Renal diseases in pregnancy DR PRAYTHIESH BRUCE MBBS

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Renal diseases in pregnancy DR PRAYTHIESH BRUCE MBBS

  1. 1. THE RENAL DISEASES IN THE KIDNEY BY PRAYTHIESH BRUCE(CRRI) DEPT OF OBG,SMIMS KULASEKHARAM
  2. 2. OVER VIEW Introduction Urinary tract infection Acute pyelonephritis Chronic pyelonephritis Acute renal failure Pregnancy in renal transplant patient Hypertension and renal disease
  3. 3. INTRODUCTION Diseases of urinary tract is common in pregnancy-structural and functional changes are normally seen in pregnancy STRUCTURAL CHANGES: Dilatation of urinary tract-iii trimester Stasis,hydronephrosis occur- due to gravid uterus and dilatation of right side ureter occur-due to dextrorotation uterus Progesterone-relaxant-smooth muscle
  4. 4. FUNCTIONAL CHANGES INPREGNANCY Renal blood flow-increases by 80% Gfr,creatinine,creatinine clearance-increases by 50% >0.9%mg/dl s.creatinine suggest renal disease Glycosuria-lowering of renal threshold Sodium and water retention Fall in osmolality
  5. 5. URINARY TRACT INFECTION Commonest infection Causative organism; Ecoli Klebsiella Pseudomonas aeroginosa TYPES A)asymptomatic bacteruria B)cystitis C)acute pyelonephritis
  6. 6. ASYMPTOMATIC BACTERURIA Occur in 5%pregnancy Must be treated as 30%can cause symptomatic infection Diagnosis: First visit:screening by urine culture and microscopy Routine mid stream urine culture of >1,00,000organisms per 1 ml (Len)leucocyte esterase nitrate dip stick test can be used if prevalence is low in the population
  7. 7. TREATMENT OF ASYMPTOMATICBACTERURIA Treatment required to prevent pyelonephritis/preterm delivery It is associated with risk of hypertension,preeclampsia,anaemia in mother and lbw in children Treatment depend on culture sensitivity report
  8. 8. TREATMENT OF ASYMPTOMATICBACTERURIA(3-5)DAYS Oral antibiotics: Ampicillin 500mg qid Amoxycillin 5oomg tds Cephalexin 250mg tds Nitrofurantoin 100mg qid Iv antibiotics: Cefuroxime 750 mg tds Coamoxyclav 1.2g tds
  9. 9. CYSTITIS Infection of lower urinary tract Characterised by burning micturition( dysuria) Frequency Urgency Complicate in 1% pregnancy
  10. 10. CYSTITIS CAUSATIVE ORGANISM Ecoli Klebsiella Pseudomonas aeroginosa DIAGNOSIS: Urine analysis shows Bacteriuria,pyuria,hematuria Urine culture and sensitivity
  11. 11. TREATMENT FOR CYSTITIS Depend on culture sensitivity report Oral antibiotics: Nitrofurantoin 100mg qid Ampicillin 500mg qid Amoxycillin 500mg tds Cephalexin 250mg tds
  12. 12. ACUTE PYELONEPHRITIS Infection of upper urinary tract involving both renal pelvis and parenchyma Incidence- 1-2% Causative organism; Ecoli Klebsiella Pseudomonas aeroginosa
  13. 13. CLINICAL FEATURES OFACUTE PYELONEPHRITIS Onset is acute, 2nd &3rd trimester of pregnancy Symptoms: Anorexia, back pain , chills & rigor with fever, dysuria, nausea & vomiting Signs: Increased temprature(101of) Urine turbid Tachycardia
  14. 14. INVESTIGATIONS FOR ACUTEPYELONEPHRITIS Urine examination: High specific gravity, acid reaction, proteinuria, leucocytes, red cells, white cell cast,bacteria Urine culture & sensitivity test: Blood examination: sign of renal dysfunction, elevated bun, creatinine & creatinine clearance
  15. 15. COMPLICATIONS OF ACUTEPYELONEPHRITIS Septic shock due to endo-toxins Pulmonary injury Chronic renal infections Adult respiratory distress syndrome Abortion, fetal growth restriction,intra-uterine fetal death Premature labour
  16. 16. TREATMENT OF ACUTEPYELONEPHRITIS Hospitalisation, bed rest, plenty of fluids, easily digestable diet, pulse oximetry 4th hrly TPR & B.P monitoring Uterine contractions, fetal monitoring, I.V.F for dehydrated & oliguric patients (crystalloids,dextrose, D.saline) I/V antibiotics Ampicillin 500mg iv 6th hrly Co amoxyclav 1.2g iv 12 hrly after patient is afebrile for 24-48 hrs oral antibiotics started
  17. 17. CHRONIC PYELONEPHRITIS Chronic diseases charecterised by severe scarring of the kidneys resulting from persistent/ recurrent infections in patients with vesico-urethral reflux Complications : Chronic hypertension Acute pyelonephritis Chronic microcytic anaemia Pre-eclampsia, hyponatraemia, glycosuria
