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Showing posts with label obstetric. Show all posts
Showing posts with label obstetric. Show all posts

Wednesday, February 17, 2016


Hypertensive Disorders in Pregnancy( a quick review)

Hypertensive disorders of pregnancy can be classified as:
1. Gestational hypertension (formerly PIH or transient hypertension)
2. Pre-eclampsia and eclampsia
3. Pre-eclampsia superimposed on chronic hypertension
4. Chronic hypertension.

Gestational hypertension: It is said to be present when BP > 140/90 mm Hg for first time during pregnancy after 20 weeks, but no proteinuria. This is transient hypertension and blood pressure returns to normal by 12 weeks postpartum.

Pre-eclampsia: It is defined as new hypertension presenting after 20 weeks with significant proteinuria [more than 300 mg per 24 hours, or persistent 30 mg/dL (1+ on dipstick)] in random urine samples.

Chronic hypertension: BP > 140/90 mm Hg before pregnancy or diagnosed before 20 weeks gestation or hypertension first diagnosed after 20 weeks of gestation and persistent after 12 weeks postpartum.

Superimposed pre-eclampsia (on chronic hypertension): All chronic hypertensive disorders regardless of their cause predispose to development of superimposed pre-eclampsia or eclampsia. Pre-eclampsia is accompanied by proteinuria.

The pathogenesis of pre-eclampsia
Theories for development of pre-eclampsia:
1.     Increased pressor responses: Women with PIH have been found to have increased vascular sensitivity to pressors.
2.     Prostaglandins: In PIH, there is decreased prostacyclin production and increased thromboxane A2; resulting in vasoconstriction and sensitivity to infused Angiotensin II.
3.Nitric oxide Decreased levels are found in PIH patients.

4. Vascular endothelial growth factor (VEGF):
VEGF has been reported to be increased in serum from women with pre-eclampsia.

5. Genetic predisposition

6. Immunological factors: PIH is probably an immune response to antigenic sites on placenta.

7.Inflammatory factors: Pre-eclampsia is considered a disease due to extreme state of activated leukocytes in the maternal circulation.

Wednesday, April 27, 2011

Management of the Parturient With Cardiovascular Disease


Management of the Parturient With Cardiovascular Disease
Lisa M. Councilman, M.D. Temple, Texas

Introduction
The incidence of clinically significant cardiac disease in the pregnant population ranges from 0.1-4%,
unchanged in decades; however, the most frequently seen etiology is now congenital heart disease (70-80%)1 due in part to advances in surgical techniques for these patients and advances in medical therapy, allowing these women to survive into childbearing age.2 Ischemic heart disease is also seen more commonly today due to both the increasing number of women of advanced maternal age who are electing to undergo pregnancy and childbirth as well as advances in medical therapy for ischemic heart disease, allowing women with this condition to carry a pregnancy to term. While the incidence of cardiac disease in pregnant patients has remained relatively unchanged, the maternal mortality from cardiac disease has decreased from 6% in the 1930s to 0.5-2.7% today.1 The last decade has shown a decline in maternal mortality from congenital heart disease, and now acquired heart disease has risen to be the leading cardiac cause of maternal death, with myocardial infarction, aortic dissection, and cardiomyopathy as the main processes.3 Unfortunately, the  cardiovascular changes of pregnancy may place additional stress on patients with underlying cardiac disease, increasing the risk of peripartum morbidity and mortality when compared with the general population, with the actual risk depending on the underlying cardiac disease process.1,2 Taking the altered physiologic processes into account, women with congenital heart disease and those with a history of ischemic heart disease require special attention and a multidisciplinary cooperation for optimal outcome during vaginal delivery or
cesarean section. The decision to perform regional or general anesthesia will ultimately depend on a thorough
understanding of the cardiac condition and condition-specific hemodynamic goals.2

Tuesday, April 19, 2011

Non obstetric surgery during pregnancy


Non obstetric surgery during pregnancy is relatively common.
The most common indications for surgery during pregnancy are either pregnancy related or pregnancy non related. Pregnancy related surgery include interventions for cervical incompetence and surgery for ovarian cyst problems.
The most common non pregnancy related indications are acute abdominal problems( most commonly appendicitis and cholecystitis), maternal trauma and surgery for malignancies.
Anaesthetists who care for pregnant patients undergoing non-obstetric surgery must provide safeanaesthesia for both the mother and the foetus.  To maintain maternal  safety the physiological and anatomical changes of pregnancy must be considered and anaesthetic techniques and drug administration modified accordingly.  Foetal wellbeing is related to avoidance of foetal asphyxia, teratogenic drugs and preterm labour.
Physiological Changes during Pregnancy


