Obstetric Conditions Flashcards
Define an obstetric complication
A health problem related to pregnancy which may be affecting the mother, baby or both.
What is the threshold for haemoglobin in anaemia during pregnancy?
During 1/3 and 2/3 it is 110g/dL
During 3/3 it is 105g/dL
Outline how anaemia may occur in pregnancy.
Adult haemoglobin synthesised slower compared to foetal haemoglobin thus physiological anaemia occurs
State the common presentation of anaemia in pregnancy
- Tired
- Palpitations
- SOB
- Dizziness
- Myalgia
- Tachypnoea
- Tachycardia
- Pallor
- Peripheral Oedema
How may you investigate someone with suspected anaemia?
- FBC
- Ferritin
- Folic Acid (B9)
- Hydroxocobalamin (B12)
How do you treat someone with anaemia in pregnancy
- Iron (PO/IM)
- B12 (IM)
- B9 (PO)
How much folic acid should someone be taking during the first trimester?
400mcg
If a previous pregnancy has resulted in a neural tube defect, what dose should this woman take during her current pregnancy?
5mg
What is a UTI?
Non-specific, umbrella term for infection occurring anywhere in urinary tract, from urethra to bladder to the ureters to the kidneys. Bacterial stasis + ascending infection due to urinary stasis, compromised ureteric valves + vesicoureteric reflux
Outline the pathogenesis of a UTI in pregnancy.
- Bladder volume increases + detrusor tone decreases
* Progestogenic relaxation of ureteric smooth muscle + pressure from uterus -> ureteric dilatation (90%)
Which pathogen is the usual cause of UTIs.
E.coli
Outline the symptoms and signs which a UTI may present with.
- Dysuria
- Frequency
- Urgency
- Suprapubic pain
- Haematuria
• NONE
How would you investigate a pregnant woman with urinary symptoms?
- MSU Culture + Sensitivity
* Urinalysis
How do you treat a UTI in pregnancy?
• Supportive: fluids + paracetamol
+
• ABX: Nitrofurantoin
When should you avoid giving nitrofurantoin in pregnancy to treat a UTI?
At term, may cause neonatal haemolysis
What is acute cystitis?
infection of urinary bladder
Which organisms are a common cause of acute cystitis?
- E. coli
- S. saprophyticus
- K. pneumoniae
- P. mirabilis
State the presentation of acute cystitis.
Symptoms:
• Dysuria
• Urgency
• Frequency
Signs:
• Flank/Abdominal/Suprapubic Pain
• Fever
What is the treatment for acute cystitis?
• Supportive: fluids + paracetamol
+
• ABX: Nitrofurantoin
-> May cause neonatal haemolysis if pregnancy at term
2nd line ABX: Amoxicillin
What is pyelonephritis?
Severe infectious inflammatory disease of kidney parenchyma, calices and pelvis which can be acute, recurrent or chronic
Outline the presentation of a patient with pyelonephritis.
- Tachycardia
- Tachypnoea
- Pyrexia
- Loin pain
- Urinary symptoms: frequency, urgency, dysuria
Which investigations may you wish to run in a patient with suspected pyelonephritis?
- MSU – culture + sensitivity
- FBC
- RFT
- CRP
• USS of renal tract
How do you manage a patient with Pyelonephritis who is pregnant?
• ABX: Cephalexin
Septic
• ABX: Metronidazole + Cephalexin
Describe hyperemesis gravidarum.
= Most severe form of NVP (morning sickness), NV in morning hours, beginning in 4th-7th week following last menstrual period; 1st 1/3 and resolves by 2/3 usually. Severe NVP entails persistent vomiting, volume depletion, ketosis, electrolyte disturbances and weight loss.
When does hyperemesis gravidarum typically present?
1/3
State 3 RFs for hyperemesis gravidarum
- FHx HG
- PMHx HG
- Multiple gestation
- Increased placental mass
- Motion sickness
- Molar pregnancies
- Gestational trophoblastic disease (GTD = abnormal cells or tumours in the womb from cells which develop into placenta)
What is a postulated cause of hyperemesis gravidarum?
• Rapidly rising HCG (placental)
What is the presentation of hypermesis gravidarum?
Symptoms:
• Nausea
• Vomiting
• Weight loss
Signs: • Dizziness • Tachycardia • Hypotension • Dry mucous membranes • Ketotic breath
What investigations would you wish to conduct in a patient presenting with Hyperemesis Gravidarum?
- FBC (normal)
- Metabolic panel: variable, hyponatremia and hypochloraemia
- Urea + Creatinine: variable, elevated in HG
- Urine or Serum Ketones: positive
- Foetal Ultrasound with Nuchal Translucency: variable, may show multiple gestation; GTD; hydrops fetalis; increased nuchal translucency
- Serum analytes: variable, abnormally high or low hCG and PAPP-A
How would you treat a patient with hyperemesis gravidarum?
• IV Fluids (IV Ringer’s lactate), replacement fluid for deficit, ongoing losses and daily fluid maintenance
+
• Anti-emetic (metoclopramide/chlorpromazine (FGA) /prochlorperazine (FGA) /Promethazine (TCA))
+
• PPI (Omeprazole)
What is implantation bleeding?
Light spotting/bleeding at day 10-14 due to fertilised egg attaching to lining of uterus
State 3 causes for early bleeding and 3 for late bleeding in pregnancy.
Bleeding in Pregnancy: Early vs Late • Implantation bleeding • Ectopic pregnancy • Molar pregnancy • Chorionic Haematoma • Miscarriage • Cervical causes – ectropian/polyp/cancer
- Placental abruption
- Placenta praevia
- Vasa praevia
- Uterine rupture
- Post-partum haemorrhage
Describe a miscarriage
involuntary, spontaneous loss of pregnancy prior to 24 weeks associated with unprovoked vaginal bleeding +/- suprapubic pain
What type of miscarriage is this, ‘miscarriage symptoms but pregnancy in situ and os closed’?
Threatened
What type of miscarriage is this, ‘pregnancy in situ with no heart beat’?
Early foetal demise
What type of miscarriage is this, ‘pregnancy still in situ however os is open and PoC can be sighted’?
Inevitable
What type of miscarriage is this, ‘products of conception passed (PoC) + Os is closed’?
Complete
What type of miscarriage is this, ‘cant identify products of conception (PoC)’?
Incomplete
What type of miscarriage is this, ‘3≤ consecutive miscarriages’?
Recurrent
State 3 RFs for a miscarriage.
- Older age
- Embryological abnormalities e.g. chromosomal causes.
- Immunological causes such as antiphospholipid syndrome.
- Infections- rubella, CMV, toxoplasmosis, listeria.
- Severe emotional upset
- Iatrogenic post chorionic villus sampling (CVS)
- Associated with smoking, alcohol, cocaine
Outline the postulated pathophysiology of a miscarriage.
• Bleeding from placental bed (chorion) causes hypoxia and placental dysfunction leading to embryonic demise.
How may a miscarriage present?
- Bleeding/ Recent post-coital bleed: may pass products
- Suprapubic pain
- Cramping
- LBP
• Positive pregnancy test
Which investigations may you wish to conduct in a patient you suspect with a miscarriage?
- TVUS: consider miscarriage when gestational sac > 25 mm diameter with no visible yolk sac/foetal pole OR embryo measures 7mm or more with no obvious heart activity
- Serum ß-hCG: Falling titres (< 50% in 24 hours) suggest failing pregnancy
- Rhesus Blood Group: Identify Rh-negative blood group in mother
How do you manage a patient who has recently had a miscarriage?
• Supportive: Emotional support/ Haemodynamic stability/ USS/ Histology/ ßhCG/ Anti-D (for future pregnancies)
+
Medical
• Mifepristone (antiprogestogenic steroid, sensitising myometrium to PG-induced contractions)
+
• Misoprostol (Synthetic PGE1 loosening foetal tissue + uterine contractions + cervical dilatation)
Surgical evacuation
• Suction aspiration (vacuum removes uterine contents through cervix)
OR
• Dilation and Curettage (D+C) (physical dilatation of cervix and curette removing uterine tissue)
How does mifepristone work?
antiprogestogenic steroid, sensitising myometrium to PG-induced contractions)
How does misoprostrol work?
Synthetic PGE1 loosening foetal tissue + uterine contractions + cervical dilatation
How may you reduce the risk of miscarriages?
- Smoking cessation
- Avoid alcohol
- Avoid drugs
- Treat/control chronic morbidities (DM, HTN, SLE etc..)
What is an ectopic pregnancy?
Implantation of fertilised ovum (blastocyst) outside uterine endometrial cavity, most commonly fallopian tube, which may lead to maternal death if undiagnosed due to rupture and intraperitoneal haemorrhage.
What is the commonest site of implantation in an ectopic pregnancy?
Fallopian tube
What are the types of ectopic pregnancy?
Tubal Ovarian Cervical Interstitial (peritoneum) Abdominal (liver etc) Hysterotomy scar pregnancy (previous surgical incision site)
State 3 RFs for an ectopic pregnancy.
- Smoking
- PMHx Ectopic
- IUD use (if pregnancy occurs with IUD in situ; lowers absolute risk of ectopic cf non-contraceptive-using population)
- PMHx genital infections
- Chronic salpingitis
- Salpingitis isthmica nodosa (SIN)
- Multiple sexual partners
How may an ectopic pregnancy present?
Symptoms:
• Dizziness
• Abdominal pain: unilateral/localised
• Shoulder tip pain (extreme cases due to diaphragmatic irritation)
• Amenorrhea (4-8 weeks prior to presentation)
• Vaginal bleeding/brown watery discharge
• Dysuria (painful wee)/Dyschezia (painful poo)
Signs:
• Abdominal tenderness: voluntary guarding
Involuntary guarding; rebound; acute abdomen findings ≈ rupture signs
• Adnexal tenderness/mass
• Blood in vaginal vault
• Pallor
• Haemodynamic instability
Which investigations may you wish to conduct in a patient presenting with suspected ectopic pregnancy?
- Urine/Serum pregnancy test: Positive
- TVUS: No IU pregnancy detected/ectopic pregnancy visualised (doughnut sign = heterogenous adnexal mass separate from two ovaries)
How would you manage an ectopic pregnancy?
• Medical management: Methotrexate (if stable, low ßhCG levels and ectopic small and unruptured)
OR
• Surgical: laparoscopic salpingectomy
What is a chorionic haematoma?
A pooling of blood between the embryo and the endometrium.
How may a chorionic haematoma present?
- Bleeding
- Cramping
- Threatened Miscarriage
- Symptoms follow severity, more blood= worse symptoms
How do you treat a chorionic haematoma?
• Supportive: Reassurance; Surveillance
What is an antepartum haemorrhage?
Umbrella term for bleeding from genital tract after 22nd week of pregnancy
State the common causes for an antepartum haemorrhage.
- Placental abruption
- Placenta praevia
- Cervicitis
- Trauma
- Vulvo-vaginal varicosities
- Genital tumours
- Infection
What is placenta praevia?
