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.

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.

case files-renal pelvis.jpeg

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.

Wednesday, July 12, 2017


A 59-year-old man with a history of frequent crack cocaine use presented with difficulty breathing for four hours. He had no prior medical problems or known allergies. He admitted to smoking crack cocaine four days before his symptoms began. He reported a one-day history of productive cough but denied chest pain, sore throat, and fever.​

​He was a well-developed man in mild distress. His temperature was 36.5°C, pulse 90 bpm, blood pressure 188/108 mm Hg, and respiratory rate 20 bpm. His oxygen saturation was 100% on four liters by nasal cannula. Inspiratory stridor was noted with supraclavicular retractions and accessory muscle use. His lungs were otherwise clear to auscultation. His oral cavity and oropharynx were normal in appearance. The remainder of his physical exam was unremarkable.​

A chest x-ray was obtained. What should be the next steps in this patient's evaluation and treatment?

The patient was diagnosed with crack cocaine-induced subglottic edema. The chest x-ray revealed a “steeple sign” (arrow) indicative of subglottic stenosis, similar to that seen in children with croup. This finding was later confirmed on CT of his chest. Initial treatment with inhaled nebulized albuterol was followed by nebulized racemic epinephrine and 10 mg IV dexamethasone. Flexible fiberoptic laryngoscopy was performed at the bedside by the otolaryngology service, which revealed only bilateral nonobstructive arytenoid edema with an otherwise normal hypopharynx, true vocal cords, epiglottis, and other supraglottic structures.

Cocaine is one of the most common illicit drugs of abuse leading to emergency department visits. The cocaine epidemic that began in the mid-1980s in the United States was fueled by the introduction of crack, a free-base form of the drug not destroyed by heat that can be inhaled. Crack cocaine use can achieve concentrations in the blood comparable with that of intravenous cocaine at a much cheaper price. Reported pulmonary complications of crack cocaine use include acute exacerbations of asthma, barotrauma, noncardiogenic pulmonary edema, diffuse alveolar hemorrhage, interstitial pneumonitis, and pulmonary infiltrates with distinct histologic features referred to as crack lung. (Curr Opin Pulm Med 2001;7[2]:43.) Thermal injury to the laryngeal and supraglottic structures of the upper airway from crack cocaine use has also been described. (Am J Emerg Med 2017;35[2]:381e5.) The mechanism of injury is similar to inhalation of hot vapors or particulate matter in a room containing fire.

Cocaine free-base melts at 98°C and vaporizes at higher temperatures. (N Engl J Med 1986;315[23]:1495.) It is typically smoked through a short pipe, with a fine mesh screen or Brillo pad placed at the bottom of the pipe bowl to protect the user from aspirating foreign material. This metal screen becomes hot and may partially disintegrate, resulting in aspiration of burning metal debris or smoldering crack particles. The combination of efficient heat dissipation in the upper airway, low heat capacity of air, and reflex closure of the larynx usually results in superheated air causing injury only to supraglottic structures, which includes the aryepiglottic folds, epiglottis, false vocal cords, and arytenoid mucosa. (Scand J Trauma Resusc Emerg Med 2013;21:31.) Thermal injury to the airway may not become evident for more than 48 hours after the initial insult. (Laryngoscope 1997;107[5]:620.)

Presenting symptoms of these injuries after smoking crack cocaine include throat pain, dysphagia, odynophagia, cough, foreign body sensation in the throat, shortness of breath, and voice change. Stridor may also be present. (Laryngoscope 1997;107[5]:620.) Symptoms, signs, and radiologic and laryngoscopic findings may mimic infectious epiglottitis. (J Emerg Med 1997;15[4]:483.) Further confusing this issue is the fact that a significant percentage of these patients may not initially report their crack cocaine use. (Laryngoscope 1997;107[5]:620.)

Management of upper airway injury secondary to inhalation of crack cocaine lacks universal guidelines, though some research has yielded recommendations for treatment. (Ear Nose Throat J 2003;82[1]:53; Laryngoscope 1997;107[5]:620.) Most patients can be managed expectantly in an intensive care setting, with intubation used as a final resort to stabilize the airway. The decision to intubate these patients should be guided by their overall clinical status. The upper aerodigestive tract should be examined by laryngoscopy for mucosal injury and the presence of foreign bodies. While controversial, corticosteroids may have a role in decreasing airway edema and should be administered. Nebulized racemic epinephrine may also be used for this purpose. Antibiotics may be given until an infectious source of the airway injury can be definitively excluded.

