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PRE ECLAMPSIA
By Ruth
DESCRIPTION
ī‚´ It’s among the hypertension disorders and occurs only in pregnancy
ī‚´ It is a disorder of widespread vascular endothelial malfunction and vasospasm that
occurs after 20 wks gestation and can present as late as 4-6 wks postpartum
ī‚´ It’s characterized basically by hypertension and proteinuria with or without
pathological edema
ī‚´ PET occurs in 3% of all pregnancies and > 10% of women develop this in their 1st
pregnancy
INCIDENCE
ī‚§ Global incidence is estimated at 5-14% of all pregnancies 10% of women develop
this in their 1st pregnancy
ī‚§ In developing countries the hypertensive disorders are the second most common
obstetrical cause of stillbirths and early neonatal deaths
ī‚§ In Kenya pre-eclampsia is the 3rd leading pregnancy-related cause of death (1st-
hemorrhage,2nd sepsis)
ī‚§ Pre-eclampsia is the cause of estimated 790 maternal deaths per 100,000 live births
accounting for 23.6%
PREDISPOSING FACTORS
ī‚´ Pre pregnancy hypertension also referred to as existing or chronic
hypertension(essential hypertension) before conception, because of damage of the
various endothelium.
ī‚´ Previous history of pre-eclampsia, because of probability of re-occurrence.
ī‚´ Family history of pre-eclampsia mostly within her nuclear family of origin.
ī‚´ Polyhygramnious
ī‚´ Pre-existing medical conditions e.g. Renal diseases due to high release of angiotensin
II.
ī‚´ Pre-existing Diabetes mellitus due to endothelial cells dysfunction and also large
placental mass.
ī‚´ Multiple pregnancy, large placental mass hence possibility vasoconstriction.
ī‚´ Hydatidform mole.
ī‚´ Maternal age below 20 years and above 35 years. Low age has negative impact on
pregnancy, while high age there is possibility of chronic HTN
Contâ€Ļ
ī‚´ Being a primigravida because of the maternal immune response to fetal antigen from
the father.
ī‚´ Change of male partner(First pregnancy from a new partner)-
The fetal antigen from the sperm sensitizes the production of antibodies by the maternal
body hence endothelial cells dysfunction leading to high sensitivity to angiotensin II=
HTN.
ī‚´ Pregnancy after assisted reproductive technology
ī‚´ Obesity
ī‚´ Women from low social economic status-start clinic late
Aetiology
ī‚´ Development of pre-eclampsia basically occurs in two stages namely:
STAGE I
ī‚´ Early in pregnancy as the decidua gets invaded by the syncytiotrophoblast for
implantation to occur .
ī‚´ The erosion of the muscular wall & endothelium of the spinal arteries is abnormal.
Finally the placenta is not appropriately supplied by oxygen though no features are
detected clinically.
STAGE II
ī‚´ Occurs between 16th-20th week the oxidatively stressed [inadequately oxygen
supplied placenta ] placenta, releases factors leading to damage of endothelial
cells which form endothelium ,in the maternal circulation.
īƒŧ Eventually the endothelial cells dysfunction and maternal systemic inflammatory
response lead to clinical features of pre-eclampsia
Clinical features
Cardinal signs
1. High blood pressure- Bp reading are
140/90 mmhg & above, taken on two
consecutive occasions, at least 2- 4 hours
apart
2. Proteinuria- Signifying renal damage
3. Edema:- Initially of ankles, later fingers, face
& legs.
īƒ˜ Finally becomes generalized edema to
include abdomen, sacral region & vulva,
results from severe fluid retention
Signs of impending/severe
pre-eclampsia
ī‚´ A sharp rise in blood pressure
ī‚´ Diminished urinary output(Oliguria)
ī‚´ Increased proteinuria on urine testing
ī‚´ Severe persistence headache usually frontal
or occipital due to increased intracranial
pressure
ī‚´ Drowsiness or confusion
ī‚´ Visual disturbances e.g. Blurred vision, flash
light and double vision. Sometimes
temporary blindness
ī‚´ Nausea and vomiting
ī‚´ Epigastric pain
DIAGNOSIS OF PRE-ECLAMPSIA
NB//
īƒ˜ The symptoms are rarely experienced by the mother until the disease have reached an advanced state
īƒ˜ Diagnosis is based on 3 cardinal signs;
1. HIGH BLOOD PRESSURE
ī‚§ Increase in diastolic pressure of 15-20mmhg above the mothers normal diastolic pressure or increase above
90mmhg on 2 or more occasions
2.PROTENURIA
ī‚§ Presence of proteins in urine in absence of UTI is diagnostic
ī‚§ The amount of protein in urine indicates the severity of pre-eclampsia
3.OEDEMA
â€ĸ It is generalized and doesn’t disappear on rest
ī‚´ Indicates high rate of fluid retention
ī‚´ Most affected areas are:- legs, face, hands, abdomen, sacral & vulva.
Lab tests
ī‚´ Urinalysis
ī‚´ Increased hemoglobin & haematocrite level.
ī‚´ Thrombocytopenia.
ī‚´ Prolonged clotting time due to over consumption of fibrinogen, since there is high
release of thromboplastin from damaged blood vessels.
ī‚´ High serum creatinine levels (>90 mmol/L) & urea levels due to poor blood flow to
the kidneys.
ī‚´ Increased serum uric acid level.
ī‚´ Abnormal liver function test results.
Pathophysiology
ī‚´ Refers to pathological changes brought about by severe state of pre-eclampsia
leading to multisystem disorders [effects].
