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HTN in Pregnancy.pptx
1. Hypertensive disorders in pregnancy
Dr Biswas Bikram Kharel
Resident 2nd year
MDGP & EM
Moderator: Dr Sanjay Kumar Gupta
2. DEFINITION
•In pregnancy, the blood pressure is considered to be raised if:
•The blood pressure is 140/90 mmHg or more
•The systolic blood pressure has increased by 30mmHg
•The diastolic blood pressure has increased by 15mmHg
3. MAGNITUDE AND IMPORTANCE
•Hypertension is the most common medical problem encountered
during pregnancy, complicating up to 10% of pregnancies
• Hypertensive disorders in pregnancy may cause maternal and fetal
morbidity and remain an important cause of maternal deaths around
the world.
6. CLASSIFICATION OF HYPERTENSIVE DISEASES
OF THE PREGNANCY
• 1. Gestational hypertension (PIH)
• 2. Pre-eclampsia
• 3. Eclampsia
• 4. Pre-eclampsia superimposed on chronic hypertension
• 5. Chronic hypertension
7. GESTATIONAL HYPERTENSION (PIH)
• Diagnosis made when the blood pressure reaches 140/90mmHg or
greater for the first time during pregnancy but in whom proteinuria
has not developed.
• Gestational hypertension is called transient hypertension if pre-
eclampsia doesn’t develop and the blood pressure returns to normal
by 12 weeks postpartum.
• BP returns to normal <12wks postpartum
• Gestation hypertension is termed as chronic if blood pressure
elevation persists beyond 12 weeks postpartum
8. PRE-ECLAMPSIA
• Hypertension associated with protenuria and oedema occurring
primarily in Nulliparous after 20th week’s gestation and most
frequently near term.
• It is a specific syndrome of reduced organ perfusion secondary to
vasospasm and endothelial activation.
• Proteinuria is an important sign of pre-eclampsia and that the
diagnosis is questionable in its absence. (significant protenuria is
defined by urine protein of 0.3g/24 hrs)
Protenuria defined by excretion of 300mg protein in 24 hrs or
persistence 30mg/dl (1+ dipstick in random urine sample).
9. • DIAGNOSTIC CRITERIA FOR PRE-ECLAMPSIA
• Minimum criteria -BP >140/90mmHg after 20wks –
• Proteinuria >300mg/24hrs or >1+ dipstick
11. CHRONIC HYPERTENSION
• Hypertension that is present before conception, before 20wks
gestation or that persists beyond 12wks postpartum.
• The diagnosis of chronic hypertension is suggested by;
• 1. Hypertension (140/90mmHg ) antecedent to pregnancy.
• 2. Hypertension detected before 20wks unless there is GTD’s.
• 3. Persistent hypertension long after delivery.
12. PRE-ECLAMPSIA SUPERIMPOSED ON
CHRONIC HYPERTENSION
• Patient prognosis (both mother and the fetus) is grave than in either
of the conditions.
•All chronic hypertensive disorders regardless of their cause predispose
to the development of superimposed pre-eclampsia or eclampsia
13. Diagnosis of superimposed pre-eclampsia
• Criteria for superimposed preeclampsia are:-
worsening Hypertension above average values before 20wks (30mmHg
systolic, 15mmHg diastolic)
Non-dependent oedema
New onset protenuria of more than 300mg in 24hrs (+1 dip stick) in
hypertensive women with no protenuria or a sudden increase in
proteinuria or BP in a woman with hypertension
14. pathophysiology
•The exact pathophysiologic mechanism is not clearly understood
Disorder of endothelial function with generalised vasospasm.
Abnormal placental development or placental damage from diffuse
microthrombosis may be central to the development of this disorder.
15.
16. • Normally, placenta liberates angiotensinase which degrade
angiotensin II.
• Vascular synthesis of prostaglandin I2 and NO neutralizes the
vasoconstrictive effect of angiotensin II.
• Increased level of VEGF restores the uteroplacental blood flow to
normal.
• All these maintain blood pressure in normal state during pregnancy.
17. • But in pre-eclampsia, there are
• Imbalance of prostaglandin I2
• Increases synthesis of thromboxane A2
• Depressed activity of angiotensinase thereby increasing vascular sensitivity
of angiotensin II.
