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.
Friday, February 28, 2014
The classic clinical presentation of infantile hypertrophic pyloric stenosis (IHPS) is an emaciated 3- to 6-week-old infant who has been experiencing immediate postprandial, nonbilious, projectile vomiting over a period of weeks. The infants remain hungry and demand to be re-fed after vomiting. Caucasian, full-term boys (4:1 to 6:1) tend to present with this condition most frequently, and these patients tend to be firstborns.
An olive-sized tumor can be felt to the right of the umbilicus, and this may best be palpable immediately after the infant has vomited. Visible peristaltic waves may also be noted. The infants are typically not otherwise ill-appearing, but they may be dehydrated with fretfulness, apathy, and loss of skin turgor. Click here to watch a video of a patient with pyloric stenosis.
The frequent and persistent vomiting puts these infants at risk for electrolyte abnormalities, specifically hypochloremia, hypokalemia, and metabolic alkalosis. Interestingly, the classic presentation of this condition would probably not include electrolyte abnormalities; they tend to be absent in the majority of patients studied. (Am J Emerg Med 1999;17:67; Pediatr Emerg Care 2013;29:465; J Pediatr Surg 1989;24:1250.) Significant electrolyte abnormalities tend to occur in infants undiagnosed for more than three weeks. Fortunately, infants are currently diagnosed earlier than in the past, and they tend to be less emaciated.
Normal laboratory values are the most common finding in hypertrophic pyloric stenosis, but it is clinically important to understand the electrolyte complications that can occur when a child is vomiting multiple times a day for weeks at a time. The loss of large amounts of gastric hydrochloric acid (HCL) results in the hypochloremic metabolic alkalosis. Renal potassium wasting appears to be the primary cause of the hypokalemia.
Another 5-week-old boy recently presented for prolonged vomiting. Sure enough, ultrasound of the gastric outlet demonstrated hypertrophy of the pylorus with a single wall thickness of 5 mm and increased length measuring up to 24 mm. The laboratory results were also notable. He demonstrated the classic findings of hypochloremic, hypokalemic metabolic alkalosis.
He also demonstrated hyperbilirubinemia, which turned out to be a great teaching point even for the old-timers. Hyperbilirubinemia is not uncommonly associated with IHPS, and is known as the icteropyloric syndrome. Unconjugated hyperbilirubinemia is more common than conjugated hyperbilirubinemia, and may be associated genetically with Gilbert syndrome. (J Pediatr 1990;117[1 Pt 1]:168; S Afr Med J 1986;69:446; Arch Dis Child 1999;81:301.)
Our ED was recently reminded that pyloric stenosis can occur in adults with exactly the same pattern of electrolyte abnormalities. The patient was a 34-year-old man with neurofibromatosis. His initial history did not confirm frequent episodes of vomiting, but his electrolyte pattern (see image below) made me think that his laboratory testing looked exactly like a pyloric stenosis patient. He later told us he had a history of intractable vomiting associated with gastric outlet obstruction secondary to pyloric strictures. Pyloric thickening in adults is associated with peptic ulcer disease, hypertrophic gastropathy, and carcinoma. (J Gastrointest Surg 2006;10:265.)
Hypochloremic, metabolic acidosis accompanied by hypokalemia is not present in every case of pyloric stenosis, but it can be helpful in confirming the diagnosis when it does occur. That goes for adults and infants.
Friday, January 31, 2014
Why I Disagree with the IDSA Guidelines for GAS in Children Under 3
IDSA Statement: Diagnostic studies for GAS pharyngitis are not indicated for children under age 3 because acute rheumatic fever is rare in children under 3 and the incidence of streptococcal pharyngitis and the classic presentation of streptococcal pharyngitis are uncommon in this age group [emphasis added]. Selected children under 3 who have other risk factors, such as an older sibling with GAS infection, may be considered for testing (strong, moderate).
The prevalence of GAS pharyngitis is significantly lower for children under 3; it ranges from 10% to 14% [emphasis added].
GAS causes only 5% to 15% [emphasis added] of cases of acute pharyngitis in adults.
My Beef: I don’t see any difference in frequency between adults and children under 3 years of age.
IDSA Statement: However, the prevalence of GAS pharyngitis is significantly lower for children under 3, ranging from 10% to 14%, and if a corresponding rise in ASO is required, the prevalence can be as low as 0% to 6% [emphasis added].
Such testing, however, is not useful in the diagnosis of acute pharyngitis because antibody titers of the two most commonly used tests, antistreptolysin O (ASO) and anti-DNase B, may not reach maximum levels until 3-8 weeks after acute GAS pharyngeal infection [emphasis added] and may remain elevated for months even without active GAS infection.
My Beef: The IDSA, to support its argument that GAS pharyngitis is uncommon in children under 3, throws in a seemingly unfair comment about a corresponding rise in ASO titer. Interestingly, in the same guidelines they recommend against testing [emphasis added] for these titers because they are usually negative for one to two months. And this will be especially true for children under 3 who are getting their GAS pharyngitis infections for the first time.
