POSTPARTUM HEMORRHAGE

Postpartum Hemorrhage

Postpartum hemorrhage is blood loss of > 500 mL during or immediately after the 3rd stage of labor in a vaginal delivery or > 1000 mL in a cesarean delivery. Diagnosis is clinical. Treatment depends on etiology of the hemorrhage.

Causes of postpartum hemorrhage :

> Uterine atony (the most common)
> Lacerations of the genital tract
> Extension of an episiotomy
> Uterine rupture
> Bleeding disorders
> Retained placental tissues
> Hematoma
> Uterine inversion
>Subinvolution (incomplete involution) of the placental site (which usually occurs early but may occur as late as 1 mo after delivery)


Risk factors for uterine atony include uterine overdistention (caused by multifetal pregnancy, polyhydramnios, or an abnormally large fetus), prolonged or dysfunctional labor, grand multiparity (delivery of ≥ 5 viable fetuses), relaxant anesthetics, rapid labor, and chorioamnionitis.

Uterine fibroids may contribute to postpartum hemorrhage. A history of prior postpartum hemorrhage may indicate increased risk.



Treatment

Ø Removal of retained placental tissues and repair of genital lacerations Uterotonics (eg, oxytocin , prostaglandins)
Ø Sometimes surgical procedures


Ø Intravascular volume is replenished with 0.9% saline up to 2 L IV; blood transfusion is used if this volume of saline is inadequate. Hemostasis is attempted by bimanual uterine massage and IV oxytocin infusion, and the uterus is explored for lacerations and retained placental tissues. The cervix and vagina are also examined; lacerations are repaired. Bladder drainage via catheter can sometimes reduce uterine atony.

Ø 15-Methyl prostaglandin F2 α250 μg IM q 15 to 90 min up to 8 doses or methylergonovine 0.2 mg IM q 2 to 4 h (which may be followed by 0.2 mg po tid to qid for 1 wk) should be tried if excessive bleeding continues during oxytocin infusion; during cesarean delivery, these drugs may be injected directly into the myometrium. Prostaglandins should be avoided in women with asthma; methylergonovine should be avoided in women with hypertension. Sometimes misoprostol 800 to 1000 μg rectally can be used to increase uterine tone.

Ø Uterine packing or placement of a Bakri balloon can sometimes provide tamponade. This silicone balloon can hold up to 500 mL and withstand internal and external pressures of ≤ 300 mm Hg. If hemostasis cannot be achieved, surgical placement of a B-Lynch suture (a suture used to compress the lower uterine segment via multiple insertions), hypogastric artery ligation, or hysterectomy may be required. Uterine rupture requires surgical repair.

Blood products are transfused as necessary, depending on the degree of blood loss and clinical evidence of shock. Infusion of factor VIIa (50 to 100 μg/kg, as a slow IV bolus over 2 to 5 min) can produce hemostasis in women with severe life-threatening hemorrhage. The dose is given q 2 to 3 h until hemostasis occurs.


Prevention

Ø Predisposing conditions (eg, uterine fibroids, polyhydramnios, multifetal pregnancy, a maternal bleeding disorder, history of puerperal hemorrhage) are identified antepartum and, when possible, corrected. If women have an unusual blood type, that blood type is made available. Careful, unhurried delivery with a minimum of intervention is always wise.

Ø After placental separation, oxytocin 10 units IM or dilute oxytocin infusion (10 or 20 units in 1000 mL of an IV solution at 125 to 200 mL/h for 1 to 2 h) usually ensures uterine contraction and reduces blood loss. After the placenta is delivered, it is thoroughly examined for completeness; if it is incomplete, the uterus is manually explored and retained fragments are removed. Rarely, curettage is required. Uterine contraction and amount of vaginal bleeding must be observed for 1 h after completion of the 3rd stage of labor.

Prepared and modified by MD. Niamul Hasan , MBBS Final Year BMCH

Oral Contraceptive Pills : Uses , Fuctions, Toxic Syndrommes..........

Oral cotraceptive pills are tablets that prevents conception. Perhaps its the most accepted contraceptive method in developing countries. Its principle function is to prevent conception and it doesn't give any protection against HIV and other STD's.

Oral Contraceptive Pills (OCP) are mainly two types.

1. Combiled OCP.

2. Progesteron OR Estrogen only Pills.

The mechanism of action of OCP is very simple. We know that female Menstrual cycle is devided into three phases.

