Recovery from pelvic bone problems after childbirth
Date updated: December 05, 2007
Bets Davis, MFA; Kathe Gallagher, MSW
Content provided by Healthwise Separated pubic symphysis
The left and right bones of your pelvic girdle are joined at the front by a narrow section of cartilage and ligament. This is called the pubic symphysis, or symphysis pubis. As the pelvic bones loosen during pregnancy, the pubic symphysis can temporarily separate. Although this is not a dangerous condition, it can be painful.
You can feel the pubic symphysis by pressing on your lower front pelvic bone, just above your genital area. Your health professional can tell when it is separated or misaligned simply by pressing on it. During pregnancy and after childbirth, you can realign your pubic symphysis by lying back on your elbows and squeezing a pillow between your raised knees. This is likely to temporarily relieve pain and pressure.
A separated pubic symphysis can take 3 to 8 months to heal on its own. For most women with this condition, pain or discomfort lingers for about 2 months after childbirth.
During childbirth, pressure from the baby's head can fracture the coccyx, or tailbone. A fractured coccyx can be quite painful and symptoms can take months to subside. Many women gain relief after about 2 months of physical therapy, nonsteroidal anti-inflammatory drugs (NSAIDs), and ice. If your pain is severe and prolonged, talk to your health professional about pain medication.
June 23, 2002
Highlights Prevalence of Disorder
Scientists Share Findings on Pain Research and New Therapies
Many women have it, but few talk about it. Some will seek out doctor after doctor-typically, about five-before getting a diagnosis.
Vulvodynia is a condition characterized by burning, stinging, irritation, or rawness of the female genital area when there is no apparent infection or skin disease that could cause these symptoms. Vulvodynia includes vulvar vestibulitis (pain on contact in the vulvar vestibule) and vulvar dysesthesia (unprovoked, generalized vulvar pain). An estimated 14 million American women may have vulvodynia at one point in their lives, although for many women the condition remains undiagnosed. Vulvodynia can have a profound impact on a woman's quality of life, hindering her ability to exercise, have sexual intercourse, and take part in social activities.
Recently, more than two hundred researchers, clinicians, and members of the public gathered at the National Institutes of Health (NIH) to take part in the workshop, "Vulvodynia-Toward Understanding a Pain Syndrome." Phyllis Leppert, M.D., Ph.D., of the National Institute of Child Health and Human Development (NICHD), and Maria Turner, M.D., of the National Cancer Institute, chaired the workshop. Participants presented an overview of the science and incidence of vulvodynia, classified the varieties of vulvar pain, devised research approaches to studying the condition, and developed strategies for alleviating vulvar pain.
The workshop was sponsored by the NICHD, along with the NIH's Office of Diseases and Office of Research on Women's Health.
Bernard Harlow, Ph.D., of Brigham and Women's Hospital's Obstetrics and Gynecology Epidemiology Center in Boston, reported that in his study, 16 percent of more than 3,000 women who responded to a survey said they had experienced chronic, or long-term, burning, knifelike pain or pain on contact that lasted three months or longer. Nearly seven percent of the respondents were experiencing pain at the time of the survey.
Dr. Harlow and his coworkers also found that Hispanic women were 80 percent more likely to experience chronic vulvar pain than were white and African American women.
The findings were published in the April issue of The Journal of the American Women's Medical Association.
Other research highlights from the conference include:
- Sophie Bergeron, Ph.D., Universite de Quebec, Montreal, reported that vulvar vestibulitis may require treatment spanning a variety of medical specialties, including group cognitive behavioral therapy, biofeedback, and vulvar surgery, to relieve pain and associated sexual impairment over the long term.
- Nina Bohm-Starke, M.D., Karolinska Institutet, Sweden, presented evidence that vulvar vestibulitis may result from inflammation (swelling) brought on by the nerves of the vulva.
- Jacob Bornstein, M.D., Carmel Medical Center, Haifa, Israel, reviewed the literature regarding the results of vestibulectomy-surgical treatment for vulvodynia. Surgery was most successful in women who were determined to have vulvar vestibulitis, but it did not help women already experiencing unprovoked, generalized vulvar pain
- David Foster, M.D., University of Rochester, presented his work on vulvar vestibulitis. He found that this disorder does not consistently show classic evidence of inflammation, such as white blood cells in the tissue. He reported that a subgroup of cells in the vulvar area near the vaginal opening show a density of prostaglandins-molecules that indicate inflammation-greater than cells in other areas of the vulva.
