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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.

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Tuesday, January 20, 2015

By Mikhail Elfond, DO; Esi Quayson, MD; & Joseph V.M. Kelly, MD, MBA

 

A 65-year-old man presented to the ED via EMS with symptoms of stroke. The paramedics stated his right-sided weakness and speech difficulty started 40 minutes prior to presentation in the ED. En route to the hospital, paramedics observed four episodes of facial twitching.

 

 

Vitals signs were significant for a rectal temperature of 100.2°F and a fingerstick blood sugar of 220 mg/dL. History of present illness was significant for a diagnosis of left otitis media treated with Augmentin and Vicodin at an urgent care center one day prior to presentation. Past medical history included hypertension, hypercholesterolemia, and diet-controlled borderline diabetes mellitus.

 

He appeared confused and did not follow commands. He had a right lateral gaze, a right pronator drift, and global aphasia. Left tympanic membrane was perforated with purulent discharge. No mastoid tenderness or overlying skin changes were noted.

 

A head CT scan without contrast was performed, and revealed an ill-defined low attenuation lesion within the posterior left temporal lobe with associated pneumocephalus. Given ipsilateral opacification of the mastoid air cell and middle ear, findings were concerning for otomastoiditis complicated by intracerebral abscess. A follow-up maxillofacial CT scan with contrast showed thinning of the overlying roof of the temporal bone with dehiscence at multiple locations. A focus of associated pneumocephalus was identified. No definite abnormal parenchymal enhancement was identified, but the findings were consistent with intracerebral abscess complicating otomastoiditis.

 

Laboratory studies including complete blood count with differential showed WBC 11.54 with 88.2% neutrophils. Pre-operative labs and blood cultures were drawn; the patient was given Levetiracetam, ceftriaxone, and vancomycin, and taken to the operating room by neurosurgery and ENT.

 

A left ear culture grew Pseudomonas oryzihabitans and Streptococcus pneumoniae. An intracranial abscess grew S. pneumoniae. The patient did well post-operatively, and was discharged home on IV antibiotics.

 

A brain abscess is a focal, suppurative collection in the brain parenchyma resulting from an infection, trauma, or neurosurgery. Approximately 1,500 to 2,000 cases of brain abscesses are diagnosed in the United States annually, with an estimated one in 10,000 being hospitalized. (Int J Infect Dis 2006;10[2]:103.) Rates are higher in certain high risks groups, including patients with HIV/AIDS. (N Engl J Med 2014;371[5]:447.)

 

Bacterial invasion is from direct or hematogenous spread. Direct spread makes up 20 to 60 percent of all abscesses, which are caused by otitis media, mastoiditis, dental and other oropharyngeal diseases, or sinusitis, and usually result in a single abscess. (Laryngoscope 1998;108[11]:1635.) Ear infections are decreasing as a cause of brain abscesses in developed countries, but sinus infections continue to be an important consideration. (Laryngoscope 1998;108[11]:1635.) When infection spreads from the mastoids or middle ear to the CNS, the cerebellum, temporal lobes, or both are most often involved. (Laryngoscope 1998;108[11]:1635.) The most frequently isolated pathogen in acute mastoiditis is S. pneumoniae, with a prevalence of approximately 30 percent with minimal variation worldwide. (Laryngoscope 1998;108[11]:1635; QJM 2002;95:501.)

 

Common symptoms and signs include headache in 70 percent of cases, mental status changes in 65 percent, focal neurological deficits in 65 percent, fever in 50 percent, seizures in 25 to 35 percent, nausea and vomiting in 40 percent, nuchal rigidity in 25 percent, and papilledema in 25 percent. (N Engl J Med 2014;371[5]:447; QJM 2002;95[8]:501.)

 

The classic triad of fever, headache, and a focal neurological finding is only present in 20 percent of patients. Fever is absent in about 50 percent of patients with brain abscess at the time of the initial presentation. (N Engl J Med 2014;371[5]:447; QJM 2002;95[8]:501.) A lesion in the temporal lobe may lead to an ipsilateral headache, aphasia, and possibly a visual field defect. Hematogenous spread from bacteremia usually leads to multiple abscesses, usually in the territory of the middle cerebral artery. (N Engl J Med 2014;371[5]:447; QJM 2002;95[8]:501.)

