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CVS selling low-cost generic epinephrine autoinjector
CVS Pharmacy is currently selling a generic epinephrine autoinjector for a price of $109.99 per two-pack, which is about one-sixth the cost of Mylan’s EpiPen two-pack.
The product, an authorized generic for Adrenaclick, is manufactured by Lineage Therapeutics, which is a wholly owned subsidiary of Fort Washington, Pa.–based Impax Laboratories. CVS Pharmacy characterized the product as having “the lowest cash price in the market” and said in a Jan. 12 statement that the move was undertaken to address the “urgent need for a less-expensive epinephrine autoinjector.”
Data from a Kaiser Family Foundation analysis found that the average total Part D Medicare spending per EpiPen prescription increased nearly fivefold, from an average of $71 in 2007 to $344 in 2014. This trend continued, and in September 2016, Mylan’s CEO Heather Bresch faced questioning on Capitol Hill about the price hikes from members of the House Oversight Committee.
“We’re encouraged to see national efforts to make epinephrine autoinjectors more affordable and more available to Americans across the country,” Cary Sennett, MD, PhD, president and CEO of the Landover, Md.–based Asthma and Allergy Foundation of America, said in the CVS statement. “Partnerships that increase access to vital medications are key in helping those suffering from life-threatening allergies.”
CVS Pharmacy is currently selling a generic epinephrine autoinjector for a price of $109.99 per two-pack, which is about one-sixth the cost of Mylan’s EpiPen two-pack.
The product, an authorized generic for Adrenaclick, is manufactured by Lineage Therapeutics, which is a wholly owned subsidiary of Fort Washington, Pa.–based Impax Laboratories. CVS Pharmacy characterized the product as having “the lowest cash price in the market” and said in a Jan. 12 statement that the move was undertaken to address the “urgent need for a less-expensive epinephrine autoinjector.”
Data from a Kaiser Family Foundation analysis found that the average total Part D Medicare spending per EpiPen prescription increased nearly fivefold, from an average of $71 in 2007 to $344 in 2014. This trend continued, and in September 2016, Mylan’s CEO Heather Bresch faced questioning on Capitol Hill about the price hikes from members of the House Oversight Committee.
“We’re encouraged to see national efforts to make epinephrine autoinjectors more affordable and more available to Americans across the country,” Cary Sennett, MD, PhD, president and CEO of the Landover, Md.–based Asthma and Allergy Foundation of America, said in the CVS statement. “Partnerships that increase access to vital medications are key in helping those suffering from life-threatening allergies.”
CVS Pharmacy is currently selling a generic epinephrine autoinjector for a price of $109.99 per two-pack, which is about one-sixth the cost of Mylan’s EpiPen two-pack.
The product, an authorized generic for Adrenaclick, is manufactured by Lineage Therapeutics, which is a wholly owned subsidiary of Fort Washington, Pa.–based Impax Laboratories. CVS Pharmacy characterized the product as having “the lowest cash price in the market” and said in a Jan. 12 statement that the move was undertaken to address the “urgent need for a less-expensive epinephrine autoinjector.”
Data from a Kaiser Family Foundation analysis found that the average total Part D Medicare spending per EpiPen prescription increased nearly fivefold, from an average of $71 in 2007 to $344 in 2014. This trend continued, and in September 2016, Mylan’s CEO Heather Bresch faced questioning on Capitol Hill about the price hikes from members of the House Oversight Committee.
“We’re encouraged to see national efforts to make epinephrine autoinjectors more affordable and more available to Americans across the country,” Cary Sennett, MD, PhD, president and CEO of the Landover, Md.–based Asthma and Allergy Foundation of America, said in the CVS statement. “Partnerships that increase access to vital medications are key in helping those suffering from life-threatening allergies.”
Children with infantile spasms or nonsyndromic epilepsy achieve similar outcomes
HOUSTON – Infants and children who had epilepsy that was not identified as being part of a syndrome fared slightly worse in developmental outcomes and pharmacoresistance than did those with West syndrome/infantile spasms, Dravet syndrome, or another type of syndromic epilepsy, according to a prospective multisite study.
But in the study of 775 patients from 17 American pediatric epilepsy centers, early age at diagnosis was associated with greater mortality, greater risk of developmental decline, and greater pharmacoresistance, regardless of seizure type.
Lead study author Anne Berg, PhD, and her colleagues wrote that they were surprised to see that children in their study population with nonsyndromic epilepsy (NSE) were slightly more likely to have pharmacoresistant seizures (PR).
Further, although logistic regression analysis showed that seizure etiology, younger age at onset, and PR all had independent contributions to developmental decline, “West/IS was not convincingly associated with developmental decline,” they said.
In a poster session at the annual meeting of the American Epilepsy Society, Dr. Berg, an epidemiologist and research professor of pediatric neurology at Northwestern University, Chicago, presented the findings of a study that examined outcomes for infants and children diagnosed with epilepsy.
Patients were prospectively identified during a 3-year period from 2012 to 2015. Patients were eligible if their epilepsy began before their third birthday, and if the epilepsy was initially diagnosed at one of the participating centers. Patient data were evaluated for seizure and developmental outcomes if the patient was followed for at least 6 months after diagnosis.
Of the 775 patients initially recruited, 367 (47.3%) were girls. The mean age of epilepsy onset (which usually meant age at first unprovoked seizure) was 11.1 months (standard deviation, 9.4). Most patients (n = 509; 65.7%) were diagnosed with epilepsy before the age of 1 year. Just 115 patients (14.8%) received their epilepsy diagnosis when they were older than 2 years.
A key outcome investigated by Dr. Berg and her colleagues was pharmacoresistance, identified as lack of seizure control (i.e., at least a 3-month seizure-free period) after trying two appropriate medications. Other outcome measures included tracking whether patients developed West/IS, and whether West/IS evolved into other seizure types. The investigators also tracked developmental delay after epilepsy diagnosis and collected data about deaths among participating patients.
About a quarter (27%) of patients had persistent PR; these were more likely to occur in children who were younger at the onset of epilepsy. PR were more common when seizures began before the age of 1 year, occurring in 30% of this patient population, whereas 20% of patients with seizure onset happening after 1 year of age had PR (P = .0008).
Other findings from the study revealed that infants whose NSE had an etiology of focal cortical dysplasia or of an acquired insult such as trauma were more than twice as likely to have their seizures evolve into WS/IS.
Of 214 children whose initial presentation was WS/IS, 49 (23%) developed new seizure types. Most of these (47 of 49) were infants. Patients with WS/IS due to tuberous sclerosis complex, infectious causes, hypoxic-ischemic encephalopathy, and cephalic brain disorders were more likely to develop new seizure types.
“At initial presentation of epilepsy, children with West/IS were more likely already to have developmental delay than children with other syndromes or NSE,” they said.
Of the 22 patient deaths that occurred during the study, all but 1 occurred in infants younger than 1 year. None of the deaths occurred in typically-developing children with unknown epilepsy etiology.
“West/IS is the only early life epilepsy with consensus guidelines for treatment,” noted Dr. Berg and her coauthors, speculating that the guidelines might contribute to the slightly better outcomes observed for this population in their study.
However, although some groups of infants and children in the study fared slightly better than others, “[F]or the most part, there are no clearly ‘low’ risk groups,” Dr. Berg and her colleagues said. “Our findings highlight that most, if not all, early life epilepsies pose serious risk for poor outcomes and are equally deserving of concerted efforts.”
Dr. Berg reported no relevant financial disclosures. The study was funded by the Pediatric Epilepsy Research Foundation, and conducted through the Pediatric Epilepsy Research Consortium.
koakes@frontlinemedcom.com
On Twitter @karioakes
HOUSTON – Infants and children who had epilepsy that was not identified as being part of a syndrome fared slightly worse in developmental outcomes and pharmacoresistance than did those with West syndrome/infantile spasms, Dravet syndrome, or another type of syndromic epilepsy, according to a prospective multisite study.
But in the study of 775 patients from 17 American pediatric epilepsy centers, early age at diagnosis was associated with greater mortality, greater risk of developmental decline, and greater pharmacoresistance, regardless of seizure type.
Lead study author Anne Berg, PhD, and her colleagues wrote that they were surprised to see that children in their study population with nonsyndromic epilepsy (NSE) were slightly more likely to have pharmacoresistant seizures (PR).
Further, although logistic regression analysis showed that seizure etiology, younger age at onset, and PR all had independent contributions to developmental decline, “West/IS was not convincingly associated with developmental decline,” they said.
In a poster session at the annual meeting of the American Epilepsy Society, Dr. Berg, an epidemiologist and research professor of pediatric neurology at Northwestern University, Chicago, presented the findings of a study that examined outcomes for infants and children diagnosed with epilepsy.
Patients were prospectively identified during a 3-year period from 2012 to 2015. Patients were eligible if their epilepsy began before their third birthday, and if the epilepsy was initially diagnosed at one of the participating centers. Patient data were evaluated for seizure and developmental outcomes if the patient was followed for at least 6 months after diagnosis.
Of the 775 patients initially recruited, 367 (47.3%) were girls. The mean age of epilepsy onset (which usually meant age at first unprovoked seizure) was 11.1 months (standard deviation, 9.4). Most patients (n = 509; 65.7%) were diagnosed with epilepsy before the age of 1 year. Just 115 patients (14.8%) received their epilepsy diagnosis when they were older than 2 years.
A key outcome investigated by Dr. Berg and her colleagues was pharmacoresistance, identified as lack of seizure control (i.e., at least a 3-month seizure-free period) after trying two appropriate medications. Other outcome measures included tracking whether patients developed West/IS, and whether West/IS evolved into other seizure types. The investigators also tracked developmental delay after epilepsy diagnosis and collected data about deaths among participating patients.
About a quarter (27%) of patients had persistent PR; these were more likely to occur in children who were younger at the onset of epilepsy. PR were more common when seizures began before the age of 1 year, occurring in 30% of this patient population, whereas 20% of patients with seizure onset happening after 1 year of age had PR (P = .0008).
Other findings from the study revealed that infants whose NSE had an etiology of focal cortical dysplasia or of an acquired insult such as trauma were more than twice as likely to have their seizures evolve into WS/IS.
Of 214 children whose initial presentation was WS/IS, 49 (23%) developed new seizure types. Most of these (47 of 49) were infants. Patients with WS/IS due to tuberous sclerosis complex, infectious causes, hypoxic-ischemic encephalopathy, and cephalic brain disorders were more likely to develop new seizure types.
“At initial presentation of epilepsy, children with West/IS were more likely already to have developmental delay than children with other syndromes or NSE,” they said.
Of the 22 patient deaths that occurred during the study, all but 1 occurred in infants younger than 1 year. None of the deaths occurred in typically-developing children with unknown epilepsy etiology.
“West/IS is the only early life epilepsy with consensus guidelines for treatment,” noted Dr. Berg and her coauthors, speculating that the guidelines might contribute to the slightly better outcomes observed for this population in their study.
However, although some groups of infants and children in the study fared slightly better than others, “[F]or the most part, there are no clearly ‘low’ risk groups,” Dr. Berg and her colleagues said. “Our findings highlight that most, if not all, early life epilepsies pose serious risk for poor outcomes and are equally deserving of concerted efforts.”
Dr. Berg reported no relevant financial disclosures. The study was funded by the Pediatric Epilepsy Research Foundation, and conducted through the Pediatric Epilepsy Research Consortium.
koakes@frontlinemedcom.com
On Twitter @karioakes
HOUSTON – Infants and children who had epilepsy that was not identified as being part of a syndrome fared slightly worse in developmental outcomes and pharmacoresistance than did those with West syndrome/infantile spasms, Dravet syndrome, or another type of syndromic epilepsy, according to a prospective multisite study.
But in the study of 775 patients from 17 American pediatric epilepsy centers, early age at diagnosis was associated with greater mortality, greater risk of developmental decline, and greater pharmacoresistance, regardless of seizure type.
Lead study author Anne Berg, PhD, and her colleagues wrote that they were surprised to see that children in their study population with nonsyndromic epilepsy (NSE) were slightly more likely to have pharmacoresistant seizures (PR).
Further, although logistic regression analysis showed that seizure etiology, younger age at onset, and PR all had independent contributions to developmental decline, “West/IS was not convincingly associated with developmental decline,” they said.
In a poster session at the annual meeting of the American Epilepsy Society, Dr. Berg, an epidemiologist and research professor of pediatric neurology at Northwestern University, Chicago, presented the findings of a study that examined outcomes for infants and children diagnosed with epilepsy.
Patients were prospectively identified during a 3-year period from 2012 to 2015. Patients were eligible if their epilepsy began before their third birthday, and if the epilepsy was initially diagnosed at one of the participating centers. Patient data were evaluated for seizure and developmental outcomes if the patient was followed for at least 6 months after diagnosis.
Of the 775 patients initially recruited, 367 (47.3%) were girls. The mean age of epilepsy onset (which usually meant age at first unprovoked seizure) was 11.1 months (standard deviation, 9.4). Most patients (n = 509; 65.7%) were diagnosed with epilepsy before the age of 1 year. Just 115 patients (14.8%) received their epilepsy diagnosis when they were older than 2 years.
A key outcome investigated by Dr. Berg and her colleagues was pharmacoresistance, identified as lack of seizure control (i.e., at least a 3-month seizure-free period) after trying two appropriate medications. Other outcome measures included tracking whether patients developed West/IS, and whether West/IS evolved into other seizure types. The investigators also tracked developmental delay after epilepsy diagnosis and collected data about deaths among participating patients.
About a quarter (27%) of patients had persistent PR; these were more likely to occur in children who were younger at the onset of epilepsy. PR were more common when seizures began before the age of 1 year, occurring in 30% of this patient population, whereas 20% of patients with seizure onset happening after 1 year of age had PR (P = .0008).
Other findings from the study revealed that infants whose NSE had an etiology of focal cortical dysplasia or of an acquired insult such as trauma were more than twice as likely to have their seizures evolve into WS/IS.
Of 214 children whose initial presentation was WS/IS, 49 (23%) developed new seizure types. Most of these (47 of 49) were infants. Patients with WS/IS due to tuberous sclerosis complex, infectious causes, hypoxic-ischemic encephalopathy, and cephalic brain disorders were more likely to develop new seizure types.
“At initial presentation of epilepsy, children with West/IS were more likely already to have developmental delay than children with other syndromes or NSE,” they said.
Of the 22 patient deaths that occurred during the study, all but 1 occurred in infants younger than 1 year. None of the deaths occurred in typically-developing children with unknown epilepsy etiology.
“West/IS is the only early life epilepsy with consensus guidelines for treatment,” noted Dr. Berg and her coauthors, speculating that the guidelines might contribute to the slightly better outcomes observed for this population in their study.
However, although some groups of infants and children in the study fared slightly better than others, “[F]or the most part, there are no clearly ‘low’ risk groups,” Dr. Berg and her colleagues said. “Our findings highlight that most, if not all, early life epilepsies pose serious risk for poor outcomes and are equally deserving of concerted efforts.”
Dr. Berg reported no relevant financial disclosures. The study was funded by the Pediatric Epilepsy Research Foundation, and conducted through the Pediatric Epilepsy Research Consortium.
koakes@frontlinemedcom.com
On Twitter @karioakes
AT AES 2016
Key clinical point:
Major finding: Infantile spasms was not independently associated with worse developmental decline compared with nonsyndromic epilepsy.
Data source: Prospective study of 775 infants and children with epilepsy.
Disclosures: Dr. Berg reported no relevant financial disclosures. The study was funded by the Pediatric Epilepsy Research Foundation, and conducted through the Pediatric Epilepsy Research Consortium.
Chest-worn seizure detection device shows promise
HOUSTON – An investigative, chest-worn device shows promise for detecting a wide range of seizure types in children with epilepsy, results from a small single-center study showed.
“Our goal is for parents to have more peace of mind, not feeling like they have to watch their kids all night long,” one of the study authors, Kristin H. Gilchrist, PhD, said in an interview at the annual meeting of the American Epilepsy Society. “There are currently many wearable devices marketed for fitness [purposes], but if we can leverage some of these heart rate monitors and use them to detect seizures with specialized algorithms, that would be ideal.”
Approximately 60% of patients had a seizure during the monitoring period. Seizures without any clinical response or those lasting less than 10 seconds (such as single myoclonic jerks or clusters) were excluded from analysis, as were subjects with multiple seizures per hour because the autonomic signals often did not return to baseline, and this seizure frequency is outside of the intended use of the monitor. After exclusions, the algorithm was evaluated on 10 children with a mean age of 12 years. For additional validation, the algorithm was also evaluated with the Massachusetts Institute of Technology, Boston, PhysioNet database with ECG from five adults with partial seizures (Neurology. 1999;53:1590-2).The algorithm without motion parameters detected all seizures classified as tonic-clonic (3/3) or atonic/clonic/tonic (4/4), and 3/9 and 7/10 of focal seizures from the CNMC and MIT subjects, respectively. In the CNMC dataset, the motion algorithm detected all seizures classified as tonic-clonic (3/3), half of those categorized as atonic/clonic/tonic (2/4), and one of nine classified as focal seizures.
In the CNMC dataset, false positives averaged one per 14 hours, however, the majority of false positives occurred in a few patients with poor sensor data quality. More than half of the subjects (70%) had no false positives. One false positive occurred in the 16.8 hours of MIT data.
“In addition to an alert application, we have a technology that can be beneficial to clinic-based studies to quantify how many seizures people are having,” Dr. Gilchrist said. “Hopefully someday it will reach the commercial market.” She reported having no financial disclosures.
HOUSTON – An investigative, chest-worn device shows promise for detecting a wide range of seizure types in children with epilepsy, results from a small single-center study showed.
“Our goal is for parents to have more peace of mind, not feeling like they have to watch their kids all night long,” one of the study authors, Kristin H. Gilchrist, PhD, said in an interview at the annual meeting of the American Epilepsy Society. “There are currently many wearable devices marketed for fitness [purposes], but if we can leverage some of these heart rate monitors and use them to detect seizures with specialized algorithms, that would be ideal.”
