Missing Blood and no mention of timing of the clamping of the cord. Why not? Similar to Chow-case-law
A child's volume of placenta blood with all the stem cells and nutrients of whole blood simply went missing in the Chow-case-law. by Donna Young
The story below, with link, reveals missing placenta blood. What parents
do not know is the child's property, placenta blood,
may be drained of the blood while the doctor and nurse are alleging to be stitching the mother, after
an episiotomy. The placenta
will be full of blood by hasty umbilical cord clamping, known, since 1801, to be harmful to the child,
and by standards of primal
birth care.
The draining of the placenta, if yet in the birth canal, takes 7 minutes. The
baby by immediate cord clamping can be losing up
to 50 percent of total blood volume. This was so and the cause of anemia in the Chow-case-law. An
award of some $8 million
dollars was granted for the child's care. The placenta in the birth canal keeps the blood warm
for faster flowing into blood
collection bags. The placenta blood may be sold to the highest bidder and the parent(s) never
informed this even went on.
It is not wise to birth alone without a birth witness, a member of the family
keeping an eye on the child, at all times. Many times
the doctors and nurse try to remove the baby away from the mother and the birth room, alleging, some
kind of emergency. The
birth attendant/witness must go too, and remain with the baby. What is done to the placenta must
be checked too. It is really best
to go back to the primal birth method, now called the Lotus Birth.
A signed birth contract protects the mother and father of no unnecessary
risk taking to their child and blood deprivation to
their child, that will be sold. Even the placenta and cord need not be detached from the child,
as the placenta is being sold, too.
The placentas are then ground up and put in centrifugal machines and tissues separated and the blood
components.
You do not have to blindly trust the hospitals and its doctors, nor your doctor,
and he/she should, by good faith, sign a birth
contract as to conflict of interest in the placenta blood. Nothing of their training or intentions
should be secret or kept from the
parents on their intended procedure of the care and the treatment to the child and his right to full
placenta transfusion into the
baby's lungs. Most doctors have been known to lie about the importance of the nutrients in the
blood to the owner/baby. They are
alleging a bogus reason for interruption of the child's lifeline. They can be required to justify their
policies and practice before a
judge. Make them do that.
The procedure and intent of the doctor need not be agreed to, if known of his
training to go along with immediate cord
clamping. The reasons are political in increased profits in selling the placenta and the placenta blood. The forewarning of the
actual birth care needs to be discussed long before the child's birth is expected.
Premature babies or c-section babies are not to be removed from their placenta
either. All babies can remain on their
placenta and cord. The removal can be done by the parent, when and if done. This is
only done for cosmetic reasons and has
risk of cord infections. The Lotus birth is a wiser decision, no cord infections. And as
long as the baby is kept warm and the
placenta, full blood transfusion will take place. This is true for babies in special life-support
equipment, to be left on their
placenta. The placenta close beside them, wrapped in a diaper.
Hospital policies cannot direct or order the placenta clamped or cut off. It is a violation of parental rights to protect their baby.
There is no harm done if the umbilical cord is not clamped or removed. This is a primal method
of care that our pioneer
grandparents did. It produced strong healthy children with full immunities. And, it is a parental
decision not a policy that can be
imposed on their child to clamp and/or amputate and cosmetically remove the placenta. This is
a simple procedure that the
parents can do themselves, when the want, if they want. Find out the policy intended or mostly
practiced in your community by
each doctor. The early clamping must be exposed in each community. Go public and the best means
to protect your baby is to
birth in the privacy of your own home. Doctors have been known to harm the mother who would not
allow hasty clamping. They
have pushed the baby back inside the womb and torn up the mother so she will not have babies again. Many medical doctors
and the nurses are infringing on rights of the parents to be in control of a harmless procedure to protect
their baby. NO clamping
of the umbilical cord ever, unless the cord tore or for placenta previa. The seldom ever happen and
an investigation ought to be
done for medical negligence. One does not need to submit to political policies to deprive the
child of his/her blood components.
The hospital can be taken to court if they violated the wishes of the parents
and removed they clamped the cord and cut it.
