Transitions Conference

This patient has osteomyelitis of the distal femur. Osteomyelitis, which is a pyogenic infection of the bone, occurs via hematogenous seeding (most common in children), seeding from a contiguous source of infection (eg, diabetic foot ulcer), or direct inoculation (eg, puncture wound, orthopedic procedure). Children will most often present with acute osteomyelitis (< 2 weeks) with signs of systemic infection such as fever and irritability in addition to localized bone pain and swelling. Adults commonly present with subacute or chronic osteomyelitis, and will have pain, swelling, as well as non-healing ulcers more frequently than they will have fever. Plain radiographs are the initial imaging choice in patients with osteomyelitis, though fewer than one third of patients will have any abnormalities in the first seven to ten days of admission. Periosteal reaction is the earliest osseous finding. The most common infecting organism in osteomyelitis for healthy hosts in all age groups except neonates is Staphylococcus aureus. Patients with sickle cell have an increased risk of osteomyelitis overall, especially from Salmonella spp. Additionally, Salmonella spp. are the most common pathogen identified in sickle cell patients with osteomyelitis. Pseudomonas (C) infection should be considered in the setting where osteomyelitis develops following a penetrating injury through a surface colonized with pseudomonas (e.g. the sole of a shoe). Haemophilus spp. (A) used to be the second most common cause of osteomyelitis, however this is no longer true secondary to the advent of the Haemophilus vaccine. Klebsiella spp. (B) and other anaerobes are rarer causes of osteomyelitis and are more frequently associated with chronic osteomyelitis, as in diabetic patients with non-healing foot ulcers.

This patient is presenting with signs and symptoms associated with pyloric stenosis. Pyloric stenosis is caused by the idiopathic hypertrophy and elongation of the pylorus causing gastric outlet obstruction. Pyloric stenosis is best diagnosed with abdominal ultrasound. Risk factors for the development of pyloric stenosis include male sex, being firstborn, and exposure to erythromycin as a neonate. Patients with pyloric stenosis generally present within the first 3 to 6 weeks of life. Signs and symptoms include projectile nonbilious emesis with persistent hunger after vomiting. There may be a palpable olive-shaped mass in the epigastrium or right upper quadrant of the abdomen; however, it is not often palpable due to patient crying during the exam. Management of pyloric stenosis is with surgical pyloromyotomy.

A CT of the abdomen (B) is generally not necessary to make the diagnosis of pyloric stenosis as it is typically easily seen with ultrasound alone. Ultrasound is also more desirable as it does not expose the child to radiation and is non-invasive. An upper GI series (C) is used to diagnose malrotation and midgut volvulus, which presents with bilious emesis. The image produced shows a corkscrew appearance of the oral contrast, revealing the diagnosis. An X-ray of the abdomen (D) is often sufficient to diagnose necrotizing enterocolitis, which presents with pneumatosis intestinalis and feeding intolerance in neonates.

This child is presenting with signs and symptoms associated with Hirschsprung disease, also known as congenital aganglionic megacolon. Hirschsprung disease is caused by the lack of ganglion cells in the colon, leading to increased muscle tone and contractility of the aganglionic segment. The majority (75%) occur in the rectosigmoid segment. The most common presenting complaint is delayed passage of meconium, greater than 48 hours after birth. Other signs and symptoms include diminished stool frequency, abdominal distension, and bilious emesis (late finding). Hirschsprung disease may be diagnosed with barium enema (reveals a cone-shaped transitional zone), rectal manometry (reveals lack of anal sphincter relaxation), or definitively on rectal biopsy. Definitive management of Hirschsprung disease is via resection of the aganglionic segment.

Incomplete rotation of intestine around superior mesenteric artery and abnormal attachment of the abdominal mesentery (A) to the abdominal wall and ligament of Trietz is the mechanism by which malrotation and midgut volvulus occurs. Ectopic gastric mucosa (B) is the most common form of ectopic tissue found within Meckel’s diverticulum and frequently ulcerates causing patients to present with painless rectal bleeding. Pyloric sphincter hypertrophy (D) is the mechanism by which pyloric stenosis occurs.