• Deficiency of NO.
• Increased synthesis of endothelin-1 (which is a potent vasoconstrictor)
• Cytokines (TNF-α, IL-6) elevated
• Oxidative stress
• All these contribute to vasospasm resulting in hypertension.
18. Abnormal Trophoblastic Invasion
• Normal implantation is characterized by extensive remodeling of the
spiral arterioles within the decidua basalis.
• first trimester (10–12 weeks) endovascular trophoblasts invades up to
decidual segments and in the second trimester (16–18 weeks) another
wave of trophoblasts invades upto the myometrial segments.
• This process replaces the endothelial lining and the muscular arterial
wall by fibrinoid formation. The spiral arterioles thereby become
distended, tortuous, and funnel- shaped. This physiological change
transforms the spiral arterioles into a low resistance, low pressure, high
flow system.
19. • In pre-eclampsia, there is failure of the second wave of endovascular
trophoblast migration and there is reduction of blood supply to the
fetoplacental unit.
20. Immunological Factor
• Normally there is maternal immune tolerance to paternally derived
placental and fetal antigens.
• Loss of this tolerance, or perhaps its dysregulation, account for
preeclampsia syndrome.
• Dysregulation include “immunization” from a previous pregnancy,
some inherited human leukocyte antigen (HLA) and natural killer (NK)-
cell receptor haplotypes, and possibly shared susceptibility genes with
diabetes and hypertension
21. Maternal risk factors for preeclampsia
• 1. First pregnancy
• 2. New partner/paternity
• 3. Age younger than 18 years or older than 35 years
• 4. History of preeclampsia
• 5. Family history of preeclampsia in a first-degree relative
• 6. Black race
• 7. Multiple pregnancy
• 8. polyhydromnious
• Interpregnancy interval less than 2 years or longer than 10 year
22. Medical risk factors for preeclampsia
• Chronic hypertension
• Secondary causes of chronic hypertension such as hypercortisolism,
hyperaldosteronism, pheochromocytoma, or renal artery stenosis
• Preexisting diabetes (type 1 or type 2), especially with microvascular
disease
• Renal disease
• Systemic lupus erythematosus
• Obesity
• Thrombophilia
25. MILD PREECLAMPSIA
•BP 140/90 to <160/110mmHg.
•Protenuria <2g/24hrs
•Normal deep tendon reflex
•Pretibial edema nil/mild
26. SEVERE PREECLAMPSIA
• systolic BP>160mmHg or diastolic 110mmHg on 2 different occasions 6hrs
apart
• protenuria >2g/24hrs or 2-4+dipstick.
• Serum creatinine >1.1mg/dl
• Oliguria <500ml/24hrs
• Cerebral or visual disturbance
• Epigastric pain
• Elevated liver enzymes
• Platelets <100,000/m3
• Retinal haemorrhage, exudates or pappiloedema
• Pulmonary edema.
27. PATHOLOGY SEEN IN Pre-eclampsia
• CNS
• Petechial haemorrhage or gross intercranial haemorrhage.
• Fibrinoid necrosis
• Thrombosis of arterioles
• Microinfacts
• Retinal haemorrhage and infarcts are less common
• cerebral oedema
• The lesions are widely distributed throughout the brain where the
cortex is much more affected
28. • Serous retinal detachments and cortical blindness
• Pulmonary edema may be due to: Protenuria or endothelial leakage--
--Fluid admin ----Decreased plasma colloidal osmotic pressure
• LIVER : Periportal hemorrhagic necrosis----Hepatic rupture ----Sub
capsular haematoma ----HELLP syndrome ---Hepatic infarction
• KIDNEYS:Glomerulosclerosis -swelling of the glomerular capillary
endothelium that causes decreased glomerular perfusion and GFR ---
Leakage of proteins through the glomeruli leading to proteinuria.
• Lesions are totally reversible after 6wks
29. • BLOOD:DIC
•Low fibrinogen
•HELLP syndrome diagnosis based on Schistocytes on peripheral blood
smears, Lactic dehydrogenase >600U/l, total bilirubin of >1.2mg/dl,
AST>70/ul and platelet counts of <100,000/mm.
