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.
Comment on a case or submit your own case following the instructions in the Submissions box to the right.
Thursday, September 18, 2014
By Joshua B. Hourizadeh, DO, & Joseph VM Kelly, MD, MBA
A 38-year-old African American man presented to the emergency department with severe left-sided inspiratory chest pain with no radiation for two days and increasing shortness of breath. The patient said he had recently broken up with his girlfriend, which lead him to smoke crack cocaine for three consecutive days.
The patient had no past medical or surgical history, but he had a past social history of illicit drug abuse, nicotine use, and social alcohol use. His heart rate was 96 bpm, blood pressure was 112/80 mm Hg, oxygen saturation was 86% on room air, his respiratory rate was 24 bpm, and his temperature was 98.7°F. Physical examination was unimpressive with the exception of diminished breath sounds on the left side. Chest radiograph (Figure 1) displayed a left-sided pneumothorax with a mediastinal shift indicating the beginning of a possible tension pneumothorax. A tube thoracostomy was placed, and water seal pressure was applied without any suction apparatus. The patient felt immediate relief once the thoracostomy tube was in place, and his oxygen saturation improved to 95%. The patient was placed on oxygen therapy at 2 l/min.
Three hours after tube thoracostomy placement, the patient complained of increasing dyspnea, and said he had pain at the thoracostomy site. Auscultation of the chest revealed inspiratory crackles on the left side. Oxygen saturation fell to 83%, and arterial blood gas analysis indicated hypoxemia. Repeat chest radiography (Figure 2) showed proper placement of the tube, that the left lung had re-expanded, and that he had ipsilateral pulmonary edema. Oxygen therapy was increased to 8 l/min, and oxygen saturation stabilized at 94%.
The patient was observed overnight. The tube was removed when no evidence of air leakage was detected. Chest radiography (Figure 3) was repeated 12 hours after the tube was removed, and showed the lung re-expanded and decreased pulmonary edema. The patient recovered and was released three days after admission. Follow-up chest radiography (Figure 4) revealed a normal chest with no pneumothorax or pulmonary edema.
Reexpansion pulmonary edema is rare and often a fatal complication that can occur after tube thoracostomy. It normally occurs on the ipsilateral side of the resolved pneumothorax, but it can occur contralaterally or even bilaterally.(Pulm Med 2012;2012:256878.) Mortality rates as high as 20 percent have been reported, even with early and appropriate medical intervention.(Ann Thorac Surg 1988;45:340.) Although not completely understood, it is believed the etiology of reexpansion pulmonary edema is caused by secretion of protein-rich fluid because of increased endothelial permeability.(Light R, “Pleural Diseases,” in Evidence-based Respiratory Medicine. Malden, MA: Blackwell Publishing Ltd, 1995, 268.)
Risk factors of pneumothorax include being male, family history, Marfan syndrome, homocystinuria, anorexia nervosa, history of previous pneumothorax, diabetes, irritation of the lungs such as smoking, and chronic obstructive pulmonary disease.(J Cardiothorac Surg 2013;1:164.) The risk of reexpansion pulmonary edema include people under 40 years old, a pneumothorax that goes without treatment for 48 hours or greater, the size of the pneumothorax, negative pleural pressure, and rapid lung reexpansion.(N Engl J Med 2014;370e19.)
Treatment consists of hemodynamic support, supplemental oxygen, asynchronous differential lung ventilation,and ventilation with positive end-expiratory pressure. Laying the patient in the lateral decubitus position with the affected side up will decrease hypoxemia, which increases oxygenation, when unilateral reexpansion pulmonary edema is present. (Pulm Med 2012;2012:256878; Ann Thorac Surg 2005;80:1933; Ann Thorac Surg 1997;63:1206.)
Thursday, September 18, 2014
By Andrew Yocum, MD & Andrew King, MD
A 69-year-old woman with a past medical history of multiple sclerosis, hypertension, hyperlipidemia, remote cerebral vascular accident, and a known abdominal aortic aneurysm was brought to the emergency department by EMS complaining of abdominal pain. Her AA was stable on imaging four months prior to presentation with a measurement of 3.8 cm.