This child is presenting with signs, symptoms, and imaging findings consistent with malrotation and midgut volvulus. Management of malrotation with midgut volvulus is with fluid resuscitation, nasogastric tube decompression, and definitively with surgical correction. The etiology of malrotation is incomplete rotation of the intestine around the superior mesenteric artery (SMA). This happens secondary to abnormal attachment of the mesentery to the abdominal wall and ligament of Treitz. In the end, malrotation causes volvulus, which occurs when the SMA is strangled by the intestine and causes midgut ischemia. Patients present with midgut volvulus 75% of the time before the age of one year. Signs and symptoms of malrotation with midgut volvulus are that of complete small bowel obstruction and include bilious emesis, abdominal pain, and abdominal distension. Blood in the stool is a late finding, suggesting gut ischemia. Sepsis and shock may occur with necrotic bowel. Diagnosis of malrotation with midgut volvulus is made on upper GI series, which reveals a “corkscrew” appearance of the contrast.

Air enema (A) is the first-line treatment for intussusception. Broad spectrum intravenous antibiotics (B) would be appropriate if you suspected perforation. Sigmoidoscopy (C) is the treatment of choice for sigmoid volvulus.

Hypoglycemia in neonates and infants should be taken seriously has symptomatic neonatal hypoglycemia is associated with brain injury and poor intellectual performance later in childhood. A high suspicion for hypoglycemia should be maintained as symptoms are nonspecific. Neonates can present with jitteriness, hypotonia, altered mental status, cyanosis, poor feeding, hypothermia, seizures, or coma. Older children may present with tachycardia, tachypnea, diaphoresis, or anxiety. The etiology of hypoglycemia in infants includes decreased oral intake, high ratio of insulin to counter-regulatory hormones including secondary to growth hormone deficiency and adrenal insufficiency, inborn errors of metabolism, and sepsis. Hypoglycemia is diagnosed with rapid bedside glucose testing and treatment should be initiated promptly before other studies are complete. However, when possible, extra tubes of blood should be drawn prior to administration of dextrose for possible further workup by the pediatric endocrinologists. The presence or absence of ketonuria can also help differentiate causes of hypoglycemia. Treatment thresholds for hypoglycemia vary slightly in the first days after birth, but generally are < 45 mg/dL in symptomatic patients and < 35 mg/dL in asymptomatic patients. If the hypoglycemia is thought to be secondary to an inborn error of metabolism, glucose should be maintained above 70 mg/dL. First-line treatment for hypoglycemia is bolus dosing of IV dextrose 0.5 g/kg in any of a number of regimens, with preference for larger volumes of less-concentrated dextrose to reduce venous injury. These regimens can be remembered by the “rule of 50s,” in that the product of the concentration of dextrose and volume per kilogram should equal 50. Neonates and infants should be given 10% dextrose at 5 mL/kg IV bolus, toddlers and children should receive 25% dextrose at 2 mL/kg IV bolus, and adolescents can be given 50% dextrose at 1 mL/kg IV bolus. Maintenance dextrose should the be started with 10% dextrose at 6–8 mL/kg/hr IV. For patients without IV access, glucagon can be given at 0.3 mg/kg intramuscularly. Glucagon is additionally beneficial as it can help determine the etiology of the hypoglycemia. If serum glucose increases with glucagon, there are appropriate hepatic glycogen stores and the problem is likely a hormonal deficiency. A lack of an appropriate increase in serum glucose indicates poor hepatic glycogen stores. Additionally, if there is concern for adrenal insufficiency as the cause of hypoglycemia, hydrocortisone should be given. Lastly, there should be a high index of suspicion for sepsis in hypoglycemic neonates and infants, and broad-spectrum IV antibiotics should be considered in these children if they are ill-appearing or have altered mental status.