- Donald C. Manning, M.D., Ph.D., University of Virginia, and Calgene Corporation, described the complexities of developing and testing new drugs for pain, some of which have the potential for treating vulvodynia.
- Barbara Reed, M.D., University of Michigan, reported that many of her patients sought out doctor after doctor for more than five years before receiving a diagnosis of vulvodynia.
- Jay P. Shah, M.D., NIH Clinical Center, discussed the role that a category of pain known as myofascial pain and dysfunction might play in vulvodynia. Vulvar myofascial pain occurs when a muscle becomes overloaded due to tense pelvic floor holding patterns or trauma, causing extremely irritable bundles of fibers to become "knotted." These bundles, known as myofascial trigger points, lead pain to other areas.
- Elizabeth G. Stewart, M.D., Harvard University, presented an overview of current therapies for vulvodynia, including estrogen, corticosteroids, acupuncture, physical therapy, biofeedback, antidepressants, and surgery. A low-oxalate diet combined with calcium pills has been helpful in some cases. Oxalates are found in certain vegetables such as eggplants.
- Karl B. Thor, Ph.D., Dynogen Pharmaceuticals, Inc., and Duke University Medical Center, presented new findings suggesting that nerve damage caused by surgery to repair injury resulting from childbirth may result in vulvodynia. He described the anatomy of the newly discovered Human Levator Ani Nerve, and theorized that damage to this nerve may play a role in vulvodynia.
- Ursula Wesselmann, M.D., Ph.D., Johns Hopkins University School of Medicine, reported on her study of chronic visceral (internal organ) pain. She discussed her finding that different types of pain caused by different pain mechanisms may occur in the same person.
This is the second NIH-sponsored workshop on vulvodynia. The first,
Current Knowledge and Future Directions," was held at NIH in April 1997. Sponsored by the NICHD, the National Institute of Arthritis and Musculoskeletal and Skin Diseases, and the Office of Research on Women's Health and the Office of Rare Diseases, NIH, the 1997 workshop explored the state of the science by reviewing definitions, epidemiology, and treatments for vulvodynia.
Primary Postpartum Haemorrhage (PPH)
Department of Obstetrics and Gynecology, Geneva University Hospital
Primary postpartum haemorrhage is still one of the leading causes of maternal mortality. The problem has recently been reviewed (1). The risk of death from PPH in Britain is about one in one million deliveries. The risk of death from PPH in women who do not have access to blood transfusion has been estimated to approximately 1 in 1000 deliveries. Although postpartum haemorrhage is usually defined as a haemorrhage of more than 500 ml, haemorrhages of less than 1 litre are usually without major consequences (1). A pregnant non-obese woman has a blood volume of approximately 80 ml/kg body weight and signs of cardiovascular shock are usually observed after a loss of more than 15% of the circulating volume. Severe symptoms of shock are usually observed after a volume loss of 30 or more per cent of intravascular volume, i.e., of between 1.5 and 2 litres in a normal pregnant woman of 70 kilos. In a hospital setting such a degree of hypovolaemia is rare as volume replacement is instituted promptly in the case of major postpartum haemorrhage. (Note: few people die of anaemia but many die of hypovolaemia.)
Anatomy and physics of postpartum haemorrhage due to placental causes and uterine atony. As these are the most common forms of postpartum haemorrhage, it is worthwhile recalling the following facts. Postpartum haemorrhage due to other than trauma arises from the placental bed which is obviously inside the uterus. The blood supply comes from outside the uterus and traverses the myometrium. Primary haemostasis from the placental bed is due to compression of the uterine vessels as they pass through the myometrium. The degree of compression of these vessels depends on the force acting on the vessels. This force obeys the Young-Laplace relationship (F= 2T / r ), where F equals the compressive force acting on the blood vessels, T is the wall tension (generated by the uterine contraction), and r is the radius of the uterus. It is apparent that the force compressing the vessels cannot be very high if r is large. Therefore, it is essential that the radius of the uterus be made small by emptying the uterus from any blood or placental tissue and increasing the wall tension of the uterus (T) by giving ecbolics. This is the scientific basis of the initial treatment and the prevention of primary postpartum haemorrhage.