The patient had intermittent generalized abdominal pain over the previous four weeks that resolved without intervention. This episode began almost 24 hours prior to presentation after the patient finished eating. She had a constant, generalized abdominal pain since that time. The patient said the pain was worst in the left lower quadrant. She described the pain as 8/10, sharp, and nonradiating with associated anorexia. She denied any nausea, vomiting, changes in bowel movements, hematochezia, melena, fevers, or chills. She also denies any urinary frequency, dysuria, or hematuria, but does intermittently self-catheterize because of her multiple sclerosis.
The patient’s primary physician prescribed her a course of steroids and Levofloxacin eight days prior to presentation for a cough, which resolved her symptoms.
The patient had a colonoscopy in 2009 that revealed a 4 mm sessile polyp, which was resected and found to be tubular adenoma. She was noted to have a tortuous sigmoid colon at that time.
The patient was normotensive but pale in the ED. Her abdominal exam revealed tenderness, which was worst in the left lower quadrant but tender throughout with deep palpation. No distention, rebound, or guarding was noted. Chemistry panel, urinalysis, complete blood count, liver function tests, and lipase were ordered. A recheck of the patient’s vital signs found she was hypotensive at 76/52 mm Hg and tachycardic to 110. Laboratory analysis revealed leukocytosis with a white blood cell count of 45.6, anemia with a hemoglobin of 10.3 g/dl, acute kidney injury, and metabolic acidosis with an anion gap of 16. The patient’s stool guaiac was negative. Central venous catheterization was performed, and IV fluid resuscitation was initiated.
The patient met SIRS criteria, so empiric antibiotics were initiated, and a chest x-ray and CT scan of her abdomen and pelvis were obtained. The CT revealed a large mesenteric hematoma measuring 10.1 x 5.5 cm with layering fluid density, free fluid consistent with hemoperitoneum, presumed blood tracking throughout the central mesentery, and an atrophic left kidney with increasing left hydronephrosis.
Immediate surgical consultation was obtained, and the patient was admitted to the surgical ICU, where she required four units of packed red blood cells. Interventional radiology was consulted, and an angiography identified a dissection aneurysm of the gastroepiploic artery that was subsequently embolized. The angiography also identified diffused small and moderated vessel irregularities of the celiac and superior mesenteric arteries consistent with vasculitis. The patient’s hemoglobin stabilized after embolization, and a course of prednisone was initiated for presumed vasculitis, although an MRI performed prior to discharge did not identify any evidence of vasculitis.
Mesenteric hematoma is a difficult diagnosis because of its rarity and highly variable presentation based on the location and size of the hematoma. Spontaneous hemorrhages have been reported in patients from ages 2 to 84 with highest prevalence in those 50 to 59. They also tend to occur more in men. (Am J Surg 1970;120:623; Ann Surg 1962;155:153.) Patients generally lack pathognomonic signs or symptoms, but typically have sudden onset abdominal pain that may rapidly progress. The pain may decrease in some patients if bleeding ceases, but others may present with abdominal mass or intestinal obstruction. The situs of mesenteric hematomas has varied in previous case reports with the gastroepiploic artery as a rare source of bleeding. (J Cardiovasc Surg 1999;40:63.)
Laboratory analysis is often of limited diagnostic value; it may be normal or may reveal nonspecific abnormalities such as anemia or leukocytosis. (Int J Surg Case Rep 2012;3:614.)
Frequently no cause is identified prior to treatment, but a thorough investigation should be done after the patient is stabilized to identify any underlying coagulopathy, vasculopathy, connective tissue disorder, or malignancy. Previous studies have noted that no underlying cause is identified in as many as one-third of all cases. (Cardiovasc Intervent Radiol 2011;34[Suppl 2]:S142.)
Having a high level of suspicion and ordering appropriate imaging is essential to making this diagnosis. CT scan is often ordered to rule out more common causes of shock in patients presenting with abdominal pain, such as acute pancreatitis, abdominal aneurysm, malignancy, and mesenteric ischemia. CT scan of the abdomen and pelvis has been shown to be effective in diagnosing hemoperitoneum and arterial extravasation. (J Med Liban 2009;57:178.) CT is typically the primary imaging modality, but an ultrasonography with a FAST exam may be useful in the unstable patient.
Managing a mesenteric hematoma is largely targeted at treating the underlying cause. Initial resuscitation is identical to any other patient with intra-abdominal hemorrhage: fluid resuscitation, initial labs, appropriate consultations, and blood transfusions, if required. Once a mesenteric hematoma has been identified, treatment varies from conservative management with serial imaging to more invasive therapy such as vessel embolization in patients who are hemodynamically stable or are not surgical candidates. (Hepatobiliary Pancreat Dis Int 2010;9:634; Diagn Interv Radiol 2012;18:121.)
