Stuart A. Bradin, DO

A study  published earlier this year in the 

 reported that girls suffer nearly  twice as many youth soccer concussions as boys. The primary maneuver  responsible for the injury and its consequences is “the header.”

 on a group of avid young female soccer players  now suffering sustained neurologic deficits after multiple concussions may  prompt soccer moms-and dads-to ask you if this popular youth sport should be  off limits for their daughter. Or, is there a way she can play safely?

What  exactly is this severe post-concussion syndrome and how common is it? Why are  teenage girls so much more susceptible to head injury than boys? How do you  counsel a parent who says, “My daughter feels fine, and she wants to play”?

Here to discuss the research and to help you answer anxious parents’  questions is Dr Stuart Bradin. Dr Bradin is Assistant Professor of Pediatrics  and Emergency Medicine at the University of Michigan Health System in Ann  Arbor.

 
 1. Marar  M, McIlvain NM, Fields SK, Comstock RD. Epidemiology of concussions among  United States high school athletes in 20 sports. 

. 2012;40:747-755.
 2. Concussion crisis growing in girls’ soccer. Rock Center with Brian  Williams, May 9, 2012. Available at: 

http://rockcenter.msnbc.msn.com/_news/2012/05/09/11604307-concussion-crisis-growing-in-girls-soccer?lite

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Young female athletes are vulnerable to concussions and other sports-related head and neck injuries. Repeated insult may lead to permanent neurologic deficit.

Post-Concussion Syndrome in Young Female Soccer Players

While the grip of winter this year has been loosened in some locales, in others the fist is tight and will bring its annual upsurge of young patients who have croup or bronchiolitis. Croup targets the upper respiratory tract; bronchiolitis threatens the small and medium lower respiratory tract passages. Both illnesses are associated with significant morbidity and mortality in high-risk patients.

This article provides an update on the diagnosis and treatment of these 2 common pediatric diseases.



Croup, or acute laryngotracheobronchitis, is the most common infectious cause of sudden upper airway obstruction in children and of stridor in febrile children.

 Croup accounts for more than 15% of pediatric respiratory illnesses.

 Children aged 6 months to 6 years--especially boys--are affected most often: the peak incidence occurs during the second year of life. About 2% of all preschoolers have croup every year, and recurrence is common. Croup can develop at any time of the year, although it classically presents in late autumn and winter.

Although croup can be caused by bacteria (eg, 

) and atypical agents, most cases are viral. (This article will address viral croup only.) The leading cause of croup, isolated from more than 80% of positive cultures, is parainfluenza virus (types 1, 2, and 3).4 Other viruses that can cause croup include adenovirus, influenza A and B viruses, respiratory syncytial virus (RSV), and rubeola virus.

The time and manner in which the child presents may yield general clues to the cause of the viral croup. For example, parainfluenza viruses predominate in the fall, whereas RSV croup peaks in the midwinter. The most severe illness is caused by influenza A virus infection.


The pediatric airway is inherently predisposed toward obstruction.

 Because a child's airway is proportionally smaller than that of an adult, a given amount of luminal swelling reduces the airway diameter much more dramatically than it does in an adult. In infants, for example, 1 mm of subglottic edema decreases the cross-sectional area of the trachea by 50%.

The narrowest portion of the pediatric airway is the subglottic region at the cricoid cartilage.

As with most respiratory infections, acute laryngotracheobronchitis begins in the nasopharynx and spreads through the respiratory tree. Diffuse inflammation, erythema, and edema develop in the tracheal walls and are most prominent in the subglottic region at the cricoid cartilage. Any swelling (mucosal and/or submucosal) in the region of the subglottic trachea encroaches on the airway, greatly restricting airflow and causing inspiratory stridor. The vocal cords become edematous and relatively immobile.


Croup typically starts with several days of nonspecific upper respiratory tract symptoms, such as rhinorrhea, pharyngitis, low-grade fever (temperature of 38ºC to 39ºC [100.4ºF to 102.2ºF]), and cough. Within 12 to 48 hours, the cough is harsh and barky (seal-like) and is accompanied by inspiratory stridor and hoarseness. A temperature that exceeds 40ºC (104ºF) and a toxic appearance are atypical and may indicate tracheitis or epiglottitis.

