by The Case Files

The Case Files: Polyarthralgias, Rash, Swelling of Joints

By Alice Chao, MD, and Ayesha Khan, MD, MPH

A 44-year-old previously healthy woman presented to the emergency department with chest pain and shortness of breath. The patient reported a two-month history of polyarthralgias and rash. She initially noted swelling and pain of her ankles that progressed to her knees, wrists, and shoulders.

The patient also reported a non-pruritic rash with erythematous borders on her extremities that would come and go (Figure 1), nodules in her skin, and intermittent fevers.

Figure 1.

She denied any insect bites or recent travel, and had no personal or family history of autoimmune disorders. She reported a sore throat two weeks prior to onset of symptoms that was not treated. The patient was found to be in sinus tachycardia (Figure 2), and she complained of chest pressure and difficulty breathing.

Figure 2.

She continued to have persistent tachycardia despite fluid hydration and pain control. A CT angiogram of the chest was negative for pulmonary embolism. The patient was admitted for persistent tachycardia and further workup of recent symptoms that were concerning for acute rheumatic fever. Laboratory tests revealed a high antistreptolysin O titer. Throat culture was positive for Streptococcus pyogenes.

She also had elevated ESR and CRP. An echocardiogram was done during the hospitalization, which revealed mild thickening of the mitral valve and aortic valve with mild mitral and aortic regurgitation. Echo also revealed minimal pericardial effusion. The treating physicians felt the patient met the criteria for acute rheumatic fever (major criteria: polyarthritis, carditis/valvulitis, erythema marginatum [Figure 3], subcutaneous nodules; minor criteria: fever, arthralgia, elevated ESR and CRP, prolonged PR interval).

Figure 3.

The patient was started on penicillin 250 mg four times a day for two weeks, followed by 250 mg BID indefinitely for prophylaxis. She was also discharged on prednisone 40 mg daily and ibuprofen 800 mg TID for symptomatic relief. The patient's arthralgias and rash improved after treatment was initiated, and she is being followed by rheumatology and cardiology as an outpatient. Acute rheumatic fever (ARF) is a delayed sequela of group A streptococcus (GAS) pharyngeal infection.

A latent period of two to three weeks precedes the first signs of ARF. ARF and subsequent rheumatic heart disease affect almost 20 million people in the developing world, and are the leading cause of cardiovascular death in patients under age 50. (Lancet Infect Dis 2005;5[11]:685.) The mean incidence is 19 per 100,000 population.

A much lower incidence of ARF is reported in the United States and developed countries, likely because of improved hygienic standard and routine antibiotic treatment of acute pharyngitis. The incidence of ARF in developed countries has been as low as two to 14 cases per 100,000, though recent local outbreaks have occurred. (Circulation 2009;119[11]:1541; New Engl J Med 1987;316[8]:421; Pediatr Infect Dis J 1990;9[2]:97.)

T. Duckett Jones, MD, first described and published diagnostic criteria for acute rheumatic fever in 1944. (JAMA 1944;126[8]:481.) The American Heart Association subsequently established guidelines for diagnosing rheumatic fever (See Table 1 at end of article). (JAMA 1992; 268[15]:2069.)

A diagnosis of acute rheumatic fever requires the presence of two major manifestations or of one major and two minor manifestations with supporting evidence of a preceding group A streptococcal infection, according to the Jones criteria. Our patient had four major criteria (polyarthritis, carditis, erythema marginatum, and subcutaneous nodules) and four minor criteria (fever, arthralgia, elevated ESR and CRP, and prolonged PR interval). She also had elevated antistreptolysin O titers and a positive throat culture for group A streptococcus, both supporting a prior GAS infection.

The three major treatment goals of acute rheumatic fever are relief of symptoms, eradication of GAS, and prophylaxis against future GAS infection to prevent recurrent cardiac disease. Aspirin or other antiinflammtory agents are the mainstay of symptomatic management because of ARF, including relief of discomfort related to arthritis and fever.

Oral penicillin V is the drug of choice for eradication of GAS pharyngitis. Amoxicillin and cephalexin are also acceptable treatments. Approved alternatives for patients with potential severe hypersensitivity to beta-lactam antibiotics are azithromycin, clarithromycin, and clindamycin. (Circulation 2009;119[11]:1541.)

Prevention of recurrent GAS pharyngitis is the most effective method to limit progression of rheumatic heart disease because patients who have had rheumatic fever are at high risk for a recurrent attack. This secondary prevention requires continuous antibiotic prophylaxis, the duration of which depends on the risk of recurrence. Patients who have had rheumatic carditis are at relatively high risk for recurrence with cardiac involvement progressing with each recurrence.

Prophylaxis in these patients should continue until the patient reaches age 21 or for a total of 10 years (whichever is longer). Our 44-year-old patient, who is older than the typically affected population (ages 5–15), will need prophylaxis for several years. The antibiotic of choice for prophylaxis is IM penicillin G every four weeks or PO penicillin V twice daily. (Circulation 2009;119[11]:1541.)

Recent resurgence of rheumatic fever in the United States after years of decline suggests increases in undiagnosed and untreated cases of streptococcus pharyngitis. Rheumatic heart disease, a preventable illness, can lead to devastating complications such as cardiomyopathy, congestive heart failure, or complete heart block. It is important for physicians to remain diligent in diagnosing and treating cases of confirmed or suspected streptococcal pharyngitis.

Dr. Chao is a second-year resident in the Stanford/Kaiser
Emergency Medicine Residency Program. Dr. Khan is
a clinical instructor in emergency medicine at Stanford
University.

Table 1. Guidelines for Diagnosing an Initial Attack of Rheumatic Fever

Major Manifestations
Carditis
Polyarthritis
Chorea
Erythema marginatum
Subcutaneous nodules

Minor Manifestations
Clinical Findings
Arthralgia
Fever
Laboratory Findings
Elevated acute phase reactants (ESR, CRP)
Prolonged PR interval

Supporting Evidence of Antecedent Group A Streptococcal Infection
Positive throat culture of rapid streptococcal antigen test
Elevated or rising streptococcal antibody titer

Tags: Polyarthralgias, Rash, Swelling of Joints, rheumatic fever

Published: 4/29/2013 9:52:00 AM

04.24.13

by The Case Files

The Case Files: Methanol or Ethanol Poisoning? Correct Diagnosis Influences Treatment

Sanaei-Zadeh, Hossein MD

A 23-year-old man presented with agitation and decreased level of consciousness four hours after consuming homemade alcohol. He was brought in by a friend who had also ingested the same alcohol and was completely symptom-free. The patient had a history of seizures controlled by sodium valproate and a ventricular septal defect repaired in childhood. He was irritable, lethargic (Glasgow coma score: 12), and hypothermic. His pulse rate was 80 bpm, his respiratory rate was 20 bpm, and his blood pressure was 70/40 mm Hg. His pupils were midsized and reactive. Radial pulse was not detected, and carotid pulse was detected with difficulty. Bedside glucometery was determined to be 180 mg/dL. The patient's electrocardiogram is shown.The patient experienced cardiopulmonary arrest about 10 minutes after hospital presentation. Advanced life support was performed as were passive external and internal rewarming. The parameters of venous blood gas analysis were pH=7.15, HCO3=14.7, pCO2=43.2, and BE=-11.3. The lab test results were white blood cells, 11.1 × 103 /mm3; hemoglobin, 15.4; platelets, 187000/mm3; CPK, 49; CPK-MB, 29; blood urea nitrogen, 16; creatinine, 1.6; AST, 21 U/L; ALT,22 U/L; Na, 156 meq/L; and K,5.3 meq/L. He developed pulseless ventricular tachycardia without response to external pacing. Serum ethanol, methanol, formate, and lactate concentrations were not available. Ethanol was administered during the resuscitation via the nasogastric tube because of suspected methanol toxicity. The patient developed asystole two hours and 20 minutes after presentation, and did not respond to resuscitation. Methanol intoxication may regularly be seen endemically or sometimes epidemically because alcohol may contain methanol in countries where alcohol consumption is prohibited or the price of the commercially available alcohol is high. (J Med Toxicol 2011;7[3]:189; J Intern Med 2005;258[2]:181.) A severely ethanol-intoxicated patient usually presents with coma, hypotension, hypothermia, hypoventilation, respiratory arrest, mild acidosis associated with hypoglycemia, and an odor of ethanol on the breath. (Goldfrank's Toxicologic Emergencies, 9th Ed., New York: McGraw-Hill, 2011.) Severely methanol-intoxicated patients in contrast often present with coma, hypotension, tachycardia, tachypnea (to compensate for severe metabolic acidosis), seizure, and elevated blood glucose. (J Med Toxicol 2011;7[3]:189; J Intern Med 2005;258[2]:181; Haddad and Winchester's Clinical Management of Poisoning and Drug Overdose. 4th Ed., Philadelphia: Saunders Elsevier, 2007; J Med Toxicol 2011;7[3]:189.) The ethanol component of these alcohols postpones the metabolism of methanol, and these patients often present six to 24 hours post-ingestion with no odor of ethanol on the breath. (J Med Toxicol 2011;7[3]:189.) The patient's friend had consumed the same alcohol without signs or symptoms of methanol intoxication. The best clinical diagnosis for this patient is ethanol but not methanol intoxication, although there was no confirmatory test. The patient's ECG findings show he certainly was suffering from hypothermia. (Goldfrank's Toxicologic Emergencies, 9th Ed., New York: McGraw-Hill, 2011.) Administration of ethanol worsened his intoxication and hypothermia. The postmortem examination found the ethanol levels of the vitrous humor and blood samples were 70 and 129 mg/dL, respectively, and no methanol was detected in the patient's toxicological samples.

Published: 4/24/2013 6:46:00 AM

01.02.13

by The Case Files

The Case Files: Syncope

Sarin, Ritu MD; Habboushe, Joseph MD, MBA

A 29-year-old woman waiting to be seen in the emergency department went to the bathroom to provide a urine specimen. While on the toilet, she vomited and then had a syncopal episode. Her husband prevented her from hitting her head when she fell off the toilet, and he called for help as she started to wake up.

The nursing staff, attending, and resident came to the bathroom to help the patient onto a stretcher. Initial vital signs showed the patient was tachycardic at 101 bpm, normotensive at 123/99 mm Hg, and afebrile at 98°F, with a respiratory rate of 22 bpm and an oxygen saturation of 100% on room air.

The common standard differential for initially assessing a patient with syncope consists of arrhythmia, hypoglycemia, anemia, vasovagal syndrome, and orthostatic hypotension. It is helpful to organize a diagnostic approach of dangerous versus benign causes, as well as painful versus painless causes, however, when dealing with an unstable patient with syncope.
Less commonly remembered are the “bad and painful” causes:

* Headache and syncope: subarachnoid hemorrhage.
* Chest pain and syncope: pulmonary embolism or aortic dissection.
* Abdominal pain and syncope: ruptured ectopic or AAA.

The Basics of Emergency Medicine: A Chief Complaint-Based Guide includes an approach to syncope and pre-syncope (see table) that uses a differential-focused workup for the dangerous causes of syncope.

A brief initial assessment of the patient indicated she had presented to the ED because of intense nonradiating lower abdominal pain for four hours. The pain had progressively worsened, and was aggravated by movement. She denied vaginal bleeding or discharge, diarrhea, dysuria, hematuria, fever, chills, dizziness, headache, chest pain, and shortness of breath. The patient noted similar pain a few weeks prior for which she was seen in the ED. She denied any significant past medical history, and did not know her pregnancy status.
The patient appeared uncomfortable and pale. Her pupils were equal and reactive, conjunctiva pink, and scelra clear. Her neck was supple without JVD, and she was tachycardic. Breath sounds were clear and equal bilaterally.

Her abdomen was diffusely tender, more so in the lower than upper quadrants, with rebound and guarding. She had no CVA tenderness. Her lower extremities were nontender without edema and had normal distal pulses. Neurologically she was intact without gross deficits.

Diagnosis and Treatment

The patient was placed on a cardiac monitor. The initial FAST ultrasound exam, performed with the patient lying supine, was negative for free fluid. Given a high pretest probability for a ruptured ectopic pregnancy in this patient with abdominal pain and syncope, the FAST ultrasound exam was repeated after the patient was put in the Trendelenburg position, revealing free fluid in Morison's pouch. (See ultrasound.)

Laboratory tests including CBC, BMP, type and screen, and beta-hCG were ordered, and two large-bore intravenous lines were placed. The patient had just urinated and was too unstable to wait for her to urinate again, so a bedside pregnancy test was run with whole blood. (See photo.) Recently described as a rapid way to test pregnancy at the bedside, studies have shown that whole blood point-of-care testing with standard urine pregnancy tests have accuracy close to that of urine, with a 95.8% sensitivity and 100% specificity, as long as a full five minutes elapse before reading the test. (J Emerg Med 2012;43[3]:478; Ann Emerg Med 2011;29[7]:840.)

The patient was bolused with two liters of normal saline and given intravenous morphine and ondansetron for symptom relief. Given the findings of a positive FAST exam and positive whole blood point-of-care pregnancy test, a diagnosis of a ruptured ectopic pregnancy was presumed. OB-Gyn was emergently consulted, and the patient was prepped for the operating room.

The patient denied any past medical or surgical history, medication use, smoking, alcohol use, or illicit drug use. She was sexually active with her husband, but did not use oral contraceptives, an IUD, or condoms. The patient's os was closed on pelvic exam and no blood or abnormal discharge was present, but she was tender to palpation diffusely in the adnexa and over the cervix.

A transvaginal ultrasound was performed by OB-Gyn while awaiting transport to the OR that revealed heterogeneous material in the cul-de-sac and left adnexa, confirming the diagnosis of ruptured ectopic.

Laparoscopic findings in the operating room showed the left fimbriated portion of Fallopian tube had ruptured. A clot approximately 1600 mL was visualized in the abdomen, including an organized clot in the cul-de-sac on the left. A partial left salpingectomy was performed, and the patient recovered without complications. Pathology did not show any gross fetal parts, but did show clotted blood, papilliferous tissue, and fallopian tube

Syncope as a Chief Complaint

Syncope or near-syncope accounts for one to two percent of ED visits annually, resulting in six percent of hospital admissions per year. The differential for syncope is extensive, with estimates of 10 percent being of cardiac origin, 21 percent vasovagal, nine percent related to orthostatic hypotension, nine percent neurological, including seizures, and up to 40 percent for unknown reasons. Patients with syncope and neurological or cardiac causes have a significant increase in mortality; patients with unknown causes have an increased risk of death of 30 percent. (Tintinalli's Emergency Medicine, 7th edition; New York: McGraw-Hill, 2011 [Ch. 56].)

Multiple clinical guidelines have been developed to help the emergency physician approach this large population of patients where missing important risk factors can have fatal consequences for the patient. The most commonly referenced decision rule in current literature is the San Francisco Syncope Rule, which can be found on MDCalc.com, a website designed by EMN's Emergentology author Graham Walker, MD. (Ann Emerg Med 2004;43[2]:224; Ann Emerg Med 2006;47[5]:448.) This rule was developed to assess adverse outcomes in patients seven and 30 days after syncope. The derivation of a clinical rule identified the several predictors of significant adverse events, primarily arrhythmias and anemia, using the acronym CHESS:

C: History of CHF.
H: Hematocrit below 30.
E: Abnormal ECG findings.
S: Shortness of breath on history or exam.
S: Systolic blood pressure below 90.

These criteria have not been well validated in the literature, but they are often referenced and used as a guideline by practitioners when approaching possible cardiac causes of syncope. (Ann Emerg Med 2008;52[2]:151.) They do not, however, address many of the more difficult-to-remember differentials for syncope, including the bad and painful.
More recently developed, the Boston Syncope Criteria used a larger list of factors to identify patients at risk for critical outcomes. (J Emerg Med 2007;33[3]:233 and 2012;42[3]:345.) Patients are considered at risk if they meet any of the following criteria:

* Signs and symptoms of acute coronary syndrome.
* Signs of conduction disease.
* Worrisome cardiac history.
* Valvular heart disease by history or physical examination.
* Family history of sudden death.
* Persistent abnormal vital signs in the ED.
* Volume depletion.
* Primary central nervous system event.

These criteria are more expansive than the San Francisco Syncope Rule and likely to assist in identifying patients at risk for adverse outcomes, but they have yet to be externally validated.

Syncope, in common practice and supported by ACEP guidelines, is commonly approached with an initial workup consisting of an ECG, cardiac monitoring, bedside glucose testing, urine pregnancy test, and CBC, with further testing focused by history and physical. (Ann Emerg Med 2007;49[4]:431.) The initial workup is fairly standard, but it only addresses the commonly remembered differential for syncope including cardiac causes, hypoglycemia, vasovagal, orthostatic hypotension, and anemia.

The differential can first be divided into the dangerous and less-dangerous causes of syncope. The dangerous differential list can be classified as painless or painful. Dangerous painless causes of syncope include cardiac arrhythmias, new valvular disease, myocardial infarction, hypoglycemia, and anemia. Cardiac causes that are often overlooked include Brugada syndrome, prolonged QT, Wolff-Parkinson-White syndrome, and signs of hypertrophic cardiomyopathy. (Am J Emerg Med 2007;25(6):688.) The history and physical exam should be focused on this differential list.

The dangerous and painful causes of syncope are often overlooked by inexperienced clinicians, and include subarachnoid hemorrhage (headache), pulmonary embolism (chest pain), aortic dissection (chest pain), ruptured ectopic pregnancy (abdominal pain), and ruptured abdominal aortic aneurysm (abdominal pain).

