What Are the Clinical Signs and Symptoms of Congenital Syphilis?

Patient Presentation
A 5-day-old male came to clinic for his well-child examination. He was taking formula every 2-3 hours and his mother complained that she was quite tired from feeding him. The past medical history showed his 19-year-old G3P1 mother had received prenatal care but was living in transitional housing. She had been working until his birth at a restaurant. She had been positive on several occasions for sexually transmitted infections including syphilis before conception and had been treated. During pregnancy she was treated at his first appointment for chlamydia and tested negative for other sexually transmitted infections including syphilis and HIV. She had been re-screened at different points during pregnancy and was negative.

The patient’s clinical course showed that he had no complications and a normal physical examination. Neonatology had been consulted and as the mother had been adequately treated before and during pregnancy, no specific evaluation or treatment for any sexually transmitted disease was recommended.

The pertinent physical exam showed a healthy male who was down 3% from his birth weight. Growth parameters were around the 25th percentile.

The diagnosis of a healthy male was made. The mother had been offered social work support during their admission and asked for additional help with transportation and food programs. The resident and the staff physician both discussed that they knew that the incidence of syphilis was increasing but had not treated anyone for it in a long time.

The patient’s clinical course showed that several health supervision appointments were missed or rescheduled, however by his 12 month appointment he had received all of his vaccines, they were now living a shared apartment, and his mother had two steady part-time jobs.

Discussion
Syphilis is caused by the spirochete Treponema pallidum. It is a very old disease that despite understanding the organism and readily available treatment, still causes disease. Syphilis is transmitted sexually. According to the Centers for Disease Control, “[i]n 2018, a total of 35,063 cases of [Primary and Secondary] syphilis were reported in the United States, yielding a rate of 10.8 cases per 100,000 population …. This rate represents a 14.9% increase compared with 2017 (9.4 cases per 100,000 population), and a 71.4% increase compared with 2014 (6.3 cases per 100,000 population).” The increase is associated with an increase in men, particularly men who have sex with men. Syphilis is also considered a risk factor for Human Immunodeficiency Virus (HIV).

Syphilis can also be transmitted to the fetus because of the maternal spirochetemia and transplacental transmission resulting in congenital syphilis if not treated. Transmission increases with the advancing pregnancy but can occur at any time. Fetuses and infants can be affected from birth or years later. “After decreasing from 10.5 to 8.4 reported congenital syphilis cases per 100,000 live births during 2008-2012, the rate of reported congenital syphilis has subsequently increased each year since 2012. In 2018, there were a total of 1,306 reported cases of congenital syphilis, including 78 syphilitic stillbirths and 16 infant deaths, and a national rate of 33.1 cases per 100,000 live births. This rate represents a 39.7% increase relative to 2017 (23.7 cases per 100,000 live births) and a 185.3% increase relative to 2014 (11.6 cases per 100,000 live births).”

Evaluation includes a detailed history and physical examination. Early congenital syphilis is also associated with anemia, thrombocytopenia, abnormal liver enzymes, and cerebrospinal fluid with pleocytosis and elevated protein. The diagnosis is made by detection of spirochetes or antibodies in body tissues or fluids. Two commonly used serological tests are rapid plasma reagin (RPR) and Venereal Disease Research Laboratory tests (VDRL). Prevention is key so all pregnant women are tested at their first prenatal appointment in the first trimester and again later in pregnancy (28-32 week gestation) if in high risk areas. Women who are positive for syphilis and their sexual partners should be screened for HIV as well and appropriately managed and treated including their newborns. Treatment for syphilis is penicillin, but the timing and length of treatment varies by clinical status including age and symptoms. Normal infants of women adequately treated before pregnancy do not need evaluation or treatment usually. Normal infants of women adequately treated during pregnancy and at least 4 weeks before delivery are not evaluated but are treated with one dose of penicillin. Infants of women with shorter durations of treatment or with abnormal physical examinations require more evaluation and longer durations of treatment.

Adolescents with sexually transmitted infections should be screened for syphilis as multi-organism infections are common. Syphilis has 3 stages. Primary syphilis has characteristic painless chancres at the site of primary inoculation. Secondary syphilis has symptoms similar to early congenital syphilis but especially a polymorphous rash on palms and soles, lymphadenopathy and fever. If untreated syphilis enters a latent stage and is not contagious during this time. Tertiary syphilis occurs 10-30 years after primary infection and classically has granulomatous skin growths and cardiac and neurological problems. Neurosyphilis can occur at any stage of symptomatic infection.

