use of other substances. (JAMA 2004;291:2114.) This syndrome has also been described by users of synthetic cannabinoid products. (J Emerg Med 2013;45:544.)
Friday, November 01, 2013
Two major problems occur with anaphylaxis: recognition and management. The recognition problem is related to the very confusing and complex diagnostic criteria that have been established. (Ann Emerg Med 2006;47:373.) I carefully reflected on these criteria, and several years ago simplified the definition for myself and our residents: If two organ systems are involved, then one has met the definition of anaphylaxis.
Adapted from Ann Emerg Med 2006;47:373.
This definition approximates the criteria and the most common presentations of anaphylaxis quite well. It doesn’t exactly fit the isolated reduced blood pressure after exposure to a likely allergen, but that scenario seems to be relatively uncommon and relatively obvious diagnostically. Nevertheless, the presence or absence of hypotension is a critical decision in managing anaphylaxis. Diagnosed anaphylaxis should be divided into another two distinct categories: anaphylaxis without hypotension and anaphylaxis with hypotension. This fork in the road becomes important in managing anaphylaxis with epinephrine.
The management problems associated with anaphylaxis boil down to epinephrine. The recommendation to administer H1 and H2 blockers comes easily to most of us, but the epinephrine recommendations are downright confusing. There is a healthy and deserved respect and fear of epinephrine. Anyone who has practiced emergency medicine for any period of time has one or more stories to tell about epinephrine administration problems.
Dosing epinephrine can be extremely confusing because of different concentrations, different dosing settings and different routes of administration. The following information deserves a much more in-depth discussion, but the mnemonic “One, Two, Three, Four” provides a structured and easily recalled format for managing an anaphylaxis patient, and is suggested as a way to organize one’s thoughts on administering epinephrine in anaphylaxis.
One mL dose of epinephrine concentrations
• 1:1,000 concentration = 1000 mcg/mL (or 1 mg/mL)
• 1:10,000 concentration = 100 mcg/mL (or 0.1 mg/mL)
• 1:100,000 concentration = 10 mcg/mL (or 0.01 mg/mL)
Epinephrine concentration per milliliter.
Much of the confusion around administering epinephrine exists because three different concentrations of epinephrine can be used for anaphylaxis. Understanding how many micrograms are in one milliliter (mL) of the three concentrations helps one comprehend the dosing recommendations for epinephrine for each clinical category or level of anaphylaxis severity.
Two Clinical Categories of anaphylaxis
• Anaphylaxis without hypotension
• Anaphylaxis with hypotension
The presence or absence of hypotension in anaphylaxis is a critical decision element that guides the route of epinephrine administration. Anaphylaxis without hypotension is treated immediately with intramuscular epinephrine. On the other hand, documented hypotension should immediately prompt the health care provider to begin preparing immediately for the intravenous infusion of epinephrine and saline by placing large-bore intravenous catheters while still administering the first dose of intramuscular epinephrine. The patient also should be placed into a supine position with legs elevated. Usually these maneuvers are sufficient, but when they aren’t, these simultaneous preparations to administer intravenous epinephrine can be life-saving.
Three epinephrine concentrations used in anaphylaxis treatment
• 1:1,000 → Anaphylaxis without hypotension (IM)
• 1:10,000 → Cardiac arrest with anaphylaxis (IV)
• 1:100,000 → Anaphylaxis with hypotension* (IV)
* Anaphylaxis with hypotension should initially be treated with IM epinephrine, the 1:1000 concentration. The intravenous route for epinephrine must be considered when hypotension persists.
Three epinephrine concentrations used in anaphylaxis management.
These three concentrations are simply sequential epinephrine dilutions by factors of 10 beginning with the 1:1000 concentration. The higher concentration of intramuscular epinephrine (1:1000) allows smaller fluid volumes for injection into the muscles. The more dilute epinephrine concentrations (1:10,000 and 1:100,000) are most appropriate for intravenous administration during advanced cardiac life support or pulse dosing for children, adolescents, and adults.
