How the State of Oregon Kidnapped Our Son

Unexplained Injury

On November 8th, 2011 we noticed my son was feeling some pain and was running a low grade fever (100.2° F). I was concerned so I called an advice nurse that my wife's insurance provided. The nurse on the line was very polite and recommended that we go to the ER because my son was only five weeks old. Her concern was that at that age a fever could mean something was seriously wrong and we needed to have it examined.

The First Hospital 

We went to the local hospital in our home town to see a doctor there. Upon arrival the triage nurse performed her introductory evaluation, noting that there were "no bruises, swelling, or any external abnormalities" while also noting that "all four extremities are moving strongly and equally." 

We were brought to a room in the ER where a doctor performed a number of tests. This included a hip flexing check and saw that the legs were pulled up tightly towards the abdomen. He explained that sometimes when babies have abdominal pain they'll pull their legs in tightly. While the doctor manipulated my son's legs he let out a very loud scream, quite unlike we had heard before. This was very different than the experience with the triage nurse just minutes before.

The doctor ordered an x-ray to view my son's abdomen and hips. The doctor's belief was that their could possible be an obstruction in my son's intestines causing the pain. 

The X-Ray Technician

My wife needed to return home at this point. In our haste to get to the ER we had forgotten to bring a change of clothes and diapers, and while there our son soiled his outfit. I stayed and the x-ray technician came in to take a number of images. At one point while we were moving my son the x-ray technician looked at me in a confused way and asked if the doctor had mentioned anything about my son's left leg. I replied that he hadn't other than a possible abdominal issue. 

The technician left after taking his initial x-rays, and came back half an hour later. He was told to take specific pictures of the leg. He then came in again one more time after another half an hour to take a clearer picture of the leg. My wife had returned at this point and the Doctor came in and told us that our son had a spiral femur fracture (We later learned that it was actually an oblique fracture and not a spiral). The doctor informed us that as protocol he had to notify the authorities and an investigation would take place. (It was also noted that he had gaseous distention from the x-rays)

The First Police Office

We spoke to the police officer that came to see us and explained that there hadn't been anything traumatic that happened. Nobody dropped him, no one fell with him, nothing happened. While we spoke to the police officer we mentioned we came in because our son was having abdominal pain, thought to be bad gas, and a low grade fever. We mentioned that he had no bruises (which was confirmed by a nurse that was in the room at the time) and we told him we had no idea there was a fracture. Our son hadn't screamed in pain as he did until the doctor manipulated his leg.

My son was only mildly more fussy than normal prior to our visit, and as young parents we thought that as long as he was eating he was okay. The night before we also noticed a fever and we went to the store so he could have baby Tylenol and Gripe Water (Natural medicine to reduce gas). This seemed to work as it lowered his temp and calmed him down.

The Children's Hospital

The Children's Hospital was notified. Their EMT crew and a pediatrician arrived and wrapped up my son's leg. My son was transferred to the Children's Hospital in an ambulance with my wife. I had to run home and pick up some things for my son, and then I drove out there myself. 

While in the ambulance, my wife was able to hear a pediatrician and an EMT discuss that they thought this was clearly abuse and that it was only protocol to bring a parent. When they arrived at the Children's Hospital a complete trauma workup was performed on my son. It was noted again that there were no bruises, swelling, lesions, abrasions, and that my son was content beyond his leg. It was noted that my son had extra cartilage on his skull but it was not trauma related, and I remember wondering what that meant. My son showed no symptoms of being in any pain or distress, though he did have a low grade fever. 

My wife had been advised to ask the ER doctor what could cause such injuries in an infant. She was rudely told that "It was either child abuse or you're lying (about there being no accident)." 

My son was sent to have a head CT done immediately. His results came back perfectly normal. There was no bleeding on the brain, no hemorrhaging, no skull fractures, or signs of trauma. My wife requested that a new doctor be placed with our son after the encounter with the previous doctor, and was given an advanced resident to look over our son. A full blood workup was run, including a spinal tap, to check for infection because of his low grade fever. My son, minus the blood drawing, remained content, fed well, and soothed easily. It was very hard for the doctors to draw blood from our son, and it took quite a lot of time for them to finally get anything, causing my son great pain in the process. On the spinal tap, one of the residents missed the spinal fluid and hit a vein, causing blood to become mixed in with the spinal fluid. They also took new x-rays while in the Children's Hospital ER. Even after taking the blood, a number of tests were lost or not valid. 

The Inpatient Room

We were eventually moved to an inpatient room. They tried to draw more blood during the night, but they didn't tell us what the blood was being drawn for. We were also informed not to feed our son throughout the night so they could reset the bone, and he cried through the night in hunger pains. We followed the directions we were given. Despite all this, he wasn't given any medication because he was still soothing himself. The room was very cold at night, yet my son maintained a high temperature and was even sweating. None of the nurses adjusted the temperature at night, nor did they tell us how. 

In the morning a new nurse came in and said my wife could feed our son. They took a full skeletal survey in the morning where they noted a number of fractures. These inculded:

• An acute left femoral diaphysis angulated oblique fracture, 
• Age-indeterminate bilateral distal femoral, 
• Probable left and right proximal tibia metaphyseal corner fractures, 
• Probable age-indeterminate left proximal humeral metaphyseal corner fracture, 
• Probable partially healed proximal right tibia and fibula fracture, 
• And healing bilateral rib fractures (Probably three). 

