Patient Presentation

An 8-year-old female came to the emergency room with a new onset seizure that was witnessed at school, when she suddenly stopped, fell towards her left side and then fell to the floor. She was not able to speak and had movements of her left upper extremities. She was given lorazepam and taken by ambulance to the local emergency room where she had left sided weakness and some abnormal eye movements noted. She was airlifted to a regional children’s center. She had a past medical history of Sturge-Weber Syndrome diagnosed because of a port-wine stain. The review of systems showed she was previously well with no seizures, headaches, auras or other neurological problems. She had no infectious disease symptoms.

The pertinent physical exam showed a child who was tired but arousable. Her vital signs were normal and her growth parameters were 10-50%. She had a port-wine nevus in the distribution of the first and second divisions of the right trigeminal nerve but it also crossed the midline. There were no obvious hemangiomas. Neurologically she had left-sided weakness of both upper and lower extremities and face. Cranial nerves were intact. Deep tendon reflexes were normal. The radiologic evaluation of a head computed tomography examination showed no changes to the previously documented right-sided leptomeningeal angioma. The work-up included normal electrolytes, calcium, phosphorous and magnesium. A video electroencephalogram showed many seizures. Ophthalmological consultation found no glaucoma or other disease. During a later patient interview, the patient said that she could remember people screaming at her during the episode. The diagnosis of Sturge-Weber syndrome and complex-partial seizures was made. She was started on Keppra®. At discharge she had mild left-sided weakness and she had started receiving physical therapy. She had had no obvious seizures for 2 days and was to continue on anti-epileptic medication.

Figure 87 - Axial image from a computed tomography scan of the brain performed with intravenous contrast shows marked enhancement of the leptomeninges in the right temporal, parietal and occipital lobes and minimal leptomeningeal enhancement in the right frontal lobe. There was mild atrophy of the right cerebral hemisphere.

Discussion
Neurocutaneous syndromes or phacomatoses are a group of congenital or hereditary diseases that develop hamartomas of various tissues and usually additional cutaneous stigmata. Most phacomatoses have quite variable phenotypical presentations for an affected individual. Those that are listed below are common for that disease process.

Learning Point
Common major phacomatosis include:

• Sturge-Weber Syndrome
  • Genetics: non-genetic
  • Neurological: seizures (often contralateral to the nevus and focal), hemiparesis (again often contralateral to the nevus), mental retardation, ophthalmological problems including glaucoma
  • Dermatological: port-wine nevus often in the trigeminal nerve’s first division, hemangiomas
  • Other clinical features: may be associated with Klippel-Trenaunay-Weber syndrome (hemangiomas with hypertrophy of the related adjacent tissues)
  • Radiological features: intracranial paired lines of calcifications often called trolley tracks caused by leptomeningeal angiomas

• Neurofibromatosis Type 1
  • Epidemiology: 1:2500-3000 - most common phacomatosis
  • Genetics: autosomal dominant with variable penetrance, associated with chromosome 17
  • Neurological: various central nervous system tumors especially neurofibromas (often benign but may act malignant because of location or size, tumors may also degenerate into a malignant variant or cause other problems such as hypothalamic problems secondary to an optic chiasm tumor ), optic nerve tumors, pheochromocytomas, mental retardation
  • Dermatological: neurofibromas, cafe-au-lait spots
  • Other clinical features: Lisch nodules of eye, other congenital anomalies may be associated including bone (rib, vertebra) and renal artery stenosis.
  • Radiological features: lesions tend to be more scattered in brain and more peripheral than tuberous sclerosis

• Neurofibromatosis Type 2
  • Epidemiology: 1-33,000-40,000
  • Genetics: autosomal dominant with variable penetrance, associated with chromosome 22
  • Neurological: bilateral vestibular nerve schwannomas, brain meningiomas and dorsal root schwannomas
  • Dermatological: various skin changes can be seen but are less consistently associated
  • Other clinical features: eye lens opacities

• Tuberous Sclerosis
  • Epidemiology: 1:5700-10,000
  • Genetics: autosomal dominant with variable penetrance, often is new mutation
  • Neurological: seizures (infantile spasms, grand mal), mental retardation, learning problems, behavior problems, autism
  • Dermatological: ash-leaf spots (depigmented spots), adenoma sebaceum (pink/yellow/brown raised nevi predominantly in butterfly distribution), shagreen patches (flesh-colored leather-like plaque)
  • Other clinical features: fibromas of other tissues include rhabdomyoma of heart
  • Radiological features: calcified periventricular lesions, lesions may also be scattered but are more central than Neurofibromatosis type 1