Approximately 60% of patients had a seizure during the monitoring period. Seizures without any clinical response or those lasting less than 10 seconds (such as single myoclonic jerks or clusters) were excluded from analysis, as were subjects with multiple seizures per hour because the autonomic signals often did not return to baseline, and this seizure frequency is outside of the intended use of the monitor. After exclusions, the algorithm was evaluated on 10 children with a mean age of 12 years. For additional validation, the algorithm was also evaluated with the Massachusetts Institute of Technology, Boston, PhysioNet database with ECG from five adults with partial seizures (Neurology. 1999;53:1590-2).The algorithm without motion parameters detected all seizures classified as tonic-clonic (3/3) or atonic/clonic/tonic (4/4), and 3/9 and 7/10 of focal seizures from the CNMC and MIT subjects, respectively. In the CNMC dataset, the motion algorithm detected all seizures classified as tonic-clonic (3/3), half of those categorized as atonic/clonic/tonic (2/4), and one of nine classified as focal seizures.
In the CNMC dataset, false positives averaged one per 14 hours, however, the majority of false positives occurred in a few patients with poor sensor data quality. More than half of the subjects (70%) had no false positives. One false positive occurred in the 16.8 hours of MIT data.
“In addition to an alert application, we have a technology that can be beneficial to clinic-based studies to quantify how many seizures people are having,” Dr. Gilchrist said. “Hopefully someday it will reach the commercial market.” She reported having no financial disclosures.
HOUSTON – An investigative, chest-worn device shows promise for detecting a wide range of seizure types in children with epilepsy, results from a small single-center study showed.
“Our goal is for parents to have more peace of mind, not feeling like they have to watch their kids all night long,” one of the study authors, Kristin H. Gilchrist, PhD, said in an interview at the annual meeting of the American Epilepsy Society. “There are currently many wearable devices marketed for fitness [purposes], but if we can leverage some of these heart rate monitors and use them to detect seizures with specialized algorithms, that would be ideal.”
Approximately 60% of patients had a seizure during the monitoring period. Seizures without any clinical response or those lasting less than 10 seconds (such as single myoclonic jerks or clusters) were excluded from analysis, as were subjects with multiple seizures per hour because the autonomic signals often did not return to baseline, and this seizure frequency is outside of the intended use of the monitor. After exclusions, the algorithm was evaluated on 10 children with a mean age of 12 years. For additional validation, the algorithm was also evaluated with the Massachusetts Institute of Technology, Boston, PhysioNet database with ECG from five adults with partial seizures (Neurology. 1999;53:1590-2).The algorithm without motion parameters detected all seizures classified as tonic-clonic (3/3) or atonic/clonic/tonic (4/4), and 3/9 and 7/10 of focal seizures from the CNMC and MIT subjects, respectively. In the CNMC dataset, the motion algorithm detected all seizures classified as tonic-clonic (3/3), half of those categorized as atonic/clonic/tonic (2/4), and one of nine classified as focal seizures.
In the CNMC dataset, false positives averaged one per 14 hours, however, the majority of false positives occurred in a few patients with poor sensor data quality. More than half of the subjects (70%) had no false positives. One false positive occurred in the 16.8 hours of MIT data.
“In addition to an alert application, we have a technology that can be beneficial to clinic-based studies to quantify how many seizures people are having,” Dr. Gilchrist said. “Hopefully someday it will reach the commercial market.” She reported having no financial disclosures.
AT AES 2016
Key clinical point:
Major finding: The algorithm without motion parameters detected all seizures classified as tonic-clonic (3/3) or atonic/clonic/tonic (4/4), and 3 of 9 classified as focal seizures.
Data source: A clinic-based study of 10 epilepsy patients with a mean age of 12 years who wore an investigative device to detect seizures.
Disclosures: The study was funded by a grant from the National Institutes of Health. Dr. Gilchrist reported having no financial disclosures.
Lab values poor surrogate for detecting pediatric Rocky Mountain spotted fever in children
The three fatalities observed in a retrospective analysis of six cases of Rocky Mountain spotted fever (RMSF) in children were associated with either a delayed diagnosis pending laboratory findings or delayed antirickettsia treatment.
“The fact that all fatal cases died before the convalescent period emphasizes that diagnosis should be based on clinical findings instead of RMSF serologic and histologic testing,” wrote the authors of a study published online in Pediatric Dermatology (2016 Dec 19. doi: 10.1111/pde.13053).
Two of the fatal cases involved delayed antirickettsial therapy after the patients were misdiagnosed with group A streptococcus. None of the six children were initially evaluated for R. rickettsii; they averaged three encounters with their clinician before being admitted for acute inpatient care where they received intravenous doxycycline after nearly a week of symptoms.
“All fatal cases were complicated by neurologic manifestations, including seizures, obtundation, and uncal herniation,” a finding that is consistent with the literature, the authors said.
Although the high fatality rate might be the result of the small study size, Ms. Tull and her coinvestigators concluded that the disease should be considered in all differential diagnoses for children who present with a fever and rash during the summer months in endemic areas, particularly since pediatric cases of the disease are associated with poorer outcomes than in adult cases.
Given that RMSF often remains subclinical in its early stages, and typically presents with nonspecific symptoms of fever, rash, headache, and abdominal pain when it does emerge, physicians might be tempted to defer treatment until after serologic and histologic results are in, as is the standard method. Concerns over doxycycline’s tendency to stain teeth and cause enamel hypoplasia are also common. However, empirical administration could mean the difference between life and death, since treatment within the first 5 days following infection is associated with better outcomes – an algorithm complicated by the fact that symptoms caused by R. rickettsii have been known to take as long as 21 days to appear.
In the study, Ms. Tull and her colleagues found that the average time between exposure to the tick and the onset of symptoms was 6.6 days (range, 1-21 days).
Currently, there are no diagnostic tests “that reliably diagnose RMSF during the first 7 days of illness,” and most patients “do not develop detectable antibodies until the second week of illness,” the investigators reported. Even then, sensitivity of indirect fluorescent antibody serum testing after the second week of illness is only between 86% and 94%, they noted. Further, the sensitivity of immunohistochemical (IHC) tissue staining has been reported at 70%, and false-negative IHC results are common in acute disease when antibody response is harder to detect.
Ms. Tull and her colleagues found that five of the six patients in their study had negative IHC testing; two of the six had positive serum antibody titers. For this reason, they concluded that Rocky Mountain spotted fever diagnosis should be based on “clinical history, examination, and laboratory abnormalities” rather than laboratory testing, and urged that “prompt treatment should be instituted empirically.”
The authors did not have any relevant financial disclosures.
The three fatalities observed in a retrospective analysis of six cases of Rocky Mountain spotted fever (RMSF) in children were associated with either a delayed diagnosis pending laboratory findings or delayed antirickettsia treatment.
“The fact that all fatal cases died before the convalescent period emphasizes that diagnosis should be based on clinical findings instead of RMSF serologic and histologic testing,” wrote the authors of a study published online in Pediatric Dermatology (2016 Dec 19. doi: 10.1111/pde.13053).
Two of the fatal cases involved delayed antirickettsial therapy after the patients were misdiagnosed with group A streptococcus. None of the six children were initially evaluated for R. rickettsii; they averaged three encounters with their clinician before being admitted for acute inpatient care where they received intravenous doxycycline after nearly a week of symptoms.
“All fatal cases were complicated by neurologic manifestations, including seizures, obtundation, and uncal herniation,” a finding that is consistent with the literature, the authors said.
Although the high fatality rate might be the result of the small study size, Ms. Tull and her coinvestigators concluded that the disease should be considered in all differential diagnoses for children who present with a fever and rash during the summer months in endemic areas, particularly since pediatric cases of the disease are associated with poorer outcomes than in adult cases.
Given that RMSF often remains subclinical in its early stages, and typically presents with nonspecific symptoms of fever, rash, headache, and abdominal pain when it does emerge, physicians might be tempted to defer treatment until after serologic and histologic results are in, as is the standard method. Concerns over doxycycline’s tendency to stain teeth and cause enamel hypoplasia are also common. However, empirical administration could mean the difference between life and death, since treatment within the first 5 days following infection is associated with better outcomes – an algorithm complicated by the fact that symptoms caused by R. rickettsii have been known to take as long as 21 days to appear.
In the study, Ms. Tull and her colleagues found that the average time between exposure to the tick and the onset of symptoms was 6.6 days (range, 1-21 days).
Currently, there are no diagnostic tests “that reliably diagnose RMSF during the first 7 days of illness,” and most patients “do not develop detectable antibodies until the second week of illness,” the investigators reported. Even then, sensitivity of indirect fluorescent antibody serum testing after the second week of illness is only between 86% and 94%, they noted. Further, the sensitivity of immunohistochemical (IHC) tissue staining has been reported at 70%, and false-negative IHC results are common in acute disease when antibody response is harder to detect.
Ms. Tull and her colleagues found that five of the six patients in their study had negative IHC testing; two of the six had positive serum antibody titers. For this reason, they concluded that Rocky Mountain spotted fever diagnosis should be based on “clinical history, examination, and laboratory abnormalities” rather than laboratory testing, and urged that “prompt treatment should be instituted empirically.”
The authors did not have any relevant financial disclosures.
The three fatalities observed in a retrospective analysis of six cases of Rocky Mountain spotted fever (RMSF) in children were associated with either a delayed diagnosis pending laboratory findings or delayed antirickettsia treatment.
“The fact that all fatal cases died before the convalescent period emphasizes that diagnosis should be based on clinical findings instead of RMSF serologic and histologic testing,” wrote the authors of a study published online in Pediatric Dermatology (2016 Dec 19. doi: 10.1111/pde.13053).
Two of the fatal cases involved delayed antirickettsial therapy after the patients were misdiagnosed with group A streptococcus. None of the six children were initially evaluated for R. rickettsii; they averaged three encounters with their clinician before being admitted for acute inpatient care where they received intravenous doxycycline after nearly a week of symptoms.
“All fatal cases were complicated by neurologic manifestations, including seizures, obtundation, and uncal herniation,” a finding that is consistent with the literature, the authors said.
Although the high fatality rate might be the result of the small study size, Ms. Tull and her coinvestigators concluded that the disease should be considered in all differential diagnoses for children who present with a fever and rash during the summer months in endemic areas, particularly since pediatric cases of the disease are associated with poorer outcomes than in adult cases.
Given that RMSF often remains subclinical in its early stages, and typically presents with nonspecific symptoms of fever, rash, headache, and abdominal pain when it does emerge, physicians might be tempted to defer treatment until after serologic and histologic results are in, as is the standard method. Concerns over doxycycline’s tendency to stain teeth and cause enamel hypoplasia are also common. However, empirical administration could mean the difference between life and death, since treatment within the first 5 days following infection is associated with better outcomes – an algorithm complicated by the fact that symptoms caused by R. rickettsii have been known to take as long as 21 days to appear.
In the study, Ms. Tull and her colleagues found that the average time between exposure to the tick and the onset of symptoms was 6.6 days (range, 1-21 days).
Currently, there are no diagnostic tests “that reliably diagnose RMSF during the first 7 days of illness,” and most patients “do not develop detectable antibodies until the second week of illness,” the investigators reported. Even then, sensitivity of indirect fluorescent antibody serum testing after the second week of illness is only between 86% and 94%, they noted. Further, the sensitivity of immunohistochemical (IHC) tissue staining has been reported at 70%, and false-negative IHC results are common in acute disease when antibody response is harder to detect.
Ms. Tull and her colleagues found that five of the six patients in their study had negative IHC testing; two of the six had positive serum antibody titers. For this reason, they concluded that Rocky Mountain spotted fever diagnosis should be based on “clinical history, examination, and laboratory abnormalities” rather than laboratory testing, and urged that “prompt treatment should be instituted empirically.”
The authors did not have any relevant financial disclosures.
FROM PEDIATRIC DERMATOLOGY
Key clinical point:
Major finding: Half of pediatric patients diagnosed with Rocky Mountain spotted fever died after treatment was delayed.
Data source: A retrospective analysis of 6 pediatric RMSF cases among 3,912 inpatient dermatology consultations over a period of 10 years at a tertiary care center.
Disclosures: The authors did not have any relevant financial disclosures. .
Adolescents, boys, black children most likely to be hospitalized in SJS and TEN
Annual hospitalization rates in the United States for Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) were shown to be higher in adolescents, boys, and black children, in a cross-sectional analysis of discharge records from more than 4,100 hospitals.
Using relevant ICD-9 codes, researchers at Harvard University identified 1,571 patients hospitalized for SJS, TEN, or both in 2009 and 2012, as listed in the Kids Inpatient Database from the Agency for Healthcare Research and Quality. The highest hospitalization rates per 100,000 in each year were for adolescents between 15 and 19 years (P = .01), boys (P = .03), and black children (P = .82). The overall risk of death from these conditions was 1.5% in 2009 and 0.3% in 2012. The data were published online in a brief report (Pediatr Dermatol. 2016 Dec 19. doi: 10.1111/pde.13050).
With the number of SJS- and TEN-related hospitalizations between 0.1 and 1.0 per 100,000, lead author Yusuke Okubo MD, MPH, and his colleagues wrote that their data aligned with previous studies; however, regarding the emphasis on demographic differences, theirs was, to the best of their knowledge, “the first study to reveal these disparities.” Compared with adults, they added, mortality was “remarkably lower” in children.
The authors had no disclosures.
Annual hospitalization rates in the United States for Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) were shown to be higher in adolescents, boys, and black children, in a cross-sectional analysis of discharge records from more than 4,100 hospitals.
Using relevant ICD-9 codes, researchers at Harvard University identified 1,571 patients hospitalized for SJS, TEN, or both in 2009 and 2012, as listed in the Kids Inpatient Database from the Agency for Healthcare Research and Quality. The highest hospitalization rates per 100,000 in each year were for adolescents between 15 and 19 years (P = .01), boys (P = .03), and black children (P = .82). The overall risk of death from these conditions was 1.5% in 2009 and 0.3% in 2012. The data were published online in a brief report (Pediatr Dermatol. 2016 Dec 19. doi: 10.1111/pde.13050).
With the number of SJS- and TEN-related hospitalizations between 0.1 and 1.0 per 100,000, lead author Yusuke Okubo MD, MPH, and his colleagues wrote that their data aligned with previous studies; however, regarding the emphasis on demographic differences, theirs was, to the best of their knowledge, “the first study to reveal these disparities.” Compared with adults, they added, mortality was “remarkably lower” in children.
The authors had no disclosures.
Annual hospitalization rates in the United States for Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) were shown to be higher in adolescents, boys, and black children, in a cross-sectional analysis of discharge records from more than 4,100 hospitals.
Using relevant ICD-9 codes, researchers at Harvard University identified 1,571 patients hospitalized for SJS, TEN, or both in 2009 and 2012, as listed in the Kids Inpatient Database from the Agency for Healthcare Research and Quality. The highest hospitalization rates per 100,000 in each year were for adolescents between 15 and 19 years (P = .01), boys (P = .03), and black children (P = .82). The overall risk of death from these conditions was 1.5% in 2009 and 0.3% in 2012. The data were published online in a brief report (Pediatr Dermatol. 2016 Dec 19. doi: 10.1111/pde.13050).
With the number of SJS- and TEN-related hospitalizations between 0.1 and 1.0 per 100,000, lead author Yusuke Okubo MD, MPH, and his colleagues wrote that their data aligned with previous studies; however, regarding the emphasis on demographic differences, theirs was, to the best of their knowledge, “the first study to reveal these disparities.” Compared with adults, they added, mortality was “remarkably lower” in children.
The authors had no disclosures.
Key clinical point:
Major finding: Hospitalization rates for SJS/TEN were highest among adolescents (aged 15-19) at 1.36 and 1.09 per 100,000 children in 2009 and 2012, respectively.
Data source: An analysis of 1,571 pediatric discharge records for 2009 and 2012 from more than 4,100 hospitals in a national database.
Disclosures: The authors had no disclosures.
IPV boost after initial OPV offers sustained protection to at least 11 months
Protection against the poliovirus is lower at 1 month but remains sustained at 6 and 11 months after an inactivated poliovirus vaccine (IPV) boost following initial oral poliovirus vaccination (OPV), according to Jacob John, MD, of Christian Medical College, Vellore, Tamil Nadu, India, and his associates.
In a randomized controlled trial from Nov. 4 and Dec. 17, 2014, 900 healthy children from ages 1 to 4 years were randomly assigned between three study groups. The groups had the children receive IPV boost at 5 months (arm A), at enrollment (arm B), or no vaccine (arm C). Poliovirus shedding in stool 7 days after challenge, determined by Fisher’s exact test, was significantly lower in arms A and B, compared with C (risk ratio, 0.68; P = .003, RR, 0.70; P = .006 for arm A vs. C and B vs. C, respectively). The reduction in shedding was more marked for serotype 3 (RR, 0.60; P = .004, RR, 0.54; P = .001 respectively) than for serotype 1 (RR, 0.72; P = .057, RR, 0.80; P = .215, respectively).
It was noted that 41 serious adverse events (11 in arm A, 17 in arm B, and 13 in arm C), including 2 deaths in arm A, were reported during the trial. However, the reported adverse events were classified as unrelated, and the deaths were from leukemia and from viral hemorrhagic fever.
“The boost to intestinal immunity against poliovirus that results from administration of IPV to OPV-vaccinated children is sustained at 6 and 11 months. It is clear that IPV is playing an increasingly important role in the polio endgame as the world transitions away from the use of OPV,” the researchers concluded. “Every effort needs to be made to ensure supply of this vaccine to meet this expanding role.”
Find the full study in the Journal of Infectious Diseases 2016. doi: 10.1093/infdis/jiw595.
Protection against the poliovirus is lower at 1 month but remains sustained at 6 and 11 months after an inactivated poliovirus vaccine (IPV) boost following initial oral poliovirus vaccination (OPV), according to Jacob John, MD, of Christian Medical College, Vellore, Tamil Nadu, India, and his associates.
In a randomized controlled trial from Nov. 4 and Dec. 17, 2014, 900 healthy children from ages 1 to 4 years were randomly assigned between three study groups. The groups had the children receive IPV boost at 5 months (arm A), at enrollment (arm B), or no vaccine (arm C). Poliovirus shedding in stool 7 days after challenge, determined by Fisher’s exact test, was significantly lower in arms A and B, compared with C (risk ratio, 0.68; P = .003, RR, 0.70; P = .006 for arm A vs. C and B vs. C, respectively). The reduction in shedding was more marked for serotype 3 (RR, 0.60; P = .004, RR, 0.54; P = .001 respectively) than for serotype 1 (RR, 0.72; P = .057, RR, 0.80; P = .215, respectively).
