ABORTION in Nursing.pptx Obstetric Nursing.

Abortion and Risk involved

1. OBSTETRIC NURSING UNIT EIGHTEEN

2. BLEEDING IN EARLY PREGNANCY

3. BLEEDING IN EARLY PREGNANCY Bleeding in pregnancy, however slight is abnormal. Patient must be taught to report without delay, the slightest vaginal bleeding. Causes of bleeding

4. Extra gestational or incidental causes of bleeding: In early pregnancy these refer to those conditions which could have caused vaginal bleeding in any woman. The incidence is high in pregnancy because of increased vascularity of the genital organs. These incidental causes are as follows:

5. 1. Cervical erosion 2. Cervical polyps 3. Carcinoma of the cervix 4. Trauma or laceration in the genital tract 5. Schistosomiasis – patient may confuse haematuria with vaginal bleeding

6. Gestational causes: These are: 1. Abortion 2. Ruptured ectopic pregnancy 3. Hydatidiform mole 4. Decidual bleeding

7. ABORTION Abortion is the most common cause of bleeding in early pregnancy. Abortion may be defined as interruption of pregnancy before the 24th (28th) week of gestation. The placenta is usually separated and this may result in the death of the fetus and its subsequent expulsion. Abortion may be spontaneous or induced

8. SPONTANEOUS ABORTION Spontaneous abortion is defined as the involuntary loss of the products of conception prior to 24 weeks’ gestation. Incidence 15% of all confirmed pregnancies are said to result in a miscarriage. The majority occur in the first trimester 1 – 2% occur in the 2nd trimester (after the 13th week).

9. CAUSES/AETIOLOGY Fetal causes and maternal causes FETAL CAUSES 1. 50% of miscarriages are due to chromosomal abnormalities of the conceptus . 2. Genetic abnormalities 3. Structural abnormalities

10. MATERNAL CAUSES 1. Maternal age – risk increases with advancing maternal age 2. Structural abnormalities of the genital tract. These include: - infantile uterus - Incompetent internal os of the cervix - Retroversion of the uterus - Bicornuate uterus - Fibroids 3. Infections, these include:

11. - Rubella - Listeria - Chlamydia - Malaria - Pyelonephritis 4. Maternal diseases - Diabetes mellitus - Renal disease - Thyroid dysfunction 5. Environmental factors Excessive consumption of alcohol and coffee Cigarette smoking Exposure to organic solvents

12. 6. Hormonal imbalance 7. Extreme emotional stress eg grief or fright 8. Violent exercises 9. Accidents 10. Certain drugs Previous obstetric history is a predictor of spontaneous abortion. Multigravidae are at higher risk than primigravidae . Miscarriage in the previous pregnancy is a prime indicator of risk (it can occur again)

13. THREATENED ABORTION In threatened abortion the disturbance to the pregnancy is slight and the pregnancy may continue to term with good management. On the other hand the damage may be progressive resulting in massive separation of the placenta and dilatation of the cervix

14. Signs and symptoms. - Scanty blood loss - There may or may not be low backache and abdominal cramps like dysmenorrhoea . - The cervix is closed on speculum examination - The uterus is soft with no tenderness when palpated - Fetal heart sound may be present

15. Management 1.Reassure patient 2.Put patient to bed and ensure complete bed rest (complete bed rest is maintained till vaginal bleeding ceases). 3.Continue to reassure patient to allay anxiety. 4.Patient is made to wear a vulva pad and remain in bed while the doctor is informed. 5.Check vital signs ½ hourly initially 6.Estimate the amount of blood loss from the sanitary pad, clothing and linen.

16. 7.Save all soiled articles for doctor’s inspection. 8.Tidy client, change clothing and make her comfortable in bed. 9.Record all findings. Prepare for speculum exam. 10.Swab vulva twice daily with antiseptic lotion. 11.Check hemoglobin level. 12.Give any prescribed analgesic. 13.Perform or assist where necessary all activities of daily living for the client. 14.Ensure patient passes urine well. 15.Prevent constipation by serving diet rich in fibre .

17. 16.Also diet should be rich in protein, vitamins and minerals. 17.Check vital signs 18.Check blood pressure daily 19.Test urine daily for albumin, sugar, and acetone 20.Prevent malaria (start IPT if not already started) and anaemia. 21Serve routine drugs If bleeding stops for 3 days allow client out of bed.

18. If she does not bleed for one week, she can be discharged home on advice. Scan is done to ascertain viability. On discharge advise patient on the following: - Rest at home. - Avoid lifting heavy objects. - Avoid any strenuous exercise. - Avoid intercourse at least one month. - Attend antenatal clinic regularly and report immediately if bleeding recurs. - Record care given.

19. INEVITABLE ABORTION In this case the pregnancy cannot be saved because a good or large portion of the placenta has been detached and the cervical os is dilating. Vaginal bleeding is heavy with clots or gestational sac containing the embryo or fetus ( conceptus may be seen or felt protruding through the dilating os during examination). The uterus if palpable may be smaller than expected.

20. -The membranes are ruptured -Severe backache and lower abdominal pain is present -Uterus is contracted -Inevitable abortion may end up as one of the following: 1) Complete abortion: In this case the whole products of conception is expelled. After expulsion, pain and vaginal bleeding decrease. -The cervix is closed -The uterus is contracted and smaller in size. -Complete abortion is more common before the 8th week of gestation.

21. 2) Incomplete abortion : In this case part of the products of conception is expelled and the placenta and membranes are retained. Bleeding continues and may become profuse because the presence of the retained products does not allow for efficient uterine contraction and retraction. -There is severe lower abdominal pain. -The uterus is bulky. -The patient’s condition depends on the amount of blood loss.

22. -If bleeding is excessive patient may be in shock and have anaemia -The pulse is weak and rapid -Patient feels cold (the skin is cold and clammy) -Air hunger may even follow. Management of inevitable and incomplete abortion Seek medical aid (inform doctor), call for help Treat for shock: - Keep patient warm, feet raised

23. -If bleeding is excessive patient may be in shock and have anaemia -The pulse is weak and rapid -Patient feels cold (the skin is cold and clammy) -Air hunger may even follow. MANAGEMENT OF INEVITABLE AND INCOMPLETE ABORTION 1.Seek medical aid (inform doctor), call for help. 2.Treat for shock. 3.Keep patient warm, feet raised.

24. 4.Take specimen of blood for grouping and haemoglobin level estimation 5.IV fluid to expand fluid volume 6.Give IM ergot 0.5mg and repeat after 20 minutes if bleeding is profuse or oxytocin may be added to the drip. 7.Give analgesic such as pethidine . 8.Soiled articles or vulval pads are saved for estimation of blood loss. 9.Check vital signs ¼ hourly 10.Wash pubic area and shave and clean with antiseptic solution.

25. 11.Counsel client. 12.Motivate client on Family Planning. 13.Inform client that fertility returns in less than 2 weeks after abortion. 14.Encourage her to choose a method especially condom if her risk of acquiring STIs is high. 15.Educate on prevention of STIs.

26. When the patient’s condition improves, Manual -Vacuum Aspiration (MVA) is performed if gestational age is 12 weeks or below 12 weeks. -Ensure bladder is emptied before procedure -After MVA procedure, monitor client’s condition, -check vital signs, -check vulva for bleeding. -Monitor the urine output to detect oliguria early. -If gestational age is more than 12 weeks, other methods may be used to evacuate the uterus.

27. Even if client wants a pregnancy she has to choose a contraceptive method to enable her recuperate before embarking on another pregnancy. Educate patient on care of the breast if the gestational age is more than 16 weeks.

28. HABITUAL OR RECURRENT ABORTION The term habitual or recurrent abortion is used when a patient has had three or more consecutive spontaneous abortions. Often the cause is not known. Incompetence of the internal cervical os resulting from previous trauma to the cervix is associated with mid trimester abortions.

29. A thorough examination is done to exclude diseases such as diabetes mellitus, nephritis, TB, cervical erosion, abnormalities of the uterus, displacement of the uterus and fibroids after the episode. Clinical features of abortions due to cervical incompetence (incompetence of the internal os) 1) The abortions occur late in the second trimester, usually between the 22nd and 24th week. 2) No previous warning such as vaginal bleeding

30. 3) The membranes may rupture suddenly followed by expulsion of the products of conception 4) The products of conception looks fresh (fetus may be alive) MANAGEMENT 1.Client is educated on diet – food rich in protein, minerals and vitamins 2.She is advised to recover from the current event before starting another pregnancy 3.She is advised to report as soon as she thinks she is pregnant and advised not to have sexual intercourse, lift heavy objects, avoid strenuous exercise, rest and avoid infection

31. In cases where the patient is unlikely to have adequate rest at home, hospital admission is recommended during the first half of the pregnancy. The treatment of incompetent cervix is the shirodkar operation. Non – absorbable suture is tied round the cervix at the level of the internal os at the 14th to 16th week of pregnancy. The operation is boldly written on the patient’s folder.

