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

Case reports should focus on:

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

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Tuesday, November 13, 2018

​BY DAVID DIAZ; JONATHAN HAVERTY, DO; & JORGE DIAZ, DO

A previously healthy 20-year-old woman presented to the emergency department with three days of bilateral thigh pain. The pain had initially started in a focal area of the anterior aspect of the lower thighs bilaterally. The next day, her pain had progressed to involve a larger area of her thighs, and she noticed redness and swelling in the same area.

She had difficulty walking and bending her legs due to the pain. She said no other muscle groups were involved and she had never experienced this before. The patient had no history of vigorous physical activity or trauma, illicit drug use, recent travel, and insect bites. She had no other symptoms or history other than a recent URI, which had resolved a week earlier.

Her vital signs were unremarkable, and she was well-appearing and in no distress. The anterior aspect of the thighs bilaterally was tender with mild swelling and erythema. Her legs were symmetric, and no joint involvement was apparent. She had intact sensation and pulses distally and only mildly diminished quad strength bilaterally, but the exam was limited due to pain.

On a hunch, a creatine kinase level was ordered and came back with a surprising result of 33,000 U/L. We then ordered a urinalysis, liver panel, CBC, basic metabolic panel, pregnancy test, and urine toxicology screen for drugs of abuse. The urine was described by the lab as clear, yellow, and dipstick positive for moderate heme with only one RBC/HPF.

The liver panel showed an elevated AST (322 U/L), ALT (92 U/L), and LDH (533 U/L) with normal bilirubin levels. The urine toxicology screen was negative. Serum potassium, BUN, and creatinine were normal. The patient was diagnosed with rhabdomyolysis of unknown etiology.

She was admitted, treated with hydration, and monitored for renal function and potassium. The inpatient team ordered a viral panel that was positive for adenovirus and echovirus, which could indicate a recent viral infection (consistent with her previous URI), but no convalescent titers were ordered to confirm this. Her workup for rheumatologic causes, inflammatory myopathies, and endocrinopathies was negative. Rheumatology was consulted and concluded that the cause of rhabdomyolysis was most likely viral myositis.

Her CK levels peaked to 44,100 U/L on her second day of admission, and then declined to less than 10,000 U/L by day four when she was discharged. Her hospital course was uneventful, and she did not develop any severe complications or renal sequelae of rhabdomyolysis.

Muscle Breakdown

Rhabdomyolysis is characterized by skeletal muscle breakdown with leakage of muscle contents, including myoglobin, sarcoplasmic elements, and electrolytes into the circulation. (N Engl J Med 2009;361:62[1]:72.) Some of the most common causes of rhabdomyolysis include trauma, immobilization, strenuous exercise, recent surgery, sepsis, hyperthermia, drugs, toxins, metabolic and electrolyte disorders, myopathies, and infections (viral and bacterial). Rhabdomyolysis has many causes, all thought to share a common final pathophysiologic process.

The mechanism of skeletal muscle injury is thought to be secondary to increased intracellular calcium caused by depletion of ATP or by direct injury to the plasma membrane. This increase in intracellular calcium leads to persistent muscle contraction and activation of calcium-dependent proteases and phospholipases that lead to irreparable cellular injury and eventually myocyte necrosis. (N Engl J Med 2009;361:62[1]:72.)

Patients may manifest symptoms as a result of this pathologic process, which include the classic triad of muscle pain, weakness, and dark urine although up to 50 percent of patients may not report any muscular symptoms. (Medicine [Baltimore] 1982;61[3]:141.)

Muscle pain when present is typically noted in the proximal muscle groups such as the thighs and shoulders. (Eur J Intern Med 2007;18[2]:90.) Other clues to the diagnosis include electrolyte abnormalities, acute kidney injury, elevations in the creatine kinase and other muscle enzymes, and urinalysis that is heme-positive but with minimal or absent RBCs.

