Cerebro placental Ratio (CPR) as an predictor for foetal outcome

 

 

Cerebroplacental ratio (CPR) is an obstetric  ,,ultrasound tool used as a predictor of adverse pregnancy outcome in both small for gestational age (SGA) and appropriate for gestational age (AGA) fetuses. An abnormal CPR reflects redistribution of cardiac output to the cerebral circulation, and has been associated with intrapartum fetal distress, increased rates of emergency cesarean and NICU admissions and poorer neurological outcomes. 

It is calculated by dividing the Doppler pulsatility index (PI) of the middle cerebral artery (MCA) by the PI of umbilical artery (UA) pulsatility index:

CPR = MCA PI / UA PI

The index will reflect mild increase in placental resistance with mild reductions in the fetal brain vascular resistance. An abnormal cerebroplacental ratio may result in the following conditions:

• low normal range MCA and upper normal range UA PI
• abnormal low MCA and normal UA PI
• abnormal low MCA and high UA PI

It follows then that detection of perinatal risk based on CPR may occur in the setting of reassuring UA PI (but abnormal MCA), or even if both UA and MCA PI are within the normal range. The essence of the capacity of a pregnancy to develop normally is that there should be adequate supply of nutrients and oxygen. The principal supply lines are the uterine and umbilical arteries. The utero-placental blood flow has been found to be decreased in hypertensive pregnancies and fetal growth restriction , where instead of the low resistance and high flow state which is seen in normal pregnancies, there is decreased umbilical and uterine blood flow (2).

In antenatal period these small babies can be identified on clinical examination and ultrasonography, but the normal small fetus cannot be distinguished from the compromised small fetus. The Doppler Velocimetry has become an important tool in the evaluation and management of high-risk pregnancies. The umbilical and uterine Doppler abnormalities have been documented in pregnancy complicated by hypertension and fetal growth restriction (3,4). As it can detect abnormal feto-placental circulation, it can be used to differentiate between normal and compromised small fetuses that are at risk of adverse perinatal outcome (5).

The study was conducted with the aims and objectives to study the doppler velocimetric indices of the uterine and umbilical artery in normotensive and hypertensive pregnancy in the third trimester; to detect the number of small for gestational age fetuses with abnormal velocimetric study in each group & correlate the relation of birth weight and Doppler velocimetric findings with perinatal outcome in both the groups.

Material and Methods

The present study was conducted in the Department of Obstetrics and Gynaecology, in collaboration with the Department of Radiology of Mahatma Gandhi Institute of Medical Sciences, Sevagram. A total of 200 cases from the women attending the antenatal outpatient department were included in the study of which 100 were hypertensive and 100 normotensive. All the women had a singleton pregnancy of >32 weeks \gestation and vertex presentation and did not have any history of medical disorder. Both primigravida and multigravida were selected for the study. Among the hypertensive group the women who had recorded blood pressure of >140 / 90 on two or more occasions six hours apart after adequate rest were selected. Baseline investigations and Doppler velocimetry of both the uterine arteries and umbilical artery was performed in both the groups. The patients were followed up till delivery. The perinatal outcome were noted and compared with the results of the Doppler velocimetry.

POD fluid in USG what does that mean to a clinician ?

 

 POD fluid in USG what does that mean to a clinician ?

Diagnosing the Cause of and Measuring Cul-de-Sac Fluid –How we should interpret??

Principle: Cul-de-Sac fluid should always be evaluated at the time of a transvaginal ultrasound, as the findings are often helpful in supporting a diagnosis. Measurements of the largest pocket of fluid were taken in three planes: height, length and depth. If the fluid surrounded the uterus and was found anterior and superior to the uterus as well, the volume of the uterus was calculated and subtracted from the measurement of the fluid pocket.

The study determined that the measurements of fluid volumes correlated with the amount of fluid instilled in the patient during the study and were reproducible. On the other hand, the absence of fluid in the pouch of Douglas may also have clinical significance. For example, in a patient with endometriosis, an obliterated cul-de-sac secondary to agglutination of the peritoneal surfaces from scarring caused by infiltrating endometriosis will prevent fluid from pooling here.

The pouch of Douglas should always be evaluated at the time of a transvaginal ultrasound, as the findings are often helpful in supporting a pelvic pain diagnosis. Because fluid from the pouch of Douglas protects the body from contamination, checking it on transvaginal ultrasound is vital.