32. The suture must be removed at about the 38th week of pregnancy or as soon as the patient goes into labour. The patient is made aware of the implication and the possible danger if the suture is not removed on time. MISSED ABORTION The term missed abortion is used when the fetus dies and is retained in utero.

33. -The signs of threatened abortion subside except for some brownish discharge which is not associated with pain. -The uterus fails to grow. -The breasts become soft and other signs of pregnancy disappear. -The dead fetus may be retained for varying periods of time (3 – 4 weeks). If it is retained for a long time it may lead to profuse vaginal bleeding as a result of hypofibrinogenaemia .

34. Oxytoncin drip is set up after insertion of prostaglandin to soften and efface the cervix. Labour is induced and the uterus is emptied. When the conceptus has been expelled and there is haemorrhage, curettage of the uterus, administration of oxytocic drugs and fresh blood or fresh frozen plasma may be used to save the woman’s life.

35. BLOOD MOLE Blood mole may arise in cases of missed abortion in which the decidua capsularis remains intact and permits the conceptus to be surrounded by layers of blood, which is referred to as a blood mole. When fluid is extracted from the blood, the fleshy, firm, hard mass is known as a carneous mole. The management is the same as for missed abortion.

36. INDUCED ABORTION Induced abortion can be therapeutic or criminal. Therapeutic abortion Therapeutic abortion is evacuation of the uterus done by a qualified medical practitioner in the interest of the mother’s life or her total wellbeing. The indications are usually medical conditions threatening the mother’s life or likely to cause gross fetal abnormalities. These conditions include cardiac disease, chronic nephritis and German measles contracted in the 1st trimester.

37. . Both the husband and wife must give written consent for the termination of the pregnancy. The are four (4) identified areas that allow grounds for ending a pregnancy before 24 weeks gestation. Two medical practitioners are required to certify that one or more of the following apply:

38. 1) Continuation of the pregnancy would involve greater risk of injury to the physical or mental health of the pregnant woman or any existing children of her family than if the pregnancy were terminated. 2) Termination is necessary to prevent grave permanent injury to the physical or mental health of the woman 3) The continuation of the pregnancy would involve risk to the life of the pregnant woman, greater than if the pregnancy were terminated

39. 4) There is substantial risk that if the child were born it would suffer such physical or mental abnormalities as to be seriously handicapped. After 24 weeks, termination of pregnancy is permitted where the woman’s life is at risk or where there is a substantial risk of the child being born seriously disabled physically or mentally. Therapeutic abortion should be performed as early as possible in pregnancy to avoid complication.

40. CRIMINAL ABORTION Is abortion illegally procured. Such abortions are often done by unqualified persons having little regard for the consequences. Risk of sepsis, uterine perforation, cervical laceration, haemorrhage, acute renal failure and sudden death are associated with criminal abortion.

41. SEPTIC ABORTION Septic abortion is usually a sequel of incomplete abortion, often criminally induced. The patient is usually anaemic , ill with a high temperature, rapid pulse, headache, vomiting and lower abdominal pain (especially if there is pelvic peritonitis). The lochia are profuse and offensive. The patient becomes jaundiced and looks toxic especially if the condition is complicated by septicaemia .

42. MANAGEMENT 1.She is confined to bed. 2.Pain is relieved. 3.Vital signs are checked 4 hourly. 4.Sponging is done when necessary ie if the temperature is above 38oc. 5.Bed bath twice daily. 6.Vulval toileting twice daily. 7.Change pad when soiled. 8.Care for the mouth.

43. 9.IV infusion to correct dehydration and electrolyte imbalance. 10.Monitor fluid intake and output to detect renal complications early. 11.Take blood for grouping and cross – matching. 12.Replace blood loss. 13.Treat infection with appropriate antibiotics. 14.Evacuation of the uterus is done when the infection is under control or under heavy antibiotic cover.

44. 15.In some cases antitetanus and anti gas gangrene sera are administered. 16.Easily digestible food rich in protein, vitamins and high in calories is offered to the patient when she starts eating. 17.Fluid intake is encouraged. 18.Routine haematinics and anti malarials are administered. 19.Family planning counselling is done when the patient recovers.

45. ECTOPIC PREGNANCY

46. Ectopic pregnancy By the end of this lesson student will be able to: - Describe what is meant by ectopic pregnancy - Identify different types of ectopic pregnancy - Discuss the risk factors for developing an ectopic pregnancy - Outline the different treatment options available and when they may be appropriate. - Discuss the nurse’s role in the care of patients with an ectopic pregnancy. Introduction

47. Ectopic pregnancy By the end of this lesson student will be able to: - Describe what is meant by ectopic pregnancy - Identify different types of ectopic pregnancy - Discuss the risk factors for developing an ectopic pregnancy - Outline the different treatment options available and when they may be appropriate. - Discuss the nurse’s role in the care of patients with an ectopic pregnancy.

48. Introduction An ectopic pregnancy is one that develops outside the uterus. The developing embryo implants in an area other than the endometrial layer of the uterus, which is the normal site for implantation and development. In ‘normal’ pregnancy, the ovum, once fertilized, proceeds along the fallopian tube. Transit of the ovum is assisted by - Peristaltic action - Fluid produced by the epithelial lining

49. - Cilia lining the fallopian tube Over the course of 4 – 5 days, the zygote develops by simple cell division, but does not increase in size. The mass of cells at this stage is called a morula , which divides into an outer and inner cell mass. A blastocyst is formed when fluid fills the space between the outer and inner cell mass.

50. The outer cell mass, referred to as the trophoblast, is involved in the implantation of the blastocyst into the prepared endometrium (the decidua) and the inner cell mass develops into the embryo, umbilical cord and amnion (inner membrane). Implantation occurs about 7 – 10 days after fertilization when the endometrium closes over the blastocyst.

51. . After implantation, the chorion (the outermost extraembryonic membrane) develop from the trophoblast. Chorionic villi develop as extensions of the chorionic blood vessels, bringing embryonic circulation to the placenta. The placenta secures the developing fetus to the uterus and provides an area for the exchange of nutrients and waste products between the fetus and the mother.

52. In ectopic pregnancy the journey along the fallopian tube is arrested or altered in some way. Between 95% and 98% of ectopic pregnancies develop in the fallopian tube. There are four parts to the fallopian tube extending from the uterus: The interstitial, isthmus, ampulla (the widest part of the tube) and the infundibulum with fimbriae which form finger- like projections from the infundibulum over the ovary.

53. The most common sites for ectopic pregnancies in the fallopian tube are the ampulla and the isthmus, followed by the fimbriated end of the tube. Reports indicate a general increase in the incidence of ectopic pregnancy. Ectopic pregnancy is a leading cause of first trimester mortality and accounts for 9% of pregnancy related deaths in the first trimester.

54. Ectopic pregnancy implantation sites - Fallopian tube - Ovary - Cervix - Abdomen Risk factors - Tubal pathology - Previous tubal surgery - Infertility - Genital or pelvic inflammatory disease or previous tubal infection

55. - Use of some reproductive technologies - Previous miscarriage - previous induced abortion - Use of an intrauterine contraceptive device - previous ectopic pregnancy - Sterilization - Smoking - Douching - Exposure to diethylstiboestrol

56. Abnormalities in fallopian tubal structure and transport are associated with ectopic pregnancy, but the specific aetiology is unknown. Women who have tubal pathology or have had tubal surgery are at increased risk of ectopic pregnancy. Fibroids in the uterus and endometriosis, sexual activity with multiple partners or at a young age. Tubal surgery increases the risk of scarring and narrowing of the fallopian tube, which may alter function.

57. Genital infection with chlamydia trachomatis, if left untreated, the infection can result in tissue damage and permanent scarring resulting in multiple sites of obstruction in the fallopian tube. An estimated 70 – 90% of women with chlamydia trachomatis infection are asymptomatic, therefore they will not receive treatment

58. DIAGNOSTIC PROCEDURES FOR SUSPECTED ECTOPIC PREGNANCY Diagnosis of ectopic pregnancy can be challenging as many patients are asymptomatic before tubal rupture. - Urine pregnancy test. - Beta – human chorionic gonadotrophin concentrations. - Transvaginal ultrasound. - Serum progesterone concentrations. - Dilatation and curettage. - Laparoscopy.

59. SIGNS AND SYMPTOMS Initial symptoms are non-specific. A period of amenorrhoea (usually 6 – 8 weeks) - Abdominal pain or tenderness (pain may be dull or sharp and may be generalized or localized to one area). - Vaginal bleeding or spotting which may be irregular. - Usual symptoms of early pregnancy eg nausea and breast tenderness may be present.

