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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.

Comment on a case or submit your own case following the instructions in the Submissions box to the right.

Thursday, October 15, 2015
By Joseph Hourizadeh, DO; Richard D. Susi, MD; Joseph Kelly, MD; & Afaq Sharieff, MD

A 56-year-old man arrived by car to the emergency department complaining of sore throat, difficulty swallowing, and fever. The patient was previously healthy and up to date with his immunizations. He reported that the pain had started roughly 14 hours earlier and had intensified.

He had taken ibuprofen and acetaminophen with no relief. He mentioned that he had pain in his throat, increasing dysphagia, and increasingly difficulty swallowing. He did not complain of any shortness of breath or difficulty breathing. Oral temperature taken at home was 100.4°F. Vital signs were normal with the exception of tympanic temperature measuring 101.6°F. The patient was alert and oriented, in pain, and leaning forward with his neck extended. The anterior cervical lymph nodes were enlarged and tender bilaterally. Physical examination was normal with the oropharynx showing no tonsillar enlargement, exudate, or erythema. Two blood cultures taken on the day of admission grew Haemophilus influenzae Type b (Hib). The patient was admitted to the intensive care unit for observation, and otolaryngology was consulted. His condition improved with intravenous hydration, antibiotics, steroids, and nebulizer treatments.

H. influenzae is serologically differentiated into six unique strains (a-f) based on structural differences in the polysaccharide envelope. (J Infect Dis 2003;187[1]:109.) Those strains without the polysaccharide envelope are labeled as nontypable and are known to cause invasive infections. The most virulent serotype, Type b, has been in decline since the early 1990s introduction of the Hib vaccine. (Pediatr Infect Dis J 1999;18[6]:490; Microb Pathog 1989;7[3]:225.) Some bacteria that have been shown to cause epiglottitis include Haemophilus parainfluenzae, Streptococcus pneumoniae, Group A streptococcus,Staphylococcus aureus, and herpes simplex virus. Ingestion of caustic materials, inhalations of hot vapors, and smoke have also been known to induce epiglottis, suggesting a noninfectious component to the overall etiology. (Int J Pediatr Otorhinolaryngol2008;72[6]:901.)

Adults presenting with acute epiglottitis tend to have similar initial symptoms as pediatric cases. Sore throat with odynophagia is the most prevalent prodromal and nonspecific symptom of all cases of epiglottitis. (J Exp Med 1931;53[4]:471; Mayo Clin Proc1996;71[12]:1155.) Other symptoms include the tripod position, the clinical sign where patients sit up on both hands while protruding the tongue with the head tilted forward, drooling from the inability to manage oral secretions, cervical lymphadenopathy, hyperpyrexia, and hypoxia. (Microb Pathog 1989;7[3]:225.)

Lateral radiographic images of the neck provided a visual confirmation of the patient's epiglottic pathology, although visual confirmation on x-ray is not always evident at initial presentation. The epiglottis is usually 3-5 mm thick on the lateral neck soft tissue radiograph. Using a criterion of 7 mm thickness, however, can provide 100% sensitivity and specificity for adult acute epiglottitis. (J Am Osteopath Assoc1997;97[4]:227.) Some signs associated with epiglottitis include the thumb/omega sign, which is a swollen epiglottis, and thickened aryepiglottic folds. An aryepiglottic fold width greater than 4.5 mm yielded 83% sensitivity and 100% specificity for adult acute epiglottitis. (J Am Osteopath Assoc 1997;97[4]:227.) A radiological sign includes the vallecula sign where you see a shallow V-shape space instead of a deep linear space extending from the tongue base almost to the epiglottis. (Figure 1.) The diagnosis of epiglottitis can be confirmed if a lack of airspace extends from the hyoid bone to the pharyngotracheal air column.

Bedside ultrasonography has been shown to be a quick and reliable tool for diagnosing epiglottitis. The sensitivity of this technique, however, is relegated to the skill and proficiency of the technician using and reading the ultrasound. (J Ultrasound Med 2012;31[1]:19.)

Airway management is the most urgent consideration followed by supplemental oxygen on initial patient interaction. Patients may deteriorate precipitously. Immediate intubation should be performed if the patient worsens and can no longer maintain oxygenation.

