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.

Friday, December 1, 2017


Symptomatic bradycardia is usually reserved for the over-the-hill crowd, but it is not entirely unheard of in the young and healthy. A 21-year-old African American man was sent to the emergency department by his primary care provider. The patient had no previous medical issues, normal vital signs, and was fine until about a week prior. He had quickly worsening shortness of breath while climbing the stairs to get to his dorm bedroom. The young man denied having been out in the woods or noting tick bites. He had no family history of cardiomyopathy or early cardiac events.​

The patient had negative toxicology and social history screens. When pressed further, he recalled malaise, stiff neck, low-grade temperature, and muscle aches for about two weeks prior to exertional dyspnea onset. As it turned out, he went to a bonfire party for his graduating college class about three weeks before presentation. He thought the malaise was just a cold, and only the exertional component brought him and his mom to his doctor for evaluation.

A heart block with a heart rate of 36 bpm was noted on an ECG in the office, which was then compared with the normal sinus rhythm from previous ECGs. The patient was directed to the emergency department for further testing. The patient appeared well, had no advantageous heart sounds, and had an essentially normal exam with no skin rash besides a heart rate of 44 bpm and a third-degree heart block on ECG.

The clinical suspicion for Lyme disease was high because no other likely source trumped the history given by the patient. Initial Lyme testing was negative, which is often the case. The patient's serology, toxicology, cardiac markers, and electrolytes were unremarkable. Chest imaging was normal, and the patient was admitted to the cardiology ICU. Further testing involved an MRI of the heart and echocardiography as well as serial cardiac markers. The patient was monitored, but did not require temporary pacing.

Lyme disease is caused by Borrelia burgdorferi, the most common parasite transmitted by ticks in the United States. The transmission route is through a bite of an Ixodes tick. Most reports of transmission come from the Northeast and upper Midwestern states. The typical symptoms are malaise and arthralgia, as well as the telltale bull's eye rash of erythema migrans. Lyme disease may present with more insidious neurological symptoms in up to 20 percent of cases, such as Bell's palsy and rare cardiac events (up to 10% of cases), such as heart block. (Expert Rev Mol Med 2004;6[2]:1; Infect Dis Clin North Am 2008;22[2]:275; Clin Lab Med 2010;30[1]:311.)

The differential for this case certainly included acquired causes such as toxidromes, electrolyte abnormalities or medical management side effects, and congenital causes such as cardiac conduction pathway malformations and conduction abnormalities. Finally, developing infiltrative or inflammatory processes or infections must be considered.

Early Diagnosis and Antibiotics

Most Lyme carditis cases resolve completely within six weeks without the need for permanent pacemaker. The block usually resolves 48-72 hours after the initiation of intravenous antibiotics, so even a temporary pacemaker is rarely needed. This stresses the importance of early diagnosis and initiation of antibiotics to avoid complications like cardiac arrest or severe heart failure. The outcome and prognosis are highly favorable when treated early with antibiotics. (Przegl Epidemiol 2004;58[4]:589; Front Biosci 2003;8:s769; Int J Cardiol 2017;232:24; Int J Cardiol 2008;129[1]:15.)

PO antibiotics can be considered for cases of mild carditis, doxycycline or amoxicillin for 21 days. IV antibiotics (ceftriaxone or cefotaxime for 14-21 days) and hospitalization are required for moderate and severe carditis, manifested by advanced heart block, cardiac arrest, congestive heart failure, and vital instability. Most of the time, the heart block improves within 72 hours of starting the intravenous antibiotic. Very rarely, a temporary pacemaker is needed, but continued cardiac monitoring is essential. Supportive therapy with intravenous hydration, supplemental oxygen, and diuretics might be needed. Severe heart failure, though rare, can require additional supportive measures, including mechanical ventilation and circulatory support. (J Emerg Med 2017;52[6]:815; Clin Infect Dis 2014;59[7]:996.)

Our patient was admitted and treated with two weeks of IV ceftriaxone. He developed a left bundle branch block (LBBB) intermittently while being closely monitored in the cardiac intensive care unit. Once the LBBB resolved, the patient entered a first-degree sinus block with an occasional Mobitz type 1 rhythm. Electrophysiology consultants recommended noninterventional observation because this rhythm transition is self-limiting and will resolve completely once the Lyme parasite load is eliminated. The patient returned to an asymptomatic state during his two-week hospital course, and was discharged home with two weeks of oral doxycycline and interval cardiologist follow-up.