CK Elevation

Diagnosis of rhabdomyolysis is typically made with a history of acute muscular illness with marked elevations in serum CK, typically five times the upper limit of normal with or without characteristic urinary findings. Elevations in serum CK levels are highly variable at presentation, ranging from 1,500 to more than 100,000 U/L, with the mean peak CK typically around 10,000 to 25,000 U/L. (Medicine [Baltimore] 2005;84[6]:377.) Other laboratory values, such as AST, ALT, LDH, aldolase, and uric acid, may also be elevated.

Prompt diagnosis of rhabdomyolysis is critical to identify patients at risk for developing severe complications, including AKI, compartment syndrome, disseminated intravascular coagulation, or severe electrolyte derangements that could lead to cardiac arrhythmias. AKI is one of the most common complications of rhabdomyolysis with a reported incidence ranging from 13 percent to approximately 50 percent of patients. (N Engl J Med 2009;361:62[1]:72.) The incidence of AKI in rhabdomyolysis was noted to be highest in patients who had used illicit drugs, alcohol, or experienced trauma. (Medicine [Baltimore] 2005;84[6]:377.)

The pathophysiological mechanisms responsible for acute kidney injury seen in rhabdomyolysis is thought to be multifactorial including ischemia due to renal vasoconstriction, renal tubular injury caused by myoglobin-induced oxidative injury, and distal tubule obstruction due to precipitation of myoglobin-Tamm-Horsfall protein complexes. Interestingly, the precipitation of the myoglobin-Tamm-Horsfall protein complexes is accelerated by the presence of acidic urine, and myoglobin's nephrotoxic effects are clinically insignificant unless the urine is acidic. (N Engl J Med2009;361:62[1]:72.) The utility of alkalinization of urine for treating rhabdomyolysis-induced AKI is controversial. Nonetheless, the mainstay of treatment for rhabdomyolysis includes aggressive fluid resuscitation to prevent AKI, correction of electrolyte abnormalities, and monitoring for other complications such as compartment syndrome.

Our patient's case was a rather unusual presentation of rhabdomyolysis. She had no history of trauma or strenuous exercise, urine toxicology was negative, and her history did not fit with that of a typical case of rhabdomyolysis. She had no apparent inciting event leading to her diagnosis other than a recent URI, and if it weren't for the chance CK ordered, this case might have been missed.

This case also highlights some important clinical pearls regarding rhabdomyolysis: Presentations of this illness can be highly variable, the inciting event leading to rhabdomyolysis may not always be obvious, and up to 50 percent of cases don't present with the classic triad of muscle pain, weakness, and dark urine. It makes sense to have a high level of suspicion and a low threshold to order a creatine kinase level.

Dr. David Diaz is a fourth-year medical student at the UCSF School of Medicine in San Francisco. Dr. Haverty is a first-year resident in the Hofstra-Northwell Emergency Medicine Residency at the Donald and Barbara Zucker School of Medicine in Hempstead, NY, and Dr. Jorge Diaz is an associate clinical professor of emergency medicine at the David Geffen School of Medicine, UCLA, and an emergency physician at Olive View-UCLA Medical Center in Sylmar, CA.

Wednesday, October 24, 2018

​BY ARJUN BHARADWAJ; MARGARET GAVOR, MBChB, MPH; & KHALID MALIK, MD

A 65-year-old man presented to the emergency department complaining of sudden-onset left-sided abdominal pain followed by a “seizure.” His abdominal pain started a few hours prior to presentation, was sharp in nature, and radiated to his back and umbilicus. The pain waxed and waned, worsened when he walked or sat up, and at its worst was a 10/10. He took a laxative and two antacids, but received no relief.

Each “seizure” episode lasted about 30 seconds and occurred every five minutes. He said he felt drained after each event but never lost consciousness. He denied any recent trauma, falls, contact sports, contact with sick individuals, or travel outside the country, but he had travelled between New Jersey and Chicago. A review of systems was positive for two days of constipation but negative for melena, hematemesis, nausea, vomiting, anorexia, fever, chills, headaches, muscle weakness, easy bruising, and rashes. Other systems were negative.