It was noted that 41 serious adverse events (11 in arm A, 17 in arm B, and 13 in arm C), including 2 deaths in arm A, were reported during the trial. However, the reported adverse events were classified as unrelated, and the deaths were from leukemia and from viral hemorrhagic fever.
“The boost to intestinal immunity against poliovirus that results from administration of IPV to OPV-vaccinated children is sustained at 6 and 11 months. It is clear that IPV is playing an increasingly important role in the polio endgame as the world transitions away from the use of OPV,” the researchers concluded. “Every effort needs to be made to ensure supply of this vaccine to meet this expanding role.”
Find the full study in the Journal of Infectious Diseases 2016. doi: 10.1093/infdis/jiw595.
Protection against the poliovirus is lower at 1 month but remains sustained at 6 and 11 months after an inactivated poliovirus vaccine (IPV) boost following initial oral poliovirus vaccination (OPV), according to Jacob John, MD, of Christian Medical College, Vellore, Tamil Nadu, India, and his associates.
In a randomized controlled trial from Nov. 4 and Dec. 17, 2014, 900 healthy children from ages 1 to 4 years were randomly assigned between three study groups. The groups had the children receive IPV boost at 5 months (arm A), at enrollment (arm B), or no vaccine (arm C). Poliovirus shedding in stool 7 days after challenge, determined by Fisher’s exact test, was significantly lower in arms A and B, compared with C (risk ratio, 0.68; P = .003, RR, 0.70; P = .006 for arm A vs. C and B vs. C, respectively). The reduction in shedding was more marked for serotype 3 (RR, 0.60; P = .004, RR, 0.54; P = .001 respectively) than for serotype 1 (RR, 0.72; P = .057, RR, 0.80; P = .215, respectively).
It was noted that 41 serious adverse events (11 in arm A, 17 in arm B, and 13 in arm C), including 2 deaths in arm A, were reported during the trial. However, the reported adverse events were classified as unrelated, and the deaths were from leukemia and from viral hemorrhagic fever.
“The boost to intestinal immunity against poliovirus that results from administration of IPV to OPV-vaccinated children is sustained at 6 and 11 months. It is clear that IPV is playing an increasingly important role in the polio endgame as the world transitions away from the use of OPV,” the researchers concluded. “Every effort needs to be made to ensure supply of this vaccine to meet this expanding role.”
Find the full study in the Journal of Infectious Diseases 2016. doi: 10.1093/infdis/jiw595.
FROM THE JOURNAL OF INFECTIOUS DISEASES
Oral Rehydration Therapy for KidsA More Palatable Alternative
A 3-year-old boy is brought in by his mother for vomiting and diarrhea that started in the middle of the night. On examination, he is slightly dehydrated but does not have an acute abdomen or other source of infection. He is drinking from a sippy cup. What fluids should you recommend?
Acute gastroenteritis is a common cause of vomiting and/or diarrhea in children, resulting in 1.5 million outpatient visits and 200,000 hospital admissions annually in the United States.2 Children with gastroenteritis are at risk for dehydration, and the recommended treatment for anything less than severe dehydration is oral rehydration therapy (ORT) and early resumption of feeding upon rehydration.2
In 2002, the World Health Organization recommended an ORT with an osmolarity of 245 mOsm/L.3 However, cultural preferences, cost, taste, availability, and caregiver and professional preference for IV hydration have all been barriers to the use of ORT.2,4-8 In fact, a study of ORT preferences in 66 children ages 5 to 10 years found that less than half of the children would voluntarily drink the ORT again.5
This study evaluated the use of diluted apple juice as a more palatable alternative to ORT in children with vomiting and/or diarrhea.
STUDY SUMMARY
In kids older than 2, apple juice will do
This study was a single-center, single-blind, noninferiority RCT conducted in the emergency department (ED) of a tertiary care pediatric hospital in Canada. The researchers compared the use of half-strength apple juice to a standard ORT for rehydration in simple gastroenteritis.1 Participants were 6 months to 5 years of age, weighed more than 8 kg (17.7 lb), and had vomiting and/or diarrhea for less than 96 hours (with ≥ 3 episodes over the past 24 hours). They also had a Clinical Dehydration Scale (CDS) score < 5 and a capillary refill of < 2 seconds (see Table).9 Of the total, 68% of the children had a CDS score of 0; 25.5%, of 1 to 2; and 6.4%, of 3 to 4. Exclusion criteria included chronic gastrointestinal disease or other significant comorbidities (eg, diabetes) that could affect the clinical state and potential acute abdominal pathology.
Children were randomly assigned to receive half-strength apple juice (intervention group, n = 323) or an apple-flavored sucralose-sweetened electrolyte maintenance solution (EMS; control group, n = 324). Immediately on triage, each child received 2 L of their assigned fluid, to be used while in the ED and then at home. The children received 5 mL of fluid every two to five minutes. If a child vomited after starting the fluid, he or she was given oral ondansetron.
At discharge, caregivers were encouraged to replace 2 mL/kg of fluid for a vomiting episode and 10 mL/kg of fluid for a diarrhea episode. At home, children in the juice group could also drink any other preferred fluid, including sports beverages. The EMS group was instructed to drink only the solution provided or a comparable ORT. Caregivers were contacted daily by phone until the child had no symptoms for 24 hours. They were also asked to keep a daily log of vomiting and diarrhea frequency, as well as any subsequent health care visits. At least one follow-up contact occurred with 99.5% of the children.
The primary outcome was treatment failure, defined as the occurrence of any of the following within seven days of the ED visit: hospitalization, IV rehydration, further health care visits for diarrhea/vomiting in any setting, protracted symptoms (ie, ≥ 3 episodes of vomiting or diarrhea within a 24-hour period occurring > 7 days after enrollment), 3% or greater weight loss, or CDS score ≥ 5 at follow-up.
Treatment failure occurred in 16.7% of the juice group, compared to 25% of the EMS group (difference, 8.3 percentage points; number needed to treat [NNT], 12), consistent with noninferior effectiveness. The benefit was seen primarily in children ≥ 24 months of age. In children < 24 months, the treatment failure for juice was 23.9% and for EMS, 24.1%. In older children (those ≥ 24 months to 5 years), the treatment failure with juice was 9.8% and with EMS, 25.9% (difference, 16.2 percentage points; NNT, 6.2).
IV rehydration in the ED or within seven days of the initial visit was needed in 2.5% of the juice group and in 9% of the EMS group (difference, 6.5 percentage points; NNT, 15.4). There were no differences in hospitalization rate or in diarrhea or vomiting frequency between groups.
WHAT’S NEW
Kids drink more of what they like
This study, in a developed country, found rehydration with diluted apple juice worked just as well as ORT. In children ≥ 24 months of age, there were fewer treatment failures.
CAVEATS
Infants may not benefit; ondansetron played a role
Children in this study were only mildly dehydrated. The study did not include infants younger than 6 months of age, and the greatest benefit was seen in children ≥ 24 months of age.
Also noteworthy was that most of the children (67.4%) received an oral dose of ondansetron (0.1 mg/kg). Although ondansetron is expensive, it would be considered cost-effective if one dose prevents a hospitalization. Previous studies of oral ondansetron show it reduces vomiting (NNT, 5); lowers the rate of IV hydration in the ED (NNT, 5); and reduces the hospitalization rate from the ED (NNT, 17).10
Lastly, there are a variety of fluid replacement guidelines. In this study, fluid replacement was 2 mL/kg for a vomiting episode and 10 mL/kg for a diarrhea episode.
CHALLENGES TO IMPLEMENTATION
Given the ease of swapping diluted apple juice for ORT, there are no foreseen barriers to implementation.
ACKNOWLEDGEMENT
The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.
Copyright © 2016. The Family Physicians Inquiries Network. All rights reserved.
Reprinted with permission from the Family Physicians Inquiries Network and The Journal of Family Practice. 2016;65(12): 924-926.
1. Freedman SB, Willan AR, Boutis K, et al. Effect of dilute apple juice and preferred fluids vs electrolyte maintenance solution on treatment failure among children with mild gastroenteritis: a randomized clinical trial. JAMA. 2016;315:1966-1974.
2. King CK, Glass R, Bresee JS, et al. Managing acute gastroenteritis among children: oral rehydration, maintenance, and nutritional therapy. MMWR Recomm Rep. 2003;52:1-16.
3. World Health Organization. New formula oral rehydration salts. WHO Drug Information. 2002;16(2). http://apps.who.int/medicinedocs/en/d/Js4950e/2.4.html. Accessed December 5, 2016.
4. Cohen MB, Hardin J. Medicaid coverage of oral rehydration solutions. N Engl J Med. 1993;329:211.
5. Freedman SB, Cho D, Boutis K, et al. Assessing the palatability of oral rehydration solutions in school-aged children: a randomized crossover trial. Arch Pediatr Adolesc Med. 2010;164:696-702.
6. Reis EC, Goepp JG, Katz S, et al. Barriers to use of oral rehydration therapy. Pediatrics. 1994;93:708-711.
7. Karpas A, Finkelstein M, Reid S. Parental preference for rehydration method for children in the emergency department. Pediatr Emerg Care. 2009;25:301-306.
8. Ozuah PO, Avner JR, Stein RE. Oral rehydration, emergency physicians, and practice parameters: a national survey. Pediatrics. 2002;109:259-261.
9. Goldman RD, Friedman JN, Parkin PC. Validation of the clinical dehydration scale for children with acute gastroenteritis. Pediatrics. 2008;122:545-549.
10. Fedorowicz Z, Jagannath VA, Carter B. Antiemetics for reducing vomiting related to acute gastroenteritis in children and adolescents. Cochrane Database Syst Rev. 2011; CD005506.
A 3-year-old boy is brought in by his mother for vomiting and diarrhea that started in the middle of the night. On examination, he is slightly dehydrated but does not have an acute abdomen or other source of infection. He is drinking from a sippy cup. What fluids should you recommend?
Acute gastroenteritis is a common cause of vomiting and/or diarrhea in children, resulting in 1.5 million outpatient visits and 200,000 hospital admissions annually in the United States.2 Children with gastroenteritis are at risk for dehydration, and the recommended treatment for anything less than severe dehydration is oral rehydration therapy (ORT) and early resumption of feeding upon rehydration.2
In 2002, the World Health Organization recommended an ORT with an osmolarity of 245 mOsm/L.3 However, cultural preferences, cost, taste, availability, and caregiver and professional preference for IV hydration have all been barriers to the use of ORT.2,4-8 In fact, a study of ORT preferences in 66 children ages 5 to 10 years found that less than half of the children would voluntarily drink the ORT again.5
This study evaluated the use of diluted apple juice as a more palatable alternative to ORT in children with vomiting and/or diarrhea.
STUDY SUMMARY
In kids older than 2, apple juice will do
This study was a single-center, single-blind, noninferiority RCT conducted in the emergency department (ED) of a tertiary care pediatric hospital in Canada. The researchers compared the use of half-strength apple juice to a standard ORT for rehydration in simple gastroenteritis.1 Participants were 6 months to 5 years of age, weighed more than 8 kg (17.7 lb), and had vomiting and/or diarrhea for less than 96 hours (with ≥ 3 episodes over the past 24 hours). They also had a Clinical Dehydration Scale (CDS) score < 5 and a capillary refill of < 2 seconds (see Table).9 Of the total, 68% of the children had a CDS score of 0; 25.5%, of 1 to 2; and 6.4%, of 3 to 4. Exclusion criteria included chronic gastrointestinal disease or other significant comorbidities (eg, diabetes) that could affect the clinical state and potential acute abdominal pathology.
Children were randomly assigned to receive half-strength apple juice (intervention group, n = 323) or an apple-flavored sucralose-sweetened electrolyte maintenance solution (EMS; control group, n = 324). Immediately on triage, each child received 2 L of their assigned fluid, to be used while in the ED and then at home. The children received 5 mL of fluid every two to five minutes. If a child vomited after starting the fluid, he or she was given oral ondansetron.
At discharge, caregivers were encouraged to replace 2 mL/kg of fluid for a vomiting episode and 10 mL/kg of fluid for a diarrhea episode. At home, children in the juice group could also drink any other preferred fluid, including sports beverages. The EMS group was instructed to drink only the solution provided or a comparable ORT. Caregivers were contacted daily by phone until the child had no symptoms for 24 hours. They were also asked to keep a daily log of vomiting and diarrhea frequency, as well as any subsequent health care visits. At least one follow-up contact occurred with 99.5% of the children.
The primary outcome was treatment failure, defined as the occurrence of any of the following within seven days of the ED visit: hospitalization, IV rehydration, further health care visits for diarrhea/vomiting in any setting, protracted symptoms (ie, ≥ 3 episodes of vomiting or diarrhea within a 24-hour period occurring > 7 days after enrollment), 3% or greater weight loss, or CDS score ≥ 5 at follow-up.
Treatment failure occurred in 16.7% of the juice group, compared to 25% of the EMS group (difference, 8.3 percentage points; number needed to treat [NNT], 12), consistent with noninferior effectiveness. The benefit was seen primarily in children ≥ 24 months of age. In children < 24 months, the treatment failure for juice was 23.9% and for EMS, 24.1%. In older children (those ≥ 24 months to 5 years), the treatment failure with juice was 9.8% and with EMS, 25.9% (difference, 16.2 percentage points; NNT, 6.2).
IV rehydration in the ED or within seven days of the initial visit was needed in 2.5% of the juice group and in 9% of the EMS group (difference, 6.5 percentage points; NNT, 15.4). There were no differences in hospitalization rate or in diarrhea or vomiting frequency between groups.
WHAT’S NEW
Kids drink more of what they like
This study, in a developed country, found rehydration with diluted apple juice worked just as well as ORT. In children ≥ 24 months of age, there were fewer treatment failures.
CAVEATS
Infants may not benefit; ondansetron played a role
Children in this study were only mildly dehydrated. The study did not include infants younger than 6 months of age, and the greatest benefit was seen in children ≥ 24 months of age.
Also noteworthy was that most of the children (67.4%) received an oral dose of ondansetron (0.1 mg/kg). Although ondansetron is expensive, it would be considered cost-effective if one dose prevents a hospitalization. Previous studies of oral ondansetron show it reduces vomiting (NNT, 5); lowers the rate of IV hydration in the ED (NNT, 5); and reduces the hospitalization rate from the ED (NNT, 17).10
Lastly, there are a variety of fluid replacement guidelines. In this study, fluid replacement was 2 mL/kg for a vomiting episode and 10 mL/kg for a diarrhea episode.
CHALLENGES TO IMPLEMENTATION
Given the ease of swapping diluted apple juice for ORT, there are no foreseen barriers to implementation.
ACKNOWLEDGEMENT
The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.
Copyright © 2016. The Family Physicians Inquiries Network. All rights reserved.
Reprinted with permission from the Family Physicians Inquiries Network and The Journal of Family Practice. 2016;65(12): 924-926.
A 3-year-old boy is brought in by his mother for vomiting and diarrhea that started in the middle of the night. On examination, he is slightly dehydrated but does not have an acute abdomen or other source of infection. He is drinking from a sippy cup. What fluids should you recommend?
Acute gastroenteritis is a common cause of vomiting and/or diarrhea in children, resulting in 1.5 million outpatient visits and 200,000 hospital admissions annually in the United States.2 Children with gastroenteritis are at risk for dehydration, and the recommended treatment for anything less than severe dehydration is oral rehydration therapy (ORT) and early resumption of feeding upon rehydration.2
In 2002, the World Health Organization recommended an ORT with an osmolarity of 245 mOsm/L.3 However, cultural preferences, cost, taste, availability, and caregiver and professional preference for IV hydration have all been barriers to the use of ORT.2,4-8 In fact, a study of ORT preferences in 66 children ages 5 to 10 years found that less than half of the children would voluntarily drink the ORT again.5
This study evaluated the use of diluted apple juice as a more palatable alternative to ORT in children with vomiting and/or diarrhea.
STUDY SUMMARY
In kids older than 2, apple juice will do
This study was a single-center, single-blind, noninferiority RCT conducted in the emergency department (ED) of a tertiary care pediatric hospital in Canada. The researchers compared the use of half-strength apple juice to a standard ORT for rehydration in simple gastroenteritis.1 Participants were 6 months to 5 years of age, weighed more than 8 kg (17.7 lb), and had vomiting and/or diarrhea for less than 96 hours (with ≥ 3 episodes over the past 24 hours). They also had a Clinical Dehydration Scale (CDS) score < 5 and a capillary refill of < 2 seconds (see Table).9 Of the total, 68% of the children had a CDS score of 0; 25.5%, of 1 to 2; and 6.4%, of 3 to 4. Exclusion criteria included chronic gastrointestinal disease or other significant comorbidities (eg, diabetes) that could affect the clinical state and potential acute abdominal pathology.
Children were randomly assigned to receive half-strength apple juice (intervention group, n = 323) or an apple-flavored sucralose-sweetened electrolyte maintenance solution (EMS; control group, n = 324). Immediately on triage, each child received 2 L of their assigned fluid, to be used while in the ED and then at home. The children received 5 mL of fluid every two to five minutes. If a child vomited after starting the fluid, he or she was given oral ondansetron.
At discharge, caregivers were encouraged to replace 2 mL/kg of fluid for a vomiting episode and 10 mL/kg of fluid for a diarrhea episode. At home, children in the juice group could also drink any other preferred fluid, including sports beverages. The EMS group was instructed to drink only the solution provided or a comparable ORT. Caregivers were contacted daily by phone until the child had no symptoms for 24 hours. They were also asked to keep a daily log of vomiting and diarrhea frequency, as well as any subsequent health care visits. At least one follow-up contact occurred with 99.5% of the children.
The primary outcome was treatment failure, defined as the occurrence of any of the following within seven days of the ED visit: hospitalization, IV rehydration, further health care visits for diarrhea/vomiting in any setting, protracted symptoms (ie, ≥ 3 episodes of vomiting or diarrhea within a 24-hour period occurring > 7 days after enrollment), 3% or greater weight loss, or CDS score ≥ 5 at follow-up.