Our patient time zero for starting the antibiotics was several hours after we interpreted his ECG and processed his history. We would like to propose empiric doxycycline to be started at the time of presentation for suspected Lyme carditis. Literature overwhelmingly advocates for antibiotics. Our role as emergency physicians should include starting the antibiotics much sooner, preferably before admission.

Dr. Singh is currently an assistant professor of emergency medicine at Hartford Hospital, University of Connecticut. She and her emergency physician-husband, Daksh Rampal, MD, own Priority Urgent Care in Ellington, CT ( Mr. Keiltyka is an emergency medicine physician assistant and a graduate of Drexel University's physician assistant program in Philadelphia.

Wednesday, October 25, 2017


A 43-year-old man presented to the ED with a rash in a C7 dermatomal pattern that was burning and painful. The patient said the rash began three weeks before the ED visit as a group of little blisters on his right upper back and extending down his right arm. The patient was worried and in mild distress as the rash continued to burn, and he reported numbness to the area. He mentioned he had received the shingles vaccine in the past.​

The patient's rash was yellow, crusty, and tender upon palpation. The area was hyperkeratotic with noticeable scabbed lesions and cracked skin. The patient had normal range of motion without motor deficits in the right arm. Herpes zoster (HZ) is caused by the reactivation of varicella zoster virus (VZV), which occurs when immunity to VZV declines because of aging and or immunosuppression. This condition most commonly affects the elderly population; more than half of the cases of HZ occur in patients over 60. (Mayo Clin Proc 2009;84[3]:274.) The condition is diagnosed clinically by the distinctive dermatomal characteristics of the rash and the painful sensation. Herpes zoster lesions contain high concentrations of VZV, which can spread through physical contact or airborne transmission. Exposure to airborne VZV can result in primary varicella infection in susceptible people. HZ is only contagious, however, from the time after the rash appears until the lesions crust.

The condition, commonly referred to as shingles, comes from the Latin word cingulum meaning belt, which describes the rash's dermatomal pattern. The shingles infection is a well-known, dreaded potential consequence of a prior VZV infection. The rash is characterized as grouped vesicles on a red base that are located unilaterally (do not cross the midline) and undergo different stages: red macule to papule within the first seven to 10 days, which then progresses to vesicles and ultimately pustules and crusty lesions. These crusty lesions may take up to four weeks or more to completely resolve. Herpes zoster presents with pruritus, dysesthesia, and pain along the involved dermatome. This pain may occur days before the onset of the rash, leading to multiple workups and misdiagnoses.

Early detection and treatment of HZ reduces the acute symptoms and severity of postherpetic neuralgia (PHN). Differential diagnoses for HZ include the herpes simplex virus, candidiasis, contact dermatitis, impetigo, autoimmune blistering diseases, and dermatitis herpetiformis. The most sensitive and specific diagnostic test to confirm the diagnosis of HZ is viral DNA PCR, but PCR is not necessary if the clinical presentation is distinctive for HZ.

Timing is Key

Common complications include postherpetic neuralgia, superinfection with Staphyloccocus aureus and Streptococcus pyogenes, scarring, and hyperpigmentation. Shingles can also lead to pneumonia, hearing problems, blindness (herpes zoster ophthalmicus), encephalitis, cranial and peripheral nerve palsies, and sometimes death. Approximately 13 percent of those 60 and older with HZ will get PHN, which mainly consists of pain persisting for more than three months after the initial shingles rash has healed. (Mayo Clin Proc 2009;84[3]:274.)

The risk of PHN increases with age and low immunity. A large population study found the rate of PHN increased from five percent in HZ patients under 60 to 10 percent in those 60-69 and to 20 percent in those 80 and older. (Mayo Clin Proc 2007;82[11]:1341.)

The pain occurs due to viral damage to the sensory nerves. The condition is refractory to most analgesics, but effective therapy often requires multiple drugs started in a systematic pattern, initially administering a low dose and increasing the dose gradually until the pain is resolved and adverse effects are noted. The medications used for PHN include topical agents, antidepressants, anticonvulsants, and opioids. During an acute episode of HZ, symptom control and disease complication prevention is achieved with a combination of antiviral therapy, corticosteroids, and analgesics. The antivirals include acyclovir, famciclovir, and valacyclovir, which inhibit viral replication and thus decrease the duration of viral shedding. This decrease allows for faster rash healing, and reduces the duration of severe pain and the risk of PHN. Antiviral treatment is specifically recommended for patients over 50 who have moderate to severe pain and facial involvement. (Mayo Clin Proc 2009;84[3]:274.)