That is not their choice to impose an unnecessary procedure on the baby. It is merely cosmetic
removal, and the parents can
control that for all babies, c-section and premature babies, too. No political policy not approved
by a Court's ruling can could risk
any child to be weaker then it ought to be by blood deprivation. The political interest
is that the baby's blood is being "robbed"
for research and compensation to the highest bidder. The price received can be dependent on the child's
ethnic group and blood
type. Russian blood may be most desired, as well as Oriental and mixed race groups.
All are factors in compensation to wanted stem cells posted on medical web sites,
known at most hospitals. Doctors know the
blood type of the babies they are delivering. The baby may be premeditated to early clamping, by the
doctor's intent to keep
his/her practices and training quiet. The C-sections babies, mostly being larger babies, are at
risk of hasty clamping, too.
Because premature babies have more stem cell blood then do full term, they are especially vulnerable
to unnecessary early
clamping. The standard of care for all premature babies has been set at 30-seconds, and they then
must be revived, as will any
child early clamped.
In the event of hasty clamping and the placenta is being drained, the mother
cannot feel the placenta being drained, because it
is not her blood. It is the infant's blood that is being deprived the child.
Failing to enforce and investigate endangering to a child under ten years of
age and endangering to a person:
Few police investigate hospital procedures and care and treatment of patients and trends and policies of the Administration as to what they are doing with the placenta and the blood trapped in them by the present trend of immediate cord clamping. Involved in concealment are the Registered-Nurses, and the Lab Technicians, who may participate in draining the placenta of the blood.
Lab Technicians simply follow orders as most of the medical staff in most hospitals,
private or public, and do not report
strange happenings of care and treatment to any patient.
Knowing this and Coroners not properly trained, most not doctors, I question
this report as to what is missing, the timing of
the clamping of the umbilical cord, and how the child was held during the c-section. If the baby is
held high the baby's blood can
run back into the placenta, causing the appearance of the cord to be premature white and to have stopped
pulsating. Too low,
and the sleepy drugged baby, is not likely going to have a strong heart beat to transfuse blood up hill
through the vein.
http://www.indianpediatrics.net/april2002/april-385-388.htm
V. Parveen
S.K. Patole
J.S. Whitehall
From the Department of Neonatology, Kirwan Hospital for Women Townsville, Queensland 4817, Australia.
Correspondence to: Dr Sanjay Patole, Department of Neonatology, Kirwan Hospital for Women Townsville, Queensland 4817, Australia.
E-mail: sanjay_patole@health.qld.gov.au
Manuscript received: July 4, 2001;
Initial review completed: August 30, 2001;
Revision accepted: September 11, 2001.
Massive fetomaternal hemorrhage (FMH) is defined as loss of over 150 ml (5 ounces) of blood;
its frequency is largely
unknown(1).
It has been reported as an unexpected cause of death in 13.8% of otherwise unexplained
fetal deaths(2). (See
Shock
)
Association of persistent pulmonary hypertension of the newborn (PPHN) with
severe anemia
following massive FMH is known
but not well documented(3,4).
We report such an association in a term neonate needing rescue therapy with high-frequency oscillatory
ventilation (HFOV) and
inhaled nitric oxide (INO).
Case Report
A 39-year-old mother (gravida-9, para-1, miscarriages-4, ectopic pregnancies-2, term-ination
of pregnancy-1). delivered a
female neonate weighing 3.3 kg at term following an emergency Caesarean section
due to decreased fetal movements with
sinusoidal pattern on the non-stress test.
A CTG done for decreased fetal movements 2 weeks prior to the delivery was normal.
Follow up CTG/biophysical profile, and ultrasonography could not be done due to patient noncompliance.
There was no history of trauma, vaginal bleeding, diabetes mellitus,
urinary tract infection, or use of non-steroidal anti-inflammatory drugs like indomethacin.
At birth, the baby was hydropic, very pale, floppy with weak peripheral pulses, and had a heart
rate of 70/minute.
Apgar scores were 1 and 5 at 1 and 5 minutes, respectively. (
Comments from Donna Young: This test may indicate immediate
cord clamping)
.
The cord pH and Hb were 7.08 and 2.5 g/dl, respectively.