Note, the only fully confirmed fracture has been the left femur fracture and an age-indeterminate posterior rib fracture. This is also the point where they say it was on oblique fracture and not a spiral. A doctor came in to look at my son's eyes. She saw no retinal hemorrhaging, but noticed a mild discoloration in his eyes. She called in a superior who also noted that there was nothing wrong with his eyes, but that he did have mild discoloration. Again, My son was only 5 weeks old at the time. 

My son had seen many different doctors in this time, all noting that he look healthy an happy. My son had been in for a 1 week check, 2 week check, at about 3 1/2 weeks he was circumcised, he had visited the hospital twice because he was jaundice, and my wife's midwife had also seen him during one of her post birth visits the day before we went to the hospital.

They attempted to draw more blood, and continued to be unsuccessful, taking a full second day to gather the blood needed to send out for the Osteogenesis Imperfecta (OI) test and a few other tests regarding bone health. He was still on no medication until they decided to put an IV in his head where they used morphine. They took an abdominal CT because my son had high liver enzymes, but his CT came back perfectly normal. He was put into a Pavlik harness to help heal his femur fracture. 

The State Intervenes

A Child Protective Services (CPS) worker, a detective, and a police captain interviewed me, my wife, and my wife's parents. They agreed that everything we have said had been consistent. There hasn't been any trauma, and certainly no outward signs abuse. The police never filed criminal charges.

We had to appear in court for an emergency hearing as requested by CPS. I had already obtained a lawyer but my wife hadn't had time yet. During the hearing the judge seemed to want to give us both of our children back. But CPS boldly lied and said there was liver damage and stated that all fractures were fact, rather than possibilities. The judge reluctantly had our son put into a "Medical" foster home, while allowing us to keep our daughter (As long as we were in sight and sound of Linda's parents with our daughter).

At 3 Months

CPS continued to hold our son, and was attacking our parenting skills and the well being of both of our children. We had 3 1-hour visits a week with our son, and during that last month we discovered that our son now had an umbilical hernia (which may have been developing while he was still with us). We asked CPS to take our son to see a doctor, but they informed us they had another appointment set up for his two month check and will have it looked at than. 

We have since discovered that our son does have low calcium, low vitamin D, high alkaline phosphatase. We have looked into many different possibilities, including OI, Rickets, Temporary Brittle Bone Disease (TBBD), and other diseases that could have caused this. The OI test came back negative, but there are other options, but at this time it was very difficult to have our son tested. 

Back in the Womb

My wife had a rough pregnancy because of his size. We discovered that she has a retroverted uterus. This made our son's birth even tougher. He was born at 41 5/7 weeks by induction with pitocin. My son had severe shoulder dystocia during birth, and had an initial APGAR score of 3, taking a full minute to even breath. During the later stages of pregnancy my son was unable to move much, but certainly was noticeable due to his large size. My son only moved at night when my wife was able to lay flat, especially during the third trimester. His birth weight was 9lbs 7oz and 21 1/2 inches. 

The Judicial Hearing

We started the Judicial Hearing Process on January 5th, 2011. The hearings were held on the 5th, 6th, 9th, 10th, 11th, and 18th. One of the worst problems with this process is that it is held in the Juvenile Courts, and rather than using "Beyond a reasonable doubt" they use "Preponderance of Evidence" which refers to balancing the evidence (50/50), and whichever side is over the 50% mark wins the case. 

We clearly should have had more than enough evidence to prove that we had not abused our son. Firstly, it was made clear that the hospital had lost blood tests, including a very important vitamin D, phosphorus, ionized calcium, and the PTH tests, all vital for diagnosing Rickets. They also noted elevated liver enzymes related to bone breaks which were elevated even higher after our son was in foster care, after declining to a normal level at the hospital. 

The Expert and the Villain

We had hired Dr. David Ayoub to testify about what he saw from the x-ray and CT images. He testified that he could see from the radiological evidence that our son had neonatal rickets. Dr. Ayoub even had images taken directly from My son's X-rays and CT scans to show these signs. 

The state provided numerous medical witnesses, and each of these witnesses, except Dr. Villain (A Child abuse Expert who has been certified by American Board of Pediatrics, Child Abuse Pediatrics since 2009), had admitted that if our son had a medical condition of bone fragility that it could explain his fractures. It was also noted that our son had no bleeding on the brain, no subdural bleeding, no retinal hemorrhaging, no bruising, no swelling, no internal organ damage, no brain damage, no cuts or lesions, and no tissue damage. The only thing noted were the unexplained bone fractures without local tissue trauma. 

It was even noted in court that there was very likely a new rib fracture after our son was placed in foster care. There was even a physician's assistant who noted that if our son did have bone fragility he himself could have accidentally broken our son's ribs during a routine well baby check. 

The ER doctor who saw our son when we brought him to the hospital still can't give a clear answer about whether or not he broke our son's femur, and when asked on the stand said "I don't believe I did." rather than a simple yes or no. The pediatrician who is currently seeing our son was even confused why they were calling this abuse when there clearly were other things that needed to be looked at first, and recommended that our son see and endocrinologist and geneticist. 

There were two doctors who testified that the obvious fact that all of the normal signs of abuse were missing meant it was unlikely to be abuse when evaluating the differential diagnosis. 

