rhesus isoimmunisation
DESCRIPTION
Powerpoint presentation on Rhesus ImmunisationTRANSCRIPT
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Rhesus Isoimmunisation
Rhesus AlloimunisationRhesus (D) disease
Rhesus incompatibilityRh Haemolytic Disease of the Newborn
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Outline
• Terminology• Pathophysiology• Causes/Risk factors• Management
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Terminology
• Rhesus – refers to the Rhesus blood group system
• Isoimmunisation/alloimmunisation – production by an individual of antibodies against constituents of the tissues of another individual of the same species
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• Erythroblastosis fetalis– Making of immature RBCs in the fetus due to
haemolysis• Hydrops fetalis
– Excessive accumulation of serous fluid in tissues or cavities of the body of the fetus
– Presents as edema in the fetus
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ABO System
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• Consists of 50 defined blood group antigens.• D, C, c, E, e most important; no d antigen• d refers to absence of D allele• Rh factor, Rh positive, Rh negative refer to D antigen ONLY
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Putting both together…
Rh IgG is only present following sensitizing event
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Taken from http://bloodcenter.stanford.edu/about_blood/blood_types.html
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How sensitization occurs Haemolysis, anemia, and high output cardiac failure
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Causes/Risk factors: sensitizing events1. Mismatched transfusion2. Transplacental transfer/FMH
• Child birth (86%)• Antepartum haemorrhage (e.g. threatened miscarriage)• Therapeutic abortion• Abdominal trauma• ECV• Ectopic pregnancy• Invasive antenatal testing (e.g. amniocentesis, CVS,
cordocentesis)• C-section
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Management
Primary goal: PREVENTION1. Early detection – screening for Rhesus
grouping at the first bookingi. If mother is Rhesus negative, assess husband’s
Rhesus status + screen for Rh antibodiesii. If both mother and father are Rhesus negative,
there is little problem.iii. If the father is Rhesus positive, close supervision
is required
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Management
2 scenarios:• Patients who are nonalloimmunised
(no antibodies)• Patients who are alloimmunised
(antibodies present)
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1. Rh –ve, no antibodies• 4 weekly screening until 30 weeks• After that, 2 weekly screening until delivery• Prophylatic anti-D immunoglobulin at 28 and 32
weeks POG.
Anti-D is given ASAP in the following conditions:• Antenatal sensitizing events• After delivery
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2. Rh –ve, with antibodies• Maternal serum antibodies dilution titers done
every 2 weeks• Antibodies titer at or below 1:16 unlikely to
cause serious fetal disease• Amniocentesis is indicated if titer more than 1:8
Assess bilirubin level using spectrophotometer. Optical density reflects degree of haemolysis plotted on Liley’s chart
• Fetal ultrasound to detect early ascites, Doppler for blood velocity (middle cerebral artery)
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Optical density for bilirubin
Gestation in weeks
mild
moderate
severe
Liley’ chart for classifying the degree of hemolysis
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• Mild region, no intervention needed, amniocentesis repeated in 2 weeks.
• Moderate or severe zones, intervention needed:i. Deliver the fetus; following that exchange
transfusion by Paediatricianii. Intrauterine transfusion – intravascular or
intraperitoneal (every 2 weeks up till 34-36 weeks)
iii. Plasma exchange of mothers for antibodies removal
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Rho(D) Immune Globulin• Eligibility: Rhesus –ve mothers, no antibodies• Indication: Within 72 hours of any sensitizing event
in the pregnancy• Dosing regiment:
– 250 IU (50ug) for events before 20 weeks– 500 IU (100ug) IM at both 28 & 32 weeks' gestation and
postpartum within 72 hours of delivery * Kleihauer-Betke test on mother’s bld shows >1 fetal cell
per 500 adult red cells (= 4 – 5 ml of packed fetal red cells) Additional 150 IU of anti-D IgG is given for each ml of the transplacental bleed > 4 mls of packed fetal red cells.
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MEDICAL DISORDERs IN PREGNANCY
JAUNDICE
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Jaundice
• Yellow discolouration of sclera, skin and mucose membrane because of raised serum bilirubin.
• Normal: 3 – 17µmol/L• Detectable clinically
>35µmol/L
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Bilirubin pathway
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Approach to jaundice in pregnany
• Similar to the non-pregnant.• Viral hepatitis and gallstones may also cause
jaundice in pregnancy.• History: blood transfusions, IVDU, body
piercing, tattoos, sexual activity, travel abroad, jaundiced contacts, family history, alcohol consumption, drug history
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Investigations
• LFT• Coagulation profile• FBC• Renal profile• Viral screen (hepatitis A, B, and C, Epstein Barr and
cytomegalovirus)• Autoimmune screen
– anti-smooth muscle antibody (autoimmune hepatitis)– antimitochondrial antibodies (primary biliary cirrhosis)
• Ultrasound of the hepatobiliary system• UFEME
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LFT in pregnancy
• For AST, ALT, GGT and bilirubin, the upper limit of normal throughout pregnancy is 20% lower than the non-pregnant range.
• The increase in ALP in pregnancy is usually placental in origin and so does not normally reflect liver disease.
• In normal pregnancy, LFTs may increase in the first 10 days of the puerperium.
