Census of India

It is estimated that 15.6 million abortions take place in India every year. A significant proportion of these are expected to be unsafe. Unsafe abortion is the third largest cause of maternal mortality leading to death of 10 women each day and thousands more facing morbidities. As many as 34 births and 10 deaths are registered in India every minute. The number goes up to 2,062 births and 603 deaths per hour, up to 49,481 births and 14,475 deaths per day and further up to 1.5 million births and 0.4 million deaths per month How many babies are born each day in India? As many as 34 births and 10 deaths are registered in India every minute. The number goes up to 2,062 births and 603 deaths per hour, up to 49,481 births and 14,475 deaths per day and further up to 1.5 million births and 0.4 million deaths per month. Per year birth is therefore 1.5

At India =50,000 birth per day × 365=   × 18,250,000=18 million Birth per annum.

The current population of India is 1,369,788,422 as of Monday, September 30, 2019, based on Worldometers elaboration of the latest United Nations data. India 2019 population is estimated at 1,366,417,754 people at mid year according to UN data.

Growth rate	1.19% (2016) (96th)
Birth rate	19.3 births/1,000 population (2016 est.)
Death rate	7.3 deaths/1,000 population (2016 est.

As per Census 2011, Gender ratio of India is 943 females per 1000 males. In rural area, there are 949 females to 1000 men, while in urban area there are 929 females to 1000 males. Rural India has 21,813,264 more males and urban India has 13,872,275 more males than females. Latvia, Lithuania, Armenia, Belarus, Russia, Ukraine and Estonia are among the countries with the largest female populations.

Vatican City is the only country in Europe with no voting or electoral rights, including no voting rights for women.

Thrombophilia and DVT

What are thrombophilias?? Ans:-It is a deficiency disorder (acquired or congenital):  : A number of isolated  deficiencies of proteins   involved    either A)  in coagulation  inhibition or   B)   Fibrinolytic system in the fibrinolytic system – collectively    referred  to a thrombophilia - . This can cause a o hyper coagulable state of affair. Some of them may lead to  recurrent venous   thrombo embolism .

What is called   Milk leg??  The other terminology is   phlegmasia alba dolens ( milk leg)-a kind of . DEEP VENOUS THROMBOSIS

 The signs    and symptoms of deep venous thrombosis involving the lower   extremity vary greatly depending    upon the degree of occlusion    and   the intensity of  the  inflammatory    response. Clinical puerperal thrombo philebitis involving   the lower   extremity   is abrupt in onset with severe pain and edema of the leg and   thigh. The thrombus typically    is left sided     and involves    much of the deep venous   system from the foot   to the iliofemoral region. Occasionally     reflex   arterial spasm causes     a pale cool extremity with diminished   pulsations-  so called phlegmasia alba dolens or milk leg.

What clinical conditions may mimic DVT but such conditions are nonthrobotic?? Ans Non thrombotic    conditions   are often demonstrated   that  explain   the clinical findings  that originally   suggest  venous thrombosis    Some  examples  include   cellulites,  edema,   hematomas   and  superficial  phlebitis.

What about Calf pain??  Most of DVT are asymtomatic because many a clot in deep veins of leg or thigh  though  there may be appreciable volume of clot   yet such clot cause  little    reaction in the form of pain , heat   or swelling      . Ans:-   calf pain is not specifc and may not be present at all and thereby causing no symptom , But pain in  the affected leg may be evoked by many causes like 

a)                 in response   to squeezing or b)  to stretching   the Achilles tendon   may be caused by  c)  or a strained    muscle   d)  a contusion f) or  thrombosis    . The latter may be    common   during the early puerperium as the consequence of   inappropriate   contact   between the calf   and the delivery  table leg  holders.

How to diagnose DVT ??  1) Compression ultrasonography    used along with duplex    color Doppler    ultrasound a the primary    test currently  used to detect   proximal  DVT. But  the limitation of    ultrasonography    used along with duplex    color Doppler    ultrasound    is this procedure  results do   not necessarily rule out pulmonary embolism frequently   originates in the iliac   veins.