Treatment failure occurred in 16.7% of the juice group, compared to 25% of the EMS group (difference, 8.3 percentage points; number needed to treat [NNT], 12), consistent with noninferior effectiveness. The benefit was seen primarily in children ≥ 24 months of age. In children < 24 months, the treatment failure for juice was 23.9% and for EMS, 24.1%. In older children (those ≥ 24 months to 5 years), the treatment failure with juice was 9.8% and with EMS, 25.9% (difference, 16.2 percentage points; NNT, 6.2).
IV rehydration in the ED or within seven days of the initial visit was needed in 2.5% of the juice group and in 9% of the EMS group (difference, 6.5 percentage points; NNT, 15.4). There were no differences in hospitalization rate or in diarrhea or vomiting frequency between groups.
WHAT’S NEW
Kids drink more of what they like
This study, in a developed country, found rehydration with diluted apple juice worked just as well as ORT. In children ≥ 24 months of age, there were fewer treatment failures.
CAVEATS
Infants may not benefit; ondansetron played a role
Children in this study were only mildly dehydrated. The study did not include infants younger than 6 months of age, and the greatest benefit was seen in children ≥ 24 months of age.
Also noteworthy was that most of the children (67.4%) received an oral dose of ondansetron (0.1 mg/kg). Although ondansetron is expensive, it would be considered cost-effective if one dose prevents a hospitalization. Previous studies of oral ondansetron show it reduces vomiting (NNT, 5); lowers the rate of IV hydration in the ED (NNT, 5); and reduces the hospitalization rate from the ED (NNT, 17).10
Lastly, there are a variety of fluid replacement guidelines. In this study, fluid replacement was 2 mL/kg for a vomiting episode and 10 mL/kg for a diarrhea episode.
CHALLENGES TO IMPLEMENTATION
Given the ease of swapping diluted apple juice for ORT, there are no foreseen barriers to implementation.
ACKNOWLEDGEMENT
The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.
Copyright © 2016. The Family Physicians Inquiries Network. All rights reserved.
Reprinted with permission from the Family Physicians Inquiries Network and The Journal of Family Practice. 2016;65(12): 924-926.
1. Freedman SB, Willan AR, Boutis K, et al. Effect of dilute apple juice and preferred fluids vs electrolyte maintenance solution on treatment failure among children with mild gastroenteritis: a randomized clinical trial. JAMA. 2016;315:1966-1974.
2. King CK, Glass R, Bresee JS, et al. Managing acute gastroenteritis among children: oral rehydration, maintenance, and nutritional therapy. MMWR Recomm Rep. 2003;52:1-16.
3. World Health Organization. New formula oral rehydration salts. WHO Drug Information. 2002;16(2). http://apps.who.int/medicinedocs/en/d/Js4950e/2.4.html. Accessed December 5, 2016.
4. Cohen MB, Hardin J. Medicaid coverage of oral rehydration solutions. N Engl J Med. 1993;329:211.
5. Freedman SB, Cho D, Boutis K, et al. Assessing the palatability of oral rehydration solutions in school-aged children: a randomized crossover trial. Arch Pediatr Adolesc Med. 2010;164:696-702.
6. Reis EC, Goepp JG, Katz S, et al. Barriers to use of oral rehydration therapy. Pediatrics. 1994;93:708-711.
7. Karpas A, Finkelstein M, Reid S. Parental preference for rehydration method for children in the emergency department. Pediatr Emerg Care. 2009;25:301-306.
8. Ozuah PO, Avner JR, Stein RE. Oral rehydration, emergency physicians, and practice parameters: a national survey. Pediatrics. 2002;109:259-261.
9. Goldman RD, Friedman JN, Parkin PC. Validation of the clinical dehydration scale for children with acute gastroenteritis. Pediatrics. 2008;122:545-549.
10. Fedorowicz Z, Jagannath VA, Carter B. Antiemetics for reducing vomiting related to acute gastroenteritis in children and adolescents. Cochrane Database Syst Rev. 2011; CD005506.
1. Freedman SB, Willan AR, Boutis K, et al. Effect of dilute apple juice and preferred fluids vs electrolyte maintenance solution on treatment failure among children with mild gastroenteritis: a randomized clinical trial. JAMA. 2016;315:1966-1974.
2. King CK, Glass R, Bresee JS, et al. Managing acute gastroenteritis among children: oral rehydration, maintenance, and nutritional therapy. MMWR Recomm Rep. 2003;52:1-16.
3. World Health Organization. New formula oral rehydration salts. WHO Drug Information. 2002;16(2). http://apps.who.int/medicinedocs/en/d/Js4950e/2.4.html. Accessed December 5, 2016.
4. Cohen MB, Hardin J. Medicaid coverage of oral rehydration solutions. N Engl J Med. 1993;329:211.
5. Freedman SB, Cho D, Boutis K, et al. Assessing the palatability of oral rehydration solutions in school-aged children: a randomized crossover trial. Arch Pediatr Adolesc Med. 2010;164:696-702.
6. Reis EC, Goepp JG, Katz S, et al. Barriers to use of oral rehydration therapy. Pediatrics. 1994;93:708-711.
7. Karpas A, Finkelstein M, Reid S. Parental preference for rehydration method for children in the emergency department. Pediatr Emerg Care. 2009;25:301-306.
8. Ozuah PO, Avner JR, Stein RE. Oral rehydration, emergency physicians, and practice parameters: a national survey. Pediatrics. 2002;109:259-261.
9. Goldman RD, Friedman JN, Parkin PC. Validation of the clinical dehydration scale for children with acute gastroenteritis. Pediatrics. 2008;122:545-549.
10. Fedorowicz Z, Jagannath VA, Carter B. Antiemetics for reducing vomiting related to acute gastroenteritis in children and adolescents. Cochrane Database Syst Rev. 2011; CD005506.
Pediatric ENT Complaints: An Update
Among all of the causes of ear, nose, and throat (ENT) complaints, acute otitis media (AOM), bacterial sinusitis, and streptococcal pharyngitis (SP) are the most common infections prompting pediatric presentation to the ED. Through a series of case scenarios, along with key questions to help guide the clinician’s work-up, this review covers the proper evaluation and management of pediatric ENT complaints.
Case Scenario 1
A 13-month-old girl presented to the ED with a 1-day history of fever and runny nose. According to her parents, the child had been continually pulling on her ears in apparent discomfort. During history-taking, the parents further informed the emergency physician (EP) that the patient started daycare 4 months earlier and had two elementary school-aged siblings. The patient’s medical history was significant for otitis media, but the parents stated she had not been on antibiotics for over 4 months.
On physical examination, the patient’s vital signs were: blood pressure (BP), 75/50 mm Hg; temperature (T), 101.3°F; slight tachycardia; and normal age-adjusted respiratory rate (RR). Oxygen saturation was 100% on room air. The lungs were clear to auscultation and heart sounds were normal and without murmur. The otolaryngologic examination revealed copious yellow discharge from both nostrils, non-erythematous posterior oropharynx, and erythema to the right tympanic membrane (TM). Questions to Guide the Work-Up: (1) What physical examination findings should be present for accurate diagnosis of otitis media? (2) Will this patient require antibiotics immediately, or is a “wait-and-see” approach indicated? (3) If treatment with antibiotic therapy is warranted, what are the appropriate therapeutic regimen and duration of therapy?
Otitis Media
Acute otitis media is one of the most common presentations in young children. Defined as the rapid onset of signs and symptoms of middle ear inflammation, in conjunction with middle ear effusion (MEE), AOM can develop secondary to a viral or bacterial infection. It is estimated that more than 80% of the pediatric population will experience at least one episode of AOM by age 3 years.1-3
Risk factors for AOM include upper respiratory infection (URI), daycare attendance, siblings, parental smoking, and formula-feeding versus breastfeeding. The patient’s history may include rapid-onset otalgia, fever, irritability, anorexia, and concurrent URI symptoms, as well as other nonspecific symptoms (eg, ear rubbing and/or pulling, crying, changes in behavior and sleep patterns).2-4 In general, otalgia and ear-rubbing in the nonverbal patient seem to have the best predictive value for AOM.3
Signs and Symptoms
A normal TM should be translucent and pearly gray, with visible landmarks of the manubrium of malleus and pars flaccida. A TM that is bulging, cloudy, and immobile is the most consistent finding in AOM, with bulging having a specificity of 97%. Redness of the tympanic membrane is not a useful predictor of AOM as this finding is noted in upward of 30% of pediatric patients on general examination but in <1% of AOM diagnoses in the absence of a bulging TM.
Diagnosis
Pneumatic otoscopy is the gold standard for diagnosing for MEE; however, this examination can be difficult in younger, often uncooperative, patients. A TM that does not perceptibly move with either positive or negative insufflation pressure greatly enhances the diagnostic accuracy for MEE over the use of visible eardrum characteristics alone.2-5
Acute otitis media is a clinical diagnosis and does not require imaging studies or laboratory evaluation unless more serious processes, such as skull fracture, mastoiditis, or intracranial abscess, are being considered.2,3
Treatment and Management
Analgesia. The first step in managing patients with AOM is to provide analgesia. In most cases, acetaminophen in patients over 2 months of age, or ibuprofen in patients over 6 months of age, are adequate choices for managing pain. When either of these analgesics is administered in the clinic/ED setting, patients should be monitored to assure adequate pain relief prior to discharge.
While topical agents such as combination antipyrine-benzocaine suspensions were commonly given in the past to alleviate the pain associated with AOM, there are limited data to support their effectiveness. As such, in July 2015, the US Food and Drug Administration ordered manufacturers to halt production on these unapproved prescription products.3,4,6 There are also no randomized controlled trials (RCTs) to support the use of decongestants or antihistamines for resolution of AOM or otalgia.3,7
Antibiotic Therapy. The most common bacteria associated with AOM are Streptococcus pneumonia, nontypeable Hemophilus influenza, and Moraxella catarrhalis. In 30% of patients, the causative etiology is viral. When the decision is made to treat AOM, high-dose amoxicillin is still considered the first-line treatment, despite ever evolving susceptibilities of bacteria. 
When a child is noted to have been treated with amoxicillin within a 30-day period or who has concurrent conjunctivitis, amoxicillin-clavulanate is considered the first-line treatment.2-4,7,8 The current American Academy of Pediatrics (AAP) guidelines recommend 10 days of antibiotic therapy for children younger than age 2 years, and 5 to 7 days for children older than age 2 years who have uncomplicated AOM. Intramuscular (IM) ceftriaxone is an acceptable first-line agent in a child who is unable to tolerate oral medications or who is suffering persistent emesis. Intramuscular ceftriaxone can be given as a single dose of 50 mg/kg, though the patient should be followed closely as studies show that a second dose may be necessary 5 to 7 days later to prevent infection recurrence. The IM dose of ceftriaxone 50 mg/kg can also be given if treatment with other antibiotics fails to resolve the AOM (failure is defined as no improvement in the patient’s condition 48 to 72 hours from treatment). In such cases, ceftriaxone is given in three consecutive doses.3,4,7
Wait-and-See Approach. Studies of patients whose AOM was confirmed via culture (19% were positive for S pneumoniae, 48% for H influenza, and 78% for M catarrhalis) showed bacterial clearance without antibiotic intervention.4 Based on these findings, the 2013 revised AAP evidence-based clinical practice guidelines indicate an initial watching-and-waiting period combined with pain management for patients older than 6 months of age who are diagnosed with unilateral AOM in the absence of severe symptoms (ie, fever is lower than 102.2˚F or patient has severe otalgia).4 A period of observation prior to treatment is also endorsed for children older than age 2 years who exhibit nonsevere symptoms—even if they have bilateral disease.4
Conversely, all patients younger than age 6 months and all children with severe symptoms should be treated with antibiotics at diagnosis.3,4 The wait-and-see approach, recommends an observation period of 24 to 48 hours for children in the lower risk group prior to antibiotic administration. Delayed antibiotic administration can be performed by a physician in an office/ED follow-up or as a safety-net antibiotic prescription (SNAP) sent home with the family on the initial ED encounter.2-4,8,9
Case 1 Resolution
Given this patient’s unilateral and nonsevere symptoms (minor otalgia, fever <102.2°F), age older than 6 months, and no recent antibiotic use), she was treated with oral ibuprofen. At discharge, the parents were given a 10-day SNAP prescription of high-dose amoxicillin (90 mg/kg/d, divided into two daily doses) and instructed to fill the prescription only if the patient’s otalgia did not improve in 1 or 2 days.
Case Scenario 2
A 5-year-old boy was presented for evaluation by his parents, who stated that their son had been sick since he had started kindergarten in the fall. The patient had a 10-day history of cough, thick runny nose, and facial pain, and a 1-day history of new-onset fever and headache. His parents further noted that the patient had been seen by his pediatrician several times over the past week. At each of these visits, the pediatrician had informed them that their son had a virus.
Vital signs on examination were: BP, 100/60 mm Hg; heart rate (HR), 112 beats/min; normal age-adjusted RR; and T, 102.6oF. Oxygen saturation was 100% on room air. The patient did not appear toxic, his lungs were clear on auscultation, and there were no other clinical signs suggestive of meningitis. The otolaryngologic examination revealed bilateral thick mucoid drainage and visible edema and erythema of the nasal turbinates. The patient was noted to have some facial pain in the maxillary area bilaterally.
Questions to Guide the Work-Up: (1) Does the patient have a prolonged URI or pediatric sinusitis, and what differentiates the two conditions? (2) What sinuses are present in a 5-year-old patient? (3) What treatment modalities are available for sinusitis? (4) Is imaging of the sinuses helpful in confirming the diagnosis?
Acute Bacterial Sinusitis
Rhinosinusitis is an inflammation of the mucosal lining of the nasal passages and paranasal sinuses. Most cases occur secondary to a viral URI and resolve spontaneously in 99% of the pediatric population.10,11
Acute bacterial sinusitis (ABS) is an inflammation of the same mucosal lining of the nasal passages secondary to bacterial overgrowth that lasts more than 10 days, with complete resolution by 30 days.12,13 When evaluating a pediatric patient for ABS, it is important to consider the sinus growth and development: If the sinus is not yet formed, it therefore cannot be the location of an ABS.13 The ethmoid and maxillary sinuses are present at birth, aerated within 4 months of life, and are fully developed by age 12 years. The sphenoid sinuses begin development around age 3 years, are aerated by age 7 or 8 years, and are fully developed by age 18 to 20 years. The frontal sinuses begin development around age 8 years and are aerated and fully developed by age 12 to 15 years.10,13,14 While most guidelines focus on children older than age 1 year (due to very small infantile sinuses), ABS does occur in children younger than age 1 year.12,14
Signs and Symptoms
Differentiation between a viral URI/rhinosinusitis and ABS is a challenge and can be based upon severity of symptoms as well as length of illness. Symptoms of ABS are typically present and persistent for more than 10 days, without improvement. Continuing illness and worsening of symptoms are identifying features of ABS given most viral URIs gradually resolve within a 10-day timeframe. Other common symptoms include milky/thick nasal discharge, fever, predominantly nocturnal cough, and headache. Other less common symptoms include facial pain, toothache, malodorous breath, and periorbital edema. On physical examination, erythema and edema of the turbinates, as well as reproducible pain over aerated sinuses, are suggestive of ABS.10-14
Diagnosis
In the acute care setting, diagnosis of ABS should be clinical in nature. Neither imaging nor laboratory work-up is generally required secondary to their poor diagnostic specificity for ABS. The bacteria involved in ABS are similar to those associated with AOM, with S pneumonia, nontypeable H influenza, and M catarrhalis being the predominant organisms.10-15
Treatment and Management
Treatment of ABS is generally recommended once the diagnosis is made, though this is based largely on expert opinion as there are limited RCTs available.13 However, available studies do show a more rapid improvement in children on antibiotic therapy than those on placebo.15,16
Antibiotic Therapy. Amoxicillin remains the antimicrobial agent of choice for first-line treatment of uncomplicated ABS forsituations in which antimicrobial resistance is not suspected. In communities with a high prevalence of nonsusceptible S pneumoniae (>10%, including intermediate- and high-level resistance), treatment may be initiated at 80 to 90 mg/kg/d in two divided doses, with a maximum of 2 g per dose.
Patients presenting with moderate to severe illness, as well as those who are younger than 2 years, attend childcare, or have recently been treated with an antimicrobial, may receive high-dose amoxicillin-clavulanate as initial therapy given the elevated beta-lactamase production of the common bacteria that cause ABS.
Second-line alternatives include azithromycin, cefdinir, and sulfamethoxizole-trimethoprim (Table 1). There are data to suggest higher rates of decreased susceptibility of S pneumonia and H influenza to third-generation cephalosporins, and the addition of clindamycin may be warranted when utilizing those medications. Treatment is recommended for 10 to 14 days, though improvement should be noted within 1 to 3 days.10-12,14-17
Adjuvant Therapy. Additional therapies include nasal irrigation, decongestants, antihistamines, and intranasal steroids; however, there are only anecdotal reports of their efficacy in providing symptom relief. Therefore, there are insufficient evidence-based data to support or refute the role of these adjuvant therapies in treating pediatric patients with ABS.9,13
Case 2 Resolution
The prolonged duration and severity of symptoms (high fever and headache) and the gradual worsening of the clinical course (ie, late-onset fever) in this patient all suggest ABS rather than a simple prolonged URI. The physical examination findings of inflamed turbinates and facial pain further increase the specificity for ABS. The patient was started on oral amoxicillin-clavulanate with planned treatment for 14 days. At discharge, his parents were instructed to follow-up with the patient’s pediatrician in 3 days to ensure a degree of clinical resolution.
Case Scenario 3
A 4-year-old boy was presented by his parents for evaluation of a 2-day history of a persistent and unimproved sore throat. The patient’s mother indicated that the child’s oral T upon returning home earlier from preschool was 101.2oF. She further noted that her 17-month-old daughter and 8-year-old son also experienced similar symptoms which had self-resolved. Triage vital signs were: T, 100.8oF, orally; BP, HR, and RR were all within normal limits. Oxygen saturation was 100% on room air.
