The Case Files
Welcome to the Case Files!
The Case Files is an anecdotal collection of emergency medicine cases to enable physicians and researchers to find clinically important information on unusual conditions.
Case reports should focus on:
- Unusual side effects or adverse interactions.
- Unusual presentations of a disease.
- Presentations of new and emerging diseases, including new street drugs.
- Findings that shed new light on a disease or an adverse effect.
Comment on a case or submit your own case following the instructions in the Submissions box to the right.
Tuesday, September 02, 2014
By Dyer, Alexandra; Berg, Kenneth MD; King, Andrew MD
Rat bite fever (RBF) is a fairly rare illness caused by Streptobacillus moniliformis or Spirillum minus. It can be a devastating and even fatal illness if left undiagnosed or untreated. Despite its name, RBF is not only transmitted by rat bites but also by contact with rat feces, ingestion of rat-contaminated food and water, or simply through direct contact with rats. (Clin Microbiol Rev 2007;20:13; Vet Microbiol 2009;133:211; BMJ Case Rep 2009; Epub Dec 17.)
The first documented outbreak in Haverhill, MA, in 1926 was believed to be caused by a pathogen named Haverhillia multiformis. It was later determined to be identical to S. moniliformis. Other outbreaks with matching symptoms have also been documented and frequently misdiagnosed. (Clin Microbiol Rev 2007;20:13.)
RBF is difficult to diagnose. Its sequelae are often nebulous — chills, rigors, and polyarthralgias — and the causative pathogens are difficult to isolate in cultures. RBF is also likely to respond to empiric therapy and it is not a reportable disease, so definitive diagnosis may never be established even if treated appropriately. (Clin Microbiol Rev 2007;20:13; Vet Microbiol 2009;133:211.) Consequently, this condition is often erroneously omitted from the differential when evaluating fevers in the ED unless the history is highly suggestive of a rat bite.
Rats are more than pests in today's society. Humans are coming increasingly into contact with rats in laboratories and even as pets. (Paediatr Child Health 2010;15:131.)
A 21-year-old man presented to the ED with chills and rigors after being bitten by a lab rat on the right hand four days previously. Surprisingly, the patient denied any significant localized symptoms around the bite itself. He also denied any experiments involving infectious pathogens being performed at his laboratory. Two days after being bitten, the patient woke with generalized fatigue, malaise, myalgias, chills, and rigors.
Aspirin at home did provide mild transient relief of his symptoms, but they continued to recur and progressively worsen as the medication wore off. His symptoms persisted, and he also developed sore throat and diaphoresis. He denied recent travel, but did say he was camping in the woods about two weeks prior to his symptoms. Nonetheless, he denied mosquito and tick bites. He also denied any nausea, vomiting, chest pain, shortness of breath, abdominal pain, rash, and urinary symptoms.
His past medical history was notable for a nephrectomy in 1992 for polycystic kidney disease. The patient also endorsed daily use of LSD, dextroamphetamine/amphetamine (Adderall), and recently recreational diphenhydramine (Benadryl) with alcohol. He reported that he had used these substances as recently as 36 to 48 hours prior to admission, and had used them in the past with no similar reactions. He also said others used the same batch of medications and drugs he did without these symptoms. The patient denied any history of intravenous drug use. His sexual history was notable for numerous female sexual partners and unprotected intercourse. He denied any history of genital or oral lesions, ulcers, discharge, or lymphadenopathy.
The patient was febrile with a temperature of 104°F rectally during his initial ED evaluation. He appeared ill, and was hypotensive at 70/40 mm Hg. He was profoundly tachycardic with a heart rate of 143 and an oxygen saturation of 90% on room air, but not in respiratory distress with a rate of 16.
He was notably diaphoretic, anxious-appearing, agitated, and mildly confused. The rat bite wound located on the right hand appeared clean, well-healing, and was not tender, warm, or erythematous. There was no drainage.
Laboratory evaluation yielded a normal white blood cell count of 5.4 and mild thrombocytopenia at 131. A urine drug screen was only positive for cotinine, a nicotine metabolite, despite the patient's admission to the use of other recreational drugs. His serum alcohol level was zero. His basic metabolic panel and electrolytes were all within normal limits. He had a very mild transaminitis with an AST of 48 and a mildly elevated creatine kinase at 223. A urinalysis showed trace blood but no signs of infection, and was otherwise negative. His initial CRP was 9.60. An x-ray of the patient's hand showed no osseous abnormality.
