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A. Uacker and A. H. Matsumoto

References

1. Goldblatt H, Lynch J, Hanzai RF, Summerville WW. Studies on experimental hypertension; production of persistent elevation of systolic blood pressure by means of renal ischemia. J Exp Med. 1934;59:347–79.
2. Textor SC, Lerman LO. Paradigm shifts in atherosclerotic renovascular disease: where are we now? J Am Soc Nephrol. 2015;26(9):2074–80.
3. Textor SC.Renal arterial disease and hypertension. Med Clin North Am. 2017;101:65–79.
4. Parikh SA, Shishehbor MH, Gray BH, White CJ, Jaff MR. SCAI expert consensus statement for renal artery stenting appropriate use. Catheter Cardiovasc Interv. 2014;84:1163–71.
5. Textor SC, McKusick MM.Renal artery stenosis: if and when to intervene. Curr Opin Nephrol Hypertens. 2016;25:144–51.
6. Messerli FH, Bangalore S. Renal denervation for resistant hyper­tension? N Engl JMed. 2014;370:1454–7.
7. Cooper CJ, Murphy TP, Cutlip DE, Jamerson K, Henrich W, Reid DM, etal. Stenting and medical therapy for atherosclerotic renal artery stenosis. The CORAL trial. N Engl JMed. 2014;370:13–22.
8. Carr TM, Sabri SS, Turba UC, Park AW, Saad WEA, Angle JF, Matsumoto AH.Stenting for atherosclerotic renal artery stenosis. Tech Vasc Interv Radiol. 2010;12:134–45.
9. Olin JW, Froehlich J, Gu X, Bacharach JM, Eagle K, Gray BH, etal. The US registry for bromuscular dysplasia: results in the rst 447 patients. Circulation. 2012;125:3182–90.
10. O’Connor SC, Gornik HL. Recent developments in the under­standing and management of bromuscular dysplasia. JAHA. 2014;3:e001259.
11. Meuse MA, Turba UC, Sabri SS, Park AW, Saad WEA, Angle JF, Matsumoto AH.Treatment of renal artery bromuscular dysplasia. Tech Vasc Interv Radiol. 2010;13:126–33.
12. Murphy TP, Cooper CC, Pencina KM, D'Agostino R, Massaro J, Cutlip DE, et al. Relationship of albuminuria and renal artery stent outcomes: results from the CORAL randomized clini­cal trial (Cardiovascular Outcomes with Renal Artery Lesions). Hypertension. 2016;68:1145–52.
13. Misra S, Khosla A, Allred J, Harmsen WS, Textor SC, McKusick MA. Mortality and renal replacement therapy after renal artery
stent placement for atherosclerotic renovascular disease. J Vasc Interv Radiol. 2016;27(8):1215–24.
14. Lewis S, Kadian-Dodov D, Bansai A, Lookstein RA. Multimodality imaging of bromuscular dysplasia. Abdom Radiol. 2016;41:2048–60.
15. Mamoulakis C, Tsarouhas K, Fragkiadoulak I, Heretis I, Wilks MF, Spandidos DA, et al. Contrast-induced nephropathy: basic con­cepts, pathophysiological implications and prevention strategies. Pharmacol Ther. 2017; 180: 99-112.
16. Idee J, Fretellier N, Robic C, Corot C.The role of gadolinium che­lates in the mechanism of nephrogenic systemic brosis: a critical update. Crit Rev Toxicol. 2014;44:895–913.
17. Noory E, Sritharan K, Zeller T.To stent or not to stent? Update on revascularization for atherosclerotic renovascular disease. Curr Hypertens Rep. 2016;18:45.
18. De Bruyne B, Manoharan G, Pijls NHJ, Verhamme K, Madaric J, Bartunek J, etal. Assessment of renal artery stenosis severity by pres­sure gradient measurements. JAm Coll Cardiol. 2006;48:1851–5.
19. Leesar MA, Varma J, Shapira A, Fahsah I, Raza ST, Elghoul Z, et al. Prediction of hypertension improvement after stenting of renal artery stenosis: comparative accuracy of translesional pres­sure gradients, intravascular ultrasound, and angiography. J Am Coll Cardiol. 2009;53:2363–71.
20. Dangas G, Laird JR Jr, Mehran R, Lansky AJ, Mintz GS, Leon MB. Intravascular ultrasound-guided renal artery stenting. JEndovasc Ther. 2001;8:238–47.
21. Raman G, Adam GP, Halladay CW, Langberg VN, Asodo IA, Balk EM.Comparative effectiveness of management strategies for renal artery stenosis. An updated systematic review. Ann Intern Med. 2016;165:635–49.
22. Tegtmeyer CJ, Selby JB, Hartwell GD, Ayers C, Tegtmeyer V. Results and complication of angioplasty in bromuscular dis­ease. Circulation. 1991;83(suppl):I155–61.
23. Trinquart L, Mounier-Vehier C, Sapoval M, Gagnon N, Plouin P.Efcacy of revascularization for renal artery stenosis caused by bromuscular dysplasia: a systematic review and meta-analysis. Hypertension. 2010;56:525–32.
24. Yang YK, Zhang Y, Meng X, Yang KQ, Jiang XJ, Wu HY, et al. Clinical characteristics and treatment of renal artery bromuscular dysplasia with percutaneous transluminal angioplasty: a long-term follow-up study. Clin Res Cardiol. 2016;105:930–7.