Note: The 1:1000 comes in a small 1 ml glass vial, and is used also to treat asthma with IM drug. The 1:10,000 is the 10 ml prepackaged vial kept in crash carts for CPR. The 1:100,000 must be mixed by the clinician, and is not commercially available.
Pulse dosing of epinephrine for anaphylaxis with mild hypotension using the most dilute epinephrine formulation (1:100,000) is also proposed as a treatment option. Pulse dosing of vasopressors is a recognized adjunct for hypotension management, but it is generally not taught in managing anaphylaxis. The use of continuous intravenous infusions of epinephrine for persistent hypotension is more often recommended, but its administration is potentially delayed by the time demands associated with the preparation processes.
The preparation of epinephrine for pulse dosing, however, is simple and rapidly accomplished. Pulse dosing allows minute-to-minute, manual management of the patient’s hypotension and increasing the epinephrine doses as indicated by the patient’s condition. This concentration is not commercially available, but it is easily prepared by the clinician. It is prepared by filling a 10 mL syringe with 9 mL normal saline. Draw up 1 mL of epinephrine from a cardiac (ACLS) ampule (1:10,000), inject this amount into the 10 mL syringe, and shake well. This creates 10 mL of epinephrine with 1:100,000. Now one can pulse dose 5-10 mcg (0.5 to 1 mL or more if clinically indicated) every few minutes with a syringe epinephrine concentration of 10 mcg/mL. Pulse dose epinephrine can also be administered manually as a continuous infusion. Pulse dose epinephrine can be the intermediate step to starting a continuous infusion that is titrated up or down.
How to mix 1:100,000 epinephrine for pulse dosing of anaphylaxis associated with hypotension.
Four levels of severity that guide epinephrine concentration and dosing used.
* Up to the entire syringe (10 ml or 100 mcg).
** These guidelines recommend the ACLS bradycardia epinephrine infusion dosing: 2-10 mcg/min.
This severity staging table is adapted from a grading system described in Lancet in 1977 for anaphylactoid reactions. (Lancet 1977;1(8009):466.) Other authors have also created similar grading systems for generalized hypersensitivity reactions. (J Allergy Clin Immunol 2004;114(2):371.)
Descriptions of the clinical presentation are linked to the recommended treatment, administration routes (intramuscular, intravenous, pulse dosing, etc.), epinephrine concentrations, specific dosing information, and frequency of administration.
* If hypotension persists, escalate pulse doses of epinephrine by two or three times (0.2 mL to 0.3 mL/kg/minute).
** Standard recommendation for pediatric epinephrine infusion is 0.1 to 1.0 mcg/kg/minute.
Relative amounts of epinephrine recommended for each severity stage of pediatric anaphylaxis.
The intramuscular dose of epinephrine would be administered first in almost all settings, as with adults, because it is the most familiar and most easily prepared (and frequently all that is needed). Immediate preparations for intravenous epinephrine should be started, however, if stage II or III anaphylaxis is not responsive to the intramuscular preparation.
The pulse dose epinephrine concentration can be used for children as well as adolescents and adults. Anaphylaxis with hypotension in children can also be treated with a continuous epinephrine infusion and the standard dosing is 0.1-1 mcg/kg/min titrated to effect. Pulse dosing, however, is potentially more timely and appropriate for the hypotensive child. The preparation of the pulse dose epinephrine concentration is the same for adults and children. The smaller pulse doses for a child would be 0.1 ml/kg/dose of the 1,100,000 pulse dose concentration. This amount is 0.001 mg/kg or 1 mcg/kg (compare with 10 mcg/kg for PALS dosing which is 0.1 mL/kg of the 1:10,000 concentration).