1.CARDIOVASCULAR
īļ General vasoconstriction leads to:
ī‚´ Enlargement of the heart as it attempts to counteract the increased peripheral
resistance.
ī‚´ General oedema, due to increased capillary permeability & loss of plasma proteins.
ī‚´ Increased coagulation activation due to damage of blood vessels & other tissues
hence high probability of DIC.
2.RENAL
īļ Reduced blood supply makes the afferent arterioles go into vasospasm leading to
damage of glomerular filtering bed hence:
ī‚´ Proteinuria.
ī‚´ Reduced creatinine clearance & urea excretion.
īƒŧ Therefore serum creatinine & uric acid levels increases.
ī‚´ Oliguria:- urinary output ranges between 400-500ml in 24hrs.
3.RESPIRATORY
ī‚´ Pulmonary oedema due to damage of blood vessels & low osmotic pressure.
ī‚´ Cyanosis , because of impaired oxygen supply.
Contâ€Ļ
Contâ€Ļ
4.GASTRO-INTESTINAL
ī‚´ Inadequate perfusion leads to oedema of the liver particularly, hence:
īƒŧ Epigastric pain.
īƒŧ Intracapsular hemorrhage.
īƒŧ Altered liver function test results.
īƒŧ Sometime jaundice.
Contâ€Ļ
5.CENTRAL NERVOUS SYTEM
īļ Hypertension and cerebrovascular endotherial dysfunction increases the blood-
brain barrier permeability leading to cerebral oedema and microhaemorrhage.
ī‚´ Generally leads to:-
īƒŧ Headaches
īƒŧ Visual disturbances.
īƒŧ Cerebral thrombosis because of fibrin & platelets deposition hence postpartum
eclampsia.
īƒŧ Convulsions.
Contâ€Ļ
6.REPRODUCTION SYSTEM
ī‚´ Reduced blood supply to placental tissues and increased pressure within the
vessels at the placental leads to:
īƒ˜ Infarcts formation, hence intrauterine growth restricts.
īƒ˜ Impaired hormonal production , affects fetal survival hence premature labour
=early birth.
īƒ˜ Placental abruption, some vessels burst at the placental bed leading to APH.
Classification of Pre-eclampsia
1. MILD
īļ Characterized by:-
ī‚´ BP reading of 140/90mmhg where;
ī‚´Systolic ranges btwn 140-149 mmHg
ī‚´Diastolic ranges btwn 90-99 mmHg
ī‚´ Protenuria ranges between trace to1+.It is below 0.5gms/1lt
ī‚´ Oedema, marked on the ankles, feet and sometimes pretibial
region.
ī‚´ No complains are presented, features are noted (elicited) during a
routine antenatal service.
ī‚´ However close follow is important.
Contâ€Ļ
2. MODERATE
ī‚´ Marked rise in BP of both systolic and diastolic
ī‚´ BP readings where Bp 140/100-160/110;
ī‚´ Systolic ranges btwn 140-160 mmHg
ī‚´ Diastolic ranges btwn 100-110 mmHg
īƒŧ Specifically rise in both systolic & diastolic pressure with about 20mmhg
is noted.
ī‚´ Proteinuria ranges between 1+ to 2+(above 0.5 gms/lt)
ī‚´ Edema is marked on legs, fingers and face hence denoted as (++)
ī‚´ Mother aware of the symptoms.
Contâ€Ļ
3. SEVERE
ī‚´ BP is 160/110mmHg or higher where;
ī‚´Systolic is > 160 mmHg
ī‚´Diastolic is â‰Ĩ110 mmHg
ī‚´ Oedema is gross(generalized), i.e. involves also, abdomen,
sacral region & sometimes vulva.
ī‚´ Proteinuria 2+ and above (3+)(0ver 1 gm/lt)
ī‚´ Presents with various impending signs as per clinical
features e.g. headache and blurred vision
Specific management
ī‚´ Provide rest and a quiet environment hence control BP.
ī‚´ Monitor disease process and take appropriate interventions as necessary.
ī‚´ Prolong pregnancy hence improve the survival rate of the fetus while also safeguarding
maternal life
ANTENATALLY
MILD PET
īļ Closely monitor noted signs through weekly ANC and advise on:
ī‚´ Bed rest at least 12-24 hours
ī‚´ Sleep in lateral position to improve renal and placental blood supply
ī‚´ Administer sedatives e.g. phenobarbitone 30mg every 8 hourly or valium 5mg nocte to
ensure rest and sleep
ī‚´ Administer antihypertensive e.g. Aldomet 250-500mg TDS or nifedipine 20mg BD
ī‚´ Balanced diet with extra-proteins, high fiber and low in salt and carbohydrates
ī‚´ Monitor fetal kicks and report if low or absent
ī‚´ Need of having somebody to assist in domestic work
Contâ€Ļ
MODERATE
ī‚´ Requires immediate admission to hospital.
ī‚´ Inform the doctor.
ī‚´ Nursed in a quiet area, preferably dim lit to facilitate rest & sleep.
īƒŧ Control visitors
īƒŧ Position-patient nursed in sitting up or left lateral position(supine)
ī‚´ Closely monitor fetal and maternal condition through:
īƒ˜ Fetal :- 4hrly F.H.S, fetal kick chart, ultrasound to monitor fetal growth, particularly
where control is not being achieved, cardiotocograph for sign of fetal hypoxia.
īƒ˜ Maternal:- 4 hourly vital signs especially BP.
īƒŧ 12 hourly urinalysis for proteinuria.
īƒŧ Occasionally, 24 hours urine collection & request for protein levels, & creatinine
clearance.