He had a history of glaucoma, benign prostatic hyperplasia, noncancerous colonic polyps, and prehypercholesterolemia but no history of mononucleosis, blood disorder, malaria, liver disease, or cancer. His family history was positive for multiple first-degree family member with colorectal cancer. The patient had had no genetic testing, but he regularly followed up with an oncologist and had frequent colonoscopies (2014 and 2016). He was taking finasteride, latanoprost, aspirin, polyethylene glycol, calcium carbonate, and red yeast rice extract. He reported drinking alcohol occasionally but did not use cigarette or illicit drugs.

His vital signs were a temperature of 98.8°F, a pulse of 85 bpm, a respiration rate of 18 bpm, a blood pressure of 106/68 mm Hg, and an oxygen saturation of 100% on room air. The patient was alert and in distress. His abdomen was soft, nondistended with mild epigastric and left upper quadrant tenderness to palpation, with guarding but no rebound tenderness. Murphy's sign was negative, percussion was tympanic, and bowel sounds were present and normal.

The patient's laboratory findings were CMP within range, WBC (14 k/μL), RBC (4.25 M/μL), Hbg (13.6 g/dL), haematocrit (41.9%), troponin (<0.03 ng/dL), magnesium (1.9 mg/dL), INR (1.0), Protime (10.2 sec), PTT (20.4 sec), lactic acid (2.3 mmol/L), and negative mononucleosis test. A head CT showed no acute intracranial changes, and an abdominal CT revealed large hematoma centered in the spleen with subcapsular and perisplenic components, with probable pooling of hemorrhagic products extending along the right and left paracolic gutters, the perihepatic region, and pelvis. (Figure 2.) There were also two hypoattenuating on the left and right hepatic lobes. (Figure 1.)

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Figure 1. Transverse cross-section of abdominal CT with IV contrast: A. Hematoma centered in the spleen with subcapsular and perisplenic components. B: Hypoattenuating lesion on the left lobe. C: Hemorrhagic blood products extended to perihepatic region. D: Nonaneurysmal abdominal aorta without evidence of a dissection flap or intramural hematoma.


Figure 2. Coronal cross-section of abdominal CT with IV contrast: A. Hematoma centered in the spleen with subcapsular and perisplenic components (11cm), B: Hemorrhagic blood product extended to right paracolic gutter. C: Non-aneurysmal abdominal aorta without evidence of a dissection flap or intramural hematoma.

The patient was diagnosed with atraumatic splenic rupture (ASR). Surgical consultation was obtained, and he was closely observed. The patient was transferred to another facility with interventional radiology capable of performing transcatheter embolization. He was managed conservatively for 24 hours and then referred back to his oncologist in New Jersey for further follow-up and management for possible solid tumor metastasis-related rupture.

Differential and Care

Splenic rupture is a potentially life-threatening condition, often associated with trauma. Spontaneous or atraumatic splenic rupture is rare and not often considered for acute abdominal pain in the absence of trauma. (Am J Case Rep2013;14:13; http://bit.ly/2NMpp26.)

Early imaging diagnosis of ASR is warranted to limit mortality, and atraumatic splenic rupture can be classified as idiopathic (7%) or pathologic (93%). (Insights Imaging 2016;7[4]:641; http://bit.ly/2zDivDEBr J Surg2009;96[10]:1114.) ASR represents the initial manifestation of a previously unknown underlying pathologic condition in most patients (90%), while “idiopathic” ASR occurs in a normal spleen without predisposing factors. (Insights Imaging 2016;7[4]:641; http://bit.ly/2zDivDEBr J Surg 2009;96[10]:1114; World J Gastroenterol 2008;14[43]:6711; http://bit.ly/2xS6nfCJ R Coll Surg Edinb 2002;47[1]:437.)