• von Hippel-Lindau Syndrome
  • Epidemiology: 1:40,000-50,000
  • Genetics: autosomal dominant
  • Neurological: hemangioblastomas of cerebellum, angioma of retina, presents usually because of increased intracranial pressure
  • Dermatological: relatively uncommon
  • Other clinical features: cystic lesions of other tissues and other central nervous system locations

Other phakomatosis include:

• Chédiak-Higashi syndrome
• Cutaneous Spinal Angiomatosis
• Epidermal Nevus Syndrome (Linear nevus sebaceous)
• Hereditary Hemorrhagic Telangectasis (Osler-Rendu-Weber Syndrome)
• Incontinentia Pigmenti
• Incontinentia Pigmenti Achromaians (Hypomelanosis of Ito)
• Neurocutaneous Melanosis
• Polyostotic Fibrosis Dysplasia (McCune-Albright syndrome)
• Sjögren-Larsson syndrome
• Wyburn-Mason Syndrome

Questions for Further Discussion
1. What are the size and number criteria for cafe-au-lait spots used for diagnosing neurofibromatosis?
2. What are the primary diagnostic criteria for diagnosing tuberous sclerosis?
3. What is the role of a general pediatrician and a geneticist in counseling a family about a phacomatosis?

Related Cases

Disease: Sturge-Weber Syndrome | Neurologic Diseases | Skin Pigmentation Disorders

Symptom/Presentation: Seizures | Pigmentary Lesions | Syndromes

Specialty: Emergency Medicine | Neurology / Neurosurgery | Radiology / Nuclear Medicine / Radiation Oncology

Age: School Ager

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Evidence-based medicine information on this topic can be found at SearchingPediatrics.com, the National Guideline Clearinghouse and the Cochrane Database of Systematic Reviews.

Information prescriptions for patients can be found at MedlinePlus for these topics: Neurological Disease and Skin Pigmentation Disorders.

To view current news articles on this topic check Google News.

To view images related to this topic check Google Images.

Rudolph CD, et.al. Rudolph’s Pediatrics. 21st edit. McGraw-Hill, New York, NY. 2003:769-774, 2344-2349.

Online Mendelian Inheritance in Man. NEUROFIBROMATOSIS, TYPE I; NF1. Available from the Internet at http://www.ncbi.nlm.nih.gov/omim/162200 (rev. 3/18/10, cited 5/27/10).
Online Mendelian Inheritance in Man. NEUROFIBROMATOSIS, TYPE II; NF2. Available from the Internet at http://www.ncbi.nlm.nih.gov/omim/101000 (rev. 3/31/10, cited 5/27/10).
Online Mendelian Inheritance in Man. STURGE-WEBER SYNDROME. Available from the Internet at http://www.ncbi.nlm.nih.gov/omim/185300 (rev. 2/26/10, cited 5/27/10).
Online Mendelian Inheritance in Man. TUBEROUS SCLEROSIS 1; TSC1. Available from the Internet at http://www.ncbi.nlm.nih.gov/omim/191100 (rev. 1/27/10, cited 5/27/10).
Online Mendelian Inheritance in Man. VON HIPPEL-LINDAU SYNDROME; VHL. Available from the Internet at http://www.ncbi.nlm.nih.gov/omim/193300 (rev. 8/18/09, cited 5/27/10).

ACGME Competencies Highlighted by Case

Patient Presentation
A 10-year-old female came to the inpatient floor with suspected spontaneous bacterial peritonitis. She had steroid responsive nephrotic syndrome that was intermittent (2 previous episodes). Over the past 2-3 weeks she had been having more fatigue, shortness of breath and for the last 3 days has had periorbital edema with her urine being > 3+ on urine dipstick. She re-started her prednisone 3 days ago. She began having mild abdominal pain last evening and this morning it was increased and was accompanied by nausea and emesis. The past medical history showed her last episode of nephrotic syndrome was 10 months ago. The review of systems was negative.