Predisposing factors. These are well known, the most important factors being previous postpartum haemorrhage, large intrauterine volume (multiple pregnancy, large baby, polyhydramnios), maternal age and obesity.
Prevention of postpartum haemorrhage. It is well accepted that active management of the third stage and routine administration of oxytocin or an ergot alkaloid, or a combination thereof, is indicated and effective. The short duration of oxytocin administered intravenously and the hypertensive effect of ergot alkaloids administered intravenously are well recognized.
Treatment of primary postpartum haemorrhage. Every obstetric unit should have a protocol for the management of postpartum haemorrhage which is well known to every member of the obstetric team. The team must be able to act as a team.
Most maternal deaths are avoidable and are due to underestimation of blood loss, inadequate volume replacement, and delay in operative intervention. Any delay in achieving haemostasis results in terminal coagulopathy (dilutional coagulaopathy and later disseminated intravascular coagulopathy due to prolonged shock). At this stage even surgery may be too late. Hence rapid and resolute action is paramount.
The key steps are as follows.
(1) Placenta - where?
Establish whether the placenta is delivered.
Establish the mother's cardiovascular status (pulse, and if immediately available, blood pressure)
(3) Source of bleeding?
Palpate the abdomen to establish whether haemorrhage is likely to come from the placental bed or the lower genital tract.
Call for help.
These four steps take less than one minute.
(5) Remove placenta
If the placenta has not been removed from the uterus and the patient's cardiovascular condition is worrying, remove the placenta. Do not wait for the anaesthetist because if you wait the patient may be dead by the time the anaesthetist arrives. In less acute cases or where the placenta has been delivered, insert a wide gauge intravenous cannula and infuse colloid and crystalloid solutions and red blood cells if available. As soon as anaesthesia is available deliver the placenta, check the uterine cavity and the lower genital tract. Meanwhile, unless bleeding is major, proceed with the following steps.
(6) Make uterus contract - treat hypovolaemia
Manually stimulate the uterus to contract, give further injections of ergometrine or Syntometrine, intravenously if deemed necessary. Start continuous infusion of oxytocin (30 units in 500 ml saline).
(7) Bimanual compression - uterine artery stretch
Bimanual compression of the uterus prevents an increase in the radius of the uterus due to bleeding in the uterus and atony. Simultaneously, the uterus is pushed cephalad, which puts the uterine arteries under tension and reduces blood flow to the uterus. Catheterise bladder.
(8) If bleeding persists and the uterus is not firmly contracted (indicating that at least part of the bleeding is due to uterine atony rather than trauma) administer the prostaglandin drug that is part of the hospital's routine.
To my knowledge, all the uterocontracting prostaglandins currently available have been used successfully in the treatment of uterine atony (2-17). The success rate for cases refractory to oxytocin and the ergot alkaloids seems to be situated between 80-90% for all prostaglandins used. The analogues (15-methyl-...PGF2a = carboprost = Prostin /15MR = HemabateR etc., 16, 16-dimethyl..PGE1 methylester = gemeprost = CervagemR etc., sulprostone = NaladorR etc., and misoprostol = CytotecR) seem to have less side effects than the natural prostaglandins (PGF2a et PGE2). Various routes of administration ro have been described, even for the same drug (intrauterine, intramyometrial, transabdominal and intracervical, transvaginal, intravenous, intramuscular, vaginal and rectal). The most interesting drug seems to be misoprostol which is cheap and does not require storage at a low temperature. Rectal administration ((5 tables of 200 m g = 1 g) is efficient in cases refractory to oxytocin and ergometrine (16). After administration of misoprostol (400 m g rectally) given prophylactically the duration of the 3d stage and blood loss were similar to that after syntometrine (1 ampoule) but the incidence of diastolic hypertension was lower (18). This is in keeping with reports on the prophylactic use of carboprost vaginally or rectally (19). Direct intramyometrial injection of prostaglandins may act faster but carries the risk of intravenous injection which may lead to several cardiovascular side effects including cardiac arrest (20-23)
(9) Uterine packing
Packing using gauze, gauze placed within a plastic bag, or using inflatable tubes (e.g., Sengstaken-Blakemore), accompanied by temporary external compression of the uterus has been recommended. It may be particularly useful in cases of placenta praevia accreta (24,25).
