Lactobacillus or Döderlein Bacilli

 White Discharge- A menace for Woman. Leucorrhoea-Persistent long term annoying white discharge with or without pruritus vulvae, may or may not be associated with Urinary symptoms .Possibly 1 in 5 cases of gynae cases seen at our clinic are of such symptoms, so also at OPD.

Lactobacilli are the most abundant bacteria present in normal vaginas of women of child-bearing age (with some exceptions due to race, geographic location and ethnic groups) .

How many of us are aware that Lactobacilli (D Bacilli)  are mainly derived from intestinal microbiota. This symptom of vaginal discharge is strongly suspicious of some common but drug resistant infections as such come to our clinic after  some treatement by one / two GP or even  occasionally by two-three consultants. It is therefore presumable that such cases are some resistant strains of bacteria or fungus and therefore warrant some uncommon investigations which are not always available in all towns(fungal culture) . Leucorrhoea / Whites are therefore --It’s a challenge for the Gynaecologists ll!

Q. 1: Vaginal Ecosystem & Immune system of vaginal mucosa and vaginal fluid is the least discussed topic.

Why and how entry of offending bacteria, parasites and viruses inside the vaginal canal are continuously prevented still remains an enigma to  even the Gnaecologists of repute.

Q.2: What are the normal vaginal Flora???

•         Let us talk about most commonly discussed bacteria- i.e. Lacto Bacilli(D. Bacilli) .

•         1) There are about 100 species of L B.

•         2) They principally produce Lactic Acid as well as Hydrogen Peroxide.

•        .

Q. 3 : Besides  Hydrogen  Peroxide and Lac acid there are  the Defensins which maintains ecosystem of vaginal mucosa .

•         Defensins: :-Usually neutrophils and macrophages of body excrete this substances to fight against any invading organism. At vaginal fluid  Lact. Bacilli also synthesize such some other antibacterial substances to kill against invading organisms

Q.4: What are Bacteriocins. Who normally liberates   Bacteriocins? It is   by Lact. Bacilli???

•         IV) Bacteriocins. These are group of anti-bacterial substances (chemical) which are produced by one strain of bacteria which are harmful against another strain of the same family.

Q.5. How the defense system is normally maintained?

•         It is already known that 1) L. Acid, 2)  H2O2, 3) Defensins, & 4) Bacteriocins .-all collectively fight with the  invasive organisms . These four are important both in prevention of overgrowth of pathogenic bact & their proliferation. Additionally one should also think of about pH of vaginal fluid- which is normally   3.5-4.5.à This high pH is key inhibitor in preventing growth of anaerobic organisms. 

Q. 6: Persistent white discharge not responding to your diagnois!!! Please do consider if she oestrogen-deficient clinically because of the fact that the population and work force of L. Bacilli &  Doderlein   bacilli depend much on estrogen.

•         If the women concerned is oestrogen deficient her conc. of Doderlein   bacilli, (L. Bacilli) , H2O2  and Lac. Acid   in vagina will be less.

•         As such, she  will be a candidate for recurrent  bacterial vaginosis not amenable to the most appropriate antimicrobials as was selected by the clinicians  .

 

Q.7: Where are the sources of normal virginal secretions?

•         After attaining adulthood--Vagina is almost always moist (oestrogen effect) . It  comes from transudation from multilayered virginal mucosa . Incidentally Vaginal mucosa do not contain any glands (in contrast to esophagus) to secrete any fluid.

 

Q.8:-What are the normal & usual sources of vaginal secretions?

•         Sources are:- Transudates from vaginal  walls, cervical secretions, Endometrial and tubal fluids, secretions from sebaceous glands, sweat glands, Skene glands of ext. urethral glands , Bartholin glands. Any such gland can pour & cause  much-  annoyance to the woman concerned.

 

Q.9:-Qualities of Normal Vaginal Fluid- How it looks and feels like? Ans: White, Thin, flocculent, without any smell/ pruritus. It contains many micro-organisms and their metabolic products that are excreted in the fluid.