The patient was given lorazepam (Ativan) for his rigors, and empirically covered with ampicillin/sulbactam (Unasyn). Acetaminophen was used to treat his fever. Aggressive resuscitation with intravenous fluids was performed given the hypotension on arrival. He was admitted to the intensive care unit for further management and workup.
The patient tested negative for EBV, HIV, adenovirus, influenza, RSV, metapneumovirus, rhinovirus, parainfluenza, gonorrhea, and chlamydia after admission. Blood cultures were drawn and showed no growth after five days. Diagnosing the patient with RBF was aided by process of elimination, literature review, and evaluation of the patient's symptoms.
The patient was discharged after receiving five days of ampicillin/sulbactam on oral amoxicillin/clavulanate for treatment of RBF. He was scheduled for follow-up as an outpatient a week after his discharge from the hospital. His symptoms had completely resolved by the time of his appointment.
The patient admitted to recent polysubstance abuse, including known hallucinogens like LSD and other stimulants. LSD intoxication has been known to resemble symptoms of schizophrenia. (Int J Neuropsychopharmacol 2013;16:2165.) This drug acts by stimulating 5-HT receptors, causing hypertension, nausea, tachycardia, tachypnea, and mydriasis, among other mostly stimulatory effects. (Int J Neuropsychopharmacol 2013;16:2165; Forensic Sci Int 2012;214[1-3]:e6.)
The patient's mental status and physiological state in this case, however, did not exactly match this classic toxidrome. His symptoms also had persisted for several days, which is atypical for LSD. His additional ingestion of alcohol and diphenhydramine, though, convoluted his presentation and produced side effects mimicking serotonin syndrome or cholinergic toxicity, QT prolongation, and rhabdomyolysis. (Conn Med 2008;72:79; Psychiatry Clin Neurosci 2012;66:244; Psychiatry Clin Neurosci 2011;65:534.) Adderall is also a stimulant that increases blood pressure and heart rate, findings not seen in this patient. Alcohol withdrawal classically presents with autonomic hyperactivity, tremors, insomnia, vomiting, transient hallucinations, psychomotor agitation, anxiety, and seizures. (Crit Care Clin 2012;28:549.)
Rat bite fever can present with variable symptoms, and is often confused for conditions such as meningococcemia, influenza, disseminated gonorrhea, Staphylococcus, and Streptococcus infections, Rocky Mountain spotted fever, brucellosis, leptospirosis, and many other viral infections, including EBV and Coxsackie. (Clin Microbiol Rev 2007;20:13; Vet Microbiol 2009;133:211.)
S. moniliformis and S. minus also frequently colonize the nasal passages and oropharynx of rats. (Clin Microbiol Rev 2007;20:13.) These causative organisms are difficult to isolate; the negative cultures in this case are common with RBF cases. An adequate history is essential in the diagnosis of RBF. Several reports have emphasized that contact with rat feces, rodent scratches, or even brief hands-on contact with rats, in addition to a rat's bite, can cause RBF. (Clin Microbiol Rev 2007;20:13; Vet Microbiol 2009;133:211; BMJ Case Rep 2009; Epub Dec 17.) There is a reported 10 percent risk of transmission following a rat bite. (Clin Pediatr 2004;43:291.)
S. moniliformis is the most common in North America, and is a pleomorphic gram-negative rod with characteristic bulbar swellings under the microscope. It is extremely fastidious, requiring microaerophilic conditions and a special medium to grow in the laboratory. (Clin Microbiol Rev 2007;20:13.) S. minus is more common in Asia, causing a disease known by many as Sodoku. This gram-negative spirochete can only be visualized with a Giemsa stain, Wright stain, or dark-field microscopy, which are not commonly done unless specifically requested by the physician. (Clin Microbiol Rev 2007;20:13.) Many new PCR techniques are being developed to help identify these organisms; unfortunately, this is not yet commonly available to most practitioners. (Microbiol Immunol 2008;52:9; Lab Anim 2002;36:200.) Sodium polyanethol sulfonate, an added anticoagulant in many culture systems, can limit the growth of S. moniliformis. (Am J Clin Pathol 1973;60:854.)