On physical examination, the child was noted to have anterior cervical lymph nodes bilaterally and an erythematous oropharynx with exudate noted on both tonsils. There were no cutaneous abnormalities, nasal edema, erythema, or drainage. Based on the clinical examination, the EP was suspicious for SP.
Questions to Guide the Work-Up: (1) Is SP diagnosed based on clinical findings alone in this patient’s age group? (2) At what age in the pediatric population is it appropriate to perform a rapid streptococcal antigen test? (3) Are there medications other than antibiotics that are beneficial in treating symptomatic SP?
Streptococcal Pharyngitis
Streptococcal pharyngitis is a clinical condition caused by group A beta-hemolytic S pyogens. This bacterium is responsible for multiple conditions, including pharyngitis, skin infections, poststreptococcal glomerulonephritis, and rheumatic fever, as well as invasive syndromes. (This case focuses solely on SP).
Pharyngitis can occur secondary to a viral or bacterial infection, and SP is the most common cause of pediatric bacterial pharyngitis. It is estimated that children aged 5 to 15 years are more commonly diagnosed with SP, although approximately 24% of children younger than age 5 years with pharyngitis symptoms will be ultimately diagnosed with SP.
Signs and Symptoms
Typical symptoms include fever, pharyngitis, generalized abdominal pain, nausea, vomiting, headache, and absence of viral URI symptoms (eg, cough, nasal discharge). However, younger patients with SP may have clinical findings of prolonged nasal drainage and excoriated nares. Examination findings may include swollen and tender anterior cervical lymph nodes; generalized edema and erythema of the posterior pharynx; tonsillar exudates; and palatal petechiae.
Diagnosis
Centor Criteria. The Centor criteria were developed to assist practitioners in identifying patients with potential SP. Criteria for patients older than age 15 years include fever, absence of cough, tonsillar exudates, and tender anterior cervical lymphadenopathy. A modified Centor criteria was later established to include children older than age 5 years, with children between ages 5 and 15 years being the fifth variable in the modified score. In general, patients with a score of 4 or 5 (presence of each variable = 1 point) are most likely to test positive for SP on rapid antigen testing (RAT) or culture.18-20
Swab, Rapid Antigen Testing, and Culture. Swabbing the throat and RAT and/or culture should be performed in most children with suspected SP because the clinical features alone do not reliably discriminate SP from viral pharyngitis. Rapid antigen testing is only specific for group A beta-hemolytic streptococcal species, which is the only streptococcal species that is routinely treated with antibiotics in the setting of acute pharyngitis. It is unlikely for a patient with a score of 0 or 1 to have SP, and several sources suggest neither testing nor treating this cohort, but rather to consider an alternative diagnosis.18-20
Within the population of children and young adolescents, due to a RAT sensitivity of 70% to 90%, a negative result should always be backed-up by a throat culture, and treatment initiated if results of the culture are later found to be positive. As the current generation of RAT tests have a high specificity, a positive RAT does not necessitate a back-up culture, and treatment is indicated without further investigation.19,20
Routine RAT is not recommended in children younger than age 3 years as patients in this age group are at low-risk of developing rheumatic fever. One notable exception for these very young children would be if there are siblings in the home with confirmed SP, in which case, RAT should be considered in the clinical context of SP.21 Adolescents over age 15 years are another cohort with a low likelihood of developing rheumatic fever, though they can develop other poststreptococcal complications, such as glomerulonephritis.
The US Centers for Disease Control and Prevention/American Academy of Family Practitioners (AAFP) guidelines suggest that pharyngitis in older adolescents can be approached in a similar fashion to adults, with empiric therapy for a Centor score of 3 or 4, RAT (without the need for follow-up culture) for Centor score of 2, and neither testing nor treating patients with a score of 0 or 1.19
Treatment and Management
Streptococcal pharyngitis is treated mainly to prevent the poststreptococcal complications of rheumatic fever, though it will not prevent poststreptococcal glomerulonephritis. Treatment of SP also facilitates resolution of symptoms and return to baseline activities.
Antibiotic Therapy. Patients who have a positive RAT or a follow-up throat culture positive for group A streptococcus should be given antibiotics. The gold standard treatment is penicillin V orally for 10 days. 
Corticosteroid Therapy. The use of corticosteroids for symptom control of SP in pediatric patients is controversial. Although the Infectious Disease Society of America does not recommend corticosteroid therapy in the treatment of SP, several studies show such therapy (namely dexamethasone), improves pain in children and adolescents diagnosed with SP, but without significant change to the overall disease course.21,23-26
Case 3 Resolution
The patient had a modified Centor criteria score of 4, as well as siblings with similar symptoms. In following current guidelines, the EP performed a RAT and back-up culture. The RAT was negative in the ED, but the back-up culture was subsequently positive, and the child was started on a 10-day course of oral amoxicillin.
Conclusion
When evaluating pediatric patients presenting with ENT signs and symptoms such as ear pain and erythema, fever, sore throat, nasal congestion and discharge, a thorough physical examination and history-taking—including recent illness of any siblings—along with testing when indicated, is essential to guide the diagnosis and determine appropriate treatment and management. In addition to administering antibiotic therapy when such is warranted, the EP should provide appropriate analgesia to manage the patient’s pain and assure relief prior to discharge.
1. Rosenfeld RM, Shin JJ, Schwartz SR, et al. Clinical practice guideline: otitis media with effusion (Update). Otolaryngol Head Neck Surg. 2016;154(1 Suppl):S1-S41. doi:10.1177/0194599815623467.
2. Acute Otitis Media Guideline Team, Cincinnati Children’s Hospital Medical Center. Evidence-based care guideline for medical management of acute otitis media in children 2 months to 13 years of age. http://f.i-md.com/medinfo/material/4f4/4eb132ba44ae4ffe12a814f4/4eb132d744ae4ffe12a814f7.pdf. August 2006. Accessed December 29, 2016.
3. Nesbit CE, Powers MC. An evidence-based approach to managing acute otitis media. Pediatr Emerg Med Pract. 2013;10(4):1-26; quiz 26-27.
4. Lieberthal AS, Carroll AE, Chonmaitree T, et al. The diagnosis and management of acute otitis media. Pediatrics. 2013;131(3):e964-e999. doi:10.1542/peds.2012-3488.
5. American Academy of Family Physicians; American Academy of Otolaryngology-Head and Neck Surgery; American Academy of Pediatrics Subcommittee on Otitis Media With Effusion. Otitis media with effusion. Pediatrics. 2004;113(5):1412-1429.
6. US Food and Drug Administration Web site. FDA: Use only approved prescription ear drops. http://www.fda.gov/ForConsumers/ConsumerUpdates/-ucm453087.htm. Updated July 10, 2015. Accessed December 15, 2016.
7. Sack F. An evidence based approach to the management of uncomplicated acute otitis media in children. Int Pediatrics. 2005;20(1):44-46.
8. Johnson NC, Holger JS. Pediatric acute otitis media: the case for delayed antibiotic treatment. J Emerg Med. 2007;32(3):279-284. doi:10.1016/j.jemermed.2006.07.029.
9. Spiro DM, Tay KY, Arnold DH, Dziura JD, Baker MD, Shapiro ED. Wait-and-see prescription for the treatment of acute otitis media: a randomized controlled trial. JAMA. 2006;296(10):1235-1241. doi:10.1001/jama.296.10.1235.
10. Brook I. Management of acute rhinosinusitis in pediatric patients. Pediatr Emerg Med Pract. 2012;9(5):1-24.
11. Ferdman RM, Linzer JF Jr. The runny nose in the emergency department: rhinitis and sinusitis. Clin Pediatr Emerg Med. 2007;8(2):123-130.
12. Acute Bacterial Sinusitis Guideline Team, Cincinnati Children’s Hospital Medical Center: Evidence-based care guideline for medical management of acute bacterial sinusitis in children 1 through 18 years of age. http://www.antibioticos.msssi.gob.es/PDF/sinusitisguideline.pdf. July 7, 2006. Accessed December 29, 2016
13. Holt KR, Murdoch Cuenca M, Cuenca PJ, Johnston GM. acute pediatric sinusitis and “the 10-day rule.” Pediatr Emerg Med Pract. 2006;3(2):1-16.
14. American Academy of Pediatrics. Subcommittee on Management of Sinusitis and Committee on Quality Improvement. Clinical practice guideline: management of sinusitis. Pediatrics. 2001;108(3):798-808.
15. Wald ER, Nash D, Eickhoff J. Effectiveness of amoxicillin/clavulanate potassium in the treatment of acute bacterial sinusitis in children. Pediatrics. 2009;124(1):9-15. doi:10.1542/peds.2008-2902.
16. Arroll B, Kenealy T. Are antibiotics effective for acute purulent rhinitis? Systematic review and meta-analysis of placebo controlled randomised trials. BMJ. 2006;333(7562):279. doi:10.1136/bmj.38891.681215.AE.
17. McQuillan L, Crane LA, Kempe A. Diagnosis and management of acute sinusitis by pediatricians. Pediatrics. 2009;123(2):e193-e198.
18. Singer JI, Fontanette R. Recognizable and suspected group A beta-hemolytic streptococcal syndromes. Pediatr Emerg Med Rep. 2010;15(11):129-144.
19. Weglowski J. An evidence-based approach to the evaluation and treatment of pharyngitis in children. Pediatr Emerg Med Pract. 2011;8(12):1-28.
20. Gerber MA, Baltimore RS, Eaton CB, et al. Prevention of rheumatic fever and diagnosis and treatment of acute Streptococcal pharyngitis: a scientific statement from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee of the Council on Cardiovascular Disease in the Young, the Interdisciplinary Council on Functional Genomics and Translational Biology, and the Interdisciplinary Council on Quality of Care and Outcomes Research: endorsed by the American Academy of Pediatrics. Circulation. 2009;119(11):1541-1551. doi:10.1161/CIRCULATIONAHA.109.191959.
21. Shulman ST, Bisno AL, Clegg HW, et al. Clinical practice guideline for the diagnosis and management of group A streptococcal pharyngitis: 2012 update by the Infectious Diseases Society of America. Clin Infect Dis. 2012;55(10):1279-1282. doi:10.1093/cid/cis847.
22. Clegg HW, Ryan AG, Dallas SD, et al. Treatment of streptococcal pharyngitis with once-daily compared with twice-daily amoxicillin: a noninferiority trial. Pediatr Infect Dis J. 2006;25(9):761-767. doi:10.1097/01.inf.0000235678.46805.92.
23. Bulloch B, Kabani A, Tenenbein M. Oral dexamethasone for the treatment of pain in children with acute pharyngitis: a randomized, double-blind, placebo-controlled trial. Ann Emerg Med. 2003;41(5):601-608. doi:10.1067/mem.2003.136.
24. Niland ML, Bonsu BK, Nuss KE, Goodman DG. A pilot study of 1 versus 3 days of dexamethasone as add-on therapy in children with streptococcal pharyngitis. Pediatr Infect Dis J. 2006;25(6):477-481. doi:10.1097/01.inf.0000219469.95772.3f.
25. Wei JL, Kasperbauer JL, Weaver AL, Boggust AJ. Efficacy of single-dose dexamethasone as adjuvant therapy for acute pharyngitis. Laryngoscope. 2002;112(1):87-93. doi:10.1097/00005537-200201000-00016.
26. Hayward G, Thompson M, Heneghan C, Perera R, Del Mar C, Glasziou P. Corticosteroids for pain relief in sore throat: systematic review and meta-analysis. BMJ. 2009;339:b2976. doi:10.1136/bmj.b2976.
Among all of the causes of ear, nose, and throat (ENT) complaints, acute otitis media (AOM), bacterial sinusitis, and streptococcal pharyngitis (SP) are the most common infections prompting pediatric presentation to the ED. Through a series of case scenarios, along with key questions to help guide the clinician’s work-up, this review covers the proper evaluation and management of pediatric ENT complaints.
Case Scenario 1
A 13-month-old girl presented to the ED with a 1-day history of fever and runny nose. According to her parents, the child had been continually pulling on her ears in apparent discomfort. During history-taking, the parents further informed the emergency physician (EP) that the patient started daycare 4 months earlier and had two elementary school-aged siblings. The patient’s medical history was significant for otitis media, but the parents stated she had not been on antibiotics for over 4 months.
On physical examination, the patient’s vital signs were: blood pressure (BP), 75/50 mm Hg; temperature (T), 101.3°F; slight tachycardia; and normal age-adjusted respiratory rate (RR). Oxygen saturation was 100% on room air. The lungs were clear to auscultation and heart sounds were normal and without murmur. The otolaryngologic examination revealed copious yellow discharge from both nostrils, non-erythematous posterior oropharynx, and erythema to the right tympanic membrane (TM). Questions to Guide the Work-Up: (1) What physical examination findings should be present for accurate diagnosis of otitis media? (2) Will this patient require antibiotics immediately, or is a “wait-and-see” approach indicated? (3) If treatment with antibiotic therapy is warranted, what are the appropriate therapeutic regimen and duration of therapy?
Otitis Media
Acute otitis media is one of the most common presentations in young children. Defined as the rapid onset of signs and symptoms of middle ear inflammation, in conjunction with middle ear effusion (MEE), AOM can develop secondary to a viral or bacterial infection. It is estimated that more than 80% of the pediatric population will experience at least one episode of AOM by age 3 years.1-3
Risk factors for AOM include upper respiratory infection (URI), daycare attendance, siblings, parental smoking, and formula-feeding versus breastfeeding. The patient’s history may include rapid-onset otalgia, fever, irritability, anorexia, and concurrent URI symptoms, as well as other nonspecific symptoms (eg, ear rubbing and/or pulling, crying, changes in behavior and sleep patterns).2-4 In general, otalgia and ear-rubbing in the nonverbal patient seem to have the best predictive value for AOM.3
Signs and Symptoms
A normal TM should be translucent and pearly gray, with visible landmarks of the manubrium of malleus and pars flaccida. A TM that is bulging, cloudy, and immobile is the most consistent finding in AOM, with bulging having a specificity of 97%. Redness of the tympanic membrane is not a useful predictor of AOM as this finding is noted in upward of 30% of pediatric patients on general examination but in <1% of AOM diagnoses in the absence of a bulging TM.
Diagnosis
Pneumatic otoscopy is the gold standard for diagnosing for MEE; however, this examination can be difficult in younger, often uncooperative, patients. A TM that does not perceptibly move with either positive or negative insufflation pressure greatly enhances the diagnostic accuracy for MEE over the use of visible eardrum characteristics alone.2-5
Acute otitis media is a clinical diagnosis and does not require imaging studies or laboratory evaluation unless more serious processes, such as skull fracture, mastoiditis, or intracranial abscess, are being considered.2,3
Treatment and Management
Analgesia. The first step in managing patients with AOM is to provide analgesia. In most cases, acetaminophen in patients over 2 months of age, or ibuprofen in patients over 6 months of age, are adequate choices for managing pain. When either of these analgesics is administered in the clinic/ED setting, patients should be monitored to assure adequate pain relief prior to discharge.
While topical agents such as combination antipyrine-benzocaine suspensions were commonly given in the past to alleviate the pain associated with AOM, there are limited data to support their effectiveness. As such, in July 2015, the US Food and Drug Administration ordered manufacturers to halt production on these unapproved prescription products.3,4,6 There are also no randomized controlled trials (RCTs) to support the use of decongestants or antihistamines for resolution of AOM or otalgia.3,7
Antibiotic Therapy. The most common bacteria associated with AOM are Streptococcus pneumonia, nontypeable Hemophilus influenza, and Moraxella catarrhalis. In 30% of patients, the causative etiology is viral. When the decision is made to treat AOM, high-dose amoxicillin is still considered the first-line treatment, despite ever evolving susceptibilities of bacteria.
When a child is noted to have been treated with amoxicillin within a 30-day period or who has concurrent conjunctivitis, amoxicillin-clavulanate is considered the first-line treatment.2-4,7,8 The current American Academy of Pediatrics (AAP) guidelines recommend 10 days of antibiotic therapy for children younger than age 2 years, and 5 to 7 days for children older than age 2 years who have uncomplicated AOM. Intramuscular (IM) ceftriaxone is an acceptable first-line agent in a child who is unable to tolerate oral medications or who is suffering persistent emesis. Intramuscular ceftriaxone can be given as a single dose of 50 mg/kg, though the patient should be followed closely as studies show that a second dose may be necessary 5 to 7 days later to prevent infection recurrence. The IM dose of ceftriaxone 50 mg/kg can also be given if treatment with other antibiotics fails to resolve the AOM (failure is defined as no improvement in the patient’s condition 48 to 72 hours from treatment). In such cases, ceftriaxone is given in three consecutive doses.3,4,7
Wait-and-See Approach. Studies of patients whose AOM was confirmed via culture (19% were positive for S pneumoniae, 48% for H influenza, and 78% for M catarrhalis) showed bacterial clearance without antibiotic intervention.4 Based on these findings, the 2013 revised AAP evidence-based clinical practice guidelines indicate an initial watching-and-waiting period combined with pain management for patients older than 6 months of age who are diagnosed with unilateral AOM in the absence of severe symptoms (ie, fever is lower than 102.2˚F or patient has severe otalgia).4 A period of observation prior to treatment is also endorsed for children older than age 2 years who exhibit nonsevere symptoms—even if they have bilateral disease.4
Conversely, all patients younger than age 6 months and all children with severe symptoms should be treated with antibiotics at diagnosis.3,4 The wait-and-see approach, recommends an observation period of 24 to 48 hours for children in the lower risk group prior to antibiotic administration. Delayed antibiotic administration can be performed by a physician in an office/ED follow-up or as a safety-net antibiotic prescription (SNAP) sent home with the family on the initial ED encounter.2-4,8,9
Case 1 Resolution
Given this patient’s unilateral and nonsevere symptoms (minor otalgia, fever <102.2°F), age older than 6 months, and no recent antibiotic use), she was treated with oral ibuprofen. At discharge, the parents were given a 10-day SNAP prescription of high-dose amoxicillin (90 mg/kg/d, divided into two daily doses) and instructed to fill the prescription only if the patient’s otalgia did not improve in 1 or 2 days.