•         Normally there is a bio-film of normal commensal (Doderlein   bacilli)  in the vaginal mucosaà prevents entry of bacteria into the mucosa.

Reproductive Hormones are the key regulators of amount, character of Discharge.

 

 

 

 

Q. 10 : The history of discovery of Lacto bacilli ?    Ans ; Lactobacilli are the most abundant bacteria present in normal vaginas of women of child-bearing age. In the last decade, there have been quite a lot of scientific advances reported regarding the immunology and pathophysiology of human vaginal microbiota. As a result, physicians have a more comprehensive understanding of the role that lactobacilli exert in the vaginal milieu and their interactions- with vaginal mucosa, pathogenic bacteria and fungi. There have been advances in vaginal microflora, vaginal epithelial cells, immunity, bacterial vaginosis (BV) and candidiasis. Additionally, recent reports regarding

Lactobacilli are the most abundant bacteria present in normal vaginas of women of child-bearing age (with some exceptions due to race, geographic location and ethnic groups) .They are mainly derived from intestinal microbiota. The significance of lactobacilli presence for a healthy vaginal milieu has been recognized ever since Albert S Doderlein discovered a vaginal bacillus that he named Döderlein, in 1892. This bacillus was subsequently renamed as Lactobacillus .

Döderlein claimed that, in normal vaginal secretions, the combination of Döderlein's bacilli and acidity was essential for keeping the vagina free of pathogenic bacteria. This fundamental concept still continues to be utilized today

Ecosystem of vagina and Bact infections of vagina

 

Q. What specific changes do occur in Bact vaginosis ?? Ans:BV is   mainly an increased prevalence of anaerobic  bacteria    including   Gardnerella vaginalis, Mycoplasma  hominis,  Prevotella,  and Peptostreptococcus 

Q.2: What is the prevalence ? Ans:Bacterial  vaginosis   is the most  common urogenital disease   affecting about 19-24%  of the women   during the reproductive age, and   occurs as a result of    imbalance  in   the vaginal    microbiota, disruption of the normal   lactobacillus and   subsequently  increase  in predominantly  anaerobic  bacteria    including   Gardnerella vaginalis, Mycoplasma  hominis,  Prevotella,  and Peptostreptococcus   have led to its occurrence.

Q.3:  Vaginal ecobiogy :--Lactobacillus is associated with supporting full term birth and healthy pregnancy,   and is the dominant microbe in the vagina ,

Q.4: What harm can occur in preg period if   BV  overrules Lactobacilli ?? Disruption of L bacilli population   increases   the risk of potentially severe   gynecological   and obstetric complications. Bacterial vaginosis is associated with an elevation   of cervico- vaginal  pro inflammatory  cytokines including   interleukin-   1 beta  and lL -8, which   initiates   the cascade   of inflammatory events   involved  in prelabour. , late   miscarriage, chorioamnionitis, premature rupture  of membranes, preterm birth and    postpartum  endometritis.

 

Q.5: What gynae harm it can do?? Bacterial  vaginosis is associated with increased risk of pelvic    inflammatory    disease, tubal factor   infertility . Antibiotic  therapy is the current  treatment for   bacterial vaginosis   , but its  uncertainty in preventing  preterm birth   in women   has been   reported. Also,    antibiotics are unable   to fully eradicate   bacterial  vaginosis  vaginal   biofilms    associated bacteria , which    can   explain  its high    recurrence   rates. Therefore , probiotics  have been  suggested as an add an to antibiotic therapy  in restoring vaginal  lactobacilli  and reversing  bacterial vaginosis.

NORMAL  VAGINAL  FLORA

 Over  50  microbial  species have been  recovered from the vaginal   tract   and lactobacillus  is the predominant   species .

BACTERIAL VAGINOSIS – DYSBIOSIS

 It is  abnormal vaginal discharge  characterized by an  overgrowth   of predominantly anaerobic organisms  in the vagina  leading   to a replacement   of lactobacilli and an increase   in vaginal  pH.

It   often   remits spontaneously , but  may present   as chronic or recurrent disease.

Often seen in women   of childbearing  age and  sometimes even menopausal  women .