30. INVESTIGATIONS
1. CBC
2. Liver function test
i. Aspartate aminotransferase (SGOT)
>72 IU/L
ii. Plasma albumin (decrease because
of hemodilution)
1. Total bilirubin > 1.2 mg/dL
iii. LDH >600 IU/L
3 Coagulation profile
• Fibrinogen levels, and fibrin
degradation products and
• Prothrombin time,(abruptio
placentae, or microangiopathic
haemolytic anaemia),
• Activated partial thromboplastin
time
4.Kidney function tests
• Blood Urea Nitrogen,
• Creatinine clearance,
• Uric acid,
• 24-hour urine collection for protein
excretion
30
31. Management of mild pre-eclampsia
• MATERNAL
• Bed rest
• Daily urine protein
• BP monitoring
• Pt education on danger signs
• LFT, Uric acid, Electrolytes, serum proteins weekly
• Coagulation studies
• Antihypertensives
33. Severe Cases
•Prevent the occurrence of seizures by using magnesium sulphate
•Control BP
•Decision to deliver depends on GA and fetal/maternal conditions.
•Accelerate lung maturity by steroids(inj Dexamethasone 12mg im 12
hrs apart)
34. Guidelines on hypertension in pregnancy were released in May
2018 by Hypertension Canada and the Society of Obstetricians
and Gynaecologists of Canada.
• A BP level of ≥160/110 mm Hg is associated with increased risk of
maternal stroke in pregnancy and is therefore considered the
diagnostic threshold of severe hypertension in pregnancy.
• Antihypertensive therapy is recommended for average SBP
measurements of ≥140 mm Hg or DBP measurements of ≥90 mm Hg
in pregnant women with chronic hypertension, gestational
hypertension, or preeclampsia.
35. • Initial antihypertensive therapy should be monotherapy from the
following first-line drugs: oral labetalol, oral methyldopa, long-acting
oral nifedipine, or other oral β-blockers (acebutolol, metoprolol,
pindolol, and propranolol).
• Other antihypertensive drugs can be considered as second-line drugs,
including clonidine, hydralazine, and thiazide diuretics.
• ACE inhibitors and angiotensin receptor blockers should not be used
in pregnant women.
36. • A DBP of 85 mm Hg should be targeted for pregnant women receiving
antihypertensive therapy with chronic hypertension or gestational
hypertension.
• Women with severe hypertension with SBP ≥160 or DBP ≥110 mm Hg
in pregnancy require urgent antihypertensive therapy because it is
considered an obstetric emergency.
37. Acute Treatment of Severe Hypertension in
Pregnancy
• In the setting of severe hypertension (SBP >160 mm Hg; DBP >110
mm Hg), antihypertensive treatment is recommended.
• The goal of hypertension treatment is to lower BP to prevent
cerebrovascular and cardiac complications while maintaining
uteroplacental blood flow (ie, maintain BP around 140/90 mm Hg).
• Drugs commonly used are Hydralazine, Labetalol, Nifedipine
38. • Hydralazine is a direct peripheral arteriolar vasodilator
• Hydralazine should be given as an IV bolus at a dose of 5-10 mg,
depending on the severity of hypertension, and may be administered
every 20 minutes up to a maximum dose of 30 mg
• Labetalol is a selective alpha blocker and a nonselective beta blocker
that produces vasodilatation and results in a decrease in systemic
vascular resistance. The dosage for labetalol is 20 mg IV with repeat
doses (40, 80, 80, and 80 mg) every 10 minutes up to a maximum
dose of 300 mg.
39. • Calcium channel blockers act on arteriolar smooth muscle and induce
vasodilatation by blocking calcium entry into the cells.
• Nifedipine is the oral calcium channel blocker that is used in the
management of hypertension in pregnancy.
• The dosage of nifedipine is 10 mg PO every 15-30 minutes, with a
maximum of 3 doses.
• Nifedipine is commonly used postpartum in patients with
preeclampsia, for BP control.
40. • In a severe hypertensive emergency, when the above-mentioned
medications have failed to lower BP, sodium nitroprusside may be given.