This patient was admitted to the intensive care unit and treated with 10 mg IV dexamethasone every eight hours and nebulized racemic epinephrine as needed. The patient's symptoms resolved within 24 hours, and he was discharged after an unremarkable of his hospital stay.

Dr. Tedla is an emergency physician at Presence St. Joseph Medical Center in Joliet, IL; Dr. Eilbert is a professor of emergency medicine at the University of Illinois at Chicago, College of Medicine; and Dr. Colla is an assistant professor of emergency medicine at the University of Illinois at Chicago, College of Medicine.

Tuesday, June 27, 2017


A 33-year-old obese woman was sent to the ED by her primary care physician with the complaint of severe abdominal pain for 10 hours. Her pain was associated with nausea and loss of appetite without vomiting. The patient had a past medical history significant for hypertension, and depression, which were treated with losartan-hydrochlorothiazide and paroxetine HCL, respectively. Her past medical history was also significant for untreated polycystic ovarian syndrome (PCOS). The patient denied ever having abdominal surgeries, but noted that her gynecologic history was significant for irregular menses.​

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Axial view showing the maximal diameter of the left ovary.

​The patient's abdomen was severely tender in the left lower quadrant with voluntary guarding and abdominal masses which were palpable approximately three centimeters above the umbilicus bilaterally. Laboratory workup over the course of the visit included beta HCG, CBC with differential, CMP, lipase, lactic acid, urinary analysis, coagulation studies, and CA-125. Laboratory results were remarkable for elevated lactic acid of 3.1 and extremely high CA-125 at 675.9. CT imaging of abdomen and pelvis with IV contrast was performed, and revealed markedly enlarged cystic ovaries, the left measuring larger at 28 cm and the right at 21cm. The immediate diagnostic concern was ovarian cancer due to the elevated CA-125. The patient was discharged home with pain medication, and instructed to meet with a gynecologic oncologist for ovarian cyst removal and staging. With the small pool of research pertinent to this patient's history of untreated PCOS, perhaps there is a need for more research into a relation between PCOS and ovarian cancer.

Occam's Razor

PCOS diagnosis is considered after the exclusion of any other entities that would cause hyperandrogenism with menstrual dysregulation and polycystic ovaries. (J Clin Endocrinol Metab 2006;91[3]:781; Hum Reprod 2004;19[1]:41.) It's estimated that five to 10 percent of all women are affected by PCOS, and with this common syndrome comes an increased prevalence in comorbidities such as diabetes, hypertension, obesity, metabolic syndrome, and infertility. The prevalence of infertility is extremely high due to oligomenorrhea and amenorrhea, and usually leads to the workup and diagnosis of PCOS. (Obstet Gynecol 1996;88[4 Pt 1]:554; Gynecol Endocrinol 2013;29[2]:145.)

A clear correlation has been made between PCOS and endometrial cancer, but little evidence suggests a link between PCOS and ovarian cancer. (Hum Reprod Update 2001;7[6]:522; Folia Histochem Cytobiol 2009;47[5]:101; Gynecol Endocrinol 2005;20[4]:200; Reprod Biomed Online 2009;19[3]:398.) The most quoted paper advocating a relationship between PCOS and ovarian cancer showed a 2.5-fold increase in the risk of epithelial ovarian cancer in PCOS, going up to as high as 10.5-fold for women who were not treated with oral contraceptives. (Obstet Gynecol 1996;88[4 Pt 1]:554.) This study has been limited for interpretation due to its small sample size and not being the primary focus of the original study.

Coronal view showing bilateral polycystic ovaries.

A more recent study compared separately the risk of PCOS and its relations to endometrial, ovarian, and breast cancers, which originally showed on analysis that ovarian cancer was not significant (OR 1.41;95% CI,0.93-2.15 p<0.11), but further stratification of the population to include only women younger than 54 showed the risk became significantly elevated (OR 2.52; 95% CI 1.08-5.89, p<0.03). (Hum Reprod Update 2014;20[5]:748.)

