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Refusal of intramuscular Vitamin K at birth is an emerging public health issue resulting in increased rates of intracranial bleeding. Parents who refuse this intervention bear epidemiologic resemblance to vaccine-refusing parents, are geographically clustered and share a mistrust of public health interventions. We review the prevalence of Vitamin K refusal and discuss individual and societal recommendations that may reduce Vitamin K refusal, adapted from vaccine hesitancy literature. We note the prevalence of misinformation on social media as a contributor to refusal and explore how changes in healthcare practices may influence growing physician mistrust. We propose solutions to the issue including state-based mandates and a pervasive social media strategy to combat misinformation as a contributor to Vitamin K refusal.

We describe a 5-week-old infant who presented in cardiac arrest and was later found to have intracranial hemorrhage due to late vitamin K deficiency bleeding. The infant had not received vitamin K prophylaxis following a home birth. Because of worsening direct hyperbilirubinemia and transaminitis, she was subsequently found to have biliary atresia. This case allows us to review the differential diagnosis of intracranial hemorrhage in infants and underscores the importance of considering whether infants presenting with any source of bleeding had received vitamin K prophylaxis. As refusal of vitamin K prophylaxis has increased in the United States over the last decade, pediatricians now play an increasingly vital role in promoting strong adherence to universal prophylaxis for newborns in their practice.

Objectives: To describe rates of newborn vitamin K prophylaxis uptake according to method of administration (intramuscular [IM], oral, refused) and identify predictors for the choice of oral administration and for refusal of vitamin K prophylaxis. Methods: A retrospective cohort study examined the relationship between method of vitamin K administration and various exposure factors (infant, maternal, socio-demographic and healthcare professional). Written and electronic data for births from a single tertiary birthing unit in New Zealand (NZ) were examined over a four-year period from January 2009 to December 2012. Results: Records for 7,089 mothers/babies were examined. Of these, 92.9% of infants received IM and 5.4% oral vitamin K. Refusal of vitamin K was associated with (OR [95%CI]): Asian ethnicity (5.87 [3.61 to 9.53] p

Background Infants may present to the emergency department (ED) with vague complaints worrisome to parents and may initially appear well, despite serious underlying pathology. Whereas sepsis and nonaccidental trauma are high on most providers' diagnostic considerations, we report a case representative of a worrisome trend secondary to the refusal of parenteral vitamin K at birth leading to significant neurologic sequelae. Case Report A 10-week-old boy presented to the ED with gradual increase in fussiness for 2 weeks and new onset of blood flecks in the stool on the day of presentation. Careful physical examination revealed a pale-appearing infant, leading to diagnostic evaluation demonstrating profound anemia and intracranial bleeding. The patient was diagnosed with late-onset vitamin K-deficient bleeding (VKDB) secondary to parental refusal of the vitamin K shot at birth. Why Should Emergency Physicians be Aware of This? Emergency Medicine providers need to add this serious treatable disease into their diagnostic consideration for fussy infants, infants with unexplained bruising or bleeding, or infants with new-onset seizures. Rapid identification of VKDB can lead to prompt treatment and halt the rapid progression of symptoms. Emergency Medicine providers should ask all parents if their infant received parenteral vitamin K in the newborn period, especially if they are exclusively breastfed or born out of the hospital.