Central Nervous System Effects

The minimal alveolar concentration (MAC) progressively decreases during pregnancy—at term, by as much as 40%—for all general anesthetic agents; MAC returns to normal by the third day after delivery. Changes in maternal hormonal and endogenous opioid levels have been implicated. Progesterone, which is sedating when given in pharmacological doses, increases up to 20 times normal at term and is probably at least partly responsible for this observation. A surge in -endorphin levels during labor and delivery also likely plays a major role
At term, pregnant patients also display enhanced sensitivity to local anesthetics during regional anesthesia; dose requirements may be reduced as much as 30%. This phenomenon appears to be hormonally mediated but may also be related to engorgement of the epidural venous plexus.
Obstruction of the inferior vena cava by the enlarging uterus distends the epidural venous plexus and increases epidural blood volume. The latter has three major effects: (1) decreased spinal cerebrospinal fluid volume, (2) decreased potential volume of the epidural space, and (3) increased epidural (space) pressure. The first two effects enhance the cephalad spread of local anesthetic solutions during spinal and epidural anesthesia, respectively, whereas the last may predispose to a higher incidence of dural puncture with epidural anesthesia

Saturday, October 23, 2010

Postpartum haemorrhrage

Postpartum haemorrhrage
Primary PPH is defined as blood loss of greater than 500 mL within 24 hours of delivery and affects about 5% of deliveries.
There are many known risk factors: prolonged third stage pf labor, preeclampsia, multiple gestation, foeceps delivery, and mediolateral episiotomy.
The three most common causes of PPH are uterine atony, retained placenta, and cervical/vaginal lacerations.

Retained placenta
This is the second most important etiology of PPH (roughly 20%–30% of cases).
It is suggested by the finding of an absent or incomplete placenta. If delivery of the placenta has not taken place, it must lead without delay to manual removal of the placenta, under anesthesia whenever possible, to ensure uterus emptying.

Uterine atony
Uterine atony is the leading cause of PPH, observed alone in 50% to 60% of cases; it presents as painless continuous bleeding, often developing slowly at the beginning.
 The other key diagnostic criterion is abdominal palpation of a soft and oversized uterus.
Prevention relies on active management of the third stage of labor.
Treatment is based on bladder emptying and oxytocin (10–20 IU; ±uterine massage). When these measures are not quickly effective cervical/vaginal lacerations must be searched for and then be followed by rapid implementation of prostaglandin treatment if bleeding still persists.

Cervical/vaginal lacerations
This is the third cause of PPH (roughly 10% of cases), and it is more likely to occur after instrumental extraction, fetal macrosomia, or quick labor and delivery before full cervical dilation.
Diagnosis is also suggested when retained placenta and uterine atony have been discarded. this diagnosis is often made much too late (the bleeding can be concealed in the vaginal wall or pelvis), when the parturient displays hemodynamic instability, coagulation disorders, and increasing pelvic pain.

Uterine inversion
This is a rare iatrogenic event (!1/1000) where the internal surface of the uterus is partially or completely exteriorized into the vagina. Clinical features include abdominal pain and often severe hemodynamic instability.
Immediate uterine reversion must be performed by the obstetrician and can be facilitated by short-time tocolysis (trinitrine as first line), using usually a potent IV vasopressor at the same time to counteract hypotension (phenylephrine or adrenaline).
Coagulation disorders
Coagulation disorders can be the cause or the consequence of PPH. Many causes can be listed (congenital, such as von Willebrand disease, or acquired,
such as HELLP syndrome, disseminated intravascular coagulopathy, anticoagulation therapy, etc). In fact, coagulation disorders are rarely a true triggering
cause of PPH.

Planning for obstetric hemorrhaged organizational aspects
The effective management of obstetric hemorrhage relies on very simple but often overlooked principles that all concur to timely treatment:
_ Simultaneous, coordinated, multidisciplinary management (ie, obstetricians, anesthesiologists, hematologists, laboratory and blood bank technicians, radiologists).
_ Consensual and practical definition of hemorrhage: any abnormal bleeding (in rate or duration) should trigger at once the diagnosis ofhemorrhage. This is particularly important after delivery where the border between physiologic bleeding and PPH must be clear-cut to avoid
any treatment delay.
_ Consensual, preplanned, step management available as a written operational protocol.