RBF caused by S. moniliformis generally presents with an abrupt fever, rigors, and migratory polyarthralgias. The incubation period on average is two to three days. (Vet Microbiol 2009;133:211.) The bite usually heals uneventfully before RBF develops. More than 50 percent of patients develop migratory polyarthralgias, and 75 percent develop a variable rash that can be maculopapular, petechial, hemorrhagic, purpuric, or desquamative. (See photo.) The rash is strongly associated with RBF and should evoke immediate suspicion of this diagnosis. Other associated symptoms are nonspecific and can include headache, nausea, vomiting, sore throat, and severe myalgias. Symptoms can be highly variable, making the diagnosis even more difficult. It should be noted that RBF caused by S. minus causes distinct findings such as a longer incubation period of 14 to 18 days, relapsing fevers with up to three to seven days of afebrile time between flares and prominent lymphadenopathy. Joint manifestations are rare in cases of RBF caused by Spirillum minus. (Clin Microbiol Rev 2007;20:13; Vet Microbiol 2009;133:211.)
The most commonly documented serious complication of RBF is endocarditis. These patients present with symptoms of RBF, and were found to have valvular disease and positive blood cultures growing S. moniliformis. (J Clin Microbiol 2007;45:3125; Indian Heart J 2013;65:442.) Many other complications of RBF have been reported, including myocarditis, systemic vasculitis, septic arthritis, pericarditis, polyarteritis nodosa, meningitis, hepatitis, pneumonia, tenosynovitis, parotitis, and focal abscesses. (Clin Microbiol Rev 2007;20:13; Vet Microbiol 2009;133:211; J Clin Microbiol 2007;45:3125; Eur J Clin Microbiol infect Dis 2006;25:791; Indian Heart J 2013;65:442.) Mortality of untreated RBF ranges from seven to 13 percent, necessitating early diagnosis and treatment of RBF. (Vet Microbiol 2009;133:211.)
RBF treatment is relatively straightforward. First-line therapy is penicillin, although S. moniliformis has shown susceptibility to many alternative antibiotics including tetracycline, ampicillin, streptomycin, tetracycline, chloramphenicol, gentamicin, cefuroxime, vancomycin, and erythromycin. (Clin Microbiol Rev 2007;20:13; Vet Microbiol 2009;133:211.) This patient was treated with ampicillin/sulbactam as an inpatient and amoxicillin/clavulanate as an outpatient, which adequately covered S. moniliformis.
RBF continues to be an elusive diagnosis, which is more common than originally thought, and can lead to significant morbidity and mortality if untreated. This condition should always be included on the differential diagnosis in the ED when a patient presents with fever, rigors, arthralgias, or rash. This is especially true if the patient has had any possible contact with rats.
Ms. Dyer is a fourth-year medical student at Ohio State University. Dr. Berg is an emergency medicine resident and Dr. King is an assistant clinical professor at Wexner Medical Center at Ohio State University.
Tuesday, August 26, 2014
Turrin, Danielle DO; Sattler, Steven DO; Amodeo, Dana DO
A 25-year-old Hispanic man presented to the emergency department with a complaint of three days of left-sided precordial chest pain. He described the pain as a constant 6/10 with pressure-like discomfort radiating to his left arm and the left side of his neck. He also experienced nausea, but denied any provocative or palliative factors. He said he had not experienced anything similar to this before.
He had no family history of heart disease, acute myocardial infarction, or sudden cardiac death. He admitted to a 1.5 pack-per-day smoking history and social alcohol use, but denied use of any illicit substances. The patient also reported a recent upper respiratory infection that had completely resolved.
The patient appeared pale, diaphoretic, and anxious. No murmurs or extra heart sounds were appreciated, and he had no chest wall tenderness, jugular venous distention, or peripheral edema. The remainder of his exam was unremarkable.
His electrocardiogram showed sinus rhythm at 66 beats per minute with diffuse T wave inversions and ST elevations greater than 1 mm in leads V1-V3. (Figure 1.) His chest radiograph was normal.
The cardiac catheterization team was activated for a presumed anterior wall MI based on his EKG findings and symptoms. The patient was placed on oxygen via nasal cannula, and labs, including cardiac enzymes, were drawn. He was given aspirin and sublingual nitroglycerin, and taken to the catheterization lab.
