Postpartum haemorrahge final

Postpartum haemorrahge

Professor: Fatma El SokkaryObstetrics and Gynecology Department

Faculty of Medicine For GirlsAl-Azhar University

Postpartum hemorrhage (PPH) is the leading cause of maternal mortality.

All women who carry a pregnancy beyond 20 weeks’ gestation are at risk for PPH and its sequelae.

Although maternal mortality rates have declined greatly in the developed world, PPH remains a leading cause of maternal mortality elsewhere.

Estimates of blood loss at delivery are subjective and generally inaccurate.

• It has been suggested that doctors consistently underestimate actual blood loss.

• Using a 10% fall in hematocrit value to define PPH, is inaccurate because this change is dependent on the timing of the test and the amount of fluid resuscitation given.

• The ability of the individual to respond to blood loss is different ,e.g a healthy woman has a 30-50% increase in blood volume in a normal singleton pregnancy and is much more tolerant of blood loss than a woman who has preexisting anemia, an underlying cardiac condition, or a volume-contracted condition secondary to dehydration or preeclampsia.

For these reasons, it has been suggested that PPH should be diagnosed with any amount of blood loss that threatens the hemodynamic stability of the woman.

What are the natural mechanisms of stopping uterine bleeding after birth?

The physiology of postpartum hemostasis following placental separation depends primarily upon:

Mechanical events mediated by hormones (oxytocin and prostaglandins ) , which induce strong uterine muscular contraction.

Apposition of the uterine walls. The activation of both the clotting cascade and

fibrinolysis ( pregnancy is a hypercoagulable state).The intermediate muscular layer of interlacing muscle

bundles of the upper uterine segment (8 figures) consisting of tiny myofibrils, around the

branches of the uterine arteries that run through the wall of the uterus to the placental area.

Apposition of the uterine walls.

Image

Activation of both the clotting cascade and fibrinolysis

Muscle fibers of the uterus .

Figure of eight

Delay in diagnosis patient has

significant tachycardia but initially not

hypotensive,

The doctor in charge can

not state the problem

clearly to all who attend emergency

There is delay in commencing

resuscitation

There is under-

estimation of blood

loss.

There is delay in

recognizing need for

transfer to theatre.

Obstetric Hemorrhage Can Be ChallengingBleeding can be rapid life threatening because:

Why there is usually a delay in diagnosis of post- partum haemorrhage?

Dilution of blood with amniotic fluid

Blood loss may be

concealed

Physiological changes of pregnancy mask the

clinical signs of hypovolemia

Difficulties in diagnosis of postpartum haemorrhage

Haemorrhage can be

difficult to quantify

• The pregnant patient is able to adapt to

haemorrhage more effectively than her non pregnant counterpart due to haemodynamic changes that accompany pregnancy ( physiologic changes during pregnancy).• These changes include increased red cell

mass, increased plasma volume and increased cardiac output ( = Stroke volume x heart rate).

• Total blood volume at term is approximately 100 ml/kg (an average 70 kg woman-total blood volume of 7000 ml). So patient has to lose large amount of blood before clinical manifestations of shock appear.

• Also, because of great plasma augmentation hemoglobin concentration and hematocrit decrease slightly. This will mask the laboratory results for diagnosis of shock.

What will happen as a response to haemorrhage?

• In early phases of haemorrhage ,the body compensates by raising systemic vascular resistance in order to maintain blood pressure and perfusion to vital organs.• As bleeding continues further

vasoconstriction is impossible resulting in drop in blood pressure, cardiac output and end organ perfusion.

Because of the physiological adaptation, the vital signs become relatively insensitive during pregnancy. Tachycardia does not develop until blood loss exceeds 1000 ml and blood pressure is usually maintained in the normal range well beyond this level.

The relative masking of signs during pregnancy hinders recognition of hypovolaemia and delays treatment, resulting in further blood loss and increased risk of haemorrhagic shock.

Consequently, hypovolaemic women who begin to decompensate, as evidenced by hypotension, will deteriorate extremely rapidly.

What are the factors which maintain tissue perfusion?

Tissue perfusion depends on four factors: •Cardiac •Vascular •Microcirculatory •Humoral

Pathophysiology of decreased tissue perfusion

Decrease O2+ nutrient.Aneaerobic metabolism.

Decreased ATP and energy.Increase membrane permeability

Influx of Na+ waterEfflex of K. Cel l edema.

Mitochondrial damage.

Intracellular acidosisLysozomal membrane rupture.

Extracellular lytic enzymes.

Extracellular acidemia.

Cell damage and death

Tissue perfusion becomes inadequate to meet nutritional requirements of the cells and remove waste products.

Metabolic changes include:• Decreased O2 consumption and

decrease body temperature.• Hyperglycemia early but

hypoglycemia later.

• Lactic acidemia and pyruvic acidemia.•Ketonemia and acidosis. ( metabolic at first later

respiratory).• Increase breakdown of certain

tissue proteins (increased blood urea nitrogen).