With PCOS affecting such a high percentage of women and this example of a possible malignant transformation in a patient of known PCOS, perhaps it warrants more studies to find an association that has eluded us so far. We must keep Occam's razor in mind before dismissing this patient's presentation as a separate occurrence of ovarian carcinoma.

Mr. Avery and Mr. Maina 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.

Tuesday, June 27, 2017


A 73-year-old man with a past medical history of hypertension, type 2 diabetes, and hyperlipidemia and a surgical history for a coronary artery bypass presented with sudden, severe lower abdominal pain. He characterized his pain as 8/10 and was tender to palpation.

Laboratory studies showed a white blood cell count of 7.51 with a glucose of 759, no bands, a platelet count of 230,000, and a lactic acid level of 6.7. Urinalysis showed +5 ketones and a glucose count of greater than 500. An abdominal CT showed possible microperforations around the cecum. The patient also had electrocardiogram changes indicative of an abnormality in the inferior wall of the heart. The patient was given 1 g of ertapenem and 1 g of ceftriaxone, and was placed on a bicarbonate drip. The clinical impression at this point was shock (septic vs cardiac).

The patient was taken emergently to the catheterization lab to rule out acute coronary artery disease. Severe three-vessel coronary artery disease, totally occluded third vein graft, and moderate to severe reduced left ventricular function with an ejection fraction of 30 to 35 percent were found. The patient was transferred to the intensive care unit, where he was evaluated by surgery. His blood pressures was in the 70s, and he was tachycardic and tachypneic. A central line was placed and dobutamine, levophed, and two liters of normal saline were administered with appropriate caution to the patient's compromised ejection fraction.

An exploratory laparotomy was scheduled. The preoperative diagnosis was a perforated diverticulitis. Ascites was drained during the procedure, and the drained fluid was brown in color without odor. No indurations were felt while palpating the abdomen, but gross contamination of the abdomen was evident. A large 3 cm stercoral ulcer with a hard, rock-like stool was identified when palpation continued toward the left colon around the sigmoid area.

Stercoral ulcers are defined as perforations of the large bowel due to pressure necrosis from fecal impaction. (Curr Gastroenterol Rep 2014;16[9]:404.) Fewer than 100 cases of stercoral ulcers have been documented. (G Chir 2011;32[8-9]:368.) Perforation most often occurs at the antimesenteric border of the sigmoid colon and rectosigmoid junction because this area has a narrower lumen, decreased blood flow, and the driest stool, increasing susceptibility to rupture. Rupture has occurred at other locations, however. (Am Surg 2012;78[12]:E515.)

These patients generally present with a history of chronic constipation, and many have a history of opioid medication use or abuse or other constipating agents along with the use of laxatives or enemas in the past. (G Chir 2011;32[8-9]:368.) Most cases are of elderly patients, but a case of a 25-year-old man with chronic constipation leading to stercoral ulcer perforation has been documented. (South Med J 2006;99[5]:525.)

The rupture of the colon subsequently leads to the release of fecal material into the peritoneal cavity, leading to peritonitis and signs of acute abdomen supported by radiographs demonstrating peritoneal free air. (Am Surg 2012;78[12]:E515.) There have been cases of stercoral ulcers without perforation through the lumen, which instead presented with gastrointestinal bleeding. (CMAJ 2011;183[2]:E134.)

Inevitable Sepsis

The treatment for stercoral ulcer perforation involves emergent exploratory laparotomy with resection of the affected colon along with repeated abdominal washout to remove feces. A colostomy is performed along with formation of a mucus plug. (South Med J 2006;99[5]:525.) Parenteral antibiotics are required during this procedure because of seeding of bacteria into the bloodstream, which inevitably leads to sepsis. (Am Surg 2012;78[12]:E515.)

The criteria of a systemic inflammatory response syndrome (SIRS) must be met to determine whether a patient is septic. (JAMA 2016;315[8]:775.) These criteria are two or more of the following:

* Temperature >38°C or <36°C

* Heart rate >90/min

* Respiratory rate >20 or PaCO2 <32 mm Hg

* WBC count >12,000/mm3 or <4,000/mm3 or >10% immature band cells

Contrast-enhanced axial CT scan demonstrates extraluminal gas (arrow) in the ileocecal area indicating perforation.