Placenta overlying cervical os which may be complete (grade 4), partial (grade 3), marginal (grade 2) or low-lying (grade 1).
State 5 RFs for placenta praevia.
- Scarred uterus/ Previous C-section
- Advanced maternal age
- Smoking
- PMHx multiple pregnancies
- Miscarriages
- Prior PP
- Infertility treatment
- Illicit drug use
How does placenta praevia present?
- Painless vaginal bleeding: severity in bleeding
* No pain
What investigations should you do in a suspected placenta praevia?
- FBC: Hb decreases <100g/dL
- ßhCG
- UUS + Doppler analysis: Position of placenta identified
How do you manage a patient with placenta praevia with bleeding currently and a grade 4 PP.
• Resuscitation and stabilisation: Antifibrinolytic, monitor foetal heart, IV fluids
-> Not stabilised, emergency caesarean section
+/- Anti-D Ig: 300mcg IM
• Urgent USS
How do you manage a patient with placenta praevia with no bleeding and a grade 3 PP.
• Supportive: Monitoring and pelvic rest \+ Corticosteroids (< 34 weeks) ± Anti-D immunoglobulin
How do you manage a patient with low-lying placenta praevia (grade 1) at term?
• Await spontaneous labour OR • C-Section ± Anti-D Ig
What is a placental abruption?
Premature separation of placenta from uterine wall occurring before delivery of foetus which can be revealed (blood escapes through vagina) or concealed (bleeding occurs behind placenta without PV bleeding) and can be partial (part of placenta) or total (entire placenta)
What are the two categories of placental abruption?
Partial (part of placenta)
Total (entire placenta)
State 5 RFs for placental abruption.
- HTN
- Pre-eclampsia
- Smoking
- Cocaine use
- Trauma
- Chorioamnionitis
- Uterine malformations
- Placental abruption
- Oligohydramnios
How may placental abruption present?
- Vaginal bleeding*
- Abdominal pain: occurs in 2/3
- Uterine contractions
- Uterine tenderness
What investigations do you wish to conduct in a patient you suspect has a placental abruption?
- Foetal monitoring – Cardiotocography (CTG), abnormalities in tracing e.g. late decelerations, loss of variability, variable decelerations, sinusoidal foetal heart tracing, foetal bradycardia (< 110bpm)
- Hb and Hct: Normal or low
- Kleihauer-Betke Test: Positive or Negative
- USS: Retroplacental haematoma (hyperechoic, isoechoic, hypoechoic), pre-placental haematoma (jiggling appearance with shimmering effect of chorionic plate with foetal movement); increased placental thickness and echogenicity
How does a Kliehaeur-Betke test work? What is its purpose?
Estimation of foetal cells in maternal circulation thus useful in foetal maternal haemorrhage
How do you manage a patient with a placental abruption in a foetus which is 32 weeks old?
Stabilise patient: keep Hb > 100g/dL, urine output > 30mL/hour, reduce bleeding, Anti-D Ig
Consider if < 34 weeks Corticosteroid \+ Tocolytic \+ Consider delivery by 37-38 weeks
OR
• Urgent CSD \+ Blood coagulation products \+ Post-placental delivery utero-tonic agent: Oxytocin (10IU IM) OR misoprostrol (800-100 mcg PV)
How do you manage a patient with a placental abruption in a foetus which is 36 weeks old?
• Conservative management: foetal heart rate monitoring, sonograms, biophysical profile; Keep Hb above 100g/dL, urine output ≥ 30mL/hour, reduce bleeding (anti-fibrinolytics given early prior to 3 hours), FFP if signs of DIC (replace clotting factors)
+
• Vaginal delivery
+
Oxytocin induction (0.5-1mU/minute then 1-2mU/minute increment PRN every 15-60 minutes; maximum 10mU/minute)
+
Blood coagulation products
+
Post-placental delivery utero-tonic agent: Oxytocin (10IU IM) OR misoprostrol (800-100 mcg PV)
+
Post-delivery haemostatic interventions: Surgical ligation (1st) OR Embolisation (2nd) OR Hysterectomy (3rd)
What is placenta accreta?
Condition whereby the chorionic villi attach to the myometrium.
If the placenta invades the myometrium, what is this called?
Placenta increta
If the placenta invades the the uterus, what is this called?
Placenta percreta
How do you manage a patient with placenta accreta?
- Prophylactic insertion of internal iliac balloon
- Caesarean hysterectomy
- Blood loss >3L expected
- Conservative management + methotrexate
What is a uterine rupture?
A full thickness opening of the uterus (including serosa. If serosa is intact termed dehiscence).
What are the risk factors for a uterine rupture?
- Previous C section/uterine surgery (myomectomy)
- Multiparity
- Use of prostaglandins/syntocin increase risk
- Obstructed labour
What is the presentation of a uterine rupture?
- Severe abdominal pain- even with epidural may be sore
- Shoulder tip pain- due to diaphragmatic irritation
- Maternal collapse
Signs of uterine rupture: • Intrapartum loss of contractions • Acute abdomen • Peritonism • Fetal distress/IUD
How do you manage a patient with a uterine rupture?
- Urgent resus- major haemorrhage protocol, IV fluids, transfuse etc
- Anti-D if rhesus negative.
What is a vasa praevia?
Unprotected fetal vessels transverse the membranes below the presenting part over the internal os. Will rupture during labour or at amniotomy. Causes include ectropion, polyp, carcinoma.
State 3 RFs for vasa praevia.
- Placental anomalies e.g. bilobed
- Low lying placenta
- Multiple pregnancy
- IVF
How do you diagnose a vasa praevia?
made at US- transabdominal and transvaginal.
How do you manage a patient with vasa praevia?
- Antenatal diagnosis
- Steroids from 32 weeks
- Deliver by elective C section at 32-34 weeks.
- If antepartum haemorrhage emergency C section
What is obstetric cholestasis?
Intrahepatic cholestasis or pregnancy (ICP) is a condition caused by bile flow stasis resulting in deposition in the skin and placenta causing a pruritic condition as the result of hormonal, genetic and environmental factors.
How may obstetric cholestasis present?
- Pruritus (sparing the face)
- Excoriation without rash
- Mild jaundice
How may you investigate a potential obstetric cholestasis?
- LFTs: elevation of transaminases up to 300u/L
- Coagulation profile: PT prolonged if vitamin K depleted
- Bile acids: elevated > 11micromol/L
- Fasting serum cholesterol: Elevated
- Hepatitis C virology: Positive in hepatitis C infection
How do you manage a patient with symptomatic mild obstetric cholestasis?
• Conservative: Foetal surveillance/ fluids/Antihistamines (diphenhydramine)
+
• Colestyramine (4-16g/day PO in 2-4 doses) + Vitamin K (phytomenadione 10mg PO/IM single dose)
± (adjunct)
• Ursodeoxycholic acid (competes with cytotoxic bile acids and improves pruritus and liver function)
±
• Corticosteroids: IM betamethasone (12mg IM every 24 hours for 2 doses = accelerate foetal lung maturity and improve neonatal outcomes)
± ≥ 37 weeks
• Surgery: Caesarean section
What are the potential complications of obstetric cholestasis?
- Meconium passage
- Small risk of stillbirth
- Premature birth (iatrogenic)
What is abnormal labour?
Umbrella term for a labour which may be premature, late, painful, fail to progress, involve foetal distress or require intervention.
Outline the stages of labour.
Normal Labour: Stage 1: Latent (irregular uterine contractions, cervical effacement) -> Stage 1: Active (regular uterine contractions, regular contractions, 1-2cm per hour until 10cm dilation; full cervical effacement) -> Stage 2: full dilation = 2 hours (nulliparous), 1 hour (multiparous) ± 1 if anaesthetic -> Expulsion of placenta and membranes = 10 minutes.
How is foetal progression described?
described in terms of abdominal 5ths. How much of the babies head is above the pubic symphysis. 5/5 is the head is completely mobile above.
What is the term used for amniotic fluid released?
Liqour
When may the membranes rupture?
Can rupture at any point- could be preterm, prelabour, in the 1st stage, 2nd stage or could be born in caul.
State 3 signs that the placenta has been expelled.
- Uterus contracts, hardens and rises
- Umbilical cord lengthens permanently
- Gush of blood (variable amount)
How much blood is usually lost in labour?
500mL
How much EBL is considered abnormal?
≥ 500mL
What is considered a significant EBL in labour?
≥ 1500mL
Outline the physiological way by which the uterus achieves haemostasis.
Clotting pathways
Tonic contraction of uterine muscle with lattice arrangement of muscle fibres to strangulate leaky vessels
What is the puerperium?
A period of recovery and repair of tissues to a non-pregnant state in 6 weeks. Patients will suffer from lochia, which is vaginal discharge containing blood, mucus and endometrial castings. Can be characterised as rubra (fresh red), serosa (brownish red, watery) or alba (yellow). This lasts for 10-14 days following birth.
Give the three characterisations of iochia?
Rubra
Serosa
Alba
Describe uterine involution.
the uterus essentially gets smaller. It reduces its weight from 1000gms to 50-100gms. Fundal height is within pelvis within 2 weeks. The endometrium regenerates within a week. The cervix, vagina and perineum regress but never return to pre-pregnancy state. Physiological diuresis occurs 2-3 days postnatally.
Describe lactation.
Initiated by placental expulsion, due to a decrease in oestrogen and progesterone. Prolactin is maintained. Colostrum (first milk) is rich in immunoglobulins.
Outline how long the second stage of pregnancy usually takes?
Primiparous - 2 hour (3 if anaesthesia)
Multiparous - 1 hour (2 if anaesthesia)
What is the aetiology of failure to progress?
- Power- inadequate contraction
- Passages- short stature, trauma, pelvic shape
- Passenger- big baby, malposition
What is the definition of failure to progress?
In the first stage of labour:
• Nulliparous women- <2cm dilation in 4 hours
• Parous women - <2cm dilation in 4 hours or failure to progress
Second stage
Primiparous - 2 hour (3 if anaesthesia)
Multiparous - 1 hour (2 if anaesthesia)
How may you assess labour progression?
Partogram
What is foetal distress?
Stress inflicted on the baby
How may you conduct an intra-partum foetal assessment?
• Doppler Auscultation of the fetal heart.
Stage 1- before and after contraction. Every 15 mins
Stage 2- at least every 5 minutes during and after a contraction for at least 1 minute. Check maternal pulse every 15 mins.
• Cardiocotography
• Colour of amniotic fluid
State 5 RFs for foetal hypoxia.
Risk Factors for fetal hypoxia: • Small fetus • Preterm/postdates • Antepartum haemorrhage • Hypertension/pre-eclampsia • Diabetes • Meconium • Epidural analgesia • Premature rupture of membranes >24 hours • Sepsis • Induction/augmentation of labour • Vaginal birth after c section (VBAC)
How do you manage foetal distress?