GI Bleeding

MichaelDarcy

Pathophysiology

Gastrointestinal bleeding (GIB) can occur anywhere along the GI tract with upper GI bleeding (UGIB) being that which occurs proximal to the ligament of Treitz and lower GI bleeding (LGIB) arising distal to that. While GI bleeding can be either arterial in origin or the result of venous variceal bleeding, this chapter will focus on arterial bleeding as vari­ceal bleeding is covered in the chapters on TIPS (Chap. 38) and BRTO (Chap. 39).
GIB is a very common problem with 100 cases of UGIB and 21–27 cases of LGIB per 100,000 adults per year [1, 2]. GIB can occur in any age group and there are many causes of bleeding. A study of 1929 patients showed that ulcers were the most common cause of UGIB (34%) followed by varices (33%), erosive esophagitis (8%), and Mallory-Weiss tear (6%) [3]. LGIB sources of bleeding are more diverse which vary depending on the part of the bowel involved, and an exact etiology is often not dened. Table 27.1 shows the pathology that was the source of bleeding in a series of 112 patients who underwent embolization for LGBI [4]. Most often bleeding is the only actual symptom, although patients may have some associated symptoms. Ulcers may present with abdominal pain, and signicant vomiting or retching may precede bleeding from a Mallory-Weiss tear. The type of bleeding is not always a good way to distinguish UGIB from LGIB.In a large study of UGIB patients [3], 55% pre­sented with hematemesis, but 42% had melena alone, and 2% had hematochezia alone. For LGIB, the color of the blood is also not very helpful to determine which part of the bowel is bleeding.
M. Darcy (*) Chief of Interventional Radiolgy, Mallinckrodt Institute of Radiology, Washington University in St Louis, St. Louis, MO, USA e-mail: darcym@wustl.edu
27
Table 27.1 Percent of pathology causing bleeding in LGIB
Small bowel Colon Rectum # of Pts 36 36 40 Diverticula 39% GI anastomosis 25% 8% 5% Post-endoscopic biopsy 22% 8% Malignancy 6% 6% Angiodysplasia/AVM 3% 8% Unspecied 72% 25% 78%
Adapted from Ref. [4]
Hematochezia may indicate a more distal source such as a rectal bleed, and melena is sometimes associated with a more proximal source, however, if the bleeding is brisk enough even an UGIB can present with hematochezia.
Given the wide range of pathology that can cause bleed­ing, the risk factors are also extremely variable, but one of the most common factors encountered is abnormality of coagulation parameters. Elevation of the INR due to medica­tions or liver disease and low platelet count from a variety of causes can precipitate bleeding from a lesion that otherwise might not bleed.
Key Point
High INR and low platelets can precipitate bleeding from a lesion that might not otherwise bleed.