These diagnoses are much less common than the dangerous and painless causes, but the patients are often much more critically ill. Getting into the habit of even briefly considering these diagnoses on all syncope patients may help increase the clinician's diagnostic accuracy for these high-mortality diseases.
The dangerous and painful cause of syncope in this case was a ruptured ectopic pregnancy. Consideration of ruptured ectopic pregnancy in a young woman with syncope and abdominal pain not only led to a FAST ultrasound very early in the patient's course of treatment, it also compelled repeating the ultrasound in the Trendelenburg position. Early consideration of a ruptured ectopic pregnancy also resulted in diagnosing the pregnancy with a drop of blood on a urine pregnancy test, leading to the correct diagnosis and timely treatment.

Ectopic Pregnancy

Ectopic pregnancy is relatively common, occurring in one in 3,000 pregnancies to one in 30,000. The history and exam tend to point the physician in the right direction, but studies have shown that women are wrong 10 percent of the time when they say there is absolutely no way they can be pregnant. (Ann Emerg Med 1989;18[1]:48.)

Multiple risk factors exist, including a history of PID, infertility for more than two years, tubal surgery or ligation, prior ectopic pregnancy, and IUD placement. Data show that 50 percent of women with ectopic pregnancy have one or more risk factors, but 25 percent of patients with an intrauterine pregnancy and threatened abortion also have one or more of these risk factors.
Most patients will present with lower abdominal pain and vaginal bleeding, but syncope can be part of the presentation. Adnexal tenderness or fullness is present in about 50 percent of patients with ectopic pregnancy and also in about 15 percent of patients with threatened abortions. (http://crashingpatient.com/ob-gyn/5358.htm.)

Patients should be screened with a stat pregnancy test, a transvaginal ultrasound, serum beta-hCG, and type and screen. All patients diagnosed with ectopic pregnancy require an OB-Gyn consultation. Some patients only require close follow-up after the OB-Gyn evaluation if they are stable enough to avoid the OR or if ultrasound findings are indeterminate because studies have shown that as many as 15 percent of indeterminate ultrasounds end up being ectopic pregnancies. (Ann Emerg Med 1989;18[1]:48.)

With a beta-hCG of 1200–1500, endovaginal ultrasound should reveal an intrauterine pregnancy; with a beta-hCG over 6500, an intrauterine pregnancy can typically be seen on simple transabdominal pelvic ultrasound. The beta-hCG level should increase by 66 percent every 1.8 to three days for the first six to seven weeks beginning eight to nine days after ovulation in normal intrauterine pregnancy. Symptomatic patients with hCG over 1500 are much more likely to have an ectopic or abnormal pregnancy. (Emergency Medicine Practice 2003;5[11].) If the beta-hCG is over 1000 and no intrauterine pregnancy is observed on ultrasound, the patient requires a two-day follow-up with OB-Gyn in two days for repeat beta-hCG levels.

Methotrexate is often the treatment of choice by OB-Gyn for patients with a beta-hCG over 3000 who are hemodynamically stable, reliable, and available for follow-up. Patients are advised to avoid folic acid, alcohol, and intercourse until the beta-hCG returns to normal. Ruptured ectopic pregnancies and ectopic pregnancies with beta-hCG over 3000, a mass over 4 cm, or cardiac activity typically require laparoscopy. Be mindful of patients in the first two weeks post-methotrexate treatment with abdominal pain and vaginal bleeding. Obtain an ultrasound and hematocrit to rule out a ruptured ectopic that failed therapy versus methotrexate side effects. If unsure, patients should be admitted and observed using serial examinations and hematocrit. (Tintinalli's Emergency Medicine, 7th edition; New York: McGraw-Hill, 2011 [Ch. 101].)

Pocket Guide for Residents

EMRA'S Basics of Emergency Medicine is a chief complaint-based pocket guide provided to all first-year emergency medicine residents in their welcome packet from the Emergency Medicine Residents' Association. It is also available for $12 ($7 for residents) on www.EMRA.org and www.ACEP.org. It was scheduled to be released as an iPhone app at the ACEP Scientific Assembly in October.

Published: 1/2/2013 10:37:00 AM

10.26.12

by The Case Files

The Case Files: Syncope and Undiagnosed Addison’s Disease

Bober, Wojciech DO; Levy, David DO; Rosenthal, Cynthia DO

A 15-year-old girl was brought by her mother to the emergency department with several days of weakness, non-bloody vomiting, and syncope. She had four syncopal episodes, all without premonitory symptoms. She had a past medical history of asthma, for which she was prescribed albuterol. She denied any past surgical history, allergies to medications, and taking any other medications. She denied complaints of chest pain, palpitations, and shortness of breath.

Her temperature was 97.6°F, pulse 110 beats per minute, blood pressure 94/68 mm Hg, and respiratory rate 18 beats per minute with O2 saturation 97% on room air. She appeared pale, but was well developed and lying comfortably on a hospital stretcher.

Her pupils were equally round and reactive to light and accommodation, sclera were anicteric, and she had no evidence of pallor. She had a normal pharynx without erythema or exudates, and her mucous membranes were somewhat dry. Her neck was supple, nontender, and without lymphadenopathy or meningitic signs. Her heart was tachycardic but regular without murmurs, rubs, or gallops. Her lungs were clear to auscultation without wheezes, rhonchi, or rales.

Her abdomen was soft with normal bowel sounds, nontender, and nondistended. Her extremities were nontender to palpation, and were without edema or erythema; capillary refill was less than two seconds. Her skin examination was unremarkable except for slight darkening of the vermillion border of her lips. She was awake, alert, and oriented, and had no focal findings on neurological examination.

She had a witnessed self-limited syncopal episode in the ED lasting approximately five seconds. No seizure activity was noted, and she did not experience a post-ictal state after. The ED workup consisted of SMA-7, CBC, UCG, urine toxicology screen, EKG, and cardiac enzymes. The SMA-7 revealed a Na+ 121 mg/dL, and her BUN and Cr were 21 and 0.8 respectively. All other tests including potassium level were within normal limits.

The patient was admitted to the pediatric unit for evaluation and treatment of hyponatremia and dehydration. Intravenous fluids and ondansetron (Zofran) were continued. Repeat lab work over the next 48 hours showed a gradual improvement of sodium level toward normal, and her nausea and vomiting resolved. She was discharged home for follow-up with her pediatrician.

She returned to the ED a week later, once again complaining of generalized weakness and inability to perform routine activities. She was again found to be hyponatremic, and was subsequently admitted to the pediatric unit and then transferred to the PICU for an in-depth evaluation of her fatigue and hyponatremia.

A pediatric endocrinologist was consulted, and a metabolic/hormonal workup was performed. The results were significant for low cortisol level, high ACTH, and high renin. The patient also tested positive for adrenal cortex antibodies. Chest radiography revealed a somewhat small heart silhouette than expected given the patient's body size and age, likely secondary to hypovolemia. Secondary causes of adrenal insufficiency were ruled out using MRI of the patient's brain showing a normal pituitary and hypothalamus. SIADH was ruled out using urine sodium and osmolality measurements, and the patient was diagnosed with Addison's disease based on the test results and clinical features.

The patient is currently being followed by a pediatric endocrinologist. She is receiving mineralocorticoid/glucocorticoid replacement, which is the treatment of choice in primary adrenal insufficiency. (New Engl J Med 2003;348[8]:727.) The patient has returned to performing her normal activities of daily living. Her weight has improved, and symptoms of weakness have completely resolved.

The incidence of Addison's disease in the United States is 40–60 cases per million. (Lancet 1968;2[7571]:744; JAMA 1997;278[22]:1931.) It is mainly characterized as a chronic endocrine disorder in which adrenal gland dysfunction leads to insufficient production of glucocorticoids and mineralocorticoids. Symptoms of Addison's disease are often insidious and nonspecific. The potassium level may be normal in a third of patients, as it was in this case. (Rosen's Emergency Medicine, 7th Ed., Vol. 2; Philadelphia: Mosby; 2010.) New onset fatigue in an otherwise healthy and active young patient should raise concern for this diagnosis. Dizziness and orthostasis because of hypotension may occasionally lead to syncope. Syncope in children is often benign and attributed to vasovagal episodes or dehydration, but other causes must be entertained.

Patients with new onset fatigue, multiple visits to the ED, and with no other identifiable causes require pediatric specialists and a more thorough workup. Addison's disease is difficult to diagnose on a single encounter, and often not entertained even after multiple visits, yet recognition is critical because an acute superimposed stress can lead to vascular collapse and death. (Rosen's Emergency Medicine, 7th Ed., Vol. 2; Philadelphia: Mosby; 2010.)

Diagnosis of Addison's disease consists of checking morning serum cortisol levels. A result of less than 3 μg/dL is diagnostic of a hypoadrenal state. Our patient's cortisol level was less than 0.2. This is typically followed by an ACTH stimulation test to confirm the diagnosis and distinguish between primary and secondary adrenal insufficiency. A high level is consistent with primary adrenal insufficiency — Addison's disease. Adrenal auto-antibodies directed against 21-hydroxylase and 17-hydroxylase also are present in most cases of primary adrenal insufficiency. (JAMA 1997;278[22]:1931.) Those were positive in our patient.

Published: 10/26/2012 8:29:00 AM

10.19.12

by The Case Files

The Case Files: Masquerading Shoulder Pain

Weinstein, Shannon DO; Saadatmand, Babak MD; Sattler, Steven DO; Levy, David DO

A 62-year-old woman with a past medical history of breast cancer presented to the emergency department with three weeks of intermittent left scapula pain. The onset was at rest, and she had no history of trauma. The pain was not made worse or relieved by change in position. She denied any associated symptoms, but a review of systems revealed a few episodes of abdominal fullness over the preceding three weeks.

She denied chest pain, shortness of breath, abdominal pain, nausea, vomiting, diarrhea, fever, chills, leg pain or swelling, and recent travel. Prior treatment for the pain included over-the-counter analgesics, which offered minimal relief. She had outpatient evaluations by a cardiologist and a neurologist for her shoulder pain before her ED visit. The outpatient doctors ordered numerous blood tests, a transesophageal echocardiogram (TEE), and an MRI of the lumbosacral spine. The indications for these diagnostic modalities were unknown to the patient.

The TEE was unremarkable, and MRI showed a clinically insignificant lumbar disc herniation. The patient had bilateral lumpectomies in 2000 and 2002, and additional past medical history included palpitations and mitral valve prolapse. She denied tobacco, alcohol, or drug abuse. The patient's vital signs on arrival in the ED were unremarkable. She was uncomfortable, her abdominal exam included normal bowel sounds, and her abdomen was flat, not obese, not distended, and nontender without palpable organomegaly.

A back exam revealed no tenderness to palpation and no deformity. The remainder of her physical exam was normal. The patient received ketorolac, oxycodone/acetaminophen, and diazepam. Blood work was drawn, and a CT of the chest with contrast to rule out PE was obtained. The labs were unremarkable except for a mild normocytic anemia. The CT of the chest was extended to the abdomen during the exam at the order of the attending doctor when the CT technologist recognized a suspicious mass on the last cuts of the CT chest.

The abdominal CT revealed a large abdominal mass measuring 13 cm x 15 cm x 24 cm in size, encasing and displacing the abdominal aorta, inferior vena cava, and the left kidney, while extending from the left diaphragmatic crus to the left iliac fossa. The patient was admitted, and underwent percutaneous biopsy. The pathology was consistent with lymphoma. The patient was subsequently discharged home with oncology follow-up as an outpatient. She is now awaiting a specialized multifaceted treatment plan from her surgeon and oncologist.

Referred pain is found in the literature as early as 1893 when Sir Henry Head, an English neurologist, included the phrase “referred tenderness and pain” in his paper, “On Disturbances of Sensation with Especial Reference to the Pain of Visceral Disease.” (Brain 1893;16:1.) Since then, it has been defined as pain perceived at a site adjacent to or at a distance from the site of origin. (Clin J Pain 2001;17[1]:11.)

Several neuroanatomical and physiological theories focus on this concept. Collective conclusions from past studies state that nociceptive dorsal horn and brainstem neurons receive convergent inputs from various tissues; therefore, higher centers cannot identify the actual input source correctly.

The best known example is pain experienced during a heart attack. Nerves from damaged heart tissue convey pain signals to spinal cord levels T1-T4 on the left side, which are the same levels that receive sensation from the left side of the chest and part of the left arm. Another example involves pain from a ruptured spleen or splenic abscess. Called Kehr's sign, it is the referred pain from abnormal spleen pathology irritating the diaphragm. The sensory fibers of one of the phrenic nerves send pain signals to the spinal cord at C3-C5. Neurons at these spinal cord levels also receive sensation from the shoulders via the supraclavicular nerves.

The patient in this case was experiencing referred pain from the large abdominal mass abutting the diaphragm, causing signals to be sent via the phrenic nerve to the brain and making the patient perceive the pain as coming from the shoulder. Unfortunately, the mass was not able to be palpated by physicians due to its posterior location in the abdomen nor was it readily distinguishable from the other abdominal organs because of the mass spanning across the entire abdomen from the diaphragm to the bony pelvis, making it critical to obtain a CT of the abdomen and pelvis.

It is important for physicians to remember the concept of referred pain when diagnosing and treating presumed musculoskeletal complaints, especially in instances when extensive diagnostic testing has elicited no cause. Had the symptom been considered before her ED visit, it may have led to the correct diagnosis and earlier intervention.

Published: 10/19/2012 12:38:00 PM

09.07.12

by The Case Files

The Case Files: Right Flank Pain and Nausea

Bremjit, Prasheeda MD; Sheele, Johnathan M. MD, MPH

A 27-year-old woman with a history of recurrent urinary tract infections presented to the emergency department with right-sided flank pain and nausea. She denied fevers, chills, urinary symptoms, diarrhea, and constipation, though she did report some mild dyspnea and cough. She reported that she had had a normal spontaneous vaginal delivery of a healthy infant two weeks earlier. Pregnancy was complicated only by a urinary tract infection.

The patient was febrile to 38.6°C. She did not have right costovertebral tenderness or right upper quadrant abdominal pain. Urinalysis was notable for positive nitrite, small leukocyte esterase, 5-10 white blood cells, 3-5 red blood cells, and positive bacteria. The urine culture ultimately grew 20,000 organisms of more than two organisms thought to be related to skin contamination. Serum laboratory testing was significant for a white blood cell count of 21,000 cells/?L, alkaline phosphatase 205 U/mL, total bilirubin 0.8 mg/dL, AST 37 U/L, and ALT 24 U/mL. The patient was given intravenous ceftriaxone in the ED for presumed pyelonephritis. One hour into her ED stay, she was noted to have tachypnea. Chest x-ray was obtained, and read as "probable mild blunting right costophrenic angle, perhaps atelectasis or small effusion. Fluid level right upper quadrant, likely within a loop of bowel or stomach."

A computed tomography scan of the chest, abdomen, and pelvis revealed several intrahepatic abscesses, with the largest measuring 8 x 10 x 11 cm in the posterior right lobe. The second largest was abutting the gallbladder with associated gallbladder wall thickening and pericholecystic fluid. The third and fourth abscesses in the tip of the right hepatic lobe were abutting the hepatic flexure and ascending colon with associated colon wall thickening. A fluid-filled borderline prominent ascending colon with moderate wall thickening was also seen.

Coronal CT images showing multiple liver abscesses.

Surgery, OB/GYN, and interventional radiology were consulted, and the patient ultimately required drainage of the abscesses. Gram stain of the liver abscesses showed many polymorphonuclear cells, innumerable gram-positive rods, innumerable gram-positive cocci, many gram-negative rods, and a few gram-negative cocci. Anaerobic and aerobic cultures grew Escherichia coli, Bacteroides thetaiotaomicron-isolated, Peptoniphilus asaccharolyticus (previously Peptostreptococcus)-isolated, and Clostridium species-isolated.

This is the first known documented case of a liver abscess occurring in an otherwise healthy woman two weeks post-partum after an uncomplicated vaginal delivery. Liver abscesses can be seen in young women, but most have underlying risk factors such as diabetes mellitus, pancreatitis, appendicitis, cholelithiasis, gastrointestinal or hepatobiliary malignancy, gastrointestinal or pelvic infections, abdominal trauma, recent abdominal surgery, or liver transplantation. (Clin Infect Dis 2004;39[11]:1654; J Clin Gastroenterol 2005;39[7]:646; Current Medical Diagnosis & Treatment. New York: McGraw-Hill; 2012; Surg Clin North Am 2010;90[4]:679.) Liver abscesses are relatively rare, but they are still the most common type of visceral abscess (with an annual incidence of 3.6 cases per 100,000 population). (Am J Gastroenterol 2010;105[1]:117.) Liver abscesses can be caused by a bacteria, parasites, and fungi (Surg Clin North Am 2010;90[4]:679), but the most common organisms to cause them in North America are Klebsiella pneumoniae and Escherichia coli. (Clin Infect Dis 2004;39[11]:1654.)

Axial CT images showing large liver abscesses.

The pathogenesis of pyogenic liver abscess is multifactorial; the liver can be infected through the bile duct, the portal vein, the hepatic artery (secondary to bacteremia), or direct extension from any alternate underlying infection. Symptoms from a pyogenic liver abscess usually develop over days to weeks, and initially are characterized by malaise, anorexia, myalgias, arthralgias, and headache. (Surg Clin North Am 2010;90[4]:679.) Late findings more characteristic of pyogenic liver abscesses are fevers, chills, and right upper quadrant abdominal pain. (Surg Clin North Am 2010;90[4]:679.)