- Change the maternal position
- Iv fluids
- Stop syntocinon (oxytocin)- contractions may be too long or too strong affecting the fetal heart rate.
- Scalp stimulation
- Consider tocolysis- terbulatine 250 micrograms. These are used to suppress premature labour.
- Maternal assessment
- Fetal blood sampling- looks at the scalp pH.
• Operative delivery
What is the threshold for foetal scalp pH regarding action?
≥ 7.25 = normal
7.25-7.20 = borderline, check in 30 minutes
≤ 7.20 = abnormal thus deliver
Describe pre-term labour.
Preterm birth occurs at 24-37 weeks gestation with 66% preterm labours being iatrogenic and 33% presenting with threatened premature labour (TPTL) progressing to actual labour and delivery.
State 3 RFs for pre-term labour.
- Infection and inflammation
- Cervical trauma
- Short cervical length
- Low maternal weight
- Multiple pregnancies
- Polyhydramnios
- PPROM (spontaneous rupture of membranes before 37 weeks of gestation in absence of regular painful uterine contractions)
- Pre-eclampsia/Eclampsia
- IUGR
How may a premature labour present?
- Uterine contractions
- Advanced cervical dilation
• PV Bleed
Which investigations may you wish to conduct in the presence of a pre-term labour.
- CTG
- Tocography: > 1 contraction per 10 minutes
- TVUS of cervix: positive if <2cm
- FBC: Decreased Hb with antenatal haemorrhage and raised WBC
- CRP: Elevated if infection
- Urine dipstick: Positive if infection
- MSU culture + sensitivity: positive growth in presence of infection
- Kleihauer-Betke test: Positive with foetal-maternal haemorrhage
How may you manage a patient with pre-term premature rupture of membranes?
• Maternal evaluation and assessment of foetal viability
+
• ABX: Erythromycin (250mg PO QDS) OR phenoxymethylpenicillin (250mg PO QDS) for 10 days
+
Corticosteroids: Betamethasone sodium phosphate (12g IM every 24 hours for 2 doses)
±
Gestation > 34 weeks or chorioamnionitis
• Consider induced labour
How may you manage a threatened premature labour?
- Maternal evaluation and assessment of foetal viability (continuous CTG + review al data concerning gestational age)
- Tocolytics: terbutaline OR nifedipine
- Steroids (foetal lung maturation)
- Magnesium sulphate (neuro protection)
Why may hypertension occur in pregnancy?
Largest CV Stress occurs in first 12 weeks of pregnancy:
• Blood volume increases
• Plasma volume increases
• Stroke volume increases
• Heart rate increases
• Cardiac output increases
• Peripheral vascular resistance increases
What are the three categories of hypertension in pregnancy?
- Pre-existing hypertension (diagnosed before pregnancy). This is more likely if hypertensive in early pregnancy. Risk of this include IUGR, abruption PET)
- Pregnancy induced (comes on with pregnancy however no pre-eclampsia symptoms). Second half of pregnancy. Resolves within 6 weeks of delivery. No proteinuria or other features of pre-eclampsia. 15% progress to pre-eclampsia.
- Pre-eclampsia- hypertension, proteinuria, oedema.
When does hypertension in pregnancy usually occur?
2nd trimester
Describe pre-eclampsia.
Multisystem disorder of pregnancy which occurs in a triad of new-onset hypertension and proteinuria either before 34 weeks (early pre-eclampsia) or after 34 weeks (late onset pre-eclampsia).
Which form of pre-eclampsia is more severe and why?
Early pre-eclampsia is uncommon. It is associated with extensive villus and vascular lesions of the placenta. Higher risk for both maternal and fetal complications than late pre-eclampsia.
State 5 RFs for pre-eclampsia.
- Primiparity
- PMHx pre-eclampsia/eclampsia
- FMHx pre-eclampsia/eclampsia
- BMI > 30
- Multiple gestation
- Diabetes Mellitus
- HTN
- Kidney disease prior to pregnancy
- SLE
- Antiphospholipid syndrome (autoimmune disorder to phospholipids)
How may pre-eclampsia present?
- Headache
- Visual disturbance
- Epigastric/RUQ pain (if there is liver involvement)
- Nausea/vomiting
- Rapidly progressing oedema
- Hypertension
- Proteinuria
- Oedema
- Abdominal tenderness
- Disorientation
- SGA
- IUD
- Hyper-reflexia/involuntary movements/clonus
Describe the pathogenesis of pre-eclampsia.
• Cytotrophoblasts fail to infiltrate thus spiral arteries are incorrectly formed leading to abnormal placentation causing a reduction in placental perfusion and resultant placental ischaemia. The placenta releases factors which induces pre-eclampsia (anti-angiogenic state). High resistance, low flow network leads to maternal blood pressure increased to increase perfusion to placenta.
How may you manage pre-eclampsia?
• Supportive: Hospital admission + monitoring: BP monitored QDS with risk-prediction PREP-S useful for decisions about admission and thresholds for intervention; Decide on delivery mode
+
Corticosteroid: Betamethasone (12mg IM ever 24 for 2 doses)
- If severe hypertension (> 160/110mmHg)
±
Labetalol (20mg IV then 40mg if BP still exceeded, then 80mg then hydralazine, then consult specialist)
Describe eclampsia
Eclampsia is the presence of tonic clonic (grand mal) seizures occurring in the presence of hypertension and proteinuria caused by cerebral vasospasm/ischaemia.
How do you manage eclampsia?
Before delivery
• Supportive: Hospital admission + monitoring: BP monitored QDS with risk-prediction PREP-S useful for decisions about admission and thresholds for intervention; Decide on delivery mode
+
Corticosteroid: Betamethasone (12mg IM ever 24 for 2 doses)
- If severe hypertension (> 160/110mmHg)
±
Labetalol (20mg IV then 40mg if BP still exceeded, then 80mg then hydralazine, then consult specialist) - If Seizures
±
Magnesium sulfate
Describe some of the complications pre-eclampsia can result in.
CNS • Eclampsia • Hypertensive encephalopathy • Intracranial haemorrhage • Cerebral oedema • Cortical blindness • Cranial nerve palsy
Renal • Decrease in GFR • Proteinuria • Increase in uric acid • Increase in creatinine, potassium, urea • Oligouria/anuria • Acute renal failure
Liver Disease • Epigastric/RUQ pain • Abnormal liver enzymes • Hepatic capsule rupture • HELLP syndrome- haemolysis, elevated liver enzymes, low platelets.
Haematological Disease • Decreased plasma volume causes haemoconcentration • Thrombocytopenia • Haemolysis • Disseminated intravascular coagulation
Cardiac/pulmonary disease
• Pulmonary oedema causes ARDS.
• Pulmonary emboli
Placental Disease
• Fetal growth restriction
• Placental abruption
• IUD
Describe gestational diabetes mellitus.
Glucose intolerance resulting in hyperglycaemia which is precipitated in pregnancy.
Outline the pathophysiology of GDM.
• Placenta secretes TNF-a, hCS causing reduced insulin and insulin resistance -> overgrowth of insulin tissues and macrosomia -> foetal metabolic reprogramming results in long-term risk of obesity, IR and diabetes.
What is the presentation of GDM.
- Polyuria
- Polydipsia
- Foetal macrosomia
Which investigations would you conduct in a patient with GDM?
- FPG: > 7mmol/L
- RPG: > 11.1mmol/L
- OGTT: > 8.5mmol/L after 2 hours
When do you conduct a OGTT in a patient who is G3 P2+1 with PMHx of GDM?
1st trimester
What is the target BM for a patient with GDM.
- FPG <5.3mmol/L
- 2-hour Post-prandial: <7.8mmol/L
- HbA1c: 48mmol/L
How do you manage a patient with GDM?
• Supportive: Diet; Weight control; Exercise; BM monitoring; Growth scan
± Uncontrolled or marked initial hyperglycaemia (RPG > 11.1mmol/L)
• Insulin: Insulin NPH + Insulin lispro
Give an example of an intermediate acting insulin and a short-acting insulin.
Insulin: Insulin NPH + Insulin lispro
State 3 potential complications which may arise due to GDM.
- Pre-eclampsia
- Polyhydramnios
- Macrosomia
- Microsomia
- Shoulder dystocia
- Neonatal hypoglycaemia
Describe what SGA means.
An infant with a birthweight that is less than the 10th centile for gestation when corrected for maternal height, weight, fetal sex and birth order.
Describe what IUGR means.
Reduced size of foetus as a result of disease which is classified as symmetrical or asymmetrical. Symmetrical meaning the whole body is small, whereas asymmetrical meaning one part of the body is normal and the other is smaller.
Poor growth could be due to maternal cause, fetal causes or placental causes.
State 3 RFs which may cause IUGR.
Maternal factors: • Lifestyle- smoking, alcohol, drugs • Height and weight • Age • Maternal disease e.g. hypertension
Fetal Factors:
• Infection e.g. rubella, CMV, toxoplasma
• Congenital anomalies e.g. absent kidneys
• Chromosomal abnormalities e.g. Downs syndrome
Placental Factors
• Infarcts
• Abruption
• Often secondary to hypertension
How may you clinically diagnose poor growth on history and examination?
- Predisposing factors
- Fundus height less than expected
- Reduced liquor
- Reduced fetal movements- a baby struggling for oxygen will lie still.
What is foetal macrosomia?
Large baby > 4.5kg or > 90th centile compared to gestational age and population based charts
State 2 risks associated with foetal macrosomia.
Risks associated with fetal macrosomia: • Maternal anxiety • Labour dystocia • Shoulder dystocia • Post-partum haemorrhage
How do you manage foetal macrosomia?
- Exclude diabetes
- Reassure
- Delivery methods depend on cases, could vaginal, could c section
What is polyhydramnios?
Excess amniotic fluid with an AFI > 95th percentile
What are the causes of polyhydramnios?
- Maternal diabetes
- Fetal anomaly
- Monochorionic twin pregnancy
- Hydrops fetalis
- Idiopathic
How may a polyhydramnios present?
- Abdominal discomfort
- Prelabour rupture of membranes
- Preterm labour
- Cord prolapse
How do you diagnose polyhydramnios?
• Ultrasound scan will confirm:
Amniotic fluid index (AFI) > 25
Deepest vertical pocket (DVP) >8cm
Fetal survery- lips, stomach
• Serology- to look for toxoplasmosis, CMV, parvovirus
• Antibody screen
• Oral glucose tolerance test- look for diabetes
How do you manage a polyhydramnios?
- Patient education/information on complications
- Serial USS- for growth, LV, presentation
- Induction of labour by 40 weeks
What are the risks of polyhydramnios?
- Cord prolapse
- Preterm labour
- PPH
What are the RF for multiple pregnancies?
- Assisted conception
- Race- African
- FHx
- Increased maternal age
- Increased parity
- Tall women > short women
What does chronicity depend on in monozygotic twins?