Doctor Parviz Lalezari, currently a clinical professor of Medicine and Pathology at Albert Einstein College of Medicine in New York, describes highlights of his research career since 1958. He became the director of the blood bank at Montefiore Hospital in New York City in 1961, director of the Division of Immunohematology until 1996, and then until 2001, was President and chief executive officer of the Bergen Community Regional Blood Center in New Jersey. Doctor Lalezari was born in Iran in 1931, and after graduation from Medical School, he came to the United States in 1956. His initial research was on leukocyte antibodies. After modifying the available antibody detection techniques, he discovered that like hemolytic disease of the newborn and neonatal immune thrombocytopenia, fetal-maternal neutrophil incompatibility can cause neonatal neutropenia. He identified the targets of these antibodies and showed that they were expressed only on peripheral blood neutrophils. Doctor Lalezari also discovered that a common form of neutropenia in early childhood was caused by development of autoantibodies, which surprisingly were directed against the same neutrophil-specific antigens involved in fetal-maternal incompatibility. In 1959, a heparin-neutralizing drug (Polybrene) was introduced to be used after open-heart surgery. Lalezari discovered that Polybrene, a quaternary ammonium polymer, reacted with sialic acid molecules on the red blood cell (RBC) surface, causing the RBCs to aggregate. Later, realizing that the repelling forces generated by the RBC surface membrane charges were responsible for failure of the small IgG antibody molecules to agglutinate the RBCs, he used Polybrene to neutralize the RBC surface negative charge to allow the IgG antibody molecules to induce hemagglutination. This became The Polybrene test, which is to be used in RBC antibody detection.

Deficiency of vitamin K predisposes to early, classic or late hemorrhagic disease of the newborn (HDN); late HDN may be associated with serious and life-threatening intracranial hemorrhage. Late HDN is characterized by intracranial bleeding in infants aged 1 week to 6 months due to severe vitamin K deficiency, occurring particularly in exclusively breastfed infants. Late HDN is still an important cause of mortality and morbidity in developing countries where vitamin K prophylaxis is not routinely practiced. In this study, we report on two siblings with intracranial bleeding who were fully breastfed without a routine supplementation of vitamin K. Vitamin K should be given to all newborns as a single, intramuscular dose of 1 mg. (c) 2006 Elsevier Inc.

Haemophilia A and B are the most common of the inherited bleeding disorders. Haemophilia in the newborn presents a number of challenges in terms of both diagnosis and management which reflect features unique to this age group. In the presence of a family history of haemophilia optimal management requires close co-operation between three individual specialist groups - obstetricians, haematologists and neonatologists, who each have an important role to play in ensuring a safe outcome for these infants. More problematic is where a family history is absent or has not been adequately elucidated in which case the diagnosis of haemophilia in the neonate will be unsuspected. Diagnostic difficulties may then arise due to failure to recognise the presence of abnormal bleeding, which is often different from that typically observed in older children with haemophilia. In addition, diagnostic investigations are complicated by physiological differences in the neonatal haemostatic system. Although major bleeding is relatively uncommon, the incidence of intracranial haemorrhage is higher during the first few days of life than at any other stage in childhood, which relates to the trauma of delivery. Controversy, however, remains on optimal strategies for both prevention and management of this potentially devastating complication.

Hemorrhage in neonates and infants is a life-threatening emergency. Vitamin K deficiency is a common cause for neonatal bleeding. American Academy of Pediatrics (AAP) recommends routine administration of vitamin K to all neonates to prevent bleeding. We report a case of an infant who was brought with bleeding from site of vaccination. The infant had received prophylactic vitamin K at birth. There were no predisposing illnesses like liver disease and malabsorption. Occurrence of late vitamin K Deficiency Bleeding (VKDB) even after vitamin K dose in a healthy infant and its sole manifestation as bleeding from injection site are rare and hence are reported in this case. He improved on treatment with vitamin K and fresh frozen plasma (FFP). a r t i c l e i n f o

Newborn care in the first 24 hours of life has been based on tradition for many years. Nurses recognize that many practices are not based on good scientific evidence and are not individualized. Instead, all newborns are treated as though they acquire potential pathogens during birth and are oblivious to noxious interventions such as intramuscular injections and heel sticks. In this article, obtaining blood samples from heel sticks and administering vitamin K and prophylaxis for ophthalmia neonatorum are presented as practices that require scrutiny by nurses to promote evidence-based care of newborns in the 1st day of life.