The State recalled two of their medical witnesses to discredit Dr. Ayoub's work simply because his current study hadn't been published in a peer reviewed journal yet. Dr. Villain (who had never actually seen our son, nor viewed his full medical history) claimed that he didn't care if our son had a medical condition. He (in a very belligerent attitude)believed that this was abuse anyways, and would not be convinced otherwise.

The Judge's Ruling

So the Judge erred on the side of caution and adjudicated my wife and I of abusing our son. We we able to keep our daughter home with us, because she was in perfect health. He even stated that we should bring new medical evidence to him should we have any.

We tried to have CPS take our son to specialist to evaluate him, and the judge even order them to do it. This never happened. We fought for our innocence, and after 17 month we got our son back. The verdict hadn't changed, but the judge had decided that we were trustworthy enough to have our son back.

The new evidence

In 2013 we finally had the opportunity to have our son evaluated by a endocrinologist at the very same children's hospital. They thought the situation was very odd. While they found no endocrine problems, they suggest that our son be evaluated for Ehlers-Danlos with a geneticist.

We finally were able to see the very busy geneticist in 2014, and they said that our son clearly has Ehlers-Danlos type-III (Hypermobility). We were told that his was very likely the reason our son was injured without a traumatic accident. We thought that it was great to finally know what we as a family were dealing with. The syndrome isn't life threatening for our son, but it isn't a simple disorder either. He deals with fatigue and soreness frequently.

We haven't been able to return to court, because it is very difficult to find an attorney who wants to reopen finished cases.

We didn't abuse our son, and they shouldn't be able to take our son like this without reasonable cause. 

Our story has been passed on, and we hope people continue to share it. So please repost and spread the word about this huge injustice to all your friends and family. This isn't about just our family anymore. This scenario is happening over and over again all across the country and internationally. So please share this story, it may help a family be saved.

Osteomalacia And Vitamin D, What Is The Link?

Dr. Michael Holick Speaks on Osteomalacia and its link to Vitamin D deficiency.

The breastfeeding mother: Breast milk as a biomarker?

Posted on June 25, 2012 by John Cannell, MD

It just never made sense to me, 40 years ago, when my professors at UNC School of Medicine casually announced human breast milk contained no vitamin D.
“How can that be? How can that possibly be? That makes no sense,” I thought. “Was primitive man supposed to give their infants vitamin D pills that didn’t even exist?”
I have written before about biomarkers, such as:

• How high does your vitamin D level have to be to maximally suppress parathyroid hormone?
• How high does your vitamin D level have to be to maximally improve calcium absorption?
•  How high does your vitamin D level have to be to prevent abnormal bones?

The answer to these questions varies from 20 ng/ml to 40 ng/ml, depending on what study you decide to quote. But what about breast milk as a biomarker? Infants need vitamin D for strong bones and general development. Without vitamin D, the infant can develop rickets. In the 21^st century, this is treatable in a clinic. In the wild, the tribe may have left a screaming baby with soft bones at the wayside.

How high does the breastfeeding mom’s vitamin D level need to be for her infant to get natural vitamin D levels? This level is a biomarker because it gives us insight on how high vitamin D levels were for species survival. If the breastfeeding mom couldn’t supply vitamin D to the infant, our species may not have survived. Whatever vitamin D level that might be, that would be the level humans evolved to have.
Professors Wagner and Hollis and colleagues did an elegant randomized controlled trial 6 years ago that we have covered before, but it should be covered often. They simply gave two different doses of vitamin D to nursing mothers and measured the vitamin D levels of their infants and mothers. They used a small sample of breast feeding women, giving half the women a prenatal vitamin (containing 400 IU) and the other half a prenatal vitamin plus an extra 6,000 IU/day of vitamin D.
The suckling infants of the mothers given only the prenatal were also given 300 IU of vitamin D directly (it would have been unethical to deprive any of the infants of vitamin D). They noted no side effects with any dose, but the 6,000 IU/day arm of the study answered my 40-year-old question.
Wagner CL, Hulsey TC, Fanning D, Ebeling M, Hollis BW. High-dose vitamin D3 supplementation in a cohort of breastfeeding mothers and their infants: a 6-month follow-up pilot study. Breastfeed Med. 2006 Summer;1(2):59-70.
The 6,000 IU/day dose of vitamin D did three things.

1. It gave the mothers natural vitamin D levels (50 ng/ml or close to).
2. It transformed breast milk into a rich source of vitamin D.
3. It gave suckling infants natural blood levels of vitamin D (45 ng/ml).

Given this, if you are now breast-feeding and not taking vitamin D, then I hope you are giving your infant at least 400 IU of vitamin D per day as the American Academy of Pediatrics (AAP) recommends. If you want your infant to start getting their vitamin D from your breast milk, I recommend the following steps:

1. Take a loading dose of 10,000 IU/day for a month.
2. After one month on 10,000 IU/day, stop supplementing your infant with vitamin D as your breast milk should now be filled with vitamin D.
3. Take 6,000 IU/day maintenance dose thereafter, except on days you get full body sun exposure.

However — and this is important — when the breastfeeding stops, you need to start supplementing your child again, as the AAP recommends, unless the child is in the sun enough to have adequate levels, and very few are.
I’d like to reiterate, can you think of a better biomarker for how much vitamin D humans need?

• “How much vitamin D do human breast–feeding mothers have to take to transform their breast milk into an adequate source of vitamin D for their infants?”