The most common causes of ASR can be grouped into six main causes: neoplasm (30.3%), infections (27.3%), inflammatory noninfectious (20%), drug-treatment related (9.2%), mechanical disorders (6.8%), and normal spleen (6.4%). (Br J Surg 2009;96[10]:1114.) ASR occurs in a wide age range, and the predominant signs and symptoms include upper or left-sided abdominal pain, tachycardia, and hypotension. Malaise, vomiting, generalized abdominal tenderness, peritonism, and progressive hemodynamic shock are present in later stages of presentation. (Insights Imaging 2016;7[4]:641; http://bit.ly/2zDivDE.) Ultrasound can be used as a rapid, noninvasive test for detecting hemoperitoneum. (Insights Imaging 2016;7[4]:641; http://bit.ly/2zDivDEAm J Case Rep 2013;14:13; http://bit.ly/2NMpp26.)

CT scan is often the ideal imaging modality to make the diagnosis, however, and the most common finding is splenomegaly with splenic lacerations and intraperitoneal or subcapsular bleeding. (Am J Case Rep 2013;14:13; http://bit.ly/2NMpp26.) The majority of ASR cases are treated surgically: total splenectomy (84%) and organ-preserving surgery (1.2%). Approximately 14.7 percent of cases are treated with conservative measures. (Insights Imaging 2016;7[4]:641; http://bit.ly/2zDivDE.) The mortality rate is reported at 12.2 percent; splenomegaly, advanced age, and neoplastic disorders are also associated with increased ASR-related mortality. (Br J Surg2009;96[10]:1114.)

Most cases of ASR represent the initial manifestation of a previously unknown underlying pathologic condition with unclear history, physical exam, and lab findings that do not accurately reflect bleeding. Increased awareness enhances diagnosis and effective triaging and treatment among watchful waiting, interventional and surgical treatment. Physicians should keep a broad differential in mind, have a high index of suspicion, and consider atraumatic splenic rupture as a differential diagnosis in patients presenting with sudden left-sided abdominal pain in the absence of trauma and any unknown underlying conditions.

Mr. Bhardwaj is a third-year medical student at the University of Medicine and Health Science, and is currently doing his emergency medicine rotation at Weiss Memorial Hospital in Chicago, IL. Ms. Gavor is a fourth-year medical student at Xavier University School of Medicine in Oranjestad, Aruba. Dr. Malik is a board-certified emergency and internal medicine physician and the director of the emergency department at Weiss Memorial Hospital, an affiliate of the University of Illinois Hospital.

Wednesday, October 24, 2018

​BY GREGORY TAYLOR, DO, & SHERIF EL-ALAYLI, DO

A 60-year-old man with a significant history of alcohol abuse, metastatic hepatocellular carcinoma, and cirrhosis presented to the emergency department complaining of vomiting up bright red blood. The patient was reportedly supposed to have an esophagogastroduodenoscopy (EGD) six months earlier but failed to follow up.

He had two episodes of melena the night before and two episodes of hematemesis that morning. He was also experiencing fatigue, weakness, and abdominal pain, which he described as achy and localized to the epigastric region. He had refused treatment for his hepatocellular carcinoma and continued to drink at least 12 beers a day.

He was afebrile and had a blood pressure of 97/58 mm Hg, a heart rate of 114 bpm, a respiratory rate of 22 bpm, a weight of 123 kg, and a pulse ox of 99% on room air. The patient appeared ill, and he was sitting up dry heaving with dried blood on his chin. His eyes revealed scleral icterus bilaterally, and he had sinus tachycardia without a murmur and clear lungs. His abdomen was soft but distended, positive fluid wave, and tenderness to palpation within the epigastric region without any peritoneal signs to suggest a bacterial peritonitis.

