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❖ Management of Shock
❖ Acute Kidney Injury (AKI)
► Causes
► Management in Obstetrics
❖ Blood Coagulation Disorders in Obstetrics
► Normal Blood Coagulation

► Pathology of Acquired Coagulopathy ► Investigations
► Treatment
❖ High-risk Pregnancy
► Screening of High-risk Cases
► Management of High-risk Cases ❖ Immunology in Obstetrics
❖ Critical Care in Obstetrics

INTRAPARTUM FETAL EVALUATION

By deflnUion, Int,apa,tum Fetal Evaluation (IFM) means to watch the fetal condition • · during labor. The goal of IFM is to detect
-
!I
hypoxia in labor and to initiate management ■ .... depending upon the severity of hypoxia. Severe hypoxia in labor when associated with metabolic acidosis can cause fetal organ damage or fetal death.
In between contractions the intraluminal pressure within the spiral artery (85 mm Hg) is higher than the intramyometrial pressure (10 mm Hg) to maintain the uteroplacental blood flow. During peak uterine contractions, myometrial pressure (120 mm Hg) exceeds the arterial pressure (90 mm Hg) causing
temporary halting of 02 delivery to the fetus through the placenta. Depending upon the intensity and duration of
contraction, fetal hypoxia may develop.
The objective of intrapartum fetal monitoring is to prevent fetal organ injury that may be caused by intrapartum fetal hypoxia.
Even in a normal labor, the baby is subjected to stress due to:
1. Uterine contractions temporarily curtailing the uteroplacental circulation.
2. Cord compression with contractions can cause intermit tent interruption of blood flow and may cause hypoxia.
Factors for the release of oxygen from hemoglobin are (factors for shift of oxyhemoglobin saturation curve to the right): (a) increased levels of 2,3-diphosphoglycerate (DPG) concentration, (b) production of lactic acid
(decreased pH), (c) increased partial pressure of CO2
(pC02).

Fetal defense mechanism to hypoxia
■ t 02 extraction by the tissues.
■ !- Non-essential activity(!- fetal movement).
11 t Sympathoadrenal activity(catecholamines). ■ t Glycogenolysis.
11 t Anaerobic metabolism (tK+, tlactate).
■ t Redistribution of blood flow (heart, brain). ■ t Use of bicarbonate to stabilize pH.
11 Metabolic acidosis.
■ Persistent acidemia, hypotension.
■ Multiorgan hypoperfusion (heart, brain, adrenals).
■ Cellular dysfunction; ion shifts, !- enzyme function, t free radicals.
■ Cell injuty, organ damage ➔ fetal death. I METHODS OF FETAL MONITORING
A. Clinical B. Biophysical C. Biochemical
A. CLINICAL: To note the FHR-intermittent Auscultation of FHR using an ordinary stethoscope or a fetoscope or a handheld Doppler can be done to note its rate and rhythm. FHR should be recorded at every 30 minutes interval initially followed by 15 min intervals in the first stage and at about 5 min intervals in the second stage. The auscultation should be made for 60 sec par ticularly before and immediately following a uterine contraction.
Normal fetal heart rate is at an average of 140 beats per minute(bpm) in between contractions with a variation between 100 and 160 per min (FIGO ACOG: 110-160 bpm). There may be slowing of FHR during a contraction (vagal stimulation) which, however, comes back to normal
when the contraction passes off.
!J Chapter 39: Special Topics in Obstetrics
Table 39.1: Causes of fetal tachycardia and bradycardia lasting for> 1 O minutes.

Causes of fetal tachycardia (FHR >160 bpm)
11 Drugs to mother:
(i) -sympathomimetic agents used to inhibit preterm labor (isoxsuprine, ritodrine); (ii) Vagolytic: atropine.
■ Maternal: Metabolic acidemia, hyperthyroidism. ■ Infection-both maternal and fetal.
11 Anemia-both maternal and fetal. ■ Fetal hypoxia.

Causes offetal bradycardia (FHR <: 110 bpm)
♦ Fetal hypoxia, acidosis. ♦ Fetal sepsis, anomalies.
♦ Drugs to mother, e.g., pethidine, antihypertensives (methyldopa,
propranolol), Mg504•
• Use of local anesthetic drugs, epidural analgesia.
♦ Fetal heart conduction defect (SLE).
♦ Maternal: Hypoglycemia, hypothermia.

Limitations of clinical methods
1. As it is a periodic observation, any transient significant abnormality in between observations is likely to be overlooked;
2. Inherent human error;
3. Difficult, at times, to count the FHR during uterine contractions or in case of obesity or hydramnios.
Evidences of distress
1. An increase in FHR to over 160/min (tachycardia
lasting for >10 minutes) or a decrease in rate to less than 100/min (bradycardia) (Table 39.1);
2. FHR takes a long time to come back to its normal rate after the contraction passes off;
3. Fetal heart rate irregularity.
Meconium in the liquor amnii: Meconium in the liquor amnii is a potential sign of fetal hypoxia. It acts as a toxin, if the fetus aspirates this particulate matter. Pathogenesis: Hypoxia ➔(t) vagal response ➔ (t) peristaltic activity and relaxation of the anal sphincter ➔ passage of meconium. The vicious circle is: Placental insuficiency ➔ oligohydramnios ➔ cord compression ➔ hypoxia ➔ thick meconium ➔ gasping breath ➔ meconium aspiration. Meconium staining of the liquor as observed following rupture of the membranes gives a crude idea of intrauterine fetal jeopardy. It is observed in about 10-20% of labors. Presence of meconium and nonreassuring FUR pattern necessitates urgent intervention. On the other hand, reassuring FUR pattern and thin meconium can be managed expectantly.
Intermittent auscultation is recommended to monitor the fetus for a woman in labor without any complications.
B. (i) BIOPHYSICAL-Ultrasound: Doppler effect is used to detect Fetal Heart Rate (FHR) from cardiac motion and major fetal vessels. This observation has to be rechecked when an abnormality is detected.
(ii) CONTINUOUS ELECTRONIC FETAL MONITORING (EFM) Indications of continuous EFM are:
a. Maternal conditions: Hypertension diabetes, previous cesarean delivery, induced labor, APH, PROM, thick MSL, pyrexia (38°C on 2 ocassions, 2 hours apart), fresh bleeding in labor, oxytocin use for labor augmentation.
b. Fetal conditions: Small fetus (FGR), oligohydramnios, multiple pregnancy, abnormal FHR on auscultation.

Two methods are applied: ♦ External: From maternal abdominal wall-noninvasive; ♦ Internal: Directly from the fetus-invasive.
Maternal position: Maternal lateral recumbent position or half sitting are preferable.
External (Fig. 35.4): Continuous tracing of FHR can be obtained using ultrasound Doppler effect. The transducers are placed on the maternal abdomen, one over thefundus and the other at a site where the fetal heart sound is best audible. Frequency of uterine contractions and uterine pressure are recorded simultaneously by tocodynamometer.
Internal: Fetal ECG tracing is made by applying a spiral pointed scalp electrode to the fetal scalp after rupturing the membranes (Fig. 39.1). Intrauterine pressure could be simultaneously measured by passing a catheter inside the uterine cavity.
CTG could be done with portable sensors that transmit signals wirelessly to a remote fetal monitor (telemetry). This allows the mother to move freely. Paper speed is 1 cm/min.
Internal scalp electrode should not be used in cases with active genital herpes infection, HIV or in a very preterm fetus ( <:32 weeks).
Categorization of FHR according to RCOG, NICE is as in Table 39.2. National Institute of Child and Human Development (2008), ACOG (2009); Three-tier FHR interpretation system.

Fig. 39.1: Scalp electrodes.
Chapter 39: Special Topics in Obstetrics

Table 39.2: Categorization of Fetal Heart Rate (FHR) features (RCOG, NICE).
-Baseline Variability
Feature (bpm) (bpm) Deceleration
Normal/ 110-160 >5-25 None or early or variable decelerations with no reassuring concerning features for <1 O min.

Accelerations
Present

Categorization of CTG Traces
Based on four features (baseline FHR, variability, decelerations, accelerations)
Normal: All four features are reassuring.

Non-reassuring

Abnormal

100-109 OR
161-180

<100 OR
>180

<5 for 30 to 50 min.
OR
>25 for 15-25 min.

<5 for >50 min OR >25 for >25 min OR sinusoidal pattern> 10 min.

Variable decelerations:
•
Dropping from baseline by s60 bpm,
recovering by s60 seconds OR >60 bpm,
recovering >60 seconds OR late decelerations. Present up to 30 minutes.
•
■ Occurring o:50% of contractions.
■ Nonreassuring variable decelerations (as
above) present even 30 min after conservative
measures OR
■ Late decelerations >30 min with >50% of
contractions OR
■ Bradycardia or a single prolonged deceleration lasting o:3 minutes.

Absence of accelerations with an otherwise normal CTG is of uncertain significance.

Suspicious: One nonreassuring and the rest are reassuring.

Pathological: Two or more features nonreassuring OR one or more abnormal categories.

Category I: Normal (baseline rate 110-160 bpm; FHR variability-moderate; no late, variable or prolonged deceleration; early deceleration±; acceleration±.
Category II: Indeterminate-all tracings not categorized as category I or III.
Category III: Abnormal (either absent baseline FHR variability and any one of the following: recurrent late/ variable decelerations, bradycardia at least for 10 min or sinusoidal pattern for at least 20 min).
Advantages of EFM over clinical monitoring ♦ Accurate monitoring of uterine contractions.
♦ Significant improvement of perinatal mortality.
♦ Can detect hypoxia early and can explain the mechanism of hypoxia and its specific treatment.
♦ Improvement of intrapartum fetal death by threefold. ♦ It is an important record for medicolegal purpose.
Drawbacks:
,. Interpretation is affected by intra- and interobserver error.
■ Due to error of interpretation (false positive) cesarean section rate (63%) and operative vaginal delivery (15%) are high.
■ Instruments are expensive and trained personnel are required to interpret a trace.
■ Mother has to be confined in bed unless portable sensors are used.
Fetal behavior states: (a) Deep sleep (no eye movements) up to 50 minutes, {b) active sleep (rapid eye movements) (c) wakefulness. All these are hall mark fetal neurological responsiveness and absence of hypoxia/ acidosis. Deep sleep is associated with stable base line, accelerations (rare) and borderline variability. Active sleep is associated with moderate number of accelerations and normal variability. Active wakefulness is rarer and

represented by a good number of accelerations and normal variability.

INTERPRETATION OF A CARDIOTOCOGRA PHY (CTG)
♦ Accelerations and normal baseline variability (5-25 bpm) denote a healthy fetus.
♦ Absence of accelerations is of unknown significance.
♦ Absence of accelerations, reduced baseline variability of <5 bpm for >50 minutes denotes a hypoxic fetus.
♦ Decreased baseline variability may be due to fetal sleep, infection, hypoxia, anomalies or due to maternal medications.
♦ Repeated late decelerations increase the risk of low Apgar score and hypoxemia.
♦ Reduced baseline variability, with late or variable deceleration lasting 3 minutes, increases the risk of hypoxia.
♦ Interpretation of the CTG should always be made in the context of clinical picture.
Baseline FHR is the mean level of FHR excluding accelerations and decelerations. It is expressed in beats per minute (bpm). Normal baseline FHR is 100-160 bpm.
Baseline variability is the oscillation of baseline FHR excluding the accelerations and decelerations. Variability is the reflex of normal cardiac behavior in response to sympathetic and parasympathetic nerve input. However, parasympathetic (vagus) has the dominant role in modulating variability. Baseline variability may be:
(A) Absent (B) Minimal ( <5 bpm) (C) Moderate (6-25 bpm) (D) Marked (>25 bpm)
Reduced baseline variability is observed in many conditions (Table 39.3).
Acceleration: Transient increase in FHR by 15 bpm or more lastingfor at least 15 seconds. Prolonged acceleration
Chapter 39: Special Topics in Obstetrics
•

Table 39.3: Factors to cause FHR changes.
Factors to cause diminished fetal heart variability Factors (maternal/fetal) to alter FHR not related to oxygenation

Maternal medications
■ Pethidine
■ Tranquilizers
■ Corticosteroids
■ Hypoxia, acidosis • Atropine
" General anesthesia

Fetal conditions • Prematurity
■ Sleep cycle Hypoxia Anemia
•
•
•
•
Metabolic acidemia Infection
" Congenital malformation

Factor(s)
• Infections Prematurity Fetal anemia Fetal sleep Heart block
•
•
•
•

Alteration in FHR
■ Tachycardia, tvariability. ■ Tachycardia, tvariability.
■ Sinusoidal pattern, tachycardia. tvariability, taccelerations.
•
■ ,,variability, bradycardia.

lasts ?.2 min but <10 min. When it lasts ?.10 min, it is called baseline change. Acceleration denotes an intact neurohormonal and cardiovascular activity and therefore, a healthy fetus (Fig. 39.2).
Deceleration: Transient decrease in FHR below the baseline by 15 bpm or more and lasting ?.15 seconds (Fig. 39.3).
Three basic types of deceleration are observed and are called early, late and variable (Fig. 39.3).
■ Early deceleration (Type I Dips), uniform, repetitive periodic slowing of FHR and, in most cases, the onset, nadir and recovery of deceleration coincides with the beginning, peak and ending of uterine contraction respectively. It is due to head compression (vagal nerve activation) (Fig. 39.3). It is usually benign (no hypoxia) in nature.
■ Late deceleration (Type II Dips), uniform, U shaped with reduced variability within the deceleration segment and with repetitive periodic slowing of FHR. It begins >20 sec after the onset of the uterine contraction. Usually, the onset, nadir and recove1y of the deceleration occur after the start, peak and end of the uterine contraction respectively. Nadir occurs 20 seconds after the peak of the contraction (acme) and FHR returns to normal after the contraction is over. It suggests uteroplacental insufficiency (Fig. 39.4) and fetal hypoxia (50%).

I
LL

2©0

180+··
160
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1©0
80

60
CGBI 100 CG46
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-
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Fig. 39.2: Reactive trace with acceleration.

160 deceleration::: II Variable 140
Ill
I
Early
:
shape
120 100

■ Causes of late deceleration:
i. Placental pathology (postmaturity, hypertension, diabetes, placental abruption);
ii. Excessive uterine contractions;

Fig. 39.3: Graphic representation showing various types of decelerations in relation to uterine contractions.

•• • ·754·1a· • • • • • • • • • • • • ;40• • • • • ·754;9 •• 75420 240 . 0 2-10
1-80 80 mo
1-50 -50 150 1-20
90
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60 60
30 0 30~
.00 mo
mo
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ZS .s 50 50 50 ff ff
0 0 0
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Admission CTG is a CTG trace done for a woman on admission in the labor ward. Admission CTG is poor in predicting fetal compromises in labor. Routine admission CTG testing is not recommended in low-risk women.

Fig. 39.4: Persistent late deceleration with loss of variability.

iii. Injudicious use of oxytocin;
iv. Regional anesthesia (spinal or epidural).
■ Variable deceleration: It is the intermittent periodic slowing (variable) of FHR (V shaped) with rapid onset and recovery (Fig. 39.3). Decelerations are variable in all respect of size, shape, depth, duration and timing to the uterine contractions. When it is 'U' shaped with reduced variability and/or duration c:3 minutes, it suggests fetal hypoxia/acidosis. It is thought to indicate cord compression and may disappear with the change in position of the patient. It is the most common type. Accelerations often precede and follow the deceleration. It is called shoulders. Concerning character of a variable deceleration: (a) Lasting >60s, (b) No shouldering, (c) Reduced baseline variability, (d) Faliure to return to baseline; biphasic (W) shape. Prolonged deceleration is the abrupt decrease in
FHR (c:15 bpm) to levels below the baseline and it lasts >3 min but <10 min. Commonly seen following: Placental abruption, Uterine rupture, Cord prolapse, Uterine hyperstimulation and Epidural top-up. It indicates
hypoxia and acidosis and require emergent intervention. Prolonged deceleration: it indicates fetal hypoxia/acidosis and require emergent intervention. Fetal pH drop by 0.01/min. If it lasts c:10 min, it is a baseline change.
Lag period: It is the time taken for the FHR to reach the nadir (the lowest point of the FHR dip) from the apex of the preceding uterine contraction (Fig. 39.3). In deceleration lag period is c:30 seconds.
Sinusoidal pattern: It resembles a sine wave (3-5 cycles/min). It has a stable baseline FHR with fixed or absent baseline variability (:55) lasting c:30 min. Accelerations are absent. It is often associated with fetal anemia, fetomaternal hemorrhage, vasa previa, fetal hypoxia (acidosis) (Fig. 39.5). It may occur when narcotics are given to mother. Such FHR showing 'sawtoothed' pattern are called pseudosinusoidal as the fetus is well-oxygenated. It is observed in fetomaternal hemorrhage, twin to twin transfusion syndrome, ruptured vasa previa and
hydrops fetalis.
Pseudosinusoidal pattern: It is more jagged "saw tooth" pattern rather than the smooth sine-wave form.
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Fig. 39.5: Sinusoidal pattern showing absence of baseline variability.

Chapter 39: Special Topics in Obstetrics

It seldom exceeds 30 minutes. It is often observed after analgesic/sedative drugs. At times it is difficult to distin guish from true sinusoidal pattern except the short duration.
C. INDUCED FETAL STIMULATION AND FHR ACCELERA TIONS: Any FHR acceleration spontaneous or induced, indicates the absence of fetal acidosis.
Vibroacoustic Stimulation (VAS) of the fetus is done using an electronic larynx placed on the maternal abdomen. Presence of FHR accelerations indicates normal blood pH.
Fetal scalp stimulation by gentle digital stroke is done before scalp blood pH test. Presence of FHR accelerations is associated with normal scalp blood pH.
Halogen light stimulation is used. FHR accelerations suggests normal pH. Positive response.
Place of auscultation of fetal heart sound versus EFM: Intermittent auscultation is an effective method for evaluation of fetal wellbeing. It is as effective as EFM. In the high-risk patient, auscultation should be done at every 15 minutes in the first stage and at every 5 minutes
in the second stage. In the low-risk group, or in the absence of adequate staff, it may be done at an interval of 30 minutes in the first stage and at every 15 minutes in the second stage. Auscultation should be done for a period of 60 seconds after a uterine contraction. When any audible abnormality is heard, continuous auscultation or conversion to EFM is recommended.
Fetuses with abnormal FHR pattern on auscultation should have EFM to detect any nonreassuring patterns.
D. BIOCHEMICAL: Fetal scalp Blood Sampling (FBS): To corroborate the significance of fetal CTG abnormality due to hypoxia. Saling, in 1962, demonstrated a simple and quick method to obtain fetal blood samples from the scalp to detect the fetal blood pH. Fetal scalp blood pH <7.20 is abnormal and indicates fetal acidosis and urgent delivery, pH between 7.21 and 7.25 is borderline and needs to be repeated within 30 minutes. pH >7.25 is reassuring and labor progress is monitored. pH to be repeated after 30 minutes to detect any changes. It has high specificity. The positive predictive value of a low scalp pH in identifying a newborn with hypoxic ischemic encephalopathy is low. If the CTG (after resuscitation effects) remain unchanged, a second FBS is indicated. FBS can be done for a maximum of 4 times. Lactate levels of the fetus are often correlated with FBS values: <4.1: Normal; >4.9: Abnormal; 4.2-4.9: Boderline. Currently it is not used in many institutions.
Procedures: Mother is in left lateral position. An illuminated plastic cone is inserted through the dilated cervix ( 4-5 cm) against the fetal head. An incision of 2 mm depth is made with a lancet. Blood is collected (35 µL may be adequate for analysis with most pH monitors) with a long capilla1y tube for pH and base excess estimation.
mJ Chapter 39: Special Topics in Obstetrics
Indications: (i) Nonreassuring CTG in labor, (ii) Bio chemical assessment of fetal hypoxia.
Contraindications:
i. When delivery is urgently indicated or spontaneous delivery is imminent.
ii. Maternal infection (HIV, hepatitis or herpes simplex virus).
iii. Fetal coagulation disorders. iv. Prematurity ( <34 weeks).
v. Cervical dialation of 4 cm.
Risks involved are: • Fetal bleeding from the incision site and maternal injury. • False prediction is about 10%.
E. FETAL ELECTROCARDIOGRAM (ECG) analysis has been done with ST segment and T wave analysis (STAN) or with T/QRS ratio. An increase in T-wave amplitude occurs in hypoxia. Each fetus has its own baseline T/QRS. A normal fetus has a T/QRS <0.25. A significant increase in T/QRS or more than two consecutive biphasic ST in fetal ECG complexes, combined with a nonreassuring FHR tracings (CTG), indicates fetal metabolic acidosis. Fetal ECG analysis (ST-segment analysis) when combined with CTG, reduces operative delivery rates compared to CTG alone. Limitations: Not used for fetus <36 weeks. Cannot be used alone for decision making.
F. Umbilical arterial cord (or neonatal) blood samples with pH <7.0 and base deficit of >12 mmol indicates profound metabolic acidemia and multiple organ dysfunction. Intrapartum umbilical artery Doppler study was poor to predict umbilical artery acidosis. A positive test increases the cesarean delivery rates. There is a correlation between NRFS and neonatal depression, but it is not related with the long-term neurologic sequelae.
G. Fetal pulse oximetry is no longer used as its accuracy is uncertain.