At the start of the 20th century the mechanisms of haemostasis were virtually unknown. Townsend had coined the term 'Haemorrhagic disease of the newborn' in 1894 but it was not until the discovery of vitamin K ('Koagulation vitamin') by Dam and others in the 1930s that the condition became understood, allowing treatment and prophylaxis. Methods of prophylaxis (preparations used, doses and routes of administration), still widely debated, have varied with time and from one country to another. The formation of the British Paediatric Surveillance Unit in the 1980s has allowed a series of prospective population studies of Vitamin K deficiency bleeding (VKDB) in the United Kingdom (UK) and Ireland which, together with contemporaneous surveys of practices of vitamin K prophylaxis, have greatly improved our understanding of the condition and informed practices of prophylaxis. In the UK prophylaxis (by injection or by mouth) is now offered to every newborn baby and VKDB is very rare, most cases occurring in breastfed babies whose parents have refused prophylaxis; by contrast, in developing countries most babies do not receive prophylaxis and VKDB is probably a common (but poorly documented) cause of death and handicap in the early months of life. Vitamin K prophylaxis should be available to all newborn babies.

Certified nurse-midwives, whose responsibility includes care of the newborn in the first days of life, should be well versed in the commonly used pharmaceutical preparations in the neonatal period. This article reviews therapeutic uses and the pharmacodynamics of vitamin K, as well as the neonatal eye preparations for prophylaxis of infections (silver nitrate, tetracycline, and erythromycin ophthalmic ointments). Preparations used in caring for the umbilical cord, as well as the commonly prescribed antibiotics ampicillin and gentamicin, are discussed. The narcotic antagonist naloxone is also reviewed, along with commonly used medications for colic and thrush. The etiology and clinical conditions that require the application of these medications are considered.

4. Ascher DP, Wilson S, Fischer GW. Comparison of bacteremia and antigen detection in a neonatal group B streptococcal sepsis model [Abstract 1602]. Society for Pediatric Research. Anaheim, Calif., May 6-11, 1990. 5. Harris MC, Deuber C, Polin RA, et al. Investigation of apparent false-positive urine latex particle agglutination tests for the detection of group B streptococcal antigen. J Clin Microbiol 1989;27:2214-7. 6. Morris B, Morris R. Macromolecular uptake and transport by the small intestine of the suckling rat. In: Hemmings WA, ed. Antigen absorption by the gut. Lancaster, United Kingdom: MTP Press, 1978:23-30. 7. Roberton M, Paganelli R, Dinwiddie R, Levinsky RJ. Milk antigen absorption in the preterm and term neonate. Arch Dis Child 1982;57:369-72. 8. Vukavic T. Timing of gut closure. J Pediatr Gastroenterol Nutr 1984;3:700-3. 9. Courcal R J, Roussel-Delvallez M, Puech F, Delecour M, Martin GR. Bacteriological analysis of amniotic fluid. Biol Neonate 1982;42:166-73.