Immediate surgical laparotomy is indicated in the hemodynamically unstable patient. (Int J Surg Case Rep 2012;3:614.) Patients who are seen in institutions where these services are not available should be rapidly stabilized and transported to institutions with necessary services available. Previous case reports have demonstrated benefit in avoiding emergency surgery in those patients who are hemodynamically stable. (South Med J 1998;91:273.)
Spontaneous mesenteric hematomas or hemorrhage are a rare cause of abdominal pain, anemia, and shock, and require a high level of suspicion for appropriate workup and treatment in the ED, even in patients who lack known predisposing factors or traumatic events.
Dr. Yocum is an emergency medicine resident at the Ohio State University Wexner Medical Center and the Ohio State University Medical Center East, where Dr. King is a clinical assistant professor of emergency medicine.
Tuesday, September 02, 2014
By Dyer, Alexandra; Berg, Kenneth MD; King, Andrew MD
Rat bite fever (RBF) is a fairly rare illness caused by Streptobacillus moniliformis or Spirillum minus. It can be a devastating and even fatal illness if left undiagnosed or untreated. Despite its name, RBF is not only transmitted by rat bites but also by contact with rat feces, ingestion of rat-contaminated food and water, or simply through direct contact with rats. (Clin Microbiol Rev 2007;20:13; Vet Microbiol 2009;133:211; BMJ Case Rep 2009; Epub Dec 17.)
The first documented outbreak in Haverhill, MA, in 1926 was believed to be caused by a pathogen named Haverhillia multiformis. It was later determined to be identical to S. moniliformis. Other outbreaks with matching symptoms have also been documented and frequently misdiagnosed. (Clin Microbiol Rev 2007;20:13.)
RBF is difficult to diagnose. Its sequelae are often nebulous — chills, rigors, and polyarthralgias — and the causative pathogens are difficult to isolate in cultures. RBF is also likely to respond to empiric therapy and it is not a reportable disease, so definitive diagnosis may never be established even if treated appropriately. (Clin Microbiol Rev 2007;20:13; Vet Microbiol 2009;133:211.) Consequently, this condition is often erroneously omitted from the differential when evaluating fevers in the ED unless the history is highly suggestive of a rat bite.
Rats are more than pests in today's society. Humans are coming increasingly into contact with rats in laboratories and even as pets. (Paediatr Child Health 2010;15:131.)
A 21-year-old man presented to the ED with chills and rigors after being bitten by a lab rat on the right hand four days previously. Surprisingly, the patient denied any significant localized symptoms around the bite itself. He also denied any experiments involving infectious pathogens being performed at his laboratory. Two days after being bitten, the patient woke with generalized fatigue, malaise, myalgias, chills, and rigors.
Aspirin at home did provide mild transient relief of his symptoms, but they continued to recur and progressively worsen as the medication wore off. His symptoms persisted, and he also developed sore throat and diaphoresis. He denied recent travel, but did say he was camping in the woods about two weeks prior to his symptoms. Nonetheless, he denied mosquito and tick bites. He also denied any nausea, vomiting, chest pain, shortness of breath, abdominal pain, rash, and urinary symptoms.
His past medical history was notable for a nephrectomy in 1992 for polycystic kidney disease. The patient also endorsed daily use of LSD, dextroamphetamine/amphetamine (Adderall), and recently recreational diphenhydramine (Benadryl) with alcohol. He reported that he had used these substances as recently as 36 to 48 hours prior to admission, and had used them in the past with no similar reactions. He also said others used the same batch of medications and drugs he did without these symptoms. The patient denied any history of intravenous drug use. His sexual history was notable for numerous female sexual partners and unprotected intercourse. He denied any history of genital or oral lesions, ulcers, discharge, or lymphadenopathy.
The patient was febrile with a temperature of 104°F rectally during his initial ED evaluation. He appeared ill, and was hypotensive at 70/40 mm Hg. He was profoundly tachycardic with a heart rate of 143 and an oxygen saturation of 90% on room air, but not in respiratory distress with a rate of 16.
He was notably diaphoretic, anxious-appearing, agitated, and mildly confused. The rat bite wound located on the right hand appeared clean, well-healing, and was not tender, warm, or erythematous. There was no drainage.
