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The Case Files

Welcome to the Case Files!
The Case Files is an anecdotal collection of emergency medicine cases to enable physicians and researchers to find clinically important information on unusual conditions.

Case reports should focus on:

  • Unusual side effects or adverse interactions.
  • Unusual presentations of a disease.
  • Presentations of new and emerging diseases, including new street drugs.
  • Findings that shed new light on a disease or an adverse effect.

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Tuesday, July 08, 2014
By Ringhauser, Holly DO; Glantz, Sanford MD; Havasy, Stephen P. MD

A 74-year-old woman presented to the emergency department with altered mental status for one week. The patient's husband said the patient had been in her usual state of health until seven days earlier, when she got lost on the way home from a restaurant that she had frequented for several decades. She had become increasingly confused and unable to care for herself, and was now unable to finish a sentence or ambulate without assistance. The patient had been seen by her primary physician and a neurologist. She had blood work, a CT scan, and an MRI performed, but her husband was not yet aware of the results of these tests.
The patient's past medical history was significant for hypertension and hypercholesterolemia, and her medications included enalapril and ezetimibe with no recent changes in dose or frequency. The patient's husband said the patient did not smoke, drink alcohol, or use any illicit drugs, and he denied any recent travel or sick contacts.

The patient's initial vital signs were within normal limits with the exception of mild hypertension (155/59 mm Hg). Her rectal temperature was 99.2°F, and she remained afebrile throughout her workup. She was confused and disoriented. She answered questions inappropriately and nonsensically. She could follow simple commands, such as opening or closing her eyes, but was unable to follow more complicated instructions, such as putting her finger to her nose. She was tremulous throughout the exam. Her gait was not formally tested, but patient's husband described a wide-based, staggering, and uncoordinated gait. The remainder of her exam was normal with the exception of 1+ pitting edema to the mid-calf bilaterally.
The patient's labs revealed the following:

The patient was evaluated in the ED by her neurologist, who recommended performing an LP to send CSF for cell count, gram stain, culture, cryptococcal antigen, AFB, and 14-3-3 protein. The patient was admitted to the hospital, and the EP requested psychiatry and physical therapy consults. The patient had an EEG the following day, which was abnormal with background slowing and periodic to pseudoperiodic sharp-wave discharges, consistent with Creutzfeldt-Jakob disease.
The outpatient MRI was reviewed by neurology, which noted increased cortical ribboning, particularly on FLAIR sequence. The patient developed akinetic mutism and startle myoclonus over the next 72 hours. Her mental status and ability to ambulate continued to deteriorate rapidly during her stay in the hospital, and the patient was ultimately transferred to a skilled nursing facility for hospice care. CSF samples were sent to the National Prion Disease Pathology Surveillance Center in Cleveland, and were found to be positive for 14-3-3 protein and Tau protein, which is consistent with Creutzfeldt-Jakob disease.
Rapidly progressive dementia can be caused by a number of conditions, including human prion diseases. Creutzfeldt-Jakob disease is a neurodegenerative transmissible spongiform encephalopathy caused by a prion, and it is categorized as sporadic or variant. (J Neurol Neurosurg Psychiatry 2001;79[6]:744.) The sporadic form of Creutzfeldt-Jakob disease (sCJD) is the most common prion disorder in humans (Infect Dis Rep 2013;5[2]:e10), and is characterized by rapidly progressive dementia, ataxia, visual disturbances, myoclonus, and extrapyramidal features. (Neurology 2012;79[6]:547.)
sCJD is caused by prion proteins that undergo conformational changes, causing spongiform encephalopathy. (J Neurol Neurosurg Psychiatry 2001;79[6]:744.) The estimated worldwide incidence is 1:1,000,000 (Neurology 2012;79[14]:1499), and human-to-human transmission can occur via direct tissue implantation, use of contaminated medical instruments, administration of contaminated human hormones, and via contaminated blood products. (Infect Dis Rep 2013;5[2]:34.) CJD has no cure, and it is universally fatal.
Histopathologic diagnosis can be performed on brain biopsy samples or at autopsy, but that exposes the pathologist to infectious materials. Several guidelines have been proposed to aid in the diagnosis using less invasive means. The World Health Organization guidelines for diagnosis include progressive dementia with two of the following: myoclonus, pyramidal/extrapyramidal deficits, visual/cerebellar deficits, or akinetic mutism, plus EEG findings of 1-2 Hz periodic pattern or positive 14-3-3 protein and no other explanation for deficits. (Centers for Disease Control and Prevention, 2013;
MRI also plays a significant role in diagnosis because it is reflected in diagnostic guidelines from the University of San Francisco and the European MRI- CJD Consortium. (Neurology 2012;79[14]:1499.) It is important to exclude the numerous alternative diagnoses that may be treatable or curable, such as multiple sclerosis, status epilepticus, Lewy body dementia, Alzheimer's disease, Parkinson disease, sepsis, tuberculosis, lupus, and certain psychiatric disorders, to name a few. (Neurology 2012;79[14]:1499.)
Altered mental status is a common chief complaint in the ED, and the differential diagnosis is broad. Our patient's symptoms of myoclonus, akinetic mutism, ataxia, and tremor are consistent with the WHO criteria for CJD. She was also found to have periodic and pseudoperiodic patterns on EEG, positive CSF biomarkers, and cortical ribboning on FLAIR-MRI. No alternative cause of her symptoms could be found.
It is important to establish this diagnosis because of the potential transmissibility of infectious prions. It is also important to exclude alternative diagnoses that may be treatable or curable.
Dr. Ringhauser is a second-year resident in emergency medicine at Good Samaritan Hospital Medical Center in West Islip, NY. Drs. Glantz and Havasy are emergency physicians at Good Samaritan Hospital Medical Center in West Islip, NY.