Learning Point
Clinical signs and symptoms of congenital syphilis include:

  • Fetal affects
    • Abortion, spontaneous
    • Still birth
    • Preterm delivery
    • Hydrops (non-immune)
    • Perinatal death
  • Early congenital syphilis or infants and children affected before 2 years of age
    • Adenopathy – especially epitrochlear nodes that are palpable
    • Dermatological findings
      • Rash – usually maculopapular and oval, it is more prominent on the palms and soles and becomes more copper- colored and has desquamation.
      • Pemphigus syphiliticus has bullous lesions that may cause cracking and peeling and wrinkling.
      • Oral mucus patches
      • Condylomata lata
    • Hepatomegaly – can occur with or without jaundice
    • Splenomegaly
    • Neurological findings – asymptomatic, cranial nerve palsies, seizures
    • Ophthalmological findings – cataract, chorioretinitis
    • Orthopaedic findings – osterochronditis, periostitis
    • Pneumonia alba
    • Rhinitis (‘snuffles”)
    • Other
      • Fever
      • Hypopituitarism and diabetes insipidus
      • Malabsorption in the gastrointestinal tract
      • Myocarditis
      • Nephrotic syndrome
      • Pancreatitis
  • Late congenital syphilis or children affected after 2 years of age
    • Dental findings – Hutchinson’s teeth*, mulberry molars
    • Rhagades – cracks in the skin particularly edges of the mouth
    • Neurological findings – cranial nerve palsies, deafness*, optic nerve atrophy, general paresis, hydrocephalus, mental retardation, seizures
    • Ophthalmological findings – healed chorioretinitis, interstitial keratitis*
    • Orthopaedic findings – facial changes including frontal bossing, saddle nose deformity, high arch palate, protuberant mandible, short maxilla, saber shins and abnormal joints

*Hutchinson’s triad of late congenital syphilis is Hutchinson’s teeth, deafness and interstital keratitis.

Questions for Further Discussion
1. Name the TORCH infections?
2. What are the most common sexually transmitted infections in your location? How common is syphilis?
3. What services are available in your community for teenage mothers?

Related Cases

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

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

Information prescriptions for patients can be found at MedlinePlus for these topics: Syphilis and Infections and Pregnancy.

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

To view images related to this topic check Google Images.

To view videos related to this topic check YouTube Videos.

Cooper JM, Sanchez PJ. Congenital syphilis. Semin Perinatol. 2018;42(3):176-184. doi:10.1053/j.semperi.2018.02.005

Heston S, Arnold S. Syphilis in Children. Infect Dis Clin North Am. 2018;32(1):129-144. doi:10.1016/j.idc.2017.11.007

Syphilis – 2018 Sexually Transmitted Diseases Surveillance. Published October 8, 2019. Accessed June 16, 2020. https://www.cdc.gov/std/stats18/syphilis.htm

Arrieta AC, Singh J. Congenital Syphilis. New England Journal of Medicine. Published online November 27, 2019. doi:10.1056/NEJMicm1904420

Author
Donna M. D’Alessandro, MD
Professor of Pediatrics, University of Iowa

What Are Systemic Disease Causes of Oral Ulcers?

Patient Presentation
A 10-year-old male came to clinic for his health supervision visit. He and his mother had no questions, but during the physical examination the mother said that he had intermittent oral ulcerations. He had them at least monthly and had had them for years. She had never asked his dentist or pediatrician as she said “she forgot about it” in between the episodes. He said that they were not painful, would occur on different parts of his lips and teeth and would go away in a few days. He denied any lesions any place else. He denied any visual problems including dry or itchy eyes. He was not having any lesions currently. The past medical history and review of systems were negative. The family history was positive for autoimmune hepatitis in his grandmother.

The pertinent physical exam showed a healthy male with normal growth parameters and vital signs. His oral examination was negative.

The diagnosis of a healthy male was made. The pediatrician said that he couldn’t remember too many reasons for chronic ulcers other than Bechet’s disease and ulcerative colitis. Both of these seemed unlikely in the boy because of his own and family history. “He doesn’t seem to have any systemic disease that would cause them, but there are also other causes. However, we probably should get to the bottom of this, so call your dentist the next time this occurs and have him or her take a look at the lesions. Then maybe we can figure out if anything else needs to be done. Maybe they can even take some pictures and if we need to, we can send them to the oral pathologist at the state dental school,” said the pediatrician.