NONREASSURING FETAL STATUS (NRFS)

DEFINITION: Fetal distress is an ill-defined !) !·) term, used to express intrauterine fetal jeopardy, a result of intrauterine fetal .Ea;;i hypoxia. Nonreassuring Fetal Status !] (NRFS) is characterized by tachycardia or bradycardia, reduced FHR variability, decelerations and absence of

accelerations (spontaneous or elicited). It must be emphasized that hypoxia and acidosis is the ultimate result of the many causes of intrauterine fetal compromise (Box39.l).
FHR patterns in labor are dynamic and can change rapidly from normal to abnormal and vice versa. Because of this uncertainty about the diagnosis of fetal distress, terminologies used are 'Reassuring' and 'Nonreassuring'.
Nonreassuring fetal heart rate pattern is associated with fetal hypoxia, acidosis and, therefore, called fetal distress (Box 39.1). Features to rule out metabolic acidosis are: (a) Presence of accelerations, (b) moderate variability, and (c) scalp blood pH >7.25.
Fetal condition at birth is assessed by blood gas values of the umbilical artery. Normal (mean) values are: pH
7.27, PC02 50; Hco- 23, base excess -3.6. The correlation
3
between the FHR and long-term neurological sequelae is poor. In many cases, asphyxia occurs prior to labor.

MANAGEMENT OF NONREASSURING FETAL STATUS (NRFS)

Ideally, management should be specific to the cause ofNRFS.
NONSURGICAL: Management is aimed to reverse the abnormality (hypoxia) by noninvasive procedures.
■ Lateral positioning avoids compression of vena cava and aorta by the gravid uterus. This increases cardiac output and uteroplacental perfusion. This also reduces umbilical cord compression.
11 Change in maternal position also reduces cord compression.
■ Oxygen is administered (6-8 L/min) for short periods
to the mother with face mask to improve fetal Sa02•
■ Correction of dehydration by IV fluids (crystalloids) improves intravascular volume and uterine perfusion.
■ Correction of maternal hypotension (following epidural analgesia) with immediate infusion of 1 liter of crystalloid (Ringer's solution).
■ Stoppage of oxytocin to improve fetal oxygenation. Fetal hypoxia may be due to strong and sustained uterine contractions. With reassuring FHR and in absence of fetal acidemia, oxytocin may be restarted.

A.Acute:
I. During pregnancy-less common
♦ Placental separation in placenta previa or abruptio placentae + Following external cephalic version due to cord entangle-
ment
♦ During oxytocin induction + Diabetes
+ Hypertension

II. During labor-common
+ Uterine tachysystole following oxytocin for augmentation of labor. + Placental abruption.
+ Uterine rupture or scar dehiscence. + Cord prolapse.
+ Injudicious administration of oxytocin, analgesics and anesthetic agents.
+ Maternal hypotension-as in epidural analgesia.

B. Chronic: The various clinical conditions which are responsible for chronic placental insufficiency and IUGR, are also linked with chronic fetal distress.
Chapter 39: Special Topics in Obstetrics JI:--- 11 Remove prostaglandins (vaginal pessa1y). patients need to be evaluated (continuous or intermittent)
11 Tocolytic (Injection terbutaline 0.25 mg SC) is given as required to exclude acidosis. Labor progress is to be when uterus is hypertonus and there is nonreassuring monitored, vaginal delivery could be done safely.
FHR. Tocolytics increase oxygen to the fetus. B. Persistence of nonreassuring pattern or the fetus • To avoid sustained pushing in the second stage of labor. becoming acidotic, patient needs immediate delivery. • Amnioinfusion can be given for NRFS. SURGICAL: Cesarean delivery should be done with a
Amnioinfusion is the process to increase the intraute 15° lateral tilt till the baby is delivered. Thirty minutes
rine fluid volume with warm normal saline (500 mL). ( Cat I) has been accepted as the gold standard for
Other indications of amnioinfusion: decision to delivery interval in cases of confirmed fetal
Pediatrician should be present.
compromise.
a. Oligohydramnios and cord compression, Limitation of cardiotocography: (a) Inter- and intra observer disagreement. (b) Criteria forinterpretation of
b. To dilute or to wash out meconium,
c. To improve variable or prolonged decelerations,
d. To reduce fetal gasping which is the result of hypoxia CTG are in identification of deceleration and evaluation due to cord compression. suspicious and pathological tracings. ( d) Suspicious and pathological tracings have a limited capacity to predict
of variability. (c) Disagreements are more with the
Advantages of amnioinjusion:
Reduces cord compres
sion, meconium aspiration, and improves Apgar score. It
also reduces cesarean section rate.
metabolic acidosis and hypoxic neurologic injury. Thus Routine prophylactic use of amnioinfusion for meco CTG has low specificity and low positive predictive value.
Continuous monitoring with CTG is not recommended
nium stained liquor is not recommended (ACOG). for all women in labor. Benefits of CTG in monitoring in If the fetal heart rate pattern remains nonreassuring, labor was reduction in neonatal seizures (50%}. Only a further tests are performed to rule out fetal acidosis. small proportion of perinatal deaths and cerebral palsies Tests are: (i) To detect FHR accelerations (CTG) are caused by intrapartum hypoxia/acidosis. On the other spontaneous or induced ( digital fetal scalp stimulation), hand continuous CTG was associated with 63% increase (ii) Scalp blood pH, (iii) Fetal ECG/ST-segment analysis in cesarean delivery and 15% increase in instrumental (STAN), combined with CTG. Above supportive measures vaginal delivery. Unnecessary obstetric intervention due
are continued and the women is revaluated. to poor CTG in interpretation confer more risks for the A. Conversion of NRFS to a reassuring pattern (RFS) and mother and the newborn. Computer analyses of CTG without any evidence of metabolic acidosis (presence of are more precise but has not improved the prediction of
accelerations, variability and scalp blood pH > 7 .25): these neonatal outcome. r:f:.,n
► lntrapartum fetal monitoring is done to evaluate the oxygenation of a fetus during labor. The sole objective is to take appropriate steps
in time so that fetal hypoxic injury is prevented.
► Continuous EFM (CTG) in labor reduces neonatal seizures by 50%.
► EFM, scalp pH and ST analysis are used to detect intrapartum fetal hypoxia.
► Methods of intrapartum monitoring includes: (1) Clinical monitoring: (a) intermittent auscultation, (bl color of the liquor (meconium). (2) Biophysical: (a) CTG, (bl induced fetal stimulation (acoustic, fetal scalp). (3) Doppler velocimetry for UA. (4) Combined fetal CTG & ECG. (5) Biochemical: (a) Fetal blood sampling (pH), (b) Lactate estimation.
► Intermittent auscultation is an effective method. Fetuses with abnormal FHR pattern on auscultation should have EFM.
► EFM has few limitations. Normal CTG indicates a healthy fetus, whereas abnormal FHR pattern in CTG does not always indicate
fetal asphyxia. Limitations are: • Inter- and intra-observer disagreement of CTG report, • Different CTG interpretation criteria, • Limited knowledge about the pathophysiology of fetal hypoxia.
► Presence of accelerations and normal variability denote a healthy fetus.
► False positive rate of EFM for predicting fetal hypoxia is high. CTG has low specificity and low positive predictive value to detect fetal acidosis.
► Loss of variability, loss of acceleration and presence of bradycardia indicate fetal compromise.
► Decelerations that occur with 50% of uterine contractions in a 20 minute window are defined as recurrent decelerations. ► Presence of accelerations of the FHR either spontaneous or induced (VAS stimulation), indicates absence of fetal acidosis.
► EFM is most reliable when FHR pattern is reassuring (category-I) and when there is fetal acidosis (category-Ill). It is most unreliable when tracings are equivocal (category-II).
► High-risk labor should be monitored continuously. Use of continuous EFM is associated with an increased rate ofoperative interventions (vacuum/forceps-15%, or cesarean delivery-63%). Only a small proportion of perinatal deaths and CP are caused by intrapartum hypoxia and/or acidosis.
► Nonsurgical measures are used to improve or reverse hypoxia.
► Persistent hypoxia or presence of metabolic acidosis needs expeditious delivery of the baby to prevent neurological injury and organ damage.
► Amnioinfusion for variable decelerations may reduce the rate of cesarean section.
fD Chapter 39: Special Topics in Obstetrics SHOCK IN OBSTETRICS
DEFINITION: Shock is defined as a state of
-
!l !l
cj

circulatory inadequacy with poor tissue ·' perfusion resulting in generalized cellular hypoxia. Circulatory inadequacy is due
to a disparity between the circulating blood volume and the capacity of the circulatory bed. The net effect of this disparity is inadequate exchange of oxygen and carbon dioxide between the intra- and extravascular compartments. The stagnation of carbon dioxide and other metabolites in the tissue leads to metabolic acidosis, cellular dysfunction and death. The series of changes
observed in shock and their clinical manifestations, are therefore, dependent on two sets of changes: (a) Circulatory inadequacy at the 'filtration' level (microvascular compartment), (b) Cellular damage and ultimately death.
Anatomy of microvascular circulation: Microvascular circulation consists of circulation of blood through a tuft of capillaries with a feeding arteriole and a draining venule at either end of the capillary bed. The flow of blood within the capillary bed is controlled by 2 sphincters-one at the arteriolar end and the other at the venular end. They are known as pre- and postcapillary sphincters. In addition to the tuft of capillaries, there is a direct communication between the arteriole and the
venule and this communicating trunk bypasses the capillary bed. This is known as metarteriole shunt or 'thorougllfare channel'. When the sphincters are closed, the metarteriole shunt operates to divert blood for supply to the vital organs, like brain, heart and kidney. The basic pattern of microcirculation is schematically represented in Figure 39.6.

I PATHOPHYSIOLOGY OF SHOCK

Pathophysiological changes in obstetric shock are predominantly associated with: (a) general changes due to hypovolemia, and (b) specific changes due to liberation of endotoxin.
Hypotension stimulates release of neuroendocrine mediators like Adrenocorticotropic Hormone (ACTH), Growth Hormone (GH), endorphin, cortisol and

Arteriole

·., 7 l
l
_ True I l
:
-,_
capillary: : Metarteriole :
I
I
I
I
: Thoroughfare
_________ J chan: nel __ -1.- U- I
I
I
capillary I
I
I
___________________ J

Fig. 39.6: Schematic diagram of a microcirculatory unit.

glucagon (Flowchart 39.1). There is also sympathoadrenal response. Presence of endotoxin (lipopolysaccharide), in septic shock activates the leukocytes through complement system. There is release of inflammatory mediators such
as proteases, superoxide (02), hydroxyl (OH-) radicals, cytokines, prostaglandins and many cytotoxic enzymes.
These interfere with the function of a number of enzyme systems and increase capillary permeability. Cytokines such as Interleukins (ILS) and Tumor Necrosis Factor (TNF) interact by autocrine and paracrine mechanism to cause cellular or organ dysfunction. In presence of hypoxia, sepsis and acidosis, lysosomal enzymes which are cytotoxic, are released. They can cause myocardial depression and coronary vasoconstriction.
Prostacyclin is a vasodilator and inhibits platelet aggregation.
Thromboxane A2 causes pulmonary vasoconstriction and platelet aggregation. Leukotrienes cause vasoconstriction, platelet
activation and increased vascular permeability. Endothelium Derived Relaxing Factor (EDRF) which is identified as Nitric Oxide (NO) is found to produce sustained vasodilatation and hypotension. Thrombosis is increased due to inhibition of antithrombin III. Thrombocytopenia is common.
In pregnancy prostaglandins and nitric oxide, upregulated by estradiol are implicated in physiological adaptation required to support the developing fetus. This may make pregnant women more susceptible to abrupt hypotension due to infection. The women suffers the risk of tissue hypoxia and organ dysfunction.
Metabolic changes: Hepatic glycogenolysis due to increased level of glucagon, catecholamine and cortisol leads to hyperglycemia. There is diminished peripheral utilization of glucose due to increased level of insulin antagonists like cortisol and growth hormone. Inadequate oxygen supply to tissue initiates anaerobic metabolism. Consequently, there is metabolic acidosis, production of lactic acid and H+ ions. Sodium pump fails to operate. Finally, the lysosomal enzymes are released. These lead to cell death.

GENERAL CHANGES IN SHOCK (WITH SPECIAL REFERENCE TO HYPOVOLEMIC SHOCK)

The changes are in four phases. The first two phases are reversible; the third one probably correctable and the fourth is irreversible:
♦ First phase: Sympathetic impulses and the level of circulating catecholamines increase in response to hypovolemia, cardiogenic or neurogenic stimulus.
♦ Second phase: As a result of excessive sympathetic stimulus, there is constriction of the pre- and postcapillary sphincters, resulting in inadequate venous return leading to diminished cardiac output, clinical manifestations of which are hypotension and tachycardia.
Compensatory mechanisms that operate at this stage to maintain the blood pressure, has been discussed in the (Flowchart 39.1).
These mechanisms attempt to correct hypovolemia, improve cardiac output and the perfusion of vital organs.
Chapter 39: Special Topics in Obstetrics

Flowchart 39.1: Pathogenesis of Septic Shock.

INFECTION (sepsis syndrome)
i
(Septic abortion, septic peritonitis, pyelonephritis, chorioamnionitis/endometritis/Necrotizing fascitis)

Gram-negative (70-80%) Gram-positive (20-30%)

(Aerobic and anaerobic)

Endotoxin (lipopolysaccharide acid}

• • 0 • N utrophils • Monocytes
•
•
..
.
.
-
l

Exotoxin (lipoteichoic acid)
• Macrophages • Endothelial cells (j.

Systemic inflammatory response (SIR)
lI
l

• Endogenous mediators • Autocrine and paracrine action
I
1 l 1
• Cytokines, chemokines (T cells, B cells).• Platelet activating factor. • Endothelin-1.
• Proinflammatory: IL 1, IL 6, IL 8, • Prostaglandins (PGE , PGl , TXA )- • Cytotoxic enzymes.
2
2 2
IL 12, TNFa, interferon. • p endorphins. • Complements C3a, C5b.
Anti-inflammatory: IL4, IL 10, TGFp. • lnterferon-y. • Nitric oxide.
i l !
Myocardial effects Vascular effects ■ Coagulation cascade activation.
■ Cardiomyocyte death. ■ Vasodilatation. ■ Vasoconstriction.
■ Myocardial contraction!-. ■ Maldistribution of blood flow. ■ Fibrin deposition.
■ Cardiomyopathy. ■ lntravascular thrombosis. ■ Microthrombi formation.
■ LV ejection fraction i. ■ Endothelial cell injury. ■ ARDS. ■ Thrombocytopenia.
■ Cardiac output ,I._ ■ Hypotension. ■ Tissue hypoperfusion. ■ DIC. ■ tcapillary permeability.
1---------_,

----------- I Irreversible phase
-,+1
I
l
Persistent hypotension Metabolic acidosis Severe myocardial depression

Multiorgan Dysfunction Syndrome (MODS)

At this stage replacement of blood volume (transfusion) and control of hemorrhage are usually effective in restoring the normal circulatory balance and tissue perfusion.
♦ Third phase: Prolonged anoxia of the tissues will lead to excessive production of lactic acid (acidosis). Lactic acid and anoxia cause relaxation of the precapillary sphincters but not the postcapillary sphincters. In addition,
thromboxane A2 and leukotrienes (endogenous mediators) cause damage to the endothelial cells of the capillaries of the
microcirculatory bed. These lead to formation of thrombus within the capillaries (diffuse intravascular coagulation) and increased capillary permeability.
♦ Fourth phase: Consequent to persistent constriction of the postcapillary sphincter, blood remains stagnant within the capillary bed. Fluid from the capillaries leaks into the tissue spaces due to increased permeability. All fluids administered intravenously will go into the interstitial spaces and circulatory blood volume cannot be restored. Clinically, this is the stage of irreversible shock. There is severe loss of systemic vascular resistance, severe

myocardial depression ( I, cardiac output), unresponsive hypotension and ultimately multiple organ system failure.
Systemic Inflammatory Response Syndrome (SIRS) is manifested by two or more of the following conditions: (1) Temperature >38°C or <36°C, (2) HR >90 bpm, (3) Respiratory rate >24/min, or (4) Serum lactate >l mmol/L, (5) WBC >12000/ µLor leukopenia: <4000/µL or more than 10% immature forms.
I CHANGES IN ENDOTOXIC SHOCK

