Pregnancy induced hypertension(PIH).pptx

pregnancy induced hypertension is high blood pressure that develops during pregnancy, usually after the 20th week. it can lead to complications like pre- eclampsia and eclampsia affecting both mother and baby.

1. PRESENTATION ON PREGNANCY INDUCED HYPERTENSION PRESENTED BY MAHPARA RASHEED MSC. NURSING 2 nd YEAR

2. INTRODUCTION Hypertension is one of the common medical complications of pregnancy and contributes significantly to maternal and perinatal morbidity and mortality.

3. DISORDER DEFINITION Hypertension BP > 140/90 mmHg measured two times with at least 4- hour interval but not more than 7 days apart. Proteinuria Urinary excretion of > 0.3 g protein/24 hours specimen or 0.1g/l Gestational hypertension BP > 140/90 mmHg for the first time in pregnancy after 20 weeks, without proteinuria. Pre- eclampsia Gestational hypertension with proteinuria. Eclampsia Women with pre- eclampsia complicated with grand mal seizures and/or coma. HEELP syndrome Hemolysis (H) Elevated liver enzymes(EL) Low platelet (LP) count. Chronic hypertension Known hypertension before pregnancy or hypertension diagnosed first time before 20 weeks of pregnancy. Superimposed pre- eclampsia or eclampsia Occurrence of new onset of proteinuria in women with chronic hypertension. Chronic hypertension with superimposed pre- eclampsia and eclampsia . New onset of proteinuria > 0.5g/24 hours specimen. Aggrevation of hypertension. Development of HELLP syndrome Development of headache scotoma , epigastric pain.

4. PRE-ECLAMPSIA It is a multisystem disorder of unknown etiology characterized by development of hypertension to the extent of 140/90 mmHg or more with proteinuria after 20 th week in a previously normotensive and non proteinuric woman.

5. INCIDENCE About 5-8 % of all pregnancies are complicated by hypertension and of these pre- eclampsia accounts for 80%. It occurs more frequently in young primigravida and in mothers over 35 years of age.

6. CAUSES/RISK FACTORS Primigravida - young or elderly(first time exposure to chorionic villi) Family history- Hypertension, pre- eclampsia Placental abnormalities obesity: BMI> 35 Kg/m2 Pre-existing vascular disease

7. CLINICAL CLASSIFICATION OF PRE-ECLAMPSIA

8. MILD PRE-ECLAMPSIA BP more than 140/90 mmHg, but less than 160/110 mmHg without significant proteinuria on two occasions of 6 hrs apart.

9. SEVERE PRE-ECLAMPSIA BP exceeds 160/110 mmHg Proteinuria(75g/day ) Oliguria(< 400 ml/24h) Platelet count less than 100,000/mm3 Elevated liver enzymes Cerebral or visual disturbances Persistent severe epigastric pain Retinal hemorrhages IURG Pulmonary edema Serum creatinine >1.1mg/dl

10. CLINICAL FEATURES

11. MILD SYMPTOMS Slight swelling over the ankles which persists on rising from the bed in the morning or tightness of the ring on the finger is the early manifestation of edema due to pre- eclampsia . Gradually, the swelling may extend to the face, abdominal wall, vulva and even the whole body.

12. ALARMING SYMPTOMS Headache- either located over the occipital or frontal region. Disturbed sleep Diminished urinary output Epigastric pain- associated with vomiting, at times coffee color , is due to hemorrhage gastritis Eye-symptoms- Blurring, scotomata

13. SIGNS Abnormal weight gain Rise of BP Edema Pulmonary edema - due to leaky capillaries and low oncotic pressure. Abdominal examination may reveal evidences of chronic placental insufficiency, such as scanty liquor or growth retardation of the fetus .

