M2E Too! Mellick's Multimedia EduBlog
The M2E Too! Blog by Larry Mellick, MD, presents important clinical pearls using multimedia.

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.

Thursday, June 1, 2017

Are you one of those clinicians who frequently finds himself frustrated with asthma patients who improve to a point but not enough to discharge home? Even though this has to be a common problem, no one seems to talk or write much about it. I was feeling deeply frustrated about these patients, and it led me to serious clinical introspection. Why does everyone write about the crashing asthma patient, but hardly anyone addresses the problematic patient with improving but recalcitrant bronchospasm?

Most articles typically cover every available therapeutic option, including the proverbial “kitchen sink” for managing severe asthma emergencies. Kitchen-sink recommendations generally include continuous albuterol nebulization, intravenous magnesium sulfate, intramuscular epinephrine or terbutaline, noninvasive (NIV) positive pressure ventilation, helium-oxygen administration, and ultimately intubation and ventilation using ketamine. It is time, however, to give “out-the-door” asthma management a little respect and attention.

Typically, emergency department asthma protocols will include repeated albuterol treatments with at least two of those treatments combined with nebulized ipratropium bromide. Corticosteroids are also administered orally or intravenously. When these initial interventions fail, most practitioners continue to treat the bronchospasm with additional doses of albuterol and ultimately continuous nebulization of the β2 agonist.

This is where logic seems to fade. Continuing to hammer the patient with the same medication and the same receptors seems a little illogical. Wouldn’t it make more sense to switch to other medications that target different pulmonary smooth muscle receptors and the inflammatory factors associated with the bronchoconstriction? Nevertheless, most clinicians maintain a relatively limited number of therapeutic tools in their toolbox when it comes to routinely managing asthma. Consequently, many patients are ultimately admitted to the hospital for ongoing management when some of them could have been discharged home.

What other options do we have? Truthfully, a lot of new magic bullets don’t really exist for acutely managing asthma. What about looking again at some of the older, proven interventions that have been benched for the newer, shinier treatments? Maybe we should be treating the known common inflammatory factors associated with asthma more aggressively. The following treatment options seem to be working anecdotally, especially for my pediatric asthma patients. Beginning with the strongest evidence first, these tools for your asthma tool box may help you get a few more patients home.

Inhaled Corticosteroids
One of the best supported asthma management options is inhaled corticosteroids. The literature is consistently positive, and appears to support nebulized steroids in addition to other systemic corticosteroids. In our pediatric emergency department, we typically give one dose of oral dexamethasone (0.6 mg/kg) up to a maximum of 16 mg for asthma exacerbations that have been ongoing for one to two days and are resistant to home management. Other options are effective, but my choice for an inhaled or nebulized corticosteroid is 0.5 mg of budesonide. A review article and a Cochrane review of the benefits of inhaled corticosteroids provide supporting evidence for routinely adding this intervention for patients with recalcitrant bronchospasm. (Respir Med 2007;101[4]:685; Cochrane Database Syst Rev 2012;12:CD002308.)

Intramuscular or Nebulized Epinephrine
Epinephrine, of course, has always worked for bronchospasm. Older clinicians will remember when subcutaneous epinephrine administered every 20 minutes was one of the few treatment options available. Despite the tears caused by the painful injections, it worked. In fact, many older papers described injected and nebulized epinephrine as being therapeutically similar to agents such as terbutaline or albuterol. (Ann Allergy 1983;50[6]:398; Clin Pharm 1983;2[1]:45.) Besides having a few more side effects, epinephrine, a nonselective β2 agonist, also fell to the wayside because it was far easier and less objectionable to nebulize medications than give painful injections to children and adults. If they use it at all, most clinicians reserve epinephrine for the patient presenting with severe and status asthma.

Nebulized epinephrine, however, probably works just as well as intramuscular epinephrine, and possibly delivers a greater quantity of epinephrine with minimal side effects. Both regular epinephrine (5 mg maximum) and racemic epinephrine (11.25 mg maximum) can be nebulized to treat asthma and croup. It seems to be much easier to use the commercially supplied preparations of racemic epinephrine for nebulization current available. Again, there is good evidence for the effectiveness of nebulized racemic epinephrine to treat asthma. (CJEM 2007;9[4]:304; Acad Emerg Med 2000;7[10]:1097; Am J Emerg Med 2006;24[2]:217; J Crit Care 2004;19[2]:99; Allergy 1980;35[7]:605.) When the effectiveness of nebulized albuterol seems to have petered out and you sense a need for something else, consider a trial of nebulized racemic epinephrine.