The pertinent physical exam showed a mildly ill-appearing female who was afebrile, blood pressure of 122/70, pulse of 100, respiratory rate of 24. Her weight was 21 kilograms up from a normal weight of 18.9 kilograms (75%). Her height was 75%. HEENT showed mild periorbital edema. Extremities appeared slightly puffy. Heart showed normal S1, S2 with no murmur. Abdomen was distended with generalized guarding. A small fluid wave was elicited, but no masses were palpable. The rest of the examination was normal.

The laboratory evaluation included a hemoglobin of 13.4 mg/dl and platelets of 432 x 1000/mm² and white blood count of 15.6 x 1000/mm², with 79% neutrophils. Her electrolytes were normal with a blood urea nitrogen of 7.0 mg/dl, creatinine of 0.4 mg/dl, total protein of 3.9 g/dl, albumin of < 1.0 g/dl, and a cholesterol of 256 mg/dl. Liver function tests were normal. Her urinalysis showed specific gravity of > 1.030, 1+ glucose and hyaline casts. The radiologic evaluation of a computed tomography examination of the abdomen was negative aside from the presence of ascites. An paracentesis was performed, and it and a blood culture eventually grew S. pneumoniae, confirming the diagnosis of spontaneous bacterial peritonitis. The patient’s clinical course showed her started on vancomycin and ceftriaxone initially and once sensitivities were known she continued on ceftriaxone for a total of 10 days of antibiotics. She received influenza vaccine in the hospital and was discharged home on prednisone to follow up in one month.

Discussion
Nephrotic syndrome is a common pediatric kidney disease affecting 16 in 100,000 children that leads to proteinuria, hypoalbuminemia, hyperlipidemia and edema. The cause is usually minimal change nephrotic syndrome (77%), focal segmental glomerulosclerosis (8%), membranoproliferative glomerulonephritis (6%) and other causes (9%).

Response to steroid therapy with normalization of urine protein levels by 8 weeks of treatment has good sensitivity and specificity of predicting minimal change nephrotic syndrome.

The nephrotic syndrome initial evaluation is recommended to include:

• All patients
  • Urine - urinalysis, urine protein/creatinine ratio (first morning)
  • Serum - electrolytes, blood urea nitrogen, creatinine, glucose, albumin, cholesterol level, complement 3 level, purified protein derivative level
• Some patients
  • Age > 10 years or with signs of Systemic Lupus Erythematosus - antinuclear antibody level
  • Age > 12 years - kidney biopsy
  • High risk populations - Hepatitis B and C levels and HIV

Prednisone is recommended for initial treatment of nephrotic syndrome. Prednisone 2 mg/kg/day for 6 weeks (with a maximum of 60 mg) and then prednisone 1.5 mg/kg every other day for another 6 weeks (with a maximum of 40 mg). Then discontinuation of prednisone is recommended.

Because of the complication risks, inactivated influenza and conjugated pneumococcal vaccines are recommended for all patients. Influenza vaccine is recommended for all household contacts too. Live vaccines are deferred until specific criteria are met, however varicella should be given in certain circumstances.

Learning Point
Spontaneous bacterial peritonitis (SBP) is a common complication associated with ascites due to various causes including nephrotic syndrome and cirrhosis. Low albumin and low complement levels are associated with SBP. In children with relapsing nephrotic syndrome the incidence is 5-17.3%.
Signs and symptoms of SBP can include any constellation of the following:

• Abdominal pain and guarding
• Abdominal distension
• Diarrhea
• Emesis
• Encephalopathy
• Fever
• Lethargy
• Poor feeding
• Sepsis

There are no reliable signs/symptoms that indicate a definitive diagnosis other than peritoneal fluid culture.

Streptococcus pneumonia is the most common organism causing SBP. Gram-negative organisms can also cause a significant amount of SBP depending on the population. One review recommends initial treatment with broad-spectrum antibiotics (Cefotaximine in particular) until culture sensitivity and specificity are known. The American Academy of Pediatrics’ RedBook® recommends that for “critically ill infants and children with invasive infections potentially attributable to S pneumoniae, vancomycin in addition to usual antimicrobial therapy (such as ampicillin, ampicillin-sulbactam, cefotaxime, or ceftriaxone) may be considered for strains that possibly are nonsusceptible to penicillin, cefotaxime or ceftriaxone.”

