Classification Gestational hypertension:>=140/90,>20 wks,no proteinuria,resolves PP Preeclampsia: above + proteinuria>=+1 Eclampsia : preeclampsia + convulsions Chronic HT : < 20 wks,ct > 12 wks PP, +/- proteinuria Chr HT + Superimposed preeclampsia : onset of proteinuria(if nonproteinuric),shootup of BP/proteinuria(if proteinuric)
CASE 1a: Mrs. A, 2O yr old primigravida,under your ANC, develops mild preeclampsia at 30 wks of pregnancy.(BP 150/94 mm Hg ,Urine proteins- +1 on random dipstick sample) Pathogenesis…. Current concepts .. Management :Role of antihypertensives?? Role of bed rest,SRD, sedatives & tranquilisers? Role of antioxidants?? Corticosteroids? Monitoring…… When to deliver?
Antihypertensive drug therapy for mild to moderate hypertension during pregnancy. Antihypertensive drugs are often used to lower blood pressure in the belief that they will prevent this progression. The review of 46 trials, involving 4282 women, found there was not enough evidence to show the benefit of antihypertensive drugs for mild to moderate hypertension during pregnancy. More research is needed. Cochrane Database of Systematic Reviews 2007, Issue 1Abalos E, Duley L, Steyn DW, Henderson-Smart DJ..
Bed rest with or without hospitalisation for hypertension during pregnancy. At present, there is insufficient evidence to provide clear guidance for clinical practice. Therefore, bed rest should not be recommended routinely for hypertension in pregnancy Meher S, Abalos E, Carroli G Cochrane Database of Systematic Reviews 2005, Issue 4
CASE 1b: Mrs. A on routine 2D USG at 31 wks show IUGR on biometry with AFI=6. Further testing?? Primary screening tool -- DOPPLER vs BPP vs NST ?? In Doppler ---uterine a. /umbilical/MCA/venous as primary value screen for fetal well being?? If umbilical flow N –What next? How freq monitoring?? If abN – What next ? Delivery timing & options ?? Role of various Rx options for oligohydramnios …. recommendations…
A study comparing fetal heart-rate monitoring, biophysical profile and umbilical artery Doppler found that only umbilical artery Doppler had value in predicting poor perinatal outcomes in SGA
Grade A(RCOG) Use umbilical artery Doppler as the primary surveillance tool. A systematic review with meta-analysis has provided evidence that the use of umbilical artery Doppler to monitor high-risk fetuses reduces perinatal morbidity and mortality. In addition, there was a significant reduction in the number of antenatal admissions and inductions of labour
RCOG Evidence level II A variety of indices of umbilical arterial Doppler waveform, such as:- Resistance index, systolic/diastolic ratio, pulsatility index and diastolic average ratio, is used for predicting perinatal outcome. Resistance index had the best ability to predict abnormal outcomes
RCOG Evidence level II Frequency of monitoring in SGA fetuses with normal Doppler need not generally be more than once every fortnight.
RCOG Evidence level Ia Grade A The biophysical profile has not been shown to improve perinatal outcome but sufficient data do not exist to rule out its value. However, there is evidence from uncontrolled observational studies that biophysical profile in high-risk women has good negative predictive value, i.e. fetal death is rare in women with a normal biophysical profile
Evidence level Ib The absence of benefit from randomised trials and since it is a time-consuming test, So it cannot be recommended for routine monitoring in low risk pregnancies or for primary surveillance in SGA When primary surveillance with umbilical artery Doppler is found to be abnormal, biophysical profile is likely to be useful given its good negative predictive value in high-risk populations. This recommendation is further supported by evidence that, in high-risk women, the biophysical profile was rarely abnormal when Doppler findings were normal.