Endotoxic shock usually follows infection with gram negative organisms (75-80%). The most common organism involved is Escherichia coli (50%). Other organisms occasionally responsible for endotoxic shock are, Pseudomonas aeruginosa, Klebsiella, Proteus, Bacteroides and Aerobacter aerogenes. Gram-positive organisms (Staphylococcus, Streptococcus), anaerobes (Bacteroides
fragilis), Clostridium group are less common (20%).
Pathophysiology of endotoxic shock has been discussed before (Flowchart 39.1). Bacterial endotoxin
•=-· ml Chapter 39: Special Topics in Obstetrics

causes selective vasospasm at the postcapillary end. Blood is pooled in the capillary bed. There is inhibition of myocardial function and cellular damage through complex biochemical changes (vide supra).
The patient in early septic shock feels warm due to vasodilatation. This is called warm shock. In the late phase, the patient feels cold due to vasoconstriction (sympathetic squeeze). This is called cold shock or late shock. Patient's skin becomes cold, clammy and ashen gray.
The various biochemical and pathological changes observed in endotoxic shock are: (i) Diffuse intravascular coagulation, (ii) Increased capillary permeability, (iii) Metabolic acidosis, (iv) Release of nitric oxide (NO) superoxide (0 -) and hydroxyl (OH-) radicals, (v) Failure of sodium pump operation, (vi) Water and electrolyte imbalance, (vii) Lowered pH, (viii) Altered enzyme function, (ix) ion shift and (x) Excessive and uncontrolled Systemic Inflammatory Response (SIR) can lead to cellular and tissue disfunction, injury and even death. Organ changes depend on the degree of hypoperfusion and extent of the underlying pathology: (a) Kidney Patchy and massive cortical necrosis leading to oliguria, anuria and azotemia. Persistent hypotension leads
2
to acute tubular necrosis and ultimately renal failure. (b) Liver-Hepatocellular necrosis and degeneration ultimately leading to hepatic failure. (c) GI tract Hypoxic mucosa! injury increases systemic sepsis by translocation of intraluminal microbes. Congestion, hemorrhage and ulceration are responsible for hematemesis. (d) Lungs-Congestion or atelectasis leads to tachypnea or dyspnea, progressive hypoxemia and reduced pulmonary compliance. ARDS results from increased capillary permeability and thickening
of the alveolar capillary membranes. Arterial Pa02 is
low ( <65 mm Hg). Mechanical ventilation is needed. (e) Coagulopathy (DIC)-It is due to diffuse endothelial injury, microvascular thrombosis and thrombocytopenia. (f) Adrenal insuficiency is due to Critical Illness-Related Corticosteroid Insufficiency ( CIR CI). CIR CI causes hypotension which is refractory to fluid replacement. Vasopressor therapy is needed. (g) Heart-Cardiac output decreases depending on the degree of hypotension, hypoperfusion and vasoconstriction. Myocardial ischemia ➔ cardiac dysfunction ➔ dysrhythmias ➔ cardiac failure ➔t Left Ventricular End-Diastolic Pressure (LVEDP) ➔ pulmonary edema ➔ tissue hypoxia (h) Ultimately, multiple organ failure develops. Endotoxins have got special affinity for kidneys and lungs for reasons which are
not very clear.
I CLASSIFICATION OF SHOCK
Based on our understanding of the basic pathophysiology of shock and its clinical correlation; shock may be classified as follows
(Box39.2):

1. Hypovolemic shock: (i) Hemorrhagic or (ii) Nonhemorrhagic. Hemorrhagic shock: Associated with postpartum or postabortal hemorrhage, ectopic pregnancy, placenta previa, abruptio placentae.
• Shock associated with disseminated intravascular coagulation. Nonhemorrhagic shock:
• Fluid loss shock-associated with excessive vomiting, diarrhea, diuresis or too rapid removal of amniotic fluid.
• Supine hypotensive syndrome.
2. Septic shock (endotoxic shock): Hypotension (systolic BP <90 mm Hg) is due to sepsis resulting in cellular and organ system dysfunction.
3. Cardiogenic shock:
• Myocardial infarction.
• Cardiac arrest (asystole or ventricular fibrillation). • Cardiac tamponade.
Characterized by I, systolic pressure(<80 mm Hg), ,I, cardiac index ( < 1.8 L/min/m2) and left ventricular filling pressure(> 18 mm Hg).
t
4. Extracardiac shock: Massive pulmonary embolism, amniotic
fluid embolism, anaphylaxis, drug overdose.
• Chemical injury: Aspiration of gastrointestinal contents during general anesthesia (Mendelson's syndrome).
• Drug-induced: Associated with spinal anesthesia.

CLINICAL FEATURES OF SHOCK: Clinical features of shock depend on the basic etiological factors and, consequently, the sequence of pathological changes occurring within the microvascular unit. In early stages, the features of hypovolemic and septic shock are different. In the irreversible (late) phase, the clinical features are the same as the final pathology is multiple organ failure. It canies mortality of 30-100%.
Hemorrhagic Shock
■ Early phase (com11ensatory phase): In the early phase, there is mild vasoconstriction and with the compensatory mechanism operating, the patient has relatively normal blood pressure but tachycardia. This phase can be easily managed by volume replacement.
■ Intermediate phase (reversible phase): If the early phase remains untreated, the patient passes into the state of
hypotension. Patient progressively becomes pale; tachycardia persists and due to intense vasoconstriction, the periphery becomes cold and there may be sweating. Due to diversion of blood to vital organs, the patient remains conscious and the urine output is within normal limits. Still with adequate
management, the shock state can be reversed.
■ Late stage (irreversible): Hypotension continues and cannot be reversed by fluid replacement (CIRCI). Extremities become cold and clammy because of vasoconstriction due to sympathetic stimulation. Metabolic acidosis, coagulopathy and thrombocytopenia are associated. Practically, imperceptible low volume pulse, oliguria, mental confusion is observed. Patient is in MODS. Treatment of any kind is practically useless in this phase and mortality varies between 3% and 100%.
NEUROGENIC SHOCK: The basic pathological factors in both hemorrhagic and neurogenic shock are more or less the same except for the fact that hemorrhagic shock is hypovolemic and neurogenic shock, initially is
Chapter 39: Special Topics in Obstetrics &BL

normovolemic, though this becomes hypovolemic in the later phase due to pooling and stagnation of blood in the microvascular capillaries.
ENDOTOXIC SHOCK: Clinically it is manifested with temperature changes, >38°C or <36°C, bounding pulse, heart rate >100 beats per min, respirato1y rate >20/min, WBC >12000/mm3 or <4000/mm3. Pathophysiology of septic shock has been described on p. 576.
SEPSIS-3: ltis defined as the septic shock with the need of vasopressor drug to maintain a mean arterial pressure (MAP 65 mm Hg). In the absence of hypovolemia and serum lactate >2 mmol/L.

MANAGEMENT OF SHOCK I HEMORRHAGIC SHOCK
Basic management of hemorrhagic shock is to stop the bleeding and replace the volume which has been lost (Tables 39.4 and 39.5). Prompt diagnosis and immediate resuscitation is essential failing which multiple organ failure develops.
■ Restore circulating volume (infusion and transfusion): Blood should be transfused, especially in hemorrhagic shock as soon as it is available. Crystalloids: Normal saline has to be infused (20-30 mL/kg) initially for immediate volume replacement. Crystalloids are the primary choice. Colloids: Polygelatin solutions (Hemaccel, Gelofusion) are iso-osmotic with plasma. They do not interfere with the coagulation system. They promote osmotic diuresis. Human albumin solutions ( 4.5%)-are less used for volume replacement.
■ Maintenance of cardiac efficiency: When a large volume of fluid or blood is to be administered, the

Table 39.4: Classification of obstetric hemorrhage based O[l th' mo r't,
e
'
of blood loss (volume deficit), considering a woman weighing 60 kg·i with a blood volume of 6lat 30 weeks of gestation (Be!)edetti-2002),'.
Blood loss (mLJ (%) Clinical
Class of blood volume presentation Management
0 <500: ( < 10%) Nil Normal loss
1 900 ml: (15%) No alteration Observation, replacement ±
2 1200-1 500 ml: ■ tPulse Immediate
(20-25%) ■ !-BP volume
■ tRespiratory repalcement +
rate Uterotonics ■ !-Urine output
3 1800-2000 ml: ■ t PR Urgent active
(30-35%) ■ -!-BP managemet Volume <!l.5 l ■ Cold, clamy
is considered as massive hemorrhage
■ t Resp. rate
4 2400ml: (40%) Features of shock Critical; active management (50%mortality if unattended )

cardiac competence or eficiency should be ascertained, otherwise there is a risk of overloading the circulation and cardiac failure. 6 liters of crystalloids may be needed for loss of 1 liter of plasma volume. One or two large bore (14 or 16 gauge) cannula are inserted for volume replacement. Packed red blood cells (specific blood component), combined with normal saline, are used for hemorrhagic shock. Hemodynamic monitoring is aimed to maintain systolic BP >90 and MAP ':60 mm
Hg, CVP 12-15 cm H2O and pulmonaiy capillary wedge
pressure 14-18 mm Hg.
■ Administration of oxygen to avoid metabolic acidosis: In the initial phase, administration of oxygen by nasal cannula at a rate of 6-8 liters per minute is started. Oxygen delivery should be continued to
maintain 02 saturation >94%. PaCO2 30-35 mm Hg and
pH >7.35. Endotracheal intubation and mechanical ventilation may be needed for patients with septic shock. Indications of mechanical ventilation are: (a) Severe tachypnea (RR >40/min), (b) altered
mental status, (c) persistent hypoxemia, despite 02 supplementation.
■ Pharmacological agents: Use of vasopressor drugs should be kept to a minimum, since peripheral vasoconstriction is already present. The role of vasoactive drugs, inotropes and corticosteroids in shock has been discussed in detail in connection with management of endotoxic shock.
■ Control of hemorrhage: Specific surgical and medical treatment for control of hemorrhage should start along with the general management of shock. The specific management of each variety of obstetric hemorrhage has been outlined in the related chapters.

Table 0 39.5:·c1assificati fo(h.emorrhagic shod (based on total
'
,
blood volume 6 L). ' '
Parameter Class I Class II Class Ill Class IV Blood volume s15 15-30 30-40 >40 loss%(ml) (<750) (750-1500) (1500-2000) (>2000)
Heart rate No Tachycardia Moderate Marked (bpm) change tachycardia tachycardia
Blood Normal Normal Decreased Decreased pressure
Respirations Normal Tachypnea Tachypnea Marked tachypnea
Mean arterial Normal Mildly <60mm Hg Decreased pressure decreased
Cardiac Normal Mildly Reduced Markedly output reduced reduced
Systemic Normal Increased Increased Increased vascular resistance
Urine output >30 20-30 5-15 Anuric (ml/hr)
Mental status Normal Anxious Confused Obtunded
ZI Chapter 39: Special Topics in Obstetrics

Monitoring: Clinical parameters like skin temperature, visible peripheral veins can be helpful to assess the degree of tissue perfusion. Urine output (>30 mL/hr) is a useful guide. Arterial blood pressure is a poor indicator to assess tissue perfusion. Invasive monitoring may not be needed in a straight fo1ward case. In a critically ill patient, however, measurement of Central Venous Pressure (CVP), to assess the adequacy of patient's circulating volume and the contractile state of the myocardium, is essential. Pulse oximeter and blood gas analysis are useful to assess tissue perfusion. Measurement of left atrial pressure (pulmonary arte1y occlusion pressure) by 'Swan-Ganz' catheters could be done in selected cases.
I ENDOTOXIC SHOCK
Investigations to organize in a patient with !] •· !] septic shock: CBC, hematocrit, coagulation
-
!]
profile, (platelet count, serum fibrinogen,
FDPs, PT, APTT), liver enzymes and renal
function tests, chest radiograph, USG, CT or MRI may be needed (for localizing pelvic pathology or pelvic abscess, pneumonia or ARDs), and also ECG monitoring to detect signs of arrhythmias or ischemia.
Biomarkers: In evaluation of obstetric sepsis, the important blood biomarkers predominantly used are: WBC count, C-Reactive Protein (CRP), Procalcitonin (PCT) and lactate. WBC and CRP are nonspecific, but PCT appears to be more specific for bacterial infection. A venous lactate >2 mmol/L suggest critical care input and a level >4 mmol/L needs the support of vasopressors, monitoring of Central Venous Pressure (CVP) and oxygen saturation.
Principles of management are: (a) To correct the hemodynamic instability due to sepsis (endotoxin), (b) appropriate supportive care, and (c) to treat and to remove the source of sepsis.
Two wide bore cannulas are sited. Foley's catheter is inserted. Oxygenation with (face mask) is to be given. Mechanical ventilation may be needed in a severe case.
Goal ofhemodynamic resuscitation is to maintain (a) Mean arterial pressure > 70 mm of Hg, (b) CVP 10 to 12 cm HzO, (c) Urine output 0.5 mL/kg/hour, (d) Central venous oxygen saturation > 70%.
This includes administration of oxygen, antibiotics, intravenous fluids, adjustment of acid-base balance, steroids, inotropes, prevention and treatment of intra vascular coagulation and toxic myocarditis, administration of oxygen and elimination of the source of infection.
■ Antibiotics: Endotoxic shock is most commonly due to gram-negative organisms. The choice of antibiotic will depend upon the sensitivity test but before the report is available, broad-spectrum antibiotics co-vering gram-positive, gram-negative and anaerobic organisms should be started. Ampicillin (2G IV every

6 hours), gentamicin (2 mg/kg N loading dose followed by 1.5 mg/kg N every 8 hours) and metronidazole (500 mg IV every 8 hours) is a good combination to start with. Alternative regimen is to give N teicoplain 12 mg/ kg 12 hourly for 3 does, then 10 mg/kg/24 hourly + IV clindamycin 1.2 g 6 hourly+ N gentamycin 5 mg/kg.
■ Intravenous fluids and electrolytes: Septic shock associated with hemorrhagic hypotension should be treated by liberal infusion and blood transfusion. Isotonic c1ystalloid (normal saline) should be given. The amount of fluid to be administered can be precisely assessed by monitoring the pulse, BP, urine output and recording the central venous pressure. Oliguria with high specific gravity is an indication for fluid administration. Impairment of renal function contraindicates administration of electrolytes. Estimation of blood electrolytes (Na, K, bicarbonate) is needed.
■ Correction of acidosis: Acidosis and hypoxemia depress myocardial contractility. Bicarbonate should be administered to correct persistent metabolic acidosis (pH <7.2) only. A reasonable first dose would be 50-100 mEq (60-110 mL of 7.5%) of sodium bicarbonate solution. Further doses will depend on the clinical state of the patient and blood gas analysis result.
■ Vasopressors: Inotropic agent is started in a critically ill patient when there is hypotension (MAP <60 mm Hg) and impaired perfusion of vital organs despite adequate volume replacement, inotropes should be used. Noradvenaline is the first line treatment because of its eficacy. A sepsis related scoring system to identify the critically ill obstetric patient has been made (Table 39.6) and for convenience a quick scoring system has also been made (Table 39.7). Noradrenaline and
dobutamine have both inotropic and vasoconstrictive
effects. Dobutamine W1 and p2 adrenergic) is used in
cardiogenic shock. Noradrenaline (5-15 microgram/
min) is used. Adrenaline is a very potent a and p agonist and is sometimes used in patients who do not respond to other drugs, especially in septic shock. Levosimendan is a novel inotropic agent. It has vasodilater and anti inflammatory effects.
Vasodilator therapy: In selected cases (MAP >70 mm Hg) afterload reduction may improve stroke volume and reduce ventricular wall tension. Sodium nitroprusside and nitroglycerin could be used for that purpose. This is done under continuous hemodynamic monitoring.
Diuretic therapy: To reduce fluid overload (preload) and pulmona1y edema, diuretics should be used. Frusemide is the drug of choice.
■ Corticosteroids: Patients with severe sepsis develop systemic inflammatory response syndrome or relative adrenal insufficiency (CIRCI). Corticosteroids could be used as anti-inflammatory agents to improve the outcome. The dose recommended in septic shock
Chapter 39: Special Topics in Obstetrics

Table 39.6: Obstetrically modified SOFA score.
A sepsis-related scoring system to identify the critically ill obstetric patient
Score
System parameter 0 1 2
Respiration: PaO/Fi02 >400 300to <400 <300
Coagulation: Platelets (x >150 100-150 <100 105/L)
Liver: Bilirubin (µmol/L) <20 20-32 <32
Cardiovascular (CVS): Mean >70 <70 Vasopressors arterial pressure (mm Hg) required
Central nervous system Alert Rousable by Rousable by voice pain
Renal: Creatinine (µmol/L) <90 91-120 >120

is 50 mg of hydrocortisone per kg body weight in
divided doses for 7 days. The advantages claimed are: (i) exerts an anti-inflammatory effect at the cellular level, (ii) stabilizes lysosomal membrane, (iii) counteracts anaerobic oxidative mechanism,
(iv) exerts positive inotropic effect to improve cardiac efficiency, (v) improves regional blood flow (micro circulation). However its absolute benefits are debated.
■ Treatment of dffuse intravascular coagulation: When there is low fibrinogen level, reduced platelet count and increased fibrin degradation products, heparin therapy should be considered. As a prophylactic measure, heparin 5000 JU subcutaneous or intravenous route at 8 hourly interval can be given safely. Alternatively, fresh frozen plasma or Packed Red Blood Cells (PRBC) transfusion could be done.
■ Treatment of myocarditis: Myocarditis most often is associated with septic hypotension. There is no specific treatment apart from the treatment of endotoxemia. In cases with congestive cardiac failure or features of atrial fibrillation or flutter, digitalis may be administered.

Table 39.7: Obstetrically modified qSOFA score.
Rapid clinical assessment before investigations to identify the critically ill obstetric patient
A score ,2 is associated with an increased risk of mortality
Score Parameter 0 1 Systolic BP (mm Hg) '.90 <90
Respiratory rate <25 breaths/ >25 breaths/minute minute
Altered mentation Alert Not alert
■ SOFA (Sequential) or qSOFA (Quick Sequential) Sepsis-Related Organ
Failure Assessment.
•
PaO = Partial Pressure of Inspired Oxygen .
2
2
■ FiO = Fraction of Inspired Oxygen.
• Society of obstetric medicine, ANZ guidelines for the investigation

the retained products of conception or hysterectomy for a case with septic abortion or puerperal sepsis should be done without delay. Removal of the source of infection may make the patient hemodynamically stable.
■ Intensive insulin therapy is done in patients with severe sepsis and septic shock to maintain normal blood glucose level. These patients often develop hyperglycemia, which further increases the risk of septicemia and death.
H -blockers: Antacids to reduce the stress ulcer of gastric mucosa either by oral or H2-blocking agents (IV) are used.
2
Nutritional support is maintained as Total Parenteral Nutrition (TPN). Usually, 20-30 kcal/kg/day is equally distributed between fat and carbohydrate. Serum electrolytes, BUN, glucose, creatinine should be monitored on a regular basis.
Admission to ICU: Selected patients need ICU admission.

■ Surgical management: Surgical intervention should be done to eliminate the source of infection. Evacuation of

Morbidity from sepsis in pregnancy has been scored to decide the need for ICU admission (Tables 39.6 to 39.8).

Table 39.8: Sepsis in obstetrics score (SOS)-a model to identify risk of morbity from sepsis and need for admission in ICU.

