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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5762_Библиотеки_им_академика_М_И_Перельмана.pdf
230
a
H. Han et al.
b
c
Fig. 10.2 Common hepatic artery aneurysm. Computed tomography
angiography (CTA) clearly demonstrated an aneurysm at the common
hepatic artery (a). Digital subtraction angiography (DSA) conrmed an
aneurysm located at the common hepatic artery, with gastroduodenal
artery branches lying anterior to the aneurysm (b). After hepatic artery
aneurysm embolization, superior mesenteric artery angiography
10.5 Pathology
showed that the aneurysm and common hepatic artery had been completely embolized with no extravasation, and the left and right hepatic
arteries are supplied by gastroduodenal artery (c). (LHA left hepatic
artery, RHA right hepatic artery, HA hepatic artery, GDA gastroduodenal artery, SMA superior mesenteric artery)
• The causes of HAA include:
– Atherosclerosis, media degeneration, arterial brodys-
10.5.1 General Features
plasia, vasculitis;
– Iatrogenic causes from surgical, endoscopic, or radio-
• The incidence of visceral aneurysms in vascular diseases
is 1–2%. Hepatic artery aneurysms account for 12–20%
logically interventional procedures.
– Trauma, inammation, and infection.
of visceral aneurysms, second to splenic aneurysms.
• The vast majority of hepatic aneurysms are isolated,
accounting for 90% and extrahepatic aneurysms are common, with a male-to-female ratio of 2:1.
Atherosclerosis is the most common cause of extrahepatic
artery aneurysms, and blunt or penetrating trauma are common cause of intrahepatic artery aneurysms.
10 Hepatic Artery Aneurysm
231
10.5.2 Staging, Grading, andClassication
• Base on the origin of aneurysm, it can be categorized as
common, left and right hepatic artery aneurysm.
– Common hepatic artery aneurysms are the most com-
mon, accounting for 63%.
– Followed by the right hepatic artery aneurysm,
accounting for 28%.
– Left hepatic artery aneurysm is accounting for 5%.
– About 4% of patients with both left and right hepatic
arteries involved.
• Hepatic artery aneurysms are classied as extrahepatic
aneurysms or intrahepatic aneurysms according to intraor extrahepatic occurrence.
• Approximately 75–80% of hepatic artery aneurysms are
extrahepatic.
• Hepatic artery aneurysms can be distinguished as true
aneurysm, pseudoaneurysm, and dissecting aneurysm
according to the existence of intact three layers of arterial
wall.
10.6 Clinical Issues
10.6.1 Presentation
• About 75% of hepatic artery aneurysms are found incidentally and have no symptoms [5].
• The clinical manifestations of hepatic artery aneurysms
are usually nonspecic, and epigastric pain is the most
common symptom.
• The triad presentation of HAA rupture consists of abdominal pain, obstructive jaundice, and hemorrhage.
Hypovolemic shock may occur with massive hemorrhage.
10.6.2 Prognosis
• Hepatic artery aneurysms have a 20–30% risk of rupture
and rupture being associated with a 35% mortality.
• It is suggested that pregnancy, increasing in size and
diameter larger than 2cm are risks for rupture of hepatic
artery aneurysms.
• Non-atherosclerotic hepatic artery aneurysms carry a
higher risk of rupture than those with atherosclerosis.
10.6.3 Treatment
• Because of the high mortality rate associated with rupture
of hepatic artery aneurysm, it is suggested that therapeutic plans should be created timely once they are detected,
no matter there are symptoms or not [6].
• HAA can be treated by surgical or endovascular treatments [7].
• Surgical methods consist of ligation, excision, venous
grafting, and hepatectomy.
Endovascular approaches comprise aneurysm emboliza-
tion with coils and stent placement [8].
The choice of treatment for HAA depends on the size and
location of the aneurysm, as well as the presence of hepatic
collateral circulation and patient clinical status [9, 10].
References
1. Kim JH, Rha SE, Chun HJ, Kim YS, Oh SN, Lee YJ, Byun JY, etal.
Giant aneurysm of the common hepatic artery: US and CT imaging
ndings. Abdom Imaging. 2010;35:212–4.
2. Palubinskas S, Rasmussen SL. Hepatic artery aneurysm causing
gastrointestinal haemorrhage – Case report and literature review.
Int J Surg Case Rep. 2017;41:12–6.
3. Warshauer DM, Keefe B, Mauro MA. Intrahepatic hepatic artery
aneurysm: computed tomography and color-ow Doppler ultrasound ndings. Gastrointest Radiol. 1991;16:175–7.
