Gastro-Hepatic conditions Flashcards
Discuss appendicitis in pregnancy
-Incidence (1)
-Complications (4)
-Obstetric complications (4)
-Management (2)
- Incidence 1:1000
- Complications
-Sepsis, perforation, abscess, peritonitis - Obstetric complications
-Fetal loss 1% if simple appendicitis, 36% if ruptured
-Miscarriage 33% in first trimester
-PTL 14% in second trimester - Management
-Surgery - laparoscopic until 34 weeks
-Open with site of incision depending on gestation
Discuss bilary colic in pregnancy
-Incidence of Gallstones in pregnancy
-Cause of gallstones in pregnancy
-Presentation in pregnancy
-Management
- Incidence
-Gallstones present in approx 20% of pregnant women
-33% of pregnant women have gallbladder sludge - Cause of gallstones in pregnancy
-Oestrogen increases gallstone formation
-Progesterone reduces gallbladder contractility - Presentation in pregnancy
-Similar to outside of pregnancy - Management
-Aim for conservative management
-Consider surgery if frequent attacks to reduce maternal morbidity
-Increased risk of gallstone pancreatitis in pregnancy with high fetal mortality
Discuss acute fatty liver of pregnancy
-Incidence
-Risk factors (4)
- Incidence
-1:7000 to 1:20000 - Risk factors
-Multiple pregnancy
-Male fetus
-Nulliparity
-Obesity
What is the pathophysiology of acute fatty liver of pregnancy
Thought to be due to an autosomal recessive disorder in the fetus where by it lacks LCHAD enzyme (Long chain 3-hydroxy acyl-CoA dehydrogenase).
This leads to a build up of medium to long chain fatty acids which enter the maternal circulation and accumulate in the maternal liver.
The gene affected most commonly is E474Q
Discuss acute fatty liver of pregnancy
-Clinical features (7)
-Investigations (9)
-Distinctive features (3)
- Clinical features
-Onset in third trimester after 30/40 or postnatal (20%)
-Gradual onset of malaise, nausea, anorexia
-Severe vomiting and abdo pain in 60%
-Pruritis or jaundice
-Polyuria or ploydipsia secondary to impaired liver being unable to metabolise vasopressin = ADH (Diabetes insipidis)
-DIC
-Hepatic encephalopathy - Investigations
-LFTs deranged 3-10x. Bilirubin can be raised
-FBC - neutrophillia
-Creatinine - raised
-Uric acid often raised more than in PET
-Coagulopathy seen in 90% - low IR, low fibrinogen, prolonged PT
-Hypoglycemia in 70%
-Blood gases - lactic acidosis
-Liver USS for fatty infiltrate
-Liver Bx for definitive diagnosis but coagulopathy may preclude this. Shows microvascular fatty infiltration - Distinctive features
-Hypoglycemia - 70%
-Hyperuricemia - 90%
-Coagulopathy in absence of thrombocytopenia - 90%
What features distinguish HELLP from AFLP
How should AFLP be managed (8 points)
- MDT with obstetric, anaesthetics, haematology, gastro / hepatologist
- Expedite delivery once maternal condition stabilised
- Correct hypoglycemia - 10% or 50% IV glucose
- Correct coags - FFP, Vit K
- Consider NAC if LFTs severely deranged
- Fluid balance and if increased polyuria consider desmopressin
- Significant sepsis risk - consider Abx
- Screen baby for LCHAD deficiency
What are the risks associated with AFLP
- Maternal mortality - was 10-20% now improved to 2%
- Fetal mortality - was 20-30% now 11%
- Most women if they survive make a full recovery
- Recurrence risk - 25%
Discuss GORD in pregnancy
-Incidence
-Causes (3)
-Management (7)
- Incidence - 60%
- Causes
-Decreased lower oesophageal sphincter pressures
-Decreased gastric emptying and peristalsis
-Enlarging uterus - Management
-Upright position after meals
-Eat small meals
-Avoid irritants
-Gaviscon or mylanta - first line
-Omeprazole - 2nd line
-Consider metocloprimide for gastric emptying
-Avoid ranitidine - cancer link
Discus HELLP disease
-Epidemiology (1)
-Definition
-Risk factors (2)
- Affects 20% of women with severe PET
- Definition
-Complication of severe PET including haemolysis, elevated liver enzymes, low platelets - Risk factors