This is a great biomarker question, one essential to the survival of our species. The answer is 50 ng/ml, which can be achieved by 6,000 IU/day for breastfeeding mothers.
Further reading:

• Taylor SN, Wagner CL, Hollis BW. Vitamin D supplementation during lactation to support infant and mother. J Am Coll Nutr. 2008 Dec;27(6):690-701. Review.

About John Cannell, MD

Dr. John Cannell is founder of the Vitamin D Council. He has written many peer-reviewed papers on vitamin D and speaks frequently across the United States on the subject. Dr. Cannell holds an M.D. and has served the medical field as a general practitioner, itinerant emergency physician, and psychiatrist.

View all posts by John Cannell, MD →

 

http://blog.vitamindcouncil.org/2012/06/25/the-breastfeeding-mother-breast-milk-as-a-biomarker/ 

Doctors Say Rickets Is Back

By Melissa Schorr
B O S T O N, Aug. 10

An exclusive diet of breast milk could be putting some babies at risk for vitamin D deficiency and thus at risk for rickets, a bone-weakening disorder that has been virtually nonexistent in the United States for decades.

Doctors nationwide are reporting a small spike in the number of breast-fed babies developing nutritional rickets, Rickets is caused by a lack of vitamin D, which is crucial for strong bone development. It can result in stunted growth, broken bones and bow legs in children.

Breast milk, though an excellent source of nutrition overall, provides little vitamin D. Babies can get the vitamin instead from a splash of sunlight or from a daily supplement.

But rickets may be on the rise, researchers believe, because of the renewed popularity of breast-feeding, along with doctors’ failure to properly prescribe vitamin D supplements to breast-feeding moms.

Dark Skin, High Risk At special risk are dark-skinned babies, whose pigmentation prevents them from using sunlight to produce the necessary vitamin D.

But babies of any race who aren’t getting enough vitamin D from their diet and aren’t getting a daily dose of sunlight are potentially at risk of developing rickets, researchers say.

Doctors at two medical centers in North Carolina report in this month’s issue of the Journal of Pediatrics that they saw 30 cases of rickets in breast-fed black infants from 1990 though 1999, with more than half of the cases occurring in the last 18 months alone.

This June, researchers at the University of Texas Southwestern Medical Center in Dallas published a report in the journal Texas Medicine about a recent outbreak of rickets among dark-skinned infants who were breast fed, despite the presence of abundant sunlight in the state.

Statewide Surge Cases of rickets have been popping up around the country, from New York to Florida, notes Dr. Robert P. Schwartz, an endocrinologist at Wake Forest University School of Medicine in Winston-Salem, N.C., lead author of the study.

Schwartz decided to study the issue along with his colleagues, Dr. Shelley Kreiter, a pediatrician at Wake Forest, and Dr. Henry Kirkman of the University of North Carolina School of Medicine in Chapel Hill.

Because of growing concerns, the Centers for Disease Control will be putting out a bulletin on rickets this fall, a spokesman says.

“This is a disease that was here 100 years ago,” Schwartz says. “It’s back.”

History of Rickets

As late as the 1940s, rickets was a common childhood ailment, killing thousands of children annually until doctors learned that that vitamin D in milk and sunlight could largely prevent it.

Today, fortified milk and prepared baby formula both contain vitamin D, largely eliminating the problem.

But because breast milk contains much lower levels of vitamin D, babies exclusively fed on it may be at risk, especially if they have darker skin that blocks out sunlight; live in northern climates and receive less light or have moms with vitamin D deficiencies themselves.

The number of African-American women who are breast-feeding has been on the rise in the past decade, from about 5 to 22 percent, the Pediatrics study reports.

“We’re glad to see that more minority women are breast-feeding, and we don’t want them scared away because they hear their breast milk is not sufficient,” says Carol Huotari, manager for the Center for Breastfeeding Information at La Leche League International, a Schaumburg, Ill.-based group that promotes breast-feeding. “It’s a simple thing to provide vitamin D supplements.”

“We don’t want to come across as against breast-feeding,” Schwartz concurs. “But we think all infants should be supplemented with vitamins.”

Since January, Schwartz’ group has provided supplements to more than 700 women in North Carolina who are exclusively breast-feeding. The supplements are paid for by the federal Health Resources and Services Administration’s Maternal and Child Health Block Grant program.

“Proving supplements to every baby seems like overkill,” says Huotari, “when it’s just a selected group of babies that would benefit.”

But Schwartz says many infants are potentially at risk and the cost has been minimal so far: about $1.50 per infant per month — far less than hospitalizing infants for fractures and broken bones.

Doctors Fail to Warn Besides the increase in breast-feeding contributing to this rise in rickets, pediatricians also may not be telling mothers to supplement the breast milk with vitamin D.

The Journal of Pediatrics study surveyed 400 North Carolina pediatricians and found that 16 percent weren’t prescribing vitamin supplements at all. Younger doctors, who may have never seen a case of rickets, were less likely to prescribe vitamin D than older ones.

“Doctors have not been led to believe it is essential,” Schwartz explains.

Schwartz says the American Academy of Pediatricians hasn’t established clear enough guidelines on supplementation.

In 1998, the academy recommended vitamin D supplements be used for breast-fed infants with dark skin or inadequate exposure to sunlight, but other earlier policy statements still in effect haven’t provided a clear mandate for vitamin use.