His rectal exam was notable for black stool, hemoccult-positive. His lab results revealed a leukocytosis of 11.2 k/μL, hemoglobin of 9.2 g/dL (baseline of 12), hematocrit 28.9%, and a thrombocytopenia of 142 bil/L (150-450 bil/L), INR of 1.7. A metabolic panel was notable for an alkaline phosphatase of 319 IU/L, aspartate aminotransferase 89 U/L (10-37 U/L), alanine aminotransferase 43 U/L (10-37 U/L), and a total bilirubin of 2.7 mg/dL. Gastroenterology was consulted for a potential sentinel variceal hemorrhage. The patient was started on a Protonix gtt, octreotide gtt, and ceftriaxone prophylaxis, and was taken for an emergent EGD.

Continued Bleeding

The EGD revealed multiple columns of large distal esophageal varices status post-band ligation x 4, with bleeding from esophageal and gastric varices with associated portal hypertensive gastropathy. He was transferred to the ICU for monitoring. The patient underwent a repeat EGD on day three after having an additional episode of hematemesis, resulting in three more bands being placed. He was ultimately discharged from the hospital on day seven after completing a seven-day course of antibiotics for spontaneous bacterial peritonitis prophylaxis. The patient returned to the ED six months later for abdominal distention, lower extremity edema, and in severe respiratory distress, with continued medical noncompliance. The patient ultimately enrolled into hospice.

Hemorrhage from ruptured esophageal varices is one of the most life-threatening complications arising from cirrhosis and a major cause of upper gastrointestinal bleeding. It is truly a medical emergency with a mortality rate from 15 percent to 20 percent, increasing up to 33 percent in patients with re-bleeds. (J Punjab Acad Forensic Med Toxicol 2010;10[2]:104; http://bit.ly/2xLgS5l.) Upper gastrointestinal bleeding is bleeding that originates proximal to the ligament of Treitz. Risk factors for upper GI bleeding include medications (aspirin, steroids, anticoagulation), ethanol abuse, and aortoenteric fistula (after aortic graft placement). (BMJ 2012;344:e3412.)

The differential of upper GI bleeding remains broad, and includes peptic ulcer disease, gastritis/esophagitis, varices, Mallory-Weiss tear, malignancy, aortoenteric fistula, Boerhaave esophagus, Dieulafoy's lesion, hemorrhagic gastritis, and portal hypertensive gastropathy. The physical exam may reveal tachycardia, hemorrhagic shock, palmar erythema, jaundice, spider angioma, and petechiae/purpura. It has been noted that 20 percent of patients with a positive hemoccult have an upper GI bleed. As a result, an upper GI bleed should not be completely ruled out in patients with a negative hemoccult. (BMJ 2012;344:e3412.)

Treatment

A retrospective study was performed by Downstate Medical Center in Brooklyn, NY, looking at the utility of nasogastric aspiration and lavage in the ED to differentiate an upper GI bleed from a lower GI bleed. They concluded that the diagnostic performance for predicting an upper GI bleed is poor, with sensitivity as low as 42% and specificity as low as 54%. They concluded there is limited utility in ruling out an upper GI bleed in patients with hematochezia or melena without hematemesis. (Acad Emerg Med 2010;17[2]:126.)

Management for a suspected esophageal variceal hemorrhage is multifactorial and involves airway, breathing, circulation, and undergoing an emergent EGD. A balloon tamponade equipped with a gastric and an esophageal inflatable balloon, called Blakemore's tube, can be used in the acute setting to control hemorrhage if endoscopy is not readily available. (Gastroenterology Rep [Oxf] 2017;5[3]:185; http://bit.ly/2R7JdL5.) Multiple medications are utilized: pantoprazole 80 mg bolus followed by an infusion at 8 mg/hr (or 40 mg BID) is recommended because it has been shown to decrease the rate of rebleeding, erythromycin 250 mg (given prior to endoscopy) has been recommended to improve gastric clearance, and vasoactive medications like octreotide (50 mcg IV followed by 50 mcg/hr continuous infusion for two to five days) is recommended because it is a splanchnic vasoconstrictor and decreases portal pressure.