Although  2)    venography  remains  the standard for confirmation of DVT  non invasive methods have largely   replaced these tests  to confirm    the clinical   diagnosis. 3) Magnetic    resonance imaging   is reserved   for specific   caes in which   the ultrasound    findings are equivocal or  with negative   ultrasound findings    but strong clinical suspicion. This   technique   allows for excellent delineation  of  anatomical   detail above   the inguinal ligament   and phase   images can be used  to diagnose   the   presence or absence   of pelvic   vein flow. An additional    advantage   is   the ability to image   in coronal   and sagittal   planes. 4) CT Scan:-Computed tomographic  scanning     may also be  used to assess the  lower   extremities  . It is   widely available     but requires   contrast   agents   and ionizing    radiation. As   discussed in Appendix   C , radiation exposure  to the fetus   is negligible unless the  pelvic  veins  are imaged.

Superficial  venous thrombosis

Thrombosis   limited strictly to the superficial veins   of the saphenous system is   differentiated   from DVT   and treated with analgesia elastic   support and rest . If  it does   not soon   subside or if deep   venous involvement   in suspected   appropriate  diagnostic    measures art taken and    heparin   is given if deep  vein  involvement   is confirmed superficial thrombophlebitis is typically seen in association   with superficial   varicosities   or as  a sequela to intravenous catheterization .

Management of DVT :- Which agent?? Ans: anyone like  either unfractionated  heparin or with low molecular   weight   heparin. Having said that treatment    of DVT  consists  of anticoagulation limited activity   and analgesia . For  all women during either   pregnancy   or postpartum initial    anticoagulation is with  either unfractionated  heparin or with low molecular   weight   heparin.  For women    during pregnancy    heparin  therapy   is continued and for those postpartum  warfarin    therapy  is given.

Most often   pain is promptly   relieved    by these   measures    . After   symptoms   have  completely  abated graded   ambulation  should be  started  with the legs fitted with   elastic  stockings and anticoagulation   continued   . Recovery   to this stage  usually   takes about 7 to  10 days.

Therapeutic dose Heparin

Treatment   of acute attack (not prophylaxis) :-thromboembolism  during pregnancy  begins with an  intravenous  heparin   bolus   followed by continuous infusion     titrated to achieve  full anticoagulation. There    are  a number of protocols   to accomplish   this . Intravenous    anticoagulation    should be maintained for at least 5 to 7 days  after which   treatment    is converted to    subcutaneous heparin Injections are given every     8  hours to prolong    the partial thromboplastin    time to at  least   1.5 to 2.5  times    control throughout   the    dosing    interval. Treatment is continued for at least    3 months after the   acute  event.

 If the  woman is still pregnant    at  this juncture   it is not known whether   it is better   to continue   with a therapeutic or a  prophylactic dose of anti coagulate   for the reminder of pregnancy.

Complications of heparin therapy include thrombocytopenia osteoporosis and hemorrhage. There are   two types   of thrombocytopenia   associated  with heparin   use. The most    common type of heparin induced   thrombocytopenia   is a  non immune benign  reversible    form that occurs within the    first few days   of therapy  and resolves  in 5 days  without cessation of therapy  . The  more severe   form of HIT   results from an immune    reaction involving   IgG   antibodies   directed   against  complexes  of platelet factor  4  and heparin . Osteoporosis develops   with long   term   administration   and is more    prevalent   in cigarette smokers. In an   attempt to avoid severe   osteoporosis    women   treated   with heparin   should   be encouraged to take supplemented calcium  of vitamin d

Low   Molecular weight  Heparin

This is a family of derivatives of   unfractionated heparin and   their   molecular   weight   average 4000  to 5000 daltons compared    with about 12,000   to 16,000   daltons   for conventional heparins. Like    standard heparin low molecular    weight heparin do not     cross the placenta.