Case Scenario 2
A 5-year-old boy was presented for evaluation by his parents, who stated that their son had been sick since he had started kindergarten in the fall. The patient had a 10-day history of cough, thick runny nose, and facial pain, and a 1-day history of new-onset fever and headache. His parents further noted that the patient had been seen by his pediatrician several times over the past week. At each of these visits, the pediatrician had informed them that their son had a virus.
Vital signs on examination were: BP, 100/60 mm Hg; heart rate (HR), 112 beats/min; normal age-adjusted RR; and T, 102.6oF. Oxygen saturation was 100% on room air. The patient did not appear toxic, his lungs were clear on auscultation, and there were no other clinical signs suggestive of meningitis. The otolaryngologic examination revealed bilateral thick mucoid drainage and visible edema and erythema of the nasal turbinates. The patient was noted to have some facial pain in the maxillary area bilaterally.
Questions to Guide the Work-Up: (1) Does the patient have a prolonged URI or pediatric sinusitis, and what differentiates the two conditions? (2) What sinuses are present in a 5-year-old patient? (3) What treatment modalities are available for sinusitis? (4) Is imaging of the sinuses helpful in confirming the diagnosis?
Acute Bacterial Sinusitis
Rhinosinusitis is an inflammation of the mucosal lining of the nasal passages and paranasal sinuses. Most cases occur secondary to a viral URI and resolve spontaneously in 99% of the pediatric population.10,11
Acute bacterial sinusitis (ABS) is an inflammation of the same mucosal lining of the nasal passages secondary to bacterial overgrowth that lasts more than 10 days, with complete resolution by 30 days.12,13 When evaluating a pediatric patient for ABS, it is important to consider the sinus growth and development: If the sinus is not yet formed, it therefore cannot be the location of an ABS.13 The ethmoid and maxillary sinuses are present at birth, aerated within 4 months of life, and are fully developed by age 12 years. The sphenoid sinuses begin development around age 3 years, are aerated by age 7 or 8 years, and are fully developed by age 18 to 20 years. The frontal sinuses begin development around age 8 years and are aerated and fully developed by age 12 to 15 years.10,13,14 While most guidelines focus on children older than age 1 year (due to very small infantile sinuses), ABS does occur in children younger than age 1 year.12,14
Signs and Symptoms
Differentiation between a viral URI/rhinosinusitis and ABS is a challenge and can be based upon severity of symptoms as well as length of illness. Symptoms of ABS are typically present and persistent for more than 10 days, without improvement. Continuing illness and worsening of symptoms are identifying features of ABS given most viral URIs gradually resolve within a 10-day timeframe. Other common symptoms include milky/thick nasal discharge, fever, predominantly nocturnal cough, and headache. Other less common symptoms include facial pain, toothache, malodorous breath, and periorbital edema. On physical examination, erythema and edema of the turbinates, as well as reproducible pain over aerated sinuses, are suggestive of ABS.10-14
Diagnosis
In the acute care setting, diagnosis of ABS should be clinical in nature. Neither imaging nor laboratory work-up is generally required secondary to their poor diagnostic specificity for ABS. The bacteria involved in ABS are similar to those associated with AOM, with S pneumonia, nontypeable H influenza, and M catarrhalis being the predominant organisms.10-15
Treatment and Management
Treatment of ABS is generally recommended once the diagnosis is made, though this is based largely on expert opinion as there are limited RCTs available.13 However, available studies do show a more rapid improvement in children on antibiotic therapy than those on placebo.15,16
Antibiotic Therapy. Amoxicillin remains the antimicrobial agent of choice for first-line treatment of uncomplicated ABS forsituations in which antimicrobial resistance is not suspected. In communities with a high prevalence of nonsusceptible S pneumoniae (>10%, including intermediate- and high-level resistance), treatment may be initiated at 80 to 90 mg/kg/d in two divided doses, with a maximum of 2 g per dose.
Patients presenting with moderate to severe illness, as well as those who are younger than 2 years, attend childcare, or have recently been treated with an antimicrobial, may receive high-dose amoxicillin-clavulanate as initial therapy given the elevated beta-lactamase production of the common bacteria that cause ABS.
Second-line alternatives include azithromycin, cefdinir, and sulfamethoxizole-trimethoprim (Table 1). There are data to suggest higher rates of decreased susceptibility of S pneumonia and H influenza to third-generation cephalosporins, and the addition of clindamycin may be warranted when utilizing those medications. Treatment is recommended for 10 to 14 days, though improvement should be noted within 1 to 3 days.10-12,14-17
Adjuvant Therapy. Additional therapies include nasal irrigation, decongestants, antihistamines, and intranasal steroids; however, there are only anecdotal reports of their efficacy in providing symptom relief. Therefore, there are insufficient evidence-based data to support or refute the role of these adjuvant therapies in treating pediatric patients with ABS.9,13
Case 2 Resolution
The prolonged duration and severity of symptoms (high fever and headache) and the gradual worsening of the clinical course (ie, late-onset fever) in this patient all suggest ABS rather than a simple prolonged URI. The physical examination findings of inflamed turbinates and facial pain further increase the specificity for ABS. The patient was started on oral amoxicillin-clavulanate with planned treatment for 14 days. At discharge, his parents were instructed to follow-up with the patient’s pediatrician in 3 days to ensure a degree of clinical resolution.
Case Scenario 3
A 4-year-old boy was presented by his parents for evaluation of a 2-day history of a persistent and unimproved sore throat. The patient’s mother indicated that the child’s oral T upon returning home earlier from preschool was 101.2oF. She further noted that her 17-month-old daughter and 8-year-old son also experienced similar symptoms which had self-resolved. Triage vital signs were: T, 100.8oF, orally; BP, HR, and RR were all within normal limits. Oxygen saturation was 100% on room air.
On physical examination, the child was noted to have anterior cervical lymph nodes bilaterally and an erythematous oropharynx with exudate noted on both tonsils. There were no cutaneous abnormalities, nasal edema, erythema, or drainage. Based on the clinical examination, the EP was suspicious for SP.
Questions to Guide the Work-Up: (1) Is SP diagnosed based on clinical findings alone in this patient’s age group? (2) At what age in the pediatric population is it appropriate to perform a rapid streptococcal antigen test? (3) Are there medications other than antibiotics that are beneficial in treating symptomatic SP?
Streptococcal Pharyngitis
Streptococcal pharyngitis is a clinical condition caused by group A beta-hemolytic S pyogens. This bacterium is responsible for multiple conditions, including pharyngitis, skin infections, poststreptococcal glomerulonephritis, and rheumatic fever, as well as invasive syndromes. (This case focuses solely on SP).
Pharyngitis can occur secondary to a viral or bacterial infection, and SP is the most common cause of pediatric bacterial pharyngitis. It is estimated that children aged 5 to 15 years are more commonly diagnosed with SP, although approximately 24% of children younger than age 5 years with pharyngitis symptoms will be ultimately diagnosed with SP.
Signs and Symptoms
Typical symptoms include fever, pharyngitis, generalized abdominal pain, nausea, vomiting, headache, and absence of viral URI symptoms (eg, cough, nasal discharge). However, younger patients with SP may have clinical findings of prolonged nasal drainage and excoriated nares. Examination findings may include swollen and tender anterior cervical lymph nodes; generalized edema and erythema of the posterior pharynx; tonsillar exudates; and palatal petechiae.
Diagnosis
Centor Criteria. The Centor criteria were developed to assist practitioners in identifying patients with potential SP. Criteria for patients older than age 15 years include fever, absence of cough, tonsillar exudates, and tender anterior cervical lymphadenopathy. A modified Centor criteria was later established to include children older than age 5 years, with children between ages 5 and 15 years being the fifth variable in the modified score. In general, patients with a score of 4 or 5 (presence of each variable = 1 point) are most likely to test positive for SP on rapid antigen testing (RAT) or culture.18-20
Swab, Rapid Antigen Testing, and Culture. Swabbing the throat and RAT and/or culture should be performed in most children with suspected SP because the clinical features alone do not reliably discriminate SP from viral pharyngitis. Rapid antigen testing is only specific for group A beta-hemolytic streptococcal species, which is the only streptococcal species that is routinely treated with antibiotics in the setting of acute pharyngitis. It is unlikely for a patient with a score of 0 or 1 to have SP, and several sources suggest neither testing nor treating this cohort, but rather to consider an alternative diagnosis.18-20
Within the population of children and young adolescents, due to a RAT sensitivity of 70% to 90%, a negative result should always be backed-up by a throat culture, and treatment initiated if results of the culture are later found to be positive. As the current generation of RAT tests have a high specificity, a positive RAT does not necessitate a back-up culture, and treatment is indicated without further investigation.19,20
Routine RAT is not recommended in children younger than age 3 years as patients in this age group are at low-risk of developing rheumatic fever. One notable exception for these very young children would be if there are siblings in the home with confirmed SP, in which case, RAT should be considered in the clinical context of SP.21 Adolescents over age 15 years are another cohort with a low likelihood of developing rheumatic fever, though they can develop other poststreptococcal complications, such as glomerulonephritis.
The US Centers for Disease Control and Prevention/American Academy of Family Practitioners (AAFP) guidelines suggest that pharyngitis in older adolescents can be approached in a similar fashion to adults, with empiric therapy for a Centor score of 3 or 4, RAT (without the need for follow-up culture) for Centor score of 2, and neither testing nor treating patients with a score of 0 or 1.19
Treatment and Management
Streptococcal pharyngitis is treated mainly to prevent the poststreptococcal complications of rheumatic fever, though it will not prevent poststreptococcal glomerulonephritis. Treatment of SP also facilitates resolution of symptoms and return to baseline activities.
Antibiotic Therapy. Patients who have a positive RAT or a follow-up throat culture positive for group A streptococcus should be given antibiotics. The gold standard treatment is penicillin V orally for 10 days.
Corticosteroid Therapy. The use of corticosteroids for symptom control of SP in pediatric patients is controversial. Although the Infectious Disease Society of America does not recommend corticosteroid therapy in the treatment of SP, several studies show such therapy (namely dexamethasone), improves pain in children and adolescents diagnosed with SP, but without significant change to the overall disease course.21,23-26
Case 3 Resolution
The patient had a modified Centor criteria score of 4, as well as siblings with similar symptoms. In following current guidelines, the EP performed a RAT and back-up culture. The RAT was negative in the ED, but the back-up culture was subsequently positive, and the child was started on a 10-day course of oral amoxicillin.
Conclusion
When evaluating pediatric patients presenting with ENT signs and symptoms such as ear pain and erythema, fever, sore throat, nasal congestion and discharge, a thorough physical examination and history-taking—including recent illness of any siblings—along with testing when indicated, is essential to guide the diagnosis and determine appropriate treatment and management. In addition to administering antibiotic therapy when such is warranted, the EP should provide appropriate analgesia to manage the patient’s pain and assure relief prior to discharge.
Among all of the causes of ear, nose, and throat (ENT) complaints, acute otitis media (AOM), bacterial sinusitis, and streptococcal pharyngitis (SP) are the most common infections prompting pediatric presentation to the ED. Through a series of case scenarios, along with key questions to help guide the clinician’s work-up, this review covers the proper evaluation and management of pediatric ENT complaints.
Case Scenario 1
A 13-month-old girl presented to the ED with a 1-day history of fever and runny nose. According to her parents, the child had been continually pulling on her ears in apparent discomfort. During history-taking, the parents further informed the emergency physician (EP) that the patient started daycare 4 months earlier and had two elementary school-aged siblings. The patient’s medical history was significant for otitis media, but the parents stated she had not been on antibiotics for over 4 months.
On physical examination, the patient’s vital signs were: blood pressure (BP), 75/50 mm Hg; temperature (T), 101.3°F; slight tachycardia; and normal age-adjusted respiratory rate (RR). Oxygen saturation was 100% on room air. The lungs were clear to auscultation and heart sounds were normal and without murmur. The otolaryngologic examination revealed copious yellow discharge from both nostrils, non-erythematous posterior oropharynx, and erythema to the right tympanic membrane (TM). Questions to Guide the Work-Up: (1) What physical examination findings should be present for accurate diagnosis of otitis media? (2) Will this patient require antibiotics immediately, or is a “wait-and-see” approach indicated? (3) If treatment with antibiotic therapy is warranted, what are the appropriate therapeutic regimen and duration of therapy?
Otitis Media
Acute otitis media is one of the most common presentations in young children. Defined as the rapid onset of signs and symptoms of middle ear inflammation, in conjunction with middle ear effusion (MEE), AOM can develop secondary to a viral or bacterial infection. It is estimated that more than 80% of the pediatric population will experience at least one episode of AOM by age 3 years.1-3
Risk factors for AOM include upper respiratory infection (URI), daycare attendance, siblings, parental smoking, and formula-feeding versus breastfeeding. The patient’s history may include rapid-onset otalgia, fever, irritability, anorexia, and concurrent URI symptoms, as well as other nonspecific symptoms (eg, ear rubbing and/or pulling, crying, changes in behavior and sleep patterns).2-4 In general, otalgia and ear-rubbing in the nonverbal patient seem to have the best predictive value for AOM.3
Signs and Symptoms
A normal TM should be translucent and pearly gray, with visible landmarks of the manubrium of malleus and pars flaccida. A TM that is bulging, cloudy, and immobile is the most consistent finding in AOM, with bulging having a specificity of 97%. Redness of the tympanic membrane is not a useful predictor of AOM as this finding is noted in upward of 30% of pediatric patients on general examination but in <1% of AOM diagnoses in the absence of a bulging TM.
Diagnosis
Pneumatic otoscopy is the gold standard for diagnosing for MEE; however, this examination can be difficult in younger, often uncooperative, patients. A TM that does not perceptibly move with either positive or negative insufflation pressure greatly enhances the diagnostic accuracy for MEE over the use of visible eardrum characteristics alone.2-5
Acute otitis media is a clinical diagnosis and does not require imaging studies or laboratory evaluation unless more serious processes, such as skull fracture, mastoiditis, or intracranial abscess, are being considered.2,3
Treatment and Management
Analgesia. The first step in managing patients with AOM is to provide analgesia. In most cases, acetaminophen in patients over 2 months of age, or ibuprofen in patients over 6 months of age, are adequate choices for managing pain. When either of these analgesics is administered in the clinic/ED setting, patients should be monitored to assure adequate pain relief prior to discharge.
While topical agents such as combination antipyrine-benzocaine suspensions were commonly given in the past to alleviate the pain associated with AOM, there are limited data to support their effectiveness. As such, in July 2015, the US Food and Drug Administration ordered manufacturers to halt production on these unapproved prescription products.3,4,6 There are also no randomized controlled trials (RCTs) to support the use of decongestants or antihistamines for resolution of AOM or otalgia.3,7
Antibiotic Therapy. The most common bacteria associated with AOM are Streptococcus pneumonia, nontypeable Hemophilus influenza, and Moraxella catarrhalis. In 30% of patients, the causative etiology is viral. When the decision is made to treat AOM, high-dose amoxicillin is still considered the first-line treatment, despite ever evolving susceptibilities of bacteria.
When a child is noted to have been treated with amoxicillin within a 30-day period or who has concurrent conjunctivitis, amoxicillin-clavulanate is considered the first-line treatment.2-4,7,8 The current American Academy of Pediatrics (AAP) guidelines recommend 10 days of antibiotic therapy for children younger than age 2 years, and 5 to 7 days for children older than age 2 years who have uncomplicated AOM. Intramuscular (IM) ceftriaxone is an acceptable first-line agent in a child who is unable to tolerate oral medications or who is suffering persistent emesis. Intramuscular ceftriaxone can be given as a single dose of 50 mg/kg, though the patient should be followed closely as studies show that a second dose may be necessary 5 to 7 days later to prevent infection recurrence. The IM dose of ceftriaxone 50 mg/kg can also be given if treatment with other antibiotics fails to resolve the AOM (failure is defined as no improvement in the patient’s condition 48 to 72 hours from treatment). In such cases, ceftriaxone is given in three consecutive doses.3,4,7
Wait-and-See Approach. Studies of patients whose AOM was confirmed via culture (19% were positive for S pneumoniae, 48% for H influenza, and 78% for M catarrhalis) showed bacterial clearance without antibiotic intervention.4 Based on these findings, the 2013 revised AAP evidence-based clinical practice guidelines indicate an initial watching-and-waiting period combined with pain management for patients older than 6 months of age who are diagnosed with unilateral AOM in the absence of severe symptoms (ie, fever is lower than 102.2˚F or patient has severe otalgia).4 A period of observation prior to treatment is also endorsed for children older than age 2 years who exhibit nonsevere symptoms—even if they have bilateral disease.4
Conversely, all patients younger than age 6 months and all children with severe symptoms should be treated with antibiotics at diagnosis.3,4 The wait-and-see approach, recommends an observation period of 24 to 48 hours for children in the lower risk group prior to antibiotic administration. Delayed antibiotic administration can be performed by a physician in an office/ED follow-up or as a safety-net antibiotic prescription (SNAP) sent home with the family on the initial ED encounter.2-4,8,9
Case 1 Resolution
Given this patient’s unilateral and nonsevere symptoms (minor otalgia, fever <102.2°F), age older than 6 months, and no recent antibiotic use), she was treated with oral ibuprofen. At discharge, the parents were given a 10-day SNAP prescription of high-dose amoxicillin (90 mg/kg/d, divided into two daily doses) and instructed to fill the prescription only if the patient’s otalgia did not improve in 1 or 2 days.
Case Scenario 2
A 5-year-old boy was presented for evaluation by his parents, who stated that their son had been sick since he had started kindergarten in the fall. The patient had a 10-day history of cough, thick runny nose, and facial pain, and a 1-day history of new-onset fever and headache. His parents further noted that the patient had been seen by his pediatrician several times over the past week. At each of these visits, the pediatrician had informed them that their son had a virus.
Vital signs on examination were: BP, 100/60 mm Hg; heart rate (HR), 112 beats/min; normal age-adjusted RR; and T, 102.6oF. Oxygen saturation was 100% on room air. The patient did not appear toxic, his lungs were clear on auscultation, and there were no other clinical signs suggestive of meningitis. The otolaryngologic examination revealed bilateral thick mucoid drainage and visible edema and erythema of the nasal turbinates. The patient was noted to have some facial pain in the maxillary area bilaterally.