Pyogenic liver abscesses are rare compared with pyelonephritis. (Am J Gastroenterol 2010;105[1]:117; Clin Infect Dis 2007;45[3]:273.) Clinical vigilance is important, or the diagnosis can easily be overlooked. Clinically, symptoms of pyogenic liver abscess are often nonspecific, but may include fever and abdominal pain. Jaundice may also be noted on physical exam in some cases. Laboratory abnormalities can include an elevated white blood cell count, erythrocyte sedimentation rate, and abnormal liver function tests. (Surg Clin North Am 2010;90[4]:679.)

Blood cultures are positive in 50-100 percent of cases. Ultrasound, CT, or MRI can be used to diagnose pyogenic liver abscess. (Current Medical Diagnosis & Treatment. New York: McGraw-Hill; 2012; Surg Clin North Am 2010;90[4]:679.) The preferred treatment is percutaneous drainage of the abscess and several weeks of antibiotic therapy. (Clin Infect Dis 2004;39[11]:1654.) Pyelonephritis was initially suspected, but subtle clinical, laboratory, and radiological findings ultimately led to the correct diagnosis. The definitive mechanism by which the pyogenic liver abscess developed in our patient was never fully elucidated.

Dr. Bremjit is a resident in internal medicine-family medicine at Eastern Virginia Medical School in Norfolk. Dr. Sheele is an assistant professor and the fellowship director of international health and wilderness medicine in the department of emergency medicine at Eastern Virginia Medical School.

Published: 9/7/2012 12:23:00 PM

08.20.12

by The Case Files

The Case Files: Swollen Legs

Himelfarb, Nadine T. MD; McGregor, Alyson J. MD

A patient comes to the emergency department with a seemingly simple chief complaint. "My legs are swollen," he said.

The patient is a 52-year-old man with alcoholic cirrhosis who had experienced increased lower extremity edema over the past week. He admitted to noncompliance with his recently prescribed medications, Aldactone and Lasix. He reported a history of "fluid in his abdomen," but denied any recent infections requiring antibiotics. He also denied fever, chills, chest pain, shortness of breath, and abdominal pain.

The patient had a temperature of 98.9°F with a pulse of 102 bpm and a blood pressure of 95/48 mm Hg. He was alert and oriented, and appeared disheveled but was in no apparent distress. Bitemporal wasting and scleral and sublingual icterus were noted. His mucous membranes were dry. Pulmonary auscultation revealed bibasilar rales. Heart sounds were normal. Abdominal exam was nontender and otherwise notable for the findings in the photos. He was noted to have 3+ pitting edema to the hips, with additional pitting edema extending up his trunk to his chest. He had full painless range of motion of his extremities. His skin was noted to be dry and icteric, with multiple bruises and scattered petechiae.

His chem 7 was reported as glucose 73, sodium 139, potassium 3.4, chloride 106, bicarbonate 25, creatinine 2.34, and BUN 43. His CBC revealed a WBC 9.0 (88% segs, 4% lymphs), Hgb 10.9, Hct 32.3, Plt 99, AST 70, ALT 41, Alk Phos 116, Tbili 2.9, Dbili 1.3, albumin 1.8, and INR 1.6

What is your doorway diagnosis? How many physical exam findings can you identify to support this diagnosis based on the photos?

This patient was in fulminant hepatic failure with all the findings of hepatic congestion: icterus, ascites, edema, portal hypertension manifested by caput medusa and spider angiomata, and gynecomastia thought to be because of increased estrogen or estrogen:testosterone ratios. Given these findings, he was admitted to the medical service for worsening hepatic failure and acute kidney injury thought to be because of either prerenal causes or hepatorenal syndrome.

He was noted to have a fever and increased WBC with a 9% bandemia on his second hospital day. A diagnostic and therapeutic paracentesis was performed that was consistent with spontaneous bacterial peritonitis, and he was started on antibiotics. A gastroenterology consult was obtained, and recommendations were made to stop diuresis given poor urine output and inability to appreciate the presence of hepatorenal syndrome.

It was determined that he was not a candidate for liver transplantation because of alcohol abuse. One week into hospitalization, he was noted to have hematemesis. An endoscopy was performed revealing grade II esophageal varices requiring banding. He responded poorly to symptomatic care, and multidisciplinary meetings were held with the patient to discuss his poor prognosis. The patient ultimately decided to begin comfort care, with the hope of transitioning to home with hospice services.

Cirrhosis is a result of irreversible scarring of the liver from many causes, among them alcohol abuse, nonalcoholic fatty liver disease, chronic viral hepatitis, biliary sclerosis or atresia, autoimmune cirrhosis, inherited disorders, and other unknown causes. Emergency physicians should maintain a high level of suspicion for spontaneous bacterial peritonitis in patients with ascites because earlier detection and treatment results in a decreased infection-related mortality. Administering antibiotics before the onset of renal failure and shock has a significant effect on improving prognosis. The one- to two-year mortality after spontaneous bacterial peritonitis remains at 70-80 percent despite these efforts. Hepatorenal syndrome is an often fatal complication of cirrhosis, and requires immediate involvement of gastroenterology or hepatology.

Dr. Himelfarb is an emergency medicine resident at Rhode Island Hospital in Providence. Dr. McGregor is an assistant professor of emergency medicine at the Warren Alpert Medical School of Brown University, also in Providence.

Published: 8/20/2012 8:12:00 AM

08.10.12

by The Case Files

The Case Files: Renal Infarct

Dubrovskiy, Aleksandr DO; Levy, David DO; Saadatmand, Babak MD

A 56-year-old man with a past medical history significant for hypertension, hyperlipidemia, and sciatica presented to the ED complaining of a sudden onset of sharp, severe, right flank pain radiating to his right groin. The pain began about 30 minutes prior to arrival and had been constant since onset. He denied any alleviating or aggravating factors, trauma, or prior occurrences.

He complained of nausea without vomiting, and review of systems was otherwise negative. He had no recent surgeries and denied any alcohol, smoking, or drug use. The patient was allergic to penicillin, and was compliant with his prescribed atorvastatin (Lipitor), aspirin, niacin (Niaspan), olmesartan (Benicar), multivitamin, folate, and fish oil. He was unsure about his family history.

His temperature was 98.6°F, pulse was 50 bpm, respiratory rate was 20, blood pressure was 123/79 mm Hg, and oxygen saturation was 100% on room air. His general appearance reflected a well-nourished but uncomfortable man who was unable to sit still secondary to pain. His pupils were equally round and reactive to light with extraocular muscles intact. He had no rhinorrhea, and his pharynx was clear. His neck was supple, nontender, and without lymphadenopathy. He had a regular heart rate with normal S1 and S2 without murmurs, rubs, or gallops. His lung sounds were clear bilaterally without wheezing, rales, or rhonchi. He had significant right costovertebral angle tenderness.

His abdomen had normal bowel sounds and was soft and nontender without rebound or guarding. The genitourinary exam revealed normal external genitalia without meatal discharge. Both testes were descended, and the right testicle was tender upon palpation. There was no cyanosis, clubbing, or edema on the extremity exam. Distal pulses were normal in all four extremities. Skin was normal for his age -- dry, warm, and without any lesions or rashes. He was awake, alert, and oriented x 3. His cranial nerves II-XII were intact, and he had no sensory or motor deficits.

Blood work was ordered, including a complete blood count, basic metabolic panel, and coagulation profile. The results showed a white count of 6.2 x10(3)/mcL, hemoglobin of 15.2gm/dL, hematocrit of 44.1%, and platelet count of 254x10(3)/mcL. The basic metabolic panel was normal with sodium of 140 mmol/L, potassium of 3.9 mmol/L, chloride of 103 mmol/L, bicarbonate of 25 mmol/L, BUN of 24 mg/dL, creatinine of 1.1 mg/dL, and glucose of 126 mg/dL. His LDH level was elevated at 530. The coagulation profile was unremarkable with a PT of 11.1 seconds, INR of 1.1, and PTT of 22.5 seconds. The patient was treated with ketorolac (Toradol) 30 mg IV push and morphine 5 mg IV push with minimal resolution of his pain. A noncontrast CT scan of the abdomen and pelvis obtained for evaluating renal colic was reported as normal. (Figure 1.) A testicular ultrasound was also normal.

Because of persistent pain, a CT scan with IV contrast was ordered to evaluate for other etiologies. The scan showed marked decrease of contrast uptake in the right kidney, signifying lack of perfusion or a right renal infarct. (Figure 2.) The patient was given additional analgesia, hydromorphone (Dilaudid) 3 mg IV push and diazepam (Valium) 2 mg IM.

The patient was admitted to the telemetry unit. He was seen in consultation by urology, hematology/oncology, cardiology, and vascular surgery. The hypercoagulable workup was negative. An echocardiogram showed an ejection fraction of 60% and no valvular or chamber abnormalities. The patient was started on heparin at a full anticoagulation dose. Three days following admission, the anticoagulation was switched from heparin to clopidogrel (Plavix). His pain resolved over the course of the admission, and he was ultimately discharged home on clopidogrel five days after admission.

His initial presentation was consistent with the common ED complaint of renal colic. Renal infarcts are rare, even more so in patients without obvious risk factors as presented in this case. The normal initial noncontrast CT was misleading. The origin of the infarct was never determined during his hospital course.

The incidence of renal infarction is rare. Patients will often complain of abdominal, low back, or flank pain. Most cases occur due to atrial fibrillation or valvular or ischemic heart disease. Previous embolism is also a common risk factor. (Nat Clin Pract Nephrol 2007;3[11]:631.)

Patients usually complain of an acute onset of severe flank or abdominal pain typically associated with nausea and vomiting. Fever also may be present. Diagnosis usually goes unnoticed due to many other common disease processes with similar symptoms. Average time for diagnosis to be made is approximately two days after initial presentation. Lab studies predominantly show elevations in WBC, creatinine, and LDH. LDH elevation without elevations in transaminases is strongly suggestive of a renal infarct, and is the most sensitive test. (Isr Med Assoc J 2002;4[10]:781.) Hematuria will generally be absent. Diagnosis is made by a contrast CT, which should be performed if a noncontrast CT is negative and the patient still has persistent severe pain. Angiography, renal scintigraphy, intravenous pyelography, and ultrasound also may be used to aid in the diagnosis.

The mainstay of treatment is IV heparin followed by warfarin until the INR is therapeutic between 2 and 3. (Nat Clin Pract Nephrol 2007;3[11]:631; Isr Med Assoc J 2002;4[10]:781; Medicine [Baltimore] 2004;83[5]:292.) An intraarterial infusion of a thrombolytic agent or a thrombectomy may be performed if systemic anticoagulation is seriously contraindicated. (Int J Urol 2006;13[2]:168.) Surgery and angioplasty are other less used alternatives.

A 2004 review of 44 patients showed an 11.4 percent mortality after the first month. The true prognosis following a renal infarction is uncertain, however, because of the rarity of cases and because renal infarction usually occurs in those with multiple comorbidities, including possibility of emboli traveling to other organs.

This case signifies the importance of maintaining broad clinical suspicion and ordering the proper imaging studies to rule out rare but harmful disease processes that may pose as non-life-threatening complaints. Insufficient information on the incidence and distribution of renal infarcts is unavailable because of the rarity of these cases, and more research is required on this topic.

Published: 8/10/2012 11:52:00 AM

07.20.12

by The Case Files

The Case Files: Abdominal Pain Isn’t Always Appendicitis

Hughes, Heather DO; McGerald, Genevieve DO; Daniel, Reethamma MD; Kutin, Neil MD

A 3-year-old girl presented to the emergency department complaining of abdominal pain for three days. The pain was constant and mainly located over the right lower quadrant. The symptoms had increased in severity over the past day. The patient also presented with nausea, loose bowel movements, and anorexia. Her medical history revealed hypothyroidism but no previous surgical history.

Tenderness of the entire abdomen was noted with the point of maximal tenderness in the right lower quadrant. Rebound tenderness was also noted. A laboratory analysis demonstrated no significant abnormalities. Abdominal computed tomography revealed inflammatory changes around the cecum with focal fluid collection without visualization of the appendix, highly suspicious for acute appendicitis.

The patient underwent surgery for appendicitis, but during surgery, the surgeon observed torsion of the omentum with areas of hemorrhage and infarction. The vasculature was congested, suggesting omental torsion and infarction. The omentum and appendix were removed. The postoperative period was uneventful, and she was discharged from the hospital without complication. The pathologist confirmed the diagnosis of omental infarction with no pathologic evidence of appendicitis.

Omental infarction is a rare condition and difficult to diagnose preoperatively. She subsequently was found to be the youngest case of omental infarction in the literature. Omental infarction is an infrequent cause of abdominal pain, presenting mainly in the third to fifth decades of life. Fewer cases are reported in children. The youngest documented case of omental infarction is age 5, largely because of the absence of omental fat in children. The omentum twists around its axis, compromising vascularity and resulting in extravasation and necrosis.

Children with omental infarction classically present with acute onset of right-sided abdominal pain and tenderness, and the tenderness is localized in most patients. The presumed diagnosis in children is usually appendicitis. Omental infarction can mimic various other causes of an acute abdomen, and physicians should generally include this in their differential diagnosis of pediatric patients with abdominal pain. Unfortunately, the symptoms and clinical findings do not present in any characteristic pattern that suggests the diagnosis. The differential diagnosis should include not only appendicitis but cholecystitis, cecal diverticulitis, and other disease. Omental infarction has an incidence of 0.0016-0.37 percent in pediatric patients with abdominal pain. (Gac Med Mex 2007;143(1):17.)

It is not possible to distinguish omental infarction from appendicitis clinically. Because CT is being used more frequently to investigate acute abdominal pain in children, knowing the characteristic imaging features of omental infarction is important in making the diagnosis preoperatively and in distinguishing omental infarction from acute appendicitis. The CT scan shows an infarcted omentum as an area of high-attenuated fat containing hyperattenuated streaks just beneath the parietal peritoneum with thickening of the overlying anterior abdominal wall in cases of omental torsion. (Abdom Imaging 2004;29[4]:502.)

Another finding can be a whirling pattern of the mesentery or fluid accumulation within the abdomen. Unfortunately, all of these findings also can be observed in various other disease processes. Acute appendicitis was the initial diagnosis made in this patient. The CT findings were not diagnostic of omental infarction, and the final diagnosis was established intraoperatively.

Theories regarding the causes of omental infarction include anomalous arterial supply to the omentum, kinking of veins associated with increased intra-abdominal pressure, or vascular congestion after large meals. (Radiology 1992;185[1]:169.) Childhood obesity has recently been identified as a predisposing factor. Other precipitating factors include trauma, coughing, sudden change in body position, and compression between the liver and the anterior abdominal wall. (Principles of Surgery. 5th ed. New York, NY: McGraw-Hill, 1989: 1495.)

Pathologic findings include congestion, hemorrhage, fat necrosis, and varying degrees of inflammatory cell infiltration. Segmental omental infarction is a self-limited, benign condition that may resolve spontaneously in most patients. The inflammatory response resolves with retraction and fibrosis leading to complete healing or autoamputation. (Radiology 1992;185[1]:169; Australas Radiol 2000;44[2]:212; J Comput Assist Tomogr 1993;17[3]:379.) Reported complications include adhesions with bowel obstruction and abscess formation. (J Comput Assist Tomogr 1993;17[3]:379; Am J Gastroenterol 1980;74[5]:443.)

Although some surgeons promote conservative treatment, many believe that laparoscopic excision is the treatment of choice. After the infarcted omentum is removed, the child's clinical symptoms resolve quickly and the risk of abscess formation or other problems, such as bowel obstruction caused by adhesions, is reduced. Recovery after removal is rapid and uneventful in most patients.

Published: 7/20/2012 7:49:00 AM

07.13.12

by The Case Files

The Case Files: A Blue Leg

Segerivas, Doni Marie DO; Sattler, Steven DO; Amblard, Louis MD

A 49-year-old woman presented to the emergency department with a complaint of color change to her left leg while walking. She was watching a parade when she developed paresthesias to her left thigh and leg, and noticed her entire left thigh and leg were discolored and blue. She denies prior occurrence or any injury or trauma to the leg. She had no headache, weakness, change in vision, chest pain, shortness of breath, palpitations, abdominal pain, nausea, vomiting, diarrhea, or urinary symptoms. She had no history of prior thromboembolism or arterial pathology. She is not a smoker, and has not seen a physician for years. She also denied recent travel, oral contraceptives, recent surgery, any medical conditions, or surgical history.

She stated that her leg appears slightly better than before, and the paresthesias have resolved. She is morbidly obese, and appears slightly anxious, with an elevated heart rate of 115 bpm. Her vital signs are otherwise within normal limits. Her entire leg from her inguinal ligament to her foot is mottled and slightly cyanotic with marked swelling. She has normal range of motion. Her leg is warm and not tender. Sensation is intact, and distal pulses are palpable. The rest of her physical exam is unremarkable.

Her EKG is sinus tachycardia without ST/T wave changes. A heparin drip is empirically ordered before the negative Doppler of the left lower extremity study for DVT. Vascular surgery is consulted, and a CT angiogram of the aorta with runoff is obtained (Fig. 1-3)

Figure 1: Transverse view of right iliac artery compressing left iliac vein against lumbar spine just distal to venous bifurcation

Figure 2: Transverse view of venous congestion in left lower extremity contributing to markedly swollen leg found on exam

Figure 3

The patient was admitted when the CT suggested a pelvic DVT. Later review of the CTA lead to the diagnosis of a left iliac vein DVT due to May-Thurner syndrome.