When cleavage takes place. 0-3 days after fertilisation is dichorionic diamniotic. Whereas 4-7 days after fertilisation is monochorionic diamniotic (MCDA). If cleavage takes place 8-14 days after fertilisation it will be Monochorionic mono amniotic (MCMA)
What is a MCDA pregnancy?
How is this determined?
1 placenta, 2 amnions
Cleavage taking place 4-7 days
What is a MCMA pregnancy? How is this determined?
1 placenta, 1 amnion
Cleavage taking place 8-14 days
What is a DCDA pregnancy?
How is this determined?
2 placenta, 2 amnions
Cleavage takes place within 0-3 days
Or dizygotic twins
How may multiple pregnancies present?
Exagerrated pregnancy symptoms
high amniotic fluid index
Large for dates uterus
Multiple fetal poles
When are DCDA twins delivered?
• DCDA are delivered between 37-38 weeks.
When are MCDA twins delivered?
• MCDA twins are delivered at 36 weeks.
Can you deliver by a C-section if one of the twins is presented cephalically?
No, bigger risk
What is a postpartum haemorrhage?
Expulsion of blood with EBL ≈ > 500mL within 24 hours of delivery to 12 weeks post-partum
What are the two categories of PPH?
1) 1º PPH: Blood loss ≥ 24 hours of delivery
2) 2º PPH: Significant vaginal bleed between 24 hours < X > 12 weeks following delivery
What are the two types of primary PPH?
- Minor: 500-1000mL + X hypovolaemic shock
- Major: ≥ 1000mL + hypovolaemic shock
What are the causes of PPH?
4 Ts
- Tone: Atonic uterus ≈ no uterine 3rd stage contraction causes lack of intramyometrial BVs and placental site
- Tissue: Retained placental tissue, inhibiting uterine contractility (atonic)
- Trauma: perineal tear/episiotomy/cervical tear; uterine incision/extension/rupture
- Thrombin (coagulopathy): DIC sepsis/placental abruption/PPH/AFE/IUD
How do you manage a PPH?
• Assess + Resuscitate mother: Observations/EBL/IV access/Fluids/Blood
+
Identify cause + manage: Placenta delivered/Uterus contracted/Trauma
May be multifactorial
+ Atonic uterus
- Mechanical compression: Bimanual/IU balloon/Brace sutures
- Pharmacological: Syntocinon (Synth. OT)/Ergometrine/Carboprost/Misoprostol (PGE1)/Tranexamic acid (antifibrinolytic)
- Interventions: Embolisation (occluding artery)/Uterine artery ligation (clamping blood supply to uterus)/Hysterectomy (removal of uterus) ± salpigo-oophrectomy
When are pre-existing medical conditions discussed in pregnancy?
- Family Planning
- Contraception
- Review medication list
- Refer for preconception counselling if essential
- Advice to start folic acid (400mcg or 500mg)
State 5 conditions in which genetic screening is advised during pregnancy?
NF
Tuberous sclerosis
Huntington’s
CF
Achondroplasia
Tay-Sachs
Friedreich’s Ataxia
CAH
G6P dehydrogenase deficiency
DMD
Fragile X syndrome
Marfan’s syndrome
What is asthma?
Heterogeneous disease characterised by chronic reversible inflammation eliciting symptoms of wheeze, dyspnoea, tightness, cough which varies with time and intensity due to variable airflow limitations
State 3 RFs for asthma.
- Serum eosinophilia
- Allergic sensitization (Atopy)
- FHx asthma
- Environmental tobacco exposure
- Triggers: U-GO-SEA
- Abnormal lung function with airway hypersensitivity
Outline the presentation of asthma in pregnancy.
- Wheezing
- Increased work of breathing
- Features of atopy: dermatitis, allergic rhinitis
- History of response to treatment within appropriate time frame
- Dyspnea on exertion
- Expiratory wheeze
- Dry night-time cough
Outline the investigations you may use in asthma.
- PEF: Absolute values
- Spirometry: Scalloping of expiratory flow volume loop; FEV1/FEVC < 0.7
- Bronchodilator-response spirometry: Inhaled corticosteroid or ß2 agonist yields reversibility (12% improvement in FEV1 or FVC)
- Bronchial provocation tests (BPT): Inhaled Mannitol (indirect) or Methacholine (PD20; Provocation Dose for 20% reduction) (direct) shows FEV1 decreased (15-20%)
- Fractional Expired Nitric Oxide (FeNO) test: Elevated (> 50ppb; normal ≈ 25ppb)
- CXR: Normal; Hyperinflation; Rule out other pathologies
- FBC: Possible eosinophilia, IgE
- Blood culture: Aspergillus
- Bronchoscopy: Normal; Look for structural abnormalities such as tracheomalacia or bronchomalacia
How do you manage a patient with asthma?
Step 1 – SABA Step 2 – ICS Step 3 – LABA Step 4 - -> ICS Step 5 – LRTA Step 6 – Biologic
• Short-Acting Beta Agonist: Salbutamol (PRN)
±
• Low-dose inhaled corticosteroid (ICS): Budesonide (0.25-0.5mg/day nebulized); Fluticasone (100-200mcg/day)
Increase ICS dose as step 4
±
• Long-Acting Beta Agonist: Salmeterol (50mcg BD)
±
• Leukotriene Receptor Antagonist (LTRA): Monteleukast (4mg PO OD)
±
• Immunomodulator (Biologics): Omalizumab (Anti-IgE mAb)
How does omalizumab work?
Biologic IgE mAb thus reduces mast cell degranulation and histamine release
PEF of 60% is what severity of asthma?
1) Mild Asthma
• PEF: 50-75%
PEF of 40% is what severity of asthma?
2) Acute Severe Features
• PEF: 33-50% predicted
Which severity of asthma is this…
42% FEV (expected), cannot complete sentences in one breath, RR 30, HR 120bpm
Acute Severe
Which severity of asthma is this…
PEF 70% (expected), completes full sentences, RR 24, HR 100bpm
Mild
HR 110bpm and RR 25 are diagnostic thresholds for acute severe asthma
Which severity of asthma is this…
PEF 30% (expected), SpO2 80%.
Life-threatening asthma
What is the immediate treatment for life-threatening asthma?
- Oxygen to maintain SpO2 @ 94-98%
- Salbutamol 5mg via oxygen-driven nebuliser
- Ipratropium bromide 0.5mg on oxygen-driven nebuliser
- Prednisolone 40-50mg or IV hydrocortisone 100mg
- No sedatives of any kind
- CXR
Give treatment regimen acutely
- Oxygen
- SABA
- ICS
- Prednisolone
- CXR
What is cystic fibrosis?
Autosomal recessive disease due to ∆CFTR, fo8und in lungs, intestines, pancreatic ducts, sweat glands and reproductive organs, causing reduced apical chloride secretion ≈ reduced osmotic gain and reduced mucous clearance ≈ accumulation of viscous mucous causing damage to respiratory and digestive systems. Common clinical manifestations: pancreatic dysfunction (malabsorption), lung disease (mucus retention) and inflammation
How do you manage CF in pregnancy?
• Supportive: Physiotherapy; ABX; foetal monitoring (31 weeks)
+
Inhaled bronchodilator: Salbutamol
+
Inhaled mucolytic: Mannitol + Dornase alfa (rhDNAse)
+
Anti-inflammatory agent: Corticosteroid/Ibuprofen/Azithromycin
±
CFTR modulator: Ivacaftor
How does ivacaftor work?
Potentiates CFTR by acting as an agonist thus increase Cl- apical secretion to reduce mucous build up
Describe Venous Thromboembolism.
Formation of a blood clot in the deep veins which is due to interaction of Virchow’s triad: stasis, hypercoagulability and endothelial damage.
Outline the aetiology of VTE.
- Venous stasis: Reduced flow/ Immobility/ Surgery/ Age
- Hypercoagulability: Increased clotting factors/ Surgery/ Oestrogen pills
- Endothelial damage: Atherosclerosis/ Catheters/ ICD/ Smoking
Describe Virchow’s Triad.
Interplay between venous stasis, hypercoagulability, endothelial damage
Outline the risk categories for VTE in pregnancy.
- High risk: Previous VTE -> Antenatal LMWH
- High risk: 3 ≥ RFs (parity > 3, smoker, varicose veins, immobility, FHx, multiple pregnancy) -> Antenatal LMWH
- Intermediate risk: Previous VTE; High risk thrombophilia; Medical comorbidities -> Consider LMWH
- Low risk: 3 ≤ RFs -> Mobilisation and avoidance of dehydration
Outline the presentation of someone with a VTE.
- Swelling
- Oedema
- Leg pain/discomfort
- Tenderness
- Increased leg temp
- Lower abdo pain
- Elevated white cell count
Which imaging technique would you use to identify a PE in pregnancy?
V-Q scan > CT-PA as reduced sensitivity but reduced exposure of radiation to breast tissue which reduces breast cancer risk
Which risk stratification tool can be used to determine a PE risk and subsequent investigations
Wells Score <4 or > 4
DAMN BC
DVT Sx (3)
Another Ddx Unlikely (3)
Mobility reduced (1.5)
kNown history of DVT (1.5)
Blood in cough (1)
Cancer (1)
How do you treat a PE in Pregnancy?
• Anticoagulation: LMWH
+
• Thrombolysis: Alteplase/ Streptokinase
± (Failed thrombolytic therapy/CI)
• Surgery: Thrombectomy
Why can you not give warfarin in pregnancy?
Warfarin is teratogenic
What changes may occur to a baby should you prescribe warfarin during pregnancy?
- Midface hypoplasia
- Short proximal limbs
- Short phalanges
- Scoliosis
What is T1DM?
Metabolic disorder characterised destruction of pancreatic ß-cells causing insulin deficiency resulting in hyperglycaemia, loss of weight, polydipsia and polyuria and secondary complications of a microvascular and macrovascular nature
Outline the pathophysiology of T1DM.
• Autoimmune pancreatic ß-cell destruction (GAD, TP, IA-2) in genetically-susceptible individuals (HLA ∆) -> reduced insulin secretion -> reduced uptake into cell -> secretion of glucagon, adrenaline, cortisol and GH -> promote glucose production (glycogenolysis, gluconeogenesis and ketogenesis) -> further raise blood glucose -> microvascular and macrovascular problems
Outline the management of T1DM in pregnancy.
• Basal bolus insulin: insulin glargine/insulin detemir/insulin degludec + insuin lispro/aspart
+
Aspirin: 75-150mg (reduce pre-eclampsia risk in 1/3)
Describe T2DM.
Progressive metabolic disease defined by defective insulin secretion and resistance leading to abnormal glucose metabolism resulting in hyperglycaemia, weight gain and vascular pathology
How do you manage T2DM in pregnancy?
• Supportive: Diet restriction/ Exercise/ Fluids/ Examination/ Monitoring
+
• Basal-bolus insulin: Insulin NPH (BDS) + Insulin lispro (pre-prandial)
What is hypothyroidism?
