Upload
reese-crowther
View
216
Download
1
Embed Size (px)
Citation preview
Pregnancy Induced Hypertension
Jun Ma
Dept. of Obstetrics & Gynecology
The First Hospital of Xi’an Jiaotong Univ
Introduction
Incidence: China: 9.4%, worldwide: 7-12% The most common and yet serious conditions seen
in obstetrics cause substantial morbidity and mortality in the
mother and fetus Death due to cerebral hemorrhage, aspiration
pneumonia, hypoxic encephalophathy, thromboembolism, hepatic rupture, renal failure
Hypertension in pregnancy
Definition Diastolic BP ≥90 mmHg Systolic BP ≥140 mmHg Or as an increase in the diastolic BP of ≥ 15
mmHg or in the systolic blood pressure of 30 mmHg, as compared to previous pressure
The increased blood pressures be present on at least two separate occasions, > 6h apart
Classification
• Pregnancy-induced hypertension
Preeclampsia
Mild
Severe
Eclampsia• Chronic hypertension preceding pregnancy• Chronic hypertension with superimposed PIH
Superimposed preeclampsia
Superimposed eclampsia• Gestational hypertension
Classification of Hypertensive Disorders in Pregnancy (ACOG)
Classification (1)1. Pregnancy-induced hypertension:
Hypertension associated with proteinuria and edema, occurring primarily in nulliparas after the 20th week or near term.
Preeclampsia
【 mild 】 BP ≥ 140/90mmHg Onset after 20 weeks’ gestation Proteinuria (>300mg/24-hr urine collection) or + Epigastric discomfort Thrombocytopenia
Classification (2)
【 severe 】 BP ≥ 160/110 mmHg Marked proteinuria (>1-2 g/24-hr urine collection or 2+
or more), oliguria Cerabral or visual disturbances such as headache and
scotomata Pulmonary edema or cyanosis Epigastric or right upper quadrant pain (probably
caused by subcapsular hepatic hemorrhage) Evidence of hepatic dysfunction, or thrombocytopenia
Classification (3)
Eclampsia
Meets the criteria of preeclampsia
Presence of convulsions, not attributable
to other neurological disease,
Occurrence: 0.5 -4 %, with 25%
occurring in the 1st 72 hs postpartum
Classification (4)
2. Chronic hypertension proceeding pregnancy (essential or secondary to renal disease, endocrine disease, or other causes)
BP ≥ 140/90 mmHg
Presents before 20 wk gestation
Persists beyond 12 wk postpartum
Classification (5)
3. Chronic hypertension with superimposed preeclampsia or eclamptia
Coexistence of preeclampsia or eclampsia with preexisting chronic hypertension
Cause greatest risk When diagnosis is obscure, it is always wise to
assume that the findings represent preeclampsia and treat accordingly.
Classification (6)
4. Gestational hypertension: not mentioned in
the ACOG
Finding of hypertension in late pregnancy in the
absence of other findings suggestive or
preeclampsia
Transient hypertension of pregnancy
May develop into chronic hypertension if
elevated BP persists beyond 12 weeks
postpartum
High risk factors
Nulliparous <18ys or >40 ys, multiple pregnancy Has previous gestational hypertensive
disorders Chronic nephritis Diabetic Malnutrition Low social status Hydatidiform mole
Etiology: UNCLEAR Immune mechanism (rejection phenomenon,
insufficient blocking Ab) Injury of vascular endothelium----disruption of the
equilibrium between vasoconstriction and vasodilatation, imbalance between PGI and TXA
Compromised placenta profusion Genetic factor Dietary factors: nutrition deficiency Insulin resistance Increase CNS irritability
Pathophysiology
Central nervous system
Raised BP disrupt autoregulation
Increased permeability due to vasospasm---thrombosis of arterioles, microinfarcts, and petechial hemorrhage
Cerebral edema: increased intracranial pressure
CT scan (1/3-1/2 positive): focal hypodensity
Cerebral angiography: diffuse arterial vasoconstriction
EEG: nonspecific abnormality (75% in eclamptic patient)
Eyes
Serous retinal detachment Cortical blindness
Pulmonary system
Pulmonary edema Cardiogenic or noncardiogenic Excessive fluid retention, decreased hepatic
synthesis of albumin, decreased plasma colloid oncotic pressure,
Often occurs postpartum Aspiration of gastric contents: the most
dreaded complications of eclamptic seizures
Kidneys
