Obs-Gyn-Conditions Flashcards
(681 cards)
Define anaemia in pregnancy?
First trimester – Hemoglobin <110 g/L (approximately equivalent to a hematocrit <33 percent)
Second trimester – Hemoglobin <105 g/L (approximate hematocrit <31 or 32 percent)
Third trimester – Hemoglobin level <110 g/L (approximate hematocrit <33 percent)
Some individuals may have a significant decrease from baseline without crossing these thresholds, and clinical judgment is required to determine the reason(s) for the decrease and the need for (and aggressiveness of) further evaluation. As an example, in an individual with a baseline hemoglobin of 14 g/dL that decreases to 11 g/dL associated with macrocytosis, checking a reticulocyte count and testing for vitamin B12 and folate deficiencies is reasonable.
Anaemia is normally <120g/L FEMALE
<140g/L MALE
PREGNANCY = RF for anaemia
Other RFs include: extremes of age, female gender, lactation, and pregnancy.
Most frequent cause of anaemia in pregnancy worldwide?
IDA
Explain the aetiology / risk factors of anaemia in pregnancy
Physiological/Dilutional - plasma volumes increase to a greater proportion than RBC volume
IDA
OTHER:
Haemoglobinopathies
- Thalassaemia
- Sickle Cell
RBC membrane disorders:
- hereditary sphere/ellipto
Acquired:
- Folate
- B12 (don’t forget crohns)
- Vit A deficiency
- A/I ie SLE / acute viral infection causing anaemia
- Hypothyroidism / CKD
Summarise the epidemiology of anaemia in pregnancy
Estimated 30% WW women of reproductive age = anaemic
WHO WW = 40% preg women
Many individuals = iron deficient but not yet ANAEMIC
Recognise the presenting symptoms/signs of anaemia in pregnancy
Palpitations Dizziness SOB Fatigue Pallor Fainting
Maternal consequences: maternal cardiovascular strain, reduced physical and mental performance, reduced peripartum blood reserves, increased risk for peripartum blood product transfusion, and increased risk for maternal mortality
Identify appropriate investigation for anaemia in pregnancy
RBC count
CBC count
Iron studies - serum ferritin (eg, <30 ng/mL [<30 mcg/L]),
TIBC, Transferrin Sat (<20%) - beware iron supplements can cause pseudo.
Extreme microcytosis (eg, mean corpuscular volume [MCV] <80 fL), suggestive of thalassemia
Macrocytosis (MCV >100 fL), suggestive of vitamin B12 or folate deficiency or reticulocytosis due to hemolysis
Other cytopenias such as thrombocytopenia or neutropenia
Abnormally high white blood cell (WBC) count or platelet count
Abnormal RBC or WBC morphologies
Failure of the anemia to correct with iron supplementation
Generate a management plan for anaemia in pregnancy
Supplemental plan for ALL WOMEN:
IRON - 30mg/day
OR 60mg/day guaranteed in FOOD
A 55 kg woman requires approximately 1 gram of additional iron from conception to delivery
BUT Rx of IDA:
Oral/IV iron
ORAL = Ferrous Sulphate 65mg-200mg daily (absorption increased with Vit C supplementation, avoidance of coffee)
IV = NOT used in 1st trimester, but low threshold in 2/3rd
Usually takes 3 weeks to correct.
Transfusion for SEVERE symptoms
OTHERS
- Folic acid supplementation
- Vit B12 supplementation
- Avoid oxidant meds if G-6PD
- SCD = transfusion
- Thal = transfusion
- A/I causes = transfusion
Continue post partum
Identify the possible complications of anaemia in pregnancy and its management
Intrauterine growth restriction, death in utero, infection, preterm delivery and neurodevelopmental damage, which may be irreversible.
Maternal death (most common cause)
Normal anaemia parameters?
Anaemia is normally <120g/L FEMALE
<140g/L MALE
PREGNANCY = RF for anaemia
Other RFs include: extremes of age, female gender, lactation, and pregnancy.
Define amniotic fluid embolism
Amniotic fluid embolism syndrome (AFES) is a rare but catastrophic condition that occurs when amniotic fluid enters the maternal circulation.
Acute pulmonary hypertension and rapid right ventricular failure ensue (usually lasting 15 to 30 minutes) followed by left ventricular dysfunction; hypoxemic respiratory failure and cardiovascular collapse quickly ensue and culminate in systemic inflammation and noncardiogenic pulmonary edema.
Explain the aetiology / risk factors of amniotic fluid embolism
Cesarean or instrumental vaginal delivery
Precipitous or tumultuous labor
Advanced maternal age (eg, ≥35 years)
Placenta previa, placenta accrete/percreta/increta, or placental abruption
Grand multiparity (≥5 live births or stillbirths)
Cervical lacerations
Fetal distress
Eclampsia
Pharmacologic induction of labor
Uterine rupture
Polyhydramnios
Miscarriage, abortion, amniocentesis
Summarise the epidemiology of amniotic fluid embolism
AFES is rare. Most studies indicate that the incidence is between 1 and 12 cases per 100,000 deliveries
90% occur during labour/immediately postpartum
Recognise the presenting symptoms/signs of amniotic fluid embolism
Aura – 1/3 = sense of sudden doom, chills, nausea and vomiting, agitation, anxiety, or change in mental status
Cardiorespiratory failure and/or arrest – Patients suddenly develop hypoxemic respiratory failure, hypotension from cardiogenic shock, and/or cardiovascular collapse/cardiac arrest.