Tuesday, July 08, 2014
By Fox, Alex MD; King, Andrew MD
CrossFit has become a workout phenomenon with more than 5,500 gyms and millions of staunch followers. Developed by Greg Glassman, CrossFit defines itself as “that which optimizes fitness, constantly varied functional movements performed at relatively high intensity.” The craze has been embraced by fitness enthusiasts and weekend warriors alike.
These intense workouts can be dangerous for those with less experience who do not have trainers to help ease them into the routine. A 2005 New York Times article, “Getting Fit, Even If It Kills You,” criticized CrossFit for placing emphasis on speed and weight hoisted instead of technique. (Dec. 22, 2005; The article later quoted Wayne Winnick, a sports medicine specialist, as saying, “There's no way inexperienced people doing this are not going to hurt themselves.” Mr. Glassman backs up the risk by stating, “It can kill you. … I've always been completely honest about that.”
Our patient was a 33-year-old man with a past medical history of migraine headaches and attention deficit hyperactivity disorder, who presented with a left temporal headache and neck tightness for one month. The headache began suddenly during an intense CrossFit regimen. He was doing heavy lifting at the time of acute onset, and was exerting himself more than his normal limits. He developed severe, throbbing pain in the left side of his head that was accompanied by neck tightness, which was different from his migraines in severity and character. He saw his primary care physician, who prescribed him a medication for migraines, but the drug proved ineffective. The headache was constant and intense for the entire month before his emergency department visit, and he only slightly responded to ibuprofen and acetaminophen. He returned to his primary physician a week before his ED visit, and his physician performed a CT head scan that was negative. Given the persistence of pain, he presented for further evaluation. The patient denied any associated neurologic sequelae including paresthesias, weakness, vision changes, and tinnitus.
Vital signs revealed tachycardia at a rate of 112 bpm, but his other vital signs were normal. His pupils were also equal, round, and reactive to light, and the extraocular muscles were intact. Cranial nerve examination involving nerves II-XII was normal. Strength and sensory testing in the upper and lower extremities was normal and symmetric. Cerebellar testing also was entirely normal. The patient exhibited a normal, brisk gait. Laboratory testing showed a normal CBC, PT/INR, and PTT. Given the persistence of his symptoms and the negative outpatient head CT, a brain and neck MRI/MRA was ordered to delineate the cause of his headache. He received intravenous prochlorperazine and diphenhydramine, which lessened his symptoms. The neck MRA revealed dissection of the distal left cervical internal carotid artery as it entered the skull base with an associated 50 percent stenosis.
The patient was started on a heparin drip, and the EP consulted a neurologist, who recommended that aspirin also be administered. The patient was admitted to the neurology service, where the heparin was discontinued. He was later discharged on Plavix and Lipitor, and given clear instructions to refrain from strenuous exercise, heavy lifting, and golf. The neurologists determined that long-term anticoagulation was not necessary, and no procedure was performed during his inpatient admission. Coagulation studies were also negative. The patient remains well with no headache or neurologic sequelae.
Our case was difficult because the patient had a known history of migraines, which could have initially explained his headache. If advanced imaging had not been pursued, a correct diagnosis was unlikely, and the patient would have been at risk for a catastrophic outcome.
Carotid dissections occur when an arterial wall loses its structural integrity, allowing blood to flow and collect between layers, usually in the subintimal plane. (Neurology 2000;54[2]:442.) Many triggers are associated as etiologies for dissection, such as minor trauma and intense physical activities. The high amount of stress placed on the body by CrossFit combined with inexperience puts lifters at risk for a carotid artery dissection.
Headache and neck pain are the most common symptoms for carotid artery dissection, occurring in 80 percent of patients. (Neurology 2000;54[2]:442.) More than the 56 percent of patients present with TIA symptoms and another 25 percent present with Horner's syndrome, both of which would lead a practitioner to consider vascular etiologies.
Spontaneous carotid dissection accounts for 20 percent of ischemic strokes in young adults, occurring in approximately 2.6 per 100,000. (Neurology 2006;67[10]:1809.) The diagnosis of our patient was clinched by the MRA of the head and neck. The pathognomonic sign to look for is the crescent sign of intramural hematoma, which forms because of an eccentric rim of hyperintensity surrounding a hypointense arterial lumen. (See Figures 1 and 2.)