Depletion of lactobacilli  population  and the presence   of  Gram – negative anaerobes, or an some cases Gram- positive  cocci, and aerobic  pathogens.

BACTERIAL  VAGINOSIS

 Depletion   of lactobacilli population

Presence  of Gram – negative   anaerobes, Gram – positive  cocci, and aerobic pathogens

SYMPTOMS

Offensive   fishy  smelling vaginal   discharge

Not  associated   with soreness, itching or irritation

Approximately 50% women   are asymptomatic.

SIGNS

Thin white   , homogenous discharge   coating  the walls   of the vagina

No evidence   of inflammation

Unpleasant  fishy  odour  of discharge

BACTERIAL  VAGINOSIS  DIAGNOSIS

CLINICAL DIAGNOSIS

AMSEL’S Criteria : At   least  three of the four  criteria   are present   for the diagnosis  to be confirmed.

Fishy   smell

Clue  cells   on wet mount   microscopy

Full blown > 20 %

Partial > 0and < 20 %

Vaginal pH > 4.5

LABORATORY   DIAGNOSIS

  Gram stained  vaginal  smear

Hay/ Ison criteria :

Grade 1  : Lactobacillus  morphotypes  are predominate 

Grade 2 :   Mixed flora  with some Lactobacilli is present. Gardnerella or Mobiluncus morphotypes  are also present

Grade 3 : Predominantly  Gardnerella and / or Mobiluncus morpho   types and few or absent Lactobacilli,

Grade 4 : Predominantly Gram – positive  cocci

The  Nugent score :

Normal  <4

Intermediate 4-6

Bacterial vaginosis >6

WHOM TO SCREEN ?

AMSEL’S   Criteria : At least three of the four criteria  are present   for the diagnosis   to be confirmed.

All symptomatic patients

Asymptomatic  with high risk

SCREENING TEST

Amsel’s criteria

COMPLICATION

 Bacterial vaginosis is not a  sexually transmitted but it may  be associated with sexually transmitted  infections  and other    genital infections.

Increased risk of acquiring human immunodeficiency virus in pregnant women.

Decrease incidence of chlamydia  have been reported  in women  treated for  asymptomatic  bacterial vaginosis

Its    prevalence  is high  in women   with pelvic  inflammatory disease.

It is   common in women   undergoing   elective   termination of pregnancy  and is associated with post – TOP endometritis  and PID.

In  pregnancy  bacterial   vaginosis is associated with late miscarriage   , preterm   birth , preterm    premature rupture of  membranes  , and postpartum endometritis

It is   associated with an increased   incidence  of vaginal cuff cellulitis and  abscess  formation   following   transvaginal   hysterectomy

It is  associated with non gonococcal  urethritis in male partners.

MANAGEMENT

 General  advice :

To avoid   vaginal   douching

Avoid   use of  shower  gel

Avoid use of antiseptic  agent  or shampoo

Treatment of    recurrence   : Co – treatment with antibiotics  and probiotics  but probiotics  is preferred.

 

Treatment for SCREEN POSITIVE –Symptomatic  pregnant /  non pregnant ,  Asymptomatic with high risk pregnancy   ,  women undergoing  some   surgical procedure

Co- treatment   with antibiotic  and probiotic

Metronidazole  400 mg  twice  daily for 5-7 days .

Or  Metronidazole 2 g single   dose

Or Intravaginal   metronidazole gel once daily for 5 days

Or Intravaginal  clindamycin  cream   once daily  for 7 days

Probiotics : Lactobacilli species like  acidophilus, rhamnosus, reuterii , fermentum etc  for 15 days,

DIAGNOSTIC  AND DIFFERENTIAL DIAGNOSIS ALGORITHM

 Vaginal  discharge – Gray  thin,  watery or yellowish – green

White  cottage- cheese appearing , homogenously thick – check pH -1)  >pH 4.5 2) < pH 4.5

>pH 4.5 –Saline microscopy -1) Trichomonads- Trichomonads vaginalis  2) Clue  cells with positive   whiff test- Bacterial  vaginosis  3) No Trichomonads  No clue cells -  Cervicitis obtains GC/ Chlamydia DNA probe, NAAT  on probe  or urine – Positive –PID. Negative – No  diagnosis

 

<pH 4.5 – Hyphae seen –Candida Vulvovaglnitis

No Hyphae seen – Obtain a yeast culture . Negative – Normal physiological

 

 

How useful is  Glucocorticoid Administration at OPU to prevet OHSS??

