Tuesday, January 31, 2012

AMNIOTIC FLUID.

OBJECTIVES:
What is amniotic fluid?
 Physical characteristic and Volume
 Chemical Composition
 Amniotic fluid production
 Amniotic fluid circulation
 Functions
 Amniocentesis
 Amniotic fluid index
 Abnormalities
Polyhydramnious
 oligohydramnious



Amniotic fluid: or liquor amnii is a clear, slightly yellowish liquid that surrounds the unborn baby (fetus) during pregnancy.
 It is the nourishing and protecting liquid
 It is found within the amniotic sac contained in the mother's womb.


Physical characteristics
 It is clear  pale yellow fluid.
 pH of is around 7.2.
 Specific gravity of 1.0069 – 1.008.


volume:
volume depends on gestation

As a very rough guide, total volumes are about:
30 ml at ten weeks,
300 ml at twenty weeks,
600 ml at 30 weeks and
about a litre at thirty-eight weeks.
Beyond this point, the volume gradually falls
It will be about 800 ml at forty weeks and lower still if the pregnancy continues to forty-one or forty­ two weeks.


Chemical composition:

The composition of the amniotic fluid changes with gestation in early pregnancy it is similar to maternal and fetal serum.
  98-99% of the amniotic fluid is  water.
A large number of dissolved substances such as: creatinine, urea, bile pigments , renin, glucose ,fructose, proteins (albumin and globulin) , lipids, hormones (estrogen and progesterone ), enzymes , minerals (Na+ ,K+  Cl- )
 un-dissolved substances like  fetal epithelial  cells .
 during the second half of gestation its osmolarity decreases and is close to dilute fetal urine  with added phospholipids and other substances from fetal lung and other metabolites .


Amniotic fluid production:
At very early stages the amniotic fluid is secreted by the amniotic cells .
- Later most of it is derived from the maternal tissue fluid by diffusion, across the amniochorionic membrane  and from the placenta.
- A little is contributed by fetal respiratory secretions through the skin which becomes less later in progressed pregnancy since the fetal skin becomes less permeable .
- By 11th week, fetus contributes to amniotic fluid by urinating into the amniotic cavity; in late pregnancy about half a liter of urine is added daily.
- After about 20 weeks, fetal urine makes up most of the fluid.

Amniotic Fluid: Circulation
The water content of the amniotic fluid changes every three hours
Large volume moves in both directions between the fetal & maternal circulations  mainly through the placental membrane
It is swallowed by the fetus, is absorbed by respiratory & GIT and enters fetal circulation. It then passes to maternal circulation through placental membrane. During final stages of pregnancy fetus swallows about 400ml of amniotic fluid per day
Excess water in the fetal blood is excreted by the fetal kidneys and returned to the amniotic sac through the fetal urinary tract





Amniotic Fluid: Functions:
Amniotic fluid is "inhaled" and "exhaled" by the fetus. It is essential that fluid be breathed into the lungs in order for them to develop normally.
Swallowed amniotic fluid also creates urine and contributes to the formation of meconium.
The fetus floats in the amniotic fluid. It allows fetus to move freely, aiding development of muscles and bones.
Acts as a cushion to protect embryo from mechanical injuries.
Permits normal fetal  development.

Acts as a barrier to infection ,(transferrin in the amniotic fluid binds iron needed by some bacteria and fungi ,fatty acids have a detergent effect on bacterial membranes and contains Ig and lysozomes that also help in fighting pathogens)
  Assists in regulation of fetal body temperature, protecting from heat loss
 Prevent adherence to the amnion
 Helps in dilatation of cervical canal at the time of birth
 Amniotic fluid is also a plentiful source of non-embryonic stem cells. These cells have demonstrated the ability to differentiate into a number of different cell-types, including brain, liver and bone



Amniocentesis:
Amniocentesis is the removal of a small amount of amniotic fluid from the sac around the baby.
 This is usually performed at 16 weeks (2nd trimester) in pregnancy.
 A fine needle is inserted under ultrasound guidance through the mothers' abdomen into a pool of amniotic fluid.