14. INVESTIGATIONS RENAL Urine quantity reduced Proteinuria of > 300 mg/24 h Urine dipstick> 1+ BLOOD Protein/ creatinine ratio> 0.3 Serum creatinine > 1.2 mg/dl Serum uric acid> 5.6 mg/dl Platelet count< 100,000/mm3 Elevated PT or PPT Decreased fibrinogen

15. LIVER ENZYME Serum AST>70U/L Antenatal fetal monitoring Opthalmoscopic examination

16. MANAGEMENT

17. REST The women should in bed preferably in left lateral position as much as possible to lessen the effects of vena cava compression. Rest is to be continued until all the pre- eclamptic manifestations subside. Rest increases the renal blood flow causing increased diuresis, increases uterine blood flow causing improved placental perfusion and reduces the BP.

18. DIET The diet should contain adequate amount of daily protein( about 100 g) Usual salt intake is permitted. Fluids need not be restricted. Total calorie app. 1600 cal /day

19. DIURETICS Furosemide(Lasix) 40 mg, given orally after breakfast for 5 days in a week In acute condition, iv route is preferred .

20. ANTIHYPERTENSIVES Laetalol 100 mg tid or qid Nifedipine 10- 20 mg bid Methyl- dopa 250-500 mg tid or qid Hydralazine 10-25 mg bid

21. HYPERTENSIVE CRISIS Labetalol 10-20 mg I/V every 10 minute Hydralazine 5 mg I/V every 30 minute Nifedipine 10 -20 mg oral, can be repeated in 30 minute Nitroglycerin 5ug/minute I/V

22. COMPLICATIONS

23. IMMEDIATE(MATERNAL) DURING PREGNANCY Eclampsia (2%) Accidental hemorrhage Oliguria and anuria Dimness of vision and even blindness Preterm labor HELLP syndrome Cerebral hemorrhage Acute respiratory distress

24. DURING LABOR Eclampsia PPH

25. DURING PUERPERIUM Eclampsia occurs within 48 hours. Shock sepsis

26. FETAL IUD- due to spasm of utero placental circulation leading to accidental hemorrhage or acute red infarction. IUGR- Due to chronic placental insufficiency Asphyxia Pre-maturity- either due to spontaneous preterm onset of labor or due to preterm induction.

27. REMOTE Residual hypertension( it may persist even after 6 months following delivery in about 50% cases). Recurrent pre- eclampsia Chronic renal disease Risk of placental abruption for those women with pre- eclampsia ranges from 5 to 20% and women with HELLP syndrome, the risk of pre- eclampsia in subsequent pregnancy is about 20%

28. ECLAMPSIA The term eclampsia is derived from a Greek word, meaning like a flash of lightening. It may occur quite abruptly, without any warning manifestations.

29. DEFINITION Pre- eclampsia when complicated with convulsion and/or coma is called eclampsia .

30. INCIDENCE The incidence varies from country to country and even between different zones of the same country. The hospital incidence of India ranges from 1 in 500 to 1 in 30. It is more common in primigravida (75%), five times more common in twins than in singleton pregnancies and occurs between the 36 th week and term in more than 50% cases.

31. PATHOPHYSIOLOGY Since eclampsia is a severe form of pre- eclampsia , the histopathological and biochemical changes are similar; although, intensified than those of C pre- eclampsia as already described.

32. CAUSES OF CONVULSION Anoxia spasm of the cerebral vessels → increased cerebral vascular resistance → fall in cerebral oxygen consumption → anoxia , Cerebral edema may contribute to irritation , Cerebral dysrhythmia increases following anoxia or edema . Excessive release of excitatory neurotransmitters (glutamate ). Loss of cerebrovascular autoregulation with forced dilatation and vasospasm

33. ONSET OF FITS Fits occur more commonly in the third trimester (> 50%). On rare occasions, convulsion may occur in early months as in hydatidiform mole . Antepartum (50%): Fits occur before the onset of labor. More often, labor starts soon after and at times, it is impossible to differentiate it from intrapartum ones . Intrapartum (30%): Fits occur for the first time during labor . Postpartum (20%): Fits occur for the first time in puerperium , usually within 48-72 hours of delivery. Fits occurring beyond 48 hours but less than 4 weeks after delivery is accepted as late postpartum eclampsia .

34. CLINICAL FEATURES

35. PREMONITORY STAGE The patient becomes unconscious. There is twitching of the muscles of the face, tongue and limbs, Eyeballs roll or are turned to one side and become fixed. This stage lasts for about 30 seconds .