• Electrolyte and water disturbances including hyponatremia, hyperkalemia, hypochloremia ,decreased secretion of sodium and water.• Blood ascorbic acid falls abruptly.• Pituitary-adrenal activity increases,

increased of some adrenal medullary and cortical hormones and antiduritic hormone.• Liver function tests are impaired.

Treatment Physiologic response Acute blood loss

Class

Minimal Dizziness, palpatations , normal blood pressure

15 % (1000cc)

1

intravenous fluids Tachcardia, tachypnea, sweating, thirst weakness, narrowed pulse pressure ,orthostatic hypotension, low blood pressure(systolic 90-80)

20-25 %( 1500cc)

2

fluids and packed RBCs

very fast heart rate, low blood pressure ,restlessness ,pallor, cool extremities ,confusion

30-35 %(2000cc)

3

aggressive in-terventions

critical blood pressure and heart rate, shock air hunger, oliguria, or anuria.

>40 %(>2500cc)

4

Hemorrhage classification and physiologic response

compensated

Mild

Moderate

Severe

Rule of 30

• 30% blood loss > moderate shock• HR –increase > 30 bpm• Respiratory rate > 30/min• Systolic BP –down 30 mm Hg• Urinary output < 30 ml/hour• Haematocrit drop > 30% & to be

kept at an absolute value of > 30

Shock index

• Shock Index = HR / Systolic BP•Normal= 0.5-0.7• Shock index > 0.9 indicates state

of shock that needs urgent resuscitation

• Microcirculatory changes during shock progress in several ways:

Compensation phase( 1000 cc):• As a result of hypovolemia the precapillary

arterial sphincters contract. As a result the filtration pressure in the capillaries decrease and the fluid moves into the vascular system under the effect of osmotic pressure of plasma proteins inside.

• The blood volume increases.

Cell distress phase:• if compensatory mechanisms are inadequate or

the shock is prolonged the organs enters into a stage of cell distress. The precapillary sphincter still closed and arteriovenous shunts are opened.

• The bypassed cells start to depend on anaerobic metabolism for energy.

• Metabolites accumulate and histamine is released from the damaged cells.

• Histamine produces closure of the postcapillary sphincters

• Blood stagnates in the capillaries.

Decompansation phase:• Just before cell death, as a result of accumulation

of metabolites and local acidosis result in reopening of the pre capillary sphincters while the post capillary sphincters remain closed.

• The endothelial cells of the capillaries are damaged by hypoxia and capillary permeability increases.

• Proteins are lost into the interstitial spaces and capillaries are distended with red cells which pile up and agglutinate ( sludge formation).

• If blood volume is restored at some point in the decompansation phase, while the effects on microcirculation are still reversible many of the damage cells can be recovered, otherwise the shock enters a state of irreversibility.

Staying PerfusedThere are four components that must be working in harmony in order to maintain

adequate perfusion.

Irreversible

Refractory stage (microcirculatory failure

stage) At this stage, the vital organs have failed

and the shock can no longer be reversed. Brain damage and cell death are occurring, and death will occur imminently.

The Golden Hour• The 'golden hour' is the time at which

resuscitation must be commenced to ensure the best chance of survival• Emergency measures should be

initiated if the estimated blood loss is more than one- third of the woman's blood volume or more than 1000 ml or a change in hemodynamic status.

Trust Guideline for the use of the Modified Early Obstetric Warning Score (MEOWS) in detecting the seriously ill and deteriorating women

• The MEOWS is calculated by scoring the values of a full set of observations carried out routinely by staff which include;

Temperature Systolic blood pressure Diastolic blood pressure Heart rate Respiratory rate Level of consciousness using AVPU scale +/- urine output • A - Alert Alert and conscious • V - Voice Responds to voice • P - Pain Responds to pain • U - Unresponsive No response to voice or pain Of all the variables the respiratory rate is the most sensitive indicator.

Guidelines for (MEOWS) in detecting seriously ill and deteriorating woman

Effect of shock on the viscera

Effect of shock on gastero-intestinal tract:• Hypoxic cell of the intestinal mucosa lose the

protective barrier for content of intestinal lumen by permitting intra and trans epithelial penetration of intestinal toxins and proteolytic enzymes.

• A mycardial depressent factor secreted from ischemic pancreas has an important role in pathogenesis of irreversibility. It depress the already weakened myocardium and augments splanchnic vasoconstriction which increase visceral ischemia.

ischemic pancreas•mycardial depressent factor• augments splanchnic vasoconstriction

Effect of shock on lung:• The early signs of shock at cellular level in the

lung is interstitial pulmonary edema.• Initially the precapillary sphincter constrict this

lead to alteration in the capillary bed with increased vascular permeability due to endothelial damage.

• Changes in alveolar type II cells which produce surfactant lead to atelectasis.

• As the shock progress in severity and duration damaged vessels leak erythrocytes into fluid filled interstitum and into the alveoli.

interstitial pulmonary edema

atelectasis.

damaged vessels leak erythrocytes

Effect of shock on kidney:• Low blood flow leads to decrease of glomerular

filtration.• There is shunting of blood through the medullary

portions of the kidneys by passing the cortical glomeruli.