The crescent sign is typically found on MRI T1-weighted sequences, but can be seen on MRI diffusion-weighted imaging or CT angiography. (J Neurol Sci 2007;253[1]:81.) A 2009 systematic review showed the diagnostic sensitivity and specificity of MRI, MRA, and CT-angio to be similar in carotid artery dissection. (AJR Am J Roentgenol 2009;193[4]:1167.) Carotid artery duplex Dopplers are a quick and cheaper bedside tool for diagnosing dissection, but sensitivity is only 70 percent in patients with a headache and no signs of ischemia. (Front Neurol Neurosci 2006;21:70.)
Our patient was stable for a month, but he could have had a devastating outcome. The emergency provider must always remember that intense physical exertion is a risk factor for carotid artery dissection and vascular headache, and that a head CT for a persistent headache will miss pathology in the neck, which could reveal the etiology. Consider obtaining imaging of the neck to rule out carotid artery dissection for patients who recently had an intense CrossFit workout presenting with a headache, neckache, or neurologic symptoms.

Dr. Fox is an emergency medicine resident at Wexner Medical Center at the Ohio State University and the Ohio State University Medical Center East. Dr. King is an assistant professor-clinical at Wexner Medical Center at the Ohio State University and the Ohio State University Medical Center East.

Tuesday, July 08, 2014
By Libertin, Nicholas MD; Haynes, Ann MD; King, Andrew MD

Emergency physicians see toxicology cases every day, and the treatment for these cases is often just symptomatic care and stopping the offending agent. Certain cases, however, require specific antidotes to prevent significant morbidity and even mortality.
Toxicology cases are in many ways just as important as diagnosing sepsis or a ST-elevation myocardial infarction. Toxic alcohol cases fit into this “immediate treatment” category, like a patient we recently saw who drank windshield wiper fluid. She survived without any major morbidity or mortality thanks to early recognition and treatment by the emergency department staff.
The early administration of fomepizole in this particular case likely prevented the harmful effects of these toxins.
As Amal Mattu, MD, says, “When other physicians hear hoof beats, they think of horses, but emergency physicians think of lions, tigers, and bears.” As emergency physicians, we are taught to think of the worst things first because we are often the first physicians to see a patient, and we often dictate the direction of their care. Many emergency department cases require prompt recognition and treatment to prevent significant morbidity and mortality.
This patient ingested a potentially toxic dose of methanol, and complications such as optic disk edema, metabolic acidosis, and anoxic brain injury were prevented simply by the prompt administration of antidote based on a thorough history and physical examination. The fomepizole was administered even before the onset of symptoms and laboratory abnormalities.
The patient was a 26-year-old woman with a history of self-reported attention deficit hyperactivity disorder who was brought in clinically intoxicated by EMS. The patient had been arguing with her boyfriend, and was visibly upset. She reported being anxious because of final examinations and other stressors she refused to identify. She argued with her boyfriend, and then ingested four 200 mg ibuprofen tablets and an unknown quantity of isopropyl rubbing alcohol. She later divulged that she also consumed an unknown but substantial amount of windshield washer fluid. The patient denied that this was a suicide attempt; she said she did this “to get a reaction” from her boyfriend. Her past medical history was significant for situational depression after a break-up several years before presentation, for which she was placed on bupropion, which was later discontinued.