Some forms of intervention There is not enough evidence to assess the value of oxygen therapy, nutrient therapy, hospitalisation and bedrest, betamimetics, calcium channel blockers, hormonal therapy and plasma volume expansion in treating growth restriction. The Cochrane Library, Issue 3, 2003
Maternal hydration for increasing amniotic fluid volume in oligohydramnios Simple maternal hydration (two litres of water/Intravenous hypotonic hydration) appears to increase amniotic fluid volume and may be beneficial in the management of oligohydramnios and prevention of oligohydramnios during labour or prior to external cephalic version. Controlled trials are needed to assess the clinical benefits and possible risks of maternal hydration for specific clinical purposes Hofmeyr GJ, Gülmezoglu AM. Cochrane Database of Systematic Reviews 2002, Issue 1.
Mrs .A develops sev preeclampsia at 32 wks.BP 160/110, urine protein +2, Admitted & Ix sent. Started on antihypertensives. Fetal Doppler N. Criteria for severe preeclampsia… Which antihypertensive would you prefer & why ?? Delivery ? Prophylactic MgSO4 ??
Features of severe Pre-Eclampsia Blood pressure >160/110 mm Hg Proteinuria >5 g/24 h Cerebral involvement (hyper-reflexia, seizures) Oliguria < 500 ml /24hr Increased serum creatinine level Pulmonary oedema Epigastric or right upper quadrant abdominal pain Evidence of hepatic injury (HELLP) Thrombocytopenia or disseminated intravascular coagulation Evidence of fetal compromise (IUGR or oligohydramnios)
Drugs for treatment of very high blood pressure during pregnancy. Until better evidence is available, the choice of antihypertensive should depend on the clinician's experience and familiarity with a particular drug, and on what is known about adverse effects. Exceptions are diazoxide, nimodipine , which are probably best avoided. Duley L, Henderson-Smart DJ, Meher S. Cochrane Database of Systematic Reviews: Reviews 2006 Issue 3
IV Labetolol Vs SL/Oral Nifedepine vs Oral hydrallazine
Interventionist versus expectant care for severe pre-eclampsia before term. There are insufficient data for any reliable recommendation about which policy of care should be used for women with severe early onset pre-eclampsia. Further large trials are needed. Churchill D, Duley L. Cochrane Database of Systematic Reviews 2002, Issue 3.
Magnesium sulphate and other anticonvulsants for women with pre-eclampsia Magnesium sulphate more than halves the risk of eclampsia, reduces risk of abruptio placenta and probably reduces the risk of maternal death. It does not improve outcome for the baby, in the short term. A quarter of women have side effects, particularly flushing. Duley L, Gülmezoglu AM, Henderson-Smart DJ.. Cochrane Database of Systematic Reviews 2003, Issue 2.
CASE 1d: After 12 hrs of admission her UOP is 300 ml/12 hrs. Bld urea is 40,s creatinine is 1.0 mg/dl,electrolytes are N.Wt :60 kgs Criteria for renal failure…..can we call this as “renal failure”?
The RIFLE classification (ADQI group) of ARF: Risk (R)- Increase in serum creatinine level X 1.5 or UO <0.5 mL/kg/h for 6 hours Injury (I) - Increase in serum creatinine level X 2.0 or UO <0.5 mL/kg/h for 12 hours Failure (F) - Increase in serum creatinine level X 3.0 or serum creatinine level > 4 mg/dL; UO <0.3 mL/kg/h for 24 hours, or anuria for 12 hours Loss (L) - Persistent ARF, complete loss of kidney function >4 wk End-stage kidney disease (E)- Loss of kidney function >3 months
In next 12 hrs UOP is 100 ml.Total 400 ml/24 hrs. Pathogenesis of ARF in preeclampsia & clinical correlation….Prerenalvs ATN vs CAN Investigations. Role of fluid challenge. Nutrition,fluid & electrolyte balance.how to judge? Role of diuretics ??? Role of renal dose dopamine ??? Dialysis … when ,which type??? Delivery..when??