4. Durkin N, Deganello A, Sellars ME, Sidhu PS, Davenport M,
Makin E.Post-traumatic liver and splenic pseudoaneurysms in children: diagnosis, management, and follow-up screening using contrast enhanced ultrasound (CEUS). J Pediatr Surg. 2016;51:289–92.
5. Nathan DP, Wang GJ, Woo EY, Fairman RM, Jackson BM.Open
and endovascular repair of hepatic artery aneurysm: two case
reports and review of the literature. Vascular. 2011;19:42–6.
6. Abbas MA, Fowl RJ, Stone WM, Panneton JM, Oldenburg WA,
Bower TC, Cherry KJ, etal. Hepatic artery aneurysm: factors that
predict complications. J Vasc Surg. 2003;38:41–5.
7. Bacalbasa N, Brezean I, Anghel C, Barbu I, Pautov M, Balescu I,
Brasoveanu V.Successful resection and vascular ligation of a large
hepatic artery aneurysm– A case report and literature review. In
Vivo. 2017;31:979–82.
8. Hashim A, Allaqaband S, Bajwa T.Leaking hepatic artery aneu-
rysm successfully treated with covered stent. Catheter Cardiovasc
Interv. 2009;74:500–5.
9. Schick C, Ritter RG, Balzer JO, Thalhammer A, Vogl TJ.Hepatic
artery aneurysm: treatment options. Eur Radiol. 2004;14:157–9.
10. Jones VS, Chennapragada MS, Lord DJ, Stormon M, Shun A.Post-
liver transplant mycotic aneurysm of the hepatic artery. J Pediatr
Surg. 2008;43:555–8.
Peliosis Hepatis
YiDong, FengMao, andWen-PingWang
11
11.1 Terminology
• Peliosis hepatis (PH) is a rare benign vasogenic lesion
characterized by the presence of cystic blood-lled cavities distributed randomly throughout the liver
parenchyma.
• PH was rst reported in the German literature in 1861 by
Wagner, and named by Schoenlank in 1916.
• “Peliosis” is a term derived from the Greek pelios, which
means “dusky” or “purple,” referring to the color of the
liver parenchyma with peliosis.
• The size of the lesion may vary from 1 mm to several
centimeters.
11.2 Imaging
11.2.1 Conventional Ultrasound Findings
• Conventional B mode ultrasound shows homogeneous
hypoechoic lesion in liver without cirrhosis, and heterogeneously hypoechoic lesions if complicated by hemorrhage. The lesion always lacks of volume effect
(Fig.11.1).
• The lesion might be single or multiple, always be detected
incidentally.
• Color ow imaging can show color ow signals both
inside the lesion and in the surrounding area of the lesion.
11.2.2 Contrast Enhanced Ultrasound Findings
• Only a few cases of peliosis hepatis have been described
using CEUS.
Y. Dong (*) · F. Mao · W.-P. Wang
Department of Ultrasound, Zhongshan Hospital, Fudan University,
Shanghai, China
e-mail: dong.yi@zs-hospital.sh.cn; mao.feng@zs-hospital.sh.cn
• Consistent with radiological performance, a typical target
sign enhancement, e.g., an early arterial-phase contrast
accumulation in the center of the lesion with a centrifugal
lling and a homogeneous enhancement in late phase was
detected by CEUS (Fig.11.2).
• In other cases, a peripheral ring enhancement could be
observed in arterial phase with centripetal lling and
homogeneous hyperenhancement in late phase (Figs.11.3
and 11.4).
11.2.3 CT Findings
• CT ndings vary with the size of masses, presence or
absence of thrombus within the cavities, and presence of
hemorrhage.
– Peliosis lesions could usually be observed as multiple
areas of low attenuation on unenhanced CT.
– In particular, peliosis lesions may appear spontane-
ously hyperattenuating in certain patients (probably
related to intralesional hemorrhage).
– Additional, when peliosis cavities are smaller than
1cm in diameter, the lesions could not be detected and
CT ndings may be normal.
– Calcications within peliosis lesions have also been
described.
• On contrast-enhanced CT, typical peliosis lesions show
early arterial-phase globular enhancement and multiple
small, central accumulations of contrast material, with a
centrifugal progression of enhancement in portal venous
phase.
– The enhancement pattern varies, depending on the
freshness of the blood that lls the peliosis cavities.
Fresh blood is associated with marked hyperenhancement, whereas retention of old blood is associated with
little or nonenhancement.