_ As a first step, the obstetric team needs to focus on the search and basic treatment of the three most common causes of PPH: retained placenta
(manual removal of the placenta and manual uterine exploration), uterine atony (bladder emptying and IV oxytocin _ uterine massage), and cervical/vaginal lacerations (examination of the vagina and cervix with
appropriate valves, and repair as needed). Simultaneously, the anesthetic team provides basic resuscitation and adequate analgesia for these obstetric interventions.
_ The second step is implemented as soon as the first step has proven ineffective at stopping the bleeding and no later than 30 minutes after initial PPH diagnosis, to improve effectiveness. It mainly relies on prostaglandin administration, either IV prostaglandin E2 (PGE2)
sulprostone or intramuscular 15-Methyl prostaglandin F2a
(PGF2a) carboprost; uterine tamponade can also be useful. More advanced resuscitation and monitoring are also usually needed and provided by the anesthetic team at this stage.
_ The third step is considered within an additional 30 minutes (and no longer than after 1 hour) if the second step has also failed to stop bleeding. It relies on invasive therapy, either surgical artery ligation _ B-lynch suture or
radiologic embolization.
_ The last step is hysterectomy; meanwhile, the use of recombinant activated factor VII (rFVIIa) can be considered.

Invasive therapy
Several invasive options are available to control PPH when medical treatment is unsuccessful at controlling bleeding: uterine balloon tamponade, arterial embolization, uterine compression sutures, and internal iliac artery ligation.

Uterine balloon tamponade
Uterine packing has long been the treatment of choice to manage PPH; it is safe, quick, and effective in a majority of cases. Various balloon devices have been used, with the Sengstaken-Blakemore esophageal catheter being the most frequently employed.
Uterine arterial embolization
Another less radical approach to control bleeding is the use of uterine artery embolization. It has become a well-recognized alternative method of treatment in the conservative management of PPH in association with
local or medical treatment, or in the event of their failure.
The reported success rate
of uterine artery embolization in the literature is more than 90%.
In most patients, fertility is preserved and normal menstruation returns almost 100%. Minor complications such as pain and transient inflammation with fever are rare (0%–10%). More severe complications such as
pelvic infection, pulmonary embolism, or uterus and bladder necrosis have been reported.

B-Lynch suture
the so-called B-Lynch uterine compression suture has been used successfully to control bleeding following failed conservative management.
This technique also allows uterus conservation for subsequent menstrual function and pregnancies and seems to be devoid of long-term sequelae.

Surgical iliac (or uterine) artery ligation
When uterine tamponade and arterial embolization fail, a laparotomy to perform iliac artery ligation is an option to preserve the uterus. It can also be performed as a first invasive option, during C-section delivery, or when
the patient is hemodynamically unstable or if embolization is not readily available.
When arterial ligation fails, hysterectomy is usually necessary. This may carry a higher risk of morbidity when compared with emergency hysterectomy performed
Without prior iliac artery ligation.

Hysterectomy
As a last resort, but decided on quickly when all other interventions have failed, peripartum emergency hysterectomy may be required to control bleeding and save lives.

Transfusion therapy and resuscitation
Transfusion should be initiated with red blood cells in all obstetric patients with signs of inadequate oxygen carrying capacity and inmost obstetric patients with a hemoglobin of less than 7 g/dL, or when blood loss is ongoing and the hemoglobin is around 7 g/dL. If
hemorrhage is accompanied by coagulation disorders, 15 to 20 mL/kg of fresh frozen plasma should be given as first-line treatment and target hemoglobin should be set higher, above 8 g/dL, to improve overall coagulation activity. Transfusion of platelet concentrates is recommended to treat active bleeding associated with thrombocytopenia below 50 G_L_1

Intraoperative cell salvage
Intraoperative cell salvage (or preoperative autologous donation in scheduled cases) has an undisputed role in obstetrics in patients with high risk such as placenta previa/accreta, massive fibroids, or rare blood type
or unusual antibodies. Intraoperative cell salvage can be also useful in the treatment of Jehovah’s Witnesses or in geographic areas where allogeneic blood supply is particularly problematic.

Recombinant factor VIIA (NovoSeven)
It was suggested that rFVIIa was often effective at
stopping or reducing the bleeding, particularly when other conventional treatments (see above) had failed. The dosage used varied roughly from 20 to 120 mcg/kg, without clear evidence of a dose-response relationship.
Nonetheless, because of lack of level 1 evidence, the use, dosage, and timing of rFVIIa are still a matter of debate.
‘‘rFVIIa may be considered as treatment for life-threatening post-partum hemorrhage, but should not be
considered as a substitute for, nor should it delay, the performance of a life-saving procedure such as embolization or surgery, nor the transfer to
a referring center.