May-Thurner syndrome is also known as iliac compression syndrome, and is a rare congenital anatomic variant that causes narrowing of the left common iliac vein by compression from the chronic pulsation of the right common iliac artery against the lumbar spine. This compression leads to swelling, pain, varicosities, and venous ulcers, and predisposes the patient to thrombus formation. Establishing the diagnosis is critical because severe complications such as phlegmasia cerulea dolens or pulmonary embolus leading to sudden death can occur.

This syndrome was first described by James Playfair McMurrich in 1908, but was named after May and Thurner in 1957 who described it after examining 430 cadavers. (Angiology 1957;8[5]:419.) They documented occurrence where the right iliac artery crossed over the left iliac vein, and hypothesized that this chronic compression impeded flow and thrombosis because of the intimal hyperplasia that ensued. It has been suggested from cadaver examinations and retrospective CT reviews that approximately 22-24 percent of the population has this variant and is asymptomatic. (J Vasc Surg 2004;39[5]:937.)

May-Thurner most commonly affects women 20-40 years old. Thrombosis occurs more commonly on the left side, and should be considered a risk factor for patients presenting with a left-sided iliofemoral DVT. (Diagn Interv Radiol 2007;13[3]:152.) Risk factors are similar to those with a lower extremity DVT such as oral contraception, obesity, pregnancy, immobilization, cancer, recent surgery, and genetic hypercoagulable states. Venography is the study of choice. Ultrasound Doppler of the extremity is usually negative.

Similar to other DVTs, patients are anticoagulated to prevent clot progression. Unfortunately, anticoagulation alone is not sufficient in these patients because reoccurrence most likely occurs from anatomical chronic compression. Localized thrombolytic therapy or catheter-directed administration of an antifibrinolytic is effective in eliminating the clot. Angioplasty with an endovascular stent can be placed after successful thrombectomy. Failure of stent placement increases the risk for rethrombosis or venous insufficiency. (J Vasc Surg 2004;39[5]:937; Diagn Interv Radiol 2007;13[3]:152.) Complications with stent placement include in-stent thrombosis, stent migration, and retroperitoneal hemorrhage. (J Vasc Surg 2007;46[4]:743.) Retrospective and prospective studies suggest that endovascular stent placement is the front-line treatment. (J Vasc Surg 2007;46[4]:743; J Cardiovasc Surg 2001;42[1]:83; AJR Am J Roentgenol 2004;183[5]:1523.)

Drs. Segerivas is a fourth-year emergency medicine resident, Dr. Sattler is an attending emergency physician, and Dr. Amblard is an attending radiologist, all at Good Samaritan Hospital Medical Center in West Islip, NY.

Published: 7/13/2012 8:42:00 AM

07.06.12

by The Case Files

The Case Files: Diagnosing with Ultrasound

Vitello, Sarah DO; McGerald, Genevieve DO; Teng, David MD

An 11-year-old boy was brought into the ED by wheelchair complaining of left hip pain after slipping and falling on the floor at home just prior to arrival. He was not able to get up. The patient also reported that he had fallen two weeks earlier while running, and had had ongoing left hip discomfort since then.

He denied any other injuries or complaints, and had no significant past medical history. He de-nied prior surgeries, allergies, and medications.

His temperature was 98.4°F, pulse 103 bpm, blood pressure 128/71 mm Hg, respiratory rate of 20 breaths per minute with O2 saturation of 99% on room air. He reported his pain as 10/10.

This overweight boy was lying uncomfortably on the stretcher, moaning in pain. His pupils were equally round and reactive to light. He had a normal pharynx with no erythema or tonsil-lar hypertrophy; his neck was supple and nontender without lymphadenopathy. His heart rate was regular with no murmurs, rubs, or gallops, and his lungs were clear to auscultation with no wheezes, rhonchi, or rales. His abdomen was soft with normal bowel sounds, nondistended and nontender.

He was lying with his left leg externally rotated, and he had left hip tenderness and limited range of motion due to pain. He was unable to bear weight but had good distal pulses, capillary refill <2 seconds, and no clubbing, cyanosis, or edema. He was awake, alert, and oriented, his deep tendon reflexes were intact, and he had normal strength and normal sensation.

An emergency bedside ultrasound was performed with the patient in the supine position. A high-frequency linear probe was placed parallel to the femoral neck and perpendicular to the groin line. Ultrasound of the right hip appeared normal. (Fig. 1.) The ultrasound of the left hip revealed a physeal step-off with posterior displacement of the proximal portion. (Fig. 2.) A plain AP radiograph of hips and pelvis was performed to confirm the diagnosis, and showed moderate slippage of the left capital femoral epiphysis. (Fig. 3.)

Figure 1

Figure 2

Figure 3

The patient underwent left hip in situ pinning of his slipped capital femoral epiphysis that day before staying the night in the pediatric unit. Day one post-surgery, he received physical ther-apy and was discharged with outpatient follow-up with his orthopedist.

The incidence of slipped capital femoral epiphysis (SCFE) in the United States is 10 cases per 100,000 children. The left hip is more commonly affected than the right, and it is twice as com-mon among boys as girls, although incidence is changing as more girls are participating in sports. (Hosp Med 1999; 60[11]:788.) The disorder is mainly characterized by hip pain, inability to bear weight or limp, and decreased range of motion. (Pediatr Ann 2006;35[2]:102.) Its clinical manifestation is caused by the instability of the proximal femoral growth plate. Swift diagnosis and definitive treatment are critical in preventing complications such as avascular necrosis, chondrolysis, and degenerative arthritis. (Curr Opin Pediatr 1998;11[1]:80.)

The diagnosis on plain radiography is made by visualizing a displaced femoral epiphysis and a fracture through the physis. Radiographic imaging can prove inaccurate because of projectional errors from the difficulty in positioning painful affected hips. (J Bone Joint Surg Br 1991;73[6]:884.) Plain radiographs have traditionally been the gold standard for diagnosis, but this case and multiple other studies demonstrate that ultrasound is a safe and ac-curate modality for the prompt clinical diagnosis of SCFE.

No step is seen between the metaphysic and epiphysis in a normal hip. A physeal slip and broadened epiphyseal plate can be visualized in a hip with SCFE using ultrasound. Some studies even suggest that measuring the anterior physeal slip can be used to grade the severity and to assess even minimal slippage. (Acta Orthop Scand 1992;63[6]:653; Radiol Med 1998;95[1-2]:16.)

Ultrasound is increasingly being used as the imaging modality of choice in the diagnosis of SCFE because of its sensitivity, repeatability, and safety because it does not impart ionizing radiation to the patient. Studies suggest that a skilled ultrasonographer, such as a trained emergency physician, is able to diagnose SCFE reliably and efficiently using ultrasound. It is essential that emergency physicians remain aware of possible alternative and supplemental imaging modalities to ensure prompt patient diagnosis and disposition for SCFE.

Published: 7/6/2012 1:12:00 PM

06.22.12

by The Case Files

The Case Files: Persistent Headache in Post-Partum Woman

Koehler, Kevin Scott MD; Lawrence, Matthew MD

A 27-year-old woman with no significant past medical history arrived at the emergency department complaining of persistent headache three days after a spontaneous vaginal delivery. The patient's recent hospital stay was notable for epidural anesthesia and epidural blood patch for lumbar puncture-induced headache performed the day after delivery.

The patient had complained of persistent headache since delivery. She denied any positional quality to the headache and any light or sound sensitivity. She had no nuchal rigidity or fevers, and had a nonfocal neurologic exam. All other reviews of systems were within normal limits. She had no family or personal history of intracranial hemorrhage or central venous thrombosis.

Our differential included pre-eclampsia, continued cerebrospinal fluid leak from failed blood patching, and meningitis. Her triage and subsequent blood pressures were elevated above her baseline, so a pre-eclampsia workup was initiated. Our initial plan was to evaluate for other causes of headache via a non-contrast head CT scan.

The pre-eclampsia workup and her labs were negative, and her pain was better controlled with parental opioids. Her head CT demonstrated pneumocephalus. This is an uncommon complication of epidural anesthesia and blood patching due to the infusion of a small amount of saline, which may contain gas bubbles, into the epidural space. Most cases of pneumocephalus are caused by trauma or neurosurgical interventions. The patient suffered no consequences from the intraventricular free air aside from a headache that subsided on hospital day five, which correlated with reabsorption of the air pocket. She was admitted strictly for pain control, and her subsequent CT scans were negative.

Published: 6/22/2012 12:13:00 PM

05.29.12

by The Case Files

A Blasting Impression

Girgis, Kareem MD; Winston, Lori MD

A 42-year-old man presented to the emergency department after sustaining multiple burns and abrasions from a firework accident earlier that day. His chief complaint included hearing loss and blood from his right ear.

Further history reveals that the patient and his brother, who worked with commercial grade fireworks, decided to fire off a few to celebrate Memorial Day. Before they could get a safe distance away, the commercial grade firework ignited, striking the brother in the face and killing him instantly. The patient, who was standing a few feet away, was showered with hot embers.

A few hours later, the patient complained of multiple small burns to the right side of his body, from his face to his legs, and a ringing and pain in his right ear.

The patient had crusted blood in the right ear canal with a ruptured tympanic membrane and multiple small superficial burns and abrasions to the right side of his face, right arm, and right lower leg. He also had two small 1 cm gaping lacerations on the lateral right lower leg. His clothes were singed in places and scattered with small shards of white matter.

An x-ray of the lower extremity revealed a small radio-opaque foreign body. The clinicians were unsure which hole housed the foreign body, and sent the patient back to x-ray with paperclips marking the wounds. The patient was given pain medication, the corresponding wound was irrigated and probed, and the foreign body was found to be about 2 cm deep. The object was removed using hemostats and traction. The foreign body was a molar: oral shrapnel from his deceased brother.

The patient's wounds were cleaned and dressed. A tetanus booster and a dose of parenteral antibiotics to cover oral flora were administered. The patient was given ENT follow-up for the blast injury to his ear.

This case is interesting not from a medical treatment and management standpoint but an emotional perspective. We had not considered the possibility of the foreign body's origin until it was extracted. The white shards covering his clothing and skin presumably were bone fragments from his brother's skull.

Published: 5/29/2012 8:04:00 AM

05.25.12

by The Case Files

The Case Files: Vision Loss in a Pregnant Patient

Davis, Frederick DO; Trivedi, Shefali MD; Glantz, Sanford MD

Clinicians must consider a number of worrisome causes when a pregnant patient presents with vision changes. But what should one do when the patient has no evidence of preeclampsia and a normal ophthalmic exam?

A 22-year-old woman G1P0 at four weeks gestation presented to the emergency department for painless vision loss that had progressed over the previous 24 hours. The patient noted that she could see shapes but no longer read. She denied any floaters, headache, or head trauma. She noted recently changing medication from metoclopramide (Reglan) to an ondansetron (Zofran) pump for hyperemesis gravidarum.

The patient had no recent fevers or upper respiratory infections. The patient denied any neck stiffness, shortness of breath, nausea, vomiting, chest pain, or abdominal pain. She denied any recent travel or sick contacts. The patient also had no history of allergies, and was on an ondansetron infusion pump for hyperemesis gravidarum.

She had a history of ADHD, and denied any surgical history. She had no previous history of ocular trauma, and did not wear glasses or contacts. The patient denied smoking, alcohol, and illicit drug use, and she had no known family history of any medical problems.

Vital signs were unremarkable with a temperature of 98.0°F, a pulse of 80 bpm, blood pressure of 102/54 mm Hg, and a respiratory rate of 18 with oxygen saturation of 100% on room air. She is Caucasian and in no apparent distress. Her head was normocephalic and atraumatic. Pupils were 5 mm and sluggishly reactive. She had a positiveconsensual reflex, with a visual acuity in the left eye of 20/100 and in the right eye of 20/70. Extraoccular muscles were intact, conjunctiva and sclera normal.

Fundoscopic exam revealed a normal optic disc. She had no photophobia and a supple, nontender neck with no lymphadenopathy. The ENT exam revealed normal tympanic membranes, normal nose, no rhinorrhea, normal dentition, no tonsillar hypertrophy, and moist mucus membranes. Cardiovascular exam revealed a regular rate and rhythm with a positive S1S2 and no murmurs.

The lung exam was clear to auscultation with normal excursion and no wheezing. Abdomen was soft, nontender with positive bowel sounds. The patient had full range of motion of the extremities with distal pulses and no edema. The patient was alert and oriented to person, place, and time.

Cranial nerves II-XII were grossly intact. She had no sensory deficits and 5/5 muscle strength in all extremities. Her skin was warm, dry, and intact.

We checked for electrolyte abnormalities after an unremarkable exam, and proceeded to imaging that might help us shed some light on this blurry situation. A complete blood count, electrolyte panel, and urine analysis were obtained. (Figure 1.)

Laboratory findings were normal. We could safely say that her vision loss was not likely due to any electrolyte abnormality or anemia. Her blood pressure was not elevated, and we felt these symptoms could not be attributed to preeclampsia. Our differential also included a cavernous sinus thrombosis because that could cause vision abnormalities from direct pressure or thrombus in the cavernous sinus or a hypercoagulable state from pregnancy leading to an ischemic cerebrovascular accident. We were concerned about radiation, and after consulting with neurology, ordered an MRI of her brain.

The patient's ondansetron infusion pump was stopped while waiting for the MRI. (Figure 2.) An hour after the ondansetron infusion was stopped, the patient reported that her vision was less blurry, and she was starting to make out shapes. She said her vision was back to baseline an hour later, and she was able to read without any correction.

The sudden loss of vision seen with increased pressure as in acute angle glaucoma or sudden experience of flashing light and floaters as in retinal detachments are serious causes for concern. Vascular abnormalities like retinal artery and retinal vein occlusions as well as amaurosis fugax, transient ischemic attacks, cerebral vascular accidents, and temporal arteritis are also worrisome. We also have to consider a progression of an infectious agent that starts out as sinusitis and progresses to cavernous sinus thrombosis or brain abscess.

Pregnant patients pose another concern because hypertensive emergencies like preeclampsia can call for emergent delivery. Changes in hormones and fluid metabolism cause changes in the curvature of the cornea and make a pregnant patient more prone to clots.

Ondansetron is an antiemetic with known side effects such as constipation, diarrhea, dizziness, drowsiness, headache, irritation, redness, pain, and burning at the site of injection. Transient visual disturbances following bolus intravenous ondansetron administration have been reported in patients undergoing chemotherapy where larger doses (up to 32 mg given as an infusion over 15 minutes) are commonly administered. (Cancer J Sci Am 1998;4[1]:52.) As far as we know, vision loss has not been described previously in a pregnant patient or those on a continuous infusion for hyperemesis gravidarum.

The mechanism by which ondansetron causes blindness is not fully understood. Hallucinogens from substances like LSD are known to cause visual disturbances by acting on the serotonergic receptors. (Brain Res 2001;896[1-2]:77.) The 5-HT3 and specifically the 5-HT3A subgroup receptor has been identified as playing a role in modulating the signaling pathway in the retina, and ondansetron does have an effect on this receptor. (Brain Res 2001;896[1-2]:77.)

A few case studies have been reported that are related to vision changes from ondansetron. This mostly included abnormal accommodation and blurred vision with long-term use or high doses as seen in patients receiving chemotherapy. The few cases of transient blindness that have been reported lasted only two to three minutes, with resolution within 20 minutes and up to 48 hours. This case highlights the importance of understanding all the possible effects even routine medications can have on patients.

Published: 5/25/2012 8:01:00 AM

05.21.12

by The Case Files

Case Report: Pain and Swelling of a Prince Albert Piercing

Patee, Allen MD; Farrah, Hillary MS-IV; Strony, Robert DO

A 25-year-old man presented to the ED complaining of pain, swelling, and erythema of his glans penis. The patient reported that this developed after having a new bar penile piercing five days earlier.

He had increased penile pain in his glans and swelling with painful bilateral inguinal lymphadenopathy for three days. The pain made it difficult for him to walk, and he was concerned because he felt his urine stream was obstructed and spraying. The patient reported that each night he was wrapping his penis in toilet paper and then placing a condom over the toilet paper as directed by his piercing studio.

Vital signs were within normal limits. Examination revealed erythema of the glans penis. Two piercings are present on the ventral surface near the base. A Prince Albert piercing with a ring was coming out of the urethral meatus on the ventral side. The new bar piercing travels transversely through the glans penis.

Body piercing dates back to at least 3000 B.C. It is documented in wall carvings, paintings, and sculptures of the body. Some sources state body piercing may have originated with the Hindu religion, but it has been documented in tribal societies on all continents, especially in Africa, Asia, and South America. These piercings have represented rites of passage from adolescence to adulthood in some cultures.

The Prince Albert, a penile ring through the urethral meatus that exits on the ventral surface, dates back to the Victorian age. The piercing is named after Queen Victoria's husband, who is rumored to have worn the ring to secure his genitals to his leg while wearing a tight uniform. Little documentation was made about piercings in western society until World War II, but it is believed that tattooing and piercings of the labia and nipple were performed before the war.

The punk movement in 1970s Europe reignited an interest in body piercing. This started with the use of safety pins, but allergic reactions prompted piercers to use different alloys to reduce undesirable reactions.