She was resuscitated using intermittent positive pressure ventilation after endotracheal intubation,
intra-tracheal adre-naline, and
transfusion of 120 ml of group O-negative packed red cells immediately over 2 hours
followed by 44 ml of cross matched red
cells over 2 hours followed by a single dose of furosemide.
The baby’s post transfusion hemoglobin was 14.6 g/dl (hematocrit = 0.43) at 14 hours of age.
The direct Coombs test was negative.
Maternal Kliehauer Betke test was positive. (Estimated fetomaternal bleed: 154 ml).
The placental histopathology was normal.
Maternal Parvovirus B19 IgM was non-reactive.
Specific IgM titers for toxoplasmosis, rubella, cytomegalovirus, and herpes simplex I and II were
negative.
The relevant laboratory investigations were as follows:
Nucleated RBC’S 542/100 WBC,
WBC count 10000/mm3,
Platelet count - 57000/mm3,
blood culture - negative,
serum creatinine-0.13 mmo1/L,
serum bilirubin - 60 mmo1/L,
total proteins - 3.2 g/L,
albumin - 1.4 g/L,
AST - 141 IU/L,
ALT 42 IU/L,
GGT - 21 IU/L,
cranial ultrasound - normal.
Sonography revealed severe ascites with no evidence of pleural/pericardial effusions.
Color Doppler study showed a structurally normal heart with evidence of PPHN (tricuspid regurgitation,
right to left flow across the
patent ductus arteriosus).
Additionally, the difference between pre and post ductal saturations by pulse oximetry was > 15%.
HFOV (MAP = 17 cm H2O,
amplitude = 59) was resorted to at 5 hours of age in view of the rising ventilatory requirements
(PIP/PEEP - 35/6 cmH2O, rate -
55/minute) and unstable oxygenation (PO2 - 24-204 mmHg) in 100% oxygen along with surfactant therapy,
sedation, muscle
paralysis, inotrope therapy.
INO was subsequently started at 6 hours of age (oxygenation index - 62) at 20 ppm and later increased
to 30 ppm.
Following a sustained improvement in oxygenation commencing at 7 hours of age, the inspired oxygen
con-centration was
reduced to 40% by 60 hours of age and the mean airway pressure was weaned to 8 cm H2O by 75 hours
of age.
Cardiovascular stability allowed inotropes (dopamine, dobutamine) to be weaned off by day 3.
INO was subsequently weaned off by day 4 and the neonate was extubated to room air on day 6.
The urine output had increased to 8-9 ml/kg/hour by day 5 with significant resolution of the generalized
edema by day 7.
Further hospital stay was uneventful and the neonate was neurologically normal at
discharge on day 12.
Discussion
FMH of over 30 ml of fetal blood occurs in normal pregnancies with a frequency of about 1 in 300(1).
Defined as the loss of more than 150 ml (or approximately 50% of the fetal blood volume),
massive FMH is rarely
suspected before fetal death(5,6).
PPHN has been reported as a consequence of massive FMH (3,4).
Frickers et al. reported massive FMH leading to marked anemia (Hb - 4.9 g/dl) and rapidly progressive
heart failure in a neonate
who developed symptoms of ‘persistent fetal circulation’ (PFC) despite blood transfusion and digoxin
therapy but survived(3).
Moya et al reported 4 cases of massive FMH presenting with severe anemia (hematocrit - 16-26%)
and signs of circulatory
failure(4).
One of these neonates with pallor (Hb - 5.5 g/dl), weak peripheral pulses, systemic hypotension, soft
systolic murmur and
hepatomegaly deteriorated rapidly, developing PPHN documented on echocardiography.
Though the mother had gestational diabetes, echocardiography of this neonate did not reveal poor
cardiac contract-ility or
cardiomyopathy that is usually seen in infants of diabetic mothers.
Red cell trans-fusion and mechanical ventilation with 100% oxygen were required to stabilize
the neonate. At discharge the
neonate was neurologically normal.
The factors associated with the patho-genesis of PPHN include acute as well as chronic hypoxia(7,8).
It is well documented that acute hypoxia causes smooth muscle contraction in pulmonary arteries through
a direct effect on
intracellular calcium levels(8).