“The nice thing is, this disease doesn’t have to occur at all,” Schwartz says. “This is 100 percent preventable.”

http://abcnews.go.com/Health/story?id=118054&page=1#.T36eC6tSSj_

By CARRIE GANN (@carrie_gann) , ABC News Medical Unit

Feb. 8, 2012

Vitamin D is the key to having healthy bones, yet many Americans don't get as much as they need.

The consequence? Broken bones, even among the young and healthy, according to two new studies presented yesterday at a meeting of the American Academy of Orthopaedic Surgeons.

In one study, researchers from South Korea studied 104 postmenopausal women with wrist fractures and found that 44 percent of the women had insufficient or deficient vitamin D levels. Only 13 percent of 107 women soft tissue injuries were found to have low vitamin D levels.

Vitamin D deficiency can be devastating among younger women and men also, according to another study presented at the AAOS meeting.

Researchers at the University of Missouri studied the medical records of nearly 900 adults, some as young as 18 years old, who were admitted to a trauma center for orthopedic injuries. Researchers found that 77 percent of them had insufficient or deficient levels of vitamin D. Nearly 40 percent were vitamin D deficient.

"We are dealing with a significant problem in our population, especially related to those individuals that sustain fractures," said Dr. Joseph Lane, chief of metabolic bone disease service at the Hospital for Special Surgery in New York City.

Vitamin D helps the body absorb calcium from food, strengthening the bones. The nutrient is found naturally in fatty fish like salmon and tuna, and in small amounts in mushrooms, cheese and egg yolks.The other natural source for vitamin D is sunshine, which causes the body to make vitamin D.

Vitamin D is also added to nearly all milk sold in the U.S.

In 2010, the Institute of Medicine recommended that children and adults up to age 70 get 600 IU of vitamin D each day, and that adults over 70 should get 800 IU per day.

Getting enough of the nutrient naturally is next to impossible, according to some experts. A cup of milk only has 100 IU of vitamin D. Drink 4 a day and you still won't meet the IOMs daily requirements.

Sunlight is also insufficient for most, said Dr. Loren Wissner Green, an associate professor at New York University School of Medicine.

"Light-skinned people generally use sunscreens that prevent the skin from manufacturing vitamin D and darker skinned people have natural melanin barriers to UV rays that allow the skin to manufacture vitamin D," Green said.

Experts say taking a vitamin D supplement is a good idea, especially for older women who are at greater risk for bone fractures.

"All postmenopausal women should be taking calcium and a multivitamin containing vitamin D," said Dr. Scott Boden, director of the Emory University Orthopaedic and Spine Center in Atlanta, Ga.

Additionally, older people, those with previous bone fractures, and others who are at an increased risk of fractures, may want to consider having a doctor check their vitamin D levels.

http://www.ajcn.org/content/80/6/1697S.long

American Journal of Clinical Nutrition, Vol. 80, No. 6, 1697S-1705S, December 2004
© 2004 American Society for Clinical Nutrition

VITAMIN D AND HEALTH IN THE 21ST CENTURY: BONE AND BEYOND

Nutritional rickets among children in the United States: review of cases reported between 1986 and 2003^1,2,3,4

Pamela Weisberg, Kelley S Scanlon, Ruowei Li and Mary E Cogswell

¹ From the Maternal Child Nutrition Branch, Division of Nutrition and Physical Activity, Centers for Disease Control and Prevention, Atlanta.

² Presented at the conference "Vitamin D and Health in the 21st Century: Bone and Beyond," held in Bethesda, MD, October 9–10, 2003.

³ Supported by a CDC federal government work study salary (PW) and CDC federal government salaries (KSS, RL, and MEC). No external funds were used.

⁴ Address reprint requests and correspondence to KS Scanlon, Maternal Child Nutrition Branch, Mailstop K-25, 4770 Buford Highway, Atlanta, GA 30341-3724. E-mail: kscanlon@cdc.gov.

ABSTRACT

Reports of hypovitaminosis D among adults in the United States have drawn attention to the vitamin D status of children. National data on hypovitaminosis D among children are not yet available. Reports from 2000 and 2001 of rickets among children living in North Carolina, Texas, Georgia, and the mid-Atlantic region, however, confirmed the presence of vitamin D deficiency among some US children and prompted new clinical guidelines to prevent its occurrence. We reviewed reports of nutritional rickets among US children <18 y of age that were published between 1986 and 2003. We identified 166 cases of rickets in 22 published studies. Patients were 4-54 mo of age, although in 17 studies the maximal age was <30 mo. Approximately 83% of children with rickets were described as African American or black, and 96% were breast-fed. Among children who were breast-fed, only 5% of records indicated vitamin D supplementation during breast-feeding. The American Academy of Pediatrics (AAP) recently recommended a minimal intake of 200 IU/d vitamin D for all infants, beginning in the first 2 mo of life. AAP recommends a vitamin D supplement for breast-fed infants who do not consume at least 500 mL of a vitamin D-fortified beverage. Given our finding of a disproportionate number of rickets cases among young, breast-fed, black children, we recommend that education regarding AAP guidelines emphasize the higher risk of rickets among these children. Education should also emphasize the importance of weaning children to a diet adequate in both vitamin D and calcium.