Lovenox warned   that its  use in pregnancy had been   associated   with congenital   anomalies  and as increased risk of   hemorrhage   . concluded   that  enoxaparin   and dalteparin  could be given  safely   during pregnancy. One  caveat    is that  low molecular    weight   should  not be used in patients with prosthetic heart   valves  because of reports   of valvular thrombosis   . Their    use may increase   the risk of spinal   hematoma  associated  with    regional    analgesia. Finally  given within  2 hours  of cesarean delivery    these agents   increase   the risk of wound hematoma.

Warfarin

Anticoagulation  with warfarin derivatives is generally  contraindicated   during pregnancy. These   drugs readily   cross the placenta    and cause fetal   death and malformation from hemorrhages. They are  safe     however    when ingested   while  breastfeeding . Postpartum  venous thrombosis can be  treated with intravenous heparin   and oral warfarin initiated simultaneously and heparin    can usually   be discontinued after 5 days  Postpartum women  have been   shown to require    a significantly  larger median total   dose   of warfarin compared to non pregnant   controls and a longer time    to achieve  the target   international    normalized ratio   after  delivery   most women    are anti coagulated  with warfarin for at least 6 weeks.

PULMONARY  EMBOLSIM

Although  it caused about 10 percent of maternal deaths  pulmonary   embolism   is relatively uncommon during pregnancy  and the puerperium. The incidence   averages about  1 in 7,000  pregnancies  with an   almost equal prevalence  for  antepartum and postpartum embolism. Clinical evidence  for DVT of the legs precedes pulmonary   Embolization in about   70 percent  of cases. In others especially  those that  arise   from deep   pelvic   iliac veins   the women   usually is asymptomatic  until symptoms of Embolization develop.

Physical  signs associated with pulmonary   embolism may   include as accentuated pulmonic closure sound rales    or friction rub . Right Axis deviation may  or may not be   evident on the  electro cardiogram . Even with massive pulmonary  embolism   signs symptoms  and laboratory  data to support  the diagnosis    may be deceivingly non specific.

Diagnosis

As with deep   venous  thrombosis   the diagnosis  of pulmonary   embolism requires   an initial high   index of suspicion  followed by objective   testing  . A chest   radiograph should be  performed if there is  underlying  suspicion  for other diagnosis . In many   centers  spiral  computed    tomography  has   replaced  the more cumbersome ventilation perfusion  lung scan .

These scans utilize   a small   dose of a radioactive    agent usually . Tc macro aggregated albumin which   is  administered intravenously  . There is  negligible  fetal  radiation   exposure  . the scan may   not provide  a definite  diagnosis  because  many   other conditions – for example pneumonia  or local   bronchospasm- can  cause   perfusion   defects.  Ventilation scan   with inhaled Xe  or Tc   are added  to perfusion   scan  in the  hope   that ventilation will be  abnormal  but perfusion normal    its  areas of pneumonia or hypoventilation . Thus   although ventilation scanning      increases  the probability     of an accurate   diagnosis   of pulmonary    embolus  in patients   with large   perfusion    defects  and   ventilation    mismatches normal    ventilation perfusions  does not   rule out pulmonary    embolism.

Spiral  computed tomography

Helical  computed  tomography       or spiral CT  allows  rapid imaging   from  the main pulmonary   arterials to at least the segmental and possibly  the sub segmetnal  branches . Fetal      radiation      exposure     with standard   single detector    spiral CT is less than with V/Q   lung scanning

We now use multi detector     spiral   CT as first    line evaluation of pregnant  women at parkland  Hospital  Although    the technique   has many advantages   we have found that the  better resolution allows  detection of previously   inaccessible  small distal  emboli that have    uncertain   clinical  significance.      DVT & PE:-Pregnancy   and the puerperium are considered  at one of the  highest   risks for otherwise healthy women to develop venous   thrombosis    and pulmonary   embolism. Indeed  thrombotic  pulmonary   embolism  caused nearly 9 percent    of the almost  623   pregancy  related    deaths in the United States during 2005.

The incidence  of all thromboembolism      is approximately  1 per 1000   pregnancies. About   half are identified antepartum and the other half    in the puerperium. Stasis is probably the  strongest   single predisposing event to  deep  venous thrombosis the frequency  of  which has decreased   remarkably  during the puerperium as early  ambulation has   become widely practiced .

