critical care preeclampsia eclampsia
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70 patients presented with mild preeclampsia,52 presented with severe preeclampsia and21 patients presented with eclampsia. All of these patients were admitted to the obstetriccare unit of the hospital. All patients of
pr ee cl am ps ia in cl ud in g mi ld pr ee cl am ps iawere regarded as possible of developing anycomplication of preeclampsia and risk of
progression of disease. Detailed history takenand examination performed on admission tolabour ward to assess severity of preeclampsiaand risk of eclampsia.
A detailed history included informationregarding the obstetric history, presenting
complaints, history of symptoms ad signs of pr eeclampsia , impend ing ec lampsia, hi storysuggestive of any organ system involvement,menstrual history, history of investigations
pe rf or me d an d tr ea tm en t ta ke n, an ysignificant past medical and surgical history,history of immunization, history of medication for hypertension,ultrasonography, tests for foetal wellbeing andsymptoms of labour.
On examination, a note is made of thegeneral condition of patient and level of consciousness. Check for pulse rate andvolume, BP in the left lateral position, pallor,oedema feet, icterus, cyanosis, and patellar reflexes. Look for tongue bite, cyanosis,
pa pi ll ar y re fl ex es , pa te ll ar an d pl an ta r reflexes, motor tone in patients witheclampsia. Check the respiratory andcardiovascular systems for aspiration andsigns of congestive cardiac failure (CCF).
On per abdominal examination look for uterine size-Gestational age (GA), foetal life,
pr es en ta ti on an d fo et al he ar t ra te , ut er in eactivity, w/f signs of abruptio placentae,ascites.
On per speculum examination, check for any evidence of leaking, bleeding per vaginum(PV), local cervico-vaginal infection. On per
vaginal examination, check the Bishop’scervical score; and pelvic adequacy in
pr imigravidas and pa tien ts with past hi storyof preterm vaginal delivery or no vaginaldelivery.
Two intravenous lines of no. 18 wereintroduced in peripheral veins. Blood wascollected for Haemoglobin, PCV, CompleteBlood Count, Bleeding Time (BT), ClottingTime (CT), platelet count, Prothrombin time(PT), clot observation test, DIC profile (whereindicated), Blood Urea Nitrogen (BUN),Serum Creatinine, Liver function test andserum electrolytes. Fundoscopy is performed.
Blood is send for grouping and cross matchand confirmed. Enquiry regarding availabilityof FFP platelet concentrates andcryoprecipitate is made. Written informedvalid consent taken, explaining both maternaland foetal prognosis. Relatives asked tomobilize more manpower and finances if required, as the general population is of lower socio-economic class and coming from distant
places.
Investigations are traced. Intrapartumfoetal heart rate monitoring (IPM) done onadmission, if non-reassuring pattern, thenVAST performed. Maternal and foetalmonitoring done every 15 minutes. Obstetricultrasonography was done in cases where the
pr es en ta ti on wa s do ub tf ul , fo et al he ar t no theard on Doppler transducer and for liquor volume, if required.
Patient maintained on liquid diet excepteclamptics, severe preeclamptics withsymptoms and signs of impending eclampsiaand those patients who are likely to need
LSCS delivery and patients on iv oxytocindrip. Patients are given complete bed rest inleft lateral position. Uterine activitymonitored. Strict Intake/Output chartmaintained and sterile pads given. Repeatedhourly questionnaire for symptoms and signs
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of impending eclampsia enquired with patientand knee jerks assessed so as whether Inj.MgSO4 therapy required or not. Sincecontinuous FHR monitoring not possible, IPMis repeated 2 hourly in active labour. Per urethral Foley’s catheter was introduced in
patients on MgSO4 therapy, eclamptics, and pa tien ts wi th low ur ine ou tput and abrupt io pl ac en ta e.