60. Late symptoms include: - Dizziness and fainting as a result of haemorrhage from tubal rupture. - Referred shoulder pain caused by blood irritating the diaphragm. - Tachycardia. - Bloated, hard abdomen. - General weakness.

61. (These late symptoms require emergency treatment). Since some women do not show early symptoms of ectopic pregnancy and the early symptoms of bleeding and abdominal pain following a period of amenorrhoea can be confused with miscarriage. Screening is important in women who are known to be at risk.

62. TREATMENT 1. Expectant management. 2. Medical treatment . 3. Surgical treatment . EXPECTANT MANAGEMENT The patient’s condition is closely monitored without treatment.

63. This is done for women who are medically stable and have access to immediate help and are willing to be followed up with USG and serial Beta HCG measurements. (Can be successful in 50 – 70% of women). Spontaneous resolution by tubal abortion or resorption can take up to 50 days. It is important to provide the woman and her family with information, reassurance and emotional/psychological support.

64. MEDICAL TREATMENT Methotrexate is commonly used in ectopic pregnancy when medical management is a possibility. This might be an option if the woman presents with haemodynamic stability, the size of the ectopic is 3 – 4cm at the widest diameter and it remains unruptured . It can be administered by IM injection or by injection directly into the ectopic pregnancy.

65. It is administered with leucovorin (an active form of folic acid). The woman need to be observed and monitored ie her vital signs to see how she is responding to the treatment. SURGICAL TREATMENT Surgical treatment involves removal of the ectopic pregnancy by laparoscopy or laparotomy.

66. Fallopian tube is removed by salpingectomy or conserved by: - Linear salpingotomy - Salpingostomy - Fimbrial evacuation EMOTIONAL SUPPORT Ectopic pregnancy is usually diagnosed early in pregnancy. With pregnancy comes the expectation of delivery of a baby and this can affect the way women and their partners deal with this event.

67. This affects women both physically and emotionally (traumatic event). There is loss of the fetus, invasive procedures to undergo and the implications in terms of fertility and future pregnancies. A feeling of loss and grief is to be expected after the event. It is helpful for nurses to be aware of various grief theories such as those of - Kubler – Ross - Parkes and Markus - Stroebe and Schut - Worden

68. To improve their understanding of possible reactions and responses of the couple and to provide appropriate support, the nurse has to provide information, advice and support, be empathetic and employ her counseling skills to help the woman accept the loss, work through her feelings and make positive adjustments. CLINICAL FEATURES OF RUPTURED TUBAL PREGNANCY. - History of amenorrhoea of about 6 to 8 weeks duration.

69. - Transient feeling of faintness and dizziness when rupture takes place. - Massive bleeding into the peritoneal cavity. - Signs and symptoms of shock. • Increase in pulse rate (weak and rapid pulse). • Severe hypotension. • Beads of cold sweat on forehead.

70. - Transient feeling of faintness and dizziness when rupture takes place. - Massive bleeding into the peritoneal cavity. - Signs and symptoms of shock • Increase in pulse rate (weak and rapid pulse) • Severe hypotension • Beads of cold sweat on forehead • Cold clammy skin

71. - Severe abdominal pain. - Pain when the cervix is moved during vaginal examination. - Rebound tenderness. - Positive abdominal tap (blood collects in the syringe when a needle attached to a syringe is introduce into the abdomen and the plunger withdrawn). - Pain which may be felt in the iliac fossa or hypogastrum and radiates to the shoulder. - Slight vaginal bleeding because of the decidual reaction in the uterus.

72. MANAGEMENT 1.Notify the doctor (call the doctor). 2.Call for help. 3.Treat for shock. Check vitals ½ hourly. 4.Set up IV infusion. 5.Take blood for grouping and cross –matching and haemoglobin estimation. 6.Administer analgesics (100mg pethidine IM). 7.Transfuse when blood is available.

73. 8.Reassure client and family members 9.Explain condition to client (family and how it will be managed). 10.Assist client/family to sign the consent form. 11.Perform general and abdominal examination if possible. 12.Inform theatre staff. 13.Prepare client for surgery.

74. - Wash abdomen and pubicarea with soap and water, shave and clean with antiseptic solution - Cover area with sterile towel. - Pass catheter. - Check for dentures (ask the woman). - If she has dentures assist her to remove them and keep according to hospital protocol or according to her wishes. - Monitor intake and output. - Send patient to theatre. - Prepare for post operative management of patient.

75. BLEEDING IN LATE PREGNACY (ANTEPARTUM HAEMORRHAGE) The term Anterpartum haemorrhage (APH) is applied to bleeding from the vagina occurring at anytime after the 24th week of pregnancy and before the birth of the child. APH may be described under three headings:

76. - Haemorrhage from a normally situated placenta. This is called placental abruption or abruptio placentae or accidental haemorrhage. The placenta is normally attached to the upper uterine segment, occupying part of the fundus and passing down onto the posterior or anterior wall. - Haemorrhage from partial separation of a placenta abnormally situated in the lower uterine segment.

77. This is termed placenta praevia or unavoidable haemorrhage. Haemorrhage is unavoidable when the lower uterine segment becomes stretched prior to the onset of labour. - Haemorrhage from a lesion of the cervix or vagina such as an erosion, a polyp or a carcinoma.

78. MANAGEMENT OF A PATIENT WITH UNCLASSIFIED BLEEDING (APH) The obstetric nurse has a duty to see to it that the patient does not lose her life and that of her baby. 1.Reassure patient. 2.Put patient to bed (complete bed rest). 3.Keep patient warm and calm in bed. 4.Raise feet to prevent shock. 5.Admit patient.

79. 6.Reassure patient/family members or significant others. Make family members comfortable. Allay anxiety. 7.Explain condition to patient/family and reason for procedures. 8.Notify the doctor (call the doctor). 9.Call for help if indicated. 10.Assess patient’s general condition. 11.Note the pulse, blood pressure, pallor and oedema .

80. 12.Set IV line depending on patient’s condition. 13.Take blood for grouping and Cross Matching and haemoglobin estimation. 14.Pass catheter and connect to urine bag. 15.Monitor intake and output and record on intake and output chart. 16.Administer analgesic if there is pain. 17.Perform a gentle abdominal exam to determine the lie of the fetus, the presentation and engagement.

81. 18.Assess for pain, tenderness, uterine consistency and malpresentation . 19.Auscultate fetal heart sound. 20.Estimate amount of blood loss from soiled sanitary pads, clothing and linen and all clothes and pads removed from the patient should be kept for the doctor’s inspection. 21.Check blood pressure, pulse and respiration ¼ hourly and record. Observe for signs of shock such as increase in pulse rate, hypotension, perspiration, cold clammy skin and sometimes air hunger.

82. 22.Give O2 if indicated. 23.Test urine for sugar, albumin and acetone. 24.Prepare for blood transfusion if necessary. 25.Tidy up client. 26.Allow significant others to see client if they want to leave. 27.Inform theatre staff. 28.Prepare patient for examination under anaesthesia . 29.Prepare patient for abdominal ultrasound (scan) to localise placenta. 30.Obtain consent from patient/relatives.

83. 31.Prepare client for emergency caesarean section if necessary. 32.Cross – match two pints of blood ready for transfusion or manage patient conservatively. 33.If C/S is done, give post operative management. 34.Report and record all findings. APH is classified according to the site or location of the placenta.

84. PLACENTAL ABRUPTION Placental abruption (accidental haemorrhage) is bleeding from premature separation of a placenta situated in the upper uterine segment. TYPES 1. Revealed accidental haemorrhage . 2. Concealed accidental haemorrhage . 3. Mixed accidental haemorrhage .

85. Due to the separation of a portion of the placenta from its uterine attachment, maternal blood escapes from the opened sinuses. This blood may track down between the membranes and the wall of the uterus and escape at the cervix (revealed haemorrhage) or the blood may remain inside the uterine cavity (concealed haemorrhage). In nearly all cases there is some external bleeding, but in concealed cases the degree of shock is out of proportion to the external loss.

86. INCIDENCE 1in 80 to 1 in 200 pregnancies (deliveries) Cause 1. About a ¼ of cases are associated with hypertension. 2. It may be caused by trauma during external version. 3. Direct blow on the abdomen or a fall. The bleeding in cases of placental abruption may be of any degree from a small retroplacental haematoma, which may not affect the fetus and which may only be discovered after the placenta is delivered;

87. to a large collection of blood which distends the uterus and kills the fetus by separating a large part of the placenta. In severe cases haemorrhage occur into the uterine wall and may extend to the perimetrium which then looks bruised and oedematous . In concealed cases the whole uterus is tense and tender but in revealed or less severe cases there is more localised tenderness over the site of haemorrhage.

