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
Q

what is the pattern of immune hydrops

A
  • 1st ascites
  • 2nd edema
  • 3rd pleural and pericardial effusions
26
Q

what is the pattern of hydrops with thoracic abnormalities

A
  • chylothorax and heart abnormalities

- pleural and pericardial effusions usually occur first

27
Q

what is chyle

A
  • milky fluid drom food is taken up during digestion

- consists of lymph fluid

28
Q

what are two other names for immune hydrops

A
  • alloimmune hydrops

- erythroblastosis fetalis

29
Q

what causes immune hydrops

A
  • 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
Q

what is hemolysis

A
  • separation of the hemoglobin from the red cells and is then found in plasma
31
Q

what is Rhesus factor

A
  • majority have red blood cell protein called Rhesus factor (Rh+)
  • minority lack the protein (Rh-)
  • immune hydrops is due to anti D antibodies
32
Q

what does the destruction of RBCs cause in the fetal

A
  • anemia
  • hepatosplenomegaly
  • erythroblastosis fetalis
33
Q

what is erythroblastosis fetalis

A
  • outpouring of many immature red blood cells

- these immatures RBC do not support or carry oxygen well

34
Q

what does erythroblastosis fetalis cause

A

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
Q

what is the assessment of immune hydrops

A
  • 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
Q

treatment of immune hydrops

A
  • 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
Q

when is non immune hydrops commonly seen

A
  • 1st and 2nd trimester spontaneously aborted fetuses
38
Q

what is the etiology of non immune hydrops

A
- varies geographically 
  \+ North America and europe
      \+ cardiovascular, infection and chromosomal 
   \+ Southeast Asia
       \+ homozygous thalassemia
39
Q

what is homozygous thalassaemia

A
  • if others parents pass the gene on to the fetus then the fetus has profound anemia resulting in death in utero
40
Q

what is heterozygous thalassemia

A
  • if only on parent passes the gene to the fetus then the fetus would have relatively mild red cell anomalies
41
Q

what are three maternal causes of non immune hydrops

A
  • severe diabetes mellitus
  • sever anemia
  • TORCH
42
Q

what are 3 placental causes of non immune hydrops

A
  • chorioangioma (benign mass in placenta blocking flow to baby)
  • venous thrombosis
  • cord torsion
43
Q

what are 8 fetal causes of NIH

A
  • 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
Q

what is the investigation of non immune hydrops

A
  • 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
Q

steps of following NIH

A
  • 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
Q

what does the therapy for NIH depend on

A
  • etiology
47
Q

treatment for NIH arrhthmyias

A
  • digoxin can be administer to mom
48
Q

treatment for NIH aneuploidy

A
  • no therapy
49
Q

treatment for NIH anemia

A
  • transfusion
50
Q

treatment for NIH chylothorax and CCAM 1

A
  • pleural drainage in utero

- prevent pulmonary hypoplasia

51
Q

treatment for NIH infections

A
  • maternal or fetal antibiotic

- some fetus have long term adverse effects if not caught soon enough

52
Q

prognosis of NIH

A
  • mortality still high
  • counselling is challenge because no specifics
  • termination offered
53
Q

what are two antenatal therapies

A
  • thoracentisis = removing fluid form fetal chest to help breathing
  • paracentesis = removing fluid from fetal abdomen prevent dystocia
54
Q

three therapies with TTTS

A
  • 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