The administration per minute should be guided by keeping in mind the standard dosing of the pediatric continuous epinephrine infusions of 0.1 to 1 mcg/kg/min titrated. Both of the recommended pulse dose calculations per minute for adults and children start the intermittent intravenous epinephrine at the high end of the continuous epinephrine infusion recommendations. This is considered appropriate because hypotension associated with anaphylaxis is notoriously resistant to epinephrine administration, and at times it will be clinically appropriate to double or triple the pulse dose epinephrine in Stage III anaphylaxis. If a child progresses to cardiac arrest, pediatric ACLS dosing for cardiac arrest is 0.01 mg/kg or 10 mcg/kg (0.1 mL/kg of 1:10,000) and can be repeated every three to five minutes.
Charles Moore, MD, the chief resident in emergency medicine at Georgia Regents University, contributed editorial assistance for this post.
Thursday, October 03, 2013
A tripwire is usually a wire stretched near ground level to ensnare someone or to activate a booby trap or detonate explosives, and some chief complaints come with their own built-in tripwires that should cause emergency physicians to stop dead in their tracks. Acute scrotal pain without a doubt is one of those chief complaints. Torsion of the testicle is not the only cause of acute scrotal pain, but it is the one that emergency physicians cannot afford to miss. Unfortunately, this condition comes with an impressive number of tripwires capable of bringing down even the most experienced clinicians:
• Clinical Overlap: The clinical presentation of testicular torsion overlaps significantly with other more benign causes of acute scrotal pain.
• Physical Examination: The physical examination for testicular torsion is not always reliable.
• Pain Honeymoon: The pain level associated with testicular torsion waxes and wanes; some patients seem to have a pain honeymoon.
• Atypical Presentations: Atypical presentations of testicular torsion are not uncommon.
Clinical Presentation Overlap
Other conditions such as epididymitis or torsion of the appendix can mimic testicular torsion and vice versa. It seems that presentations of epididymo-orchitis (EO) or torsion of the appendix (TAT) more commonly mimic testicular torsion (TT), but gradual onset and absence of nausea and vomiting are also reported with testicular torsion. Cass et al reported that 16 percent of their patients with testicular torsion had a gradual onset, and sudden onset was described in 51 percent of their patients with acute epididymitis. (J Urol 1980;124:829.)
Mushtaq et al reported documented vomiting in 33 percent of the testicular torsion patients and 14 percent of the epididymitis-orchitis patients. (ANZ J Surg 2003;73[1-2]:55.) Waldert et al reported nausea and vomiting in 32 percent of TT patients, three percent of TAT patients, and 12.5 percent of EO patients. (Urology 2010;75:1170.) The overlap in clinical presentation between testicular torsion and other less urgent conditions is a major tripwire capable of deceiving the very best.
The physical examination can be confirmatory for testicular torsion if one actually palpates the testicle. Simply looking at the scrotum is almost never helpful early in the disease process. On the other hand, the visual diagnosis of a problem becomes a more realistic possibility once tissue edema, hydroceles, and associated erythema of the overlying skin have developed and the testicle is necrotic. Nevertheless, visual examination of the scrotum will be deceptively benign in the acutely torsed testicle. This will be especially true when the scrotum is retracted by the dartos muscle, making the torsed testicle appear similar to its domestic partner.
Early testicular vascular congestion, abnormal lie, and disproportionate tenderness become apparent only with palpation of the scrotal contents. Unfortunately, the epididymis can also be markedly swollen and tender in TT patients on examination and ultrasound, causing further concern about the diagnosis. Multiple ultrasound studies have documented enlargement of the epididymis in testicular torsion. (Urology 2010;75:1170; Pediatr Radiol 2005;35:302; J Urol 1997;157:1369.) A transverse lie is common in testicular torsion, but so is a vertical lie. (Br J Urol 1988;61:148; Med Princ Pract 2005;14:177.) Abul et al reported that a transverse elevated lie of the testis was observed in only four (36.4%) TT patients. (Med Princ Pract 2005;14:177.)