88. SIGNS AND SYMPTOMS(REVEALED HAEMORRHAGE) - With or without any obvious cause the woman notices blood coming from the vagina. - The woman complains of a sudden attack of abdominal pain. - The blood is dark red in colour . - There is abdominal discomfort and tenderness over the site. - The head of the fetus may be engaged in late pregnancy. - Fetal distress or fetal death.

89. Signs and symptoms – concealed haemorrhage.  The abdomen is tense and boardlike (hard like a board).  There is tenderness of the abdomen.  There is constant excruciating abdominal pain due to uterine distension.  The degree of shock is out of proportion to the amount of blood loss.  The woman is in shock due to haemorrhage and pain.  The blood pressure may be normal.

90.  Pulse is weak and rapid.  The uterus may be larger than would be expected for the period of gestation reached and more globular in outline.  Fetal parts cannot be palpated.  Fetal heart sound cannot be heard.  Protein may be present in the urine. In many cases the bleeding is partly concealed and partly revealed and the signs and symptoms are mixed. The severity of the case should be judged by the general condition of the woman.

91. MANAGEMENT All cases of APH should be admitted to hospital. A vaginal examination should not be made. In severe cases (severe shock), blood transfusion or plasma expanders or IV fluid should be given. In most severe cases the fetus is already dead and need not be considered. Analgesics may be given to relieve pain.

92. The object of treatment is to empty the uterus, contract and retract it with as little bleeding as possible and with no risk to the mother. Examine her to see if she is in labour and monitor labour (no C/S if fetus is dead). If she is not in labour, labour is induced by rupturing the membranes and setting up oxytocin drip. If bleeding is profuse, C/S may be done after treating for shock or if there is slight bleeding and the fetus is in distress and woman is not in labour.

93. The 2nd stage of labour may be shortened by vacuum extraction. Active management of the 3rd stage of labour is employed with IV injection of oxytocin. Monitor woman’s condition for 24 hours after delivery – check vital signs and amount of blood loss.

94. COMPLICATIONS Postpartum haemorrhage (PPH). Disseminated intravascular coagulopathy (DIC) Hypofibrinogenaemia (failure of blood clotting). Renal cortical necrosis or lower nephron necrosis resulting in anuria.

95. PLACENTA PRAEVIA

96. COMPLETE PARTIAL MARGINAL LOW LYING

97. PLACENTA PRAEVIA In this condition the placenta is wholly or partially situated in the lower uterine segment. The stretching and dilatation of the lower uterine segment during the later weeks of pregnancy (last 12 weeks of pregnancy) causes premature separation of the placenta which results in bleeding. The bleeding is not associated with any pain or exertion. The first few episodes of bleeding are usually slight but subsequent episodes may be profuse.

98. Diagnosis 1) By ultrasound 2) The placenta can be felt through the cervical os. However, such an exam should only be carried out in an operating theatre ready for C/S with some amount of blood available for transfusion. 3) Clinical features Clinical features 1) History of painless recurrent haemorrhages which occur without any cause. It can occur at rest

99. 2) The general condition of the patient is directly proportional to the amount of vaginal bleeding 3) The following will be found on abdominal exam: a) A high freely mobile presenting part which cannot be made to enter the pelvic brim easily. The head is not engaged The breech may present b) Abnormal lie of the fetus eg transverse or oblique lie

100. c) The uterus is neither hard nor tender on palpation d) The fetal parts are easily felt and fetal heart sounds are usually heard 4) Hypertension or proteinuria are not usually present. Causes The cause of implantation of a placenta in the lower uterine segment is not clearly understood. It is more common in multiparous women.

101. In multiple pregnancy the large placental site may encroach into the lower uterine segment. History of C/S

102. Types of placenta praevia Four types have been described: 1. Type I or lateral placenta praevia In this type the placenta is situated mainly in the upper uterine segment with only a tip of it encroaching on the lower uterine segment. In type I two varieties are described: a. Type I anterior b. Type I posterior

103. 2. Type II or marginal placenta praevia A greater part of the placenta is attached to the lower uterine segment in such a way that its lower margin extends to the undilated internal os. Two varieties are described: a. Type II anterior b. Type II posterior

104. 3. Type III or complete placenta praevia The placenta completely covers the undulated internal os ( it covers the os up to 6cm dilatation but not when it is fully dilated). 4. Type IV or central placenta praevia The placenta completely covers the undilated internal cervical os and the margin cannot be reached by the examining finger. It completely covers the entire os even at full dilatation.

105. Management The management depends on the ff. 1. Amount of blood loss 2. The maturity of the fetus 3. Degree (type) of placenta praevia . Active management Active management ie immediate termination of the pregnancy. This is done when the bleeding is severe or the patient fails to respond to conservative treatment.

106. IV line is secured, blood is taken for grouping and x-matching and haemoglobin estimation (or patient should have x-matched blood ready at the bank). IV infusion is administered until blood is ready. Record intake and output. Patient is reassured and condition explained to her. She is kept warm and calm in bed

107. Check vital signs ¼ hourly Inform theatre staff to set up theatre for vaginal examination under anaesthesia and possible C/S. Prepare patient for C/S and send her to the theatre after she has signed the consent form. An urgent vaginal examination under general anaesthesia is performed. If the type is II posterior, III or IV C/S is carried out to avoid massive haemorrhage and fetal death.

108. Ultrasonic scan may be used to locate the placenta or diagnose the type. The reason for doing a C/S in type II posterior placenta praevia is that the bleeding is difficult to control and the descending head could compress the placenta against the sacral promontory resulting in fetal hypoxia and intrauterine death.

109. If the bleeding is controlled and there is no cephalopelvic disproportion (CPD), artificial rupture of membranes ( amniotomy ) is done for type I anterior or posterior and type II anterior placenta praevia , whether the fetus is alive or dead. The patient usually goes into labour and delivers spataneously . Prepare for resuscitation of the baby.

110. If the bleeding is controlled and there is no cephalopelvic disproportion (CPD), artificial rupture of membranes ( amniotomy ) is done for type I anterior or posterior and type II anterior placenta praevia , whether the fetus is alive or dead. The patient usually goes into labour and delivers spataneously . Prepare for resuscitation of the baby.

111. Expectant or conservative treatment Expectant or conservative treatment is given to a patient whose bleeding is slight and the gestational age is less than 36 weeks. Expectant treatment is an attempt to prolong the pregnancy, prevent prematurity and give the baby a chance of survival. Patient is usually admitted and kept under careful supervision.

112. She is reassured and her condition explained to her. Complete bed rest is ensured. Abdominal examination (a gentle abdominal exam) noting the size of the fetus and fetal heart sounds is done twice daily. Vital signs are checked and recorded twice daily. Urine testing is done daily to exclude albuminuria. Diet rich in protein, vitamins, minerals and high in fibre with fruits is served.

113. . perineal pad is inspected at least four times daily noting evidence of fresh bleeding. If fresh bleeding occurs perineal pads are kept for doctor’s inspection. Vulval toileting is done twice daily. Routine drugs are served as ordered. IPT is completed. Patient is encouraged to sleep under ITN (insecticide treated bed nets).

114. Patient is allowed out of bed 3 days after cessation of bleeding and kept under close observation. About the 38th week of gestation an examination under general anaesthesia is carried out in the theatre which is set for C/S. The patient should be having blood transfusion at the time of the exam and another 1 or 2 pints of blood are kept handy in an ice box in the theatre ready for transfusion.

115. Equipment for resuscitation of a collapsed patient and asphyxiated baby, should also be ready.

116. Complications Haemorrhage 1.APH 2.PPH. PPH occurs because the lower uterine segment does not contract and retract efficiently. Puerperal sepsis as a result of haemorrhage, anaemia Renal failure Fetal hypoxia Still birth

117. VASA PRAEVIA A rare cause of APH occurs when there is a velamentous insertion of the cord and the vessels lie in the membranes covering the internal os infront of the presenting part. When the membranes rupture, these may be torn and vaginal bleeding occurs. The blood lost is fetal blood and the fetus may become exsanguinated. The fetus should be delivered as quickly as possible, probably by C/S.

118. HYPERTENSIVE DISORDERS OF PREGNANCY Hypertension is defined as a sustained elevation of blood pressure that is greater or equal to 140/90mmHg or an increase of 30mmHg systolic or 15mmHg diastolic taken on two different occasions. Women with a rise of 30mmHg systolic and 15mmHg diastolic need close observation, especially to rule out proteinuria and raised uric acid level.

119. INCIDENCE Hypertension is the commonest medical condition in pregnancy complicating approximately 10% of all pregnancies. In Ghana it has become a major cause of maternal mortalities especially in the major institutions. Hypertensive disorders are also an important cause of maternal morbidity.