Typical clinical findings include oxygen desaturation, dyspnea, tachypnea, cyanosis, crackles, and occasionally, wheeze.
Hypoventilation is unusual unless in the setting of respiratory arrest. Those with cardiac arrest can present with bradycardia, tachycardia, ventricular fibrillation, pulseless electrical activity (PEA) and/or asystole. If patients survive the initial cardiorespiratory event, noncardiogenic pulmonary edema often develops (worsening dyspnea and tachypnea, crackles) as left ventricular failure resolves.
Hemorrhage from disseminated intravascular coagulation (DIC) typically occurs shortly after the development of cardiorespiratory compromise but may be the initial presentation [1,2,5,43].
Prolonged bleeding from sites of invasive interventions and bruising are the most common manifestations of DIC.
Neurologic manifestations – Tonic-clonic seizures (30 percent) and stroke (rare) .
Levels of zinc coproporphyrin-1 and sialyl Tn antigen increased in some
Identify appropriate investigations for amniotic fluid embolism and interpret the results
INC WCC
Anaemia
DIC - inc D-dimer, low fibrinogen (<200g/L), thrombocytopenia <150-400
ABG - hypoxaemia, pos met acidosis if cardiac arrest
Radiographic - pos bilateral oedema/haemorrhage
ECG - tachy / pos arrhythmia
FETAL signs:
- decelerations
- loss of variability
- bradycardia
Typical investigations include complete blood count, chemistries, renal and liver function tests, cardiac enzymes, brain natriuretic peptide levels, chest radiography, arterial blood gases, electrocardiography, and/or bedside ultrasonography (if available). The primary purpose of initial investigations is to narrow the differential since AFES is a diagnosis of exclusion.
Generate a management plan for amniotic fluid embolism
- Prompt delivery of child if viable
- Supportive
- Examination
- Small fluid boluses 250-500ml, inotrope, vasopressor therapy, etc etc
Potential transfusion with DIC, replacement of blood, fresh frozen plasma, platelets, and cryoprecipitate should be available in the operating room.
Identify the possible complications of amniotic fluid embolism and its management
Leading cause of maternal deaths in developed countries
Cardiogenic shock / cardiac arrest
Potential neurological injury.
20-50% neonates die.
Summarise the prognosis for patients with amniotic fluid embolism
Leading cause of maternal deaths in developed countries
85% have neurological injury.
Define Asherman’s syndrome
Intrauterine adhesions
IUAs, or intrauterine synechiae, is a condition in which scar tissue develops within the uterine cavity. Intrauterine adhesions that are accompanied by symptoms (eg, infertility, amenorrhea) are referred to as Asherman syndrome. The degree of adhesion formation and the impact of the adhesions on the contour of uterine cavity vary greatly. Minimal disease is characterized by thin strands of tissue stretched across the uterine cavity while severe disease is characterized by complete obliteration of the cavity, with the anterior wall of the uterus densely adherent to the posterior wall.
Explain the aetiology / risk factors of Asherman’s syndrome (Intrauterine adhesions)
IUAs appear to result from trauma to the basalis layer of the endometrium
Pregnancy
Intrauterine procedures - curettage / fibroid removal / myomectomy
Infection: Endometritis, Genital TB,
Uterine compression sutures (used to treat postpartum haemorrhages)
Summarise the epidemiology of Asherman’s syndrome (Intrauterine adhesions)
- 5 percent = incidental finding at hysterosalpingogram
21. 5 percent with a hx of postpartum uterine curettage
Recognise the presenting symptoms of Asherman’s syndrome (Intrauterine adhesions)
An ovulatory woman who develops secondary amenorrhea or hypomenorrhea after an intrauterine procedure, particularly if the procedure was performed on a gravid uterus.
Sx Uterine bleeding Infertility Cyclical pelvic pain / dysmenorrhoea Recurrent pregnancy loss Incidental finding
Identify appropriate investigations for Asherman’s syndrome and interpret the results (Intrauterine adhesions)
Direct visualization of IUAs with hysteroscopy is the gold standard for the diagnosis
USS - thin endometrium
Estrogen/progestin withdrawal test takes too long.
Physical examination may show difficulty passing dilator
Generate a management plan for Asherman’s syndrome
HYSTEROSCOPIC RESECTION — The standard treatment of symptomatic intrauterine adhesions is lysis under direct hysteroscopic visualization
Estrogen therapy — The rationale for postoperative estrogen therapy is that the hormone will promote regrowth of the endometrium over the denuded surface.
Intra-uterine catheter — Catheters (eg, size 8 pediatric bladder catheter with a 5 cc balloon or Malecot catheter) can be inserted into the uterine cavity immediately after adhesion lysis.
Intrauterine gel — Both hyaluronic acid gel and polyethylene oxide-sodium carboxymethylcellulose gel have appeared to reduce the reformation of IUAs,
Prevention: Surgical techniques - cold loop adhesion rather than cautery.
Semisolid (gel) adhesion barriers
Identify the possible complications of Asherman’s syndrome and its management
Infertility
Menstrual abnormalities
Recurrence 1/3-2/3
Obstetric outcomes