Questions for Further Discussion
1. What is in the differential diagnosis of ascites?
2. What are other common complications of nephrotic syndrome?
3. How common is peritonitis in patients treated with peritoneal dialysis?

Related Cases

Disease: Spontaneous Bacterial Peritonitis | Nephrotic Syndrome | Kidney Diseases

Symptom/Presentation: Edema | Infections | Mass or Swelling | Abdominal Pain | Vomiting

Specialty: Infectious Diseases | Nephrology / Urology | Pharmacology / Toxicology

Age: School Ager

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Evidence-based medicine information on this topic can be found at SearchingPediatrics.com, the National Guideline Clearinghouse and the Cochrane Database of Systematic Reviews.

Information prescriptions for patients can be found at MedlinePlus for this topic: Kidney Diseases.

To view current news articles on this topic check Google News.

To view images related to this topic check Google Images.

Gorensek MJ, Lebel MH, Nelson JD. Peritonitis in children with nephrotic syndrome. Pediatrics. 1988;81 (6):849 - 856.

Cavagnaro F, Lagomarsino E. Peritonitis as a risk factor of acute renal failure in nephrotic children. Pediatr Nephrol. 2000 Dec;15(3-4):248-51.

Leonis MA, Balistreri WF. Evaluation and management of end-stage liver disease in children. Gastroenterology. 2008 May;134(6):1741-51.

American Academy of Pediatrics. Pneumococcal Infections, In Pickering LD, Baker CJ, Kimberlin DW, Long SS, eds. Red Book: 2009 Report of the Committee on Infectious Diseases. 28th edit. Elk Grove Village, IL: American Academy of Pediatrics; 2009;529.

Gipson DS, Massengill SF, Yao L, Nagaraj S, Smoyer WE, Mahan JD, Wigfall D, Miles P, Powell L, Lin JJ, Trachtman H, Greenbaum LA. Management of childhood onset nephrotic syndrome. Pediatrics. 2009 Aug;124(2):747-57.

ACGME Competencies Highlighted by Case

Patient Presentation
A 6-year-old male came to clinic with a 2 day history of painful right eyelid swelling. His mother noticed the top lid was red, swollen in 1 discrete area and was mildly painful. He denied any problems seeing and his mother agreed that he did not have problems walking or doing other activities because of visual problems. They noticed some debris on the lashes that was crusted especially when awakening. He had not had any prior eyelid or other ophthalmological problems. The review of systems was negative for fever or other current or recent infectious diseases.

The pertinent physical exam showed a well-appearing male. Vital signs were normal and growth parameters were 50-90% for age. Visual acuity was 20:20 by Snellen chart. Extra ocular movements were intact. The left eyelid margin showed one 2-3 mm swelling with a central area that pointed outward that was slightly yellowish. There was mild erythema of the swelling and surrounding tissue. There were no other lesions noted with eversion of the eyelid. The right eye was normal as was the rest of the examination. The diagnosis of a simple external hordeolum was made. The family was instructed to do warm compresses for 15 minutes four times/day. They were to call if the swelling or pain increased, or if changes in vision or generalized symptoms such as fever developed. They were also instructed to call if the hordeolum did not appear to be improving in about 3 days.

Discussion
There is confusion with the terms stye, hordeolum and chalazion because of the general public usage and the most precise medical usage. Even in the more precise usage, there is difficulty because of the overlap in the anatomy.

Hordeola and chalazia can be caused by blepharitis or generalized eyelid inflammation. A differential diagnosis of blepharitis can be found here.

Learning Point
Stye is a term used often by the general public to denote a small localized swelling/inflammation of the eyelid.

A hordeolum (or a stye) is term used by the medical profession to denote a localized inflammation and/or infection of the hair follicles of the eyelid or the meibomian glands. It is usually an acute problem but can be recurrent. These are usually somewhat painful with erythema and the entire general eyelid may be edematous. Generalized cellulitis can also occur. In 90-95% of cases, Staphylococcus aureus is the cause. Treatment is mainly with warm compresses (four times/day), but sometimes incision to aid drainage is needed. Topical antibiotics may be helpful for recurrent or actively draining hordeola. Ophthalmologic consultation is recommended if not improving in 2-3 days.