Clinical trials have demonstrated the effectiveness of treatment 72 hours after rash onset, though this timing is not always feasible in a clinical practice setting. Initiating antiviral treatment after 72 hours of rash onset and its benefits have not been studied, but patients with severe HZ symptoms should be started on antivirals regardless of timing, especially if there is new vesicle formation. Valacyclovir and famciclovir may be administered in an outpatient setting because they require less frequent dosing than acyclovir. Immunocompromised patients require a more aggressive IV treatment. Corticosteroids do not have any effect on PHN; their only benefit is assisting a faster resolution of the acute symptoms when combined with antiviral therapy. NSAIDs are ineffective in treating acute HZ pain; instead, acute pain can be relieved by antivirals, and associated HZ pain can be treated with opioids.

Decreased Efficacy

The shingles vaccine is a protective measure recommended for those 60 and older. (​.) The shingles vaccine, Zostavax, is a live attenuated vaccine given as a one-time subcutaneous injection. It is composed of an antigen glycoprotein E (IgE) and an adjuvant system. Zostavax has been the only shingles vaccine approved in the United States since 2006. A 2016 study by Cunningham, et al., found that the herpes zoster subunit vaccine reduces the risks of herpes zoster by 89.8 percent and postherpetic neuralgia by 88.8 percent among adults 70 and older. (N Engl J Med 2016;375[11]:1019.) The 2015 Shingles Prevention Study gathered individuals 60 and older who received the shingles vaccine, and determined that the vaccine significantly reduced the incidence of shingles. The shingles vaccine decreases the risk of contracting shingles and PHN by 51 percent and 67 percent, respectively. (

These results suggest a benefit associated with early vaccination, but a study by Morrisson, et al., showed there is still a risk of reactivation of VZV resulting in shingles. (Clin Infect Dis 2015;60[6]:900.) One of the causes for shingles infection in vaccinated adults is the issue of decreased vaccination efficacy over time. The Morrisson study highlights the decline of the vaccine's efficacy from years seven to 11 post-vaccination (46% decline in efficacy year seven to 14% decline in efficacy in year 10). The downward trend of the vaccine's efficacy throughout the years may be due to decreasing levels of vaccine-induced immunity and or a decline in the host's immunosenescence.

HZ vaccination is recommended for the elderly population as a preventive measure against shingles, though vaccination does not prevent all shingles infections. Current guidelines do not support revaccination with Zostavax, but future studies may allow researchers to assess the long-term protection of the HZ vaccine as well as the possible benefit of revaccination.

The patient in this case was discharged with tramadol, acyclovir ointment, clindamycin, and oral acyclovir. He was instructed to follow up with his primary care physician in one to two days.

Ms. Cazeau, Ms. Roman Hernandez, Ms. Scheuermann, and Ms. Ijaz are third-year medical students at the University of Medicine and Health Sciences in St. Kitts. Dr. Raziuddin is an internist and emergency physician at Weiss Memorial Hospital, Gottlieb Memorial Hospital, and Westlake Hospital, all in Illinois.

Wednesday, October 11, 2017


A 16-year-old boy presented to a rural ED with a swollen jaw, painful blisters in the mouth, and earache for the past day. One week before, he had a fever with chills, sore throat, and dry coughs. He was not taking any medications, and his immunizations were up-to-date. He had a mild learning disorder but no significant past medical or surgical history.​

case files-matsumoto.jpeg

An apthous ulcer, the most common and one of the earliest signs of Behçet's disease.

The patient's vital signs were within normal limits, and his physical examination revealed anterior cervical lymphadenopathy, sinus congestion, and small erythematous vesicles in bilateral tympanic membranes. There were vesicular clusters in the oral mucosa and a few shallow ulcers in the buccal mucosa and posterior pharynx. There was no evidence of facial edema, drooling, or airway compromise.

The patient was prescribed a narcotic pain reliever, and was discharged in stable condition with instructions to follow up promptly with dermatology to consider other diagnoses and treatments. Herpetic gingivostomatitis was suspected.

Two days later, the patient began having dysuria, followed by the appearance of genital lesions. He was admitted to the hospital where an evaluation by an infectious disease specialist revealed painful genital lesions in the urethra, similar lesions in the esophagus per endoscopy, and bilateral conjunctival injection. The patient was diagnosed with Behçet's disease, and was treated with colchicine.