Another physical examination tripwire is the belief that the presence of a cremasteric reflex essentially rules out a testicular torsion. In fact, a number of series report that 100 percent of patients presenting with testicular torsion lost their cremasteric reflex. (Indian J Pediatr 2009;76:407; J Urol 1984;132:89; J Pediatr Surg 1984;19:581.) And these authors tout the loss of the cremasteric reflex as a highly reliable sign diagnostic for testicular torsion. Unfortunately, this isn’t true. Besides being a subtle and fickle examination finding that often requires a good imagination, it is absent in many normal males and in many patients with TAT and EO. (J Pediatr Surg 2001;36:863; J Urol 1994;152[2 Pt 2]:779.)
Most importantly, however, is the fact that the cremasteric reflex is commonly absent in scrotal pain conditions other than TT, but it is also persistent in a significant number of patients with testicular torsion. Multiple small studies describe patients with dead or dying testicles who still had a cremasteric reflex. (Pediatr Surg Int 2006;22:413; Pediatr Surg Int 1999;15[5-6]:353.) The bottom line is that the cremasteric reflex cannot be relied on to evaluate patients presenting with scrotal pain.
I have had the opportunity to review a number of testicular torsion cases over the past few years that have gone to litigation and after a pain honeymoon has become apparent. In fact, the patient may have several days of relatively normal activity and a full night's sleep before the testicle becomes markedly swollen and painful again. The patient returns at this time walking with the broad gait of a saddle-sore cowboy. More specifically there appears to be a period of decreased pain as the testicle becomes increasingly ischemic although the first episode of pain was excruciating at onset. Watch a video of a patient with a 720-degree torsion and minimal pain.
The most common atypical presentation is isolated abdominal pain. Lower abdominal pain without reported pain in the testicle is a formidable tripwire. Negative CT scans of the abdomen are common, and even surgery to remove the appendix has been reported. Cass et al reported that 12.5 percent of their TT patients presented with only abdominal or inguinal pain. (J Urol 1980;124:829.)
Anderson et al reported that 32 of 597 patients (5%) with testicular torsion did not describe any scrotal pain, and 22 percent of the entire group had abdominal pain, which often preceded and exceeded the scrotal pain. (Br J Surg 1988;75:988.) In fact, the appendix was removed in three patients before the true diagnosis was made. Similarly, inguinal pain alone was described in six percent of cases. (Br J Surg 1988;75:988.)
A more complete discussion of the myths associated with diagnosing and managing testicular torsion can be reviewed in an article I published in January 2012 that can be accessed at http://bit.ly/19w9y8P.
Tuesday, September 03, 2013
Many of my pediatric patients with nasal foreign bodies present to the emergency department for chief complaints unrelated to the nose. The young man shown below, for example, presented several years ago for the evaluation of dog bite wounds to the face. I could see the telltale signs and symptoms of a chronic unilateral nasal drainage the minute I walked in the room. (Figure 1.)
Figure 1. Nasal drainage is the telltale sign of a nasal foreign body.
I questioned the patient and his father, and they offered no history to confirm insertion of a nasal foreign body. Nevertheless, a wad of mummified Halloween candy wrappings inserted a month earlier was removed after significant effort that required the assistance of our ENT colleagues. (Figure 2.)
The family will uniformly complain that the patient has an offensive body odor after the nasal foreign body has been present for weeks to months. A purulent unilateral nasal drainage will also be observed and reported. The foreign body can be found in any area of the nasal cavity, but will most predictably be located below the inferior turbinate or immediately anterior to the middle turbinate.
Three different types of techniques are used to remove a foreign body: manual removal with a curette, forceps, hemostats, or suction; positive air pressure techniques, and balloon catheter techniques. The equipment that may be required for the different techniques are:
• Bulb syringe
• Katz extractor
• Alligator forceps
• Bayonet forceps
• Suction tip (e.g., Frazier)
• Mother’s mouth
• Topical skin adhesive
Patient cooperation and preparation are crucial. Procedural sedation is often required in the ED, but sedation with nasal midazolam alone may be sufficient. Apply it with an atomizer. The affected naris should be treated with a topical nasal vasoconstrictor such as oxymetazoline, and the mucosa should be anesthetized with a patient-weight-appropriate amount of 4% lidocaine, again using the atomizer.