Variable
Score +4
Temp( C) >40.90 SBP(mm Hg)
°
HR(bpm) >179 RR (breaths/minute) >49
SpO2 (%)
Leukocytes (number/µL) >39.9
Immature neutrophils (%)
Lactic acid (mmol/L)

+3
39-40.9

150-179
35-49

130-149

25-39.9 2'10%
::4

+1
+38.5-38.9

120-129 25-34

17-24.9

Value
0(normal)
36-38.4 >90
sl 19 12-24 ::92
5.7-16.9
<10%
<4

+1
34-35.9

10-11 90-91
3-5.6

+2
32-33.9 70-90

6-9

1-2.9

+3 +4 30-31.9 <30
<70

:55 85-89 s85
sl

Patients with an SOS score 2c6 are more likely to be admitted to intensive care. [Albright et. al. (2014)].
(SBP: Systolic Blood Pressure in mm Hg; HR: Heart Rate; bpm: beats per minute; RR: Respiratory Rate).
mJ Chapter 39: Special Topics in Obstetrics
ACUTE KIDNEY INJURY {AKI) (Syn: Acute Renal Failure in Obstetrics)
I

DEFINITION: Acute kidney injury (failure) is !] J!]
®
ti
■ ·· --
clinically accepted as a condition in which the urine volume falls below 400 mL in 24 hours, the minimum amount necessary for
the excretion of the normal solute load. Currently AKI is considered as the fall in urine output below <0.5 mL/kg/ hr for 6 hours. There is associated rise in serum creatinine ::0.3 mg/dL from the baseline or rise in serum creatinine 2 times the normal (I.I mg/dL). Oliguria is the term given to the clinical condition. Anul'ia is the absence of excretion of urine in 12 hours.
Acute Kidney Injury (AKI) is manifested with the sudden impairment in kidney function resulting in retention of waste products (BUN) and potassium. There is abnormal fluid and electrolyte balance with loss of body acid-base equilibrium.
Effects of AKI on pregnancy are: Miscarriage, low birth weight, IUGR, preterm labor and still birth. ARF carries high maternal mortality therefore it needs to be prevented and treated aggressively.
Acute renal failure: (a) Urine output <400 mL/24 hours, (b) Rise in serum creatinine (at least 1.5 fold) and BUN. Prerenal failure: Patient is hypovolemic and hypo tensive. Laboratory tests: Serum BUN to creatinine >20, urinary sodium <20 mEq/L and FENa <l %. Fractional Excretion of Sodium (FENa) reflects the amount of sodium excreted as compared to the creatinine. In pre renal failure, the sodium excretion is less compared to creatinine ( <l %). In cases with renal cause, kidneys will not be able to resorb sodium and the fractional sodium excretion will be elevated(> 1% ).
Renal causes of failure may be due to: (a) Glomerular, (b) tubular, (c) interstitial, and (d) vascular. In all these causes FEN a is >l %. In all glomerular causes urine analysis revealed: REC, casts and protein.
Bl CAUSES OF ACUTE KIDNEY INJURY (AKI)
Causes are broadly classified into: (A) Causes unrelated to the pregnant state and (B) Causes peculiar to the

pregnant state. The second group may be divided into three categories: (1) Prerenal ARF, (2) Intrinsic renal ARF, and (3) Postrenal ARF (Table 39.9).
Prerenal ARF is due to hypovolemia and/or low cardiac output resulting in renal hypoperfusion.
PATHOLOGY OF ARF: Prerenal is the most common form of AKI (ARF). It is due to mild-to-moderate degree of renal hypoperfusion. Mild and even moderate ischemia with acute tubular necrosis are reversible. In severe ischemia, renal cortical tissue is damaged and this pathology is irreversible.

CHARACTERISTICS OF THE RENAL AND SPLANCHNIC CIRCULATION: Under normal conditions it is strongly auto regulated, but in emergency situations the generalized intense sympathetic vasoconstriction overrides the renal auto regulatory mechanism; With gentle falls in BP, the renal auto regulatory mechanism is maintained; The renal venous pO2 is high because this tissue is normally over-perfused for its metabolic needs.

ACUTE TUBULAR NECROSIS: It is the most common pathology in obstetrics. Acute tabular necrosis is due to several causes such as: ischemic insult; shock, surgery, toxins, drugs (aminoglycosides ), NSAIDS. Urinary sodium is >25 mEq/L and FENa is >l. The lesion begins in Henle's loop, especially in the intermediate zone, involving particularly the ascending limb and distal convoluted tubules and is fully developed after 48 hours.

ACUTE CORTICAL NECROSIS: It is relatively uncommon and seen in abruptio placentae and endotoxic shock following gram-negative septicemia. Usually diffuse ischemic necrosis occurs all over the cortex. The glomerular afferent vessels are end arteries and thus the damage that occurs in the segment of the nephron supplied by these arteries is irreversible, hence the ultimate fatality. This condition is best diagnosed by Contrast Enhanced CT Scan (CECT) as the 'rim sign'.

CLINICAL FEATURES: When anuria is reversible, the clinical condition can be divided into four phases:
♦ Incipient phase ♦ Phase of anuria
♦ Phase of diuresis ♦ Phase of recovery

Table 39.9: Cau;es of acut kidney injury (failure) in-'pregnancy' (prere- a1'.? , :_ , ;;; :' \) -, :;:., ) : ' = s: ,, J -
- ' " ' ' - < •
;:

0 '. > o- l y" . • ',
c
I
_, '
J

Early pregnancy Late pregnancy and labor Other causes in pregnancy
■ Acute and massive hemorrhage: ■ Acute and massive hemorrhage: Postpartum ■ Mismatched blood transfusion. Abortion, ectopic pregnancy, hemorrhage, placenta previa, traumatic ■ Thrombotic microangiopathy. hydatidiform mole. delivery, obstetric shock. Hemolytic Uremic Syndrome (HUS) .
•
•
■ Severe dehydration: Hyperemesis ■ Abruptio placentae:The pathological basis of Renal: Renal disease, DIC, hypoperfusion, gravidarum, acute pyelonephritis. ARF are: (a) Hypovolemia; (b) DIC. ischemia, toxins, obstetric pathology
superimposed on pre-existing renal disease
(interstitial nephritis), (interstitial nephritis, SLE). ■ Septic abortion: Septicemia, • Severe pre-eclampsia, eclampsia, HELLP ■ Postrenal (obstructive): Accidental ligature
endotoxic shock, hypotension. syndrome. of the ureters during cesarean section,
■ Acute Fatty Liver of Pregnancy (AFLP). hysterectomy for rupture of uterus (rare). • Urosepsis, nephritis (pre-existing) . ■ Severe infection: Chorioamnionitis, pyelonephritis. ■ Drugs: NSAIDs, aminoglycosides.

Table 39.10: Criteria, for differentiation between prerenal and renal causes of dysfunction.

Chapter 39: Special Topics in Obstetrics -

Endogenous protein catabolism

Criteria
Urine specific gravity.
Urine osmolality (mOsm/kg}.
Urine sodium (mmol/L}.

Pre-renal Renal >1.0020 <1.010 >500 <350
<10 >20

INCIPIENT PHASE: The phase is short-lasting. There is marked diminution in urinaty output.
PHASE OF ANURIA: This phase lasts from a few hours to as long as 3 weeks. A urinaty output is less than 30 mL/hours. Initially, the patient remains alert and looks well. There is rise in serum BUN and potassium levels. Gradually the patient develops anorexia, vomiting and diarrhea.
Blood biochemical changes: There is gradual rise in the concentration of plasma urea, potassium, creatinine and phosphate as a result of endogenous protein catabolism (Table 39.10). The rise in plasma potassium is aggravated by the retention of hydrogen ions which are forced into the cells in exchange of intracellular potassium ions. The plasma concentration of bicarbonate diminishes. Acidosis occurs due to shifting of hydrogen ions intracellularly. Simultaneously, there is rise of phosphate which leads to lowering in plasma calcium. The fall in calcium and rise in potassium level have got a combined adverse effect on the cardiac function which may cause death. A simultaneous rise of plasma magnesium potentiates the harmful effect of rising plasma potassium.
INVESTIGATIONS
■ Blood: Leukocytosis may be evident and is a better index of infection than the rise of temperature.
■ Urine: Physical examination shows scanty and dark colored urine. Specific gravity is 1020 or more in prerenal causes and 1010 or less in renal causes. Protein is present in va1ying amounts. Presence of casts and red cells on microscopic examination suggests glomerular pathology.
■ Blood biochemical findings (Fig. 39. 7): Urine sodium concentration is <10 mmol/L in prerenal and >20 mmol/L in renal causes. Urine osmolality is more than 500 mOsmol/L in prerenal and less than 350 mOsmol/L in renal causes. Urine: Plasma creatinine ratio is >40 in prerenal ARF and <20 in intrinsic renal causes.
There is raised sodium (normal 136-145 mEq/L); potassium (normal 3.5-5 mEq/L); and urea level (normal 20-25 mg%). Standard bicarbonate level falls resulting in acidosis (normal 24-32 mEq/L). Arterial blood gases are done to detect acidosis (Table 41.11).
■ ECG-for evidence of rise in plasma potassiwn: Serial electrocardiographic tracing is important. The findings are: (a) Gross peak of the 'T' waves, (b) Absence of 'P' waves, (c) Prolonged 'QRS' complex to 0.2 seconds.
PHASE OF EARLY DIURESIS: In this phase, tubular function (reabsorption) is delayed. The only favorable feature

(-}
--{ Bicarbonate pH-I, Urea Potassium Phosphate
l
Acidosis Magnesium Potentiates1 Lowers
- ->
plasma
Cardiotoxic __ calcium

Fig. 39.7: Effects of acute renal failure of blood biochemical changes.

is the increased excretion of dilute urine. But the rise of potassium, sodium, creatinine (BUN) and chloride continues and the specific gravity of the urine is still low.

THE PHASE OF LATE DIURESIS: The phase is as hazardous as the previous one. The causes of diuresis are:
1. Osmotic diuresis due to high blood urea,
2. Functional inadequacy of tubular reabsorption,
3. Release of surplus fluid and electrolytes, particularly sodium and potassium.
CLINICAL FEATURES: Clinical features and complications are anorexia, nausea, vomiting, cardiac arrhythmia, anemia, thrombocytopenia, metabolic acidosis and electrolyte imbalance (hyponatremia, hyperkalemia, hypermagnesemia, hyperphosphatemia).
PHASE OF RECOVERY: Tubular epithelium regenerates and tubular function is re-established along with the establishment of glomerular activity. The concentration of the electrolytes either in the plasma or in the urine gradually returns to normal values and so also the specific gravity of the urine. It may take about 1 year for restoration of full function.

MANAGEMENT OF AKI IN OBSTETRICS (Prerenal)

Prevention of ARF
■ Decline in the number of septic abortion cases with liberalization of MTP plans and medical methods of abortion.
■ Selection of high risk cases and judicious termination of cases with severe pre-eclampsia and hypertension in pregnancy.
■ Appropriate management of cases with abruptio placentae.
ED Chapter 39: Special Topics in Obstetrics

■ Early volume replacement and intervention in cases with hemorrhage in pregnancy, labor and postpartum.
■ Facilities of blood transfusion.
TREATMENT: The first thing is to exclude retention of urine (obstruction). The possibility of inadvertent injury to the ureters during surgery should also be excluded by ultrasonographic study.
ACTUAL MANAGEMENT: Emergency management inclu des correction of causes of acute renal failure ( obstetric hemorrhage).
■ Surgical measures: Correction obstetric sepsis, hypovolemia or uterine bleeding. Patient may need dilatation and curettage, laparotomy for hysterectomy to remove the source of sepsis.
■ Medical measures: Fluid and electrolyte balance to be restored. Fluid intake is calculated from urinary output, loss of fluid from other sources (e.g., diarrhea, vomiting, insensible loss of about 500 mL/day along with correction of fever. Intake output record is to be maintained carefully. Hyperkalemia is controlled with the use of glucose and insulin. Diet should be with optimum calories containing carbohydrates, low proteins and electrolytes. Patient may need parenteral therapy due to nausea and vomiting. Antibiotics without renal toxicity should be given, if needed to control sepsis.
PLACE OF DIALYSIS:
Dialysis is no longer a last resort. The following are the accepted indications (Table 39.11):
Hemodialysis in pregnancy often causes wide fluctuation of blood pressure. Continuous EFM should be continued during dialysis. Dialysates containing glucose and bicarbonate are preferred to avoid loss of bicarbonate. Patient must have at least 70 g of protein and 1 .5 g of calcium daily. Hematocrit should be above 25%. Packed red cell transfusion or Iron (IV) may be given. Risk of preterm labor is high as progesterone is removed during dialysis. Parenteral progesterone therapy is advocated in patients with dialysis. Maternal complications are placental abruption, heart failure and sepsis. Women need more frequent dialysis.
POSTPARTUM RENAL FAILURE (Ch. 30, p. 416) (postpartum hemolytic uremic syndrome)
It is a clinical condition of acute irreversible renal failure occurring within the first 6 weeks postpartum.

Table 39.11: Indications of dialysis. ,
Criteria for dialysis in antepartum Serum levels cases with continuing pregnar,cy
■ Potassium 6.5 mEq/L In such a case dialysis is instituted ■ Sodium sl 30 mEq/L earlier considering fetal wellbeing.
• Bicarbonate s 13 mEq/L No specific criteria have been
firmly established. One criteria is Daily increments of 30 mg/dl rise of BUN >60 mg/dl.
BUN ,,120 mg/dl or
■
Blood urea 150 mg/dl

The exact cause is still obscure. Thrombocytopenic Purpura-Hemolytic Uremic Syndrome (TTP-HUS)-is an unexplained combination of thrombocytopenia and microangiopathic hemolytic anemia. Renal failure is caused by microangiopathy. The pantad findings of TTP-HUS are: (a) Microangiopathic hemolytic anemia; (b) Thrombocytopenia; (c) Neurologic abnormalities (headache, confusion, fever, seizures); (d) Fever and (e) Renal dysfunction. The mortality of TTP is high (90%). The optimal therapy for TTP-HUS is delivery. Plasma pheresis has improved survival (80%).

OBSTRUCTIVE RENAL FAILURE: Obstructive anuria due to ureteric ligation should be dealt with promptly. If the general condition permits, delegation or implantation of the ureters into the bladder can be carried out after prior confirmation by cystoscopy and ureteric catheterization. If the general condition is too poor, bilateral nephrostomy is the life-saving procedure.
In obstetrics, overall mortality due to ARF is about 15% and slightly high in sepsis-related ARF. Renal parenchymal injury is associated with high mortality. Prognosis of the fetus is unfavorable and mortality is about50%.
!]m!]

BLOOD COAGULATION DISORDERS IN OBSTETRICS

Disseminated Intravascular Coagulation
(DIC), is a clinicopathologic syndrome . .. '-•: characterized by widespread intravascular
fibrin deposition in response to excessive .t
blood protease activity that overcomes the natural anticoagulant mechanism.
The commonly used terminology: Consumptive coagulopathy, where there is actual consumption of procoagulants within the vascular system. Activation of fibroholytic system is the other cause of defibrination syndrome.
The plasmin activity usually declines until after deli very. The plate count either remains static or there is a slight fall (15%) in pregnancy.
Control of blood loss from the vessels depends on the following:
■ Muscular contraction
+ Vascular contraction ( vasoconstriction)
+ Myometrial contraction (adjacent to the vessels) ■ Tissue pressure
■ Platelet functions
■ Blood coagulation mechanism (Fig. 39.8)
Physiological changes: Procoagulant factors markedly increased in pregnancy are I, VII, VIII, IX and X. Factors either unchanged or mildly increased are II, V and XII. Factors that decline are XI and XIII.
Chapter 39: Special Topics in Obstetrics :I Xll➔Xlla

( Intrinsic pathway ) ( Extrinsic pathway )

Ca2• §}--v11
XI Xia Tissue
Thromboplastin

VIia/tissue factor

IX IXa

VIII ----+ VIiia

Common pathway
I
I

- - ----- x

Va------ V

Prothrombin (II)

Thcomr (Ila)

aPTTIPT

Fibrinogen
n

Cross-linked fibrin clot

FOP,
0-dimers
Plasmin
l

Plasminogen

Fibrin polymer

Xllla

Plasminogen activator inhibitors (EACA)

Fibrin monomer

Fibrinolysis

Plasminogen activator (urokinase)

Fig. 39.8: Coagulation cascade and laboratory assessment of clotting factor deficiency activated Partial Thromboplastin Time (aPTT ), Prothrombin Time (PT) and Thrombin Time (TT).

The plasmin activity usually declines until after delive1y. The platelet count either remains static or there is a slight fall (15%) in pregnancy.

Table 39.12: Complications and trigger factors for DIC.
Release of Release of Endothelial injury thromboplastin phospholipids

Initiation of pathological coagulation: There is release of tissue factor from the damaged subendethelial layer of the blood vessels. Cytokines are released from the endothelium. The cascade of coagulation and fibrinolysis {Fig. 39.8) is initiated. Ultimately the coagulation factors and platelets are depleted to manifest the fetuses of consumptive coagulopathy. Obstetric complications that trigger consumptive coagulopathy are many (Table 39.12).

♦ Pre-eclampsia, eclampsia, HELLP syndrome.
♦ Sepsis syndrome • Septic abortion
• Chorioamnionitis • Pyelonephritis
♦ Hypovolemia.

♦ Amniotic fluid embolism.
♦ Dead fetus syndrome.
♦ Abruptio placentae. ♦ Hydatidiform mole. ♦ Cesarean section.
♦ Intra-amniotic hypertonic saline.
♦ Shock.

♦ Fetomaternal bleed.
♦ Incompatible blood transfusion.
♦ Hemolysis. ♦ Septicemia.
--·· ED Chapter 39: Special Topics in Obstetrics
I NORMAL BLOOD COAGULATION

Normal intravascular blood coagulation is linked with three different interrelated systems.

These are:
• Coagulation system
• Coagulation inhibitory system • Fibrinolytic system.
Pathological disturbance of one or more of the systems leads to intravascular coagulation or a tendency to bleed.

COAGULATION MECHANISM: The complex system of blood coagulation, 'Enzyme cascade theory' involves two different pathways, viz. intrinsic and extrinsic. Both are initiated by different stimuli and ultimately they culminate into a common pathway for final conversion of inert prothrombin to thrombin.

COAGULATION INHIBITORY SYSTEM: There are a number of naturally occurring anticoagulants in blood, to counterbalance the hypercoagulable state in pregnancy. Antithrombin III (AT III) is a main physiological inhibitor of thrombin and factor Xa. Protein C combined with protein S and thrombomodulin inactivates factors V and VIII. Their deficiency is associated with recurrent thromboembolism.

PLASMA FIBRINOLYTIC SYSTEM: Tissue plasminogen is activated to plasmin by tissue activators ( urokinase, streptokinase). In turn, plasmin lyses fibrinogen and Fibrin-to-fibrin Degradation Products (FDP). Serum FDPs are detected by immunoassays as D-dimers. Blood coagulation and fibrinolysis work side-by-side to maintain hemostasis and patency of microcirculation. There are several plasminogen inhibitors like Epsilon Aminocaproic Acid (EACA) and tranexamic acid (AMCA).
I PHYSIOLOGICAL CHANGES IN PREGNANCY
During pregnancy, there is increase in concentration of clotting factors II, V, VII, VIII, IX, X and XII. Plasma

fibrinogen level is significantly increased. There is a small decrease in platelet count, due to low-grade intravascular coagulation. Plasma fibrinolytic activity is suppressed during pregnancy and labor. It returns to normal within 1 hour of delive1y of the placenta. This is due to liberation of plasminogen inhibitor from the placenta (Fig. 39.8).

PATHOLOGICAL CONDITIONS OF ACQUIRED COAGULOPATHY

Initiation of pathological coagulation: There is release of tissue factor from the damaged subendothelial layer of the blood vessels. Cytokines are released from the endothelium. The cascade of coagulation and fibrinolysis (Fig. 39.8) is initiated. Ultimately the coagulation factors and platelets are consumed (depleted) to manifest the features of consumptive coagulopathy.
Obstetric complications and trigger factors for DIC are many (Table 39.12). All these clinical conditions may trigger the delicate hemostatic mechanism either by endothelial injury or by release of thromboplastin and phospholipids. It is always a secondary phenomenon and never primary. Because of the hypercoagulable state in pregnancy, presence of any provocative factor can easily upset the normal balance culminating into Disseminated Intravascular Coagulopathy (DIC). It is sometimes called 'defibrination syndrome' but because other constituent factors, besides fibrin, are also consumed, a better nomenclature would be 'consumptive coagulopathy'. The blood fibrinogen level of 100 mg/ dL is arbitrarily considered to be a critical level.
Chronic DIC is a compensated state commonly observed in a case with dead fetus syndrome. Plasma levels of FDP, D-dimers are raised, aPTT, PT and fibrinogen are within the normal range. There may be mild thrombocytopenia and red cell fragmentation (Flowchart 39.2).