With resistance to ampicillin increasing, third-generation cephalosporins and beta-lactamase penicillins have become the preferred choice in treating Haemophilus influenzae. (Am J Emerg Med 1996;14[4]421.) Acute setting medications, such as corticosteroids, racemic epinephrine, and beta-agonists, have not been proven to be effective treatment options. Rifampin is suggested as prophylactic treatment for anyone exposed and has been shown to be effective as a four-day course in preventing colonization and sequelae of infection. (J Pediatr 1981;98[3]:485.)

The severity of initial presentation is staged and graded allowing for appropriate treatments. The initial concern is airway management, and respiratory rate is an invaluable indicator of staging. Friedman's staging uses respiratory rate, physical examination findings such as stridor, retractions, and perioral cyanosis, along with levels of consciousness, to categorize the aggressiveness of epiglottis and dictating the immediacy of intervention. (Ear Nose Throat J1989;67[12]:873.) Our case presentation suggests the patient is stage II on the Friedman's classification because of his increased respiratory rate. (Figure 2.)

Tuesday, July 14, 2015
By Anthony Congeni, Alex Fox, MD, & Andrew King, MD

Naloxone is given routinely in the hospital and prehospital setting without much concern for significant morbidity. Many providers are unaware of its potential complications, including pulmonary edema, and may be caught off guard when respiratory distress occurs in an awake patient who was previously rescued with naloxone.

The use of naloxone is now common in anesthesiology and emergency medicine for patients with concern for opiate toxicity. Its use, however, is not without occasional morbidity, particularly cardiopulmonary complications including pulmonary edema. (J Toxicol Clin Toxicol 1996;34[4]:409; Expert Opin Drug Saf 2007;6[2]:125; Oral Surg Oral Med Oral Pathol 1981;52[6]:602; Anesthesiology1977;47[4]:376.)

Among reported cases, these episodes have occurred more frequently after postoperative opiate intoxications, though non-postoperative cases have also been described. (Anaesthesist 2012;61[2]:129.) The pathogenesis of naloxone-associated pulmonary edema remains controversial, and the emergency medicine literature on this phenomenon, including its potential emergence in the pre-hospital setting, is limited.

Our patient was a 37-year-old previously healthy male inmate. He was “roughhousing” when he struck his head and went to sleep. Sometime later, the patient was witnessed sliding out of bed, unresponsive. Bystanders reported that the patient had taken heroin prior to the episode, and the facility's nursing staff reported small pupils on exam. EMS arrived and performed chest compressions for an unknown period of time. No epinephrine was given. EMS then gave two doses of naloxone 1mg IM with resulting arousal. An ECG showed normal sinus rhythm.

The patient was taken to the ED of an outside hospital. He was hypoxic en route, with an oxygen saturation in the high 80s despite oxygen. Initial assessment revealed no abnormal neurological or cardiopulmonary findings. Shortly after arrival, he received another dose of naloxone, this time 1 mg IV, as well as 1 L of normal saline. Initial vital signs in the ED were normal with blood pressure of 115/76 mm Hg, heart rate of 86/min, and respiratory rate of 15/min. Initial SaO2, however, was 76% on nasal cannula at 6 L/min. He was switched to a 100% nonrebreather mask with improvement of SaO2 to the mid-90s. The patient then developed a cough with pink sputum, so a chest x-ray was ordered showing severe bilateral pulmonary edema.

The patient was then given a 40 mg IV dose of furosemide and 3 mL nebulized ipratropium/albuterol. A head CT was unremarkable. A drug screen was negative, so the patient was given a diagnosis of “nontoxic overdose,” and transferred to our tertiary care center.

On our initial examination, the patient had rales bilaterally in all lung fields. Repeat chest x-ray (Figure 1) showed a hazy right mid-lung opacity, which was read as asymmetric pulmonary edema versus pneumonia, without evidence of rib fractures or pneumothorax. He was then given another 40 mg IV dose of furosemide. A bedside transthoracic echocardiogram demonstrated no wall motion or valvular abnormalities and a grossly normal ejection fraction, which was later confirmed by a comprehensive echocardiogram. The patient's SaO2stayed in the low-to-mid-90s on nasal cannula at 6 L/min. Other laboratory findings including troponin, BNP, and chemistries were unremarkable. A second drug urine screen collected nine hours after the initial incident was negative. The patient later admitted to taking some form of narcotics earlier in the day, however. He was admitted to an inpatient medicine service. After a one-day stay without complications, his oxygen was weaned and he was discharged in stable condition on room air.