Behçet's Disease

Behçet's disease is an idiopathic chronic inflammatory disorder that was first identified in 1936 by the Turkish dermatologist Hulusi Behçet. Symptoms are multisystemic, with vasculitis underlying its pathophysiological characteristics. Presentation usually includes recurrent aphthous oral and genital ulcerations, arthritis, cutaneous and ocular lesions, and an exaggerated skin response to minor injury known as pathergy. Median age of presentation is 25 to 35 years old, and it is more common and severe in men. Other forms of clinical manifestations may be present in cardiac (pericarditis, endocarditis, myocarditis, venous and arterial occlusions), gastrointestinal (aphthous stomatitis), and neurological systems (aseptic meningitis, parenchymal lesions). (Arthritis Res Ther 2003;5[3]:139.)

The etiology of Behçet's disease is unknown, although it is characterized as a genetically related, excessive T-cell-mediated inflammatory disorder involving veins and arteries. Studies have shown possible linkage of Behçet's disease to polymorphisms of genes HLA-B51, GIMAP, and IL12A. (Arthritis Rheum 2009;61[10]:1287; Ann Rheum Dis 2013;72[9]:1510.) Prevalence of Behçet's disease is recognized worldwide, but it is higher in Asian, Mediterranean, and Middle Eastern populations (80-370 per 100,000 in Turkey, 2-30 per 100,000 in Japan, Korea, Iran, Iraq, and Saudi Arabia), and is extremely rare in the United States (one per 100,000). (Ann Med Interne [Paris] 1999;150[6]:488.) Delaying treatment may lead to long-term complications such as blindness, stroke, and vascular thrombosis.

No specific tests currently confirm the diagnosis. Instead it is based on clinical findings specified as the International Clinical Criteria for Behçet's disease. The patient should present with recurrent oral ulcerations (aphthous or herpetiform) at least three times in one year, plus any two of the following: recurrent genital ulcerations, eye lesions (uveitis or retinal vasculitis), skin lesions found in adult patients not being treated with corticosteroids (erythema nodosum, pseudofolliculitis, papulopustular lesions, acneiform nodules), and a positive pathergy test read by a physician within 24-48 hours of testing. (Lancet 1990;335[8697]:1078.)

Severity of Behçet's disease varies from patient to patient, and treatment depends on the severity of the manifestations and organ systems involved, which can be minor or major. Much of the management is symptomatic and focuses on reducing discomfort and preventing serious complications. As with this patient, minor manifestations are those that interfere with the patient's quality of life but do not threaten any vital organ function, such as arthritis, oral aphthae, and genital and skin lesions. The recommended treatment is colchicine, while glucocorticoids and other immunosuppressives may be considered. Major manifestations are those with the risk of major organ damage, such as uveitis, encephalitis, and carditis, which require more specific treatment regimens. (Ann Rheum Dis 2008;67[12]:1656.) Behçet's disease affects a multitude of systems, so it is common to have various specialists treating the affected area within their field of expertise. It is helpful to have a primary care physician or rheumatologist to coordinate the treatment and monitor the patient's progress.

Arytenoid cartilage ulcers (left) and the epiglottic ulcers (right) shown via endoscopy.

According to the Arab American Institute and U.S. Census, Middle Easterners ranked third among the fastest growing immigrant groups in the United States from 2010-2014, so physicians will be seeing an increased number of medical diseases unique to those populations if this trend in growth continues, particularly in urban areas where most live. The current prevalence of Behcet's disease in the United States is uncommon, but as at-risk populations increase, it would be prudent for clinicians to become more familiar with its presentation and treatment to avoid treatment delays and complications which may result in catastrophic patient outcomes.

Ms. Matsumoto is a medical student at Touro University of Nevada College of Osteopathic Medicine, where Dr. Meeks is an assistant professor, the chair of department of specialty medicine, and the director of clinical systems.

Wednesday, September 13, 2017


The patient had been playing a round of golf a week earlier, and thought he had strained a muscle in his right lower back while swinging a golf club. The patient continued his golf workouts throughout the week, which included lifting weights and swinging a golf club with minimal pain.​

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The day prior to ED presentation, he began having worsening right-sided back pain, and began ibuprofen and ice treatment, which helped minimally. The patient woke up experiencing worsening back pain that radiated from his right flank to his right lower abdominal area. He reported increased pain with ambulation, and on presentation was experiencing sweats and a fever. His mother reported that the patient had a temperature of 101°F.

