The gentlebirth.org website is provided courtesy of
Ronnie Falcao, LM MS, a homebirth midwife in Mountain View, CA
An interactive resource for moms on easy steps they can take to reduce exposure to chemical toxins during pregnancy.
Other excellent resources about avoiding toxins during pregnancy
These are easy to read and understand and are beautifully presented.
Judy Slome Cohain, CNM
Abstract: Improved outcomes from Technological birth reached
the point of diminishing returns in year 2000 when the increasing cesarean
rate increased MMR in the presence of an unchanged PMR. Hospital birth
was successfully sold to women in western cultures since the 1950s, but
has failed to show any safety advantage over planned attended homebirth.
Planned attended homebirth is safer than hospital birth for low risk women
and their single, head down fetus between 37+0 and 42+0 weeks gestation.
An accurate assessment of the current relative dangers of hospital birth
for low risk women compared to homebirth are summarized.
The first evidence that hospital birth offered no advantage for mother or baby over attended homebirth for low risk women were the statistical analyses by the British statistician Majorie Tew (1). She compared all available evidence from before and after the move to hospital birth and analyzed comparable populations in terms of maternal and perinatal mortality. She was neither able to find any improved outcomes for birth in hospital settings, nor any journal willing to publish her analysis.
Until 1940, women who could afford it had attended homebirths because it was known to be far safer than hospital birth, a service provided for poor women. Around 1750 Dr Semelweiss ‘discovered’ handwashing, which slowly improved hospital outcomes as it was adopted. Hand washing, which had been practiced by midwives for centuries, was slowly adapted in hospitals. The maternal mortality rate in Sweden in the early 1900s was one third that in the United States, a recognized result of competent midwives attending home deliveries.(2)
Uterine infection and postpartum hemorrhage (PPH) were the 2 leading causes of maternal death in industrialized nations up to the Second World War. In the late1940s and early 1950s, the distribution of two major medical discoveries greatly improved the outcomes of the birth process: Penicillin against infection and Pitocin against hemorrhage. Those two additions to the midwife’s bag brought down the maternal and perinatal mortality rates. Around the same time, medical organizations lobbied to close down midwifery schools in an effort to change the balance of power so the medical profession could control birth. Women in the US were being convinced to birth in the hospital setting with doctors. The advent of penicillin and pitocin and improved nutrition, social and sanitary conditions caused a great decrease in deaths, which happened simultaneously with the increase in hospital birth, but the timing was serendipitous. Hospital birth offers no advantage over home, no advantage in terms of ability to give penicillin or pitocin, and exposes the woman and newborn to strangers and their pathogenic bacteria not encountered in the own home.
From 1940-2000 following the addition of antibiotics and drugs to contract the uterus after birth, maternal mortality dropped, reaching a low of 10 per 100,000 in the US in 1977 which was maintained until 2000. Then, the rate started to rise for the first time in 60 years reaching 13 per 100,000 live births in 2003, and 14 per 100,000 in 2004.
Maternal mortality rates include any pregnant woman who dies of any cause including homicides, suicides, infectious diseases, traffic accidents, in addition to deaths at the time of birth. The US does not require maternal mortality to be reported by cause, therefore an increase in Maternal death from birth would not be able to be differentiate a flu epidemic from increased domestic violence. No government, other than the UK has made any effort to clarify the causes of the increasing maternal mortality rate. A popular cover up is to say that the rates are increasing because of improved reporting which is suspicious since maternal mortality continues to be consistently underreported in all western countries except the UK. In the UK, a law was passed in 1952 forcing every case of maternal mortality to be reported along with the cause of death, in an idealistic effort to decrease maternal mortality. As a result, the UK statistics are the only ones available that show the increase in the number of women dying at birth is a result of increased hemorrhage following cesarean surgery. The UK Maternal Death rate for 1997- 1999 was 11.4 per 100,000 maternities. The overall maternal mortality rate for the United Kingdom for 2000-2002 is 13.1, 2003-2005 is 14 maternal deaths per 100,000 maternities (3) with the increase in the category of direct deaths from bleeding and anesthesia after cesarean, most usually as a result of placenta previa and placentas implanting into the uterus at the scar from a previous CS. All the women who died of placenta previa between 2000-2002 had previous cesareans.
