M2E Too! Mellick's Multimedia EduBlog
E 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.
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
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.
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.
Tuesday, November 1, 2016
I have immense respect for a few pediatric emergency conditions. Post-surgical bleeding following a tonsillectomy and adenoidectomy (T&A) has given me several memorable patient care experiences over the years. Honestly, the word "memorable" is actually a euphemism for terrifying.
Part of the problem with post-T&A bleeding is the patient. Typically, it's a pediatric patient who for hours has been quietly bleeding into the posterior pharynx while quietly swallowing the evidence (e.g., blood). By the time the patient presents to the ED, a significant but unknown percentage of the child's total blood volume has been lost. We cannot begin to guess how much blood has actually been lost until the patient starts vomiting. Suddenly realizing that your pediatric patient is already in compensated shock is a frightening experience.
The problem with T&A surgery is that bleeding can come from four locations. Two adenoids and two tonsils are removed. The bleeding can occur immediately after the surgery or, more commonly, days to weeks later. Bleeding can occur in the nose and the mouth, and these are not easily accessible for applying direct pressure to stop the bleeding.
My most recent patient was a 5-year-old who presented with a nosebleed three weeks after her tonsillectomy and adenoid surgery. The nosebleed had already been going on for three hours by that time. Her mother had already applied oxymetazoline, an adrenergic receptor agonist, eight to 10 times her nose without success. Then the vomiting began. Emesis after emesis of large amounts of blood continued for the next hour while we waited for the ENT consultant to arrive.
The ENT's initial advice was to apply more oxymetazoline, a potentially dangerous medication, and he asked over the phone if we had tried to pack the nose, a silly question as far as I was concerned. Packing the nose of a frightened little girl with nares smaller than the tip of my little finger just wasn't going to happen without sedation. Nasal packing also didn't seem like the correct therapeutic intervention for bleeding from a post-surgical adenoidectomy site.
How do you stop bleeding from a post-surgical adenoidectomy site? This scenario is similar to stopping the bleeding of posterior epistaxis. My plan, if her condition deteriorated, was to insert a pediatric Foley catheter, blow up the balloon, and apply traction. Besides placing two of the largest intravenous catheters possible, I ordered a 20 mL/kg normal saline bolus and a blood type and cross. Her initial hemoglobin was 11.1 g/dL, and I briefly considered O-negative blood as her heart rate climbed and her pulse pressure narrowed. Thankfully, the signs of compensated shock subsided and the bleeding slowed before she was taken to the operating room to have her left bleeding adenoidectomy site treated. I checked a day or two later, and her hemoglobin had settled at 8.0 g/dL, a 3 g/dL drop.
What else could I have done? Using forceps to apply an epinephrine-soaked gauze to the posterior pharynx apparently works for bleeding tonsillectomy sites. Access to the adenoidectomy site is not guaranteed, however. Next time, I will use a laryngotracheal mucosal atomization device placed through the bleeding nares to deposit 1:10,000 or 1:100,000 epinephrine to my patient's posterior nasopharynx. Another potential but unproven option is the topical application of hemostatic agents such as fibrin sealant or thrombin with the mucosal atomization device. Intravenous tranexamic acid is also a consideration. The topical application of tranexamic acid has been used successfully in surgery to stop or slow bleeding.
Watch a video of a patient with post-T&A bleeding.
Monday, October 3, 2016
Ankle dislocations are usually the result of high-energy trauma that cause plantar flexion of the ankle combined with an inversion or eversion stress. These dislocations are typically described according to the direction of displacement of the talus and foot in relation to the tibia. Consequently, dislocation may be upward, posterior, medial, lateral, posteromedial, or anterior.
Posterior dislocation of the talus is the most common form of ankle dislocation. Associated fractures are the rule rather than exception, and ligamentous disruption varies according to the type of dislocation. One of the most dramatic joint dislocations is the open, dislocated ankle. A principal concern, in addition to timely reduction, is the possibility of a neurovascular injury. Radiographs should not delay reduction in cases where vascular compromise or skin tenting is present. After reduction, reassessment of the neurovascular status, splinting, ankle elevation, and post-reduction radiography are accomplished.
The reduction procedure is accomplished with the patient lying supine. After procedural sedation and analgesia, the knee is flexed to 90 degrees. Distraction of the foot, followed by a gentle force reversing direction of the dislocation is sometimes all that is needed, though a more forceful maneuver may be needed. Many open ankle fractures and dislocations will not be reduced unless the injury mechanism is first recreated.
This important tenet of orthopedic surgery is frequently overlooked. When that happens, the joint dislocation reduction can be nearly impossible to accomplish. This video shows the initial failures of open ankle fractures and dislocation reductions by emergency medicine and orthopedic residents. Only after the operators regrouped and recreated the mechanism of injury were the open ankle dislocations successfully reduced.
Watch a video showing an ankle injury being recreated so that the open dislocation can be reduced.
Thursday, September 1, 2016
How could a Lyme disease lookalike rash and anaphylaxis to meat have anything in common? As I found out recently, they do. They both have a common vector, the Lone Star Tick, which is also known by its formal name, Amblyomma americanum, and is found predominately in the East, Southeast, and Southwest. It is an aggressive tick that loves humans.
In fact, all three growth stages (adult, nymph, and larva) are known to feed on humans. Besides the common signs of irritation that often accompany a tick bite, a rash similar to the rash of Lyme disease has been commonly described. This "bull's-eye" rash is often accompanied by systemic symptoms such as fatigue, fever, headache, muscle, and joint pains. Even though the rash looks almost identical to the erythema migrans of Lyme disease, it isn't caused by Borrelia burgdorferi. In fact, researchers still have not isolated out the etiology of STARI or Southern Tick-Associated Rash Illness.
Treatment with doxycycline seems to be associated with disappearance of the rash and relief of the associated signs and symptoms. Yet, whether to treat is still considered the prerogative of the physician.
The Lone Star Tick is also implicated in causing growing numbers of humans to develop a strange allergy to meat. More specifically, the allergy is to a carbohydrate present in mammalian meat called galactose-alpha-1,3-galactose, or Alpha-Gal for short. The reaction may be delayed for several hours after eating mammal meat, causing confusion and misdiagnosis. As with any anaphylaxis condition, it can be severe and life-threatening.
This is what I love about medicine: the never-ending list of new discoveries that occur on a daily basis.
Watch this video showing removal of a female Lone Star Tick from a child, and hear a discussion of STARI and Alpha-Gal.