Questions to Guide the Work-Up: (1) Does the patient have a prolonged URI or pediatric sinusitis, and what differentiates the two conditions? (2) What sinuses are present in a 5-year-old patient? (3) What treatment modalities are available for sinusitis? (4) Is imaging of the sinuses helpful in confirming the diagnosis?
Acute Bacterial Sinusitis
Rhinosinusitis is an inflammation of the mucosal lining of the nasal passages and paranasal sinuses. Most cases occur secondary to a viral URI and resolve spontaneously in 99% of the pediatric population.10,11
Acute bacterial sinusitis (ABS) is an inflammation of the same mucosal lining of the nasal passages secondary to bacterial overgrowth that lasts more than 10 days, with complete resolution by 30 days.12,13 When evaluating a pediatric patient for ABS, it is important to consider the sinus growth and development: If the sinus is not yet formed, it therefore cannot be the location of an ABS.13 The ethmoid and maxillary sinuses are present at birth, aerated within 4 months of life, and are fully developed by age 12 years. The sphenoid sinuses begin development around age 3 years, are aerated by age 7 or 8 years, and are fully developed by age 18 to 20 years. The frontal sinuses begin development around age 8 years and are aerated and fully developed by age 12 to 15 years.10,13,14 While most guidelines focus on children older than age 1 year (due to very small infantile sinuses), ABS does occur in children younger than age 1 year.12,14
Signs and Symptoms
Differentiation between a viral URI/rhinosinusitis and ABS is a challenge and can be based upon severity of symptoms as well as length of illness. Symptoms of ABS are typically present and persistent for more than 10 days, without improvement. Continuing illness and worsening of symptoms are identifying features of ABS given most viral URIs gradually resolve within a 10-day timeframe. Other common symptoms include milky/thick nasal discharge, fever, predominantly nocturnal cough, and headache. Other less common symptoms include facial pain, toothache, malodorous breath, and periorbital edema. On physical examination, erythema and edema of the turbinates, as well as reproducible pain over aerated sinuses, are suggestive of ABS.10-14
Diagnosis
In the acute care setting, diagnosis of ABS should be clinical in nature. Neither imaging nor laboratory work-up is generally required secondary to their poor diagnostic specificity for ABS. The bacteria involved in ABS are similar to those associated with AOM, with S pneumonia, nontypeable H influenza, and M catarrhalis being the predominant organisms.10-15
Treatment and Management
Treatment of ABS is generally recommended once the diagnosis is made, though this is based largely on expert opinion as there are limited RCTs available.13 However, available studies do show a more rapid improvement in children on antibiotic therapy than those on placebo.15,16
Antibiotic Therapy. Amoxicillin remains the antimicrobial agent of choice for first-line treatment of uncomplicated ABS forsituations in which antimicrobial resistance is not suspected. In communities with a high prevalence of nonsusceptible S pneumoniae (>10%, including intermediate- and high-level resistance), treatment may be initiated at 80 to 90 mg/kg/d in two divided doses, with a maximum of 2 g per dose.
Patients presenting with moderate to severe illness, as well as those who are younger than 2 years, attend childcare, or have recently been treated with an antimicrobial, may receive high-dose amoxicillin-clavulanate as initial therapy given the elevated beta-lactamase production of the common bacteria that cause ABS.
Second-line alternatives include azithromycin, cefdinir, and sulfamethoxizole-trimethoprim (Table 1). There are data to suggest higher rates of decreased susceptibility of S pneumonia and H influenza to third-generation cephalosporins, and the addition of clindamycin may be warranted when utilizing those medications. Treatment is recommended for 10 to 14 days, though improvement should be noted within 1 to 3 days.10-12,14-17
Adjuvant Therapy. Additional therapies include nasal irrigation, decongestants, antihistamines, and intranasal steroids; however, there are only anecdotal reports of their efficacy in providing symptom relief. Therefore, there are insufficient evidence-based data to support or refute the role of these adjuvant therapies in treating pediatric patients with ABS.9,13
Case 2 Resolution
The prolonged duration and severity of symptoms (high fever and headache) and the gradual worsening of the clinical course (ie, late-onset fever) in this patient all suggest ABS rather than a simple prolonged URI. The physical examination findings of inflamed turbinates and facial pain further increase the specificity for ABS. The patient was started on oral amoxicillin-clavulanate with planned treatment for 14 days. At discharge, his parents were instructed to follow-up with the patient’s pediatrician in 3 days to ensure a degree of clinical resolution.
Case Scenario 3
A 4-year-old boy was presented by his parents for evaluation of a 2-day history of a persistent and unimproved sore throat. The patient’s mother indicated that the child’s oral T upon returning home earlier from preschool was 101.2oF. She further noted that her 17-month-old daughter and 8-year-old son also experienced similar symptoms which had self-resolved. Triage vital signs were: T, 100.8oF, orally; BP, HR, and RR were all within normal limits. Oxygen saturation was 100% on room air.
On physical examination, the child was noted to have anterior cervical lymph nodes bilaterally and an erythematous oropharynx with exudate noted on both tonsils. There were no cutaneous abnormalities, nasal edema, erythema, or drainage. Based on the clinical examination, the EP was suspicious for SP.
Questions to Guide the Work-Up: (1) Is SP diagnosed based on clinical findings alone in this patient’s age group? (2) At what age in the pediatric population is it appropriate to perform a rapid streptococcal antigen test? (3) Are there medications other than antibiotics that are beneficial in treating symptomatic SP?
Streptococcal Pharyngitis
Streptococcal pharyngitis is a clinical condition caused by group A beta-hemolytic S pyogens. This bacterium is responsible for multiple conditions, including pharyngitis, skin infections, poststreptococcal glomerulonephritis, and rheumatic fever, as well as invasive syndromes. (This case focuses solely on SP).
Pharyngitis can occur secondary to a viral or bacterial infection, and SP is the most common cause of pediatric bacterial pharyngitis. It is estimated that children aged 5 to 15 years are more commonly diagnosed with SP, although approximately 24% of children younger than age 5 years with pharyngitis symptoms will be ultimately diagnosed with SP.
Signs and Symptoms
Typical symptoms include fever, pharyngitis, generalized abdominal pain, nausea, vomiting, headache, and absence of viral URI symptoms (eg, cough, nasal discharge). However, younger patients with SP may have clinical findings of prolonged nasal drainage and excoriated nares. Examination findings may include swollen and tender anterior cervical lymph nodes; generalized edema and erythema of the posterior pharynx; tonsillar exudates; and palatal petechiae.
Diagnosis
Centor Criteria. The Centor criteria were developed to assist practitioners in identifying patients with potential SP. Criteria for patients older than age 15 years include fever, absence of cough, tonsillar exudates, and tender anterior cervical lymphadenopathy. A modified Centor criteria was later established to include children older than age 5 years, with children between ages 5 and 15 years being the fifth variable in the modified score. In general, patients with a score of 4 or 5 (presence of each variable = 1 point) are most likely to test positive for SP on rapid antigen testing (RAT) or culture.18-20
Swab, Rapid Antigen Testing, and Culture. Swabbing the throat and RAT and/or culture should be performed in most children with suspected SP because the clinical features alone do not reliably discriminate SP from viral pharyngitis. Rapid antigen testing is only specific for group A beta-hemolytic streptococcal species, which is the only streptococcal species that is routinely treated with antibiotics in the setting of acute pharyngitis. It is unlikely for a patient with a score of 0 or 1 to have SP, and several sources suggest neither testing nor treating this cohort, but rather to consider an alternative diagnosis.18-20
Within the population of children and young adolescents, due to a RAT sensitivity of 70% to 90%, a negative result should always be backed-up by a throat culture, and treatment initiated if results of the culture are later found to be positive. As the current generation of RAT tests have a high specificity, a positive RAT does not necessitate a back-up culture, and treatment is indicated without further investigation.19,20
Routine RAT is not recommended in children younger than age 3 years as patients in this age group are at low-risk of developing rheumatic fever. One notable exception for these very young children would be if there are siblings in the home with confirmed SP, in which case, RAT should be considered in the clinical context of SP.21 Adolescents over age 15 years are another cohort with a low likelihood of developing rheumatic fever, though they can develop other poststreptococcal complications, such as glomerulonephritis.
The US Centers for Disease Control and Prevention/American Academy of Family Practitioners (AAFP) guidelines suggest that pharyngitis in older adolescents can be approached in a similar fashion to adults, with empiric therapy for a Centor score of 3 or 4, RAT (without the need for follow-up culture) for Centor score of 2, and neither testing nor treating patients with a score of 0 or 1.19
Treatment and Management
Streptococcal pharyngitis is treated mainly to prevent the poststreptococcal complications of rheumatic fever, though it will not prevent poststreptococcal glomerulonephritis. Treatment of SP also facilitates resolution of symptoms and return to baseline activities.
Antibiotic Therapy. Patients who have a positive RAT or a follow-up throat culture positive for group A streptococcus should be given antibiotics. The gold standard treatment is penicillin V orally for 10 days.
Corticosteroid Therapy. The use of corticosteroids for symptom control of SP in pediatric patients is controversial. Although the Infectious Disease Society of America does not recommend corticosteroid therapy in the treatment of SP, several studies show such therapy (namely dexamethasone), improves pain in children and adolescents diagnosed with SP, but without significant change to the overall disease course.21,23-26
Case 3 Resolution
The patient had a modified Centor criteria score of 4, as well as siblings with similar symptoms. In following current guidelines, the EP performed a RAT and back-up culture. The RAT was negative in the ED, but the back-up culture was subsequently positive, and the child was started on a 10-day course of oral amoxicillin.
Conclusion
When evaluating pediatric patients presenting with ENT signs and symptoms such as ear pain and erythema, fever, sore throat, nasal congestion and discharge, a thorough physical examination and history-taking—including recent illness of any siblings—along with testing when indicated, is essential to guide the diagnosis and determine appropriate treatment and management. In addition to administering antibiotic therapy when such is warranted, the EP should provide appropriate analgesia to manage the patient’s pain and assure relief prior to discharge.
1. Rosenfeld RM, Shin JJ, Schwartz SR, et al. Clinical practice guideline: otitis media with effusion (Update). Otolaryngol Head Neck Surg. 2016;154(1 Suppl):S1-S41. doi:10.1177/0194599815623467.
2. Acute Otitis Media Guideline Team, Cincinnati Children’s Hospital Medical Center. Evidence-based care guideline for medical management of acute otitis media in children 2 months to 13 years of age. http://f.i-md.com/medinfo/material/4f4/4eb132ba44ae4ffe12a814f4/4eb132d744ae4ffe12a814f7.pdf. August 2006. Accessed December 29, 2016.
3. Nesbit CE, Powers MC. An evidence-based approach to managing acute otitis media. Pediatr Emerg Med Pract. 2013;10(4):1-26; quiz 26-27.
4. Lieberthal AS, Carroll AE, Chonmaitree T, et al. The diagnosis and management of acute otitis media. Pediatrics. 2013;131(3):e964-e999. doi:10.1542/peds.2012-3488.
5. American Academy of Family Physicians; American Academy of Otolaryngology-Head and Neck Surgery; American Academy of Pediatrics Subcommittee on Otitis Media With Effusion. Otitis media with effusion. Pediatrics. 2004;113(5):1412-1429.
6. US Food and Drug Administration Web site. FDA: Use only approved prescription ear drops. http://www.fda.gov/ForConsumers/ConsumerUpdates/-ucm453087.htm. Updated July 10, 2015. Accessed December 15, 2016.
7. Sack F. An evidence based approach to the management of uncomplicated acute otitis media in children. Int Pediatrics. 2005;20(1):44-46.
8. Johnson NC, Holger JS. Pediatric acute otitis media: the case for delayed antibiotic treatment. J Emerg Med. 2007;32(3):279-284. doi:10.1016/j.jemermed.2006.07.029.
9. Spiro DM, Tay KY, Arnold DH, Dziura JD, Baker MD, Shapiro ED. Wait-and-see prescription for the treatment of acute otitis media: a randomized controlled trial. JAMA. 2006;296(10):1235-1241. doi:10.1001/jama.296.10.1235.
10. Brook I. Management of acute rhinosinusitis in pediatric patients. Pediatr Emerg Med Pract. 2012;9(5):1-24.
11. Ferdman RM, Linzer JF Jr. The runny nose in the emergency department: rhinitis and sinusitis. Clin Pediatr Emerg Med. 2007;8(2):123-130.
12. Acute Bacterial Sinusitis Guideline Team, Cincinnati Children’s Hospital Medical Center: Evidence-based care guideline for medical management of acute bacterial sinusitis in children 1 through 18 years of age. http://www.antibioticos.msssi.gob.es/PDF/sinusitisguideline.pdf. July 7, 2006. Accessed December 29, 2016
13. Holt KR, Murdoch Cuenca M, Cuenca PJ, Johnston GM. acute pediatric sinusitis and “the 10-day rule.” Pediatr Emerg Med Pract. 2006;3(2):1-16.
14. American Academy of Pediatrics. Subcommittee on Management of Sinusitis and Committee on Quality Improvement. Clinical practice guideline: management of sinusitis. Pediatrics. 2001;108(3):798-808.
15. Wald ER, Nash D, Eickhoff J. Effectiveness of amoxicillin/clavulanate potassium in the treatment of acute bacterial sinusitis in children. Pediatrics. 2009;124(1):9-15. doi:10.1542/peds.2008-2902.
16. Arroll B, Kenealy T. Are antibiotics effective for acute purulent rhinitis? Systematic review and meta-analysis of placebo controlled randomised trials. BMJ. 2006;333(7562):279. doi:10.1136/bmj.38891.681215.AE.
17. McQuillan L, Crane LA, Kempe A. Diagnosis and management of acute sinusitis by pediatricians. Pediatrics. 2009;123(2):e193-e198.
18. Singer JI, Fontanette R. Recognizable and suspected group A beta-hemolytic streptococcal syndromes. Pediatr Emerg Med Rep. 2010;15(11):129-144.
19. Weglowski J. An evidence-based approach to the evaluation and treatment of pharyngitis in children. Pediatr Emerg Med Pract. 2011;8(12):1-28.
20. Gerber MA, Baltimore RS, Eaton CB, et al. Prevention of rheumatic fever and diagnosis and treatment of acute Streptococcal pharyngitis: a scientific statement from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee of the Council on Cardiovascular Disease in the Young, the Interdisciplinary Council on Functional Genomics and Translational Biology, and the Interdisciplinary Council on Quality of Care and Outcomes Research: endorsed by the American Academy of Pediatrics. Circulation. 2009;119(11):1541-1551. doi:10.1161/CIRCULATIONAHA.109.191959.
21. Shulman ST, Bisno AL, Clegg HW, et al. Clinical practice guideline for the diagnosis and management of group A streptococcal pharyngitis: 2012 update by the Infectious Diseases Society of America. Clin Infect Dis. 2012;55(10):1279-1282. doi:10.1093/cid/cis847.
22. Clegg HW, Ryan AG, Dallas SD, et al. Treatment of streptococcal pharyngitis with once-daily compared with twice-daily amoxicillin: a noninferiority trial. Pediatr Infect Dis J. 2006;25(9):761-767. doi:10.1097/01.inf.0000235678.46805.92.
23. Bulloch B, Kabani A, Tenenbein M. Oral dexamethasone for the treatment of pain in children with acute pharyngitis: a randomized, double-blind, placebo-controlled trial. Ann Emerg Med. 2003;41(5):601-608. doi:10.1067/mem.2003.136.
24. Niland ML, Bonsu BK, Nuss KE, Goodman DG. A pilot study of 1 versus 3 days of dexamethasone as add-on therapy in children with streptococcal pharyngitis. Pediatr Infect Dis J. 2006;25(6):477-481. doi:10.1097/01.inf.0000219469.95772.3f.
25. Wei JL, Kasperbauer JL, Weaver AL, Boggust AJ. Efficacy of single-dose dexamethasone as adjuvant therapy for acute pharyngitis. Laryngoscope. 2002;112(1):87-93. doi:10.1097/00005537-200201000-00016.
26. Hayward G, Thompson M, Heneghan C, Perera R, Del Mar C, Glasziou P. Corticosteroids for pain relief in sore throat: systematic review and meta-analysis. BMJ. 2009;339:b2976. doi:10.1136/bmj.b2976.
1. Rosenfeld RM, Shin JJ, Schwartz SR, et al. Clinical practice guideline: otitis media with effusion (Update). Otolaryngol Head Neck Surg. 2016;154(1 Suppl):S1-S41. doi:10.1177/0194599815623467.
2. Acute Otitis Media Guideline Team, Cincinnati Children’s Hospital Medical Center. Evidence-based care guideline for medical management of acute otitis media in children 2 months to 13 years of age. http://f.i-md.com/medinfo/material/4f4/4eb132ba44ae4ffe12a814f4/4eb132d744ae4ffe12a814f7.pdf. August 2006. Accessed December 29, 2016.
3. Nesbit CE, Powers MC. An evidence-based approach to managing acute otitis media. Pediatr Emerg Med Pract. 2013;10(4):1-26; quiz 26-27.
4. Lieberthal AS, Carroll AE, Chonmaitree T, et al. The diagnosis and management of acute otitis media. Pediatrics. 2013;131(3):e964-e999. doi:10.1542/peds.2012-3488.
5. American Academy of Family Physicians; American Academy of Otolaryngology-Head and Neck Surgery; American Academy of Pediatrics Subcommittee on Otitis Media With Effusion. Otitis media with effusion. Pediatrics. 2004;113(5):1412-1429.
6. US Food and Drug Administration Web site. FDA: Use only approved prescription ear drops. http://www.fda.gov/ForConsumers/ConsumerUpdates/-ucm453087.htm. Updated July 10, 2015. Accessed December 15, 2016.
7. Sack F. An evidence based approach to the management of uncomplicated acute otitis media in children. Int Pediatrics. 2005;20(1):44-46.
8. Johnson NC, Holger JS. Pediatric acute otitis media: the case for delayed antibiotic treatment. J Emerg Med. 2007;32(3):279-284. doi:10.1016/j.jemermed.2006.07.029.
9. Spiro DM, Tay KY, Arnold DH, Dziura JD, Baker MD, Shapiro ED. Wait-and-see prescription for the treatment of acute otitis media: a randomized controlled trial. JAMA. 2006;296(10):1235-1241. doi:10.1001/jama.296.10.1235.