 

 

 

Point 1:     Role of 3D?? With the development and advancement of ultrasound technology, assessment of the type and amount of fluid in the pouch of Douglas has improved our ability to categorize what's found there. At the same time, 3D ultrasound has reduced the number of invasive and often painful procedures performed via the posterior vaginal fornix. Increased amount of fluid in pelvis

 

 

Point 2;  How best to define ascites?? The ultrasound definition of ascites has been described as fluid filling the pouch of Douglas and extending beyond the fundus of the uterus. A better definition or actual quantification of the fluid is needed as the size of a uterus varies from individual to individual. In 2010, a study published in the journal Ultrasound in Obstetrics & Gynecology determined that patient height and weight did not appreciably affect the calculation of pelvic fluid volumes up to 1 liter.

 

 

 

 

Q.1:  What is POD?? Ans : The pouch of Douglas exists between the uterus and the rectum and is the most dependent area of the pelvis, where fluids pool.

 

Q 2: Etiology of fluid collection?? Ans: Physiologic and pathologic cul-de-sac fluid takes many forms. 1) Menstrual blood that has refluxed through the fallopian tubes and 2)  fluids related to ovulation or 3)  ruptured cysts settle in it. 4)  blood from a ruptured ectopic pregnancy, 5) inflammatory debris from a pelvic or appendiceal infection and 6) ascites due to malignancy, liver or 7) cardiac failure may collect here.

 

Q,3: What will be amout ?? The amount may be copious or simply a small bit that is noted on routine ultrasound evaluation.

Transvaginal ultrasound image of small amount of fluid in cul-de-sac (arrow)

 

Q. 4: What Is the Pouch of Douglas? 

The area in question is situated in close proximity to the posterior vaginal fornix, which provides a potential keyhole for access to the pelvic cavity.

Q.5: Clinical Relevance of POD?? Diagnostic culdocentesis, drainage of cul-de-sac fluid collections and abscesses, and biopsies of cul-de-sac masses are examples of procedures that can be performed. Even minimally invasive actions, such as egg retrievals for IVF or bilateral tubal ligations, have been accomplished via this route.

Q.7: Who was Douglas??  Ans; This small, seemingly insignificant and shapeless space was named after an esteemed 18th-century Scottish physician and anatomist who lived in London and cared for women during childbirth. Dr. James Douglas was the queen's personal doctor. He also performed dissections in his home and published his findings and observations on a broad range of subjects. His surviving papers and anatomic drawings are preserved at the University of Glasgow and his immortality assured with several anatomic landmarks carrying his name, including the pouch of Douglas.

Q.8: What to Look for in the Pouch of Douglas during USG?

Studies published in 1982 in Radiology and in 1998 in the Journal of Ultrasound in Medicine demonstrated that A) echogenic masses and B)  cul-de-sac fluid on transvaginal ultrasound are highly predictive of the finding of clotted blood and hemoperitoneum. C) Inflammatory effusions can have a variety of ultrasound features depending on the stage of the disease process. The discovery of filmy adhesions in the cul-de-sac fluid is suggestive of a past or chronic infection.

 

Q.9: What mstakes may occur?? A full urinary bladder may displace pelvic fluid out of the pouch of Douglas. This could lead to the mistaken diagnosis of ascites, which would have significant clinical implications.

 

Fluid (arrow) and ovary in cul-de-sac

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LH hypersecretion in PCO

  

 Is LH hypersecretion is the chief cause of PCO : The possible pathogenesis LH hypersecretion which in turn leads to  ovarian hyperandrogenism in PCOS. The cardinal clinical features of PCOS are menstrual irregularity from anovulation and occasionally hirsutism. Obesity occurs in approximately 50% of hyperandrogenic anovulatory women, some of whom also have non-insulin-dependent diabetes mellitus.

Underlying these clinical findings are several biochemical abnormalities, including LH hypersecretion, hyperandrogenism, acyclic estrogen production, decreased SHBG capacity, and hyperinsulinemia, all of which contribute to increased ovarian production of androgens, particularly T. A fundamental mechanism of ovarian hyperandrogenism in PCOS is LH hypersecretion.

 Whether the central nervous system is a possible locus for initiating LH hypersecretion remains unclear, because exaggerated LH secretion is temporarily reversed by induced ovulatory cycles or physiologic luteal concentrations of progesterone.

 

Is PCO initiates in utero- diseases of PCO is imprinted on female foetus?? Reasons:, desynchronization of pulsatile LH secretion from sleep in girls with PCOS and an exaggerated (e.g., masculinized) early LH response to GnRHa testing in women with hyperandrogenic anovulation and congenital adrenal virilizing disorders suggest that events occurring before puberty, perhaps during fetal life, may irreversibly alter neuroendocrine function. Hyperinsulinemia from insulin resistance is an important regulatory mechanism governing ovarian hyperandrogenism.