A man presented to the emergency department on his 89th birthday in early 2013 with 2 days of persistent bleeding from a minor scalp laceration sustained during a mechanical fall at home. He had undergone elective carpal tunnel release surgery 1 week before, which was followed by progressive swelling and bruising of the left hand. He had a history of idiopathic bile acid malabsorption diagnosed on selenium homocholic acid tauroselcholic acid (SeHCAT) scan, and was taking cholestyramine and vitamin D replacement but no other medication. On examination he had no bleeding from any site other than the scalp wound. CT head showed no intracranial bleed. Blood tests showed anaemia with a polychromatic fi lm, in keeping with haemorrhage. Platelet count and white cell count diff erential and morphology were normal. The prothrombin time (PT) was long (>180 s; normal 12·5 –15·1 s), as was the activated partial thromboplastin time (APTT) (132·5 s; 23·0–37·0 s). Thrombin time (TT) was normal. A 50:50 mix of normal plasma with patient plasma corrected APTT to normal, in keeping with clotting factor defi ciency rather than an inhibitor or lupus anticoagulant. We diagnosed vitamin K defi ciency, stopped the patient’s cholestyramine, and started 10 mg intravenous vitamin K immediately, then daily for three consecutive days. In view of the active bleeding we gave one dose of prothrombin complex concentrate (PCC) 30 units/kg (composed of the vitamin K dependent clotting factors II, VII, IX, and X in a lyophilised, virally inactivated formulation) and 2 units of packed red cells for symptomatic anaemia. Repeat coagulation studies taken 20 min after PCC showed PT and APTT were normal. Bleeding stopped immediately after PCC treatment, and the patient was discharged home 5 days later. Vitamin K defi ciency was confi rmed by severe defi ciency of clotting factor II (2%; normal 50–200%), factor VII (3%; 50–200%), factor IX (6%; 50–200%), and factor X (1%; 50–200%), with preserved clotting factors V, VIII, XI, and XII. Protein Induced by Vitamin K Absence II (PIVKA-II) was greater than 10 au/mL (normal 0·0–0·2 au/mL), in keeping with vitamin K defi ciency. The patient was also defi cient in fat soluble vitamin A (0·90 umol/L; 1·40–3·84), but not vitamin E or D. We prescribed watersoluble oral vitamin K replacement (menadiol sodium phosphate) to prevent further episodes of bleeding, which the patient is still taking. At last follow-up in May, 2014, he remains well, without symptomatic bleeding and with normal PT and APTT. Vitamin K is necessary for the hepatic synthesis of coagulation factors II, VII, IX, and X. Its importance in haemostasis was identifi ed by Danish scientist Henrik Dam in 1929. Investigating the role of cholesterol by feeding chickens a cholesterol-depleted diet, he noticed that chickens kept on this diet developed bleeding. He attributed the bleeding to defi ciency of a vitamin, which he named “Koagulationsvitamin”, later shortened to “vitamin K”. Vitamin K is a fat soluble vitamin, absorbed in the terminal ileum, and is dependent on functioning villi, bile acid, and fat absorption. Cholestyramine is a bile acid sequestrant used in the management of bile acid malabsorption. Both bile acid malabsorption and cholestyramine can be associated with vitamin K defi ciency. “Haemorrhagic disease of the newborn” (now called vitamin K defi ciency bleeding), has been reported since the late nineteenth century. Vitamin K prophylaxis for neonates, recommended since the 1960s, is supported by a Cochrane review. The UK national programme of vitamin K replacement at birth is associated with a decrease in the incidence of vitamin K defi ciency bleeding, most importantly intracranial haemorrhage, with associated improvements in perinatal mortality, and short-term and long-term morbidities (1·2 to 1·8 per 100 000 births). In patients with bile acid malabsorption and those taking c holestyramine, defi ciency of all fat soluble vitamins (K, A, D, and E) should be considered and replaced appropriately.

The objective of this cohort study of a consecutive sample of infants exposed during pregnancy to anticonvulsant drugs was to determine if the mother received late pregnancy prophylaxis with vitamin K, and if any infants had signs of hemorrhagic disease. The medical records of 204 neonates exposed to anticonvulsant drugs in utero and 77 unexposed control neonates were retrospectively reviewed. No hemorrhagic disease was observed, and the incidence of bleeding tendencies was not higher in infants exposed to these drugs compared with control infants, despite no prenatal vitamin K supplementation in all but 1 epileptic woman.

THE TERM "hemorrhagic disease of the newborn" was first used in 1894 when Townsend ~ reported 50 infants with bleeding during the first two weeks of life. The hemorrhage usually began on the second o? third day of life and most commonly was from the gastrointestinal tract. The observation that this disorder was self-limiting led Townsend to differentiate acquired hemorrhagic disease from inherite d hemophilia. Vitamin K was not discovered until 1929 when Dam 2 serendipitously observed bleeding in chickens fed a fat-free diet. Soon afterward, Brinkhous et al. 3 documented low prothrombin levels in normal newborn infants. Others demonstrated that these low levels could be elevated by the administration of vitamin K. 4,5 Hemorrhagic dise~e caused by vitamin K deficiency was subsequently differentiated from bleeding secondary to other causes, 6, 7 and the effectiveness of vitamin K administration in the prevention of vitamin K-deficiency bleeding was established? .9 In 1961 the Committee on Nutrition of the American Academy of Pediatrics 9 reviewed the role of vitamin K in the newborn period. The Committee suggested that HDN be defined as a "hemorrhagic disorder of the first days of life caused by a deficiency of vitamin K and characterized by deficiency of prothrombin and proconvertin and probably of other factors?' It recommended that prophylactic

