Transcript The Eclamptic Patient and Management: local and international

The Ecliptic Patient and
Management: local and
international practices
Dr. Chisale Mhango FRCOG
NPC Training in MNH
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Definition of Eclampsia
New onset of grand mal seizure activity
and/or unexplained coma during
pregnancy or postpartum in a woman with
signs or symptoms of preeclampsia
It typically occurs at ≥ 20th week of
gestation.
It is considered a complication of severe
preeclampsia.
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Prevalence
• 10% of all pregnancies are complicated
by hypertension.
• Eclampsia and preeclampsia account for
about half of these cases worldwide.
• Preeclampsia affects approximately 4.5
to 11.2% of pregnancies in
industrialized countries [ 33]
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Presentation
• Seizure or postictal state (100%)
– tonic-clonic spasms like epilepsy
• Headache (83%), usually frontal
• Vision disturbance (44%), such as blurred
vision and photophobia
– Nurse patient in a darkened room
• Amnesia and other mental status changes
• Coma (unconsciousness)
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Presentation cont.
Physical signs
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
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Physical signs cont.
9. Oliguria or anuria
10. Localizing neurologic deficits
11. Right upper quadrant or
epigastric abdominal
tenderness with nausea
(20%)
12. Generalized oedema (49%)
13. Small fundal height for the
estimated gestational age
14. Apprehension
15. Marked proteinuria
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Aetiology
1.
2.
3.
4.
5.
Genetic predisposition,
Immunology,
Endocrinology,
Nutrition,
Abnormal trophoblastic
invasion,
6. Coagulation
abnormalities,
7. Vascular endothelial
damage,
8. Cardiovascular
maladaptation,
9. Dietary deficiencies or
excess, and infection
have been proposed as
etiologic factors for
preeclampsia/eclampsia
[2]
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Risk Factors for Eclampsia
The following are considered risk
factors for eclampsia:
The following pre-existing medical
conditions are also considered risk
factors[4] :
• Family history of
preeclampsia, previous
preeclampsia and
eclampsia[2]
• Multifoetal gestations,
• hydatidform mole,
• foetal hydrops,
• Teen pregnancy
• Primigravida/Nulliparity
• Patient older than 35 years
•
•
•
•
•
•
Low socioeconomic status
Obesity
Renal disease
Gestational diabetes
underlying hypertension
chronic illnesses such as
– autoimmune disease
– diabetes mellitus
– renal disease.
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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 reported in the
United Kingdom.[5]
• Similarly, hypertension was absent in 16% of cases
reviewed in the United States.[4]
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Differential Diagnosis
1. Cerebral malaria
2. Subarachnoid
Haemorrhage
3. Cerebellar
Haemorrhage
4. Encephalopathy,
Hypertensive
5. Encephalitis
6. Hypoglycaemia
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7. Meningitis
8. Stroke, Haemorrhagic
9. Stroke, Ischemic
10. Metabolic Disorders
11. Undiagnosed Brain
Tumour e.g.
Gestational
Trophoblastic
Neoplasia
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Laboratory studies to guide
management [60]:
1.
2.
FBC with platelet count
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[2]
iv. Elevated levels due to
hepatocellular injury and
HELLP syndrome
v.
Fibrinogen levels, and fibrin
degradation products and
vi. Prothrombin time,(abruptio
placentae, or
microangiopathic
haemolytic anaemia),
vii. Activated partial
thromboplastin time
3.
Kidney function tests
a. Blood Urea Nitrogen,
b. Creatinine clearance,
c. Uric acid,
d. 24-hour urine collection for
protein excretion
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Maternal and Neonatal Outcomes
Maternal mortality
Neonatal mortality
Maternal death is largely a
result of
• complications from
abruptio placentae,
• hepatic rupture, and
• Eclampsia
• Delivery likely to be
preterm. Sequelae of
prematurity include
– Cerebral oedema
– respiratory distress
syndrome,
– chronic lung disease,
– intraventricular haemorrhage,
– cerebral palsy,
– sepsis,
– necrotizing enterocolitis.
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Management
Supportive care
• Delivery is only
definitive treatment
for eclampsia (i.e. removal
of the placenta from the uterus).