 

As many as 85 organisms have been cultured from blood, CSF, or infection sites of patients with brain abscesses. The most common organisms are Streptococcus spp and Staphylococcus spp. (N Engl J Med 2014;371[5]:447.) A meta-analysis by Brouwer, et al. found Pseudomonas spp in only two percent of all cultured bacteria. P. oryzihabitans is rare and opportunistic, and is an interesting isolate in our case. It is most commonly associated with catheters, other foreign body causes of bacteremia, and is interesting because this patient had no previous implantation of surgical objects. (Microb Ecol 2011;62[3]:505.)

 

 

Case fatality rates from brain abscesses have decreased from 40 to 10 percent, with rates of full recovery increasing from 33 to 70 percent over the past 50 years. These improvements have been attributed to advancement in antibiotics, stereotactic biopsies, and advanced imaging techniques such as MRIs and CT scans. (N Engl J Med 2014;371[5]:447.)


 

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Wednesday, January 07, 2015

By Mikhail Elfond, DO, & Joseph V.M. Kelly, MD, MBA

 

A 63-year-old woman presented to the ED via ambulance with complaint of a draining abscess from her groin that had worsened over the past day. She also reported subjective fever and chills. The patient said she first noticed the abscess two days earlier.

 

The patient had had an appendectomy in 1994 and a hysterectomy in 2000, and she had type II diabetes, hypercholesterolemia, and hypertension. The patient was not compliant with her medications, and was not sure what they were. Her body mass index was 33.2, respiration rate was 18 bpm, oral temperature was 100.5°F, pulse was 108 bpm, blood pressure was 173/94 mm Hg, and pulse oximetry was 97% on room air. Physical examination was significant for a foul-smelling draining abscess in the perineal region that was tender, erythematous, and edematous with crepitus surrounding the site of drainage and copious amounts of pus that were expressed with light pressure during palpation.

 

Laboratory results were significant for a blood glucose level of 395 mg/dL and a white blood count of 20.3 cells/ml. A CT scan of the abdomen and pelvis with contrast showed multiple foci of air in the right lower anterior pubic region that was suspicious for a gas producing infection.

 

 

The diagnosis of Fournier’s gangrene was confirmed, and the patient was immediately started on broad-spectrum IV antibiotics, insulin, and IV fluids.

 

The patient was transferred to surgery where, after consulting with urology, a decision was made to perform a radical debridement of necrotic tissue and to drain the area surgically. The patient was stabilized after debridement and released from the ICU. The patient underwent reconstructive surgery, and was released three weeks after admission. The patient also received education on managing her chronic conditions. Because of immediate identification and intervention, the patient recovered.

 

Fournier’s gangrene is a rare form of necrotizing fasciitis with rapid onset and progression. Venereologist Jean Alfred Fournier was the first to describe a rapidly progressing case of necrotizing fasciitis in 1883. (AJR Am J Roentgenol 1998;170[1]:163.) This form of necrotizing fasciitis is caused by anaerobic and aerobic microorganisms. The infection often begins as a simple cellulitis from a defect or break in the skin of the perineal or genital region, providing entry for bacteria. Because of the aggressive nature of the bacteria, even with early intervention, mortality rates remain high.

  

Multiple organisms can be present in the infection and may act synergistically, encouraging growth. The most common bacteria present are Escherichia coli, Bacteroides, Proteus, Staphylococcus, Enterococcus, Streptococcus, Pseudomonas, Klebsiella, and Clostridium species. (EMN 2005;27[5]:24.) The byproducts of an anaerobic metabolism lead to soft tissue gas formation that is composed of hydrogen, hydrogen sulfide, and nitrous oxide.  (AJR Am J Roentgenol 1998;170[1]:163.)

 

It is important that surgical debridement be performed as soon as possible once Fournier’s gangrene is identified. Diagnosis can be made through physical examination, blood tests such as a CBC, imaging such as sonograms and CT scans that can provide evidence of the extent of subcutaneous infection, and a thorough history to help establish comorbidities such as diabetes, alcohol abuse, or immunodeficiency.

