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132 S. Puppala
Pre-procedural Care
1. Informed consent: patients should be fully informed of the risks of PES and
its variable occurrence and severity. It is helpful to establish what the patient
understands about PES and target explanation to any gaps in their knowledge.
2. Hydration: crucial in PES due to the risks of contrast nephropathy fluid loss from
vomiting, loss of appetite, and secondary dehydration.
3. Analgesia: prophylactic analgesics are essential.
• A combination of oral, IV, epidural, and/or patient-controlled analgesia can
be used.
• A local regime should be established with the pain control team and ward, and
angiography staff should be familiar with the chosen protocol.
• Our practice is to administer a non-steroidal analgesics either paracetamol
(acetaminophen) 1 g IV or diclofenac 50 mg PR for procedures that are typically painful such as hepatic and renal tumor embolization. Acetaminophen
helps control pain, reduces the inflammatory response, and provides an
antipyretic action.
• Patient-controlled analgesia (PCA) is set up and connected before the
procedure.
• Additional opiate analgesia is given from the start of the procedure according
to patient requirement.
4. Sedation:
• A small dose of intravenous benzodiazepine such as midazolam is given at the
start of the procedure.
• Additional doses are given as indicated.
5. Antibiotics: broad spectrum antibiotics may prevent infection but there is little
evidence to support routine use.
Management of PES: Intraprocedural
Analgesia: PCA pump using morphine sulphate set at 1 mg/5 min lockout. This
should be supplemented by additional opiate analgesia titrated to control pain. If a
PCA pump is not used, then IV short-acting opiate and benzodiazepine protocols
may be advantageous. It is essential that someone other than the operator takes
responsibility for pain control.
Antiemetics: an IV antiemetic, e.g., Cyclizine 50 μg should be given.
Ondansetron sodium is an alternative and administered as 16 mg per rectally or
as 8 mg slow i ntravenous injection.
13 Management of Post-embolization Syndrome 133
Management of PES—Post-procedure
Analgesia: should be continued until the patient is comfortable. PCA is discontinued
when patient is able to tolerate oral analgesia. Use of an opiate combined with a
NSAID is usually better than a single agent.
Antiemetics: should be continued as required using IV or IM routes until oral
intake has resumed.
Hydration: is essential, intravenous fluids should be prescribed for sedated
patients or those unable to manage oral fluids.
Reassurance: remind patients that PES is a normal and self-limiting side effect
of embolotherapy.
Keypoints
• Post-embolization syndrome is an important and common side effect of
embolization. It is a self-limiting phenomenon, and effective supportive
measures for control of pain and nausea improve the overall outcome and
also the quality of life after embolization. It is essential to have a clear
local strategy for management pre-, peri- and post-procedure.
• Efforts should be focused on prevention of pain and sickness and supportive post-procedural care. It is essential not to discharge patients before
symptoms have resolved sufficiently for them to be cared for at home.
Further analgesics and antiemetics should be provided as necessary and
the patient should be given clear verbal and written instructions regarding
the normal evolution of PES.
Bibliography
1. Hemingway AP, Allison DJ. Complications of embolization: analysis of 410 procedures.
Radiology 1988 Mar; 166(3):669–72.
2. Sohara N, Takagi H, Abe T, Hashimoto Y, Kojima A, Takahashi H, Nagamine T, Mori M.
Nausea and vomiting induced by arterial chemo-embolization in patients with hepatocellular
carcinoma and the antiemetic effect of ondansetron hydrochloride.
Support Care Cancer 1999 Mar; 7(2):84–8
3. Romano M, Giojelli A, Tamburrini O, Salvatore M. Chomoembolization for hepatocellular
carcinoma: effect of intrarterial lidocaine in peri and post procedural pain and hospitalization.