– In addition, some lesions were described with a cen-
tripetal enhancement mimicking hepatic hemangio-
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2021
W.-P. Wang et al. (eds.), Contrast-Enhanced Ultrasound Imaging of Hepatic Neoplasms,
https://doi.org/10.1007/978-981-16-1761-4_11
233
234
a
a
b
Fig. 11.1 Different kinds of echogenicity of peliosis hepatis lesions, including hypoechoic (a) and isoechoic (b)
b
Y. Dong et al.
c
d
Fig. 11.2 A case of peliosis hepatis with target sign enhancement on
contrast enhanced ultrasound. B mode ultrasound revealed a slightly
hyperechoic focal lesion (arrow) in right lobe of liver (a). The lesion
showed centrifugal lling hyperenhancement during arterial phase (b–
e). In portal venous and late phases, the lesion showed isoenhancement
(f, g)
11 Peliosis Hepatis
g
235
fe
Fig. 11.2 (continued)
mas or with atypical enhancement patterns, which
were not suggestible for any typical hepatic tumor
type.
– In delayed phase, late diffuse homogeneous hyperat-
tenuation can be observed in the phlebectatic type of
peliosis hepatis (because of the lack of hemorrhagic
parenchymal necrosis).
– In some instances, small peliosis lesions (<2cm) may
also show hyperattenuation in both arterial and portal
venous phases.
– If there is thrombosis, a non-enhancing nodule will be
seen within the lesion.
11.2.4 MRI Findings
• On MR examination, the signal intensities of the lesions
largely depend on the age and status of the blood
component.
– PH lesions may appear hypointense on T1WI for sub-
acute hemorrhage, and hyperintense on T2WI, which
is suggestive of the presence of hemorrhagic necrosis.
– The signal intensity features on DWI and the ADC val-
ues on the ADC maps of focal peliosis hepatis are also
variable and nonspecic, probably due to its content,
including different degrees of thrombus and
hemorrhage.
– Although peliosis hepatis is benign, ADC values are
lower than normal hepatic parenchyma, probably due
to its content including thrombus and hemorrhage.
– Both uid–uid levels and low ADC values are related
to old and new blood products in the lesions on MR
images.
• On T1WI after contrast material injection, peliosis lesions
usually show typical centrifugal enhancement similar to
CT appearance.
– In other cases, the lesions could be observed progres-
sive centripetal enhancement with restricted diffusion
236
a
fe
Y. Dong et al.
b
c
d
g
Fig. 11.3 A case of peliosis hepatis with centripetal lling enhancement on CEUS.B mode ultrasound revealed a hypoechoic focal lesion
near the surface of right hepatic lobe (a). Color ow signals could be
detected in the peripheral area of the lesion (b). Arterial Doppler spec-
trum with resistance index (RI) as 0.61 was measured (c). The lesion
showed a peripheral rim-like enhancement and centripetal lling immediately during arterial phase (d–f). The lesion showed homogeneous
hyperenhancement in the late phase (g)
ab
cd
fe
11 Peliosis Hepatis
237
g
Fig. 11.4 A case of peliosis hepatis with iso-enhancement in arterial
phase of contrast enhanced ultrasound (CEUS). B mode ultrasound
image revealed a heterogeneous hypoechoic lesion in right lobe of liver
(a). Color ow signals could be detected inside the lesion (b). On CEUS,
the lesion showed complete isoenhancement during arterial phase (c–e).
It was detected slightly wash-out in portal venous and late phases (f, g)
238
Y. Dong et al.
that was unusual and can lead to puzzling in differentiating the lesion from hemangioma or malignancy.
– An enhancing rim may be revealed in cystic cavities
that represent a hematoma.
– Both hemorrhagic parenchymal necrosis and throm-
bosed cavities could be observed as non-enhanced
areas.
11.2.5 Other Imaging Findings
• On angiography, peliosis lesions could be detected as
multiple vascular nodules (i.e., accumulations of contrast
material) in late arterial phase. Typical enhancement of
peliosis lesions is more distinct in parenchymal phase and
persists during portal venous phase.
• If PH was just a blood-lled cyst without any inammatory focus or malignant transformation, 18F-FDG PET/
CT would reveal PH lesions isometabolic with surrounding hepatic parenchyma. Otherwise, PH might show
increased 18F-FDG uptake with cholestasis, hepatic failure, hemorrhagic necrosis or clumps of microorganisms
(Bartonella henselae or B. quintana) that may present
with lymphadenopathy.
11.3 Dierential Diagnosis
11.3.1 Hepatic Adenoma
• Similar to peliosis, hepatic adenoma might also be associated with the long-term use of estrogens.
• In the case of diffuse peliosis hepatis, the differential
diagnosis is relatively easy.