 

Treatment consists of broad-spectrum antibiotics, surgical debridement of necrotic tissue, and surgical drainage. Hyperbaric oxygen therapy is not a mainstay of treatment, but it can be beneficial and reduce mortality. (J Urol 1997;158[3 Pt 1]:837.) Primary closure of the skin is done once granulation tissue begins to form after surgical debridement. Depending on the amount of debridement, local skin flap coverage or skin grafts can be used for closure of surgical site. Differential diagnosis of Fournier’s gangrene includes cellulitis, abscess, hernia, hydrocele, orchitis, testicular torsion, balanitis, fungal infections, and vulvovaginitis. Patients should have appropriate surgical and urological follow-up.

 

Dr. Elfond is the associate medical director and director of Academic Affairs in the Department of Emergency Medicine at Nassau University Medical Center in East Meadow, NY. Dr. Kelly works at Premier Care, an urgent care office in New York.

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Wednesday, January 07, 2015

By Tamara Halaweh, MD, & Ashish Panchal, MD

 

A 53-year-old man with fair control of his diabetes presented with three-and-a-half weeks of scrotal pain. He reported difficulty sitting, and complained of significant dysuria and inability to initiate a urine stream. He was also constipated, but had no fevers or chills.

 

A rectal exam was consistent with an exquisitely tender and boggy prostate and significant perineal tenderness. His labs were consistent with a leukocytosis of 20,000. A CT scan with rectal contrast displayed a prostate abscess measuring 5.6 x 6.2 x 6.1 cm in maximum dimensions with extension into the puborectalis sling.

 

 

The patient was given intravenous antibiotics, and had a drain placed by Interventional Radiology transrectally. A total of 120 mL of purulent fluid was aspirated before a 10-French pigtail catheter was inserted using real-time ultrasound guidance. Culture of the aspirate grew methicillin-resistant Staphylococcus aureus (MRSA). The patient received broad-spectrum antibiotic treatment with Zosyn and ciprofloxacin in the hospital, and he did well after a month course of doxycycline. He was admitted two weeks later to the hospital for hyperglycemia and had a repeat CT at that time, which showed resolution of his prostatic abscess, and his perirectal drain was removed.

 

Prostatitis is a common presentation for emergency physicians, and a large prostate abscess was quite an unexpected finding in this patient with almost a month of symptoms prior to presentation. Prostatic abscesses have been noted in the literature previously, but none with the size demonstrated in this case. Escherichia coli and sexually transmitted infections, especially Neisseria gonorrhea, are described as the most common etiologies of prostatitis. (Harefuah 2008;147[7]:594.) A few case reports have also demonstrated the presentation of emphysematous prostatic abscesses in alcoholic diabetics and grew Klebsiella pneumoniae. (J Infect 2007;54[1]:e51.)

 

Community-acquired MRSA as the responsible organism in prostatic abscesses is seen in less than five previous case reports. (Int J Case Rep Images 2012;3[2]:20.) Few case reports discuss size and volume of aspirated fluid, with the largest being 50 mL of thick fluid with average of 12 mL depending on abscess size. (Cent European J Urol 2012;65[4]:224; J Ultrasound Med 2000;19[9]:609.)

 

With the time frame, size, and uncommon bacterial etiology, it is remarkable that the patient did not present with constitutional symptoms or even sepsis in the face of his immunocompromised status. This case provides a humbling example of how an immunocompromised patient could mask a significant infection. Had the emergency physicians treated this patient as uncomplicated prostatitis, he likely would have had a far worse outcome and delayed management.

 

Considering the presentation of complicated prostatitis, emergency physicians need to pay particular attention to a number of signs and symptoms that may indicate a possible deep space abscess. Diagnosis of this process is often difficult because it mimics lower urinary tract infections. Possible deep space infection are indicated not just by the common complaint of tender prostate but also by associated complaints of dysuria, fever, new onset symptoms of benign prostatic hypertrophy (hesitancy, weakened stream), and generalized perineal pain. (Harefuah 2008;147[7]:594.)

 

The patient did well with proper drainage and follow-up despite his late presentation. In-hospital broad-spectrum antibiotic treatment and outpatient treatment with doxycycline, with known penetration to the prostate, treated the infection to complete resolution in two weeks.

 

Dr. Halaweh is a third-year emergency medicine resident at the Wexner Medical Center at the Ohio State University, and Dr. Panchal is an assistant professor of emergency medicine, also at Wexner Medical Center.