She denied headache, dizziness, visual changes, chest pain, nausea, vomiting, diarrhea, hematemesis, and melena. Her vital signs in the ED were blood pressure of 134/76 mm Hg, heart rate of 91 bpm, temperature of 36.7°C, and a respiratory rate of 20 bpm. She had an oxygen saturation of 95% on room air, and her physical examination was unremarkable. She was alert and oriented with an intact neurologic examination, and had no positive findings for optic disk edema, abdominal tenderness, peritoneal signs, or Kussmaul breathing.
Treatment in the emergency department consisted of a fomepizole loading dose of 15 mg/kg over 30 minutes and 10 mg/kg maintenance infusion over the next 12 hours. The patient was also treated with a loading dose of magnesium for QT prolongation on ECG.
She was admitted to the hospitalist service, and eventually was medically cleared after another dose of fomepizole and a discussion with the poison control center. No metabolic acidosis or osmolar gap was appreciated on subsequent laboratory studies likely because fomepizole was promptly administered. No neurologic or ophthalmologic sequelae were appreciated on future physical examinations. The patient was eventually seen by psychiatry, and was diagnosed with poor coping skills. Her physician recommended 24-hour observation with discharge the next day.
Methanol is used in many different formularies across North America because of its low freezing point. It can be found in common items such as antifreeze, glass cleaner, solvents, de-icers, homemade alcohol (moonshine), and windshield wiper fluid. The initial presentation of methanol poisoning is frequently nonspecific with symptoms such as nausea, vomiting, and abdominal pain. (CJEM 2002;4[1]:34.) Fomepizole is currently viewed as efficacious as ethanol in toxic alcohol poisoning without the risk of hepatotoxicity, hypoglycemia, or intoxication. (New Engl J Med 2001;344[6]:424.)
An index of suspicion should always be maintained for methanol toxicity because untreated patients are at risk for blindness from optic nerve toxicity, coma, retinal injury, seizures, cardiopulmonary arrest, and severe metabolic acidosis. Early administration of fomepizole can prevent conversion of methanol to formaldehyde and subsequent conversion to its toxic metabolite, formic acid, by inhibiting alcohol dehydrogenase. (CJEM 2002;4[1]:34.) It is well known that the degree of toxicity correlates with the amount of methanol ingested, but data show that this does not correlate well with presenting methanol levels. The lethal dose of methanol is reported to be 1–2 mL/kg, though ingestion of as little as 0.1 mL/kg has resulted in permanent blindness. (Medline 2009;52[3]:125.)
Some guidelines state that a methanol level of 20 mg/dl could be an arbitrary cutoff for treatment, but few data support this practice. We followed the recommendations of the Central Ohio Poison Center for our patient, which were an initial dosing of 15 mg/kg of fomepizole, followed by 10 mg/kg every 12 hours for 48 hours, and continuation of 15 mg/kg every 12 hours until the methanol level is less than 20 mg/dl. They recommend fomepizole administration for asymptomatic methanol levels of 20–50 mg/dl. They recommend fomepizole and hemodialysis for patients with end-organ damage, elevated osmolal gap, or levels greater than 50 mg/dl.
Our patient's report of how much methanol she ingested and when she ingested it were likely unreliable because of her concomitant ethanol ingestion. Her ethanol intake may have inadvertently provided a temporary protective effect against her methanol ingestion because ethanol also inhibits alcohol dehydrogenase.
The prompt diagnosis of methanol toxicity may have prevented severe end-organ damage in this patient, and emergency physicians should suspect it in any patient where ingestion of antifreeze, glass cleaner, solvents, de-icers, homemade alcohol, or windshield wiper fluid is reported or suspected. The data for treating asymptomatic individuals with levels above is 20 mg/dl are lacking, but this seems to be standard of care given the severe repercussions of not administering the antidote. We recommend administering this medication and treating all toxic alcohol ingestions in cooperation with your local poison control center because practice patterns may vary in different locations.
Dr. Libertin is an emergency medicine resident at the Ohio State University Wexner Medical Center and the Ohio State University Medical Center East. Dr. Haynes is an assistant professor at the Ohio State University Medical Center East. Dr. King is an assistant professor-clinical at the Ohio State University Wexner Medical Center and the Ohio State University Medical Center East.