Body piercing has increased in all age and socioeconomic groups in western society. Several studies cited a range 33 percent to 51 percent in the number of Americans getting at least one piercing in their lifetime.

Complications depend on the experience of the piercer, sterility of the piercing technique, and wound care by the customer. The most common complications associated with piercings are local infection and bleeding. Local infection was reported in 10 percent to 30 percent of piercings. The most commonly isolated species are Staphylococcus aureus, group A streptococci, and Pseudomonas.

Case reports also have documented the transmission of hepatitis B and C through piercings, but several other methods of transmission are possible for these cases. Additional research is needed to evaluate body piercing as a risk factor for viral hepatitis. Risks of acquiring hepatitis and other sexually transmitted diseases also depend on the hygiene practices of the individuals with piercings.

Case reports stemming from body piercings include sepsis, endocarditis, toxic shock syndrome, and pneumonia. Those with pre-existing cardiac disease are at substantial risk of developing endocarditis after a piercing. These patients should refrain from piercings or be pretreated with prophylactic antibiotics prior to the procedure.

Over the past decade, metal allergies associated with piercings have increased. The most frequent contact allergen is nickel sulfate at 13 percent. Gold also has been on the rise recently with rates of 0.78 percent to 13 percent. The European Nickel Directive set threshold values for nickel content, but limits are often ignored. These restrictions do not exist in the United States. Piercing also can be the cause of sensitization to an allergen. One study found metal sensitization of four percent in men without piercings, 11.1 percent in men with one piercing, and 14.6 percent in men with two or more piercings.

Genital piercings may show pronounced delay in wound healing, which may take up to one year. This can be delayed further by sexual intercourse and bike riding. Local and systemic infection can arise; episodes of Fournier gangrene have been reported. Genital piercings also have been documented to initiate paraphimosis.

Hemorrhage is another complication of penile piercing. Where the piercing crosses through the glans (known as a Palang), the spongy body of the penis can be damaged, leading to massive hemorrhage. One young man developed a case of traumatic hypospadias after a piercing was torn out during sexual intercourse. This injury required surgical repair for a glandular hypospadias.

Skin traumatized by piercing may increase the susceptibility of papillomavirus infection. One 22-year-old man presented with a 5 mm exophytic growth on his penis. The patient had a previously healed piercing over the area; he was treated with liquid nitrogen and podophyllin.

Another incident involved an uncircumcised man who presented with paraphimosis three days after he had the ventral portion of the glans of his penis pierced. The swelling caused by the piercing prevented him from retracting his foreskin. Following a penile block, his foreskin was manually reduced.

Piercing as a potential source of HIV-1 transmission also has been documented. One patient, who was reportedly not sexually active, received multiple piercings to multiple areas of his body; he had piercings to his penis, scrotum, nipples, umbilicus, tongue, chin, eyebrows, and nasal septum done at three different piercing parlors. Although the sources of his HIV-1 transmission was not confirmed, there is a high suspicion that he obtained HIV from one of the piercings.

Regulations vary from state to state. The industry is highly unregulated, and no agency is responsible for certification in piercing, which leads to a wide variation in piercing practices. No standards on sterilization methods and antibiotic use exist either. This is left up to interpretation by the piercer. Although several associations exist and online interest groups share sterilization techniques and hygiene, only a few states have regulations in place for body-piercing establishments.

Dr. Patee is an emergency medicine resident at Geisinger Medical Center; Ms. Farrah a fourth-year medical student at the Philadelphia College of Osteopathic Medicine; and Dr. Strony is an associate professor of emergency medicine at Geisinger Medical Center.

Published: 5/21/2012 8:18:00 AM

05.14.12

by The Case Files

Black and Blue: A Case Report of a Spontaneous Right Internal Jugular Vein Thrombus

Keehn, Steven DO; Margulies, Jeffrey MD; Levy, David DO; Dvorkin, Ronald MD

A 74-year-old man was brought to the ED by ambulance complaining of swelling and ecchymoses to his arms and left knee beginning on the same day. He also complained of mild, dull, intermittent right-sided neck pain, and had noticed some "extra heart beats."

He denied abdominal pain, chest pain, dyspnea, headache, nausea, vomiting, diarrhea, and fever, but he had been released earlier that day from the same hospital after an admission for evaluation of chest pain, during which he had had a negative stress test. He was discharged on warfarin, and had received a dose of enoxaparin prior to discharge when his INR was subtherapeutic. He had a past medical history of atrial fibrillation, hypertension, diabetes, cholecystectomy, appendectomy, spine surgery, and wisdom tooth removal.

He was compliant with his warfarin therapy, and denied trauma. He had no recent invasive procedures or other symptoms. The patient had no allergies and was taking nitroglycerine, amiodarone, warfarin, pantoprazole, fish oil, and vitamin E on a regular basis. The patient denied tobacco, alcohol, or illicit drug use. He was retired, and was visiting from out of state. He had no family history of hematologic disorders.

On physical exam, his blood pressure was 164/80 mm Hg, heart rate was 70 bpm, his temperature was 99.4 F, and respirations were 18 per minute with an O2 saturation of 94% on room air. He appeared well developed and well nourished and in no apparent distress. His pupils were equal and reactive, conjunctiva pink and sclera anicteric.

He had a normal pharynx without tonsillar hypertrophy. His neck was supple, nontender, carotid pulses 2+ without cervical lymphadenopathy, JVD, or carotid bruits. His heart was irregularly irregular without murmurs, rubs, or gallops. Breath sounds were clear and equal bilaterally with normal chest excursion. His abdomen had normal bowel sounds, and was not distended; there was no abdominal or costovertebral angle tenderness.

His extremities revealed a normal range of motion, were nontender, and had 2+ distal pulses and no edema. His skin was warm and dry, with good turgor. Ecchymoses was noted over both antecubital fossa, with the left arm more severe than the right, and on the abdominal wall where he had received the previous enoxaparin injections. He was awake, alert, and oriented. His cranial nerves were intact, and no gross deficits were identified.

Hospital Course

Laboratory tests were ordered, including a CBC, chemistry panel, coagulation profile, liver function tests, urinalysis, and an ultrasound of his upper extremities. (Fig. 1.) The CBC included a WBC of 9.4 x10(3)/mcL, hemoglobin of 14.1gm/dL, hematocrit of 42.4%, and platelet count of 200x10(3)/mcL. The chemistry panel was unremarkable with sodium of 140 mmol/L, potassium of 4.1 mmol/L, calcium of 9.0 mg/dL, chloride of 105 mmol/L, bicarbonate of 25 mmol/L, BUN of 19 mg/dL, creatinine of 1.2 mg/dL, and glucose of 106 mg/dL.

Figure 1: Ultrasound of Right Upper Extremity

Figure 2: Ultrasound Left Upper Extremity

His coagulation profile showed a mildly subtherapeutic PT of 15.8 seconds, INR of 1.6, and PTT of 34.2 seconds. His liver function tests revealed an AST of 20 units/L, ALT of 44 units/L, alkaline phosphatase of 59 units/L, total bilirubin of 0.5 mg/dL, direct bilirubin of 0.0 mg/dL, indirect bilirubin of 0.6 mg/dL, total protein of 6.9 gm/dL, and albumin of 3.8 gm/dL. His total CPK revealed 145 unit/L, troponin-I <0.015 ng/mL, and magnesium 2.3 mg/dL. Urinalysis revealed a specific gravity of 1.006, pH of 5.5, no protein, no blood, no glucose, trace ketones, bilirubin negative, nitrite negative, leukocyte esterase negative, and RBC of <1/HPF.

The upper extremity ultrasound revealed a thrombus without detectable blood flow in the inferior right jugular vein. During his admission, vascular surgery, hematology, and medicine services were consulted. He was placed on enoxaparin 100 mg subcutaneously every 12 hours as well as his usual dose of warfarin. During his admission, his INR dropped from 1.6 to 1.2, and his PT dropped from 15.8 to 12.6.

A full hypercoagulable workup was held until he returned to his out-of-state home. The patient had follow-up scheduled with his private medical doctor and cardiologist. At discharge, the patient's INR was therapeutic at 2.5. He was discharged with final diagnoses of DVT of his right internal jugular vein, atrial fibrillation, hypertension, and chronic low back pain.

Diagnosis and Treatment

This patient's neck pain and ecchymosis was eventually determined to be an unusual occurrence of a spontaneous right internal jugular (IJ) vein thrombosis. IJ thrombosis can be caused by previous central venous line placement, malignancy, trauma, infection, neck massage, intravenous drug abuse, or hypercoagulable states, which this patient did not have. He had been on anticoagulation for two years, and denied a clear-cut antecedent manipulation of his arm. He also denied chest pain, dyspnea, headache, dizziness, fever, chills, diaphoresis, abdominal pain, excessive bleeding, and night sweats.

The first case of an IJ thrombosis was diagnosed in 1936 by Lemierre. It was a feared complication from acute oropharyngeal infection leading to septic thrombophlebitis, and little could be done secondary to lack of antibiotics at the time.

Complications of an IJ thrombosis include pulmonary embolism, subclavian vein thrombosis, superior sagittal sinus thrombosis, pseudotumor cerebri, laryngeal and lower airway edema, and infected thrombophlebitis. An infected thrombophlebitis can lead to systemic sepsis syndrome, septic emboli to other organs and tissues, and other pathologic conditions. The outcome for patients with this condition is good when anticoagulated. The risk of pulmonary embolism is reported as approximately 0.5 percent for isolated IJ thrombosis.

Bruising and neck pain in the emergency department is a seemingly benign complaint. The bruising could easily be assumed to be the result of over-anticoagulation, but in this patient, it was associated with a thrombosis of the right internal jugular vein. A spontaneous internal jugular vein thrombus without any risk factors is rare. It is prudent for the physician to perform a detailed history and physical examination routinely, and maintain a broad differential and a high level of suspicion for uncommon conditions. Physicians should not be led astray by the use of anticoagulants or other apparently simple etiologies

Comments about this article? Write to EMN at emn@lww.com.

Drs. Keehn, Margulies, Levy, and Dvorkin are from the department of emergency medicine at Good Samaritan Hospital Medical Center in West Islip, NY.

Published: 5/14/2012 8:28:00 AM

05.07.12

by The Case Files

Necrotic Penile Lesion: What a Culture Swab Will Not Reveal

McGregor, Alyson J. MD; Ruskis, Jennifer MD

A 42-year-old man presents complaining of a painful penile lesion. There are no associated fevers, rashes, or recent illness. He denies penile discharge, dysuria, and hematuria. He is sexually active with one female partner. He has no history of sexually transmitted infections. The patient revealed that five days prior to presentation, the dorsum of the penile body (shaft) skin became entrapped in his pants zipper. He spent three hours attempting to disengage the zipper by forcibly removing the skin from the zipper teeth. A closer examination of the wound reveals granulation tissue along the periphery with a center of dried blood that was easily removed with local wound care.

Zipper entrapment injuries of the penis, while uncommon, pose a unique problem to the patient and the practitioner on the best method to remove the zipper and salvage penile skin tissue. These injuries are most commonly seen in prepubertal boys, and can cause bruising, abrasions, localized swelling, and less frequently necrosis. Skin loss, as seen in the photograph, is also rare for these types of injuries if managed appropriately.

Treatment of zipper entrapment includes local anesthesia and prompt removal of the teeth. Prevention of a prolonged entrapment is critical to minimizing edema, which can lead to a more challenging procedure. Topical anesthetic creams or local infiltration of lidocaine can provide effective anesthesia with penile blocks reserved for severe injuries.

Removal techniques depend in part on the component of the zipper involved. Cutting the cloth around the zipper will open the teeth and allow removal of the skin. Mineral oil combined with gentle traction or a wire cutter may be necessary if the fastener is involved. Local wound care with topical antibiotic ointment is the recommended treatment for post-procedure care. Prompt urologic consultation is necessary if any injuries involve the urethra or if significant tissue loss is present.

Comments about this article? Write to EMN at emn@lww.com.

Dr. McGregor is an assistant professor of emergency medicine at the Warren Alpert Medical School of Brown University, Rhode Island Hospital, and the Miriam Hospital. Dr. Ruskis is an emergency medicine resident at Warren Alpert.

Published: 5/7/2012 8:47:00 AM

04.30.12

by The Case Files

Case Report: A Rare Transmission of Group A Streptococcus

By Chantel O'Shea, DO; David Levy, DO; Sarah Arzt, DO; & Sandra Deniz, MD

A 34-year-old woman with no significant past medical history presented to the emergency department with fever, dizziness, and abdominal pain for three days. The patient stated that her pain was located in her lower abdomen and radiated to her groin, legs, and left flank. During each episode, she experienced fever and dizziness. She also noted foul-smelling urine and a slight vaginal discharge for the past several weeks.

She denied nausea or vomiting. There was no frequency, urgency, or dysuria, and no headaches or loss of consciousness. She did note several episodes of diarrhea, the last occurring while in the emergency department. The only sick contact that she could recall was her husband who had been diagnosed with pharyngitis several weeks earlier.

Upon presentation, the patient's vital signs were significant for a temperature of 102.2 F, pulse of 115, and blood pressure of 96/65 mm Hg. She appeared comfortable and in no apparent distress. She had a normal physical exam, with the exception of her abdominal exam, which was significant for right lower quadrant tenderness with a lesser degree of suprapubic and left lower quadrant tenderness. There were normal bowel sounds, no distention, no palpable organomegaly, or CVAT. There was also no guarding, rebound, or rigidity.

Her genitourinary exam was significant for slight vaginal bleeding, although the patient did begin her menstrual cycle the day before. No other vaginal discharge was noted, and the cervical os was closed. There was mild cervical motion tenderness but no adnexal tenderness or masses.

The patient initially received a 2000 ml normal saline bolus and 975 mg acetaminophen. Her temperature decreased to 98.4 F, and her tachycardia improved. Significant laboratory results included a white blood cell count of 11.2 x109/L with a bandemia of 39. Urinalysis was positive for moderate blood. Basic metabolic panel, coagulation studies, and hepatic function panel were normal. Lactic acid was 1.8 mmol/L. The patient had a transvaginal sonogram, which was normal. She also had a contrast enhanced CT of the abdomen and pelvis which showed dilation of the large and small bowel consistent with an ileus pattern but without evidence of obstruction. There was also a small amount of presacral fluid. No abscesses were seen.

She was started on ertapenem (Invanz) in the emergency department, and was admitted to the hospital. She was evaluated by consultants from OB/GYN, surgery, and infectious disease. The patient continued to have pain and spike fevers. She was taken to the OR the following day for an exploratory laparoscopy. A large amount of intra-abdominal purulent material was removed and cultured. There was also diffuse erythema of all the peritoneal surfaces. The appendix, uterus, ovaries, and Fallopian tubes appeared normal, and no obvious source of infection was noted.

The patient's blood cultures were positive for Group A Streptococcus, as were her intra-abdominal and vaginal cultures. Upon further questioning, the patient stated that her husband's pharyngitis had been positive for Group A Streptococcus. The patient later admitted that she and her husband had engaged in oral-genital contact while he was ill.

Streptococcus pyogenes, or Group A streptococcus (GAS), is known to be associated with a variety of human illnesses, including invasive disease associated with high morbidity and mortality. (Sex Transm Dis 2002;29[8]:483.) Cunnilingus is a well known means of transmission of a multitude of pathologic organisms. (Sex Transm Dis 2002;29[8]:483.) Organisms may be transmitted from the oropharynx to the genitals and vice versa. Three other case reports of oral sex have been reported as the mechanism of transmission from a man with oropharyngeal GAS to a woman's genitourinary tract, leading to invasive disease. In two of the reports, serological typing of the GAS strains was identical in the couples. In one case, an intrauterine device was implicated as the portal of infection entry and also tested positive for the same strain. (Sex Transm Dis 2002;29[8]:483.) In the earliest case, serological typing was not yet available so the relationship was based on speculation. (Sex Transm Dis 2002;29[8]:483.)

Acute pelvic inflammatory disease is usually caused by organisms ascending from the vagina and cervix along the mucosa of the endometrium to the oviduct. Inflammatory conditions possible as a result of this ascending infection could be endometritis, salpingitis, tubo-ovarian/uterine abscess, and peritonitis. Secondary spread and associated disease, such as with bacteremia and streptococcal toxic shock syndrome, are also possible. (Sex Transm Dis 2002;29[10]:606; Scand J Infect Dis 1995;27[2]:171.) GAS colonization of post-operative wounds and the oropharynx is common. The organism is not, however, considered part of the normal vaginal flora. (Eur J Clin Microbiol Infect Dis 2001;20[6]:437.) Genitourinary tract colonization serving as a reservoir for GAS as a sole causative organism leading to ascending infection, bacteremia, and invasive disease is distinctly unusual. (Sex Transm Dis 2002;29[10]:606.)

Scarce reports exist of recovery of GAS from the female reproductive tract above the vagina. Disseminated GAS infection likely requires some minor trauma to the skin or mucous membranes as a portal of entry. When isolated as the single etiologic agent, there is usually some history of associated gynecologic instrumentation. (Sex Transm Dis 2002;29[8]:483; 2002;29[10]:606.) Host immunity factors involved in susceptibility of invasive GAS disease are not well understood so the question remains why most carriers of GAS remain asymptomatic while others may develop severe invasive and sometimes fatal disease. (Sex Transm Dis 2002;29[8]:483; 2002;29[10]:606; Scand J Infect Dis 1995;27[2]:171.)