1. Proliferative phase : Here estrogen is secreted by Ovary , which causes uterine endrometrial growth. After this phase there is sudden withdrwal af estrogen which causes Ovulation ( It is the fall of mature ovum into Peritoneal Cavity , which ultimately comes into the uterine tube and finally in uterus ).

2. Secretory phase : Here both Progesterone and Estrogen Causes more and more growth if endometrium and increase secretion by the uterine glands.

3. The Menstrual phase : Here sudden Withdrawal of Progesterone cause increase uterine contraction and shedding out of uterine endometrium with mature Ovum , which is visible as bleeding.

Now, OCP maintains a steady concentration of estrogen and progesterone into the body. Though , Ovulation occur due to sudden withdrawal of estrogen and OCP maintains estrogen level , so , there is no ovulation in the body. And , there is menstruation due to sudden withdrawal of progesterone , because , OCP intake should be stopped after 21 days. After this , the women will take 7 Iron tablets , and by this period there is sudden withdrwal of progesterone in the body. So , there is menstruation but without any ovulation.

Now, though there is no ovulation so , so Sperms inters into the vagina and uterus they can not find any mature ovum in female genital tract. So , there is no fertilization in the body. So, that women will not conceve .

By this way OCP maintains Contraception into the body.

Overweight and Its Relation to CHD

UNDERSTANDING CORONARY HEART DISEASE (CHD)

According to current estimates, 64.4 million Americans have one or more types of cardiovascular disease. Within cardiovascular diseases, coronary heart disease (CHD) is the single largest killer of Americans. CHD caused 502,189 deaths in the US in 2001 – about 1 in every 5. The American Heart Association estimates that 13.2 million Americans have CHD. In fact, up to half of all sudden, out-of-hospital cardiac deaths occur in people with no prior diagnosis of heart disease, and over two-thirds of heart attach sufferers have blockages in their arteries considered to be clinically “insignificant” in terms of plaque burden and percent stenosis. Until recently, it was widely held that most heart attacks were caused by a gradual build-up of atherosclerotic plaque within the arteries of the heart (“hardening of the arteries”), impedes blood flow, and eventually results in blocked blood vessels that can cause acute ischemic events such as unstable angina, heart attack, stroke, peripheral vascular disease, and a variety of other related debilitating conditions.

Source: Association for the Eradication of Heart Attack

Scientists now know that life-threatening cardiac events are very often linked to unstable, rupture-prone arterial deposits known as “vulnerable plaques.” These unstable plaques are associated with enlargement of the arterial vessel wall, and consist of soft, biologically active, thrombogenic fatty material covered by a thin fibrous cap and characterized by a large infiltration of activated macrophages, indicating a high level of inflammation. Inflammation leads to an accumulation of proteolytic enzymes, which leads to a breakdown or sudden rupture of the fibrous cap, without warning, resulting in the release or erosion of the fatty lipid core into the blood stream. Exposure to the thromboemboli cascade promotes the formation of blood clots that can cause acute ischemic events, such as unstable angina or myocardial infarction.

Researchers believe that these vulnerable plaques are responsible for 85% or more of all heart attacks, and that the same types of plaque deposits in the carotid and cerebral arteries may account for the majority of ischemic strokes.

Research 06 : Diabetes Can Be Cured Parmanantly.

Diabetes Mellitus ..... Its a very common name for some peoples of this world. Because its on the diseases that is also called a " silent killer ". But proper care can relives its symptoms. Let us Know what is Diabetes Mellitus (DM). Simply its a disease of Pancreatic B- Cells where there is less production of Insulin. As a result , blood glucose is not properly metabolised. So, there is extra amount of blood glucose which causes several symptoms. 

Now , DM is a great challenge to treat. Now a days one in every 300 aged person has Insulin Dependant Type-I Diabetes (IDDM-I) . So redical cure of it can save thousands of People. Still today the only prophylaxis that causes symptomatic releive is Controlling DM. But, Researchers have reached beyond the limit. Experiment of Animals like Rat , shows that a B-Celll transplantation can prodeces sufficient amount of Insulin . And its sufficient to meet the peripheral demand of Insulin in the body. As a result glucose metabolism will be restored to previous normal level. So it can relieve DM.......................

To BE Continued...................