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Fetal Malpresentation and positions
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OBSTETRIC NURSING EXAM REVIEW |care of women during pregnancy and childbirth and in the diagnosis and treatment of diseases of the female reproductive organs
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Pre-eclampsiaPre-eclampsia = mulL-system disease; usually manifests as HTN and proteinuri
delivery. Blood vessel endothelial cell damage, in assoc with exaggerated mate
inc capillary permeability and clo_ng dysfuncLon. Can affect all maternal orga
and complicaLons. Inc vascular resistance à HTN, inc vascular permeability à
blood flow for IUGR and reduced cerebral perfusion for eclampsia. 2 stages dis
Stage 1: dev of disease; occurs <20 weeks; causes no symptoms. In normal pre
spiral arterioles à vasodilataLon of vessel walls. In pre-eclampsia, this invasion
maternofetal trophoblast interacLon may be caused by altered immune respon
may contain atheromatous lesions. Result = decreased uteroplacental blood flo
BP normally changes in pregnancy: BP dep on systemic vasc resistance + Stage 2: manifestaLon of the disease; Ischaemic placenta, probably via exagge
cardiac output; usually falls to minimum level in 2nd tri (by 30/15mmHg) induces widespread endothelial cell damage à vasoconstricLon, inc vasc perm
due to dec vasc resistance; occurs in both normotensive + chronically HTN = sign rather than disease; occasionally absent unLl late stages; early dise
hypertensive women. By term, BP inc again to pre-pregnant levels. HTN Establishing diagnosis of pre-eclampsia: BP rises > 140/90mmHg with Proteinu
due to pre-eclampsia – largely due to inc systemic vascular resistance. Courses and Degrees of disease:
Protein excreLon in normal pregnancy = inc, but in absence of underlying Disease = progressive; variable and unpredictable. HTN usually precedes prote
renal disease = <0.3g/24h. develop life-threatening disease at 24 weeks; others develop mild HTN at term
Classifica8on and degrees of pre-eclampsia
Pre-exis8ng HTN in pregnancy: HTN: Mild (140/90-149/99 mmHg), moderate (150/100-159/109mmHg) or sev
BP already treated/ >40/90mmHg before 20 weeks. Underlying HTN Mild: proteinuria and mild/moderate HTN
present in 5% pregnancies. More common in older + obese women, Moderate: proteinuria and severe HTN with no maternal complicaLons
posiLve FH or in those who develop HTN taking combined OCP. PaLents Severe: proteinuria and any HTN <34weeks of with maternal complicaLons
with pregnancy-induced HTN have underlying predisposiLon to HTN; Epidemiology: Pre-eclampsia variably affects 6% nulliparous women. Less com
may need Rx later in life. addiLonal RFs present. Approx 15% recurrence rate (up to 50% if severe pre-ec
Ae8ology: Primary or ‘idiopathic’ HTN = most common cause. Secondary Principal RF for pre-eclampsia: nulliparity; previous history; family history; old
HTN commonly assoc with obesity, DM or renal disease causes e.g. diabetes; twin pregnancies; autoimmune disease (esp anLphospholipid syndro
polycysLc disease, renal artery stenosis or chronic pyelonephriLs. Rare pregnancies with a large placenta (twins, fetal hydrops, molar pregnancy).
cases: phaechromocytoma, Cushing’s syndrome, cardiac disease and Assessment of Urinary Protein:DipsLcks (bed); Trace: seldom significant; 1+: p
aorLc coarctaLon. >2+: signif proteinuria likely: quanLfy; Protein: creaLne raLo (PCR) >30mg/nmo
Clinical features: HTN inc in late pregnancy. Symptoms usually absent; 24h collecLon >0.3g/24h: confirmed significant proteinuria
look for fundal changes, renal bruits; radiofemoral delay; proteinuria in Clinical Features: History: pre-eclampsia is usually asymptomaLc. Late stage: h
pt with renal disease is usually present at booking disturbances, nausea/vomiLng; epigastric pain
Complica8ons: principle risks – worsening HTN and pre-eclampsia: risk ExaminaLon: HTN usually first sign; occasionally absent unLl late stages. Oedem
inc 6x. In absence of these, perinatal mortality is only marginally inc. in pre-eclampsia may be massive, not postural or of sudden onset. The presenc
Inves8ga8ons: to idenLfy secondary HTN: in severe cases, exclude suggesLve of impending complicaLons. Urine dipsLck tesLng for protein to be
phaeochromocytoma: at least 2x 24-h urine collecLons for VMA: Complica8ons:
maternal mortality phaeochromocytoma is very high Maternal: Early onset disease tends to be more severe; Occurrence of any of fo
To idenLfy pre-eclampsia: quanLficaLon of any proteinuria at booking together) = indicaLon for delivery whatever the gestaLon:
and uric acid level allow for comparison in later pregnancy - Eclampsia: grand mal seizures (0.05% of all pregnancies in UK); prob result
Management: HTN: ideally, medicaLon changed pre-pregnancy; ACEI = Mortality can result from hypoxia and concomitant complicaLons of severe
teratogenic + affect fetal urine producLon. Labetalol = normally used; and intensive surveillance for other complicaLons
nifedipine = 2nd line agent. Meds may not be req in second trimester due - Cerebrovascular haemorrhage: due to failure of cerebral blood flow autore
to physiological fall in BP. >140mmHg. Treatment of HTN should prevent this.
