STEP WISE PELVIC

DEVASCULARISATION
 Dr. Niranjan Chavan
MD, FCPS, DGO, DFP, MICOG, DICOG, FICOG
Professor and Unit Chief, L.T.M.M.C & L.T.M.G.H
Chairperson, FOGSI Oncology and TT Committee (2012-2014)
Treasurer, MOGS (2017- 2018)
Chair and Convener, FOGSI Cell- Violence against Doctors (2015-2016)
Chief Editor, AFG Times (2015-2017)
Editorial Board, European Journal of Gynecologic Oncology
Editor of FOGSI FOCUS, MOGS, AFG & IAGE Newsletters
Member, Managing Committee, IAGE (2013-2017)
Member , Oncology Committee, AOFOG (2013 -2015)
Recipient of 6 National & International Awards
Author of 15 Research Papers and 19 Scientific Chapters
Course Co-Ordinator, of 11 batches, of MUHS recognized Certificate Course of
Basic Infertility Management Including Endoscopy (BIMIE) at LTMGH
 INTRODUCTION

• Postpartum hemorrhage (PPH)

• World’s leading cause of maternal

mortality

• 1/3rd of all maternal deaths

worldwide PPH

• 60% of all maternal deaths in

developing countries
Countdown to 2015: Maternal, Newborn and Child Survival, WHO, 2012
 INTRODUCTION
• Majority of these deaths occur within 4
hours of delivery.

• A Practice Bulletin from the ACOG 2011,

places the estimate at 140,000 maternal
deaths per year or 1 woman every 4
minutes due to postpartum haemorrhage.
 POST PARTUM HEMORRHAGE

• Blood loss

• Vaginal deliveries > 500mL (3-5%)

• Caesarean section deliveries >1000mL (5-

7%)

• For clinical purposes, any blood loss that has the

potential to produce hemodynamic compromise

should be considered a PPH.

 TYPES OF PPH

• Primary (immediate) postpartum

haemorrhage

• Excessive bleeding that occurs within the

first 24 hours after delivery

• 70% due to uterine atony (failure of the

uterus to contract adequately after the
child is born)
 TYPES OF PPH

• Secondary (late) postpartum haemorrhage

• Excessive bleeding occurring between 24

hours after delivery of the baby and 6 weeks
postpartum

• Due to retained products of conception, or

infection, or both combined.
POSTPARTUM HAEMORRHAGE
PRESENTS AS
SHOCK
 SHOCK : SYMPTOMS
Mild (<20% Blood Volume Moderate (20–40% Blood Severe (>40% Blood Volume)
Cool extremities Same, plus: Same, plus:

Increased capillary refill time Tachycardia Hemodynamic instability

Diaphoresis Tachypnea Marked tachycardia

Collapsed veins Oliguria Hypotension

Anxiety Postural changes Mental status deterioration (coma)

CAUSES OF POSTPARTUM
HAEMORRHAGE
 ETIOLOGICAL CAUSE CLINICAL RISK FACTORS
Over distended uterus Polydramnios
Multiple gestation
Macrosomia
Uterine muscle exhaustion Prolonged labor
Precipitate labour
ABNORMALITY OF High parity
UTERINE Intra-amniotic infection Fever
CONTRACTION (70%) Prolonged rupture of membranes

Functional or anatomic distortion Fibroid uterus

of the uterus Placenta previa or abruptio
Uterine anomalies
Distended bladder may prevent
contraction of the uterus

Uterine-relaxing medications Halogenated anaesthetics,

nitroglycerin, magnesium sulphate
 ETIOLOGICAL CAUSE CLINICAL RISK FACTORS

•Retained products •Previous uterine surgery

•Abnormal placentation •High parity
•Retained cotyledon or •Abnormal placenta on ultrasound
RETAINED PRODUCTS OF succenturiate lobe •Retained blood clots
CONCEPTION (20%) •Incomplete placenta at delivery •Atonic uterus
 ETIOLOGICAL CAUSE
•Tears (lacerations) of the cervix,
vagina, or perineum
•Ruptured vulval varicosities
CLINICAL RISK FACTORS
•Precipitous delivery
•Operative delivery
•Mistimed or inappropriate use of
episiotomy