All 10 large studies of planned homebirth (4) as well as this years 2 Canadian RCT studies of planned homebirth (4, 5) have shown homebirth is not associated with an increased risk of adverse perinatal outcomes. There are no studies showing hospital to have better outcomes than planned homebirths. In the studies where CS rates are reported, the CS rate is always significantly lower for planned homebirths.
Planned homebirth Planned hospital
6% 15% hospital ( 6)
1% 2% Hospital birth (7)
5% 14% (8)
2% 7% (9) (4th deg.tear: 0.3 home VS 2.7%)
7% 11% (4)
5% 8% (5)
The 17 contributing factors contributing to unnecessary cesarean surgery / high CS rates in hospitals have been elaborated elsewhere (12). When one examines the effect of hospital birth in terms of long term sequellae, hospital birth no longer remains on an equal footing with planned hospital birth. Hospital birth always involves a higher CS rate and CS causes higher rates of placenta previa, placenta accreta, third trimester stillbirth and increased isoimmunization to blood factors even in the presence of Rhogam administration (13), on the next pregnancy, which result in higher rates of Maternal death and increased perinatal mortality.
Although we do not have direct maternal mortality reports by cause in the US, large studies of 15,000 women studied the maternal mortality rate from elective repeat CS. The reported frequency of maternal death resulting from elective repeat CS was 1/2,250 for 1999 through 2002 year(14). The deaths were from hemorrhage, anesthesia problems or amniotic fluid embolisms. In a population of Medicaid recipients in a Tennessee hospital in 1991 the maternal mortality among 7,441 cesareans was 1 per 930. (15) For the same years, the death rate of US women at vaginal births was 1 in 50,000. In a retrospective cohort study of 308,755 Canadian women over a 12-year period maternal in-hospital death rate from elective cesarean section was 1/18,000 whereas only 1/128,000 died following vaginal birth.(16) Overall reported maternal mortality in Canada is half the rate in the US or approximately 7 per 100,000 live births. (jrooks in press)
The American College of OBGYN (ACOG) gives lip service to supposedly wanting to lower the cesarean rate, but its policy statements reflect no such desire. Although the many published studies of planned homebirth show equally good outcomes to hospital birth and that it safely protects against unnecessary cesarean surgery, in 2008, ACOG reiterated its official position statement against homebirth for all women. (17)
Some midwifery organizations currently are participating in the misinformation of women as well. The so-called ‘debate’ between hospital birth and homebirth, referred to by Deanne R. Williams, former ACNM Executive Director, in the July August 2009 issue of JMWH does not exist. (18) One could debate the definitions of high risk. But when it comes to a head down, singleton pregnancy at term there is no debate. The outcomes have always been shown to be statistically equivalent for either setting, with hospital births having many more interventions like CS. The rhetoric of some midwifery organizations does not reflect the facts.
President Obama gives lip service to wanting to lower health spending, but his proposals carefully avoid the obvious and effective. The most common reason for hospitalization is childbirth and the most common surgical procedure is cesarean section (CS). Currently, in the US, there are 1,500,000 cesareans per year, with a national average cost (2004) $12,500 each without complications, $16,000 (2004) each with complications, adding up to 22 billion dollars per year, and 95% of them are completely unnecessary surgery if attended homebirth were available. The average birth center birth is $1,600 (2004). There are no rent and upkeep costs at a homebirth. A homebirth attendant could be paid $500 plus transportation, would nicely reimburse her since transportation and time are her only costs. If homebirth were supported, there would be no reason for malpractice insurance for homebirth midwives, since malpractice insurance does not improve outcomes, it is being used as an indirect method to eliminate the homebirth option in many states. If the 3,000,000 annual low risk vaginal births planned to deliver at home, the savings in hospital room costs alone would be in the tens of billions. Not only that, but the rate of breastfeeding would increase, which lowers childhood disease as well as breast, ovarian and uterine cancer. CS delivery has also been shown to increase the rate of asthma in children.