Studies of the cells obtained from the amniotic fluid permit:
1- Chromosomal analysis of the  cells which can be performed to investigate the following;
§Diagnosis of sex of the fetus
§Detection of chromosomal abnormalities e.g. trisomy 21(Down’s syndrome)
§DNA studies
2- The cells may be cultured and analyzed for enzymes, or for other materials that may indicate genetically transmitted diseases
§( Inherited disorders e.g Cystic Fibrosis).
3-To check for developmental problems e.g. Spina Bifida . Babies born with spina bifida have a backbone that did not close properly. Serious complications of spina bifida can include leg paralysis, bladder and kidney defects, brain swelling (hydrocephalus), and mental retardation.
§
4- Other studies can be done directly on the amniotic fluid including measurement of alpha-fetoprotein
high levels of alpha-fetoproteins indicate the presence of a severe neural tube defect
whereas low levels of alpha-fetoproteins may indicate chromosomal abnormalities  .




Who is the proper candidate for an Amniocentesis investigation? 1-Those whom are suspected to have possible problems indicated by certain tests conducted previously ,(e.g If  pregnancy is complicated by a condition such as Rh-incombatibility, the doctor can use amniocentesis to find out if the baby's lungs are developed enough to endure an early delivery). 
2- Family history of genetic abnormalities (in this case would be advisable to seek genetic counseling before becoming pregnant)
3-Those that have been exposed to certain risk environmental factors that might lead to fetal abnormalities



What are the risks of amniocentesis?
Like any invasive procedure there are risks, which are:
- Abortion: about 1 in 200 to 400 women aborted (higher risk if done in the first quarter)
- Uterine infection: 1 in 1000
When are the results be obtained?
 It might take two weeks or shorter depending on the test required .Having it done in minimum time   is  important so that the decision  can be made at the proper time depending on the outcome
   
Examples of Other Tests performed on the amniotic fluid :
a)Measurements of the lecithine/sphingomyelin ratio  ( as the lung matures the concentration of  phospholipids especially lecithin increases since it is the major  lung surfactant). This test is done to assess the maturation of the fetal lungs , a ratio 4/1 indicates mature lungs and a ratio less than 4/1 indicates immature lungs.
 b) Measurements of bilirubin indicates the degree of fetal red blood cell destruction ,where abnormally high levels could indicate serious cases such as mother fetal blood incompatibility

Amniotic Fluid Index:
Amniotic fluid index (AFI) is a rough estimate of the amount of amniotic fluidand is an index for the fetalwell-being. It is a part of the biophysical profile.
AFI is the score (expressed in cm) given to the amount of amniotic fluid seen on pregnant uterusand calculated by a ultrasonograph (aka ultrasound). To determine the AFI, doctors may use a four-quadrant technique , when the deepest, unobstructed, vertical length of each pocket of fluid is measured in each quadrant and then added up to the others , or the so called "Single Deepest Pocket" technique


A normal AFI is about 12.
But 8-18 is normal
AFI < 5-6 = oligohydramnios (oligo, less; hydramnios, fluid)
AFI > 18-22 = polyhydramnios
 (poly, much or many)

ABNORMALITIES
Polyhydramnios:
Polyhydramnios means having too much amniotic fluid in the uterus (womb) more than 1500-2000 ml

Polyhydramnios signs and symptoms:
 Are a result of pressure being exerted within the uterus and on nearby organs, may cause:
 Shortness of breath or the inability to breathe, except when upright
 Swelling in the lower extremities, vulva and abdominal wall
 Decreased urine production

CAUSED BY:
 A birth defect that affects the baby's gastrointestinal tract or central nervous system
Maternal diabetes
 Twin-twin transfusion — a possible complication of identical-twin pregnancies in which one twin receives too much blood and the other too little
A lack of red blood cells in the baby (fetal anemia)
Blood incompatibilities between mother and baby
Infections that affect baby, such as rubella, cytomegalovirus toxoplasmosisand syphilis
the placenta may have developed a tumour
§ there may be a problem with the arteries in the umbilical cord resulting in polyhydramnios. 