He had no appetite, was nauseated, and complained of pain in the right flank area that radiated to the right lower abdominal area. The patient's heart rate was 104 bpm, blood pressure was 115/49 mm Hg, oxygen saturation was 97% on room air, and his temperature was 99.3°F orally. The patient denied testicular pain, dysuria, hematuria, diarrhea, constipation, and URI symptoms. He had an unremarkable past medical history, no prior surgeries, no significant family history or social history, and was not sexually active.

Physical exam findings revealed an unremarkable ENT exam. He was tachycardic without any murmurs, and his lungs were clear to auscultation. The patient's abdominal exam revealed pain at McBurney's point, no rebound, and no peritoneal signs with diminished bowel sounds. No inguinal hernias were present on exam, and his testicles are bilaterally descended with no pain to palpation; he had no penile discharge. Musculoskeletal exam revealed tenderness to palpation along the right paraspinal muscles of the lower thoracic and lumbar area. He had some pustular acne around the area of discomfort with no signs of cellulitis or induration. He had no pain to palpation about the bony thoracic or lumbar spine. He is neurologically intact with no focal deficits.

IV fluids were started and labs were obtained, ketorolac was given for pain, and a CT scan of the abdomen and pelvis was ordered for possible retrocecal appendicitis. The patient's blood work revealed a leukocytosis of 13.03, his lactate level was normal at 0.8, and all other labs were unremarkable. While awaiting CT scan, the patient spiked a temperature of 103°F, at which time acetaminophen, rebolus of IV fluids, and Unasyn were started for suspicion of an acute appendicitis. A CRP and CPK were added because the patient also complained of pain when he moved, adding myositis to the differential, and he was given morphine for pain. The CRP was elevated at 145.6, and the CPK was normal. CT scan of the abdomen and pelvis with IV contrast was interpreted by the radiologist as unremarkable with a normal-appearing appendix and negative for presence of acute pathology.

Now we had a dilemma. We had a patient with fever, right-sided back and lower abdominal pain who now cannot walk without extreme pain and who has an elevated CRP and WBC count with no help so far from advanced imaging. The differential diagnosis now included psoas muscle abscess, epidural abscess, discitis, and viral myositis. We chose to do an MRI with and without contrast of the lumbar spine for further advanced diagnostic imaging and arranged for an inpatient admission.

MRI to the Rescue

MRI revealed extensive muscle edema involving the right posterior paraspinal muscles originating from L1 to the sacrum. Findings were consistent on MRI for cellulitis and myositis. A focal abscess was also found on the posterior psoas muscle abutting the right facets of L5-S1 measuring 3 cm in greatest dimension. Edema extended into the neural foramen at L4-L5 and L5-S1 on the right.

Vancomycin was added to his antibiotic regimen, and an ultrasound-guided right paraspinal abscess drainage was ordered. This revealed 2 mL of purulent specimen that was sent to the lab and revealed MSSA (methicillin-sensitive Staphylococcus aureus). Blood cultures also isolated S. aureus. A psoas muscle abscess is a rare condition that is becoming more common. The classic triad of presenting symptoms—fever, limp, and back pain (Buffalo Med Surg J 1881;21:202)—was actually present in our patient. Many patients also present with pyrexia, malaise, and progression of symptoms to include worsening abdominal and flank pain, pain with hip movement and a hip held in a flexed and externally rotated posture.

Psoas muscle abscesses can fit into either a primary or secondary classification. Primary psoas muscle abscesses occur from the hematogenous or lymphatic spread of an organism from a distant site (in this case, probably pustular acne). Secondary psoas muscle abscesses occur from a nearby infectious or inflammatory process that has directly spread into the psoas muscle (most commonly appendicitis). Approximately 30 percent of all psoas muscle abscesses are primary. Eighty-three percent of psoas muscle abscesses occur in patients under 30.

Primary cases that occur in children are usually due to the patient being immunocompromised or having HIV (our patient was tested and negative) or diabetes. One of the most common risk factors for developing a primary psoas abscess is muscle trauma (our patient was swinging a golf club rigorously and weightlifting). Secondary cases are more common in the elderly and occur from an intra-abdominal bowel inflammation (Crohn's or diverticulitis) or infection such as appendicitis.

Advanced diagnostic imaging is needed for making the diagnosis and providing a focused treatment plan. MRI is more sensitive and specific than CT scan for providing more accurate delineation of inflammatory changes. CT scans can also have false negative results (as in our case) when the abscesses do not contain air or have a low attenuation, which makes it difficult to see on CT scan images. Direct aspiration of the abscess with gram stain and culture provides the most accurate directed means of guiding treatment. (Appl Microbiol 1974;28[6]:943.)

