Are Doctors Causing Infant Brain Damage By Clamping The Umbilical Cord Prematurely?

Newborn lungs exist in a “compacted state” suitable for the womb. When the infant is born, the placenta and cord pulse for up to 20 minutes, delivering a burst of blood volume to the infant’s system. This blood burst is just what is needed for the lungs of the newborn to expand.

Unfortunately, many hospitals and doctors don’t understand the mechanics of this and are engaging in early umbilical cord clamping — often within one minute of birth.

Without the burst of blood from the placenta, the infant suffers a drop in blood pressure as its lungs fail to open as they should, creating a chain reaction of effects that can include brain damage and lung damage. Immediate cord clamping can cause hypotension, hypovolemia and infant anemia, resulting in cognitive deficits. Some have even theorized that the rise in autism could be linked at least in part to early cord clamping.

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When a baby is born, one of the first procedures performed is the clamping and cutting of the umbilical cord. In hospitals, this task is often done before 30 seconds have elapsed because it’s believed it will reduce the mother’s risk of excess bleeding and the baby’s risk of jaundice.

Very often cords are clamped early also to collect cord blood and cord stem cells to be used for various medical and commercial purposes.

However, research is increasingly revealing that clamping the umbilical cord prematurely, before two or even three full minutes have elapsed, robs your baby of much-needed blood and oxygen.

Today there is absolutely no consensus about the optimal time to clamp the umbilical cord after birth, yet over 200 years ago in 1801, Erasmus Darwin (Charles Darwin’s grandfather) shared some wise words on the topic that have been largely overlooked:

“Another thing very injurious to the child, is the tying and cutting of the navel string too soon; which should always be left till the child has not only repeatedly breathed but till all pulsation in the cord ceases.

As otherwise the child is much weaker than it ought to be, a portion of the blood being left in the placenta, which ought to have been in the child.”

Suffocating Baby at Birth?

One of the primary arguments for delaying cord clamping has to do with the way a baby breathes just before and after being born.

Before birth, the baby’s lungs are filled with fluid and very little blood flows through them; the child receives oxygen from its mother through the placenta and cord. This placental oxygen supply continues after the child is born until the lungs are working and supplying oxygen — that is, when they are filled with air and all the blood from the right side of the heart is flowing through them.

After birth, when the child is crying and pink, the cord vessels clamp themselves. During this interval between birth and natural clamping, blood is transfused from the placenta to establish blood flow through the baby’s lungs. The natural process protects the baby’s brain by providing a continuous oxygen supply from two sources until the second source is functioning well.

However, according to George M. Morley, M.B., Ch. B., FACOG of Cordclamping.com, immediate cord clamping at birth instantly cuts off the placental oxygen supply and the baby remains asphyxiated until the lungs function. Blood, which normally would have been transfused to establish the child’s lung circulation, remains clamped in the placenta, and the child diverts blood from all other organs to fill the lung blood vessels.

While most full-term babies have enough blood to establish lung function and prevent brain damage, the process often leaves them pale and weak. For premature babies, the process can be even more devastating. And no matter what, immediate cord clamping will cause some degree of asphyxia and loss of blood volume because it:

1. Completely cuts off the infant brain’s oxygen supply from the placenta before lungs begin to function.

2. Stops placental transfusion — the transfer of a large volume of blood (up to 50% increase in total blood volume) that is used mainly to establish circulation through the baby’s lungs to start them functioning.

Injuries Related to Immediate Cord Clamping

Keeping valuable oxygen and blood from an infant by clamping the umbilical cord prematurely increases the baby’s risk of brain hemorrhage and breathing problems. It has also been implicated as a contributing factor to:

• Autism
• Cerebral Palsy
• Anemia
• Learning disorders and mental deficiency
• Behavioral disorders
• Respiratory distress

Immediate cord clamping has even been identified as causing brain injuries that lead to death, according to Morley.

Are You Seeking Natural Childbirth Options?

Given the overwhelming research about the potential harms of early cord clamping, both the World Health Organization and the International Federation of Gynecology and Obstetrics (FIGO) have dropped the practice from their guidelines.

But it is still widely done in the United States and other developed countries, especially if you give birth in a hospital with an obstetrician (specially trained surgeons). This is one of many reasons why you may want to consider having a midwife deliver your baby instead.

There is not a single report in the scientific literature that shows obstetricians to be safer than midwives for low risk or normal pregnancy and birth. So if you are among the more than 75 percent of all women with a normal pregnancy, the safest birth attendant for you and your baby is in fact not a doctor but a midwife or doula.

A midwife will be more accommodating to your wishes, such as waiting for two to three minutes, or until the umbilical cord has stopped pulsating, before it is cut. Caesarean rates and use of other drug and surgical interventions also tend to be lower when you use a midwife.

One study in the British Medical Journal even found that a woman’s risk of death during delivery is three to five times higher during caesarean than a natural delivery, her risk of hysterectomy four times higher, and her risk of being admitted to intensive care is two times higher.

Fortunately, there are many excellent resources out there for anyone who is planning a natural childbirth, including delayed cord clamping, and here are some to get you started.

Source:

http://m.kenyon.webnode.com/umbilical-cord-articles/

The Stepchildren Of Modern Medicine, As Applied To Shaken Baby Syndrome (SBS)/Non-Accidental Injury (NAI)

Harold E. Buttram, MD

July 20, 2010

Abstract: In hospital emergency rooms throughout the USA it is standard procedure to attribute infantile brain hemorrhages, with or without retinal hemorrhages, to inflicted child abuse, generally referred to as Shaken Baby Syndrome/Non-Accidental Injury (SBS/NAI) in the absence of a known major accident. However, beginning with the work of A. Kalokerinos, Australian health officer among the Australian aborigines, who reduced a 50 percent infant mortality to 3 percent by avoiding vaccines during viral illnesses, supplementing children with vitamin C, and giving vitamin C injections during crises. In a study by Pourcyrous et al (2006) involving 239 preterm infants, it was found that 70 percent of infants administered single vaccines and 85 percent of infants administered multiple vaccines had elevated C-Reactive proteins (markers of inflammation). Among the general population, surveys have been conducted showing general and significant inverse relations between C-Reactive proteins and blood levels of vitamin C and other antioxidants. By the inherent nature of the human infant brain, it is highly vulnerable to lipid peroxidation. Vaccine adjuvants are designed to enhance and prolong immune responses to vaccines, which are inherently pro-inflammatory. It is the hypothesis of this paper that many infant brain hemorrhages now being attributed to inflicted child abuse are actually from adverse vaccine reactions.

Historical Perspectives

Ignatz Semmelweiss was an Austrian obstetrician who practiced his profession at a birthing center in Vienna in the mid-nineteenth century, a time when maternity death rates were an appalling 30 percent from “childbed fever,” due to poor sanitary practices and conditions of the times. Semmelweiss observed that medical students would perform autopsies on the victims of childbed fever and then often go to maternity wings and deliver babies without washing their hands. Deeply troubled about the losses at the birthing center, it occurred to him that the students might be carrying some noxious substance on their hands to the mothers in the delivery wards. Acting upon this impression, he mandated that no doctor should touch a woman in labor without first washing his hands in the rather harsh soap of the times. As a result the mortality rate soon dropped from 30 percent to approximately 3 percent, while other wings in the birthing center continued with their usual 30 percent mortalities. In spite of this enormous humanitarian contribution, his work was ignored, and he became ostracized from his colleagues and remained so until his death.

Although in the field of nutrition rather than infectious disease, the story of A. Kalokerinos, an Australian health officer who worked among the Australian aborigines in the 1960s and 1970s, is quite similar. When he first began his work Kalokerinos similarly became appalled by the nearly 50 percent infant mortality that was taking place. Noting signs of scurvy among some of the infants, and observing that they frequently died following immunizations, especially if ill with a viral illness, Kalokerinos began administering vitamin C supplements to the children, improving their diets, avoiding vaccines during viral illnesses (even if just a runny nose), and administering vitamin C injections during crises. Subsequently death rates dropped to three percent in his district.(1)

The Australian government awarded Kalokerinos a medal of merit for his work. Also, in 1989 his work gained academic validation with the publication of a 3-volume work, Vitamin C, by CAB Clemetson.(2) However, much after the experiences of Semmelweiss, the work of Kalokerinos has been largely overlooked or ignored by the medical profession. In my opinion this is tragic, as similar deaths among children are still taking place, although they are now in many instances being attributed to Shaken Baby Syndrome/Non-Accidental Injury (SBS/NAI).

In my 10+ years of experience with over 100 case reviews involving SBS/NAI areas, I have found record of only one case in which vitamin C blood level was tested, and even this was several weeks following hospital admission of the infant and therefore irrelevant. When the truth of this issue does become known, as it will be, I believe that vitamin C, administered orally, intramuscularly, or intravenously depending on the situation, will be found to play an indispensable protective role in the complications now being attributed to SBS/NAI.

While the recommended 30 mgs of vitamin C per day is generally adequate for a healthy infant, it may be rapidly consumed and totally inadequate when the infant is stressed or ill, as with viral or bacterial infections, or toxic chemical exposures. The common cold, for instance, has been shown to reduce vitamin C levels in the blood by 50 percent.(3) Vaccines contain numerous toxic adjuvants, (to be reviewed below) which create pro-inflammatory free radicals. All vaccine adjuvants are pro-oxidants that drain the body’s supply of antioxidants including vitamin C.(4) Another risk factor may be the use of microwave ovens for heating infant formulas. Also, fruits and vegetables need to be reasonably fresh, as vitamin C content declines with their aging.