Complications of polyhydroamnios
 Polyhydramnios may increase the risk of:
 Premature birth
 Pregnancy-induced high blood pressure
 Urinary tract infections during pregnancy
 Premature rupture of membranes
 Excess fetal growth
 Placental abruption — when the placenta peels away from the inner wall of the uterus before delivery
 Umbilical cord prolapse — when the umbilical cord drops into the vagina ahead of the baby
 C-section delivery
 Stillbirth
Heavy bleeding due to lack of uterine muscle tone after delivery

TREATMENT of polyhydroamnios:
Drainage of excess amniotic fluid.
 Medication. 
oral medication indomethacin to help reduce fetal urine production and amniotic fluid volume




Oligohydramnios:
A deficiency in the amount of amniotic fluid in the gestational sac during pregnancy less than 400ml.

AETIOLOGY:
FETAL
PROM (50%)
CHROMOSOMAL ANOMALIES
CONGENITAL ANOMALIES
IUGR
IUFD
POSTTERM PREGNANCY

MATERNAL
PREECLAMPSIA
APLA SYNDROME
CHRONIC HT

PLACENTAL
CHRONIC ABRUPTION
TTTS
CVS

DRUGS
PG SYNTHETASE INHIBITORS
ACE INHIBITORS
IDIOPATHIC


COMPLICATIONS:
FETAL
Abortion
Prematurity
IUFD
Deformities –CTEV,contractures,amputation
Potters syndrome- pulmonary hypoplasia
Malpresentations
Fetal distress
MSAF – MAS
Low APGAR

MATERNAL
Increased morbidity
Prolonged labour: uterine inertia
Increased operative intervention
(malformations, distress)

TREATMENT:
ADEQUATE REST – decreases dehydration
HYDRATION – Oral/IV Hypotonic fluids(2 Lit/d)
                         temperory increase
                         helpful during labour,prior
                         to ECV, USG
SERIAL USG – Monitor growth,AFI,BPP
INDUCTION OF LABOUR/ LSCS
                                       Lung maturity attained
                                       Lethal malformation
                                       Fetal jeopardy
                                       Sev IUGR
                                       Severe oligo



AMNIOTIC FLUID EMBOLISM:
AFE is thought to occur when amniotic fluid , fetal cells, hair, or other debris enter the maternal circulation
Presentation:
there will be profound respiratory failure with:
 deep cyanosis  
 cardiovascular shock 
 convulsions and
 profound coma

Causes:
Ruptured membranes (a term used to define the rupture of the amniotic sac)
Ruptured uterine or cervical veins
A pressure gradient from uterus to vein
A maternal age of 35 years or older,
 caesarean or
placenta previa or abruption,
eclampsia, and

Time of event:
    - During labor.
    - During C/S.
    - After normal vaginal delivery.
    - During second trimester TOP. 
 AFE syndrome has been reported to occur as late as 48 hours following delivery.



Risk factors of AFE:
Advanced maternal age
Multiparity
Meconium
Cervical laceration
Intrauterine foetal death
Very strong frequent or uterine tetanic contractions
Sudden foetal expulsion (short labour)
Placenta accreta
Polyhydramnios
Uterine rupture
Maternal history of allergy or atopy
Chorioamnionitis
Macrosomia
Male fetal sex
Oxytocin  (controversial)

Nevertheless, these and other frequently cited risk factors are not consistently observed and at the present time  
Experts agree that this condition is not preventable



Tuesday, May 3, 2011

INFARCTION:
The word "infarction" comes from the Latin "infarcire" meaning "to plug up or cram."
An infarction is the formation of an infarct, that is, an area of tissue death (ischemic necrosis) due to a local lack of oxygen caused by obstruction of the tissue's BLOOD SUPPLY  i.e Arterial supply or Venous drainage.