Laboratory evaluation yielded a normal white blood cell count of 5.4 and mild thrombocytopenia at 131. A urine drug screen was only positive for cotinine, a nicotine metabolite, despite the patient's admission to the use of other recreational drugs. His serum alcohol level was zero. His basic metabolic panel and electrolytes were all within normal limits. He had a very mild transaminitis with an AST of 48 and a mildly elevated creatine kinase at 223. A urinalysis showed trace blood but no signs of infection, and was otherwise negative. His initial CRP was 9.60. An x-ray of the patient's hand showed no osseous abnormality.
The patient was given lorazepam (Ativan) for his rigors, and empirically covered with ampicillin/sulbactam (Unasyn). Acetaminophen was used to treat his fever. Aggressive resuscitation with intravenous fluids was performed given the hypotension on arrival. He was admitted to the intensive care unit for further management and workup.
The patient tested negative for EBV, HIV, adenovirus, influenza, RSV, metapneumovirus, rhinovirus, parainfluenza, gonorrhea, and chlamydia after admission. Blood cultures were drawn and showed no growth after five days. Diagnosing the patient with RBF was aided by process of elimination, literature review, and evaluation of the patient's symptoms.
The patient was discharged after receiving five days of ampicillin/sulbactam on oral amoxicillin/clavulanate for treatment of RBF. He was scheduled for follow-up as an outpatient a week after his discharge from the hospital. His symptoms had completely resolved by the time of his appointment.
The patient admitted to recent polysubstance abuse, including known hallucinogens like LSD and other stimulants. LSD intoxication has been known to resemble symptoms of schizophrenia. (Int J Neuropsychopharmacol 2013;16:2165.) This drug acts by stimulating 5-HT receptors, causing hypertension, nausea, tachycardia, tachypnea, and mydriasis, among other mostly stimulatory effects. (Int J Neuropsychopharmacol 2013;16:2165; Forensic Sci Int 2012;214[1-3]:e6.)
The patient's mental status and physiological state in this case, however, did not exactly match this classic toxidrome. His symptoms also had persisted for several days, which is atypical for LSD. His additional ingestion of alcohol and diphenhydramine, though, convoluted his presentation and produced side effects mimicking serotonin syndrome or cholinergic toxicity, QT prolongation, and rhabdomyolysis. (Conn Med 2008;72:79; Psychiatry Clin Neurosci 2012;66:244; Psychiatry Clin Neurosci 2011;65:534.) Adderall is also a stimulant that increases blood pressure and heart rate, findings not seen in this patient. Alcohol withdrawal classically presents with autonomic hyperactivity, tremors, insomnia, vomiting, transient hallucinations, psychomotor agitation, anxiety, and seizures. (Crit Care Clin 2012;28:549.)
Rat bite fever can present with variable symptoms, and is often confused for conditions such as meningococcemia, influenza, disseminated gonorrhea, Staphylococcus, and Streptococcus infections, Rocky Mountain spotted fever, brucellosis, leptospirosis, and many other viral infections, including EBV and Coxsackie. (Clin Microbiol Rev 2007;20:13; Vet Microbiol 2009;133:211.)
S. moniliformis and S. minus also frequently colonize the nasal passages and oropharynx of rats. (Clin Microbiol Rev 2007;20:13.) These causative organisms are difficult to isolate; the negative cultures in this case are common with RBF cases. An adequate history is essential in the diagnosis of RBF. Several reports have emphasized that contact with rat feces, rodent scratches, or even brief hands-on contact with rats, in addition to a rat's bite, can cause RBF. (Clin Microbiol Rev 2007;20:13; Vet Microbiol 2009;133:211; BMJ Case Rep 2009; Epub Dec 17.) There is a reported 10 percent risk of transmission following a rat bite. (Clin Pediatr 2004;43:291.)
S. moniliformis is the most common in North America, and is a pleomorphic gram-negative rod with characteristic bulbar swellings under the microscope. It is extremely fastidious, requiring microaerophilic conditions and a special medium to grow in the laboratory. (Clin Microbiol Rev 2007;20:13.) S. minus is more common in Asia, causing a disease known by many as Sodoku. This gram-negative spirochete can only be visualized with a Giemsa stain, Wright stain, or dark-field microscopy, which are not commonly done unless specifically requested by the physician. (Clin Microbiol Rev 2007;20:13.) Many new PCR techniques are being developed to help identify these organisms; unfortunately, this is not yet commonly available to most practitioners. (Microbiol Immunol 2008;52:9; Lab Anim 2002;36:200.) Sodium polyanethol sulfonate, an added anticoagulant in many culture systems, can limit the growth of S. moniliformis. (Am J Clin Pathol 1973;60:854.)