The most common lie made by professional organizations to scare women out of giving birth at home is that ‘in the case of a serious emergency, being in the hospital could save the mother’s life or the life of the baby. ‘(19)
There is no rare but very serious emergency that could have better outcomes
on maternal mortality if the woman starts in the hospital and only one
very very rare case of an emergency in which the baby may have better outcomes
if the birth takes place in hospital.
1. There are No Rare and Serious complications at homebirth endangering the mother in the presence of a competent attendant i.e. in the absence of blatant malpractice:
Since the distribution of antibiotics in 1945 and pitocin in 1953, low risk women don’t die from vaginal births except if she is conned into delivering in hospital. A woman with a Hgb of 11 or 12 at the start of birth, can lose a liter of blood and not even have symptoms of blood loss. Any low risk woman with a single baby in head down position at term who died in childbirth was a result of hospital intervention or unattended homebirth or blatant malpractice. Maternal mortality of women at planned homebirths with a skilled attendant has never been documented in the absence of malpractice. In the worst case scenario of a sudden, massive hemorrhage, pitocin and methergine are administered, IV fluids are administered, an ambulance is called and the woman is stabilized before transfer.
Amniotic fluid embolism is associated with high risk women who should not be having a baby at home, or low risk women who go to hospital to give birth, who are sectioned or given IV pitocin in the presence of ruptured membranes. Amniotic fluid embolism was identified for the first time in 1941 and has never been documented to have happened during a planned homebirth. Currently, AFE is responsible for about 10% of maternal deaths in the United States.
Birth is unpredictable and therefore, AFE could theoretically happen at an attended homebirth, but the likelihood is infinitesimal. AFE is associated with first and foremost with caesarean section, then multifetal pregnancy, placenta previa, placental abruption, eclampsia, and large cervical laceration, none of which should take place at an attended homebirth with a competent midwife following safe protocols. If the woman starts having tachycardia at home, the first sign, she will be transferred to hospital for appropriate care. The maternal death rate from AFE is 10% and 30% of their fetuses die. The estimated incidence of AFE is 1:15,200 in North America vs 1:53,800 deliveries in Europe.
The chance of a rare but serious complication at a planned homebirth of a low risk women which would have better outcomes in hospital only regards the survival of the fetus and never concerns the mother’s life.
2. Rare but serious complication of the fetus at homebirth
In the rare and sudden case of a massive, complete placental abruption before crowning, whether the woman is at home or in the hospital makes no difference because complete anoxia causes the fetus to be brain damaged in 4 minutes and dead in 5 minutes. In the case of a marginal, incomplete placental abruption of less than 50%, even a 2 hour drive to hospital has not been shown to affect outcomes.
There is only one case and it most likely occurs less than 1 in 500,000 births, in the absence of malpractice. The only case in which planned homebirth is riskier than hospital birth for a low risk fetus is the when she experiences a sudden, painless, incomplete (<50% separation) placental abruption, with no apparent bleeding in which no one was listening to the fetal heart rate. In the rare case of an assymptomatic placental abruption at home in which the FHT is being monitored, the fetus will survive a 45 minute transfer with the mother treated with oxygen. Threatening incomplete placental abruptions have fetal heart decelerations. If there is no bleeding apparent, the woman happened to feel none of the usual severe pain associated with placental abruption, and the fetal heart was not monitored, then yes, the baby will die at home, whereas if the woman happened to be on a monitor in the hospital, the fetus could be saved in a hospital. There is no research to know if this has ever happened. There are no case studies published about this, therefore one can only make an educated guess or estimate.