25% dextrose at 2 mL/kg IV bolus (B) is an appropriate dose as it meets the “rule of 50s,” however, it is a highly concentrated solution and has a high risk of causing venous injury. Neonates and infants should receive a bolus of 10% dextrose at 5 mL/kg. 5% dextrose at 5 mL/kg IV bolus (C) is too small of a dose and is too dilute to be an effective therapy in this symptomatic hypoglycemic patient. Using the “rule of 50s,” this regimen would only provide half the insulin needed to treat this patient’s hypoglycemia. Additionally, dextrose 5% should not be used for bolus dose treatment of hypoglycemia. It is indicated for maintenance fluids in normoglycemic patients to prevent hypoglycemia, especially while they are being kept NPO in the hospital. Glucagon 0.3 mg/kg intramuscularly (D) can be used to treat hypoglycemia but generally should be reserved for patients without IV access. While there are some benefits to glucagon in that it can be both therapeutic and diagnostic of the etiology of hypoglycemia, IV dextrose remains first-line therapy when IV access is present, as in this patient.

Pediatric patients are at an increased risk of spinal cord injury without radiographic abnormalities (SCIWORA) as compared to adults. SCIWORA was originally defined as clinical evidence of a spinal cord injury (e.g., neurologic deficits, including transient deficits) without abnormalities on cervical spine CT or flexion-extension X-rays. More recently, with the use of MRI, we have found that most SCIWORA patients have visible acute spinal cord injuries, including those with transient symptoms and normal neurologic exams by presentation. Pediatric patients are at higher risk for SCIWORA secondary to larger head-to-body ratios, more elastic spinal ligaments, shallow vertebral facets that predispose to subluxation, as well as higher spinal canal diameter-to-spinal cord diameter, allowing movement of the cord within the canal. As such, it is important to maintain a high index of suspicion for spinal cord injuries in pediatric patients with significant mechanism (e.g., axial loading, high-risk motorized vehicle collision), or those with neurologic symptoms and normal preliminary spine imaging. Pediatric patients are also at higher risk for higher-level cervical spine injuries. As the head-to-body ratio decreases with age, the cervical spine fulcrum moves from C2–C3 at birth to C5–C6 by approximately 8 years of age.

Injury to C6–C7 (B) is more common in adults, as their smaller head-to-body ratio lowers the fulcrum in their cervical spine. Young children, less than 8 years old, are more likely to have higher cervical spinal injuries, as described above. Injury to spinal cord at T4–T5 (C) would cause symptoms at and below that spinal level. The arms are innervated by nerves arising from the brachial plexus, which originates from nerve roots C5–T1. Therefore, an injury below T1 (e.g., T4–T5) would not cause upper extremity paralysis or numbness. Normal MRI (D) would not likely be seen, as this patient had neurologic deficits, albeit transient. As discussed above, the majority of pediatric patients with high-risk mechanisms for cervical spine injury, even transient neurologic deficits and normal cervical spine CT scans, have been found to have cervical spinal cord injuries on MRI.

Child abuse is a common and serious emergency department diagnosis accounting for between 2% and 10% of pediatric ED visits. It is an important diagnosis to recognize, both for the safety of the child and due to mandatory physician reporting in all 50 states. Historical clues as well as injury patterns can help the clinician differentiate unintentional trauma and intentional trauma. Bruising in a child less than 6 months of age has a very high likelihood of being related to intentional trauma. Patients under 6 months are nonmobile and therefore unlikely to fall or pull objects onto themselves. This falls into the TEN-4 mnemonic (bruising to the torso, ears, neck or under 4 months), which has a sensitivity of 97% in detecting intentional trauma. Young age is the most significant risk factor for intentional trauma.

Intentional bruises are more likely to be found in clusters, on the back, and in symmetric patterns versus anterior and isolated bruising such as on the central forehead (B), which can commonly occur from falls during early ambulation. Burns to the face and neck (C) can be seen in children who are cruising (8–16 months) as they unintentionally pull hot objects down. Spiral tibia fracture (D), also known as a toddler fracture, is an unintentional fracture with a twist and fall mechanism in children 9 months to 3 years. Toddler fractures typically present with refusal to bear weight.