S. pyogenes has an array of defense mechanisms that allow

invasion of host tissues and evasion of the neutrophil-mediated phagocytosis. The bacterial cell wall structure components, peptidoglycan and lipoteichoic acid, are proinflammatory agents, and play a major role in host activation. The capsule, composed of hyaluronic acid, is essential to the organism's invasiveness. S. pyogenes is also known to produce a family of superantigenic exotoxins capable of activating a large quantity of CD4+ lymphocytes. This mechanism results in massive cytokine release, leading to the induction of septic shock. (Sex Transm Dis 2002;29[10]:606.)

Dr. O'Shea is a fourth-year emergency medicine resident at Good Samaritan Hospital in West Islip, NY.

Published: 4/30/2012 7:56:00 AM

04.27.12

by The Case Files

Case Report: Odontogenic Cyst

Bair, Jacob DO; Decena, Eric MD; Ruotolo, Rachel MD; Miller, Sarah PA; Henesch, Stephen M. DO

A 10-year-old boy with no past medical or surgical history presents to the emergency department, accompanied by his mother, complaining of right-sided facial swelling for the past two months. The mother reports that he was enrolled in a beginner boxing class, and was punched in the face with a soft glove two months prior to presentation.

Right facial swelling in 10-year-old boy.

Since he was struck, she has noticed a progressive swelling to the right side of his face. The patient denied any change in speech, pain with chewing, difficulty swallowing, or sensitivity to cold or hot foods and liquids, and he had no history of fever, chills, dental pain, or recent dental work performed. The child had been seen by his pediatrician multiple times over the few weeks prior to ED presentation, and was initially treated for a hematoma. The swelling did not improve with conservative measures, and the child was eventually referred to see a surgeon, but the mother was unable to obtain an appointment with one.

His vital signs were normal, and his physical exam demonstrated a well appearing, well developed boy in no distress. Examination of his face revealed marked swelling over the right cheek without any discernible border, erythema, warmth, or tenderness. The mouth revealed deviation of the first and second molars with increased spacing between the two teeth. No erosions, abscesses, drooling, bleeding gums, or malocclusion were present.

Basic laboratory studies included a complete blood count, electrolytes, renal function, and coagulation profile, which were all within normal limits. A contrast enhanced facial bone CT scan was obtained, and revealed an expansile, septated hypo-attenuated mass measuring approximately 9.2 × 4.7 × 5.1 cm in craniocaudal, transverse, and anterior-posterior dimensions, respectively, centered around the right mandible and mildly displacing surrounding structures.

Results of the CT and blood work were explained to the patient and his mother, and the patient was discharged to follow up with a pediatric plastic surgeon with subspecialty in craniofacial procedures.

Right mandibular mass in the sagittal and coronal planes.

Odontogenic cyst is a broad term describing a variety of cysts defined as epithelial-lined structures derived from odontogenic epithelium. Odontogenic cysts can be divided into inflammatory and developmental categories. Inflammatory cysts include radicular (periapical) and paradental. Developmental cysts include dentigerous (follicular), developmental lateral periodontal, odontogenic keratocyst, and glandular odontogenic cyst. Included in the differential of the mandibular mass of this patient are traumatic bone cyst, central giant cell granuloma, and the malignant tumors that affect the area described. (Laryngoscope 1998;108[2]:280.) Most odontogenic cysts are defined more by their location than by any histologic characteristics, and the surgeon must provide the pathologist with appropriate history and radiographs when submitting such specimens for examination.

The most important concept in managing odontogenic pathology is obtaining a complete history and thorough physical examination, which should include careful inspection, palpation, and percussion of the affected part of the jaw and overlying dentition. Radiologic examination is usually the first procedure of choice in evaluating jaw-related cysts and tumors. In general, well-demarcated lesions outlined by sclerotic borders suggest benign growth while aggressive lesions tend to be ill-defined lytic lesions with possible root resorption. Finally, fine-needle aspiration, open biopsy, or excisional biopsy may be necessary for definitive diagnosis, which is needed to determine appropriate medical or surgical therapy. (J Dent Child [Chic] 2009; 6[3]:217.)

Dental displacement noted in bone windows.

This patient's cyst is significant for the growth rate and large size at presentation to the ED. Because panorex radiography is difficult to interpret and rarely available to the emergency physician, contrast-enhanced CT scan is the most appropriate diagnostic modality for evaluation of facial masses. Patient follow-up is of utmost importance because odontogenic masses are often deforming, may be malignant, and may sometimes require extended treatment.

Drs. Bair, Decena, Ruotolo, and Henesch, and Ms. Miller are from the department of emergency medicine at Good Samaritan Hospital Medical Center in West Islip, NY

Published: 4/27/2012 7:54:00 AM

04.23.12

by The Case Files

The Importance of Being Vigilant

Goldstein, Scott DO

A 51-year-old computer programmer was hanging a latch on a door when he slipped off a ledge, landing on his back. He presented to the emergency department by ambulance, and complained of upper back pain, described as "aching and weird" without any other symptoms.

The patient denied shortness of breath, chest pain, abdominal pain, numbness, tingling, head injury, or loss of consciousness. The patient's initial vital signs were normal and stable throughout his stay in the emergency department.

The patient underwent chest x-ray to rule out thoracic injury, including pneumothorax or upper thoracic vertebral injury. After review of the chest x-ray, a CT scan of the chest was ordered because of air in the subcutaneous space on the left side of the neck. The scan showed numerous rib fractures, including bilateral first rib fractures and pneumomediastinum with accompanying pneumothorax and subcutaneous air. The patient was transferred to the trauma center, and admitted to the ICU for monitoring.

Chest x-ray showing air in the supraclavicular space.

CT scan showing pneumomediastinum

The extensive and severe injury from a seemingly minor accident and normal vital signs stresses the importance of being vigilant for occult injury and underlying disease even when a patient presents in no distress. Also, all x-rays should be looked at the same way each time so minor finds that could be devastating such as subcutaneous air in the neck are not missed.

Dr. Goldstein is the chief of tactical medicine in the division of disaster medicine and EMS at Albert Einstein Medical Center in Philadelphia.

Published: 4/23/2012 1:05:00 PM

04.20.12

by The Case Files

Fatal Drip: Sinusitis and Meningitis

Rivas, Doni Marie DO; McGerald, Genevieve DO; Reid, Patrick MD; Winslow, Jason MD; Benanti, Michael DO; Rispoli, Loretta NP

A 48-year-old woman presented to the emergency department complaining of a five- to six-week history of persistent nasal drip, with fever and intermittent headaches for one month. She described a throbbing occipital headache radiating to the periorbital area bilaterally. She had been treated with several different antibiotics in the preceding four months for a presumptive diagnosis of sinusitis. Symptoms improved while on the medication, but then would quickly return once the antibiotic course was finished.

At presentation, the patient had a temperature of 102.0°F, and her skin was flushed and hot to the touch. She appeared uncomfortable, lying on the stretcher holding her head. Nasal congestion with surrounding erythema and clear rhinorrhea were noted. Her tympanic membranes were normal bilaterally, and her pharynx appeared normal with no tonsillar hypertrophy or exudate. Her neck was supple with no tender lymphadenopathy. Her heart maintained normal rhythm and rate, and her lungs were clear to auscultation bilaterally. She was neurologically intact. The rest of her physical exam was unremarkable.

Laboratory studies demonstrated a leukocytosis of 23.6 × 103/mcL with 89% segmented neutrophils and 6% lymphocytes. Besides an elevated alkaline phosphatase at 158, the rest of her laboratory evaluation and a CT scan of her brain were unremarkable. A lumbar puncture was attempted but unsuccessful. Ceftriaxone 2 g was given, and the patient was admitted for an MRI and fluoroscopic-guided lumbar puncture. An MRI of the brain subsequently demonstrated a left superior ethmoid cell defect causing CSF leakage through the ethmoid sinuses. (Photo.) CSF analysis was suggestive of bacterial meningitis, but no organisms were found. She was transferred to a tertiary care facility where she was successfully treated with endoscopic endonasal repair without recurrence of symptoms.

Photo: MRI brain coronal view of left superior ethmoid cell defect.

Cerebrospinal fluid (CSF) fistulas can occur from traumatic and atraumatic causes. Although the occurrence of a CSF fistula is rare, traumatic causes are the most common etiology, occurring in 70 to 80 percent of cases. CSF fistulas can also occur from eroding tumors, congenital defects, ENT infections, or increased intracranial pressures such as those with pseudotumor cerebri. In any of these cases, there is a destruction or breakdown of the bony architecture resulting in a defect of the cribriform plate. Immediate action is necessary to prevent ascending meningitis, which occurs in a third of patients with CSF leaks.

Whatever the cause of a CSF leak, patients most commonly present with unilateral clear rhinorrhea, which can easily be confused for allergic rhinitis. The fluid may be tested for beta-2 transferrin to confirm the CSF leak. The second most common presentation is active meningitis or a history of meningitis. Defects are most commonly in the sphenoid sinus and the ethmoid roof.

Management depends on etiology. If due to traumatic events, patients who present with small fistulas may be treated conservatively with head elevation, bed rest, and antibiotics. For those who do not respond to conservative management or who have large or nontraumatic fistulas, immediate surgical repair is needed. IV acetazolamide is given for those with pseudotumor cerebri to attempt to decrease intracranial pressure. A VP shunt is placed for those who present with recurring leaks or who do not respond appropriately to diuretics.

The etiology of this patient's CSF leak still remains uncertain. There was no recent trauma to suggest that a physical defect occurred. Cases of CSF leaks have been known to occur 20 years after a traumatic head injury, however, and this patient admitted to such an event 22 years previously. According to the patient, past CT scans and MRIs of the brain were negative, although small fistulas may be missed by radiological studies.

Our patient was also obese, and admitted to occasional headaches, which may also suggest pseudotumor cerebri as a cause. Our patient also had a history of sinus infections for more than four months, which also could be the source of the defect. Unfortunately, the mystery remains on whether the leak was present prior to the sinusitis causing similar symptoms. One thing, however, is certain. The multiple courses of antibiotic regimens that she received saved her life.

The authors are from the emergency medicine residency at Good Samaritan Hospital Medical Center in West Islip, NY.

Published: 4/20/2012 12:39:00 PM

04.16.12

by The Case Files

Sometimes You Don’t Have to Look for the Zebra

Keehn, Steven DO; Mackoff, Robin DO; Levy, David DO; Womack, Lawrence MD; Hegazy, Manal MD

A 41-year-old man with history of a left-sided nephrectomy presented to the emergency department complaining of abdominal pain that suddenly began four hours before arrival. He described the pain as a constant but progressively worsening, dull, "burning" discomfort in the mid-epigastric area. The pain radiated bilaterally to the lower quadrants, and had no exacerbating or relieving factors. He complained of associated nausea, diaphoresis, and constipation. He had taken Pepto-Bismol and Gas-X without relief.

His left nephrectomy was performed at three months of age secondary to an atropic left kidney. His past medical history also included a left ankle fracture and surgery on his left wrist and right hand. He denied any allergies, and was not taking any medications on a regular basis. His social history was non-contributory for tobacco, alcohol, or illicit drug use. He was employed as a computer executive. He had no family history of hemostasis disorders, but his father had coronary artery disease with a myocardial infarction at age 54.

On physical exam, he was noted to be mildly hypertensive at 149/90 mm Hg with a heart rate of 60 bpm. He was afebrile at 97.1°F, respirations were 16 with an oxygen saturation of 100% on room air. On initial evaluation, the patient appeared well-developed and well-nourished but in mild distress.

His pupils were equally round and reactive, conjunctiva were pink and sclera anicteric. His otic examination was unremarkable. He had a normal pharynx without tonsillar hypertrophy. His neck was supple, nontender, without cervical lymphadenopathy, JVD, or carotid bruits. His heart revealed a normal S1/S2 without murmurs, rubs, or gallops. Breath sounds were clear and equal bilaterally with normal chest excursion.

His abdomen had normal bowel sounds, and was nondistended but diffusely tender over bilateral lower quadrants with an equivocal Rovsing's sign. He did not exhibit any guarding, rebound, or rigidity, and had no costrovertebral angle tenderness. His extremities revealed normal range of motion. They were nontender to palpation, with normal distal pulses, and were without edema. His skin was warm and dry, with good turgor, and no apparent lesions. Neurologically, he was awake, alert, and oriented. His cranial nerves were intact, and no gross deficits were identified.

Laboratory tests were ordered, including a CBC, chemistry panel, coagulation profile, liver function tests, amylase, lipase, urinalysis as well as a CT of the abdomen and pelvis with oral and IV contrast. (Figure 1.) The CBC revealed an elevated WBC count of 14.5×10(3)/mcL, hemoglobin of 15.8 gm/dL, hematocrit of 45.7%, and platelet count of 285×10(3)/mcL. The chemistry panel was unremarkable, with a sodium of 138 mmol/L, potassium of 4.1 mmol/L, calcium of 9.5 mg/dL, chloride of 100 mmol/L, bicarbonate of 26 mmol/L, BUN of 14 mg/dL, creatinine of 1.2 mg/dL, and glucose of 119 mg/dL. His coagulation profile was typical, and revealed a PT of 10.5 seconds, INR of 1.0, and PTT of 24.1 seconds.

Figure 1. CT of the abdomen revealing a splenic infarction, shown as a large triangular area of decreased enhancement at the spleen (see inset).

His liver function tests revealed an AST of 35 units/L, ALT of 49 units/L, alkaline phosphatase of 75 units/L, GGT of 26 units/L, LDH of 175 units/L, total bilirubin of 0.5 mg/dL, direct bilirubin of 0.0 mg/dL, indirect bilirubin of 0.5 mg/dL, total protein of 7.5 gm/dL, albumin of 4.7 gm/dL, and globulin of 2.8 gm/dL.

His amylase level was 72 units/L, and lipase was 232 units/L. Urinalysis revealed a specific gravity of 1.024, pH of 7.0, trace protein, no blood, no glucose, ketones of 40, bili negative, nitrite negative, leukocyte esterase negative, RBC of 1/HPF, and rare mucous. The abdominal-pelvis CT scan revealed a splenic infarction, shown as a large triangular area of decreased enhancement at the spleen. The celiac axis was poorly visualized. He had a normal appendix and no colonic diverticulitis or intestinal obstruction. The left common iliac artery had a 2.5 cm fusiform aneurysm.

Anticoagulation was initiated, and he was admitted to the hospital. During his hospital course, he was evaluated and followed by surgery, cardiology, and medicine services. Cardiology performed a bedside echocardiogram in the ED, which was normal. The echo was repeated the next morning, and was again normal. Cardiology was concerned about a hypercoagulable state and the possibility of paroxysmal atrial fibrillation. A CT scan of his chest with IV contrast was ordered on admission to rule out a pulmonary embolism because the patient began to complain of dyspnea. (Figure 2.)

Figure 2. The chest CT revealed a filling defect of the right lower lobe consistent with pulmonary embolism.

The chest CT revealed a filling defect of the right lower lobe consistent with pulmonary embolism. Lower extremity venous Dopplers were negative. A subsequent MRI/MRA of the mesentery revealed possible celiac access dissection with occlusion at the distal portion, including the splenic artery, resulting in splenic infarction. (Figure 3.) There was also the suggestion of aneurysms of the left common iliac and right internal iliac arteries. Anticoagulation with heparin was continued, and he was then started on warfarin as well. He subsequently developed heparin-induced thrombocytopenia (HIT), and the anticoagulation was changed. Enoxaparin was stopped, and the patient was continued on warfarin, and started on argatroban until his INR was therapeutic, at which time the argatroban was discontinued. Analgesics were prescribed for worsened abdominal pain.

Figure 3. MRA of the mesentery showing possible celiac access dissection with occlusion at the distal portion, including the splenic artery, resulting in splenic infarction.

At discharge, the patient's INR was therapeutic at 2.3. He was discharged with final diagnoses of pulmonary embolism, splenic infarction, abdominal pain, constipation, HIT, and suspected hypercoagulable state. Subsequent hypercoagulable workup was normal.

The cause of abdominal pain is rarely celiac artery thrombosis leading to a splenic infarction. Although pulmonary embolisms are not uncommon (approximately 1:1000), splenic infarctions are considerably rare. What makes this case more interesting is that he had both conditions simultaneously without a documented hypercoagulable state. Aneurysms of the celiac artery are an uncommon clinical problem, and fewer than 180 cases have been reported in the medical literature. It was first described in 1745. Aneurysms of the celiac artery only account for 3.6 percent to 4 percent of splanchnic artery aneurysms with an annual incidence of 0.005 percent to 0.01 percent. This patient's pulmonary embolism was believed to be from lower leg trauma the patient sustained while previously exercising.

After hospital discharge, the patient was evaluated by multiple vascular surgery specialists in New York City. A CT of his abdomen and pelvis six months following his hospitalization revealed a celiac artery aneurysm. He underwent angiography to delineate his anatomy further, and was found to have a rare variant of his hepatic artery, precluding embolization of the aneurysm and needing an open surgical repair with graft tissue. A full hypercoagulable workup was repeated six months following discharge, and was completely normal. The patient's hematologist believed that the initial hypercoagulable workup revealed abnormalities as a result of the patient's HIT at that time, but would otherwise have been normal.