Placenta abruption has an overall incidence of 3/1000 births. Most are minor separations during pregnancy in which the pregnancy continues normally. The cause is not known. It is associated with (20):
1. Hypertension (present in 50% of abruptions that caused fetal death)
2. Multiple pregnancy- e.g. placenta separates after first baby delivers
3. Trauma and Car Accidents
4. Smoking during pregnancy
5. Rare: short umbilical cord less than 5 inches or 14 cm, uterine anomaly or tumor, sudden decompression of the uterus or sudden pressure of large uterus on the inferior vena cava while laying on back.
Serious abruptions are usually not asymptomatic and show 1 or more of the following signs (20)
70% Severe abdominal pain
70% Abnormal fetal heart
27% Vaginal bleeding
20% Hypertonia of the uterus
14% No contractions
Cord prolapse: Does not have better outcomes in the hospital than at home, because almost all cord prolapse happens to either low or high risk women either before labor starts ie before an attendant is present, which has no relevance to setting… or from hospital interventions during labor, typically routine AROM.
Umbilical Cord prolapse (UCP) is the event in which the cord slips down next to the fetal head or rump easily, but as labor progresses, the cord may be compressed in the birth canal, compromising the blood flow through the umbilical vessels, or the cord may vasospasm from cooler temperature in the vagina. In both cases cord compression can easily be detected by decelerations in the fetal heart rate. UCP is a rare occurrence- with an overall rate of between 1/750 - 1/1000 births (21)
Cord prolapse is associated with the following situations(22), none of which is appropriate for planned homebirth
1. breech or transverse presentation (50% of cases are
breech or transverse. The risk of UCP in breech is 5% more with footling
and less with complete breech, the risk of UCP in transverse presentation
3. multiple pregnancy
4. Artificial rupture of membranes
5. Labor induction
Therefore, the rate of cord prolapse occurring at attended homebirths has never been published and may be 1 in 10,000 or less.
If it happens : Recommended interventions are those that decrease pressure on the cord which are all easily carried out in a home setting if the practitioner is trained to diagnose the problem, then treatment is simple: Elevating the presenting part , Adopting the knee-chest & head-down position, Filling the bladder, and transfer to hospital unless the prolapse happened during crowning and the birth is expected to take place within 5 minutes. In a recent UK hospital study(22), it was possible to decrease diagnosis to delivery time DDT, but decreasing the DDT time from 25 minutes to 15 minutes until delivery did not statistically improve the fetal outcomes (22). In this study of 59 recent cord prolapses, 65% were delivered by CS, the rest vaginally, because sometimes the cervix is fully dilated and the babies are often small. Three/59 (5%) died, the rest were fine. Speeding up the diagnosis to delivery time did not improve fetal mortality or morbidity or the number of low apgars. Again, all the risk factors listed above which are associated with cord prolapse should not be taking place at home anyway. But if lowering the time from 25 minutes to 15 minutes made no difference, it is unclear whether there is a difference in outcomes between 25 minutes and 60 minutes. The critical factor seems not to be time, but early diagnosis and correct management . Outcomes are thought to be dependent on how vulnerable the baby is in terms of gestational age and viability. Turbo delivery has not been shown to improve outcomes.