A meta-analysis revealed the most common cause to be S. aureus and the second most common to be Escherichia coli. (Int J Gerontology 2011;5[2]:75.) Primary psoas abscess results from hematogenous or lymphatic spread of infection from a distant source. Primary abscesses are often monomicrobial, with S. aureus as the predominant organism. The rich blood supply of the iliopsoas muscles predisposes it to primary infection. Secondary psoas abscess results from contiguous spread from nearby musculoskeletal, gastrointestinal, genitourinary, and vascular structures, and are typically polymicrobial. S. aureus still accounts for 88 percent of secondary cases.

Treatment should begin with broad-spectrum empiric antibiotics targeting staphylococcal (primary and secondary due to skeletal infections) and enteric organisms (secondary to intra-abdominal infection). Ticarcillin-clavulanic acid 3.1 g IV q6h, piperacillin-tazobactam 3.375 g IV q6h, or meropenem 1 g q8h are effective initial treatment. Dual therapy with a third-generation cephalosporin, such as ceftriaxone 1 g IV q12-24h with metronidazole 500 mg IV q8h, is also adequate. Treat MRSA infection with vancomycin 15 mg/kg IV q8-12h. Daptomycin 6 mg/kg IV once daily or linezolid 600 mg IV/PO twice daily are alternatives. Most cases require percutaneous (PCD) or open surgical drainage with parenteral antibiotic treatment (16-20% success rate with antibiotics if abscess<3 cm). CT-guided PCD is the initial procedure of choice. Successful decompression is noted in at least 50 percent of cases and almost all following a second drainage.

Our patient was initially started on broad-spectrum antibiotics, but those were changed to Ancef after the organism was identified. He was discharged home on Ancef with a PICC line, and made a full recovery.

Dr. Grant is an assistant clinical professor at Michigan State University COM/CHM. He and Ms. Carignan work with the Michigan-based group Independent Emergency Physicians.

Tuesday, July 25, 2017

​BY Dhimitri A. Nikolla, DO

An 82-year-old man with a history of dementia, multiple urinary tract infections, insulin-dependent diabetes mellitus, and an admission a month earlier for Fournier gangrene presented to the emergency department with reports of confusion and hypotension from his nursing home. His vital signs were normal, but he was disoriented with a mildly tender abdomen. His genital examination revealed a suprapubic catheter without evidence of soft tissue infection. A CT with contrast of the abdomen and pelvis revealed the images shown.

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What is the diagnosis? What is the treatment?

The CT images demonstrated a left casting calculus extending into the proximal ureter with air in the renal pelvis consistent with emphysematous pyelitis. Vancomycin, piperacillin/tazobactam, and ceftriaxone were started in the ED based on his previous urine cultures and sensitivities. Later that day, the patient received a left ureteral stent. Urine cultures eventually grew Klebsiella pneumoniae, Escherichia coli, Enterococcus faecalis, and Candida tropicalis with multiple resistances. He was discharged after five days with cefdinir, amoxicillin, and fluconazole, but received a left percutaneous nephrostomy tube 17 days after ED presentation due to persistent hydronephrosis.

Emphysematous pyelitis is a gas-producing infection of the renal pelvis. It is rarely reported in the literature, possibly because it is not always recognized as its own entity but as a subtype of emphysematous pyelonephritis where infection extends into the renal parenchyma. (Arch Intern Med 2000;160[6]:797; Radiology 1996;198[2]:433; Biomed Imaging Interv J 2008;4[4]:e24; CJEM 2017;19[1]:63.)

The most common risk factors are diabetes mellitus and urinary obstruction, but the causative bacteria is usually E. coli or Klebsiella. (J Urol 2008;179[5]:1844.) Mortality is significantly lower in emphysematous pyelitis compared with emphysematous pyelonephritis—18 percent versus 69 percent—and it usually resolves with antibiotic therapy alone. (Radiology 1996;198[2]:433 & 2001;218[3]:647.) Those who develop emphysematous pyelonephritis will likely require percutaneous drainage and possibly nephrectomy. (J Urol 2007;178[3 Pt 1]:880; BJU Int 2010;105[7]:986.)

Dr. Nikolla is an emergency medicine resident at St. Vincent Hospital, a part of the Allegheny Health Network, in Erie, PA.