  18. 18. TREATMENT OF CHRONICPYELONEPHRITIS Maternal & fetal prognosis depends on the extent of the renal damage Cap. Ampicillin 500mg/tab.nitrofurantoin 100mg/cap. Cephalexin 500mg -1cap. Every night for the duration of pregnancy
  19. 19. ACUTE RENAL FAILURE Rare complication in pregnancy in which sudden decrease in renal function with oliguria over a period of hours or days Diagnosis: Oliguria, hyperkalemia, metabolic acidosis,rising blood urea &creatinine
  20. 20. CAUSES OF ACUTE RENALFAILURE Obstetric haemorrhage Infection Septic abortion Pre eclampsia Drugs-nsaids Renal diseases Post renal(obstructive uropathy)
  21. 21. TYPES OF ACUTE RENAL FAILUREACUTE TUBULAR RENAL CORTICALNECROSIS NECROSISLess serious seriousReversible Irreversiblea/w sepsis & htn a/w obstetric causes& pre-eclampsiaKidney lesion- focal, Kidney lesion-dilatation & flattening of focal,patchyepethelium of confluent/gross resultingDCT,pigmented cast in from thrombosis of renallower part of nephrons vascular system
  22. 22. TYPES OF ACUTE RENAL FAILUREACUTE TUBULAR RENAL CORTICALNECROSIS NECROSISPatint have high grade Oliguria which can lead totemperature, vomiting, anuria, azotoemiadiarhoea &consumptive coagulopathyShock occurs rapidly & Extra-renal manifestationsmay have mild jaundice, like cardic dilatation, CHF,pallor& cyanosis lethargy, convulsionsMost patient respond to _volume resuscitation&vigorous antibiotics inICU
  23. 23. CLINICAL FEATURES OFACUTE RENAL FAILURE Oliguria- sign of acute impaired renal function Input /output chart Patient is warm to touch, thirsty, irritable, lethargic Rise in blood urea &serum potassium level which causes muscular & ECG changes In diuretic phase there is excess of passage of urine, but blood urea remains high
  24. 24. MANAGEMENT OF ACUTE RENAL FAILURE Early diagnosis is important Blood volume replacement is required for hemorrhage, control of B.P& delivery for pre- eclampsia, stoppage of nephro-toxic drugs Patient needs intensive care with hydration Assessment of fluid balance by C.V.P line is important Liberal fluids given in hemorrhagic shock Infection should be controlled by antibiotics in septic abortion & puerperal sepsis Blood levels of electrolytes, urea, creatinine should be checked daily Help of nephrologist is sought Peritoneal/hemodialysis is performed to keep BUN to 50mg/dl If not already delivered, delivery should be expedited after stabilising her general condition
  25. 25. PREGNANCY IN RENALTRANSPLANT PATIENT More women are expected to come for pregnancy with more liberal use of renal transplant They should delay pregnancy for 1-2 years after transplantation to allow the graft function to stabilise &immunosupperession reach maintenance level Cyclosporine, azathioprine, prednisolone are considered safe in pregnancy Women on Cyclosporine should not breast feed
  26. 26. CHRONIC RENAL DISEASE IN PREGNANCY  Incidence: 0.2%  Effect of pregnancy on kidney disease:Mild Moderate SevereRisk of renal Risk of renal Risk of renalfailure is low failure is 10% failure is 50%(<5%)Serum creatinine Serum creatinine Serum creatinine<125 micromol/lit 125-250 >250 micromol/lit micromol/lit
  27. 27.  Super-imposed pre-eclampsia prognosis is worse Primary glomerulo-nephritis has better prognosis Focal glomerulo sclerosis, immune nephropathy, membrano-proliferative glomerulo-nephritis has poor prognosis
  28. 28. Effect of kidney disease onpregnancy Effect of pregnancy depends upon the severity of renal diseases, serum creatinine levels, hypertension & proteinuria Super-imposed pre-eclampsia- perinatal mortality is 50% In severe kidney disease risk of abortion, IUGR, pre- term labour Careful pregnancy surveillance, proper treatment, improved neonatal care& colaboration with nephrologist has improved prognosis of mother & newborn
  29. 29. TREATMENT OF CHRONIC RENALDISEASE IN PREGNANCY Pre-conceptional counselling Mild to moderate kidney disease- regular assessment of kidney function Women with severe kidney disease adviced against contraception Therapeutic abortion justified in early pregnancy Anti-hypertensive drugs given for hypertension Fetal monitoring performed each visit Management of labour is like pre-eclampsia with the aim of vaginal delivery