ī‚´ Maintain records and consult PRN.
Contâ€Ļ
ī‚´ Drugs:
īƒ˜ Administer antihypertensive e.g. Aldomet 250-500mg TDS or nifedipine 20mg BD
-If diastolic of 110 and above give apresoline 10-20mg 1.m or slow I.V infusion
īƒ˜ Sedatives-phenorbarbitone
īƒ˜ Anti-convulsant therapy diazepam 10-20mgs
ī‚´ Offer psychological support to control anxiety.
ī‚´ Maintain fluid balance chart and weigh on alternate days to monitor edema
,oliguria
ī‚´ Regularly evaluate the progress through interviewing and physical examination
findings.
Contâ€Ļ
ī‚´ Monitor urine-tested twice per day for proteins,sugar,acetone and other
abnormalities
ī‚´ Diet-Rich in proteins and vitamins and low in carbohydrate and salts
ī‚´ Control achieved before term, discharge to continue with review visits at the
antenatal clinic.
īƒ˜ Encourage to report back incase of abnormality.
ī‚´ Control not well achieved and at term.
īƒ˜ Either induction is attempted at 38 weeks, but if complications then emergency
caesarean section is carried out.
NB: Induction at 38 weeks is aimed at preventing I.U.F.D thereafter, since placental
functions are impaired.
Contâ€Ļ
SEVERE:
ī‚´ Admit at first contact because she is at the verge of developing eclampsia.
ī‚´ Inform the doctor immediately for medical management.
ī‚´ Nurse in a quite dimmed lit area and on complete bed rest.
ī‚´ Encourage lateral position to improve blood supply to kidneys & placental bed.
ī‚´ Maintain records of observations and consult PRN.
īƒ˜ Vital signs every2 hours –Bp 2hrly or more frequent
īƒ˜ Urinalysis on every specimen.
īƒ˜ State of oedema through phy exam + daily weighing.
īƒ˜ Fluid chart & for gross oedema, restrict fluid intake to 2L×24hrs.
ī‚´ Enquire for symptoms e.g. headache, epigastric pain etc.
ī‚´ Fetal:-F.H.S every 3hrs, fetal kick/movement, instruct client on maintaining record.
Contâ€Ļ
ī‚´ If facilates are available ,occasionally carry out:
īƒ˜ Cardiotocography.
īƒ˜ Doppler ultrasound, to measure the efficiency of blood flow to the placenta, hence
determine fate of the fetus & effect delivery appropriately.
ī‚´ Diet, as in moderate
ī‚´ Psychological support.
ī‚´ Hygiene
Contâ€Ļ
DRUGS:-
ī‚´ Parental antihypertensive i.e. hydrallazine 10mg i.v slowly stat.
ī‚´ Anti-convulsant- magnesium sulphate 20% solution 4gm IV for 10-15 minutes.
īƒ˜ Then follow promptly with 10 gm of 50% solution MgSo4 , 5gm on each buttock, deep
IM with 2% lignocaine in the same syringe.
NB: Observe usual precautions before giving mgso4 i.e
1) Respiration should not be below 16/min
2) Urine output –not less than 40/ml within the last 4 hrs
3) Reflexes-patellar reflexes should be present
ī‚´ closely monitors BP every 15 to 30 minutes in order to diagnose signs of sudden
hypotension which is dangerous to both mother & fetus.
ī‚´ As soon as the diastolic pressure stabilizes to a range of 90-100mhg then change to oral
antihypertensive e.g. aldomet 500mg TDS or nifedipine 20mg BD either sublingually or
orally.
ī‚´ Sedation e.g. phenobarbitone 30mg TDS.
Contâ€Ļ
ī‚´ For preterm delivery anticipation, administer steroid=dexamethesone 4mg BD 1.m
for 4/7 to prevent respiratory distress syndrome.
īƒ˜ However, the condition is a stressor leading early maturation of the lungs, so not
always necessary.
ī‚´ Evaluate the progress daily.
ī‚´ As the condition gets controlled re-introduce to limited daily activity and allow
pregnancy to continue to term.
ī‚´ However if she is admitted at term or condition doesn’t improve irrespective of the
gestation age emergency caesarean section is highly recommended.
Emergency treatment of severe pre-eclampsia
ī‚´ Pre-load the woman with 200-250 mL of Ringer’s Lactate solution over 30 minutes.
ī‚´ Give Nifedipine 100 mg orally
ī‚´ Give a loading dose of Methyldopa 1 gram orally
ī‚´ Consider giving magnesium sulphate
ī‚´ Transfer the woman to a well equipped hospital urgently
ī‚´ Measure her BP every 10 minutes
ī‚´ Aim for a diastolic pressure of 90-100 mmHg
ī‚´ Repeat Nifedipine 10 mg after 30 minutes if necessary.
Labor/ intrapartum care
ī‚´ The mode of delivery is dependent on the maternal & fetal condition as well as the
gestation of the pregnancy, regardless of the classification & where possible,
spontaneous onset of labour & vaginal birth is preferable.
ī‚´ MW should remain with the client throughout labour as PET can suddenly worsen any
time.
Indications for imminent delievery in pre-eclampsia are:-
īļ Pregnancy â‰Ĩ 32 wks in severe pre-eclampsia
īļ Estimated fetal wt â‰Ĩ1.5 kg in severe pre-eclampsia
īļ Eclampsia
īļ Cerebral oedema
īļ H.E.L.L.P syndrome
īļ Renal dysfunction
īļ Thrombocytopaenia
īļ Uncontrollable HTN
īļ Fetal compromise
īļ Dead fetus
First stage:
ī‚´ Usual care is given and have resuscitative equipment within reach because sudden
eclampsia may occur.