• Nitroprusside results in the release of nitric oxide, which in turn causes
significant vasodilation.
• Preload and afterload are then greatly decreased.
• The onset of action is rapid, and severe rebound hypertension may result.
• Cyanide poisoning may occur subsequent to its use in the fetus.
• Therefore, sodium nitroprusside should be reserved for use in postpartum
care or for administration just before the delivery of the fetus.
41. INDICATIONS OF DELIVERY IN SEVERE CASES
• BP consistently higher than 100mmHg diastolic in 24hrs period or
confirmed higher than 110mmHg
• Raising serum creatinine
• Persistent or severe headache
• Epigastric pain
• Abnormal liver function test
• Thrombocytopenia
• HELLP syndrome
• Pulmonary edema
• Eclampsia
• Abnormal CTG
42. Eclampsia
• Eclampsia as the occurrence of 1 or more generalized, tonic-clonic convulsions
unrelated to other medical conditions in women with hypertensive disorder of
pregnancy.
FEBRUARY 2022 American Journal of Obstetrics & Gynecology
• Convulsive state of pre-eclampsia is called eclampsia.
• Pre-eclampsia is complicated by generalized tonic and clonic convulsions and coma .
• Up to 38% of cases of eclampsia can occur without premonitory signs or symptoms
of pre-eclampsia—that is, hypertension, proteinuria, and oedema.
43. Incidence
• More common in primi-gravida
• Five time more common in twins
• developed countries 1.6 to 10 per 10,000 deliveries
• developing countries from 50 to 151 per 10,000 deliveries
• responsible for up to 14% of all maternal deaths worldwide
44. • Outcome is poor for mother and child.
• Almost one in 50 women suffering eclamptic seizures die,
• 23% will require ventilation and
• 35% will have at least one major complication including pulmonary
oedema, renal failure, disseminated intravascular coagulation, HELLP
syndrome, acute respiratory distress syndrome, stroke, or cardiac
arrest.
• Stillbirth or neonatal death occurs in approximately one in 14 cases
of eclampsia.
45. • It is extremely difficult to predict which women with pre-eclampsia
will develop eclamptic seizures.
• Consequently, it is almost impossible to devise strategies for seizure
prophylaxis in pre-eclamptic women.
• Although this has been recently answered in the “Magpie” trial
which showed clear advantages in the use of Magnesium Sulfate in
severe pre-eclampsia reduced the relative risk of eclampsia by 58%
and of maternal death by 45%
46. Pathophysiology
• Not well understood
• One proposed model - alteration of autoregulation in the cerebral
circulation similar to hypertensive encephalopathy with blood-brain
barrier (BBB) disruption and passage of fluid, ions, and plasma
proteins into the brain parenchyma
• Autoregulation of the cerebral circulation is a mechanism to maintain
constant cerebral blood flow during changes in blood pressure
47. Physical signs:
• Eclamptic seizure
• The patient may have 1 or more seizures.
• Seizures generally last 60-75 seconds.
• The patient's face initially may become distorted, with protrusion of
the eyes.
• The patient may begin foaming at the mouth.
• Respiration ceases for the duration of the seizure.
48. • The seizure may be divided into 2 phases:
• Phase 1 lasts 15-20 seconds and begins with facial twitching. The
body becomes rigid, leading to generalized muscular contractions.
• Phase 2 lasts approximately 60 seconds. It starts in the jaw, moves to
the muscles of the face and eyelids, and then spreads throughout the
body. The muscles begin alternating between contracting and relaxing
in rapid sequence.
49. •A coma or a period of unconsciousness follows phase 2.
•Unconsciousness lasts for a variable period.
•Following the coma phase, the patient may regain some
consciousness.
•The patient may become combative and very agitated.