Key Words: Vitamin D deficiency • rickets • breast-feeding • case reports • children • African American children

INTRODUCTION

Recent studies reported high rates of hypovitaminosis D among adolescents and adults in the United States, particularly among black subjects (1-3). National data on the prevalence of hypovitaminosis D among children are not yet available; however, published reports from 2000 and 2001 of cases of clinical nutritional rickets among young children living in North Carolina (4), Texas (5), Georgia (6–8), and the mid-Atlantic region (9) confirmed the presence of severe vitamin D deficiency among some US children and stimulated renewed interest in the disease and new American Academy of Pediatrics (AAP) clinical guidelines to prevent its occurrence (10).

Rickets is associated with biochemical abnormalities, bone deformities, impaired growth, developmental delays, and, late in the course of the disease, seizures. Vitamin D₃ functions with parathyroid hormone (PTH) to maintain intracellular and extracellular calcium concentrations within a physiologically acceptable range (11). When vitamin D concentrations are inadequate, intestinal absorption of calcium is decreased. The slight decrease in serum calcium concentrations that results stimulates PTH secretion, which in turn mobilizes calcium and phosphorus from bone to restore serum calcium concentrations to normal levels. Serum alkaline phosphatase (ALP) concentrations increase once clinical signs of rickets are apparent. Low serum 25-hydroxyvitamin D [25(OH)D] concentrations can confirm vitamin D deficiency as the cause of rickets if treatment with vitamin D has not yet been initiated, whereas serum 1,25-dihydroxyvitamin D concentrations can be low, normal, or elevated in vitamin D deficiency (11). The biochemical abnormalities detected vary, depending on the stage of deficiency and the PTH response in mobilizing calcium and phosphorus. The characteristic bone changes of rickets include bowing of the legs, rachitic rosary of the rib cage, frontal bossing, and epiphyseal enlargement of the wrists and ankles.

Vitamin D is available to humans through the photochemical action of sunlight or ultraviolet light on 7-dehydrocholesterol in skin and through dietary sources such as fish liver oils, fatty fish, and foods fortified with vitamin D, particularly liquid cow's milk, infant formula, and breakfast cereals (11, 12). Infants with darkly pigmented skin are at elevated risk for deficiency because melanin in the skin competes with 7-dehydrocholesterol for ultraviolet-B photons, thus decreasing vitamin D₃ synthesis in the skin (12, 13).

In 1985, Cosgrove and Dietrich (14) reviewed 65 clinical cases of nutritional rickets that were reported between 1975 and 1985, in 11 publications, from medical centers in 9 US states. The children with rickets were 2-45 mo of age and were still breast-feeding or were consuming a milk-free vegetarian diet at the time of diagnosis. Among the 44 children for whom race was reported, 40 were described as black. The purpose of our study was to review all cases of nutritional rickets reported in the literature between 1986 and 2003 and to provide an expanded review of characteristics common to its occurrence. Information on common factors associated with rickets in the United States should help health care providers educate families regarding the new AAP clinical guidelines on preventing rickets and vitamin D deficiency, by emphasizing the children who are at greatest risk of deficiency.

METHODS

This review includes published case reports of nutritional rickets among children in the United States. The MEDLINE database was used to identify all case reports of rickets published between 1986 and 2003. Key words used in the MEDLINE search were rickets and vitamin D deficiency. The search was limited to reports of children <18 y of age, in the United States. Eighteen articles met our selection criteria. Another 6 articles were identified from the references of the articles, for a total of 24 articles published between 1986 and 2003. The 24 publications reported on 22 case studies; 3 articles (6–8) reported on different cases and aspects of one case group. The cases reported were identified from inpatient and outpatient clinical records with various methods. We reviewed all reports to examine the region, month, and year of diagnosis, clinical findings, age, sex, race/ethnicity, infant feeding and supplementation practices, and exposure to sunlight. Abnormal clinical findings were designated by the medical laboratory or clinic making the assessment and were limited to those reported in the article. Reference ranges for the laboratory assays used varied among the studies, but there was insufficient information for individual cases to set standard cutoff values for this review. Furthermore, not all studies provided information on the biochemical assays performed.

RESULTS

Characteristics of the clinical rickets cases reported in the literature between 1986 and 2003 are presented in Table 1. The cases were ascertained through case findings and clinical encounters in at least 17 states and at 1 center representing the mid-Atlantic region (4–9, 15–32). The 17 states that reported cases represented all regions of the United States. A total of 166 cases of rickets were reported in the 22 case reports. Patients presented to the hospital or clinic with clinical signs such as delayed growth or motor development, inability to walk, bone abnormalities, or seizures and were diagnosed on the basis of radiographic, biochemical, or clinical evidence of rickets. Of the 159 cases with radiographs (one study had no radiographs for 7 cases) (18), all except 3 showed radiographic evidence of rickets, including metaphyseal flaring, cupping, or fraying. Of the 3 cases with no radiographic evidence, one involved an 8-mo-old child with normal radiographic findings but biochemical evidence of hypovitaminosis D, hypocalcemia, hyperparathyroidism, and elevated ALP concentrations who responded to vitamin D and calcium supplementation (23), one involved a 4-mo-old child with normal radiographic findings but biochemical evidence of hypocalcemia and elevated ALP concentrations who responded to vitamin D and who was described as a child with "biochemical rickets" by the authors (27), and one involved a 7-mo-old child with normal scout films of the abdomen and chest who presented with a hypocalcemic seizure, elevated ALP and PTH concentrations, and low serum 25(OH)D concentrations and who responded clinically to combined vitamin D and calcium supplementation (26).