CAUSES OF INFARCTION:
ARTERIAL CAUSES: 
The supplying ARTERY
 may be blocked by an obstruction (e.g. an arterial embolus, thrombus, or atherosclerotic plaque)
may be mechanically compressed (e.g. tumor, volvulus, or hernia)
ruptured by trauma (e.g. atherosclerosis or vasculitides)
vasoconstricted (e.g. cocaine vasoconstriction leading to myocardial infarction)
 
venous causes:
§Occluded venous drainage (e.g. venous thrombosis) can cause infarction but more often induce congestion only (due to rapid blood flow through collaterals).
§ Infarcts due to venous thrombosis are  more likely in organs with single venous outflow, such as testis or ovary.
 
INFARCT MORPHOLOGY:
Morphologically, the necrotic tissue of an infarct swells, and the infracted area often protrudes above  the surface of the organ.
As an infarct ages it undergoes fibrosis, reduces in size, and ultimately shrinks below the surface of the organ.


CLASSIFICATION OF INFARCTION
Classified according to colour and the presence or absence of infection
 1. WHITE INFARCT OR ANEMIC INFARCT
2. RED INFARCT OR HEMORRHAGIC INFARCT.

Red  OR Hemorrhagic infarct occurs:
- In venous occlusion ( Example: ovarian torsion)
In loose tissues (such as lungs, placenta)
-  In tissues with dual circulation (Example: lungs and small intestine)
In tissues previously congested because of sluggish venous outflow.
At a site of previous occlusion and necrosis when flow is re-established i.e repurfusion  injury


White infarctions (anemic infarcts) affect solid organs with end arterial circulation such as the
spleen , kidneys and Heart.
wherein the solidity of the tissue  substantially limits the amount of nutrients (blood/oxygen/glucose/fuel) that can flow from adjoining capillaries into  the area of  ischemic necrosis

 
SEPTIC INFARCTION:
An area of necrosis resulting from vascular obstruction caused by emboli consisting of clumps of bacteria or infected material.
E.G: infected cardiac valve
In these cases the infarct is converted into an abscess and Abscess slowly organize to SCAR.


 
Pathogenesis and pathology of red infract:
-Arterial obstruction causes fall of distal blood pressure to capillary pressure with dilation of capillaries causing injury due to anoxia.  This is the commonest cause.
-
-Blood from the veins accumulates in the dilated and injured capillaries with outpouring of fluid and RBC into the surrounding tissue.
-
-Thus, the area becomes red, engorged and even hemorrhagic with venous blood, hence the term RED infarction


  white infarct pathology:
 > Atherosclerotic  plaque is injured, ulcerates, or is ruptured
> leading to  platelet aggregation, fibrin deposition, spasm (clot formation and  occlusion)
> cells robbed of O2 begin relying on anaerobic glycolysis
 > after 10 seconds, fuel is depleted and cells become stunned
 > stunned cells unable to participate in contraction
 reversible if O2 supply is restored
 > if O2 is not restored then INFARCTION (MI) occurs
  and in this cells become necrotic




Gross features:  
-All infarcts tend to be wedge-shaped, the occluded vessel marks the apex, and the organ periphery forms the base.
-Lateral margins may be irregular reflecting the pattern of adjacent vascular supply.
e.g This is a recent spleen infarct, showing the classic triangular or wedge shape and the distinctly pale appearance. The reaction zone here is not too apparent, because it is obscured by marked sinusoidal hyperemia




Factors that influence development of an infarct:
1. Pattern of vascular supply:
§ Organs with dual circulation (lung, liver) or anastomosing circulation (radial and ulnar arteries, circle of Willis, small intestine) are protected against infarction.
§ Organs supplied with end arteries (spleen, kidneys) usually develop infarct after occlusion of the arterial supply.    
§
2. Rate of development of occlusion:
Slowly developing occlusions less often cause infarction by providing time to develop alternate perfusion pathways.
 (Example: collateral coronary circulation).

3.  Changes due to hypoxia:
§ Neurons undergo irreversible damage after 3 to 4 minutes of ischemia
§ myocardial cells die only after 20 to 30 minutes.
§ In contrast, fibroblasts within ischemic myocardium are viable even after many hours.
4. Oxygen content of blood:
Anemia, cyanosis, or congestive heart failure (with hypoxia) may cause infarction.