Discussion
Oral ulcers are common problems seen by dentists but pediatricians also see them. Usually families have are concerned because they are painful and acute. Ulcers are sometime noticed by the physician and not the family as in the case of herpangina or hand-foot and mouth disease. Chronic or recurrent ulcerations present less commonly and therefore it may be more difficult to determine their etiology. Many of the systemic disease causes of oral ulcers are overall infrequent and/or not common in the pediatric age range.

Ulcers can be classified in several ways but acute ulcers are usually painful and last less than 2 weeks and chronic ulcers may or may not be painful and lasts more than 2 weeks. Minor ulcers are considered to be 5 mm, can be deep, usually are single lesions and can heal with scaring. They heal within 7-10 days.

Trauma (e.g. mechanical, heat, chemical) is one of the most common reasons for ulcers. These generally heal quickly unless there is ongoing trauma such as a habit.

Recurrent apthous stomatitis (RAS) or canker sores present clinically as shallow with a necrotic center and red halo surrounding the ulceration. They are very commonly seen in younger children. The cause is unknown but probably the patient has genetic susceptibility with another health problems that exacerbates the stomatitis and/or other agents that trigger then such as medication, food, etc. Herpetiform aphthous ulcers are a variation of RAS that are < 1 mm and occur in clusters.

Treatment for minor ulcers is usually palliative good oral hygiene, and potentially antibiotic oral rinses, silver nitrate cauterization or topical corticosteroids. For major ulcers, corticosteroids or other medications such as azothioprine, mycophelylate, and others are used. Dental referral can be considered if usual treatment does not work or the clinical presentation is not clear.

Learning Point
The differential diagnosis of leukoplakia also overlaps oral ulcers and can be reviewed here.

The differential diagnosis of oral ulcers includes:

  • Trauma – one of most common
  • Recurrent aphthous stomatitis including Herpetiform aphthous ulcers
  • Hormonal
    • Puberty
    • Oral contraceptives
    • Pregnancy
  • Immune problems
    • Lichen planus, oral
    • Pemphigus vulgaris
    • Erythema multiforme
  • Infectious disease
    • Coxsackie A
    • Cytomegalovirus
    • Epstein-Barr virus
    • Herpes simplex 1 and 2
    • Human immunodeficiency virus
    • Varicella
    • Syphilis
    • Tuberculosis
    • Fungal
  • Neoplasm – Squamous cell carcinoma
  • Systemic diseases
    • Acute necrotizing ulcerative gingivitis
    • Bechet’s syndrome
    • Celiac disease
    • Cyclic neutropenia
    • Inflammatory bowel disease – Crohn’s and ulcerative colitis
    • Immunoglobulin A deficiency
    • Iron deficiency anemia
    • Pernicious anemia
    • MAGIC syndrome – oral and genital ulcers with inflamed cartilage
    • Reiter syndrome
    • Sweet syndrome – neutrophilic dermatosis with fever
    • Wegner’s granulomatosis

Questions for Further Discussion
1. How do you treat skin pressure ulcers? A review can be found here
2. How does ulcerative colitis present? A review can be found here
3. How common are gastric ulcers in children? A review can be found here
4. What are indications for referral to a dentist?

Related Cases

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

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

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

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

To view images related to this topic check Google Images.

To view videos related to this topic check YouTube Videos.

Siu A, Landon K, Ramos DM. Differential diagnosis and management of oral ulcers. Semin Cutan Med Surg. 2015;34(4):171-177. doi:10.12788/j.sder.2015.0170

Fitzpatrick SG, Cohen DM, Clark AN. Ulcerated Lesions of the Oral Mucosa: Clinical and Histologic Review. Head Neck Pathol. 2019;13(1):91-102. doi:10.1007/s12105-018-0981-8

Minhas S, Sajjad A, Kashif M, Taj F, Waddani HA, Khurshid Z. Oral Ulcers Presentation in Systemic Diseases: An Update. Open Access Maced J Med Sci. 2019;7(19):3341-3347. doi:10.3889/oamjms.2019.689

Author
Donna M. D’Alessandro, MD
Professor of Pediatrics, University of Iowa

What is the Allergen Cross-Reactivity Rate of Legumes?