GENITAL TRACT TRAUMA (10%)

•Extensions, lacerations at •Malposition

caesarean section •Deep engagement

•Uterine rupture •Previous uterine surgery

•Uterine inversion •High parity

•Fundal placenta
 ETIOLOGICAL CAUSE CLINICAL RISK FACTORS
Pre-existing states History of hereditary
- haemophilia A coagulopathies
-von Willebrand‘s disease1 • History of liver disease
ABNORMALITIES OF
COAGULATION (<1%)
Acquired in pregnancy •Bruising
- Idiopathic thrombocytopenic •Elevated BP
purpura2 •Elevated BP
- Thrombocytopenia with •Foetal demise
preeclampsia •Fever
- Disseminated intravascular •Elevated white blood cells
coagulation •Antepartum hemorrhage
- Preeclampsia •Sudden collapse
- Dead foetus in utero
- Severe infection/sepsis
- Placental abruption
- Amniotic fluid embolus

Therapeutic anticoagulation History of thrombotic disease

MANAGEMENT OF POSTPARTUM
HAEMORRHAGE
 IMMEDIATE RESUSCITATION
• The primary treatment of PPH is to control the source
of bleeding as soon as possible and to replace fluid. Crystalloids restore
• Maintain airway, breathing and circulation volume in a 3:1 ratio
• Large bore IV Line: Fluid replacement
• O2 Inhalation Colloids restore
volume in a 1:1 ratio
• Crystalloid is the first fluid of choice for resuscitation.
Immediately administer 2 L of isotonic sodium chloride
solution or lactated Ringer’s solution in response to
shock from blood loss
• Blood transfusion
MEDICAL MANAGEMENT
 MANAGEMENT OF PPH
• External and internal bi-manual uterine massage

• Aortic compression

• Umbilical vein injection (injection of uterotonic into the

umbilical cord attached to the undelivered placenta)

• Manual exploration of the uterus and manual removal of the

placenta

• Repair of perineal trauma including repair of episiotomy

• Repair of cervical and high vaginal tears

 TEMPORIZING MEASURES

• Temporizing measures recommended for intractable atonic and non-atonic PPH

include:
1. External aortic compression
2. Bimanual uterine compression
3. Non-pneumatic anti-shock garment (NASG)
 SURGICAL MANAGEMENT OF PPH

• Uterine compression sutures

• Systematic pelvic devascularization

• Uterine artery embolization

• Total or sub-total hysterectomy

 SYSTEMATIC PELVIC DEVASCULARIZATION

• Uterine and utero-ovarian artery ligation followed

by internal iliac artery ligation.

• One of several uterus-conserving techniques.

• Relatively simple and effective procedure should

be taught during Obstetric and Gynaecologic
training.
 UTERINE ARTERY LIGATION

• Expose the lower part of the broad ligament.

• Feel for pulsations of the uterine artery near the junction of the
uterus and cervix.
• Pass a needle loaded with Catgut No 1-0 around the artery and
through 2–3 cm of myometrium (uterine muscle) at the level
where a transverse lower uterine segment incision would be
made. Tie the suture securely.
• Place the sutures as close to the uterus as possible because the
ureter is generally only 1 cm lateral to the uterine artery.
• Repeat on the other side.
 UTERINE ARTERY LIGATION

• 1ST Step in systematic pelvic

devascularisation.

• uterine arteries which provide

approximately 90% of uterine blood flow.

• Ligation of uterine arteries alone has

success rate of 80% in controlling PPH
SITES FOR LIGATING UTERINE ARTERY
 UTERO OVARIAN ANASTOMOSIS

• If the artery has been torn, clamp and tie the bleeding ends.

