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Rhesus Alloimunisation Rhesus (D) disease Rhesus incompatibility Rh Haemolytic Disease of the Newborn
Outline
Terminology Pathophysiology Causes/Risk factors Management
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
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
ABO System
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
Management
Primary goal: PREVENTION 1. Early detection screening for Rhesus grouping at the first booking
i. If mother is Rhesus negative, assess husbands Rhesus status + screen for Rh antibodies ii. If both mother and father are Rhesus negative, there is little problem. iii. If the father is Rhesus positive, close supervision is required
Management
2 scenarios: Patients who are nonalloimmunised (no antibodies) Patients who are alloimmunised (antibodies present)
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
Fetal ultrasound to detect early ascites, Doppler for blood velocity (middle cerebral artery)
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 Paediatrician ii. Intrauterine transfusion intravascular or intraperitoneal (every 2 weeks up till 34-36 weeks) iii. Plasma exchange of mothers for antibodies removal
Jaundice
Yellow discolouration of sclera, skin and mucose membrane because of raised serum bilirubin. Normal: 3 17mol/L Detectable clinically >35mol/L
Bilirubin pathway
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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)
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.
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
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.
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
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
Complications:
Acute renal failure Hepatic encephalopathy DIVC Coma and death PPH Neonatal hypoglycemia
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
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
Complications:
DIVC Renal failure Abruptio placenta Liver subcapsular hematoma
Management:
Definitive treatment: delivery
Maturity of pregnancy
Yes
If severe disease
No
Maintain BP < 160/110 mmHg by IV hydralazine or labetalol IV dexamethasone PE profile CTG fetal monitoring Any complications emergency caesarean section
Hyperemesis Gravidarum
Pathological vomiting during pregnancy a/w liver dysfunction & jaundice. Liver dysfunction resolves when vomiting subsides.
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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
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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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2-10% of newborns develop clinical hepatitis 90% of infected infants will become chronic carriers
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