īƒ˜ They include:
īƒŧ Anticonvulsants, e.g parenteral magnesium sulphate.
īƒŧ Antihypertensives e.g apressoline (hydrallazine).
īƒŧ Sedatives e.g parenteral phenobarbitone.
īļ To handle the emergency to the best:-
īƒŧ various instruments should be available:-artificial airway, mouth gag padded
spatulla.
īƒŧ Other resources are gauze, cotton wool, gloves,branula,syringe & needles,strapping
and intravenous infusion of normal saline 1/2litre or hartman’s solution.
contâ€Ļ
ī‚´ Oxygen+apparatus, suction machine + correct tubings.
ī‚´ Closely monitor BP every 2 hours, fetal heart sound 1/4hrly and general progress of
labour, maintain records & consult.
ī‚´ Withhold oral feeds , instead commence intravenous infusion of 10% dextrose to
provide energy.
ī‚´ Keep doctor informed of the progress and report promptly:-
īƒ˜ Sudden sharp rise of BP.
īƒ˜ Restless/abnormal eyes movements.
īƒ˜ Fetal hypoxia signs.
īƒ˜ Intrapartum haemorrhage=placental separation.
ī‚´ If fetal hypoxia occurs at the end of 1st stage,increase the rate of the
drip,administer oxygen,prepare for neonatal resuscitation.
Second stage:
ī‚´ Preparation as usual but be ready to resuscitate also the mother.
ī‚´ Closely monitor maternal & fetal conditions to early diagnose signs of impending
eclampsia & fetal hypoxia respectively.
ī‚´ Hasten delivery through elective episiostomy and vacuum extraction.
Third stage:
ī‚´ Use natural methods of controlling bleeding.
ī‚´ If severe bleeding occurs administer synitocinon 5-10i.u, i.v & commence a drip of same
20.IU at 30dpm.
POSTNATALLY
ī‚´ Closely monitor vital signs i.e. 1/4hrly in 4th stage and every 2 hrly for at least 24hrs,
specifically BP & respiratory efforts respectively.
īƒŧ Aim of respiratory effort monitoring, is to early diagnose pulmonary oedema.
Contâ€Ļ
īƒ˜ Thereafter every 4 hourly.
īƒ˜ Urinary output, urinalysis BD, state of oedema, & lactation.
īƒ˜ Signs of postpartum haemorrhage.
ī‚´ Facilitate complete bed rest for at least 2 hours.
ī‚´ CT with antihypertensives and haematinics.
ī‚´ Plan for discharge when stable through sharing on:
īƒŧ Follow up BP monitoring and maintain records.
ī‚´ Compliance, with medication instruction on discharge, review visit schedule,ie
medical clinic & MCH/FP clinic.
ī‚´ Rest and to avoid strenuous duties to facilitate BP control.
ī‚´ Diet, to restrict on salt.
ī‚´ Early booking of future ANC & hospital delivery.
ī‚´ Family planning-avoid COC
ī‚´ The doctor discharges the patient to continue with review as per schedule.
EFFECTS ON THE MOTHER .[COMPLICATION-
MOTHER]
ī‚´ Development of eclampsia if condition not controlled.
ī‚´ Antepartum haemorrhage and intrapartum haemorrhage due to reduction of the
placental site before labour & in labour respectively= placental abruption.
ī‚´ Postpartum haemorrhage, because of the coagulation defect brought about by the
placental abruption leading to damage of uterus muscle.
ī‚´ Renal failure
ī‚´ Cardiovascular accident
ī‚´ Development of disseminated intravascular coagulation due to increased
consumption of platelets leading to thrombocytopenia .
ī‚´ Failure of any of the vital organs resulting from poor blood flow for a long period
due to vasospasms and deposits of platelets & fibrin.
ī‚´ Temporary blindness, severe damage of capillaries within the eyes fundus.
EFFECT-FETUS/NEONATE
ī‚´ Fetal hypoxia which leads to fetal distress due poor placental functions.
ī‚´ Intra-uterine fetal death or still birth because of severe placental dysfunction.
ī‚´ Preterm birth (early delivery) due to either severe pre-eclampsia, eclampsia or
antepartum haemorrhage.
ī‚´ Low birth weight baby-I.U.G.R or early birth.
COMPLICATONS PREVENTIVE MEASURES
ī‚´ Control and management of hypertension
ī‚´ Early diagnosis and accurate interventions.
ī‚´ Effective referral system for those with predisposing factors to a hospital based
ANC after thorough explanation.
ī‚´ Effective control of various social factors which may hinder antenatal services
attendance.
īƒ˜ For distant organize for mobile services at a central point.
SUMMARY- important to note
īą Methyldopa is the most widely used drug in women with mild to moderate
gestational hypertension.
īą An Îą and β blocker such as Labetalol is an alternative and considered safe in
pregnancy except for women with asthma or congestive heart failure.
īą Atenolol used over the long-term is NOT recommended as it’s linked with fetal
growth restriction
īą The use of ACE inhibitors are contraindicated in pregnancy.
īą Calcium channel blockers e.g. Nifedipine are increasingly used to treat severe
hypertension in pregnancy.
The principles of pre-eclampsia mgt are:-
ī‚´ Early detection of the symptomless syndrome.
ī‚´ knowledge of the serious nature of the condition in its severest form.
ī‚´ Adherence to agreed guidelines for admission to hospital, investigations and
antihypertensive/anticonvulsant prescription.