Antihistamines
The triggers of an asthma exacerbation are commonly divided into allergic and nonallergic etiologies. In fact, it is possible that allergies trigger asthma attacks in 60 to 90 percent of children and 50 percent of adults. (Medscape. April 13, 2017; http://bit.ly/2oXKp4s.) Mite and cockroach antigens are known to increase asthma morbidity, and are commonly found in the environment. (J Allergy Clin Immunol 2015;136[1]:38.) Histamine is a known inflammatory mediator in the pathophysiology of asthma. IgE binds to high-affinity receptors on the surface of mast cells and basophils, leading to mast cell and basophil degranulation. Mast cell mediators, histamine, pro-inflammatory cytokines, and proteases are released, leading to an early allergic response.

Consequently, it seems intuitive that antihistamines could play a role in treating asthma. Unfortunately, evidence for the benefit of first-generation antihistamines in asthma is relatively limited. This may be secondary to the fact that antihistamines were avoided in asthma for many years. Clinicians were taught to avoid antihistamines out of concerns for possible drying and inspissation of airway secretions. Current research on second-generation antihistamines suggests benefit, however. (Am J Med 2002;113[Suppl 9A]:2S; Curr Opin Allergy Clin Immunol 2002;2[1]:53; Treat Respir Med 2006;5[3]:149; J Allergy Clin Immunol 2003;112[4 Suppl]:S96.) Clinical studies have shown mixed results, but no detrimental effects were noted. Despite weaker evidence, the addition of intravenous or oral antihistamines during an acute asthma event seems safe, reasonable, and disease mechanism-based. And it is possible that antihistamines could prove to be synergistic with other anti-inflammatory interventions.

Ibuprofen or NSAIDs
Another even more controversial option is the use of the anti-inflammatory drug, ibuprofen, in asthma. Ibuprofen is a nonselective inhibitor of the enzyme cyclooxygenase (COX), which is required for the synthesis of prostaglandins via the arachidonic acid pathway. This pathway is active in the pathogenesis of asthma. (Pharmacotherapy 1997;17[1 Pt 2]:3S.) (Figure 1.)

mellick-ibuprofen.png
Figure 1. Stylized cell depicting the mechanism of action of ibuprofen. (Pharmacogenet Genomics 2015;25[2]:96.)  Pharmacodynamics ©PharmGKB. Reprinted with permission from PharmGKB and Stanford University.

Ibuprofen is often immediately rejected as a therapeutic intervention for asthma because of concerns about exacerbating asthma in the context of aspirin sensitivity. Literature analysis seems to indicate that the use of ibuprofen in the pediatric population does not exacerbate asthma morbidity. (Paediatr Drugs 2004;6[5]:267; Clin Ther 2007;29[12]:2716.) As stated by one author: "Given the infrequent occurrence of aspirin/NSAID sensitivity in children with asthma, it seems reasonable to allow the use of ibuprofen in this population unless there is a personal or family history of aspirin-induced asthma. In addition, the inflammatory pathogenesis of asthma, anti-inflammatory effect of ibuprofen, and evidence suggesting ibuprofen may reduce morbidity in children with asthma raises the intriguing possibility that ibuprofen might actually have therapeutic benefit for at least some children with asthma." (Paediatr Drugs 2004;6[5]:267.)

A paper by Lesko, et al., stated that rather than supporting the hypothesis that ibuprofen increases asthma morbidity among children who are not known to be sensitive to aspirin, their study suggested that compared with acetaminophen, ibuprofen may reduce such risks. (Pediatrics 2002;109[2]:E20.) Finally, another study recommended that ibuprofen be withheld for at least 24 hours prior to investigations utilizing allergen bronchoprovocation because a single dose of ibuprofen was found to inhibit early and late asthmatic responses to allergen bronchoprovocation. (Allergy Asthma Clin Immunol 2016;12:24.) The evidence is limited, but ibuprofen should theoretically decrease the inflammatory factors causing bronchospasm in asthma through its actions on the arachidonic acid pathway.​

If you find yourself regularly frustrated with asthma patients who only partially improve, consider putting back into the game some or all of these older, previously benched bronchodilators and anti-inflammatory treatment modalities.




Wednesday, May 3, 2017

The differential list of potential causes of abdominal pain is pretty long. Like most differentials, though, it usually boils down to a handful of more common etiologies benign and serious. Potentially life- or organ-threatening conditions such as appendicitis, diverticulitis, or ovarian or testicular torsion simply cannot be misdiagnosed and usually aren't missed.