Investigations BLOOD CBC Urea,creatinine,uric acid Electrolytes LFT S.proteins Coagulation profile ABG RBS Osmolality URINE sp.gravity osmolality electrolytes proteins pigment casts c/s ECG
Prerenal failure Adequately replace fluid losses,maintain BP. Lasix challenge trial to d/d b/w reversible prerenal failure & established ATN (provided oliguria <48 hrs & U:P osmolality > 1.05) If diuresis (>50ml/hr or doubling) established within 3 hrs,maintain NS infusion acc to UOP & replace electrolytes acc to urinary loss estimations. If unsuccessful –objective is to support the functionally anephric pt till kidneys recover.
Diuretics Diuretics commonly have been given in an attempt to convert the oliguric state to a nonoliguric state. However, diuretics have not been shown to be beneficial, and they may worsen outcomes. In the absence of compelling contradictory data from a randomized, blinded clinical trial, the widespread use of diuretics in critically ill patients with acute renal failure should be discouraged. Useful only in management of fluid-overloaded patients Cantarovich F, Rangoonwala B, Lorenz H, Verho M, Esnault VL. High-dose furosemide for established ARF: a prospective, randomized, double-blind, placebo-controlled, multicenter trial. Am J Kidney Dis 2004;44:402-9. Kellum JA. Systematic review: The use of diuretics and dopamine in acute renal failure: a systematic review of the evidence. Critical Care1997;1(2):53–9.
DOPAMINE Dopamine traditionally has been used to promote renal perfusion(1-5 mcg/kg/min ) However, systematic reviews of dopamine treatment in critically ill patients and in patients with sepsis do not support the use of dopamine to prevent renal insufficiency, morbidity, or mortality. In the majority of ARF studies, dopamine was associated only with an increase in urine output. Kellum JA, Decker MJ. Use of dopamine in acute renal failure: a meta-analysis. Crit Care Med 2001;29:1526-31. Denton MD, Chertow GM, Brady HR. "Renal-dose" dopamine for the treatment of acute renal failure: scientific rationale, experimental studies and clinical trials. Kidney Int 1996;50:4-14.
Low-dose dopamine for women with severe pre-eclampsia. It is unclear whether low-dose dopamine therapy for pre-eclamptic women with oliguria is worthwhile. It should not be used other than in prospective trials. Steyn DW, Steyn P. Cochrane Database of Systematic Reviews 2007, Issue 1
Management Restore or maintain fluid balance The maintenance of electrolytes and acid base balance The maintenance of nutritional support Prevention of infection Avoid renal toxins (including NSAIDS) Instigate renal replacement therapies
Nutrition INTAKE 1500 cal (protein free) Oral/parenteral If vol limitation-50%D via central vein Essential L-aminoacids: K,Mg,P:Improve wound healing, hasten recovery Protein intake of 0.6 g per kg per day
Indications for Renal Replacement Therapy Acidosis unresponsive to medical therapy Acute, severe, refractory electrolyte changes (e.g., hyperkalemia) Encephalopathy Significant azotemia (blood urea nitrogen level >100 mg per dL [36 mmol per L]) Significant bleeding Uremic pericarditis Volume overload
Early “Prophylactic” Dialysis Allows more liberal fluid, protein & salt intake. Prevent hyperkalemic emergencies. Reduces infectious Cx. Improves comfort & survival
Hemodialysis Vs Peritoneal dialysis Limited usefulness if hypotension C/I in actively bleeding pt. Controlled anticoagulation reqd Volume shifts-careful Faster correction • Can be used in preg/PP pt. • Easily available • Simple,inexpensive • Lower Cx rate • Minimises rapid metabolic pertubations & fluid shifts • Insert cath high direct vision
Delivery Development of ARF in obs pt is indication of delivery in majority cases. Deliver if UOP<20 ml/hr >2hrs despite adequate vol expansion & immediate delivery not expected Redistribution of CO – better renal perfusion. Remove fetus from hostile environment. Neonate increased urea –osmotisdiuresis -dehydration
CASE 1e: Decision of LSCS taken. Coagulation profile N . Intraopretroplacentalhaematoma 100 gms .Rest uneventful.Post op after 4 hrs continuous trickling p/v present .Rpt coagulation profile sent. PC : 70000/cumm… APTT 70 ,control 40…PT 25 , control 15…Fibrinogen 60 mg/dl. Hb 8.5, Haematopathology ….. MANAGEMENT— FFP…CRYOPPT…PLATELETS ???? How much of above required? Target values?? Monitoring… Other Mx options.. Expected complications??