ī‚´ Accurately timed delivery to avoid serious complications to either mother or fetus.
ī‚´ Postnatal follow up of hypertension, expected to settle at most, after 6 months and
counseling for future pregnancies.
THE END

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PRE ECLAMPSIA .pptx

  • 2. DESCRIPTION ī‚´ It’s among the hypertension disorders and occurs only in pregnancy ī‚´ It is a disorder of widespread vascular endothelial malfunction and vasospasm that occurs after 20 wks gestation and can present as late as 4-6 wks postpartum ī‚´ It’s characterized basically by hypertension and proteinuria with or without pathological edema ī‚´ PET occurs in 3% of all pregnancies and > 10% of women develop this in their 1st pregnancy
  • 3. INCIDENCE ī‚§ Global incidence is estimated at 5-14% of all pregnancies 10% of women develop this in their 1st pregnancy ī‚§ In developing countries the hypertensive disorders are the second most common obstetrical cause of stillbirths and early neonatal deaths ī‚§ In Kenya pre-eclampsia is the 3rd leading pregnancy-related cause of death (1st- hemorrhage,2nd sepsis) ī‚§ Pre-eclampsia is the cause of estimated 790 maternal deaths per 100,000 live births accounting for 23.6%
  • 4. PREDISPOSING FACTORS ī‚´ Pre pregnancy hypertension also referred to as existing or chronic hypertension(essential hypertension) before conception, because of damage of the various endothelium. ī‚´ Previous history of pre-eclampsia, because of probability of re-occurrence. ī‚´ Family history of pre-eclampsia mostly within her nuclear family of origin. ī‚´ Polyhygramnious ī‚´ Pre-existing medical conditions e.g. Renal diseases due to high release of angiotensin II. ī‚´ Pre-existing Diabetes mellitus due to endothelial cells dysfunction and also large placental mass. ī‚´ Multiple pregnancy, large placental mass hence possibility vasoconstriction. ī‚´ Hydatidform mole. ī‚´ Maternal age below 20 years and above 35 years. Low age has negative impact on pregnancy, while high age there is possibility of chronic HTN
  • 5. Contâ€Ļ ī‚´ Being a primigravida because of the maternal immune response to fetal antigen from the father. ī‚´ Change of male partner(First pregnancy from a new partner)- The fetal antigen from the sperm sensitizes the production of antibodies by the maternal body hence endothelial cells dysfunction leading to high sensitivity to angiotensin II= HTN. ī‚´ Pregnancy after assisted reproductive technology ī‚´ Obesity ī‚´ Women from low social economic status-start clinic late
  • 6. Aetiology ī‚´ Development of pre-eclampsia basically occurs in two stages namely: STAGE I ī‚´ Early in pregnancy as the decidua gets invaded by the syncytiotrophoblast for implantation to occur . ī‚´ The erosion of the muscular wall & endothelium of the spinal arteries is abnormal. Finally the placenta is not appropriately supplied by oxygen though no features are detected clinically. STAGE II ī‚´ Occurs between 16th-20th week the oxidatively stressed [inadequately oxygen supplied placenta ] placenta, releases factors leading to damage of endothelial cells which form endothelium ,in the maternal circulation. īƒŧ Eventually the endothelial cells dysfunction and maternal systemic inflammatory response lead to clinical features of pre-eclampsia
  • 7. Clinical features Cardinal signs 1. High blood pressure- Bp reading are 140/90 mmhg & above, taken on two consecutive occasions, at least 2- 4 hours apart 2. Proteinuria- Signifying renal damage 3. Edema:- Initially of ankles, later fingers, face & legs. īƒ˜ Finally becomes generalized edema to include abdomen, sacral region & vulva, results from severe fluid retention Signs of impending/severe pre-eclampsia ī‚´ A sharp rise in blood pressure ī‚´ Diminished urinary output(Oliguria) ī‚´ Increased proteinuria on urine testing ī‚´ Severe persistence headache usually frontal or occipital due to increased intracranial pressure ī‚´ Drowsiness or confusion ī‚´ Visual disturbances e.g. Blurred vision, flash light and double vision. Sometimes temporary blindness ī‚´ Nausea and vomiting ī‚´ Epigastric pain
  • 8. DIAGNOSIS OF PRE-ECLAMPSIA NB// īƒ˜ The symptoms are rarely experienced by the mother until the disease have reached an advanced state īƒ˜ Diagnosis is based on 3 cardinal signs; 1. HIGH BLOOD PRESSURE ī‚§ Increase in diastolic pressure of 15-20mmhg above the mothers normal diastolic pressure or increase above 90mmhg on 2 or more occasions 2.PROTENURIA ī‚§ Presence of proteins in urine in absence of UTI is diagnostic ī‚§ The amount of protein in urine indicates the severity of pre-eclampsia 3.OEDEMA â€ĸ It is generalized and doesn’t disappear on rest ī‚´ Indicates high rate of fluid retention ī‚´ Most affected areas are:- legs, face, hands, abdomen, sacral & vulva.
  • 9. Lab tests ī‚´ Urinalysis ī‚´ Increased hemoglobin & haematocrite level. ī‚´ Thrombocytopenia. ī‚´ Prolonged clotting time due to over consumption of fibrinogen, since there is high release of thromboplastin from damaged blood vessels. ī‚´ High serum creatinine levels (>90 mmol/L) & urea levels due to poor blood flow to the kidneys. ī‚´ Increased serum uric acid level. ī‚´ Abnormal liver function test results.