The great majority of children have mild symptoms, which tend to worsen at night and when the child becomes agitated. Symptoms typically peak by the third to fifth day of illness and last for 7 to 10 days. Airway obstruction develops in a small subset of children with croup. Severe hypoxia and death from croup are rare.

Spasmodic croup begins abruptly, generally occurs at night, and has a relatively mild course. The child may have had a previous respiratory tract infection. Between 1% and 5% of children hospitalized with croup require intubation for airway management.

The diagnosis of croup is clinical: the barking cough is distinctive and easily recognized by parents and clinicians. Nonetheless, it is still important to exclude other potentially life-threatening conditions, such as epiglottitis or foreign body ingestion, that require intervention.

Radiographs of the neck can help confirm the diagnosis of croup and exclude other causes of the croup syndrome. The anteroposterior view may demonstrate subglottic narrowing--the classic "steeple sign" of croup 

). Lateral films may demonstrate an overly distended hypopharynx.

Keep in mind that in approximately 50% of children with croup, the steeple sign is not visible on radiographs (giving a false-negative result). Moreover, subglottic narrowing can be present in children who do not have croup (giving a false-positive result). This suggests that radiographs should be used judiciously in the diagnosis of croup and are best reserved for children with atypical presentations.

Croup scores are a subjective measurement of severity. The most commonly used is the Westley Score.

 Independent risk factors for respiratory failure include:

Airway management is the primary goal for children with croup. Hospitalization is indicated if any risk factors are present. Treatment has traditionally included mist therapy and inhaled epinephrine as well as corticosteroids.

. Mist has been widely used and is often the initial treatment before the child arrives in the emergency department (ED). While mist can soothe and moisten an inflamed airway, it can also increase respiratory distress by provoking anxiety and agitation in young children. Recent studies have questioned its efficacy.

. This is now standard therapy for children with moderate to severe croup. A dose of 0.5 µL of racemic epinephrine is equivalent to 5 µL/L of epinephrine (1:1000). Inhaled epinephrine works quickly and can dramatically reduce inspiratory stridor and retractions. However, as the effects of epinephrine wane – typically over 2 to 4 hours from time of administration – symptoms may begin to escalate and stridor, particularly when the child is at rest, may return. Recent studies suggest that the use of epinephrine does not mandate admission to the hospital and that children can be discharged after 2 to 4 hours of observation in the ED provided a corticosteroid has been administered and there is no return of stridor at rest or increased respiratory distress.

Children can be managed as outpatients if they are clinically stable, have no distress or stridor at rest, are not hypoxic, and have normal mentation. They also must have received a dose of dexamethasone.

 Favorable efficacy, tolerability, and cost explain why corticosteroids are the treatment of choice, even for children with mild croup. Other benefits provided by corticosteroids include a decrease in croup score and a reduced need for hospitalization. For children who do require hospitalization, corticosteroids shorten the length of stay and reduce the need for admission to the ICU.

The preferred preparations are intramuscular or oral dexamethasone and nebulized budesonide. Intramuscular and oral dexamethasone are similarly effective. The standard dose of dexamethasone is 0.6 mg/kg with a maximum of 10 mg. A single dose is usually given. However, several recent studies suggest that lower doses of 0.15 to 0.3 mg/kg work just as well. At present, however, the accepted dose remains 0.6 mg/kg.

Budesonide is also effective in the treatment of croup. However, because of the expense of nebulized budesonide and its delivery system, this agent is not used to treat patients with croup.

Bronchiolitis is one of the most common and serious viral infections to affect the small and medium airways of the lower respiratory tract in young children.