Radio Med (Torino) 2003 Apr; 105(4):350–5
4. Bissler JJ, Racadio J, Donnelly LF, Johnson ND. Reduction of post embolization syndrome
after ablation of renal angiomyolipoma. Am J Kidney Dis 2002 May; 39(5):966–71
5. Rauh S, Duhem C, Ries F, Dicato M. Complications and hospitalisation duration
after chemoembolization for liver metastasis. Bull Soc Sci Med Grand Duche Luxemb
1999;(2):29–36
6. Sundset A, Haanaes OC, Enge I. Embolization of bronchial arteries in severe and recurrent
haemoptysis. Tidsskr Nor Laegeforen 1992 Sep 30; 112(23):2958–62
134 S. Puppala
7. Leung DA, Goin JE, sickles C, Raskay BJ, and Soulen MC. Determinants of post embolization syndrome after hepatic chemoembolization. Journal of vascular interventional radiology
2001 Mar; 12(33):321–6
8. Marcio H M, Stanley P, Steel D A, Ortega JA. Feasibility and toxicity of chemoembolization
for children with liver tumours. J clin oncol March 2000;18(6):1279–1284
9. Coldwell DM, Kennedy A, Vanecho D. Comparative side effects of yttrium-90 based intraarterial brachytherapy. J Clin Oncol (July 15 Supplement) 2004;22(14S): 3760
10. Huo T-I, Wu J-C, Lee P-C, C hang F-Y, Lee S-D. Incidence and risk factors for acute renal failure in patients with hepatocellular carcinoma undergoing transarterial chemoembolization: a
prospective study. Liver Int June 2004;24(3):210–215(6)
11. Ganguli S, Faintuch S, Rabkin DJ, Lang EV. Post-Embolization Syndrome: Leukocytosis
after Uterine Artery Embolization
12. Kimura F, Itoh H, Ambiru S et al. Long term results of initial and repeated partial
splenic embolization for the treatment of chronic idiopathic thrombocytopenic purpura. AJR
2002;179:1323–6.
13. Wah et al. Image guided percutaneous radiofrequency ablation and incidence of post ablation
syndrome: prospective survey. Radiology 2005;237(3):1097.
14. Ganguli S, Faintuch S, Salazar GM, Rabkin DJ. Postembolization syndrome: changes in white
blood cell counts immediately after uterine artery embolization. J Vasc Interv Radiol. 2008
Mar;19(3):443–5.
15. The British National Formulary reference can easily be found by you
http://bnf.org/bnf/bnf/current/104945.htm
Section II
Chapter 14
Peripheral Vascular Malformations
Peter Littler and Peter Rowlands
Background
• Peripheral vascular malformations are uncommon lesions and are thought to be
due to a focal persistence of primitive vascular elements.
• Vascular malformations are not neoplastic. They are subdivided into high-flow
and low-flow lesions. High-flow lesions are arterial; low-flow lesions are venous,
capillary, or lymphatic.
• It is important that these lesions are evaluated and treated by a specialist with
experience in embolotherapy working within a multidisciplinary team with
access to anesthetic support and plastic surgery.
• The purpose of diagnostic evaluation is to assess suitability for treatment and to
evaluate if the lesion is high flow (arteriovenous malformation) or low flow, as
treatments are different for each group.
Low-Flow Lesions
Clinical Features
• Include venous, lymphatic (Chapter 46), and capillary malformations.
• Common sites of involvement include the limbs and head and neck.
• Patients with a venous or lymphatic malformation often present with swelling
and/or pain.
• Other reasons for presentation include aesthetic appearance or hemorrhage.
• Pregnancy may exacerbate symptoms, particularly with lower limb lesions.
Transcatheter Embolization and Therapy,
Techniques in Interventional Radiology, DOI 10.1007/978-1-84800-897-7_14,
C
Springer-Verlag London Limited 2010
137
138 P. Littler and P. Rowlands
Diagnostic Evaluation
Clinical Review
• A comprehensive history of the lesion is taken together with relevant past medical
and drug history.
• The lesion is examined clinically for site, size, and appearance.
• Ultrasound (Fig. 14.1) should be considered to be a part of the clinical
examination.
a
b
c
Fig. 14.1 (a) Ultrasound and (b) MRI demonstrating a venous malformation in a patient with
Klippel–Trenaunay syndrome (Chapter 17). Note the right leg hypertrophy and large popliteal
vein (c)
Laboratory
• It is important to check the platelet count in patients with very large vascular
malformations as there can be a low platelet count secondary to sequestration.
14 Peripheral Vascular Malformations 139
• Clotting measurements and routine blood tests can be relevant if intervention is
planned.
Imaging
• Ultrasound with greyscale and Doppler is a key step in evaluation of a peripheral vascular malformation (Fig. 14.1). Together with clinical examination, most
lesions can be easily differentiated by ultrasound into high- and low-flow lesions.
Limitations occur when evaluating deep lesions when the full extent of the lesion
cannot be visualized.
