The following paper on vitamin K is obviously not exhaustive. I am not a researcher and I am very aware of it’s simplicity and lack of elegance. Therefore, I ask for your input not only on the subject, but on how to be better at research, and presentation of ideas. It would be nice to be able to write about a subject in a way that is palatable and understandable. That said, here is my vitamin K paper.
Neonatal Vitamin K Prophylaxis
Annie sewell
NSG 225
24 February 2006
The presence of turbulent blood flow through neonatal alternate circulation, which lasts up to two days post partum is a direct contraindication for the administration of prophylactic vitamin K in neonates.
While it is not in the scope of this paper to expound upon the nuances of vitamin K synthesis, blood coagulation, and fetal blood coagulation as it relates to intestinal flora and fat synthesis in the liver, the above topics will be touched on as much as needed to discuss the efficacy of neonatal vitamin K prophylaxis.
Standardized vitamin K prophylaxis: A history
In the 1930’s, hemorrhagic disease of the newborn (HDN) was the diagnosis given to several neonatal deaths from intracranial hemorrhage (Rothville, K.,2006). In an effort to eliminate HDN, scientists found that these infants all had low levels of vitamin K and prothrombin, which was the only similarity found among the babies, and so concluded that this was the cause (Rothville, K.,2006). In 1961, the American Academy of Pediatirics, in response to growing alarm over several infant hemorrhagic deaths, recommended that an IM vitamin K preparation called, phytomenadione, be given to all neonates (Hey, E.,2003).
The estimated number of deaths from HDN before vitamin K prophylaxis was 411 out of 100,000 live births (Pereira,SHearer, Williams, & Mie-Vergani, 2003), and those statistics have only been reduced to 1.4-6.4 out of 100,000 live births since the implementation of prophylaxis (American Academy of Pediatrics, 2003). To add to the dubious nature of the standardization of vitamin K prophylaxis, it has been found that half to three quarters of babies who presented with HDN were found to have an underlying liver malabsorption disorder (Hey, E., 2003).
Vitamin K and coagulation
Vitamin K, one of the four fat-soluble vitamins stored in the liver, is responsible for the proper functioning of the clotting factors II, VII, IX and X (Booth, S.L., 2000). Vitamin K is a co-factor needed to activate surface agents of the vitamin K dependent coagulation proteins, which enables them to stick to membrane surfaces (Bowen, R. 1999). This ability to adhere to one another and to damaged endothelium is important, as it is through adherence that the chronological reactions of coagulation and clotting take place (Bowen, R., 1999). It is important to note that the intrinsic pathway of coagulation is activated when the blood “detects an insult” via contact with an unevenness or break of the blood vessel endothelium. The intrinsic clotting pathway is initiated by non vitamin K dependent factor XII and platelets (Guyton, A.C., 1987). Coagulation factors XI, XII, and XIII appear in low levels in fetal blood, while platelets and factors X, VII and fibrinogen are at adult levels (Olds, S., London, M., Ladewig, P., Davidson, M., 2004).
Because vitamin K is fat soluble, it cannot be activated unless the liver is functioning properly in conjunction with adequate bile and pancreatic enzyme activity to ensure proper absorption and synthesis of vitamin K (Rothvill, K., 1999). In order for vitamin K to be absorbed from the intestines, natural bacteria and adequate amounts of medium chain fatty acids must be present in the intestines (Rothville, K., 1999). Breast milk, especially colostrum and hind milk, contain large amounts of vitamin K as well as being a rich source of fatty acids and lipase which aid with early and complete fat digestion in the human gut (Hey, E., 2003). Fetal intestines are full developed with adequate enzyme activity to metabolize nutrients by 36-38 weeks, therefore early feedings will provide the bacteria needed for proper synthesis and uptake of fat soluble vitamins i.e., vitamin K (Olds, S., et al, 2004).