 

Hyperinsulinemia in hyperandrogenic anovulatory women potentiates ovarian hyperandrogenism by enhancing LH secretion; potentiating 17-hydroxylase and, to a lesser extent, 17,20-lyase activity; and suppressing SHBG capacity. It is a key component of hyperandrogenic anovulation caused by a type of insulin resistance that in independent and additive to that of obesity alone. Although the mechanisms governing insulin action on ovarian steroidogenesis are unknown, abnormalities of intracellular insulin signaling or cytochrome P450c 17[alpha] activity may render the 17-hydroxylase/17,20-lyase enzyme complex more sensitive to insulin.

  :  Why so much abdominal fat ?? Hyperinsulinemia in hyperandrogenic anovulatory women is accompanied by upper-body obesity characterized by an increased amount of abdominal fat. Upper-body obesity is an important independent risk factor for CVD and diabetes. Although genetic and environmental factors affect fat distribution, sex steroids, particularly androgens, regulate lipid metabolism, suggesting yet another link between the hormonal and metabolic abnormalities of hyperandrogenic anovulation. A careful history and physical examination guide the extent of diagnostic testing. Slowly progressive hirsutism with anovulation of peripubertal onset usually reflects hyperandrogenic anovulation. This type of clinical presentation requires an evaluation to rule out other endocrinopathies (e.g., virilizing tumors, adult-onset CAH, hyperprolactinemia, and Cushing's syndrome). Virilization or severe rapidly progressive hirsutism requires immediate investigation to rule out a possible virilizing tumor. The ultimate goals of therapy for hyperandrogenic anovulatory women are to normalize the endometrium, antagonize androgen action at target tissues, reduce insulin resistance, and correct anovulation, if necessary. Obesity is a common cause of anovulation in developed countries. It has been estimated that 50% of women who are more than 20% over their ideal weight will be anovulatory or have luteal insufficiency. Often a 20% reduction in body weight is all that is required to restore fertility. Because obesity is associated with PCO, PCOS and insulin resistance, these disorders must be ruled out or treated first before attempting OI

NAC-N Acetyl cysteine as an insulin sensitizers ,and antioxidants : Role of NAC in PCOS , Diabetes and NASH

 NAC-N Acetyl cysteine  as an insulin sensitizers ,and antioxidants  : Role of NAC  in PCOS , Diabetes and NASH (Non Alcoholic Stato hepatitis N-Acetyl Cysteine is considered as one of the insulin sensitizers. Further NAC is believed  as antioxidant as well . As such NAC alone or more commonly with metformin is used in Ovulation induction but not routinely. So, it is felt that NAC is used occasionally in PCO women to potentiate the action of insulin.

Such NAC containg agents i.e. branded drugs as available in Indian  market are followings:  :-A) Chrominac-A (TTK) B) Met PCO Care (metformin 500, NAC 500 and C) Chirocyst Myoinositol  550 mg, DCI 13.8, NAC 600 mg

A)      NAC is used along with either CC and or letrozole to promote ovulation and improved oocyte quality NAC is also recognized as an antioxidants and researchers believe it prevents cellular injury in men and women with high blood sugar. High blood sugar causes glucose toxicity. However NAC and the antioxidant α[alpha ]-lipoid acid have  been in this way proposed and clinically used as an insulin sensitizer. 

 

B)         Can NAC be used along with  CC in unexplained subfertility ?? 

 

C)         Following are the comments in Fertility and Sterility

D)         Volume 86, Issue 3, September 2006, Pages 647-650

E)           

F)           Ovulation induction

G)         Clomiphene citrate plus N-acetyl cysteine versus clomiphene citrate for augmenting ovulation in the management of unexplained infertility: a randomized double-blind controlled trial

H)         Author links open overlay panel::  AhmedBadawyM.D.^aAbuBaker El NasharM.D.^bMohamedEl TotongyM.D.^a

I)             Show more

J)            https://doi.org/10.1016/j.fertnstert.2006.02.097Get rights and content

K)         Objective

L)          To compare clomiphene citrate with N-acetyl cysteine vs. clomiphene citrate alone for augmenting ovulation in management of unexplained infertility.

M)       Design

N)         Prospective randomized double-blind controlled trial.

O)         Setting

P)           Department of obstetrics and gynecology in a university medical faculty in Egypt.

Q)         Patient(s)

R)         Four hundred four patients as a study group (clomiphene citrate plus N-acetyl cysteine group) and 400 patients as a control group (clomiphene citrate–alone group). All women had unexplained infertility.

S)           Intervention(s)

T)          Patients in the study group were treated with clomiphene citrate (50-mg tablets) twice per day and with N-acetyl cysteine (1,200 mg/d orally) for 5 days starting on day 2 of the cycle. Patients in the control group were treated with clomiphene citrate with sugar powder.

Main Outcome Measure(s)

The primary outcomes were number and size of growing follicles, serum E₂, serum P, and endometrial thickness. The secondary outcome was the occurrence of pregnancy.