• External hordeolum - a hordeolum of hair follicles that usually has its leading edge pointing externally to the eyelid. It affects the sebaceous glands of Zeis or the apocrine sweat glands of Moll which both service the hair follicles. There is often purulent material on the eyelashes and lid margin.
• Internal hordeolum - a hordeolum of the meibomian glands lying within the tarsal plates that usually has its leading edge point internally to the eyelids. Purulent material may be seen on the conjunctival surface of the eyelid.
• Hordeola may also be bi-directional.

A chalazion is a term used by the medical profession to denote a swelling caused by blockage of sebaceous glands and formation of granulomas. It usually occurs in the meibomian glands in the tarsal plates, but also can occur in the sebaceous glands of Zeis. It is a chronic problem and it is usually painless. Internal hordeola may lead to chalazia. Chalazia can become quite large and put pressure on the cornea and thereby cause visual changes.
Chalazia usually are treated with warm compresses (4 times/day). Washing the eyelashes with a baby shampoo may also help with lid hygiene and improves control of seborrheic dermatitis if present. Antibiotics are usually not used unless there is an additional secondary infection. Ophthalmologic referral is usually made after 2 weeks and treatment at that time may include surgical drainage or steroid injection.

Questions for Further Discussion
1. What are indications for ophthalmology consultations?
2. When can a child’s visual acuity be evaluated in a health supervision visit?

Related Cases

Disease: Hordeolum | Eye Lid Disorders

Symptom/Presentation: Mass or Swelling | Eye Pain

Specialty: General Pediatrics | Ophthalmology

Age: School Ager

To Learn More

To view pediatric review articles on this topic from the past year check PubMed.

Evidence-based medicine information on this topic can be found at SearchingPediatrics.com, the National Guideline Clearinghouse and the Cochrane Database of Systematic Reviews.

Information prescriptions for patients can be found at MedlinePlus for this topic: Eyelid Disorders

To view current news articles on this topic check Google News.

To view images related to this topic check Google Images.

Bessette MJ. Hordeolum and Stye. eMedicine.
Available from the Internet at http://emedicine.medscape.com/article/798940-overview (rev. 2/24/2010, cited 5/24/2010).

Fansler JL, Schraga ED, Santen S. Chalazion. eMedicine.
Available from the Internet at http://emedicine.medscape.com/article/797763-overview (rev. 4/27/2010, cited 5/24/2010).

Dictionary.com. Chalazion - http://dictionary.reference.com/browse/chalazion,(cited 5/24/2010)

Dictionary.com. Hordeolum - http://dictionary.reference.com/browse/hordeolum,(cited 5/24/2010)

ACGME Competencies Highlighted by Case

Patient Presentation
A 25-month-old male came to the emergency room with increased somnolence and breaththrough seizures.
The patient had known congenital hydrocephalus secondary to neonatal meningitis, and usually had well-controlled generalized tonic-clonic seizures on Keppra®.
He had increasing somnolence for 24 hours and 2 seizures in the last 6 hours. He was able to eat and drink with no emesis, and his mother said that he would awaken but was more irritated. He did not complain of pain and had no infectious disease symptoms.
The past medical history showed no previous shunt revisions, but evaluations for possible shunt malfunction had happened 3 times in the past.

The pertinent physical exam showed a small but normal appearing male who was sleeping in his mothers lap. Heart rate was 130 beats per minute with a normal blood pressure and temperature. Growth parameters were 10-25%. HEENT showed 3 mm reactive pupils and a ventriculoperitoneal shunt on the right side. With palpation, no discontinuity of the shunt was noted in the head or neck. Abdomen showed a small scar in the mid right abdomen that was well healed. Abdomen was soft without obvious masses or distention. Neurological examination revealed cranial nerves 3-12 were intact, and deep tendon reflexes were slightly increased in upper and lower extremities with 2 beats of clonus in the feet, consistent with previous examinations. He was easy to arouse but very cranky and wanted to return to sleep. The diagnosis of probable shunt malfunction was made. The radiologic evaluation of a head computed tomography exam showed a discontinuous proximal shunt at the angle of the reservoir and ventriculomegaly. He was taken to the operating room and had the shunt replaced. He did well and was discharged home. The patient’s clinical course one week later revealed him returning to the emergency room with fever and increased somnolence. Head computed tomography at that time showed an intact shunt and he was diagnosed with a viral upper respiratory tract infection. He was well at his last follow-up appointment at 6 months.