Naloxone has been used for treatment of opiate overdose since the 1960s. (Anaesthesist 2012;61[2]:129.) The first known case of pulmonary edema after its administration was published by JW Flacke et al. in 1977. (Anesthesiology 1977;47[4]:376.) Other cardiopulmonary complications associated with the drug, including various arrhythmias and hypertensive crisis, have also been described. (J Toxicol Clin Toxicol 1996;34[4]:409; Ann Thorac Surg1974;18[6]:608; JAMA 1974;228[1]:25; Anesth Analg 1979;58[6]:524;Am J Med Sci 1985;290[2]:70.)

A review by Lassen et al. in 2012 found 24 published cases of naloxone-associated pulmonary edema. Nineteen occurred in postoperative patients, while five occurred in non-postoperative patients. Three cases resulted in fatality. (Zhonghua Yi Xue Za Zhi1997;60[4]:219; Anesth Analg 1980;59[10]:782; Anaesth Intensive Care 1989;17[3]:374.)

Cases have occurred with as little as 80 μg of IV naloxone, and onset of symptoms after administration has ranged from 1 to 60 minutes. (Anaesthesist 2012;61[2]:129; J Clin Anesth 1995;7[4]:356;Anesthesiology 1986;65[6]:709.)

The majority have occurred in previously healthy men below age 50. (Anaesthesist 2012;61[2]:129.) In three postoperative cases, opiates were not used prior to naloxone. (Minerva Anestesiol 1982;48[1-2]:43;Lakartidningen 1995;92[42]:3919.) Our patient initially denied but later admitted to opiate use, despite having an undetectable level on the urine screen. It is probable that it was opiate intoxication that caused the unresponsive episode necessitating chest compressions and naloxone administration by EMS. Based on the time course, imaging, and unremarkable echocardiogram, it is likely that our patient is another case of naloxone-associated pulmonary edema in the prehospital setting.

Many past case reports have attempted to explain the pathophysiology of non-cardiogenic pulmonary edema after naloxone. After the earliest cases, it was proposed that the pathophysiology is a catecholamine surge induced by abrupt awakening and return of painful stimuli, causing increased pulmonary blood pressure and capillary permeability. (Anesthesiology 1977;47[4]:376; Minerva Anestesiol 1982;48[1-2]:43.) Later it was proposed that the catecholamine surge was neurally mediated, with naloxone antagonizing endogenous opioid receptors in the central nervous system leading to catecholamine release from the brainstem and adrenal medulla. (Anesthesiology 1984;60[5]:485.) The general principles of this mechanism were agreed upon by authors of several other case reports of naloxone-associated pulmonary edema in the 1990s and 2000s. (Chest 2007;132[4_MeetingAbstracts]:692; Anaesth intensive Care 1991;19[4]:578; Anesth Analg 1997;84[1]:218.)

The 2012 review by Lassen et al. debated this mechanism. It stated that the evidence for a catecholamine surge after naloxone is controversial, with some animal studies showing increased catecholamine production, but one showing a decrease. (Anesthesiology 1998;88[5]:1154; Br J Anaesth 1977;49[6]:525;Anesth Analg 1988;67[8]:730; Acta Anaesthesiol Scand2006;50[10]:1271.) They pointed out that in the only basic science study relating pulmonary capillary permeability to naloxone, the drug did not increase capillary blood flow or pressure. (Prog Clin Biol Res1990;328:389.) The authors also mentioned that no experimental studies have been done where naloxone alone was able to induce pulmonary edema. (Anaesthesist 2012;61[2]:129.)

They stated that hypoxia, which is not caused by naloxone, is a common precipitant for other types of non-cardiogenic pulmonary edema including that induced by opiates. They argue that hypoxia from opiates themselves may be the driving pathophysiology for pulmonary edema and not naloxone in many of the cases described. They are not the first to make this argument; similar points were made in a 1989 letter to the editor in Annals of Emergency Medicine and as a review of naloxone complications in the same journal in 2005. (18:116; 22[9]:612.)

It is probable that a catecholamine surge has a pathophysiologic role in the development of naloxone-associated pulmonary edema. The only experimental study on the relationship between naloxone and pulmonary capillary permeability showed no link between the two, but catecholamine surge leading to pulmonary edema has been established in experimental studies on neurogenic pulmonary edema. (Lancet 1975;2[7938]:749.) Also, in several of the cases described, including ours, patients develop signs compatible with a catecholamine surge including tachycardia, elevated blood pressure, and diaphoresis. (Anesthesiology 1977;47[4]:376; Anesthesiology1984;60[5]:485; Chest 2007;132:692; Ann Emerg Med1987;16[11]:1294.)