Elevated Blood Histamine as Cause of Capillary Fragility and Bleeding from Scurvy

Far from being uncommon, vitamin C deficiency still does occur in the Western World. When people attending a Health Maintenance Organization (HMO) clinic in Tempe, Arizona, were tested for plasma vitamin C, it was found to be depleted (between 0.2 and 0.5 mgs/100 ml) in 30 percent of subjects, and to be deficient (below 0.2 mgs/100 ml) in 6 percent.(5)

As reviewed by Clemetson, when the human plasma ascorbic acid level falls below 0.2 mg/ml, the whole blood histamine level is doubled or quadrupled.(6) Blood histamine is also increased by vaccines or toxoids, by stresses such as heat or cold, and by various drugs in guinea pigs.(7) Vitamin C has been shown to inactivate tetanus toxin (8) and diphtheria toxin.(9) It has been shown that bleeding from scurvy results from increased blood histamine, or histaminemia, which causes separation of endothelial cells from one another in capillaries and small venules.(10) This process may result in subperiosteal hemorrhages, the latter resulting in callus-like bone swellings commonly misinterpreted as fractures, extensive spontaneous bruising, and subdural hemorrhages, which were included in early descriptions of classical scurvy.(11-12)

The Human Infant Brain: Uniquely Susceptible to Lipid Peroxidation

Although an infant’s brain receives 15 percent of normal cardiac output, it utilizes nearly 25 percent of the body’s oxygenation.(13) In addition to being a highly oxygenated organ, the vulnerability of the human brain to harmful peroxidation rests on the fact that it has by far the highest fat content of any organ of the body with membrane lipids constituting 60 percent of the solid matter.(14) In addition, both brain and retina contain a relatively high percentage of the omega-3 polyunsaturated fatty acid, docosahexaenoic acid (DHA),(15-21) which serves as a primary building block of the membranes of these structures. The DHA and other polyunsaturated fatty acids are high in energetics, but they are far more unstable and prone to pro-inflammatory peroxidation (rancidity) than saturated fats.(15-21)

By way of explanation, the term “lipid peroxidation” refers to free-radical generation from a series of chain reactions, which can be very damaging if the process is prolonged. “Free-radicals” in turn refer to atoms with unpaired electrons, which results in heightened instability and reactivity. The end result of abnormally prolonged lipid peroxidation may be abnormal brain inflammation and brain swelling.

In essence, the brain might be compared with highly inflammable dry grass or brush enclosed with elevated oxygen levels, needing only a spark to set off a conflagration of inflammatory lipid peroxidation. In all likelihood, vaccine adjuvants provide this spark far more often than generally realized.

In addition, the infant’s immature brain and nervous system tissues are going through an extended period of rapid growth and development, which also bring heightened vulnerability to cellular damage. As reported by R.I. Haynes et al (22)(2005)(Journal of Comparative Neurology), cerebral axons (lengthy extensions of brain cells) achieve approximately one-fourth of adult level from the 24th to the 34th weeks during pregnancy, with rapid axonal growth and elongation taking place between 21 weeks during pregnancy and 24 weeks following birth. Onset of myelin development (fatty coating that protects nerve cells and provides nerve impulse insulation), does not commence until 14 weeks following birth with gradual progression to adult-like staining at 32 to 52 weeks. It is during this period of furious brain growth, limited myelin protection, and increased vulnerabilities that infants receive over 21 vaccines, according to today’s recommended schedule.

Hazards of Free Iron In and Around the Brain

Standard pediatric texts list prolonged labor, fetal malpresentation, and large babies as risk factors for significant brain hemorrhages. Tauscher et al reported an association between histologic chorioamnionitis (inflammation of the placenta) and brain hemorrhage in preterm infants.(23) Intracerebral hemorrhage occurs in up to 50 percent of very low-birth-weight infants and is thought to represent a substantial cause of morbidity and mortality in these infants.(24) Small subdural hemorrhages (SDH) are not uncommon in uncomplicated births and asymptomatic term newborns. Based on magnetic resonance imaging (MRI), Whitby et al (25)(2004) reported subdurals in 9 of 111 infants in 2004, all of which had resolved favorably when MRIs were repeated one month later.

V.J. Rooks et al (26)(2008) performed MRI scans on 101 term infants at 72 hours, 2 weeks, one month, and 3 months. Forty-six had asymptomatic SDH within 72 hours of delivery. All 46 had supratentorial SDH in the posterior cranium. Forty-three percent also had infratentorial SDH. Most SDH were < 3 mm in sizes, all of which were resolved within one month. Larger hematomas dissolved within 3 months.

Consequently, small hemorrhages are not uncommon even in uncomplicated childbirths, but little consideration has been given to the residual iron. As the red blood cells begin to lyse (break up) and release their iron following a hemorrhage, a process that takes place in two or three weeks, the iron is scavenged by white blood cells and carried into nearby tissues in the form of hemosiderin.(27)

Free-iron in and around the brain also may result when there are critical drops in levels of vitamin C following administration of vaccines, followed in turn by a precipitous rise in serum histamine bringing increased capillary fragility and leakage of blood into and around the brain.

It is known that iron overload in the liver, pancreas, and kidneys can be very destructive, a condition known has hemochromatosis. The concern here is that residual iron in and around the brain from an earlier brain hemorrhage, such as from birth trauma, may act as a lighted fuse that could ignite a firestorm of lipid peroxidation in the brain following vaccines.(28)

Vaccine Adjuvants and Their Role in Causing Prolonged Immune Responses to Vaccines and their Potentially Adverse Consequences

In what may be the most comprehensive review to date on the pathophysiology of adverse vaccine reactions, Russell Blaylock has compiled a mass of evidence that repeated stimulation of the systemic immune system results in intense reactions of microglial and astraglia cells, which serve as the brain’s immune system, with each successive series of vaccinations. This is the result of vaccine adjuvants that are added for that purpose.(29-30)

In explanation, microglia and astrocytes are first-line-immunological responder cells located in the brain that defend against foreign infectious invaders. Normally this response, such as to a viral infection, is of limited duration and harmless to the brain. However, when microglia and astrocytes are over-stimulated for prolonged periods, which vaccine adjuvants are designed to bring about, this extended activation can be very destructive to the brain.

Because of the critical dependence of the developing brain on a timed sequence of cytokine and excitatory amino acid fluctuations, according to Blaylock, sequential vaccinations can result in alterations of this critical process that will not only result in synaptic and dendritic loss, but abnormal (nerve) pathway development. When microglia are excessively activated by vaccines, especially chronically, they secrete a number of inflammatory cytokines, free radicals, lipid peroxidation products, and the two excitotoxins, glutamate and quinolenic acid, which may become highly destructive when activated for prolonged periods. (Emphasis added) This process was suggested as the principle mechanisms resulting in the pathological as well as clinical features of autism.(29)

Vaccine adjuvants are substances added to vaccine formulations during manufacturing that are designed to boost and prolong the overall immune system response when the vaccine is injected. These substances include albumin, several forms of aluminum, formaldehyde, various amino acids, DNA residues, egg protein, gelatin, surfactants, monosodium glutamate (MSG), Thimerosal (50 percent ethyl mercury, which is still in a number of vaccines)(31), and various antibiotics. Regarding mercury, even if it is not added as a preservative, it is commonly used in the manufacturing process, which leaves “traces” as residues. Even these trace amounts are potentially toxic because of the universally recognized principle of toxicology that combinations of toxins will increase toxicity exponentially; that is, two toxins will increase toxicity 10-fold, or three toxins increase toxicity 100-fold. In vaccines special attention should be given to the two toxic heavy metals, aluminum and mercury, each noted for its potential toxicity. The same principle applies in other classes of toxic chemicals.(32-34)

In view of these findings, R. Blaylock has referred to the inconsolable, high-pitched cry that commonly occurs following infant vaccinations as an “encephalitic cry.”

The Pourcyrous Study: The First of Its Kind, Presents a Unified Theory of Adverse Vaccine Reactions

It has long been known from animal studies that vaccines can cause brain inflammation,(35-37) which has now been confirmed in human infants in a study on primary immunization of 239 premature infants with gestational ages of less than 35 weeks by M. Pourcyrous et al. (38)(Journal of Pediatrics, 2007) The study was designed to determine the incidence of cardio-respiratory events and abnormal C-Reactive protein (CRP) elevations associated with administration of a single vaccine or multiple vaccines simultaneously at or about two months age. (CRP is a standard blood test indicator for body inflammation, which in the present study would represent brain inflammation.) CRP levels and cardio-respiratory manifestations were monitored for three days following immunizations in a neonatal intensive care unit sponsored by the University of Tennessee. Elevations of CRP levels occurred in 70 percent of infants administered single vaccines and in 85 percent of those given multiple vaccines, 43 percent of which reached abnormal levels. Overall, 16 percent of infants had vaccine-associated cardiorespiratory events with episodes of apnea (cessation of breathing) and bradycardia (slowing of pulse). It can be reasonably assumed that the cardio-respiratory events and CRP elevations primarily reflected brain inflammation and swelling following the vaccines. Most important for our present topic, intraventricular (brain) hemorrhages occurred in 17 percent of infants receiving single vaccines, with 24 percent incidence in those receiving multiple vaccines.

The first study of its kind, The Pourcyrous study provides evidence for a unified theory of adverse vaccine reactions:

• Brain inflammation, as indicated by elevations of C-Reactive proteins.
• Brain swelling (edema), as one of the cardinal manifestations of inflammation.
• Potentially lethal cardio-respiratory events (bradycardia & apnea).
• Intraventricular brain hemorrhages.

The study also raises a question: Why were the brain hemorrhages in the Pourcyrous study intraventricular rather than subdural? The answer is that the Pourcyrous study was performed on preterm infants, some born at less than 30 weeks term, in whom intraventricular hemorrhages are known to be characteristic. This may be due to the significant differences in the infant brain/skull interactions at these different stages of development. In preterm infants the skull would be highly flaccid, providing little if any resistance to a swollen (edematous) brain.

In term infants, in contrast, the inner surface of the skull presents a relatively firm surface, and when brain inflammation and edema takes place from vaccines,(35-37) it would require very little brain swelling for the outer surface of the brain to impact against the inner surface of the skull and, tourniquet-like, to cut off the passive outflow of blood in the subdural venous network. With cranial arterial blood coming in at much higher pressures, this would bring a precipitous rise in intracranial venous pressure, this in turn causing an extrusion of blood into the subdural spaces. According to W. Squier and J. Mack,(39) most infant subdural hemorrhages take place as a result of blood seepage into the immature subdural membranes, which in infancy are made up of 10 to 15 layers of loosely arranged flake-like cells with fluid-filled spaces between the layers. These open spaces readily allow seepage of blood in between the subdural membranes.

As final pieces of evidence connecting the pro-inflammatory effects of vaccine adjuvants with antioxidant deficiencies, as the true cause of many subdural brain hemorrhages now being attributed to inflicted child abuse, in a cross-sectional analysis of the third National Health and Nutrition Examination Survey data, Ford et al (40) reported that C-Reactive Protein concentrations were inversely and significantly associated with concentrations of retinaol, retinyl esters, vitamin C, alpha carotene, beta carotene, lycopene, cryptoxanthin, lutein or zeaxanthin, and selenium C after adjustment for age, gender, race-ethnicity, education, body mass index (BMI), leisure-time physical activity, and aspirin use. Furthermore, Wannamethee et al(41) reported a significant inverse association of dietary and plasma vitamin C and fruit and vegetable intakes with biomarkers of inflammation in a cross-sectional study of 3258 men aged 60-69 years who had no history of cardiovascular disease or diabetes. Wannamethee et al concluded that vitamin C has anti-inflammatory effects and is associated with an attenuation of endothelial dysfunction.