36. TONIC STAGE The whole body goes into a tonic spasm- the trunk- opisthotonus , limbs are flexed and hands clenched. Respiration ceases and the tongue protrudes between the teeth. Cyanosis appears. Eyeballs become fixed . This stage lasts for about 30 seconds.

37. CLONIC STAGE All the voluntary muscles undergo alternate contraction and relaxation. The twitchings start in the face then involve one side of the extremities and ultimately the whole body is involved in the convulsion. Biting of the tongue occurs. Breathing is stertorous and blood stained frothy secretions fill the mouth; cyanosis gradually disappears. This stage lasts for 1-4 minutes.

38. STAGE OF COMA Following the fit, the patient passes on to the stage of coma. It may last for a brief period or in others deep coma persists till another convulsion. On occasion, the patient appears to be in a confused state following the fit and fails to remember the happenings. Rarely, the coma occurs without prior convulsion.

39. DIFFERENTIAL DIAGNOSIS The diseases, which are associated with convulsions and/or coma are to be borne in mind while arriving at the diagnosis of eclampsia . Such diseases are: Epilepsy Encephalitis Meningitis Puerperial cerebral thrombosis Intracranial tumors Absence of previous history of convulsion with presence of edema , hypertension and proteinuria along with fits or coma during pregnancy or soon after, points to the diagnosis of eclampsia . In doubtful cases, it is desirable to place the patient in the obstetric unit for observation until the final diagnosis is made.

40. MANAGEMENT The patient, if at home or in the peripheral health centers, should be shifted urgently to the referral hospitals. The patient must be heavily sedated before moving her to the hospital. The aims of immediate management in the hospital are to : Clear and maintain the airway Prevent hypoxia Prevent injury Arrest convulsions Effect delivery in 6-8 hours.

41. The midwife must remain with the mother constantly. In the first instance, all effort is devoted to the preservation of the mother's life : The patient should be placed in a railed cot in an isolated room, protected from noxious stimuli, which might provoke further fits. The patient is to be positioned in semiprone position in order to facilitate drainage of saliva and vomit. Side lying position helps to minimize vena caval compression. If the patient is unconscious, the position should be changed at intervals to prevent hypostatic pneumonia and bedsore. Airway is maintained and oxygen administered to prevent severe hypoxia . Detailed history is to be taken from the relatives relevant to the diagnosis of eclampsia -duration of pregnancy, number of fits and the medications administered outside . After the patient is properly sedated, thorough, but quick general, abdominal and vaginal examinations are done. A self-retaining catheter is introduced and the urine is tested for protein. Continuous drainage is established for measurement of the urinary output, periodic urinary analysis and for prevention of soiling of the bed due to incontinence likely to occur during fits.

42. Vital signs check (pulse, respiration and blood pressure) is to be done at every 30 minutes and recorded. Progress of labor and output is to be noted hourly. must be monitored. Urinary Fluid balance: Crystalloid solution (Ringer's lactate) is started as a first choice. Total fluids should not exceed the previous 24 hours urinary output plus 1,000 mL (insensible loss through lungs and skin). Normally, it should not exceed 2 L in 24 hours. In preeclampsia and eclampsia , although there is hypovolemia , the tissues are overloaded . Anticonvulsant therapy is given to control the fit and to prevent its recurrence. Magnesium sulfate is the drug of choice. It reduces motor end-plate sensitivity to acetylcholine and thereby reduces neuromuscular irritability. Magnesium sulfate induces cerebral vasodilation, dilates uterine arteries and inhibits platelet activation. It has no detrimental effects on the neonate within therapeutic level.