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TABLE 1 Reports of rickets cases in the United States published between 1986 and 2003¹

Biochemical indicators reported in the studies included low serum 25(OH)D concentrations for 68% of the children tested (67 of 98 children), hypocalcemia for 55% of those tested (77 of 141 children), hypophosphatemia for 64% of those tested (95 of 148 children), elevated ALP concentrations for 99% of those tested (142 of 144 children), and hyperparathyroidism for 94% of those tested (74 of 79 children). Biochemical studies were sometimes performed after treatment with vitamin D had been initiated, as was the case for the 4 children with normal serum 25(OH)D concentrations in the North Carolina study (4). Clinical findings included seizures, failure to thrive, delay or regression in motor development, weight-for-age or length-for-age less than the 5th percentile, and bone abnormalities, such as bowing of the legs, fractures, rachitic rosary, frontal bossing, or widened wrists and ankles.

The children with rickets described in the 22 case studies ranged from 4 to 54 mo in age at the time of diagnosis (Table 1). In 17 studies, however, the maximal age at diagnosis was <30 mo. Only 3 studies presented cases involving children <6 mo of age (4, 27, 32). When mean ages were reported (15 studies), they ranged from 10.5 to 25 mo. Among the 12 studies that reported the length of gestation for all cases (5, 6, 9, 17, 19, 21–24, 30–32), all except 2 cases were described as full term (37 wk of gestation completed). The 2 preterm cases were 35-wk gestations (data not shown) (32).

Most studies provided the sex and racial/ethnic distribution of cases, indicating that overall 54% of cases (80 of 148 cases) with reported sex were male and 83% (138 of 166 cases) were African American or black, 4% nonwhite (of African American or Indian decent), 6% white, 2% Hispanic, 2% Alaskan native, and ≤1% Middle Eastern, Asian, or unknown. The 5 studies that reported cases among white children were reports from northern states, ie, Washington, Minnesota, New York, Connecticut, and New Hampshire (18, 23, 27, 30, 32).

A common characteristic among cases was that the dietary history indicated that the children were breast-fed without vitamin D supplementation. All except 7 cases (96%, 152 of 159 cases) for which this information was reported involved children who were breast-fed. Among the 151 children who were breast-fed and for whom it was reported whether supplementation was used, only 8 (5%) received a vitamin D supplement during the breast-feeding period, as indicated in the medical records or by the parent (18, 25, 27, 32). Administration of the supplement was reported as sporadic or intermittent for 2 of those children. Among the studies that reported on liquids introduced after weaning (6, 15, 17,18, 25, 30), consumption of vitamin D-fortified milk was reported by the parents for only 3 children (15, 18, 25) and a vitamin D-enriched soy beverage was reported by the parent of 1 child (30). The authors of 5 studies made qualitative comments about poor overall dairy consumption among the patients (5, 17, 24,27, 32). Kreiter et al (4) reported poor intake of fortified cow's milk and other dairy foods among patients ≥1 y of age.

Twelve studies provided information on sunlight exposure, but they varied greatly in how they reported exposure (5, 6, 16, 17, 19–22, 24, 27, 29, 31). Parents interviewed by Tomashek et al (6) responded that sun exposure was minimal for 3 of 6 children with rickets. The mother of one child with rickets presented by Bhowmick et al (19) reported that she restricted sunlight exposure for the first 8 mo of her infant's life, and the mother of the child presented by Hayward et al (16) reported that she remained indoors with her child most of the time. In 7 other studies, the authors provided qualitative reports that some of the children with rickets were not outside very often (20, 21, 27, 29, 31) or had "limited sunlight exposure" (16, 17). Shah et al (5) reported that there was no evidence of reduced sunlight exposure for the 9 children with rickets in their study.

All except 3 studies (6, 22, 32) reported on the responses of all cases to treatment (data not shown). Those studies reported resolution of the radiographic and biochemical features of all rickets cases with vitamin D treatment. The vitamin D was administered with or without the addition of a calcium supplement or dairy foods. DeLucia et al (32) reported on responses to treatment for 3 of the 43 cases presented and found that 1 case responded to calcium supplementation without vitamin D.

DISCUSSION

In a 1985 review, Cosgrove and Dietrich (14) described characteristics of 65 cases of nutritional rickets reported in the literature between 1975 and 1985. The cases described involved children 2-45 mo of age who had been breast-fed and either were still breast-feeding or were consuming a milk-free vegetarian diet at the time of diagnosis. Among the 44 children for whom race was reported, 91% were described as black. We found similar characteristics among the 166 clinical cases of rickets published in the literature between 1986 and 2003, and we expanded our review to include information on vitamin D supplementation and details of clinical presentation and responses to treatment. The clinical cases we reviewed occurred among children 4-54 mo of age; 83% were described as black, and 96% were breast-fed. Among breast-fed infants, only 5% of records indicated that the infant received supplementation with vitamin D during breast-feeding. When additional dietary information was available, we noted that often these children were weaned onto a diet low in vitamin D and calcium. All except 3 cases showed radiographic evidence of rickets. In the 19 studies with information on responses to treatment, all rickets cases treated with vitamin D responded clinically and biochemically to treatment. The vitamin D was administered with or without added calcium or dairy foods. One case responded to calcium without vitamin D (32). The authors of nearly all case reports indicated that the rickets resulted from severe vitamin D deficiency; however, we cannot rule out low calcium intake as a contributor to the development of rickets in some US cases (32, 33).