Rizk (1993) has found no protective effect of intravenous glucocorticoid. They considerd that the  pathophysiology suggest the involvement of an inflammatory mechanism during the development of the fluid leakage associated with the syndrome. Therefore, investigators hypothesized that glucocorticoids could possibly prevent OHSS in patients at high risk. Tan et al. (1992) also in a prospective randomized trial investigated the usefulness of glucocorticoids in the reduction of the rate of OHSS. Thirty-one patients, who were stimulated with hMG and who were desensitized with GnRH agonists and developed more than 20 follicles > 12 mm and/or had serum estradiol of > 10 000 pmo1/1 on the day of hCG administration, were recruited. The patients were randomized into two groups.

Group A (n= 17) were administered intravenous hydrocortisone immediately after transvaginal ultrasound oocyte recovery. Prednisolone 10 mg three times daily was given for five days, starting on the day of oocyte recovery, followed by prednisolone 10 mg twice daily for three days and 10 mg once daily for two days.

Group B (n =14) did not have any intravenous or oral gluco­corticoid treatment. Luteal phase support was given in the form of intra­muscular Gestone 100 mg/day. Seven of the 17 patients (41.2%) who received glucocorticoids developed OHSS compared with six of the 14 patients (42.9%) who did not. The authors concluded that the administration of glucocorticoids to high-risk patients did not diminish the risk of developing OHSS.

But can glucocorticoid administration prior to OPU say commencing from day 6 of COH reported that methylprednisolone 16 mg/day, starting on the 6th day of controlled ovarian hyperstimulation and tapered to day 13 after embryo transfer, was effective in reducing OHSS significantly to 10%, compared with 43.9% in the control group.

 

OHSS-Prevention

 

OHSS:---Prevalence:-upto 10% especially if agonists are used along with  Gonadotrophins in high dose as is usually done(long protocol) . But prevalence will be less in other methods of Ov Induction  protocol.

A)      Who are more prone &  in which cases doctor should be more cautious?

 1) Lean PCOS,2)  Hyperandrogenic women 3) Young age ,4)  Low  BMI 5)   6) P/H/O OHSS 7) Rapidly rising E2 & if on the day of trigger E2 is > 6000 pg/ml.( Normal ON DAY OF Trigger of plasma E2 will be  about 500-1500 pg/ml) .8) USG prior to oV Induction and selection of protocol.—if exhibit  PCOM/-Pcos type of USGà but no systemic symptoms or sign of PCOS . Therefore women who exhibit polyfollicular features  which are insignificant metabolically or have no menst disorders per se in non-preg state. Such women with polyfollicular pattern these PCOM women while on stimulation will hyperresponders in 40% cases.

 

 

B)        Doctor is an experienced and wel aware of the fact thwt Ms XYZ can deveop OHSS . Then , how she / he will prevent OHSS if there is any risk factor/ factors are already present?

1)                   Daily USG including search for ascites 2) Hematocrit 3) To opt for  Chr low dose protocol in next cycle-more so who are more prone for OHSS e.g. Lean PCOS, 2) Hyperandrogenic women 3) Young age, 4) Low BMI   4) Coasting: - Stop administering further gonadotrophins-watch but if one gives trigger that must be administered by 72 hrs after stoppage of HMG (i.e. initiation of coasting)  5) Can Cancel the cycle. 6) IVM –In vitro maturation after aspirating immature oocytes 7) Cryopreservation-all Freeze->Transfer  in later cycles. 8) Plasma Expanders. 9) Trigger by agonist-e.g. Decapaptyl-0.5 mg to 0.1 mg; but not r-LH neither  HCG:

But the problem is that this agonist trigger will not work if the cycle was down regulated by Long protocol (Long agonist suppression) or Antagonist protocol 10) Aspirate all follicles 11) If down regulated with agonist –one can continue the agonist even after HCG triggerà this policy will lessen the release of vasoactive substances.