Characteristic lesion of preeclampsia: glomeruloendotheliosis
Swelling of the glomerular capillary endothelium
Decreased GFR Fibrin split products deposit on basement
membrane Proteinuria Increase of plasma uric acid, creatinine,
Liver
The spectrum of liver disease in preeclampsia is broad
Subclinical involvement
Rupture of the liver or hepatic infarction
HELLP syndrome: hemolysis, elevated liver enzymes and low platelets
Cardiovascular system
Generalized vasoconstriction, low-output, high-resistance state
Untreated preeclamptic women are significantly volume-depleted
Capillary leak Cardiac ischemia, hemorrhage, infarction,
heart failure Increased sensitivity to vasoconstrictor effects
of angiotensin
Blood (1)
Volume: reduced plasma volume Normal physiologic volume expansion
does not occur Generalized vasoconstriction and capillary
leak Hematocrit
Blood (2): coagulation Isolated thrombocytopenia: <150,000/ml Microangiopathic hemolytic anemia DIC (5%) HELLP syndrome: in severe preeclampsia
1. schistocytes on the peripheral blood smear
2. lactic dehydrogenase > 600 u/L
3. total bilirubin > 1.2 mg/dl
4. aspartate aminotransferase >70 U/L
5. platelet count <100,000/mm3
Misdiagnosis: hepatitis, gallbladder disease, ITP
Endocrine system
Vascular sensitivity to catecholamines and other endogenous vasopressors such as antidiuretic hormone and angiotensin II is increased in preeclampsia
Disequilibrium of prostacyclin/ thromboxane A2
Placenta perfusion
500 mm vs 200 mm Acute atherosis of spiral arteries: fibrinoid
necrosis of the arterial wall, the presence of lipid and lipophages and a mononuclear cell infiltrate around the damaged vessel----vessel obliteration---- placental infarction
Fetus is subjected to poor intervillous blood flow
IUGR or stillbirth
Clinical findings (1)Symptoms and signs
1. Hypertension
Diastolic pressure ≥ 90 mmHg or
Systolic pressure ≥ 140 mmHg or
Increase of 30/15 mmHg
2. Proteinuria >300 mg/24-hr urine collection or + or more on dipstick of a random urine
Clinical findings (2)
3. Edema Weight gain: 1-2 lb/wk or 5 lb/wk is
considered worrisome Degree of edema Preeclampsia may occur in women with
no edema Most recent reports omit it from the
definition
Clinical findings (3)
4. Differing clinical picture in preeclampsia-eclampsia crises: patient may present with
Eclamptic seizures Liver dysfunction and IUGR Pulmonary edema Abruptio placenta Renal failure Ascites and anasarca
Clinical findings (4)
Laboratory findings (1)
Blood test: elevated Hb or Hct, in severe cases, anemia secondary to hemolysis, thrombocytopenia, FDP increase, decreased coagulation factors
Urine analysis: proteinuria and hyaline cast, specific gravity > 1.020
Liver function: ALT and AST increase, alkaline phosphatase increase, LDH increase, serum albumin
Renal function: uric acid: 6 mg/dl, serum creatinine may be elevated
Clinical findings (5)
Laboratory findings (2)
Retinal check:
Other tests: ECG, placenta function, fetal maturity, cerebral angiography, etc
Differential diagnosis
Pregnancy complicated with chronic nephritis
Eclampsia should be distinguished from epilepsy, encephalitis, brain tumor, anomalies and rupture of cerebral vessel, hypoglycemia shock, diabetic hyperosmatic coma
Complications
Preterm delivery Fetal risks: acute and chronic
uteroplacental insufficiency Intrapartum fetal distress or stillbirth IUGR Oligohydramnios
Predictive evaluation (1)
1. Mean arterial pressure, MAP= (sys. Bp + 2 x Dia. Bp) /3
MAP> 85 mmHg: suggestive of eclampsia
MAP > 140 mmHg: high likelihood of seizure and maternal mortality and morbidity
Predictive evaluation (2)
2. Roll over test: ROT Preeclamptic patients are more
sensitive to angiotensin II Difference between Bp obtained at
left recumbent position and supine position (at a 5 min interval)
Positive: > 20 mmHg
3. Urine calcium/ creatinine < 0.04
Prevention
Calcium supplementation: not effective in low risk women bur show effect in high risk group
Aspirin (antithrombotic): uncertain Good prenatal care and regular visits Baseline test for high-risk women Eclampsia cannot always be prevented, it
may occur suddenly and without warning.