Central venous line (Cavafix) wasintroduced unhesitantly in indicated cases i.e.severe preeclamptics and eclampticsundergoing LSCS, patients with oliguria,Antepartum haemorrhage, and malignant
hypertension. Watch is kept on all organsystems to see whether their function isaffected by progression of preeclampsia. Clotobservation test repeated 4 hourly. Renal,liver function tests, platelet count repeated12 hourly.
Inj. MgSO4 by Pritchard’s regime wasstarted in patients who presented with or developed eclampsia during labour, patients
presenting or developing symptoms and signsof impending eclampsia, severe preeclampsiawith no symptoms and signs of impendingeclampsia, severe preeclampsia but BP of 160/110 mmHg or more on presentation or later on in labour. Patients whose coagulation
prof il e showed abnormal ity were given In j.MgSO4 by University of Tennessee regimeor given Inj. Phenytoin i.e. drip (loading dose)followed by Inj Phenytoin 100 mg iv 8 hourly.
Poor maternal prognostic factors were- pr es en ce of as ci te s, ha em at ur ia , ol ig ur ia ,elevated BUN, S Creatinine, Jaundice, visualdisturbances, prolonged BT and CT,
thrombocytopenia, altered DIC profile,altered level of consciousness, Adultrespiratory distress syndrome.
Patients with mild preeclampsia either had pr es en te d in la bo ur or were in du ce d at 37completed weeks of gestation.
Patients with severe preeclampsia alsoeither had presented in labour or were inducedin view of completed 37 weeks, completed 34weeks or more with severe IUGR andoligohydramnios or foetal well being testsshowing foetal compromise or if anygestational age but developing symptoms andsigns of impending eclampsia or increasingascites or uncontrolled BP or worsening
bi oc he mi ca l pa ra me te rs .
Patients with eclampsia if not inspontaneous labour were induced. Inj.Betamethasone 12 mg i.m. stat and repeatafter 24 hours given to all preeclamptics and
eclamptics with gestational age (GA) less than34 weeks.
Induction of labour was done by Foley’scatheter no. 18 introduction transcervical(Balloon inflated with 30 ml normal saline)and hitched onto the anterior abdominal wall. 1
In patients with Bishop’s cervical score of 9or less. Foley’s catheter was removed 6 hourslater, followed by low artificial rupture of membranes and iv oxytocin drip. In patientswith Bishop’s cervical score of more than 9,labour was induced with low artificial ruptureof membranes and oxytocin iv dripaugmentation of labour.
LSCS was performed for obstetricindications as needed but only if the maternalrisk was low; not at the cost of mother. Secondstage of labour was cut short usinginstrumental delivery. Liberal use of concentrated Oxytocin iv drip and Inj. PG F2 α
po st pa rt um to pr ev en t po st pa rt umhaemorrhage.
Postpartum strict vigilance is still
continued for 24 hours in mild preeclampsia;for 48-72 hours in patients with severe
pr ee cl am ps ia an d ec la mp si a. A co mb in edteam approach helps to achieve a goodmaternal and perinatal outcome whichincludes consultations by Obstetrician,
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Haematologist, Intensivist, Nephrologist andany other specialist consultants, if required.
R e s u l t sThere were 143 patients with preeclampsia-
eclampsia of 1357 deliveries. 70 patients pr es en te d wi th mi ld pr ee cl am ps ia , 52 pr es en te d wi th se ve re pr ee cl amps ia an d 21 presented with ecl ampsia. Tab le 1 shows thecharacteristics of study population.
Of the 70 patients with mild preeclampsia,16 of them had preeclampsia relatedcomplications intrapartum as shown in Table2. No patient had postpartum haemorrhage.Of the 52 patients with severe preeclampsia,30 had no preeclampsia related complications.The remaining 22 patients had single or multiple complications related to
preeclampsia (Table 3). Of the 21 patients who presented with eclampsia, 10 had no further complications. Of the remaining 11eclamptics, 8 had DIC, 2 HELLP syndromeand 2 had impending renal failure (Table 4).3 patients developed Congestive cardiacfailure (CCF), of which 2 patients requiredlife support systems and could not pull
through and died. An unregistered patientwho presented in advanced labour with severe
preeclampsia, jaundice, oligur ia and deranged
coagulation profile expired inspite of allcritical care offered (Table 5).