  • 10. Pathophysiology ī‚´ Refers to pathological changes brought about by severe state of pre-eclampsia leading to multisystem disorders [effects]. 1.CARDIOVASCULAR īļ General vasoconstriction leads to: ī‚´ Enlargement of the heart as it attempts to counteract the increased peripheral resistance. ī‚´ General oedema, due to increased capillary permeability & loss of plasma proteins. ī‚´ Increased coagulation activation due to damage of blood vessels & other tissues hence high probability of DIC. 2.RENAL īļ Reduced blood supply makes the afferent arterioles go into vasospasm leading to damage of glomerular filtering bed hence:
  • 11. ī‚´ Proteinuria. ī‚´ Reduced creatinine clearance & urea excretion. īƒŧ Therefore serum creatinine & uric acid levels increases. ī‚´ Oliguria:- urinary output ranges between 400-500ml in 24hrs. 3.RESPIRATORY ī‚´ Pulmonary oedema due to damage of blood vessels & low osmotic pressure. ī‚´ Cyanosis , because of impaired oxygen supply. Contâ€Ļ
  • 12. Contâ€Ļ 4.GASTRO-INTESTINAL ī‚´ Inadequate perfusion leads to oedema of the liver particularly, hence: īƒŧ Epigastric pain. īƒŧ Intracapsular hemorrhage. īƒŧ Altered liver function test results. īƒŧ Sometime jaundice.
  • 13. Contâ€Ļ 5.CENTRAL NERVOUS SYTEM īļ Hypertension and cerebrovascular endotherial dysfunction increases the blood- brain barrier permeability leading to cerebral oedema and microhaemorrhage. ī‚´ Generally leads to:- īƒŧ Headaches īƒŧ Visual disturbances. īƒŧ Cerebral thrombosis because of fibrin & platelets deposition hence postpartum eclampsia. īƒŧ Convulsions.
  • 14. Contâ€Ļ 6.REPRODUCTION SYSTEM ī‚´ Reduced blood supply to placental tissues and increased pressure within the vessels at the placental leads to: īƒ˜ Infarcts formation, hence intrauterine growth restricts. īƒ˜ Impaired hormonal production , affects fetal survival hence premature labour =early birth. īƒ˜ Placental abruption, some vessels burst at the placental bed leading to APH.
  • 15. Classification of Pre-eclampsia 1. MILD īļ Characterized by:- ī‚´ BP reading of 140/90mmhg where; ī‚´Systolic ranges btwn 140-149 mmHg ī‚´Diastolic ranges btwn 90-99 mmHg ī‚´ Protenuria ranges between trace to1+.It is below 0.5gms/1lt ī‚´ Oedema, marked on the ankles, feet and sometimes pretibial region. ī‚´ No complains are presented, features are noted (elicited) during a routine antenatal service. ī‚´ However close follow is important.
  • 16. Contâ€Ļ 2. MODERATE ī‚´ Marked rise in BP of both systolic and diastolic ī‚´ BP readings where Bp 140/100-160/110; ī‚´ Systolic ranges btwn 140-160 mmHg ī‚´ Diastolic ranges btwn 100-110 mmHg īƒŧ Specifically rise in both systolic & diastolic pressure with about 20mmhg is noted. ī‚´ Proteinuria ranges between 1+ to 2+(above 0.5 gms/lt) ī‚´ Edema is marked on legs, fingers and face hence denoted as (++) ī‚´ Mother aware of the symptoms.
  • 17. Contâ€Ļ 3. SEVERE ī‚´ BP is 160/110mmHg or higher where; ī‚´Systolic is > 160 mmHg ī‚´Diastolic is â‰Ĩ110 mmHg ī‚´ Oedema is gross(generalized), i.e. involves also, abdomen, sacral region & sometimes vulva. ī‚´ Proteinuria 2+ and above (3+)(0ver 1 gm/lt) ī‚´ Presents with various impending signs as per clinical features e.g. headache and blurred vision
  • 18. Specific management ī‚´ Provide rest and a quiet environment hence control BP. ī‚´ Monitor disease process and take appropriate interventions as necessary. ī‚´ Prolong pregnancy hence improve the survival rate of the fetus while also safeguarding maternal life ANTENATALLY MILD PET īļ Closely monitor noted signs through weekly ANC and advise on: ī‚´ Bed rest at least 12-24 hours ī‚´ Sleep in lateral position to improve renal and placental blood supply ī‚´ Administer sedatives e.g. phenobarbitone 30mg every 8 hourly or valium 5mg nocte to ensure rest and sleep ī‚´ Administer antihypertensive e.g. Aldomet 250-500mg TDS or nifedipine 20mg BD ī‚´ Balanced diet with extra-proteins, high fiber and low in salt and carbohydrates ī‚´ Monitor fetal kicks and report if low or absent ī‚´ Need of having somebody to assist in domestic work
  • 19. Contâ€Ļ MODERATE ī‚´ Requires immediate admission to hospital. ī‚´ Inform the doctor. ī‚´ Nursed in a quiet area, preferably dim lit to facilitate rest & sleep. īƒŧ Control visitors īƒŧ Position-patient nursed in sitting up or left lateral position(supine) ī‚´ Closely monitor fetal and maternal condition through: īƒ˜ Fetal :- 4hrly F.H.S, fetal kick chart, ultrasound to monitor fetal growth, particularly where control is not being achieved, cardiotocograph for sign of fetal hypoxia. īƒ˜ Maternal:- 4 hourly vital signs especially BP. īƒŧ 12 hourly urinalysis for proteinuria. īƒŧ Occasionally, 24 hours urine collection & request for protein levels, & creatinine clearance. ī‚´ Maintain records and consult PRN.
