scholarly journals INTRACEREBRAL BLEEDING IN LATE HEMORRHAGIC DISEASE OF THE NEWBORN

2019 ◽  
pp. 1-2
Author(s):  
Jayashree Nadkarni

1 Vitamin K Ad Hoc Task Force. Controversies concerning vitamin K and the newborn. Pediatrics 1993; 91: 1001-1003. 2. Isarangkura PB, Pintadit P, Tejavej A, Siripoonya P. Chulajata C, Green GM. Vitamin K prophylaxis in the neonate by oral route and its significance in reducing infant mortality and morbidity. J Med Assoc Thai 1986; 69: 56-61. 3. Ijland MM, Pereira RR, Cornelissen EA. Incidence of late vitamin K deficiency bleeding in new-borns in the Netherlands in 2005: Evaluation of the current guideline. Eur J Paediatr 2008; 167: 165-169. 4. Waseem M. Vitamin K and hemorrhagic disease of new-borns. South Med J 2006; 99: 1199. 5. Lane PA, Hathaway WE. Vitamin K in infancy. J Pediatr 1985; 106: 351-359. 6. Singh M. Vitamin K during infancy: Current status and recommendations.Indian Pediatr 1997; 34: 708-712. 7. Bor O, Akgun N, Yakut A, et al. Late hemorrhagic disease of the new-born.Paediatr Int 2000; 42: 64-66. 8. D?Souza IE, Rao SD. Late hemorrhagic disease of new-born. Indian Paediatr 2003; 40: 226-229. 9. Flood VH, Galderisi FC, Lowas SR, et al. Hemorrhagic disease of the new-born despite vitamin K prophylaxis at birth. Paediatr Blood Cancer 2008; 50: 1075-1077. 10. Zengin E, Sarper N, Türker G, et al. Late haemorrhagic disease of the new- born. Ann Trop Paediatr 2006; 26: 225-231. 11. Sutor AH, Dagres N, Niederhoff H. Late form of vitamin K deficiency bleeding in Germany. KlinPediatr 1995; 207: 89-97

2017 ◽  
Vol 37 (1) ◽  
pp. 104-107 ◽  
Author(s):  
Sudhir Adhikari ◽  
Eva Gauchan ◽  
Tejesh Malla ◽  
Brijesh Sathian ◽  
Kalipatanam Seshagiri Rao

Vitamin K deficiency bleeding (VKDB) can manifest as intracranial hemorrhage (ICH) and is still prevalent in poor resource countries. Infants aged one to twelve months with the diagnosis of ICH from 1st July 2011 to 30th June 2016 were included. There were 16 cases of ICH attributed to vitamin K deficiency. Clinical presentations were anemia16 (100%), bulged fontanel 13(81.3%), seizures 10(62.5%), vomiting 8(50%) and fever 9(56.3%). Mean INR at admission was 8.575±7.267 and 1.868±0.838 after three doses of vitamin K administration. Sites of intracranial bleed were parenchymal 5(31.3%), subdural 4(25%), extradural 2(12.5%), ventricular 2(12.5%). In 3(18.8%) of cases bleeding was more extensive involving more than one site. Mortality was 4(25%) and 3(18.8%) had abnormal neurological findings at discharge. There is an urgent need for national policy for vitamin K prophylaxis at birth.


2016 ◽  
Vol 36 (S1) ◽  
pp. S29-S35 ◽  
Author(s):  
M J Sankar ◽  
A Chandrasekaran ◽  
P Kumar ◽  
A Thukral ◽  
R Agarwal ◽  
...  

2011 ◽  
Vol 53 (6) ◽  
pp. 897-901 ◽  
Author(s):  
Daijiro Takahashi ◽  
Akira Shirahata ◽  
Susumu Itoh ◽  
Yukihiro Takahashi ◽  
Tomizo Nishiguchi ◽  
...  

1999 ◽  
Vol 81 (03) ◽  
pp. 456-461 ◽  
Author(s):  
Rüdiger von Kries ◽  
Marlies Cornelissen ◽  
Andrew McNinch ◽  
Maureen Andrew ◽  
Anton Sutor