Fetal Circulation
There are three distinct alterations in fetal blood flow: 1) the ductus venosus which bypasses the liver, (providing only half the amount of extra uterine blood supply to the liver), 2) the foramen ovale which is an opening between the right and left atrium and, 3) the ductus arteriosis which shunts the bulk of the blood flow returning from the pulmonary circulation to the descending aorta (Fetal blood and circulation, 2006). These alternate pathways, while normal in fetal circulation, have serious consequences for the newborn if they do not close properly. It must be emphasized, however, that while closure of the three alternate pathways of fetal blood flow is imperative for survival, the normal time frame for closure can be up to several weeks after birth (Verklan, T., 2002).
Neonatal blood flow and dynamics
During the transition from intrauterine to extra uterine life, neonatal hemodynamics undergoes dramatic, and at times, unstable shifts as the lungs take over respiration (Verklan, T., 2002). Neonates have a high pulmonary vascular resistance (McConnell, M., Elixson, E., 2002), as well as the possibility of right to left shunt termed, “bidirectional flow”, through the ductus arteriosis (Olds et al., 2004, p 772), and possible prolonged closure times of alternate blood flow pathways as before stated.
Neonatal coagulation and turbulent blood flow
One of three factors must be present for thrombus formation: endothelial injury, turbulent blood flow or hypercoagulable blood, collectively referred to as Virchows Triad (Demark, T., 1999). As was discussed above, direct insult to blood precedes the activation of the intrinsic pathway of coagulation, which is non vitamin K dependent. Turbulent blood flow is an insult to blood as proven by Virchow’s Triad. Neonatal blood is arguably not hyper coagulated, and in the absence of endothelial injury, the neonate is, amazingly, at risk via bidirectional blood flow, (turbulent blood flow), for thrombus formation.
Putting the pieces together
It would seem that the obvious is staring us in the face. Neonates, at birth, have lower levels of vitamin K, prothrombin and clotting factors XI, XII and XIII, and it is agreed that this is normal. It is agreed too, that at birth, neonates have high pulmonary vascular resistance to overcome and bidirectional blood flows that may not resolve for weeks. At the first feeding, bacterial flora are established aiding the liver and gut in synthesis and uptake of vitamin K, thus activating the full compliment of blood coagulation factors. There is a two to five day post-birth nadir of prothrombin in neonatal blood (Olds, et al., 2004), and vitamin K levels as well as coagulation factors are not fully developed until nine months (Olds, et al., 2004).
Rather than being the cause of unexplained hemorrhage, low vitamin K and clotting factor levels appear to protect the neonate from thrombus formation during a time of hemodynamic transition. In no other time of life do we have normal changes in blood flow pathways, and if blood flow pathway changes do occur, they are treated immediately with anticoagulation. In no other case of turbulent blood flow or high pulmonary blood pressures is coagulation therapy implemented, it simply is not common sense.
Conclusion
The efficacy of neonatal prophylactic vitamin K therapy is controversial at best. While it is true that neonates have low vitamin K levels and low coagulation levels, these findings are normal, and occur in all neonates. HDN is a frightening phenomenon and one that cannot be disregarded as fluke. However, the evidence would suggest that rather than focusing on blood coagulation, the research ought to aim at discovering the similarities in lifestyle, diet, and medication and prenatal care of those babies who do hemorrhage.
Vitamin K therapy has proved successful in treating bleeding disorders in neonates and ought to be considered for infants who have sustained trauma during birth. A thorough maternal history will alert the nurse to any predisposing factors to HDN such as certain medications, and drug or alcohol abuse. Nurses also ought to be familiar with the signs and symptoms accompanying acute hemorrhage, which does respond rapidly to vitamin K therapy (Hey, E., 2003).
As part of the nursing standard of care, we are to first, “do no harm”. The two populations most in need of advocacy are the young and the old, and it is the nurse’s responsibility to provide theat evidnece-based advocacy.
Excellent nursing practice requires that the nurse be aware of current trends and practices and be able to tell the difference between those practices that are based in sound reasoning from those that are not. It also requires that the nurse speak on behalf of sound practices.
Questioning the efficacy of neonatal vitamin K prophylaxis seems archaic, since the practice has been so long accepted. Widely accepted, often unquestioned nature of many medical practices ought to cause the nurse to begin to reevaluate accepted standards of practice with an eye to understanding if they are truly based in sound reasoning.