Almost 85% of all reported cases of bronchiolitis are caused by RSV. However, parainfluenza virus, adenovirus, influenza A virus, and rhinovirus can also be responsible. Bronchiolitis targets young children, particularly those aged 2 to 6 months. Most children are infected by age 3; roughly 10% have clinically diagnosed bronchiolitis during the first year of life. Bronchiolitis is a seasonal illness: the peak incidence occurs in winter and early spring.

Infection is usually mild and self-limited, although cough may linger for weeks. However, bronchiolitis is the most common cause of hospitalization among infants. Furthermore, rates of hospitalization have risen dramatically over the past 2 decades. The associated economic burden is enormous; estimated costs for direct hospital charges alone exceed $3 million annually.

In the United States, 2 of 100,000 infants die of complications related to bronchiolitis. Mortality among infants hospitalized for bronchiolitis is less than 1%; however, this rate escalates to nearly 4% for high-risk infants. Those at greatest risk for severe disease are the very young, the premature, and the chronically ill. These children tend to have small airways and poor ability to clear respiratory secretions, and they are predisposed to apnea.

 Not surprisingly, the emotional distress and anxiety experienced by the family members and caregivers of these children are substantial.

The child with bronchiolitis typically presents with a several-day history of clear, profuse rhinorrhea and congestion. Fever may be present. Over the next 3 to 4 days, cough, tachypnea, wheezing, retractions, and respiratory distress may develop. Poor feeding and decreased appetite can result in dehydration. Secondary otitis media and pneumonia may develop. Infants younger than 3 months are especially prone to apnea, which may be the only sign that the child has RSV infection. Signs and symptoms of bronchiolitis are usually most intense by the fifth day, although children are usually sick for 10 to 14 days.

Bronchiolitis is a clinical diagnosis. While the cause of infection can be identified by sending a nasopharyngeal swab for viral culture or for a rapid antigen detection test, this does not change clinical management or outcome.

Chest radiographs often reveal airway abnormalities, including peribronchial cuffing, atelectasis, and hyperinflation 

. However, their value for confirming the diagnosis or deciding on a management strategy remains controversial, since these findings do not distinguish between bronchiolitis and bacterial infection.

Most children with RSV infection experience only mild to moderate symptoms and can be managed at home. Supportive care and careful monitoring for complications are the cornerstones of therapy. Adequate hydration, supplemental oxygen to correct hypoxia, and pulmonary toilet are often sufficient. Hospitalization is indicated for children with any of the following risk factors for severe disease:
• Very young age (increased risk of apnea).

• Significant comorbidities (immunodeficiency, cardiac disease, chronic lung disease).

Hospitalization is also prudent for children whose parents may not reliably seek follow-up care.

The American Academy of Pediatrics (AAP) recommends passive immunization and prophylaxis with RSV immunoglobulin and humanized monoclonal antibody (palivizumab) in a select group of high-risk infants. The cost-effectiveness of RSV prophylaxis remains unknown, although it is associated with a reduced rate of hospitalization for respiratory illnesses in high-risk children. Vaccines to prevent RSV infection are now being developed.

Bronchiolitis management has sparked many controversies, especially concerning the effectiveness of bronchodilators, the role of corticosteroids, and the risk of serious bacterial infection in febrile infants with bronchiolitis.

Evidence for the effectiveness of albuterol in children with bronchiolitis is conflicting. A meta-analysis performed by Kellner and colleagues

 showed some benefit, while a meta-analysis by Flores and Horwitz

 showed none. Bronchodilators may not help everyone with bronchiolitis, but a subset of patients--especially those with recurrent wheezing--may benefit. If there is no response after 1 or 2 initial treatments, there is no need to continue albuterol.

Several studies suggest that racemic epinephrine might be better than albuterol when used short-term in children with moderate to severe bronchiolitis. However, recent studies show no significant difference in clinical parameters following epinephrine use versus that of albuterol or placebo. I use racemic epinephrine as a rescue medication for the hospitalized child who is not responding to albuterol.