2)                   When to withhold trigger? If there are > 2 DF above 18 mm in IUI cycles .

Tamoxifene -How useful as an ovulation inducing agent

 

Tamoxifen when? Scope & Indications of Tamoxifen as ovulogen:-:- In present day the main and possibly the only indication of prescribing TMX is when there are side effects with CC particularly visual /neurological side effects . Scintillating Scotoma are the main contraindications of CC. Though, in such situation both the drugs (CC & TMX) are to be withheld forthwith but one can use either agent at a lower dose after a gap of 3-6 cycles couple of months..

Gonadotrophins are quite effective in CC resistant cases but costly . CC has failed after couple of cycles. Now, what are the practical options open to young women in Indian perspective? Once counselling done after several cycles of failed CC, many Indian couple (even uneducated couple) does realize that gonadotrophin is badly needed for them but repent because they are simply unable to afford for G cycle. Put in such a situation (after CC resistant cases) the option remaining to the treating physician to prescribe TMX (as an alternative to Gonadotrophin) and make some compromise. Doctor feel-“Watch- what happens”-.

Not to speak of Gonadotrophins : Many Indians cannot afford further tests so as to why CC resistance has followed: in her case--Unfortunately, many Indian couple cannot afford for usual tests at this juncture - so as to why CC failed in their case. Such tests, if not carried out earlier are 1) AMH .2) AFC, 3) Insulin Resistance, 4) high D2 LH & testosterone 5) DHEASO4, & 6) PRL --not to speak of other costly tests. In such cases further tests so as to find the etiology of CC resistant in particular women. We, Indian doctors have to make many compromises at every step of clinical practice not only in the discipline of reproductive medicine.

Like CC TMX is also an competitive estrogen Antagonist –TMX ,like CC also competitively block the estrogen binding sites at the level of arcuate nucleus of hypothalamus, and stimulate GnRH receptors located at Pit for accentuated release of Pit FSH & LH.

Is there any differential expression of LH over FSH –particularly in CC failure cases? In fact there is about 3-4 fold rise of FSH & LH while someone is on CC. But the differential expression FSH & LH in the aforesaid two types of oral Ovulogens is still under study. I have a feeling this part of CC /TMX have not been adequately explored. It is hoped by many researcher that CC failure is due possibly to over expression of LH in fair number women and is a major cause of CC failure à poor oocyte quality. Those who are biased for TMX they claim such disproportionate rise of LH on cycle days 8-11 is not the case with TMX. I admit that I personally do not know about the differential expression of FSH vs. LH in CC cycles against TMX cycles. But many researcher believe that CC in fair no. of cases more rise of LH during the cycle days of Day 8-Day 10 thereby interfering the oocyte quality. Similarly in some cases of CC induced cycle serum E2 remain at supraphysiological levels –explain partly the reasons of failure of CC cycles. In such women one can use TMX as an iterative if the age of the female partner is< 25 yrs or she cannot afford for gonadotrophin cycle. Some also have claimed that LUF is more than TMX.

Miscarriages rate and multiple preg rates are more or less same with CC and Tamoxifen :- e.g. 10% & ABOUT 22% respectively depending on other associated factors like age of female partner, BMI, androgen excess disorders, Hyperinsulinaemia, serum testosterone etc. But for the oral Ovulogens to be effective the D2 serum E2 should be ideally> 50 pg/ml and not less. Additionally, Women who are contraindicated for CC may also be prescribed few cycles of TMX RY after due counselling. Such contraindications of CC are 1) impairment of hepatic enzymes 2) Eye changes after CC .

