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.

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.​


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.

Wednesday, January 4, 2017

Conversion reactions are commonly seen conditions in health care and come in various forms and presentations. Two common conversion reactions seen in the emergency department are conversion coma and psychogenic nonepileptic seizures (PNES). Both mimic life-threatening conditions and require rapid differentiation. Premature anchoring and wrong diagnoses can result in potentially harmful outcomes or expensive and unnecessary procedures, workups, and evaluations.

Conversion disorder, or functional neurological symptom disorder, is categorized under the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition, (DSM-5) under the category of "Somatic Symptom and Related Disorders." Conversion disorder is characterized by physical symptoms or deficits affecting voluntary motor or sensory function that resemble those of a nervous system disorder. Common examples of conversion symptoms are blindness, diplopia, paralysis, amnesia, coma, aphonia, seizures, pseudocyesis, and others. These physical signs and symptoms are typically triggered by emotional or mental factors such as conflict or other stressors. Unlike factitious disorders and malingering, the symptoms of somatoform disorders are not intentional or under the patient's conscious control.

Psychogenic Nonepileptic Seizures (PNES)

Patients presenting with PNES may show symptoms that look similar to those of epileptic seizures. They can mimic absence seizures, complex partial seizures, or tonic-clonic seizures. Abnormal brain electrical discharges are not the cause of PNES, however, and this can be confirmed with an EEG.​

Many patients with PNES will have a specific traumatic event, such as physical or sexual abuse, incest, divorce, or the death of a loved one. My most recent patient with psychogenic nonepileptic seizures was found "seizing" in the bathroom outside of the intensive care unit where her daughter, the victim of a home invasion and multiple gunshot wounds, was being treated. Characteristics of patients with PNES can include the following:

  • Side-to-side shaking of the head
  • Bilateral asynchronous movements (e.g., bicycling)
  • Limb or truncal movements
  • Facial movements with or without movements of the limbs or trunk
  • Weeping or stuttering
  • Arching of the back
  • Preserved awareness
  • Eyelid fluttering
  • Episodes affected by bystanders (intensified or alleviated)
  • Tongue-biting and infrequent incontinence

Conversion Coma

Patients presenting in a comatose state that is, in reality, a conversion disorder often have characteristic findings. They can be extremely difficult to differentiate from other more serious causes of coma. We typically use nociceptive or noxious stimuli to help differentiate the etiology of the altered mental status, but other history and physical signs and symptoms can be helpful. Conversion coma patients may have the following exam findings:

  • May be observed to "slump" to the floor and avoid hitting their heads.
  • Often resist examination and make semi-purposeful avoiding movements.
  • Have normal pupils, corneal reflexes, plantar reflexes, and sphincters.
  • Keep their eyes closed tightly and resist attempts to open them while in organic coma; eye closure is slow and difficult to simulate.
  • Have Bell's phenomenon, e.g., eyes roll up when lids are raised while the eyes of patients with true coma remain in a neutral position
  • Display geotropic eye movements.
  • Their hands will often just miss when dropped toward their faces.
  • Respond with purposeful movement to painful stimulation and avoid unpleasant stimuli
Conversion coma is perhaps as difficult to diagnose as psychogenic nonepileptic seizures and should be diagnosed through exclusion. A short list of potential emergency conditions to be ruled out includes intracranial hemorrhage, toxic ingestions, hyperosmolar hyperglycemic nonketotic coma, meningitis, hypoxia or hypercarbia, hepatic encephalopathy, and uremia.

Diagnostic and therapeutic goals for managing these patients are to rule out true medical and surgical emergencies, or to confirm the existence of a conversion disorder using laboratory testing, physical examination findings, and noxious or nociceptive stimuli. Noxious or nociceptive stimuli have been part of the neurologic examination for centuries. In fact, painful stimuli are central to the Glasgow Coma Scale.

Using of pain as a diagnostic tool may seem contrary to the basic tenets of medicine, but it can be a lifesaving maneuver. Painful stimuli can assist with the neurologic examination to demonstrate true paralysis or other evidence of a stroke. It can also confirm a conversion disorder and protect the patient from the administration of unnecessary medications, unneeded clinical and imaging studies, and potentially dangerous procedures and emergency interventions.

The video demonstrates the following noxious and nociceptive tests: the drop arm test, sternal rub, nipple squeeze, nail bed compression, and the Soto saline sign. The Soto saline sign is a new test described by Mario Soto, MD, in which saline is squirted into the eye of a comatose or seizing patient. It has been proven to be surprisingly effective in our shop.