Patient Presentation
A 6-month-old female came to clinic for her health supervision visit. The mother was worried about food allergies. The mother had tried to feed the infant jarred peas for the first time and the infant had a rash around her mouth and face within a few hours. The rash resolved but recurred the next 2 days when fed peas and the rash seemed to come on quicker and was spreading down her neck. The mother wasn’t sure if she was itching but she did not have any problems with breathing or swallowing. The infant had been receiving only breast milk and other foods such as cereals, carrots and sweet potatoes which she had not had any reactions to in the past. The mother reported eating a general diet. The father had some seasonal allergic rhinitis and the older brother did not have any problems with food. He enjoyed eating peanut butter. There was no history of eczema or asthma in the family.

The pertinent physical exam showed a healthy female with normal growth patterns in the 75-90%.She had a minor diaper dermatitis but no other rashes. Her examination was normal.

The diagnosis of a healthy female with possible pea sensitivity or allergy was made. The pediatrician counseled, “I don’t know the exact percentage of children with pea allergy but it does happen. Usually around now we also recommend starting peanut butter containing foods and both peas and peanuts are legumes and therefore may have some cross-reactivity. She didn’t have any breathing or swallowing problems and no one else in the family has any food allergies and they also don’t have eczema or asthma. I also bet she’s been exposed to peanut butter because of her brother eating it too. Usually the allergy doctors tell us to take precautions but also use reasonable judgment because we know that being exposed to some of these foods actually decreases the allergies long-term. I wouldn’t give her any more peas, but I do think you can start to give her peanut containing foods. I’ll give you detailed instructions about how to do this and signs to watch her closely for. I’m also going to give you an Epi-pen® to have in case there is a problem, and if she has problems you are going to call 911. I would rather you give her the peanut food now and watch her, than she gets it by accident later and she has a reaction when you aren’t expecting it.” The patient’s clinical course showed at her 9-month appointment she didn’t have any reactions to peanut or soy foods.

Discussion
There are 8 common foods which compromise 90% of food allergens with those being peanuts, soybeans, cow’s milk, eggs, fish, crustacean/shellfish, wheat and tree nuts. Some people believe that lupin (a legume) is 9th.

Legumes belong to the Fabaceae family. They provide protein, fat, vitamins other essential nutrients and therefore are used in the human diet throughout the world.

“[A]llergenicity due to consumption of legumes in decreasing order may be peanut, soybean, lentil, chickpea, pea, mung bean and red gram.” Other common legumes include alfalfa, clovers, beans, lupins, mesquite, carob, and red kidney bean. Different legumes are consumed in different countries and therefore the prevalence of allergenicity to those legumes will be different. For example, legumes have a higher sensitization rate in Spain (5th most common reason for allergies) and India. Lupin is grown in Mediterranean countries and has a high rate of allergens in this area particularly Italy. Lupin seeds are eaten as a snack or it is ground and used as flour. It is becoming more commonly consumed in other Western European countries and in the same geographical areas there are also an increase of people with these allergies. In India, allergies to lentils, chickpeas, red gram and moong are more common.

The allergenicity of legumes is IgE mediated. The protein allergens are characterized into 4 main groupings including storage proteins (i.e. seed storage), profilins or other proteins. There is cross reactivity among the legumes themselves. There is also cross-reactivities with legume proteins and other botanicals including legume seed storage proteins cross-reacting with some tree and groundnuts. Cooking changes the allergenicity. For example, boiling or frying peanuts decreases the allergenicity whereas roasting increases it. Boiled legumes such as lentils, peas, and chickpeas can be decreased but it also depends on the length of time.

Legume allergy symptoms are similar for all legumes and range from mild to life threatening including urticaria, rhinorrhea, asthma exacerbation, angioedema, and anaphylaxis. Oral consumption is the main exposure to legume allergens but inhalation from flour, powder or vapor can also cause problems. People who are allergies have to be careful of hidden allergens. Not only because there might be contact with the production and processing of the foods, but because other ingredients may be included but not be required to be listed on food labels. These include lupin and pea, as well as celery, mustard, colorings, preservatives and spices. For example, fenugreek is a legume that is often part of spice mixtures.

Learning Point
“Although extensive serological IgE cross-reactivity among legume species has been found using in vitro methods, the rate of clinically relevant cross-reactivity to multiple legumes has been reported to be low.” For peanuts (the most common legume studied), the rates of cross-reactivity with another legume was 5-7.9%. Cross-reactivity between certain legumes also appear to be more clinically relevant.
Peas have cross-reactivity especially to lentils and chickpeas as they have similar allergens within them from the cupin superfamily of allergens.