A nasal speculum, otoscope, and head lamp are other essential tools for visualizing and performing the procedure. The patient should be positioned and his head immobilized, and then various tools — alligator or bayonet forceps, wire loops, or right-ankle hooks — can be used to remove the object manually. Bending the tip of an 18-gauge needle will create a cheap and effective right-angle hook. (Figure 3.)
Figure 3. Right-angle hook made from the tip of an 18-gauge needle.
Common complications are bleeding, barotrauma, and dislodged foreign bodies that can be aspirated or swallowed. Mucosal trauma and epistaxis are common occurrences, but can often be avoided or minimized by careful preparation of the nasal mucosa. (Figure 4.)
Dislodged foreign bodies are a real concern, and airway compromise is always a risk. I clearly remember one such event early in my career. I had successfully removed wood screws from the nose of a screaming toddler, but they dropped from my hemostat directly into her open mouth. She promptly swallowed them, and after a few anxious moments, we were able to confirm that the screws had safely made their way to the child’s stomach and not the right main stem. Safe passage of the screws occurred several days later.
Figure 4: Epistaxis following attempts at removing a well-entrenched foreign body.
Pediatric nasal foreign body removal is clearly within the realm of emergency medicine, but if you encounter a stubbornly entrenched foreign body that resists all your tricks, it is important to request that your ENT colleagues help out with their tools of the trade.
Wednesday, July 24, 2013
My suspicions smoldered for years. I even doubted myself and thought maybe the problem resided with me. My self-doubt was with my skills at removing entrapped skin from zippers. Zipper mechanisms on rare occasion become attached to penile skin, more commonly in prepubertal males but also in grown men. Every major clinical procedures textbook has instructed us for decades to use wire cutters to release the median bar of the zipper mechanism to release entrapped skin and clothing. I have never been successful using this approach, and the cause of the failure was not clear. Two years ago, however, I had a sentinel patient whose zipper dilemma totally clarified the source of the problem. The so-called authoritative textbooks were just plain wrong.
My patient was a middle-aged man who had been drinking at a bar with a lady friend. A trip to the restroom resulted in entrapping his penile skin, so he pulled out his knife and desperately cut the zipper out of his pants. Nevertheless, it was too late. His bladder had emptied, and his date night was over. He spent a fitful night trying to remove the zipper mechanism on his own, but then he gave up and presented to the emergency department. Here is where my personal crisis in faith began. No matter how hard we tried, we simply could not cut through the median bar of the zipper mechanism with our wire cutters. After an hour of trying, we finally zipped up the detached zipper through the remaining teeth and the skin was successfully released.
Still stinging from this failure, I reviewed the literature and to my surprise found that this recommended technique is rarely successful. I then experimented with the procedure using several zippered jackets languishing in the lost and found box in our pediatric emergency department. The wire cutters simply couldn’t cut through the median bar of the zippers. We recorded a video of this experiment so you could learn the truth for yourself.
So, what does work? Wedging a flat head screwdriver between the zipper plates and prying them apart worked quite well. The zippered teeth and entrapped skin can be removed once the plates are separated. Our review of the literature on this topic was published in the Pediatric Emergency Care. (2011;27:451.) Other techniques reported to work are described in the article, which can be accessed for free at http://bit.ly/12DYAZS or http://bit.ly/1ao25do.
“A new nonsurgical technique for managing zipper injuries,” Eur J Emerg Med Aug 29, 2013 (Epub ahead of print). Abstract: http://bit.ly/14yZqP3.
This study advocates using a new technique to release of entrapped penile skin from a zipper by cutting the zipper tape and teeth immediately superior and inferior to the zipper connector and using a needle holder to pull the zipper apparatus apart following the application of lubrication and appropriate use of local analgesia.
Dr. Mellick comments: The technique described involves completely cutting out the zipper leaving minimal zipper tape, lubricating and then tugging on the remaining zipper tape while stabilizing with your hand. We recommended separating the zipper mechanism with a flat head screw driver, but this recommendation seems to be an excellent alternative method.