• In addition, the presence of fat in some adenomas could
be used as a sign to make a differential diagnosis.
• However, in certain instances, it is difcult to differentiate
focal peliosis from adenomas. In these patients, biopsy is
often required to reach a denitive diagnosis.
11.3.2 Hemangioma
• Opposite of peliosis hepatis, the typical enhancement pattern of hemangiomas is peripheral ring, or globular
enhancement with centripetal progression. Therefore, differential diagnosis can be achieved in most patients.
• In addition, hemangiomas may be rather large lesions
with a mass effect on the hepatic vessels, while there is
usually no mass effect on hepatic vessels in peliosis
lesions.
11.2.6 Best Imaging Protocol Advices
• The variable imaging ndings of peliosis hepatis depend
on the pathologic patterns of disease, various degrees of
the blood component of the lesions, and concomitant
hepatic steatosis.
• In review of some literatures, whether in dynamic MRI/CT
or CEUS, the enhancement patterns of PH lesion in arterial
phase could be divided into two categories: quick hyperenhancement type whether presented with globular enhancement or central enhancement, homogeneously or
heterogeneously; and mild iso/hypo-enhancement type.
• Meanwhile, both types showed a tendency of homogeneous
enhancement in the late phase in dynamic MRI/CT while
gradually becoming hypoechoic in delayed phase in CEUS.
• Fresh and actively circulating blood within the dilated
sinusoid could result in hyperenhancement in arterial
phase of dynamic CT or MRI, whereas old and stagnated
blood within the peliosis hepatis could cause persistently
low or slow centripetal enhancement in portal or delayed
phase.
• Nevertheless, the diagnosis of atypical lesions often
remains problematic, so percutaneous liver biopsy is
more reliable to establish a denite diagnosis, but the
bleeding risk should be considered.
11.3.3 Focal Nodular Hyperplasia
• Typically homogeneously hyperattenuating masses on the
arterial phase, focal nodular hyperplasia is isoattenuation
on the portal venous and delayed phases.
• Often with a central scar with low attenuation on the arterial and portal venous phases, these lesions has enhancement on the delayed phase images.
• On color Doppler ultrasound, FNH was characterized by
the presence of abundant blood ow signals exhibiting
dendritic and spoke-wheel patterns.
• The most common arterial enhancement pattern on CEUS
was centrifugal or homogeneous enhancement in FNH.
• Atypical forms of focal nodular hyperplasia may not
show the characteristic enhancement patterns and the central scar just described, however, and thus pose some
problems in the differential diagnosis with peliosis
hepatis.
11.3.4 Hepatic Abscess
• It is important to differentially diagnose peliosis hepatis
and hepatic abscess, to avoid the percutaneous drainage
11 Peliosis Hepatis
239
of peliosis lesions, which can be dangerous and even
fatal.
• With regard to imaging criteria, a pyogenic abscess usually presents as a mass with a multiseptated or cluster-ofgrapes appearance with non-enhancing contents.
11.3.5 Hypervascular Metastases
• Although mild hyperattenuating in the delayed phase can
be shown in some hypervascular metastases with brotic
change, hypervascular metastases are usually totally
hypo- or isoattenuation in the delayed phase of contrast
enhancement because of the rapid wash-out of contrast
material.
• In general, peliosis lesions are rarely confused with
hypervascular metastases.
11.3.6 Hepatocellular Carcinoma
• With rapid wash-out in the portal venous phase, hepatocellular carcinoma is usually hyperattenuating in the arterial
phase, and iso- or hypoattenuation in the delayed phase.
• Although rare, it was reported the possibility that peliosis
hepatis may mimic the presence of hypervascular hepatocellular carcinoma in the literature. In these patients,
biopsy is often necessary to reach a denitive diagnosis.
11.3.7 Arteriovenous Malformations
• The appearance on conventional angiography differs from
that of arteriovenous malformations.
11.4 Pathology
11.4.1 General Features
• Microscopically, blood-lled cysts and hemorrhagic
necrosis were observed, and the adjacent peliosis spaces
had no endothelial lining, which are important pathological characteristics of PH.
• Pathologists classied two types of PH for different
causes of this rupture: phlebectatic type associated with
the intrinsic weakness of the bers of endothelial wall;
parenchymal type associated with focal hepatocyte
necrosis.
• The pathogenesis of peliosis hepatis remains unclear. The
possible mechanisms include:
– Congenital malformation, vascular varicosity with or
without prior angitis.
– Hepatocellular necrosis leading to cavity formation.
– Outow obstruction at sinusoidal level and central
vein of the hepatic lobule.