Dysregulation of thyroid resulting in reduced production of T3 and T4 of multifactorial cause
Outline the pathophysiology of hypothyroidism.
• Autoimmune thyroiditis/Drugs = Thyroid dysregulation -> Lymphocyte infiltration + Antithyroid peroxidase or antithyroglobulin Ab -> reduced thyroid hormone synthesis (Amiodarone)/Secretion (Lithium) -> reduced T4 and T3 in target tissues
State the potential presentation of hypothyroidism.
- Weakness
- Lethargy*
- Cold sensitivity*
- Constipation
- Weight gain*
- Depression
- Facial oedema
- Glossitis
- Coarse hair
- Goitre
- Oligomenorrhea/amenorrhoea
- Infertility
- Bradycardia
- Diastolic hypertension ± narrow pulse pressure
Which investigations will show hypothyroidism?
- TSH: Elevated*
- Free T4: Low*
- FBC: Leukocytosis (autoimmune lymphocytes); Anaemia
How do you manage an obstetric patient with hypothyroidism?
• Levothyroxine: 1.6mcg/kg/day PO
- > Normalises TSH
- > Measure TSH ever 6/52 and may need to increase dose
What is Hyperthyroidism?
Condition whereby excessive production of thyroid hormones by thyroid gland
What interventions are necessary in a pregnant patient with underlying hyperthyroidism?
- Specialist review
- Anti-thyroid Rx
- Foetal monitoring
- Radioactive Iodine contraindicated in Pregnancy
What hormonal derangements occur in hyperthyroidism? Which investigations may you wish to conduct.
- T3/T4: High*
- TSH: Low*
- US-Thyroid: Vascularised/Diffuse/Enlarged
Outline the symptoms and signs a pregnant patient with hyperthyroidism may display?
- Heat intolerance*
- Sweating*
- Weight loss*
- Palpitations*
- Tremor
- Diffuse goitre
- Exophthalmos
- Scalp hair loss
- Tachycardia
- Wide pulse pressure
How would you manage a pregnant patient with hyperthyroidism?
Manage closely - therapy may not be indicated if T4 levels are close to the normal range in pregnancy.
• Propylthiouracil: 500-1000mg PO loading dose + 250mg PO every 4 hours
+
• Labetalol: 60-80mg PO 4-6 hours
State 5 RFs for hypertension.
- Advanced age
- Sex (M)
- FHx
- Ethnicity
- Obesity
- Dyslipidemia
- Dietary fiber
- Iatrogenic (NSAIDs/Oral steroids/Venlafaxine/Soluble drugs/Illicit Drug Use
- Alcohol intake
- Salt intake
What is the threshold for stage 2 hypertension?
160-179/100-109
What is the threshold for stage 1 hypertension?
140-159/90-99
What is the threshold for stage 3 hypertension?
180-209/110-119
What is the threshold for stage 4 hypertension?
≥ 210/ ≥ 120
What treatment algorithm may be used to decide the choice of drug to treat hypertension?
A + B –> C + D
A: Age < 55 or T2DM -> ACEi/ARB
C: Caribbean or Black or Age 55 < = CCB
Then add in A/C/D
What is peripartum cardiomyopathy? (PPCM)
New onset of heart failure between 24th week of pregnancy and 6 months post-delivery with no cause
State 3 RFs for peripartum cardiomyopathy.
- Maternal Age
- Hypertension
- Multiparity
- Multiple pregnancy
Outline the presentation a patient with peripartum cardiomyopathy may have.
- SOB
- Poor exercise tolerance
- Palpitations
- Peripheral and pulmonary oedema
- Raised JVP
- Basal crackles on lung auscultation
What is antiphospholipid syndrome?
Autoimmune disease caused by antibodies targeting the phospholipid cell membrane which causes arterial and venous thrombosis. This can be primary or secondary to other immune disorders.
Which two antibodies are pathognomonic of antiphospholipid syndrome?
anti-cardiolupin (anti-cl)
lupus anticoagulant (LA)
Outline the potential presentation of a pregnant woman with antiphospholipid syndrome.
- Arterial/venous thrombosis
- Stroke
- TIA
- MI
- Valvular heart disease
- DVT
- Budd-Chiari Syndrome (occlusion of hepatic veins -> ascites, abdo pain + hepatitis)
- Recurrent miscarriages
- Recurrent early pregnancy loss
- Late pregnancy loss- usually preceded by FGR
- Placental abruption
- Severe early onset pre-eclampsia
- Severe early onset fetal growth restriction
Which investigations may be run and suggestive of a pregnant patient with antiphospholipid syndrome?
- ßhCG: Positive
- APTT: Increased
- FBC: Thrombocytopenia
- Antibodies: Anti-cardiolipin; Lupus anticoagulant (LA)
Lab tests must be positive on two occasions
How do you manage a pregnant woman with antiphospholipid syndrome?
• Supportive: Foetal surveillance; Mobility; TED stocking; Stop Warfarin;
+
• COX-1i: Aspirin 75mg
± (Thrombotic event)
• Anticoagulant: LMWH
Describe rheumatoid arthritis.
Chronic inflammatory condition affecting small joints of hands and feet which is characterised by joint pain, swelling and persistent morning swelling resulting in reduced mobility and reduced quality of life.
State 3 RFs for Rheumatoid Arthritis.
- Advanced age: 50-55 years
- Female
- Genetic: FHx RA
Outline the pathophysiology of rheumatoid arthritis.
• Aberrant immune response causing inflammation which drives synovial changes via angiogenesis (VEGF/VEGT), cellular hyperplasia, inflammatory influx and interleukin expression -> Results in: erosions; tendon rupture; soft tissue damage; joint instability; pannus formation
Outline the presentation of rheumatoid arthritis.
• Joint pain: Painful on movement
• Joint swelling: Tender + swollen
-> Bouchard’s Nodes (PIP)
• Stiffness: > 1 hour of joint stiffness
- Swan neck deformity: DIP hyperflexion + PIP hyperextension
- Boutonniere’s deformity: DIP hyperextension + PIP hyperflexion
Non-Articular Manifestations
- Fever
- Fatigue
- Weight loss
- Sjogren’s Syndrome
- Scleritis
- Carpal tunnel syndrome
- Atlanto-axial subluxation
- Polyneuropathy
- Lymphadenopathy
- Felty’s Syndrome (RA + Splenomegaly + Neutropenia)
- Anemia
- Thrombocytosis
- Pleural effusion
- Lung fibrosis
- Rheumatoid pneumoconiosis (Caplan’s Syndrome)
- Pericarditis
- Pericardial effusion
- Raynaud’s Syndrome
• Analgesic nephropathy
- Leg uclers
- Gangrene
Which joint changes occur in Boutonniere’s deformity?
DIP hyperextension + PIP hyperflexion
Which joint changes occur in Swan neck deformity?
DIP hyperflexion + PIP hyperextension
Which investigations will be conducted in a pregnant patient with rheumatoid arthritis? What may they show?
- ßhCG: Positive
- Rheumatoid factor (RF): Positive
- Anti-cyclic citrullinated peptide (anti-CCP) Ab: Positive
- XR/CT: Erosions
How would you manage a pregnant woman with rheumatoid arthritis?
Pregnancy
• Corticosteroid: Prednisolone
Describe epilepsy.
Continuing tendency to have seizures (convulsion/transient abnormal event caused by paroxysmal discharge of cerebral neurons)
Is there an increased risk of seizures during pregnancy?
No, pre-pregnancy and during pregnancy rates remain similar
Well controlled 1st trimester can greatly reduce seizures within pregnancy
Why should you be cautious of anti epileptics in pregnancy?
AEDs may be teratogenic thus use safer ones such as lamotrigine, not sodium valproate or valproic acid which may cause foetal valproate syndrome.
Which additional drug should all pregnant women with epilepsy take?
Folic Acid 5mg
What is a generalised tonic-clonic seizure?
rigid tonic phase + jerking (clonic phase) with muscle jerking rhythmically and eyes remain open then stuporous state (post-ictal depression). Lasts seconds to minutes and associated with: tongue biting, urinary incontinence, post-ictal flaccidness, confusion or drowsiness and headache
What are the three phases of a generalised tonic-clonic seizure?
Tonic then Clonic then Stuporous
What is a petit mal seizure?
childhood with ceasing activity (absence), staring and going pale and atonic (loss of tone). These seizures last for seconds. Despite being ‘absence’ these seizures still have excitation detected by EEG with 3Hz spikes. Children tend to develop generalized tonic-clonic seizures in adult life.
Which group are petit mal seizures more commonly seen in?
Children
In petit mal seizures, children tend to go on to develop which other form of seizure?
Grand mal seizures
Describe myoclonic seizures.
Isolated muscle jerking (myoclonic)
Describe tonic seizures.
rigidity
Describe focal seizures.
Focal seizure: type of partial seizure which may be complex or partial. Symptoms depend on area of brain affected
Describe a Jacksonian seizure.
Jacksonian seizure originates in motor cortex with jerking movement, corner of mouth or thumb and index finger spreading to contralateral side of epileptic focus. These may last for hours (= Todd’s paralysis).
Describe a temporary lobe seizure.
olfactory/visual hallucinations, blank staring, feeling of unreality (jamais-vu), undue familiarity (deja-vu) with surroundings
Outline the potential presentation of a patient with epilepsy.
- LOC
- Tonic stiffening (Grand mal)
- Clonic jerking (Grand mal)
- Stupurous state (Grand mal)
- Ceasing activity/atonic (Petit mal)
- Myoclonic (MTA seizures)
- Tonic (MTA/Grand mal)
- Akinetic (MTA)
- Fever (Febrile seizure)
- Jerking movements spreading to contralateral side (Jacksonian/Motor cortex seizure) + Lasts for hours (Todd’s paralysis)
- Deja-vu (Temporal lobe seizure)
- Jamais vu (Temporal lobe seizure)
- Tongue biting/urinary incontinence/stupurous state (Grand Mal associated)
- Stares and pales (Petit mal associated)
- Loss of memory
- Aura
- Visual disturbances
State 5 risks which may occur from generalised maternal seizures.
- Maternal abdominal trauma
- Preterm premature rupture of the membranes
- Hypoxia/acidosis
- Major and minor congenital malformations
- Adverse perinatal outcomes
- Long term developmental effects
- Haemorrhagic disease of the newborn
- Risk of childhood epilepsy
How would you manage a pregnant patient with epilepsy?
• AEDs: Lamotrigine/Carbamazepine (Partial; All seizures in pregnancy)
± Seizure
• IV Benzodiazepine: IV Lorazepam
Which AED should you not prescribe in pregnancy.
Sodium valproate
Phenytoin
If a patient has an epileptic fit in pregnancy, what should you immediately administer?
• IV Benzodiazepine: IV Lorazepam
What is gestational anaemia?
Development of Anaemia, low Hb > 2SD from mean) during pregnancy
110g/dL 1/3 and 2/3
105g/dL 2/3
How may gestational anaemia present?