Treatment
A. Mild preeclampsia: bed rest & delivery Hospitalization or home regimen Bed rest (position and why) and daily weighing Daily urine dipstick measurements of proteinuria Blood pressure monitoring Fetal heart rate testing Periodic 24-h urine collection Ultrasound Liver function, renal function, coagulation
A. Mild preeclampsia: bed rest & delivery
Observe for danger signals: severe headache, epigastric pain, visual disturbances
Sedatives: debatable
B. Severe preeclampsia:
Prevention of convulsion: magnesium sulfate or diazepam and phenytoin
Control of maternal blood pressure: antihypertensive therapy
Initiation of delivery: the definitive mode of therapy if severe preeclampsia develops at or > 36 wk or if there is evidence of fetal lung maturity or fetal jeopardy.
Magnesium sulfate
1. Decreases the amount of acetylcholine released at the neuromuscular junction
2. Blocks calcium entry into neurons
3. Vasodilates the smaller-diameter intracranial vessels
Magnesium sulfate
1. Prevent convulsion
2. Virtually ineffective on blood pressure
3. i.v. or i.m. 5g loading dose 5-10 min, i.v. 1-2g/hr constant infusion Total dose: 20-30 g/d
Toxicity: Diminished or loss of patellar reflex Diminished respiration Muscle paralysis Blurred speech Cardiac arrest
How to prevent toxicity? Frequent evaluation of patellar reflex and
respirations Maintenance of urine output at >25 ml/hr
or 600 ml/d Reversal of toxicity:
1. Slow i.v . 10% calcium gloconate
2. Oxygen supplementation
3. Cardiorespiratory support
Antihypertensive therapy: reduce the Dia. pressure to 90-110 mmHg
Indication Bp> 160/110 mmHg Dia. Bp > 110 mmHg MAP > 140 mmHg Chronic hypertension with previous
antihypertensive drugs usage
Antihypertensive therapy
Medications: Hydrolazine: initial choice Labetolol Nifedipine Nimoldipine Methyldoe Sodium nitroprusside
Medication Mechanism of action
Effects
hydralazineDirect peripheral vasodilation
CO, RBF maternal flushing, headache, tachycardia
labetalol, -a b adrenergic
blocker
CO, RBF maternal flushing,headache, neonatal depressed respirations
nifedipineCalcium channel blocker
CO, RBF maternal orthostatic hypotensionHeadache, no neonatal effects
methyldopaDirect peripheral arteriolar vasodilation
CO, RBF maternal flushing,headache, tachycardia
sodium nitroprusside Direct peripheral vasodilation
Metabolite (cyanide) toxic to fetus
Plasma expander Diuretics
Delivery
Indication of termination of pregnancy
1. Preeclampsia close to term
2. <34 wk with decreased placental function
3. 2 hs after control of seizure
Delivery
Induction of labor
1. First stage: close monitor, rest and sedation
2. Second stage: shorten as much as possible
3. Third stage: postpartum hemorrhage Cesarean section
1. Induction of labor unsuccessful
2. Induction of labor not possible
3. Maternal or fetal status is worsening
Eclampsia
No aura preceding seizure Multiple tonic-clonic seizures Unconsciousness Hyperventilation after seizure Tongue biting, broken bones, head
trauma and aspiration, pulmonary edema and retinal detachment
Management
Control of seizure Control of hypertension Delivery Proper nursing care