A quick sequential organ failure assessment (qSOFA) can be used to aid in assessing the severity of organ failure and mortality rates. A qSOFA ≥2 has been correlated with a 10 percent increase in mortality. The qSOFA criteria are:

* Respiratory rate ≥22/min

* Altered mentation

* Systolic blood pressure ≤100 mm Hg

The criteria for a patient to be in septic shock are:

* Meet the criteria for sepsis

* Hypotension and requiring vasopressors to maintain MAP ≥65 mm Hg

* Lactate levels >2 mmol/L

All these criteria must be met despite adequate volume resuscitation, and are associated with an increase in mortality more than 40 percent. (JAMA 2016;315[8]:775.) The mortality rates of sepsis are higher among adults over 60. Those who survive often experience a decline in functional status in the first year after discharge. (Open Forum Infect Dis 2016;3[1]:ofw010.)

Treatment of septic shock is centered around maintaining perfusion of organs and preventing the three septic shock criteria from occurring. This is done by fluid resuscitation, use of vasoactive drugs, and red cell transfusion. A meta-analysis looking into early goal-directed therapy rather than waiting for symptoms to occur and treating accordingly found no difference in mortality rates. (N Engl J Med 2015;372[14]:1301.) This patient demonstrated a case of stercoral ulcer perforation, which subsequently led to severe septic shock in an elderly man with an extensive past medical history.

A Must for Differential Diagnosis

The affected areas were transected, which included the ulcerated and contaminated parts of the mesentery, small bowel, and colon. The abdomen was irrigated with about 15 liters of normal saline until the fluid became completely clear. A circular incision was made on the left lower quadrant through all layers of the abdomen, and the proximal aspect of the colon was brought out to complete a colostomy. Lastly, a Jackson-Pratt drain was placed in the pelvis.

No significant changes were observed over the next five days; the patient remained in critical condition with shock, on a ventilator with multiple medications for blood pressure support, and strict NPO. On postoperative day five, the patient developed worsening hypotension, bradycardia, hypoxemia despite maximum vasopressors, bicarbonate, steroids, antibiotics, and intravenous fluid resuscitation. Subsequently, the patient's family requested a DNR; continuous renal replacement therapy was discontinued five minutes later. The patient showed no signs of life and was pronounced dead after 15 minutes.

Chronic constipation leading to fecal impaction is potentially life-threatening. Risk factors for fecal impaction include the elderly, incapacitated patients, and the use of constipating agents. Fecal impaction, if not promptly discovered and treated, can lead to complications of feces leakage or stercoral ulcer rupture. Ruptured stercoral ulcer has a very high mortality due to severe peritonitis and septic shock. (Curr Gastroenterol Rep 2014;16[9]:404.) The risk factors for stercoral ulcer perforation should be identified in patients who are high-risk for prevention and resolution of the underlying constipation.

Contrast-enhanced sagittal CT scan demonstrates the site of the perforation and a fecaloma (arrow) in the proximal sigmoid colon, and due to pressure necrosis, signs of adjacent colonic wall thickening (arrowhead) are noticed.

It is also important to be aware of the different presentations of stercoral ulcers. If the ulcer has not completely ruptured, it may present as chronic constipation with accompanying rectal bleeding. (CMAJ 2011;183[2]:E134.) Stercoral ulcers also have no underlying pathology because they occur without any polyps or colon cancer causing the weakness of the affected viscus. (Am Surg 2012;78[12]:E515.) Patients with a ruptured stercoral ulcer will have peritoneal signs and an acute abdomen; later complications will evolve into septic shock. (G Chir 2011;32[8-9]:368.) Differentials for these presentations include diverticulitis, appendicitis, and perforated peptic ulcer. Due to its rarity, clinicians often do not keep a ruptured stercoral ulcer in mind, but its high mortality rate if missed should warrant its permanent place on a list of differential diagnoses.

Clinicians should also be aware of how to identify and treat a stercoral ulcer once an exploratory laparotomy has begun. Ruptured stercoral ulcers will lead to evisceration of feces into the peritoneal cavity that will likely be widely noticeable. An ulcer will most likely be located at the antimesenteric border of the sigmoid colon and rectosigmoid junction, with feces present at the opening. (Am Surg 2012;78[12]:E515.) The patient may also have evident megacolon leading up to the location of the ulcer. (South Med J 2006;99[5]:525.) The ruptured viscera must be resected and the abdomen properly irrigated to remove the remaining feces from the peritoneal cavity. Lastly, a colostomy must also be formed. (G Chir 2011;32[8-9]:368.)