Result(s)

There were no statistically significant differences between the two groups in the number of follicles sized >18 mm, mean E₂ levels, serum P, or endometrial thickness. Pregnancy rate was comparable in both groups (22.2% vs. 27%). Miscarriage rate was comparable in both groups (6.7% in the study group vs. 7.4% in the control group).

Conclusion(s)

N-Acetyl cysteine is ineffective in inducing or augmenting ovulation in patients with unexplained infertility and cannot be recommended as an adjuvant to clomiphene citrate in such patients.

 

NAC is used in various indications and one of the uncommon indication is  NASH(non‐alcoholic steatohepatitis (NASH) which may appear in 4/5^th decades of life in PCO women . It has been observed that combination of N‐acetylcysteine and metformin improves histological steatosis and fibrosis in patients with non‐alcoholic steatohepatitis

There is no proven medical therapy for the treatment of non‐alcoholic steatohepatitis (NASH). Oxidative stress and insulin resistance are the mechanisms that seem to be mostly involved in its pathogenesis of liver injury in long standing PCO or Diabetes mellitus in either sex, . There have been studies  to evaluate the efficacy of  treatment. N ‐acetylcysteine (NAC) in combination with metformin (MTF) in improving the aminotransferase and histological parameters (steatosis, inflammation, hepatocellular ballooning, and fibrosis)

 

Methods: months. A low calorie diet was prescribed for all patients. months. All patients underwent evaluation of serum aminotransferase, fasting lipid profile and serum glucose, anthropometric parameters, and nutritional status at 0 and 12 mg/day) were given orally for 12 g/day) and MTF (850–1000 years [36–68] and body mass index [BMI] 29 [25–35]) with biopsy‐proven NASH were enrolled in the study. NAC (1.2 2 ± Twenty consecutive patients (mean age 53

Results: NAC along with Metformin may yield to  modest reduction of followings like serum alanine aminotransferase, high‐density lipoprotein, insulin, and glucose concentrations and the  homeostasis model assessment–insulin resistance (HOMA‐IR) index .The BMI  too declined, but without statistical significance. Where NAC are ineffective?? Aspartate aminotransferase, gamma‐Glutamyl Transferase, alkaline phosphatase, cholesterol, and triglycerides levels are  not altered with the treatment by combination of  NAC & metformin . Liver steatosis and fibrosis decreased ( P <0.05), but no improvement was noted in lobular inflammation or hepatocellular ballooning. The NASH activity score was significantly improved after treatment. 

Conclusion: Based on the biochemical and histological evidence of different studies  NAC in combination with MTF appears to ameliorate several aspects of NASH, including fibrosis.

What is glucose toxicity in DM & longstanding  PCO  and  role of antioxidants    α[alpha ]-lipoid acid & NAC ??  Long standing high glucose in blood leads to Oxidative stress. This oxidative stress (ROS)  has been implicated in glucose toxicity. It is presumable that  certain antioxidants may prevent insulin-resistant glucose transport that develops in adipocytes after sustained exposure to high glucose, provided insulin is present.

The antioxidant α[alpha ]-lipoid acid has been proposed as an insulin sensitizer. In research settings 3T3-L1 adipocytes were preincubated 18 hours in media containing insulin (0.6 nmol/L) with low (5 mmol/L) or high (25 mmol/L) glucose with or without [alpha ]-lipoate, dihydrolipoate (each 0.1 to 0.5 mmol/L), or N-acetylcysteine (1 to 5 mmol/L). After extensive re-equilibration in insulin and antioxidant-free media, basal and maximally insulin-stimulated (100 nmol/L) glucose transport was measured.

Insulin was quantified by radioimmunoassay. Preincubation with   α [alpha ]-lipoate and dihydrolipoate but not N-acetylcysteine increased subsequent basal glucose transport; the effect was much smaller than that of acute maximal insulin stimulation.

 

Preincubation in high glucose without antioxidants inhibited acutely insulin-stimulated glucose transport by 40% to 50% compared with low glucose. This down- regulation was partially or completely prevented by each antioxidant. In cell-free media, the 2 reluctant, dihydrolipoate and N-acetylcysteine, rapidly decreased immunoreactive insulin, but [alpha ]-lipoate was ineffective. However, during incubation with adipocytes, [alpha ]-lipoate, and dihydrolipoate promoted the decline in immunoreactive insulin nearly equally.

Because insulin and high glucose are synergistic in inducing insulin resistance in this model, the reduction in immunoreactive insulin probably contributed to the protective effect of the antioxidants. 3T3-L1 adipocytes efficiently metabolize [alpha ]-lipoate to dihydrolipoate, which may be released into the medium. The stimulation of glucose transport by [alpha ]-lipoid acid may represent redox effects in sub cellular compartments that are accessible to dihydrolipoate.

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