– Rupture of reticular ber, thus resulted in sinusoidal
dilation.
– Breakdown of sinusoidal borders and increased endo-
thelial cell permeability with numerous red blood cells
in the space of Disse.
• In immunohistochemistry, the lesion is shown to be negative for CD31, CD34, CD117, DOG-1, PCK, EMA,
HMB45, and F8in the sinusoidal dilation area, but it was
positive in the normal sinusoidal area.
11.5 Clinical Issues
11.5.1 Presentation
• The pathogenesis of PH remains unknown, and its pathogenic factors vary. They can be divided into three categories: drug-related, autoimmune, and infectious roughly.
– PH has been associated with the use of hormones and
immunosuppressive medications, especially α-alkyl
steroid hormones and thiopurin.
– Autoimmune factors are those associated with second-
ary immunodeciency result from certain potential
consumptive diseases, for example, tuberculosis,
hematological malignancies, acquired immunodeciency syndrome, immune deciency after transplantation, and hepatocellular carcinoma.
– Infectious factors include Bartonella infection, which
leads to cat-scratch disease. PH has also been observed
in dogs infected with Bartonella.
• One or several factors may cause hepatocyte necrosis
which then leads to the formation of cysts; in addition, the
dysfunctional endothelial cells in the hepatic sinus may
lead to angiectasis and hyperemia, the formation of mass
blood-lled cysts in the hepatic parenchyma.
• Microscopically, there exist two types of peliosis: “parenchymal peliosis” and “phlebectatic peliosis,” the main difference being whether the cavities are lined by
endothelium or brotic tissue.
– The characteristics of the parenchymal pattern are
irregular blood-lled spaces, lined by brous tissue
rather than the endothelium, which neither communicate with the central veins nor compress adjacent
parenchymal cells. Instead, there are associations
between many areas of focal necrosis in the surrounding hepatic tissue and them.
– The second morphological type is the phlebectatic pat-
tern, showing minimal hepatocyte necrosis. The regularly spherical, centrilobular blood-lled spaces are
lined by endothelial cells and/or brotic tissue and
240
Y. Dong et al.
freely communicate with hepatic sinusoids. As an integral part of the central vein, they cause compression of
the adjacent parenchymal cells, and contain mural
brin clots.
• Patients may be asymptomatic or present with hypodynamia, cholestasis, hepatomegaly, portal hypertension,
ascites, liver failure, hepatic encephalopathy, or fatal
intraperitoneal hemorrhage.
• Severe abdominal pain may be related to rupture and
intraperitoneal hemorrhage.
• In the case of bacillary peliosis, the typical ndings are
lymphadenopathy with B. henselae and neurologic symptoms with B. quintana.
• Peliosis hepatis can occur at any age and sex.
11.5.2 Prognosis
• After drug withdrawal, the natural course of peliosis
hepatis is regression, cessation of steroid therapy, or resolution of associated infectious disease.
• A pseudotumoral and hemorrhagic evolution has also
been described.
• Complications include portal hypertension, liver failure,
and liver rupture leading to hemoperitoneum or shock.
11.5.3 Treatment
• Patient with ruptured lesion or suspected bleeding should
be treated promptly with transcatheter super-selective
embolization or even surgical hemostasis if necessary.
• If conservative treatment proved to be inefcient, or
tumor growth was detected during monitoring, surgery is
an effective way to prevent associated complications.
• In severe cases, liver transplantation would be the last
resort for life saving.
• If the cause is unknown or conservative treatment is
ineffective, surgery should be performed. Surgery is the
most effective treatment for the prevention of massive
hemorrhage caused by lesion rupture, and hepatic
failure.
• In HIV-related peliosis hepatis caused by B. henselae,
clinical improvement has been documented with the use
of antibiotics (i.e., erythromycin) [1–3].
References
1. Loizides A, Glodny B, Zoller H, Zelger BG, Junker D, Henninger
B, Putzer D, etal. Contrast enhanced ultrasound of a rare case of
Peliosis hepatis. Med Ultrason. 2017;19:114–6.
2. Kim SH, Lee JM, Kim WH, Han JK, Lee JY, Choi BI.Focal peliosis
hepatis as a mimicker of hepatic tumors: radiological-pathological
correlation. J Comput Assist Tomogr. 2007;31:79–85.
3. Battal B, Akgun V, Sari S.Peliosis hepatis: one pathology, a thousand faces, and a clinical and radiological diagnostic challenge. J
Dig Dis. 2014;15:281–2.
• In those who had a medical history of possible etiologies,
treating the cause is expected to have lesion resolved
(e.g., infection and related drug practice).