                                                                                                                                                                                                                                                                                                                                                                                       

Hyperthyroidism

Hyperthyroidism : Women    thyroid   stimulating   antibody  activity  declines during pregnancy   associated  with chemical    remission.  When   mild thyrotoxicosis may be difficult to diagnose   during pregnancy    overt can be easily diagnosed. The  diagnosis   is confirmed when   an abnormally  low thyroid    stimulating hormone level is accompanied by abnormally  high serum  triiodothyronine levels -   . The   major  cause of hyperthyroidism   in pregnancy     is Graves disease an organ specific   autoimmune process   usually associated with   thyroid  stimulating    antibodies. In many  women    thyroid   stimulating   antibody  activity  declines during pregnancy   associated  with chemical    remission.

Pregnancy    outcomes depend  upon   whether    metabolic   control is achieved   .women   who remain hyperthyroid  despite therapy    and in those whose   disease   is  untreated    there is a higher   incidence  of preeclampsia heart failure    and adverse   perinatal outcomes. Thyroid   storm is encountered only  rarely in untreated   women  with Graves disease. Heart  failure is  more common  than T storm cases.

How common is subclinical hypothyroidism

Iodide fortification   of table   salt    and bread products   has diminished   and iodide deficiency has been   identified in some of the population. Adequate   iodide is requisite for normal   fetal neurological   development    beginning soon after conception.

The   recommended daily intake during   pregnancy is at least 220  ug/day  . Severe   deficiency    is associated with  endemic cretinism. Although   not quantified   it is presumed that moderate deficiency has intermediate and variable    effects    on intellectual and psychomotor function. Although    it is doubtful that mild deficiency causes intellectual impairment supplementation   prevents  fetal  goiter

CLINICAL  HYPOTHYROIDISM

  Clinical   or overt  hypothyroidism   complicates  approximately  2 per  1000  pregnancies . Clinical    hypothyroidism    is diagnosed when   an abnormally  high    serum thyrotropin level is   accompanied  by an abnormally low free thyroxine  level.  The most   common  etiology is glandular   destruction   by  autoantibodies or Hashimoto    thyroiditis  . Thyroid    peroxidase   antibodies   have been   identified  in 5 to 15   percent of pregnant  women up to half  of whom later    in life develop   an autoimmune    thyroiditis.

Overt   hypothyroidism is associated   with infertility. When    pregnancy   does occur there are   increased   rates of maternal and fetal  complications to include preeclampsia placental   abruption   cardiac dysfunction    stillbirth  and prematurity . Fortunately     perinatal  outcomes  are usually normal  with adequate treatment . Replacement therapy is with    thyroxine   50 to 100   ug daily . Serum   TSH   and free thyroxine    levels   are measured at 4 to 6  week intervals    and thyroxine   adjusted    by 25 to 50 ug increments   until normal values  are reached. Pregancy is associated with an increase  in thyroxine    requirements  of about   a third however   care  should be individualized  as not all   women require an adjustment in therapy.

SUBCLINICAL  HYPOTHYROIDISM

 Subclinical hypothyroidism   is defined  by an abnormally  elevated  TSH level  with normal serum   free T in an asymptomatic woman. The prevalence   of subclinical  hypothyroidism  in pregnancy   is approximately  2.3   percent. Approximately 2 to  5 percent   of reproductive   age women with   subclinical disease   per year   progress   to overt    thyroid failure. Heredity is a potent risk factor    . Other    risk factors  for  thyroid     failure include  type -1  diabetes and thyroid   peroxidase antibodies . Effects    of subclinical    hypothyroidism   on pregnancy   outcome are not  clear. Pregnancies   with subclinical   hypothyroidism on pregnancy  outcome are not   clear. Pregnancies   with  subclinical hypothyroidism   may be   at increased risk for  preterm   birth    or placental  abruption. Effect of  maternal hypothyroidism   on the fetus   and infant . Hypothyroidism – either   overt  or subclinical -  has been   reported  to   cause   sub normal mental  development    Elevated  maternal   TSH  values have been associated    with  offspring     who have   diminished  school performance   reading recognition  and intelligence   quotient   scores as compared   with matched controls.