The rush to delivery is not even always life saving. In a recent case at 23 weeks, the womans water broke and a loop of umbilical cord with a pulse was seen in the vagina. Since the baby was not viable, the hospital recommended delivery. The woman refused delivery. She was put in Trendelenburg position with head lowest, body angled at a downward position. Fetal heart tones were checked every 4 hours from 23 weeks and Two 12-mg intramuscular doses of betamethasone were administered 24 hours apart. The umbilical cord was prolapsed approximately 4 cm past the cervix. The cord never regressed into the uterus and the continued prolapse was documented on multiple examinations. At 25 weeks, the patient had some bleeding, contractions and moderate variable decelerations and underwent CS. The baby was discharged 11 weeks later in good condition. (22)
In a series of 132 cases of umbilical cord prolapse at varying gestational ages (23–42 weeks) treated only with either elevation of the presenting part or knee-to-chest position, “Murphy etal reported that only one stillbirth/neonatal death (0.7%) could be directly attributed to the UCP. Duval et al described 67 cases of UCP and reported that when the fetus was alive at the time of UCP diagnosis, elevation of the fetal presenting part resulted in a perinatal mortality rate of only 1.5% (one of 67). This procedure may be tedious for the obstetrician (sic) or uncomfortable for the mother if the time from UCP diagnosis to delivery is prolonged.” (22)
High fetal mortality of 45% associated with Cord Prolapse has been reported in the literature both for homebirths (including unattended) as well as some hospitals(22). It appears that hospital setting does not decrease mortality from cord prolapse. Since there are bad outcomes even in the presence of quick diagnosis to delivery times, there must be other factors involved. Perhaps the degree of cord compression, length of the cord that has prolapsed also influence neonatal outcome. In the only study of long-term outcome in children whose perinatal course was complicated by UCP, a 2-year neurodevelopmental follow up was done on 13 infants delivered because of prolonged premature rupture of membranes and UCP, in which the diagnosis to delivery interval ranged from 10 to 720 minutes and the gestational age at delivery ranged from 24 to 34 weeks. One infant died of complications from prematurity and the remaining 12 had normal 2-year neurodevelopmental outcomes.
Some researchers have suggested that cords that prolapse happen in fetuses
that are compromised previous to the cord prolapse. They suggest
that poor oxygenation and acidemia CAUSES UCP, not the other way
around. They said that cord that are not getting enough oxygen are more
rigid therefore less buoyant and therefore prolapse more. (22)
The research suggests but does not conclude that faster delivery is
the key to less fetal mortality. Cesarean delivery appears
to have brought down the fetal mortality rate from UCP. Since UCP
is most likely to happen in high risk clients who have no option of a planned
homebirth, until research shows otherwise, it is incorrect to use UCP as
an excuse to say a woman would be safer in hospital.
Ruptured uterus – The most common cause of ruptured uterus is previous CS and the next most common cause is stimulation of labor with pitocin, in particular when used, against protocol on women with a predisposition for uterine rupture, such as previous major surgery on the cervix or uterus including cesarean section, overdistention of the uterus, grand multiparity, or past history of uterine sepsis or of traumatic delivery.. Williams Textbook of Obstetrics puts it simply, “The previously untraumatized, spontaneously laboring uterus will not persist in contracting so vigorously as to destroy itself.” If it were to occur in a low risk woman at a planned homebirth, lets say with a history of a D&C that damaged the uterine wall, for example, it is so easily diagnosed by listening to the fetal heart, bleeding and lack of contractions, that is not a “rare but serious complication of homebirth that will have better fetal outcomes in hospital. Ruptured uterus happens 1 / 20,000 in the second and third trimesters, and is always associated with a previous CS or other uterine damage, placenta previa or placenta accreta. Despite this risk, we do not recommend that all high risk women spend their entire pregnancy in hospital based on the premise that this rare and serious complication has better outcomes if the woman is already in hospital.
Placenta accreta can happen at a homebirth, in which case, the placenta does not deliver, the woman is transferred to hospital if the placenta fails to deliver by 30 minutes. A 1-2 hour transfer time does not affect outcomes.
Fetal Anoxia or distress
It was hypothesized that a 33% CS rate would lower the cerebral palsy rate at least a drop, but it hasn’t. The rate of cerebral palsy of baby’s born at term is the same as 100 years ago.