(10) Aortic compression
Transabdominal compression of the aorta against the promontorium is done in preparation for laparotomy if required. In all cases the uterus must be closely supervised i.e., a midwife must be with the patient with her hand on the patient's uterus and ensuring that the uterus does not relax and fill with blood.
(11) Treat anaemia, coagulopathy, thrombocytopenia
(12) Operative procedures
Operative procedures are required in cases of refractory uterine atony and in cases of pathological placentation (the worst cases being those of placenta previa accreta/increta). Hysterectomy and ligation of the internal iliac arteries are well known procedures but not necessarily the best, particularly not in the case of placenta praevia. Hysterectomy may not be necessary while ligation of the internal iliac arteries may be ineffective (65% success rate in one report (26)), particularly in cases of uterine atony and placenta praevia where the already rich collateral circulation is particularly well developed. If internal iliac artery ligation is carried out the artery should be ligated quite distally from its origin from the common illiac arteries as the uterine arteries originate from distal branches of the internal iliac. This is technically difficult.
I. Bilateral mass ligation of the uterine arteries. This has been used in cases of bleeding during Caesarean sections (n=265 over 30 years (27)). Sutures including 2-3 cm of myometrium are placed 2-3 cm below the uterine incision.
II. Stepwise uterine devascularisation. This consists of (1) unilateral and, if required (2) bilateral uterine vessel ligation, followed by (3) low bilateral uterine vessel ligation after mobilisation of the bladder, and (4) unilateral or bilateral ovarian vessel ligation (28) Both techniques allow revascularisation of the ligated vessels with subsequent normal uterine function.
III. Uterine compression sutures. A technique used in cases of uterine atony has been described by B-Lynch (29,30). A similar method has been used also ( 31)
IV. Arterial embolisation. This effective technique is often impractical for primary massive haemorrhage for organisational reasons. It should be considered in cases of protracted primary PHH and in cases of secondary PPH (32-34). A highly skilled invasive radiologist is required.
1. Drife J. Management of primary postpartum haemorrhage (Commentary). Br J Obstet Gynaecol 104:275-277, 1997.
2. Markos AR. Prostaglandin E2 intrauterine suppositories in the treatment of secondary postpartum haemorrhage. J R Soc Med 82(8):504-505, Aug 1989.
3. Peyser MR, Kupferminc MJ. Management of severe postpartum hemorrhage by intrauterine irrigation with prostaglandin E2. Am J Obstet Gynecol 162(3):694-696, 1990.
4. Sarkar PK, Mamo J. Successful control of atonic primary postpartum haemorrhage and prevention of hysterectomy, using i.v. prostaglandin E2. Br J Clin Pract 44(12):756-757, Dec 1990.
5. Meinen K, Lange R, Breinl H. Intramyometrial PGF2 alpha administration in the control of severe atonic postpartum hemorrhage. Geburtshilfe Frauenheilkd 48(4):268-270, April 1988.
6. Schonegg W, Wessel J, Schmidt-Gollwitzer K. Experiences with intravenous sulprostone administration in massive postpartal hemorrhage. Geburtshilfe Frauenheilkd 47(11),789-791, Nov 1987.
7. Buttino L Jr, Garite TJ. The use of 15 methyl F2 alpha prostaglandin (Prostin 15M) for the control of postpartum hemorrhage. Am J Perinatol 3(3):241-243, Jul 1986.,
8. Bigrigg A, Chissell S, Read MD. Use of intra myometrial 15-methyl prostaglandin F2 alpha to control atonic postpartum haemorrhage following vaginal delivery and failure of conventional therapy. Br J Obstet Gynaecol 98(7):734-736, Jul 1991.
