Module 15 : Hydrops Flashcards

1
Q

what is the definition of hydrops

A
  • abnormal accumulation of serous fluid in at least 2 body cavities or tissue
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2
Q

is serous fluid amniotic fluid

A
  • no
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3
Q

what are 4 examples of collections of fluid in fetus

A
  • pleural effusion
  • abdominal ascites
  • pericardial effusion
  • edema
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4
Q

what are the two classifications of hydrops and what are they based on

A
  • based on etiology

- immune vs non immune

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5
Q

is hydrops common or rare

A
  • common

- each specific etiology that causes it is rare

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6
Q

when is hydrops usually seen in fetus

A
  • terminal stage for many conditions

- signifies fetal decomposition

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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
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8
Q

why is investigation important with hydrops

A
  • important for management and future counselling
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9
Q

what are 2 important aspects of the investigation

A
  • ultrasound

- fetal blood sampling

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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
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11
Q

what is ascites

A
  • fluid collecting in the fetal abdomen
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12
Q

where might we see the fluid first with ascites and why

A
  • pelvis

- gravity = most dependent

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13
Q

what might ascites cause in males

A
  • fluid tracks down into scrotum causing hydrocele
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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

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15
Q

what is a pleural effusion

A
  • fluid in plural space around the lungs
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16
Q

what does the pleural effusion cause in regards to pressure

A
  • increase in pleural effusion&raquo_space; increase in pressure on the mediastinum, thoracic vasculature and heart
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17
Q

what three things pleural effusion cause

A
  • upper body edema
  • poly
  • pulmonary hypoplasia
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18
Q

where can subcutaneous edema be located

A
  • general, local

- limited to the upper or lower body depending on eitology

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19
Q

what is anasarca

A
  • general edema
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20
Q

where is edema first seen

A
  • fetal scalp and face

- then abdomen and limbs

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21
Q

what is placental edema a sign of

A
  • late sign of hydrops
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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