Base treatment on need to:– – Maintain fibrinogen level above 1 g/l. – Maintain PT and APPT less than 1.5 times control value – Stop persistent active bleeding
Guidelines: FFP Use Usual dosing: 10-15ml/Kg 15-20% rise in factor levels Usually does not correct laboratory coagulation status to “normal” Evidence for its use as prophylaxis in nonbleeding patients, is limited
Cryoprecipitate 10-15 ml per unit (bag) Fibrinogen 250 mg Factor VIII 80-120 units Von Willebrand Factor 40-70% of FFP Factor XIII 20-30% of FFP Fibronectin 20-40 mg
Cryoprecipitate: Dosing 1-2 Units / 10 Kg Expect 60-100 mg/dl rise in fibrinogen Goal: Fibrinogen 70-100 mg/dl Patients on massive transfusion protocol and receiving greater than 10 units of FFP generally do not need additional cryoprecipitate, having received an adequate bolus of fibrinogen in the large quantity of FFP.
Platelets: Risk of Spontaneous Hemorrhage CountSite > 40,000 Minimal 20-40,000 GI Mucosa 5-20 Skin,Mucus Membranes < 5 CNS, Lung
Prophylactic Platelet TX Guidelines Platelet Count/μlRecommendation 0-5,000 Always 5-10,000 If Febrile or Minor Bleeding 11-20,000 If coagulopathy / minor procedure >20,000 If Major Bleed / invasive procedure
Transfused Platelets/Survival 6 units = 1 single donor unit (SDP); available as ¼, ½ and full SDP Dose: adult 1 unit/8-10 kg Lifespan: 7-10 Days Native 2-3 Days Transfused Factors shortening Lifespan: Fever, Sepsis HLA, Platelet Specific Abs DIC Product Age?
CASE 2: 26 yr primi,32 wks pregnancy ,mild preeclampsia,comes with vague symptoms –malaise,epigastricpain,vomiting, giddiness. On Ix--- Hb 9.5,PCV 30, PC 80000,S.Br 2.8, SGPT 45,SGOT 80, RFT N, Coagulation profile N Probable Diagnosis?? Differential diagnosis?? Would you ask for any other Ix?? Pathophysiology …
Laboratory Findings in HELLP Hemolysis Abnormal peripheral smear Total bilirubin > 1.2 mg/dl LDH > 600 IU/L Liver Enzymes AST (SGOT) > 70 IU/L Platelet count < 100,000
Etiology and Pathogenesis Thehemolysisin HELLP syndrome is a microangiopathic hemolytic anemia. Red blood cells become fragmented as they pass through small blood vessels with endothelial damage and fibrin deposits. The peripheral smear may reveal spherocytes, schistocytes, triangular cells and burr cells. Increase in Bilirubin and lactic dehydrogenase levels. Haptoglobin
Etiology and Pathogenesis The elevated liver enzymelevels in the syndrome are thought to be secondary to obstruction of hepatic blood flow by fibrin deposits in the sinusoids. This obstruction leads to periportal necrosis and, in severe cases, intrahepatic hemorrhage, subcapsular hematoma formation or hepatic rupture.
Etiology and Pathogenesis The thrombocytopenia has been attributed to increased consumption and/or destruction of platelets. With platelet activation, thromboxane A and serotonin are released, causing vasospasm, platelet agglutination and aggregation, and further endothelial damage.