9. Bates A, Johansen K. The use of gemeprost pessaries to arrest postpartum haemorrhage. Br J Obstet Gynaecol 101(3):277-278, Mar 1994.,
10. El-Lakany N, Harlow RA. The use of gemeprost pessaries to arrest postpartum haemorrhage. Br J Obstet Gynaecol 101(3):277, Mar 1994.
11. Phuapradit W, Saropala N, Randsipragarn R. Treatment of atonic postpartum hemorrhage with a prostaglandin E2 analogue. J Med Assoc Thai 76(6):303-
307, Jun 1993.
12. Oleen MA, Mariano JP. Controlling refractory atonic postpartum hemorrhage with Hemabate sterile solution. Am J Obstet Gynecol 162(1):205-208, Jan 1990.
13. Trivedi AN. Gemeprost pessaries for postpartum haemorrhage. N Z Med J 111(1065):175, 1998.
14. Goffinet F, Haddad B, Carbonne B, et al. Utilisatioin pratique du sulprostone dans le traitement des hémorragies de la délivrance. J Gynecol Obstet Biol Reprod 24(2):209-216, 1995.
15. Kupferminc MJ, Gull I, Bar-Am A, et al. Intrauterine irrigation with prostaglandin F2-alpha for management of severe postpartum hemorrhage. Acta Obstet Gynecol Scand 77(5):548-550, May 1998.
16. O'Brien P, El-Refaey H, Gordon A, et al. Rectally administered misoprostol for the treatment of postpartum hemorrhage unresponsive to oxytocin and ergometrine: a descriptive study. Obstet Gynecol 92(2):212-214, Aug 1998.
17. Barrington JW, Roberts A. The use of gemeprost pessaries to arrest postpartum haemorrhage. Br J Obstet Gynaecol 100(7):691-692, 1993.
18. Bamigboye AA, Merrell DA, Hofmeyr GJ, et al. Randomized comparison of rectal misoprostol with Syntometrine for management of third stage of labour. Acta Obstet Gynecol Scand 77(2):178-181, Feb 1998.
19. Liu C, Wang D, Li X. Clinical study on reduction of postpartum bleeding by methyl carprost suppository. Chung Hua Fu Chan Ko Tsa Chih 32(1):22-24, Jan 1997.
20. Kilpatrick AW, Thorburn J. Severe hypotension due to intramyometrial injection of prostaglandin E2. Anaesthesia 45(10):848-849, Oct 1990.
21. Popat MT, Suppiah N, White JB. Cardiac arrest following myometrial injection of prostaglandin E2. Anaesthesia 46(3):236. Mar 1991.
22. Veber B, Gauthe M, Michel-Cherqui M, et al. Severe hypertension during postpartum haemorrhage after i.v. administration of prostaglandin E2. Br J Anaesth 68(6):623-624, Jun 1992.
23. Chen FG, Koh KF, Chong YS. Cardiac arrest associated with sulprostone use during caesarean section. Anaesth Intensive Care 26(3):298-301, Jun 1998.
24. Druzin ML. Packing of lower uterine segment for control of postcesarean bleeding in instances of placenta previa. Surg Gynecol Obstet 169(6):543-545, Dec 1989.
25. Bobrowski RA, Jones TB. A thrombogenic uterine pack for postpartum hemorrhage. Obstet Gynecol 85(5 Pt 2):836-837, May 1995.
26. Chattopadhyay SK, Deb Roy B, Edrees YB. Surgical control of obstetric hemorrhage: hypogastric artery ligation or hysterectomy? Int J Gynecol Obst 32:345-351, 1990.
27. O'Leary JA. Uterine artery ligation in the control of postcesarean hemorrhage. J Reprod Med 40:189-193, 1995.
28. AbdRabbo SA. Stepwise uterine devascularization: a novel technique for management of uncontrollable postpartum hemorrhage with preservation of the uterus. Am J Obstet Gynecol 171:694-700, 1994.
29. B-Lynch C, Coker A, Lawal AH, et al. The B-Lynch surgical technique for the control of massive postpartum haemorrhage: an alternative to hysterectomy? Five cases reported. Br J Obstet Gynaecol 104:372-375, 1997.