We frequently find ourselves walking into the patient's room at the end of an extensive and exhaustive workup and announcing the good news that the cause of the pain isn't one of these more serious causes. As emergency physicians working in an uncontrolled and tactical environment, we get used to reassuring patients that it isn't something serious even though we are unable to provide a definitive diagnosis.

If we admit it, deep down we share a little bit of the frustration expressed by our internist colleagues who by self-report experience a degree of psychic pain when stuck with a differential list instead of a definitive diagnosis for a patient's complaint. We may also find ourselves quietly avoiding our frustration with having exposed the patient to the CT scan's radiation or the expense of sequential tests such as a screening ultrasound only to find "enlarged lymph nodes," "a small amount of free fluid," or a few normal appearing ovarian cysts.

Epiploic appendagitis is one diagnosis, albeit rare, that allows the emergency physician to give the patient pretty much all-around good news. Making the diagnosis of this condition caused by a twisting or necrosis of the fat appendages hanging off the colon allows us to give the patient a definitive diagnosis and the good news that they have a condition that will not require admission or surgical intervention. In fact, the treatment for this condition is ibuprofen, rest, and time. Epiploic appendagitis can be responsible for an "acute abdomen" presentation, but the associated condition is self-limited and requires only pain and inflammation management. In fact, ibuprofen is frequently sufficient. The condition is rare enough that the few times that we've made the diagnosis before confirmation by CT scan were considered "high-five" moments. Most recently, the diagnosis was made in a 17-year-old boy sent to the emergency department because of suspicion for appendicitis. (See video​.)

What's the skinny on this condition that frequently causes your colleagues and the patient to correct your suspected mispronunciation of "appendicitis"?

-Epiploic appendagitis (EA) is frequently a condition unknown to clinicians. (AJR Am J Roentgenol 2009;193[5]:1243.)
-The term "epiploic appendagitis" is attributed to Lynn, et al., in 1956 who described a primary inflammatory disease of the fatty colonic appendages. (Surg Gynecol Obstet 1956;103[4]:423.)
-EA has other aliases such as appendicitis epiploica, hemorrhagic epiploitis, epiplopericolitis, or appendagitis. (Surg Gynecol Obstet 1956;103[4]:423.)
-EA is the result of ischemic infarction of an epiploic appendage following torsion or spontaneous thrombosis of the central draining vein.
-The epiploic appendages are finger-like projections of adipose tissue typically arranged in parallel rows along the colon. (Arch Surg 1985;120[10]:1167.)
-Numbering between 50 to 100, these appendages cover the entire adult colon but are larger and most abundant on the transverse and sigmoid colon.
-Epidemiologic studies suggest that the true incidence of EA is not known, but it has been reported in two percent to seven percent of patients initially suspected of having acute diverticulitis. (Nat Rev Gastroenterol Hepatol 2011;8[1]:45.)
-This condition usually occurs more commonly in men in the fourth and fifth decades of life, but also occurs in women and children.
-Sudden focal, nonmigrating lower abdominal pain and tenderness with a dull and colicky pain that waxes and wanes may be described by the patient. (Dig Dis Sci 2004;49[2]:347.)
-Ultrasound of EA has characteristic findings and MRI appears to be a reliable tool, but CT is the current imaging study of choice.
-Classically the findings of epiploic appendagitis on CT is a fat-density oval lesion called a “ring sign” consisting of a central fatty core (between 1.4 cm and 3.5 cm in length) surrounded by inflammation and located on the anterior aspect of the sigmoid colon. (Radiol 2005;237[1]:301; AJR Am J Roentgenol 2004;183[5]:1303.) A central dot corresponding to a thrombosed appendage vein is sometimes evident. (Radiology 1997;204[3]:713.)

When your colleagues try to correct your "mispronunciation" of appendicitis, your response should be, "Heck no, I meant to say appendagitis. Go look it up!"

Watch a video interview with a young patient with epiploic appendagitis.