Figure 85 - AP radiograph of the skull demonstrates the tip of the VP shunt to be disconnected from its reservoir.

Figure 86 - CT scan of the brain performed without intravenous contrast demonstrates marked dilation of the lateral, third and fourth ventricles in axial (top), coronal (middle), and sagittal (bottom) planes.

Discussion
Hydrocephalus can occur for many reasons including congenital anomalies (e.g. spina bifida, aqueductal stenosis, Arnold-Chiari or Dandy-Walker malformations), trauma, intraventricular hemorrhage and meningitis. The common pathway is cerebrospinal fluid accumulation causing pressure effects on the central nervous system. While not perfect, ventriculoperitoneal shunts allow many children with hydrocephalus to live symptom free lives and many others to have much improved quality of life. In the pre-shunt era, only 20% of children survived to adulthood and 50% had brain damage.
One major improvement was the development of the DWT pressure valve by Roald Dahl (the famous author), Stanley Wade (engineer particularly of hydraulic pumps) and Kenneth Till (first full-time pediatric neurosurgeon in Great Britain) valve (DWT)

Any medical device can have complications. For shunts these are divided into 3 categories, infective, overdrainage and mechanical.

• Shunt infections occur in 5-10% of surgeries usually within the first 3 months after surgery and more commonly in younger patients. Staphylococcus is the most common organism, and common symptoms include abdominal pain, nuchal rigidity, and swelling, drainage or erythema of the shunt site.
• Overdrainage of the ventricles can cause subdural hematomas and excessive siphoning can actually cause mechanical shunt obstruction.
• Mechanical problems can be caused by disconnection of the parts of the shunt system, breakage of the tubing, and obstructions at either end of the tubing (especially glialependymal tissue in the brain).
  Children with acute mechanical shunt malfunctions can present in several ways including headache, emesis, personality changes, papilledema and cranial nerve palsies. New onset seizures or changes in the patients normal seizure pattern should also raise concerns. Chronic malfunction may present with loss of developmental milestones, abnormally increased head growth, papilledema or optic atrophy and again changes in seizure patterns.

Learning Point
Of the shunts placed about 80% will have a need for revision with 30% of these occurring in the first year. The average child over their childhood will have 2-3 operations for shunt revisions. This would come out to be 1-1.25 shunt revision surgeries per week for a large neurosurgical practice following 500 children. The number of evaluations for possible shunt malfunction because of seizures, headaches etc. to identify a child who needs a shunt revision is even higher.

Questions for Further Discussion
1. What is the role of a general pediatrician in shunt management and evaluation for possible shunt malfunctions?
2. What are the sports and activities limitations recommended for children with shunts?

Related Cases

Disease: Hydrocephalus

Symptom/Presentation: Mental Status Changes | Seizures

Specialty: Developmental Disabilities | Emergency Medicine | Medical History | Neurology / Neurosurgery | Radiology / Nuclear Medicine / Radiation Oncology

Age: Toddler

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Evidence-based medicine information on this topic can be found at SearchingPediatrics.com, the National Guideline Clearinghouse and the Cochrane Database of Systematic Reviews.

Information prescriptions for patients can be found at MedlinePlus for this topic: Hydrocephalus

To view current news articles on this topic check Google News.

To view images related to this topic check Google Images.

Prusseit J, Simon M, von der Brelie C, Heep A, Molitor E, Volz S, Simon A. Epidemiology, prevention and management of ventriculoperitoneal shunt infections in children.
Pediatr Neurosurg. 2009;45(5):325-36.

Obituary of Kenneth Till. Guardian Newspaper. August 26, 2008. Available from the Internet at: http://www.guardian.co.uk/society/2008/aug/26/health

Conant, Jennet. The Irregulars. Roald Dahl and the British Spy Ring in Wartime Washington. Simon & Schuster. New York, NY. 2008;343.

Kramer LC, Azarow K, Schlifka BA. Management of Spina Bifida, Hydrocephalus and Shunts. eMedicine. Available from the Internet at http://emedicine.medscape.com/article/937979-overview (rev. 11/19/2009, cited 5/20/2010).

ACGME Competencies Highlighted by Case