Cases of arrhythmias and hypertensive emergency associated with naloxone not resulting in pulmonary edema have also been reported. (Ann Thorac Surg 1974;18[6]:608; JAMA 1974;228[1]:25; Anesth Analg 1979;58[6]:524; Am J Med Sci 1985;290[2]:70.) It is possible, however, that opiate-induced hypoxia is also a component in naloxone-associated pulmonary edema. Our patient was likely hypoxic after being unresponsive prior to naloxone administration. He was also known to be hypoxic en route to the ED, prior to symptoms of pulmonary edema. Catecholamines and hypoxia play roles in vasoconstricting the pulmonary vasculature, so it is possible that these factors may contribute or be additive to inducing pulmonary edema in patients who receive naloxone after opiate intoxication. The full cause may not be elucidated until more basic science experiments are conducted in this area.

The majority of case reports of naloxone-associated pulmonary edema have occurred in the postoperative period, but five non-postoperative cases have been reported. (Anaesthesist 2012;61[2]:129.) Four of those occurred in the emergency department. (J Toxicol Clin Toxicol1996;34[4]:409; Chest 2007;132(4_Meeting Abstracts]:692; Med Clin (Barc) 1990;94[16]:637; J Opioid Manag 2013;9[5]:369.) Only one previously published case was the result of naloxone administration by EMS in the field, similar to our case. (Chest 2007;132:692.) The patients were quickly brought to EDs before the onset of symptoms and received treatment and supportive care in a controlled environment in these cases. Field administration presents a new set of difficulties in diagnosing and treating a patient with complications from naloxone. Pulmonary edema or other cardiopulmonary complications could occur after naloxone in patients who are not in a position to receive emergent medical care shortly thereafter.

Legislation in various parts of the United States has now made naloxone available with civil and criminal protection from liability to bystanders or first responders such as police officers and EMS personnel, with the goal of bringing faster treatment to potentially lethal opiate intoxications. (J Opioid Manag 2013;9[5]:369.) It is well established in emergency medicine that recreational overdose on opiates is often deadly, usually before prehospital care is initiated. Severe cardiopulmonary complications from naloxone are rare, but fear of complications should never preclude the use of naloxone in suspected overdose, even in the prehospital setting by bystanders and first responders. It would be meaningful for first responder personnel to be aware of the potential complications of naloxone, and to have a plan to activate the proper emergency services in the event of an arrest or severe dyspnea. This could further limit the morbidity and mortality from recreational opiate intoxication.

Our patient is another case of pulmonary edema associated with naloxone administration in the ED. It was previously thought that a catecholamine surge is the cause of the complication, but the mechanism remains controversial. Hypoxia from the opiates themselves has also been proposed to be the driving pathophysiology.

This is the second-known case of pulmonary edema after administration of naloxone in the field. As naloxone use becomes more common among bystanders and first responder personnel, it is important to stress the need for emergent medical care should cardiopulmonary complications arise.

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Tuesday, June 23, 2015

By Charles Burtis, MD; Ann Haynes, MD & Andrew King, MD

A 59-year-old woman presented to the emergency department complaining of worsening abdominal pain and distension as well as four episodes of syncope and lightheadedness. The patient reported a past medical history of hypertension and hypothyroidism, but denied other comorbidities. The patient reported that she was walking her dog the previous night when the dog bolted forward, causing her to lose her balance and fall forward.

The patient reported that she was able to tuck into a ball and roll, sustaining minor trauma only to her right side. She denied any head trauma or loss of control after falling. She was able to walk home, and she felt fine apart from some bruising on her right lower ribs. Over the course of the evening, however, the patient's pain began to worsen. She had several episodes of nausea and non-bloody, non-bilious emesis. The next morning she began to feel short of breath, and her abdominal pain continued to worsen. She reported two episodes of syncope, which she attributed to the severity of her pain or because she was breathing too quickly.

The patient's systolic blood pressure was in the 80s when she arrived in the ED, and her heart rate was 130 bpm. Her respiratory rate was 26 bpm, and her SPO2 was 85% on room air. The patient was in distress and started on oxygen, intravenous access was obtained, and she was resuscitated with normal saline. She had significant abdominal pain that seemed to localize to the right upper quadrant, and a bedside FAST exam was positive for intra-abdominal fluid.