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Friday, March 31, 2017

Hanging out with cardiopulmonary researchers effectively imprinted on my psyche that we fail our patients during cardiopulmonary resuscitation in many ways. Unfortunately, too many patients who could have walked out of the hospital after experiencing death don't because of our mistakes in CPR. It's critical to find the resuscitation sweet spot for each patient and to never waver during a CPR event. These are the ways we can kill our patients during cardiopulmonary resuscitation:

Too Slow or Too Fast

The recommended heart rate for cardiopulmonary resuscitation was 60 compressions/minute in 1960. (JAMA 1960;173:1064.) Observational human studies relating compression rate to outcomes, however, have established a sweet spot somewhere between 100 and 120 compressions per minute. (Crit Care Med 2015;43[4]:840.) External chest compressions are the primary intervention performed in cardiopulmonary resuscitation, and not doing them correctly has the greatest impact on the outcome. Without any doubt, compressing too slow or too fast is deadly during CPR.

Too Shallow or Too Deep

Part of the problem with compressing too fast is that the depth of compressions suffers dramatically, and the compressions become too shallow. (Crit Care Med 2015;43[4]:840.) Too deep compressions simply don't appear to add any benefit to resuscitation end-points and may cause unwanted trauma such as broken ribs and increased intracranial pressure (ICP), resulting in reduced cerebral blood flow. Compressions that are too shallow are simply not effective in moving blood into and out of the heart. The AHA recommended compression depth is 2.0 to 2.4 inches or 5 to 6 centimeters. (http://bit.ly/2mZwT3U.) The evidence is strong that the depth of chest compressions makes a difference in survival outcomes. (Circulation 2014;130[22]:1962.)

Too Many or Too Slow

It is almost counterintuitive to think that breathing more frequently for a patient during CPR has the potential to guarantee the patient a trip to the morgue. Ventilating too rapidly or prolonging slower respirations has a dramatic impact on physiology that has been repeated and easily demonstrated in resuscitation laboratories. Positive pressure ventilation in the laboratory increases intrathoracic pressure and intracranial pressure and decreases venous blood return to the right heart.

A decrease in cerebral and coronary artery perfusion pressure occurs during the ventilation process. We need to look at ventilations during cardiopulmonary resuscitation as a necessary evil that they temporarily negate the benefits of our chest compressions while providing oxygen and keeping the airways open for gas exchange. Animal studies unequivocally demonstrate that high ventilation rates can be uniformly lethal in the ventricular fibrillation cardiac arrest model. (Crit Care Med 2004;32[9 Suppl]:S345; Circulation 2004;109[16]:1960.)

Leaning on the Chest

Not allowing full recoil can also be detrimental to effective CPR. It is a subtle and easy not to recognize the error of continuing to put downward pressure and prevent full recoil of the chest. This happens when the rescuer continues to lean on the chest between compressions. Incomplete chest wall recoil or leaning increases ICP and lowers right atrial pressure, decreasing cerebral and coronary perfusion pressures.

Too Many Interruptions

Too many and too long interruptions can negate the benefits of performing spot-on chest compressions. These interruptions ultimately result in the same outcomes as compressing the chest too slowly. No compressions mean no heartbeat.

Giving Up Too Soon

Just how long should we perform cardiopulmonary resuscitation? This partially depends on the patient and his condition. Longer CPR attempts are appropriate from a prehospital perspective, and excellent neurologic recovery is possible for those with the best conditions of shockable rhythms and bystander resuscitation. (Circulation 2016;134[25]:2084.) Hospitalized patients also appeared to benefit from longer CPR, which was associated with greater return of spontaneous circulation and survival to discharge even for the patients in asystole. Efforts to systematically increase the duration of resuscitation could improve survival in this high-risk population. (Lancet 2012;380[9852]:1473.)

In reality, the brain is probably a little more resilient than we think. Resuscitation researchers describe porcine research subjects that go about their activities of daily living after prolonged periods of ventricular fibrillation and delayed resuscitation. They also have scores of stories of human patients down for prolonged periods who received effective resuscitation and eventually recovered after prolonged periods of unconsciousness in the intensive care unit. (Resuscitation 2014;85[2]:211.) Reperfusion injury to the brain, however, does happen, and research on how to prevent such injuries is ongoing.

Too Slow Adaptation

It's true that adapting new technologies too soon or before they are adequately vetted with good research is potentially dangerous, but it is also true that good research based on bad CPR can slow the acceptance of potentially useful new resuscitation tools. (Resuscitation 2015;94:106; http://bit.ly/2mZSglK; N Engl J Med 2015;373[23]:2203.) Several decades of work has yielded irrefutable evidence that good things happen to the cerebral perfusion pressure and the coronary perfusion pressure with the impedance threshold device and active compression decompression CPR. (West J Emerg Med 2014;15[7]:803.) And elevating the head simultaneously with the application of an impedance threshold device also clearly improves those physiologic parameters that are associated with better outcomes. (Resuscitation 2016;102:29.) Evidence, finally, is accumulating to validate the decades of work of these resuscitation researchers. (Resuscitation 2017;110:95; Circ J 2016;80[10]:2124.)