• Admit to intensive
care setting for
supportive care and
treatment until
delivery (do not leave woman
alone).
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1. Secure an intravenous (IV)
line with a large-bore
catheter, - Ringer lactate or
normal saline 30 drops/min.
or 1 litre in 6-8 hrs.
2. Administer oxygen, and (iii)
keep patient in left lateral
decubitus position.
3. Supportive care for ecliptic
convulsions includes the
following:
–
–
–
–
Close monitoring
Maintain airway at all times
Anticonvulsant therapy
Blood pressure (BP) control
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Management cont.
1. BP should be assessed with the goal of maintaining the
systolic BP at ≤ 170 mmHg; diastolic BP ≤ 110 mm Hg with
antihypertensive medications as needed (e.g., hydralazine
(apresoline), labetalol, nifedipine).
– NB: Excessive decrease of BP can cause inadequate uteroplacental
perfusion and foetal distress.[13]
2. Antenatal steroids may be administered in anticipation of
delivery at less than 34 weeks gestation.
– Betamethasone (12 mg IM q24h × 2 doses) or dexamethasone (6 mg
IM q12h × 4 doses) is recommended.
3. Keep nil by mouth (including medications) until patient is
stabilized or delivered, to reduce risk for aspiration when
postictal.
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Management cont.
Maternal monitoring
Foetal monitoring
• Monitor
• Foetal heart rate should
be monitored
continuously.
– (a) fluid intake and
urine output
– (b) maternal
respiratory rate, and
– (c) uterine
contractions status.
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– If the foetal heart tracing
does not improve following
a seizure, further
evaluation should be
undertaken.
• Abruption may be
present where uterine
hyperactivity and foetal
bradycardia persists. 14
Management cont.
Pharmacotherapy goals
• reduce morbidity,
• prevent complications,
and
• correct eclampsia.
The drug of choice
• MgSO4 is drug of
choice.[13]
• Control of hypertension
is essential to prevent
further morbidity or
possible mortality.
– Most recommended
antihypertensive agents
are hydralazine,
labetalol, and nifedipine.
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Management of Hypertension
1. Hydralazine 5 mg IV over 3-4 minutes, if not
possible give IM every 30 minutes until BP ≤
170/90. MAXIMUM total dose 20 mg.
2. If hydralazine not available give Labetalol 10 mg
IV
a. If inadequate response after 10 minutes, repeat 20
mg, if ten minutes later still adequate increase to
40mg, then 80 mg ten minutes later if still
inadequate
3. Nifedipine 5 mg orally. If no response after 10
minutes, repeat dose
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Monitor patient closely
1. Assess pregnancy status. If pregnant
a. Deliver as soon as patient is stabilised
b. Deliver regardless of gestation
2. Measure temperature 4 hrly
a. If ≥ 38 degrees C, treat for fever (antimalarial or
antibiotic)
3. Assess the cervix
a. If soft, thin and partially dilated do ARM (Bishop score
4)
b. If unfavourable, ripen cervix with cytotec/misoprostol
c. If there is foetal distress do C/S
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Delivery (antepartum or intrapartum
eclampsia)
• Adequate pain relief for labour and delivery is vital and
may be provided with either systemic opioids or
epidural anaesthesia.
• In the absence of foetal malpresentation or foetal
distress, oxytocin or prostaglandins may be initiated to
induce labour.
• Caesarean delivery recommended in patients with an
unfavourable cervix and a gestational age of 30 weeks
or less.
– When emergency caesarean delivery is indicated,
substantiating the absence of coagulopathy before the
procedure is important.[16]
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Anaesthesia
• For non-emergency caesarean delivery, epidural or
combined techniques of regional anaesthesia are
preferred.
• Regional anaesthesia is contraindicated in the presence
of coagulopathy or severe thrombocytopenia (< 50,000
platelets/µL).
• General anaesthesia in women with eclampsia
increases the risk of aspiration, and airway oedema
may make intubation difficult. It also can produce
significant increases in systemic and cerebral pressures
during intubation and extubation.