120. CLASSIFICATION Cardiovascular alterations which occur as a result of pregnancy may induce hypertension in women who have been normotensive prior to pregnancy, or may aggravate existing hypertensive conditions. Hypertensive disorders include a variety of vascular disturbances such as:

121. 1. Gestational hypertension(Pregnancy Induced Hypertension – PIH) 2. Pre- eclampsia 3. HELLP syndrome 4. Eclampsia Chronic hypertension Pre- eclampsia superimposed on chronic hypertension

122. GESTATIONAL HYPERTENSION This is the development of hypertension without other signs of pre- eclampsia . It is diagnosed when, after resting, the blood pressure rises above 140/90mmHg on at least two occasions, no more than one week apart after the 20th week of pregnancy in a woman known to be normotensive.

123. PRE ECLAMPSIA This is diagnosed on the basis of hypertension with proteinuria. Proteinuria measured as > + on a dipstick. >0.3g/L of protein in a random clean catch specimen of urine (midstream). 0.3g protein per 24 hour collection of urine. In the absence of proteinuria, pre eclampsia is suspected when hypertension is accompanied by symptoms including:

124. Headache Blurred vision Abdominal/ Epigastric pain Altered biochemistry especially low platelet count and abnormal liver enzyme levels. That is ALT – Alanine aminotransferase AST – Aspartate aminotransferase GGT – Gamma glutamic transpeptidase

125. The above signs and symptoms together with blood pressure greater than 160mmHg systolic or greater than 110mmHg diastolic and proteinuria of two plus (++) or three plus (+++) on a dipstick demonstrate the more severe form of the disease (severe pre- eclampsia ).

126. ECLAMPSIA This is defined as a new onset of convulsions during pregnancy or post partum unrelated to other cerebral pathological conditions in a woman with pre eclampsia. CHRONIC HYPERTENSION This is known hypertension before pregnancy or a rise in blood pressure greater than 140/90mmHg before 20 weeks gestation and persisting 6 weeks after delivery.

127. PRE-ECLAMPSIA SUPERIMPOSED ON CHRONIC HYPERTENSION This may occur in women with pre existing hypertension (less than 20 weeks gestation) who develop:

128. 1. New proteinuria > 0.3g/24 hours urine collection 2. Sudden increases in pre existing hypertension and proteinuria. 3. Thrombocytopenia (platelet count less than 100x109/L) 4. Abnormal liver enzymes

129. ETIOLOGY The placenta is generally considered to be the primary cause of the hypertensive disorders of pregnancy because after delivery, the condition subsides. The pathophysiology of hypertensive disorders of pregnancy is poorly understood. It may be due to the following factors:

130. - Abnormal placentation - Maternal immune response to fetal antigens Abnormal Placentation In normal pregnancy, the decidua is invaded by the trophoblast during early pregnancy. The muscular walls and endothelium of the spiral arteries are eroded so that the villi can float in a pool of blood and have access to oxygen and nutrients.

131. A second phase of this invasive process occurs between 16 and 20 weeks of the spiral arteries. This leads to the loss of the musculoelastic tissue of the spiral arteries. The loss of this musculoelastic tissue results in dilated vessels that are not able to contract so they remain dilated. Thus a system of low pressure and high blood flow into the placental bed is produced with maximal placental perfusion.

132. . In pre- eclampsia , trophoblastic invasion of the spiral arteries is inhibited resulting in decreased placental perfusion because the vessels do not dilate but they are contracted which may lead to lack of oxygen and nutrients.

133. Maternal Immune Response The abnormal placentation is caused by a genetically predetermined maternal immune response to fetal antigens derived from the father and expressed in normal placental tissue. The maternal immune response triggers the release of one or more factors or substances that damage endothelial cells.

134. Endothelial cells from the endothelium which lines the blood vessels and serous cavities of the body. These cells play an important role in regulating capillary transport, controlling plasma volume and modulating vascular smooth muscle reactivity in response to various stimuli.

135. They also synthesize prostacyclin and nitrous oxide which are mediators in vasodilation and inhibit platelet aggregation, thus preventing blood clot formation. Damage to the endothelial cells will

136. 1. Reduce the production of prostacyclin and nitrous oxide. 2. Increase vascular sensitivity to angiotensin II – (control BIP and the excretion of salt and water from the body). 3. Activate the coagulation cascade and the production of thromboxane a potent vasoconstrictor.

137. The combined effects of these events will cause vasospasm and increased blood pressure, abnormal coagulation, thrombosis and increased permeability of the endothelium leading to: - Oedema - Proteinuria - Hypovolaemia

138. These are the characteristic features of pre – eclampsia which become manifest throughout the body resulting in pathological changes consistent with a multisystem disorder. Predisposing factors (conditions) - Primigravidae - Diabetes mellitus - Thrombophilia

139. - Previous history of hypertension - Multiple pregnancy - Hydatidiform mole (Gestational trophoblastic disease). Mild Pre- eclampsia – B/P greater or equal to 140/90 but not more than 159/109mmHg Severe pre- eclampsia – B/P = 160/110mmHg or more.

140. HELLP Syndrome – Haemolysis, Elevated Liver enzymes, Low Platelet count Signs of impending Eclampsia - Sharp rise in blood pressure - Diminished urinary output less than 30mls per hour (oliguria) - Increased proteinuria - Severe frontal headache which is persistent

141. - Drowsiness - Confusion - Flashes of light - Epigastric pain

142. Effects of Hypertensive Disorders on the mother (pathological changes) Pathological changes occur in the ff. The blood Coagulation system Kidneys Liver Brain Fetoplacental unit

143. THE ROLE OF THE NURSE IN ASSESSMENT AND DIAGNOSIS Hypertensive disorders are unlikely to be prevented, thus early detection and appropriate management can minimise the severity of the condition (prevention of onset of eclampsia). A high standard of ANC will contribute to the maintenance of optimum health.

144. The nurse is in a unique position to identify these women with a predisposition to pre – eclampsia. A comprehensive history taken at the first or booking visit will identify: a. Adverse social circumstances or poverty which could prevent the woman from attending ANC regularly

145. b. The mother’s age and parity c. Primipaternity and partner related factors d. A family history of hypertensive disorders e. A past history of pre – eclampsia f. The presence of underlying medical conditions eg renal disease, diabetes.

146. On subsequent visits, the midwife must note any other risk factors such as multiple pregnancy. Hypertension and proteinuria are assessed for at each visit (Diagnosed after 20 weeks, before 20 weeks chronic hypertension). At every visit, the B/P should be checked, urinalysis is done, weight is checked.

147. Oedema in non dependent anatomical areas such as the face, hands, lower abdomen, vulva and sacral areas is significant. NB B/P should not be taken immediately after a woman has experienced anxiety, pain, a period of exercise or has smoked. A ten minutes rest is needed. The woman should be sitting or lying left lateral not supine or right lateral.

148. Laboratory Tests Alterations in the haematological and biochemical parameters are indicative of pre- eclampsia . - Increased haemoglobin and haematocrit levels - Thrombocytopenia - Prolonged clotting times - Raised serum creatinine and urea levels

149. - Raised serum uric acid level - Abnormal liver function tests particularly raised transaminases.

150. MANAGEMENT During the antenatal period, the condition of the woman and her fetus has to be monitored closely to prevent the hypertensive disorder from worsening. Appropriate interventions and treatments are used when necessary. Care and management will vary depending on the degree of pre – eclampsia

151. REST The woman is advised to rest as much as possible and may be admitted to hospital to facilitate rest.

152. DIET A diet rich in protein, fiber and vitamins. Prophylactic fish oil – act as an antiplatelet agent. Calcium supplementation – good for women at high risk of developing hypertension in pregnancy. Vitamins C and E supplementation – decrease oxidative stress and improve vascular endothelial function thereby preventing the development of pre –eclampsia.

153. WEIGHT GAIN (Monitoring the weight useful for monitoring the progression of pre – eclampsia) A high initial BMI is a useful predictor of hypertension in pregnancy. BLOOD PRESSURE Monitored at every visit and four hourly if admitted.

154. URINALYSIS Urine is tested for protein at every visit, if protein is detected in a midstream specimen of urine, a 24 hour urine collection is done in order to determine renal function. The level of protein indicates the degree of vascular damage. Reduced kidney perfusion leads to reduced creatinine clearance and increased serum creatinine and uric acid.

155. ABDOMINAL EXAM Is carried out at every visit or daily if on admission. Tenderness or discomfort may indicate placental abruption. Upper abdominal pain is indicative of HELLP syndrome and fulminating (rapid onset) pre – eclampsia.

