MRI of Hepatobiliary and Pancreatic Disorders in Pregnancy

Localizer T2 SSFSE

T2 2D SSFSE

T2 2D

FS FSE

T1 2D

SPGR Dixon

DWI b50, 600

T1 3D SPGR FS

Plane of acquisition

Axial, coronal, sagittal

Axial

Coronal

Axial

Coronal

Axial

Matrix

256 × 128

256 × 160

256 × 192

320 × 160

256 × 160

128 × 128

256 × 160

TR/TE (ms)

828/63

1000/60

2200/87

180/4.36 (in), 2.06 (out)

4100/64

3.63/1.73

Flip angle (°)

90 to >150–180

ST/SG (mm)

5.0/10.0

4.0/5.0

7.0/9.0

3.0/7.5

8.0/10.0

2.0/1.6

NEX

0.6

1 (b50)

3 (b600)

0.7

RBW

651

488

122.1

244

1953

300

Phase direction

A to P, R to L, A to P

A to P

R to L

A to P

Echo train length

115

160

128 (b50) 384 (b600)

112

FOV (mm)

650

350–400

Respiration

Fat saturation

–

Concatenation^a

2–3

1–2

Parallel imaging (acceleration factor)

–

1.7/2.1

Abbreviations: A to P anterior-to-posterior, BH breath-hold, Fat sat spectral selective fat saturation, DWI diffusion-weighted imaging, FOV field of view, NEX number of excitations, RBW receiver bandwidth in Hertz/pixel, R to L right to left, SSFSE half single-shot fast spin-echo sequence, ST/SG slice thickness and slice gap in millimeters, TE echo time, TR repetition time, 3D 3-dimensional, 3D SPGR DIXON 3-dimensional, nonfat-saturated, spoiled gradient-echo sequence for chemical shift imaging, 3D SPGR FS fat-saturated, 3-dimensional, spoiled gradient-echo T1-weighted sequence for postcontrast, 2D 2-dimensional

^aConcatenation is the number of interleaved acquisitions or number of breath-holds

Table 21.2

Parameters for pancreas and biliary imaging on 1.5 T MR imaging scanner

	Localizer T2 SSFSE	T2 2D SSFSE	T2 2D SSFSE	T1 2D SPGR dixon	DWI b50, 600	T1 3D SPGR FS	MRCP 2D thick slab	MRCP 3D thin slab
Plane of acquisition	Axial, coronal, sagittal	Axial	Coronal	Axial	Coronal	Axial	Coronal	Coronal
Matrix	256 × 128	256 × 160	256 × 192	256 × 160	128 × 128	256 × 160	384 × 256	256 × 256
TR/TE (ms)	1500/60	1000/62	1000/60	180/4.36 (in), 2.06 (out)	4100/64	3.65/1.75	2284/600	3750/400
Flip angle (°)	90 to >150–180	90 to >150–180	90 to >150–180	80	90	15	90	90
ST/SG (mm)	7.0/12.0	4.0/5.0	4.0/5.0	6.0/7.5	8.0/10.0	3.2/1.6	50/51	1.4/0.7
NEX	0.6	0.6	0.6	1	1.3	0.7	0.6	1
RBW	651S	390	390	488	1953		244	300
Phase direction	A to P, R to L, A to P	A to P	A to P	A to P	R to L	A to P	A to P	A to P
Echo train length	76	96	115	160	128 (b50) 384 (b600)	112	154	256
FOV (mm)	450–500	350–400	350–400	350–400	350–400	350–400	350–400	350–400
Respiration	BH	BH	BH	BH	BH	BH	BH	BH
Fat saturation	–	–	–	–	–	+	+	+
Concatenation^a	1	2–3	2	2	1–2	1	5	1
Parallel imaging (acceleration factor)	–	–	–	–	–	1.7/2.1	–	3

Abbreviations: A to P anterior-to-posterior, BH breath-hold, Fat sat spectral selective fat saturation, DWI diffusion-weighted imaging, FOV field of view, MRCP magnetic resonance cholangiopancreatography, NEX number of excitations, RBW receiver bandwidth in Hertz/pixel, R to L right to left, SSFSE half single-shot fast spin-echo sequence, ST/SG slice thickness and slice gap in millimeters, TE echo time, TR repetition time, 3D 3-dimensional, 3D SPGR DIXON 3-dimensional, nonfat-saturated, spoiled gradient-echo sequence for chemical shift imaging, 3D SPGR FS fat-saturated, 3-dimensional, spoiled gradient-echo T1-weighted sequence for postcontrast, 2D 2-dimensional

^aConcatenation is the number of interleaved acquisitions or number of breath-holds

21.3 Liver

Physiological changes that accompany pregnancy should not be confused with liver dysfunction (Table 21.3). Increase in serum alkaline phosphatase levels up to three to four times above normal, due to placental production, and mild increase in fibrinogen and ceruloplasmin levels are typical for normal pregnancy, as well as changes in serum alpha-fetoprotein levels. Mild decrease in factors participating in fibrinolysis – antithrombin III and protein S – is also typical, although there is no change in prothrombin time.