The patient underwent emergent left heart catheterization, ventriculography, and root aortography for presumed coronary artery disease and acute myocardial infarction. His left ventricle was found to be hypercontractile and mildly hypertrophied. Apical obliteration was present, and the apex was noted to have a spade-shape Figure 2.) The coronary arteries were normal, and no aortic stenosis was present. Trace aortic insufficiency was present, however, and the aortic root was of normal caliber. The patient was diagnosed with apical hypertrophic cardiomyopathy, or Yamaguchi Syndrome.
Two hours post-cardiac catheterization, the patient was discharged home with instructions to follow up with the cardiologist for an outpatient echocardiogram and genetic testing. The patient was also instructed to abstain from sports and other athletic activity until cleared by cardiology.
The patient did not keep his appointments with cardiology, and returned to the ED twice with the same complaint of left-sided chest pain. The patient was seen by cardiology in the ED on both occasions, and MI was subsequently ruled out.
Hypertrophic cardiomyopathy (HCM) is a heterogeneous disease of the cardiac sarcomere with a variable clinical course that is dependent on several factors, including genetics, location, and degree of left ventricular outflow obstruction. (Circulation 1995;92:1680.)
Apical hypertrophic cardiomyopathy (ApHCM) is a relatively rare subtype of HCM (J Am Coll Cardiol 2002;39:638) in which the abnormality is confined to the apex of the left ventricle, causing a nonobstructive cardiomyopathy. (South Med J 2003;96:828.)
ApHCM has been described primarily in Japanese patients but manifests in other populations with significantly less frequency. (J Am Coll Cardiol 1990;15:91.) ApHCM constitutes up to 25 percent of cases of HCM in Japanese patients and only three percent in the rest of the population. (South Med J 2003;96:828.) This is likely how ApHCM came to be called Yamaguchi Syndrome, named for Sakamoto Yamaguchi, who first described the typical features of ApHCM. (J Am Coll Cardiol 2002;39:638.)
ApHCM most commonly presents in young male patients as angina (16%), atypical chest pain (14%), palpitations (10%), dyspnea (6%), or syncope/presyncope (6%). (J Am Coll Cardiol 2002;39:638.) A variety of mechanisms are thought to contribute to anginal symptoms, including imbalances between oxygen supply and demand as a consequence of hypertrophied myocardium with normal coronary arteries. (South Med J 2003;96:828.)
These patients have some characteristic findings, including giant T wave inversions on electrocardiogram, which are most prominent in V4, and a spade-shaped left ventricular cavity at end diastole seen on ventriculography. (J Am Coll Cardiol 2002;39:638.)
Evaluation for HCM patients typically includes a transthoracic Doppler echocardiogram to determine the location and extent of hypertrophy, systolic and diastolic function, degree of obstruction if present, atrial size, and valvular abnormalities. (Circulation 1995;92:1680.)
Occasionally, 2D echocardiogram will not provide adequate information, and the patient will require cardiac MRI, which has been found to provide better overall assessment of left ventricular hypertrophy in HCM patients. (J Am Coll Cardiol 2002;39:638; Circulation 1995;92:1680.)
Cardiac catheterization and angiography are generally reserved for cases with diagnostic uncertainty or in which myocardial infarction is suspected. (Circulation 1995;92:1680.)
Sudden cardiac death is the most common cause of death in HCM patients, but ApHCM is not associated with sudden cardiac death, and has a benign prognosis for cardiovascular mortality. (J Am Coll Cardiol 2002;39:638.) Approximately one-third of ApHCM patients go on to develop complications including MI, arrhythmias, and stroke. (J Am Coll Cardiol 2002;39:638.)
Several treatment options for HCM exist, including medical therapy with beta blockers, calcium channel blockers and antiarrhythmics, pacemakers, and a myectomy. (Circulation 1995;92:1680.) Treatment is generally based on patient symptoms and whether the patient has obstructive or nonobstructive disease. (J Am Coll Cardiol 2002;39:638.) A majority (75%) of patients with HCM have the nonobstructive type. It is important to note, however, that HCM is not a static disease manifestation. It can appear at any age, and increase or decrease dynamically throughout life. (JAMA 2002;287:1308.)