Chickpea allergy is almost never seen alone but is associated with other allergies particularly lentil allergy.

Peanuts are associated with lentil, chickpea, pea and soy allergies. Lupin (44%) and fenugreek have high cross-reactivity with peanut. Lupin has a 44% cross-reactivity with peanut.

Cross-reactivities with other common allergens can be found here.

Questions for Further Discussion
1. What are risk factors for latex allergy? A review can be found here
2. What are common food allergies in your location?
3. How do you instruct families to introduce peanut containing foods? A review can be found here

Related Cases

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

Evidence-based medicine information on this topic can be found at SearchingPediatrics.com and the Cochrane Database of Systematic Reviews.
Information prescriptions for patients can be found at MedlinePlus for this topic: Food Allergy

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

To view images related to this topic check Google Images.

To view videos related to this topic check YouTube Videos.

Verma AK, Kumar S, Das M, Dwivedi PD. A comprehensive review of legume allergy. Clin Rev Allergy Immunol. 2013;45(1):30-46. doi:10.1007/s12016-012-8310-6

Bar-El Dadon S, Pascual CY, Reifen R. Food allergy and cross-reactivity-chickpea as a test case. Food Chem. 2014;165:483-488. doi:10.1016/j.foodchem.2014.05.138

Cabanillas B, Jappe U, Novak N. Allergy to Peanut, Soybean, and Other Legumes: Recent Advances in Allergen Characterization, Stability to Processing and IgE Cross-Reactivity. Mol Nutr Food Res. 2018;62(1). doi:10.1002/mnfr.201700446

Skypala IJ. Food-Induced Anaphylaxis: Role of Hidden Allergens and Cofactors. Front Immunol. 2019;10:673. doi:10.3389/fimmu.2019.00673

Author
Donna M. D’Alessandro, MD
Professor of Pediatrics, University of Iowa

What Is In A Ketogenic Diet?

Patient Presentation
A 9-month-old female came to clinic for her 9-month health maintenance examination.

The past medical history was significant for a history of hypoxic-ischemic encephalopathy at birth but she had been doing well overall. She was followed by the neonatal intensive care follow-up team as well as receiving physical therapy services for some gross motor delays. She was also followed by neurology for seizures and had been on Keppra® since birth. Her mother was overall happy with her progress but had noted increased numbers of seizures that lasted from several seconds up to one minute and were generalized tonic-clonic in activity. She had been having 3-4 a day but now was having 8-10 per day that the family was aware of. The mother asked what the general pediatrician thought about starting a ketogenic diet. The family history was positive for a paternal uncle with seizures as a child but “grew out of them” as he got older.

The pertinent physical exam had normal growth parameters around the 50%. She was a smiling infant who would say consonants and vowels, would sit by herself once placed into a seated position but wouldn’t consistent roll into that position nor get into a crawling position. Her tone was good as was her strength. Deep tendon reflexes were +2/+2 and cranial nerves were intact.

The diagnosis of a 9-month old with a significant past medical history and increasing seizures was made. The pediatrician didn’t feel comfortable offering an opinion about the ketogenic diet as he knew this was a specialized treatment and decisions needed to made by the neurologist and dietician. “I do know that it can be helpful for some children but I don’t know enough to give you an informed opinion. I can tell you that if you start the diet that usually this is done in a hospital to monitor people closely, and people stay on the diet for a while. I am happy to continue to follow her for her well child appointments and to help her when she gets sick. I can work with you and the neurologist together,” he explained.

The patient’s clinical course at her next neurology appointment, she was switched to another anti-epileptic medication. She continued to have more seizures and around 18 months of age, she began a ketogenic diet. At 24 months of age, her seizures had decreased to 1-2 per day.

Discussion
Epilepsy is a common problem for the general pediatrician. Its incidence is estimated at 41-87/100,000 children. While many children are controlled with medication, it is also estimated that up to 1/3 will develop drug-resistant epilepsy. Some children may have an identifiable seizure focus that may be amenable to surgery, but many others do not. One option for potential control is a ketogenic diet (KD).