The vitamin D content of breast milk from a mother with adequate vitamin D status is ∼22 IU/L (34) and thus cannot provide, by itself, the adequate intake of 200 IU/d recommended for infants (12). Most breast-fed infants may obtain adequate vitamin D through sunlight exposure. However, the amount of vitamin D synthesized through sunlight exposure is affected by the time spent outside, the amount of skin exposed, air pollution, cloud cover, time of day, latitude, and skin pigmentation (6).

Specker et al (35) estimated that white infants require ∼30 min of sunlight per week to obtain adequate vitamin D if they are wearing only a diaper and they require 2 h per week if they are fully clothed with no hat. However, because melanin in skin decreases the amount of vitamin D₃ synthesized from sunlight, infants with dark skin need to spend more time exposed to sunlight to synthesize the same amounts of vitamin D₃ as infants with light skin. One study suggested that an adult with dark skin would need to spend at least 6 times as long a time exposed to sunlight to synthesize the same amount of vitamin D as an adult with white skin (36). Comparable figures are not available for infants. Furthermore, infants living at northern latitudes in the US synthesize less vitamin D₃ from sunlight because more ultraviolet-B photons are absorbed by the atmosphere (5,11). In our review, we noted that all rickets cases involving white infants occurred among infants living at northern latitudes. Finally, breast-fed infants may not obtain adequate vitamin D₃ from sunlight because exposure is limited, because of parental concerns about air quality or subsequent skin cancer risk. In fact, the AAP recommends that infants <6 mo of age be kept out of direct sunlight to reduce the risk of skin cancer (37).

Recommendations for vitamin D supplementation for infants have varied somewhat since 1963, when the AAP recommended that all infants receive supplementation with vitamin D (38). The recommendation was modified in 1978, when vitamin D was listed as a possible supplement for breast-fed infants (39). In 1997, the AAP Work Group on Breastfeeding (40) recommended that all infants be breast-fed for a minimum of 12 mo and noted that vitamin D might need to be given before 6 mo of age to infants whose mothers have vitamin D deficiencies and those with inadequate exposure to sunlight. Near the same time, the 1998 AAP Pediatric Nutrition Handbook was released, which recommended vitamin D supplementation at 400 IU/d for all breast-fed infants in the chapter on vitamins but limited the recommendation to dark-skinned infants, particularly if they are exposed to minimal sunlight, in the chapter on breast-feeding (41).

In April 2003, as a result of continued reports of rickets in the United States and inconsistent recommendations regarding who should receive supplementation with vitamin D, the AAP published new guidelines on preventing rickets and vitamin D deficiency among children (10). The AAP (10) recommended that, "all infants, including those who are exclusively breastfed, have a minimum intake of 200 IU of vitamin D per day beginning during the first 2 months of life" (p. 908). Because the adequate intake of 200 IU/d cannot be met with human milk alone and the adequacy of sunlight exposure is difficult to determine for all breast-fed infants, the AAP recommended that all breast-fed infants be given supplemental vitamin D by 2 mo of age unless they are consuming at least 500 mL of vitamin D-fortified formula or milk (10). In addition, non–breast-fed infants who consume <500 mL of vitamin D-fortified formula or milk should be given a vitamin D supplement. The AAP recognizes that variations in this guideline may be appropriate in specific circumstances (10). Evaluation of physician advice regarding vitamin D supplementation for infants since the release of the new guidelines will be important, as will continued surveillance of hypovitaminosis D and rickets cases in the United States.

Currently, there is no national surveillance of diagnosed clinical cases of nutritional rickets in the United States. The National Hospital Discharge Survey (NHDS) data can be used to provide national estimates of hospitalizations for diagnosed conditions, including rickets (42). Scanlon and Grummer-Strawn (unpublished data cited in reference 43) used the NHDS data to estimate that 9 children per 1 million children in the population were hospitalized with rickets between 1990 and 1998. However, they concluded that the rarity of rickets diagnoses in the NHDS (ie, 20 cases in 9 y) results in an unstable estimate of rickets that should be interpreted with caution (43). Furthermore, rickets cases resulting from nutritional deficiency cannot be distinguished from rickets cases resulting from other causes in the NHDS. Only one of the case groups we reviewed provided an estimate of the incidence of nutritional rickets in the population (7). In that study, the rate of 5 cases per 1 million children 6 mo to 5 y of age reflects hospitalized cases of nutritional rickets in one US state during a 2.5-y period (7).

Breast-feeding is the preferred method of infant feeding and provides infants with important nutrients and immunologic factors (44, 45). Breast milk alone, however, does not provide infants with adequate vitamin D (10). Most breast-fed infants do not develop clinical vitamin D deficiency rickets because sufficient vitamin D is synthesized through casual sunlight exposure or obtained from a supplement. As noted above, however, environmental conditions and concerns, as well as skin pigmentation and covering, make it difficult to rely on sunlight as a source of vitamin D for exclusively breast-fed infants. Our review identified breast-feeding without vitamin D supplementation among black children as a key similarity among cases. The biologic mechanisms relating these factors to vitamin D deficiency are well established. The new AAP clinical guideline to provide a minimal intake of 200 IU/d vitamin D for all infants, beginning in the first 2 mo of life, should be emphasized in the education of all families but particularly the families of children at greatest risk of vitamin D deficiency. Furthermore, children should be weaned to a diet adequate in both vitamin D and calcium.

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