30. Goddard R, Stafford M, Smith R. The B-Lynch surgical technique for the control of massive postpartum haemorrhage: an alternative to hysterectomy? Five cases reported. (Letter). Br J Obstet Gynaecol 105:125-128, 1998.
31. Schnarwyler B, Passweg D, von Castelberg B. Successful treatment of drug refractory uterine atony by funds compression sutures. Geburtshilfe Frauenheilkd 56(3):151-153, Mar 1996.
32. Marpeau L, Rhimi Z, Larue L, et al. Place de l'embolisation artérielle pelvienne dans le traitement des hémorragies graves de la délivrance. J Gynecol Obstet Biol Reprod 21:233-235, 1992.
33. Yamashita Y, Harada M, Yamamoto H, et al. Transcatheter arterial embolization of obstetric and gynaecological bleeding: efficacy and clinical outcome. Br J Radiol 67:530-534, 1994.
34. Collins CD, Jackson JE. Pelvic arterial embolization following hysterectomy and bilateral internal iliac artery ligation for intractable primary postpartum haemorrhage. Clin Radiol 50:710-714, 1995.-------------------------------------------------------------------------------------------------------------------
Basically, it looks like what used to be my inner vulva were completely ripped away by the baby . The inside of my vagina is now the outside: bulges of flesh covered with mucus membranes . What happened to the skin that used to be there? There is a lot more mess in my panties. Water gets in when I bathe (seems unhygienic).
I have never seen this discussed in any website. Is this what is meant by the vague items like "you may lose some vaginal muscle tone"??!! More like had my privates replaced by completely different ones. I feel freaked out and alienated from my body now.
I did have what the doc described as a 2nd degree tear , which she stitched and okayed at the checkup later. childbirth" 10 months ago -- Should the appearance of my inner vulva , urethra, vaginal opening be so different compared to before the birth ? The urethra is about 1/2 inch higher up. The vaginal opening, which used to be a small (0 - 1cm) opening which I could clench shut at will, now takes up the entire cleft , no matter how many Kegels I do.
Yeah, nobody ever tells you about this stuff. I had an episiotomy and then tore all the way through to my rectum. Took them just about as long to sew me up as it took to push out my son. My opening is very large too, sorry. My Dr. will actaully be repairing it after this one, hopefully, and stitching it smaller. I almost need 2 tampons to keep them in, so not cool. I would bring it up to your Dr. ,but some of the changes aren't going to be fixed, that's a lot of trauma for your body to go through. I keep reminding myself of how lucky I am to have my son and another one on the way, but it's still hard. I won't ever wear a bikini either. I keep telling my DH that I'm getting a tummy tuck and new boobs when we are done, I think he thinks I'm kidding...
my god imma mess..everyone always says how pretty i am but under my clothes.. im jus disgusted..im only 22! i have 2 beautiful children and im a proud mother but my breasts sag and my stomach looks like a butt.. a flabby saggy butt! lol man.. but i dont know what to do.. i dont have the money for a tummy tuck or a boob job.. not to mention those ugly skin tags on my anal region. its hard to except this.. when i bend over i look skinny if you just cut off that layer of skin hanging from abdomen.. its embarassing.. and it jus cant be helped without surgery .. ive tried to tighten up but nothin helps when it comes to those areas.. i have a relationship with my boyfriend and he's all nice and fit.. and here i am with my blub, i guess im just bitchin but neede to get it out ya know? my inner lips hang outside my vagina a lil... can any of this be helped without the cost of surgery ?
This is all very true. Just had 2nd baby urethral prolapse, but now it's healing with estrace cream, but things look so swollen . don't know what to do. and things down there are way diff than 1st baby . Bulging urethra looks swollen all around. I can see up my vagina. It looks completely diff. I've been to doc 2x telling him that I think something is wrong. Also feeling a lot of pressure down there, as if something's falling out. II had a
ok i have to say I'm SOOO glad I'm not
alone in this. Up until I read this thread i though I was just
loosing my mind.