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Tuesday, December 09, 2014

By Brian Ichwan, MD & Andrew King, MD

A 35-year-old woman with a history of congenital hydrocephalus with bilateral ventriculoperitoneal (VP) shunts, morbid obesity, and a ventral hernia after multiple abdominal surgeries presented to the ED with three weeks of abdominal pain and distention that had acutely worsened over the previous two days. Her vital signs revealed a temperature of 100.4°F, blood pressure of 107/60 mm Hg, pulse rate of 118 bpm, and oxygen saturation at 95%. Her exam was significant for a large ventral hernia with a large exquisitely tender area of erythema and necrosis with bulla formation. (Figure 1.)

 

Figure 1

 

She was emergently transferred to an associated Level I trauma center for direct admission with general surgery for her sepsis with a suspected necrotizing soft tissue infection (NSTI). She was started on IV vancomycin and cefepime, IV resuscitation, and pain medication in the ED. Her initial blood work showed WBC 27.9, lactate 3, BUN 26, and creatinine 2.13.

The time from initial assessment in the tertiary ED to the academic hospital OR was six hours. The patient underwent an exploratory laparotomy with incision and drainage. Multiple large and small bowel fistulas were found secondary to a necrotic incarcerated bowel in the ventral hernia, which was complicated with an adherent VP shunt at the abdominal end. She was admitted to the surgical ICU and underwent four additional surgeries during her admission for multiple small and large bowel resections, abdominal wall resections, VP shunt externalization, and right ventriculopleural shunt placement.

Antibiotics were broadened to piperacillin/tazobactam and vancomycin, which were subsequently narrowed to ertapenem after cultures grew Bacteroides, Prevotella, Klebsiella, and alpha-hemolyticStreptococcus. The patient ultimately recovered well with neurologic stability, and was discharged to a long-term acute care facility with complications, including having 70 percent of her abdominal wall and skin excised (Figure 2), multiple enterocutaneous fistulas, and a ventriculopleural shunt.

 

Figure 2

 

Necrotizing soft tissue infections occur by direct microbial invasion of the subcutaneous tissues by trauma or direct inoculation. The cause in this case was direct inoculation via perforated viscous. (J Am Coll Surg2009;208[2]:279.) It is a rare disease with an incidence of approximately 1,000 cases per year in the United States but a morality of greater than 25 percent. (Arch Surg 2005;140[2]:151.)

The most common etiology of NSTI is polymicrobial, which includes anaerobic, gram-negative, and gram-positive cocci. Depending on the organism, multiple different exo- and endotoxins are produced, all resulting in tissue ischemia and liquefactive necrosis that allows for accelerated soft tissue invasion. This local necrosis leads to thrombosis of a large number of capillary beds because of the local hypercoagulability, platelet plugging, and increased interstitial pressure that synergistically act to decrease end tissue perfusion. (Curr Opin Crit Care 2007;13[4]:433.) The thrombosis of perforating vessels to the skin is the key sign found in necrotizing soft tissue infections. These signs may give the unseasoned physician a false sense that there is no urgency to the situation because the underlying soft tissue infection is usually much wider than shown on the surface because large numbers of capillary beds must fail before necrotic skin changes manifest.

NSTI of the abdomen secondary to strangulated bowel perforation is extremely rare, with almost all occurring post-operatively. (Hernia2003;7[4]:220.) One case of NSTI on a lower extremity secondary to a perforated inguinal hernia was reported, and a handful of case reports have been reported on perforations causing NSTI, including rectal cancer, diverticulitis, and trauma. (Hernia 2011;15[5]:571; J Plast Reconstr Aesthet Surg 2012;65[12]:1731; J Emerg Med2008;34[1]:95, Singapore Med J 2009;50[8]:e270.) This is the first case to our knowledge of documented abdominal NSTI secondary to hernia not in a post-operative setting.

An NSTI is often misdiagnosed in the early stages, leading to the high mortality rates because of delayed or inadequate treatment. The most common sign includes tender local erythema with edema, which can easily be misdiagnosed as a non-necrotizing cellulitis. A retrospective study found that 86 percent of patients who were discharged with NSTI were initially misdiagnosed as having cellulitis or simple abscess. (Ann Surg 1996;224[5]:672.) The classic presentation is a rapidly decompensating patient with pain out of proportion associated with anxiety and diaphoresis. (Ann Surg 1995;221[5]:558.) Some patients, however, may become insensate to pain as tissue necrosis progresses and desensitizes nerve fibers.