Almost 10% of preeclampsia women (45)required LSCS. 38 patients requiredinstrumental delivery. There wre 18
perina ta l deaths . 8 pe rina ta l deaths were of foetuses less than 32 weeks of gestation(prematurely and low birth weight); 4foetuses had presented with intrauterinefoetal demise. 4 foetuses had foetal distresswhere LSCS was deferred in view of poor
Table 1 : Characteristics of study population
Total deliveries 1357
Patients with PIH 143
Mild Preeclampsia 70
Severe Preeclampsia 52
Ecla mpsia 21
Nu ll ip ar a wi th PI H 80
Table 2 : Complications in patients with mildp r e e c l a m p s i a
Complicat ion No. of patients
Abruptio placentae 4
HELLP syndrome 3
Intrapartum eclampsia 4
Postpartum eclampsia 2
Severe preeclampsia 10
Table 3 : Complications in patients withsevere preeclampsia
Complicat ion No. of patients
Isolated Thrombocytopenia 1
Asci tes 3
HELLP syndrome 5
D I C 10
Congestive cardiac failure 3
Impending Eclampsia 12
Ecl ampsia 2
Impending renal failure 4
Abnormal l iver function tests 3
Maternal mortal ity 3
Venti lator support 2
Table 4 : Eclampsia related complications
Complicat ion No. of patients
D I C 8
HELLP syndrome 2
Impending renal failure 2
H y p e r m a gn e s a e m i a 1
Table 5 : Lapse in critical care
Complicat ion No. of patients
Congestive cardiacfailure (maternal mortal ity) 1
H y p e r m a gn e s a e m i a 1
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maternal health and 2 babies died of meconium aspiration syndrome. Each patientof PIH has a probability of having any of itsvarying single or multiple complicationsirrespective of severity. Risk of complicationsin patient with severe PIH is 40% and
pa ti en ts wi th mi ld pree clampsia deve lopingcomplications are 20-22%.
D i s c u s s i o n
Severe pregnancy induced hypertension isa disease which is now treated in the intensivecare unit rather than with sedation in thedark room. The pathophysiology is now wellunderstood and allows for better and more
effective management. 2 It is important thatcentres that care for critically ill pregnantwomen should form a strategy to coordinateobstetric and medical care for this unique
po pu la ti on . Each pa ti en t of PI H ha s a probability of having any of its varying singleor multiple organ system involvementirrespective of its severity. In our study, risk of complications in patient with severe
preeclampsia is 40% and pa tien ts with mi ld pr ee cl am ps ia de ve lo pi ng co mp li ca ti on s ar e20-22%.
A uniform baseline protocol is followed for all patients of preeclampsia, eclampsia inlabour and postpartum as already mentionedin the material and methods. Importantdictum in those extremely critical
pr ee cl am pt ic s- ec la mp ti cs is ma te rn al ri sk outweighs foetal risk.
The following steps help to reduce maternalmorbidity by quantity; and quality-
1 . Appropr iate t imely cont inued maternalfoetal monitoring intrapartum and
postpartum.
2. Judicious t imely delivery.
3 . Training of labour ward personnel ,resident doctors in high risk pregnancymanagement . 3
4. To keep vigilance on all body systems i.e.an overview on the whole body and not
just labour progress, Hypertens ion, foetalheart rate.
5 . Perform clot observation test 4 hour ly,IPM 2 hourly. Repeat PIH profile 12hourly; intrapartum and immediate
postpartum.
6. Avoid LSCS for foetal reasons, if high possibil ity of maternal compromise.
7 . Init ial consulta tion by a consultantobstetrician a must, repeat consultations
personal or te lephon ic as required .