Summary Terminology. Replace the term “Hemorrhagic Disease of the Newborn” (HDN) by “Vitamin K Deficiency Bleeding” (VKDB), as neonatal bleeding is often not due to VK-deficiency and VKDB may occur after the 4-week neonatal period. Definition. VKDB is bleeding due to inadequate activity of VK-dependent coagulation factors (II, VII, IX, X), correctable by VK replacement. Diagnosis. In a bleeding infant a prolonged PT together with a normal fibrinogen level and platelet count is almost diagnostic of VKDB; rapid correction of the PT and/or cessation of bleeding after VK administration are confirmative. Warning signs. The incidence of intracranial VKDB can be reduced by early recognition of the signs of predisposing conditions (prolonged jaundice, failure to thrive) and by prompt investigation of “warning bleeds”. Classification. VKDB can be classified by age of onset into early (<24 h), classical (days 1-7) and late (>1 week <6 months), and by etiology into idiopathic and secondary. In secondary VKDB, in addition to breast feeding, other predisposing factors are apparent, such as poor in-take or absorption of VK. VK-Prophylaxis: Benefits. Oral and intramuscular VK (one dose of 1 mg) protect equally well against classical VKDB but intramuscular VK is more effective in preventing late VKDB. The efficacy of oral prophylaxis is increased with a triple rather than single dose and by using doses of 2 mg vitamin K rather than 1 mg. Protection from oral doses repeated daily or weekly may be as high as from i.m. VK. VK-Prophylaxis: Risks. VK is involved in carboxylation of both the coagulation proteins and a variety of other proteins. Because of potential risks associated with extremely high levels of VK and the possibility of injection injury, intramuscular VK has been questioned as the routine prophylaxis of choice. Protection against bleeding should be achievable with lower peak VK levels by using repeated (daily or weekly) small oral doses rather than by using one i.m. dose. Breast feeding mothers taking coumarins. Breast feeding should not be denied. Supervision by pediatrician is prudent. Weekly oral supplement of 1 mg VK to the infant and occasional monitoring of PT are advisable. Conclusion. VKDB as defined is a rare but serious bleeding disorder (high incidence of intracranial bleeding) which can be prevented by either one i.m. or multiple oral VK doses.


Nutrients ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 4109
Author(s):  
Simon Fiesack ◽  
Anne Smits ◽  
Maissa Rayyan ◽  
Karel Allegaert ◽  
Philippe Alliet ◽  
...  

Neonatal vitamin K prophylaxis is essential to prevent vitamin K deficiency bleeding (VKDB) with a clear benefit compared to placebo. Various routes (intramuscular (IM), oral, intravenous (IV)) and dosing regimens were explored. A literature review was conducted to compare vitamin K regimens on VKDB incidence. Simultaneously, information on practices was collected from Belgian pediatric and neonatal departments. Based on the review and these practices, a consensus was developed and voted on by all co-authors and heads of pediatric departments. Today, practices vary. In line with literature, the advised prophylactic regimen is 1 or 2 mg IM vitamin K once at birth. In the case of parental refusal, healthcare providers should inform parents of the slightly inferior alternative (2 mg oral vitamin K at birth, followed by 1 or 2 mg oral weekly for 3 months when breastfed). We recommend 1 mg IM in preterm <32 weeks, and the same alternative in the case of parental refusal. When IM is perceived impossible in preterm <32 weeks, 0.5 mg IV once is recommended, with a single additional IM 1 mg dose when IV lipids are discontinued. This recommendation is a step towards harmonizing vitamin K prophylaxis in all newborns.


2010 ◽  
Vol 95 (Suppl 1) ◽  
pp. A67.2-A68
Author(s):  
A Busfield ◽  
R Samuel ◽  
A McNinch ◽  
J Tripp

PEDIATRICS ◽  
1993 ◽  
Vol 91 (5) ◽  
pp. 1001-1002
Author(s):  

Vitamin K deficiency may cause unexpected bleeding (0.25% to 1.7% incidence) during the first week of life in previously healthy-appearing neonates (classic hemorrhagic disease of the newborn [HDN]). The efficacy of neonatal vitamin K prophylaxis (either oral or parenteral) in the prevention of classic HDN is firmly established. It has been the standard of care since the recommendation by the Committee on Nutrition was adopted as policy by the American Academy of Pediatrics in 19611 Late HDN, a syndrome defined as unexpected bleeding due to severe vitamin K deficiency in infants aged 2 to 12 weeks, occurs primarily in exclusively breast-fed infants who have received no or inadequate neonatal vitamin K prophylaxis. In addition, infants who have intestinal malabsorption defects (cholestatic jaundice, cystic fibrosis, etc) may also present with late HDN. The rate of late HDN (often manifested by sudden central nervous system hemorrhage) ranges from 4.4 to 7.2 per 100 000 births based on reports from Europe and Asia. When a single dose of oral vitamin K has been used as neonatal prophylaxis, the rate has decreased to 1.4 to 6.4 per 100 000 births. Parenteral neonatal vitamin K prophylaxis prevents the development of late HDN, with the rare exception of infants with severe malabsorption syndromes. Oral regimens that have a similar efficacy as parenteral vitamin K in prevention of late HDN include the repeated administration of oral vitamin K1 (Germany) or K2 (Japan) at birth, 1 week, and 2 to 4 weeks. In 1990 Golding et al2 reported a study of a 1970 birth cohort in Britain in which they noted an unexpected association between childhood cancer and pethidine given in labor and the neonatal administration of vitamin K. Subsequently, Golding and others3 conducted a case-control study designed to examine the risk of cancer associated with intramuscular vitamin K administration among infants born in two hospitals in Avon between 1965 and 1987 and diagnosed with cancer between 1971 and 1989.


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