Why oral Ovulogens in lieu of gonadotrophins:- The advantages of CC/ Tamoxifen are low incidence of multiple gestations, OHSS, low cost, minimal monitoring, .But we are all aware of the fact that whatever agent we use in fair number of subfertile women CC/TMX become resistant despite appropriate dosage e.g Ov insufficiency, Hyperandrogenism, Insulin resistance ,Elderly women and women with BMI> 30 Kg/M2. In such cases one prescribes oral Ovulogens mostly CC but the doctor concerned is skeptical right from the beginning that CC/TMX may not work.

What to do in CC resistant cases? The causes are Treatment:- one can 50 mg of IM progesterone daily in late luteal phase to suppress LH & FSH levels. But usually gonadotrophins is the usual protocol.

Carry home message: Those who are biased for TMX they claim that CC ingestion cause preferential expression of LH mote than FSH from Pit so there is anovulation with CC . But such disproportionate rise of LH on cycle days 8-11 is not the case with TMX

 

How useful NAC in improving ovulation rate n PCO

 

Those with negative HOMA-index may be benefited by prescribing NAC rather than Metformin.

The choice of oral insulin sensitizers!!! Which agent as first line!!! A day may come when Metformin may be replaced by classical ISA (insulin sensitizing Agent) like metformin.

NAC has “Noninsulin-related mechanisms”

Is NAC going to replace traditional Metfromin in subfertile anovulatory women who exhibit hyperinsulinemia?? Which oral agent will be more effective in promoting fertility –Metformin or NAC??

Many feel that in Indian women many women do not respond to conventional Metformin. That is the experience of many of us . What to do in such subfertile women with impaired laboratory documented Carbohydrate metabolism? Should we jump to costly gonadotrophins keeping in mind that such PCOS women are ”Hyperinsulinemic PCOS” ??

Those patients may undergo HOMA test. Those with negative HOMA-index may be benefited by prescribing NAC rather than Metformin.

Why at all Metformin fails and become less successful? The explanation is that path of action at cellular level is absolutely different. The association NAC + Inositol + folic acid , regardless of insulin-resistance state, seems to improve ovarian function in PCOS patients. Therefore, inositol and NAC may have additional noninsulin-related mechanisms of action that allow achieving benefits also in those patients with negative HOMA-index.

Carry home message is :--Those with negative HOMA-index may be benefited by prescribing NAC rather than Metformin.

 What are the factors that can predict successful Ovulation induction & Prognosis of Oocyte quality. Forced Ovulation by any means do not equate with live baby rate. There may increased Miscarriage rate, karyotypic abnormality and other cog abnormality as a woman ages . Remeber this before you enrol your name for DM/ Ph D /FNB

1)                   Age:-  Most important predictor, Because the good quality ova are released in early part of life. After 35 yrs-biological aging of ova are immense and  besides  the age factor (biological clock) exposure to many deleterious toxic agents since childhood to her current age  do affect oocyte surrounded by follicular cells . Follicular cells do not any way protect the oocyte much for passage of pollutant particles be it food related / environmental toxins (automobile smokes in articular,. One solution is freezing the eggs.

2)                   BMI:-. Obese women are less fertile, One solution is freezing the eggs. both by natural methods & by OI, ; require higher dose of stimulation and more prone to miscarriage. Eighty per cent of obese women have IR & hyperinsulinaemia. Many have stigma of hyperandrogenism. More insulin à More LH secretion and decreases SHBG with resultant Free Testosterone conc.

 

3)                   Central Obesity & high BMI are major associations of IR & hyperandrogenism. There are two problems with Obese women A) in IR women:--They require higher dose of stimulation and B) In obese women: - If one initiates with low dose ten poor preg rate & increased misc rates. Even low dose Ry may cause multifollicular response, high Cycle cancellation rate, If one tries seriously it is not impossible to  lose wt of 10.2 Kg by 6 months!.  But a great motivation is required. Those who were able to lose wt the miscarriage rate will hopefully come  to  say 20%  from about  75% those who failed to lose Wt and insist to doctors it initiate  with Ov induction . Metformin, is now widely used in infertile women woman associated with PCOs particularly who are obese.

 

4)                   Smoking & Drug Abuse.  Effects of Pollution.

 

5)                   Decreasing seminal parameters with aged husband. Increased divorce rate is also an indication of late childbearing.