The mechanisms of pulmonary endothelial adaptation to sustained hypoxia include reduction in nitric
oxide production, possibly
through reduced activity of formative enzyme nitric oxide synthase that may enhance the development
of secondary pulmonary
hyper-tension(8).
Cardiac output and hemoglobin are the key elements in determining systemic oxygen transport(9).
Additionally hypovole-mic, anemic hypoxia (e.g., hemorrhagic shock) is less well tolerated compared
to hypoxic hypoxia(9).
Given this evidence, prompt correction of anemia/hypovolemia and aggressive prevention (e.g., management
of
hypoglycemia, hypothermia) and management of PPHN is warranted in cases of FMH(7,9,10).
Contributors: VP performed the literature search and prepared the initial draft of the manuscript. SKP
and JSW helped in final
drafting of the manuscript. SKP will act as the guarantor for the manuscript.
Funding: None.
Competing interests: None stated.
Key Messages
• Association of persistent pulmonary hypertension of newborn (PPHN) with severe anemia following massive fetomaternal hemorrhage (FMH) is known but not well documented.
• As hypovolemic, anemic hypoxia (e.g., hemorrhagic shock) is less well tolerated compared
to hypoxic hypoxia,
prompt correction of anemia, hypovolemia to maintain systemic oxygen transport and aggressive prevention
of
PPHN is warranted in cases of FMH.
References
1. Giacoia GP. Severe fetomaternal hemorrhage: A review. Obstet Gynecol Surv 1997; 52: 372-380.
2. Laube DW, Schauberger CW. Fetomaternal bleeding as a cause for "unexplained" fetal death.
Obstet Gynecol 1982; 60: 649-651.
3. Fricker HS, Zumofen W, Hofmann E. Severe neonatal anemia associated with feto- maternal transfusion
and persistent fetal
circulation. Helv Pediatr Acta 1983; 38: 179-183.
4. Moya FR, Perez A, Recece EA. Severe fetomaternal hemorrhage. A report of four cases. J Reprod Med
1987; 32: 243-246.
5. Cardwell MS. Fetomaternal hemorrhage: When to suspect, how to manage. Postgrad Med 1987; 82: 127-130.
6. Elliot JP. Massive fetomaternal hemorrhage treated by fetal intravascular trnasfusion. Obstet Gynecol
1991; 78: 520-523.
7. Yu VY. Persistent pulmonary hypertension in the newborn. Early Hum Dev 1993; 33: 163-175.
8. Higenbottam T, Cremona G. Acute and chronic pulmonary hypertension. Eur Respir J 1993; 6: 1207-1212.
9. Anderson C. Critical Hemoglobin thresholds in premature infants. Arch Dis Child Fetal and Neonatal
Ed 2001; 84: F146-F148.
10. Kinsella JP, Abman SH. Inhaled nitric oxide and high frequency oscillatory ventilation in persistent
pulmonary hypertension of
the newborn. Eur J Pediatr 1998; 157(Suppl): S-28-S-30.
___________
Search this www.lotusbirth.com web site for
: AAP policy, SOGC policy, ACOG policy; Placenta; Fetus to Neonate
Circulation; 30-second clamping; World Health Organization and Dupont ; Circumcision ; Dr. Sarah Buckley's
Declaration ; pH
receptors ; References ; Canadian Criminal Codes and when a baby is a person; and any other subject
you may be interested in
child birth.
Search Lotusbirth
(Reference from Protect Babies
http://www.123-baby-birth.com)
Search at Google this web site for the " No Policies " on equal
protection to babies from the various government officials who appointed representatives to protect
the public on medical
policies and practices; also the "No policies" of the various medical associations, societies,
and colleges did not live up to no
form of discrimination to women or the child of any kind. It is believed medical persons had a
duty to have a policy of equal
protection and security of person, regardless of: age, mental or physical disadvantages ; race,
color, social or marital status of
the pregnant lady ; or belief or faith of the family, or genetic type of blood sought for by medical
researchers, for stem cell
matching, and use of white cells, mature red cells, platelets, enzymes, hormones, and plasma.
contact: dyoung@pris.ca
Home Page: www.lotusbirth.com
A medical web site to visit:
A Petition to Protect Canadian Babies and Mothers, Too:
www.thepetitionsite.com/takeaction/102580814