ISDA Statement: The risk of a first attack of ARF is extremely low in adults, even with an undiagnosed and untreated episode of streptococcal pharyngitis. Accurate diagnosis of streptococcal pharyngitis followed by appropriate antimicrobial therapy is important for preventing acute rheumatic fever; for the prevention of suppurative complications [emphasis added] (e.g., peritonsillar abscess, cervical lymphadenitis, mastoiditis, and, possibly, other invasive infections); to improve clinical symptoms and signs; for the rapid decrease in contagiousness; for the reduction in transmission of GAS to family members, classmates, and other close contacts of the patient; to allow for the rapid resumption of usual activities; and for the minimization of potential adverse effects of inappropriate antimicrobial therapy.
When a patient is prescribed an antibiotic for treatment of streptococcal pharyngitis, a clinical response is usually achieved within 24-48 hours of therapy. It is important to note that streptococcal pharyngitis is usually a self-limited disease. Even without treatment, fever and symptoms commonly resolve within a few days of the onset of illness.
My Beef: Acute ARF is also extremely low in adults. The IDSA justifies treating GAS in adults to prevent suppurative complications, reduce transmission, and allow rapid resumption of usual activities. Why not use the same arguments for children under 3?
Source: “Clinical Practice Guideline for the Diagnosis and Management of Group A Streptococcal Pharyngitis: 2012 Update by the Infectious Diseases Society of America.” Clin Infect Dis 2012:55: e86.
Original Blog Post: We see a definite uptick in Group A Streptococcal (GAS) infections of the pharynx at this time of year. This is one of those conditions that has been much debated over the years, and it seems more recently that there is a trend to downplay its overall importance. Nevertheless, timely treatment is still recommended to prevent acute rheumatic fever and suppurative complications such as peritonsillar abscesses, cervical lymphadenitis, and mastoiditis. (Clin Infect Dis 2012;55:1279.)
Thousands of papers have been written about this condition, but some important and fresh aspects of this infection still deserve discussion, such as treating children under 3, presentation, the Centor criteria, and treatment guidelines.
Blanket statements that the disease does not occur under age 3 are flat-out wrong. Careful analysis of the literature and current national guidelines actually acknowledge that GAS pharyngitis does occur in 10-14 percent of this age group, though a portion of these may be carriers based ASO testing. (Clin Infect Dis 2012;55:1279; Red Book: 2012 Report of the Committee on Infectious Diseases. Pickering LK, ed. 29th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2012.) Interestingly, this is not too different from the five to 15 percent of cases of GAS acute pharyngitis in adults. (Clin Infect Dis 2012;55:1279.)
These facts are frequently overlooked or misinterpreted, however. These resources do discourage routine testing of children under 3 because acute rheumatic fever and the incidence of the classic presentation of streptococcal pharyngitis are uncommon. (Clin Infect Dis 2012;55:1279; Red Book: 2012 Report of the Committee on Infectious Diseases. Pickering LK, ed. 29th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2012.)
Children under 3 do get the infection, however, and testing and treatment are recommended if a child has an older sibling with GAS infection. The Infectious Diseases Society of American and the American Academy of Pediatrics also acknowledge that exudative pharyngitis is rare in this age group, but GAS infection in children under 3 is often associated with fever, mucopurulent rhinitis, excoriated nares, and diffuse adenopathy, a condition called streptococcal fever or streptococcosis. (Clin Infect Dis 2012;55:1279; Red Book: 2012 Report of the Committee on Infectious Diseases. Pickering LK, ed. 29th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2012.)
“Toddlers (1 through 3 years of age) with GAS respiratory tract infection initially can have serous rhinitis and then develop a protracted illness with moderate fever, irritability, and anorexia (streptococcal fever or streptococcosis). Acute pharyngotonsillitis is uncommon in children younger than 3 years of age.” (Red Book: 2012 Report of the Committee on Infectious Diseases. Pickering LK, ed. 29th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2012.)
This presentation is uncommon in my experience, but it sure sounds like a presentation of pediatric sinusitis that should be treated with antibiotics. We should be very careful not to jump on the bandwagon with those who believe that GAS disease does not occur in children under 3.
I started out as a general pediatrician before I went back for training in emergency medicine, and I realized that the textbook descriptions of GAS pharyngitis were lacking. Almost all sources describe circumoral pallor attributed to sparing by the scarlet fever rash, but the commonly associated prominence and sometimes swelling or slight engorgement of the lips are typically not reported. (Pediatr Emerg Care 2009;25:621; http://bit.ly/1aH2N7W.) It continues to be my opinion that the rash sparing the areas surrounding of the lips and the increased prominence of the lips contribute to the appearance of circumoral pallor. (See photo below.)
Circumoral pallor and prominent red lips in a 15-month-old with GAS pharyngitis.
I have also noted over the years that not all scarlet fever is scarlet or like fine sandpaper in texture. In fact, the rash described as fine erythematous papules or “goose flesh on sunburn” in African-Americans is frequently diffuse, coarse papules that have less-than-obvious erythema. (See photo below.)
Coarse sandpaper appearance without apparent associated erythema.