Dr. Mario Soto, Medical College of Georgia at Augusta University, described the new Soto saline sign test to confirm a conversion disorder. Watch a video of a demonstration of this new diagnostic tool.

Thursday, December 1, 2016

I recently treated a patient with hemiplegic migraines successfully with bupivacaine cervical injections, a novel therapeutic technique using paraspinous cervical injections. The technique employs deep intramuscular injections of 1.5 mL of 0.5% bupivacaine bilaterally into the paraspinous muscles of the lower neck. (Read more in my October 2012 blog and see it demonstrated in a video at http://bit.ly/2ewC5n1.)

This headache and orofacial pain treatment was first described in 1996 by my twin brother, Gary Mellick, DO, a neurologist who did a pain fellowship. The exact mechanism is unknown, but the treatment appears to work centrally on the brain based on convincing observations. Evidence of central effects include resolution of cortical-related signs and symptoms such as nausea, photophobia, and allodynia. The first three cervical nerves that innervated the neck and scalp travel directly into the brain stem and the trigeminal caudate nucleus, a relay center important to other successful headache medications. This relay center in the brain stem also has synapses with cranial nerves 5, 7, 9, and 10 and antinociceptive centers such as the periaqueductal gray, nucleus raphe magnus, and the rostroventral medulla synapse, which have a profound antinociceptive effect. Neural connections to the cerebral cortex are also documented.

Until now, no actual physical evidence has documented central activity other than patient-reported relief of headache and nausea, photophobia, phonophobia, and allodynia. This recent pediatric patient with hemiplegic migraine demonstrated dramatic physical examination changes after the injection that were undeniable. He had been admitted before after presenting with right-sided headache and left-sided hemiplegia, but this time had other known complications of this condition when he came to the ED: He was altered and only slightly responsive to painful stimuli. Because this 12-year-old basketball player was quite tall for his age, four health care providers were required to lift him from the wheelchair to the gurney because he was incapable of assisting or following directions.

I consulted with his parents, and we decided to try the bilateral cervical injections with bupivacaine. The patient demonstrated only a slight painful response to the first injection, but he was able to have a conversation with his father and move all four extremities 15 minutes after the injections. He was able to stand shortly after that, but still had difficulty walking because of residual left-sided weakness. He was admitted for further evaluation and observation.

Hemiplegic migraine has two forms, the familial hemiplegic migraine and the sporadic hemiplegic migraine. The familial form is dominantly inherited, and genetic studies have implicated mutations in the genes that encode proteins involved in ion transportation. This type of migraine headache is usually accompanied by an aura featuring a motor deficit and at least one other symptom such as aphasia, vertigo, tinnitus, or visual and sensory problems. Protracted motor deficit, confusion, coma, and seizures or status epilepticus can also occur during a severe crisis. Diagnosis of this condition is made by the process of elimination. The patient, however, may simplify the situation by presenting with the diagnosis already established. Other family members, usually first- and second-degree relatives, may have been previously diagnosed with this condition.

My patient's two older brothers also have the condition. The neurologic deficit is real and may last for minutes to hours. Prolonged speech deficits and residual motor weakness can occur depending on which cerebral hemisphere is involved. Headaches develop during or after the deficit and are often accompanied by typical migraine signs and symptoms. Severe crises, however, can present with altered mental status and even a Glasgow coma score of 3. Patients also can experience hyperthermia (41°C), respiratory failure, major confusion, agitation, hallucinations, vomiting with the risk of aspiration, and seizures, including partial or generalized status epilepticus.

Workup includes documenting absence of hypoglycemia, a battery of standard laboratory tests and toxicology screens, and CT scan and MRI. A lumbar puncture is recommended in the presence of fever and altered mental status. Other potential studies include an EEG, ECG, and chest x-ray.​

This was the first hemiplegic migraine patient I had ever treated with cervical injections, and the outcome of headache relief and subsequent neurologic recovery was clinically dramatic. This patient's response provided further evidence supporting the centrally acting mechanism of this therapeutic intervention.

mellick migraine.JPG

This 12-year-old with hemiplegic migraine could not even walk upon arrival at the ED, but could raise his arms and move his legs 15 minutes after a bupivacaine cervical injection. Watch a video of that and of his father explaining his history.​