. Studies have shown no clear benefit for corticosteroids in the treatment of bronchiolitis. However, a recent meta-analysis suggested a small but statistically significant improvement in clinical symptoms, length of stay, and duration of symptoms in hospitalized patients. Schuh and colleagues10 showed that a large dose of dexamethasone (1 mg/kg) improved clinical symptoms at 4 hours in patients with moderate to severe bronchiolitis and may also decrease hospitalization rates.

A multicenter study to determine the effectiveness of oral dexamethasone and clarify the role of corticosteroids in bronchiolitis was conducted through the federally supported Pediatric Emergency Care Applied Research Network (PECARN).

This study showed that a single dose of 1 mg/kg of dexamethasone given orally did not significantly change the rate of hospitalization, degree of respiratory distress, or later outcomes.

 Thus, the AAP does not recommend that corticosteroids be used routinely in the management of bronchiolitis.

Ribavirin, antibiotics, antihistamines, and oral decongestants have all been shown to be ineffective treatments for viral bronchiolitis.

Hypertonic saline has the potential to reduce airway edema and mucous plugging. In hospitalized patients, several studies have shown a benefit with nebulized bronchodilator administered with 3% or 5% saline compared with nebulized normal saline. Results of studies in the ambulatory or ED environment, however, have been mixed. Additional studies are in order to determine whether this therapy is truly beneficial.

. What is the risk of serious bacterial infection (bacteremia, urinary tract infection [UTI], or meningitis) in the infant who is younger than 2 months and who has concurrent bronchiolitis? The results of numerous studies suggest that the risk of concomitant UTI remains high in children younger than 2 months who contract bronchiolitis.

 showed a substantial risk of UTI in febrile infants: this rate was unchanged despite concurrent bronchiolitis. Levine and associates

 showed in a PECARN study that the risk of serious bacterial infection was high in neonates as well as in 29- to 60-day-old infants with concomitant bronchiolitis. Although febrile infants with bronchiolitis may be at lower risk for serious bacterial infection, the rate of serious bacterial infection--and UTI especially--remains significant and warrants evaluation.
 

1. Rothrock SG, Perkin R. Stridor: a review, update, and current management recommendations. Pediatr Emerg Med Rep. 1996;1:29-40.

2. Gorelick MH, Singh SB. Respiratory emergencies. In: Selbst SM, Cronan K, eds. Pediatric Emergency Medicine Secrets. Philadelphia: Hanley & Belfus; 2001:241-252.

3. Cantor RM, McQuillen KK, Dobiesz VA. Respiratory emergencies. In: Strange GR, ed. Pediatric Emergency Medicine-Just the Facts Self-Assessment & Board Review. New York: McGraw-Hill; 2004:123-127.

4. Malhotra A, Krilov LR. Viral croup. Pediatr Rev. 2001;22:5-12.

5. Linzer JF, Guthrie CG. Managing a winter season risk: bronchiolitis in children. Pediatr Emerg Med Rep. 2003;8:13-24.

6. Coffin SE. Bronchiolitis: in-patient focus. Pediatr Clin North Am. 2005;52:1047-1057.

7. Guerguerian AM, Farrell C, Gauthier M, Lacroix J. Bronchiolitis: what's next? Pediatr Crit Care Med. 2004;5:498-500.

8. Kellner JD, Ohlsson A, Gadomski AM, Wang EE. Efficacy of bronchodilator therapy in bronchiolitis. A meta-analysis. Arch Pediatr Adolesc Med. 1996;150:1166-1172.

9. Flores G, Horwitz RI. Efficacy of beta2-agonists in bronchiolitis: a reappraisal and meta-analysis. Pediatrics. 1997;100(2 pt 1):233-239.

10. Schuh S, Coates AL, Binnie R, et al. Efficacy of oral dexamethasone in outpatients with acute bronchiolitis. J Pediatr. 2002;140:27-32.

11. Corneli HM, Zorc JJ, Mahajan P, et al. A multicenter, randomized, controlled trial of dexamethasone for bronchiolitis. N Engl J Med. 2007;357:331-339.