The patient was expeditiously transferred to a trauma center where she underwent a CT with IV contrast for the abdomen and pelvis. A large smoothly marginated cystic lesion was noted on the dome of the right hepatic lobe measuring 13.1 x 8.6 cm. A grade 3 liver laceration was noted at the base of the hepatic cysts with a surrounding large hematoma. Moderate amounts of fluid were noted in Morrison's pouch, the surrounding paracolic gutter, and the pelvis. A fracture was also noted in the right eighth rib that was not displaced.

The patient's hemoglobin levels continued to drop, and she was taken to interventional radiology, where she was noted to have a small pseudoanuerysm of a segmental branch of the right hepatic artery within the hepatic cyst, with evidence of active intraperitoneal extravasation. The patient then underwent an embolization of the segmental branch of the right hepatic artery, and hemostasis was successfully obtained.

The patient's hemoglobin levels stabilized after the embolization, and she was able to resume a regular diet. She was discharged on hospital day six with the plan to follow up with trauma surgery.

Unintended falls are the most common cause of injury in the United States. They lead to 7.9 million emergency department visits per year and 860,000 hospitalizations. (Acad Emerg Med 1998;5[11]:1064.) In our particular case, what appeared to be a benign mechanism resulted in a serious injury because of the presence of a benign hepatic cyst that the patient didn't know about. Simple hepatic cysts are believed to be present in five to 10 percent of the population, with increasing incidence with age. (J Clin Ultrasound 1996;21[2]:115.) Common complications of hepatic cysts include rupture, contained hemorrhage, and obstructive jaundice. (J Nippon Med Sch 2010;77[3]:181; West J Med 1982;136[3]:246; Am J Gastroenterol 1988;83[1]:93.)

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Multiple cases of traumatic rupture of hepatic cysts are reported, but these are typically contained within the cyst. Few reports exist suggesting hemoperitoneum after cyst rupture. In our case, the rupture of the hepatic cyst was accompanied by a liver laceration, which led to extravasation of blood leading to hemoperitoneum. (HPB Surg 1988;1[1]:81; South Med J 1989;82[5]:667.) Focused bedside ultrasonography and strong clinical suspicion assisted in expediting a transfer to a trauma center where intervention corrected the problem.


Dr. Burtis is a third-year emergency medicine resident at the Ohio State University East Medical Center and the Ohio State University Wexner Medical Center, where Drs. Haynes and King are assistant professors of emergency medicine.



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Tuesday, May 26, 2015

By Mohammed Hassan-Ali, MSC & Ahmed Raziuddin, MD

A 56-year-old black man presented to the ED complaining of face and neck swelling. An initial history was difficult to obtain because the patient did not speak English fluently and had slurred speech. Symptoms started approximately a week earlier when the patient was at his nursing home. He denied dysphagia or odynophagia, he had no rashes, pruritus, dyspnea, or peripheral edema, his face was flushed, and he had visibly-engorged neck veins. He noticed that his tongue was mildly swollen, so he took Benadryl for a week with no relief. The patient said he believed that the symptoms might have been because a nurse gave him an incorrect medication at the nursing home. He had been a pack-a-day smoker for 30 years, and had a history of schizoaffective disorder, bipolar disorder with psychotic features, and GERD.

A CBC with differential, PT, PTT, BMP, and UA were all within normal limits. A chest x-ray confirmed a large mediastinal mass, and a soft tissue neck CT scan with contrast found a large mass in the upper mediastinum with extensive adenopathy in the base of the right side of his neck on the right, a right lobe thyroid mass, and occlusion of the superior vena cava and left subclavian vein. The report suggested that the findings were consistent with aggressive lymphoma or lung cancer.

The patient was admitted to the hospital with a scheduled emergent biopsy of the neck mass/lymph nodes. He was diagnosed with superior vena cava (SVC) syndrome and small cell lung carcinoma (SCLC) by tissue biopsy and pathology.