The need for parenteral antibiotics must also be addressed because these patients have a high risk of mortality due to septic shock. (G Chir 2011;32[8-9]:368.) They should be assessed for SIRS criteria and qSOFA to maintain blood pressure and prevent organ failure. (Open Forum Infect Dis 2016;3[1]:ofw010.)

Mr. Macias, Mr. Zhang, and Ms. Hughes are medical students at the University of Medicine and Health Sciences (UMHS) in St. Kitts. Dr. Khan is a graduate of UMHS. Dr. Jacome is a bariatric and general surgeon at the department of surgery at Doctors Hospital of Augusta in GA. 

Tuesday, June 13, 2017


New recommendations on fluid resuscitation in septic children were included in the last pediatric resuscitation guidelines published by the American Heart Association. (Circulation 2015;132[16 Suppl 1]:S177.) Early and rapid intravenous administration of isotonic fluids has been widely accepted as a cornerstone in treating septic shock. A large randomized controlled study revealed that the administration of intravenous fluid boluses in pediatric patients with severe febrile disease in a resource-limited setting might be associated with poor outcomes. (Indian Pediatr 2015;52[11]:965.) The recommendation of administrating 20 to 60 mL/kg fluid boluses in septic shock is based on the observational studies conducted in developed countries (Crit Care Med 2013;41[2]:580; Intensive Care Med 2008;34[6]:1065) and contradicts the results of a prospective randomized controlled study conducted in pediatric patients with severe febrile illness in underdeveloped countries. (N Engl J Med 2011;364[26]:2483.)

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A total of 3,141 pediatric patients were included in this Fluid Expansion as Supportive Therapy (FEAST) study conducted in Africa. Sixty-two percent were debilitated, 15 percent were comatose, 83 percent had respiratory distress, 52 percent had multiple signs of impaired perfusion (significant tachycardia and cold extremities), 51 percent had moderate to severe lactic acidosis, 39 percent had severe lactic acidosis (≥5 mmol/L), 57 percent had malaria, and four percent were HIV-positive with a mean hemoglobin level of 7.1 g/dL. Patients were divided into two groups to receive fluid loading (group I: 20-40 ml/kg/hour 0.9% NaCl administration or fluid loading with 5% albumin) or maintenance fluids (group II: 2.5-4.0 ml/kg/hour maintenance fluids).

The signs and symptoms were improved at the end of the first hour in more patients who had received bolus fluids compared with those who had received maintenance fluids (43% vs. 32% respectively, P<0.001), but 48 hours later and at the end of the fourth week, the mortality rate was higher among the patients who had received bolus fluids when compared with the patients who had received maintenance fluids, which were 48 percent and 20 percent respectively (RR 2.40; 95% CI 0.84, 6.88). (N Engl J Med 2011;364[26]:2483.) No significant differences were found between the patients who received 5% albumin and those who received normal saline solution in the bolus group in neurological sequelae, pulmonary edema, increased intracranial pressure, and mortality rates.

The new guidelines emphasize that fluid treatment should be tailored to each patient and that frequent clinical assessments are required. This recommendation still emphasizes the importance of intravenous fluid resuscitation in pediatric patients in septic shock, but it states that aggressive fluid boluses may be associated with complications in febrile patients if intensive care support, appropriate equipment, and expert specialists are unavailable. (Circulation 2015;132[16 Suppl 1]:S177.) Individualizing fluid treatment to each patient, frequent clinical assessment before, during, and after fluid treatment, and predicting the need for other treatment options (e.g., inotropic treatment) as well as timely initiation of these treatments are recommended.

In the case of limited access to intensive care unit resources such as mechanical ventilation or inotropic support, intravenous fluid boluses may cause harm in children with febrile disease, and should be administered with caution in these patients. (Pediatr Emerg Care 2008;24[10]:647; BMJ 2014;348:f7003.)

Dr. Biçer is an associate professor in the department of pediatrics at Yeditepe University Faculty of Medicine in Istanbul and a training coordinator in the department of pediatric emergency medicine at Marmara University Faculty of Medicine. Dr. Söğütlü is a pediatric emergency specialist at Marmara University Faculty of Medicine. Mr. Şah is a research assistant in the department of pediatrics at Marmara University.