  30. 30. RENAL DISEASE ANDHYPERENSION DEFINITION-blood pressure of more than140/90mmhg or greater or an increase of 30 mm hg sysolic or 15 mm hg diastolic over the baseline value on atleast two occations
  31. 31. TYPES OF HYPERTENSIVE DISEASE INPREGNANCY 1-Gestationalhypertension/pregnancy induced hypertension 2-pre eclampsia 3-Eclampsia 4-preclampsia superimposed on chronic hypertension 5-chronic hypetension
  32. 32. ** INCIDENCE: 5-10% 0f all pregnancies . 20% recurrence This is the third most important cause of maternal mortality worldwide** DEFINITION OF HYPERTENSION:  D.B.P. > 90 mmHg or  S.B.P. > 140 mmHg along with** PROTIENUREA: Proteinurea is defined as urinary excretion 0.3 g protein or greater in a 24-hour 30 mg/dl (+1 or greater on urine dip specimen) +/-** OEDEMA: 90% pregnancy. progressive
  33. 33. INCIDENCE 6-8%RISK FACTORSPre eclampsia occurs in & of all live birthRISK FACTORS  Multiple pregnancy  twins 13 Extremes of reproductive age vs 6% 15 < & >35 Y  Hydatidiform mole Nulliparity  Nonimmune hydrops fetalis Black race  Obesity  4.3%  BMI < 19.8 Hx of PET in a 1st degree female kg/m² relative  13.3%  BMI ≥ 35 Hx of PET in prior pregnancy kg/m² DM  Smoking  ↓ risk of HPT Chronic renal disease Ch HPT
  34. 34. •Abnormal trophoblast invasion…first 12 weeks, the decidual segments of the spiral arteries are invaded…elastic and muscular wall replaced by fibinoid walls… by 20 weeks trophoblast invades intramyometrial segment of spiralarteries(high resistance low flow-low resistanc high flow) increase in uteroplacental flowIn pre eclampsia- trophoblast invasion is patchy & spiral arteries retaintheir muscular walls….
  35. 35. PATHOGENESIS Endothelial cell injury ↓ ↓ prostacyclin & ↑ thromboxaneA2 Vasospasm and endothelial cell dysfunction>>> platelet activation and micro aggregate formation Rejection phenomenon (inadequate matenal Ab response) Compromised placental perfusion Altered vascular reactivity  ↑sensitivity to vasopressin EPN, NEPN & angiotensin ↓ GFR with retention of salt & water ↓ intravascular volume ↑ CNS irritability DIC Uterine muscle stretch & ischemia Dietary factors Genetic factors
  36. 36. PATHOGENESISSummary of current hypothesis: Immunological disturbance  abnormal placentalimplantation ↓ placental perfusion  production ofsubstances that activate or injure endothelial cells of theblood vessels  multiple organ system involvement
  37. 37. SYMPTOMS & SIGNS↑ BP Proteinuria Edema of the face & hands ( but it has been dropped of the definition due to poor predictive value) Headache Visual disturbance Epigastric pain Exaggerated reflexes
  38. 38. CLASSIFICATION OF PEECLAMPSIASEVERE PRE ECLAMPSIA-Systolic BP >160 mmHg or diastolic >110 mmHg on two occasions at least 6 hrs apart Proteinuria ≥ 5 g/24 hrs Oliguria < 500 cc /24 hrs Cerebral or visual symptoms Epigastric or Rt upper quadrant pain Pulmonary edema or cyanosis Low PLt IUGR MILD PRE ECLAMPSIA  any pre eclampsia that is not considered severe
  39. 39. •Why screening•Accuracy. Uterine artery doppler at 24 weeks, notching on both uterinearteries identifies 80% who will develop pre clampsia,,, 5% false positive
  40. 40. Management of pre eclampsiaOBJECTIVES Birth of an infant who subsequently thrives Complete restoration of health to the mother terminaton of pregnancy with the least possible trauma to the mother & fetus1- Hospitalization Women with new onset BP ≥ 140/90 Worsening BP Development of proteinuria in addition to existing BP
  41. 41. INITIAL HOSPITALMANAGEMENT Observe for headache , visual disturbance, epigastric pain & rapid wt gain Wt daily Analysis for proteinuria every 2 days / daily BP in sitting position every 4 hrs except during sleep Blood investigations  Hct, Plt, S creatinine, liver enzymes Frequent evaluation of fetal size & AF Reduced physical activity but not absolute bed rest N diet & fluid intake