Some organization    have recommended prenatal    screening and treatment    for subclinical   disease. However the American College   of Obstetricians     and Gynecologists continues   to recommend   against routine screening  . Randomized placebo    controlled   trials  to determine risks  or benefits   of detecting    and treating  subclinical   thyroid  dysfunction    in pregnancy  are in progress.

Urinary Stress Incontinence

SUI:-Let us first refresh out knowledge of anatomy & neuronal control of bladder (emptying ) evacuation?:-To put in other way round how the continence is maintained?

Causes of GSI:- A diseases of theories:-First Theory::: .(theory of Enhorning). Theory of hyper mobility of bladder neck and descent of bladder neck from abdomen to pelvis:-Childbirth damage / Senile changes in nulliparous women cause  pubourethral ligament & Levator Any muscles weakness .This is the  first step: This theory presupposes that bladder neck is  intra-abdominal in  position ;     Theory of hyper mobility of bladder neck and descent of bladder neck and proximal urethra with rise of inure-abd. pressure.(theory of Enhorning).

 So what? During sneezing/coughing the intraluminal pressure in proximal urethra is raised above the pelvic floor pressure. Therefore continence is achieved. No leakage of urine. To be continent & effective the level of proximal urethra should be at the level of pelvic floor. If prox. Urethra comes below/down the level of P. floor then SUI will occur.

To be effective the proximal urethra must be within the intra-abdominal pressure zone and should not prolapse further down. If there is damage to pelvic floor muscles or end pelvic fascia then proximal urethra will be hyrermotile and will sag down and therefore out of intraabdominal    pressure zone.

 SECOND THEORY of SUI:---Hammock Theory: vaginal fascia act like a hammock on bladder neck which is pulled during coughing.  -- Loss of angle between Bladder & Internal urethral opening :--Relevance of vaginal fasciae , pubourethral ligament , Pubococcygeus   ms. These ligaments along with vaginal fascia act like a hammock on bladder neck which is pulled during coughing.  This concept is based on the fact that bladder neck though becomes mobile in diff. dis. Conditions the proximal urethra is basically remaining as an immobilized part of soft tissue. Normally with cough/sneezing- vaginal fasciae along with the bladder neck is pulled backwards and downwards while proximal urethra remains in fixed .Therefore normal angulations between neck and urethra is maintained and continence is  achieved.

Third Theory:::  Stress incontinence is a mid urethral disease  Supports of midurethra is poor with increasing age- Support of mid urethra:- pubourethral ligament  is normal and uninjured. Loss of  supports mid urethra is te cause of Stress.. Then SUI.

CLINICAL TESTS FOR SUI:

Bonney’s Test, 2) Miyazaki  Bonney’s Test – by using sponge forceps, 3) Q-Tip cotton swab test- lubricated cotton swab n the urethra-evaluates urethral hyper motility. 4) Foley’s catheter Test_ Paid. Foley six 8- 5ml. Saline-withdraw easily comes- Denotes sphincter deficiency.

 If catheter comes easily then consider the test as +.

If + Q Tip Test and negative Foley test then COLPOSUSPENSION Will help her

LIST of Investigation to be done in a case suspected to be suffering from SUI. Unfortunately there is no clinical test which is highly sensitive and specific. Most are lab oriented.,

 Urine RE.C/S 2) Whole Abd. USG & Post void urine must be below 100ml. If excessive then revise the diag in favour of overflow incontinence.

Voiding/Bladder diary:- a) Normal bl. Capacity is 300-500 ml. That she can measure. B) Volumetric summary of diurnal urinary frequency. C) Volumetric summary of nocturnal urinary frequency. C) Any provocative/Associated events /activities.