Conclusions

The human infant brain has heightened vulnerability to inflammation due to its relatively high oxygen levels and high fat content, a large portion of which consists of polyunsaturated fatty acids, which are high in energetics but relatively unstable and susceptible to damaging peroxidation.

The Pourcyrous study, the first of its kind, provides a unified theory of adverse vaccine reactions with documented brain inflammation, as indicated by increases levels of C-Reactive protein in 70 percent of infants administered a single vaccine and 85 percent of those administered multiple vaccines; brain swelling (edema) would follow as one of the cardinal markers of inflammation; the brain swelling would immediately impact against the inner surface of the skull, cutting off (tourniquet-like) the passively outflowing of blood through the subdural venous network, this in turn resulting in a precipitous rise in intravenous venous pressure, the true cause of subdural hemorrhages in many of these cases, in my opinion.

Very sadly, the potential protective role of antioxidants in these situations is being largely overlooked and ignored.

References

(1) Kalokerinos A. Medical Pioneer of the 20th Century, an Autobiography. Melbourne, Australia, Biology Therapies Publishing, 2000: 11-26.
(2) Clemetson CAB. Vitamin C, Volumes I, II, & III. CRC Press, Boca Raton, 1989.
(3) Hume R, Weyers E. Changes in the leucocyte ascorbic acid concentration during the common cold. Scot Med J, 1973; 18:3.
(4)Clemetson CAB. Barlow’s Disease, Medical Hypothesis. 2002; 59(1):52-56.
(5) Johnston DS, Thompson MS. Vitamin C status of an out-patient population. American J Clinical Nutrition, 1998; 17:366-370.
(6) Clemetson, CAB. Histamine and ascorbic acid in human blood. Journal of Nutrition, 1980; 110:662-668.
(7) Chaterjee JB, Majunder AK, Nandi BK, Subramanian N.. Synthesis and some major functions of vitamin C in animals, Annals New York Academy of Science, 1975; 258:24-47.
(8) Dey, PK. Efficacy of vitamin C in counteracting tetanus toxin toxicity, Naturwissenschaften, 1966; 53:319.
(9) Jungblut CW, Zweemer RL. Inactivation of diphtheria toxin in vivo and in vitro by crystalline vitamin C (ascorbic acid), Proceedings of the Society of Experimental Biology & Medicine, 1935; 32:1229-1234.
(10) Gore I, Tanaka Y, Fujinami T, Shirahama T. Endothelial changes produced by ascorbic acid deficiency in guinea pigs. Arch Pathology, 1965; 80:371-376.
(11) Barlow T. On cases described as ‘acute rickets,’ which are probably a combination of scurvy and rickets; the scurvy being an essential and rickets being a variable element. Med Chir Trans, 1883; 66:159.
(12) Hart C, Lessing O. Der Scorbut der Kleinen Kinder (Moller-barlowsche Krankheit). Stuttgart: Verlag von Ferdinand Enke, 1913.
(13) O’Brien JS. Stability of the myelin membrane; Science. 1965; 147:1099-1107.
(14) Stocker JT, Dehner LP. Eds, Pediatric Pathology, Vol. 2, Philadelphia, PA.: Lippincott Williams & Wilkins, 2002:1449.
(15) Nolty J. The Human Brain, an Introduction to Its Functional Anatomy. Fifth Edition, Mosby Publ, Philadelphia, PA:129.
(16) Yavin E, Brand A, Green P. Docosahexanenoic acid abundance in the brain: a biodevice to combat oxidative stress. Nutr Neurosci, 2002; 5(3):149-157.
(17) Cunnane SC, Francescutti V, Brenna T, Crawford MA. Breast-fed infants achieve a higher rate of brain and whole body docosahexanenoate accumulation than formula-fed infants not consuming dietary docosahexaenoate. Lipids, 2000; 35(1):1-5-111.
(18) Innis SM. The role of dietary n-6 and n-3 fatty acids in the developing brain. Devel Neurosci, 2000; 22(5-6):474-480.
(19) Crawford MA, Bloom M, Cunnane S, Holmsen H, Ghebremeskel, Schmidt, WS. Docosahexanenoic acid and cerebral evolution. World Rev Nutr Diet,2001; 88:6-17.
(20) Yavin ES, Glozman S, Green PN, Cunnane SC. Docosahexaenoic acid accumulation in the prenatal brain: prooxidant and antioxidant features. J Mol Neurosci, 2001, 16(2-3):229-235:279-284.
(21) Larque EH, Demmelmair H, Koletzko B. Perinatal supply and metabolism of long-chain polyunsaturated fatty acids; importance for the early development of the nervous system. Ann NY Acad Sci, 2002; 967:299-310.
(22) Haynes RI, Borenstein NS, Desilva TM, Folkerth RD, Liu LG, Volpe JJ, Kinney HC, . Axonal development in the cerebral white matter of the human fetus and infant. Journal of Comparative Neurology, 2005; 484:156-167.
(23) Tauscher MK, Berg D, Brockmann M, Seiden-Spinner S, Speer CP, Vollard E. Association of histologic chorioamnionitis: Increased levels of cord blood cytokines, and intracerebral hemorrhage in preterm neonates. Bio Neonate, 2003; 83:166-170.
(24) Maternal-Fetal Medicine, Principles and Practice. Creasy RK, Reznik R Editors, Philadelphia: W.B. Saunders, 1994:1169.
(25) Whitby EH, Griffiths PD, Rutter S, Smith H, Sprigg A, Ohadike P et al Frequency and natural history of subdural haemorrhages in babies and relation to obstetric factors. Lancet, 2004; 8:363:846-851.
(26) Rooks, VJ, Eaton, JP, Ruess, L, Petermann GW, Keck-Wherley J, Pedersen RC. Prevalence and evolution of intracranial hemorrhage in asymptomatic term infants. American Society of Neuroradiology, American Journal Neuroradiology, 2008; http://www.ajnr.org
(27) Forensic Pathology, Principles and Practice. Dolinak D, Matshes E, Lew E. Elsevier Academic Press, New York, 2005: 431-435.
(28) Rensburg, SJ van, Zyl J van, Hon D, Daniels W, Hendricks J, Potoknic F, et al. Biochemical Model for Inflammation of the Brain: the effect of iron and transferrin on monocytes and lipid peroxidation. Metabolic Brain Disease, 2004; 19(1/2):97-112.
(29) Blaylock, RI, The danger of excessive vaccination during brain development. Medical Veritas, 2008; April, 5(1):: 1727-1741.
(30) Blaylock, RI, Chronic microglial activation and excitotoxicity secondary to excessive immune stimulation: possible factors in Gulf War Syndrome and autism. Journal American Physians and Surgeons, 2004; 9(2):46-52.
(31) King PG. Thimerosal in vaccines: Inconvenient reality. Medical Veritas, 2008; 5(2): 1816-1820.
(32) Schubert J, Riley EJ, Tyler SA. Combined effects in toxicology: A rapid systematic testing procedure: cadmium, mercury and lead. Journal of Toxicology and Environmental Health, 1978; 4:763-776.
(33) Abou-Donia MB, Wilmarth KR, Ochme F, Jensen KF, Kurt, TI. Neurotoxicity resulting from coexposure to pyridostigmine bromide, DEET, and permithrin: Implications of Gulf War chemical exposures. Journal of Toxicology and Environmental Health, 1996; 48:35-56.
(34) Arnold SF, Koltz DM, Collins B, Vonier PM, Guilette LJ, McLachlan JA. Synergistic activation of estrogen receptor with combinations of environmental chemicals. Science, 1996; 272: 1489-1492.
(35) Iwasa S, Ishida S, Akama K. Swelling of the brain caused by pertussis vaccine: its quantitative determination and the responsible factors in the vaccine. Japan J Med Sci Biol, 1985; 38(2):53-65.
(36) Levine S. Hyperacute encephalomyelitis. Amer J Pathol, 1973; 37:247-250.
(37)Munoz JJ, Bernard CE, Mackay IR. Elicitation of experimental encephalomyelitis in mice with aid of pertussigen. Cellular Immunol, 1984; 83:92-100.
(38) Pourcyrous M, Korones SB, Kristopher LA, and Bada HS. Primary immunization of premature infants with gestational age <35 weeks: Cardiorespiratory complications and C-reactive protein responses associated with administration of single and multiple separate vaccines simultaneously. J Pediatr, 2007; 151:167-172.
(39) Squier W, Mack J. The neuropathology of infant subdural haemorrhage. Forensic Science International, 2009, in press, doi:10.1016/j.forsciint.2009.02.005.
(40) Ford ES, Liu S, Mannino DM, Giles WH, Smith SJ. C-Reactive protein concentration and concentrations of blood vitamins, carotenoids, and selenium among United States adults. Europ. J.Clin. Nutr. 2003; 57:1157-1163.
(41) Wannamethee SG, Lowe GDO, Rumley A, Bruckdorfer KR, Whincup PH. Association of vitamin C status, fruit and vegetable intakes, and markers of inflammation and hemostasis. Am J. Clin. Nutri., 2006; 83:567-574.

Source:

http://imcv.info/de/vaccination/articles/the-stepchildren-of-modern-medicine-as-applied-to-shaken-baby-syndrome-sbsnon-accidental-injury-nai.html

Doctor Gagged For Doubting Shaken Baby Syndrome

29 July 2010 by Andy Coghlan

A PATHOLOGIST in the UK who argues that the trademark triad of symptoms of “shaken baby syndrome” (SBS) can have an innocent cause has been prevented from testifying in court as an expert witness. The restriction could stand until January 2012.

Yet, according to researchers and lawyers contacted by New Scientist, there are serious doubts about the safety of many shaken baby convictions. This is despite the fact that the triad of symptoms has been taken as evidence of murder for 40 years.

The pathologist in question, Marta Cohen of Sheffield Children’s Hospital, learned of the restrictions following a private hearing on 22 July before the General Medical Council, the body that investigates complaints against doctors in the UK.

“The decision is appalling,” says John Plunkett of the Regina Medical Center in Hastings, Minnesota, who has shown that short falls can cause the trademark symptoms said to be exclusive to child abuse.

The fear of similar outcomes means that British-based pathologists who dispute SBS are unwilling to take on cases of alleged child abuse. “It means that no one will take any head injury cases,” said one, who asked not to be named. “If you disagree with the prosecution, you risk being called before the GMC.”

The verdict appears under Cohen’s registration details on the GMC website, stating that: “She must not give evidence as an expert witness in cases where there is alleged non-accidental head injury to an infant or child.” It also makes clear that the restrictions are temporary precautions while the complaints against her are further investigated by the GMC.

It is not clear who complained to the GMC, but the motivation appears to come from criticisms circulated to prosecution services by a judge, Justice Eleanor King, following cases last year in which Cohen gave evidence. King’s criticisms included accusing Cohen of developing a “scientific prejudice”, of being “disingenuous” in her citing of research and unwilling to defer to prosecution expert witnesses.

The GMC will not explore the validity of the competing scientific theories about SBS, and will simply investigate Cohen’s “fitness to practice”. The GMC’s ruling comes at a time when evidence is mounting that innocent events such as the birth process itself, choking, short tumbles and breathing difficulties can cause the classic symptoms (BMJ, vol 2, p 430).

A triad of markers

The three markers for a shaken baby diagnosis are retinal haemorrhages in both eyes; subdural haemorrhages between the fibrous dura layer that protects the brain and the brain surface beneath; and swelling of the brain. Subdural haemorrhages are said to arise from ripping and shearing of so-called bridging veins. New lines of evidence challenge this hypothesis with the discovery that subdural bleeds are much more common in babies than generally appreciated, and for a host of innocent reasons (see “Anatomy of a murder?”).

Last year, Cohen and co-researcher Irene Scheimberg of Barts and the London NHS Trust examined post-mortem tissue from fetuses and newborns and found subdural haemorrhages in 16 of the 25 fetuses and 20 of the 30 newborns. They also found haemorrhages within the dural layer itself, suggesting that the bleeding started here (Pediatric and Developmental Pathology, DOI: 10.2350/08/08/0509.1). The research is just the latest of many reports to show that subdural bleeds can occur without shaking (see “Anatomy of a murder?”).

No one doubts that frenzied shaking could cause the triad of symptoms, but only after severe accompanying damage to the neck. A baby’s head striking a solid surface would also cause such damage but then there would be other evidence of an impact. For these reasons, there is increasing pressure for the triad not be used as evidence of guilt in the absence of any other evidence of child abuse. The American Academy of Pediatrics last year called for the phrase “shaken baby syndrome” to be replaced with “abusive head trauma”. In the UK, the Royal College of Pathologists last December cautioned against viewing the triad as “absolute proof of traumatic head injury in the absence of any other corroborative evidence”.

No independent witness has ever seen a shaken baby with such symptoms, the only evidence has come from confessions. Of 54 cases globally in which defendants admitted shaking a baby, only 11 had no signs of other injuries (The American Journal of Forensic Medicine and Pathology, DOI: 10.1097/01.paf.0000164228.79784.5a).

In 2001, Plunkett published 18 reports of all or some of the key symptoms in infants who had died after falling 60 centimetres to 3 metres (The American Journal of Forensic Medical Pathology, vol 22, p 1). In the same journal in 2004, (vol 25, p 89) Plunkett described evidence from a family video of a toddler with all the symptoms dying after a short fall.

The original concept of shaken baby syndrome arose not from research on babies but from road safety research published in 1968 on what happened to brains of adult monkeys when cars decelerated rapidly (Journal of the American Medical Association, vol 204, p 285). Since then, biomechanical studies using dummies as surrogates have concluded that shaking alone doesn’t cause the classic symptoms. Oxygen shortage has been proposed as a possible cause of brain damage in infants by Jennian Geddes, a retired pathologist formerly of the Royal London Hospital. Although dismissed by the UK Supreme Court in 2005, some concepts behind Geddes’s hypotheses have since been followed up.

In the US, momentum is building for a reappraisal of the status and validity of SBS as a way of diagnosing child abuse. There are also moves to reopen cases in which the triad may potentially have led to unsafe convictions.

The US Innocence Project, a nationwide network originating in New York City to identify and investigate potentially unsafe convictions, confirmed last week that they are looking into cases of SBS. “We believe there were a number of false scientific assumptions about these cases,” says Barry Scheck, a founder of the Innocence Project.

“I’m involved in conversations around the possibility of creating an ‘innocence commission’ to look specifically into SBS,” says Deborah Tuerkheimer of DePaul University College of Law in Chicago, and author of a recent law review calling for such a commission. She estimates that approximately 1500 Americans are serving sentences for SBS.

Tom Bohan, past president of the American Academy of Forensic Sciences, has been fighting for SBS to be reviewed for more than a decade. “All I’ve wanted is an impartial examination, as I’ve come to the conclusion that SBS is bogus,” he says.

All I want is an impartial examination. I’ve come to the conclusion that shaken baby syndrome is bogus

Shaking won’t damage vital brain veins

A central tenet behind the original concept of shaken baby syndrome is that the abuse would sever bridging veins that drain blood from the brain and direct it back to the heart via a channel in the brain.

Research is now showing that the bridging veins of infants are strong and seldom break when subdural haemorrhages occur. Julie Mack of Penn State Hershey Medical Center and her team found networks of hitherto unrecognised fluid channels and capillaries that develop in the protective dura about 30 weeks after birth. This is the time many shaken baby cases come to light (Forensic Science International, DOI: 10.1016/j.forsciint.2009.02.005).

These blood vessels are much more fragile and leaky than bridging veins. They can easily haemorrhage if lack of oxygen raises blood pressure, for example, which can happen if a baby is choking or a blood clot blocks the oxygen supply. In 2008, Veronica Rooks of the Tripler Army Medical Center in Honolulu, Hawaii, showed that in a group of 101 healthy newborn babies, 46 had subdural haemorrhages, presumed to be from the rigours of birth, all of which had disappeared by 3 months. These findings back up the suggestion that some of these fragile vessels can bleed again later in babyhood, perhaps after a fall or a choking episode.

Retinal haemorrhages too are proving to be more common than supposed. Evan Matshes of Southwestern Institute of Forensic Sciences in Dallas, Texas, re-examined 123 child deaths and found retinal haemorrhages are not limited to children who die of head injuries through abuse (Proceedings of the American Academy of Forensic Sciences, vol 16, p 272). Matshes says these injuries may be seen in a variety of situations.

Source:

http://www.newscientist.com/article/mg20727713.600-doctor-gagged-for-doubting-shaken-baby-syndrome.html?full=true

Metabolic Bone Disease In Preterm Newborn: An Update On Nutritional Issues

Authors:

Valentina Bozzetti

Paolo Tagliabue

Abstract:

Osteopenia, a condition characterised by a reduction in bone mineral content, is a common disease of preterm babies between the tenth and sixteenth week of life. Prematurely born infants are deprived of the intrauterine supply of minerals affecting bone mineralization.

The aetiology is multifactorial: inadequate nutrients intake (calcium, phosphorus and vitamin D), a prolonged period of total parenteral nutrition, immobilisation and the intake of some drugs.

The diagnosis of metabolic bone disease is done by biochemical analysis: low serum levels of phosphorus and high levels of alkaline phosphatase are suggestive of metabolic bone disease. The disease can remain clinically silent or presents with symptoms and signs of rachitism depending on the severity of bone demineralisation.

An early nutritional intervention can reduce both the prevalence and the severity of osteopenia.

This article reviews the pathophysiology of foetal and neonatal bone metabolism, focuses on the nutrient requirements of premature babies and on the ways to early detect and treat osteopenia.

Background:

The continuous advances in intensive care of preterm newborns have led to a progressive decline of mortality in Institutions where facilities and expertise for respiratory resuscitation and respiratory distress syndrome are available. Infant mortality dropped among all races between 1980 and 2000. The survival rate depends on the gestational age of the newborn; actually the survival rates for very low birth weight (VLBW) are the following: for those weighing 501 – 750 g is 56% and for the ones above 750 is 88% [1]. However, the success in the survival achieved through an aggressive intensive care is not always paralleled by a subsequent fully healthy development of the newborn.

Among the common conditions of morbidity due to the prematurity (cerebral impairment, bronchopulmonary dysplasia, growth failure, retinopathy…) a growing interest is focusing now on the metabolic bone disease of the prematurity (MBD), also called osteopenia of prematurity.

This condition is characterised by a reduction in bone mineral content (osteopenia), with or without rachitic changes, and is caused by several nutritional and biomechanical factors.

An inadequate supply of nutrients (vitamin D, calcium and phosphorus), a prolonged period of total parenteral nutrition, immobilisation and the intake of some drugs are the main factors involved in the pathogenesis of osteopenia [2].

The MBD usually occurs between tenth and sixteenth week of life, but it may remain silent until severe demineralisation (a reduction of BMD of 20 – 40%) occurs.

The clinical picture is various, ranging from a totally silent condition to a clinical picture of overt rickets, with multiple fractures and other alterations, when the demineralisation is severe.

The purpose of this review is to focus on the recent advances in the understanding of the bone tissue metabolism and on the nutritional approach to prevent and to treat the MBD.

Magnitude Of The Problem:

The prevalence of MBD varies depending on gestational age, birthweight and kind of alimentation.

It occurs in up to 55% of babies born with weight under 1000 g [3] and 23% of infants weighing < 1500 g at birth [4] and it is especially frequent in babies under 28 weeks of gestation. The prevalence is 40% in premature infants who are breastfed, in contrast to 16% of those fed with a formula designed for preterm infants and supplemented with calcium and phosphorus [5,6].

Preterm infants with a complicated medical course and delayed nutrition are also at high risk for MBD. Actually in western countries there is a trend of decrease of gestational age and birthweight, so the frequency of the MBD is expected to further increase.

Homeostasis of calcium -phosphorus

The homeostasis of calcium, phosphorus and magnesium is fundamental for structural matrix of the bone.

Calcium and phosphate represent the major inorganic constituents of bone. The highest amount of calcium (99%) and of phosphorus (80%) of the whole body is in the bone as microcrystalline apatite.

Only 1% of the total body calcium is within the extracellular fluids and soft tissues. About the 50% of total serum calcium is in the ionised form and represents the biologically active part. A further 8–10% is bounded to organic and inorganic acid and the remaining percentage of calcium is protein-bound (80% to albumin, 20% to globulin).

The formation of the apatite takes place if calcium and phosphorus are simultaneously available in optimal proportions.

Also magnesium is part of the bone matrix and the 60% of total body magnesium is in the bone.

Calcium and phosphorus homeostasis is a function of hormones, vitamin D and dietary intake, and depends on the intestinal absorption, skeletal accretion and reabsorption, and urinary excretion. [7]

Parathyroid hormone (PTH) is synthesised and secreted from the parathyroid glands in response to a reduction of serum level of ionised calcium. PTH regulates mineral metabolism and skeletal homeostasis through its action on target cells in bone and kidneys. It stimulates the reabsorption of calcium and excretion of phosphorus in the kidney and bone reabsorption of calcium. PTH also is able to activate the synthesis of calcitriol via stimulation of renal 25 (OH) D3-1-alpha-hydroxylase activities.

In its active form, 1, 25(OH) 2 vitamin D, stimulates the renal reabsorption of calcium and phosphorus. The synthesis of calcitriol is inhibited by elevated serum levels of calcium and phosphorus.

The combined actions of PTH and calcitriol maintain the adequate concentration of calcium in the extracellular fluids.

Kidneys contribute to maintain homeostasis of calcium; urinary calcium is one third derived from diet and the remaining from body stores, mostly bone.

Diuretics, as furosemide, increase renal calcium excretion.

Prenatal bone physiology

The amounts of minerals required for a correct accretion of the skeleton are widely different depending on the age of the babies.

The period of greater skeletal development is during the intrauterine life and specifically during the last trimester. The bone volume increases significantly with gestational age and the high net bone formation activity is mainly due to modelling, with a rapidly increasing trabecular thickness (the trabecular thickening rate being approximately 240 times faster in the foetus than in the children).

The mineralization process is determined by synthesis of the organic bone matrix by osteoblasts (osteoid) onto which calcium and phosphate salts are deposited. This process increases exponentially between 24 and 37 weeks of gestation, reaching the 80% of mineral accretion in the third trimester [8].

During gestation the developing fetus receives supplies of energy, protein and mineral for adequate growth (1.2 cm/week) and bone development.

At term the newborn skeleton has a high physical density (expressed as bone mass divided by bone volume).

The foetal accretion of calcium and phosphate during the last three months of gestation is about 20 g and 10 g respectively, which represents accretion rates of 100–120 mg/kg/day for calcium and 50–65 mg/kg/day for phosphate [9].

A very important role in skeletal accretion of the foetus is played by the placenta. In fact the transfer of calcium from the mother to the foetus through the placenta occurs via an active transport done by the calcium pump in the basal membrane [10]. There is a 1:4 maternal to foetal calcium gradient [11].

Moreover, the placenta is able to convert vitamin D to 1,25-dihydrocholecalciferol which is fundamental for transferring phosphate to the foetus [12].

The foetus is maintained hypercalcemic in a high calcitonin and estrogen environment which promotes the modelling/remodelling ratio in favour of modelling and thus increasing the endocortical bone [13].

As a result, infants born prematurely will be deprived of the intrauterine supply of calcium and phosphorus affecting bone mineralization.

It is well known that a chronic damage to the placenta may alter the phosphate transport; this explains why babies with intrauterine growth restriction may be osteopenic.

Demineralization is also observed in infants born from mother with chorioamniositis and placental infection [14].

Maternal dietary intake of calcium is a factor implied in foetal bone accretion. A supplement of calcium (2 g from before 22 weeks of gestation) to women with a low dietary calcium intake resulted in higher bone mineral content (BMC) of the total body in infants born at term [15].

After birth the physical density of term newborns bones decreases by 30% in the first 6 months of life [13]. This is mostly due to an enlargement of the marrow cavity size, which occurs faster than the increase in the cross-sectional area of the bone cortex [16]. In term infants these postnatal changes are not accompanied by an increase in bone fragility and occur because bone is exposed to different conditions before and after birth.

First, there are important changes of hormonal environment: the reduction of maternal estrogens [17] and a postnatal increase of PTH level mainly due to a reduction of the calcium supply by the placenta [18].

As the serum calcium levels falls in the first day of life, PTH secretion is stimulated. During this transition the response of the parathyroid gland to falling levels of ionised calcium is blunted, as emphasized in a recent review article [19]. This finally results in a physiological nadir in neonatal serum calcium levels within the first 48 hours of life. Of note, PTH level is still within the normal range for term babies or adult, but represents a decrease from foetal levels.

Many factors affect calcium absorption including the maternal vitamin D status, solubility and bioavailability of calcium salts, quality and quantity of calcium, amount and type of lipids and, obviously, gut function.

Calcium absorption from the intestine occurs both passively and through a vitamin-D dependent active transport mechanism. In a newly born preterm the low mineral content of human milk associated with a poorly efficient absorption of the developing gut determine a net reduction of calcium and phosphorus supply.

Absorption of phosphorus takes place in the jejunum and depends on the dietary intake. The phosphorus supply regulates calcium absorption and retention: the higher is the phosphorus content of the diet, the higher is the calcium retention. However, an excessive amount of one decreases the absorption of the other.

Moreover, while in utero fetus experiments mechanical stimulation by kicking against the uterine wall, this kind of training is missing during the extrauterine life since preterm babies usually stay in the incubator [20,21]. Inactivity due to immobilisation stimulates bone reabsorption by osteoclasts and urinary calcium excretion; furthermore the reduced muscle activity prevents the addition of new bone tissue [22]. Conditio sine qua non for the physical activity to be beneficial is that an adequate mineral intake is guaranteed [23].

The figure figure11 shows that during the third trimester of gestation, bone mineral apparent density (BMAD) increases at a faster rate in utero (term infants) than ex utero (preterm infants) according to gestational age.

Physiological evolution of DEXA apparent bone mineral density during the last trimester of gestation (filled squares) and during the first year of life in healthy term infants (upper triangles) compared to that observed in preterm infants (open squares

BMAD is an estimation of volumetric BMD (g/cm3) calculated as bone mineral content/bone area (BMC/BA). The figure figure11 also shows that there is a sharp reduction in BMAD in neonatal age followed by a stabilization that lasts all the first year of life (“black triangles”). A similar event occurs in preterm babies: from birth to the term, mineral retention sharply diminishes comparing with the foetal life, while the skeletal growth remains high. This leads to a reduction of bone density (“white squares”). A catch up mineralization occurs after discharge of VLBW so BMC spontaneously improves (“white rhombs”).

Among the other pathogenic factors, also problems related to inadequate supply of calcium to babies, which require parenteral nutrition and interference of several drugs, may contribute to determine preterm osteopenia with an increasing risk of bones fractures.

The drugs mostly implied in pathogenesis of MBD include steroids, methylxanthines and diuretics. They stimulate osteoclasts activation, decrease calcium absorption, reduce osteoblasts proliferation and increase calcium renal excretion and hence increase the risk of poor bone mineralization [24-26].

Neonatal mineral requirements

The requirements of calcium and phosphorus are based on demands for matching intrauterine bone mineral accretion rates.

Supplying calcium and phosphorus in parenteral nutrition is a challenge because of limited solubility of these two minerals. Calcium and phosphorus’s solubility in nutrition admixtures depends on temperature, type and concentration of aminoacid, glucose concentration, pH, type and concentration of calcium salts, and presence of lipid and so on…

In parenteral nutrition calcium is administered as inorganic salt and phosphorus may be administered as inorganic sodium and potassium phosphate or sodium-glucose phosphate or glycerolphosphate, which are quite soluble in water.

The addition of cystein to lower pH of the parenteral admixtures improves the solubility of calcium and phosphorus.

For all such reasons it is not possible to supply these minerals according to the physiologic requirements of the preterm to reach an adequate bone mineralization.

In the transition period, most of VLBW neonates receive full or partial parenteral nutrition with the goal to maintain normal levels of calcium and phosphorus. Hypocalcaemia, in fact, is a common event during the first days of life because of the sharp decrease of the calcium supply by the placenta and the delayed release of PTH due to the immature response of the parathyroid glands.

Parenteral administration of 50–75 mg of calcium/kg/day can prevent early neonatal hypocalcaemia in preterm infants.

Through the parenteral administration of calcium and phosphorus (40–70 mg/kg/day and of 25–45 mg/kg/day respectively) it is possible to achieve 60 – 70% of intrauterine mineralization [27]. The best calcium to phosphorus ratio for bone mineralization is 1.7:1 [28-30].

In preterm babies receiving parenteral nutrition only limited amounts of vitamin D are required since calcium is given by vein and there is no need of calcitriol to facilitate the intestinal uptake.

Moreover only the parent compound needs to be administered since the preterm infant is able to hydroxylate the inactive form to the active one since the 24th week of gestation. It is now generally accepted the daily recommended dose of vitamin D is 400 U.I./day [18].

For the transitional period, when infants are weaned from parenteral nutrition to the enteral one, the aim usually is to maintain an adequate serum level of calcium and phosphorus. However the serum level of calcium is not a good marker of adequacy of calcium intake since the level is maintained stable at the expense of the bone. Therefore the clinicians should be aware that a normal serum level of both calcium and phosphorus are not guarantee for an adequate whole body accretion as in intrauterine life.

The enteral administration of calcium is fraught with many problems as regards the calcium bioavailability. Vomiting, large gastric aspirates, constipation and abdominal distension are quite common in preterm babies and the gut absorption capacity is impaired due to the immaturity of the gastrointestinal mucosa.

Calcium absorption depends on vitamin D status, solubility of calcium salts, quality and quantity of lipid intake. Moreover, in preterm babies, vitamin D demands are influenced by body contents at birth which depends on the duration of gestation and maternal vitamin status.

Current estimates of requirements for calcium, phosphorus and vitamin D in growing premature infants vary among international sources of recommendations [31-34] (Table 1).

Minerals and vitamin D recommended intakes in growing preterm infants.

The human milk content is inadequate for preterm requirements since the content of calcium and phosphorus in preterm human milk is 31 mg/100 kcal and 20 mg/100 kcal [18] while the Life Science Research Office [31] suggests, for premature formulas, a dose approximately 4–6 times higher (123 to 185 mg Ca/100 kcal and 80 to 110 mg P/100 kcal). Even when VLBW are fed at high feeding volumes (180–200 mL/Kg), assuming calcium and phosphorus absorption of 70% and 80% respectively, this would provide only one-third of the in utero level of absorbed calcium and phosphorus [6]. Formula milk is richer in calcium and phosphorus than human one, but bioavailability is quite different. In formula fed infants, calcium absorption is usually less than with human milk, ranging from 35 to 60% of the intake. Hence the human milk intake has to be promoted, but a fortification with mineral and protein fortifier is necessary to achieve adequate nutrient intake.

With the current human milk fortifiers, containing highly soluble calcium glycerolphosphate, calcium retention reaches a level of 90 mg/kg/day (88% of the overall intake).

However the new human milk fortifiers available in the market still do not allow intakes of calcium comparable with the values achieved during the last trimester of gestation (100–120 mg/kg/day) which are considered the target mineral accretion for preterm infants, nevertheless the use of multinutrient fortification of human milk for premature infants is currently recommended.

A Cochrane systematic review and metaanalysis of human milk fortifiers, which however included studies on children who were not extremely preterm (the class at major risk) stated that the effects on bone mineralization were not conclusive [35].

Finally, it must be noted that high calcium supplementation of milk is not well tolerated; it is associated with high faecal calcium, prolonged gastrointestinal transit time and impaired fat absorption. All these effects are potential risk factors for developing necrotizing enterocolitis.

Clinical features and diagnosis

MBD remains silent until a severe demineralisation occurs. The most evident clinical findings of osteopenia are deformity of the skull (diastasis of the suture, enlargement of the sagittal fontanelle and frontal bosses, craniotabe), thickening of the chondrocostal junctions and of the wrists, rib and long bones fractures. Softening and/or fractures of the ribs can cause pulmonary changes and respiratory distress, typically between 5 and 11 weeks of age [36].

Diagnosis of osteopenia is mainly done by serum analysis. Biochemically osteopenia is characterised by low serum levels of phosphorus and by an increase in serum levels of alkaline phosphatase that can reach values 5 times higher than the upper reference range used for adults [37]. It is useful dosing the isoenzimes of alkaline phosphatase since this enzyme is synthetised also by the liver and by the gut.

Backstrom and colleagues suggested that serum alkaline phosphatase levels higher than 900 U.I/l associated with a serum phosphate level lower than 1.8 mmol/l have a diagnostic sensitivity of 100% and specificity of 70% [38]. However the opinions in literature about the reliability of alkaline phosphatase to predict the status of bone mineralization are still conflicting [39,40]

Serum level of calcium is usually within the normal range due to effects of PTH on the bone. Low concentrations of calcium and phosphorus in the urine suggest an inadequate intake. This is manly due by an increase of the tubular reabsorption of phosphate because of the low dietary intake and by an increase of PTH level that stimulates the reabsorption of calcium. Markers of nutritional status should be assessed baseline, and then weekly during the initial phase; once the newborn is stable, assessment must be done at the starting of total enteral nutrition and successively every 2–3 weeks. If MBD is diagnosed and nutritional supplementation is started, a periodic assessment of laboratory data is necessary to evaluate the response to treatment also when babies are discharged from hospital. The key clinical goal is to maintain normocalcemia and normophosphatemia and to avoid an excessive calciuria.

Once levels of ALP, calcium and phosphorus normalize, serum analysis can be performed monthly up to 6 months of age and then every 3 months.

X-rays examination may show fractures, thin bones and other alterations as reduction of thickness of the cortical, enlargement of the epiphysis, irregular border between growth cartilage and bony metaphysis [41].

Dual energy X-ray absorbitometry (DEXA) is able to determine the bone mass content of neonates and can predict the risk of fractures [39,42] since it is sensitive in detecting small changes in BMC and BMD. Its use is now validated in neonates both term and preterm ones.

DEXA reflects most accurately the state of bone mineralization in preterm infants [43] but the examination involves radiations for the baby and the device is not portable.

Quantitative ultrasound is simpler than DEXA and is non-invasive; it can be used bedside without moving the baby. Reference values are now available for infants. Quantitative ultrasound gives information about structure of the bone and about bone density [44].

Osteopenia has a good prognosis since the disease is self-resolving, provided that calcium, phosphates and vitamin D are appropriately administered to the babies.

It is still controversial the need for high calcium and phosphorus intakes in preterm infants after hospital discharge. Few data are available about the optimal length, quantity and methods of providing supplemental minerals for preterm infants who are in stable growth.

There are studies that show increased bone mineral mass in infants who receive formulas containing more minerals that the traditional ones up to 9 months [45,46].

It has been shown, with studies assessing bone mineralization with quantitative ultrasound and DEXA, that preterm infants show a catch-up mineralization for the first year of life. There is no difference in late childhood of bone mineralization between term and ex-preterm infants [47] even though the biochemical evidence of metabolic bone disease during the neonatal period may have a long-term stunting effect which continues up to 12 years later. A recent study published on Journal of Perinatology [48] stated that children who were born prematurely with birth weights less than 1.5 kg tend to be significantly smaller for age and have lower lumbar spinal bone mineral content and density compared with children born at term gestation.

The long duration of this complication provides further rationale for implementing any practice that can prevent this condition [49].

In the case of BMD of prematurity nutrition is both therapy and prevention. An adequate intake of minerals and of vitamin D, with breast milk fortifier or formula with a content of minerals suitable for preterm infant’s requirements, are necessary for a correct bone mineralization.

A regular physical stimulation, when the preterm infant is clinically stable and is receiving adequate doses of calcium, phosphate and vitamin D, should also be included in the standard preventive approach.

Conclusion

An adequate nutritional intake of calcium, phosphorus and vitamin D and passive physical exercise may prevent abnormal bone-remodelling activity during first weeks of life and may optimize growth potential of preterm infants. It is important to recognize the biochemical signs of osteopenia in an early stage in order to be able to precociously implement the dietary intake and reduce the risk of bones fractures. The determination of alkaline phosphatase and of phosphoraemia seems to be useful in assessing the risk of metabolic bone disease and serum analysis need to be performed periodically in order to assess response to nutritional treatment. Through DEXA and quantitative ultrasound it is also possible to determine the state of bone mineralization and therefore to plan a nutritional intervention.

Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

VB and PT equally contributed at the article, analyzing the literature and writing the paper. All authors read and approved the final manuscript.

Acknowledgements

We are grateful to Prof. G. Weber, University Vita-Salute, San Raffaele Scientific Institute of Milan, Italy, for her helpful advice.

References

• Neonatal Research Network From Avery’s disease of the Newborn. 8. Elsevier Saunders; 2004. Perinatal, mortality and morbidity information for infants born in the National Institute of child Health and Human Development (NICHD) Neonatal Research Network from 1997 to 2000; pp. 3–5.
• Demarini S. Calcium and phosphorus nutrition in preterm infants. Acta Paediatr Suppl. 2005;94:87–92. doi: 10.1080/08035320510043619. [PubMed] [Cross Ref]
• Mc Intosh N, DeCurtis M, Williams JR. Failure of mineral supplementation to reduce incidence of rickets in very low birth weight infants: conservative management and outcome. J Pediatr. 1989;9:326–9.
• Koo WWW, Sherman R, Succop P, Krug-Wispe S, Tsang RC, Steichen JJ, Crawford AH, Oestreich AE. Fractures and rickets in very low birth weight infants: conservative management and outcome. J Pediatr Orthop. 1989;9:326–30. [PubMed]
• Takada M, Shimada M, Hosono S. Trace elements and mineral requirements for very low birth weight infants in rickets of prematurity. Early Hum Dev . 1992;29:333–338. doi: 10.1016/0378-3782(92)90188-M. [PubMed] [Cross Ref]
• Abrams AS. In utero physiology role in nutrient delivery and fetal development for calcium, phosphorus and vitamin D. Am J Clin Nutr. 2007;85:604S–7S. [PubMed]
• Portale AA. Blood calcium, phosphorus and magnesium. In: Favus MJ, editor. Primer on the metabolic bone diseases and disorders of mineral metabolism. 4. Philadelphia: Lippincott William and Wilkins; 1999. pp. 115–8.
• Greer FR, Tsang RG. Calcium, phosphorus and vitamin D requirements for the preterm infants. In: Tsang RC, editor. Vitamin and minerals requirements in preterm infants. NY: Marcel Deer; 1985. pp. 99–136.
• Sparks JW. Human intrauterine growth and nutrient accretion. Semin Perinatol. 1984;8:74–93. [PubMed]
• Kovacs CS, Kronenberg HM. Maternal-fetal calcium and bone metabolism during pregnancy, puerperium and lactation. Endocr Rev. 1997;18:832–72. doi: 10.1210/er.18.6.832. [PubMed] [Cross Ref]
• Care AD. The placental transfer of calcium. J Dev Physiol. 1991;15:253–7. [PubMed]
• Weisman Y, Harell A, Edelstein S, David M, Spirer Z, Golander A. 1 alpha, 25-Dihydroxyvitamin D3 and 24,25- Dihydroxyvitamin D3 in vitro synthesis by human deciduas and placenta. Nature. 1979;281:317–9. doi: 10.1038/281317a0. [PubMed] [Cross Ref]
• Rigo J, Senterre J. Nutritional needs of premature infants: current issues. J of Pediatrics. 2006;149:S80–88. doi: 10.1016/j.jpeds.2006.06.057. [Cross Ref]
• Ryan S, Congdon PJ, James J, Truscott J, Horsman A. Mineral accretion in human fetus. Arch Dis Child. 1988;63:799–808. doi: 10.1136/adc.63.7.799. [PMC free article] [PubMed] [Cross Ref]
• Koo WW, Walters JC, Esterlitz J, Levine RJ, Bush AJ, Sibai B. Maternal calcium supplementation and fetal bone mineralization. Obstet Gynecol. 1999;94:577–582. doi: 10.1016/S0029-7844(99)00371-3. [PubMed] [Cross Ref]
• Rigo J, De Curtis M. Disorders of calcium, phosphorus and magnesium metabolism. In: Martin RJ, Fanaroff AA, Walsh MC, editor. Neonatal-Perinatal medicine: disease of the fetus and infanth. 8. Philadelphia: Elsevier; 2006. pp. 1492–1523.
• Toth P, Erdei G, Vasarhelyi B. Potential consequences of the sudden postnatal drop of estrogens level in preterm neonates. Orv Hetil. 2003;144:1719–24. [PubMed]
• American Academy of Pediatrics, Committee on Nutrition Nutritional needs of LBW infants. Paediatrics. 1985;75:975–6.
• Hsu SC, Levine MA. Perinatal calcium metabolism: physiology and pathophysiology. Seminars in Neonatology. 2004;9:23–26. doi: 10.1016/j.siny.2003.10.002. [PubMed] [Cross Ref]
• Miller ME. Hypothesis: fetal movement influences fetal and infant bone strength. Med Hypotheses. 2005;65:880–6. doi: 10.1016/j.mehy.2005.05.025. [PubMed] [Cross Ref]
• Miller ME. The bone disease of preterm birth: a biomechanical perspective. Pediatr Res. 2003;53:10–5. [PubMed]
• Rauch F, Schoneau E. Skeletal development in premature infants a review of bone physiology beyond nutritional aspects. Arch Dis Child Fetal Neonatal Ed . 2002;86:F82–F85. doi: 10.1136/fn.86.2.F82. [PMC free article] [PubMed] [Cross Ref]
• Specker BL, Mulligan L, Ho M. Longitudinal study of calcium intake, physical activity and bone mineral content in infants 6–18 months of age. J Bone Miner Res . 1999;14:569–576. doi: 10.1359/jbmr.1999.14.4.569. [PubMed] [Cross Ref]
• Weiler HA, Wang Z, Atkinson SA. Dexamethasone treatment impairs calcium regulation and reduces bone mineralization in infant pigs. Am J Clin Nutr. 1995;61:805–11. [PubMed]
• Zanardo V, Dani C, Trevisanuto D. Methylxanthines increase renal calcium excretion in preterm infants. Biol Neonate. 1995;68:169–74. [PubMed]
• Venkataraman PS, Han BK, Tsang RC, Daugherty CC. Secondary hyperparathyroidism and bone disease in infants receiving long-term furosemide therapy. Am J Dis Child. 1983;137:1157–61. [PubMed]
• Riefen RM, Zlotkin S. Microminerals. In: Tsang RC, Lucas A, Uauy R, editor. Nutritional Needs of the Preterm Infant. Baltimore, Williams and Wilkins; 1993.
• Rigo J, De Curtis M, Nyamugabo K, Pieltain C, Gerard P, Santerre J. Premature bone. In: Bonjour JP, Tsang RC, editor. Nutrition and bone development Nestlè nutrition workshop Series. Vol. 41. Philadelphia: Vevey/Lippincott-Raven; 1999. pp. 83–97.
• Koo WW, Tsang RC. Calcium, magnesium, phosphorus and vitamin D. In: Tsang Rc, Lucas A, Uauy R, Zlotkin S, editor. Nutrition needs of preterm infant Scientific basis and practical guidelines. Baltimore: Williams & Wilkins; 1993. pp. 135–155.
• Rigo J, De Curtis M, Pieltain C, Picaud J, Salle BL, Santerre J. Bone mineral metabolism in micropremie. Clin Perinatol. 2000;27:147–70. doi: 10.1016/S0095-5108(05)70011-7. [PubMed] [Cross Ref]
• Klein CJ. Nutrient requirements for preterm infants formulas. J Nutr. 2002:1395S–577S. [PubMed]
• European Society of Paediatric Gastroenterology and Nutrition, Committee on Nutrition of the Preterm Infant Nutrition and feeding of preterm infants. Acta Paediatr Scand Suppl. 1987;336:6–7.
• Atkinson S, Tsang RC. Calcium and phosphorus. In: Tsang RC, Uauy R, Koletzko B, Zlotkin SH, editor. Nutrition of the preterm infant: scientific basis and practice. 2. Cincinnati: Digital Educational Publishing; 2005. pp. 245–275.
• Rigo J, Pieltain C, Salle B, Senterre J. Enteral calcium, phosphate and vitamin D requirements and bone mineralization in preterm infants. Acta Paediatr. 2007:969–974. doi: 10.1111/j.1651-2227.2007.00336.x. [PubMed] [Cross Ref]
• Kuschel CA, Harding JE. Multicomponent fortified human milk for promoting growth in preterm infants. Cochrane Database Syst Rev. 2004;1:CD000343. [PubMed]
• Glasgow JS, Thomas PS. Rachitic respiratory distress in small preterm infants. Arch Dis Child. 1977;52:268–273. doi: 10.1136/adc.52.4.268. [PMC free article] [PubMed] [Cross Ref]
• Bishop N. Bone disease in preterm infants. Arch Dis Child. 1989;62:1403–9. doi: 10.1136/adc.64.10_Spec_No.1403. [PMC free article] [PubMed] [Cross Ref]
• Backstrom MC, Kouri T, Kuusela AL, Sievanen H, Kiovisto AM, Ikonen RS, Mäki M. Bone isoenzyme of serum alkaline phosphatase and serum inorganic phosphate in metabolic bone disease of prematurity. Acta Paediatr. 2000;89:867–73. doi: 10.1080/080352500750043792. [PubMed] [Cross Ref]
• Ryan SW, Truscott J, Simpson M, James J. Phosphate, alkaline phosphatase and bone mineralization in preterm neonates. Acta Paediatr. 1993;82:518–21. doi: 10.1111/j.1651-2227.1993.tb12740.x. [PubMed] [Cross Ref]
• Faerk J, Peitersen B, Petersen S, Michaelsen KF. Bone mineralisation in premature infants can be predicted from serum alkaline phopshatase or serum phosphate. Arch Dis Child Fetal Neonatal. 2002;87:F133–6. doi: 10.1136/fn.87.2.F133. [Cross Ref]
• Ardran GM. Bone destruction not demonstrable by radiography. Br J Radiol. 1951;24:107–9. doi: 10.1259/0007-1285-24-278-107. [PubMed] [Cross Ref]
• Rigo J, Nyamugabo K, Picaud JC. Reference values of body composition obtained by DEXA in preterm and term neonates. J Pediatr Gastroenterol Nutr. 1998;27:184–90. doi: 10.1097/00005176-199808000-00011. [PubMed] [Cross Ref]
• Bruton JA, Bayleys HS, Atkinson SA. Validation and application of dual-energy X-ray absorpiometry tto measure bone mass and body composition in small infants. Am J Clin Nutr. 1993;58:839–45. [PubMed]
• Rubinacci A, Moro GE, Bohem G, De Terlizzi F, Moro GL, Cadossi R. Quantitative ultrasound for the assessment of osteopenia in preterm infants. Eur J Endocrinol. 2003;149:307–15. doi: 10.1530/eje.0.1490307. [PubMed] [Cross Ref]
• Kurl S, Heinonen K, Lansimies E. Pre- and post-discharge feeding of very preterm infants: impact on growth and bone mineralization. Clin Physiol Funct Imaging. 2003;23:182–9. doi: 10.1046/j.1475-097X.2003.00493.x. [PubMed] [Cross Ref]
• Lapillonne A, Salle BL, Glorieux FH, Claris O. Bone mineralization and growth are enhanced in preterm infants fed an isocaloric, nutrient-enriched preterm formula through term. Am J Clin Nutr. 2004;80:1595–603. [PubMed]
• Fewtrell MS, Prentice A, Jones SC, Bishop NJ, Stirling D, Buffenstein R, Lunt M, Cole TJ, Lucas A. Bone mineralization and turnover in preterm infants at 8–12 years of age: the effect of early diet. J Bone Miner Res. 1999;14:810–20. doi: 10.1359/jbmr.1999.14.5.810. [PubMed] [Cross Ref]
• Chang JM, Armstrong C, Moyer-Mileur L, Hoff C. Growth and bone mineralization in children born prematurely. J Perinatol. 2008;28:619–23. doi: 10.1038/jp.2008.59. [PubMed] [Cross Ref]
• Fewtrell MS, Cole TJ, Bishop NJ, Lucas A. Neonatal factors predicting childhood height in preterm infants: evidence for a persisting effect of early metabolic bone disease? J Pediatr. 2000;137:668–73. doi: 10.1067/mpd.2000.108953. [PubMed] [Cross Ref]

Source:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2729305/

53 Wrongly Accused Articles

The symbol of Justice is that of a blindfolded woman with a sword and scales.  Supposedly, the blindfold prevents Justice from being swayed by the outward appearance of persons so that all can be treated impartially and without prejudice.  Sadly, there are times that the blindfold may prevent Justice from looking upon hidden agendas of police, lawyers and judges.  As the science of forensics continues to advance and as the criminal justice system continues to be scrutinized by the public, the media and by those that work in it, there have been cases when those accused and even imprisoned wrongly have been exonerated.  Below are sites that tell the stories of such individuals.

1. Gothamist.com – Describes the travail of several Hofstra University students falsely accused of rape.
2. MyPhillyLawyer – A Florida man wrongly accused is freed after 35 years in prison.
3. Idaho Criminal Defense Blog – Article discusses issues with testing for impaired driving.
4. LawCrossing - Article discusses the Innocence Project.
5. Glenn Sacks – Discussion of frequency of false rape accusations.
6. True Slant – Restitution for those wrongfully accused.
7. Justice on Trial – Several issues regarding those wrongfully accused.
8. BlackPerspective.net – Discussion of a case in Mississippi.
9. The Life After Innocence Project – Experiences after ones have been exonerated.
10. The Defenders Online – Several issues regarding abuse of law enforcement power.
11. Museum of Contemporary Photography – Pictorial essay of some wrongfully accused.
12. California Criminal Lawyer Blog – Various tales of abuse of the law and wrongful accusation.
13. Michigan Sex Crimes Attorneys – Some wrongfully accused of sex crimes are discussed here.
14. I Was Falsely Accused – How one man was exonerated from a child abuse accusation.
15. Southern California Defense Blog – Remedies for those wrongfully accused.
16. Wrongfully Accused – More examples from a source in Georgia.
17. Law Memo – Wrongful accusations in the workplace.
18. Abuse-Excuse.com – Help for those wrongfully accused.
19. Bluhm Blog – scholarly discussion of this issue.
20. KariSable.com – Many articles and resources relative to false accusations.
21. Caught.net – cases of misconduct in the legal system are discussed here.
22. Stories of the Wrongfully Convicted – Stories, pictures and videos on this site.
23. Falsely-Accused.net – Resources for those falsely accused of abuse.
24. Falsely Accused Dad – A father discusses his case.
25. Bill Coleman – One man on a hunger strike due to being wrongfully accused.
26. Kirstin’s Story – A young woman’s story of false accusation.
27. Reason.com – Parents try to get removed from a list of child abusers.
28. S.P.A.R.C. – Steps to take when wrongfully accused in a custody case.
29. Probable Cause – Several discussions on wrongful accusations.
30. Reversing a Wrongful Conviction – Steps to take for those wrongfully accused.
31. What’s The Harm? – Instances of induced testimony used in court.
32. Windy Citizen – A 14-year-old’s story.
33. AmFOR.net – Articles and resources for those wrongfully accused.
34. Resources for Cases of Innocence – A page dedicated to the wrongly accused.
35. Catholic Online – A man is freed after 22 years on Death Row.
36. DNA Center – how DNA helps free those wrongly accused.
37. LauraJames.com – A crime historian writes on this subject.
38. DanaRoc.com – Article on a filmmaker’s desire to tell stories of the wrongly accused.
39. P.A.T.R.I.C.K. Crusade – Resources for those needing help with false accusations.
40. Social Science Research Network – College professor posts several articles on this subject.
41. The Injustice Line – More resources for victims of injustice.

Forensic Truth Foundation – Help for those accused of Shaken Baby Syndrome.

SBSDefense.com – Another resource relative to Shaken Baby Syndrome.

FreeKenMarsh.com – Story of a man unjustly accused of a child’s death.

The Yurko Project – Another man unjustly accused of child murder.

42. Proving Innocence – A group that helps the wrongly accused get justice.
43. TheLoop21.com – Article discusses several cases of wrongful accusations.
44. Illegal Procedure – A defense attorney weighs in on this issue.
45. BruceRichland.com – The process of defending one wrongly accused.
46. Robbery of Freedom – An Alabama woman’s story.
47. Southern Injustice – Cases are presented for review for the reader to reason on.
48. Bode Technology – How DNA helped free some unjustly accused.
49. F.A.S.T – Team that helps those wrongly accused.

Source:

http://www.criminaldefenseattorney.net/?p=47

Contrecoup Injuries Of The Brain In Infancy

Hippocrates Treats His Patient

CYRIL B. COURVILLE, MD

Coroner-Medical Examiner’s Office, Los Angeles County, and the Department of Pathology (Cajal Laboratory of Neuropathology), Los Angeles County Hospital.

THE TERM “contrecoup” has long been associated with the mechanism of craniocerebral injury. Its first use was in reference to the occurrence of “contrecoup” fracture by Hippocrates,¹ in which a linear fracture appears opposite the point of a traumatic impact. It was used in this sense from the 16th to the 19th centuries.² It is not clear exactly when the term was applied to soft tissue contusions, but contrecoup lesions were the subject of numerous contributions by French surgeons during the middle of the 18th century.³ Here the matter rested until the early 20th century when the treatise of Le Count and Apfelbach⁴ on automobile injuries of the head and brain again called attention to the subject.

http://archsurg.highwire.org/cgi/content/summary/90/1/157

Coup And Contre-Coup Injury: Observations On The Mechanics Of Visible Brain Injuries In The Rhesus Monkey

Authors:

Ayub K. Ommaya, M.D., F.R.C.S., Robert L. Grubb, Jr., M.D., and Ronald A. Naumann, M.D.

The distribution of coup and contre-coup contusions and subdural hematomas after frontal and occipital impacts has been studied in the rhesus monkey. The effect of skull fracture on these lesions is noted, and the data compared to known postmortem observations in man. The translation/cavitation theory for brain injury as presently conceived is not supported by these data. The skull distortion and head rotation hypothesis offers opportunities for developing a better theory for brain injury by direct as well as indirect impact. The significance of these observations for design of protective devices is briefly discussed.

Source:

http://thejns.org/doi/abs/10.3171/jns.1971.35.5.0503

Ayub K. Ommaya, 78; Neurosurgeon and Authority on Brain Injuries

By Joe Holley

Washington Post Staff Writer
Monday, July 14, 2008

Dr. Ayub Khan Ommaya, 78, a neurosurgeon, an internationally known expert on brain injuries and the inventor of a device that facilitates treatment of brain tumors, died July 10 at his home in Islamabad, Pakistan, of complications from Alzheimer’s disease.

The longtime Bethesda resident was a retired chief of neurosurgery at the National Institute of Neurological Disorders and Stroke and professor of neurosurgery at George Washington University.

Before Dr. Ommaya’s work in the 1960s, there was no effective way to deliver chemotherapy treatments for brain tumors. His invention of the Ommaya reservoir, a plastic dome-shaped device with a catheter attached to the underside, made possible the delivery of chemotherapy to the brain and spinal cord. In addition, the device served as a prototype for all medical ports now in use.

Dr. Ommaya also developed the centripetal theory of traumatic brain injury, which allowed scientists to understand and model how brains are affected by blunt force. As chief medical adviser to the National Highway Traffic Safety Administration and director of NHTSA’s head injury prevention program, he created a model for brain injuries that led to design changes and the development of safety devices in motor vehicles worldwide.

Known as the “singing neurosurgeon,” Dr. Ommaya was a trained opera tenor who often sang before and after surgery, to the delight of patients and their families and his hospital colleagues.

Born in Rawalpindi, Pakistan, he was a national champion swimmer. He received his medical degree from King Edward Medical College in Pakistan in 1953 and, as a Rhodes Scholar, received his master’s degree from Balliol College, Oxford University, in 1956. During medical school, he trained as an amateur boxer and was a member of the crew team at Balliol.

He came to the United States in 1961 as a visiting scientist at the National Institutes of Health and later became an associate neurosurgeon. He was chief of neurosurgery from 1974 to 1979 and began teaching at George Washington University in 1970.

In 1977, Dr. Ommaya was part of a team of GWU surgeons that saved the life of a Rochester, N.Y., teacher by removing a snake-like tangle of blood vessels at the base of his brain, a rare abnormal growth that had paralyzed both his arms and legs and was threatening to cut off his breathing. In a history-making operation that lasted 19 hours, the man was chilled for a time to 65 degrees, his heart and lung were stilled and his brain activity was halted.

Dr. Ommaya, who told The Washington Post that he got through the surgery on just a couple of candy bars, said that it was “like dissecting out hundreds of tiny snakes — you have to dissect them out individually without cutting them or damaging the nerves and the spinal cord.”

As a transportation safety expert, he commissioned “Injury in America” (1985), a report that led to the creation of the Centers for Disease Control and Prevention’s National Center for Injury Prevention and Control. The center provides synthesis, direction and funding for the field.

He also invented an inflatable collar, similar to an airbag, that attaches to motorcycle helmets as a protection against spinal injury.

In 1997, Dr. Ommaya was called as a defense expert witness in the highly publicized trial of Louise Woodward, a British au pair accused of killing an 8-month-old baby in her care. He maintained that the child, Matthew Eappen, could not have been killed by violent shaking, as prosecutors claimed.

Sitting in the witness stand of a Cambridge, Mass., courtroom, he bounced a wad of Silly Putty on the floor to illustrate the damage that could be caused by impact. “The demonstration elicited a burst of laughter from jurors and observers — a rarity in a trial that has featured emotionally wrenching testimony from the baby’s parents and others,” the Patriot Ledger (Quincy, Mass.) reported at the time.

Dr. Ommaya retired in 2001.

His marriages to Parvaneh Modaber and Wendy Preece ended in divorce.

Survivors include his wife of 28 years, Ghazala N. Ommaya of Bethesda and Islamabad; three children from his second marriage, David Ommaya of Los Angeles, Alexander Ommaya of Bethesda and Shana Ommaya of Vienna; three children from his third marriage, Asha Ommaya of London and Iman Ommaya and Sinan Ommaya, both of Bethesda and Islamabad; two brothers; a sister; and five grandchildren.

Source:

http://www.washingtonpost.com/wp-dyn/content/article/2008/07/13/AR2008071301791.html

Predisposition To Subdural Hematomas

Enlarged Cerebrospinal Fluid Spaces In infants with subdural hematomas

Authors

Kapila A, Trice J, Spies WG, Siegel BA, Gado MH
Radiology 1982; 142:669-72.

Abstract
Computed tomography in 16 infants with subdural hematomas showed enlarged basal cisterns, a wide interhemispheric fissure, prominent cortical sulci, and varying degrees of ventricular enlargement. Radionuclide cisternography in eight of the 16 patients showed findings consistent with enlargement of the subarachnoid space rather than those of communicating hydrocephalus. Clinical findings and brief follow-up showed no convincing evidence for cerebral atrophy in 13 patients. These findings suggest that the enlarged subarachnoid space, which is encountered in some infants and may be a developmental variant, predisposes such infants to subdural hematomas.

Source:

http://www.ophsource.org/periodicals/ophtha/medline/record/MDLN.6977789

Subdural Hematomas In Infants With Benign Enlargement Of The Subarachnoid Spaces Are Not Pathognomonic For Child Abuse

Authors:

McNeely PD, Atkinson JD, Saigal G, O’Gorman AM, Farmer JP
AJNR Am J Neuroradiol 2006; 27:1725-8.

Abstract

BACKGROUND AND PURPOSE: Patients who have benign enlargement of the subarachnoid spaces (BESS) have long been suspected of having an increased propensity for subdural hematomas either spontaneously or as a result of accidental injury. Subdural hematomas in infants are often equated with nonaccidental trauma (NAT). A better understanding of the clinical and imaging characteristics of subdural hematomas that occur either spontaneously or as a result of accidental trauma may help distinguish this group of patients from those who suffer subdural hematomas as a result of NAT. The purpose of this study is to describe the clinical and imaging characteristics of subdural hematomas that occur either spontaneously or as a result of accidental injury in infants with BESS. METHODS: We conducted a retrospective review of all patients with BESS complicated by subdural hematomas evaluated at a single institution from 1998 to 2004. Data concerning the patient’s clinical presentation, physical findings, imaging, and management are described. RESULTS: During the study period, 7 patients with BESS complicated by subdural hematoma were identified. Their mean age at identification of the subdural hematoma was 7.4 months of age. In 5 cases, there was no recognized trauma before identification of the subdural hematoma. In 3 cases, baseline CT or MR imaging was available, showing prominent subarachnoid spaces without any evidence of subdural hemorrhage. CONCLUSION: Although suspicious for NAT, subdural hematomas can occur in children either spontaneously or as a result of accidental trauma. Caution must be exercised when investigating for NAT based on the sole presence of subdural hematomas, especially in children who are otherwise well and who have BESS.

Author Address
Division of Neurosurgery, Department of Surgery, IWK Health Centre, Dalhousie University, Halifax, Nova Scotia, Canada. dmcneely@dal.ca

Source:

http://www.ophsource.org/periodicals/ophtha/medline/record/MDLN.16971622

Cerebral Hemorrhage With No Evidence Of Trauma, Abuse Or Shaking

Is Pericerebral Hemorrhage A Cause Of Severe Malaise In Infants?

Authors:

Closset M, Leclerc F, Hue V, Martinot A, Vallée L, Pruvo JP.

Service de réanimation infantile, hôpital Calmette, Lille, France.

Abstract

The authors report 7 cases of infants presenting with an apparent life-threatening event associated with acute pericerebral haemorrhage (subarachnoid haemorrhage and/or subdural hematoma) without evidence of traumatism, abuse, or shaking. Clinical characteristics were the same in all cases, including limpness, severe dysautonomic disorders, and pallor; all infants had retinal and pre-retinal haemorrhages. Two infants died; the five survivors have severe neurologic sequelae. The symptoms revealing an infant’s pericerebral haemorrhage are usually axial hypotonia and pallor. Traumatism remains the most common aetiology and must be searched for. Non-traumatic aetiologies are unusual and were excluded in these reported cases. The ‘shaken baby’ syndrome is not the sole aetiology of an apparent spontaneous pericerebral haemorrhage: a slight bump associated with predisposing vascular factors particular to infancy could be involved. When confronted with an apparent life-threatening event associating limpness and pallor, one must consider the diagnosis of pericerebral haemorrhage.

Source:

http://www.ncbi.nlm.nih.gov/pubmed/1331965