• Ligate the utero-ovarian artery just below the point where the ovarian
suspensory ligament joins the uterus.

• Repeat on the other side.

• Observe for continued bleeding or formation of hematoma.

• Close the abdomen in layers.

 INTERNAL ILIAC ARTERY LIGATION

• Experiments in the 1960’s by Burchell,

ascertained that ligating the hypogastric
artery turned the pelvic circulation like a
venous system, thereby aiding clotting and
controlling PPH.
• It is effective in Uterine atony, midline
perforation, large broad ligament or lateral
pelvic wall haematoma, multiple cervical tears
and lower segment bleeding.
 INTERNAL ILIAC ARTERY LIGATION

• Bilateral ligation results in 85% reduction in

pulse pressure and 50% reduction in blood
flow in the arteries distal to the ligation.
• Internal iliac artery ligation also helps the
vaginal bleeding as the vagina is supplied by
the vaginal branch of internal iliac.
• The reported success rate of bilateral internal
iliac artery ligation varies widely from 42% to
93%.
INTERNAL ILIAC ARTERY LIGATION
 POST-OPERATIVE CARE

• Antibiotics

• Analgesics

• Assess hemoglobin and labs for DIC

• Transfusion
 AUTHORS YEAR METHOD NO. OF SUCCESS RATES
WOMEN
Evans et al 1985 Internal iliac artery ligation 14 6/14 (42.8%)

Clark et al 1985 Bilateral hypogastric artery ligation 19 8/19 (42.1%)

Fahmy 1987 Uterine artery ligation 25 20/25 (80%)

Fernandez et al 1988 Internal iliac artery ligation 8 8/8 (100%)

Chattopadhyay et al 1990 Bilateral hypogastric aretry ligation 29 19/29 (65%)

AbdRabbo 1994 Step-wise uterine devascularisation 103 103/103 (100%)

Ledde et al 2001 Bilateral hypogastric artery ligation 48 43/48 (89.5%)

Hebisch et al 2002 Vaginal & uterine artery ligation 13 12/13 (92.3%)

Pennet et al 2004 Bilateral uterine artery ligation 5 2/5 (40%)

TOTAL 264 83.7%

 CONCLUSION

• Blood loss is consistently underestimated.

• Underestimation may result in inadequate treatment

resulting in complications or death.

• Ongoing trickling can lead to significant blood loss.

• Anaemia and other underlying health conditions may

profoundly affect a woman‘s ability to tolerate any amount

of blood loss.
 CONCLUSION

• Systematic pelvic devascularisation is an effective and uterus

conserving surgical method to control PPH.

• All health care providers providing maternity care require to

learn this life-saving skill to enable them to make a significant
contribution to reducing maternal deaths and to promote safe
motherhood.
 REFERENCES
• Countdown to 2015: Maternal, Newborn and Child Survival, WHO, 2012
• Lu M C, Fridman M, Korst L M. et al. Variations in the incidence of postpartum hemorrhage
across hospitals in California. Matern Child Health J. 2005;9:297–306.
• Sivan E, Spira M, Achiron R, Rimon U, Golan G, Mazaki-Tovi S, et al. Prophylactic pelvic artery
catheterization and embolization in women with placenta accreta: can it prevent cesarean
hysterectomy? Am J Perinatol 2010;27:455–61
• Harrisons Principle of Internal Medicine, 19th edition
• Global causes of maternal death: a WHO systematic analysis Lale et al.The Lancet Global
Health June 2014 , Volume 2 , Issue 6 , e323 - e333
• Iwata A, Murayama Y, Itakura A, Baba K, Seki H, Takeda S. Limitations of internal iliac artery
ligation for the reduction of intraoperative hemorrhage during cesarean hysterectomy in
cases of placenta previa accreta. J Obstet Gynaecol Res. 2010 Apr;36(2):254-9.