The four-factor algorithm known as the Centor criteria predicts a positive result with an accuracy of 32-56 percent. (Med Decis Making 1981;1:239.) Current guidelines recommend using the rapid antigen detection test (RADT) the standard for the treatment decision. Researchers believe using the Centor criteria would result in treating an unacceptably large number of adults with non-streptococcal pharyngitis. Treatment is considered an undesirable result in this age group, which has a low prevalence of GAS pharyngitis and a very low risk of rheumatic fever or rheumatic carditis. (Clin Infect Dis 2012;55:1279.)
This makes a lot of sense in light of national data that show primary care physicians treat approximately 75 percent of their patients presenting with a sore throat with expensive broad-spectrum antibiotics. (Arch Intern Med 2006;166:1374.)
I have remained loyal to plain old, humble penicillin when treating GAS pharyngitis. GAS is still sensitive to penicillin, and it is the least broad-spectrum antibiotic of all the options. That is the case even with children when I use the liquid formulation. Many argue that the taste is a problem, but I have never been convinced that it caused a major problem with compliance. That may change now that all major guidelines give the option for once-daily amoxicillin at 50 mg/kg or a maximum dose of 1,000 mg or 1 g. (Clin Infect Dis 2012;55:1279; Red Book: 2012 Report of the Committee on Infectious Diseases. Pickering LK, ed. 29th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2012.)
I really like the idea of a single dose of a decent-tasting antibiotic for my pediatric patients with GAS pharyngitis, even the ones under 3.
Thursday, January 02, 2014
I recently spent some time with a group of academicians in Raleigh-Durham, NC. Jonathan Singer, MD, a recently clinically retired pediatric emergency medicine physician and faculty at the Wright State Emergency Medicine program, was part of the group. He has impressed me over the years as a tough, no-nonsense academician with a penchant for clinical photography and writing poetry and Broadway plays. The group got into a discussion about pediatric bowel intussusceptions during the meeting, and I was surprised to learn that Dr. Singer wrote one of the first papers describing the altered mental status associated with intussusception. (Pediatrics 1979;64:93; Pediatr Emerg Care 1987;3:118.)
I have always been fascinated by this presentation, but pediatric patients with altered mental status and bowel intussusception have escaped me over the years. Thanks to Dr. Singer and others who have highlighted this, however, I eventually had an opportunity to help one of our own.
Last year just before Christmas one of our nurses and her husband presented to the emergency department with their lethargic 7-month-old daughter. Their concerns were intermittent episodes of pain and that they could not keep her awake. She would briefly rouse, and then her head would immediately flop back down on her chest. I asked the resident working with me to do a rectal examination.
The stool on the glove was dark, soft, and bloody. (Figures 1 and 2.) Our diagnosis was made, and it all took place within a few minutes. The diagnosis happened so quickly that the distraught parents were incredulous at first and questioned the diagnosis. Air contrast enema confirmed our suspicions, and reduced the intussusception successfully. Watch a video of this sleeping child and the history as given by her mother.
Figure 1: Currant jelly stool with positive Hemoccult test.
Figure 2: Currant jelly stool passed by a patient with intussusception.
Diagnosing intussusception is frequently complicated by atypical presentations. The classic presentation of a relatively healthy 3- to 12-month-old presenting with paroxysms of abdominal pain associated with pulling up his legs, passing currant jelly stools, and a right upper quadrant palpable mass is straightforward, but these patients frequently contradict the textbook. (Pediatr Emerg Care 2012;28:842.) Lethargy or altered mental status appears to occur more commonly in children under a year of age, and less than 50 percent of presenting patients will have this complaint. (Pediatr Emerg Care 2012;28:842.)
The altered mental status or “knocked out” appearance was actually described before Dr. Singer’s articles, but the earlier articles mentioned lethargy in the context of sepsis, dehydration, and pre-shock. Thurston et al described 73 of 116 (63%) cases of acute intussusception in infants and children as “limp, drowsy, listless, lethargic, depressed, obtunded, stuporous, and unresponsive”. (Pediatrics 1980;65:1057; AMA Arch Surg 1953;67:68.) It was the Singer articles that correctly documented the altered mental status as occurring earlier in the course of the illness and recognized that the lethargy was a potent red herring. (See Figure 3.) The etiology of the altered mental status remains unknown, and toxins or endogenous opioids have been postulated. (Pediatr Emerg Care 1987;3:22; 1993;9:15.)
Figure 3: A common mnemonic for pediatriccoma adapted to include intussusception.
The timely diagnosis of intussusception is critical. I saw my first and only death from intussusception early in my career while serving as a pediatrician in Germany with the United States Army. A little girl had been sent home at least twice with the diagnosis of gastroenteritis. She returned vomiting bright red blood and died in the emergency department. Her autopsy demonstrated a large section of necrotic small bowel, the intussusceptum. The bottom line is that the presentation may not be classic and the only clue might be a comatose-appearing infant even though intussusception is the second most common cause of pediatric bowel obstruction. This presentation has the potential to trip up even the most astute clinician.
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.