Half of all children who develop cerebral palsy are among the 85-90% of babies born at full term and the other 50% are among the 7-15% (varies by country) of babies born before 37 weeks who are not appropriate for homebirth. Among children born at term, the incidence of cerebral palsy is reported to be between 1.1 per 1000 and 1.5 per 1000 deliveries. (23) It is estimated by 5 international studies that 66% of cerebral palsy is due to a defect that develops long before birth and CS will not prevent CP because there is no oxygen deprivation at the birth- as measured by cord blood pH for example(23). For the other 33% or 1 /2,500 births, CP is thought to be caused by conditions or events that happens before, during or soon after birth. The birth asphyxia displays itself in late decelerations or severe bradycardia usually associated with inductions and/or placental abruption, and damage can sometimes be prevented with quick diagnosis and speedy cesarean. Research shows that in about 60% of these cases the CP was preventable, but hospital care givers did not respond to the signs of distress. (23) Sometimes it is caused by a placental abruption that happens at home before labor starts and a cesarean performed within 45 minutes of the event, is enough to save the baby but not to protect the brain from damage. Currently, it appears that cesareans are saving as many babies from brain damage, as they are saving babies with brain damage who previously would have died, which may explain the lack of change in the cerebral palsy rate.
The effect of neonatal care is similarly uncertain. Expert neonatal care probably prevents brain damage from developing in some critically ill neonates. In other cases, however, intensive neonatal care, by preventing the death of critically ill babies may lead to survivors who develop cerebral palsy.
The hope in 1960, when technological fetal monitoring became accepted as routine practice was to diagnose fetal distress and prevent fetal damage from birth and lower the rate of cerebral palsy. This hope was never actualized. Six decades later it is clear that continuous fetal monitoring of low risk women definitely raises the cesarean rates wherever it is used, which increases uterine rupture and placenta previa, which increase cases of fetal hypoxia. Electronic fetal monitoring has never been shown to decrease brain damage. It may slightly lower the rate of neonatal seizures after birth, but has not been shown to improve long term health.
Autism is on the rise, and is certainly is not being prevented by hospital birth.
In summary, there is no truth the statement: ‘in the case of a serious emergency, being in the hospital could save the mother’s life and very little evidence that ‘in the case of a serious emergency, being in the hospital could save or the life of the baby of a low risk woman. Unfortunately, giving birth in hospital has been proven to always involve more interventions and more cesareans. In the absence of a basis to recommend low risk women to deliver in hospital, it is also encumbent upon practitioners to inform women of the outcomes that happen to them as a result of choosing hospital birth:
3.Common, serious complications to the low risk mother of hospital birth:
Postpartum Hemorrhage (PPH)
In the latest RCT study of low risk women, PPH occurred at the rate of 3.8% in planned homebirth vs 6% in the planned hospital group. (4) The speed and method of the delivery of the placenta, and not the routine prophylactic administration of Pitocin, has been shown to be the critical factor at preventing PPH. In attended homebirth practice, delivering the placenta in squatting position between 4 to 5 minutes postpartum, has resulted in 0% (none) PPH at all among 300 consecutive homebirths. (24)
The biggest risk factors for blood loss of > 1,500 ml are (25):
1. Emergency caesarean delivery (X3.6 )
2. von Willebrand’s disease Rate: 1/10,000 women- very low platelets (X3.3),
3. Elective caesarean delivery (X2.5),
4. Multiple pregnancies (X2.3) and
5. Anaemia (haemoglobin <9 g/dl) during pregnancy (2.2).
6. Slightly higher risk: Birth weight of >4.5 kg, Delivery by forceps or vacuum, induced and prolonged labour, previous Caesarean delivery, cardiac diseases prior to pregnancy and HELLP syndrome
In addition to the increased risk of death from CS, 2 of the top 3 biggest risk factors for severe obstetric PPH are greatly increased at hospital births. Severe PPH usually requires blood transfusion, which has rare but severe side effects. Post partum hemorrhage weakens the woman at a time when she is vulnerable to uterine and breast infections. PPH is likely to cause death, anemia, fatigue, depression , failure to breastfeed. Large postpartum hemorrhages cause Sheehans syndrome, in which the pituitary does not get enough blood and the woman does not make the hormones necessary to produce milk to breast feed.