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Pregnancy-related causes• Intrahepatic cholestasis of pregnancy• Acute fatty liver of pregnancy• Pre-eclampsia a/w HELLP syndrome• Hyperemesis gravidarum
Non-pregnancy related• Other cause: acute viral hepatitis – most
common
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Intrahepatic Cholestasis of Pregnancy
• Slowing or blockage of bile in small ducts of liver• Generally manifests in the 3rd trimester• Multifactorial:
– Genetic mutation in MDR3 gene– Hormonal factor – high estrogen level
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• Symptoms: – Generalized pruritus, especially of palms and
soles, worse at night– Jaundice (10-25%), pale stool, dark urine– Others: abdominal pain, steatorrhea
• Investigations: Abnormal LFT. Liver transaminases mildly ↑ (<300 U/L) in 60%. Bilirubin ↑ in 25% (conjugated).
• Symptoms and abnormal LFT resolve after delivery.
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• Management:– Measure LFTs weekly until delivery– Ursodeoxycholic acid (UDCA) – improve pruritus
and LFT– Cholestyramine – improve pruritus– If PT prolonged, give Vitamin K 10mg PO BD to the
mother, 1mg IM to the baby at birth– CTG daily– Aim for delivery at 37 weeks
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Acute Fatty Liver of Pregnancy
• Rare but grave (incidence: 1:6600 – 13000 deliveries); mortality 90%
• Usually occur at late 3rd trimester (>35 wks)• Unknown aetiology• Risk factors: older maternal age, multiple
pregnancy, pre-eclampsia, male fetus, being underweight, and a history of AFLP
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• Symptoms: nausea, vomiting, anorexia, lethargy, abdominal pain, ascites, and progressive jaundice
• Diagnosis: – Liver aminotransferase levels are moderately
elevated (typically 300-500 U/L)– High serum bilirubin – Hypoglycaemia, thrombocytopenia, coagulopathy,
uremia (RBS, FBC, PT/APTT, RFT)– Ultrasound scan of hepatobiliary system– Liver biopsy – diagnostic but rarely performed
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• Complications: – Acute renal failure– Hepatic encephalopathy– DIVC– Coma and death– PPH– Neonatal hypoglycemia
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• Management:– Continuous fetal monitoring – Supportive treatment for liver & renal failure – Treat hypoglycemia vigorously– Correct clotting disorders– Expedite delivery (epidural & regional anesthesia
are contraindicated)– Monitor postpartum
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Pre-eclampsia with HELLP syndrome
• Pre-eclampsia: Increased BP (>140/90 mmHg) with proteinuria (>300mg/24hour)
• H – hemolysis• E – elevated• L – liver enzymes• L – low • P – platelet
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• Pathogenesis: – Endothelial injury with fibrin deposit
microangiopathic hemolytic anemia– Endothelial injury platelet activation and
consumption thrombocytopenia, clotting system activation clotting factors consumption DIVC
– Fibrin deposits obstruct hepatic sinusoids hemorrhage liver necrosis
• Symptoms: epigastric pain, nausea and vomiting, malaise, headache, jaundice
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• Investigation: (PE profile)– FBC: ↓ platelet (<100 x 109/L), ↓ Hb– LFT: ↑ AST & ALT, ↑elevated bilirubin– RFT:↑ urea, creatinine, uric acid– ↑ LDH (>600 U/L)
• Complications: – DIVC– Renal failure– Abruptio placenta– Liver subcapsular hematoma
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• Management: – Definitive treatment: delivery
Maturity of pregnancy
Term (>37 weeks) Preterm (<37 weeks)
If severe disease
MgSO4 and deliveryExpectant management
until term/ delivery
No
Yes
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• Maintain BP < 160/110 mmHg by IV hydralazine or labetalol
• IV dexamethasone• PE profile• CTG – fetal monitoring• Any complications – emergency caesarean
section
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Hyperemesis Gravidarum
• Pathological vomiting during pregnancy a/w liver dysfunction & jaundice.
• Liver dysfunction resolves when vomiting subsides.
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Acute viral hepatitis
• Most common cause of jaundice in 3rd trimester.
• Clinical features: nausea, vomiting, fever, fatigue and jaundice, epigastric/right hypochondrium pain
• Common aetiology:– Hepatitis A– Hepatitis B
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Hepatitis A• RNA Picornavirus• Spread by fecal-oral route• Incubation period 15-50 days (average 30 days)• Acute symptoms:
– Nausea & Vomiting– Anorexia– Headache– Flu-like illness
• Detected by anti-HAV IgM
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• Self-limiting disease• No chronic infection; lifelong immunity• Practically no maternal-fetal transmission
– anti-HAV immunoglobulin (Ig) G antibodies present during the initial stages of HAV infection cross the placenta and provide protection to the infant after delivery
• No evidence of congenital HAV infection• No intervention needed
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Hepatitis B• DNA Hepadnavirus• Spectrum range from asymptomatic to
fulminant hepatic failure• Transmission:
– Vertical transmission– Through percutaneous or parenteral contact with
infected blood, body fluids & sexual intercourse• HBV does not cross placenta; breaks in
maternal-fetal barrier (e.g. amniocentesis, delivery) permit transmission
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• Factors favouring vertical transmission:– Infection in late pregnancy– HBeAg positive (90% likelihood of newborn
becoming infected)– High titers of HBsAg– High HBV DNA
• 2-10% of newborns develop clinical hepatitis• 90% of infected infants will become chronic
carriers
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• Investigations:– LFT: ↑AST, ALT– Hepatitis screening
• Prevention:– Antenatal screening– IM HBIG at birth within 12 hours– Vaccination for infant at 0, 1, 6 months– Offer vaccination to all the family
• Breastfeeding is not contraindicated