Risk of pre-eclampsia: pregnancy treated as ‘high-risk’; screening using - Liver and coagula8on problems: HELLP syndrome. DIC, liver failure and live
uterine artery Doppler and addiLonal antenatal visits are usual. Low- typically experiences severe epigastric pain. Haemolysis turns urine dark. R
dose aspirin advised. Pre-eclampsia suggested by worsening HTN, and prophylaxis against eclampsia. ICU therapy is required in severe cases.
confirmed by finding of significant proteinuria for first Lme 20 weeks. - Renal failure: idenLfied by careful fluid balance monitoring and creaLnine
Delivery usually undertaken by 40 weeks (benefits of this are debated). required in severe cases
- Pulmonary oedema: severe pre-eclampLc parLcularly vulnerable to fluid o
treated with O2 and frusemide; assisted venLlaLon may be required. ARDS
Hypertensive disorders in pregnancy maternal mortality associated with pre-eclampsia.
Pregnancy induced HTN: pre-eclampsia; gestaLonal HTN; When BP rises Fetal: Perinatal mortality &morbidity of fetus inc: pre-eclampsia = 5% sLll-birth
>140/90mmHg aSer 20 weeks; Can be due to pre-eclampsia/ transient In pregnancies affected <34weeks, IUGR. Preterm delivery oSen req; spontane
HTN. Pre-eclampsia = disorder in which HTN and proteinuria (>0.3g/24h) At term, pre-eclampsia affects fetal growth less; assoc with increased morbidit
appear in second half of pregnancy, oSen with oedema. Eclampsia = increased risk of placental abrupLon.
occurrence of epilepLform seizures: most dramaLc complicaLon. Inves8ga8on: bedside dipsLck urinalysis; exclude infxn- urine culture andquan
Occasionally proteinuria absent, e.g. early disease - not always (PCR) on single sample (30mg/nmol roughly equivalent to approx 0.3g/24h pro
disLnguished from gestaLonal HTN (new HTN presenLng aSer 20 weeks absent in early disease so repeat test. Monitor maternal complicaLons: blood t
without proteinuria). high; rapid fall in platelets due to platelet aggregaLon on damaged endothelium
Pre-exis8ng or chronic HTN: Primary/ Secondary; Present when BP in LFT (ALT) suggests impending liver damage of HELLP. LDH levels rise with live
>140/90mmHg before pregnancy or <20 weeks gestaLon, or woman is funcLon oSen mildly impaired; rapidly rising creaLnine suggests severe compli
already on anL-hypertensive medicaLon. This may be primary HTN or fetal complicaLons: US scan helps esLmate fetal weight at early gestaLons- use
may be secondary to renal/ other disease. May also be pre-exisLng artery Doppler; if abnormal, CTG required to evaluate fetal well-being
proteinuria due to renal disease. PaLents with underlying HTN are at Screening and preven8on: All pregnant women, esp. high risk, have regular BP
increased risk (6x) of ‘super-imposed’ pre-eclampsia tests = relaLvely inaccurate. Most commonly used = uterine artery Doppler at 2
Low-dose aspirin (75mg) starLng before 16weeks modestly reduces risk of pre-
Management: Women with new HTN >140/90mmHg = assessed in ‘day assess
HELLP Syndrome H (Haemolysis): dark urine, raised lacLc dehydrogenase
invesLgaLons performed. PaLents without proteinuria and with mild/moderat
(LDH), aneamia; EL (Elevated Liver enzymes): epigastric pain; liver
managed as OP. BP and urinalysis repeated 2xweek, US performed every 2-4 w
failure; abnormal clo_ng; LP (low platelets): Normal self-limiLng
Admission: Criteria for admission in pre-eclampsia or suspected pre-eclampsia
on dipsLck; or >0.3mg/24h on 24h collecLon; Diastolic BP >160/110mmHg; Sus
Postnatal care of the pre-eclamp8c pa8ent
An8hypertensives: if BP reaches 150/110mmHg; urgently req 160/110mmHg.
Delivery= only cure for pre-eclampsia; oSen takes 24h+ for severe
recommended. Oral nifedipine is used for iniLal control, with IV labetalol as 2n
disease to improve; may worsen during this Lme. Blood test: Liver enz,
Magnesium sulphate: used both for Rx and in severe disease, prevenLon of ec
platelets, renal funcLon are monitored closely. Low platelet levels usually
anLconvulsant, but by inc cerebral perfusion, probably treats underlying patho
return to normal within a few days. Fluid balance monitoring is essenLal:
resulLng in resp depression and hypotension, but is preceded by loss of patella
pulmonary oedema and resp failure may follow uncontrolled
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