Keywords
Fisherman's Waders - prostate adenocarcinoma - IVC syndrome - soft tissue uptake on
bone scintigraphy - osseous metastatic disease
This interesting image illustrates an unusual case of inferior vena cava (IVC) syndrome
from prostate cancer retroperitoneal adenopathy initially identified on skeletal scintigraphy.
IVC syndrome is an infrequent occurrence resulting from extrinsic compression or intraluminal
occlusion of the vessel. Whole-body planar skeletal scintigraphy showed a stable left
sacroiliac metastasis and increased soft-tissue uptake throughout the lower hemibody
up to the lower chest level. Computed tomography (CT) demonstrated extrinsic compression
of the IVC from metastatic retroperitoneal adenopathy. This represents a rare presentation
of IVC syndrome in prostate cancer with characteristic appearance on skeletal scintigraphy
of Fisherman's Wader's sign that should prompt confirmatory anatomic imaging.
A 66-year-old male with metastatic prostate cancer in the retroperitoneal nodes and
left iliac bone on investigational immunotherapy presented to the hospital with progressively
worsening disease despite optimal therapy. Whole-body planar bone scintigraphy with
832.5 MBq of methylene diphosphonate [Figure 1a] demonstrated a stable left sacroiliac region metastasis (white arrow). In addition,
an unusual differential diffuse soft-tissue uptake, greater in the lower hemibody
than upper hemibody (black arrow highlighting the line of demarcation in the lower
chest), was noted. CT scan performed [Figure 1b] confirmed that this unusual scintigraphic appearance was secondary to IVC syndrome
caused by conglomerate metastatic retroperitoneal nodal disease (black arrow). Diffuse
stranding throughout the subcutaneous fat on CT (white arrow) correlated well with
the distribution of abnormal uptake on skeletal scintigraphy. Bone scintigraphy [Figure 2a] and contrast-enhanced CT imaging [Figure 2b] demonstrated that the lower hemibody uptake and subcutaneous fat stranding were
not present 5 months prior in the setting of an adequately patent IVC (black circle)
with less extensive retroperitoneal adenopathy (white arrow). Subtraction venography
[Figure 3a] demonstrated an abrupt filling defect in the mid IVC with extensive collateralization,
while imaging following stent placement [Figure 3b] demonstrates contrast flowing through a patent IVC into the right atrium. The patient
responded favorably with near-complete resolution of clinical symptoms after stenting
of the obstructed IVC.
Figure 1 (a) Inferior vena cava syndrome on anterior and posterior whole-body skeletal scintigraphy.
Black arrows highlight the line of demarcation with increased activity throughout
the lower hemibody and white arrow demonstrates a known left sacroiliac metastasis.
(b) Axial and coronal computed tomography images demonstrating inferior vena cava
syndrome. Black arrows demonstrate retroperitoneal adenopathy compressing the inferior
vena cava, while white arrows demonstrate subcutaneous fat stranding
Figure 2 (a) Five months prior. Anterior and posterior whole-body skeletal scintigraphy without
evidence of inferior vena cava syndrome. Left sacroiliac metastasis was visible at
this time point (black arrow). (b) Five months prior. Axial and coronal computed tomography
images without evidence of inferior vena cava syndrome. White arrows demonstrate less
extensive retroperitoneal adenopathy, with black oval demonstrating patent inferior
vena cava as evidenced by contrast opacification
Figure 3 (a) Subtraction venography with black arrow demonstrating abrupt filling defect in
the mid inferior vena cava and white arrow highlighting extensive collateralization.
(b) Postprocedure subtraction venography with black arrow demonstrating stent in the
inferior vena cava which is now patent, with white arrow demonstrating contrast flowing
into the right atrium
IVC syndrome is an infrequent occurrence resulting from extrinsic compression or intraluminal
occlusion of the vessel. Extrinsic compression may result from retroperitoneal adenopathy
or fibrosis, aneurysms, and pregnancy, whereas intraluminal occlusion may result from
malignant intracaval thrombi from malignancies (e.g., gastric or renal cancer).[1],[2],[3] Clinical signs include hepatic congestion, ascites, lower body anasarca, pooling
in the lower extremities from elevated pressure in the IVC, and tachycardia; this
results from reduced preload due to decreased venous return. Optimal medical treatment
is not well defined and depends on mitigating the underlying cause (e.g. radiation
and chemotherapy for extrinsic masses or anticoagulation for thrombi),[4] while invasive surgical alternatives include endovascular stenting and bypass grafting.[5]
Only a few cases of IVC syndrome on skeletal scintigraphy have been demonstrated in
literature. Rodman et al. reported the first case of IVC syndrome on skeletal scintigraphy
secondary to tumor thrombus from renal cell carcinoma.[6] In a report of a 61-year-old male with nephrotic syndrome causing hypercoagulability
resulting in IVC thrombosis, Chu andHu coined the term “Fisherman's Waders” sign for
the finding of increased uptake of radiotracer in soft-tissue uptake below the level
of the lower thorax on bone scan.[7] Another study reported Fisherman's Waders' sign in a lymphoma patient complicated
by IVC obstruction seen on CT and bone scans and in nonthrombotic portal hypertension.[8] This represents a rare report of Wader's sign from IVC syndrome in metastatic prostate
cancer highlighting its characteristic imaging appearance that should prompt confirmatory
anatomic imaging.
