1
Q
what is the definition of hydrops
A
- abnormal accumulation of serous fluid in at least 2 body cavities or tissue
2
Q
is serous fluid amniotic fluid
A
- no
3
Q
what are 4 examples of collections of fluid in fetus
A
- pleural effusion
- abdominal ascites
- pericardial effusion
- edema
4
Q
what are the two classifications of hydrops and what are they based on
A
- based on etiology
- immune vs non immune
5
Q
is hydrops common or rare
A
- common
- each specific etiology that causes it is rare
6
Q
when is hydrops usually seen in fetus
A
- terminal stage for many conditions
- signifies fetal decomposition
7
Q
how long does it take for demise to occur when decomposition starts in fetus
A
- progression of hydrops is rapid and demise can occur within 24-48 hours
8
Q
why is investigation important with hydrops
A
- important for management and future counselling
9
Q
what are 2 important aspects of the investigation
A
- ultrasound
- fetal blood sampling
10
Q
7 sonographic features of hydrops
A
- ascites
- pleural effusion
- pericardial effusion
- subcutaneous edema
- placental edema
- arterial or venous doppler abnormalities
- low BPP scores
11
Q
what is ascites
A
- fluid collecting in the fetal abdomen
12
Q
where might we see the fluid first with ascites and why
A
- pelvis
- gravity = most dependent
13
Q
what might ascites cause in males
A
- fluid tracks down into scrotum causing hydrocele
14
Q
what is pseudoascites
A
< 2mm hypo echoic ring around muscular layer of the abdominal wall
- change probe angle to assess if its really free fluid
15
Q
what is a pleural effusion
A
- fluid in plural space around the lungs
16
Q
what does the pleural effusion cause in regards to pressure
A
- increase in pleural effusion»_space; increase in pressure on the mediastinum, thoracic vasculature and heart
17
Q
what three things pleural effusion cause
A
- upper body edema
- poly
- pulmonary hypoplasia
18
Q
where can subcutaneous edema be located
A
- general, local
- limited to the upper or lower body depending on eitology
19
Q
what is anasarca
A
- general edema
20
Q
where is edema first seen
A
- fetal scalp and face
- then abdomen and limbs
21
Q
what is placental edema a sign of
A
- late sign of hydrops
22
Q
what does placental edema look like
A
- ground glass appearance and > 4cm thick
23
Q
what will the placenta look like if the hydrops is of fetal etiology
A
- whole placenta should be thick
24
Q
what will placenta look like if hydrops is due to placenta vascular malformation
A
- only that part of the placenta looks hydropic
25
what is the pattern of immune hydrops
- 1st ascites
- 2nd edema
- 3rd pleural and pericardial effusions
26
what is the pattern of hydrops with thoracic abnormalities
- chylothorax and heart abnormalities
| - pleural and pericardial effusions usually occur first
27
what is chyle
- milky fluid drom food is taken up during digestion
| - consists of lymph fluid
28
what are two other names for immune hydrops
- alloimmune hydrops
| - erythroblastosis fetalis
29
what causes immune hydrops
- when rhesus sensitized mother has antibodies to fetal red blood cells
- mom is Rh -
- hemolysis occurs when maternal immunoglobulin antibodies cross the placenta and attack antigen positive fetal red cells
30
what is hemolysis
- separation of the hemoglobin from the red cells and is then found in plasma
31
what is Rhesus factor
- majority have red blood cell protein called Rhesus factor (Rh+)
- minority lack the protein (Rh-)
- immune hydrops is due to anti D antibodies
32
what does the destruction of RBCs cause in the fetal
- anemia
- hepatosplenomegaly
- erythroblastosis fetalis
33
what is erythroblastosis fetalis
- outpouring of many immature red blood cells
| - these immatures RBC do not support or carry oxygen well
34
what does erythroblastosis fetalis cause
1 = tissue hypoxia
+ immature RBC can carry oxygen to tissues
2 = hydrops
+ fluid leaks out of cells causing hydrops
3 = cardiac
+ fluid does not get back to heart so heart works harder to compensate and goes into failure