Dr. Turrin is a second-year emergency medicine resident, Dr. Sattler is an emergency physician and the associate research director, and Dr. Amodeo is an academic faculty member, all at Good Samaritan Hospital Medical Center.
Tuesday, August 26, 2014
Robbins, Shari MD; King, Andrew MD
Delineating a specific cause when evaluating patients with bradycardia in the emergency department can often be difficult. Unlike tachycardia, which often accompanies sepsis, fever, dehydration, and other common presentations, bradycardia is less frequently encountered, and can provide a challenge for the emergency practitioner.
Physicians must re-examine the potential causes when a patient is refractory to initial treatments, and ensure accurate vital signs to rule out a commonly missed but easily reversible cause. Bradycardia is initially overlooked because many patients present in stable condition, and the most frequently encountered cause is physiologic bradycardia in athletes or other healthy individuals. Bradycardia may also be medication-induced, a frequent event in patients taking beta blockers. Initial vital signs in emergency departments often omit temperature because of inaccessible rectal thermometer probes and the inability to obtain oral temperatures on patients. Our patient demonstrated the need for accurate vital-sign monitoring as the initial step in management.
The patient was a 63-year-old woman with significant comorbid history including coronary artery disease, hypertension, congestive heart failure, chronic kidney disease, and ischemic cardiomyopathy. She presented to the emergency department with a chief complaint of shortness of breath and elevated blood sugar. She was a difficult historian, but was able to provide a two-day history of shortness of breath and difficulty maintaining glycemic control. She denied fevers, cough, urinary symptoms, chest pain, and leg swelling.
Initial vital signs in the emergency department were a blood pressure of 105/43 mm Hg, a pulse of 36, a respiratory rate of 16 bpm, and oxygen saturation of 100% on room air. Triage was unable to obtain a temperature orally, and she had no significant changes in mental status. Pulmonary and cardiovascular exams were without pitting edema in the lower extremities or signs of pulmonary congestion.
Her pulse stayed in the 30s, ranging from 29-38 in the first minutes following arrival, so atropine was immediately attempted twice without success. The family disclosed that she had complained of feeling hot for the past few days, and had been turning down the thermostat inside her home for three days. Family members had been wearing outerwear in the house because of the declining temperatures. A rectal thermometer probe was used, followed by a temperature-sensing Foley catheter, and determined an initial core temperature of 87°F.
The patient was then placed in a bear hugger, and underwent active and passive rewarming measures including warmed IV fluids. She was found to have a urinary tract infection, and was presumed septic in addition to profoundly hypothermic. She was admitted to the intensive care unit, where she had an acute code blue with unresponsiveness secondary to bradycardia. Her heart rate and temperature normalized after approximately 36 hours of rewarming, and she was discharged after four days without any additional rhythm or rate abnormalities.
Hypothermia is an infrequently encountered, potentially life-threatening, and reversible etiology of refractory bradycardia. Elderly individuals are at especially high risk for developing hypothermia secondary to decreased physiologic reserve, chronic diseases, and medications impeding regulatory responses in addition to social isolation According to the Centers for Disease Control, an average of 689 deaths per year are attributed to exposure to excessive natural cold, which makes this a rare but significantly life-threatening scenario when presenting to the emergency department for care. (MMWR 2005;54:173.) Common EKG changes seen in hypothermic patients include bradycardia, Osborn waves, and prolonged QT interval. Osborn waves appear as a second positive deflection on the EKG, which occurs directly after the QRS complex. (Clin Med Res 2008;6[3-4]:107.) Though not uniformly present, a 2005 study found Osborn waves present on EKGs of 80 percent of patients with temperatures less than 30°C (86°F). (Resuscitation 2005;64:133.) These patients are often refractory to treatment with nodal agents such as atropine, and respond exclusively to active and passive rewarming measures. The identification of hypothermia as the etiology of bradycardia becomes paramount in managing these patients.
Our patient's presentation was difficult because she was elderly with multiple comorbid conditions in a state of bradycardia unresponsive to treatment. It took re-evaluation, collateral information from family, and invasive temperature measurement to delineate an etiology and properly direct treatment. She could have likely suffered a negative outcome if this had not been properly detected and managed.
Dr. Robbins is an emergency medicine resident and Dr. King is an assistant clinical professor of emergency medicine, both at the Ohio State University Wexner Medical Center and the Ohio State University Medical Center East.