Clinical Indication

The presentation of GI bleeding can range from occult bleed­ing detectable only by testing the stool with a hemoccult test all the way up to massive life-threatening bleeding. Physical exam is often unrevealing but may provide some clues. Hepatomegaly, splenomegaly, or scleral icterus could indi­cate liver disease and suggest a variceal rather than arterial source. A rectal exam is important for patients with LGIB since 40% of rectal cancers can be palpated on digital exam.
© Springer International Publishing AG, part of Springer Nature 2018 N. A. Keefe et al. (eds.), IR Playbook, https://doi.org/10.1007/978-3-319-71300-7_27
305
306
M. Darcy
Table 27.2 Advantages and disadvantages of the imaging modalities
used to detect GI bleed
Tagged RBC scan CTA Angiography
Rate of detection 0.1cc/min 0.3cc/
Localization of bleeding vessel Radiation exposure Low Medium High
Poor Best Good
min
1.0cc/min
Imaging is rarely needed early in the evaluation of UGIB as endoscopy detects the source of bleeding in the majority of cases. For LGIB, the imaging approach depends on if it is chronic minor bleeding versus major bleeding (bleeding causing signicant drop in hematocrit or hemodynamic instability). For chronic bleeding, if colonoscopy fails to yield a diagnosis, CT can be used to further study the colon and with reconstruction can provide a virtual colonoscopy. The small bowel can also be looked at by CT or CT entero­clysis, which involves lling the small bowel lumen with water or polyethylene glycol to provide contrast, which allows identication of a lling defect [5].
Key Point
It is important to understand variceal vs. arterial GI
bleeding. Look for evidence of liver disease including
hepatosplenomegaly, scleral icterus, and abdominal
varices.
Tagged RBC nuclear medicine scans are the most sensi­tive tests for detecting bleeding (0.1cc/min); however many feel that these are too sensitive (Table27.2). Angiography usually requires 1cc/min of bleeding for visualization, so it is fairly common to have a negative angiogram follow a positive tagged RBC scan. A recent study with 84 positive tagged RBC scans reported that angiography revealed bleeding in only 20 patients and only 9 of those were able to have successful hemostatic embolization [6]. An additional problem with tagged RBC scans is that incorrect localiza­tion of the source of bleeding is common which may mis­lead subsequent angiographic interrogation. The primary indication for tagged RBC scans currently is to try to local­ize slow or intermittent bleeding that is not localized by any other test.
For more active bleeding, CTA is preferred. CTA detects
0.3cc/min of bleeding [7], so it is a more realistic predictor of a positive arteriogram. Also the localization of the bleed­ing is better with CTA than tagged RBC scans [8]. Furthermore, it has the advantage of sometimes being able to specically identify the pathology that is bleeding, which allows both better triage and prediction of prognosis
Fig. 27.1 Abdominal CT in a patient with LGIB revealed a small
bowel tumor (arrow). Since the patient was not bleeding extensively, she was able to be triaged to surgery rather than angiography
(Fig.27.1). Finally, CTA can provide detailed arterial anatomy that often allows the angiographer to target the specic vessel that is bleeding. However, once a CTA is positive, all efforts should be made to perform the arteriogram expeditiously. If performed within 90 min of the CTA, 88% of arteriograms will be positive, but only 45% percent are positive when the arteriogram is delayed more than 90min after the CTA [9].
GI bleeding will often stop spontaneously, so the patient who is not massively bleeding should at least initially be managed conservatively. Indications to treat include bleed­ing that causes a signicant drop in the hemoglobin/hemato­crit, requires transfusions, or leads to hemodynamic instability. Less severe but chronic bleeding may also require treatment since it may cause anemia. The decision when to treat has to be tempered by the clinical condition of the patient. A young otherwise healthy patient can tolerate blood loss much better than an older person with coronary or carotid atherosclerotic disease in whom hypotension or decreased oxygen carrying capacity of the blood could lead to coronary ischemia or stroke.

Conventional Therapy

Endoscopy should usually be the rst step for UGIB.It can both localize the source of bleeding and identify the pathol­ogy in the majority of cases. Additionally the bleeding can often be treated with a variety of endoscopic techniques including injection of vasoconstrictors or sclerosants, thermal or electrocoagulation, or by application of constrictive clips or clamps. Additionally, gastric acid suppression through the use of intravenous proton pump inhibitors is recommended
27 GI Bleeding
307
as they have been shown to reduce the rate of rebleeding and mortality [10].
Surgery is indicated in several situations, the rst being if bleeding is massive and life-threatening and immediate control is needed. This, of course, requires that the source of bleeding has been identied so that the surgeon knows which vascular pedicle to control or what part of the intestinal tract needs to be resected. Another reason for surgical treatment is if the bleed­ing pathology is something that will not respond well to embo­lization. Examples include diffuse bleeding from a non-focal pathology such as inammatory bowel disease or if the bleed­ing is likely to be venous bleeding as with a bowel tumor. Also while embolization can stop bleeding, if the pathology is some­thing that requires a curative resection, then it may make sense to triage the bleeding patient to surgery. Studies show that angiographic embolization and surgery demonstrate compara­ble control of bleeding, but embolization is associated with lower morbidity and mortality [11, 12]. Thus, if there are no specic indications for surgery, patients more often are referred for the less invasive interventional radiologic option.