43. ADMINISTRATION OF MAGNESIUM SULPHATE REGIMEN LOADING DOSE MAINTENANCE DOSE Intramuscular(Pritchard) 4 g (20% solution) IV over 3-5 minutes followed by 10 g (50%) , deep IM 5g in each buttock) 5 g (50%) IM 4 hourly in alternate buttock. Intravenous ( Zuspan or Sibai ) 4-6 g IV slow over 15-20 minute 1-2 g/h IV infusion

44. ANTIHYPERTENSIVES AND DIURETICS In spite of anticonvulsant and sedative regimen, if blood pressure remains more than 160/110 mm Hg, antihypertensive drugs are administered. Hydralazine 5mg IV is given slowly and repeated after 20 minutes with 10 mg, if there is no response. The blood pressure should be monitored at every 5 minutes. Hydralazine is repeated whenever the diastolic pressure rises to 110mmHg, Alternatively, labetalol is given by slow IV route 20 mg/h smooth control of blood pressure. Presence of pulmonary edema requires diuretics. In such cases, frusemide is administered in doses of 20-40 mg intravenously and repeated at intervals .

45. ROLE OF MIDWIFE The woman should be placed in a sound protected room to minimize auditory stimulation . Eye pads to be applied to minimize optic stimulation The room should be well-lighted so as not to miss the development of cyanosis . 4 . Bed railings to be padded in order to minimize physical injury during convulsion . 5 . Patient to be placed in semiprone position and the position to be changed at every 2 hours, if the patient is heavily sedated or in deep coma to avoid hypostatic pneumonia and bedsores . 5 . Keep Foley's catheter in the urinary bladder and make chart of urinary output every hour . Minimal handling and stimulation in order to reduce the risk of occurrence of another convulsion. Maintain an IV line patent preferably in a central vein. Keep a tracheotomy tray available . Apply a thromboelastic stocking to prevent deep vein thrombosis.

46. MANAGEMENT DURING A FIT In the premonitory state, a mouth gag is to be placed in between the teeth to prevent tongue bite and should be removed after the clonic phase is over . The air passage is to be cleared off the mucus with a mucus sucker after convulsion . The patient's head is to be turned to one side and the pillow taken off. Raising the foot end facilitates postural drainage of the upper respiratory Oxygen is to be given until cyanosis subsides,

47. COMPLICATIONS OF ECLAMPSIA Injuries: Tongue bite, injuries due to falling out of bed . Cardiovascular : Vasospasm, pulmonary embolism Renal : Oliguria, renal failure Hematological : Hypovolemia , hemoconcentration , thrombocytopenia, DIC Hepatic : Subcapsular hematoma, hepatic necrosis Respiratory : Pneumonia (aspiration, hypostatic or infective) Sensory: Disturbed vision due to retinal edema or detachment (usually reversible ) Puerperal : Sepsis, psychosis Fetal : Placental abruption, intrauterine growth retardation, fetal distress, intrauterine death.

48. MORTALITY Maternal mortality is very high in India and varies from 20 to 30%, and more in rural hospitals. Causes for maternal death are : Cardiac failure Pulmonary edema Aspiration and/or septic pneumonia Cerebral hemorrhage Anuria Pulmonary embolism Postpartum shock Puerperal sepsis . Perinatal mortality is very high to the extent of abo30-50%. The causes are : Prematurity Intrauterine asphyxia due to placental insufficiency Effects of drugs used to control convulsions Trauma during operative delivery.

49. BIBLIOGRAPHY Annamma Jacob A comprehensive textbook of Midwifery& Gynecological Nursing 5 rd edition . Jaypee Brothers Medical publisherspage no.249-260 D.C.Dutta’s "Textbooks of Obstetrics" 9 th edition Jaypee brothers page no.207-227 A.K Debdas "Drug handbook in Obstetrics”,3’ d edition.Jaypee brothers and medical publishers private limited, New Delhi. wolter Kluwer “Drug handbook"32 edition.lippincot . www.medicine.tcd.ie/ pharmacoIogy therapeutics/ Obs&G NET REFRENCES Wikieducator.org/antepartum hemorrhage   Britanica.com/topic/PIH Ncbi.nlm.nih.gov/PubMed Resources.intensescholl.com JOURNAL REFERENCE TNNMC Journal obstetrics and gynecology , Jan-June 13, VOL-1, Page No.11-14 Journal of obstetrics and gynecology , Feb Vol.46, Page No.75-76