Abdominal pain in the emergency department is a very common complaint, but having it attributed to two concurrent but anatomically isolated pathologies (splenic infarction from a celiac thrombosis and pulmonary embolism) is exceedingly rare. It is prudent for the emergency physician to routinely perform a detailed history and physical examination, and maintain a high level of suspicion for the uncommon.

Published: 4/16/2012 7:53:00 AM

04.13.12

by The Case Files

A Case of Organoaxial Gastric Volvulus

McGrane, Owen MD; McGrane, Karen MD

A 26-year-old active-duty man presents with acute onset abdominal pain with nausea, bloating, and excessive belching. He has a six-month history of episodic abdominal cramping, diarrhea, and melena. These intermittent paroxysms of abdominal pain are associated with a difficulty tolerating his diet and a 19-pound weight loss over the previous six months. Episodes are typically severe enough to debilitate him for several hours at a time, and have been gradually worsening.

The patient has had numerous imaging exams -- endoscopy, colonoscopy, and abdominal x-rays -- and has been evaluated extensively by the gastroenterology service, carrying a diagnosis of irritable bowel syndrome. He denies heartburn, reflux, regurgitation, dysphagia, anorexia, or early satiety. The patient has been taking anti-diarrheals, antispasmodics, and proton pump inhibitors without relief. He has no other past medical history, and has never had abdominal surgeries.

He has no known familial inflammatory bowel disease or gastrointestinal cancer. The patient does not smoke or chew tobacco, drinks alcohol in moderation, and denies regular use of aspirin, acetaminophen, over-the-counter NSAIDs, and herbal products.

On physical exam, he was alert and oriented, and had abdominal pain but no acute distress. Heart and lung exams were normal. His abdomen was soft, nontender to palpation, not distended, and with active bowel sounds, most prominent in the left upper quadrant. Previously normal laboratories included TSH, stool culture, and O&P; a screen for celiac disease was negative. Initial studies included a normal CBC and serum chemistries, and he was negative for fecal occult blood. After double-contrast upper GI series and small bowel follow-through, the diagnosis was found: organoaxial gastric volvulus.

Gastric volvulus is a rare condition in which the stomach twists on itself, causing a closed-loop obstruction. There are two types, organoaxial and mesenteroaxial. Organoaxial volvulus is the more common type, representing approximately 60 percent of cases. Organoaxial volvulus occurs when the stomach rotates 180 degrees around the long axis. A diaphragmatic hernia is frequently associated with this condition.

Symptoms are typically acute in onset, and gastric ischemia is a potential complication. In mesenteroaxial volvulus, the stomach rotates around its short axis. This type of volvulus is more likely to be incomplete and intermittent with chronic symptoms.

The overall mortality of gastric volvulus has been estimated to be between 15 percent and 20 percent. Peak incidence occurs in the fifth decade of life. It may occur in children under a year old, and is typically associated with a congenital diaphragmatic defect. The incidence of this condition is unknown due to its intermittent nature, and many cases go undiagnosed.

Patients presenting with gastric volvulus typically complain of acute onset of upper abdominal pain, distention, and vomiting. The symptoms referred to as Borchardt's triad include sudden onset of severe upper abdominal pain, recurrent retching with production of little vomitus, and inability to pass a nasogastric tube. These symptoms should raise clinical suspicion for gastric volvulus. Hematemesis may be present in cases of esophageal injury related to retching or with associated gastric mucosal ischemia. In cases of chronic volvulus, patients may present with nonspecific symptoms such as epigastric discomfort, bloating, dysphagia, and dyspepsia after meals.

Plain films may demonstrate a gas-filled loop of bowel in the abdomen or chest. Barium swallow will confirm the diagnosis with visualization of the abnormality. There are no specific laboratory abnormalities associated with this condition.

Gastric volvulus is considered a surgical emergency. Treatment of gastric volvulus includes decompression of the stomach with a nasogastric tube, if possible. Endoscopic detorsion can be attempted if there are no signs of gastric infarction. Surgical detorsion with fixation of the stomach to prevent further episodes is the definitive treatment.

Published: 4/13/2012 8:10:00 AM

04.09.12

by The Case Files

Drug-Induced Gingival Hyperplasia

McGregor, Alyson J. MD, MA; Hsu-Hung, Ellen MD

A 37-year-old Spanish-speaking man presented with a complaint of tender, bleeding, and swollen gums. He had had an orthotopic heart transplant in 1997. His current mediations include Cyclosporine 125 mg bid and amlodipine 5 mg qd as well as CellCept, aspirin, and allopurinol for gout. Gingival overgrowth, also known as gingival hyperplasia, has been well described in the literature.

The most recognized cause is drug-induced gingival enlargement from phenytoin (Dilantin), which is commonly used to treat patients with epileptic seizures. Less known drugs that contribute to this phenomenon are Cyclosporine, a potent immunosuppressant used in organ transplant recipients, and calcium channel blocker agents. The interaction of these medications with epithelial keratinocytes, fibroblasts, and collagen can lead to an overgrowth of gingival tissue, particularly in patients with poor oral hygiene, periodontal disease, and malpositioned teeth.

Treatment for gingival hyperplasia includes discontinuing the drug or reducing its dose. In those for whom this is not possible, good oral hygiene and referral for surgical gingivectomy remain the only treatment. Gingival hyperplasia should be considered when treating organ transplant recipients on immunosuppressant therapy.

Dr. McGregor is an assistant professor of emergency medicine at the Warren Alpert Medical School of Brown University and an attending at Rhode Island Hospital and the Miriam Hospital. Dr. Hsu-Hung is a resident in emergency medicine at the Warren Alpert Medical School of Brown University.

Published: 4/9/2012 12:17:00 PM

04.03.12

by The Case Files

Don’t be Fooled: Take Serial FAST Scans in Blunt Flank Trauma

Rossi, Jennifer K. MD; Gharahbaghian, Laleh MD

A 38-year-old man presented to the emergency department after a horse kicked him in the left flank. He denied chest and abdominal pain. His heart rate was 85 bpm, blood pressure was 139/93 mm Hg, and oxygen saturation was 99%. He had tenderness over a 4 cm contusion on his left flank at the 10th posterior rib. His abdomen was not tender. The assessment was otherwise unremarkable.

The initial focused assessment for sonography in trauma (FAST) scan was negative. (Image 1: Right upper quadrant.) A computed tomography (CT) scan illustrated a grade 3 splenic laceration without active extravasation, perisplenic hematoma, small hemoperitoneum, and left 9th and 10th rib fractures. (Image 2.) A repeat FAST scan 10 minutes later was positive in the right upper quadrant only. (Image 3: Right upper quadrant.) The patient was admitted to the intensive care unit where his hematocrit fell to a nadir of 36.4 % (normal 35.0-47.0%). He was discharged on hospital day three.

Figure 1 - Initial ultrasound of Morrison's pouch, right upper quadrant

Figure 2 - Computed tomography of abdomen. Arrow indicates a grade 3 splenic laceration without active extravasation. Asterisks indicate large perisplenic hematoma.

Figure 3 - Repeat ultrasound of Morrison's pouch demonstrating intraperitoneal fluid (arrow).

Patients can present after blunt torso trauma with solid organ injury without abdominal tenderness or hypotension. The spleen is the most commonly injured organ, comprising one-third of such injuries. Splenic injury management includes observation, angiography and embolization, or laparotomy depending on the degree of injury and hemodynamic stability. The FAST scan is an accepted screening tool for trauma evaluation. (Curr Opin Crit Care 2007;13[4]:399.)

The right upper quadrant view is the most sensitive in a supine patient no matter the location of injury due to the anatominal attachment of the posterior mesentery. In experienced hands, 250 ml of fluid can be detected with an overall sensitivity and specificity of 86% and 98%, respectively. (J Trauma 2001;50[1]: 108.) As this case illustrates, it is imperative to perform repeat FAST scans to increase sensitivity. (J Trauma 2004;57[5]:934; J Emerg Med 2000;18[1]:79.) In hemodynamically stable patients with a positive FAST, CT can diagnose the specific injury and evaluate the retroperitoneal space because FAST scans only evaluate the intraperitoneal space. When the physician has a high degree of suspicion for intra-abdominal injury but does not have access to CT or surgical services, the FAST scan should be repeated as to avoid missing life-threatening injury.

Drs. Rossi and Gharahbaghian are emergency physicians in the department of surgery, division of emergency medicine, at Stanford University Medical Center. Dr. Gharahbaghian is also the associate director of Emergency Ultrasound and a director of the Emergency Ultrasound Fellowship at Stanford.

Published: 4/3/2012 7:50:00 AM

03.27.12

by The Case Files

Paronychia Rupture Following Blood Pressure Cuff Inflation

McKie, Robert MD

A 38-year-old man presented to the emergency department with a two-day history of pain and swelling in his distal left fifth finger. He rated the severity of his pain as approximately 4/10. The patient related no history of trauma, but he wore heavy gloves and worked as a repo man, and believed that he may have sustained minor trauma during the course of his work. He had no fever, chills, loss of function, or other complaints.

The patient had a history of type 2 diabetes, hyperlipidemia, and hypertension. He used NPH insulin, metformin, and glipizide for diabetes, which is poorly controlled on this regimen. The patient also takes lisinopril and hydrochlorothiazide for hypertension and simvastatin for hyperlipidemia. He is allergic to aspirin, and recently completed a course of prednisone and valacyclovir for Bell's palsy.

The patient had a pulse of 97 bpm, a blood pressure of 140/75 mm Hg, and a temperature of 97.1°F. On examination, the fifth digit of the patient's left hand was tender and erythematous. The patient's cardiovascular, respiratory, and lymphatic systems were normal.

During the patient's intake examination, a blood pressure cuff was inflated on his left arm. When the cuff fully inflated, the patient's paronychia ruptured and produced a small volume of purulent discharge. The patient experienced immediate pain relief, and the discharge was sent to the lab for gram stain, culture, and sensitivity. Repeat inflation of the blood pressure cuff resulted in another small amount of purulent matter being expressed from the paronychia.

Gram stain of the purulent material revealed a few polymorphonuclear leukocytes (PMNs), 2+ epithelial cells, and 2+ gram positive cocci in clusters. Culture grew 4+ Staphylococcus aureus, which was sensitive to cefazolin, ampicillin and sulbactam, ciprofloxacin, clindamycin, linezolid, oxacillin, tetracycline, sulfamethoxazole-trimethoprim, and vancomycin.

Gram stain of the purulent material revealed a few polymorphonuclear leukocytes (PMNs), 2+ epithelial cells, and 2+ gram positive cocci in clusters.

After acute drainage, the affected finger was soaked in warm sterile saline. A dressing with bacitracin ointment was placed, and the patient was sent home with sulfamethoxazole-trimethoprim 160/800 (DS), one tablet twice daily for seven days.

A paronychia is an infection of the lateral nail fold. It can be both acute and chronic. Acute infections usually involve S. aureus and Streptococcus pyogenes. If the fingers are exposed to the mouth, oral flora also should be considered as possible causative agents. Chronic paronychia is often associated with eczema.

The patient's paronychia ruptured when a blood pressure cuff was inflated on his arm, circumventing the need for I&D.

The differential diagnosis of paronychia includes felons, herpetic whitlow, and onychomycosis. Felons are serious infections of the soft tissue pulp of the distal finger. These must be treated with prompt incision and drainage to prevent osteomyelitis, finger infarction, and other complications. Herpetic whitlow is a herpes virus infection of the finger. These infections typically have vesicles similar to other herpetic infections.

Treatment of paronychia typically involves warm soaks and pain control. Topical and oral antibiotics may be used, especially in immunocompromised patients. If an abscess is present, this should be drained under appropriate anesthesia. If purulent material is drained from a paronychia, it should be sent for culture and sensitivity.

By occluding venous return, blood pressure cuff inflation likely increased the pressure on the paronychia and caused it to rupture. Blood pressure measurement is a routine part of patient evaluation, and it is reasonable to attempt ipsilateral blood pressure cuff inflation in patients with paronychia. If this causes the paronychia to rupture, the patient may be able to forgo incision and drainage.

I am calling this the Wenzel maneuver after Tom Wenzel, the emergency nurse who performed it on this patient.

Published: 3/27/2012 8:51:00 AM

03.23.12

by The Case Files

Back Pain that Takes Your Breath Away

Keehn, Steven DO; Weinstein, Lenny DO; Levy, David DO; Zimmerman, Steven MD

A 62-year-old man with history of chronic lymphocytic leukemia (CLL), hypothyroidism, transient ischemic attack, and treated pulmonary tuberculosis presented to the emergency department with a complaint of low back pain for one month. The pain had worsened on the morning of presentation, and was described as a constant dull ache, 9/10 in severity, on the left paraspinal muscle region without radiation.

Pathologic specimen: Nocardia farcinica

The pain had been improving, but started to worsen again over the past week, intensifying that morning when he sneezed and twisted toward the left. He also admitted to a two-week history of painless hematuria without other urinary symptoms, and feeling weak and tired with a poor appetite for several days. He had completed treatments for CLL a year earlier. He denied recent travel or sick contacts.

His tuberculosis infection had occurred 20 years earlier, and was treated with two drugs for one year. A cervical lymph node biopsy was his only surgery. The patient denied any allergies, and was only taking aspirin and levothyroxine. His last chemotherapy treatment was also a year earlier. The patient was a smoker who had cut down from two packs to half a pack a day. He denied illicit drug use, but did admit to social alcohol consumption. He had no family history of hypertension, diabetes, or premature coronary disease. He was retired and used to work as a toll booth attendant in the Bronx.

On physical exam, he was noted to be tachycardic with a heart rate of 119 bpm. He was normotensive at 120/68 mm Hg, afebrile at 98.3°F, respiring at 20 with an O2 saturation of 95% on room air. At first glance, the patient appeared cachectic and thinly built but in no apparent distress. His pupils were equal and reactive, conjunctiva pink and sclera anicteric. His otic exam showed no signs of infection.

He had poor dental hygiene and a normal pharynx. His neck was supple, nontender, without cervical lymphadenopathy, JVD, or carotid bruits. His heart revealed a normal S1/S2 without murmurs, rubs, or gallops. Breath sounds were clear and equal bilaterally with normal chest excursion. His abdomen revealed normal bowel sounds, it was nondistended but diffusely tender without rebound or guarding.

Interestingly, his back was tender diffusely over the lumbar area, which was worse on the left side. There was no ecchymosis or other lesions. There was mild dextroscoliosis present. The patient did not have costrovertebral tenderness and the left paravertebral muscles were boggy. His extremities revealed normal range of motion. They were nontender to palpation, with normal distal pulses and without edema. His skin was warm, dry, with good turgor, and no apparent lesions or exudates. Neurologically, he was awake, alert, and oriented. His cranial nerves were intact, and no gross deficits were identified.

Hospital Course

Laboratory tests were ordered, including a CBC and chemistry panel as well as lumbar spine x-rays. (Fig. 1.) The CBC included a WBC of 11.0 × 103/mm3, hemoglobin of 10.2 g/dL, hematocrit of 29.2%, and platelet count of 394 × 103/mm3. The chemistry panel revealed that the patient was hyponatremic with a sodium level of 124 mEq/L. The remainder of the chemistry panel was normal, and included a potassium of 4.4 mEq/L, chloride of 87 mEq/L, bicarbonate of 0.8 mEq/L, BUN of 9 mg/dL, creatinine of 0.8 mg/dL and glucose of 123 mg/dL. Because the patient had hyponatremia, he was given a 500 ml bolus of normal saline and placed on maintenance fluids with normal saline at 100ml/hr. His pain was moderately controlled with two tablets of oxycodone/acetaminophen 5/325.

Figure 1: L-spine x-ray

The patient had an admission chest x-ray performed which interestingly showed an 8 cm mass. (Fig. 2.) Consultations were requested, and he was admitted to the hospital. A chest CT scan (Fig. 3) was performed, which corroborated with the chest x-ray finding of an 8 cm mass. Further imaging performed including a renal ultrasound, which revealed a large heterogeneous mass posterior to the left kidney. Subsequently, a CT scan of the abdomen/pelvis was performed (Figures 4 and 5), revealing a large complex cystic paraspinal mass within the left psoas muscle with an accompanying epidural collection and bony erosion (Fig. 5) along the anterior L4 vertebra.

Figure 2: Admission chest x-ray.

Figure 3: CT lung mass

Figure 4: CT identifying psoas abscess

Figure 5: CT vertebral body destruction.

Brain CT revealed a focal low density within the left lentiform nucleus extending into the left corona radiata without mass effect or hemorrhage. The patient was started on sulfamethoxazole/trimethoprim (Bactrim), penicillin G, and metronidazole (Flagyl), but developed neutropenia thought to be secondary to the sulfamethoxazole/trimethoprim. The regimen was changed to amikacin (Amikin) and imipenem-cilastin (Primaxin) and continued on penicillin G until final identification of the organism. Blood and respiratory cultures grew out Nocardia farcinica. Despite aggressive treatment, the patient expired following two months of hospitalization.

Diagnosis and Treatment

Systemic and pulmonary nocardiosis is an uncommon gram-positive bacterial infection caused by aerobic actinomycetes. The classification is based on the location and extent of the disease and includes pulmonary, CNS, cutaneous, and disseminated disease. Risk factors include chronic lung diseases, alcoholism, malignancy, HIV, solid organ or hematopoietic stem cell transplantation, diabetes mellitus, or glucocorticoid therapy. Approximately one-third of infected patients are immunocompetent.