This patient presents with signs and symptoms concerning for an obstruction secondary to a volvulus and requires emergent surgical evaluation. Malrotation is a relatively common occurrence (1 in 500 live births) and about 75% of patients with malrotation will develop volvulus. During embryonic development, rotation of the gut arrests. This allows for the small bowel to twist around the superior mesenteric artery causing an acute obstruction. Patients will present with sudden onset of abdominal distension and bilious emesis. These infants will be ill-appearing and possibly toxic on presentation. Although a number of diagnostic modalities can be employed for definitive diagnosis, the priority in an ill-appearing infant with bilious emesis is emergent surgical consultation. All other interventions risk delaying definitive management. While waiting for the surgical consultation, the patient should have an IV placed, fluid resuscitation begun and a nasogastric tube placed for decompression of the stomach. Additionally, broad spectrum antibiotics should be administered. After consultation, an upper GI series may be obtained for definitive diagnosis.

Stool cultures (B) are useful when there is a suspicion for infectious process such as a parasitic or bacterial infection. Laboratory studies (C) will provide limited data and should not delay definitive management by a surgeon. The patient should receive intravenous hydration, not oral rehydration (D) as there is a high likelihood that this patient will be taken to the operating room. As such, the patient should be kept NPO.

Intussusception is when part of the intestine telescopes into itself. Ileocolic intussusception is the most common type which occurs when the small intestine prolapses through the ileocecal valve. It usually occurs in children under the age of 2 years with a peak incidence between 6 and 9 months. It can, however, occur at any age, especially if there is a lead point such as a Meckel’s diverticulum or a polyp. The classic presentation of abdominal pain, bilious emesis, an abdominal mass, and blood in the stool is rare. Most toddlers present with colicky abdominal pain and one or two of the other symptoms to aid in the diagnosis. Infants, in particular, may present with only lethargy and vomiting often being confused with sepsis. In premature neonates it can be easily confused with necrotizing enterocolitis. Most ileocolic intussusception can be successfully treated nonoperatively with an air enema if identified and reduced within 48 hours. Recurrence is rare but typically occurs within the first 48 hours and, if primarily successful, an air enema can be repeated. A small bowel intussusception is treated somewhat differently as it is less likely to respond to an air enema and more likely to spontaneously reduce.

The clinical manifestations of meningitis (B) typically include fever. Vomiting is also a possibility but it is not bilious in nature as seen in our patient. The presence of guaiac positive stool also is not consistent with meningitis. Intracranial subdural hematoma from non-accidental trauma (C) or a toxic ingestion (D) should be considered in patients this age with nonbilious vomiting and lethargy, however findings of bilious vomiting and guaiac positive stool makes intussusception more likely in this patient.

This child is presenting with signs, symptoms, and imaging findings consistent with malrotation and midgut volvulus. Diagnosis of malrotation with midgut volvulus is made on an upper gastrointestinal series, which reveals a “corkscrew” appearance of the contrast. Abdominal X-ray may show a “double-bubble” sign, but it is not a definitive study as this may also be seen in duodenal atresia. The etiology of malrotation is incomplete rotation of the intestine around the superior mesenteric artery (SMA). This happens secondary to abnormal attachment of the mesentery to the abdominal wall and ligament of Treitz. In the end, malrotation causes volvulus, which occurs when the SMA is strangled by the intestine and causes midgut ischemia. Patients present with midgut volvulus 90% of the time before the age of one year. Signs and symptoms of malrotation with midgut volvulus are that of complete small bowel obstruction and include bilious emesis, abdominal pain, and abdominal distension. Blood in the stool is a late finding, suggesting gut ischemia. Definitive management of malrotation with midgut volvulus is with surgical correction.

Abdominal ultrasound (A) is used in diagnosing intussusception or pyloric stenosis. It can also be used in children to diagnose appendicitis. CT scan of the abdomen (B) is usually a secondary study in children when you are still concerned after a primary (less invasive) study is inconclusive. X-ray of the abdomen (D) is used to evaluate for free air or pneumatosis intestinalis.