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Management of PreeclampsiaEclampsia According to Severity (1)
Severity
Gestational age at
diagnosis
Mild preeclampsia
<38 wk without maternal
(≥140mm Hg/90mm Hg – or foetal compromise (a)
≤160mm Hg/110mm Hg)
Management
Hospitalization for bed
rest and close observation
Maternal glucocorticoid
therapy at 24-34 wk for
foetal lung maturation
≥38 wk without maternal
or foetal compromise
Delivery
Magnesium sulphate
seizure prophylaxis
intrapartum and
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Management of PreeclampsiaEclampsia According to Severity (2)
Severity
Gestational age at
diagnosis
<32 wk
Management
Hospitalization with close maternal
and foetal surveillance, ideally in a
tertiary care centre
Maternal glucocorticoid therapy for
foetal lung maturation if ≥24 weeks
Delivery if maternal or foetal
compromise
Severe preeclampsia (b)
(≥ 160 mm Hg/110 mm Hg)
32-36 wk
Delivery
Magnesium sulphate
Antihypertensive therapy
Maternal glucocorticoid therapy for
foetal lung maturation if <34 weeks
In selected women, cautious delay
in
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delivery until foetal lung maturity is
Management of PreeclampsiaEclampsia According to Severity (3)
Severity
Gestational age at
diagnosis
Management
≥36 wk
Delivery
Magnesium sulphate
seizure
Antihypertensive therapy
≥20 wk
Eclampsia
Stabilization and
expedient delivery
Magnesium sulphate
seizure
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Antihypertensive therapy
References
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2000; 183: S1-S22.
4. MacKay AP, Berg CJ, Atrash HK. Pregnancy-related mortality from preeclampsia and eclampsia. Obstet Gynecol 2001; 97: 533-538.
5. Committee on Technical Bulletins of the American College of Obstetricians and Gynecologists. ACOG technical bulletin: Hypertension in
pregnancy-Number 219: January 1996 (replaces no. 91, February 1986). Int J Gynaecol Obstet 1996; 53: 175-183.
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Services, revised July 2000. Available at: http://www.nhlbi.nih.gov/health/prof/heart/hbp/hbp_preg.pdf. Accessed June 24, 2003.
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MacDonald MG (eds): Neonatology: Pathophysiology and Management of the Newborn. Philadelphia, Lippincott Williams & Wilkins, 1999, ed
5, pp 125-131.
14. Pirani BB, Campbell DM, MacGillivray I. Plasma volume in normal first pregnancy. J Obstet Gynaecol Br Commonw 1973; 80: 884-887.
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1989; 256: H1060-H1065.
32. Centers for Disease Control and Prevention. Maternal mortality: United States, 1982-1996. MMWR Morb Mortal Wkly Rep 1998; 47: 705707.
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and Welfare, Public Health Service, National Institutes of Health, 1972.
35. Trupin LS, Simon LP, Eskenazi B. Change in paternity: A risk factor for preeclampsia in multiparas. Epidemiology 1996; 7: 240-244.
43. Tyni T, Ekholm E, Pihko H. Pregnancy complications are frequent in long-chain 3-hydroxyacyl-coenzyme A dehydrogenase deficiency. Am J
Obstet Gynecol 1998; 178: 603-608.
44. Pridjian G, Puschett JB. Preeclampsia: Part 2-Experimental and genetic considerations. Obstet Gynecol Surv 2002; 57: 619-640.
45. Pridjian G, Puschett JB. Preeclampsia: Part 1-Clinical and pathophysiologic considerations. Obstet Gynecol Surv 2002; 57: 598-618.
53. Katz M, Berlyne GM. Differential renal protein clearance in toxaemia of pregnancy. Nephron 1974; 13: 212-220.
54. Cunningham FG, Gant NF, Leveno KJ, et al. Hypertensive disorders in pregnancy, in Williams Obstetrics. New York, McGraw-Hill Health
Professions Division, 2001, ed 21, pp 567-618
60. Barron WM, Heckerling P, Hibbard JU, et al. Reducing unnecessary coagulation testing in hypertensive disorders of pregnancy. Obstet23
Gynecol 1999; 94: 364-370.
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