12. Piedra PA, Stark AR. Bronchiolitis in infants and children: treatment; outcome; and prevention. http://www.uptodate.com/contents/bronchiolitis-in-infants-and-children-treatment-outcome-and-prevention. Accessed February 10, 2012.

13. Hall CB, Hall WJ. AAP Textbook of Pediatric Care. Chapter 243: Bronchiolitis. http://www.pediatriccareonline.org/pco/ub/view/AAP-Textbook-of-Pediatric-Care/394243/all/Chapter_243:_Bronchiolitis. Accessed February 10, 2012.

14. DeNicola LK. Pediatric bronchiolitis treatment and management. http://Emedicine.medscape.com/ article/961963-treatment. Updated June 21, 2011. Accessed February 9, 2012.

15. Dayan PS, Roskind CG, Levine DA, Kuppermann N. Controversies in the management of children with bronchiolitis. Clin Pediatr Emerg Med. 2004;5:41-53.

16. Levine DA, Platt SL, Dayan PS, et al. Risk of serious bacterial infection in young febrile infants with respiratory syncytial virus. Pediatrics. 2004;113:1728-1734.

Articles

Parainfluenza virus is the most common cause of croup, while bronchiolitis is usually caused by respiratory syncytial virus. Read about diagnosis and treatment of these conditions.

Croup and Bronchiolitis: Classic Childhood Maladies Still Pack a Punch

Figure - X-ray film shows endotracheal tube at tip of carina, cardiomegaly, patchy densities, and increased air in stomach.

An almost 3-year-old girl with a benign medical history was referred by her pediatrician to the emergency department (ED) because of concerns about possible pneumonia. The pediatrician reported that the patient had been normotensive despite tachycardia and tachypnea; she was also "clammy," panting, and intermittently grunting. She was afebrile.

 The patient had an episode of mild nausea, emesis, and diarrhea 6 days earlier that had resolved. Her mother reported that since then, the child had been lethargic, sleepy, and generally "not herself." The child's appetite had markedly decreased and her skin was cold and pale.

On arrival in the ED, the child was normotensive. She was in moderate respiratory distress and was grunting and moaning. She was pale, diaphoretic, and had perioral cyanosis despite normal oxygen saturation (pulse oximetry reading on room air, 100%). She had poor perfusion with cold extremities, and a delayed capillary refill (greater than 5 seconds). Her respiration rate was 50 to 60 breaths per minute.

Within 30 minutes of her arrival at the ED, the child's health had deteriorated to the point that her blood pressure could no longer be measured without Doppler ultrasonography. Tachycardia (160 beats per minute) persisted despite fluid resuscitation with nearly 50 mL/kg of normal saline and pressor support with an epinephrine drip. External jugular veins were prominent.

Cardiac examination revealed no gallop, no muffled heart sounds, and no murmur. There was no ankle edema.

The child's liver was initially palpable 4 cm below the costal margin. After fluid resuscitation, empiric antibiotic therapy, and airway control, her liver was palpable 7 to 8 cm below the costal margin.

Laboratory test results were as follows: white blood cell count, 18,300/?L; hemoglobin, 12.3 g/dL;platelet count, 317,000/?L; erythrocyte sedimentation rate (ESR), 6 mm/h (normal, 0 to 20 mm/h); C-reactive protein level, 0.1 mg/L (normal, 0.0 to 0.6 mg/L); electrolyte panel, normal; blood urea nitrogen, 26 mg/dL; creatinine, 0.6 mg/dL (normal, 0.2 to 0.6 mg/dL); aspartate aminotransferase, 88 U/L (normal, 5 to 60 U/L); alanine aminotransferase, 63 U/L (normal, 7 to 35 U/L); creatine kinase-MB fraction, 3.2 ng/mL (normal, 0.0 to 4.9 ng/mL); and cardiac troponin I level, 0.48 ng/mL (normal, 0.00 to 0.29 ng/mL).

All physical findings in this child were the result of cardiogenic shock secondary to viral myocarditis. Myocarditis usually results from viral infections. The most common are those caused by Enteroviruses (ie, coxsackievirus), adenoviruses, and influenza virus.