This is a bit TMI but I'm desperatly trying to find answers to this. I have the 'buldging' out of my vagina too. It actually sticks out and somtimes rbs on my panties. Hurts and makes the whole thing sore honestly. I've asked my GYN about it and he just blows it off as not knowing what I'm talking about. BUT for some reason when I'm standing up, it sticks out, if I lay down it goes back in??? Anyone gone through this???? Any tips on what to tell my gyn to get him to understand? It's horrible having sex too, makes it really painful most of the time, when I told him that all he did was give me estragen cream. Sorry that doesn't help the big spot that is getting irrated. And no it's not from lack of being 'wet' either, it just seems that the actual act makes it hurt.
I have one kid who is 18 months so I know I've had plenty of time to recover from childbirth and do kegels yet it doesn't help.
im22 gt2kids. goin for a boob job on 23rd ov month. am a b cup bt realy saggy, i boob to th ground, breast fed fr6wks.stomach is bigger thn b4 wen i bend over its so saggy, it discusts me. i had 2 vaginal birhs. one with an epesiotomy and forceps vagina looks realy messed up loads ov skin it looks like a pile ov mince to b honest. sex ? lucky i have sex once a month, no enjoyment fr me or my partner he let slip one time and said have u ever had a tight one? i was upset, i think he thought i knew i had a big1, not until thn i didnt. ive sufferd rely bad depression as i didnt want my last prregnancy coz i knew it would do ths to my body. i feel my partner owes me big time for disforming me a such.im a young girl with an old womans body. ppl say im lucky bt tthey dnt c underneath my clothes. i just wish sum1 told me b4i had kids
© 2005 International Anesthesia Research Society
Single-Dose, Sustained-Release Epidural Morphine in the Management of Postoperative Pain After Elective Cesarean Delivery: Results of a Multicenter Randomized Controlled Study
Brendan Carvalho, MBBCh, FRCA*, Edward Riley, MD*, Sheila E. Cohen, MBChB, FRCA*, David Gambling, MB, BS, FRCPC, Craig Palmer, MD, H. Jane Huffnagle, DO, Linda Polley, MD||, Holly Muir, MD¶, Scott Segal, MD#, Christine Lihou, CCRA**, Garen Manvelian, MD** for the DepoDur Study Group
*Department of Anesthesia, Stanford University School of Medicine, Stanford, California; Sharp Mary Birch Hospital for Women, San Diego, California; Department of Anesthesiology, University of Arizona Health Sciences Center, Tucson, Arizona; Department of Anesthesiology, Thomas Jefferson University, Philadelphia, Pennsylvania; ||Department of Anesthesiology, University of Michigan Medical School, Ann Arbor, Michigan; ¶Department of Anesthesiology, Duke University, Durham, North Carolina; #Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women’s Hospital, Boston, Massachusetts; and **SkyePharma, Inc., San Diego, California
Address correspondence and reprint requests to Brendan Carvalho, MBBCh, FRCA, Department of Anesthesia, Stanford University School of Medicine,300 Pasteur Dr., Stanford, CA 94305. Address e-mail to firstname.lastname@example.org
In this multicenter, randomized, controlled study, we compared the analgesic efficacy and safety profile of a new single-dose extended-release epidural morphine (EREM) formulation (DepoDurTM) with that of epidural morphine sulfate for the management of postoperative pain for up to 48 h after elective cesarean delivery. ASA physical status I or II parturients (n = 75) were anesthetized with a combined spinal/epidural technique. Parturients received intrathecal bupivacaine 12–15 mg and fentanyl 10 µg for spinal anesthesia and a single epidural injection of either 5 mg of standard (conventional preservative-free) morphine or 5, 10, or 15 mg of extended-release morphine after cord clamping for postoperative pain control. Single-dose EREM 10 and 15 mg groups significantly decreased total supplemental opioid medication use and improved functional ability scores for 48 h after surgery compared with those receiving 5 mg of standard morphine. Visual analog scale pain scores at rest and with activity at 24 to 48 h after dosing were significantly better in the 10- and 15-mg single-dose EREM groups versus the standard morphine group. There were no significant differences between the two 5 mg (single-dose EREM and standard morphine) groups. Single-dose EREM was well tolerated, and most adverse events were mild to moderate in severity. Single-dose EREM is a potentially beneficial epidural analgesic for the management of post-cesarean delivery pain and has particular advantages over standard morphine for the period from 24 to 48 h after surgery.
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