156. FETAL ASSESSMENT Fetal heart sounds are checked at every visit and daily on admission. The following can be done to determine fetal well being. - Kick count (kick chart) - CTG monitoring

157. - Serial ultrasound scan to check fetal growth - Assessment of liquor volume - Assessment of fetal breathing movement - Doppler flow studies to determine placental blood flow.

158. LABORATORY STUDIES It includes: Full blood count Platelet count Clotting time Urea, Electrolyte and creatinine levels Liver function test Albumin levels in urine

159. ANTIHYPERTENSIVE THERAPY Necessary to prevent increase in B/P, prevent development of severe hypertension. Reduce the risk of cerebral haemorrhage - Methyldopa - Beta blockers such as atenolol and labetanol - Nifedipine is used to treat severe hypertension in pregnancy.

160. - Antithrombotic agents (use of anticoagulants) Early activation of the clotting system may hasten the pathological changes of pre – eclampsia. Anticoagulants or antiplatelet agents are used to prevent early pathological changes and fetal growth restriction. Aspirin is thought to inhibit the production of the platelet aggregating agent thromboxane A2.

161. MANAGEMENT DURING LABOUR The nurse should remain with the woman throughout the course of labour as pre – eclampsia can suddenly worsen at any time. Maternal and fetal conditions should be monitored carefully. Any deviation should be noted and medical assistance sought.

162. Vital signs Blood pressure is checked ½ hourly, every 15 – 20 minutes in severe pre – eclampsia. The mean arterial pressure (MAP) i.e. the systolic blood pressure plus twice the diastolic blood pressure divided by three. If it exceeds 125 mmHg, hypertensive encephalopathy will occur. MAP reflects the systemic perfussion pressure, and therefore the

163. degree of hypovolaemia (manual measurement of diastolic pressure alone is a better indicator of the degree of hypertension). Pulse and respiration are recorded ½ hourly. Temperature is recorded hourly In severe pre – eclampsia, examination of the optic fundal can give an indication of cerebral oedema. Cerebral irritability can be assessed by the degree of hyperreflexia or the presence of clonus.

164. Fluid balance Because of the damaged blood vessels, IV fluids should be administered with care because it can result in circulatory overload, pulmonary oedema, adult respiratory distress syndrome and death. Recommended fluid intake in severe pre – eclampsia is 85mls / hour. Oxytocin should be administered with caution, as it has an antidiuretic effect. Urinary output should be monitored.

165. . Urine should be tested for protein, ketones and glucose every 4 hours In severe pre – eclampsia, a urinary catheter should be in situ and urine output measured hourly. A volume greater than 30mls/hour reflects adequate renal function.

166. Plasma volume Expansion Clear fluid will leak out and aggravate pre existing oedema. Therefore gelatine solutions such as Haemacel and Gelofusin may be used. These solutions increase the colloid osmotic pressure and pull fluid back into the circulation thereby reducing the oedema and increasing the blood volume.

167. Although women with pre – eclampsia have oedema, they are hypovolaemic (the blood volume is low). Pain Relief Pain should be relieved to help reduce the blood pressure. Epidural analgesia may be given.

168. Fetal Condition The fetal heart rate should be monitored every 30 minutes (½ hourly) In severe pre – eclampsia, ¼ hourly. Deviations from the normal should be reported and acted on:

169. Birth plan Towards the end of the first stage, the obstetrician and paediatrician should be notified. Vacuum extraction or forceps delivery may be performed. NB If the maternal or fetal condition deteriorates during the first stage, a C/S should be done to shorten the second stage. Baby will need resuscitation, so prepare .

170. Oxytocin is the preferred agent for the management of the third stage of labour. Ergometrine and syntometrine will cause peripheral vasoconstriction and increase hypertension. They should be used only if there is severe haemorrhage.

171. Management During The Immediate Post Partum Period The mother’s condition should be monitored every 15 minutes for the first 6 hours and then 4 hourly for the next 24 hours as there is still the potential danger of the mother developing eclampsia. The baby’s vital signs should also be monitored and should be kept warm. Breastfeeding should be initiated as soon as the condition of the baby and mother permits.

172. SIGNS OF IMPENDING ECLAMPSIA A sharp rise in blood pressure Diminished urinary output which is due to acute vasospasm. Increase in proteinuria Headache which is usually severe, persistent and frontal in location. Drowsiness or confusion due to cerebral oedema.

173. Visual disturbances such as blurring of vision or flashing of light due to retinal oedema. Epigastric pain which denotes liver oedema and impairment of liver function. Nausea and vomiting.

174. HELLP SYNDROME H – Haemolysis EL – Elevated Liver Enzymes (Liver transaminases – AST, ALT and GGT) LP – Low Platelet count It is a variant of the pre – eclampsia/eclampsia syndrome. It occurs between 32 to 34 weeks gestation. 30% of cases occur post partum.

175. SIGNS AND SYMPTOMS The woman complains of Malaise Epigastric or right upper quadrant pain Nausea and vomiting Hypertension and proteinuria may or may not be present.

176. Diagnosis/Investigation FBC Platelet count Liver Function Test Complications Subcapsular liver haematoma Rupture of the liver.

177. Patient will present with severe epigastric , neck and shoulder pain. Radiographic imaging of the liver will show the extent of liver damage. Surgical intervention or liver transplant will be required to prevent haemorrhagic shock and liver failure. Serious maternal morbidity and mortality may result from DIC, Acute Renal failure, pulmonary oedema. Baby is often small for gestational age and at risk of perinatal asphyxia.

178. Treatment If pregnancy is less than 34 weeks, conservative treatment is employed. Plasma volume expanders and antihypertensives are used. Corticosteroids are also given. Laboratory studies are done to assess improvement in condition In term pregnancy or if the maternal or fetal condition deteriorates immediate delivery by C/S is recommended.

179. ECLAMPSIA The new onset of convulsions during pregnancy or post partum unrelated to other cerebral pathological conditions, in a woman with pre – eclampsia Incidence In developing countries, it is more prevalent than in developed countries from 1:100 to 1:700 deliveries.

180. . Usually pre – eclampsia is diagnosed and treatment instituted to prevent eclampsia but occasionally pre – eclampsia is so rapid in onset and progress that eclampsia ensues before any action can be taken. In this case, pre – eclampsia is termed Fulminating.

181. CAUSE The cause is unknown but there is a link between the hypertension and cerebral disease – Hypertensive Encephalopathy

182. STAGES OF ECLAMPSIA AURA TONIC CLONIC COMA Sometimes the aura stage is very difficult to notice in the client unlike those with epilepsy.

183. CARE OF A WOMAN WITH ECLAMPSIA a. Doctor Call for help b. Nurses c. Others Prevent the mother from injury, clear and maintain the mother’s airway. This may be achieved by placing the mother in a semi prone position in order to facilitate the drainage of saliva and vomitus. Administer oxygen and prevent severe hypoxia.

184. The nurse must remain with the mother and provide assistance with medical treatment. The woman will need intensive care or high dependency care as she may remain comatous for a time following the seizure or may be heavily sedated.

185. Observation Check vital signs Pass catheter Urinalysis IV infusion (plasma volume expanders) Take blood for grouping and cross matching Monitor intake and output

186. Perform abdominal examination:- - Fundal height - Maturity - Presentation, contraction, fetal condition (fetal heart rate) Laboratory tests – clotting time Fits chart (parts of the body involved, duration).

187. Anticonvulsant therapy Magnesium sulphate Diazepam Phenytoin Diazepam is used to control other types of seizures and has a sedative effect. Phenytoin is effective in controlling convulsions and has no sedative effect

188. Magnesium sulphate is thought to aid vasodilation thereby reducing cerebral ischaemia. Mg So4 is administered intravenously according to the hospital’s protocol. Loading dose: 4 grams is given IV over 5 – 10 minutes then 10grams is given IM, 5 grams in each buttock, followed by a maintenance dose of 5g every 4 hours (in alternate buttock) until 24 hours following delivery or the last seizure

189. IV Normal saline is given. Recurrent seizures should be treated with a further bolus of 2 grams IV. Mg So4 has toxic effects. The following should be monitored hourly: - The deep tendon reflexes - Urine output - Respiratory rate (> 16 breaths/min) - The oxygen saturation level (should be > 95%) Calcium gluconate is the antidote for magnesium toxicity and should be readily available.

190. Antihypertensive therapy Antihypertensive therapy. IV hydralazine 5mg administered slowly and B/P monitored every 5 minutes until the diastolic pressure reaches 90mmHg. Labetelol may also be used. 20mg is given IV then 40mg after 10 minutes, 80mg after another 10 minutes then 80 mg (up to a cumulative dose of 300mg.