  • 20. Contâ€Ļ ī‚´ Drugs: īƒ˜ Administer antihypertensive e.g. Aldomet 250-500mg TDS or nifedipine 20mg BD -If diastolic of 110 and above give apresoline 10-20mg 1.m or slow I.V infusion īƒ˜ Sedatives-phenorbarbitone īƒ˜ Anti-convulsant therapy diazepam 10-20mgs ī‚´ Offer psychological support to control anxiety. ī‚´ Maintain fluid balance chart and weigh on alternate days to monitor edema ,oliguria ī‚´ Regularly evaluate the progress through interviewing and physical examination findings.
  • 21. Contâ€Ļ ī‚´ Monitor urine-tested twice per day for proteins,sugar,acetone and other abnormalities ī‚´ Diet-Rich in proteins and vitamins and low in carbohydrate and salts ī‚´ Control achieved before term, discharge to continue with review visits at the antenatal clinic. īƒ˜ Encourage to report back incase of abnormality. ī‚´ Control not well achieved and at term. īƒ˜ Either induction is attempted at 38 weeks, but if complications then emergency caesarean section is carried out. NB: Induction at 38 weeks is aimed at preventing I.U.F.D thereafter, since placental functions are impaired.
  • 22. Contâ€Ļ SEVERE: ī‚´ Admit at first contact because she is at the verge of developing eclampsia. ī‚´ Inform the doctor immediately for medical management. ī‚´ Nurse in a quite dimmed lit area and on complete bed rest. ī‚´ Encourage lateral position to improve blood supply to kidneys & placental bed. ī‚´ Maintain records of observations and consult PRN. īƒ˜ Vital signs every2 hours –Bp 2hrly or more frequent īƒ˜ Urinalysis on every specimen. īƒ˜ State of oedema through phy exam + daily weighing. īƒ˜ Fluid chart & for gross oedema, restrict fluid intake to 2L×24hrs. ī‚´ Enquire for symptoms e.g. headache, epigastric pain etc. ī‚´ Fetal:-F.H.S every 3hrs, fetal kick/movement, instruct client on maintaining record.
  • 23. Contâ€Ļ ī‚´ If facilates are available ,occasionally carry out: īƒ˜ Cardiotocography. īƒ˜ Doppler ultrasound, to measure the efficiency of blood flow to the placenta, hence determine fate of the fetus & effect delivery appropriately. ī‚´ Diet, as in moderate ī‚´ Psychological support. ī‚´ Hygiene
  • 24. Contâ€Ļ DRUGS:- ī‚´ Parental antihypertensive i.e. hydrallazine 10mg i.v slowly stat. ī‚´ Anti-convulsant- magnesium sulphate 20% solution 4gm IV for 10-15 minutes. īƒ˜ Then follow promptly with 10 gm of 50% solution MgSo4 , 5gm on each buttock, deep IM with 2% lignocaine in the same syringe. NB: Observe usual precautions before giving mgso4 i.e 1) Respiration should not be below 16/min 2) Urine output –not less than 40/ml within the last 4 hrs 3) Reflexes-patellar reflexes should be present ī‚´ closely monitors BP every 15 to 30 minutes in order to diagnose signs of sudden hypotension which is dangerous to both mother & fetus. ī‚´ As soon as the diastolic pressure stabilizes to a range of 90-100mhg then change to oral antihypertensive e.g. aldomet 500mg TDS or nifedipine 20mg BD either sublingually or orally. ī‚´ Sedation e.g. phenobarbitone 30mg TDS.
  • 25. Contâ€Ļ ī‚´ For preterm delivery anticipation, administer steroid=dexamethesone 4mg BD 1.m for 4/7 to prevent respiratory distress syndrome. īƒ˜ However, the condition is a stressor leading early maturation of the lungs, so not always necessary. ī‚´ Evaluate the progress daily. ī‚´ As the condition gets controlled re-introduce to limited daily activity and allow pregnancy to continue to term. ī‚´ However if she is admitted at term or condition doesn’t improve irrespective of the gestation age emergency caesarean section is highly recommended.
  • 26. Emergency treatment of severe pre-eclampsia ī‚´ Pre-load the woman with 200-250 mL of Ringer’s Lactate solution over 30 minutes. ī‚´ Give Nifedipine 100 mg orally ī‚´ Give a loading dose of Methyldopa 1 gram orally ī‚´ Consider giving magnesium sulphate ī‚´ Transfer the woman to a well equipped hospital urgently ī‚´ Measure her BP every 10 minutes ī‚´ Aim for a diastolic pressure of 90-100 mmHg ī‚´ Repeat Nifedipine 10 mg after 30 minutes if necessary.
  • 27. Labor/ intrapartum care ī‚´ The mode of delivery is dependent on the maternal & fetal condition as well as the gestation of the pregnancy, regardless of the classification & where possible, spontaneous onset of labour & vaginal birth is preferable. ī‚´ MW should remain with the client throughout labour as PET can suddenly worsen any time. Indications for imminent delievery in pre-eclampsia are:- īļ Pregnancy â‰Ĩ 32 wks in severe pre-eclampsia īļ Estimated fetal wt â‰Ĩ1.5 kg in severe pre-eclampsia īļ Eclampsia īļ Cerebral oedema īļ H.E.L.L.P syndrome īļ Renal dysfunction īļ Thrombocytopaenia īļ Uncontrollable HTN īļ Fetal compromise īļ Dead fetus
  • 28. First stage: ī‚´ Usual care is given and have resuscitative equipment within reach because sudden eclampsia may occur. īƒ˜ They include: īƒŧ Anticonvulsants, e.g parenteral magnesium sulphate. īƒŧ Antihypertensives e.g apressoline (hydrallazine). īƒŧ Sedatives e.g parenteral phenobarbitone. īļ To handle the emergency to the best:- īƒŧ various instruments should be available:-artificial airway, mouth gag padded spatulla. īƒŧ Other resources are gauze, cotton wool, gloves,branula,syringe & needles,strapping and intravenous infusion of normal saline 1/2litre or hartman’s solution.