RBF caused by S. moniliformis generally presents with an abrupt fever, rigors, and migratory polyarthralgias. The incubation period on average is two to three days. (Vet Microbiol 2009;133:211.) The bite usually heals uneventfully before RBF develops. More than 50 percent of patients develop migratory polyarthralgias, and 75 percent develop a variable rash that can be maculopapular, petechial, hemorrhagic, purpuric, or desquamative. (See photo.) The rash is strongly associated with RBF and should evoke immediate suspicion of this diagnosis. Other associated symptoms are nonspecific and can include headache, nausea, vomiting, sore throat, and severe myalgias. Symptoms can be highly variable, making the diagnosis even more difficult. It should be noted that RBF caused by S. minus causes distinct findings such as a longer incubation period of 14 to 18 days, relapsing fevers with up to three to seven days of afebrile time between flares and prominent lymphadenopathy. Joint manifestations are rare in cases of RBF caused by Spirillum minus. (Clin Microbiol Rev 2007;20:13; Vet Microbiol 2009;133:211.)
The most commonly documented serious complication of RBF is endocarditis. These patients present with symptoms of RBF, and were found to have valvular disease and positive blood cultures growing S. moniliformis. (J Clin Microbiol 2007;45:3125; Indian Heart J 2013;65:442.) Many other complications of RBF have been reported, including myocarditis, systemic vasculitis, septic arthritis, pericarditis, polyarteritis nodosa, meningitis, hepatitis, pneumonia, tenosynovitis, parotitis, and focal abscesses. (Clin Microbiol Rev 2007;20:13; Vet Microbiol 2009;133:211; J Clin Microbiol 2007;45:3125; Eur J Clin Microbiol infect Dis 2006;25:791; Indian Heart J 2013;65:442.) Mortality of untreated RBF ranges from seven to 13 percent, necessitating early diagnosis and treatment of RBF. (Vet Microbiol 2009;133:211.)
RBF treatment is relatively straightforward. First-line therapy is penicillin, although S. moniliformis has shown susceptibility to many alternative antibiotics including tetracycline, ampicillin, streptomycin, tetracycline, chloramphenicol, gentamicin, cefuroxime, vancomycin, and erythromycin. (Clin Microbiol Rev 2007;20:13; Vet Microbiol 2009;133:211.) This patient was treated with ampicillin/sulbactam as an inpatient and amoxicillin/clavulanate as an outpatient, which adequately covered S. moniliformis.
RBF continues to be an elusive diagnosis, which is more common than originally thought, and can lead to significant morbidity and mortality if untreated. This condition should always be included on the differential diagnosis in the ED when a patient presents with fever, rigors, arthralgias, or rash. This is especially true if the patient has had any possible contact with rats.
Ms. Dyer is a fourth-year medical student at Ohio State University. Dr. Berg is an emergency medicine resident and Dr. King is an assistant clinical professor at Wexner Medical Center at Ohio State University.
Tuesday, August 26, 2014
Turrin, Danielle DO; Sattler, Steven DO; Amodeo, Dana DO
A 25-year-old Hispanic man presented to the emergency department with a complaint of three days of left-sided precordial chest pain. He described the pain as a constant 6/10 with pressure-like discomfort radiating to his left arm and the left side of his neck. He also experienced nausea, but denied any provocative or palliative factors. He said he had not experienced anything similar to this before.
He had no family history of heart disease, acute myocardial infarction, or sudden cardiac death. He admitted to a 1.5 pack-per-day smoking history and social alcohol use, but denied use of any illicit substances. The patient also reported a recent upper respiratory infection that had completely resolved.
The patient appeared pale, diaphoretic, and anxious. No murmurs or extra heart sounds were appreciated, and he had no chest wall tenderness, jugular venous distention, or peripheral edema. The remainder of his exam was unremarkable.
His electrocardiogram showed sinus rhythm at 66 beats per minute with diffuse T wave inversions and ST elevations greater than 1 mm in leads V1-V3. (Figure 1.) His chest radiograph was normal.
