Antepartum Hemorrhage , Eclampsia and Sepsis .pptx

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1. APH , Eclampsia and sepsis management

2. Antepartum hemorrhage Obstetric hemorrhage is one of the leading causes of maternal morbidity and mortality throughout the world. Antepartum hemorrhage has both maternal and fetal implications. Primary causes of antepartum hemorrhage include placental abruption, placenta previa, placenta accreta syndrome, and vasa previa. Rapid assessment of potential etiologies and initiation of postpartum treatment protocols can mitigate complications .

3. PREGNANCY-RELATED HEMODYNAMIC CHANGES Pregnancy is associated with five significant hemodynamic changes . 1. The first of these is plasma volume expansion. As early as the fourth week of gestation , plasma volume begins to expand. It peaks and plateaus at 40 % to 50% above baseline by 30 weeks of gestation. 2. An increase in red blood cell (RBC) mass accompanies this expansion. With appropriate substrate availability, RBC mass can be expected to increase 20% to 30 % by the end of pregnancy. Since the RBC mass increase is less than the plasma volume expansion, a physiologic anemia occurs by the early third trimester.

4. 3. Maternal cardiac output rises by the late second trimester due to increased stroke volume and increased heart rate. The average rise in cardiac output is 30% to 50% above nonpregnant levels. 4. As cardiac output increases and plasma volume expands, systemic vascular resistance declines . This decline is due to systemic vasodilation from hormonal influences and maternal postural changes related to the gravid uterus. 5. Finally , fibrinogen and other procoagulant blood factors (II, V, VII, VIII, X, and XII) increase during pregnancy. These five hemodynamic changes protect the mother and allow her to adapt to obstetric hemorrhage.

5. CLASSIFICATION OF HEMORRHAGE Understanding the physiologic responses that accompany different degrees of volume deficit can assist the clinician in managing obstetric hemorrhage. By 30 weeks of gestation, the average 70-kg pregnant woman maintains a blood volume of 6000 mL (85 mL/kg ). Class 1 hemorrhage corresponds to approximately 1000 mL of blood loss. This blood loss equates to a 10% to 15% volume deficit. Women with this amount of volume deficit exhibit mild physiologic changes , such as dizziness and palpitations, owing to the hemodynamic adaptations that accompany normal pregnancy.

6. Class 2 hemorrhage is characterized by 1500 mL of blood loss, or a 20% to 25% volume deficit. Early physical changes that occur during a class 2 hemorrhage include tachycardia and tachypnea. Narrowing of the pulse pressure is another sign of a class 2 hemorrhage. The pulse pressure represents the difference between the systolic and diastolic blood pressures. Systolic blood pressure is a good representation of stroke volume and β1 stimulation . Diastolic blood pressure reflects systemic vasoconstriction; therefore the pulse pressure represents the interrelationship between these entities.

7. With a class 2 volume deficit, the sympathoadrenal system is activated, resulting in a diversion of blood flow away from nonvital organs (skin, muscle, and kidney) and a redistribution of the circulation to vital body organs (brain and heart ). The result of this activation is increased vasoconstriction, increased diastolic blood pressure, maintenance of systolic blood pressure, and a narrowing of the pulse pressure. A final physiologic response of class 2 hemorrhage is orthostatic hypotension .

8. Although blood pressure comparisons can be made in the supine, sitting, and standing positions to document this response, a practical approach is to assess the time needed to refill a blanched hypothenar eminence on the patient’s hand. Typically a woman with normal blood volume can refill her hypothenar eminence within 1 to 2 seconds after pressure is applied. A patient with a class 2 hemorrhage and orthostatic hypotension will have a significant reperfusion delay

9. Class 3 hemorrhage is defined as a blood loss of 2000 mL and corresponds to a volume deficit of 30% to 35%. Within this hemorrhage class, the physiologic responses noted in class 2 hemorrhage are exaggerated. Patients demonstrate significant tachycardia (120 to 160 beats/min ), tachypnea (30 to 50 breaths/min), overt hypotension, restlessness , pallor, and cool extremities. Class 4 hemorrhage is characterized by more than 2500 mL of blood loss . This amount of blood loss exceeds 40% of the patient’s total blood volume. The clinical manifestations of this volume deficit include absent distal pulses, shock, air hunger, and oliguria or anuria.

10. Advanced trauma life support classification   The Advanced Trauma Life Support manual describes four classes of hemorrhage to emphasize the progressive signs and symptoms leading to the shock state . The following classes were derived from nonpregnant populations and may be somewhat different in postpartum women: Class I hemorrhage involves a blood volume loss of up to 15 percent. The heart rate is minimally elevated or normal, and there is no change in blood pressure, pulse pressure, or respiratory rate. Class II hemorrhage occurs when there is a 15 to 30 percent blood volume loss I s manifested clinically as tachycardia (heart rate of 100 to 120), tachypnea (respiratory rate of 20 to 24), and a decreased pulse pressure, although systolic blood pressure changes minimally if at all. The skin may be cool and clammy, and capillary refill may be delayed. An increasing maternal heart rate and tachypnea with stable systolic blood pressure should be regarded as evidence of compensated shock and should prompt investigation and institution of a PPH protocol, even if only light vaginal bleeding is observed.