10. Brook I. Management of acute rhinosinusitis in pediatric patients. Pediatr Emerg Med Pract. 2012;9(5):1-24.
11. Ferdman RM, Linzer JF Jr. The runny nose in the emergency department: rhinitis and sinusitis. Clin Pediatr Emerg Med. 2007;8(2):123-130.
12. Acute Bacterial Sinusitis Guideline Team, Cincinnati Children’s Hospital Medical Center: Evidence-based care guideline for medical management of acute bacterial sinusitis in children 1 through 18 years of age. http://www.antibioticos.msssi.gob.es/PDF/sinusitisguideline.pdf. July 7, 2006. Accessed December 29, 2016
13. Holt KR, Murdoch Cuenca M, Cuenca PJ, Johnston GM. acute pediatric sinusitis and “the 10-day rule.” Pediatr Emerg Med Pract. 2006;3(2):1-16.
14. American Academy of Pediatrics. Subcommittee on Management of Sinusitis and Committee on Quality Improvement. Clinical practice guideline: management of sinusitis. Pediatrics. 2001;108(3):798-808.
15. Wald ER, Nash D, Eickhoff J. Effectiveness of amoxicillin/clavulanate potassium in the treatment of acute bacterial sinusitis in children. Pediatrics. 2009;124(1):9-15. doi:10.1542/peds.2008-2902.
16. Arroll B, Kenealy T. Are antibiotics effective for acute purulent rhinitis? Systematic review and meta-analysis of placebo controlled randomised trials. BMJ. 2006;333(7562):279. doi:10.1136/bmj.38891.681215.AE.
17. McQuillan L, Crane LA, Kempe A. Diagnosis and management of acute sinusitis by pediatricians. Pediatrics. 2009;123(2):e193-e198.
18. Singer JI, Fontanette R. Recognizable and suspected group A beta-hemolytic streptococcal syndromes. Pediatr Emerg Med Rep. 2010;15(11):129-144.
19. Weglowski J. An evidence-based approach to the evaluation and treatment of pharyngitis in children. Pediatr Emerg Med Pract. 2011;8(12):1-28.
20. Gerber MA, Baltimore RS, Eaton CB, et al. Prevention of rheumatic fever and diagnosis and treatment of acute Streptococcal pharyngitis: a scientific statement from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee of the Council on Cardiovascular Disease in the Young, the Interdisciplinary Council on Functional Genomics and Translational Biology, and the Interdisciplinary Council on Quality of Care and Outcomes Research: endorsed by the American Academy of Pediatrics. Circulation. 2009;119(11):1541-1551. doi:10.1161/CIRCULATIONAHA.109.191959.
21. Shulman ST, Bisno AL, Clegg HW, et al. Clinical practice guideline for the diagnosis and management of group A streptococcal pharyngitis: 2012 update by the Infectious Diseases Society of America. Clin Infect Dis. 2012;55(10):1279-1282. doi:10.1093/cid/cis847.
22. Clegg HW, Ryan AG, Dallas SD, et al. Treatment of streptococcal pharyngitis with once-daily compared with twice-daily amoxicillin: a noninferiority trial. Pediatr Infect Dis J. 2006;25(9):761-767. doi:10.1097/01.inf.0000235678.46805.92.
23. Bulloch B, Kabani A, Tenenbein M. Oral dexamethasone for the treatment of pain in children with acute pharyngitis: a randomized, double-blind, placebo-controlled trial. Ann Emerg Med. 2003;41(5):601-608. doi:10.1067/mem.2003.136.
24. Niland ML, Bonsu BK, Nuss KE, Goodman DG. A pilot study of 1 versus 3 days of dexamethasone as add-on therapy in children with streptococcal pharyngitis. Pediatr Infect Dis J. 2006;25(6):477-481. doi:10.1097/01.inf.0000219469.95772.3f.
25. Wei JL, Kasperbauer JL, Weaver AL, Boggust AJ. Efficacy of single-dose dexamethasone as adjuvant therapy for acute pharyngitis. Laryngoscope. 2002;112(1):87-93. doi:10.1097/00005537-200201000-00016.
26. Hayward G, Thompson M, Heneghan C, Perera R, Del Mar C, Glasziou P. Corticosteroids for pain relief in sore throat: systematic review and meta-analysis. BMJ. 2009;339:b2976. doi:10.1136/bmj.b2976.
First-trimester blood glucose predicts congenital heart disease risk
NEW ORLEANS – A single, random, first-trimester maternal plasma glucose measurement is superior to an oral glucose tolerance test later in pregnancy as a predictor of congenital heart disease in newborns, Emmi Helle, MD, reported at the American Heart Association scientific sessions.
This finding from a large retrospective study, if confirmed in a prospective data set, is likely to be practice changing. At present, a 1-hour oral glucose tolerance test in the second or third trimester is considered the best means of identifying pregnant women who ought to undergo fetal echocardiography for prenatal diagnosis of congenital heart disease, noted Dr. Helle of Stanford (Calif.) University.
An elevated random plasma glucose value in the first trimester was broadly predictive of increased risk for a variety of congenital heart anomalies, not just, for example, cyanotic conditions.
Fetal heart development is completed during the first trimester, Dr. Helle observed.
Her study received a warm reception. Michael A. Portman, MD, singled it out in his final-day wrap-up of the meeting’s highlights in the field of congenital heart disease.
Several studies have demonstrated that prenatal diagnosis of congenital heart disease results in improved surgical outcomes in newborns. The question is, how to get the right women – those at increased risk – to diagnostic fetal echocardiography. Guidelines suggest but don’t mandate on the basis of weak evidence that an oral glucose tolerance test performed in the second or early third trimester may be a useful means of screening mothers for fetal imaging. Dr. Helle’s study points to a better way.
“Hopefully we can change our guidelines and make them more scientific for identification of mothers who should undergo fetal echocardiography,” said Dr. Portman, professor of pediatrics at the University of Washington, Seattle, and director of pediatric cardiovascular research at Seattle Children’s Hospital.
Dr. Helle and Dr. Portman reported having no relevant financial interests.
NEW ORLEANS – A single, random, first-trimester maternal plasma glucose measurement is superior to an oral glucose tolerance test later in pregnancy as a predictor of congenital heart disease in newborns, Emmi Helle, MD, reported at the American Heart Association scientific sessions.
This finding from a large retrospective study, if confirmed in a prospective data set, is likely to be practice changing. At present, a 1-hour oral glucose tolerance test in the second or third trimester is considered the best means of identifying pregnant women who ought to undergo fetal echocardiography for prenatal diagnosis of congenital heart disease, noted Dr. Helle of Stanford (Calif.) University.
An elevated random plasma glucose value in the first trimester was broadly predictive of increased risk for a variety of congenital heart anomalies, not just, for example, cyanotic conditions.
Fetal heart development is completed during the first trimester, Dr. Helle observed.
Her study received a warm reception. Michael A. Portman, MD, singled it out in his final-day wrap-up of the meeting’s highlights in the field of congenital heart disease.
Several studies have demonstrated that prenatal diagnosis of congenital heart disease results in improved surgical outcomes in newborns. The question is, how to get the right women – those at increased risk – to diagnostic fetal echocardiography. Guidelines suggest but don’t mandate on the basis of weak evidence that an oral glucose tolerance test performed in the second or early third trimester may be a useful means of screening mothers for fetal imaging. Dr. Helle’s study points to a better way.
“Hopefully we can change our guidelines and make them more scientific for identification of mothers who should undergo fetal echocardiography,” said Dr. Portman, professor of pediatrics at the University of Washington, Seattle, and director of pediatric cardiovascular research at Seattle Children’s Hospital.
Dr. Helle and Dr. Portman reported having no relevant financial interests.
NEW ORLEANS – A single, random, first-trimester maternal plasma glucose measurement is superior to an oral glucose tolerance test later in pregnancy as a predictor of congenital heart disease in newborns, Emmi Helle, MD, reported at the American Heart Association scientific sessions.
This finding from a large retrospective study, if confirmed in a prospective data set, is likely to be practice changing. At present, a 1-hour oral glucose tolerance test in the second or third trimester is considered the best means of identifying pregnant women who ought to undergo fetal echocardiography for prenatal diagnosis of congenital heart disease, noted Dr. Helle of Stanford (Calif.) University.
An elevated random plasma glucose value in the first trimester was broadly predictive of increased risk for a variety of congenital heart anomalies, not just, for example, cyanotic conditions.
Fetal heart development is completed during the first trimester, Dr. Helle observed.
Her study received a warm reception. Michael A. Portman, MD, singled it out in his final-day wrap-up of the meeting’s highlights in the field of congenital heart disease.
Several studies have demonstrated that prenatal diagnosis of congenital heart disease results in improved surgical outcomes in newborns. The question is, how to get the right women – those at increased risk – to diagnostic fetal echocardiography. Guidelines suggest but don’t mandate on the basis of weak evidence that an oral glucose tolerance test performed in the second or early third trimester may be a useful means of screening mothers for fetal imaging. Dr. Helle’s study points to a better way.
“Hopefully we can change our guidelines and make them more scientific for identification of mothers who should undergo fetal echocardiography,” said Dr. Portman, professor of pediatrics at the University of Washington, Seattle, and director of pediatric cardiovascular research at Seattle Children’s Hospital.
Dr. Helle and Dr. Portman reported having no relevant financial interests.
AT THE AHA SCIENTIFIC SESSIONS
Key clinical point:
Major finding: For every 10-mg/dL increase in maternal plasma glucose on a random first-trimester measurement, the risk of giving birth to a baby with congenital heart disease rose by 8%.
Data source: A retrospective study of 19,197 pregnancies, 811 of which resulted in congenital heart disease in the offspring.
Disclosures: The presenter reported having no financial conflicts of interest regarding the study.
Guidelines for diagnosing TB in adults, children
A clinical practice guideline for diagnosing pulmonary, extrapulmonary, and latent tuberculosis in adults and children has been released jointly by the American Thoracic Society, the Centers for Disease Control and Prevention, and the Infectious Diseases Society of America.
The American Academy of Pediatrics also provided input to the guideline, which includes 23 evidence-based recommendations. The document is intended to assist clinicians in high-resource countries with a low incidence of TB disease and latent TB infection, such as the United States, said David M. Lewinsohn, MD, PhD, and his associates on the joint task force that wrote the guideline.
Even though the case rate is relatively low in the United States and has declined in recent years, “an estimated 11 million persons are infected with Mycobacterium tuberculosis. Thus … there remains a large reservoir of individuals who are infected. Without the application of improved diagnosis and effective treatment for latent [disease], new cases of TB will develop from within this group,” they noted (Clin Infect Dis. 2016 Dec 8;64[2]:e1-33. doi: 10.1093/cid/ciw694).
Among the guidelines’ strongest recommendations:
• Acid-fast bacilli smear microscopy should be performed in all patients suspected of having pulmonary TB, using at least three sputum samples. A sputum volume of at least 3 mL is needed, but 5-10 mL would be better.
• Both liquid and solid mycobacterial cultures should be performed on every specimen from patients suspected of having TB disease, rather than either type alone.
• A diagnostic nucleic acid amplification test should be performed on the initial specimen from patients suspected of having pulmonary TB.
• Rapid molecular drug susceptibility testing of respiratory specimens is advised for certain patients, with a focus on testing for rifampin susceptibility with or without isoniazid.
• Patients suspected of having extrapulmonary TB also should have mycobacterial cultures performed on all specimens.
• For all mycobacterial cultures that are positive for TB, a culture isolate should be submitted for genotyping to a regional genotyping laboratory.
• For patients aged 5 and older who are suspected of having latent TB infection, an interferon-gamma release assay (IGRA) is advised rather than a tuberculin skin test, especially if the patient is not likely to return to have the test result read. A tuberculin skin test is an acceptable alternative if IGRA is not available, is too expensive, or is too burdensome.
The guideline also addresses bronchoscopic sampling, cell counts and chemistries from fluid specimens collected from sites suspected of harboring extrapulmonary TB (such as pleural, cerebrospinal, ascetic, or joint fluids), and measurement of adenosine deaminase levels.
This work was supported by the American Thoracic Society, the Centers for Disease Control and Prevention, and the Infectious Diseases Society of America, with input from the American Academy of Pediatrics. Dr. Lewinsohn reported having no relevant financial disclosures; his associates reported ties to numerous industry sources.
A clinical practice guideline for diagnosing pulmonary, extrapulmonary, and latent tuberculosis in adults and children has been released jointly by the American Thoracic Society, the Centers for Disease Control and Prevention, and the Infectious Diseases Society of America.
The American Academy of Pediatrics also provided input to the guideline, which includes 23 evidence-based recommendations. The document is intended to assist clinicians in high-resource countries with a low incidence of TB disease and latent TB infection, such as the United States, said David M. Lewinsohn, MD, PhD, and his associates on the joint task force that wrote the guideline.
Even though the case rate is relatively low in the United States and has declined in recent years, “an estimated 11 million persons are infected with Mycobacterium tuberculosis. Thus … there remains a large reservoir of individuals who are infected. Without the application of improved diagnosis and effective treatment for latent [disease], new cases of TB will develop from within this group,” they noted (Clin Infect Dis. 2016 Dec 8;64[2]:e1-33. doi: 10.1093/cid/ciw694).
Among the guidelines’ strongest recommendations:
• Acid-fast bacilli smear microscopy should be performed in all patients suspected of having pulmonary TB, using at least three sputum samples. A sputum volume of at least 3 mL is needed, but 5-10 mL would be better.
• Both liquid and solid mycobacterial cultures should be performed on every specimen from patients suspected of having TB disease, rather than either type alone.
• A diagnostic nucleic acid amplification test should be performed on the initial specimen from patients suspected of having pulmonary TB.
• Rapid molecular drug susceptibility testing of respiratory specimens is advised for certain patients, with a focus on testing for rifampin susceptibility with or without isoniazid.
• Patients suspected of having extrapulmonary TB also should have mycobacterial cultures performed on all specimens.
• For all mycobacterial cultures that are positive for TB, a culture isolate should be submitted for genotyping to a regional genotyping laboratory.
• For patients aged 5 and older who are suspected of having latent TB infection, an interferon-gamma release assay (IGRA) is advised rather than a tuberculin skin test, especially if the patient is not likely to return to have the test result read. A tuberculin skin test is an acceptable alternative if IGRA is not available, is too expensive, or is too burdensome.
The guideline also addresses bronchoscopic sampling, cell counts and chemistries from fluid specimens collected from sites suspected of harboring extrapulmonary TB (such as pleural, cerebrospinal, ascetic, or joint fluids), and measurement of adenosine deaminase levels.
This work was supported by the American Thoracic Society, the Centers for Disease Control and Prevention, and the Infectious Diseases Society of America, with input from the American Academy of Pediatrics. Dr. Lewinsohn reported having no relevant financial disclosures; his associates reported ties to numerous industry sources.
A clinical practice guideline for diagnosing pulmonary, extrapulmonary, and latent tuberculosis in adults and children has been released jointly by the American Thoracic Society, the Centers for Disease Control and Prevention, and the Infectious Diseases Society of America.
The American Academy of Pediatrics also provided input to the guideline, which includes 23 evidence-based recommendations. The document is intended to assist clinicians in high-resource countries with a low incidence of TB disease and latent TB infection, such as the United States, said David M. Lewinsohn, MD, PhD, and his associates on the joint task force that wrote the guideline.
Even though the case rate is relatively low in the United States and has declined in recent years, “an estimated 11 million persons are infected with Mycobacterium tuberculosis. Thus … there remains a large reservoir of individuals who are infected. Without the application of improved diagnosis and effective treatment for latent [disease], new cases of TB will develop from within this group,” they noted (Clin Infect Dis. 2016 Dec 8;64[2]:e1-33. doi: 10.1093/cid/ciw694).
Among the guidelines’ strongest recommendations:
• Acid-fast bacilli smear microscopy should be performed in all patients suspected of having pulmonary TB, using at least three sputum samples. A sputum volume of at least 3 mL is needed, but 5-10 mL would be better.
• Both liquid and solid mycobacterial cultures should be performed on every specimen from patients suspected of having TB disease, rather than either type alone.
• A diagnostic nucleic acid amplification test should be performed on the initial specimen from patients suspected of having pulmonary TB.
• Rapid molecular drug susceptibility testing of respiratory specimens is advised for certain patients, with a focus on testing for rifampin susceptibility with or without isoniazid.
• Patients suspected of having extrapulmonary TB also should have mycobacterial cultures performed on all specimens.
• For all mycobacterial cultures that are positive for TB, a culture isolate should be submitted for genotyping to a regional genotyping laboratory.
• For patients aged 5 and older who are suspected of having latent TB infection, an interferon-gamma release assay (IGRA) is advised rather than a tuberculin skin test, especially if the patient is not likely to return to have the test result read. A tuberculin skin test is an acceptable alternative if IGRA is not available, is too expensive, or is too burdensome.
The guideline also addresses bronchoscopic sampling, cell counts and chemistries from fluid specimens collected from sites suspected of harboring extrapulmonary TB (such as pleural, cerebrospinal, ascetic, or joint fluids), and measurement of adenosine deaminase levels.
This work was supported by the American Thoracic Society, the Centers for Disease Control and Prevention, and the Infectious Diseases Society of America, with input from the American Academy of Pediatrics. Dr. Lewinsohn reported having no relevant financial disclosures; his associates reported ties to numerous industry sources.
FROM CLINICAL INFECTIOUS DISEASES
Key clinical point: jointly by the American Thoracic Society, the Centers for Disease Control and Prevention, and the Infectious Diseases Society of America.
Major finding: The clinical practice guideline includes 23 evidence-based recommendations concerning diagnostic testing for latent, pulmonary, or extrapulmonary tuberculosis in adults and children.
Data source: A compilation of 23 evidence-based recommendations about diagnostic testing for tuberculosis.
Disclosures: This work was supported by the American Thoracic Society, the Centers for Disease Control and Prevention, and the Infectious Diseases Society of America, with input from the American Academy of Pediatrics. Dr. Lewinsohn reported having no relevant financial disclosures; his associates reported ties to numerous industry sources.