Table 21.3

Physiologic changes of pregnancy

Increase

Serum alkaline phosphatase (from placental production)

Clotting factors: factor I (fibrinogen), factors VII, VIII, X, and XII, Von Willebrand factor, protein S-binding protein, plasminogen activator inhibitor (PAI)-1 and PAI-2 (PAI-2 is produced by the placenta)

Ceruloplasmin

Transferrin

Alpha-fetoprotein

Blood volume, heart rate, cardiac output

Decrease

Fibrinolytic factors: antithrombin III and protein S

Uric acid

Gallbladder contractility

Albumin and total serum protein (due to dilution effect from increased blood volume)

Hemoglobin (due to dilution effect from increased blood volume)

Systemic vascular resistance

Blood pressure

No change

Liver transaminases: aspartate aminotransferase (AST), alanine aminotransferase (ALT)

γ-Glutamyl transferase (GGT)

Bilirubin

Prothrombin time (PT)

Platelet count (may decline slightly due to dilution effect from increased blood volume)

Serum amylase

Three to 5 % of pregnancies are complicated by truly abnormal liver function tests, caused by a variety of hepatobiliary diseases, including infectious, autoimmune, neoplastic, and inherited causes (Table 21.4).

Table 21.4

Causes of hepatobiliary disease in pregnancy

Unique to pregnancy

Hyperemesis gravidarum

Intrahepatic cholestasis of pregnancy

Acute fatty liver of pregnancy

Preeclampsia

HELLP syndrome (hemolysis, elevated liver enzyme levels, low platelet count)

Coincidental with pregnancy

Gallstone-associated disease:

Cholelithiasis

Choledocholithiasis

Cholecystitis

Ascending cholangitis

Liver abscess

Acute pancreatitis

Acute viral hepatitis

Budd-Chiari syndrome

Portal vein thrombosis

Focal lesion (hepatic adenoma, HCC)

Preexisting disease

Chronic viral hepatitis B and C

Cirrhosis and portal hypertension

Autoimmune hepatitis

Primary biliary cirrhosis

Primary sclerosing cholangitis

Wilson’s disease

Neoplasia (hemangioma, FNH, hepatic adenoma)

focal nodular hyperplasia (FNH), hepatocellular carcinoma (HCC)

Although uncommon, any liver disease can occur coincidentally in the pregnant patient, as well as pregnancy may occur in a patient with preexisting underlying chronic liver disease. However, most liver dysfunction in pregnancy is pregnancy induced and due to one of the five liver diseases unique to the pregnant state: hyperemesis gravidarum, intrahepatic cholestasis of pregnancy, acute fatty liver of pregnancy, preeclampsia/eclampsia, and the Hemolysis, Elevated Liver enzymes and Low Platelets (HELLP) syndrome. These conditions are complications of the pregnancy itself, and all have a characteristic timing in relation to the length of the pregnancy: hyperemesis gravidarum in the first trimester, intrahepatic cholestasis of pregnancy in the second half of pregnancy, and the remaining three in the third trimester (Table 21.5).

Table 21.5

Hepatobiliary disorders unique to pregnancy

Disorder	Gestational status	Prevalence	Symptoms	Outcome	Definite treatment
Hyperemesis gravidarum	1st trimester Primiparous	0.3 %	Intractable nausea and vomiting	Benign for mother and fetus	Supportive, total parenteral nutrition
Intrahepatic cholestasis of pregnancy	2nd trimester	0.7 %	Pruritus	Benign for mother and fetus; increased gallstone disease	Ursodiol; delivery
Acute fatty liver of pregnancy	3rd trimester Primiparous 50 % have eclampsia	1:10,000–15,000	Nausea, vomiting, right upper quadrant or epigastric pain, malaise; quick progression to fulminant hepatic failure, DIC	Maternal mortality 20 %; fetal mortality up to 45 %	Delivery Test for LCHAD
Preeclampsia	Late 2nd and 3rd trimester Multiparous Multifetal	5 %	High blood pressure, proteinuria, edema, seizures, renal failure, pulmonary edema	Maternal mortality 1 %; prematurity; fetal death 30 %	Delivery
HELLP syndrome	Late 2nd and 3rd trimester, postpartum 12 % have eclampsia Multiparous Multifetal	0.5 %	Abdominal pain, seizures, renal failure, pulmonary edema, liver hematoma, and rupture	60 % maternal mortality when hepatic rupture; fetal death 30 %	Delivery

DIC disseminated intravascular coagulation, HELLP syndrome hemolysis, elevated liver enzyme levels, low platelet count, LCHAD long-chain 3-hydroxylacyl-CoA dehydrogenase

21.3.1 Hepatic Conditions Unique to Pregnancy

In general, MRI in patients with hyperemesis gravidarum and intrahepatic cholestasis of pregnancy does not have a role other than to exclude possible differential diagnoses that may cause hepatic dysfunction.

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