191. Birth plan The nurse must observe for periodic restlessness associated with uterine contractions which indicates that labour has begun. The woman’s partner should be kept informed and the nurse will need to give emotional support through this unexpected and anxious time. C/S would be done to expedite delivery as soon as possible – once the condition has been stabilized by the above measures.

192. Post natal care The woman needs intensive care. Parameters to monitor are: - A return to normal B/P - An increase in urine output - A reduction in oedema - A return to normal laboratory indices.

193. Thromboelastic stockings should be worn to prevent deep vein thrombosis. All the usual post partum care is given. As soon as the mother’s condition permits, she should see her baby. Complications Pulmonary oedema, Renal failure, Hepatic failure DIC, PPH, HELLP syndrome, Brain haemorrhage.

194. Effects of pre – eclampsia on the blood - Decrease in plasma colloid pressure and increase in oedema - Reduction in intravascular plasma causing hypovolaemia - Haemoconcentration - Congestion of lung with fluid, leading to development of pulmonary oedema. - Oxygenation impairment and occurance of cyanosis.

195. Effects of pre – eclampsia on the kidney - It leads to vasospasm of the afferent arterioles resulting in decreased renal blood flow. - Glomeruloendotheliosis (Glomerular endothelial damage) allows plasma protein in the form of albumin to filter into the urine producing protenuria - Renal damage is reflected by reduced creatinine clearance and increased serum creatinine and uric acid level - There is renal ischaemia which may result in oliguria.

196. Effects of pre – eclampsia on the coagulation system Endothelial damage leads to increased consumption of the clotting factors. Platelet consumption which produces thrombocytopenia and may be responsible for the development of Disseminated intravascular coagulation (DIC) which causes low platelet, prolonged prothrombin time and low fibrinogen level.

197. As the process progresses, fibrin and platelets are released leading to the formation of more blood clots in the system. As the small clots consume all the available coagulating platelets, normal coagulation is disrupted and abnormal bleeding occurs from the blood vessels and blood supply to many organs especially kidney, liver, brain and placenta is altered.

198. DIC: When there is damage to endothelial lining, blood clots are formed at areas of damage using the clotting factors. As this progresses, the clotting factors are used up leading to bleeding.

199. Effects on the brain 1. Hypertension combined with cerebrovascular endothelial dysfunction increases the permeability of the blood – brain barrier resulting in cerebral oedema characterized by the onset of severe headache, visual disturbances and convulsions

200. 2. When the mean arterial pressure exceeds 123mmHg, the autoregulation of cerebral flow is disrupted resulting in cerebral vasospasm and blood clot formation.

201. Effects on the Feto – placental unit - Ischaemia - Thrombosis and infarction in the capillaries of the chorionic villi. - Impaired hormonal output e.g. Human placental lactogen (HPL). A combination of these leads to preterm labour and birth. - Fetal hypoxia due to decreased blood flow. - Intrauterine growth retardation. - Intrauterine death.

202. CHRONIC HYPERTENSION This is known hypertension before pregnancy or a rise in blood pressure >140/90 mmHg before the 20th week of gestation and persisting 6 weeks after delivery. Causes It has two possible causes

203. 1. It may be a long standing problem, present before the beginning of the pregnancy e.g. essential hypertension which account for 5% of the causes of hypertension in pregnancy. 2. It may be secondary to existing medical problem such as renal disease, coarctation of the aorta, pheochromocytoma (tumour of adrenal medulla).

204. DIAGNOSIS 1. - A blood pressure of 140/90 mmHg or more on two occasions more than 24 hours apart during the first 20 weeks of pregnancy. 2. - History may reveal a known medical condition 3. - Women with chronic hypertension tend to be older, multiparous and have a family or personal history of hypertension.

205. 4. - Doctor’s physical examination may reveal effects of hypertension such as: - Retinopathy - Ischemic heart disease - Renal damage Renal function test may reveal normal serum urate level – (serum urate levels do not rise in chronic hypertension as they do in pre – eclampsia)

206. MANAGEMENT 1. Frequent antenatal visits are recommended in order to monitor the maternal condition. This includes blood pressure monitoring, urinalysis and blood test to measure haematocrit and renal function. 2. Antihypertensive Drug therapy, sedatives to reduce anxiety and help the woman to rest. 3. Monitoring fetal well being and placental function.

207. 4. If early delivery is deemed necessary induction of labour is preferred to C/S.

208. CORD PRESENTATION This occurs when the umbilical cord lies infront of the presenting part with the fetal membrane still intact. This is diagnosed on vaginal examination the intact membranes. It is however rarely detected. It may be associated with fetal bradycardia which occurs if the cord becomes compressed.

209. Management 1. The membranes should not be ruptured 2. Vaginal examination should be stopped to decrease the risk of rupturing the membranes 3. Seek medical aid (call for help)

210. 4. Monitor fetal heart rate (continuous monitoring may be employed) particularly during contractions. 5. Help the mother into a position that will decrease the likelihood of cord compression eg knee – chest position, exaggerated Sim’s position.

211. CORD PROLAPSE The cord lies infront of the presenting part and the fetal membranes are ruptured. Occult cord prolapsed is said to occur when the cord lies alongside the presenting part, but not infront of the presenting part.

212. Predisposing factors Any situation where the presenting part is neither well applied to the cervix nor well descended in the pelvis may make it possible for a loop of cord to slip down infront of the presenting part. Such situations include:

213. - High or ill–fitting presenting part - High parity - Prematurity - Malpresentation - Multiple pregnancy - Polyhydramnios

214. DIAGNOSIS It is made when the cord is felt below or beside the presenting part on vaginal examination. The cord is more commonly felt in the vagina or in cases where the presenting part is very high, it may be felt in the cervical os.

215. Whenever there are factors present that predispose to cord prolapsed, a vaginal examination should be performed immediately on spontaneous rupture of the membranes. A loop of cord may be visible at the vulva immediate Actions To Be Taken

216. 1. Call for assistance 2. Explain findings to the mother and relatives on emergency measures that will be needed 3. If an oxytocic drip is in progress it should be stopped. 4. Carry out vaginal examination and assess the degree of dilatation and identify the presenting part and descent. 5. Note the time 6. Handle the cord as little as possible (

217. 6. Handle the cord as little as possible (spasm of cord may occur through handling or due to reduction in temperature) 7. If the cord lies outside the vagina, then it should be gently replaced to maintain the temperature 8. Check fetal heart rate and record

218. 9. Relieve pressure on the cord. To do this, the nurse keeps her fingers in the vagina and especially during a contraction, holds the presenting part off the umbilical cord. 10. The mother is helped to change position so that her pelvic and buttocks are raised. 11. The knee – chest position causes the fetus to gravitate towards the diaphragm (fundus) relieving the compression on the cord

219. 12. The mother can be helped to lie on the left side with a wedge or pillow elevating her hips (exaggerated Sim’s position). 13. The foot of the bed may be raised. These measures needs to be maintained until the delivery of the baby, either vaginally or by cls . The risks to the fetus are: 1. Hypoxia

220. POSTPARTUM HAEMORRHAGE (PPH) Definition: Blood loss in excess of 500ml (excessive blood loss after delivery - 500mls or more ) after vaginal delivery and 1000mls or more after c/s. For clinical purposes Any blood loss with the potential to cause haemodynamic instability.

221. Incidence: About 11% of live deliveries. Bleeding is the leading cause of maternal death Types 2. Primary postpartum haemorrhage 3. Secondary postpartum haemorrhage

222. Aetiology /causes of PPH Tone - uterine atony Tissue – retained tissue/clots Trauma – laceration, rupture, inversion Thrombin – coagulation defects (coagulopathy)

223. Risk factors 1. Polydramnions , multiple gestation, macrosomia causing overdistension of the uterus 2. Rapid or prolonged labour, high parity causing uterine muscle exhaustion 3. Prolonged rupture of membranes causing intra amniotic infection 4. Fibroids, placenta praevia, uterine anomalies causing functional/anatomic disruption of the utrus

224. 5. Incomplete placenta, previous history of retained products, abnormal placenta causing retained products ( eg abnormal placentation, retained cotyledon succenturiate lobe). 6. Atonic utrus full bladder causing retained blood clots 7. Precipitous delivery, operative delivery causing laceration of the cervix, vagina or perineum

225. 8. Malposition, deep engagement causing extension, of incisions/lacerations at c/s 9. Previous uterine surgery causing uterine rupture. 10. High parity, fundal placenta causing uterine inversion 11. Hereditary coagulopathy, history of liver disease causing clotting problems 12. Bruising, elevated blood pressure, IUD and APH causing low platelet counts and DIC

226. 13. Previous/present deep vein thrombosis (DVT) treatment with anticoagulants causing clotting problems. 2/3 of women with PPH have no identifiable risk factors 90% if cases of PPH are due to uterine atony (atonic uterus) Obstetric haemorrhage is usually underestimated. PPH can lead to death within 2 hours after delivery because at term about 500 – 800mls of blood flow through the uterus per minute.