 

6)                   Lab aids to diagnose dwindling Ovarian Reserve (Impending POF). There are two tests (Static & dynamic). Static test implies age (independent predictor of for quality of oocytes & preg rate) whereas dynamic tests include AMH, AFC. Rising FSH (day 2) . These three test (dynamic) tests including poor response with high dose of gonadotrophins are indirect predictors of Ov reserve  but not quality of oocyte releases and therefore do not correlate with   preg rate. Clinically this (early dwindling ovarian function ) may be anticipated by frequent cycles due to decreasing conc of inhibin B (secreted by Primordial Follicle)-thereby rise of FSHà Rapid /augmented growth of Dev Foll—Rise of E2 and premature Luteinization & Polymenorrhoea.

 

Carry home message : Marry by 28 yrs and be mother / father by 30 yrs , Be merry at Doshera,

 

 

 

 News and views on FETAL MUSCULOSKELETAL EVALUATION : :  How many of us really read and interpret   at the report page of USG  ON Foetal foot length ?? 

Q.1: What is the importance of FL in USG?  Ans.  It  is the measurement of the ossification center of the femoral diaphysis.  FL is ordinarily included in routine obstetric sonography to assist in a) determining gestational age and b) growth between ultrasound examinations because it reliably corresponds to menstrual age.

An abnormal FL or configuration is often the c) first clue to a fetal musculoskeletal abnormality. Careful sonographic measurement of the femoral diaphyseal ossification center is needed to obtain accurate femur measurement and configuration assessment.

Q,2: Caution :--Proper ultrasound technique must avoid obliquity and exclude the cartilaginous epiphyses.

Q.3: what are the common pitfalls?   Common pitfalls such as a mildly curved appearance of the femur when imaging from the medial aspect of the femoral diaphysis should not mistaken for a limb abnormality. Charts correlating FL with other parameters of gestational age assessment head circumference can be used to determine whether there is limb shortening . Measurements of other long bone diaphyseal ossification centers is useful for selected cases at risk for limb length abnormality either generalized or non generalized.

Q.4: When to consider Limb shortening in the second trimester? Ans:  Limb shortening in the second trimester should raise suspicion of a fetal abnormality . Mild shortening of the femur or the humerus may be indicative of a chromosomal aberration or a syndrome .

Point 1: On Femur”  If mild femoral shortening  is present there is a 1 % risk of trisomy 21  in a high risk population and a 3% risk of trisomy 21 in a low risk population .

Point 2: On Humerus:  Mild humeral shortening is even more specific than femoral shortening in predicting trisomy 21. If mild humeral shortening is identified there is a 3% risk of trisomy 21 in a high risk population  and a 1% to 2% risk of trisomy 21 in a low risk population.

Point 3: May be normal variant in the third Trimester if slight shortening  : In the third trimester one should remember that the femur is subject to the same biologic variability as other biometric markers. It is not unusual on occasion for the FL measurement to be slightly less than other biometric markers in the absence of a morphologic abnormality. This is particularly true if the remainder of the sonographic evaluation of the fetus is normal.

Q.5:  How many of us really lookat the report page OF usdg ON Foetal foot length ??  What we should remember while interpreting Foetal foot length??  Ans : We know that  the fetal foot length is approximately equal to the FL throughout gestation . So Foot length   may be useful in detection of a fetus with skeletal dysplasia. Fetal foot length correlates with gestational age and FL . It is certain that FL :  Foot length ratio should be 1. If this ratio is <0.9 skeletal dysplasia is possible . If it is 0.9 to 1.0 it may represent a constitutionally small fetus or symmetric IUGR.

Evaluation of fetal posture and fetal movements are very important in prenatal ultrasound. Abnormal posture or movement may be the first clues to either a focal or generalized fetal musculoskeletal abnormality . Contractures or abnormal fetal movements may provide definitive diagnosis of affected fetuses for genetically transmitted muscular or musculoskeletal disorders such as some of the arthrogryposis syndromes , Pena shokeir syndrome congenital myotonic dystrophy and amyoplasia