Surgical debridement is the mainstay therapy; antibiotic therapy won't work because of the extensive tissue ischemia inhibiting adequate delivery of antibiotics to the site of infection. A delay in treatment of as little as six to 12 hours has been shown to contribute to high morbidity and mortality. Many patients will develop a massive systemic cytokine response to the large microbial toxin exposure resulting in a systemic inflammatory response syndrome, which can quickly escalate to septic shock and multiorgan dysfunction. (J Bone Joint Surg Br2001;83[5]:709; World J Emerg Surg 2011;6[1]:46.) It is important for EPs to consider NSTI in the differential for skin lesions, including cellulitis and simple abscesses, with emergent and aggressive referral to surgery for debridement, if suspected.

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Friday, November 21, 2014

By Ashley Heaney, MD & Andrew King, MD 

 

A 41-year-old woman with a past medical history of chronic low back pain and migraines presented with a headache. She had had a L4-L5 epidural steroid injection performed for her chronic lower back pain, but complained of a headache immediately after the procedure. The headache was in the front of her head and associated with photophobia. She stated that she had multiple epidural steroid injections in the past with no prior post-procedure headache. She denied neck pain, vision changes, extremity numbness, or extremity weakness.

The patient had a temperature of 98.1°F, a pulse of 76 bpm, a blood pressure of 99/63 mm Hg, a respiratory rate of 16 bpm, and an oxygen saturation of 99% on room air. She was alert and oriented. Her speech was fluent, her cranial nerves were intact, and she had full strength in all extremities. She had normal sensation to dull and light touch in all extremity dermatomes, and her neurologic examination was nonfocal. She also had full range of motion of her neck with no meningismus.

A head CT was obtained, and showed pneumocephalus ventral to the pons and medulla. Pneumocephalus was also present throughout the posterior fossa. She received IV Toradol, Valium, Benadryl, and opiate pain medication with only minimal symptom relief. The patient was evaluated by neurosurgery based on the amount of pneumocephalus present on the CT scan. They recommended inpatient observation and symptom control. The patient was placed supine, and provided with supplemental oxygen and pain medications as needed. After three days, her symptoms had significantly improved, and she was able to be discharged from the hospital.

 

 

 

Headache is a frequently encountered chief complaint in the emergency department. Migraine, subarachnoid hemorrhage, dural venous sinus thrombosis, meningitis, subdural hematoma, epidural hematoma, and carotid artery dissection are all diagnoses that every emergency medicine physician must consider when evaluating a patient presenting with headache. Headaches can be the result of procedures, most commonly lumbar punctures. Cephalgia may also result from epidural puncture from injection or anesthesia. At times, pneumocephalus may result from accidental puncture of the dura mater during a procedure. Post-procedural pneumocephalus is not a frequently encountered diagnosis, and it rarely makes the differential diagnosis of headache in the emergency department.

Pneumocephalus is the accumulation of intracranial air. (Clin Neurol Neurosurg 2009;111[3]:309.) There are multiple etiologies of pneumocephalus, the most common being trauma. Other etiologies include craniotomy, injection of air during a procedure, placement of VP shunts, CSF-pleural fistula, nasopharyngeal cancer with invasion of the skull base, nasal sinus surgery with perforation of the skull base, and otogenic causes. Injection of air can occur from accidental dural puncture during epidural anesthesia, during a blood patch procedure, epidural saline infusions, or spinal anesthesia. (Can J Neurol Sci2002;29[3]:278.)

Pneumocephalus can cause a severe headache, and no direct correlation exists between the amount of air and the presence or severity of the headache. (Can J Neurol Sci 2002;29[3]:278.) It has also been shown that increasing the amount of inspired air oxygen concentration decreases the amount of time needed to absorb intracranial air, decreasing the duration of the patient's headache. This study showed that the duration of absorption of 50 ml of air decreased from 5.8 to 1.9 weeks by 40% FiO2 from 1.9 to 0.6 weeks on room air and 100% FiO2, respectively. (Anesthesiology 1996;84[2]:442.)

 

 

Several diagnoses should be added to the headache differential diagnosis in the case of a patient receiving recent epidural spinal injections. Post-procedural headache or low-pressure headache, as well as pneumocephalus, should be added to the differential. The patient can be easily placed on a face mask to expedite air resorption, and can be provided symptom control as needed. This patient was successfully managed using supplemental oxygen and analgesia.

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