8. Patient with mild preeclampsia are at 20-22% risk of progressing to severe
pr ee cl am ps ia an d it s co mp li ca ti onint rapar tum.
9. Patients should be under surveillance for the first 48 hours postpartum. Prolongedsurveillance required in patients withsevere preeclampsia with multiorgansystem involvement and eclampsia.
10. Judicious unhesitant introduction of central venous line for Central venous
pressu re (CVP) moni to ring.
11. Catering to illiterate, low socio-economicstatus women. It is important to useclinical acumen, use bedside tests and thelimited laboratory resources availableduring emergency hours to the best. It isessential to mobilize relatives, monetary,funds, blood and blood components,laboratory reports.
12. Appropriate continued counseling of pa ti en ts an d re la ti ve s al l th ro ug h an dafter labour.
Resultant early diagnosis and treatmentof complication with no disability limitationand no prolonged rehabilitation required.
In a study by Heinonen et al ,4 the overallneed for maternal intensive care was 0.9 per
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1000 deliveries during the study period. Themost common admission diagnoses wereobstetric haemorrhage (73%) and
pr ee cl am ps ia re la te d co mp li ca ti on s (3 2% ).They concluded that although several risk factors associated with maternal intensivecare were documented, most cases occurredin low risk women which imply that the risk is relevant to all pregnancies.
Okafor, Aniebue 5 had a total of 816 patientsadmitted to the intensive care unit duringthe period under review. Eighteen (2.2%) wereobstetric patients. Nine of them (50%) were
pr ee cl am pt ic an d ec la mp ti c pa ti en ts ; fo ur
(22.2%) had obstetric haemorrhage. 5 others(27.8%) presented with the following: asthma, po st op er at iv e re sp ir at or y di st re ss , ce rv ic alincompetence, gestational diabetes andhypertension, and caesarean section for terminal carcinoma of the breast. There weresix deaths (mortality rate 33.3%).Preeclampsia-eclampsia accounted for four deaths (44% mortality rate amongst
preeclampt ics/ec lamptics ), while two deathsaccounted for a 50% mortality rate in theobstetric haemorrhage group. This study
confirms similar reports from the advancednations and Asia that preeclampsia/eclampsiaand obstetric haemorrhage are the leadingcauses of admission to the intensive care unit.The mortality rate in this study is however higher.
Naylor Jr, Olson 6 emphasized that care of the critically ill pregnant patient requires atrue multidisciplinary approach for optimaloutcomes. Alvarez, Marin 7 concluded thatwomen with pregnancy hypertension must becarefully managed by expert physicians,
particularly if they are more than 30-35 yearsold, overweight, with previous history of hypertension or nulliparous in order todecrease the several complications. Theyemphasized that their evaluation and strategy
for evaluation and management of pr ee cl am ps ia , ec la mp si a is a we ll de fi ne d, practical approach .
Mourad 2 addressed the need for stricthaemodynamic monitoring and managementrequired to prevent complications such aseclampsia, DIC, HELLP syndrome, maternaland foetal death. The nurse’s role in themanagement of severe PIH is alsoemphasized.
Moller, Hartmann-Andersen 8 concludedthat the frequency of haemodynamiccomplications in this analysis illustrated the
potent ially disastrous effect of preeclampsia
in itself. Early delivery should always beconsidered in patients with even minor symptoms of treatment failure, regardless of the age of gestation. Should haemodynamiccomplications occur despite this, referral toan intensive care unit should be considered.