The SVC drains venous blood from the head, neck, upper extremities, and thorax. Obstruction of the SVC is usually because of neoplasms that invade the tissue wall or put pressure on the SVC. (J Clin Oncol1984;2[8]:961.) SCLC accounts for 25 percent of SVC syndrome because of malignancy. (HemOnc Today Feb. 10, 2012;http://bit.ly/1H3Uggt.) Clinical features of SVC syndrome include facial edema, difficulty swallowing, engorged neck veins, cough, and dyspnea. (Int J Radiat Oncol Biol Phys 1987;13[4]:531.) Obstruction of the SVC can divert blood flow to the azygous veins, internal mammary veins, superior and inferior epigastric veins, or femoral and vertebral veins, but the venous pressure remains elevated. Complications of this condition include cerebral edema, coma, and death. (Joint Bone Spine 2002;69[4]:416.)

The patient presented with only neck swelling and difficulty speaking. The speech impediment was most likely from the combination of SVC syndrome and right-sided thyroid mass occluding the right recurrent laryngeal nerve. The prognosis of SVC syndrome is poor because of the underlying neoplasm. The patient was promptly started on a dose of approximately 2900 cGy in 13 fractions to the mediastinum and neck nodes and scheduled to receive chemotherapy. After three weeks, he was medically stabilized, and had tolerated chemotherapy and radiation. The SVC syndrome did not compromise his breathing. The patient was advised that he could be discharged with a PORT-A-CATH for future chemotherapy, but the prognosis of his condition remained poor.

Lung cancer is the leading cause of cancer-related death in the United States. (CA Cancer J Clin 2008;58[2]:71.) Its incidence is decreasing, but 13 percent of all new cancers are still from lung cancer. (“Lung Cancer Statistics,” American Cancer Society, March 4, 2015;http://bit.ly/1JSd82D.) Even with current screening techniques, approximately half of patients have a metastatic presentation and a 45 percent five-year survival rate. Approximately 90 percent of lung cancer patients are active smokers or had recently stopped.

Signs and symptoms of this cancer include shortness of breath, cough, bone pain, weight loss, fatigue, and neurologic dysfunction. (Medscape, March 26, 2014; http://bit.ly/1dPWx29.) None of these were present in the patient. Most SCLCs are metastasized by the time of diagnosis, and are not curative by surgery. A combination of chemotherapy and radiation therapy is required. SCLCs are centrally located masses found in the lung parenchyma. (J Clin Oncol2006;24[28]:4526.) These pale gray tumors are fusiform-shaped and quite fragile. They can also express neuroendocrine markers and secrete polypeptide hormones that can cause paraneoplastic syndromes (PNS), such as syndrome of inappropriate antidiuretic hormone (SIADH). (Chest 2003;123[1 Suppl]:97S.)

The time frame of disease development was unclear, but this patient's presentation was unique because he had nonthreatening symptoms. Lung cancer and SVC syndrome symptoms are usually aggressive, and can compromise the quality of life for patients. Our patient is now being treated to try to prevent the expected disease outcomes.


Mr. Hassan-Ali is a third-year medical student at the Windsor University School of Medicine in Cayon, Saint Kitts. Dr. Raziuddin is an internist specializing in emergency medicine at Louis A. Weiss Memorial and Thorek Memorial hospitals in Chicago.



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Tuesday, January 20, 2015

By Mikhail Elfond, DO; Esi Quayson, MD; & Joseph V.M. Kelly, MD, MBA


A 65-year-old man presented to the ED via EMS with symptoms of stroke. The paramedics stated his right-sided weakness and speech difficulty started 40 minutes prior to presentation in the ED. En route to the hospital, paramedics observed four episodes of facial twitching.



Vitals signs were significant for a rectal temperature of 100.2°F and a fingerstick blood sugar of 220 mg/dL. History of present illness was significant for a diagnosis of left otitis media treated with Augmentin and Vicodin at an urgent care center one day prior to presentation. Past medical history included hypertension, hypercholesterolemia, and diet-controlled borderline diabetes mellitus.


He appeared confused and did not follow commands. He had a right lateral gaze, a right pronator drift, and global aphasia. Left tympanic membrane was perforated with purulent discharge. No mastoid tenderness or overlying skin changes were noted.


A head CT scan without contrast was performed, and revealed an ill-defined low attenuation lesion within the posterior left temporal lobe with associated pneumocephalus. Given ipsilateral opacification of the mastoid air cell and middle ear, findings were concerning for otomastoiditis complicated by intracerebral abscess. A follow-up maxillofacial CT scan with contrast showed thinning of the overlying roof of the temporal bone with dehiscence at multiple locations. A focus of associated pneumocephalus was identified. No definite abnormal parenchymal enhancement was identified, but the findings were consistent with intracerebral abscess complicating otomastoiditis.