The cardiac catheterization team was activated for a presumed anterior wall MI based on his EKG findings and symptoms. The patient was placed on oxygen via nasal cannula, and labs, including cardiac enzymes, were drawn. He was given aspirin and sublingual nitroglycerin, and taken to the catheterization lab.
The patient underwent emergent left heart catheterization, ventriculography, and root aortography for presumed coronary artery disease and acute myocardial infarction. His left ventricle was found to be hypercontractile and mildly hypertrophied. Apical obliteration was present, and the apex was noted to have a spade-shape Figure 2.) The coronary arteries were normal, and no aortic stenosis was present. Trace aortic insufficiency was present, however, and the aortic root was of normal caliber. The patient was diagnosed with apical hypertrophic cardiomyopathy, or Yamaguchi Syndrome.
Two hours post-cardiac catheterization, the patient was discharged home with instructions to follow up with the cardiologist for an outpatient echocardiogram and genetic testing. The patient was also instructed to abstain from sports and other athletic activity until cleared by cardiology.
The patient did not keep his appointments with cardiology, and returned to the ED twice with the same complaint of left-sided chest pain. The patient was seen by cardiology in the ED on both occasions, and MI was subsequently ruled out.
Hypertrophic cardiomyopathy (HCM) is a heterogeneous disease of the cardiac sarcomere with a variable clinical course that is dependent on several factors, including genetics, location, and degree of left ventricular outflow obstruction. (Circulation 1995;92:1680.)
Apical hypertrophic cardiomyopathy (ApHCM) is a relatively rare subtype of HCM (J Am Coll Cardiol 2002;39:638) in which the abnormality is confined to the apex of the left ventricle, causing a nonobstructive cardiomyopathy. (South Med J 2003;96:828.)
ApHCM has been described primarily in Japanese patients but manifests in other populations with significantly less frequency. (J Am Coll Cardiol 1990;15:91.) ApHCM constitutes up to 25 percent of cases of HCM in Japanese patients and only three percent in the rest of the population. (South Med J 2003;96:828.) This is likely how ApHCM came to be called Yamaguchi Syndrome, named for Sakamoto Yamaguchi, who first described the typical features of ApHCM. (J Am Coll Cardiol 2002;39:638.)
ApHCM most commonly presents in young male patients as angina (16%), atypical chest pain (14%), palpitations (10%), dyspnea (6%), or syncope/presyncope (6%). (J Am Coll Cardiol 2002;39:638.) A variety of mechanisms are thought to contribute to anginal symptoms, including imbalances between oxygen supply and demand as a consequence of hypertrophied myocardium with normal coronary arteries. (South Med J 2003;96:828.)
These patients have some characteristic findings, including giant T wave inversions on electrocardiogram, which are most prominent in V4, and a spade-shaped left ventricular cavity at end diastole seen on ventriculography. (J Am Coll Cardiol 2002;39:638.)
Evaluation for HCM patients typically includes a transthoracic Doppler echocardiogram to determine the location and extent of hypertrophy, systolic and diastolic function, degree of obstruction if present, atrial size, and valvular abnormalities. (Circulation 1995;92:1680.)
Occasionally, 2D echocardiogram will not provide adequate information, and the patient will require cardiac MRI, which has been found to provide better overall assessment of left ventricular hypertrophy in HCM patients. (J Am Coll Cardiol 2002;39:638; Circulation 1995;92:1680.)
Cardiac catheterization and angiography are generally reserved for cases with diagnostic uncertainty or in which myocardial infarction is suspected. (Circulation 1995;92:1680.)
Sudden cardiac death is the most common cause of death in HCM patients, but ApHCM is not associated with sudden cardiac death, and has a benign prognosis for cardiovascular mortality. (J Am Coll Cardiol 2002;39:638.) Approximately one-third of ApHCM patients go on to develop complications including MI, arrhythmias, and stroke. (J Am Coll Cardiol 2002;39:638.)
Several treatment options for HCM exist, including medical therapy with beta blockers, calcium channel blockers and antiarrhythmics, pacemakers, and a myectomy. (Circulation 1995;92:1680.) Treatment is generally based on patient symptoms and whether the patient has obstructive or nonobstructive disease. (J Am Coll Cardiol 2002;39:638.) A majority (75%) of patients with HCM have the nonobstructive type. It is important to note, however, that HCM is not a static disease manifestation. It can appear at any age, and increase or decrease dynamically throughout life. (JAMA 2002;287:1308.)
