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MANAGEMENT OF COMPLICATIONS OF PIH : AN OVERVIEW

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Presentation on theme: "MANAGEMENT OF COMPLICATIONS OF PIH : AN OVERVIEW"— Presentation transcript:

1 MANAGEMENT OF COMPLICATIONS OF PIH : AN OVERVIEW

2 DR.VANDANA WALVEKAR Former Dean, Nowrosjee Wadia Maternity Hospital,
Former President, Mumbai Obs and Gyn society, Consultant, Bhatia Hospital, Mumbai

3 PIH PIH can occur without warning at any time during pregnancy or early postpartum period.It also occurs as a chronic form, gradually becoming worse with advancing pregnancy In its mild form it causes NO significant deleterious effect on the mother and the baby BUT inn the severe form plays havoc in their lives with complications

4 PIH What is more the complications are unpredictable!!!
Am JOB 2006 Aug:Ganzewoot etal 216 women with cntrols with HELLP Adverse fetal outcome:g.age :ODratio 0.4 Adverse mat outcome:parity :ODratio 0.4 Hence prediction of clinical course and development of complications is NOT FEASIBLE

5 PIH : COMPLICATIONS Maternal complications: Obstetric:
Abruptio placentae, Eclampsia, Preterm labour, PPH,DIC and coagulopathy HELLP Non Obstetric: acute pulm. Edema,CVA, blindness, ARF, acute pancreatitis, acute Cholecystitis Fetal coplications: IUGR, Prematurity, IUFD, neonatal/childhood neurological deficits

6 PIH : PATHOPHYSIOLOGY It is a multisystem disease with vasospas
& coagulation defects begins with endothelial dysfunction : platelet activation: release of thromboxane A &serotonin: vasospasm: pl. aggregation: damage with coagulopathy multiorgan failure: TERMINATES WITH DELIVERY

7 ABRIPTIO PLACENTAE Commonest, most often mixed APH, occ. Concealed :USG usually confirms the diag. & indicates severity MGT: depends on g.age, parity, inducibility with Bishop’s score, fetal heart +/- Hypertension prophylaxis, supportive mgt with transfusion if needed, ARM/LSCS as delivery only will sort the problem

8 PPH Simple, atonic: preterm labour,ut. Inertia, incoordinate ut. Action, ass. with abruptio Usually responds to standard mgt. with oxytocics etc. 2-5% severe needing surgical measures: B.Lynch suture, stepwise devscularisation of uterine, hysterectomy or int. iliac ligation Ass. With APH: couvelaire uterus: HELLP

9 ECLAMPSIA 5% approx. :ante, intra post partum epileps
Mgt with magsulph Pritchard/modified Pritchard has stood the test of time:RCTS Invest: PT, PTT, FDP, Fibrinogen, D-dimer Mgt: supportive measures, IV 4-6gm Mgso4, foll by 4-6gm im 4-6hrly with close monitoring till under control Induction/LSCS: g.age, FHS +/-,Bishop’s, Intercurrent ecl: R Bhatt: in rare cases

10 ECLAMPSIA ECLAMPSIA in UK - 2006 229 hospitals, 2205-2006 feb
Incidence: 2.7/10,000 38% proteinuria seen only one week prior 99% treated with Mgso4 NO mortality Non eclampsia related compl :10% PNMR:59/10,000

11 help.. HELP.. HELLP Syndrome
Dr. Vandana Walvekar

12 Wein Stein : 1982 H = Hemolysis EL = Elevated liver enzymes LP = Low platelets in a women with pre- eclampsia / eclampsia Appears 24 wks. – post partum (1wk -33%) Maternal Mortality of 24-40% Perinatal Mortality of 30-80%

13 Classification – Mississippi, Tennesse
I. < 50,000 /ml platelets, altered LFT microangiopathic anemia – highest MMR PNMR II. > 50,000 m/1 platelets < 100,000/ml. III. > 100,000 m/1 platelets < 150,000 LFT-LDH > 600 I.U./l, AST ³ 70 I.U./l, ALT ³ 40 I.U./l Partial HELLP: one or two of the features

14 Considered a Variant of P.E. & Eclampsia
Prognosis:- Failure of platelet count to ­ with in 96 hrs. denotes multiorgan non compensatory dysfunction Also occurs : Severe sepsis, Lung injury, multiorgan failure with DIC

15 HELLP – Pathophysiology
Vascular endothelial dysfunction ® ® Platelet aggregation ® fibrin activation & consumption ® Selective organ (Liver) insufficiency ® clinical HELLP

16 Clinical Spectrum Disease of multipara  tension > 150/90
Proteinuria Convulsion Epigastric pain Vomiting Abruptio placenta Retinal detachment with acute blindness Hemolysis Pt’s with ART techniques – donor egg, new partum more prone  MSAFP & ­­ HCG more prone

17 Laboratory Diagnosis Platelets < 100,000/ul LDH >600 I.U./1
AST >70 I.U. ALT > 40 I.u. Uric acid > 7.8mg % Creatinine > 1.0 mg%

18 Maternal Mortality : 25-40%
Causes : Cardio pulm. failure DIC CVA Hepatic rupture Post caesarean shock Multiorgan failure Associated conditions – complement

19 Early disease can be only suspected as the diagnostic symptoms come too late in the course of the diseases

20 Laboratory Evidence Peripheral smear : burr cells LDH (­ sensitive)
S. Haptoglobins ¯¯ early, sensitive Thrombocytopenia  prothrombin time, partial thromboplastin time, ¯ Fibrinogen, ­ FDP AST ³ 70 IU/l ALT ³ 40 I.u./l S. creatinine ­­