50. Most common symptoms
• Headache (66%),
• Visual disturbance (27%),
• And right upper quadrant or epigastric pain (25%)
• However, although hypertension is the hallmark for the diagnosis of
eclampsia, it may be absent in up to 15-25% of cases
51. 1. Sustained systolic BP greater than 160 mm Hg or diastolic BP greater
than 110 mm Hg
2. Tachycardia
3. Tachypnea
4. Rales
5. Hyperreflexia (80%)
6. Clonus
7. Papilledema
51
• Physical signs
8 Oliguria or anuria
9. Localizing neurologic deficits
10. Right upper quadrant or epigastric abdominal
tenderness with nausea (20%)
11. Generalized oedema (49%)
12. Small fundal height for the estimated
gestational age
13. Apprehension
14. Marked proteinuria
52. Time of Onset
• The onset of eclamptic convulsions can be in the antepartum,
intrapartum, or postpartum period
• 38% antepartum;
• 18% during labour
• 44% postpartum. Rare cases of eclampsia have occurred over a week
after delivery.
• Almost all cases of antepartum eclampsia will occur after 28 weeks of
gestation
53. • Eclampsia that occurs before 20 weeks of gestation is usually
associated with a molar pregnancy, with or without a coexistent fetus.
• Preeclampsia and eclampsia were believed to occur only within 48
hours following delivery.
• Late postpartum eclampsia can occur >48 hours but <6 week after
delivery
54. Presentation and Diagnosis
1. Eclampsia manifests as 1 seizure or more, with each seizure
generally lasting 60-75 seconds.
2. Hypertension ≥ 140/90
3. Proteinuria ≥ 2+
• with or without coexisting systemic abnormalities of the kidneys,
liver, or blood
• Eclampsia in the absence of hypertension with proteinuria occurs
in 38% of cases
• Similarly, hypertension absent in 15-25% of cases
54
55. Principles of management
• Stabilise mother and then deliver foetus
• Treat and prevent fits
• Treat blood pressure
• Attention to fluid balance
• Be aware of and prevent complications
56. Prevention of Eclampsia
•Primary prevention
• Aims:
• To prevent disease or injury before it ever occurs.
• Low-dose aspirin (dosage ranging 60-150 mg daily) reduce the risk of
preeclampsia 10% to 15%.
• Low-dose aspirin is recommended to women with a history of preeclampsia,
• Multifetal gestation,
• Chronic hypertension,
• Type 1 or 2 diabetes, renal disease, and autoimmune disease (ie, systemic lupus
erythematosus, antiphospholipid syndrome)
• Ca supplementation.
57. • Secondary prevention
Aim:
• intervention for early detection of the disease and reducing the impact of
a disease.
• weekly monitoring
a. gestational hypertension or preeclampsia,
b. antihypertensive medications for blood pressure regulation,
c. timely delivery,
d. and prophylactic use of magnesium sulfate during labor and immediately
after delivery in women with preeclampsia with severe features.
58. • women with gestational hypertension or preeclampsia will have
weekly follow-up with close monitoring of blood pressure,
• weekly laboratory test (complete blood count, serum creatinine,
aspartate aminotransferase [AST], alanine transaminase [ALT]),
• serial ultrasound to determine fetal growth every 3 to 4 weeks,
• and weekly antepartum testing. If there is no progression to
preeclampsia with severe features,
• induction of labor at 37 weeks of gestation is recommended.
59. • If there are signs or symptoms for preeclampsia with severe features
(ie, SBP of 160 mm Hg or DBP of 110 mm Hg
• thrombocytopenia, impaired liver function, renal insufficiency,
pulmonary edema, new-onset headache, or visual disturbances),
• the patient should be admitted to the hospital and managed
according to the guidelines
60. Acute care during a seizure
• Airway patency,
• Ensuring oxygenation,
• And avoiding aspiration.
• During this time, the bedside rails should be elevated and padded
• Adequate oxygenation should be maintained during the convulsive
episode, oxygen administration through a facemask at 8 to 10 L/min
• Pulse oximetry can be used for monitoring.
• Arterial blood gas analysis (oxygen saturation of< 92%).
• Foley’s catheterization
61. Treatment of convulsions
• Magnesium sulfate is the drug of choice to prevent subsequent
convulsions in women with eclampsia.
66. • In case of recurrent fits half loading dose : 2gm more
intravenously as 20% solution is given.
• 4 ml of 50% w/v (2 gm of magnesium sulphate) dissolved in
6 ml of saline to make 2 gm of 20% w/v solution( 2gm in 10
ml)
• Magnesium sulphate should be continued for 24 h after
delivery/ last seizure, whichever is later.