Aside from deemphasizing death rates, the risks of postpartum hemorrhage from cesarean are glossed over for the purposes of making cesareans appear to be safe. Universally the definition of postpartum hemorrhage is more than 500 cc. However, the definition of postpartum hemorrhage at a cesarean has arbitrarily been set at over 1000 cc, because all cesareans involve blood loss of more than 500 cc, therefore every woman undergoing cesarean has a postpartum hemorrhage of 500 cc, whereas only 5-13% of women have postpartum hemorrhages at vaginal hospital births. This redefinition of PPH for cesareans is justification for not including in the cesarean consent form the fact that every single cesarean will have a postpartum hemorrhage and its long term affects. Instead the definition of hemorrhage was raised to artificially hide this fact from women. A case appears in the literature of a mother who lost so much blood at a cesarean that she went completely blind for 24 hours and partially blind for another 24 hours(26).
Whilst uterine atony is responsible for the majority of primary PPH, surgical obstetrical causes such as episiotomy comprise about 20% of all primary PPH. Episiotomy increases risk of PPH as well as near death from infection (27). Women who planned a homebirth and had a vaginal birth had a 3% episiotomy rate compared to 7%rate among vaginal births for the hospital group using the same practitioners. (4)
INDUCTION / AUGMENTATION WITH PITOCIN
The majority of women in hospital receive oxytocin in labor, whereas no women receive oxytocin during labor at home. Receiving synthetic oxytocin during labor for a prolonged time during labor increases risk of postpartum hemorrhage because of reduced uterine response to oxytocin. (28) Routine prophylactic pitocin has been shown to decrease breastfeeding rates by 6-8%.(29)
Planned homebirth involved a 0.7% rate of uterine infection vs 2.7% rate for hospital birth for low risk women (4). The 4 times increase of infection between homebirth and hospital birth happens also to be the same as the difference in infection rates between vaginal birth 1.8% and after cesarean delivery =8%(14). Maternal infection carries with it the risk of death or long term infertility. Infection has been shown to be associated with hospital routines such as AROM, internal monitoring, and routine vaginal checks. A significant risk factors for UTI was receipt of more than 5 vaginal digital examinations. (30) Hospital acquired nosocomial infections, by definition are absent at homebirths.
EPIDURALS: Common side effects: Common side effects are temporary or long lasting back pain, temporary or long lasting continence. 15% of those who have an epidural 5 hours or more will have a fever, which may cause seizures in the newborn afterbirth, 5% will have a migraine afterwards lasting a few days to a week. Rare side effects :.
Bupivacaine has caused several deaths by cardiac arrest when epidural anesthetic has been accidentally inserted into vein instead of epidural space in the spine. (31)
Epidural Hematomas: epidural hematoma, 1 in 168,000;
deep epidural infection, 1 in 145,000;
persistent neurologic injury, 1 in 240,000;
transient neurologic injury, 1 in 6,700 (32 )
How often would the baby have had a better outcome at an attended homebirth?
4. Common, serious complications to the baby at hospital birth:
50% of births in which the fetus suffers anoxia and Apgar scores below 7 at birth have been documented to be a result of IV Pitocin. (33) Approximately half of all paid obstetric litigation claims involve allegations of oxytocin misuse. Although hospital birth brings with it the availability of expert doctors trained at infant resuscitation, this has not been shown to improve outcomes for low risk births, since it is well established that infant mortality at planned homebirths matches infant mortality at hospital births. There is evidence from Sweden that the presence of skilled personnel in cases of asphyxia in the hospital does not improve outcomes because of insufficient compliance or adherence to guidelines for neonatal resuscitation and slow paging of skilled personnel, including delayed initiation of excessive resuscitation, lack of satisfactory ventilation, and untimely interruption of resuscitation.” (34)
In summary in his letter to the editor in a recent BJOG, Dr Groenendaal(35)
poignantly points out that well-trained teams of medical specialists in
hospital should be able to perform better in dealing with unexpected medical
emergencies such as perinatal asphyxia than caregivers at home. Since the
research shows they are not performing better, then perhaps our most important
challenge is to find out why and do something about it. Hear hear.