  • 29. contâ€Ļ ī‚´ Oxygen+apparatus, suction machine + correct tubings. ī‚´ Closely monitor BP every 2 hours, fetal heart sound 1/4hrly and general progress of labour, maintain records & consult. ī‚´ Withhold oral feeds , instead commence intravenous infusion of 10% dextrose to provide energy. ī‚´ Keep doctor informed of the progress and report promptly:- īƒ˜ Sudden sharp rise of BP. īƒ˜ Restless/abnormal eyes movements. īƒ˜ Fetal hypoxia signs. īƒ˜ Intrapartum haemorrhage=placental separation. ī‚´ If fetal hypoxia occurs at the end of 1st stage,increase the rate of the drip,administer oxygen,prepare for neonatal resuscitation.
  • 30. Second stage: ī‚´ Preparation as usual but be ready to resuscitate also the mother. ī‚´ Closely monitor maternal & fetal conditions to early diagnose signs of impending eclampsia & fetal hypoxia respectively. ī‚´ Hasten delivery through elective episiostomy and vacuum extraction. Third stage: ī‚´ Use natural methods of controlling bleeding. ī‚´ If severe bleeding occurs administer synitocinon 5-10i.u, i.v & commence a drip of same 20.IU at 30dpm. POSTNATALLY ī‚´ Closely monitor vital signs i.e. 1/4hrly in 4th stage and every 2 hrly for at least 24hrs, specifically BP & respiratory efforts respectively. īƒŧ Aim of respiratory effort monitoring, is to early diagnose pulmonary oedema.
  • 31. Contâ€Ļ īƒ˜ Thereafter every 4 hourly. īƒ˜ Urinary output, urinalysis BD, state of oedema, & lactation. īƒ˜ Signs of postpartum haemorrhage. ī‚´ Facilitate complete bed rest for at least 2 hours. ī‚´ CT with antihypertensives and haematinics. ī‚´ Plan for discharge when stable through sharing on: īƒŧ Follow up BP monitoring and maintain records. ī‚´ Compliance, with medication instruction on discharge, review visit schedule,ie medical clinic & MCH/FP clinic. ī‚´ Rest and to avoid strenuous duties to facilitate BP control. ī‚´ Diet, to restrict on salt. ī‚´ Early booking of future ANC & hospital delivery. ī‚´ Family planning-avoid COC ī‚´ The doctor discharges the patient to continue with review as per schedule.
  • 32. EFFECTS ON THE MOTHER .[COMPLICATION- MOTHER] ī‚´ Development of eclampsia if condition not controlled. ī‚´ Antepartum haemorrhage and intrapartum haemorrhage due to reduction of the placental site before labour & in labour respectively= placental abruption. ī‚´ Postpartum haemorrhage, because of the coagulation defect brought about by the placental abruption leading to damage of uterus muscle. ī‚´ Renal failure ī‚´ Cardiovascular accident ī‚´ Development of disseminated intravascular coagulation due to increased consumption of platelets leading to thrombocytopenia . ī‚´ Failure of any of the vital organs resulting from poor blood flow for a long period due to vasospasms and deposits of platelets & fibrin. ī‚´ Temporary blindness, severe damage of capillaries within the eyes fundus.
  • 33. EFFECT-FETUS/NEONATE ī‚´ Fetal hypoxia which leads to fetal distress due poor placental functions. ī‚´ Intra-uterine fetal death or still birth because of severe placental dysfunction. ī‚´ Preterm birth (early delivery) due to either severe pre-eclampsia, eclampsia or antepartum haemorrhage. ī‚´ Low birth weight baby-I.U.G.R or early birth.
  • 34. COMPLICATONS PREVENTIVE MEASURES ī‚´ Control and management of hypertension ī‚´ Early diagnosis and accurate interventions. ī‚´ Effective referral system for those with predisposing factors to a hospital based ANC after thorough explanation. ī‚´ Effective control of various social factors which may hinder antenatal services attendance. īƒ˜ For distant organize for mobile services at a central point.
  • 35. SUMMARY- important to note īą Methyldopa is the most widely used drug in women with mild to moderate gestational hypertension. īą An Îą and β blocker such as Labetalol is an alternative and considered safe in pregnancy except for women with asthma or congestive heart failure. īą Atenolol used over the long-term is NOT recommended as it’s linked with fetal growth restriction īą The use of ACE inhibitors are contraindicated in pregnancy. īą Calcium channel blockers e.g. Nifedipine are increasingly used to treat severe hypertension in pregnancy.
  • 36. The principles of pre-eclampsia mgt are:- ī‚´ Early detection of the symptomless syndrome. ī‚´ knowledge of the serious nature of the condition in its severest form. ī‚´ Adherence to agreed guidelines for admission to hospital, investigations and antihypertensive/anticonvulsant prescription. ī‚´ Accurately timed delivery to avoid serious complications to either mother or fetus. ī‚´ Postnatal follow up of hypertension, expected to settle at most, after 6 months and counseling for future pregnancies.