Tuesday, August 26, 2014
Volpe, Michael DO; Golden, Jonathan MD; Amodeo, Dana DO
A 17-year-old Caucasian man with no significant past medical history or hospitalization presented to the ED complaining of abdominal pain, bloating, and diarrhea for five days. The patient said his pain was located in his upper abdomen; it was cramping, constant, and worse when he laid down, with a 7/10 intensity.
He reported more than 10 episodes of watery, brown, non-bloody diarrhea daily since the onset of his symptoms. He said he had nausea and had one episode of non-bloody and non-bilious vomiting prior to arrival. He denied fever, chills, headache, sore throat, back pain, genital pain, weight loss, and rash. He recalled similar symptoms that occurred five months earlier that lasted for one week and resolved without intervention. He had no associated trauma, sick contacts, recent travel, or family history of abdominal problems.
The patient's vital signs were stable with a temperature of 98°F, a pulse of 80 bpm, a respiratory rate of 16 bpm, a blood pressure of 130/66 mm Hg, and an oxygen saturation of 100 percent on room air.
The patient appeared uncomfortable during the physical exam. Heart sounds were normal, and lung fields were clear bilaterally. No bowel sounds were heard. He had marked abdominal distention in the epigastric region, and the abdomen was diffusely tender, firm to palpation, and tympanic to percussion, with guarding. A fluid wave was not appreciated. His mucous membranes were moist, and his skin had good turgor.The remainder of the physical exam was normal.
Intravenous fluid was started, labs were drawn, and x-rays of his abdomen with decubitus and erect views were ordered. The patient was given morphine for pain control and ondansetron (Zofran) for nausea. The laboratory results were unremarkable except for a mild elevation in total bilirubin of 1.4 mg/dL. The x-ray showed marked constipation with moderate large bowel predominant air dilation, with the absence of gas in the rectum. (Figure 1.) A CT abdomen and pelvis with oral and IV contrast was ordered. The CT revealed significant distention of the entire colon, with a sigmoid diameter of 10 cm. A transition was seen at the rectosigmoid junction, and no air fluid levels were present. A mesenteric twist was seen at the base of the sigmoid, consistent with a sigmoid volvulus. (Figure 2.)
The patient was admitted to the pediatric in-patient service. IV piperacillin/tazobactam and metronidazole were started. A barium enema was performed, but the volvulus was unable to be reduced. (Figure 3.) A flexible sigmoidoscopy and rectal suction biopsy was performed, which was successful in decompressing the sigmoid colon. The next day, the patient had a large bowel movement, which caused significant improvement in his distention. Rectal biopsies were negative for Hirschsprung's disease. The patient's diet was slowly advanced, and the patient was discharged home after three days on a high-fiber diet to prevent constipation, which was believed to be the precipitating factor. Ultimately, the patient did not require further intervention.
Sigmoid volvulus is a rare diagnosis in the pediatric population, with only 63 reported cases in patients under 18 years of age from 1940 to 2000. The median age of diagnosis in a previous review was found to be 7 years old, with a strong male predominance of 3.5:1. (J Am Coll Surg 2000;190:717.) The etiology of pediatric sigmoid volvulus differs from that seen in the adult population. It is most commonly caused by constipation in adults, and has also been associated with a high-fiber diet in developing countries. It is believed to be caused by a redundancy of the sigmoid colon, a long mesentery with a narrow base, or a lack of fixation of the mesentery to a portion of the colon in children. Children with Hirschsprung's disease are also at risk. (J Pediatr Surg 2004;39:1434.)
Sigmoid volvulus most commonly presents with the symptoms of abdominal pain, bloating, and vomiting. Less common signs and symptoms include abdominal tenderness, diarrhea, nausea, and fever. (J Am Coll Surg 2000;190:717.) A plain film will most commonly show dilated loops of colon, and may demonstrate the coffee bean sign, referring to the two distended sigmoid compartments with the central double walls of the colon. Plain films can make a diagnosis in 35–60 percent of cases. A CT is the preferred modality for diagnosis in the emergency department, nearing 100 percent accuracy, and can exclude other causes of abdominal pain. (J Emerg Med 2013;44:611.)