21 Management of HELLP Syndrome (Univ. of Mississippi Medical Center)
Anticipate the disease Laboratory evidence to evaluate severity of maternal disease Fetal management: depends on G.age Severity of mat.disease ≥ 34 – deliver within 24 hrs. irrespective of class of disease vag/abd. del. 24-34 – hospitalise, monitor, steroids : Dexa 10 mg 12 hrly till mat. Condition improves

22 HELLP Management (contd.)
Steroids : Fetal; ­­ lung maturity. Mat: platelet count stabilised, AST/ALT ¯¯ Gain time for induction of labour Gain time transfer to III institution Vital to continue post partum to prevent rebound phenomena Nitric Oxide – reverse platelet destruction & promote vasodilation Admin. Of FFP – provide other factors removal of angiopathic debris Platelet transfusion: essential if < pt for immediate C.S., bleeding from I.V. sites, vag del. Imminent, after delivery : for 24 hrs. till pt. Stabilise at ³ 50,000 in C.S. ³ 20,000 in vag.del. Refractory pts. Plasma change as a desperate measure

23 Control of ­ Tension To minimise Abruptio Alpha-dopa/ Labetelol
Nifedepine : sublingual /oral ® normalises platelet count, ­ urine output Control of convulsions: MgSO4 is the drug of choice 4-6gm iv foll. by im 4-6gm every 4-6 hrs. Monitoring is essential IV fluids to maintain output, restriction in cases of renal involvement

24 Management of Labour & Delivery
Delivery is the only way deterioration can be stopped ≥ 34 wks. – expeditions delivery 68% LSCS rate ≤ 34 wks. –cortisone – induction of labour Dexamethazone amelicrates the process & allows time for cervical ripening LSCS Spontaneous expulsion of placenta In situ repair of incision Mass closure of abd.wall Ascitic fluid loss to be compensated Regional anaesthesia safer Look for hepatic haemorrhage

25 Post Partum HELLP PE to be monitored till Post partum corticosteroids
Platelet count > 100,000 LDH ¯ ¯ Diuresis ³ 100 ml/hr ³ 150 £ 100 BP Clinical improvement Post partum corticosteroids ? D&C to remove decidual tissue Hepatic complications: rupture-surgery Recurrent risk: preeclampsia –42%, HELLP – 19-27% Higher risk in del. < 32 wks

26 HELLP:ASSORTED FACTS Essentially: supportive mgt, seizure prophylaxis, BP control, termination Pulm. Edema: IV immunoglobulin viable Refractory HELLP: pl.<30,000,ele. LFT, also need rpt. Transfusions for hematcrit maintenance Hepatic imaging & liver biopsy DO NOT correlate the sverity of HELLP Anasthesia: GA with sevoflurane without epidural/epidural

27 CARDIOVASCULAR COMPLICATIONS
Acute pulm. Edema, usually associated with eclampsia, acute hypertensive crisis without convulsions, can occur postpartum MGT: multidisciplinary, ICU Rapid digitalisation, diuretics, supportive Not advisable to terminate unless pt. stable irresp. of g.age, vag del preferred Surgical mgt only if mandatory Fluid restriction at induction, (conentrated oxytocic admn) no data with misoprostol

28 PE AND FUTURE CARDIOVASCULAR RISK
NEWSTEAD et el:mar2007:Ex,Rev.cardiovascular therapy Pregnancy is a metabolic and vascular “STRESS TEST” for the woman. Those who “FAIL” are at a risk of long term cardiovascular complications ,obesity adds a further risk

29 CEREBROVASCULAR ACCIDENTS
Usually asociated with eclampsia Acute hypertensive crisis without convulsions: mged with MgSo4, sublingual nifedepine, termination VigilPE, GraciaP :RCT :mgt. of severePE IV Hydralazine (apresoline) or labetelol 82 women SPE,HELLP: IV hydralazine5mg. Slow bolus every 20mts for 5 doses IV labetelol20mg bolus:40mg if no hypotension in 20mts:foll by 80mg every 20mts till max 300mg Safe & effective in postpartum period With intracranial hage: LSCS with decompression; Dai etal :nov2007, cl. hypertension

30 FOOTPRINTS IN THE URINE
Acute renal failure: with eclampsia or SPE No positive clinical findings, anuria, hypertension, renal profile abnormal only after hrs Multidisciplinary approach, hemodialysis essental for reversal as anuria is prerenal

31 VISUAL CALAMITIES ..AND Blurring of vision &temp blindness are known and are reversible totally Permanat blindness: rare: associated with SPE & HELLP : reports by Moseman etal OBGY,nov2007 vol100 Acute pancreatitis, cholecystitis can occue due microvascular disturbances even with splanchnic circulation

32 SEVERE PE WITH IUGR Expectant mgt of SPE with IUGR:AMJ mar2007,Hadad et al 239 pts, 24-33wks expectantly managed with steriods till del Maternal outcomes similar by way of labour and other complications to controls Fetal :higher death rath with severe IUGR

33 NEONATES AND PIH MOTHER
Ind j of pediatrics:july2007,vol 74, s. shivkumar: Babies of PIH mothers Thrombocytopenai:22%,higher in preterm No correlation in mat & fetal pl counts Neutropenia:well documented Nucleated RBCs :22% polycythemic in term IUGR: due to chronic asphxia: duration to produce polycythemia not knkwn: Philips et al

34 FUTURE THOUGHTS In this erratic, unpredictable entity it is posible that Serum, urine InhibinA may provide a marker: HamaB et al AmJObGy Dec2006 Plasmaferresis: in severe SPE, refractory HELLP, DIC Aspirin early in pregnancy :evidence inconclusive

35 COMMON PROBLEM UNPREDICTABLE MULTIPLE MANAGEMENT MODALITIES CHALLENGE TO THE OBSTETRICIAN!!! THANK YOU

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