Systemic nocardiosis (two or more sites involved) accounts for 32 percent of cases with a mortality rate varying from seven percent to 44 percent. It is uncommon to obtain a positive blood culture during the first several days, and blood cultures should be held for about four weeks. Patients with systemic nocardia may develop retroperitoneal and psoas abscesses. The mean time of diagnosis ranges from 42 days to 12 months; this case took 31 days. Two-drug therapy is recommended, and three-drug therapy if life-threatening infection is present. For a severe infection not involving the central nervous system, Bactrim plus Amikacin or Imipenem plus Amikacin is recommended. The duration of treatment depends on the patient's response, severity of the disease, and the relapsing nature of nocardia, but a prolonged course for at least a year is recommend. Some suggest indefinite suppressive therapy.

Interestingly, this patient's last chemotherapy treatment was more than a year earlier, his TB infection was 20 years earlier, and he was not on steroids or calcitonin inhibitors. He was erroneously diagnosed with a mass on chest x-ray approximately a year before presentation, which was attributed to his CLL. The patient did admit to symptoms consistent with the disease such as fever, fatigue, anorexia, weight loss, and cough. He denied night sweats, dyspnea, hemoptysis, or pleuritic chest pain. This is usually misdiagnosed as TB because upper lobe involvement is common. The first case of nocardia spondylodiscitis accompanied by a psoas abscess secondary to spread from pulmonary nocardiosis was described in January 2007. Fortunately in that case, the patient's clinical condition improved after one year of treatment.

Back pain is a common complaint in the emergency department, and it is often rapidly diagnosed and treated in fast tracks. Occasionally the etiology, though, is secondary to significant pathology, as in this case. It is prudent for tthe physician to routinely perform a detailed history and physical, and maintain a high level of suspicion for the uncommon.

Published: 3/23/2012 9:33:00 AM

03.19.12

by The Case Files

A Rare Cause for Alarm

Davis, Frederick DO; Havasy, Stephen MD; Levy, David DO

A 45-year-old woman presented to the ED with a sore throat she'd had for two days. Her husband reported that she complained of throat pain and inability to swallow, and had decreased oral intake secondary to pain. The patient confirmed the pain as 10/10, burning in nature located to the posterior oral pharynx area. On the day of presentation, the patient was unable to complete full sentences.

She denied any fevers, headaches, prior upper respiratory infection, dyspnea, nausea, vomiting, chest pain, or abdominal pain. The patient also denied any recent travel or sick contacts. No allergies were noted. While the patient did have a past medical history of hypothyroidism, she denied taking any medication. Her past medical history was consistent for a tonsillectomy, appendectomy, and C-section, all of which had occurred more than five years ago. She stopped smoking four years previously, and denied any illicit drug use. She also denied any significant family medical history.

On physical exam, this Caucasian woman was in moderate distress with an inability to swallow or control her own secretions. The patient was afebrile at 98.7°F, but she was noted to be tachycardic at 115 bpm with a blood pressure of 144/78 mm Hg. Respiratory rate was noted at 20 respirations per minute, with an oxygen saturation of 97% on room air. Tenderness was appreciated to left auditory canal with mild erythema. Tympanic membranes were nonbulging. The patient had a normal nasal exam, no rhinorrhea, and normal dentition. There was erythema and edema to the posterior pharynx with inability to fully visualize secondary to swelling. There were no exudates that could be seen. There was tenderness appreciated with palpation of the anterior aspect of the neck. Heart exam showed tachycardia but no murmurs, rubs, or gallops. Lung exam revealed clear lungs bilaterally. Normal bowel sounds were appreciated on the abdominal exam with no tenderness or guarding. The patient had no cyanosis, clubbing, or edema of the extremities. Skin was warm, dry, and intact. She was awake, alert, and oriented to person, place, and time.

Noting the distress that this patient was having with her sore throat, the inability to complete full sentences, and the edema noted on physical exam, an IV line was immediately established and both morphine and dexamethasone were given. At that time, a basic metabolic panel and complete blood count were drawn.

The CBC and the electrolyte panel were nonspecific as shown in Figure 1. After a B-hCG returned negative, a chest and lateral neck x-ray were taken. Both of these revealed no explanation for this patient's distress. The chest x-ray showed no signs of infiltrates, as can be seen in Figure 2, and the lateral neck film showed no foreign bodies or soft tissue prominence, such as the classic "thumb print sign" of epiglotitis, as one might expect from this presentation, as displayed in Figure 3. With concern for the patient and the need to establish an etiology for her symptoms, a contrast CT of the neck was obtained.

Figure 1: Lab Results

Figure 2: Normal Chest X-Ray

Figure 3: Normal Lateral Chest X-Ray

The CT proved to be the definitive test. Cystic fluid in the area of the tongue was identified, shown in Figures 4 and 5. It was noted to be an abscess of the geniohyoid muscle.

Figure 4: CT of the neck with contrast. This lateral view of the CT of the neck demonstrates a cystic structure in the muscle of the tongue as indicated by the white arrow.

Figure 5: CT of the Neck with Contrast. This coronal view of the CT of the neck demonstrates a cystic structure in the muscle of the tongue as indicated by the white arrow.

Otolaryngology was consulted. The patient was started on piperacillin/tazobactam 3.375g IV Q8H, and continued on dexa-methasone 6mg IV Q6H. She underwent an ultrasound-guided drainage of the abscess, cultures of which grew Streptococcus intermedius. After five days, the patient was able to maintain her own airway, and continued to improve throughout her hospital course. She was discharged on amoxicillin/clavulanate 875mg BID for 10 days, Bacid 2 tabs daily for 10 days, and Percocet 5/325mg Q4H prn pain.

Discussion: An abscess of the tongue is a very rare condition. Over the past 30 years, only 50 cases of glossal abscess have been reported in the English literature. (Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2004;97[5]:570.) Most of these occurred in immunocompromised patients or in healthy persons with pierced tongues. (J Emerg Med 2001;20[4]:409.) To a lesser extent, there have been cases reported after injury to the glossal area from bones while eating. What makes this case even more unique is that this patient had neither of these inciting factors, perhaps the first of its kind from what could be found in a literature search. The patient reports no tongue piercings or recent lacerations.

The differential diagnosis of a tongue abscess includes other entities that may present as lingual swelling, such as a tumor, infarction, edema, hemorrhage, metabolic macroglossia in hyperpituitarism or hypothyroidism, or developmental macroglossia in lingual thyroid or ectopic lymphoid tissue. Abscesses located in the anterior part of the tongue are easy to diagnose by direct visualization. Abscesses that present on the base of tongue may pose a diagnostic challenge because the symptoms are less specific and other inflammatory processes, such as peritonsillitis or infection of the floor of the mouth, may be indistinguishable. (Br J Oral Maxillofac Surg 1993;31[5]:321.)

Infections of the tongue are rare, and their spread to other areas of the neck is a concern for possible airway obstruction. The submandibular space consists of two areas, the sublingual space and the submylohyoid space, separated by and freely communicating around the posterior border of the mylohyoid muscle. Infections to this area most commonly originate from odontogenic structures or from the submandibular gland. Most patients do not report a recent history of URI. The time of onset of symptoms until the time of presentation is also variable, but it usually ranges from two days to two weeks. Specific symptoms and signs depend on the space involved, but symptoms generally include pain (76%), fever (64%), swelling (62%), dysphagia/odynophagia (42%), trismus (14%), respiratory distress (14%), and dental problems (8%), while physical findings include swelling (90%), dental abnormality (29%), fluctuance (27%), oropharyngeal abnormality (22%), trismus (18%), laryngeal abnormality (pooling of secretions, edema, etc.) (18%). (Laryngoscope 1988; 98[8 Pt 1]:877.)

While AP and lateral neck films are useful in delineating the course and caliber of the airway, as well as the degree of soft tissue edema, CT remains the gold standard imaging study in evaluating neck space infections. Sensitivity and specificity of CT are excellent in the delineation of involved spaces, and contrast allows enhancement of abscess walls.

Treatment of such abscesses consists of airway control and drainage. The most commonly found organisms are predominantly Streptococci species with Peptostreptococcus, Fusobacterium, and Bacteroides to a lesser extent. Antibiotics should cover for polymicrobial oral flora and agents such as penicillin and metronidazole, piperacillin/tazobactam, or ampicillin/sulbactam. For those suspected of IV drug abuse, the IV antibiotic of choice remains high-dose penicillin with nafcillin. Clindaymcin would be the alternative for those with penicillin allergy.

Complications include spread to other neck spaces causing a Ludwig's angina, mandibular osteomyelitis, and airway obstruction leading to asphyxia. Early detection through high suspicion and early antibiotics and drainage is necessary to prevent this course. If infections with the Streptococcus milleri group (Streptococcus intermedius, Streptococcus constellatus, or Streptococcus anginosus) are isolated in blood cultures, an abscess should strongly be considered and sought for. (Infect Dis Clin North Am 1992; 6[3]:705.)

This case highlights the symptoms of potential airway obstruction secondary to an uncommon abscess. A patient presenting with dysphagia should prompt immediate airway control and eventual CT imaging for possible deep neck space infections. If suspected, early antibiotics and consult with ENT for surgical drainage can help prevent the possible course of further spread and infection.

Published: 3/19/2012 11:11:00 AM

02.27.12

by The Case Files

A Pressing Headache

By Joshua Bozek, DO; Steven Zimmerman, MD; Andrew Rogove, MD, PhD; & Elliott Eisenberger, MD

A 58-year-old woman presented to the emergency department with the complaint of headaches for one day. She was brought to the ED by her son after she told him about her severe headaches. She was not answering all questions appropriately so the son provided most of the history. She was able to state that the headaches began the day before she came to the ED and that they were intermittent, 10 of 10 on the pain scale, and sharp to the back of her head. The son stated she was acting strangely and complained of worsening headaches while in the car on the way to the ED and then developed blurry vision. The son stated she has had headaches in the past, but never anything that required her to come to the ED.

She denied vomiting, diarrhea, recent colds, runny nose, cough, chest pain, shortness of breath, or weakness. The patient had no allergies to medications, but she did have a history of hypertension and anemia. The son stated she had been taking medication for her blood pressure, but neither he nor the patient could recall the names. She had no surgical history, was a former smoker of 1 pack of cigarettes a day for 20 years, but quit 20 years before. Both denied any drug or alcohol use. The son did not recall any family history of serious headaches, CVA, or brain cancers.

On physical exam, this patient was well nourished and in no apparent distress, but she was unable to concentrate for long periods of time. She would stare off into the distance, and had difficulty cooperating with the staff. Her vital signs were: 97.6°F, pulse 94 bpm, blood pressure 150/90 mm Hg (sitting), and respiratory rate 20 bpm with an oxygen saturation of 98% on room air. The head was atraumatic and normocephalic. Examination of the eyes, however, was difficult to assess because she could not track a finger, perform a finger-to-nose test, or cooperate with a visual acuity examination. The patient was oriented to person only. Cranial nerves did appear to be intact grossly, but she did not fully cooperate with the neurologic examination. There was no nuchal rigidity. Cardiac, respiratory, and abdominal examinations were within normal limits. She did not have a gait disturbance and extremity strength was 5/5x4, with full range of motion.

Given the patient's inability to cooperate fully with her examination, her change in mental status, and her blurry vision, intravenous access was established immediately and blood was sent for CBC, complete metabolic panel, PTT/PT/INR, CK, troponin I, and serum alcohol level. The patient was sent for a stat brain CT without contrast. The patient arrived back from CT scan, and repeated vital signs showed a rectal temp 99.2°F, pulse 116 bpm, respiratory rate 22 bpm, and blood pressure 220/118 mm Hg (supine). Shortly after her return, the patient began to have a tonic-clonic seizure. Lorazepam 2 mg IVP was administered, and the seizure abated. The brain CT showed no evidence of CVA, hemorrhage, or mass. (Fig. 1.) The chest x-ray revealed clear lungs with no focal infiltrate (Fig. 2), and labs were reviewed. (Fig. 3.) Given these findings, a stat lumbar puncture was performed, and fluid was sent for analysis. (Fig. 4.)

Figure 1: CT of the brain without contrast.

Figure 2: Chest x-ray.

Figure 3: Laboratory values.

Figure 4: CSF Results.

The patient had another tonic-clonic seizure 30 minutes after the lumbar puncture, Lorazepam 2 mg IVP was again administered, and the patient was given a loading dose of phenytoin 1 gram IVPB. Repeat vital signs showed pulse 114 bpm, respiratory rate 20 bpm, and blood pressure 180/100 mm Hg. The patient had a fever of 102.4°F rectally three hours later. Urinalysis showed no evidence of infection, and urine toxicology screen was negative. She was admitted, and neurology consultation was obtained. Given the cluster of symptoms and most notably the headache, altered mental status, elevated blood pressure, and seizures, the diagnosis of possible posterior reversible encephalopathy syndrome (PRES) was entertained. MRI of the brain was completed, and showed evidence of posterior cerebral edema consistent with PRES. (Fig. 5.)

Figure 5: MRI of brain on day of admission showing posterior cerebral white matter edema.

The patient was restarted on her blood pressure medications, resulting in the return of her blood pressure to a normal level. Blood cultures were negative for bacteremia, and the patient had no other episodes of fever. The patient's neurological status and overall condition improved after two days. She was discharged home on day five. In discussion with the patient after her mental status returned to baseline, she stated she was often not compliant with her blood pressure medications. She was advised of the extreme importance to be strict with her blood pressure medication regimen to avoid future episodes of the syndrome. The patient had subsequent follow-up appointments with her neurologist, and a repeat MRI was completed two months later. (Fig. 6.) This MRI showed no further evidence of posterior cerebral edema, indicating this was indeed a case of PRES.

Figure 6: MRI of brain two months later. No cerebral edema noted.

Posterior reversible encephalopathy syndrome (PRES) is also known as posterior leukoencephalopathy syndrome, reversible posterior cerebral edema syndrome, hyperperfusion encephalopathy, and brain capillary leak syndrome. PRES is described as a clinical syndrome of abrupt onset of headache, confusion or decreased level of consciousness, visual changes, and seizures. It is necessary to have all four criteria to diagnose PRES clinically. Typically, these symptoms are associated with some characteristic neuroimaging findings consistent with posterior cerebral white matter edema on MRI. PRES has been described in several conditions including hypertensive encephalopathy, eclampsia, and the use of cytotoxic drugs and immunosuppressant drugs.

PRES is being increasingly recognized throughout the world, and the exact incidence is still unknown. It has been described in patients from ages 2 to 90, and women are affected more than men even when eclamptic women are removed from the statistics. (J Child Neurol 2007;22[4]:406; Intern Med J 2005;35[2]:83.) Risk factors for PRES include hypertensive disorders, renal disease, and immunosuppressive therapies. PRES is a relatively new diagnosis, but it has been described in various case reports for many years, and was defined as a single syndrome in 1996. (N Engl J Med 1996;334[8]:494.)

The pathogenesis of the syndrome is still not understood. There are data to suggest that endothelial dysfunction may play a major role. In several disorders, there is disruption of the endothelial lining of blood capillaries and seems to be more common in eclampsia and cytotoxic drug administration. (J Child Neurol 2007;22[4]:406.) In eclampsia, a release of fibronectin, tissue plasminogen activator, thrombomodulin, endothelin-1, and von Willebrand factor may damage the endothelial lining of blood vessels. (Am J Obstet Gynecol 1988;159[4]:908.) Cytotoxic drugs are believed to have direct toxicity on the vascular endothelium, which leads to capillary leakage, blood-brain barrier disruption, and axonal swelling. (J Child Neurol 2007;22[4]:406.) Acute hypertension and endothelial damage when combined will result in hydrostatic edema. This is characterized by the forced leakage of serum through capillary walls into the brain interstitium, and is a form of vasogenic edema. If enough fluid accumulates, it will become radiographically evident.

If vascular injury to the blood-brain barrier endothelium is unregulated, it will lead to edema, protein extravasation, and fibrinoid necrosis. (J Neurol Sci 1970;10[3]:215.) Because the cortex is more tightly packed than the white matter, it resists accumulation of edema, which is why edema is seen in the white matter. (Med Biol 1986;64[2-3]:133.)In episodes of hypertensive encephalopathy, blood pressure rises beyond the upper limits of cerebral autoregulation, which also leads to vasogenic edema. The primary involvement of the posterior regions of the brain is still not understood.

As noted in the name, the condition is reversible if treated early and damage to the brain from additional seizures can be avoided. Control of blood pressure is imperative in patients with hypertensive encephalopathy and eclampsia. Discontinuation of the cytotoxic drugs for those on such therapy can reverse the syndrome in these cases as well.

This current case highlights the symptoms necessary to make the clinical diagnosis of posterior reversible encephalopathy syndrome. The patient had all of the signs and symptoms, and after ruling out an infectious etiology, it was considered in the differential diagnosis. Knowing this cluster of symptoms is particularly useful in the emergency setting because early treatment of elevated blood pressure can help reduce the chance of additional seizures.

A patient presenting with onset of headache, confusion or decreased level of consciousness, visual changes, and seizures should prompt the emergency physician to consider treating blood pressure aggressively. Neurology consultation should be obtained, and an MRI of the brain should be done as soon as possible after CT scan fails to diagnose the cause.

Dr. Bozek, a second-year emergency medicine resident; Dr. Zimmerman, an emergency physician; Dr. Rogove, a neurologist, and Dr. Eisenberger, a radiologist, all practice at Good Samaritan Hospital in West Islip, NY.

Published: 2/27/2012 4:12:00 PM

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