Tuesday, July 08, 2014
By Moises, Moreno DO; Glantz, Sanford DO

A 66-year-old woman with a history of osteoarthritis presented to the emergency department with progressively worsening left hip pain that had started five days prior to arrival. The pain was non-radiating and worse with movement, and it was associated with chills and anorexia. She had progressive difficulty walking because of pain. She had not had similar symptoms in the past, and attributed her pain to osteoarthritis. She denied recent trauma, back pain, leg swelling, numbness, and paresthesias. She also denied fever, abdominal pain and distention, nausea, vomiting, diarrhea, constipation, urinary symptoms, allergies, alcohol, and drug use.
She was a well-appearing obese woman in no acute distress. Her blood pressure was 158/100 mm Hg, and her temperature was 100.2°F. She had left lower quadrant abdominal tenderness without distention, guarding, or rigidity; she also had no costovertebral angle tenderness, hernias, or masses. Her pain was greatest with active range of motion of the left hip. The remainder of her physical exam was unremarkable.
The patient's white-cell count was 16,140 per cubic millimeter without a left shift or bandemia. X-rays of left hip and pelvis were unremarkable. A non-contrast CT of the abdomen and pelvis was obtained because of her abdominal tenderness. The CT revealed a 3.9 cm fine linear foreign body within a loop of small bowel in the upper pelvis that appeared to extend through the lateral wall abutting the adjacent left psoas, causing a psoas abscess.
The emergency physician suspected the foreign body might be a fish bone, and the patient revealed that she frequently ate fish with bones. The patient was started empirically on ertapenem, and surgery was consulted. She was taken for an exploratory laparotomy, and had extensive lysis of adhesions, a small bowel resection, and drainage of the psoas abscess. A culture of the abscess specimen grew Klebsiella pneumoniae, and intravenous antibiotics were continued for several days. The patient's symptoms resolved, and she was discharged home on cefpodoxime and metronidazole. She recovered well.

Psoas abscess is a rare condition with high morbidity and mortality. The clinical manifestations are often variable and nonspecific, which makes it difficult to diagnose on physical exam alone. Symptoms include malaise, anorexia, weight loss, nausea, back pain, and abdominal pain. The classical clinical triad consisting of fever, back pain, and a limp is present in only 30 percent of the patients with a psoas abscess. (Postgrad Med J 2004;80[946]:459.) The diagnosis could be even more challenging when the patient also has a history of arthritis, lumbar strain, vertebral osteomyelitis, or abdominal/urologic disorders suggesting an alternative pathology. This can lead to a delayed diagnosis that carries a much higher mortality. (Am J Emerg Med 1997;15[1]:83.) A high index of suspicion and a detailed history are crucial for the correct diagnosis. CT is the optimal radiographic modality; laboratory testing is unreliable in diagnosing psoas abscess.
Psoas abscess in the United States is usually caused by other disease processes, with Crohn's disease being the most common, followed by appendicitis, nephrolithiasis, diverticulitis, and colon cancer. Most patients tend to be older, and often have poorer outcomes, with mortality approaching 20 percent. (Am J Emerg Med 1997;15[1]:83.) Only two case reports have described psoas abscesses caused by duodenal perforation from foreign bodies (toothpick and wooden skewer.) (Aust N Z J Surg 1992;62[8]:662;G Chir 2008;29[4]:180.)
Psoas abscesses caused by Klebsiella pneumoniae also carry a higher mortality rate because of their ability to form gas and the increased risk of septic metastasis, including to the aorta. Early recognition and prompt drainage or debridement are essential, and should be performed in a timely manner. (J Microbiol Immunol Infect 2001;34[3]:201.) This is especially relevant when patients have a history of diabetes mellitus or alcoholism because these disease processes predispose the patient to infection with this organism.
Psoas abscess is an uncommon etiology of hip pain that is easy to overlook because of its rarity. This case differs from an isolated case of a psoas abscess because a foreign body was seen within the small bowel wall adjacent to left psoas muscle, causing the abscess. Physicians need to maintain a high index of suspicion for a psoas abscess because its signs and symptoms are highly nonspecific, and delaying the diagnosis may be fatal.