4 = demise
+ leads to demise
35
what is the assessment of immune hydrops
- assess maternal antibody titers by a blood test
- detailed fetal sonographic assessment for signs of hydrops
- MCA doppler - WITH SEVERE ANEMIA VELOCITY INCREASES due to decreased viscosity of blood
- OOD amnio is performed to assess bilirubin level in amniotic fluid
36
treatment of immune hydrops
- fetal blood sampling and blood transfusion in utero (PUBS = percutaneous umbilical blood sampling)
- with transfusion many hydropic fetuses survive and many non hydropic fetuses will survive
37
when is non immune hydrops commonly seen
- 1st and 2nd trimester spontaneously aborted fetuses
38
what is the etiology of non immune hydrops
```
- varies geographically
+ North America and europe
+ cardiovascular, infection and chromosomal
+ Southeast Asia
+ homozygous thalassemia
```
39
what is homozygous thalassaemia
- if others parents pass the gene on to the fetus then the fetus has profound anemia resulting in death in utero
40
what is heterozygous thalassemia
- if only on parent passes the gene to the fetus then the fetus would have relatively mild red cell anomalies
41
what are three maternal causes of non immune hydrops
- severe diabetes mellitus
- sever anemia
- TORCH
42
what are 3 placental causes of non immune hydrops
- chorioangioma (benign mass in placenta blocking flow to baby)
- venous thrombosis
- cord torsion
43
what are 8 fetal causes of NIH
- cardiac (malform, arrhtym, high output failure)
- thorax and neck (any anomaly of the chest that causes compression)
- urinary (prune belly)
- chromosomal
- infection (CMV, parvovirus, toxoplasmosis)
- skeletal dysplasia
- fetal hypokinesis
- idiopathic
44
what is the investigation of non immune hydrops
- history (provide clues to etiology)
- detailed scan for markers and anomalies
- fetal echo
- karyotypes
+ FISH = fluorescent in situ hybridization (technique to count chromosomes)
- fetal blood sampling
- fetal blood transfusion
- cavity aspiration
- pathology (placneta)
- autopsy (if demise occured)
45
steps of following NIH
- asses change in degree of hydrops
- cardiothoracic ratios for cardiomegaly
- doppler for cardiac failure
- doppler to asses arterial pulsations in detuses with tricuspid regurge
- perform color over TV for regurge
46
what does the therapy for NIH depend on
- etiology
47
treatment for NIH arrhthmyias
- digoxin can be administer to mom
48
treatment for NIH aneuploidy
- no therapy
49
treatment for NIH anemia
- transfusion
50
treatment for NIH chylothorax and CCAM 1
- pleural drainage in utero
| - prevent pulmonary hypoplasia
51
treatment for NIH infections
- maternal or fetal antibiotic
| - some fetus have long term adverse effects if not caught soon enough
52
prognosis of NIH
- mortality still high
- counselling is challenge because no specifics
- termination offered
53
what are two antenatal therapies
- thoracentisis = removing fluid form fetal chest to help breathing
- paracentesis = removing fluid from fetal abdomen prevent dystocia
54
three therapies with TTTS
- serial therapeutic amniocentesis for recipient twin
- fetoscopic laser ablation of communicating vessels in placenta
- cord occlusion with TRAP syndrome to prevent cardiac failure od donor twin
Ob/Gyne 2
flashcards
Decks in class (19)
# Cards
-
Module 1 : Uterine Pathology55
-
Module 2 : Ovarian Pathology51
-
Module 3 : Extra Pelvic Pathology46
-
Module 4 : Fertility Management59
-
Module 4.1 : Contraception24
-
Module 5 : Fetal Neuro Pathology85
-
Module 5.1 : Fetal Spinal Pathology46
-
Module 6 : Chromosomal Abnormalities31
-
Module 7 : Fetal Chest Pathology47
-
Module 8 : Fetal GI Pathology52
-
Module 9 : Fetal GU Pathology95
-
Module 11 : Fetal Face and Neck Pathology90
-
Module 12 : Fetal Cardiac Abnormalities73
-
Module 13 : Multiple Gestation Complications58
-
Module 14 : Amniotic Fluid25
-
Module 15 : Hydrops54
-
Module 16 : Placenta Pathology49
-
Module 17 : Gestational Trophoblastic Neoplasia42
-
Module 18 : Nuchal Lucency20