67. adverse effects of magnesium sulfate
• Respiratory depression
• Cardiac arrest( come largely from its action as a smooth muscle relaxant.
• Deep tendon reflexes are lost at a serum magnesium level of 9 mg/dl (7
meq/l),
• Respiratory depression occurs at 12 mg/dl (10 meq/ L),
• And cardiac arrest occurs at 30 mg/dl (25 meq/L).
• Patients at risk of impending respiratory depression
intubation and emergency correction with calcium gluconate 10% solution,
10 ml iv over 10 minutes.
• Recommend monitoring magnesium levels every 4 to 6 hours .
68. Fluid Management
• Despite the presence of peripheral edema, patients with
preeclampsia are intravascularly volume depleted, with high
peripheral vascular resistance. Diuretics should be avoided.
• Aggressive volume resuscitation may lead to pulmonary edema,
which is a common cause of maternal morbidity and mortality.
• A central venous pressure (CVP) of 5 mm Hg in women with no heart
disease indicates sufficient intravascular volume, and maintenance
fluids alone are sufficient.
• Total fluids should generally be limited to 80 mL/h or 1 mL/kg/h.
69. Other Regimens-
• Lytic cocktail- Is a combination of chlorpromazine, promethazine
and pethidine
• Diazepam
• Phenyton- in1000mg, iv infusion in one hour, 500mg oral after 10
hrs ,24hrs postpartum
70. Management of the eclamptic patient after a
seizure
• The presence of eclampsia would be an indication for delivery but is
not an indication for cesarean delivery.
• The decision to perform a cesarean delivery should be based on
gestational age,
• fetal condition,
• presence of labor,
• and cervical bishop score.
• Once the maternal and fetal status are stable, and the patient is alert
and oriented to person, place, and time, induction should be started
71. Delivery
• Assess pregnancy and assess cervix
• Vaginal delivery or CS?
• Vaginal if no maternal or fetal distress, no obstetric contraindication
and cervix favourable
• CS if repeated fits, fetal distress or unfavourable cervix
72. • Patients with eclampsia before 30 weeks of gestation who are not in
labor with an unfavorable cervix (bishop score of <5)
Cesarean delivery is recommended.
• Uncontrolled fits
• Unconscious patient and poor prospect for vaginal delivery
• Obstetrics indications
73.
74. • When preeclampsia with severe features is diagnosed after 34 weeks
gestation, delivery is most appropriate.
• The mode of delivery should depend on the severity of the disease
and the likelihood of a successful induction.
• Whenever possible, however, vaginal delivery should be attempted
and cesarean section should be reserved for routine obstetric
indications.
75. • Women with preeclampsia with severe features who have
nonreassuring fetal status, ruptured membranes, labor, or maternal
distress should be delivered regardless of gestational age.
• If a woman with preeclampsia with severe features is at 32 weeks'
gestation or more and has received a course of steroids, she should
be delivered as well.
76. Maternal and Neonatal Outcomes
Maternal mortality and
morbidity
• Placental abruption10%
• Pulmonary edema5%
• Neurological deficit7%
• aspiration pneumonia7%
• Cardiopulmonary arrest4%
• acute renal failure4%
• hepatic rupture
• Cerebral oedema
Neonatal mortality and
morbidity
• Delivery likely to be preterm.
Sequelae of prematurity include
• respiratory distress syndrome,
• chronic lung disease,
• intraventricular haemorrhage,
• cerebral palsy,
• sepsis,
• necrotizing enterocolitis.
• IUFD
76
77. • Post-Natal Care and Follow-Up
• The management of eclampsia in the post-natal period can be divided
into inpatient and outpatient care:
• Inpatient care:
• Regular symptom review – e.g headaches, epigastric pain.
• Bloods 72 hrs post-partum – CBC, LFTs, creatinine.
• Pre-conceptual counselling – advice regarding minimising risk
factors and prophylaxis for future pregnancies.
78. • Outpatient care:
• Consider CT Head – if persistent neurological deficit.
• Measure BP – blood pressure is checked daily for 2 weeks post-
partum.