Unfortunately, the confounding variables and uncontrolled environment of prehospital cardiac arrest research has slowed the validation and acceptance of important new techniques and technologies as well as something seemingly obvious such as continuous chest compressions during CPR. (Resuscitation 2015;94:106; http://bit.ly/2mZSglK; N Engl J Med 2015;373[23]:2203.)

A commentary by Goodloe, et al., addresses possible options to address the unique challenges of resuscitation research: "This is not to say that high-quality research attempts should not continue, but rather that treatments that appear beneficial to a consensus of resuscitation leaders should not be withheld until benefit is fully demonstrated in primary and confirmatory randomized controlled trials. The unwillingness to adopt new ideas and therapies until they are proven beyond any doubt via randomized clinical trials also holds back progress. Overwhelming evidence is often years in coming, and while we wait, patients die. The context in which resuscitation scientists work is dynamic, complex, and even sometimes chaotic, yet we have made great strides in discovering new processes and technologies that have resulted in better outcomes." (West J Emerg Med 2014;15[7]:803.)

CPR Physiology

Part of the problem with failure to perform the best CPR possible is that the vast majority of emergency health care providers probably operates with an incomplete understanding of the pathophysiology of cardiac arrest and the physiology of resuscitation. We are much more vulnerable to these mistakes without this complete understanding.

Watch a video showing how conventional CPR works — and doesn’t.​


Watch a video with tips for code team organization during​ CPR.



Wednesday, March 1, 2017

​A number of older clinical concepts may be unfamiliar to younger clinicians, but these clinical concepts are useful in pediatric medicine. Some of these concepts showed up in the medical literature for the first time nearly a century ago. Physicians should feel free to question the potential value and validity of older clinical concepts that aren't at the forefront of medical education, but my experience of more than 30 years practicing pediatrics and emergency medicine has repeatedly affirmed to me that these are valuable in emergency medicine.​

Parenteral Diarrhea

The concept of parenteral diarrhea has been around for at least a century. (Can Med Assoc J 1922;12[8]:554; Proc R Soc Med 1944;37[9]:479; Pediatrics 1948;2[5]:525.) It is often not recognized, acknowledged, or discussed as an important clinical entity, however. This type of diarrhea is caused by infections outside the gastrointestinal tract. The pathophysiology is unclear, but infections elsewhere in the body such as otitis media or (more frequently) urinary tract infections are often associated with diarrhea.

The diarrhea, however, can be characterized as different from the diarrhea patterns commonly seen with gastrointestinal diseases. Parenteral diarrhea is typically only two or three loose stools a day rather than the five to 10 watery stools seen with most cases of acute gastroenteritis. Parenteral diarrhea can also occur in concordance with occasional vomiting and fever. I have seen this pattern so many times that I immediately begin looking for other etiologies when parents describe only two or three episodes of diarrhea a day.

Unfortunately, this diarrhea presentation is frequently labeled as viral gastroenteritis, and associated infections are not sought. My experience is that urinary tract infections are the most common infection presenting as parenteral diarrhea. Of concern is that 60 percent of febrile urinary tract infections in children are upper tract disease or pyelonephritis. I am confident that thousands of pediatric urinary tract infections have been missed because the associated parenteral diarrhea served as a red herring that befuddled the clinician. My investigations have been rewarded scores of times when following this clinical clue. Parenteral diarrhea is admittedly not at the forefront of clinical teaching, but it is found in current editions of reputable pediatric textbooks such as Fleisher and Ludwig's Textbook of Pediatric Emergency Medicine.​

Conjunctivitis-Otitis Syndrome

Another clinical concept that doesn't seem to get a lot of respect is the conjunctivitis-otitis syndrome. The association of otitis media and conjunctivitis has been described since the early 1980s. (Pediatrics 1948;2[5]:525.)