Manifestations of myocarditis are nonspecific. A child may initially present with flu-like symptoms or gastroenteritis. Within 1 to 4 weeks, fever, malaise, shortness of breath, tachypnea, pallor, and poorly perfused cool extremities may develop.Infants may appear critically ill, with poor feeding, fever, grunting respirations, and listlessness; symptoms of congestive heart failure are usually present. Sinus tachycardia (especially that unresponsive to fluids), jugular venous distention, weak pulses, cyanosis, poor perfusion, and hepatosplenomegaly are often found.

Chest films show cardiomegaly, interstitial pulmonary edema, or an engorged pulmonary venous pattern. In this patient's case, the chest film showed an endotracheal tube at the tip of the carina, cardiomegaly, patchy densities, and increased air in the stomach.

An echocardiogram typically shows global cardiac enlargement with poor ventricular contractility. The white blood cell count, ESR, and C-reactive protein levels may be elevated but are nonspecific.

Acute management includes diuretics and inotropic support for heart failure. The use of corticosteroids and immunosuppressive agents is still controversial. Mortality approaches 35% and transplantation may be needed for patients with end-stage cardiomyopathy.

This unfortunate child required extracorporeal membrane oxygenation support. She subsequently had a cerebrovascular accident. Three months later, she was still dependent on an assisted ventricular device in the pediatric ICU and was awaiting transplantation.

Shock is not defined by blood pressure and may exist in the presence of "normal" blood pressure. In the emergency department, blood pressure is often the last vital sign we look at. Unexplained tachycardia is the first sign of shock followed by compensatory tachypnea in response to acidosis. This is followed by signs of decreased end-organ perfusion, a change in mentation, poor urine output, and delayed capillary refill. Blood pressure will be maintained, even in children who are hemorrhaging, until over half to three quarters of total blood volume is lost. Thus, a fall in blood pressure is a very late and ominous finding: many would argue it is a premorbid finding. 

Pump failure is a primary mechanism for cardiogenic shock: decreased contractility makes adequate delivery of oxygen impossible. 

Consider myocarditis in a patient with unexplained tachycardia and tachypnea, especially if these conditions do not respond to fluid resuscitation. 

Bachur R. Shock. Cardiogenic myocarditis. In: Roback MG, Teach SJ, eds. 

Olympia R, Zaotis T, Klein J, Eppes S. Infectious disease emergencies. In: Selbst SM, Cronan K, eds. 

. Philadelphia: Hanley & Belfus; 2001:189-190. 

Selbst SM. The septic appearing infant. In: Fleisher GR, Ludwig S, eds. 

. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2002:228-230. 

Toepper WC, Barbosa J, McQuillen KK, et al. Congestive and inflammatory heart diseases. In: Strange GR, ed. 

Pediatric Emergency Medicine: Just the Facts Self-Assessment & Board Review

Cardiogenic Shock Secondary to Viral Myocarditis

A 14-year-old boy with no known medical problems was found lying unresponsive in his bedroom, vomitus on his shirt. His mother recalled that he had been drinking and urinating frequently over the past several weeks and that his clothes had been "hanging off him." The patient had missed the past few days of school because of fatigue, malaise, abdominal pain, and a general feeling of being unwell. The patient's doctor told the family that the boy had the flu, and would feel better in a few days.

When the patient was found unconscious, his mother called the emergency response team. Initial vital signs were: heart rate, 130 beats per minute; respiratory rate, 32 breaths per minute; blood pressure, 90/65 mm Hg; temperature, 37ºC (98.6ºF); weight, 55 kg.

The patient was somnolent but could be aroused and open his eyes on command. His breath had a fruity odor. His airway was patent, with no stridor. His breathing was tachypneic, with Kussmaul respirations. His skin was clammy and cool; there was no evidence of rash or injury. Capillary refill time was 4 seconds. His lips were parched and his eyes sunken. His abdomen was not distended but was diffusely tender. Bowel sounds were present in all 4 quadrants. His pupils were 3 to 4 mm bilaterally. The Glasgow Coma Score (GCS) was 12 to 13.