There is no indication that malpractice takes place more often at homebirths than hospital births. The intimacy of being in the client’s territory would logically tend to improve the accountability of the attendant. Malpractice in either setting can take the form of: Fundal pressure, episiotomy, drug errors, non-attendance to fetal heart, infant breathing or bleeding.
Learning from our mistakes:
An elderly man and woman, both in their 70's, walk into a sex therapist's office. The doctor asks, 'What can I do for you?'
The man says, 'Will you watch us have sexual intercourse?'
The doctor raises both eyebrows, but he is so amazed that such an elderly couple is asking for sexual advice, that he agrees.
When the couple finishes, the doctor says, 'There's absolutely nothing wrong with the way you have intercourse.' He thanks them for coming, charges them $50, and says good bye.
A week later the couple returns and asks the sex therapist to watch again.
The sex therapist is a bit puzzled, but agrees.
This happens several weeks in a row. The couple makes an appointment, has intercourse with no problems, pays the doctor, then leave.
Finally, after 3 months of this routine, the doctor says, 'I'm sorry, but I have to ask. Just what are you trying to find out?'
The man says, 'We're not trying to find out anything. She's married and we can't go to her house. I'm married and we can't go to my house. The Holiday Inn charges $98. The Hilton charges $139. We do it here for $50, and I get $43 back from Medicare.
The punchline makes it clear that in the absence of pathology or financial
distress, no one would have sex with a stranger watching. The same
goes for birth. Even when the management and the care givers are the same,
such as in the Janssen research (4), medical outcomes are not as good in
the hospital as at planned, attended homebirth. This must be brought
to light to optimize outcomes.
1. Tew M. Safer Childbirth? a Critical History of Maternity Care. Chapman & Hall. 1990.
2. Högberg U. The decline in maternal mortality in Sweden: the role of community midwifery. Am J Public Health. 2004 Aug;94(8):1312-20.
4. Janssen PA, Saxell L, Page LA, et al. Outcomes of planned home birth with registered midwife versus planned hospital birth with midwife or physician. CMAJ 2009;181(6-7):377-383.
5. Hutton EK, Reitsma AH, Kaufman K.Outcomes associated with planned home and planned hospital births in low-risk women attended by midwives in Ontario, Canada, 2003-2006: a retrospective cohort study.Birth. 2009 Sep;36(3):180-9.
6. Janssen PA, Lee SK, Ryan EM, et al. Outcomes of planned home births versus planned hospital births after regulation of midwifery in British Columbia. CMAJ 2002;166:315-23.
7. Wiegers TA, Kierse MJ, van der Zee J, et al. Outcome of planned home and planned hosptial births in low risk pregnancies: prospective study in midwifery practices in the Netherlands. BMJ 1996;313:1309-13.
8. Ackermann-Liebrich U, Voegeli T, Gunter-Witt K, et al. Home versus hospital deliveries: follow up study of matched pairs for procedures and outcome. BMJ 1996;313:1313-8.
9. Lindgren H, Radestad I, Christensson K, et al. Outcome of planned home births compared to hospital births in Sweden between 1992 and 2004. A population-based register study. Acta Obstet Gynecol Scand. 2008; 87: 751-9.
10. Cohain JS. Cesareans and Low Risk Women In Israel. The Practising Midwife.2004. 7:7:28-31.
11. Shiftan A, Tel-Oren A, Sheiner E, Hadar A. [Planned home deliveries in Israel between the years 2003-2007]Harefuah. 2009 Jun;148(6):362-6, 413. Hebrew.
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