Antibiotic prophylaxis is key because up to 40 percent of cirrhotic patients presenting to the ED with upper gastrointestinal bleeding will go on to develop an infection. Ceftriaxone is currently recommended for seven days following admission for patients with cirrhosis admitted with an upper gastrointestinal bleed. Other treatment options include a transjugular intrahepatic portosystemic shunt, termed TIPS, as the current treatment of choice for variceal bleeding refractory to the above. As a result of a high risk for rebleeding, initiating secondary prophylaxis is necessary after the first episode. Propranolol is often used for this reason because it results in decreased portal pressure through bradycardia, decreased cardiac output, and ultimately splanchnic vasoconstriction. (Gastroenterology Rep [Oxf] 2017;5[3]:185; http://bit.ly/2R7JdL5.)

Dr. Taylor is completing his emergency medicine residency at Beaumont Hospital in Farmington Hills, MI, a teaching hospital of Michigan State University. He also serves as a captain and physician in the United States Air Force. Dr. El-Alayli is an emergency physician at Beaumont Hospital and a clinical instructor in emergency medicine at Michigan State University.

Tuesday, October 16, 2018

​BY ARJUN BHARADWAJ & KHALID MALIK, MD

A 58-year-old man who lived at a nursing facility came to the emergency department complaining of abdominal pain for three days. His pain was localized to the epigastrium and periumbilical regions. The nursing home staff indicated that he was hypotensive and possibly hypoxic.

The patient said he never had similar pain before, which he said pain was mild and constant in severity and did not radiate to the chest, back, pelvis, or shoulders. He also reported nausea but no trauma, falls, vomiting, fever, chills, dizziness, chest pain, shortness of breath, trouble walking, or change in bowel movements or urination.

He had a history of schizoaffective disorder, type 2 diabetes mellitus, hypertension, and hyperlipidemia. He said he did not use illicit drugs and that he had quit smoking more than three years before. He used to consume ethanol daily, but had stopped when he was admitted to the nursing home two years earlier. His vital signs were a heart rate of 116 bpm, a blood pressure of 70/42 mm Hg, a temperature of 97.1°F, a respiration rate of 29 bpm, an oxygen saturation of 97% on two L nasal cannula, and pain severity of 2/10.

His neck and pharynx were normal, and he had no tenderness to chest or chest wall palpation. His breathing was not labored, but he had decreased bilateral breath sounds. A cardiac exam showed a regular rate and rhythm, he had no peripheral edema, and his peripheral pulses were equal bilaterally. His abdomen was soft, flat, and without organomegaly, and bowel sounds were normo-active. There was mild tenderness in the epigastric region without rebound, and Murphy's sign was negative. Rectal sphincter tone was maintained, and the guaiac test was negative. His skin was warm, dry, and of normal color. The remainder of the examination was normal.

He was taking simvastatin, metformin, insulin detemir/aspart, lactulose, haloperidol, fenofibrate, divalproex, clozapine, chlorpromazine, benztropine, aspirin, and multivitamin-min-iron-FA-vit K. Based on his history and physical exam, the differential diagnosis was narrowed to pneumonia with sepsis, pulmonary embolism, myocardial infarction, and intra-abdominal sepsis.

Labo results showed a WBC count of 8.3 k/μL, Hct of 30.5%, Hbg of 10.4 g/dL, RBC count of 3.71 M/μL, lactic acid of 9 mmol/L, PT of 12 s, and troponin of <0.03 ng/dL. An ECG revealed sinus tachycardia without ischemic changes. Chest x-ray showed near-complete left hemithorax opacification (Fig. 1), which was evocative of massive pleural effusion or consolidation of the left lung. The patient at this time had a Glasgow Coma Scale score below 7, and was intubated and placed on a ventilator. Abdominal and pelvic CT revealed pneumomediastinum in the posterior mediastinum (Fig. 2) and with minor extension into the superior peritoneum. (Fig. 3.) Decompressed small bowels were also noted in Figure 3.