• MRI of the lesion is routinely performed to assess morphology (Fig. 14.1) and
any feeding and draining vessels (Fig. 14.2).
Fig. 14.2 T2-weighted
coronal MRI of the head and
neck demonstrating a large
high-signal cervical venous
malformation causing
pharyngeal narrowing. There
are multiple low-signal
phleboliths within the lesion
(arrow)
• Useful MRI sequences include T1 for anatomical detail, and fat-suppressed T2
that allows excellent visualization of the lesion, which is of high signal intensity
compared with the lower signal of surrounding tissue. Intravenous contrast is
rarely required.
Indications for Embolization
• If the patient is having pain, swelling, hemorrhage, or finds the lesion aesthetically intolerable, then it is reasonable to proceed after a risk benefit analysis.
140 P. Littler and P. Rowlands
• Platelet consumption.
• A significant proportion of patients do not require any intervention.
Alternative Therapies
• Conservative management: if the patient is relatively asymptomatic.
• Surgical resection: best for small superficial lesions. Frequent recurrence is a
problem.
• Laser: effective in treating capillary vascular malformations such as the “port
wine stain.”
• Radiotherapy: rarely used due to limited effectiveness and post-radiotherapy skin
changes.
Cautions/Contraindications
• Patent foramen ovale or other right-to-left shunts are relative contraindications. When injecting the sclerosant, you must be sure not to fill a
draining vein.
Specific Complications
• Superficial skin ulceration can rarely occur if the sclerosant tracks into the subcutaneous tissues. This is seen more commonly with alcohol than with sodium
tetradecyl sulfate (STD).
• Nerve damage rarely occurs if alcohol sclerosant is injected immediately adjacent to a nerve. This should be discussed specifically in the consent process.
Temporary facial nerve palsy is a rare complication of sclerotherapy of facial
lesions and is due to direct pressure of a swollen vascular mass on the facial
nerve.
• Swelling frequently occurs post-treatment. This is r arely a problem and resolves
in a few days. However, when treating a lesion in the head and neck, prophylactic
steroids are given to prevent obstruction of the airway.
Anatomy
• Dependent on site.
• It is crucial to understand the normal vascular anatomy and to recognize adjacent
structures that may be damaged.
14 Peripheral Vascular Malformations 141
Equipment
• 21-G butterfly needle for superficial lesions.
• A 20-G spinal needle can be used with ultrasound guidance for deeper lesions.
Embolic agents: low-flow malformations are treated using sclerosant agents.
• STD 1% or 3%, either in liquid or foam.
• Absolute alcohol.
Medication
• Pain control: simple analgesics as required post-procedure.
• Steroids: if head and neck lesion. 8 mg of dexamethosone IV during procedure
and a 5-day course of 40 mg oral prednisolone. Use with caution in diabetics.
Angiography
The procedure is often performed under general anesthetic due to discomfort during
sclerotherapy. This is usually required if a head and neck lesion is treated.
Access
• Ultrasound-guided percutaneous puncture using a 21-G butterfly or 20-G spinal
needle under aseptic conditions. Once venous backflow is achieved, then angiography can be performed.
Angiography
• Magnified DSA, usually at two frames per second. Continue until a draining
vein fills.
• It is important to note the volume and rate of contrast injection, as this guides the
injection of sclerosant.
Assessing the Lesion
Angiographic Appearance
• Angiography reveals abnormal filling of dilated vascular structures. A draining
vein or veins are often seen (see Fig. 14.3).
142 P. Littler and P. Rowlands
Fig. 14.3 (a) DSA via a 21-G
butterfly needle
demonstrating a venous
malformation, (b) early filling
ofadrainingveinvia
alternative puncture site in the
same patient
a
b
Treatment Plan and Technique
• The ultimate aim is to fill the entire lesion with sclerosant.
• Small areas of the lesion (two or three sites) are treated at each procedure to avoid
excessive swelling and the risk of tissue ulceration.
• Several sessions may be needed to treat the entire lesion.
• The sclerosant is mixed with contrast and injected under DSA guidance until a
draining vein is seen. As a guide, the volume and injection rate should be similar
to that injected in the initial DSA run.
• In low-flow lesions contrast often remains pooled in the lesion from the initial angiogram. If this has washed out then consider diluting the sclerosant with
contrast.
• Occasionally a torniquet is applied to control venous outflow by temporally
occluding a draining vein.