• Follow-up at 6 weeks – check BP, proteinuria and creatinine.
Repeat CBC, LFTs and creatinine if not previously returned to
normal
80. Long-term Maternal Prognosis
• Women with a history of eclampsia are at increased risk of
preeclampsia in a subsequent pregnancy.
• Rate of preeclampsia in subsequent pregnancies is about 25%
With higher risk if the onset of eclampsia was in the second trimester
of pregnancy.
• Rate of recurrent eclampsia is 2%.
81. Recent Updates
• The National Institute for Health and Care Excellence (NICE)
recommends Early administration of prophylactic aspirin in high-risk
women prior to 16 weeks’ gestation appears to reduce the risk of pre-
eclampsia by 17%. Furthermore, there is an 8% relative risk reduction
of preterm birth and a 14% reduction in fetal and neonatal death
• A recent study demonstrated that women who developed pre-
eclampsia had a significantly lower vitamin D concentration at 14
weeks compared with women in the control group
• Women with levels below 30 nmol/L compared with those with at
least 50 nmol/L had a greater risk of developing pre-eclampsia
82. • Low dietary calcium and low serum calcium concentrations are associated
with pre-eclampsia.
• It has been shown that high-dose calcium supplementation reduces pre-
eclampsia in women from areas with low dietary calcium intake
• A novel “point of care” test used for the prediction of pre-eclampsia is the
measurement of glycosylated fibronectin (GlyFn) serum levels in the first
trimester.
• Increased GlyFn(Glycosylated fibronectin) levels were significantly
associated with blood pressure and small-for-gestational-age neonates.
Analysis of measurements in mild pre-eclampsia showed a weekly change
of 81.7 mg/mL versus 195.2 mg/mL for severe pre-eclampsia.
83. References
• Williams OBSTETRICS 25th edition
• Ian Donald’s 8th edition
• DC Dutta’s 9th edition Obstet Gynecol 2015.
• American Journal of Obstetrics & Gynecology FEBRUARY 2022
• American College of Obstetricians and Gynecologists’ Committee on
Practice Bulletins—Obstetrics. Gestational hypertension and preeclampsia:
ACOG Practice Bulletin, number 222. Obstet Gynecol 2020;135:e237–60.
• Pritchard JA, Cunningham FG, Pritchard SA. The Parkland Memorial
Hospital protocol for treatment of eclampsia: evaluation of 245 cases. Am J
Obstet Gynecol 1984;148: 951–63
Editor's Notes
Speaker’s notes:Elevated levels due to hepatocellular injury and HELLP syndrome
The serum creatinine level is elevated because of a decreased intravascular volume and reduced glomerular filtration rate (GFR).
Speaker’s notes:
SLIDE
After the coma phase, the patient may regain some consciousness, and she may become combative and very agitated. However, the patient will have no recollection of the seizure.
A period of hyperventilation occurs after the tonic-clonic seizure. This compensates for the respiratory and lactic acidosis that develops during the apnoeic phase.
Seizure-induced complications can include (a) tongue biting, (b) head trauma, (c ) broken bones, and (d) aspiration.
Speaker’s notes:
SLIDE
Ecliptic seizures may be divided into 2 phases. Phase 1 lasts 15-20 seconds and begins with facial twitching. The body becomes rigid, leading to generalized muscular contractions.
Phase 2 lasts about 60 seconds. It starts in the jaw, moves to the muscles of the face and eyelids, and then spreads throughout the body. The muscles begin alternating between contracting and relaxing in rapid sequence.
Proteinuria, primarily due to increased glomerular permeability and damage,[53] is an integral part of the diagnosis of preeclampsia. Oliguria, defined as <500 ml/24 h, may occur secondary to hemoconcentration and decreased renal perfusion. Persistent oliguria may indicate acute tubular necrosis, the most common type of acute renal failure seen in preeclampsia.[54]
Carriers of certain inherited metabolic disorders Specifically, women who are heterozygote carriers for β-oxidation disorders, particularly long-chain 3-hydroxyacyl-coenzyme A dehydrogenase deficiency,[43] are at risk for preeclampsia and acute fatty liver of pregnancy.