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Figure 1. AP view of the chest x-ray displaying hemithorax opacification of the left lung (A).

case files-bharawaj esophageal tear2.jpg

Figure 2. Transverse CT displaying pneumomediastinum in the posterior mediastinum.

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Figure 3. Coronal cross-section of the abdomen and pelvic CT displaying encroachment of pneumomediastinum into the superior peritoneum and a decompressed small bowel.

Imaging revealed a pneumomediastinum and pleural effusion, which are indicative of a lower transmural esophageal tear. The patient was admitted to the ICU for sepsis and hypotension. Surgery was consulted for lower transmural esophageal tear and possible small bowel obstruction. (Fig. 3.) The patient was placed on broad-spectrum antibiotics, and a chest tube was placed on the left side. The esophageal stent was placed though an endoscopic procedure.

No small bowel obstruction was found. The diagnosis was actually an adynamic ileus secondary to the esophageal perforation, which was validated when the bowel movement spontaneously returned. The probable cause of esophageal rupture was combining anticholinergic and antipsychotic medications. The anticholinergic effect of these medications resulted in lower esophageal sphincter weakening and led to esophagitis. (Ann Intern Med2000;133[3]:165.) Antipsychotic medication also causes retching and forceful vomiting. (Comprehensive Hospital Medicine: An Evidence-Based Approach. Philadelphia: Saunders Elsevier; 2007.) A combination of the two may have resulted in transmural tear of the lower esophagus, which is known as Boerhaave syndrome. (Ann Surg1976;183[4]:401; http://bit.ly/2xVoJwn.) A surprising aspect of the case was that the patient displayed pain disproportionate to the severity of the problem. (Integr Physiol Behav Sci 1993;28[2]:118.)

Mr. Bhardwaj is a third-year medical student at the University of Medicine and Health Science, and is currently doing his emergency medicine rotation at Weiss Memorial Hospital in Chicago, IL. Dr. Malik is a board-certified emergency and internal medicine physician and the director of the emergency department at Weiss Memorial Hospital, an affiliate of the University of Illinois Hospital.

Tuesday, October 16, 2018

​BY GREGORY TAYLOR, DO, & FRANK SCHELL, DO

A 30-year-old woman presented to the ED complaining of pelvic pain. She said she felt an acute onset of sharp lower right pelvic pain during intercourse two days earlier. The pain continued to worsen, becoming diffuse. She was also experiencing nausea, vomiting, malaise, anorexia, and vaginal spotting. She had no history or concern for sexually transmitted disease, and had no fever or vaginal discharge. She had had a previous Cesarean section and bilateral tubal ligation.

Her vital signs were a heart rate of 110 bpm, a respiratory rate of 25 bpm, a blood pressure of 113/88 mm Hg, and a pulse ox of 100% on room air. She was in distress, lying flat, and diaphoretic, and she did not want to move. Her abdominal exam revealed a mildly distended abdomen, diffuse tenderness to palpation, with a palpable mass in the right lower quadrant with guarding and rebound. Her genital/urinary exam revealed clotted blood within the posterior vaginal vault, right adnexal tenderness, and no evidence of cervical motion tenderness.

A bedside FAST exam showed no evidence of free fluid within her abdomen or pelvis, but showed a large cystic mass within the right lower quadrant. Urine hCG and total beta hCG were negative. Transvaginal ultrasound revealed a multiloculated right adnexal cystic mass measuring 9 cm x 8 cm x 6 cm with little evidence of adequate blood flow to the ovary. (Image A.)

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Image A. Transvaginal ultrasound revealed a multiloculated right adnexal cystic mass with little evidence of adequate blood flow to the ovary.

The patient was taken emergently to the operating room for a diagnostic laparoscopy, removal of the cystic mass, and reduction of the ovarian torsion. (Image B.) The right adnexal mass was most likely a mucinous tumor that had undergone an ovarian torsion during intercourse. Her hospital stay was uncomplicated; she did well post-operatively and was discharged on day two.