- Fatigue
- NV
- Dyspnoea (SOBE)
- Nail changes: koilonychia (spoon nails)
- Angular cheilitis
- Glossitis
- Gastric difficulties: Gastritis/Achlorhydria
- Hair loss
- Pica
- Restless legs syndrome
Which investigations may you wish to conduct in a patient you suspect has gestational anaemia?
- FBC: Hb: < 130g/dL (m)/< 120g/dL (np-w)/ <110g/dL (p-w); MCV < 80fl (may not show in pregnancy); MCH (low); MCHC (low)
- Smear: Microcytic, hypochromic pencil red cells
- Serum Iron: Decreased
- Ferritin: Low (< 12 ng/mL)
- Urinalysis: Blood loss?
How do you manage a patient with gestational anaemia?
• Iron replacement: Ferrous sulfate (2-3mg/kg/day)/Ferrous gluconate(2-3mg/kg/day)/ Ferrous fumarate (2-3mg/kg/day)
Note: Pregnant women take Pregaday (Iron 322mg/ Vitamin B9 0.35mg)
±
Ascorbic acid: 500mg PO BDS-QDS
+
• Supplements: Folic Acid 400mcg
What is immune (idiopathic) thrombocytopenic purpura?
Haematological disorder caused by thrombocytopenia (< 100 x 109/L) in the absence of a known cause (idiopathic) which is secondary to an autoimmune phenomenon involving antibody-mediated destruction of peripheral platelets
What is the main risk of ITP to the foetus?
Neonatal thrombocytopenia due to IgG Abs travelling across the placenta
What are the RFs of ITP which relate to pregnant women?
- Women of childbearing age
* Pregnancy
Outline the pathophysiology of ITP
antiplatelet Abs directed against GPIIb-IIIa/ impaired platelet production (suppression of megakaryocyte development)/ T-cell mediated destruction of platelet and megakaryocyte in bone marrow.
How may ITP be classified?
- 1º ITP: Unknown cause
* 2º ITP: ITP secondary to a known disease
How may a patient with ITP present?
- Bleeding: Bruising/Petechiae/Haemorrhagic bullae
* Rash: Purpura – non-blanching, flat rash
Which investigations may you wish to conduct in a pregnant patient with ITP?
• FBC: Platelet count <100 x 109/L
Consider…
• HIV serology
• H. pylori breath test/stool antigen test
• Hepatitis C serology
• TFTs: Hypo or Hyper -> Test prior to elective splenectomy (exclude reversible causes of thrombocytopenia)
• Pregnancy test
How do you treat a patient with newly diagnosed ITP who is has bleeding but platelets are > 30x10^9L?
• Supportive: Observation, watch and wait
+
• Corticosteroid: Prednisolone
How do you treat a patient with newly diagnosed ITP who is has bleeding but platelets are 15x10^9L?
• Supportive: Observation, watch and wait \+ (Bleeding but platelets > 30 x109/L) • Corticosteroid: Prednisolone ± IVIG \+ (Platelets < 30 x109/L) • IVIG+Corticosteroid OR Anti-D Ig
A patient with known ITP becomes haemodynamically unstable with diffuse bleeding.
How will you manage them?
• IVIG ± Corticosteroids: Prednisolone/Methylprednisolone/Dexamethasone ± Platelet transfusion
Describe Thrombotic Thrombocytopenic Purpura (TTP).
Syndrome typified by microangiopathic haemolytic anaemia and thrombocytopenia purpura
Thus thrombosis and low platelets
Which are the key pentad of clinical features of Thrombotic Thrombocytopenic Purpura?
Fever
Anaemia
Thrombocytopenia
Renal insufficiency
Neurological dysfunction
State 3 RFs for TTP.
- Obesity
- Female gender
- Pregnancy
- Cancer therapies
- HIV infection
- Antiplatelet agents
Outline the pathophysiology of TTP.
• ∆ADAMTS-13 + Environmental change (pregnancy/ infection/ autoimmune condition) -> reduced ADAMTS-13 -> increased vWF -> increased coagulation status -> microangiopathic haemolytic anaemia due to shear stress sites -> microangiopathic haemolytic anaemia + fever + thrombocytopenia + anaemia + renal insufficiency + neurological dysfunction
How may TTP present in pregnancy?
- Fever
- Headache
- Bruising + Bleeding (-> Thrombocytopenia)
- Confusion
- Anaemia (fatigue/pica/angular stomatitis/headaches)
- Coma (Severe neurological)
- Focal abnormalities (Severe neurological)
- Seizures (Severe neurological)
- NVD (HUS)
- Abdominal pain (HUS)
How may you investigate TTP in a pregnant woman?
- ßhCG: Positive
- FBC: Thrombocytopenia (< 100 x 109/L); Low Hb (-> Anaemia)
- Haptoglobin: Decreased
- Peripheral smear: Microangiopathic blood film + schistocytes
- Reticulocyte count: Raised
- Urinalysis: Proteinuria
- Urea + Creatinine: Increased
- Direct Coombs’ test: Negative
How do you manage a patient with TTP in pregnancy?
• Plasma exchange: 24 hours of presentation; ineffective in children with suspected HUS (exclude); should respond within 3 weeks
+
Corticosteroids: Prednisolone/Methylprednisolone
±
Aspirin: 75-300mg PO OD ( reduce platelet aggregation)
±
Folic acid: 3-5mg PO OD
Why is plasma exchange useful in TTP?
Replace the ADAMTS-13 enzyme
Describe Disseminated Intravascular Coagulation.
Acquired syndrome caused by activation of coagulation pathways resulting in intravascular thrombi, depletion of platelets and coagulation factors which may lead to vascular obstruction/ischaemia and multi-organ failure.
How may you classify DIC.
- Acute DIC: rapid-onset generalised bleeding + micro/microcirculatory thrombosis -> hypoperfusion, infarction and end-organ damage
- Chronic DIC: subacute bleeding + diffuse thrombosis
Outline the pathophysiology of DIC.
• Extrinsic tissue factor (VIIa) pathway increases thrombin -> cleaves fibrinogen -> fibrin + reduced fibrinolytic pathway
-> Positive feedback + depletion of procoagulants + platelets ≈ fibrin deposition widespread = multi-organ failure
• Fibrinolytic system malfunction: Increased plasminogen activator inhibitor type 1 (PAI-1) = reduced plasminogen -> plasmin (conversion) = reduced plasmin -> reduced D-dimers (+ FDPs)
• Inflammatory pathways potentiate coagulation: IL-6 and TNF-a + Protein C (anti-inflammatory, inhibition of cytokine production) depression + coagulation products (Xa, thrombin, fibrin -> pro-inflammatory cytokine release from endothelium) -> activate coagulation
How do you have haemorrhage and thrombosis simultaneously in DIC?
Consumption of platelets due to hypercoagulability of blood secondary to (extrinsic clotting pathways + fibrinolytic system depletion + inflammatory pathways) causes imbalance in platelets throughout the vasculature (some more at the site of clots and few elsewhere)
Outline the potential presentation of DIC in a patient.
• S of generalised bleeding: Petechiae/Purpura/Ecchymosis/oozing/haematuria
• Delirium/coma (systemic S of micro/macrovascular thrombosis)
• Oliguria (systemic S of circulatory collapse)
• Tachycardia (systemic S of circulatory collapse)
• Hypotension (systemic S of circulatory collapse)
• Gangrene (systemic S of micro/macrovascular thrombosis)
• Acral cyanosis (systemic S of micro/macrovascular thrombosis)
• Purpura fulminans (systemic S of micro/macrovascular thrombosis)
-> thrombotic purpura in small vessels leading to skin necrosis and DIC
Which investigations would you run in a patient with DIC and what may it show?
- FBC: Thrombocytopenia/ Fibrinogen reduced
- PT: Increased
- aPTT: Unpredictable (prolonged sometimes)
- D-dimer: Elevated
How do you treat a pregnant woman with DIC presenting acutely.
• Rx underlying disorder \+ • Platelet transfusion -> if count < 20 x 109/L \+ Coagulation inhibitors: FFP/CryoPpt
Describe Haemolytic Disease of the Newborn.
Rhesus incompatibility is a condition featuring destruction of foetal red blood cells (RBCs) from transplacental passage of maternally derived IgG Abs due to mother being RhD negative and baby being RhD positive thus IgG Abs produced against RhD antigen of baby.
Outline the pathophysiology of haemolytic disease of the newborn.
RhD -ve (M) + RhD +ve (Fetus) -> B lymphocyte clones recognising RBC antigen promoting IgG Abs against Rhesus D antigen -> attach to fetal RBCs + macrophages sequester in fetal spleen = extravascular haemolysis -> foetal anaemia -> compensates for loss by extramedullary haematopoiesis ≈ HSM, portal hypertension, cardiac compromise, tissue hypoxia, hypoviscosity and increased brain perfusion -> hydrops fetalis and IU fetal death may occur unless corrected
Outline the risk factors for haemolytic disease of the newborn.
- FMH
- Invasive fetal procedures PMHx: Amniocentesis (2%) vs CVS (14%)
- Placental trauma
How may a foetus present with haemolytic disease of the newborn?
- Anaemia signs
- Jaundice signs
- Lethargy
- Low muscle tone
- CTG changes (?)
What investigations would you want to conduct if suspicious of haemolytic disease of the newborn.
- Maternal blood type: Rh-negative
- Maternal serum Rh Ab screen: Positive screen
- Klaihauer-Betke test: Variable – Positive
Which diagnostic test will suggest foetal maternal haemorrhage thus useful in haemolytic disease of the newborn?
• Klaihauer-Betke test: Variable – Positive
How do you manage a woman with haemolytic disease of the newborn?
• Anti-D immunoglobulin
Why may an airway be more challenging to secure in pregnancy?
Venous engorgement and mucosal oedema creates a more challenging and vulnerable airway
Why may breathing be more difficult in pregnancy?
Increased minute ventilation
Increased O2 consumption
Why may circulation be more difficult in pregnancy?
Increased PVR Increased volume Increased HR Increased SV Increased CO
These show signs of hypovolaemia late
How do you assess a pregnant patient in an emergency?
ABCDE
What are the causes of maternal collapse in pregnancy?
Hypoxia
Hypovolaemia
Hyper/Hypokalaemia
Hypothermia
Thromboembolism
Toxins
Tension pneumothorax
Tamponade
What is post-partum depression?
development of a depressive illness 1 month following childbirth (including bipolar but more commonly unipolar illness)
What is the aetiology of PPD?
- Psychosocial: isolation/sexual+physical violence/socioeconomic disparity
- Psychiatric illness: PMHx + FHx (environmental)
- Genetic: May be familial
- Sleep deprivation
- Complications of pregnancy and birth: Risk
- Young maternal age: u16 ≈ risk
How may PPD present?
