You are on page 1of 46

Rhesus Isoimmunisation

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

Putting both together

Rh IgG is only present following sensitizing event

Taken from http://bloodcenter.stanford.edu/about_blood/blood_types.html

How sensitization occurs

Haemolysis, anemia, and high output cardiac failure

Causes/Risk factors: sensitizing events


1. Mismatched transfusion 2. 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

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

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 Lileys chart

Fetal ultrasound to detect early ascites, Doppler for blood velocity (middle cerebral artery)

Optical density for bilirubin

severe moderate mild

Gestation in weeks Liley chart for classifying the degree of hemolysis

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

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 mothers 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.

MEDICAL DISORDERs IN PREGNANCY


JAUNDICE

Jaundice
Yellow discolouration of sclera, skin and mucose membrane because of raised serum bilirubin. Normal: 3 17mol/L Detectable clinically >35mol/L

Bilirubin pathway

23

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

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

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

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

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

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

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

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

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

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

Management:
Definitive treatment: delivery
Maturity of pregnancy

Term (>37 weeks)

Preterm (<37 weeks)

Yes

If severe disease
No

MgSO4 and delivery

Expectant management until term/ delivery

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.

40

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

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


42

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

43

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
44

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

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

You might also like