  42. 42. FURTHER MANAGEMENTDepends on: Severity of pre eclampsia Duration of gestation Condition of the Cervix Complete resolution of the signs & symptoms does not occur till after deliveryLines of management Termination of pregnancy Antihypertensive therapy Anticonvulsant therapy Home health care if BP improved within few days Pt can be managed as outpatient Home BP & urine protein monitoring . Instruction to come to hospital if she has waning symptoms . Rest at home
  43. 43. Termination of pregnancyIndications Term pregnancy with mild or severe Pre eclampsia Severe Pre eclampsia regardless of the gestational age Warning signs  headache , visual disturbance, epigastric pain, oliguria Eclampsia Pt must be stabilized & delivered immediatelyPreterm with mild Pre eclampsia  Assess fetal wellbeing by NST, BPP, DopplerMethods of termination IOL with prostaglandines to ripen the Cx followed by IV oxytocin Elective CS  Severe Pre eclampsia with unfavorable cervix
  44. 44. Antihypertensive therapy forsevere pre eclampsia Hydralazine  IV infusion or IV 5-10 mg bolus at 15-20 min interval  when diastolic BP ≥100-110 mm Hg or systolic BP ≥ 160 mmHg Nifedipine 10 mg po repeated in 30 min Labetalol 10 mg IV / 20 mg after 10 min/ 40mg after 10min/80 mg (not to exceed 220 mg) Nitroprusside used only in PT not responding to other drugs Diuretics not recommended because intravascular volume depletion already exists in Pre eclampsia
  45. 45. Antihypertensive therapyMild pre eclampsia-There is no benefit of antihypertensive therapy Reduction in the maternal BP with labetalol or nifedipine IUGR ACI contraindicated  IUGR, boney malformations, limb contracture, PDA, pulmonary hypoplasia, RDS, hypotension &deathSevere pre eclampsia-Antihypertensive therapy is used to control BP untill the Pt delivers or in preterm for 48 48 hrs to allow time for glucocorticoid administration for fetal lung maturity then delivery
  46. 46. Fluid therapy Hyperosmoticagents not recommended because intravascular influx of fluid subsequent escape of fluid to vital organs pulmonary edema & cerebral edema LR60-120 ml/hr Excessive fluid administration pulmonary edema & cerebral edema
  47. 47. Definitions Chronic hypertension:  A sustained BP > 140/90 that can antecedes pregnancy or persists postpartum (beyond 6 weeks). HTN that is present before the 20th week of pregnancy may also be included as CHTN.
  48. 48. Chronic Hypertension Oftenseen in patients who have other medical complications: obesity, diabetes, hyperlipidemia, cigarette smoking.  Essential HTN – majority will have normal pregnancies.  Secondary HTN – parenchymal renal disease, pheochromocytoma, Cushing’s syndrome, hyperthyroidism, etc.
  49. 49. Chronic Hypertension Ifend-organ disease is present (renal, cardiac, cerebrovascular), there is an increased risk of morbidity and mortality.  Maternal – superimposed preeclampsia, placental abruption, congestive heart failure  Fetal – intrauterine growth restriction, prematurity and fetal death
  50. 50. Preconception Care of CHTN Review the medical history: diagnosis and duration of hypertension, ongoing pharmacological treatment, known existence of organ damage or other compounding illnesses. Review obstetrical history.
  51. 51. Preconception Care of CHTN Physical exam and laboratory evaluation  Urine analysis, urine culture/sensitivity, 24 hour urine for total protein and creatinine clearance  CBC  Diabetes screening  If the patient has severe hypertension, significant proteinuria or prior poor obstetric outcome more extensive tests may be offered.
  52. 52. Preconception Care of CHTN Optimize control with recommended medications.  Methyldopa (Aldomet): extensively studied in pregnant women, treatment of choice if needed. Central adrenergic inhibitor  Hydralazine: potent vasodilator, which acts directly on vascular smooth muscle.  Calcium channel blockers (Nifedipine): inhibits transmembrane calcium ion influx which causes vasodilation.
  53. 53. Antihypertensives  B-Adrenoreceptor blockers (e.g. atenolol, propranolol): possible fetal IUGR, neonatal respiratory depression, bradycardia and hypoglycemia  Angiotensin-converting enzyme inhibitors: not recommended for use in pregnancy  Thiazides diuretics: not recommended for use in pregnancy.
  54. 54. THANK YOU

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