Flowchart 39.2: Pathophysiology of DIC.

Interaction between coagulation and fibrinolytic pathways
l
Widespread intravascular thrombin generation

l Deposition of Secondary fibrinolysis
fibrin in microcirculation
l
l
l

lschemic tissue damage Vessel Diffuse FOP(+)
patency bleeding D-dimer (1')

Multiorgan dysfunction

j Multiorgan failure (kidney) I

l l
RBC damage Consumption of and platelets and
hemolysis cMg"'' factorn
T
j Diffuse bleeding I

I MECHANISM OF ACQUIRED COAGULOPATHY ABRUPTIO PLACENTAE: Mechanism
■ Massive retroplacental clot: Not only the fibrinogen along with other procoagulants is consumed in the clot but after the clot retraction, the serum component is absorbed into the circulation, thereby further reducing the circulatmy procoagulant.

Chapter 39: Special Topics in Obstetrics ED RETAINED DEAD FETUS: There is gradual fall in fibrinogen
level. It usually becomes evident following retention of the dead fetus for more than 4 weeks. There is gradual absorption of thromboplastin liberated either from the placenta or from amniotic fluid or decidua. This results in consumption not only of fibrinogen but also the Factor VIII and platelets. In response to DIC, there
is enhanced fibrinolytic activity which, in turn, reduces

■ Thromboplastin liberated from the clot, damaged decidua and uterine musculature enters into the circulation and produces DIC.
■ Because of precipitating shock, synthesis of the essential coagulation factors fails to occur promptly.

the fibrinogen level further.
SALINE INDUCED ABORTION (MTP): Thromboplastin is released from the placenta, fetus and the decidua due to necrobiotic effect. It gains access into the circulation and causes defibrination.

■ Fibrinolysis (activation of plasmin): It serves as a protective mechanism to dissolve the fibrin clot so as to restore patency in the microcirculation.
■ Level of Fibrin Degradation Products (FDP) is raised. It inhibits myometrial contraction.
■ Pre-eclampsia, eclampsia and HELLP syndrome: Endothelial injmy is the underlying pathology. It results in thrombocytopenia and rise in fibrin degradation products.
AMNIOTIC FLUID EMBOLISM
Mechanism: Liquor amnii is forced into the maternal circulation either through a rent in the membranes or placenta. Thromboplastin-rich liquor amnii containing the debris, blocks the pulmonary arteries and triggers the complex coagulation mechanism leading to DIC. There is massive fibrin deposition distributed throughout the entire pulmonary vascular tree. If the patient survives from the severe cardiopulmonary embarrassment which stimulates thromboembolic phenomenon, there will be severe clotting defect with profuse bleeding per vaginam or through the venepuncture sites due to consumption of coagulation factors.
From the damaged endothelium of the pulmonary arteries, massive fibrinolytic activators are produced which excite the fibrinolytic system converting the plasminogen to plasmin, which in turn, produces lysis of fibrin, fibrinogen and even the Factor V and Factor VIII. Thus, there is secondary fibrinolysis on top of primary fibrinogen depletion arising out of DIC.
ENDOTOXEMIA-Mechanism: (I) Hypercoagulable state in pregnancy adversely reacts with endotoxin and leads to DIC. There is release of thromboplastin into maternal circulation from the placenta, fetus and decidua. There is extensive DIC and deposition of fibrin in the renal vascular system. (2) In obstetric sepsis , the endothelium of the capillaries in the microcirculation is damaged due to anoxia. There is activation of coagulation system. (3) Increased production of activators from the damaged capillary endothelium triggers the fibrinolytic activity and causes defibrination (fibrinolysis).

CESAREAN SECTION: Primary defibrination following cesarean section may be due to: (1) Entry of thromboplastin or amniotic fluid into the circulation through the open vessels on the uterine wound, (2) Excess production of plasminogen activators from the injured uterine site.
CLINICAL MANIFESTATIONS: The manifestations of blood coagulation disorder are evidenced by hemorrhage from various sites.
Before delivery: There are signs of bruising, prolonged bleeding at the injection sites (venepuncture or intramuscular), gum or nose bleeding or hemorrhage from catheterization the gastrointestinal tract and persistent hypotension.
After delivery: Apart from the manifestations already described, there is postpartum hemorrhage (traumatic bleeding being excluded). The hemorrhage usually occurs 1-2 hours following delivery. There may be bleeding from the suture sites (episiotomy wound) or hematoma formation in the abdominal wound following cesarean section or formation of a vulva! hematoma following vaginal delive1y.
I INVESTIGATIONS
Bedside tests, to evaluate the blood coagulation disorders can give useful information to the diagnosis. Detailed laborato1y investigations are needed for the diagnosis.
Bedside tests that may be done are: (1) Bleeding time, (2) Coagulation time, (3) Clot observation test, (4) Peripheral smear, (5) Circulatory fibrinolysis test.
Clot observation test (Weiner): It is a useful bedside test. It can be repeated at 2-4 hours intervals. 5 mL of venous blood is placed in a 15 mL dry test tube and kept at 37°C. Usually, blood clot forms within 6-12 minutes. This test provides a rough idea of blood fibrinogen level. If the clotting time is less than 6 minutes, fibrinogen level is more than 150 mg%. If no clot forms within 30 minutes, the fibrinogen level is probably less than 100 mg%.
Peripheral blood smear: Peripheral blood smear when stained with Wright's stain may be of help. {i) If less than four platelets per high-power field are seen,
ml Chapter 39: Special Topics in Obstetrics

thrombocytopenia is diagnosed. Thrombocytopenia is a feature of DIC but not of fibrinolytic process. (ii) RBC morphology-in DIC, the cell shape will be 'helmet shaped' or fragmented whereas in fibrinolytic process, the cell morphology will be normal.
Essential laboratory tests to know the specific defects in the coagulation mechanisms are: (1) Platelet count, (2) Activated partial thromboplastin time (intrinsic coagulation), (3) Prothrombin time (extrinsic coagulation) (4) Thrombin time, (5) Fibrinogen estimation, (6) Fibrin degradation products (FDP), (7) D-dimer.
Measurement of FDP is an indirect evidence of fibrinolysis. The determination of a low platelet count is of far more diagnostic significance than the finding of a raised FDP level. The most valuable and rapid clotting screen is thrombin time, where thrombin is added to citrated plasma. Thrombin time of normal plasma is 10-15 seconds. Thrombin time is prolonged where fibrinogen is depleted. Normal values of blood coagulation profile are given in page 608.
Thromboelastometry and thromboelastography are used as adjuncts to other laboratory tests.
I TREATMENT
PREVENTIVE: Blood coagulation disorders in obstetrics of suficient magnitude to cause hemostatic failure, have been reduced to a great extent. The responsible factors in prevention are the changes in the trends of obstetric management:
■ Abruptio placentae: (a) Massive blood transfusion, (b) To expedite early delivery by low rupture of the membranes supplemented by oxytocin drip, (c) Libera lization of cesarean section.
■ Intrauterine death: (a) Early delivery, (b) Availability of potent oxytocics (prostaglandins) to empty the uterus (p. 313).
■ Better understanding of the pathophysiology of shock and early institution of treatment. Early restoration of blood loss to treat hypovolemia and replacement of the procoagulants.
■ Severe pre-eclampsia, eclampsia and HELLP syn drome have been substantially reduced by effective care and judicious timing of delivery.
■ Emptying the uterus and controlling the infection early with antibiotics in cases with sepsis syndrome.
■ Avoiding instillation of hypertonic saline for induction of abortion.
Adjuvant therapies (vitamin K): The vitamin K dependent factors II, VII, IX, X are consumed in DIC. 5-10 mg of injection vitamin K given (IM), can help to replenish these procoagulants.

CURATIVE: The management goal is to identify and to correct the underlying pathology with priority. Women

with severe DIC are treated for hemodynamic parameters, respiratory support and surgical intervention when needed. In most cases, delivery of the fetus brings the resolution of coagulopathy. The other part of the management is to achieve a platelet count >50,000/µL and a fibrinogen level > 100 mg/dL.
ACTUAL MANAGEMENT
■ Volume replacement
■ Blood component therapy ■ Heparin
■ Fibrinolytic inhibitors
• Volume replacement by crystalloids (Ringer's solution) or by colloids (hemaccel or gelofusine or human albumin 5%) will reduce the amount of whole blood needed to restore the blood volume. The crystalloids remain in the vascular compartment less compared to colloids. Dextran should be avoided as they adversely affect platelet function and blood cross matching tests. Two large bore N catheters are sited.
• Whole blood transfusion is given to replenish not only the fibrinogen but also the other procoagulants. 500 mL of fresh blood raises the blood volume, the fibrinogen level approximately by 12.5 mg/100 mL rise in hematocrit by 3-4% and adds 10,000-15,000 platelets/mm3• Whole blood is less commonly used in present day obstetrics practice.
• Fresh-Frozen Plasma (FFP) is extracted from whole blood. It contains all the clotting factors including fibrinogen. It is commonly used in cases with consumptive and dilutional coagulopathy. However, it is not used as volume expander. It is usually given for women with fibrinogen level <150 mg/dL or with abnormal PT or a PTT. One unit of FFP (250 mL) raises the fibrinogen by 5-10 mg/dL. FFP needs to be ABO or Rh compatible. Shelf life is 12 months.
• Cryoprecipitate and fibrinogen concentrate: It is obtained from thawed FFP. It is rich in fibrinogen, factor VIII, von Willebrand's factor, and XIII. Cryoprecipitate provides less volume (40 mL) compared to FFP (250 mL). So it should not be used for volume replacement. Each 10-15 mL of cryoprecipitate contains 200 mg of fibrinogen and no platelets. Shelf life is 12 months.
• Platelet concentrates may be given to a patient with very low platelet count ( <50,000/mL) and persistent bleeding. Platelets should be given rapidly over 10 minutes. It should be ABO and Rh specific. Transfusion of a single unit of platelets is expected to raise the count between 5,000 and 10,000/mL. In case of sensitization Rh-immunoglobulin 300 µg is given. Several units (5-10 units) of platelet concentrates are to be transfused, as one unit (50 mL) raises the platelet count by 7,500/mL.
Single donor concentrates are preferred as the
Chapter 39: Special Topics in Obstetrics -

immunogenic and antigenic risks are low. Shelf life is 5 days.
+ Packed Red Blood Cells (PRBC) are most effective to improve oxygen-carrying capacity. Oxygen-carrying capacity is reduced when hemoglobin level is <8 g/dL even in an euvolemic patient. Transfusion reactions are less compared to whole blood transfusion. Each unit contains about 300 mL (250 mL RBC and 50 mL of plasma). One unit of PRBC will raise the hemoglobin by 1 g/ dL and hematocrit by 3%. PRBC has less fibrinogen, no platelets. It must be ABO compatible. Shelf life of red cells is 35 days.
+ Massive transfusion protocols: The commonly used protocol is: 5 units of PRBCs, 3 units of FFP and 1 unit of platelet concentrate (5:3:1). Cryoprecipitate may be added to this regimen.
+ Recombinant-activated Factors VIIA (rFVIIA): (60-100 µg/kg IV) can reverse DIC within 10 minutes as it is a precursor for extrinsic clotting cascade which is replaced. It also activates platelets and the coagulation cascade. It has rapid bioavailability (10-40 minutes) but the half-life is short (2 hours). rFVIIA is not effective when plasma fibrinogen level is <50 mg/ dL and platelet count is <30,000/mL.
+ Autotransfusion is the collection of blood from the operative field (blood salvage), filter the blood and then transfusing the red cells back to the patient. The device for autotransfusion is called cell saver. The advantages are: less risks of infectious disease transmission and immunological reactions. Cell salvage and autologous blood storage for transfusion has not been found useful.
+ Alternative oxygen carriers or artificial hemoglobin solutions have short intravascular half-life. Recent meta-analysis has revealed a significant risk of mortality and myocardial infarction.
Heparin: It should be used when the vascular compartment remains intact. In acute condition such as amniotic fluid embolism, intravenous heparin 5000 units repeated 4-6 hours intervals is useful to stop DIC and may be lifesaving. In retained dead fetus, there is progressive but slow defibrination due to DIC. In such cases, the process can be arrested by intravenous heparin. In acute DIC, heparin may aggravate bleeding.
Fibrinolytic inhibitors: Place of fibrinolytic inhibitors is very limited. Fibrinolysis may be a protective phenomenon. Commonly available antifibrinolytic agents are-(1) EACA-inhibits plasminogen and plasmin, (2) Trasylol-inhibits plasmin, (3) Aprotinin-nonspecific enzyme inhibitor. Fibrinolytic inhibitors are mainly indicated in postpartum hemorrhage following traumatic hemorrhage or abruptio placentae in spite of a firm and contracted uterus and when blood fibrinogen level is 200 mg% or more. However, these drugs can increase the risk of thrombosis.

Conclusion: Prompt restoration of blood volume and replacement coagulation factors is an important step in the management of coagulation disorders in obstetrics. Management of the triggering factor ( e.g., immediate delive1y in a case of abruptio placentae) should be done along with. This will improve the hemostatic competence in vast majority of cases. With adequate perfusion of vital organs, there is accelerated synthesis of procoagulants, also especially by the liver. Treatment with c1ystalloids only, may lead to dilutional coagulopathy due to depletion of platelets and clotting factors.
Whole blood-restores blood volume and fibrinogen and increases hematocrit by 3-4%. FFP-restores blood volume and fibrinogen.
Risks of blood transfusion: The adverse reactions are: (A) Immune-mediated reactions: (a) Febrile, (b) Allergic, (c) Anaphylactic, (d) Hemolytic, and (e) Transfusion related lung injmy (TRALI), which is an immune-mediated condition and causes ARDS. (B) Transfusion-related infections: Virus (HBV, HCV, CMV, HIV), parasites (malaria), bacteria. (C) Others: (a) Fluid overload, (b) Hypothermia, (c) Electrolyte imbalance (Kt, Cat), and (d) Acidosis.

HIGH-RISK PREGNANCY
ASSESSMENT OF PREGNANCY AT RISK: High-Risk Pregnancy (HRP) is one in which the mother, fetus or the newborn is/or may possibly be at increased risk of morbidity
or mortality before, during or after delive1y. Factors for increased risks are many (Box 39.3 and Table 39.13). The important causes of maternal deaths are: hypertensive disorders, hemorrhage, sepsis and the medical disorders.

A. Maternal: Diabetes, hypertension, cardiac, endocrine (thyroid), preterm labor.
B. Fetal: Structural anomalies; chromosomal abnormalities; genetic syndromes; multiple gestation and infection.
C. Maternal-fetal: Preterm birth, PPROM, cervical insufficiency, stillbirth; IUGR; abnormalities of placentation; pre-eclampsia.

Table 39.13: Assessment of high-risk factors in l bor. General physical examination Pelvic examination
■ Height: Below 150 cm, particularly ■ Uterine size below 145 cm in our country. disproportionately
■ Weight: Overweight or smaller or bigger. underweight ■ Genital prolapse. Body mass index (BMI): Weight/ ■ Lacerations or
(height)2 BMI: 20-24 is accepted as dilatation of the cervix. normal. ■ Associated tumors.
• High blood pressure. ■ Infected labor.
a Anemia ■ Liquor meconium ■ Cardiac or pulmonary disease. stained.
■ Orthopedic problems. ■ Pelvic inadequacy.
li Chapter 39: Special Topics in Obstetrics

The important causes of infant deaths (since birth to 1 year of age) are: preterm birth, prematurity related conditions, sepsis and congenital malformations.
EXAMINATION
Risk assessment starts with a good history taking and examination. Investigations are then organized for management (Table 39.14).
Maternal age: Extremes of maternal age increase the risks of maternal or fetal morbidity and mortality. Adolescents are at increased risk of pre-eclampsia, IUGR, women with increasing age are at higher risk for pre-eclampsia, diabetes, cesarean delive1y, placenta previa, accreta (PAS).
The risk of fetal aneuploidy increases with increasing maternal age. These women are offered prenatal screening which includes: serum analyte testing, cell free DNA, ultrasound and/or invasive testing following counseling.
Type of conception: Pregnancy in a women following spontaneous conception need to be differentiated from Assisted Reproductive Technology (ART). Risks of pregnancy following ART are: Increased preterm birth, multifetal gestation, low birth weight, congenital anomalies and increased perinatal mortality.
Past medical and surgical history: Past medical and surgical disorders can complicate the course of present pregnancy affecting both the mother and the fetus (Table 12.2, p. 104).
Family history: Detailed information is helpful to determine the risks of inheritable disease (diabetes, thalassemia, cystic fibrosis).
Past-obstetric history: (a) Woman with recurrent miscarriages, needs investigation following 2 losses. (b) Previous still birth. (c) Rh alloimmunization. (d) Previous infant with genetic disorder.
Physical examination: (Ch. 10). Antenatal management:
■ First trimester screening: Nuchal Translucency (NT)
°
is measured between 11 17 and 13617 weeks, combined

with maternal serum free -hCG and Pregnancy Associated Plasma Protein A (PAPP-A). Increased NT is associated with higher risks of cardiac defects, diaphragmatic hernia, fetal skeletal dysplasia and other genetic syndromes. Patients with an abnormal screening result is offered invasive testing like CVS for
earlier confirmation of aneuploidy.
■ Second trimester screening: "Quad screen" can detect fetuses with NTD and certain chromosomal abnormalities (Trisomy 21). Integrated aneuploidy screening is suggested.
■ Cell free DNA for aneuploidy screening-for trisomy 21, 18 and 13. Detection rate of >98% with false-positive rate of 0.2-0.5%.
■ Detection of preterm labor is commonly done by: (a) measurement of cervical length by TVS and {b) fetal fibronectin detection in cervicovaginal discharge.
■ Screening for gestational diabetes.
■ Assessment of fetal wellbeing: Ultrasonography is commonly used. Real-time sonography with 2 dimensional (2D) image to demonstrate fetal anatomy, fetal growth, weight, movements and liquor volume. Three-dimensional sonogrpahy 3D and 4-D have many other advantages. Fetal Doppler study, biophysical profile (BPP), fetal echocardiogram are of specialized study for other information.
■ Sonographic markers of aneuploidy screening are identified.
■ Invasive tests for prenatal diagnosis are: (a) Chori onic villus sampling {b) Amniocentesis and (c) Fetal blood sampling.
■ Antenatal fetal wellbeing: (a) Fetal movement assessment; {b) Nonstress test; (c) Biophysical profile (BPP); {d) Modified biophysical profile; (e) Growth profile and (f) Doppler studies.
11 Intrapartum management:
(A) Fetal heart rate monitoring-clinical and electronic fetal monitoring (EFM) (Box 39.4).
(B) VAS, (C) Fetal scalp blood sampling and fetal ECG.

Table 39.14: High-risk factors in pregnancy.
Reproductive history Medical disorders in pregnancy Previous surgery

■ Two or more previous miscarriages or Diseases
previous induced abortion. These cases ■ Pulmonary disease-tuberculosis run the risk of further abortion or preterm ■ Renal disease (pyelonephritis) delivery. ■ Thyroid disorders
■ Previous stillbirth, neonatal death or birth ■ Psychiatric illness of babies with congenital abnormality. ■ Cardiac disease
■ Previous preterm labor or birth of an IUGR ■ Epilepsy
or macrosomic baby. ■ Viral hepatitis
■ Grand multiparity ■ Pre-eclampsia, eclampsia ■ Previous cesarean section or hysterotomy. ■ Anemia
■ Third-stage abnormalities (PPH)-this has ■ Infections in pregnancy (malaria, HIV) a particular tendency to recur.
■ Previous infant with Rh-isoimmunization or ABO incompatibility.