- Low mood
- Anhedonia
- Anergia/fatigue
- Suicidal ideation
- Low self-esteem
- Inappropriate guilt
- Poor concentration
- Weight change (gain or loss)
- Change in appetite
- Sleep disturbance
What investigation may you use to screen for PPD?
• Whooley Questions (Identification Q’s): Feeling down, depressed or hopeless in last month? + Little interest and pleasure in doing things in last month?
What investigation may you use to diagnose PPD?
• Edinburgh Postnatal Depression Scale: Score > 12
Which investigations may you use to diagnose PPD?
- Whooley Questions (Identification Q’s): Feeling down, depressed or hopeless in last month? + Little interest and pleasure in doing things in last month?
- Edinburgh Postnatal Depression Scale: Score > 12
How would you manage a patient with PPD?
SSRIs
What is post-natal blues?
minor mood disturbance occurring 3-10th day PP
How do you manage postpartum blues?
• Spontaneous resolution
What is postpartum psychosis?
Development of psychosis shortly postpartum (7-14 days)
How may postpartum psychosis present?
- Tangentiality
- Hallucinations
- Reduced reality
- Emotional control (incongruous effect)
- Arousal/Anxious
- Disorganised behaviour/ Delusions
- Loss of volition/social settings/Low mood
- Emotional flatness
- Speech slowed (alogia)
- Slowness in thought (cognitive deficit)
How do you manage postpartum psychosis?
• 1st episode: Anti-psychotics (Aripiprazole) + Psychological interventions
What is cytamegalovirus?
ß-herpes virus infecting majority (50%) humans which is usually asymptomatic but immunocompromised individuals yield reactions when re-activation from latent stage occurs or primary infection occurs.
In which patient groups is CMV prevalent?
Immunocompromised
HIV
Immunosuppressants
How may CMV be transmitted?
person-to-person/vertical transmission/blood transfusion/transplantation (organ or haematopoietic stem cell) then CMV triggers humoral and cell-mediated adaptive immunity to control viral infection thus latency
How may CMV present in both mother or foetus?
Often asymptomatic
- Maculopapular rash/Blueberry muffin rash
- Malaise
- Fever
- Diarrhoea
- Visual floaters + blindness
- Microcephaly
- Hypotonicity + Poor motor function w/ abnormal head lag
- Hearing loss/deafness
- Intracerebral calcification
- Microcephalus
- IUGR
- Retinitis
- HSM
- Hepatitis
- Petechiae/purpura
Which tests should you conduct in a patient with suspected CMV?
- FBC: Anaemia/Leukopenia/Thrombocytopenia
- NAAT: No. genomic copies per volume of specimen
- Serology (ELISA): CMV-IgM/CMV-IgG
Why conduct an FBC in CMV regarding management?
Baseline monitoring however CMV Rx with Ganciclovir leads to bone suppression
How do you manage a patient with CMV?
• Antiviral: IV Ganciclovir/PO Valganciclovir
What is toxoplasmosis?
Condition caused by protozoan parasite Toxoplasma gondii whereby cats are the hosts, contaminating and water food with bradyzoites (tissue cysts) which is usually unnoticed as asymptomatic unless immunocompromised
What is the term for the tissue cysts which contaminate water and food that transmits T. gondii?
Bradyzoites
How is T. gondii spread?
Vertical/Food ingested
How may T. gondii present?
Signs of encephalitis in the mother
• Chorioretinitis: Lesions in fundus w/ proof of Toxoplasmosis
-> Consider other differentials
• Blurry vision
• Slurred speech (encephalitis)
• Headache (encephalitis)
• Confusion (encephalitis)
• Focal neurological deficit (encephalitis)
• Unsteady gait/imbalance (encephalitis)
Foetal abnormalities in the neonate. • Foetal microcephaly • Foetal intracranial calcification • Foetal hydrocephalus • Foetal IUGR • Cataracts • Retinitis • Pneumonitis • Myocarditis • Hepatitis • Jaundice • Hepatitis • Maculopapular rash • Anaemia • Bone abnormalities
How would you diagnose T. gondii regarding investigations?
- Serology: anti-Toxoplasma IgG elevated + anti-Toxoplasma IgM elevated
- CT/MRI-Brain: Ring-enhancing brain lesion(s) – often multiple, in the basal ganglia
How do you treat a pregnant woman with a T. gondii infection.
DHFR inhibitor: Pyrimethamine \+ DHP synthetase inhibitor: Sulfadiazine \+ THF: Calcium folinate
What is rubella?
= mild, self-limiting, systemic infection caused by rubella virus which is often asymptomatic but can precipitate symptoms in immunocompromised individuals.
How is rubella virus transmitted?
direct or droplet contact with infected body fluids (commonly nasopharyngeal secretions) -> infectious for 7-30 days post-infection/7 days pre-rash and 10 days post-rash -> replicates in local lymph nodes and spreads haematogenously
How may rubella present?
- Maculopapular rash: erythematous, discrete, maculopapular ± pruritic/accentuated by heat; face
- Koplik spots (gray spots on buccal mucosa)
- Fever: Low-grade
- Malaise
- Arthralgia: Fingers/Wrists/Knees
- Lymphadenopathy: Post-auricular/posterior cervical/occipital
- Conjunctivitis: Non-purulent conjunctivitis
- Intracerebral calcification
- Hydrocephalus
- Growth restriction
- Hydrocephalus
- Microcephalus
- Cataracts
- Microphthalmia
- Retinitis
- Cardiomegaly
- PDA
- Maculopapular rash/Blueberry muffin rash (maculopapular rash of magenta colour due to persistent dermal erythropoiesis)
- Hepatomegaly
- Jaundice
- Hepatitis
- Virus in urine
Which diagnostic test will confirm Rubella?
• Serology (ELISA): Elevated Rubella-specific IgM positive (acute) / IgG (x4 increase
How do you manage rubella in a pregnant woman?
- Specialist referral
* IM Ig
What is Varicella Zoster Virus?
Human alpha herpes virus (varicella zoster) causing an exanthematous condition (chickenpox) or shingles featuring fever, malaise, pruritic, vesicular rash with worse outcomes in immunocompromised people.
How is VZV transmitted?
Contact/Vertical then spread to regional lymph nodes leading to 1º viraemic phase -> spread to liver, spleen and reticuloendothelial system cells then 2º viraemic phase: mononuclear cells transport VZV to skin and mucous membranes ≈ vesicular rash – vasculitis of small blood vessels and degeneration of epithelial cells ≈ fluid-filled vesicles
Where may VZV lay dormant? What may this cause?
Dorsal root ganglion;
Shingles
How may VZV infection present?
- Fever
- Vesicular rash: Dew drop on a rose petal; appears central (face, scalp or truncal) then spreads distally (accral); lesions scab over as new peripheral lesions develop
- Vesicles on mucous membranes: Nasopharynx/Conjunctiva/Mouth/Vulva
- Pruritus
- Fatigue/Malaise
- Tachycardia
How would you describe VZV rash?
Vesicular rash: Dew drop on a rose petal; appears central (face, scalp or truncal) then spreads distally (accral); lesions scab over as new peripheral lesions develop
How do you clinically diagnose VZV?
- PCR: Positive for virus DNA
* Viral culture: positive for VZV
How do you manage a VZV infection in a pregnant woman?
• Antiviral: Aciclovir
±
Supportive care: Paracetamol + Diphenhydramine
What is parvovirus?
Slapped cheek syndrome caused by parvovirus B19
Outline how parvovirus may present.
- Fever
- Coryza
- Muscle aches
- Erythematous rash (slapped cheeks): Spreads from cheek to trunk and limbs
How do you treat Parvovirus?
• Conservative: Analgesia + Fluids
Which is the causative pathogen of Hand, Foot and Mouth disease?
Hand, foot and mouth disease caused by Coxsackie A virus which presents with tiredness, dry cough, fever, ulcers and red spots across the body.
How may Coxsackie virus present?
- Fever
- Ulcers and spots
- Dry cough
How do you treat Coxsackie virus?
• Supportive: Fluids; Analgesia; Isolation
How long does a child remain infective for with chickenpox?
2 days pre-rash
What is the incubation period of chickenpox?
7-21 days
What is the incubation period of rubella?
14-21 days
For how long is a child infective with rubella?
7 days pre-rash and 10 days post-rash
How long is a child infective for with slapped cheek syndrome?
10 days before day of rash
What is chlamydia?
Urogenital chlamydia infection common STI caused by Chlamydia trachomatis (gram negative bacillus) which is usually asymptomatic
How is chlamydia transmitted?
• Unprotected sex with infected
How does chlamydia present in a female?
- Vaginal/Anal discharge
- Post-coital bleeding
- Abdnominal/Pelvic Tenderness
- Reiter’s Syndrome (arthritis; cervicitis; urethritis and conjunctivitis)
- Proctitis
- Pharyngitis
What is Reiter’s Syndrome?
Arthritis
Cervicitis
Urethritis
Conjunctivitis
What complications may Chlamydia cause in pregnancy regarding a neonate?
- Conjunctivitis (5-12 days)
* Pneumonia (1-3 months)
Which investigations are used to diagnose Chlamydia?
- NAAT: VVS/ECS/FCU
* Direct immunofluorescence
How do you manage a pregnant woman with chlamydia?
Azithromycin
What is the transmission of gonorrhoea?
• Unprotected sex with carrier -> adherence to urogenital epithelium -> phagocytosed by macrophages and neutrophils -> neutrophil-rich (purulent) exudate -> transmission across epithelial membrane
Outline the presentation of gonorrhoea in a pregnant patient.
- Dysuria
- Mucopurulent discharge **
- Post-coital bleeding**
- Septic arthritis** (single joint)
- Lower abdominal pain
- Rectal infection
- Salpingitis
- PID
- Pharyngeal infection
Which diagnostic test can be used to prove the infection of gonorrhoea?
- NAAT: FCU/ECS/VVS/PS
* Culture + Light microscopy: Negative gram stain diplocci
How do you treat gonorrhoea in a pregnant woman?
• Ceftriaxone: 250mg IM
+
• Azithromycin: 1g PO orally
How may HSV infection present in a pregnant patient?
- Genital ulcer (vesicular)
- Oral ulcer
- Tingling neuropathic pain
- Lymphadenopathy
- Febrile flu-like prodrome
- Neuropathic tingling pain
- Dysuria
- Bilateral crops of painful blisters
- Lymphadenopathy
- Local oedema
- Discharge
How would you clinically diagnose HSV infection in a pregnant woman?
- Viral culture
- HSV PCR
- Serology: Glycoprotein G with Ab to HSV-1/HSV-2
What is the management of HSV?
• Aciclovir: 400mg PO TDS 7-10 days
What is HIV?
Retrovirus which is RNA inserting into DNA of host, which is an opportunistic infection transmitted by vertical and horizontal transmission, mediated by CD4+ T-helper cells.
State 3 High Risk HIV Groups.