Laboratory studies including complete blood count with differential showed WBC 11.54 with 88.2% neutrophils. Pre-operative labs and blood cultures were drawn; the patient was given Levetiracetam, ceftriaxone, and vancomycin, and taken to the operating room by neurosurgery and ENT.


A left ear culture grew Pseudomonas oryzihabitans and Streptococcus pneumoniae. An intracranial abscess grew S. pneumoniae. The patient did well post-operatively, and was discharged home on IV antibiotics.


A brain abscess is a focal, suppurative collection in the brain parenchyma resulting from an infection, trauma, or neurosurgery. Approximately 1,500 to 2,000 cases of brain abscesses are diagnosed in the United States annually, with an estimated one in 10,000 being hospitalized. (Int J Infect Dis 2006;10[2]:103.) Rates are higher in certain high risks groups, including patients with HIV/AIDS. (N Engl J Med 2014;371[5]:447.)


Bacterial invasion is from direct or hematogenous spread. Direct spread makes up 20 to 60 percent of all abscesses, which are caused by otitis media, mastoiditis, dental and other oropharyngeal diseases, or sinusitis, and usually result in a single abscess. (Laryngoscope 1998;108[11]:1635.) Ear infections are decreasing as a cause of brain abscesses in developed countries, but sinus infections continue to be an important consideration. (Laryngoscope 1998;108[11]:1635.) When infection spreads from the mastoids or middle ear to the CNS, the cerebellum, temporal lobes, or both are most often involved. (Laryngoscope 1998;108[11]:1635.) The most frequently isolated pathogen in acute mastoiditis is S. pneumoniae, with a prevalence of approximately 30 percent with minimal variation worldwide. (Laryngoscope 1998;108[11]:1635; QJM 2002;95:501.)


Common symptoms and signs include headache in 70 percent of cases, mental status changes in 65 percent, focal neurological deficits in 65 percent, fever in 50 percent, seizures in 25 to 35 percent, nausea and vomiting in 40 percent, nuchal rigidity in 25 percent, and papilledema in 25 percent. (N Engl J Med 2014;371[5]:447; QJM 2002;95[8]:501.)


The classic triad of fever, headache, and a focal neurological finding is only present in 20 percent of patients. Fever is absent in about 50 percent of patients with brain abscess at the time of the initial presentation. (N Engl J Med 2014;371[5]:447; QJM 2002;95[8]:501.) A lesion in the temporal lobe may lead to an ipsilateral headache, aphasia, and possibly a visual field defect. Hematogenous spread from bacteremia usually leads to multiple abscesses, usually in the territory of the middle cerebral artery. (N Engl J Med 2014;371[5]:447; QJM 2002;95[8]:501.)


As many as 85 organisms have been cultured from blood, CSF, or infection sites of patients with brain abscesses. The most common organisms are Streptococcus spp and Staphylococcus spp. (N Engl J Med 2014;371[5]:447.) A meta-analysis by Brouwer, et al. found Pseudomonas spp in only two percent of all cultured bacteria. P. oryzihabitans is rare and opportunistic, and is an interesting isolate in our case. It is most commonly associated with catheters, other foreign body causes of bacteremia, and is interesting because this patient had no previous implantation of surgical objects. (Microb Ecol 2011;62[3]:505.)



Case fatality rates from brain abscesses have decreased from 40 to 10 percent, with rates of full recovery increasing from 33 to 70 percent over the past 50 years. These improvements have been attributed to advancement in antibiotics, stereotactic biopsies, and advanced imaging techniques such as MRIs and CT scans. (N Engl J Med 2014;371[5]:447.)


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About the Author

Lisa Hoffman
Editor, Emergency Medicine News


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    • All relevant information about the patient in the case being reported, as well as a full description of the patient's symptoms, diagnosis, treatment, and outcome.
  • A discussion that provides context for the case being reported and an explanation of specific treatment decisions.
    • Authors must ensure that references are complete and accurate. References should be cited within the text, not with footnotes or a reference list at the end of the article, in this format: (EMN 2012;34[2]:18.)
    • Figures and tables should be submitted in the Word file with the case report, not as separate attachments. Tables should not be formatted, but included as text at the end of the file.
  • All authors must disclose any potential conflicts of interest.
  • All submissions will be edited for grammar, style, and clarity.