Results of a dipstrip registered "high" (ie, too high to register a number). There was no evidence that the patient had ingested any toxic or unusual/illicit substances.

The emergency team started the patient on oxygen, delivered via face mask. They also started 2 intravenous lines that were run wide open with normal saline as the patient was transported to the emergency department (ED). Despite these measures, the patient became responsive to pain only. His GCS had dropped to 5, and his pupils were unequal. His heart rate was 75 beats per minute, blood pressure was 135/95 mm Hg, and he had agonal respirations. On arrival at the ED, his pH was 7.02, PCO

 was 22 mm Hg, and base excess was 18 mEq/L. 

As this case illustrates, diabetic ketoacidosis (DKA)--ketoacidosis associated with varying degrees of dehydration

--can be the first sign of disease in children with diabetes. DKA is also the most common complication of diabetes.

 Its consequences are serious and can be catastrophic.

 For instance, DKA is the most common cause of hospitalization in diabetic patients younger than 20 years,

 and it is the leading cause of death in diabetic patients younger than 21 years.

 Most of these patients die of cerebral edema.

DKA, formerly considered a complication of type 1 diabetes, is now recognized in both type 1 and type 2 diabetes.

 DKA occurs in 25% to 40% of children with new-onset disease, for an overall incidence of 8 per 100 person-years.

Prevention of DKA--as well as early recognition and treatment of its complications when they do occur--is the primary goal of diabetes management in children.

Nonadherence with treatment, most problematic during adolescence, is the most common reason for DKA in children with known type 1 diabetes.

 Other contributors include stress, intercurrent illness, and limited knowledge and understanding of diabetes.

In DKA, lack of insulin prohibits cellular use of glucose. Levels of counterregulatory hormones, including glucagon, epinephrine, cortisol, and growth hormone, increase. Hepatic gluconeogenesis and glycogenolysis occur, and lipolysis in fatty acids creates ketoacids. Insulin deficiency prevents tissues from using glucose and ketones, ultimately leading to hyperglycemia and ketonemia. Glucose in the kidney tubules draws water and electrolytes into the urine, creating an osmotic diuresis that depletes both volume and electrolytes.

 Hyperglycemia, with a blood sugar level that exceeds 200 mg/dL

 Metabolic acidosis, with a pH of less than 7.30, 

 Bicarbonate level of less than 15 mEq/L (

These findings are accompanied by glucosuria, ketonuria, ketonemia, and electrolyte abnormalities,

 which lead to hyperosmolality and volume depletion. DKA is generally classified by the severity of acidosis. In mild DKA, the pH is less than 7.3 and the bicarbonate level is below 15 mEq/L. DKA is considered severe when the pH is below 7.1 and bicarbonate levels are less than 5 mEq/L.

Clinical manifestations of DKA are related to the degree of dehydration and acidosis,

 Patients with previously undiagnosed DKA may have a history of fatigue, weight loss, and polyuria and/or polydipsia for weeks before seeking medical attention.

 Often, symptoms mimic other common ailments, including gastroenteritis, appendicitis, hyperventilation, and a toxic ingestion or poisoning.

Suspect DKA in patients who have vomiting, dehydration, dyspnea, abdominal pain, effortless tachypnea, or altered mentation.

 In fact, any patient with diabetes and vomiting should be presumed to have DKA until proved otherwise.

 In young children or infants, weight loss; decreased activity or irritability with signs of dehydration; and severe, persistent candidal diaper rash suggest diabetes.

The approach to managing DKA is unique in children because of the potential for the most dreaded complication--acute cerebral edema, which affects only youngsters

 and complicates 1 in 100 episodes of pediatric DKA (

 Acute cerebral edema is lethal in 20% to 50% of children (this rate has remained constant for years).

 A third of affected children suffer serious neurologic sequelae and disability.

Although many factors historically have been considered to contribute to cerebral edema (ie, rapid intravenous hydration, a quick change in sodium or glucose levels during treatment, and young patient age

), there is no documented association between any of these and cerebral edema.