-Increased risk with increasing age and parity
Discuss HELLP disease
-Clinical features
-Onset
-Severe complications
-Rates of maternal and fetal mortality
- Clinical features
-Epigastric pain most common
-Headache, nausea, vomiting, oedema, haematuria
-Jaundice, HTN
-Diabetes insipidis (Liver unable to metabolise ADH - Onset
-15% second trimester, 50% third trimester, 35% postpartum - Severe complications
-Renal failure
-DIC
-Abruption
-Pulmonary oedema
-Liver capsule haematoma and rupture - Mortality rates
-Maternal mortality - 1-10%
-Fetal mortality 8-60%
Discuss investigations for HELLP
1. Bloods
2. Urine
3. USS
- Bloods
-FBC - anemia, thrombocytopenia
-Bloods film - fragmented red cells
-Haemolysis screen - LDH, reticulocyte count, bilirubin
-LFTs - derranged
-Coags - DIC present in 20% - Urine - protienuria
- Liver USS to assess for subcapsular haematoma
Discuss management for HELLP
- Management same as for severe PET
- Stabilise mother and expidite delivery
- Control BP
- Careful fluid balance
- Seizure prophylaxis - MgSO4
- Steroids for fetal prematurity (Can also improve thrombocytopenia)
- Correct haematology
- If platelets <20 consider platelet transfusion
What is the risk of recurrence for HELLP
Risk of recurrence for HELLP is low 3-27% compared to PET which is high at 42%
What is the effect of pregnancy on inflammatory bowel disease (5)
-Chron’s disease - not change in risk of flare
-Ulcerative colitis - double the risk of relapse in pregnancy (35%). 6 times the risk of PP flare
-Malabsorption of fat, fat soluble vitamins and B12
-Obstruction of ileostomy as pregnancy progresses
-Peristomal cracking and bleeding due to abdominal wall stretching
What is the effect of inflammatory bowel disease on pregnancy (4)
-Reduced fertility if IBD active
-Increased miscarriage rate if active disease at time of conception
-Increased risk of PTD in active disease
-Most women have normal pregnancies
How should a pregnancy be managed for a woman with inflammatory bowel disease
-Pre-conception
-Antenatally
-Intrapartum
-Post natally
- Pre conception
-Encourage conception during times of remission
-5mg folate per day if on sulfasalazine
-Review medications and stop those contra-indicated in pregnancy (Methotrexate) - Antenatal
-Monitor fetal growth
-If on anti-TNF agents stop in third trimester to allow fetus to clear prior to delivery - Intrapartum
-Avoid vaginal birth and episiotomy in severe perianal disease
-Prepare for surgical issues in previous abdominal surgery - Postpartum
-Monitor for UC flare
-Avoid live vaccines in babies exposed to anti-TNF agents for 6/12
Discus the safety of IBD medications in pregnancy and breast feeding
-Mesalazine
-Sulfasalazine
-Corticosteriods
-Thiopurines (Azathioprine, mercaptopurine)
-Anti TNF agents (Infliximab, adalumamab
-Methotrexate
- Meselazine - low risk in both
- Sulfasalzine - low risk in both
- Corticosteriods - Low risk in both
- Thiopurines - low risk in both
- Anti TNF agents. Low risk in pregnancy. Stop in third trimester or earlier if in remission. Limited data for breastfeeding. Likely low risk
- Methotrexate - contra-indicated in both
Discuss intrahepatic obstetric cholestasis
-Incidence (2)
-Risk factors
- Incidence
-0.7% in multiethnic populations
-1.2-1.5% of South Asian women - Risk factors (5)
-Ethnicity
-Family Hx (>30% have affected siblings, OR 12)
-Multiple pregnancy (RR 5)
-Hep C
-Gallstones
-Genetics
Discuss the clinical presentation of intrahepatic obstetric cholestasis (7)
-Pruritis - typically trunk and limbs but esp. palms and souls of feet. Worse at night. NB 25% of women have pruritis in pregnancy
-Absence of skin rash
-Jaundice, dark urine, steatorrhoea, pale stools = rare
-Raised bile salts >18
-LFT derangement
-Liver failure sx - prolonged PT or hypoglycemia = very rare in IOC
-More common in 3rd trimester. 5% in 1st T