Indications for KD usually are for drug-resistant epilepsy including partial and complex seizure patterns as well as some metabolic disorders such as glucose transport 1 deficiency syndrome. It has also found to be useful for some epileptic encephalopathies such as Doose, Dravet, Lennox-Gastaut, Ohthahara and West syndromes. KD is contraindicated in other conditions such as primary carnitine deficiency and other carnitine disorders, beta-oxidation defects, pyruvate carboxylase deficiency and porphyria.

The exact mechanism for the KD efficacy is not known but ketone bodies, mainly beta-hydroxybutyrate, cross the blood brain barrier. They become the main energy source for the brain and regulate various neurotransmission processes including accelerated re-uptake of neurotransmitters and neuronal inhibition. KD can be effective with up to 50% reduction in seizures for patients with drug-resistant epilepsy within 6 months. The diet is used usually for a minimum of 2 years.

Learning Point
A KD needs to have dieticians and neurologists with expertise to oversee them.
A KD consists mainly of calories from fat and a low percentage from proteins and carbohydrates. The classic diet is 80-90% fat and 10-20% proteins and carbohydrates. However other variations, which have a lower fat content, are used and can be effective. Most diets are 4:1 (fat: protein/carbohydrate) or 3:1. Basically the diet is mainly fat such as butter, whipping cream, mayonnaise, oils and protein such as eggs, meat, cheese and ground nuts. There is a lower concentration of fruits and vegetables and those chosen need to have other high quality nutrition such as vitamins and minerals associated with them such as such as avocado, broccoli, green beans, etc. Ground nuts and egg whites are often substituted for carbohydrates such as creating pizza dough or pancakes. Sugar free substitutes can be used but the type of substitute and amount needs to be scrutinized. This includes innocuous looking products such as gum or mints. Beverages usually are water, whipping cream or similar. Patients on a KD also need to have medications with the lowest sugar or carbohydrates in them.

Similar to other health conditions such as diabetes that need to be managed closely when a child is ill; children on a KD have special needs when they are ill. Breaking the KD when the child is ill may cause seizure frequency to increase. Oral rehydration solutions have low amounts of glucose but this still needs to be accounted for as part of the total day’s carbohydrates. Common medications such as acetaminophen, ibuprofen etc. may also have sugar or other carbohydrates in them and again need to be accounted for. Over the counter medications are a common reason that KD is broken. A child coming into the emergency room needs to have their fluids evaluated and replaced as necessary, but 0.9 NS and/or 0.45 NS should be used without glucose similar to a patient with diabetes. Close monitoring is very important.

Usually a KD diet is initiated in the hospital so the initial laboratory evaluations can be completed and monitored as the diet is initiated. The diet can be started by fasting, but also can be done by changing the content of the diet over from normal to 1:1, 2:1, and eventually 3:1 or 4:1. Metabolic problems associated with the diet include hypoglycemia, metabolic acidosis, excessive ketosis, electrolyte imbalances and dehydration. KD is associated with constipation because it is a low food and fiber diet. It is also associated with kidney stones especially if used for longer periods of time. Low Vitamin D, calcium, selenium and carnitine are also associated with the diet. Long-term effects on lipid profile are not clear.

Questions for Further Discussion
1. What are the various classifications of seizures? A review can be found here
2. What causes spells? A review can be found here
3. What are indications for a clinical dietician consultation?

Related Cases

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

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

Information prescriptions for patients can be found at MedlinePlus for these topics: Epilepsy and Seizures.

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

To view images related to this topic check Google Images.

To view videos related to this topic check YouTube Videos.

Martin K, Jackson CF, Levy RG, Cooper PN. Ketogenic diet and other dietary treatments for epilepsy. Cochrane Database Syst Rev. 2016;2:CD001903. doi:10.1002/14651858.CD001903.pub3

van der Louw E, van den Hurk D, Neal E, et al. Ketogenic diet guidelines for infants with refractory epilepsy. Eur J Paediatr Neurol. 2016;20(6):798-809. doi:10.1016/j.ejpn.2016.07.009

Luat AF, Coyle L, Kamat D. The Ketogenic Diet: A Practical Guide for Pediatricians. Pediatr Ann. 2016;45(12):e446-e450. doi:10.3928/19382359-20161109-01

Barry D, Ellul S, Watters L, Lee D, Haluska R, White R. The ketogenic diet in disease and development. Int J Dev Neurosci. 2018;68:53-58. doi:10.1016/j.ijdevneu.2018.04.005

Author
Donna M. D’Alessandro, MD
Professor of Pediatrics, University of Iowa