Pad test. = International Continence Society Pad Test: - . Allow her to drink Na free water 500ml. in 15 mats. Then ask her to perform strenuous exercises. If after one hour  The wt. of pad ≥ 2Gms. Then diag of SUI is confirmed.-

  Urolowmetry  :Normal Figures are Residual ≤ 50ml., First desire after filling of 150-200ml. Total capacity 400ml,

Leak Point Pressure:     This test is aimed to test the resistance of urethral sphincter and also diagnoses intrinsic sphincter deficiency. Placement of intavesical  & intravaginal catheters and assess by Valsalva method.

INFERENCE OF UROFLOWMETRY REPORTS & EVALUATION THEREOF;

SUI=  Leakage only during raised intraabdominal. Pressure in absence of Detrusor contr.

Bladder Neck Hypermobility:  High Valsalva Leak point pressure. or High maximum urethral closure pressure.

Intrinsic Sphincter deficiency:- Low Valsalva Leak point pressure or Low  maximum urethral closure pressure.

Urge Urinary Incontinence:- Incontinence due to involuntary .  detrusor . Contractions . If there is associated urge then termed as Det. Over activity.

Mixed Incontinwence . SUI & Urge Incontinence

Cysto-Urethroscopy -Bladder pathology ? Sensory urgency

Micturating  cryptography. –Any fistulae/ diverticulum.

TREATMENT OF URGE INCONTINNENCE

Usually surgical but it will be prudent to try with medicines as because the Tr. Outcome with surgery is unpredictable and it is  not a life threatening condition.

  Anti incontinent Surgeries. Plicatin  /urethropexy /needle suspension/ pubovaginal  slings/bulking agents

Inj. Of bulking agents (FDA approved)  /

 Later came Urethral placation  Surgeries(Plicatin of Suburethral  tissues)-Kelly 1914; Kennedy 1937;

 Retro Pubic Urethropexy:-  a) MMK-   1949     Marshall-Marchetti-Kranitz procedure-fixes fix such tissue with back of S.Pubis periosteum b. ) BURCH-modification of MMK on in 1961 Periurethral and per vesicular fibro muscular tissues are fixed to ileo-pectineal line. Instead of periosteum/cartilage of S. Pubis as was done in MMK procedure

  Trans vaginalis needle suspension  procedures    RETRO PUBIC SUSPENSION   Urethropexy/ Colposuspension operations   e.g.PEREyRA / Stamey procedure  .

.

PUBOVAGINAL  SINGS:-   Approach is through retropubic space , Either R. Sheath/ Fascia Lata is used to make a sling under the urethra. PARAVAGINAL Defect Repairs        Abdominal  Approach to correct lateral  vaginal support  –mostly abd. Route: now mostly used for Prolapse repair

MIDURETHRAL SLINGS.    TVT/TOT    (Mid-Urethral SLINGS).  Midurethal placement of MESH

This is very popular method because it takes care of all the three important structure that support bladder neck and proximal urethra. Such 3 structures are a) pubourethral ligaments b) suburethral  vaginal hammock, abd c) Pubococcygeus muscles. I) TVT (Tension- free vaginal tape)- Retropubic approach   via trocar and ii) TOT(Transobturator tape)—Vaginal/Obturator approach.

Vaginal approach TVT May be OPD procedure.    Possibly TOT is superior,

Transobturator Approach:- insert the mesh from  out-to-in method or better  in-to-out method . Polypropelene  mesh-----But limitation of this method is that this type of surgery cannot possibly correct  where SI is due to intrinsic sphincter defects.

Minimally invasive Slings:-also called micro sling/minis ling:-Vaginal approach- no trocar- 8 cm long strip of Polypropelene mesh is placed beneath the midurethra. TVT- Secur.

What is ISD or intrinsic sphincter deficiency?  To diagnose one should assess following 3 tests e.g.( Preoperatively always assess a)  MUCP(Maximal Urethral Closure Pressure Profile  If there is poor intrinsic sphincter deficiency then Obturator technique may fail. Also assess    b) VLPP (Valsalva - Low Leak point Pressure –will suggest ISD     c) additionally if there is Low-Q-tip angle then also think of ISD and there is little urethral hypermotility.

Sacral Neuromodulation- only when all other modes of Ry for Urge .Incon fails, Electrical nerve stimulation   pump device also available-FDA approved.