Dildy, Cotton 9 states that pregnancyinduced hypertension is a disorder of unknown aetiology unique to pregnantwomen. Classic clinical manifestations includehypertension, proteinuria and oedema. Earlyrecognition and proper management of thisdisease may serve to avoid serious maternalcomplications. Ultimate maternal treatmentdepends on delivery of the foetus and
pl ac en ta . Ad va nc ed st ag es of th is di se as eresult in multiorgan system dysfunction thatmay be life threatening to the mother andfoetus. Such maternal complications of PIHinclude severe hypertension, oliguria or anuria, HELLP syndrome, eclamptic seizures,liver rupture, pulmonary oedema, cerebraloedema, and abruptio placentae. A
multidisciplinary approach of the critical careteam often will effect a reduction in maternalmorbidity and mortality.
C o n c l u s i o n
This study establishes and reaffirms that
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all preeclamptics require vigilanceintrapartum and postpartum preferably in anobstetric intensive care unit.
Primary prevention is a Herculean task.Secondary prevention is not always possibleas most of the patients are referrals withother organ involvement. But correctingthese complications and limiting the disabilityis possible i.e. tertiary prevention.
R e f e r e n c e s
1. Bhatiyani B, Shah Parul , Kansaria JJ, Parulekar SV. Induction of labor, Foley’s catheter. Bo mb ay
Ho spit al Jo ur na l 2003; 45 (2) : 297-300.
2 . Mourad O. The in tens ive care management of
severe pregnancy induce hypertension. Au st Cr it Care 1992; 5 (1) : 20-3.
3. Surratt N. Severe preeclampsia: implications for critical care obstetric nursing. J Ob st et Gy ne co l
Neona ta l Nur s 1993; 22 (6) : 500-7.
4 . Heinonen S , Tyrva inen E , Saar ikoski S ,Ruokonen E. Need for maternal critical care inObstetrics: a population based analysis. Int J Obstet
Ane sth 2002; 11 (4) : 260-4.5 . Okafor UV, Aniebue U. Admiss ion pa t tern and
outcome in critical care obstetric patients. In t J Obstet Anesth 2004; 13 (3) : 164-6.
6. Naylor DF Jr, Olson MM. Crit ical care obstetr icsand Gynecology. Crit Care Clin 2003; 19 (1) :127-49.
7 . Alvarez Navascues R, Mar in R. Severe maternalcomplications associated with preeclampsia: analmost forgotten pathology? Ne fr ol og ia 2001; 21(6) : 565-73.
8. Moller LM, Hartmann-Andersen JF. Treatmentof women with severe preeclampsia in an
intensive care unit during a 3 year period. Ugeskr Lae ger 1990; 152 (38) : 2735-7.
9. Dildy III GA, Cotton DB. Management of severe pree cl am ps ia and ec la mpsi a. Crit Care Clin 1991;7 : 829-50.
DIAGNOSIS OF DUCTAL CARCINOMA IN SITU
`MRI helps [to diagnose] lesions that, if left undetected, would progress to invasive breast cancer'
The standard method for diagnosis of ductal carcinoma in situ (DCIS) is mammography; other br ea st im ag in g te ch ni qu es ha ve be en sh ow n to be un re li ab le . Ch ri st ia ne Ku hl an d co ll ea gu es di d a pros pe ct iv e ob se rv at io na l st udy to as se ss th e se ns it iv it y of MRI an d of ma mm og ra ph y in di ag no si ngDCIS, and to compare the biological profiles of mammography-diagnosed DCIS versus DCIS detected
by MR I al on e. Th ey fo un d th at , of th e 16 7 in tr ad uc ta l ca nc er s th at we re id en ti fi ed , 72 (4 3% ) we remammographically occult but were diagnosed by MRI alone, and that a high proportion of thosediagnosed by MRI alone were high-grade lesions at high risk of developing into invasive cancer. Theresearchers conclude that MRI could help improve the ability to diagnose DCIS, especially DCISwith high nuclear grade. In a Comment, Carla Boetes and Ritse Mann conclude that MRI should nolonger be regarded as an adjunct to mammography but rather as a distinct method to detect breastcancer in its earliest stage.
Lancet Oncol, 2007; 8 : 459, 485.