■ Myomectomy.
■ Repair of complete perinea! tear. ■ Repair of vesicovaginal fistula.
■ Repair of stress incontinence.
■ In all these conditions, fetal or maternal outcome or both may be affected.
Family history
■ Socioeconomic status-patients belonging to low socioeconomic status have a higher incidence of anemia, preterm labor, growth-retarded babies.
■ Family history of diabetes, hypertension or multi-pie pregnancy and congenital malformation.

COMPLICATIONS OF PREGNANCY AND LABOR: The cases should be reassessed during late pregnancy and labor (Box 39.5). Attention is given to detect the risks that may develop during labor. Some important points to consider are:
■ Patient having induction or acceleration of labor. 11 Patients having no antenatal care.
■ Presence of anemia, pre-eclampsia or eclampsia. 11 Premature or prolonged rupture of membranes. 11 Chorioamnionitis.
■ Meconium-stained liquor.
■ Abnormal presentation and position.
■ Disproportion, floating head in labor.
■ Multiple pregnancy. ■ Preterm labor.
■ Abnormal fetal heart rate.
■ Patients with prolonged or obstructed labor.
■ Rupture uterus.

Intrapartum complications: ■ Intrapartum fetal distress
■ Delivery under general anesthesia ■ Dificult forceps or breech delivery ■ Failed forceps
■ Postpartum hemorrhage or retained placenta
■ Prolonged interval from the diagnosis of fetal distress to delivery. Interval more than 30 minutes since the recognition of fetal distress to delivery, the mortality increases three-folds.
POSTPARTUM COMPLICATIONS: An uneventful labor may suddenly turn into an abnormal one in the form of PPH, retained placenta, shock or uterine inversion or sepsis. The condition of the neonate should be assessed after delivery. The following categories of neonates are at high risk (Box 39.6).

I MANAGEMENT OF HIGH-RISK CASES
For improvement of obstetric results, the high-risk cases should be identified and given additional antenatal, intranatal and neonatal care. But, in general, they need not be admitted to specialized centers and their care can be left to properly trained midwives and medical officers in health centers, or general practitioners. A simple checklist should be prepared for them to fill

■ Cases with uteroplacental insufficiency. ■ IUGR.
■ Hypertension.
■ Antepartum hemorrhage. ■ Prolonged pregnancy.
■ Extremes of maternal age: <15, >30 years.
■ Previous stillbirth.
■ Multiple pregnancy.
■ Diabetes mellitus.
11 Alloimmunization in pregnancy.
■ Polyhydramnios/oligohydramnios.
■ Hematological disorders in pregnancy.

Chapter 39: Special Topics in Obstetrics il--

A. Hemorrhage D. Hypertensive disorders • APH • Severe pre-eclampsia. • PPH • Eclampsia.
Nearly 75% of obstetric patients • HELLP syndrome. admitted in ICU are postpartum.
B. Sepsis syndrome E. Cardiopulmonary
• Postabortal. • Heart disease in
• Pregnancy (chorioamnionitis, pregnancy.
pyelonephritis). • Thromboembolism. C. Trauma F. Puerperal sepsis

■ Apgar score below 7. ■ Convulsions.
■ Hypoglycemia. ■ Neonatal infection.
11 Anemia. ■ Respiratory distress syndrome. ■ Birth weight <2.5 kg or ■ Persistent cyanosis.
>4kg. ■ Jaundice.
■ Major congenital
abnormalities.

up; arrangement should be made for early examination of the high-risk cases. The health centers or the clinics should have periodic specialist cover from teaching or nonteaching hospitals, as well as district and subdivisional hospitals. The general practitioner or medical officer of health centers, in collaboration with the specialists, will decide what type of cases (with a comparatively lower risk) can be managed at the health centers. Cases with a significantly higher risk should be referred to specialized referral centers. Cases from rural areas may be kept at maternity waiting homes close to the referral centers. The organizational aspect may be summarized as follows:
■ Strengthen midwifery skills, community participation and referral (transport) system.
■ Proper training of residents, nursing personnel and community health workers.
■ Arranging periodic seminars, refresher courses with participation of workers involved in the care of these cases.
■ Concentration of cases in specialized centers for management.
■ Availability of perinatal laboratory for necessary investigations; availability of a good pediatric service for the neonates.
Folic acid ( 4 mg/day) therapy should be started in the prepregnant state and is continued throughout the pregnancy. Early in pregnancy after the initial clinical examination, routine and special laboratory investigations should be undertaken.
Assessment of maternal and fetal wellbeing: This should be done at each antenatal visit according to the guidelines given in the appropriate chapter; maternal complications should be looked for and treated, if necessary.
MANAGEMENT OF LABOR: It is evident that elective cesa rean section is necessary in a high-risk case. Some cases
Chapter 39: Special Topics in Obstetrics

may need induction of labor after 37-38 completed weeks of gestation. Those cases who go into labor spontaneously or after induction, need close monitoring during labor for the assessment of progress of labor or for any evidence of the fetal hypoxia (Box 39.4).
If there is any evidence of fetal hypoxia in the first stage or labor: going to be prolonged, cesarean section is necessaiy. The condition of the neonate is assessed immediately after delive1y. Many of these babies need expert neonatal care. Delive1y is conducted in an institute with equipped neonatal care unit.

IMMUNOLOGY IN OBSTETRICS
Many obstetric problems are now explained with the complexity of immunology. In this chapter a short review of the selected areas will be made highlighting the imm unological explanations.
BASIC IMMUNOLOGY OF PREGNANCY: One tissue that is repeatedly grafted and repeatedly tolerated is the fetus. The mysterious mechanism of the immune system that prevents rejection offetus remains unknown to the immunobiologists. The immune system is generally divided into two arms:
(i) Innate, and (ii) Adaptive.
The innate immune system is the: (a) First line of host defense against infection. (b) It works fast once it recognizes the pathogens. (c) It cannot identify the self vs nonself (nonspecific). (d) It involves complement system. The immune cells involved are: phagocytic (neutrophils, monocytes and macrophages) cells, natural killer cells (NK cells), eosinophils and basophils. The immune responses are by the release of cytokines (TNFa, IL-1, IL-6) and chemokines (IL-8, MIP-la, MCP-1). The phagocytic cells ingest and digest microorganisms with lysosomal enzyme. The NK cells can recognize and distinguish between normal cells and cells infected with a virus or tumor (self or nonself) through the expression of MHC Class I antigens. The NK cells destroy cells that are deficient in HLA Class I molecules.
Adaptive immune system: (a) It works as a second line defense against infection; (b) It has delayed response; (c) It can discriminate 'self' from 'nonself'; (d) It prevents re-infection through 'immunological memory'. It is contributed mainly by two types of cells. Lymphocytes (B and T lymphocytes) and antigen-presenting cells (APC). T lymphocytes are classified into T-helper (Th) and T cytotoxic (Tc) cells. Th cells have two subtypes-Th-I and Th-2. Th-1 cells activate macrophages and are involved in cell-mediated immunity. Th-2 cells activate B-cell differentiation and are involved in humoral immunity. When pathogens (viruses) replicate inside the cells and are inaccessible to antibodies, are destroyed by T cells.
Major Histocompatibility Complex (MHC) is a complex of genes with multiple loci. It is located on the chromosome 6. MHC encodes two types of membrane proteins. Those are known as Human Leukocyte Antigens (HLA) Class I and Class II. The process of graft rejection

generally involves recognition of foreign MHC molecules by host TI hymphocytes.
(1) IMMUNOLOGY IN PREGNANCY
• Pregnancy is not an immunodeficient state. Women are able to respond to both humoral and cell-mediated immunity against the paternal antigen.
• Specific types of NK cells (large granular lymphocytes) are present in the decidua mainly at the site of implantation. These NK cells (uterine NK cells) are different from blood NK cells. These U-NK cells control the trophoblast proliferation, invasion when they interact with the trophoblast HLA Class I molecule. The U-NK cells depend on progesterone for survival. U-NK cells contribute to maternal tolerance of the fetus and maintenance of pregnancy. NK cells share many antigenic and functional similarities to 'T' cells. There is high (30%) proportion of NK cells in fetal circulation (13 weeks). Due to their high number, early presence and the ability to kill cells, it is likely that these NK cells are very important in fetal innate immune system.
Uterine macrophages are the major source of nitric oxide and prostaglandins.
• Trophoblast cells are derived from the fetal tissue and invade the decidua. These trophoblast cells (placenta) form the interface between the fetus and the mother. Thus the placenta forms an efficient barrier against the transmission of immunocompetent cells between the fetus and the mother.
• The trophoblast covering the chorionic villi (villous trophoblasts) comes in contact with the maternal blood in the intervillous space and interacts with maternal systemic immune response. It does not express HLA Class I or Class II molecules.
• The trophoblast in contact with the decidua (extravil lous trophoblast) expresses HLA Class I molecules but not HLA Class II molecule. This interacts with maternal local uterine immune response.
• Placenta presents no immunocompetent cells due to lack of HLA antigens. Placenta acts as an efficient immunological barrier.
• During pregnancy, maternal immune response is shifted (immunomodulation) from Th-1 (cell mediated) to Th-2 (humoral mediated) type. Th-2 type response is beneficial due to the production of anti-inflammatory cytokines. Immunomodulation results in improvement of woman with rheumatoid arthritis in pregnancy.
• During pregnancy there is production of antibodies of paternal antigens. These are anti-HLA antibodies and antibodies against sensitized T cells. These antibodies have no major effect on pregnancy outcome.
• Immunological mechanisms involved in pregnancy are not the same as that of organ transplantation. Immunological tolerance through complement and cytokines regulation is protective for pregnancy.
Chapter 39: Special Topics in Obstetrics ED

Other Postulations
■ Maternal fetal cell trafficking and microchimerism: Maternal tolerance of fetus is due to bidirectional cell trafficking between the mother and fetus. Cell Free Fetal DNA (Cff DNA) and also infant fetal cells are detected in maternal circulation during entire pregnancy. The existence of two-cell populations in a single person is known as microchimerism. It is likely that microchimerism may have beneficial effects.
■ Immunosuppressive factors that operate in preg nancy are: estradiol, progesterone, hCG and prolactin. Fetal tolerance is probably due to the presence of alpha fetoprotein. A number of pregnancy associated glyco
proteins, e.g., a2 macroglobulin and placental interferon
have immunosuppressive properties. Amniotic fluid is rich in immunosuppressive phospholipids.
Immune Tolerance
• Immune tolerance of normal pregnancy at the maternal-fetal interface is maintained by the interaction of HLA-G with uterine NK cells. This effect predominates in a normal pregnancy.
• The levels of complements and cytokines (proinflam matory factors) are often raised during pregnancy. Inhibition of such complements and cytokines by the placenta reduces the immune-mediated pregnancy complications.
In a normal pregnancy, there is suppression of Th-1 and activation ofTh-2 cytokine response. In cases with preterm labor, Th-1 cytokine profile is activated.
■ Inhibition of complement activation contributes to fetal tolerance.
■ Fetal red blood cells (CD 71+) produce an enzyme arginase. CD 71+ cells appear to protect the neonate from excessive inflammation.
■ Influx of T cells into the fetal membranes may cause loss of fetomaternal tolerance. Development of chorioammonitis due to influx T cells (TL-1 , IL-6, TNFa)results in preterm labor and fetal death.
(2) ABO HEMOLYTIC DISEASE OF THE NEWBORN: Jaundice in newborn within 24 hours of birth may be due to ABO isoimmunization of the mother. The incidence is higher in group 'O' mothers carrying group A fetuses.
(3) Rh-lSOIMMUNIZATION: Though entry of fetal blood in maternal circulation can take place at any time during pregnancy, fetomaternal bleed is common in the third trimester, particularly during separation of the placenta. 0.1 mL of Rh-positive fetal blood is sufficient to bring about immunization in Rh-negative mother. Immunization.
(4) PRE-ECLAMPSIA/ECLAMPSIA: In pre-eclampsia, the abnormal immunological response develops in two stages:
A. Abnormal placentation and spiral artery remode ling: This is due to decreased placental HLA-G expression. HLA-G has a major role in placentation and blood flow

development as observed in a normal pregnancy. There is failure of extravillous trophoblasts invasion and spiral arte1y remodeling. This is due to failure of interaction of extravillous trophoblasts with uterine NK cells and HLA-C receptors.
B. Pre-eclampsia is associated with widespread systemic inflammation and endothelial dysfunction. The immune dysfunction in pre-eclampsia are as follows:
• There is decrease in regulatoryT cells both in number and function.
+ There is insufficient shift from Th-1 to Th-2 as opposed to normal pregnancy.
• There is a higher level of cytokine abnormalities with increased concentration ofTNFa, IL-6, IL-1 , IL-8 and lower concentration ofIL-10.
(S) SPORADIC AND RECURRENT MISCARRIAGE:There are some observations suggesting an immunological interaction in cases with sporadic and recurrent miscarriages.
• Cytokines are immune molecules. Th-1 cells produce proinflammatory cytokines whereasTh-2 cells produce anti-inflammatory cytoldnes. In a normal pregnancy there is a shift of Th-1 response to Th-2 response. Progesterone has an immunomodulatory role to induce a pregnancy protective shift from Th-1 cytokine response to more favorable Th-2 cytokine response.
+ Women with recurrent miscarriage produce low levels ofTh-2 cytokines (IL-4 and IL-10).
+ Women with recurrent miscarriage have a decreased population of NK cells in the decidua. This indicates an altered immune environment within the decidua.
• NK cells differ from T and B lymphocytes cells. NK cells do not have clonally distributed receptors for foreign antigens and can lyse target cells without prior sensitization.
■ Cord blood transplantation: Fetal blood contains a high number of hematopoietic stem cells as well na·ive T cells and NK cells. For this, cord blood is an ideal source of cells for hematopoietic cell transplantation.
■ Solid organ transplantation in pregnancy: This is long-term persistence of fetal cells in the mother and the maternal cells in her pregnancy.
• Coexistence of two cell population in a single per son has been observed. This is referred to as Microchimerism (MC). A pregnant woman with solid organ transplantation has at least three sources of MC (fetal MC, maternal MC and the donor allograft). Uterine transplantation has now been performed.
• Maternal T cells and B cells through regulation (T REG cells and B REG cells) suppress the antigen specific immune response. In pregnancy there is expansion of
T REG cells (>100 fold). B REG cell expansion occurs in early pregnancy with rise in hCG. Combined together these help in pregnancy (maternal-fetal) tolerance and
continuation.
f mJ Chapter 39: Special Topics in Obstetrics
(6) ANTIPHOSPHOLIPID SYNDROME (p. 161,328,435): In SLE antiphospholipid antibodies, e.g., lupus anticoag
ulant 2 glycoprotein, and anticardiolipin are important. These antibodies act by dysregulation of coagulation
pathways. This causes thrombosis of uteroplacental vessels and poor placental perfusion. Obstetric complications are due to this pathology.
(7) MATERNAL AUTOIMMUNE DISEASE AND FETUS
• Incidence of neonatal thyrotoxicosis is higher in babies born of a thyrotoxic mother.
• A baby born to a mother with ITP will, in all probability, suffer from the same disease through transplacental transfer of antiplatelet antibodies.
+ Myasthenia gravis also has some such relationship due to transplacental transfer of acetylcholine-blocking factor.
Babies born of mothers suffering from systemic lupus e1ythematosus often develop congenital heart block due to transplacental transmission of anti-Ro and anti-LA (anti-SS-A and anti-SS-B) antibodies. SLE patients, very often, have exacerbation of disease activity during pregnancy or in the early postpartum phase. All the diseases listed in this group manifest transiently in the newborn.

CRITICAL CARE IN OBSTETRICS

Overall, 1-3% obstetric patients are admitted in Intensive Care Unit (ICU). Among these patients, the risk of death ranges from 2% to 11%.

Selection Criteria of Obstetric Women for ICU Admission
ICU admission should be restricted to a critically ill woman who is likely to be benefited (Box 39.7).
Some institutes have their own guidelines for transfer to ICU (ACOG). Antenatal transfer to ICU rather than with newborn transfer is preferred except in a situation, where maternal transport is unsafe or impossible.

Table 39, 1 S: Arterial Blood Gases (ABG) during nonpregnant state and pregnancy.
ABG variables Nonpregnant state Pregnancy pH 7.35-7.43 7.40-7.47
PaC02 (mm Hg) 37-40 27-34 Pa02 (mm Hg) 94 101-106 HC03-(mEq/L) 22-26 17-18 Base deficit (mEq/L) 1 3

cardiologists, pulmonologists, intensivists, respiratory therapists, pharmacists and nurses. Obstetric critical care unit involves obstetricians, obstetric nurses and neonatologists.
There are three levels of adult critical care (ACOG).
Level 1: Highest level of care: Severely ill patients are managed with the involvement of multidisciplinary team members.
Level 2: Intermediate care or High Dependency care Units (HDU): This is the post-ICU step down unit. These are within the labor ward. Care is provided by the obstetricians and nurses who are experienced.
Level 3: Other intensive care units: For patients requiring long-term ventilator support.
Arterial Blood Gases (ABGs) values during nonpregnant state and pregnancy varies (Table 39.15). It is important while managing a woman during pregnancy in ICU.

OBJECTIVE PARAMETERS (SELECTED) FOR ADMISSION OF A PATIENT (NON-PREGNANT) IN AN ICU

Laboratory values and physiologic parameters are changed in pregnancy. Hemodynamic changes in a normal nonpregnant and pregnant women at term are significant: These values are important while managing an obstetric patient in ICU (Box 39.7). Cardiovascular changes and respiratory system changes are important. Use of pulmonaiy artery catheter (Swan-Ganz) is used,

The essential requirements for transfer are: continu ous pulse oximet1y monitoring, ECG monitoring, venous access, and confirmed position of endotracheal tube when a woman is under mechanical ventilation.

Organization of a Critical Care Unit
A qualified intensive care physician is to manage ICU, though it is not mandatory. However, it is observed that high-intensity ICU physician staffing is associated with lower ICU mortality and decreased hospital stay, when compared with low-intensity ICU physician staffing.
Critical care unit involves multidisciplinary appro ach: The team members involve physicians, anesthetists,

A. Vital signs
• Heart rate (HR) <40 bpm
or >1 SO bpm.
• BP <80 mm Hg systolic or > 120 mm Hg diastolic.
• Mean arterial pressure <60 mm Hg.
• Respiratory rate > 35 breaths/minute.
B. Physical findings • Anuria
• Coma
• Uncontrolled seizures • Cardiac arrest
• Cyanosis

C. Laboratory values
• Serum Na+ <110 or > 170
mEq/L.
• Serum K+ <2 or >7 mEq/L. • Pa0 <50 mm Hg.
2
• pH <7.1 or >7.7.

D. Imaging studies
• CT/MRI: Cerebral
hemorrhage.
• Electrocardiography: Complete and heart block, complex arrhythmia, CCF.

especially in cases with severe pre-eclampsia, eclampsia, respiratory distress syndrome and amniotic fluid embolism.
Pulmonary artery catheter values: Normally, pulmonary capillary wedge pressure (mm Hg) at term pregnancy is 7.5 ( +18% rise from nonpregnant state) and CVP is 3.6 mm Hg (-2%). There is fall in systemic vascular resistance (-21 % ) and pulmonary vascular resistance (-35%) at term pregnancy compared to a nonpregnant
adult. It is an invasive procedure.
Indications of invasive hemodynamic monitoring (ACOG)
11 Shock (septic, hemorrhagic, cardiogenic). 11 Pulmonary edema.
■ Severe PIH with persistent oliguria. ■ ARDS.
■ Severe cardiac disease.
Causes of acute lung injury and ARDS in obstetrics
■ Pre-eclampsia-eclampsia.
■ Obstetric sepsis (septic abortion, chorioamnionitis, pyelonephritis, puerperal sepsis (Box 39.8).
■ Massive hemorrhage [shock, Transfusion Related Lung Injury (TRALI)].
■ Tocolytic therapy.