- MSM
- Female partners of bisexual men
- PWID
- Partners of those with HIV
- Adults from endemic areas
- Children from endemic areas
- Sexual partners from endemic areas
Outline the Pathophysiology of an HIV infection.
HIV is detected by an APC which presents to CD4+ T-helper cells via gp120, CCR5 co-receptor and CXCR4 co-receptor -> recognises MHC-2 APCs to activate B cells and CD8+ (Cytotoxic) T cells to release cytokines and antibodies -> HIV uses RTase to integrate proviral RNA into host DNA -> during infection, inserted RNA is transcribed and translated from host DNA which buds off and infects more host cells -> HIV demonstrates viral tropism (high mutation rate thus several strains of virus)
Why are CD4+ cells, called this?
This is a glycoprotein found on a variety of cells such as macrophages, dendritic cells and T-helper cells
Which protein allows HIV to bind the CD4 receptor on cells?
gp120
Which co-receptors may HIV bind to?
CCR5
CXCR4
gp120
How does HIV mediate its effects primarily?
Retrovirus - Reverse transcriptase
Budding
Viral tropism
Outline the acute phase of the HIV infection.
Virus transmitted via sexual contact -> R5 strain binds CCR5 co-receptor infection macrophages and dendritic cells in mucosal and epithelial surfaces -> return to lymph nodes -> presents to T-helper cells -> large spike of virus in patient blood -> Flu-like symptoms: Fever, Rash, Myalgia, Pharyngitis, Headache
Outline the chronic phase of HIV infection.
Immune system upregulated -> reduced level of virus in blood (viral load) + return of CD4+ T-cells to normal level
Outline the AIDS phase of the HIV infection.
CD4+ T-cell count reduces (≤ 200 cells/mm3) -> immunocompromised + opportunistic infections: Pneumocystis PNA, TB, Cerebral toxoplasmosis, CMV, Skin infections, Neurological disease, Kaposi’s sarcoma, Cervical cancer, Non-Hodgkin’s Lymphoma
Outline the phases of an HIV infection
Acute: Virus transmitted via sexual contact -> R5 strain binds CCR5 co-receptor infection macrophages and dendritic cells in mucosal and epithelial surfaces -> return to lymph nodes -> presents to T-helper cells -> large spike of virus in patient blood -> Flu-like symptoms: Fever, Rash, Myalgia, Pharyngitis, Headache
Chronic: Immune system upregulated -> reduced level of virus in blood (viral load) + return of CD4+ T-cells to normal level
AIDS: CD4+ T-cell count reduces (≤ 200 cells/mm3) -> immunocompromised + opportunistic infections: Pneumocystis PNA, TB, Cerebral toxoplasmosis, CMV, Skin infections, Neurological disease, Kaposi’s sarcoma, Cervical cancer, Non-Hodgkin’s Lymphoma
Describe the effect HIV has on other immune cells.
- CD4 + cells aggregate in lymphoid tissues- reducing circulating numbers
- Reduction in CD8 T cells (cytotoxic T cells), leading to a dysregulated expression of cytokines and increased susceptibility to viral infections
- Reduction ß-cell efficacy: in antibody class switching- meaning there is a reduced affinity of antibodies produced.
- Chronic immune activation
How is HIV transmitted?
- Vertical (MTCT – intrauterine/intrapartum/postpartum)
* Horizontal: Blood-borne/Contaminated needles/Sexual intercourse
When testing for HIV, which markers may be used?
Antibodies - IgG/IgM (Chronic)
Viral load (Acute)
Antigen p24 (Acute)
Which tests can be used for HIV?
- ELISA for Antibodies (best in chronic infection) -> IgM and IgG = 20-25 days window (exposure till detection)
- Rapid Testing: Blood/saliva with results in 20-30 minutes with 4th generation being ‘combined’
- Recent Infection Testing Algorithm (RITA): Identify infection in previous 4-6 months measuring Abs and affinity of Abs.
How may HIV present?
- Fevers and night sweats
- Weight loss/Wasting syndrome (≥ 10% loss of BW unexplained)
- Skin rash(es): HZV/Dermatitis/Fungal infections (Tinea corporis etc..)
- Kaposi’s sarcoma: pink/violaceous patch on skin/mouth
- Oral signs: thrush, ulcers and leukoplakia
- Recurrent opportunistic infections -> M. tuberculosis/Atypical mycobacterial infections/Noncardiosis/Salmonella/HSV/CMV/VZV/Pneumocystis jiroveci/Histoplasmosis/Candidiasis/Cryptococcosis/Coccidiomycosis
What is the causative agent of Pneumocystis Pneumonia?
Pneumocystic Jirovecii
When does Pneumocystic Pneumonia occur in HIV?
AIDS - ≤ 200 cells/mm3
Outline how Pneumocystic Pneumonia presents?
What will a CXR show?
Symptoms will include insidious onset of SOB and dry cough. Signs will include oxygen desaturation on exercise. CXR may be normal or show interstitial infiltrates and reticulonodular markings. Sometimes resembles heart failure with bat wing sign, alveolar oedema with/without cardiomegaly.
How do you diagnose Pneumocystic Pneumonia?
Diagnosis is made by broncheoalveolar lavage +/- immunofluorescence.
CXR
How do you treat Pneumocystic Pneumonia?
high dose co-trimoxazole and steroids. Prophylactic treatment is low dose co-trimoxazole
What is the causative agent of cerebral toxoplasmosis?
T. gondii
When may you get Cerebral toxoplasmosis in HIV?
AIDS - ≤ 150 cells/mm3
How may Cerebral toxoplasmosis present?
- Headache
- Fever
- Focal neurology
- Seizures
- Reduced consciousness
- Raised ICP
What are the symptoms of CMV infection in AIDs?
- reduced visual acuity
- floaters
- abdominal pain
- diarrhoea
- PR bleeding.
What is HIV-associated neurocognitive impairment?
Presents as reduced short-term memory with/without motor dysfunction.
What is Progressive Multifocal Leukoencephalopathy?
How does it present?
Causative organism: JC virus.
CD4 <100
Reactivation of latent infection. White matter changes likely. Can resemble MS. Rapidly progressing focal neurology, confusion and personality change.
- Distal sensory polyneuropathy
- Mononeuritis multiplex
- Vacuolar myelopathy
- Aseptic meningitis
- Guillan Barre syndrome
- Viral Meningitis
- Crytococcal meningitis
- Neurosyphilis
What is slims disease?
Multiple aetiologies including metabolic causes such as chronic immune activation, anorexia, malabsorption/diarrhoea, hypogonadism.
What Kaposi’s sarcoma?
Which organism causes it?
How is it managed?
Human herpes virus 8 (HHV8).
CD4 threshold- any but increased incidence with increased immunosuppression
Usually presents on the skin as spongy raised nodules/papules. It is a vascular tumour. Can present cutaneously, but also mucosally and viscerally (pulmonary, GI).
Treatment- HIV needs treated, local therapies can be used and possibly systemic chemotherapy
Which malignancies are related to HIV?
Kaposi’s Sarcoma
Cervical Cancer
Non-Hodgkin’s Lymphoma
What is neonatal sepsis?
Clinical syndrome resulting from infection and subsequent dysregulated immune response
What is the difference between early-onset and late-onset sepsis?
birth-72 hours = EOS
72 hours - 1 month = LOS
Outline the presentation of neonatal sepsis?
- Fever: ≥ 37.5ºC
- Tachypnoea
- Tachycadia
- Hypotension
- Bradycardia (neonates and infants)
- Altered mental state/behaviour: Reduced cerebral oxygen delivery
- Decreased peripheral perfusion
- Change in feeding pattern of neonate
- Dry nappies/decreased urine output
- Low oxygen saturation
- Mottling of skin/ashen appearance/cyanosis
- Tachypnoea
- Tachycardia
- Hypotension
How do you manage neonatal sepsis?
Management: • Fluids \+ • Oxygen \+ • IV ABX: Ceftriaxone
Describe mastitis?
inflammation of breast
How does mastitis occur?
• blocked duct/engorgement/breast abscess
How may mastitis present?
- Redness (erythema)
- Tender on palpation
- Systemic Sx: fever, rigors, lethargy, muscle aching
- Depression
- Nausea
- Headache
How do you manage mastitis?
- Drainage of breast: feeding frequency, attachment improved, positioning chin towards blockage (tongue wall-like movement to breast), heat applied before feed (improve flow), focus on area or feeding by pump and massage
- US: heat to area
- ABX: Flucloxacillin 500mg PO QDS 5/7 (Clindamycin if allergic to penicillin)
What is a mechanical feeding problem?
How do you manage a mechanical feeding problem?
Anatomical or process problem leading to nipple/breast damage
• Supportive:
Mother: body supported (reduced tension + support infant body) + cradle hold (infant head on forearm and mother supports infant back)
Infant position: (body faces mother + straight + chest close to mother + nose in line with mother’s nipple + chin close to breast)
Should a HSV infection of the breast occur showing painful sores around the nipple on a background of erythema, what changes should be made to manage this?
- Avoid breastfeeding until sores resolved
- Express milk and discard to maintain milk supply
- Self-resolves
What is dermatitis?
(= Dermatitis/Eczema characterised by papules and vesicles on an erythematous base due to underlying atopy (allergic rhinitis/eczema/hay fever
How does dermatitis occur?
• 1º genetic defect in filaggrin protein ≈ dryness + increased permeability + loss of barrier function -> increased permeability ≈ inflammation + scratching
How may dermatitis present?
- Pruritic
- Erythematous
- Dry scaly patches
- Common on face and extensor in children
- Common in flexor compartment in adults
- Scratching
- Excoriations and lichenifications
How do you manage dermatitis?
- Avoid exposures + triggers
- Oil/soap substitute
- Steroids (mometasone PO OD 10/7)
- Oral therapies (H2-As)
How may a fungal infection occur in the breast?
Outline the presentation and management.
• Colonisation with C. albicans (often following ABX Rx)
Signs and Symptoms:
• Burning pain in nipple
• Pain occurs during and after feeds
• Pain radiates into breasts
- Infant has white lesions on buccal mucosa
- Topical antifungal (fluconazole) for both
What is the cause of nipple vasospasm?
How may this present?
How will you manage this?
• Idiopathic vasospasm (Raynaud’s phenomenon) causing change of bloodflow to alter and reduce causing blanching
-> Occur in women with poor circulation or FHx; may be present before; exacerbated by cold
Signs and Symptoms:
• Nipple colour change (purple/blue/blanching)
• Radiation to breast
Management
• Supportive: cover after feeds, heat applied, warm clothes and environment
• CCB: Nifedipine PO OD 20mg slow release
State 3 causes of low milk supply.
- Hypoplastic breasts (wide-spaced + prominent areolas)
- Breast reduction surgery ≈ hyposensitive breasts
- Placental remains ≈ interference with lactogenesis
- Compromised thyroid function
- PPH ≈ pituitary hypoperfusion
- Abnormal autocrine regulation (asymmetrical production)