• Angiotensin II is formed under the effect of renin released from the ischemic kidneys.

• Angiotensin II aggravates the vasospam which is deleterious.

• The kidney function is impaired as a result of tubular necrosis with subsequent sodium and potassium retention, uremia and aggravates acidosis.

Effect of shock on central nervous system:• Total arrest for 4 minutes at normothermia

results in permanent cerebral damage.• Many patients who have apparently had

circulatory arrest for more than 10 minutes have been resuscitated without irreversible brain damage.

• It must be noted that total arrest of circulation has more severe effect than perfusion with hypoxic blood.

• The neuronal functions are abolished according to the phylogentic age of the structures archipallium being the most resistant.

Red: archipallium (The Reptilian Brain) Yellow: paleopallium (The Mammal Brain )Green: neopallium( The Cerebral Brain)

Intravascular clotting:• During shock platelets agglutinate

and become destroyed releasing platelet factors and serotonin.• Platelet factors contribute to

disseminated intravascular coagulation and serotonin produces uniform arterial vasoconstriction which aggravates the effect of shock on vital organs.

Measuring Blood Loss A key step to EFFECTIVE TREATMENT…..

Blood Loss: 1. Visual EstimationOverestimation may result in

unnecessary and costly interventions. underestimation may delay

identification and diagnosis of what is truly a hemorrhage.

Visual Estimation

The accuracy of this method can be improved by standardization and training.

The observer needs to be trained in determining the blood loss using a single collecting container and fixed-sized gauze pads of size

10 × 10 cm.

Soakage characteristics of 10 × 10 cm pads

Another method of calculation is by allowing blood to drain into a fixed collecting container . Blood losses on the delivery table, garments and floor should also be assessed at the end of one hour.

Blood lost is estimated by totaling up the blood in the container, in the sponges and secondary blood spillage on the delivery table, garments and floor.

Disadvantage is underestimation.

Blood drained into a fixed collecting container

2. Direct collection of blood into bedpan or plastic bags:

Blood loss was measured from the time of delivery until the mother was transferred to postnatal care This period was generally up to 1 hour postpartum.

Immediately after the cord was clamped and cut, the blood collection was started by passing a flat bedpan under the buttocks of a woman delivering in a bed or putting in place an unsoiled sheet for a woman delivering on a delivery table.

The collected blood was poured into a standard measuring jar provided by WHO and its volume measured. Any available small gauze swabs soaked with blood were put into the measuring jar and included in the measurement together with the blood and clots.

• Disadvantages of direct collection of blood into bedpan or plastic bags: :

The errors in estimating blood loss arise fromfailure to collect all the blood in stainedlinen, incomplete extraction from the collectiondevice, ignoring maternal blood within theplacenta (approximately 153 ml), confusionrelated to the mixing of blood contaminatedwith amniotic fluid and urine, and technicalinaccuracies associated with transfer of thecollection to a measuring device.

Photograph of noncalibrated drape containing 500 mL of blood and calibrated drape containing 1000 mL of blood. In addition to blood, drapes also contained 100 mL of simulated urine and surgical sponges.

THE BRASSS-V DRAPE A low cost calibrated plastic

blood collection drape.

Measuring Blood Loss in PPH

Goudar, Eldavitch, Bellad, 2003

Advantages of Brasss-V•Simple and practical•Low cost: ( Plastic)•Accurate:•Provides a hygienic delivery

surface

3. Gravimetric method:This method involves weighing sponges

before and after use. The difference in weight provides a rough

estimate of blood loss.Inaccuracies can arise at several steps in

this procedure, including lack of international standardization of size and weight of gauze, sponges and pads

weighing balabce1gm=1ml

Chux Pads Kendall maternity pad

cloth soaker pad dry lap sponge graduated container volume

4.Acid hematin method:This method is based on collected blood

being mixed with a standardized solution which converts hemoglobin to acid hematin or cyanmethemoglobin.

This in turn can be measured by a spectrophotometer or colorimeter

( PRINCIPLE Compare the color of acid hematin solution obtained using the collected blood sample with the standard solution color of the Sahli hemometer.)

Sahli hemometer

5.Plasma volume changesThe plasma volume can be

determined before and after delivery using radioactive tracer elements.

6.Measurement of tagged erythrocytes

Blood loss can be measured by using 51Cr-tagged erythrocytes

7.Determination of changes in hematocrit and hemoglobin

The changes in values before and after delivery of the hematocrit and hemoglobin levels provide

quantitative measurements of blood loss.

8.Tablet-Based Technology Gauges Surgical Blood Loss(An optical scanner for Apple’s iPad tablet computer)

Technology ISSUE: NOVEMBER 2012 VOLUME: 38:11

Conclusion:• Because hemorrhage is a significant cause of maternal

mortality, methods to accurately measure blood loss of PPH are needed.

• The methods that can be implemented with the least equipment and education turn around direct measurement and weighing.

• A combination of the two methods may be the most practical.

• Objective data, such as vital signs and hematocrit changes, are helpful in the clinical management of patients with large blood loss over time; however, they are not helpful in the measurement of blood loss in clinical practice or research.

Thank you