Dr. Turrin is a second-year emergency medicine resident, Dr. Sattler is an emergency physician and the associate research director, and Dr. Amodeo is an academic faculty member, all at Good Samaritan Hospital Medical Center.
Tuesday, August 26, 2014
Robbins, Shari MD; King, Andrew MD
Delineating a specific cause when evaluating patients with bradycardia in the emergency department can often be difficult. Unlike tachycardia, which often accompanies sepsis, fever, dehydration, and other common presentations, bradycardia is less frequently encountered, and can provide a challenge for the emergency practitioner.
Physicians must re-examine the potential causes when a patient is refractory to initial treatments, and ensure accurate vital signs to rule out a commonly missed but easily reversible cause. Bradycardia is initially overlooked because many patients present in stable condition, and the most frequently encountered cause is physiologic bradycardia in athletes or other healthy individuals. Bradycardia may also be medication-induced, a frequent event in patients taking beta blockers. Initial vital signs in emergency departments often omit temperature because of inaccessible rectal thermometer probes and the inability to obtain oral temperatures on patients. Our patient demonstrated the need for accurate vital-sign monitoring as the initial step in management.
The patient was a 63-year-old woman with significant comorbid history including coronary artery disease, hypertension, congestive heart failure, chronic kidney disease, and ischemic cardiomyopathy. She presented to the emergency department with a chief complaint of shortness of breath and elevated blood sugar. She was a difficult historian, but was able to provide a two-day history of shortness of breath and difficulty maintaining glycemic control. She denied fevers, cough, urinary symptoms, chest pain, and leg swelling.
Initial vital signs in the emergency department were a blood pressure of 105/43 mm Hg, a pulse of 36, a respiratory rate of 16 bpm, and oxygen saturation of 100% on room air. Triage was unable to obtain a temperature orally, and she had no significant changes in mental status. Pulmonary and cardiovascular exams were without pitting edema in the lower extremities or signs of pulmonary congestion.
Her pulse stayed in the 30s, ranging from 29-38 in the first minutes following arrival, so atropine was immediately attempted twice without success. The family disclosed that she had complained of feeling hot for the past few days, and had been turning down the thermostat inside her home for three days. Family members had been wearing outerwear in the house because of the declining temperatures. A rectal thermometer probe was used, followed by a temperature-sensing Foley catheter, and determined an initial core temperature of 87°F.
The patient was then placed in a bear hugger, and underwent active and passive rewarming measures including warmed IV fluids. She was found to have a urinary tract infection, and was presumed septic in addition to profoundly hypothermic. She was admitted to the intensive care unit, where she had an acute code blue with unresponsiveness secondary to bradycardia. Her heart rate and temperature normalized after approximately 36 hours of rewarming, and she was discharged after four days without any additional rhythm or rate abnormalities.
Hypothermia is an infrequently encountered, potentially life-threatening, and reversible etiology of refractory bradycardia. Elderly individuals are at especially high risk for developing hypothermia secondary to decreased physiologic reserve, chronic diseases, and medications impeding regulatory responses in addition to social isolation According to the Centers for Disease Control, an average of 689 deaths per year are attributed to exposure to excessive natural cold, which makes this a rare but significantly life-threatening scenario when presenting to the emergency department for care. (MMWR 2005;54:173.) Common EKG changes seen in hypothermic patients include bradycardia, Osborn waves, and prolonged QT interval. Osborn waves appear as a second positive deflection on the EKG, which occurs directly after the QRS complex. (Clin Med Res 2008;6[3-4]:107.) Though not uniformly present, a 2005 study found Osborn waves present on EKGs of 80 percent of patients with temperatures less than 30°C (86°F). (Resuscitation 2005;64:133.) These patients are often refractory to treatment with nodal agents such as atropine, and respond exclusively to active and passive rewarming measures. The identification of hypothermia as the etiology of bradycardia becomes paramount in managing these patients.
Our patient's presentation was difficult because she was elderly with multiple comorbid conditions in a state of bradycardia unresponsive to treatment. It took re-evaluation, collateral information from family, and invasive temperature measurement to delineate an etiology and properly direct treatment. She could have likely suffered a negative outcome if this had not been properly detected and managed.
Dr. Robbins is an emergency medicine resident and Dr. King is an assistant clinical professor of emergency medicine, both at the Ohio State University Wexner Medical Center and the Ohio State University Medical Center East.
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