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Image B. The patient was taken emergently to the operating room for a diagnostic laparoscopy, removal of the cystic mass, and reduction of the ovarian torsion.

An ovarian torsion represents about three percent of all gynecological emergencies. Ovarian torsion is the result of a partial or complete rotation of the ovary at its pedicle leading to obstructed venous and arterial vascular flow that can ultimately end in ischemia, necrosis, hemorrhage, peritonitis, and septic shock. (BMJ Best Practice September 2017; http://bit.ly/2Qe1cyh.) Venous and lymphatic flow is affected first in torsion. Arterial flow is maintained because the arteries' thick, muscular walls are less collapsible. This leads to ovarian edema and ovarian enlargement, causing increased pressure on the ovary and eventually leading to an obstruction of arterial flow. (Radiographics2008:28[5]:1355; http://bit.ly/2DxVt4U.)

Underlying abnormalities, like neoplasms and ovarian cysts, represent the majority of all cases. (BMJ Best PracticeSeptember 2017; http://bit.ly/2Qe1cyh.) Major risk factors include ovarian neoplasms larger than 5 cm in diameter, which represent 40 percent of all cases of ovarian torsion, and ovarian cysts larger than 5 cm in diameter, which represent another 40 percent of ovarian torsion cases. It is considered rare to see torsion in patients with a cyst smaller than 5 cm. (Radiographics 2008:28[5]:1355; http://bit.ly/2DxVt4U.) Other risk factors include infertility treatment (secondary to ovarian enlargement), pregnancy, strenuous exercise, intercourse, and sudden increases in intra-abdominal pressure (secondary to defecating, vomiting, coughing, and hiccups, causing the ovary to rotate about the pedicle). (BMJ Best Practice September 2017; http://bit.ly/2Qe1cyh.) Our patient had a preexisting 9 cm adnexal mass that resulted in ovarian torsion during intercourse.

The majority of patients will present to the ED with a sudden onset of abdominal pain located within the lower quadrant and pelvis associated with nausea and vomiting. The pain can be constant or intermittent, acute or chronic, and radiating to the flank, back, or groin. Left-sided ovarian torsion is less common because the sigmoid colon occupies the space in the left lower quadrant, leaving less space for rotation at the pedicle.

Diagnosis requires a thorough clinical history, ultrasound, and high index of suspicion in any female patient with risk factors and presenting with lower quadrant abdominal pain. No specific labs indicate ovarian torsion, but they are often performed to rule out other causes of lower abdominal pain. A transvaginal ultrasound is performed to evaluate for vascular flow and ovarian cysts, but the findings depend on the degree and duration of the torsion. (BMJ Best Practice September 2017; http://bit.ly/2Qe1cyh.)

Routine imaging findings necessary to make the diagnosis are often not present in many cases. Early in the process, the most commonly detected finding seen on ultrasound is unilateral ovarian enlargement larger than 4 cm. (Radiographics 2008:28[5]:1355; http://bit.ly/2DxVt4U.) As it progresses, other findings may include free fluid (87% of cases), a twisted vascular pedicle, and a string of pearls sign. A retrospective study of 21 patients with surgically confirmed ovarian torsion found that 10 had a normal ultrasound with Doppler findings. (Fertil Steril 2000;73[5]:1047; http://bit.ly/2zyPVTD.) The presence of vascular flow on ultrasound does not rule out an ovarian torsion, but it may suggest that the ovary is still viable if intervention is performed quickly.

Prompt recognition and immediate treatment can yield an excellent prognosis. The likelihood of saving a viable ovary decreases over time with some evidence suggesting that symptoms lasting more than 48 hours results in irreversible ischemia (more than six hours for testicular torsion). (Obstet Gynaecol 2012;14[4]:229; http://bit.ly/2zA8Jlx.) Ovarian torsion is a diagnostic challenge, especially in patients with intermittent symptoms. A high index of suspicion and clinical judgment are paramount in saving an ovary.