Managing sigmoid volvulus in children is controversial because of its rarity. Fluid resuscitation and antibiotics should be given because of its association with bowel ischemia, gangrene, and perforation. Early consultation to surgery and gastroenterology is recommended. Nonoperative management should be considered first. Barium enema can be diagnostic and therapeutic, and was successful in reducing the volvulus in 77 percent of patients in a previous study. (J Am Coll Surg 2000;190:717.)
A flexible sigmoidoscopy is also an option, with a success rate of 78 percent, but it has a 2.4 percent risk of traumatic perforation. Nonoperative treatment has a high recurrence rate of 35 percent in children and up to 70 percent in adults. Definitive treatment is sigmoidectomy, and should be considered in most patients to prevent recurrence. (World J Surg 2010;34:1923.)
Sigmoid volvulus, though rare in children, should be considered in any patient presenting with symptoms of bowel obstruction. Early diagnosis and decompression is vital to prevent complications such as bowel ischemia, gangrene, or perforation.
Dr. Volpe is a second-year emergency medicine resident, Dr. Golden is an attending pediatric emergency physician, and Dr. Amodeo is an attending emergency physician at Good Samaritan Hospital Medical Center in West Islip, NY.
Tuesday, August 26, 2014
Hourizadeh, Joshua B. DO; Kelly, Joseph VM MD, MBA
An 81-year-old man presented to the emergency department complaining of acute onset abdominal pain, vomiting for one day, and subjective fever and chills. The patient had had non-bloody bowel movements, and was able to pass flatus. The patient said the pain started suddenly the day before, and that it was accompanied by two episodes of bilious non-bloody vomiting.
The patient had a surgical history, including bilateral inguinal hernia repair in 1974, a repeat left inguinal hernia repair in 1996, and lip cancer surgery in 2009. His vitals were normal except for a rectal temperature of 101.6°F. Physical examination was significant for abdominal distension, abdominal tenderness, guarding over the right lower quadrant and inguinal region, and hyperactive bowel sounds. Routine blood work was normal, with the exception of an elevated white blood count of 14.6, lactate of 4.4, BUN of 12, and creatinine of 0.6. Urinalysis showed a slight increase of ketones. Radiological imaging was obtained in the form of an abdominal CT that showed a bowel loop extending through the abdominal wall.
Purulent fluid was present once we entered the peritoneal cavity during an exploratory laparotomy. Investigation of the right lower quadrant identified a portion of antimesenteric wall of the small bowel located in the right inguinal hernia sac. Necrotic regions of the small bowel with perforations were noted. A palpable, movable mass was found within the necrotic regions. The hernia was closed as the area of diseased small bowel was excised.
Discovered within the excised portion of the bowel was a phytobezoar identified as an apricot that measured approximately 4 cm in length. Postoperatively and upon further questioning, the patient said he stopped wearing his dentures after the lip surgery and was placed on a puree diet. He had been eating apricots while visiting his brother the day before the pain started.
Richter first described hernias where a portion of the bowel was strangulated in 1785. (Ann Surg 2000;232:710.) Richter's hernias can progress to gangrene faster when compared with other types of hernias. They most commonly affect the ileum, but any part of the bowel can be affected. (Nyhus and Condon's Hernia. Philadelphia: Lippincott, 1989; 305.) The lumen of the hernia remains free of preventing obstruction. With no intestinal obstruction between onset, symptoms, and identification, there is more time for bowel necrosis to set in and progress.
Richter's hernias are divided into four groups. (Ann Surg 2000;232:710.) The obstructive group has symptoms of intestinal obstruction that lead to early diagnosis. The danger group is where symptoms are vague and delay identification and treatment, which increases mortality. The post-necrotic group is where perforation leads to formation of a fistula. The fourth is called the unlucky perforation group, in which a post-necrotic abscess leads to sepsis or peritonitis. (Ann Surg 2000;232:710.)
Immediate intervention is required when a Richtner's hernia is suspected. The patient's symptoms, physical examination, lab results, and CT scan in this case indicated that immediate surgical intervention was required. The patient recovered, and was discharged three days later.
Dr. Hourizadeh works at Premier Care, an urgent care office in New York, and is also a professor at New York College of Osteopathic Medicine and the New York Institute of Technology. Dr. Kelly also works at Premier Care.
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