11. Class III hemorrhage involves a 30 to 40 percent blood volume loss R esulting in a significant drop in blood pressure and changes in mental status. Any hypotension (systolic blood pressure less than 90 mmHg) or drop in blood pressure greater than 20 to 30 percent of the measurement at presentation is cause for concern. While diminished anxiety or pain may contribute to such a drop, the clinician must assume it is due to hemorrhage until proven otherwise. Heart rate (≥120 and "thread") and respiratory rate are markedly elevated, while urine output is diminished. Capillary refill is delayed. Class IV hemorrhage involves more than 40 percent blood volume loss L eading to significant depression in blood pressure and mental status. Most patients in class IV shock are hypotensive (systolic blood pressure less than 90 mmHg). Pulse pressure is narrowed (≤25 mmHg), and tachycardia is marked (>120 ). Urine output is minimal or absent. The skin is cold and pale, and capillary refill is delayed

12. ANTEPARTUM HEMORRHAGE Placental Abruption refers to the premature separation of a normally implanted placenta from the uterus prior to delivery of the fetus. The diagnosis is typically reserved for pregnancies greater than 20 weeks of gestation. Abruption is characterized by defective maternal vessels in the decidua basalis , which rupture and cause the separation . On rare occasions, the separation may be caused by a disruption of the fetal-placental vessels .

13. Clinical Manifestations The clinical manifestations of placental abruption are determined by several factors, including the temporal nature of the abruption (acute vs. chronic), the clinical presentation (overt vs. concealed), and the severity .

14. Diagnosis Placental abruption is primarily a clinical diagnosis that is supported by radiographic, laboratory, and pathologic studies. Any findings of vaginal bleeding, uterine contractions, abdominal and/or back pain, or trauma should prompt an investigation for potential placental abruption. Vaginal bleeding may range from mild to severe.

15. Radiology. Ultrasound can identify three predominant locations for placental abruption : subchorionic (between the placenta and the membranes ), retroplacental (between the placenta and the myometrium), and preplacental (between the placenta and the amniotic fluid ).

16. Retroplacental hematomas are associated with a worse prognosis for fetal survival than subchorionic hematomas. The size of the hemorrhage is also predictive of fetal survival. Large retroplacental hematomas (> 60 mL) have been associated with a 50% risk of fetal mortality, whereas similarly sized subchorionic hematomas carry less than a 10 % risk. Magnetic resonance imaging (MRI) can be used for the diagnosis of placental abruption when sonography is equivocal

17. Placenta Previa Definition and Pathogenesis Placenta previa is defined as the presence of placental tissue over the cervical os. Contemporary classification of placenta previa consists of two variations: placenta previa, in which the internal cervical os is covered by placental tissue, and low-lying placenta, in which the placenta lies within 2 cm of the cervical os but does not cover it. Although not a true placenta previa, a low-lying placenta is associated with an increased risk for bleeding and other adverse pregnancy events

18. The exact cause of implantation of the placenta in the lower segment is not known. The following theories are postulated . Dropping down theory The fertilized ovum drops down and is implanted in the lower segment. Poor decidual reaction in the upper uterine segment may be the cause. Failure of zona pellucida to disappear in time can be a hypothetical possibility. The is explains the formation of central placenta previa.

19. Persistence of chorionic activity In the decidua capsularis and its subsequent development into capsular placenta which comes in contact with decidua vera of the lower segment can explain the formation of lesser degrees of placenta previa. Defective decidua Results in spreading of the chorionic villi over a wide area in the uterine wall to get nourishment. During this process, not only the placenta becomes membranous but encroaches onto the lower segment. Such a placenta previa may invade the underlying decidua or myometrium to cause placenta accreta, increta or percreta . Big surface area of the placenta As in twins may encroach onto the lower segment.

20. The term placental migration has been used to explain this “resolution ” of placenta previa noted near term. Two theories have been suggested to account for this phenomenon. The first proposes that as the pregnancy advances, the stationary lower placental edge relocates away from the cervical os with the development of the lower uterine segment. The second theory suggests that trophotropism, or the growth of trophoblastic tissue away from the cervical os toward the fundus , results in resolution of the placenta previa

21. Clinical Manifestations Placenta previa typically presents as painless vaginal bleeding in the second or third trimester. The bleeding is believed to occur from disruption of placental blood vessels in association with the development and thinning of the lower uterine segment. Nearly 90% of patients with placenta previa will have at least one bleeding episode. About 10% to 20% of patients present with uterine contractions before the onset of bleeding, and fewer than 10% remain asymptomatic until term.