Hypoprothrombinemia occurs in newborn infants, but it is unclear whether this is the result of reduced production of Factor II precursor or a vitamin K deficient state. In this study, 76 cord blood specimens were analyzed for functional factor coagulant activity and levels of Factor II antigen as determined by electroimmunoassay. In 40 normal term infants, CA = 30% +/- 1.6 (mean +/- SEM) and Ag = 44% +/- 2.3; in 17 normal preterm infants CA = 30% +/- 1.0 and Ag = 31% +/- 4.2; and in 50 normal adults CA = 83 +/- 3 and Ag = 91 +/- 4. In the term infants the average ratio of CA:Ag was 0.90 and in the preterm infants 0.96, both values being similar to those in adults and suggesting underproduction of the precursor form. In 19 term infants who experienced complications of pregnancy and/or delivery, the ratio was 0.76; seven of these ratios were less than 0.70 (range 0.40 to 0.69). These data show that hypoprothrombinemia is common in infant cord blood and is most marked in preterm infants. In the normal infants the CA:Ag ratios were normal, suggesting that the hypoprothrombinemia is the result of reduced production of the protein and not of vitamin K deficiency. However, term infants with complications of labor and delivery had reduced CA:Ag ratios that were suggestive of vitamin K deficiency.

A 6-week-old infant is described who had autoimmune hemolytic anemia manifested by severe anemia, a low reticulocyte count, an anerythroid bone marrow, and a strongly positive direct antiglobulin reaction of the red cells. Mild ABO hemolytic disease had been present at birth. However, the panagglutinin in the child's serum was shown to be distinct from any antibody in the mother. The autoimmune hemolytic anemia persisted beyond the age of 17 months. The infant did not respond to large doses of prednisone, but improved with ACTH therapy. Despite the usual low antigenic capacity of the newborn, severe autoimmune hemolytic anemia may occur in this age period.

Summary Orally administered phytonadione in doses of 2 mg. of an emulsion given in a dextrose feeding formula on the first day of life is as effective as menadiol sodium biphosphate given intramuscularly in doses of 2.5 mg. in preventing abnormal elevations of the prothrombin time during the first five neonatal days. This same dose of phytonadione rapidly and effectively reduced to normal limits the abnormally high prothrombin times of 9 of a control group of 52 newborn infants who had not received any form of vitamin K.

Plasma thromboplastin antecedent (Factor XI) levels were determined in cordblood, in the blood of women before and during the last trimester of pregnancy, and, at term, and in the blood of infants in the neonatal period and early infancy. The neonatal levels were significantly lower than the maternal levels at term and rose gradually within 60 days to near normal adult values. Vitamin K did not appear to alter the levels within the first 5 days of life and had no effect on the rate of rise. Findings in three infants suggest that decreased activity of PTA in the newborn infant may be responsible for bleeding symptoms similar to those associated with hemorrhagic disease of the newborn, and that it cannot be prevented by administration of vitamin K.

Breech presentation continues to seriously concern obstetricians, particularly since various neurological abnormalities have been found in these children years after birth. This clinical study concerns 208 primigravidas with single breech presentation. The corrected perinatal mortality was 13 per cent compared with an over-all perinatal mortality of 3.3 per cent. Cerebral trauma and anoxia are implicated as serious hazards associated with delivery of the aftercoming head. Breech extraction was associated with a prohibitively high perinatal wastage. Intravenous oxytocin was employed to augment labor of a very small and very select group of patients with no associated perinatal loss. A 100 per cent fetal salvage following cesarean section compared with the perinatal loss associated with vaginal delivery, even in a small series such as this, warrants liberalization of cesarean section in the management of breech presentation in the primigravida.