Decision Making and Patient Care in ICU
For a pregnant woman, ICU team members should plan for management including delivery which may be needed long before the EDD. Safe delivery of a woman needs consideration of period of gestation (fetal survival), place and mode of delivery (vaginal or cesarean). Vaginal delive1y or operative vaginal delive1y (forceps, ventouse) after at least 34 weeks of gestation within the ICU set up when possible is always beneficial. Cesarean delivery in the ICU is often faced with the problem of space for anesthesia, operative facilities, neonatal resuscitation arrangements and the risk of infection. Cesarean delive1y in ICU may have to be done where transport of patient is not possible or for perimortem procedures.

Chapter 39: Special Topics in Obstetrics

■ CNS: Confusion, altered sensorium.
■ CVS: Tachycardia, hypotension, warm or cool peripherals. 11 Respiratory: Tachypnea, hypoxia.
11 Renal: Oliguria, anuria.
11 GI: Abnormal LFTs, jaundice, nausea, vomiting.
■ Metabolic:
• Lactic acidosis.
• Hypo-/hyperglycemia. • Hypocalcemia.
11 Hematology:
• Abnormal WBC count.
• Reduced platelets, fibrinogen, DIC.
• Increased D-dimer. ■ Skin:
• Hyperthermia. • Hypothermia.

Fetal Care in ICU
11 Fetal gestational age assessment is essential to estimate the approximate fetal survival rate following delivery. Effects of obstetric medications need to be carefully judged in terms of risks and benefits.
■ Drug-related side effects that may arise are: beta ago nists (tachycardia), indomethacin (platelet dysfunction, reduced renal perfusion), beta blockers (IUGR). Bene fits of antenatal corticosteroids are established and it is to be given in the event ofpreterm delive1y ( <34 weeks).
■ Maternal drugs (sedatives), acidemia, hypoxia, blood pH, may alter the CTG tracings. Correction of mater nal hypoxia, acidemia may improve fetal condition. Howeve1; fetal interest comes second and essential med ications should not be withheld to the pregnant woman.
Place of perimortem cesarean delivery: There is no such clear guideline regarding this issue. However, it is observed that cesarean delivery should be considered for both maternal and fetal benefits about 5 minutes within a pregnant woman has experienced total cardiopulmona1y arrest in the third trimester.

► Women with multisystem pathology need improved care with technology and expertise of critical care obstetrics.
► Common indications for admission in ICU (based on objective parameters) are: Need of cardiac, circulatory, pulmonary or multiorgan support arising out of obstetric complications (hemorrhage, hypertensive disorders or sepsis).
► The comparative values of hemodynamic changes in nonpregnant and pregnant women at term are important in the management. Pulmonary artery catheterization are of immense value in the management.
► Critical care unit management involves multidisciplinary approach. High-intensity ICU staffing can reduce ICU mortality and decrease hospital stay. Obstetrician, intensivist, specialty nurses, and neonatologists are involved.
► Acute Respiratory Distress Syndrome (ARDS) may be due to pneumonia, sepsis, pre-eclampsia, embolism or drugs. Vigorous antimicrobial therapy, oxygen delivery (early intubation and ventilation for woman with respiratory failure) and support of circulatory volume (IV crystalloids and blood) are essential considerations.
► Fetal care in ICU needs consideration of fetal gestational age, drug-related side effects, and timing, place and mode of delivery. ► Benefit of antenatal corticosteroids in the event of preterm delivery (<34 weeks) is established and should be used.
► Nearly 7S% of obstetric ICU patients admitted are postpartum.
► Hemorrhage, hypertension and sepsis are the most common causes of admission in obstetric ICU.
► Necessary medications should not be withheld to a pregnant woman because of fetal concerns. So also necessary imaging studies. However, attempts should be made to limit fetal exposure (drugs/radiation) as much as possible.
► For antimicrobial therapy-Read more Dutta's Clinics in Obstetrics, Ch. 71 and Clinics in Gynecology, Ch. 59.

Current Topics in Obstetrics

CHAPTER

CHAPTER OUTLINE
❖ Medical Ethics
❖ Effective Clinical Communication ❖ Pregnancy Following Assisted
Reproductive Technology (ART)
❖ Antibiotic Prophylaxis in Cesarean Section

❖ Day-care Obstetrics
❖ Legal and Ethical Issues in Obstetric Practice
❖ Audit in Obstetrics
❖ The Preconception Counseling Prenatal Diagnostic Techniques

❖ Umbilical Cord Blood Stem Cells in Transplantation and Regenerative Medicine
► Stem Cells and Therapies in Obstetrics

I MEDICAL ETHICS
The word ethics (derived form the Greek word 'ethos'), means custom, habit, character or disposition.
Ethics consists of moral principles which are concerned with individuals and society. It is a system which helps us to tell right from wrong, good from bad and gives practical guidance to our lives.
Principles of medical ethics:
(1) Respect for autonomy; (2) Nonmaleficence; (3) Beneficence and ( 4) Justice, are the four principles of medical ethics (Tom Beauchamp and James Childress-1985). Along with these, confidentiality and truth-telling are also included. Medical ethics is meant to profit and defend human dignity and patient's rights and it is a set of norms, values and principles to avoid harm.
Need for ethics: To have norms which everyone should follow both as an individual and as a society, otherwise it will end up in chaos.
■ Beneficence: It is a moral obligation to act for the benefit of others, e.g., holding the hand of a dying person.
■ Nonmaleficence: There is an obligation not to infilict harm on others "primum non nocere" (first, do no harm).
■ Autonomy: It involves respecting patient's view, allowing or enabling them to make their own decision-it is a shared decision
■ Justice: According to health care, ethics is divided into three categories (Gillon-1994): distributive justice, rights based justice and legal justice.
Distributive justice means fair distribution of scarce resources, rights based justice is respect for people's rights and legal justice means respect for morally acceptable laws.
Alperovitch (2009) described two more elements: Equality and Equity. There should be equal access to the treatment and the patients should be treated equally.
It is vital that healthcare professionals must have knowledge and training about ethics and its challenges so that the patients receive the best care. Role of healthcare ethics will change in future and will gain increased importance.

EFFECTIVE CLINICAL COMMUNICATION

To have a good patient-physician relationship, effective communication is the cornerstone. Students need to develop communication strategies and the skill throughout the medical course. Nowadays, effective clinical communication skill is considered as the utmost important and it is also to be assessed.
Steps for effective clinical communication are: (1) To greet and to introduce one self; (2) Initiate the reason for discussion; (3) Building the relationship; ( 4) Providing information; (5) Explaining the risks; (6) To assist with decision making; (7) Closing the consultation.
Decision making with patients is guided both by the ethics of beneficence and the ethics of respect to autonomy.
Simple consent: Where clinical management poses no significant risk to the patient ( measurement of BP).
Informed consent: Where clinical management entails clinically significant risks, including the risk of mortality , disability or sufferings.
Example: (A) To give information regarding: Instrumental (forceps/ventouse) vaginal delivery to cut short the delay in second stage of labor.
Steps involved
1. First greet and introduce yourself: Establish the reason for consultation.
2. Building the relationship: Assess the woman's and her attenders knowledge for about the forceps/ventouse delivery. Establish their ideas about this, their expectations and their concerns.
3. Providing informations: Frame an organized consultation. Give a clear information about the use and benefits of instrumental vaginal delivery. It should be in simple words. Medical terminology is to be avoided as much as possible. Use visual aids (when needed). Explain the procedure to relieve her apprehension: For example, to avoid pain, appropriate analgesic will be given during the procedure. There is no need of general anesthesia. There would not be much need of straining as the instrument will help her during the procedure. It also reduces the time for the baby under stress.

Instrumental delivery facilitates early ambulation and less hospital stay. She can go home within 2-3 days.
4. Explaining the risk:
• A small cut is made at the birth passage. It is repaired at the end. It heals soon.
• Analgesics (oral) are sufficient enough to take care of her pain following delivery.
5. Assist with decision-making:
• Time should be given to the woman to respond on the information provided.
• Encourage her. Help her to make the decision.
6. Closing the consultation
• Invite some more questions from them. • Discuss and agree to her plan.
• Get signature.
• Thank the patient.
(B) Breaking the bad news: For example, Intrauterine Fetal Death (IUFD)
1. Initiating session:
• Introduce yourself.
• Provide a comfortable room for all.
• Establish rapport with her and her spouse/accompanying person.
2. Assess whether they already have any information about the condition:
• Assess what is their concern, ideas and their expectations. • Briefly tell them what has happened in simple words.
3. Delivering bad news
• Give the news in simple straightforward manner.
• Give reason for patient's condition (intrauterine death). • Give some time to the patient to process the information. • Show empathy.
4. Explore the patient's initial emotions
• Allow the woman to express her initial emotions. • Try and identify her emotions.
• Recognize how the patient feels after hearing the news. • Show concern.
5. Giving information
• Find out whether the patient needs some more information. • Provide clear explanation (visual aid)
• Offer other medical options/additional investigations
6. Assist in taking decision
• Give enough time to the patient to reflect on the information provided.
• Assist in arriving at her plan (shared decision).
7. Inviting further questions
• Invite some more questions from them. Discuss and agree to the plan.
8. Closing the consultation:
• Inform the patient about the plan of subsequent management.
• Discuss about the patient's support and follow-up. • Get the signature.
• Thank them.

Chapter 40: Current Topics in Obstetrics ml

■ Gestational Diabetes Mellitus (GDM-20%).
11 Gestational hypertension, pre-eclampsia (2%). 11 Complications related to multiple pregnancy.
■ Hemorrhage (placenta previa, placenta accreta, abruption). ■ Cesarean delivery.
• Admission to Intensive Care Unit (ICU-33%).

11 Genetic and chromosomal abnormalities (Trisomy 21). ■ Structural malformations (7%).
■ Fetal Growth Restrictions (FGR).
11 Low birth weight babies (<2500 g). ■ Stillbirth.
■ Preterm births (11 %, spontaneous and indicated). ■ Increased perinatal mortality (2-3 fold).

babies have been conceived through IVF. Assisted Reproductive Technology (ART) is now an established procedure in the management of couples with infertility. It is proved to be an effective and relatively safe procedure. The number of babies born from ART worldwide has increased significantly since 1980s. However ART has got certain risks associated (Boxes40.1 and40.2).
Conceptions following ART are at increased risk of maternal and fetal complications (Boxes 40.1 and 40.2). Early pregnancy complications are few (Table 40.1). A special care is needed when such a woman is seen in the antenatal clinic. Such woman need to be seen by a senior obstetrician.
Management issues: Risk assessment of individual woman is needed. Prenatal screening procedures are to be done. Pregnancy monitoring with standard surveillance procedure is recommended. Individual woman may be benefitted with aspirin, progesterone (recurrent miscarriage). Heavier women with recurrent miscarriage, antiphospholipid syndrome are benefitted with LMWH/heparin therapy.
Multifetal gestation following ART is high (20 times) compared to spontaneous conception. Risk of monozygotic twins (mono chorionic monoamniotic twins) appears to be higher (3%) following Elective Single Embryo Transfer (ESET) than in natural conceptions (0.4%). Risk of ectopic and heterotopic pregnancy is increased following ART treatment. Maternal risk factors such as smoking, PID, endometriosis, impaired tubal function further increase the risk. ART related factors (alterations of hormonal micro environment following controlled ovarian stimulations), embryo quality, multiple embryo transfer and embryo transfer techniques are also associated with increased risk.
ART and cancer risk in women: No increased risk for breast, ovarian or endometrial cancer has been associated. Possible increased risk of ovarian borderline tumor has been noted.

Table 40.1: Conception following ART and the early pregnancy complications.
Condition Risk

PREGNANCY FOLLOWING ASSISTED REPRODUCTIVE TECHNOLOGY

■ Miscarriage 15-20%
■ Ectopic pregnancy 2-8%

More than 3 million babies are born following ART procedures since the birth of the first baby in 1978. Overall 1-5% of the

■ Ovarian Hyperstimulation Syndrome (OHSS) 3-8%
Woman need counselling before and after ART procedure
Chapter 40: Current Topics in Obstetrics

Early menopause: No significant association between the women of ART cycles and menopause has been observed.
Venous Thromboembolism (VTE): ART doubles the risk of VTE during pregnancy. Risk is high in the first trimester (four fold). Presence of additional risk factor indicates prophylactic anticoagulation therapy (LMWH). Additional risk factors are: BM! >30 kg/m2, age >35 years, Parity ?3, estrogen provoked VTE, thrombophilia and multiple pregnancy.

ANTIBIOTIC PROPHYLAXIS IN CESAREAN SECTION

Prophylactic use of antibiotics effectively reduces postoperative infectious morbidity and hospital stay both for the mother and the neonate. Postoperative morbidity like fever, endometritis, wound infection, peritonitis, and also pelvic abscess can significantly
be reduced. However, an institution, where infection rate is high, should primarily improve the surgical and aseptic technique. Emergency cesarean section is associated with higher rate of infection than the elective procedure. Similarly, cases with prolonged rupture of membranes and in prolonged labor are at higher risk of infection.
Infective agents are mostly polymicrobial, including gram positive, gram-negative aerobes and anaerobes. Generally, antibiotics with broad-spectrum activity are better. Single dose therapy of ceftriaxone (1 g), cefuroxime (1.5 g) or co-amoxiclav (1.2 g) by intravenous route is a reasonable choice. Shorter courses of 1-3 doses may be given. This can reduce the cost compared to a full 7 days course. First dose to the mother is given 60 minutes before the skin incision is made. Ideally, the antibiotic infusion should be timed so that a bactericidal serum level is reached by the time skin incision is made. It is recommended that prophylactic antibiotic should be administered within 60 minutes of the start of the cesarean delivery. When this is not possible, it should be started as soon as possible (ACOG). This avoids antibiotic exposure to the baby. Bacteriology pattern and antibiotic sensitivity need to be monitored regularly by the microbiology laboratory. Antibiotic prophylaxis has no deleterious effects on the mother or the neonate.

DAY-CARE OBSTETRICS

It is designed to provide inpatient care to a pregnant woman, on an outpatient basis throughout the day. It is a new concept. This is similar to today's care surgery, as done for minor operations.
DEVELOPMENT OF A DAY-CARE UNIT: Significant number of antenatal inpatient load is due to pregnancies complicated by hypertension. Objective is to provide rest, risk assessment and treatment to avoid any complication. When such a patient is seen in the day-care unit, repeated blood pressure measurement is done. Examination of urine for protein, blood for uric acid and platelets, and LFT are also done. Fetal wellbeing is assessed by clinical examination and also with cardiotocography and ultrasonography for liquor volume and fetal weight. Finally, the patient's risk is assessed and management is done accordingly.
Similarly, women with diminished fetal movements could be assessed in a day-care unit. She could be assessed with all parameters of histoty, clinical examination (fetal growth, liquor volume, auscultation of FHR), ultrasonographic study (BPP),

and Doppler flow study of umbilical artery and ductus venosus depending upon the case.
PROCEDURES FOR RISK EVALUATION IN DAY-CARE OBSTETRICS
♦ It requires an organized setup with quick access to laboratory and other monitoring parameters.
♦ It is essential that an experienced obstetrician should assess the pregnant women in a day-care unit.
♦ A high-risk patient should be admitted from the day-care unit for subsequent management.
♦ A moderate-risk patient could be seen for repeat day-care assessment.
♦ A low-risk patient without any maternal or fetal compromise is referred back to routine care.
Advantages: (a) This acts as a safety net for assessment of obstetric complaints, (b) Reduces inpatient overcrowding and workload, especially in a busy hospital, (c) Reduces the stress of the woman due to separation from the family, ( d) It reduces concomitant costs.

LEGAL AND ETHICAL ISSUES IN OBSTETRIC PRACTICE
Currently, there is growing concern in the relationship of caregiver (Doctor) and the care-receiver (Client) in medical practice, in terms of mutual trust and understanding. This is due to great expectations of the society with progressive technological advancement. Medicolegal problems in obstetric practice are, therefore, rising both in the developed and in the developing world.
The doctor owes to his patient a duty of care. Care and attention must be according to the established norms available at that time and place. When the doctor fails to exercise that duty properly, he/she is found to be negligent. The failure to perform the proper duty to patient care may be due to his incompetence or malpractice or mere negligence. The failure to provide a standard care may again be either by acts of omission or commission.
Adverse outcomes of medical care are often due to: (i) System errors (inadequate staff, physician or operating room, etc.) or (ii) Healthcare personnel's error.
Once the act of substandard care due to system error, negligence, malpractice or incompetence is proved in the court of law, the plaintiff has to be compensated.
COMMON AREAS OF LEGAL THREAT IN OBSTETRICS: There are certain areas where claims are frequent and, sometimes, ve1y high. These are in the field of: (a) Perinatal inju1y, (b) Maternal injuty or (c) Both.
a. Perinatal injury: (I) Stillbirth and neonatal death, (2) Brain damage to a baby, (3) Injury following vaginal breech delive1y, (4) Operative vaginal delivery.
b. Maternal injw)': (I) Maternal trauma, (2) Maternal death, (3) Episiotomy, (4) Forgotten packs in abdominal cavity or within the vagina.
c. Both: (l) Instrumental delivery, (2) Operative delivery, (3) Anesthesia.
MEASURES TO MINIMIZE THE MEDICOLEGAL PROBLEMS
a. Communication-must be made in a clear and understandable way to the client (patient) and the relatives about the management decision.
Chapter 40: Current Topics in Obstetrics ED
I

b. Informed and written consent-must be taken before any agreed management decision or investigations.
c. Legal and ethical:
♦ Her consent must be following a clear understanding of the proposed procedures or therapy, its risks to herself and her fetus, the alternatives, success rates and the likely problems or complications.
♦ Obstetrician should not perform any procedure that is refused by the pregnant woman. Surgery without consent is an assault.
♦ The physician must provide information to the parents in relation to genetic counseling and prenatal diagnosis.
♦ Patient's privacy and autonomy must be protected. No information, obtained in genetic counseling and screening, should be disclosed to any third party without the patient's authorization.
♦ Where conflicts arise, the doctor should seek help of and advice from other professional colleagues.
d. Proper documentation of facts in the patient's file clearly and legibly in respect of date and time.
e. Strict adherence to established management protocol (evidence based) is essential. When there is any deviation, it must be documented showing suficient reasons.
f. Careful record maintenance in institution as it may be required later on.
g. Adequate training and supervision of juniors, especially involved in labor ward patient care. Seniors must be available for consultation or direct involvement as and when asked for.
h. Consultation with another physician in the specialty when any difficulty is faced as regards the patient care.
i. Regular audit and meetings-should be done to update the knowledge of all the staff involved in patient care. Audit will help to improve the quality of care.