22. Diagnosis The timing of the diagnosis of placenta previa has undergone significant change in the past five decades. Painless third-trimester bleeding was a common presentation for placenta previa in the past, whereas most cases of placenta previa are now detected antenatally with ultrasound prior to the onset of significant bleeding

23. Radiology. Transabdominal and transvaginal ultrasound provide the best means for diagnosing placenta previa. Although transabdominal ultrasound can detect the majority of placenta previa cases, transvaginal ultrasound has a reported diagnostic accuracy that approaches 100 %.

24. Management of hemorrhagic shock Shout for help ABCDE of life Open double large bore IV catheter Take 10ml of blood sample during iv line for CBC , BG & Rh and cross match Shock position Intranasal O2 Bladder catheterization for fluid balance Resuscitation with iv fluid Preparing blood Detect the cause and arrest hemorrhage

25. Fluid Resuscitation and Transfusion All obstetricians will encounter antepartum and postpartum hemorrhage. In most instances, fluid resuscitation and blood component therapy are lifesaving ; therefore every physician should have a thorough understanding of appropriate volume resuscitation, transfusion therapy, and alternative treatment options.

26. Volume Resuscitation Initial management of a bleeding patient requires appropriate volume resuscitation. Two large-bore IV catheters are recommended. Typically warmed crystalloid solution in a 3 : 1 ratio to the estimated blood loss should be infused. Goals of therapy are to maintain an adequate maternal blood pressure (systolic blood pressure >90 mm Hg) and urine output (at least 30 mL/h). If the hemorrhage is easily controlled, this may be the only therapy needed. The patient should have serial assessments of her vital signs and hematologic profiles to confirm hemodynamic stability. Large volume replacement (usually >3 to 4 L) can promote dilutional coagulopathy , electrolyte imbalances, and hypothermia

27. Colloid Solutions. Colloid solutions contain larger particles, colloids , which are less permeable across vascular membranes. These solutions provide a greater increase in colloid oncotic pressure and plasma volume; however , they are more expensive than crystalloids and may be associated with anaphylactoid reactions. Examples of colloid solutions include albumin and dextran.

28. Blood replacement

29. PIH ECLAMPSIA Is the occurrence of convulsions or coma unrelated to other cerebral conditions with signs and symptoms D efined as the development of convulsions or unexplained coma during pregnancy or postpartum in patients with signs and symptoms of PE.

30. Cerebral Pathology Autoregulation of the cerebral circulation is a mechanism for the maintenance of constant cerebral blood flow during changes in BP, and it may be altered in eclampsia . Precise cause of seizures - not clearly understood – The cause of eclampsia is unknown Two theories have been proposed to explain these cerebral abnormalities Forced dilation and vasospasm, and The forced dilation theory suggests that the lesions in eclampsia are caused by loss of cerebrovascular autoregulation

31. Two models - proposed, based on the central role of hypertension – First model Hypertension causes a breakdown of the autoregulatory system of the cerebral circulation, leading to hyperperfusion , endothelial dysfunction, and vasogenic and/or cytotoxic edema. – Second model Hypertension causes activation of the autoregulatory system, leading to vasoconstriction of cerebral vessels leading to hypoperfusion , localized ischemia, endothelial dysfunction, and vasogenic and/or cytotoxic edema Cerebral inflammation may also play a role

32. 1. General measures: ABC of life 2. Control of convulsions and Management of persistent seizures 3. Correction of hypoxia & acidosis 4. Antihypertensive therapy 5. Monitor Fluid balance & diuresis 6. Delivery 7. Prophylactic IV antibiotics 8. Manage Complications

33. sepsis Sepsis : SIRS plus a proven or suspected microbial etiology Sever sepsis : Sepsis with one or more signs of organ dysfunction (oliguria , hypoxemia , encephalopathy , metabolic acidosis, DIC) or hypotension Septic shock : sepsis with hypotension that is unresponsive to fluid resuscitation , along with organ dysfunction

34. Principle of sepsis management 1.Recognize patients with sepsis and septic shock 2 . Antibiotics 3 . R esuscitation 4 . Monitoring

35. Fluid Resuscitation targets Improved BP: mean arterial pressure (MAP) ≥ 65 mmHg SBP > 100 mmHg. Adequate urine output: ≥ 0.5 mL/kg/hr. Skin examination: capillary refill < 2–3 sec absence of skin mottling well felt peripheral pulses warm dry extremities. Improved sensorium Normalized lactate levels (if initial level high)

36. Monitor woman and fetus. Once maternal BP or SpO 2 are reduced, then fetus will become rapidly distress ed Early recognition and resuscitation are essential. During pregnancy, there is an overall increase in blood volume, HR and cardiac output, and reduction in oncotic pressure

37. Management of pregnant woman with shock Ensure adequate hydration, use IV fluids as necessary: Close attention to fluid balance to prevent fluid overload and pulmonary edema Vasopressors – use cautiously with appropriate available monitoring: May decrease uterine perfusion. Administer with IV fluids – uteroplacental flow will not be adequate with vasopressors alone. Must monitor fetus when administering.

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