227. Diagnosis of PPH Consider risk factors Observe/measure blood loss Look for hidden blood loss in the uterus, vagina, broad ligament. (Ongoing trickling losses or continuous trickling of blood can become excessive.

228. Check vital signs – vital signs may appear stable despite significant blood loss rennin, ADH and catcholamines help maintain plasma volume, cardiac output and perfusion pressure. Hypotension and tachycardia are late indicators of blood loss in pregnancy.

229. Prevention of PPH ANC Comprehensive history taking to identify women at risk for management/referral. CHECK Hb , BF, sickling and stool for worm infestation. Do diet assessment and educate on diet Do blood group and Rehsus factor. If you detect anaemia, treat do more frequent Hb checks.

230. IPT – Give 3 doses of SP Educate on benefits of taking routine drugs regularly and prescribe enough routine drugs to last till next visit. Educate on personal and environmental hygiene and proper use of foot wear. Labour Monitor first stage and plot on partograph to prevent prolonged labour. Proper management of the second stage of labour

231. Recognise factors that cause delay in the second stage of labour such as: - Rigid perineum - Persistent occipito – posterior position - Deep transverse arrest - Abnormal presentation (breech presentation) - Uterine inertia (hypertonic or hypotonic uterus and act quickly to avoid undue delay.

232. Active management of the third stage of labour (AMTSL) Administer a uterus contracting drug ( uterotonic ) within one minute after birth. Apply controlled cord traction (CCT) and counter traction to the uterus. Massage the uterus through the abdomen after delivery of the placenta every 15 minutes for 2 hours.

233. 4th stage – monitor for any signs of bleeding put 20IU of syntocinan in 500mls of N/S 40dpm for 3 – 4 hours. Educate on personal hygiene with emphasis on perineal care, frequent changing of perineal pad to keep the place dry, cleaning the anal region towards the buttocks and hand washing with soap and water.

234. Benefits of active management of the 3rd stage of labour (AMTSL) Reduces incidence of PPH by up to 60%. Reduces the quantity of blood loss thereby decreasing incidence and severity of anaemia Reduce emergencies and related cost transport Reduce the use of blood transfusion

235. Management Be prepared - Anticipate problems - Be conversant with management protocol - Have a haemorrhage trolley or PPH set - Intrauterine tamponade pack. Haemorrhage trolley or PPH set should have the following:

236. 1. Oxytocics (oxytocin 10 IV IM, 20 IV/L Crystalloid IV; Misoprostol 800 to 1000 mcg; Ergometrine 0.5mg 2. IV infusions and wide bore canula 3. Sutures 4. Sterile packs with - several syringes - sterile vaginal examination pack - several sterile sponge forceps - diagrams/instructions for various tamponade techniques/compression sutures.

237. 1. Oxytocics (oxytocin 10 IV IM, 20 IV/L Crystalloid IV; Misoprostol 800 to 1000 mcg; Ergometrine 0.5mg 2. IV infusions and wide bore canula 3. Sutures 4. Sterile packs with - several syringes - sterile vaginal examination pack - several sterile sponge forceps - diagrams/instructions for various tamponade techniques/compression sutures.

238. For the high risk mother Check the current FBC/ Hb , clotting time etc in labour Get a good IV access Cross match blood or group and save Check for availability of blood/specific blood products Call for help or inform senior personnel on duty Transfer to a unit better equipped for the possible complication.

239. Do active management of the third stage of labour (AMTSL) Give syntocinon infusion post delivery for 2 – 4 hours Suture lacerations early Watch or monitor the 4th stage properly. For a sudden onset of PPH Do a quick assessment – Remember your ABCS. Act quickly or speedily Get help, shout for help (many hands on deck) massage uterus to contract of placenta delivered Resuscitate

240. Place 1 or 2 large bore periphearal intravenous canula (gauge 14 or 16) Intiate rapid crystalloid infusion (RL or N/S) Elevate and pressurize fluids if required Infuse 3x the estimated blood loss. Colloids infuse 1x the estimated blood loss Take blood for laboratory studies – clotting time, grouping and x – match etc.

241. Do a bedside clotting test if indicated. Decide early if surgery is indicated Inform anaesthetist , doctor, theatre staff early or immediately. Test results or blood should not delay surgery. Rapid fluid administration is more important than the choice of fluid or immediate haemodynamic monitoring. In Africa patients die because they were not resuscitated aggressively enough with IV fluids

242. Diagnose the cause and treat quickly (speedily) If it is due to uterine atony : - if placneta is delivered: Rub up a contraction (rub the uterus to contract) Pass Foleys catheter Give 10 IV, then 20 IU in 500mls N/Saline at 30 drops per minute for 3 – 4 hours. Ergometrine 0.5mg can be given IM

243. Prostaglandin F2x can also be given Empty clots from the uterus Continue rubbing the uterus Continue resuscitation urine output Record IV fluid and an intake and output chart Do a more accurate measurement of the amount of blood loss. Tilt the head of the mother downwards Administer oxygen by face mask

244. Cover the patient to keep her warm. Bimanual uterine compression – unternal and A ortic compression Condom catheter can also be employed Surgical option that can be employed are: - hypogastric artery ligation - B – Lynch brace - Uterine artery ligation - Total/subtotal hysterectomy - Embolisation of uterine vessels

245. If it is due to retained placenta: Repeat delivery of placenta by CCT Give a strong analgesic and muscle relaxant and perform manual removal of placenta if not delivered by CCT Give injection oxytocin IV Send blood for x – match and set up IV fluid

246. Retained placenta can be caused by - Previous history - Uterine inertia – mismanagement of the third stage of labour - Full bladder - Presence of constriction ring - Morbidly adherent placenta

247. If it is due to trauma ( ie bleeding with a firmly contracted uterus) Explore the lower genital tract under a good source of light Give analgesia or local anaesthesia and perform appropriate surgical repair - Cervical tear – repair - Perineal tears – repair 1st and 2nd degree tears. 3rd and 4th tears should be repaired in theatre.

248. Repair episiotomy If bleeding is due to uterine rupture Repair with/without BTL Total/subtotal hysterectomy If it is doe to coagulopathy (there will be bleeding in the presence of a firmly contracted uterus) Do a bedside clotting test abnormal if not clotted within 7 – 10 minutes or clot is unstable Transfuse with fresh blood and other blood products Treat the underlying cause.

249. SECONDARY PPH Causes: - Retained products of conception - Puerperal sepsis – SVD, C/S - Infected submucosal fibroid Treatment - Resuscitate patient - Administer antibiotics - Exploration of the uterus – EOU - Lapanotomy - Hysterectomy

250. SHOCK Shock is a complex syndrome involving a reduction in blood flow to the tissue. It may resul in irreversible organ damage and progressive collapse of the circulatory system. If not treated it will result in death Shock can be classified as follows:

251. 1. Hypovolaemic – this is the result of a reduction in intravascular volume such as in severe obstetric haemorrhage (PPH,APH) 2. Cardiogenic shock 3. Neurogenic shock 4. Septic or toxic shock – occurs due to severe generalised infection ( eg septic abortion) 5. Anaphylactic shock Hypovolaemic shock and septic shock can develop as a result of childbirth as in PPH, puerperal sepsis

252. Stages of shock 1. Initial stage 2. Compensatory stage 3. Progressive stage 4. Irreversible stage – multisystem failure and cell destruction are irreparable. Death ensues Effect of shock on organs and systems Shock affects the brain, lungs, kidneys, GIT and liver

253. Management of Hypovolaemic shock. The patient will need urgent resuscitation The patient is to: 1. Call for help 2. Maintain patent airway – turn onto her side and give 40% o2 at a rate of 4 – 6 L/min. If unconscious insert an airway 3. Replace fluid loss – gain venous access and two wide – bore connulae . Immediate rapid infusion of fluid is needed to correct loss.

254. 4. Keep the woman warm but not overwarmed or warmed too quickly, as this will cause peripheral vasodilatation and result in hypotention . 5. Arrest for coagulopathy and correct 6. Manage the underlying cause 7. Observation - Assess level of consciousness. Any signs of restlessness or confusion should be noted.

255. - Assess respiratory rate, depth and pattern. Humidified oxygen should be used if oxygen therapy is prolonged. - Monitor blood pressure continuously or at least every 30 minutes. Take not of any drop in B/P - Check the pulse every 15 minutes - Measure urine output hourly, using an indwelling catheter

256. - Check termperature hourly - Observe for further bleeding, including lochia or oozing from a wound or puncture sites - Take blood for haemoglobin and haematocrit to assess the degree of blood loss.