Dr. Moreno is a second-year resident in the Emergency Medicine Residency Program at Good Samaritan Hospital Medical Center in West Islip, NY, where Dr. Glantz is an attending emergency physician.

Monday, June 23, 2014
By Osgood, James Gale MD, MBA; Robison, Matthew MD; Siethel, Michelle PA

A 19-year-old woman presents with right knee pain and a laceration after a fall. She states that she was drinking alcohol at a local bar, and fell and cut her knee on broken glass on the bathroom floor. She denies loss of consciousness or other injuries. The patient is able to bear weight, but has increased pain when moving her knee. She denied distal numbness or weakness. The patient also denied other medical problems, and her last tetanus was four years earlier.
Physical exam revealed a stable knee with several lacerations and abrasions with mild tenderness to palpation only near the laceration sites. ROM was mildly limited by pain. The sensation to the distal extremity was intact to light touch, and dorsalis pedis and posterior tibial pulses were 2+. X-rays of the knee were obtained. What is your diagnosis?

The x-ray demonstrates normal bony alignment without cortical disruption. A radiopaque foreign body was seen in Hoffa's fat pad, or the infrapatellar fat pad of the knee joint, which physically separates the antero-inferior synovial membrane of the knee from the patella. It is intraarticular but extrasynovial. Functionally, the infrapatellar fat pad may provide some cushioning to the articulating surfaces of the knee, but it also helps distribute synovial fluid during knee movement.
Orthopedics was consulted given the intraarticular position of the foreign body and a concern for possible violation of the synovium. The joint was injected with 160 mL of sterile saline without observed fluid extravasation, and the joint was thought to be intact. The wound was explored, but the foreign body was not found. The lacerations were left open. The orthopedist prescribed cephalexin for one week, and the patient was discharged with precautions to watch for signs of infection and follow-up.

Traumatic wounds are one of the most common reasons for an ED visit. Wound care accounts for five percent to 20 percent of all ED malpractice settlements against emergency physicians and for three percent to 11 percent of all claim dollars paid. A wound foreign body increases the risk of infection so any mechanism that suggests possible foreign body mandates judicious wound exploration, effective irrigation, and radiologic investigation, including the use of ultrasound, CT, or MRI for nonradiopaque material.
Studies found that retained glass was found in seven percent to 15 percent of wounds in patients injured by broken glass. Plain x-rays have 90% sensitivity in visualizing nonleaded glass with higher miss rates of small volume particles (15 mm3 or less). No randomized trials have examined the role of antibiotic prophylaxis, and its use is left to the discretion of the treating physician.
Warn the patient about an increased risk of infection before closing, and discuss signs and symptoms that warrant immediate reevaluation, with or without repair, if the mechanism suggests a possible retained foreign body. Consider delayed closure or leaving the wound open. Have a low threshold for specialty consultation and for early wound rechecks.
Dr. Osgood is an assistant professor of clinical emergency medicine, Dr. Robison is an associate professor of clinical emergency medicine, and Ms. Siethel is a physician assistant, all at University Hospital in Columbia, MO.
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Lisa Hoffman
Editor, Emergency Medicine News

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