PRECONCEPTION COUNSELING, PRENATAL DIAGNOSTIC TECHNIQUES (PCPNDT)
Objectives
1. The Act provides the prohibition of sex selection/determi nation before or after conception and prevent the misuse of prenatal diagnostic technique for sex selective abortions.
2. It regulates the use of prenatal diagnostic techniques, like ultrasound and amniocentesis by allowing them only to detect: (a) Chromosomal abnormalities, (b) Genetic abnormalities, (c) Metabolic disorders, {d) Certain congenital malformations, (e) Hemoglobinopathies, (f) Sex-linked disorders, {g) Any other abnormalities or diseases as may be specified by the central supervis01y board.
3. The techniques must be conducted by qualified persons only.
4. Every center/institute conducting these tests must be registered under the Act.
5. Every center/institute must display a notice delineating that sex determination/selection is prohibited under law.

Salient Features of the Act
■ Absolute prohibition of sex determination/selection and no communication can be made about the sex of the fetus in any manner.

11 A copy of the Act and rules must be available in the center/ institute.
■ Signage board in English and in the local language must be displayed indicating the fetal sex is not disclosed in the clinic.
■ Prohibition of sale of equipments/machines, etc., to anyone who is not registered under the act.

Penalities
Ii If any person acts contrary to the prohibitions listed above he/she will be punished with imprisonment which may extend to 3 years and fine which may extend to'( 10,000.00.
11 Any subsequent conviction entails, imprisonment which may extend to 5 years and fine which may extend to'( 50,000.00.
■ In case of a registered medical practitioner, his/her name shall be reported by the Appropriate Authority to the State Medical Council concerned for taking necessary action including suspension of the registration and for the removal of his name from the register of the council on conviction for the period of five years for the first offence and permanently for the subsequent offence.
■ Any person who puts an advertisement for prenatal and preconception sex determination facilities in any form, can be imprisoned for up to 3 years and fined no,000.00.
11 The Act mandates compulsory registration of all diagnostic laboratories, all genetic counselling centers, genetic laboratories, genetic clinics and ultrasound clinics.

AUDIT IN OBSTETRICS

Progress in clinical care cannot be achieved without a change. Many outdated practices in clinical medicine should be removed for betterment. Audit (clinical review) is an effective tool to indicate that change is essential.
DEFINITION: Audit is defined as the systematic and critical analysis of the quality of medical care. Objective of carrying out an audit is to improve the quality of clinical care. It is done by changing and strengthening many aspects of hospital practice and administration. Audit should not be confused with research, which involves new experiments, investigations and treatment.
Audit could be medical where scrutiny is done over the medical aspect of the work performed by the doctors. It could be clinical, where scrutiny is done over the work done by all health professionals including the doctors.

STRUCTURING AN AUDIT: Audit has to be structured beforehand. It should be based on available resources including personnel and finance. Important aspect to organize an obstetric audit is motivation of all doctors, midwives and other health professionals. Proper documentation of facts and figures must be there. Audit should be kept confidential and is considered as an educational tool.
EXAMPLE: Subject-'Hypertensive pregnant women must have their Blood Pressure (BP) checked at least 4-6 hours interval'. With this subject a standard (best practice) has to be adopted. The indicators are: BP measurement, hypertensive pregnant women and the time, so staff and equipment (resources) should be made available. A target is set up to include maximum number (95%) of the patients in the study. Monitoring methods should be strictly followed. The components are documentation and data collection. There must be an individual (Registrar/ Senior Resident/Lecturer) assigned for canying out the audit.
Chapter 40: Current Topics in Obstetrics

Accept a standard (best practice)

Implement Analyze the change existing practice
J

Compare
the existing practice with the standard

Fig. 40.1: Audit cycle.

Finally, this existing practice is critically analyzed, interpreted and then compared with the standard. Use of computers is helpful in data processing. Once the problems are identified and solved, better clinical care would emerge (Fig. 40.1).
AUDIT CYCLE
Importance of Carrying Out an Audit
1. A well-structured and efficient audit is based on scientific evidences with facts and figures.
2. It can replace the out-of-date clinical practice with the better one.
3. It can remove the disbelieving and agnostic attitudes between hospital management and professionals and also amongst the professionals.
4. It improves awareness between doctors and patients. 5. It is an efficient educational tool.
LIMITATIONS: Unless the audit is a simple one, it requires a lot of time, staff commitment and technology.

UMBILICAL CORD BLOOD STEM CELLS IN TRANSPLANTATION AND REGENERATIVE MEDICINE

Cord blood collection is done from the ex-utero separated placenta following delivery. Umbilical cord blood banking of Stem Cells (SC), gives benefit to treat many diseases. Allogeneic Hematopoietic Stem Cells (HSC) derived from umbilical cord blood have been used in the treatment of more than 70 indications. The common indications are: (1) Malignancies of the hematopoietic and lymphatic systems, (2) Metabolic disorders, (3) Immunodeficiencies, (4) Tumors, (5) Hemoglobinopathies, and (6) Genetic disorders.
Advantages of umbilical cord blood: (a) It is more readily available than bone marrow, (b) Better tolerated than bone marrow due to its immunological immaturity, (c) It is as effective and safe when compared to bone marrow. Fresh (not previously frozen) cord blood is a promising source of non-hematopoietic stem cells. Allogeneic stem cells from cord blood are best suited for the therapeutic use in regenerative medicine.
Common uses in regenerative medicine: (a) Myocardial infarction, (b) Heart valve replacement, (c) Diabetes mellitus, (d) Neurological disorders (stroke, Parkinson's disease, Alzheimer's disease, spinal cord injuries). With the current state

of knowledge, it is not essential to store the umbilical cord blood in private blood bank, for donor's own use.
In summary, the uses of umbilical cord blood are:
■ The allogeneic hematopoietic stem cells from umbilical cord blood are used in the treatment of hematopoietic disorders (childhood leukemia).
■ Autologous hematopoietic stem cells from cord blood are unsuitable for the treatment of hematopoietic disorders.
a Non-hematopoietic stem cells can be produced from fresh (not previously cryopreserved) allogeneic cord blood donations. These non-hematopoietic stem cells are used in regenerative medicine.
■ Current state of knowledge suggests if a child needs transplant, it is better to use the blood of a healthy allogeneic donor.
♦ Allogeneic: Donor and recipient of a transplant are not identical (they may be related or not related)
♦ Autologous: Donor and recipient are identical.
I STEM CELLS AND THERAPIES IN OBSTETRICS

Reproductive tissues are the important source of stem cells (progenitor cells). Stem cells have the potential to be used in the field of regenerative medicine. A stem cell has the ability to renew (reproduce) itself for long periods.
Potentials for the use of stem cells in regenerative medicine 1. Treatment of inherited genetic disorders
2. Treatment of hematological diseases. Properties of stem cells
a. Ability to self-renew (undergoing numerous cell divisions) maintaining the undifferentiated state.
b. Multipotency: Capacity to differentiate into a mature cell type.
Sources of stem cells
(A) Embryonic tissues, (B) Fetal tissues, (C) Extrafetal tissues, (D) Adult gonads.
A. Emb1yonic tissues: Inner Cell Mass (ICM) of the blastocyst, embryo and yolk sac.
B. Fetal stem cells: Human Fetal Hematopoietic Stem Cells (hf HSC) are primarily obtained from bone marrow and liver. Virtually, eve1y part of the developing fetus has higher proliferative capacity. These cells have higher amount of telomerase activity and have longer telomeres compared to their adult counterparts. Moreover, these tissues can differentiate efficiently into neuronal, muscle and osteogenic lineages.
Primitive hf MSC are transduced by integrating vectors and they do not express HLA-Il. They can be used for ex vivo gene therapy as well as postnatal bone tissue engineering.
C. Extrafetal tissues: Amniotic membranes, placenta, trophoblasts, amniotic fluid cells, all contain progenitor cells. These Mesenchymal Stem Cells (MSC) can differentiate into most cell types of mesodermal lineages.
Stem cell sample collection and banking
Currently, the use of stem cells in regenerative medicine is regulated through institutional regulatory boards.
■ Umbilical Cord Blood (UCB) collection and banking is an established source of HSC and MSC. This is used for

treatment of hematological diseases like leukemia and bone marrow failure.
■ Fetal tissues can be obtained following medical termination of pregnancy. Stem cells from fetal tissues can be harvested. Intrauterine transplantation of Human Fetal Mesenchymal Stem Cells (hfMSC), collected from liver, can be used for the treatment of hemoglobinopathies.
Intrauterine Stem Cell Transplantation (IUSCT) can be used to correct genetic disorders (monogenic diseases) (Box 40.3).
Use ofhfMSC has been explored for diseases having mesen chymal origin (Box 40.3). hf MSC undergoes site-specific differentiation and contributes to repair tissues in such diseases (muscular dystrophy, osteogenesis imperfecta).
Allogeneic transplantation of HSC in the treatment of mono genie disorder has certain advantages. It has high tolerance and less rejection rate as it is done before the onset offetal immune maturity (first trimester).
Autologous stem cells from fetal cord blood sampling or fetal liver biopsy in early pregnancy is done and the cells are harvested. An ex-vivo gene transfer may be done thereafter. This also reduces the risk of immune rejection. Howevet; fetal HSC in first trimester has favorable engraftment kinetics.

Chapter 40: Current Topics in Obstetrics

■ Hemoglobinopathies (a thalassemia, thalassemia, sickle cell anemia).
■ Mucopolysaccharidoses (MPS). ■ Inherited immune deficiencies. ■ Osteogenesis imperfecta.

In the first trimester, fetal hematopoietic stem cells are highly proliferative and they circulate in significant numbers. Therefore, these cells are the important source of autologous HSC.
Fetal mesenchymal stem cells can be bioengineered and used for the disease of bone, skin, liver and heart.
The potential to use stem cells for the fabrication of tissues or organ implants may prove helpful in the treatment of several diseases like genetic, immunodeficiency syndromes, urinary incontinence, infertility and structural repair.
However, till date, it is essential to understand its known lim itations, putative benefits and the unknown risks. Until there is sufficient evidence on the efficacy of therapy, each case should be considered on an individual basis.
Imaging in Obstetrics (USG, MRI, CT, Radiology), Amniocentesis and Guides to Clinical Tests

CHAPTER

CHAPTER OUTLINE
❖ Ultrasound in Obstetrics ► Three-dimensional
Ultrasonography
► First Trimester, Midtrimester and Third Trimester

❖ Magnetic Resonance Imaging (MRI) ❖ Computed Tomography (CT) in
Obstetrics
❖ Radiology in Obstetrics ❖ Amniocentesis

❖ Guides to Clinical Tests
❖ Tests for Blood Coagulation Disorders ► Collection of Blood Sample
► Samples for Blood Sugar Estimation ❖ Cervical and Vaginal Cytology

Imaging in obstetrics is indicated for the purpose of diagnosis and/or therapy to the fetus or the mother. Most (USG and MRI) of the imaging studies are harmless. The primaty imaging modality in obstetrics are 2-dimensional, 3- and 4-Dimensional (3D/4D). Magnetic Resonance Imaging (MRI) are used in situations where enhanced imaging are needed. Use of Computed Tomography (CT) and radiology in Obstetrics are limited because of safety issue.
PRINCIPLES OF DIAGNOSTIC IMAGING IN OBSTETRICS
+ Ultrasound is the most commonly used imaging tool in obstetrics.
+ MRI is useful for high soft tissue contrast and acquisition of images. Study of fetal neuroanatomy is best done with MRI.
• USG and MRI, both are safe in all the trimesters of pregnancy.
• There is no documented harmful effects to the fetus from diagnostic ultrasound and MRI (p. 629).

ULTRASOUND IN OBSTETRICS
The ultrasound is a sound wave beyond the human audible range of frequency greater than 2 MHz ( cycles per second). SONAR stands for 'Sound, Navigation and Ranging'. The clinical application of ultrasound in obstetrics was introduced and popularized by Ian Donald in Glasgow in 1958.
Ultrasound is produced by the vibration of a synthetic piezoelectric crystal in response to a rapidly altering electrical potential situated in the transducer of an ultrasound machine probe. The transducer converts electrical energy to mechanical energy ( ultrasound) and vice versa. The commonly used frequency range in obstetrics is 3-5 MHz for abdominal transducers and 5-7 MHz for vaginal transducers. When the frequency

(number of ultrasound waves per second) increases there is improvement in image resolution but due to rapid wave attenuation, deeper structures are not properly visualized. This is due to poor penetration. In medical imaging, the transducer both sends and receives ultrasound waves (pulse echosonography). Sound travels through the tissues of the body at 1,540 meters per second.
The echo strength (strength of the reflected sound) depends mainly on the following four factors: (a) acoustic impedance mismatch (e.g., soft tissue-bone interface causes maximum ultrasound reflection producing bright echogenic structure), (b) the angle at which the ultrasound beam strikes a reflecting interface (more the ultrasound beam is perpendicular to the reflector, more echogenic the structure), (c) the strength of the ultrasound, and ( d) size of the reflector (fetal femur is more echogenic whereas renal pelvises scatter the ultrasound to give speckle).
In clinical practice, standard ultrasound images are:
■ B-mode (brightness mode display)-two-dimensional (2D) images (width and brightness) are obtained.
■ M-mode is used to study the moving organs, e.g., fetal heart. This results in a wavy pattern in the presence of motion.
■ Color Doppler and pulse wave ultrasound ( Christian J Doppler-1942) is based on the principle of Doppler frequency shift. Doppler ultrasound is used to measure the speed at which blood is moving within a vessel. The most common fetal arterial Dopplers measured are: umbilical artery, middle cerebral artery. The most common fetal venous Doppler is the ductus venosus. Umbilical artery Dopplers are a reflection of the placental circulation. Ductus venosus Dopplers reflect cardiac compliance and cardiac after load. This may increase with the pathology of the placenta. The Doppler shifted audible signals can be converted
Chapter 41: Imaging in Obstetrics (USG, MRI, CT, Radiology), Amniocentesis and Guides to Clinical Tests ED to visual signals and are known as Flow Velocity
Waveform (FVW).

Safety of ultrasound: The effects of ultrasound on tissues are: temperature elevation, formation of microbubbles and cavitation. However, there is no clear evidence till date that diagnostic ultrasound examination during pregnancy is harmful. Ultrasound should be done with shortest duration possible to avoid unnecessary exposure, especially with the Doppler.

The choice of the probe generally depends on the structure to be studied and its distance from the probe. Early pregnancy study is done best by using TV probe, whereas fetal study in third trimester is best done with transabdominal imaging.

Transvaginal Ultrasound (TVS) is superior to transabdominal ultrasound for early pregnancy evaluation (when uterus is within the pelvis). There is very little attenuation of sound waves because the distance between the probe and the concepts is very close. This makes tissue resolution better.

■ Intrauterine pregnancy.
■ Suspected ectopic pregnancy.
■ Vaginal bleeding (in all trimesters). ■ Fetal anomalies (anencephaly).
■ Suspected molar pregnancy. ■ Gestational age.
■ Multiple pregnancy (chorionicity). ■ To confirm cardiac activity.
■ Screening of aneuploidy.
■ Evaluation of pelvic/adnexal masses (all trimesters).

Table 41.1: Fetal features on Transvaginal Sonography (TVS) for dating in pregnancy.
Mean Sac Diameter (MSDJ Findings
6mm Yolk sac.
12mm Embryo with cardiac activity.
Embryo CRL 2:4 mm Cardiac activity.
GS should increase by 1.1 mm in diameter per day.
Gestational age and embryonic structures are identified by Transvaginal Sonography (TVS).

I 3D/4D ULTRASONOGRAPHY
3D can produce more life-like images of the fetus in utero. The ultrasound beam is swept in two orthogonal planes to capture a block or volume of echoes (depending on the required volume), which are digitally stored. This volume of echoes can be resliced in any plane. Reconstruction of a 3D image from a subvolume of images can be made using computer software. 3D images have multiple advantages:
a. Complex structure can be viewed in a single image, e.g., no need of mental reconstruction to define a defect.

Menstrual age(weeks)
4

5 5.5 6
7

8
9

CRL(mm) -

--
5 10

16
24

Fetal structures
Choriodecidual thickness, chorionic sac.
Gestation sac.
Yolk sac.
Fetal pole, cardiac activity.
Lower limb buds, midgut herniation (physiological).
Upper limb buds, stomach.
Spine, choroid plexus.

b. The stored volume tissue (organ) can be reviewed at any plane later on without needing the patient. This helps to get second opinion if required.
c. Prenatal diagnosis of certain anomalies is improved.
d. Lifelike photos of 3D images improves antenatal parental bonding.
e. It calculates tissue and fluid volumes, e.g., fetal lung volume measurement could be done to predict pulmonary hypoplasia.
f. This is also an important teaching tool.
I FIRST TRIMESTER ULTRASONOGRAPHY
Common indications are mentioned (Box 41.1).
An Intrauterine Gestational Sac (GS) is visible by Transvaginal Sonography (TVS) by
as early as 5 weeks of pregnancy (Table 41.1). Yolk sac is seen by 5.5 weeks and the fetal pole is seen by 6 weeks of pregnancy (Fig. 42.46). Definite diagnosis of intrauterine pregnancy is possible as early as 29-35 days of menstrual age (Table 41.1). True gestational sac (GS) is eccentric in position within the endometrium of fundus or body of

the uterus. Double decidua sign of the gestational sac is due to the interface between the decidua and the chorion which appears as two distinct layers of the wall of the gestation sac. Presence of yolk sac or fetal pole within the gestation sac confirms pregnancy. True gestational sac size increases 1 mm/day. Pseudogestational sac or pseudosac is irregular in outline, usually centrally located in the uterus, has no double decidua sign and the sac remains empty. The rate of early ( <12 weeks) pregnancy loss (miscarriage) diminishes steeply with the progressive appearance of fetal structures (e.g., with only GS = 11.5% and with emb1yo >10 mm= 0-5%). Fetal anatomy and viability (Table 41.1).
Gestational age for dating in pregnancy: Ultrasound examination is the best method to estimate the gestational age dating (Table 41.1). The error with LMP is due to late ovulation (>14 days after LMP). CRL (Fig. 41.lA) is most accurate with an error of 2.1 days in the first trimester. Biparietal Diameter (BPD), Femur Length (FL), Head Circumference (HC) and Abdominal Circumference (AC) are commonly used for dating thereafter. Transcerebellar Diameter (TCD) is an accurate predictor of gestational
t__ GD Chapter 41: Imaging in Obstetrics (USG, MRI, CT, Radiology), Amniocentesis and Guides to Clinical Tests
r

Figs. 41.1A to C: (A) Sonograph (TVS) demonstrating crown-rump length (between crosses) of an 8-week fetus. Yolk sac is seen in the near field (arrow); (B) Sonograph showing femur length; (C) Biparietal diameter at the level of cavum septum pellucidum.

age when measured between 14 weeks and 28 weeks. IVF pregnancy is dated by the date of embryo transfer minus 14 days to get LMP and to calculate EDD by Naegele's rule.
An ultrasound can show the number of gestational sacs, number of yolk sacs and the number of fetal poles with cardiac activity. The presence and absence of dividing membranes between the fetuses can be seen. This is characterized by T sign or lambda sign or twin peak sign.

Ultrasound markers for fetal anomalies
USG can detect the soft markers that can be associated with aneuploidy. For soft markers of fetal aneuploidy.
Nuchal translucency (Fig. 41.2): Increased fetal nuchal skin thickness (in the first trimester) >3 mm by TVS is a strong marker for chromosomal anomalies (trisomy 21, 18, 13, triploidy and Turner's syndrome).
Other indications:
Multiple pregnancy: Identification of two gestational sacs indicates twin birth in 52-63% of case. Anemb1yonic pregnancy (blighted ovum).