What is unique is the temporal association of the two infections. The infectious agent is most commonly nontypable strains of Haemophilus influenza. (Pediatrics 1982;69[6]:695; Pediatrics. 1985;76[1]:26.) The role of sinusitis in this association is suspected, but doesn't seem to be widely discussed. My experience is that the conjunctivitis-otitis syndrome can often be diagnosed from across the room. These children will have impressive amounts of purulent drainage from their reddened eyes and ears. The amount of drainage and crusting around the eyes is consistently more dramatic than that seen with typical viral infection. A history that sounds like sinusitis with nasal drainage longer than 10 days is often associated in my clinical experience. Polymyxin B/trimethoprim provides reasonable coverage against the ocular pathogens, and amoxicillin/clavulanate should be used for the sinusitis.​


Double Sickening

Double sickening is currently seen mostly in patients with sinusitis. Historically, it is seen in a clinical setting where the patient is apparently improving or stable and then suddenly worsens. Sinusitis commonly presents with double sickening, but bacterial pneumonia also presents with this clinical pattern. (Clin Infect Dis 2012;54[8]:e72.)

These patients typically have three to four days of an upper respiratory tract infection and appear to be improving. Then they suddenly have a fever, and the patients appear and feel sicker. The bottom line is that double sickening is a valuable clue that should prod the clinician to dig a little deeper looking for sinusitis or to order imaging searching for evidence of pneumonia.

High-quality randomized controlled trials are practically nonexistent for important clinical concepts with only older observational studies available. Nevertheless, these older clinical concepts have withstood the test of time, have validated themselves clinically, and deserve respect.

This video shows another oldie but goodie tip for how to position a child properly for ear cleaning.​


Listen in as Dr. Mellick talks with a mother about her daughter's double sickening.​

mellick double sick.jpg


Wednesday, February 1, 2017

I want to reawaken awareness of a disappearing but highly contagious infectious disease — varicella. Thanks to immunizations for the wild-type varicella virus and shingles, or herpes zoster, younger health care providers are less aware of the appearance and clinical presentations of this viral infection.

Presentations of this viral disease have markedly declined and presentations are often atypical since the advent of immunizations for varicella in 1995. This DNA virus within the herpes virus family is generally a mild childhood disease but can wreak physical havoc in adults, especially pregnant women. Immunosuppressed adults and children can also experience life-threatening complications.

Thankfully, the rate of infection, hospitalizations, and mortality have all declined. Nevertheless, we should not let our guard down. The disease is still out there and presents to the emergency department in less obvious or clear-cut presentations, ready to trip up the unsuspecting clinician.

Most recently, a 6-year-old boy who had been vaccinated presented to our pediatric emergency department with the virus. I treated a febrile girl on chemotherapy for acute lymphocytic leukemia during the same shift, and one of the nurses working with us was pregnant. Thankfully, the infectious varicella patient did not come into contact with either of them. Nevertheless, the story could have been very different.

Chickenpox is highly contagious, and secondary attack rates in households are as high as 90 percent. (MMWR Recomm Rep 1996;45[RR-11]:1.) Transmission is by contact with aerosolized droplets from nasopharyngeal secretions or by direct contact with vesicle fluid from skin lesions.

Again, the problem is that we don't see as many disease presentations of this virus anymore, and varicella has dropped way down on our differential for rashes presenting to the ED. Our previous hyper-awareness of the disease has lessened, and immediate infectious disease precautions may not be as rapidly activated.

The typical chickenpox presentation is a generalized pruritic rash in a febrile child that begins as macules on the head, chest, and back after a short prodrome. The rash then spreads to the rest of the body in successive crops while transforming in appearance from macules to papules and vesicular lesions that eventually crust over. New vesicle formation usually stops within four days, and most lesions are fully crusted by day six.

Breakthrough varicella infections are defined as an infection by the wild virus that occurs at least 42 days after vaccination. The patient is typically afebrile or will have only a low-grade temperature, the number of skin lesions present are usually less than 50, and the duration of the illness is usually shorter. Consequently, the clinical diagnostic features are mild, and the diagnosis can be difficult to confirm on clinical presentation alone. Laboratory testing is becoming increasingly necessary. Unfortunately, this disease presentation remains contagious, as does herpes zoster or disseminated disease in immunosuppressed patients.

Treatment and prevention recommendations can be found in several excellent sources online:

Two rare presentations of the varicella virus are presented: disseminated varicella in a vaccinated 6-year-old with breakthrough chickenpox and an HIV patient with herpes zoster. Both patients had clinical presentations different from the now-uncommon garden-variety varicella.

Watch a video of disseminated varicella in an HIV patient.​

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Watch a second video of breakthrough chickenpox in a 6-year-old boy who was vaccinated.


Watch a third video showing several patients with typical varicella presentations. These children were filmed during a recent medical mission trip to Haiti where vaccination for varicella is neither mandatory nor widespread.