 Variations in treatment may worsen an ongoing process, but there is no evidence to suggest that cerebral edema is caused by treatment.

 The only intervention to be linked with cerebral edema is bicarbonate therapy and an increase in the severity of dehydration, as reflected by an elevation in blood urea nitrogen levels and a decrease in serum carbon dioxide pressure when the patient presents.

It has been hypothesized that cerebral edema is related to brain ischemia. Children are more affected than adults because they have higher baseline oxygen requirements. Many other theories exist, but as yet not one is fully supported by current data.

Some patients have subclinical brain edema even before treatment is initiated. Therefore, treatment may exacerbate but does not cause cerebral edema. Watch for signs and symptoms of increased intracranial pressure (eg, headache, hard to arouse, vomiting, change in mentation). Affected children need emergent CT scans of the head as well as neurosurgical consultation. Care must be taken not to hyperventilate an intubated patient. Hyperventilation decreases cerebral blood flow, which exacerbates ischemia.

Management efforts are directed at correcting dehydration, acidosis, and any metabolic derangements while minimizing adverse outcomes.

 Much controversy exists regarding optimal fluid therapy.

 Protocols vary greatly between institutions and physicians.

 The greatest controversy remains how best to administer fluids and prevent increased intracranial pressure.

 The approach I recommend is outlined in 

 Scarfone RJ, Kelly A. The recognition and management of diabetic ketoacidosis in children. 

 Jeha G, Haymond MW. Treatment and complications of diabetic ketoacidosis in children. Available at: http://www.uptodate.com. Accessed December 12, 2005.
 

 Rosenbloom AL, Hanas R. Diabetic ketoacidosis: treatment guidelines.

 Brown TB. Cerebral oedema in childhood diabetic ketoacidosis: is treatment a factor? 

 Hafeez W, Vuguin P. Managing diabetic ketoacidosis: a delicate balance. 

 Dunger DB, Sperling MA, Acerini CL, et al. ESPE/LWPES consensus statement on diabetic ketoacidosis in children and adolescents. 

 Quintana EC. Factors associated with adverse outcomes in children with diabetic ketoacidosis- related cerebral edema. 

 Baumann EE, Thorp F. Endocrine and metabolic emergencies. In: Strange GR, ed. 

Pediatric Emergency Medicine: Just the Facts.

 Levitsky LL. Symptomatic cerebral edema in diabetic ketoacidosis: the mechanism is clarified but still far from clear. 

 Glaser N, Barnett P, McCaslin I, et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. 

 Felner EI, White PC. Improving management of diabetic ketoacidosis in children. 

 Glaser NS, Wootton-Gorges SL, Marcin JP, et al. Mechanism of cerebral edema in children with diabetic ketoacidosis. 

 Lawrence SE, Cummings EA, Gaboury L, Daneman D. Population-based study of incidence and risk factors for cerebral edema in pediatric diabetic ketoacidosis. 

 Kamat P, Vats A, Gross M, Checchia PA. Use of hypertonic saline for the treatment of altered mental status associated with diabetic ketoacidosis. 

 Charfen MA, Fernandez-Frackelton M. Diabetic ketoacidosis. 

 Koves IH. The accuracy of clinical assessment of dehydration during diabetic ketoacidosis in childhood. 

 Grimberg A, Cerri RW, Satin-Smith M, Cohen P. The "two bag system" for variable intravenous dextrose and fluid administration: benefits in diabetic ketoacidosis management. 

As our children are becoming fatter, diabetes is becoming more common. Diabetic ketoacidosis (DKA) can lead to cerebral edema, a complication unique to the pediatric population and a common cause of death in this young group.

Stuart A. Bradin, DO

Articles

Post-Concussion Syndrome in Young Female Soccer Players

Croup and Bronchiolitis: Classic Childhood Maladies Still Pack a Punch

Cardiogenic Shock Secondary to Viral Myocarditis

Diabetic Ketoacidosis in Children: