legaljustice4john.com's
The Shaken Baby Syndrome Myth
renamed "Abusive Head Trauma" or "Non-Accidental Injury"

WAS

SBS: EVERTHING IS BROKEN

* SBS began as an unproven theory and medical opinions, now discredited by biomechanical engineering studies
* No DIFFERENTIAL DIAGNOSIS done to eliminate other causes, abuse assumed without evidence
* Shaken Baby diagnostic symptoms not caused by shaking
* Child protective agencies snatch children, destroy families based on medical accusations without proof of wrong-doing
*Poor or deceptive police investigations, falsified reports, perjured testimony threaten legal rights, due process
* Prosecutors seek "victory", over justice; defense attorneys guilty of ineffective counsel, ignorance, lack of effort
* Care-takers threatened, manipulated, in order to force plea bargains, false confessions
* A fractured criminal justice system--a big piece for the rich, a small piece for the poor, and none for alleged SBS cases.

Read First
1. SBS "MYTH" WEBSITE SUMMARY 
2. ARTICLE ABOUT PEDIATRIC ACADEMY SBS FRAUD

3. SUMMARIZED HISTORY OF THE SHAKEN BABY SYNDROME THEORY
4. BREAKING THE SILENCE: POLICE MISCONDUCT--DJT (coming soon)


SUBJECT: Newborns: Vitamin K Injection Dangers
  1. Vitamin K --Is this really safe and necessary?
  2. The comprehensive resource for physicians, drug and illness information Illnesses information
  3. National standard mandates newborn vitamin K injection
  4. Phytonadione Therapy in a Multiple-Drug Overdose: Adverse Effects of Vitamin K
  5. Anaphylactoid Reactions to Vitamin K
  6. Neurosurgeon, Dr. Russell Blaylock, shares the science on how particular vaccine ingredients lead to convulsions, seizures, ADD, ADHD, autism...etc.
    Vitamin K and Hepatitis B are mandated in most states to be given to newborns before they go home with mom. This has been proven to be a dangerous procedure at best. Potentially lethal.
  7. Vitamin K: controversy? what controversy?
  8. ON PLACENTAS, STEM CELLS AND BREASTMILK--Why Vit K injections may interfere
  9. Antibiotics destroy an infants capacity to produce Vit K naturally
  10. Vitamin K deficiency/intercranial bleeding/vitamin K at birth may be insufficient to prevent late HDN

"The blood of the innocents": Vitamin K injections can cause symptoms ranging from minor to DEATH. The benefit of K shots can be tracked all the way to the bank. Modern medicine and Big Pharma are damaging and killing babies for profit.

http://www.vaccination.inoz.com/VitaminK.html

Vitamin K --Is this really safe and necessary?
Bronwyn Hancock October 2003

The reason given for administration of Vitamin K is to prevent hemorrhagic disease
in newborns. However consider the following points:

The form of Vitamin K injected

· The body does not readily utilize synthetic vitamins and minerals. The vitamin K
administered by hospitals to newborns is the synthetic phytonadione. The natural forms of vitamin K that are found in many foods, particularly in vegetables such as collard greens, spinach, broccoli, asparagus, brussels sprouts and salad greens, are a different form – they are called phylloquinone or menaquinone. Certain bacteria in the intestinal tract also produce menaquinones.

· Apart from its synthetic nature, it is based on plant Vitamin K and injected. The body utilizes vitamins and minerals that are found in plants and creates the human form it needs, but this is after they go through the digestion process, which obviously does not occur with injections.

· "Little is known about the metabolic fate of vitamin K. Almost no free unmetabolized vitamin K appears in bile or urine," states both the 1988 and 1998 Physician's Desk Reference (PDR). "This is especially important due to the fact that it is a fat-soluble vitamin and therefore can accumulate in the body," wrote Vitamin K Resources (VKR) in the extremely well-documented and footnoted 1999 article, Intramuscular Vitamin K Injection: Is K OK?

Toxic ingredients accompanying the Vitamin K

· The vitamin K injections administered by hospitals and manufactured by Merck and Roche and Abbott contain benzyl alcohol as a preservative. The 1989 PDR states that, "there is no evidence to suggest that the small amount of benzyl alcohol contained in AquaMEPHYTON (Merck's vitamin K injection product), when used as recommended, is associated with toxicity." Interestingly, in November 1988, the French medical journal, Dev Pharmacol Ther, published a paper regarding benzyl alcohol metabolism and elimination in babies. The report stated that "...we cannot directly answer the issue of safety of 'low doses' of benzyl alcohol as found in some medications administered to neonates. This study confirms the immaturity of the benzoic acid detoxification process in premature newborns."

· Roche's vitamin K product KONAKION contains ingredients such as phenol (carbolic acid-a poisonous substance distilled from coal tar), propylene glycol (derived from petroleum and used as an antifreeze and in hydraulic brake fluid) and acetic acid (an astringent antimicrobial agent that may drastically reduce the amount of natural vitamin K that would have otherwise been produced in the digestive tract). As reported in the PDR and as published in the IM vitamin K packet inserts for Merck, Roche and Abbott, "Studies of carcinogenicity, mutagenesis or impairment of fertility have not been conducted with Vitamin K1 Injection (Phytonadione Injection, USP)."

· The Vitamin K injection can be in a base of polyethoxylated castor oil.

· Vitamin K injections also contain hydrochloric acid and lecithin.

Effects of Vitamin K administration

· The manufacturers warn on the product insert: "Severe reactions, including fatalities, have occurred during and immediately after intravenous injection of phytonadione even when precautions have been taken to dilute the vitamin and avoid rapid infusion.."

· The Vitamin K shot has been linked to leukemia, including acute lymphoblastic leukemia, which is characterized by an increased number of white corpuscles in the blood, and accounts for about 85 percent of childhood leukemia. Research carried out by Dr. Louise Parker, of the Sir James Spence Institute of Child Health in Newcastle upon Tyne, produced the most startling results. Dr. Louise Parker was quoted in the British Medical Journal in 1998 as stating, "It is not possible, on the basis of currently published evidence, to refute the suggestion that neonatal IM vitamin K administration increases the risk of early childhood leukemia.".

The British Journal of Cancer published "Factors associated with childhood cancer" by J. Golding, et al, in 1990. The report indicated that universally administered IM vitamin K injections significantly increase our children's chances of developing childhood cancer. A follow-up study published two years later in the British Medical Journal (Golding J, Paterson K, Greenwood R, Mott M. Intramuscular vitamin K and childhood cancer. BMJ 1992; 305:341-346.) reinforced the findings of the previous study. The authors' comments, in keeping with scientific style, are conservatively stated, but parents who are concerned about the health of their babies will read "danger" between the following lines: "The only two studies so far to have examined the relation between childhood cancer and intramuscular vitamin K have shown similar results and the relation is biologically plausible. The prophylactic benefits against hemorrhagic disease are unlikely to exceed the potential adverse effects from intramuscular vitamin K..."

The chance of your child developing leukemia from the Vitamin K shot is estimated to be about one in 500 (MIDIRS Midwifery Digest, Vol 2 #3, September 1992)

· Animal studies have linked large doses of vitamin K to a variety of conditions that include anemia, liver damage, kidney damage and death.

· Interestingly the common problem that occurs these days of jaundice in newborns has only been reported since the introduction of Vitamin K administration.

· According to the product insert, adverse reactions include hemolysis (or hemolysis - American spelling) (meaning breakdown of red blood cells), hemolytic anemia (a disorder characterized by chronic premature destruction of red blood cells), hyperbilirubinemia (too much bilirubin in blood) and jaundice (yellow skin and eyes resulting from hyperbilirubinemia), and allergic reactions include face flushing, gastrointestinal upset, rash, redness, pain or swelling at injection site and itching skin. It also warns that large enough doses can cause brain damage in infants and/or impairment to liver function. Hypoxia has also been published as having occurred in infants after Vitamin K administration.

The necessity (or lack of necessity) for administration of Vitamin K

· The bleeding condition the Vitamin K shot is supposed to prevent occurs at a rate that is far lower (in a non-Vitamin K injected child) than the rate of occurrence of leukemia.The hemorrhaging condition may occur in approximately 1 in 10,000 live births.

· The condition also will not necessarily be prevented by Vitamin K because it can be caused by other factors than a lack of Vitamin K (e.g. See Arch Dis Child 1999; 81:278 (September)). In fact, vaccination is a major cause of hemorrhaging.

· The bacteria that should quickly colonize the gut (in a baby who is breast fed and not given antibiotics directly or as one of the ingredients in vaccines, including most likely the Hepatitis B vaccine) produces Vitamin K anyway, as mentioned above.

· As early as April 17, 1977, an article in one of the world's most esteemed medical journals, the Lancet, discredited the policy of routine vitamin K injections. "We conclude that healthy babies, contrary to current beliefs, are not likely to have a vitamin K deficiency.. the administration of vitamin K is not supported by our findings.." Van Doorm et al stated in the Lancet article. VKR cited 21 peer-reviewed reports that had been published in prominent medical journals. All of them concur that policies that mandate the universal injection of newborn babies are not based on sound science. There has been much peer-reviewed evidence generated which questions the efficacy of routine vitamin K injections as sound public health policy.

· Naturopathic physicians and others who successfully adhere to a more natural approach to healthcare advocate that high-risk mothers should increase the amount of vitamin K available to the foetus, and then the breastfeeding infant, by eating adequate amounts of green leafy vegetables and other foods high in Vitamin K, such as alfalfa, brussels sprouts, cabbage, cauliflower, spinach, turnip greens, asparagus, oats and green tea.

· Commonsensically, VKR poses the question, "...how could God (or nature) have erred so badly as to give all newborn babies only an infinitesimal fraction of their required vitamin K? Surely the human race could not have survived to this point if all newborns were born with this deficiency and none being administered at birth until very recently." So ironically, when a Vitamin K deficiency does occur the probable cause(s) would be some other artificial, unnecessary interference, which just so happens to be something that one might say is fairly characteristic of modern medical treatments.


http://tinyurl.com/y8a5x56

The comprehensive resource for physicians, drug and illness information Illnesses information


VITAMIN K
General Monograph,
Phytonadione
Hypoprothrombinemia Therapy

"Action And Clinical Pharmacology: Vitamin K compounds are fat soluble naphthoquinones. Phytonadione (vitamin K1 ) and vitamin K2 occur in a variety of natural materials and are synthesized by certain bacteria in the gastrointestinal tract; however, commercially prepared phytonadione is synthetically produced..."

Manufacturers' Warnings In Clinical States: Severe reactions, including fatalities, have occurred during and immediately after i. v. phytonadione injection even when precautions have been taken to dilute the phytonadione solution and to avoid rapid infusion. These severe reactions, which may occur in patients receiving phytonadione for the first time, resemble hypersensitivity or anaphylaxis, including shock and cardiac or respiratory arrest. Therefore, use of the i. v. route should be restricted to those situations where other routes are not feasible and the serious risk involved is considered justified.

Benzyl alcohol contained in some products has been associated with toxicity in newborns. Toxicity appears to have resulted from administration of large amounts (100 to 400 mg/kg daily) of benzyl alcohol in these neonates. Products containing benzyl alcohol should be used cautiously in newborns who are also receiving other benzyl alcohol-containing medications. In each case, the attending physician must weigh the potential benefits against the possible risks.

Precautions: Because the liver is the site of prothrombin biosynthesis, hypoprothrombinemia resulting from hepatocellular damage is not corrected by administration of vitamin K. Repeated large doses of vitamin K are not warranted in liver disease if the response to initial use of the vitamin is unsatisfactory. Failure to respond to vitamin K may indicate that a coagulation defect exists or that the condition is unresponsive to vitamin K.

Vitamin K does not counteract the anticoagulant effect of heparin. Dietary supplements high in vitamin K (³0.7 mg/day) can block the effect of oral anticoagulants.

Vitamin K1 promotes the synthesis of prothrombin by the liver but does not directly reverse the effects of oral anticoagulants. Immediate coagulant effect should not be expected. It takes up to 2 hours for a measurable improvement in the prothrombin time. Whole blood or component therapy may also be necessary if bleeding is severe or if there is no response to phytonadione. Vitamin K1 is not a clotting agent, but overzealous therapy with phytonadione may restore conditions which originally permitted thromboembolic phenomena. Keep dosage as low as possible, and check prothrombin time regularly as clinical conditions indicate.

Newborns should be observed for vitamin K deficiency. The incidence of vitamin K deficiency is higher in breast-fed infants. This increase may be partly due to lower concentrations of vitamin K in human milk than in cow's milk formula or it may be due to the smaller volume of milk infants may receive in their first few days of life, especially those exclusively breast-fed. Therefore, because an infant's milk intake cannot be predicted at birth, it is recommended that vitamin K prophylaxis be given to all newborns. (Infants have been breast fed since the beginning of time.)

Drug Interactions: Anticoagulants (coumarin): Anticoagulant effects are antagonized by vitamin K. Temporary resistance to prothrombin depressing anticoagulants may result from vitamin K administration, especially when relatively large doses have been given. Therefore, when reinstituting anticoagulant therapy, it may be necessary to use larger doses of the prothrombin depressing anticoagulant or to use one that acts on a different principle, such as heparin.

Broad Spectrum Antibiotics, Quinidine, Quinine and High Dose Salicylates: Requirements for vitamin K may be increased. (see Indications).

Children: In newborns, particularly premature infants, hyperbilirubinemia and hemolytic anemia have been reported. The risk is much less with phytonadione than other vitamin K preparations unless high doses (10 to 20 mg) are given.

Pregnancy: Inadequate information exists as to whether vitamin K may affect fertility in human males or females or have a teratogenic potential or other adverse effect on the fetus. Large amounts of vitamin K in pregnancy, however, can cause jaundice in the newborn.

Lactation: Vitamin K may appear in human breast milk. Problems in humans have not been reported with the intake of normal daily requirements.

Adverse Reactions: Deaths have occurred following i. v. administration of phytonadione (see Warnings).

Transient flushing sensations and peculiar sensations of taste have been observed following phytonadione injection as well as rare instances of dizziness, rapid and weak pulse, profuse sweating, brief hypotension, dyspnea, and cyanosis. Bronchospasm, shock, cardiac and/or respiratory arrest may also occur.

Pain, swelling, and tenderness at the injection site may occur. The possibility of allergic sensitivity (i.e., rash, urticaria), including an anaphylactoid reaction, should be kept in mind.

Large doses of vitamin K or its analogues may further depress liver function in patients with severe hepatic disease and thereby further decrease the concentration of prothrombin.

Neonates: In infants (particularly premature babies), excessive doses of vitamin K analogs during the first few days of life may cause hyperbilirubinemia; this in turn may result in severe hemolytic anemia, hemoglobinuria, kernicterus, leading to brain damage or even death. Immaturity is apparently an important factor in toxic reactions to vitamin K analogs, as full term and larger premature infants show greater tolerance than smaller premature infants.


http://proliberty.com/observer//19990710.htm
From the July 1999 Idaho Observer:

National standard mandates newborn vitamin K injection
Ignorance becomes tacit consent for the questionable neonatal procedure

by Don Harkins

In cooperation with a “national standard,” most, if not all states have mandated that U.S. hospitals routinely administer to all newborns a synthetic, fat-soluble vitamin K injection (generic name phytonadione) that exceeds an infant's recommended daily dietary intake of the vitamin by 100 times.

Peer reviewed journals have linked large doses of vitamin K to childhood cancers and leukemia. Animal studies have linked large doses of vitamin K to a variety of conditions that include anemia, liver damage, kidney damage and death.

“Little is known about the metabolic fate of vitamin K. Almost no unmetabolized vitamin K appears in bile or urine,” states both the 1988 and 1998 Physician's Desk Reference (PDR).

“This is especially important due to the fact that it is a fat-soluble vitamin and therefore can accumulate in the body,” wrote Vitamin K Resources (VKR) in the extremely well-documented and footnoted 1999 article, Intramuscular Vitamin K Injection: Is K OK?

In the 1988 PDR, Merck's literature states that “A single intramuscular dose of AquaMEPHYTON (Merck brand vitamin K injection) 0.5 to 1 mg within one hour of birth is recommended.”

Merck's 1998 PDR entry for AquaMEPHYTON has removed adverse reaction liability from the pharmaceutical giant by stating, “The American Academy of Pediatrics (AAP) recommends that Vitamin K1 be given to the newborn.”

Vitamin K injections are ostensibly administered to newborns to prevent vitamin K deficiency bleeding (such as hemophilia) that may occur in approximately 1 in 10,000 live births. “This figure would probably be much lower if high risk newborns were excluded [from this figure],” wrote VKR.

Parents who wish to refuse the shot must do so in writing prior to the birth of their baby. Parental ignorance of the state-mandated injection is considered by hospitals as tacit consent authorizing them to administer the potentially damaging synthetic vitamin dose to newborns.

Five post partem nurses from hospitals in Idaho, Washington and Oregon stated that they “routinely administer vitamin K injections to newborns,” as if all of them were reading from the same script. According to a seasoned Sacred Heart Medical Center (Spokane, WA) Birthplace nurse named Terri, “Routine vitamin K injections are in cooperation with the federal standard.”

She also said that Washington hospitals are mandated by state code to provide the injections to all newborns. Terri acknowledged that parents who wish to refuse the shot must present the refusal to the hospital in writing before the baby is born.

Scientists question intelligence of universal IM vitamin K injections

Dr. Louise Parker was quoted in the British Medical Journal in 1998 as stating, “It is not possible, on the basis of currently published evidence, to refute the suggestion that neonatal IM vitamin K administration increases the risk of early childhood leukemia.”

The British Journal of Cancer published “Factors associated with childhood cancer” by J. Golding, et al, in 1990. The report indicated that universally administered IM vitamin K injections significantly increase our children's chances of developing childhood cancer.

A follow-up study published two years later in the British Medical Journal reinforced the findings of the previous study. The authors' comments, in keeping with scientific style, are conservatively stated, but parents who are concerned about the health of their babies will read “danger” between the following lines: “The only two studies so far to have examined the relation between childhood cancer and intramuscular vitamin K have shown similar results and the relation is biologically plausible. The prophylactic benefits against hemorrhagic disease are unlikely to exceed the potential adverse effects from intramuscular vitamin K...”

Both studies recommend that policies should be adopted to administer IM vitamin K injections only to high risk babies. Babies who have been identified as being at risk for vitamin K deficiency include those born to mothers who took drugs or antibiotics during pregnancy, premature babies and babies who are born cesarean. Mothers who had maternity diets low in high vitamin K foods or had diets that were low in fat have also been identified as being more likely to bear vitamin K deficient babies.

Naturopathic physicians and others who successfully adhere to a more natural approach to healthcare advocate that high-risk mothers should increase the amount of vitamin K available to the fetus during pregnancy by eating adequate amounts of green leafy vegetables. It is also recommended that mothers continue to eat vitamin K rich foods after giving birth so that their infants will receive the natural form of the vital vitamin through their breast milk.

As early as April 17, 1977, an article in one of the world's most esteemed medical journals, the Lancet, discredited the policy of routine vitamin K injections. “We conclude that healthy babies, contrary to current beliefs, are not likely to have a vitamin K deficiency....the administration of vitamin K is not supported by our findings...” Van Doorm, et al stated in the Lancet article.

VKR cited 21 peer-reviewed reports that had been published in prominent medical journals. All of them concur that policies which mandate the universal injection of newborn babies are not based in sound science.

There has been much peer-reviewed evidence generated which questions the efficacy of routine vitamin K injections as sound public health policy. Why, then, since publication of the July, 1987 article in Pediatrics “Health codes for newborns” when it was stated that only five states required hospitals to administer neonatal vitamin K injections, are they now mandated by most, if not all states?

Commonsensically, VKR poses the question, “...how could God (or nature) have erred so badly as to give all newborn babies only an infinitesimal fraction of their required vitamin K? Surely the human race could not have survived to this point if all newborns were born with this deficiency and none being administered at birth until very recently.”

Although there seems to be no evidence to support universal IM vitamin K injections among the newborn from a public health standpoint, the medical establishment, as informed by the Food and Drug Administration, the AAP and as supplied by the pharmaceutical companies such as Merck, Roche Laboratories and Abbott Laboratories, continues to endorse state mandated, routine IM vitamin K injections.

Eye of newt, spleen of bat?

The body most readily utilizes vitamins and minerals that are found in plants. The body less readily utilizes synthetic vitamins and minerals. The vitamin K administered by hospitals to newborns is the synthetic phytonadione. The natural forms of vitamin K that are found in many foods, particularly in vegetables such as collard greens, spinach, broccoli, asparagus, brussels sprouts and salad greens, are called phylloquinone or menaquinone. Certain bacteria in the intestinal tract also produce menaquinones.

The vitamin K injections administered by hospitals and manufactured by Merck and Roche and Abbott are not only synthetic but, according to the packet inserts and the PDR, contain benzyl alcohol as a preservative.

The 1989 PDR states that, “there is no evidence to suggest that the small amount of benzyl alcohol contained in AquaMEPHYTON (Merck's vitamin K injection product), when used as recommended, is associated with toxicity.”

Interestingly, in November, 1988, the French medical journal Dev Pharmacol Ther published a paper regarding benzyl alcohol metabolism and elimination in babies. The report stated that “...we cannot directly answer the issue of safety of 'low doses' of benzyl alcohol as found in some medications administered to neonates. This study confirms the immaturity of the benzoic acid detoxification process in premature newborns.”

The 1998 PDR still states, contrary to the published findings of French scientists in 1988, “there is no evidence to suggest that...”

There has been little reason to study the toxicological effects of benzyl alcohol over the last decade since state legislators have provided synthetic vitamin K manufacturers with the guaranteed marketplace of nearly every child born in a U.S. hospital.

Vitamin K injections manufactured as recently as 1995 contain hydrochloric acid “for pH adjustment.”

Roche's vitamin K product KONAKION contains ingredients such as phenol (carbolic acid -- a poisonous substance distilled from coal tar), propylene glycol (derived from petroleum and used as an antifreeze and in hydraulic brake fluid) and acetic acid (an astringent antimicrobial agent that may drastically reduce the amount of natural vitamin K that would have otherwise been produced in the digestive tract).

As reported in the PDR and as published in the IM vitamin K packet inserts for Merck, Roche and Abbott, “Studies of carcinogenicity, mutagenesis or impairment of fertility have not been conducted with Vitamin K1 Injection (Phytonadione Injection, USP).”

The purpose of this article is to alert expectant parents that their ignorance of federally-suggested, state mandated hospital policy is enough assent to authorize health care professionals to administer what may be a lethal or damaging overdose of a synthetic substance that comes with the following warning from the manufacturers: “Severe reactions, including fatalities, have occurred during and immediately after INTRAVENOUS injection of phytonadione even when precautions have been taken to dilute the vitamin and avoid rapid infusion...”

Please pass the preceeding information onto anybody you know who is expecting a baby. Afterall, we have the right to know what substances are being injected into our babies within the first hour of their lives. If we feel that a substance may be injurious to our baby, we have the right to refuse it.


http://www.medscape.com/viewarticle/409632_7

Phytonadione Therapy in a Multiple-Drug Overdose: Adverse Effects of Vitamin K

Severe adverse effects are associated with intravenous phytonadione, such as cardiac irregularities, chest pain, cyanosis, decreased level of consciousness, circulatory collapse, rapid weak pulse, hypotension, and cardiac or respiratory arrest.[13] It is not known if these reactions are due to the drug or the injection vehicle.[13] Earlier reactions to vitamin K were thought to be due to polyoxyethylated castor oil (cremophor).[29-32]

The literature contains numerous cases of anaphylactic reactions[29, 30, 32-38] as well as fatalities[34, 35] with parenteral phytonadione. The recommended infusion rate of vitamin K is no faster than 1 mg/minute[13]; however, anaphylactic reactions have occurred with slower infusion rates[33, 37] as well as with repeated exposure to intravenous vitamin K.[30, 33, 34, 37]

Dermatologic reactions were reported after intravenous, subcutaneous, and intramuscular administration of vitamin K.[39] Two distinct types of local cutaneous reactions have been described. The more common one is a pruritic, erythematous, eczematoid, indurated plaque measuring 6-20 cm around the site of injection.[39-52] The acute reaction may resolve in 2-4 weeks with treatment with high-potency corticosteroids (e.g., fluocinonide, betamethasone dipropionate). The second type appears as a scleroderma or morphea-like reaction.[53-56] The onset can be weeks to months, and the skin change may last for years.[39] Dose does not appear to bear a relationship to the onset of these reactions. Liver disease was associated with most reports of vitamin K cutaneous hypersensitivity,[39, 41] but the pathophysiology is unclear.


http://www.springerlink.com/content/v16l551682716431/

Anaphylactoid Reactions to Vitamin K

Louis D. Fiore1, Michael A. Scola1, Colleen E. Cantillon1 and Mary T. Brophy1
(1) Massachusetts Veterans Epidemiology Research and Information Center (MAVERIC), VA Boston Healthcare System, 150 South Huntington Avenue, Boston, MA, 02130

Abstract Anaphylactoid reactions in patients receiving intravenously administered vitamin K have been reported in the literature. To summarize the known data on anaphylactoid reactions from administration of vitamin K, we reviewed all published and unpublished reports of this adverse reaction. Published reports were obtained through medline (1966–1999) and EMBASE (1971–1999) searches of the English language literature and review of references from identified case reports. Unpublished reports were obtained using the Spontaneous Reporting System Adverse Reaction database of the United States Food and Drug Administration (FDA) between August 1968 and September 1997. All adverse drug reactions to vitamin K were categorized by route of drug administration, dose and standard adverse reaction code. In the FDA reports, we defined anaphylactoid reactions as any adverse drug reaction coded as either anaphylaxis, allergic reaction, apnea, dyspnea, death, heart arrest, hypotension, shock or vasodilatation. Additionally, all fatal and life-threatening FDA reported reactions were reviewed to determine if they could represent an anaphylactoid reaction missed by the above definition.
The literature review uncovered a total of 23 cases (3 fatal) of anaphylactoid reactions from intravenous vitamin K. The FDA database contained a total of 2236 adverse drug reactions reported in 1019 patients receiving vitamin K by all routes of administration. Of the 192 patients with reactions reported for intravenous vitamin K, 132 patients (69%%) had a reaction defined as anaphylactoid, with 24 fatalities (18%%) attributed to the vitamin K reaction. There were 21 patients with anaphylactoid reactions and 4 fatalities reported with doses of intravenous vitamin K of less than 5[emsp4 ]mgs. For the 217 patients with reactions reported due to vitamin K via a non-intravenous route of administration, 38 patients had reactions meeting the definition of anaphylactoid (18%%), with 1 fatality (3%%) attributed to the drug.
The absolute risk of an anaphylactoid reaction to intravenous vitamin K cannot be determined by this study, but the relatively small number of documented cases despite widespread use of this drug suggest that the reaction is rare. Anaphylactic reactions and case fatality reports were found even when intravenous vitamin K was given at low doses by slow dilute infusion. The pathogenesis of this reaction is unknown and may be multifactorial with etiologies including vasodilation induced by the solubilizing vehicle or immune-mediated processes. We conclude that use of intravenous vitamin K should be limited to patients with serious hemorrhage due to a coagulopathy that is secondary to a relative or absolute deficiency of vitamin K.


http://poisonevercure.150m.com/vaccines7.htm
Neurosurgeon, Dr. Russell Blaylock, shares the science on how particular vaccine ingredients lead to convulsions, seizures, ADD, ADHD, autism...etc.

Vitamin K and Hepatitis B are mandated in most states to be given to newborns before they go home with mom. This has been proven to be a dangerous procedure at best. Potentially lethal.

Vitamin K

The marketed purpose of the Vitamin K injection is that newborns have very little to begin with. Vitamin K is essential for the ability of blood clotting should any injury occur. Another marketed purpose is the prevention of hemorrhagic diseases of the newborn (HDN). HDN is a bleeding disorder associated with low levels of vitamin K in newborn babies. It was first defined in 1894 by Townsend as spontaneous external or internal bleeding occurring in newborn infants. Diagnosis was based solely on the opinion of the attendant medical personnel because there was no criteria in determining the cause of hemorrhaging. Townsend did not label hemophilia as a cause of HDN. The vaccine is also marketed to be essential prior to surgery. Thus, supposedly prevents excessive bleeding.

Vitamin K is naturally stored and metabolized by the liver. The cell division that rapidly continues after birth depends on precise amounts of vitamin K to proceed at the proper rate. Introduction of levels that are 20,000 times the newborn level, the amount usually injected, can have devastating consequences.

Nursing naturally raises the infant's vitamin K levels very gradually after birth so that no disregulation occurs that would encourage leukemia development. This is the way the Creator designed it to be. The clotting system of the healthy newborn is well planned, and healthy breastfed infants do not suffer bleeding complications, even without any supplementation. While nursing infants demonstrate lower blood levels of vitamin K than the "recommended" amount, they show no signs of vitamin K deficiency. This can only lead to the question of how and where the “recommended” amount was brought about.

Vitamin K vaccinations are also marketed for newborns to prevent vitamin K deficiency bleeding (such as hemophilia) that may occur in approximately 1 in 10,000 live births. Hemophilia is the oldest known hereditary bleeding disorder of which there are two types: A and B (Christmas Disease). Low levels or the absence of a blood protein, essential for clotting, causes both. Patients with hemophilia A lack the blood clotting protein, factor VIII, and those with hemophilia B lack factor IX. There are about 20,000 hemophilia patients in the United States. Each year, about 400 babies are born with this disorder. Approximately 85% have hemophilia A and the remainder has hemophilia B.

The severity of hemophilia is related to the amount of the clotting factor in the blood. About 70% of hemophilia patients have less than one percent of the normal amount which leads to severe hemophilia. A small increase in the blood level of the clotting factor, up to five percent of normal, results in mild hemophilia with rare bleeding except after injuries or surgery. The most important challenges facing the hemophilia patient, health care provider, and research community today are safety of products used for treatment, management of the disease including inhibitor formation, irreversible joint damage, and life-threatening hemorrhage. Bleeding into the brain occurs mainly from three to seven weeks after birth in just over five out of 100,000 births. Forty percent of these infants suffer permanent brain damage or death.

The vitamin K inoculations administered by hospitals and manufactured by Merck and Roche and Abbott are synthetic. According to the packet inserts and the PDR, it contains benzyl alcohol as a preservative. In November, 1988, the French medical journal, Dev Pharmacol Ther, published a paper on benzyl alcohol metabolism and elimination in infants. The report stated, "...we cannot directly answer the issue of safety of ‘low doses’ of benzyl alcohol as found in some medications administered to neonates. This study confirms the immaturity of the benzoic acid detoxification process in premature newborns."

Vitamin K vacciness also contain hydrochloric acid "for pH adjustment." Roche’s vitamin K product KONAKION contains ingredients such as phenol, propylene glycol (derived from petroleum and used as an antifreeze and in hydraulic brake fluid) and acetic acid (an astringent antimicrobial agent that may drastically reduce the amount of natural vitamin K that would have otherwise been produced in the digestive tract). Phenol is a carbolic acid and is a poisonous substance which is distilled from coal tar. It has the ability to inhibit phagocyte activity, meaning it is toxic to all cells. Phenol is capable of disabling the immune system's primary response mechanism. It can also cause systemic poisoning, headache, shock, weakness, convulsions, kidney damage, cardiac failure, kidney failure, or death. Propylene glycol can cause serious damage to liver, heart and central nervous system.

The inoculations exceed an infants recommended daily dietary intake by over 100 percent. Peer reviewed journals have linked large doses of vitamin K to childhood cancers and leukemia. Animal studies have linked large doses of vitamin K to a variety of conditions that include anemia, liver damage, kidney damage and death.

There is possibly an 80 percent increased risk of developing childhood leukemia. Several controlled studies have shown this correlation to be most likely the case while many others suggest that it is unlikely. Six different studies suggest it is a 10 percent or 20 percent increased risk.

Cancer researchers say that the synthetic vitamin K vaccine may significantly increase the risk of childhood cancer. Researchers in 1990 noted an increased incidence of childhood cancer in children given vitamin K inoculations at birth. They also found that the vitamin K injection doubled the incidence of leukemia in children less than ten years of age. A study in 1992 revealed the same association between injected vitamin K and cancer. Literature reveals that there are 1.5 extra cases of leukemia per 100,000 children due to vitamin K injections.

Recent studies in England have pointed out an increased risk of childhood leukemia with Vitamin K inoculations. Numerous studies have failed to dispute the statistical link.

Britain started a national cohort study of 16,193 infants born in one week in April in 1970. Thirty-three of the children had developed cancer by age 10 and were compared with 99 control children. The authors of the study approached Roche, the manufacturers of Konakion, for funding for a further trial to examine the findings more closely. Naturally Roche was not interested until, a few months later, the media reported the results of the study and that vitamin K given to babies might cause childhood cancer. The new study was a case-control study of 195 children with cancer born at either of two hospitals in Bristol, England, compared with 588 healthy children also born at these hospitals. One hospital administered vitamin K orally and the other intramuscularly. A nearly two-fold risk of leukaemia was found in children who had received intramuscular vitamin K.

Golding calculated that the extra cases of leukaemia caused by vitamin K injection could be as many as 980 in the UK alone. These results were supported by reports of the potential carcinogenicity of vitamin K from Israels et al. Pizer et al concluded that his study was too small to show any real effect. After an intramuscular dose of vitamin K, the baby’s plasma levels are almost 9000 times the normal adult levels. Many criticized Golding’s study. Despite the fact that assumptions were made for some cases because administration of vitamin K was not accurately recorded, expert epidemiologists considered that the results were plausible and so they could not be dismissed even in the slightest.

Two studies had carefully matched controls and more accurate information on whether vitamin K had been given or not, and by which route. One of the studies reported no association between intramuscular vitamin K and childhood cancer and the other found a risk of leukaemia, but only when cases were compared with local controls (i.e. from the same hospital) and not with controls randomly selected from the whole area under study. This was dismissed. It was then assumed and decided that worries about any potential cancer risk should be abandoned.

At that time, four more studies on vitamin K and cancer were in progress. The results were published in 1998. One of the studies showed a twofold risk of acute lymphoblastic leukaemia among 1-6 year olds, another showed a significant risk for all cancers.

There are two problems in giving vitamin K orally. It is not a licensed oral formulation for one. Compliance with three oral doses is low since many physicians are reluctant to give an unlicensed formula. The use of unlicensed preparations could lead to litigation in the event of prophylactic failure or adverse events.

Roche, the manufacturers of Konakion, state that they do not recommend the administration of Konakion solution orally. Their reasons are:

* that they have no clinical studies to support oral use,
* phenol, which has been reported to be an irritant to newborns mouths, is used as a preservative,
* the variability in the production of bile salts in newborns may affect absorption,
* that Konakion given orally has a small association with anaphylactic reactions.

The oral formula is distasteful and infants would instinctively spit it out or regurgitate it resulting in only half of an orally administered dose being absorbed. Still, the plasma concentrations in babies who were given oral vitamin K reached 300 times the adult levels, before dropping off slightly after about 24 hours.

The number of children currently developing cancer during childhood is much higher than the number developing a life threatening or permanently disabling problem as a result of late onset HDN. The risk of childhood cancer is estimated to be 1.4 per 1000, from the 1970 British cohort. (Yet, it is difficult to determine amongst all pediatric cancer patients if they developed their life threatening condition from vitamin K injection, the polio or other by other vaccines containing foreign RNA and DNA).

The only known reported cases of vitamin K toxicity result from having used the synthetic inoculated form. Vitam K inoculations can cause possibly fatal allergic reactions even during injection. The risks of injecting vitamin K into a newborn baby are nerve or muscle damage because it is injected deeply into the muscle, not subcutaneously under the skin.

wpe49F.jpg (16360 bytes)On the product insert, some reactions are listed: You may notice pain, swelling and tenderness at the injection site for a few days. Notify your doctor if you experience any of the following while taking this drug: chest pain, flushing, strange movements, rapid pulse, tightness of the chest, cramps. In the unlikely event you have an allergic reaction to this drug, seek medical attention immediately. nerve and muscle damage as the Vitamin K injection must be given deeply into the muscle. However, should a newborn experience any of these, it is incredibly difficult for them to “notify” anyone, difficult for the parents to see or understand the reason behind a newborns cries, and difficult for physicians to see these signs in infants. Majority of physicians are not educated or trained to fully examin an infant in discomfort for vaccine related symptoms. Instead, they are most likely to dismiss any vaccination link.

The following are from the vaccine product insert:

* Clinical Pharmacology: "little is known about the metabolic fate of Vitamin K".
* Contraindication: "Hypersensitivity to any component of this medication".
* Precautions: "Studies of carcinogenicity, mutagenesis, or impairment of fertility have not been conducted with phytonadione."
* Pediatric Use: "Hemolysis, jaundice, and hyperbiliruminemia in newborns, particularly in premature infants, may be related to the dose of phytonadione."
* Adverse reactions: "Deaths have occurred after intravenous administration…The possibility of allergic sensitivity should be kept in mind…Hyperbilirubinemia has been observed in the newborn following administration of phytonadione…"

Newborns are not pre-screened for allergic hypersensitivity.

Vitamin K1 in the form of Phytonadione, is a popular medication used to promote blood clotting. Preparations of Phytonadione are sold under trade names Mephyton, AquaMephyton, and Konakion.

Vitamin K is not a clotting agent in itself, and Vitamin K levels are not measured directly; only levels of other blood proteins with known dependence on Vitamin K

Jaundice is a common symptom of Vitamin K overdose. A recent pediatric statistic indicated the presence of clinical jaundice in more than half of all infants. Vitamin K shots are administered within an hour or so after birth. Clinical jaundice presents itself in the first few days after birth.

Tulchinsky paper: It was found that 12 of the 34 newborns (35%) whose medical records were reviewed already received a Vitamin K injection before presentation of any hemorrhaging symptoms. 16 of the newborns (47%) received Vitamin K after the onset of hemorrhagic symptoms. 6 newborns (18%) had no mention of Vitamin K in their medical records.

It was assumed that injection of Vitamin K had not been given if medical records contained no mention of it, even though the practice was popular at the time. There is no mandate to maintain accurate medical records of Vitamin K injection making the assumption worthy of great concern.

Then, in the mid-1950’s, circulating reports of increased jaundice and kernicterus (brain damage caused by high bilirubin levels) in infants given vitamin K prophylaxis began resulting in wide spread concern and lack of confidence in the procedure. Reviews of maternity units found that some were giving Synkavite in doses exceeding 50mg. It was established that high doses of Synkavite caused haemolysis (destruction of red blood cells) and high serum bilirubin levels.

Researchers and medical professionals questioned the safety aspects of vitamin K, and there were many conflicting reports on the appropriate dosages. Some researchers questioned the need for vitamin K at all.

Eventually, a newer preparation, intramuscular vitamin K1 (phytomenadione), was developed and approved with the presumption that it appeared to cause less haemolysis. Phytomenadione (trade names Konakion (Roche) or Aquamephyton (Merck, Sharpe & Dohme)) is a synthetic petrochemical derived from 2-methyl 1,4-naptha-quinone in a polyethoxylated castor oil base. In the US, polysorbate-80 is used as a base instead of polyethoxylated castor oil.

Despite the lack of long term trials of these formulations, the American Academy of Pediatrics recommended that phytomenadione be administered prophylactically to all newborn babies. The intramuscular route was deemed safer.

Merck’s 1998 PDR entry for AquaMEPHYTON has removed adverse reaction liability by stating, "The American Academy of Pediatrics (AAP) recommends that Vitamin K1 be given to the newborn."

Infant Formulas are supplemented with unnaturally high levels of vitamin K. The breastfed infant can be supplemented with several low oral doses of liquid vitamin K1 (possibly 200 micrograms per week for five weeks, totaling 1 milligram, even more gradual introduction may be better). Alternatively, the nursing mother can take vitamin K supplements daily or twice weekly for 10 weeks. (This does not alter fetal levels but supplementation of the nursing mother does increase breast milk and infant levels.)

Either of these provides a much safer rate of vitamin K supplementation. Maternal supplementation of 2.5 mg per day, recommended by one author, provides a higher level of vitamin K through breast milk than does formula. Formula provides 10 times the U.S. recommended daily allowance.


Vitamin K: controversy? what controversy?
By Karin Rothville DipCBEd.

For the last 40 or 50 years, it has become a generally accepted fact that vitamin K prevents haemorrhagic disease of the newborn, and routine administration of vitamin K to all newborns has been recommended. 3, 6, 21, 34, 72 This recommendation has been questioned because results released in 1990 from a study by Golding and colleagues26 in the UK showed a two to three times increased risk of childhood cancers, especially leukaemia, in children given prophylactic drugs (usually intramuscular vitamin K) in their first week. A further study in 1992 seemed to confirm this risk.25

There was widespread anxiety among parents when these findings were published. Parents were, understandably, reluctant to have their baby receive a substance that could predispose it to cancer in childhood, and many health workers were also reluctant to give, without prescription, a possibly cancer-causing substance to prevent a disease that few, if any, of them had ever seen. These concerns are not the first time that vitamin K safety has been questioned. So, what is the controversy about vitamin K? And does it predispose babies to childhood cancer?

WHAT IS VITAMIN K AND WHAT DOES IT DO?

Vitamin K is a fat-soluble substance which triggers off the blood-clotting process. Blood clotting is a complex process and can be described as a sequence of three stages, requiring up to 12 different coagulation factors.72 The liver needs vitamin K to synthesise four of these factors. Vitamin K is also needed for the formation of other proteins found in plasma, bone and kidney.33, 58

As with other fat-soluble vitamins, a normal flow of bile and pancreatic juice is necessary for digestion, and the presence of dietary fat, especially short-chain fatty acids, enhances absorption. Absorbed vitamin K is transported via the lymph into the systemic circulation.58

Normally, a significant portion (up to 55%) of absorbed vitamin K is excreted so the amount in the body is small and its turnover is rapid (about 30 hours).58 Vitamin K is stored and re-utilised in the body for 3-4 weeks.33

Vitamin K is found in many foods. Leafy, dark green and deep yellow vegetables are the best sources.58 Alfalfa18 is a good source; and milk and dairy products, eggs, cereals, fruits and other vegetables also provide small but significant amounts. As the liver of adults contains about equal amounts of plant and animal forms of Vitamin K, it is assumed that vitamin K is produced in the intestinal tract by bacterial flora. One of the reasons given for the low levels of vitamin K in newborn babies is because their gut has not yet been colonised by the required bacteria.

Recommended daily dietary intakes of vitamin K58
Category 
Age
Amount (mg)
Infants
0 - 1
10
Children
1 - 3
15
4 - 6
20
7 - 10
25
Adolescents
11 - 14
30
15 - 18
35
Adult Male
19 - 70+
45
Adult Female
19 - 70+
35
Pregnancy

+ 10

Lactating

+ 20


The dietary requirements for vitamin K in infants and children are estimates and are based on weight and growth rates as compared to adults. Many unsupplemented breasfed infants do not show clinical signs of vitamin K deficiency on intakes of less than 3 mg daily and the mean requirement for infants is estimated to be 5 mg daily based on weight. The higher amount of 10mg is recommended for prevention of Haemorrhagic Disease of the Newborn.58

WHAT IS HEMORRHAGIC DISEASE OF THE NEWBORN?

Haemorrhagic Disease of the Newborn (HDN) is a bleeding disorder associated with low levels of vitamin K in newborn babies. It was first defined in 1894 by Townsend69 as spontaneous external or internal bleeding occurring in newborn infants not due to trauma, accident or inherited bleeding disorders such as haemophilia. Previously, there were no generally agreed upon criteria to determine causes of haemorrhaging, so any diagnosis was based solely on the opinion of the attendant medical personnel.

Infants are born with low levels of vitamin K 23 compared to adults and this is termed 'vitamin K deficiency'. Up to 50% of babies develop this 'vitamin K deficiency', but bleeding occurs in only a fraction of these cases. 37 In most it starts after birth, becomes progressively more severe over 48-60 hours, then spontaneously corrects itself by 72-120 hours. 9

HDN has always been rare - in Britain where maternity units practised a selective policy of vitamin K administration, the incidence was no more than 1 in 20,000 in the years 1972-80. Estimates for late onset HDN are 4-8 per 100,000.45 Incidence also seems to vary from country to country.

HDN is divided into three categories:

1. Early onset HDN occurs in the first 24 hours. It is very rare and mainly associated with mothers who have taken anticonvulsant, antibiotic, antituberculous or anticoagulant drugs during pregnancy.
2. Classic HDN occurs in the first week after birth. It is manifested by the oozing of blood from the intestines, the nose, the cord site and broken skin sites. Bruising at sites where there has been no trauma can also appear.
3. Late onset HDN occurs after the first week, with a peak incidence between the second and sixth weeks, and about half the cases present with intracranial bleeding (bleeding into the brain).

WHAT ARE THE RISK FACTORS FOR HDN?

There has been some debate over the years as to whether or not HDN is actually caused by vitamin K deficiency. Certainly, giving vitamin K does arrest bleeding in the majority of cases, but this does not mean that vitamin K deficiency causes HDN. One may as well say that an antibiotic deficiency causes bacterial infection. There is also no consensus as to what level of vitamin K in plasma protects against HDN. Some researchers have found no evidence of vitamin K deficiency in babies in their studies 43, 49 and other factors have also been suggested.52, 73, 74

Most, if not all, of the reported cases of late onset HDN have presented with problems which affect the baby's ability to absorb or utilise vitamin K.45, 56 These include: hepatitis, cystic fibrosis, chronic diarrhoea, bile duct atresia, alpha-1-antitrypsin deficiency, coeliac disease of insufficient plasma transport capacity. Subclinical cytomegalovirus has also been implicated. Vitamin K-responsive bleeding syndrome has been well documented after antibiotic therapy, especially with cyclosporins.33

There are other factors which place the newborn at higher risk. These include pre-term birth (as the liver is very immature), low birth weight, instrumental or traumatic delivery, bruised or bleeding in the first few days after birth, requiring surgery or circumcision, taking inadequate feeds and breastfeeding. 33

BREASTFEEDING - WHY IS IT A RISK?

Several authors have noted the higher incidence of HDN in solely breastfed babies. 9, 30 The incidence has been quoted as 1 in 1200. 30 Studies comparing breastmilk with formula and cow's milk have shown that breastmilk is lower in vitamin K. 22, 28, 32 Breastmilk substitutes are heavily supplemented with vitamin K, however, it is possible that, like iron, vitamin K is biologically more available to the baby from breastmilk, and so such high levels are not necessary.

Measured levels of vitamin K in breastmilk seemed to vary depending on the type of measurement used; however, they all come out lower than cow's milk. Fournier22 and Greer28 found levels of around 8-9mg/l, which would mean that if a baby was taking in about 500ml per day, it would be getting the recommended 3-5mg daily.

Vitamin K content and availability are greater in the hind milk because of its higher fat content and vitamin K levels are also higher in colostrum.32 As an extra plus, breastmilk contains thromboplastin, one of the factors in blood clotting.18

Vitamin K levels in the breastmilk rise markedly in response to the mother eating vitamin K rich foods or taking vitamin K supplements.29, 54 Nishiguchi found no cases of low vitamin K levels in breastfed infants whose mothers had been given supplements, as opposed to infants who had only been given 1 or 2 doses of oral vitamin K.54

Unrestricted access to the breast in the early days after birth is important, due to the higher levels of vitamin K in colostrum. The importance of early feeding has been recognised since the 1940's. Babies who have been fed within their first 24 hours have significantly better coagulation times than babies not fed until after 24 hours.24

It is essential that, to receive the full complement of vitamin K in breastmilk, the baby completely finishes one breast before being offered the other. Any practice that involves restricting either the baby's time at the breast or the number of feeds will not allow the baby to receive optimum amounts of vitamin K and will also prolong the time it takes for the baby's intestine to be colonised by friendly, vitamin K manufacturing bacteria.

THE HISTORY OF VITAMIN K USE TO PREVENT HDN.

The search for the cause of HDN began in 1913 when Whipple82 postulated that a lack of prothrombin activity could be a cause of HDN. In 1929, Henrik Dam14 noticed that chicks fed a fat-free diet suffered subcutaneous and intramuscular haemorrhages, which could be prevented if the chicks were fed seeds, cereals and green, leafy plants. Dam described the condition as a vitamin deficiency and named the deficient vitamin 'vitamin K', from the Danish word 'koagulation'.

Research in 19378 found that prothrombin times in normal neonates were between 30-60% adult levels, falling to 15-30% on day two, and then gradually rising again until about day 10. This research led to the continuing belief that these low levels in the newborn are a deficiency and need to be corrected.

In 1939, vitamin K1 was isolated from alfalfa by Dam, for which he later received the Nobel Prize, along with Edward Doisy, who isolated vitamin K2.45 Further research in 1939 by Waddell and Guerry81 found that low plasma prothrombin levels could be elevated by the administration of oral vitamin K.

Armed with this 'proof' that vitamin K deficiency caused HDN, vitamin K was synthesised and various trials were commenced to ascertain which was the most effective amount and route to use in prophylaxis.

It is difficult for us to assess these trials nowadays as they were mostly neither double blind nor well controlled. The dosage of vitamin K given, the route of administration and the time of administration all varied. In many cases, the conclusions did not seem to match the results.72

Some of the studies assessed the effect on neonatal vitamin K levels if the mother was given vitamin K during labour.72 Results varied, with the effectiveness of the vitamin K given depending on how soon the woman gave birth and the dosage given. More recent studies have shown increases in cord blood levels where mothers were supplemented antenatally with vitamin K.1, 66 Two showed a significant difference between the supplemented and unsupplemented groups and found that the effect of prenatal vitamin K persisted until the fifth day after birth.1

Because of the variations in results from these early studies, further research focussed on treating the baby after birth. One particular study done in 194231 was intended to determine the minimal effective oral dose of Synkavite (K3), a water-soluble synthetic form of vitamin K. The results showed that very small daily doses were effective and that a dose of 5mg daily would probably prevent the development of HDN, except in early onset cases. The study also found that 1.25mg was effective in lowering an excessively high prothrombin time to normal. However, the author admitted that several workers found prothrombin deficiencies in babies with no abnormal bleeding.

By 1950, most maternity units had a policy of giving infants oral vitamin K (usually Synkavite) immediately after birth.70 This prevented the fall in prothrombin levels that occurred in the first few days and, presumably, the risk of excessive bleeding. This risk was higher in male babies because of routine circumcision, and, indeed, vitamin K proved to be of great clinical value in preventing post-circumcision bleeding.75

Then, in the mid-1950's, reports of increased jaundice and kernicterus (brain damage caused by high bilirubin levels) associated with vitamin K prophylaxis began circulating. Reviews of maternity units found that some were giving Synkavite in doses exceeding 50mg.70 It was established that high doses of Synkavite caused haemolysis (destruction of red blood cells) and high serum bilirubin levels.48

Researchers and medical professionals queried the safety aspects of vitamin K, and there were many conflicting reports on the appropriate dosages. Some researchers queried the need for vitamin K at all, quoting results from studies that showed no difference in prothrombin times or vitamin K plasma levels between babies that bled and babies that didn't.72

Eventually, a newer preparation, intramuscular vitamin K1 (phytomenadione), was developed and approved for use, solely on the grounds that it appeared to cause less haemolysis. Phytomenadione (trade names Konakion (Roche) or Aquamephyton (Merck, Sharpe & Dohme)) is a synthetic petrochemical derived from 2-methyl 1,4-naptha-quinone in a polyethoxylated castor oil base.18 In the US, polysorbate-80 is used as a base instead of polyethoxylated castor oil.15

In spite there being no long term trials of these preparations, the American Academy of Pediatrics recommended that phytomenadione be administered prophylactically to all newborn babies.72 The use of oral vitamin K preparations fell out of favour in the USA and the 'safer' intramuscular route became the route of choice.

In Britain, after the jaundice scare of the1950's, many maternity units began to practice a selective policy, giving vitamin K only to babies at risk of haemorrhaging. McNinch reported in 1980 that less than half the maternity units in the UK gave vitamin K to all newborns.47 Some of these babies were given oral prophylaxis and some were given intramuscular prophylaxis.

In Germany, almost all newborn infants who required medical care and instrumental deliveries were given intramuscular vitamin K, and some healthy newborns also received it.76 Records have not always been kept in New Zealand hospitals, so it is impossible to say whether or not vitamin K was given routinely and by which route.17

Although vitamin K use seemed to prevent most cases of HDN, there was still controversy. Not everyone believed vitamin K deficiency was the cause of HDN. In 1977, van Doorm et al 52, 73, 74 suggested that HDN could be caused by a heparin-like inhibitor in the newborn and he concluded that babies given their first feed soon after birth do not have a vitamin K deficiency. Other researchers agreed with van Doorn.49 In 1980, Malia et al43 could find no evidence of vitamin K deficiency in babies in their study and concluded that low levels of vitamin K dependent clotting factors were due to the immature liver. The authors of these studies questioned whether vitamin K prophylaxis was really necessary for healthy newborns.

Then, starting in November 1980, there was a cluster of six cases of HDN in Britain, all within 17 months.46 Half of these cases were classic HDN, the other half were a new manifestation of HDN - late onset.

LATE ONSET HDN

Late onset HDN was first reported in 1977.5 It mainly occurs in breastfed infants and ¯ to ¾ of cases have an underlying liver disorder or malabsorption syndrome,15 rather than insufficient dietary intake of vitamin K. This means the liver cannot adequately synthesise blood clotting factors or store adequate amounts of vitamin K. Liver function cannot be easily diagnosed at birth without a range of invasive tests and thus there exists an unknown risk of haemorrhaging.

Many factors contribute to poor liver function, including hepatitis, cystic fibrosis, antibiotic therapy, biliary atresia, alpha-1-antitrypsin deficiency, a-beta-lipoproteinaemia, coeliac disease, chronic diarrhoea and exposure to pharmacologic agents such as anticonvulsants, rifampin, isoniazid cephalosporins and coumarin compounds33 When tested, most of the reported cases of late onset HDN had hepatitis, liver malfunction or enzyme deficiencies.6, 35, 51, 80

Birkbeck6 believes there are two processes at work - low levels of prothrombin and vitamin K-dependent clotting factors VII, IX and X at birth, and a further fall in these in the neonatal period. In his view the initial low levels are not due to vitamin K deficiency as levels of 2 other non-vitamin K-dependent factors, XI and XII are also often reduced. Thus, the situation at birth may be simply due to hepatic immaturity.

Birkbeck6 also reports that HDN is almost unknown in central Africa and he suggests an environmental mechanism as the cause. Associated with this, a discussion paper from the University of Amsterdam42 raises the idea that by-products of our industrial society such as PCBs, PCDDs and PCDFs are the cause of late onset HDN. These chemicals can induce enzymes in the liver which cause liver damage and prolong prothrombin time. Although overseas studies have reported contamination of breastmilk by these pollutants, a NZ Department of Health study on breastmilk reported that levels of these contaminants were at the lower end of the scale.7 The Health Department is currently conducting another study to see if levels have changed over the past few years.

There seems to be a seasonal variance, with most cases of late onset HDN occurring in the warmer months.6 It has been suggested that the mother could have contracted a viral infection during pregnancy in the colder months and this has crossed the placenta. Since viruses have an affinity for the liver and mucous membranes, they can affect intestinal absorption and liver function.67

Another suggested cause of late onset HDN includes use of the food antioxidant BHT (butylated hydroxytoluene), which has produced vitamin K deficiency.68 BHT is present in many processed foods, including margarine. Our Western diets consist of a lot of processed food, and to reduce fat intakes, margarine is recommended rather than butter. The polyunsaturated fat in margarine is an inhibitor of vitamin K absorption.68 Both of these factors could have an effect on the amount of vitamin K available to pass through to the baby. A high level of vitamin K in the mother's blood is necessary to ensure adequate transplacental transfer of vitamin K.9, 33 It is important for the baby to have adequate stores of vitamin K in its liver at birth to prevent bleeding until its feeding and gut flora are established.

Of the six cases of HDN in Britain in 1980-1982, all were breastfed and none had received vitamin K at birth.46 Two of the cases were in the high-risk group - one was born by caesarean section and had an epileptic mother treated with phenytoin, and the other had an alcoholic mother who had taken anti-depressants - and obviously should have received vitamin K at birth.

These cases prompted a call for the re-introduction of routine prophylaxis. Many opposed the idea of unnecessarily injecting otherwise healthy babies so studies40, 47, 55, 79 were therefore conducted to determine whether oral vitamin K was as effective as intramuscular. It was also proposed that oral vitamin K would be more cost-effective and thus better suited for use in Third World countries.55 Results of these studies varied. Some showed that oral vitamin K was effective in preventing classic haemorrhagic disease but not as effective as intramuscular vitamin K in preventing late onset HDN.47, 55, 78 Others found oral as effective, especially a 10 year study conducted on 38,000 infants in Sweden where no cases of HDN were observed over that period.40 Tripp and McNinch reported no cases in 25,000 babies in their maternity unit where only those at risk were given intramuscular prophylaxis and the rest oral prophylaxis.70

In spite of these findings that oral vitamin K prophylaxis was not effective in preventing late onset HDN, it continued to be used in British maternity units, especially for low risk infants.

RISKS OF VITAMIN K PROPHYLAXIS

Konakion ampoules contain phenol, propylene glycol38 and polyethoxylated castor oil as a non-ionic surfactant. Studies in animals given polyethoxylated castor oil have shown a severe anaphylactic reaction associated with histamine release. Strong circumstantial evidence implicates polyethoxylated castor oil in similar reactions in humans. Polyethoxylated castor oil, when given to patients over a period of several days, can also produce abnormal lipoprotein electrophoretic patterns, alterations in blood viscosity and erythrocyte aggregation (red blood cell clumping). Individuals sensitive to this base are contraindicated from using Konakion. New Ethicals Compendium also warns that the use of Konakion can cause jaundice and kernicterus in infants.53 Other listed side effects include flushing, sweating, cyanosis, a sense of chest constriction, and peripheral vascular collapse. Local cutaneous and subcutaneous changes may occur in areas of repeated intramuscular injections.

This synthetic, injectable vitamin K formulation was never subjected to a randomised, controlled trial. In new drugs that are to be used for prophylaxis, the usual risk/benefit analysis does not apply, since the individual is not ill. The ethical principle of non-maleficence (primum non nocere - first do no harm) applies and the trials must thus be larger in order to identify any previously unrecognised side effects.65 Since this did not happen, nor was there any long term follow up, we actually have little idea of the effects of this drug on newborn babies.

The risks of injecting vitamin K into a newborn baby are nerve or muscle damage as the preparation must be injected deeply into the muscle, not subcutaneously under the skin. There is also the documented risk of injecting the baby with the syntocinon intended for the mother.30, 70 As stated in the product information,53 infants can suffer from jaundice or kernicterus (brain damage from a build-up of bile pigments in the brain) from Konakion. Infants who have the enzyme deficiency G6PD (glucose 6 phosphate dehydrogenase) are at particular risk from vitamin K.30 The other risk factor is the possible increased chance of childhood cancer.

THE LINK BETWEEN CHILDHOOD CANCER AND INTRAMUSCULAR VITAMIN K

In 1970, a national cohort study of 16,193 infants born in one week in April was begun in Britain.26 This study was to test hypotheses about childhood cancers and their associated factors. Thirty-three of the children had developed cancer by age 10 and were compared with 99 control children, matched on maternal age, parity and social class. One of the unlooked-for risk factors was the administration of prophylactic drugssuch as vitamin K in the first week after birth - a nearly three-fold risk. This association fitted no prior hypothesis and the authors recommended that their finding be tested in another series of cases.

The authors of the study approached Roche, the manufacturers of Konakion, for funding for a further trial to examine the findings more closely. Roche was not interested until, a few months later, the media reported the results of the study and that vitamin K given to babies might cause childhood cancer. Roche then decided to fund a new study.27

The new study25 was a case-control study of 195 children with cancer born at either of two hospitals in Bristol, England, compared with 588 healthy children also born at these hospitals. One hospital predominantly gave vitamin K orally and the other intramuscularly. The authors found a nearly two-fold risk of leukaemia in children who had received intramuscular vitamin K.

These findings were extremely worrying. Golding calculated that the extra cases of leukaemia caused by vitamin K injection could be as many as 980 in the UK alone.25 These results were supported by reports of the potential carcinogenicity of vitamin K from Israels et al, who suggested that low vitamin K levels in the newborn protect against the risk of mutations during a period of rapid cell growth and division.39 Pizer et al did not find any association between the route of vitamin K administration and mutations in cells but concluded that his study was too small to show any real effect.62 Another study reported no increase in abnormalities in newborn infants, but, with only 12 infants, the study was too small to show any real effect.10 It is worth noting that after an intramuscular dose of vitamin K, the baby's plasma levels are almost 9000 times the normal adult levels.47 It has also been suggested that the cancer-causing agent could be a metabolite, N-epoxide, or some other component of the solution other than vitamin K itself.15

Golding's study was criticised by many. One of the reasons was that the authors had to make assumptions for some cases, as the information on vitamin K administration was not clearly recorded. In spite of this, expert epidemiologists considered that the results were plausible and so could not be lightly dismissed.15 Further studies were proposed to answer the question of cancer and vitamin K.

In 1993, results from three retrospective studies on vitamin K and childhood cancer were published. The studies were done in the USA, Denmark and Sweden.41, 57, 19 These studies, although large, did not confirm the association between intramuscular vitamin K and childhood cancer. One of the studies not only showed no association between IM vitamin K and childhood cancer, it also showed no association between maternal smoking and childhood cancer, a finding totally at odds with the results from many other studies.19 The other two studies were also not comparable to the British study. One because of differences in type of vitamin K given41 and the other because of the use of birth cohorts with differing regimens of vitamin K usage.57

Because of the design flaws in these studies, there was still a need for further case-control studies. Results from two were published in 1996.2, 77 They had carefully matched controls and more accurate information on whether vitamin K had been given or not, and by which route. One of the studies2 reported no association between intramuscular vitamin K and childhood cancer and the other77 found a risk of leukaemia, but only when cases were compared with local controls (i.e. from the same hospital) and not with controls randomly selected from the whole area under study. This, although suggestive, was not followed up but dismissed as a chance finding related to multiple testing.

The suggestion was then put forward that, as these studies had failed to show a definite association between intramuscular vitamin K and childhood cancers, worries about any potential cancer risk should be abandoned.83

At that time, four more studies on vitamin K and cancer were in progress.44, 59, 60, 61 The results from these four studies were published in 1998. Two of them failed to confirm any increased risk of childhood cancers.44 61 One of the other studies showed a twofold risk of acute lymphoblastic leukaemia among 1-6 year olds,59 the other showed a significant risk for all cancers.60

So, the jury is still out on whether there is an increased risk of childhood leukaemia with the intramuscular form of vitamin K. Some recommend that intramuscular vitamin K should still be used, as the risk of leukaemia “seems more hypothetical than real”.76 Others believe that public confidence in IM vitamin K has been severely shaken and will be difficult to restore fully. They recommend an oral regimen similar to that used in the Netherlands of 25mg daily, given by the mother. This would avoid the grossly unphysiological peaks of vitamin K from both the IM route and the present oral route.71

ORAL VITAMIN K VS INTRAMUSCULAR

The two main problems with giving vitamin K orally are that there is no licensed oral formulation, meaning that babies receive the intramuscular form orally, and that compliance with three oral doses is poor as many doctors and midwives are reluctant to give an unlicensed formula.13 The use of unlicensed preparations may theoretically expose professionals to litigation in the event of prophylactic failure or unforeseen adverse events.2

Roche, the manufacturers of Konakion, state that they do not recommend the administration of Konakion solution orally.63 Their reasons are:

* that they have no clinical studies to support oral use,
* phenol, which has been reported to be an irritant to newborns mouths, is used as a preservative,
* the variability in the production of bile salts in newborns may affect absorption,
* that Konakion given orally has a small association with anaphylactic reactions.

The preparation was also unpleasant to taste and babies were inclined to spit it out82 or to vomit it back up. Only about half of an orally administered dose is absorbed.47 Even so, the plasma concentrations in babies who were given oral vitamin K reached 300 times the adult levels, before dropping off slightly after about 24 hours.47

After the publication of Golding's studies, further trials were done on oral vitamin K prophylaxis and whether it gave longer term protection. In 1992, Cornelissen11 found plasma vitamin K concentrations were higher in the group given IM vitamin K than the oral group, but blood coagulability, activities of factors VII, X and PIVKA-II concentrations showed no differences. By 3 months follow-up, vitamin K levels had dropped in both groups but more in the oral group. He suggests that neither give long term protection. One would assume that babies should be producing their own vitamin K by 3 months and, if not, what other mechanism could be hindering this process.

Von Kries et al78 studied repeated oral vitamin K prophylaxis in Germany, with 3x 1 mg doses and found that it was not as effective as a 1mg intramuscular dose at birth. Another study by Cornelissen et al12 reported on the effectiveness of differing regimens of oral vitamin K in four different countries - the Netherlands, Germany, Switzerland and Australia (two differing regimes). In the Netherlands, babies are given 25 mg daily oral vitamin K for 3 months with I mg given at birth either orally for healthy newborns or intramuscularly for unwell babies. In Germany, the regime is 3 x 1 mg oral doses as was also the case in Australia from 1993 to 1994. In Switzerland 2 oral doses of a new 'mixed-micellar' oral vitamin K is given. The Netherlands had the lowest failure rate - 0 per 100,000. In Australia, where the regime was changed in 1994 from oral to IM, the failure rate was 1.5 per 100,000 for oral and 0.9 per 100,000 for IM, showing that 3 oral doses are less effective at preventing late onset HDN than one IM dose of vitamin K. Even if Roche are persuaded to bring the mixed-micellar preparation into New Zealand, results from Switzerland (failure rate of 1.2 per 100,000)12 show that further study needs to be done on the most effective timing of the doses.

If New Zealand parents wish their baby to receive oral vitamin K, the recommended regimen is for 3 x 1mg doses, 1 at birth, 1 at 5 days and 1 at 6 weeks.6, 20 It is up to parents to ensure that their baby receives all 3 doses if they choose this form of prophylaxis.

CONCLUSION

It would seem an anachronism that babies are born with a deficiency of such an essential vitamin and require supplementation. In fact, although there have been many studies on differing aspects of vitamin K prophylaxis, there has only been one39 on the possible reasons for and the advantages (if any) of the physiological levels of vitamin K in newborns.

The risks of prophylaxis for the majority of babies who are at low risk of HDN are also not understood. As plasma vitamin K levels in newborns reach 300 times normal adult levels for oral and almost 9000 times for IM vitamin K47, some research needs to be done on the effects this may have. Studies have shown that physiological levels of vitamin K maintain a careful balance between coagulation and anti-coagulation and we have no idea what the effects of upsetting that delicate balance would be.

The number of children currently developing cancer during childhood is much higher than the number developing a life threatening or permanently disabling problem as a result of late onset HDN. The risk of childhood cancer is estimated to be 1.4 per 1000, from the 1970 British cohort. If IM vitamin K caused cancer, there would be 100 extra cases of cancer per case of HDN prevented.16 This could mean that giving IM vitamin K to every baby would be doing more harm than good.36

The decision rests on parents' shoulders - the link between intramuscular vitamin K and childhood cancer has not been definitively proved, nor has it been completely disproved. It may be that an oral regimen as suggested by Tripp and McNinch71 could be the answer to the dilemma. If this is the case, then Roche needs to be lobbied to make the European preparations available in New Zealand. In the meantime, the choice is between no vitamin K, with the mother being aware of her dietary intake of vitamin K, an oral regimen or the intramuscular formulation.

BIBLIOGRAPHY

1. Anai T, Hirota Y, Yoshimatsu J et al. Can prenatal vitamin K1 supplementation replace prophylaxis at birth? Obst Gynec 1993;81:251-4.
2. Ansell P, Bull D and Roman E. Childhood leukaemia and intramuscular vitamin K: findings from a case-control study. BMJ 1996;313(7051):204-5.
3. Barton J, McNinch A. and Tripp J. Oral vitamin K prophylaxis and frequency of late vitamin K deficiency bleeding (letter). Lancet 1994 343(8906):1168.
4. Barton J, Tripp J. and McNinch A. Neonatal vitamin K prophylaxis in the British Isles: current practice and trends. BMJ 1995; 310(6980):632-3.
5. Bhanchet P, Tuchinda S, Hathirat P et al. A bleeding syndrome in infants due to acquired prothrombin complex deficiency. Clin Pediatr 1977;16:992 in, Hathaway W. New insights on vitamin K. Hematol Oncol Clin North Am 1987;1(3):367-379.
6. Birkbeck J. Vitamin K prophylaxis in the newborn: a position statement of the Nutrition Committee of the Paediatric Society of New Zealand. NZMJ 1988;101:421-2.
7. Birkbeck J. Despite the contamination breastmilk remains the best. NZ Doctor July 1990.
8. Brinkhous K, Smith H and Warner D. Plasma prothrombin level in normal infancy and in hemorrhagic disease of the newborn. Am J Med. Sci 1937;193:475-479 in, Ruby C. Vitamin K prophylaxis: a historical perspective. MIDIRS;7:3.
9. Clarkson P and James A. Parenteral vitamin K1: the effective prophylaxis against haemorrhagic disease for all newborn infants. NZMJ 14 March 1990.
10. Cornelissen M, Smeets D, Merkx G et al. Analysis of chromosome aberrations and sister chromatid exchanges in peripheral blood lymphocytes of newborns after vitamin K prophylaxis at birth. Pediatr Res 1991;30:550-3.
11. Cornelissen EAM, Kollée LAA, DeAbreu RA et al. Effects of oral and intramuscular vitamin K prophylaxis on vitamin K, PIVKA-II, and clotting factors in breastfed infants. Arch Dis Child 1992;67:1250-54.
12. Cornelissen M, von Kries R, Loughnan P et al. Prevention of vitamin K deficiency bleeding: efficacy of different multiple oral dose schedules of vitamin K. Eur J Ped 1997;156(1):126-30.
13. Croucher C. and Azzopandi D. Compliance with recommendations for giving vitamin K to newborn infants. BMJ 1994;308(6933):894-895.
14. Dam H, Dyggve H, Larsen H and Plum P. The relationship of vitamin K deficiency to hemorrhagic disease of the newborn. Adv Pediatr 1952;5:129-153 (abstract).
15. Darlow B. Vitamin K deficiency haemorrhage: dilemmas over prophylaxis continue. NZ Practice Nurse February 1995:35-37.
16. Darlow B. and Nobbs P. The neonatal vitamin K debate: IM vs. oral: two views. New Ethicals May 1993:11-18.
17. Dockerty J, Broadbent R and McNoe B. New Zealand hospital records insufficient for vitamin K study. NZMJ 10 May 1995.
18. Donley J. Vitamin K in relation to haemorrhagic disease of the newborn. NZCOM Journal December 1992.
19. Ekelund H, Finnstrom O, Gunnarskog I. et al. Administration of vitamin K to newborn infants and childhood cancer. BMJ 1993;307(6896):89-91.
20. Fetus and Newborn Committee of the Paediatric Society of New Zealand. 1992. Vitamin K administration in the newborn.
21. Foetus and Newborn Society, Canadian Pediatric Society. The use of vitamin K in the perinatal period. Canad MAJ 1988;139:127-130.
22. Fournier B, Sann L, Guillaumont M and Leclerq M. Variations of phylloquinone concentrations in human milk at various stages of lactation and in cow's milk at various seasons. Am J Clin Nutr 187;45:551-8.
23. Garrow D, Chisholm M. and Radford M. Vitamin K and thrombotest values in full term infants. Arch Dis Child 1986;61:349-51.
24. Göbel U, Sonnenschein-Kosenow S, Petrich C and von Voss H. (Letter). Lancet 1977;i:187-8.
25. Golding J, Greenwood R, Birmingham K. et al. Childhood cancer, intramuscular vitamin K and pethidine given during labour. BMJ 1992;305 (6849):341-6.
26. Golding J, Paterson M and Kinlen L. Factors associated with childhood cancer in a national cohort study. Brit. J Cancer 1990;62:304-8.
27. Greenwood R. Vitamin K and childhood cancer. MIDIRS 1994;4(3):258-9.
28. Greer F, Marshall S, Cherry J and Suttie J. Vitamin K status of lactating mothers, human milk, and breast-feeding infants. Pediatrics 1991;88(4);751-6.
29. Greer F, Marshall S, Foley A et al. Improving the vitamin K status of breastfeeding infants with maternal vitamin K supplements. Pediatrics 1997;99(1);88-92.
30. Hall M. and Pairaudeau P. The routine use of vitamin K in the newborn. Midwifery 1987;3(4):170-7.
31. Hardwicke S. et al. Studies on the minimal effective dose of a water-soluble vitamin K substitute in the prevention of hypoprothrombinemia in the newborn infant. J Pediatr 1944;24:259-269 (abstract).
32. Haroon Y, Shearer M, Rahim S et al. The content of phylloquinone (vitamin k1) in human milk, cow's milk and infant formula foods determined by high performance liquid chromatography. J Nutr 1982;112:1105-17.
33. Hathaway W. New insights on Vitamin K. Hematol Oncol Clin North Am 1987;1(3):367-379.
34. Henderson-Smart, D. Giving vitamin K to newborn infants: a therapeutic dilemma. MJA 1996;165:414-5.
35. Heron P, Cull A., Bourchier D and Lees H. Avoidable hazard to New Zealand children: case reports of haemorrhagic disease of the newborn. NZMJ 1988;101:507-8.
36. Hey, Edmund. Vitamin K - the debate continues. MIDIRS 1998;8(2):234-6.
37. Hilgartner, M. Vitamin K and the newborn. New Eng J Med 1993;329(13):957-8.
38. Hull D. Vitamin K and childhood cancer. BMJ 1992;305:326-7.
39. Israels l, Friesen E., Jansen A. and Israels E. Vitamin K1 increases sister chromatid exchange in vitro in human leukocytes and in vivo in fetal sheep cells: a possible role for 'vitamin K deficiency' in the fetus. Pediatr Res 1991;30:550-3.
40. Jorgensen F, Fielding P, Vinther S et al. Vitamin K to neonates. Peroral versus intramuscular administration. Acta Pediatr Scand 1991;80(3):304-7.
41. Klebanoff M, Read J, Mills J. et al. The risk of childhood cancer after neonatal exposure to vitamin K. New Eng J Med. 1993;329(13):905-8.
42. Koppe J, Pluim E and Olie K. Breastmilk, PCBs, dioxins and vitamin K deficiency: discussion paper. J Royal Soc. Medicine 1989;82:416-419 in, Donley, Joan. Vitamin K in relation to haemorrhagic disease of the newborn. NZCOM Journal Dec 1992.
43. Malia R, Preston F and Mitchell V. Evidence against vitamin K deficiency in normal neonates. Thromb Haemost 1980;44:159.
44. McKinney P, Juszczak E, Findlay E, Smith K. Case-control study of childhood leukaemia and cancer in Scotland: findings for neonatal intramuscular vitamin K. BMJ 1998;316:173-7.
45. McNinch A and Tripp J. Haemorrhagic disease of the newborn in the British Isles: a two year prospective study. BMJ 1991;303(6810):1105-1109.
46. McNinch A, Orme R and Tripp J. Haemorrhagic disease of the newborn returns. Lancet 1983;i:1089-90 (abstract).
47. McNinch A, Upton C, Samuels M et al. Plasma concentrations after oral or intramuscular vitamin K1 in neonates. Arch Dis Child 1985;60:814-818.
48. Meyer T and Angus J. The effect of large doses of Synkavit in the newborn. Arch Dis Child 1956;31: 212-5 in, Ruby, C. Vitamin K: a historical perspective. MIDIRS 1997;7(3):362-4.
49. Mori P, Bisogni C, Odino S et al. (letter). Lancet 1977;ii:188.
50. Motohara K, Endo F and Matsuda I. Screening for late neonatal vitamin K deficiency by acarboxyprothrombin in dried blood spots. Arch Dis Child 1987;62:370-375.
51. Motz R. Late haemothorax after oral vitamin K. NZMJ 11 November 1992:459.
52. Muller A., van Doorm J and Hemker H. Heparin-like inhibitor of blood coagulation in normal newborn. Nature 1977;267:616-7.
53. New Ethicals Compendium; 3c: 303-304.
54. Nishiguchi T, Saga K, Sumimoto K. et al. Vitamin K prophylaxis to prevent neonatal vitamin K deficient intracranial haemorrhage in Shizuoka prefecture. Brit J Obstet Gynec 1996;103 (11):1078-84.
55. O'Connor M. and Addiego J. Use of oral vitamin K1 to prevent hemorrhagic disease of the newborn infant. J Pediatr 1986;108:616-9.
56. O'Connor M, Livingstone D, Hannah J. and Wilkins D. Vitamin K deficiency and breastfeeding. Am J Dis Child 1983;137:601-2
57. Olsen J, Hertz H, Blinkenberg K. et al. Vitamin K regimens and incidence of childhood cancer in Denmark. BMJ 1994;308(6933):895-6 in, Greenwood, R. Vitamin K and childhood cancer. MIDIRS 1994;4(3):258-260
58. Olson J. Recommended dietary intakes (RDI) of vitamin K in humans. Am J Clin Nutr 1987;45:687-92.
59. Parker L, Cole M, Craft A, Hey E. Neonatal vitamin K administration and childhood cancer in the north of England: retrospective case-control study. BMJ 1998;316:189-93.
60. Passmore S, Draper G, Brownbill P, Kroll M. Case-control studies of relation between childhood cancer and neonatal vitamin K administration: retrospective case-control study. BMJ 1998;316:178-84.
61. Passmore S, Draper G, Brownbill P, Kroll M. Ecological studies of relation between hospital policies on neonatal vitamin K administration and subsequent occurrence of childhood cancer. BMJ 1998;316:184-9
62. Pizer B, Boyse J, Hunt L. and Mott M. Neonatal vitamin K administration and in vivo somatic mutation. Mutat Res 1995;347:135-9.
63. Roche Products Ltd. Position statement re: Konakion injection given orally.
64. Roche Products Ltd. New oral vitamin K formulation for newborns (press release). Welwyn Garden City, 30 Aug 1996.
65. Ruby Christine. Vitamin K prophylaxis: a historical perspective. MIDIRS 1997;7(3):362-4.
66. Shearer M. et al. Plasma vitamin K1 in mothers and their newborn babies. Lancet 1982:460-3 in, Hathaway, W. New insights on vitamin K. Hematol Oncol Clin North Am 1987;1(3):367-379.
67. Stevenson, J. The vitamin K conundrum. Maternity Alliance Action Newsletter July/August 1992.
68. Suzuki H, Nakao T and Hiraga K. Vitamin K deficiency in male rats fed diets containing butylated hydroxytoluene (BHT). Toxicol Appl Pharmacol 1979;50:261-6 in, Birkbeck J. Vitamin K prophylaxis in the newborn: a position statement of the Nutrition Committee of the Paediatric Society of New Zealand. NZMJ 1988;101:421-2.
69. Townsend C. The hemorrhagic disease of the newborn. Arch Pediatr 1894;11:559-562 in, Birkbeck J. Vitamin K prophylaxis in the newborn: a position statement of the Nutrition Committee of the Paediatric Society of New Zealand. NZMJ 1988;101:421-2.
70. Tripp J. and McNinch A. Haemorrhagic disease and vitamin K. Arch Dis Child 1987;62:436-7.
71. Tripp J and McNinch A. The vitamin K debacle: cut the Gordian knot but first do no harm. Arch Dis Child 1998;79:295-299.
72. Vail, B. Vitamin K prophylaxis and hemorrhagic disease of the newborn. ICEA Review 1985;9(3).
73. Van Doorm J and Hemker H. Vitamin K deficiency in the newborn (letter). Lancet 1977;ii:708-9.
74. Van Doorm J, Muller A. and Hemker, H. Heparin-like inhibitor, not vitamin-K deficiency, in the newborn (letter). Lancet 1977;i:852-3.
75. Vietti T, Murphy T, James J and Pritchard J. Observations on the prophylactic use of vitamin K in the newborn. J Pediatr 1960;56(3);343-6 (abstract).
76. Von Kries R. Neonatal vitamin K prophylaxis: the Gordian knot still awaits untying. BMJ 1998;316 (7126):161.
77. Von Kries R, Göbel U, Hachmeister A. et al. Vitamin K and childhood cancer: a population based case-control study in Lower Saxony, Germany. BMJ 1996;313(7051):199-203.
78. Von Kries R, Hachmeister A and Göbel U. Repeated oral vitamin K prophylaxis in West Germany: acceptance and efficacy. BMJ 1995;310 (6987):1097-8.
79. Von Kries R, Kreppel S, Becker A, Tangermann R and Göbel U. Acarboxyprothrombin activity after oral prophylactic vitamin K. Arch Dis Child 1987;62: 938-40.
80. Von Kries R, Shearer M and Göbel U. Vitamin K in infancy. Eur J Pediatr 1988;147:106-12.
81. Waddell W. and Guerry D. The role of vitamin K in the etiology, prevention and treatment of hemorrhage in the newborn infant. J Ped 1939;15:802 in, Ruby, C. Vitamin K prophylaxis: a historical perspective. MIDIRS 1997;7(3):362-4.
82. Whipple G. Hemorrhagic disease; antithrombin and prothrombin factors. Arch Intern Med. 1913;12:637-641 in, Birkbeck, J. Vitamin K prophylaxis in the newborn: a position statement of the Nutrition Committee of the Paediatric Society of New Zealand. NZMJ 1988;101:421-2.
83. Zipursky A. Vitamin K at birth. BMJ 1994;313(1051):179-180.


HILARY BUTLER

Another Vit K injection connection: "ON PLACENTAS, STEM CELLS AND BREASTMILK"

http://www.beyondconformity.org.nz/_blog/Hilary%27s_Desk/post/On_placentas,_stem_cells_and_breastmilk/

The function of the placenta is an overlooked non-thought, because the medical system considers it redundant the minute a baby's head makes an appearance. Don't you think that strange, given that for nearly nine months, the placenta has provided nutrients, oxygen and... stem cells to the baby? This magnificent organ provides an amazing service, which is utterly abused, particularly when it comes to ... multipotent and lineage-committed stem cells. That the placenta contains stem cells should present no surprises to anyone. After all, where do the medical profession think stem cells come from? Thin air? Perhaps they "just appear" and are unique to, a developing embryo? Nope. Cord blood from the placenta, has been described as the baby's first natural stem cell transplant. Which is why anyone who understands placental physiology would never clamp a cord. So why do they? And we also also know that one of the consequences of immediate cord cutting, is brain ischaemia, which can cause brain damage for life.

But we're dealing with a system which appears to be functionally illiterate, yet loves dramatic solutions fit for TV dramas,.... so.... wouldn't you know it. ... ? Drum roll here.... A flurry of medical articles this year, has shown that administration of stem cells can treat neonatal ischemic brain damage! (click on this link, and then click on related articles to see the others). And of course, it will have to be... injected!

Is this why obstetricians are so enthusiastic about cord blood banking?

Because... they need a commercial source of a compound to fix the mistakes they make by immediately clamping the cord and depriving the baby of a natural bolus of those same stem cells?

Isn't it time the medical system came to terms with the fact that the placenta, which makes those pluripotent stem cells, AND provides oxygen and nutrient to the in-utero baby all that length of time..., doesn't need to be immediately amputated from the baby, when it still has a job to do?

This stem cell bolus transplant that the baby will get at birth is there for a very good reason.

What might that be?

Simple.

Any foetus which gets being wrung out like a wet towel while travelling down a narrow drain pipe, can incur damage in any part of the body, including in the brain, and needs an in-built fix-it. And stem cells cross the brain blood barrier. In fact, stem cells can go ... anywhere!!! Amazing don't you think. God's design has solutions for situational problems. Three solutions, actually. The second is the fact that naturally, in the first few days, a baby's blood clotting factors are lower than normal.

But ... paediatricians consider this a ... "defect" ... so want to give vitamin K which results in blood nearly 100 times thicker than an adult's. This vitamin K injection, so they say ... (like they say immediate cord clamping is safe, and normal, and delayed cord clamping is an unproven intervention) ... is because the baby wasn't designed right, and if you don't give a vitamin K injection, the baby "could bleed to death".

It's not for nothing that the vitamin K syringe, sits right alongside that cord clamp and the scissors!

But there is an unanswered question: "Why are blood clotting factors in babies low in the first few days after birth? Why has a baby got much thinner blood as a result?"

Might a logical hypothesis be, that thinner blood allows freer and quicker access of cord blood stem cells to any part of the body damaged during birth? After all, why should stem cells have to fight through a baby's blood which is now 100 times thicker than any adult's, courtesy of another needle?

Seemingly, these doctors think that stem cells should be injected into babies, but I note that none of the baby animals used in these experiments, were ALSO given vitamin K injections at birth as well! .... Other experiments injected the cells directly into the brain, ... which sounds much more "efficient", and much more dramatic. Much more "life saving"! And what with boys and toys, might well become the preferred solution, all in the name of being the white knight on a silver steed, huh?

However, these stem cells don't need to be injected. If they can migrate across the brain blood barrier, after being injected into the stomach of rats, they can cross the human blood brain barrier, after being naturally infusing down the unclamped umbilical cord, into the baby's stomach, during which time the obstetrician holds the door frame up while warming hands in pockets!

Of course, God's solutions don't just stop there. To cover all options for "treatment" of a wrung out baby, for however long a mother breastfeeds, her baby drinks lots of stem cells in breastmilk. Talk about multi-route brilliant, natural solutions... which the medical system didn't think of, and which has served to populate this world very successfully in the past.

So why don't obstetricians explain to mothers WHY the best and safest way for healthy mothers to give birth is, vaginally - with the cord not clamped until it's shrivelled hard and dry, (and then only to keep the obstetrician happy) and that mothers should breastfeed for a long time?

Problem is, if all mothers do this, some obstetricians might have to get a new job.

Oh yeah, and cut out the vitamin K injection as well. If your diet during pregnancy is right, your baby will not have a problem. After all, we survived very well before the vitamin K injection came along with the clamp and the scissors, didn't we?

Perhaps one day, some scientist will come along with an elegant, blindingly obvious physiological reason as to why babies blood shouldn't be thicker than normal in the first little while after birth!

Don't let anyone in the medical system tell you that immediate cord cutting is safe, your baby has a natural vitamin K deficiency, or that formula is healthy and a superb" breast milk equivalent", because that just ain't so.

Formula might save a life, but it certainly won't provide all the various immune enhancements and in-built "fix-its" that breastmilk can.

And on that note, don't you think it strange that many third world countries run efficient breastmilk banks, but you won't even find one, in a by-pass called New Zealand? How pathetic is that?


Gopakumar H, Sivji R, Rajiv PK. Vitamin K deficiency bleeding presenting as impending brain herniation. J Pediatr Neurosci [serial online] 2010 [cited 2012 Apr 15];5:55-8. Available from: http://www.pediatricneurosciences.com/text.asp?2010/5/1/55/66681

While there seems to be important reasons not to automatically inject vit K in newborns, this article explains how and why normal, timely Vit K production by bacteria that takes place in an infant's gut can be damaged by drug treatment. --djt

Abstract

It is presently a universal practice to administer vitamin K at birth. Hence, the serious bleeding manifestations from vitamin K deficiency are nowadays very rare. We describe a case of late vitamin K deficiency bleeding presenting as intracranial hemorrhage with impending coning and the related review of literature. Such severe bleeding episodes due to vitamin K deficiency are associated with multiple cranial involvement and impending brain herniation is probably rare.

Introduction


A 2-month-old male child was admitted with history of excessive cry and lethargy of two days and poor feeding of one day duration. Baby also had abnormal posturing of limbs and asymmetry of eye opening since one day. Parents had noticed progressive pallor over the previous two days. They attributed the complaints to a history of insect bite on thighs two days back for which the child received supportive treatment from a nearby hospital. There was no history of fever or head trauma. There was no significant past illness.

In view of abnormal posturing and progressive pallor, baby was referred to our hospital. Baby was born to a primi mother by emergency LSCS, indication being cephalopelvic disproportion. Baby cried soon after birth. Immediate postnatal period was uneventful. Baby was exclusively breast fed from birth. Mother was not sure whether vitamin K was administered at birth.

At the time of admission in our hospital, baby had irritable cry with intermittent decorticate posturing. He had severe pallor. There were no obvious bleeding manifestations. There was no icterus. Anterior fontanel was bulging and non pulsatile. There were frequent episodes of bradycardia with high blood pressure and irregular respiration. Capillary refill time was less than 2 sec. Detailed neurological examination revealed facial asymmetry, right sided ptosis with ipsilateral dilated pupils. Findings were consistent with right sided third nerve palsy with uppermotor neuron facial palsy. Tone was increased in all four limbs with exaggerated deep tendon reflexes.

Blood investigations showed unduly prolonged PT, APTT with no detectable clot. Other blood investigation showed hemoglobin value of 4.62 gm%, Hematocrit - 12.5%, total count - 21, 000 / cmm, C Reactive protein - 15 mg / l, Serum creatinine - 0.43 mg / dl, SGPT - 29.6 mg / dl, SGOT - 48.8 mg / dl, alkaline phosphatase - 408. 3, serum bilirubin - 1.6 mg / dl (direct - 0.8 mg / dl), serum albumin - 4.3 gm/dl, serum globulin - 2.3 gm/dl, protein - 6.6 gm/ dl, serum sodium - 133 meq / dl, serum potassium - 5.1meq/dl plasma urea - 32 mg / dl, serum calcium - 9.3 mg / dl, platelet count - 7.11 lakhs / cmm, differential count (neutrophills - 54.9%, lymphocytes - 37.1, monocytes - 6.71%, eosinophills - 0.013% and basophils - 1.25%) plasma fibrinogen activity - 387

In view of prolonged prothrombin time and APTT in an otherwise well child, the possibility of late onset vitamin K deficiency bleeding was considered. He was administered 15 ml / kg of fresh frozen plasma and vitamin K with which PT, APTT and INR improved dramatically (13.6 / 14.6, 26.6 / 32.2 and 0.92 respectively), further confirming our diagnosis. Packed cell transfusion was also given in view of clinically significant anemia.

Initial CT scan [Figure 1] and [Figure 2] showed extensive acute subdural hemorrhage involving the right convexity (frontoparieto occipital region). Blood fluid level was noted in the right frontal subdural bleed, suggestive of acute on chronic bleed. Subdural hemorrhage was also noted along the inter hemisphere fissure. Right tentorial subdural hemorrhage was also seen. Subdural hemorrhage was also noted in left frontal region with blood fluid level. The right lateral ventricle was completely effaced with midline shift of 1.02 cm. The suprasellar and ambient cistern were effaced, suggestive of bilateral uncal herniation.

A diagnosis of late onset vitamin K deficiency causing bilateral subdural hemorrhage with attendant uncal herniation clinically manifested as right third nerve palsy and left hemiparesis was made. Subdural hematoma was more on right than left.

Seizures were controlled with phenobarbitone, phenytoin and midazolam. Baby was electively intubated and measures to decrease intracranial pressure were given.

Baby was taken up for emergency drainage of subdural bleed under cover of mannitol. A right Frontotemporoparietal craniotomy and evacuation of SDH with lax duroplasty was done. Peroperative findings included very tight brain, with various ages of clot. Brain was bulging out of the craniotomy due to excess tension. Pulsation was very feeble. Sub dural membrane was adherent with dura mater and brain surface in few areas. A left extraventricular drainage was also placed.

Underlying brain was found to be friable. External ventricular drainage with intracranial pressure monitoring was continued postoperatively. The preoperative findings suggested that baby had minor episodes of bleeding previously as well, which was not severe enough to cause clinical manifestations.

In the initial 48 h, intracranial pressure was very high with continuous draining of CSF through external ventricular drainage. Child also had uncontrolled focal seizures that required midazolam infusion and muscle relaxants.

After 48 h, intracranial pressure came down. External ventricular drainage was minimal. Baby was free of seizures, right ptosis improved and pupils were equal and reactive bilaterally. His conscious level improved. Neurosonogram was repeated which showed no midline shift. Repeated CT scan [Figure 3] showed small amount of persisting subdural bleed. There was no midline shift. PT and APTT repeated twice were reported normal.

Baby was extubated on sixth postoperative day. External ventricular drainage was removed. Feeds was started and increased as per tolerance to full feeds. Baby was discharged on fourteenth postoperative day. At the time of discharge, baby was active and feeding well. Pupils were equal and reactive bilaterally. There was mild facial asymmetry with left sided hemiparesis. There were no further episodes of seizures. Baby is kept on regular neurodevelopmental follow up.


Discussion


Vitamin K is a fat soluble vitamin essential for the synthesis of functional prothrombin, factor VII, factor IX and factor X in the liver. Because of the short half-life of these factors, and the small amounts of vitamin K that can be stored in the body, inadequate intake of vitamin K can result in deficiency in a short period of time. PIVKA, inactive precursor proteins induced in vitamin K absence, are measurable and can be used as an indicator of vitamin K deficiency.

Vitamin K deficiency can occur in persons of any age. Infants are at higher risk for hemorrhagic disease of newborn, caused by a lack of vitamin K reaching the fetus across the placenta, the low level of vitamin K levels in breast milk, immature liver and low colonic bacterial synthesis.

The bleeding manifestations associated with vitamin K deficiency can occur in three general time frames. Early onset vitamin K deficiency bleeding that occurs less than 24 h after birth is rare and is almost always associated with maternal medications that interfere with vitamin K metabolism. The various drugs include anticonvulsants, anticoagulants, and antibiotics. Postnatal administration of vitamin K has no effect in preventing early-onset disease. Vitamin K supplementation to at risk mothers, administered prenatally may prevent this form of vitamin K deficiency bleeding.

The classic onset of vitamin K deficiency bleeding occurs between second and seventh day after birth in breastfed infants. Clinical manifestations include bleeding in to the skin or from mucosal surfaces, circumcision, or venipuncture sites. [1]

Late-onset vitamin K deficiency bleeding occurs two weeks after birth. It can, however, occur as late as 3 months postpartum. In addition to breastfeeding, risk factors include diarrhea, hepatitis, cystic fibrosis (CF), celiac disease, and alpha - 1-antitrypin deficiency or absence of prophylaxis in otherwise healthy infants. Late-onset vitamin K deficiency bleeding tends to be more severe than early-onset or classic disease and has a high frequency of intracranial hemorrhage. Intracranial hemorrhage is observed in more than 50% of infants with late-onset disease.

Almost all neonates are vitamin K deficient, presumably as a result of deficient vitamin K nutrition in the pregnant mother during the third trimester and because of the lack of colonization of the colon by bacteria that produce vitamin K in the neonate. [2] However, this deficiency is further aggravated in some patients by inadequate dietary intake of vitamin K. This disorder is more prevalent in breast-fed babies, as human milk, in contrast to cow's milk, contains only 15 µg/l of vitamin K. [3]

The risk of vitamin K deficiency bleeding in babies whose mothers are exposed to anticonvulsants during pregnancy appears to be because of competitive inhibition of the synthesis of the calcium-binding gamma-carboxyglutamic acid residues to the precursors of the clotting factors II, VII, IX, and X and by the induction of fetal microsomal enzymes, which degrade vitamin K. The pattern of the bleeding in anticonvulsant-exposed newborn infants differs from hemorrhagic disease of unexposed infants: the bleeding occurs earlier, often within the first hours of life; the extent of the hemorrhage is greater; the sites of the bleeding are different and include intrabdominal, intracranial, and intrathoracic locations. [4] Supplementation with vitamin K, 10 mg/day during the last month of pregnancy, has been recommended by the American Academy of Neurology. [5] Other drugs implicated to cause the deficiency in newborns include maternal intake of oral anticoagulants and large doses of aspirin.

Malabsorption syndromes are commonly associated with vitamin K deficiency. Defects in the enterohepatic circulation because of biliary disease interfere with absorption of fat-soluble vitamins in the ileum. Primary biliary cirrhosis, cholestatic hepatitis, and other causes of cholestasis can lead to impaired absorption of vitamin K. Furthermore, intestinal malabsorption, as in sprue or regional enteritis, impairs vitamin K use. Older adults also have evidence of mild vitamin K deficiency, presumably because of intestinal malabsorption. [6]

Bacteria in the large intestine produce functional forms of vitamin K. In the absence of dietary vitamin K, small amounts of vitamin K in the large intestine are absorbed passively and prevent severe vitamin K deficiency. This source is eliminated in patients who are on antibiotics, that deplete the intestinal flora capable of vitamin K synthesis. Thus, a common setting of vitamin K deficiency is the case of a patient with inadequate or minimal dietary intake, who is also on treatment with antibiotics.

This form of vitamin K deficiency occurs within 1 to 3 weeks, after depletion of body stores of vitamin K.

Neonates with vitamin K deficiency have a prolonged prothrombin time and partial thromboplastin time (PTT). However, it is critical to distinguish whether the prolongation of these parameters is a manifestation of the deficiency of the vitamin K-dependent proteins because of vitamin K deficiency or to decreased synthetic capacity of the liver in newborns. Elevation of the abnormal (des-?-carboxy) prothrombin (PIVKA-II) antigen level is indicative of vitamin K deficiency, as this form of prothrombin appears only when post-translational modification is impaired but not when protein synthesis is impaired. We could not do this test in our baby due to lack of facility for the same. Liver function tests done to rule out any liver pathology causing vitamin K deficiency was reported negative.

A confirmed case of VKDB should fulfill the diagnostic criteria of having a PT that is >4 the control value and display at least one of the following: (1) Normal or raised platelet count, normal fibrinogen and absent fibrin degradation products. (2) PT returning to normal after VK administration. (3) PIVKA (usually that of factor II) level exceeding normal controls. A probable case of VKDB is defined as one in which the PT and APTT are abnormal for age and one of the three extra criteria listed above is present. [7] Recently, the British Paediatric Surveillance Unit (BPSU) for their current survey (October 2006-2008) have provided a simplified definition for vitamin K deficiency bleeding 'Any infant under six months of age with spontaneous bruising/bleeding or ICH associated with prolonged clotting times (PT at least twice control value) and normal or raised platelet count, NOT due to an inherited coagulopathy or disseminated intravascular coagulation'. Our case satisfies this definition of prolonged prothrombin time along with a raised platelet count.

Administration of vitamin K (100 µg) corrects the deficiency state and usually does not need to be repeated in the otherwise healthy infant. In our patient, a single injection of vitamin K normalized the coagulation parameters. In practice, deficiency of vitamin K is confirmed by showing that the prolonged prothrombin time is rapidly corrected in 6 to 24 h after parenteral administration of Vitamin K

Vitamin K (100 µg to 1 mg) is administered intramuscularly to the newborn immediately after birth. At these doses, vitamin K administration carries little morbidity and can prevent hemorrhagic disease of the newborn.

The approach to the treatment of vitamin K deficiency depends on the clinical setting and the severity of bleeding. Except in the face of serious internal bleeding, reversal of the vitamin K deficiency by the administration of vitamin K is generally adequate. If there is no hepatic dysfunction, its administration is followed by an increase in prothrombin time above the minimal level required for hemostasis within 3 to 4 h, and usually a return to normal in about 24 h. The response to treatment should be determined in all cases by repeating the prothrombin time test 24 h after commencement of treatment.

If the prothrombin time (PT) is significantly prolonged to indicate that a bleeding complication may be induced by intramuscular injection, this route should be avoided. Because the delivery of vitamin K by the subcutaneous route is variable, intravenous administration of vitamin K 1 is the recommended approach, as it ensures rapid delivery. However, intravenous administration of vitamin K1 does require monitoring, because of certain reports of severe allergic reactions. Care must be given to initiate rapid reversal of an untoward reaction.

Serious bleeding complications attributed to vitamin K deficiency, such as intracranial bleeding, must be reversed immediately. Despite the rapid action of vitamin K, administration of vitamin K should be preceded by the infusion of fresh frozen plasma. This blood component contains all the vitamin K-dependent clotting proteins. In sufficient quantities, fresh frozen plasma can correct, or nearly correct, the PT, as well as the bleeding tendency.

Patients with vitamin K deficiency without bleeding manifestations can be treated with oral vitamin K or, as in patients with chronic vitamin K deficiency secondary to malabsorption syndromes, with subcutaneous vitamin K.


References

1. American Academy of Pediatrics. Committee statement, Committee on Nutrition. Vitamin K supplementation for infants receiving milk substitute infant formulas and for those with fat malabsorption. Pediatrics 1972;48:483-7. Back to cited text no. 1
2. Shearer MJ, Rahim S, Barkhan P, Stimmler L. Plasma vitamin K1 in mothers and their newborn babies. Lancet 1982;2:460-3. Back to cited text no. 2 [PUBMED]
3. Keenan WJ, Jewett T, Glueck HI. Role of feeding and vitamin K in hypo- prothrombinemia of the newborn. Am J Dis Child 1971;121:271-7. Back to cited text no. 3 [PUBMED]
4. Moslet U, Hansen ES. A review of vitamin K, epilepsy andpregnancy. Acta Neurol Scand 1992;85:39-43. Back to cited text no. 4 [PUBMED]
5. Practice parameter: management issues for women with epilepsy (summary statement). Report of the Quality Standards Subcommittee of the American Academy of Neurology. Epilepsia 1998;39:1226-31. Back to cited text no. 5 [PUBMED]
6. Krasinski SD, Russell RM, Furie BC, Kruger SF, Jacques PF, Furie B. The prevalence of vitamin K deficiency in chronic gastrointestinal disorders. Am J Clin Nutr 1985;41:639-43. Back to cited text no. 6 [PUBMED] [FULLTEXT]
7. Cornelissen M, von Kries R, Loughnan P, Schubiger G. Prevention of vitamin K deficiency bleeding: efficacy of different multiple oral dose schedules of vitamin K. Eur J Pediatr 1997;156:126-30.


http://www.springerlink.com/content/ajfny9uvp5v9j3m4
Annals of Hematology
Volume 75, Numbers 1-2 (1997), 65-66, DOI: 10.1007/s002770050314

Published in partnership with GTH, DGHO, and OeGHO

CASE REPORT
Late hemorrhagic disease of the newborn as a cause of intracerebral bleeding

P. Solves, A. Altés, G. Ginovart, J. Demestre and Jordi Fontcuberta

Abstract

We report a case of a 4-week-old female who presented with late hemorrhagic disease of the newborn (HDN). The newborn was previously healthy, and she received 1 mg of intramuscular vitaminK at birth. She was exclusively breast-fed. At 4 weeks she began bleeding at the umbilicus and 4 days after she suffered an intracranial hemorrhage. Coagulation studies showed a deficiency of vitamin K-dependent coagulation factors, and the normalization of all clotting studies after administration of vitamin K confirmed the diagnosis of HDN. Our conclusions are that physicians must be alert to mild bleeding in newborns and that prophylaxis with 1mg of intramuscular vitamin K at birth may be insufficient to prevent late HDN.


Dianne Jacobs Thompson  Est. 2007
Also http://truthquest2.com (alternative medicine featuring drugless cancer treatments)
Author publication: NEXUS MAGAZINE "Seawater--A Safe Blood Plasma Substitute?"