Interventional Therapy

In the early years of interventional therapy, bleeding was often controlled by intra-arterial infusion of vasopressin to constrict the arteries feeding the bleed. The problems with this are that it required prolonged arterial catheterization (24–48 h) and recurrent bleeding was high (often up to 40% of the time) after the infusion was stopped [13]. The rst embolization proce­dure to stop GI bleeding was reported by Baum etal. in 1974 [14]. Since that time arterial embolization has expanded to become one of the dominant tools for managing GI bleeding because of renements in angiographic imaging as well as the catheters and embolic agents used for embolization.
For UGIB, the usual indication for angiography is inabil­ity to control the bleeding with endoscopic techniques or rapid recurrence after endoscopic therapy. Rarely, a patient may be referred to angiography without rst undergoing endoscopy. However, if the endoscopist feels that the bleed­ing is so massive that they will not be able to visualize the bleed, angiography is performed.
Key Point
Indication for UGIB angiography:
• Inability to control the bleeding with endoscopy
• Rapid recurrence after endoscopic therapy
Indication for LGIB angiography:
• First-line therapy for bleeding
• Bleeding demonstrated on tagged RBC scan or CTA
LGIB is harder to evaluate with endoscopy because of blood owing toward the scope. One study of urgent colonos­copies showed that even with water-jet pumps and suction, complete colonoscopy to the cecum was possible in only 69% of patients and a source of bleeding was identied in only 39% of patients [15]. Therefore, in many institutions, angio­graphic embolization will be the front-line therapy. Which technique is utilized rst will depend in part on the local expertise of the interventional radiologists versus the endos­copists. Typically, the indication to proceed with angiography for LGIB is demonstration of bleeding on either a tagged RBC scan or a CTA.If bleeding is not demonstrated on either of those screening tests, then it is usually not indicated to pro­ceed with angiography since those tests are 3–10 times more sensitive at detecting bleeding than angiography.
For UGIB, technical success (occluding the target artery) ranges from 69% to 100%, while clinical success (clinical evidence that bleeding stopped) ranges from 63% to 97% [16]. Clinical success is lower than technical success because some patients continue to bleed despite successful occlusion of the artery. If the vessel suspected to be the source of bleeding cannot be identied on angiogram, empiric embolization may be performed, although this is still up for debate. Typically, empiric embolization is guided by prior identication of the bleeding source by endoscopy. The success rate for empiric embolization is comparable to embolizing a vessel that is seen to be extravasating on angi­ography [17].
For LGIB, several series on embolization have shown good technical success (89–100%) and slightly lower clini­cal success (68–96%) [1823]. This good technical success is primarily because modern micro-catheters allow the emboli to be delivered very close to the bleeding site, often in the vasa recta in the wall of the bowel (Fig.27.2). More specically for LGIB, the efcacy depends on the location in the bowel and the etiology of the bleeding. Lesions with a focal blood supply (like a diverticular bleed) are more effec­tively treated than lesions that have multiple vessels feeding it. Examples of the later include angiodysplasias, tumors, and inammatory bowel. A meta-analysis of 25 studies of embolization for LGIB reported that the rate of recurrent bleeding after embolization was only 15% for diverticular bleeds but 45% for angiodysplasias and other lesions [24]. Regarding location, embolization tends to be less successful in the small bowel (because of a richer collateral network) and cecum (because bleeding in that location is often due to angiodysplasia) [25]. Another series reported that rebleeding rates were 15% in the large bowel versus 60% in the small bowel [26]. Empiric embolization is rarely performed for LGIB due to the risk of ischemic bowel.
The results of embolization for both the UGIB and LGIB also depend on coagulation status and the type of embolic agent used. Some emboli like coils do not actually occlude
308
Fig. 27.2 (a) SMA arteriogram shows active extravasation (arrow) into the ascending colon. (b) Arteriogram done after embolization with micro-
coils shows the coils (arrow) in the vasa recta in the bowel wall and no further bleeding
M. Darcy
ow and rely on formation of thrombus on the coils. If a patient has a coagulopathy, embolization with coils alone is associated with a higher rate of rebleeding. Multiple studies have shown that n-butyl cyanoacrylate glue (super-glue) can more effectively occlude vessels in the face of coagulopathy [2729]. However, safe use of glue requires considerable expertise. Coils are usually able to be placed very precisely and tend to be used more frequently.
Pre-procedure management starts with the initial consult. The goals during that patient evaluation would be to determine if the patient is bleeding enough to warrant an arteriogram, if they have any severe contraindications to an arteriogram (such as history of life threatening contrast reaction), and if they have other medical conditions that could complicate an arte­riogram or the sedation. If the patient has a severe cardiac or respiratory condition that would not allow safe performance of an arteriogram with conscious sedation, then enlisting the assistance of an anesthesiologist should be considered. Anesthesia support can also be invaluable if the patient needs ongoing resuscitation during the arteriogram. During the consult, the procedure and its risks need to be discussed in detail in order to obtain informed consent from the patient.
Baseline hemoglobin and hematocrit levels are important not only to assess the initial degree of bleeding but for comparison to assess the results of therapy. Platelet count, PT, PTT and INR are necessary to determine if there is an underlying coagulopathy or to see if a patient is excessively anticoagulated. Correction of coagulopathy is important
since that alone may stop the GI bleeding but also because embolization is less effective in the coagulopathic patient. Serum creatinine must be checked since diagnostic angiography and interventions involve a high contrast load. Renal failure is only a relative contraindication to angiography since embolization may be lifesaving.
The patient must be kept NPO since the procedure will typically require sedation. If there is a history of contrast reaction, steroid premedication should be considered; an emergency premedication may be administered in the life­threatening situation.
Post procedure, the patient has to be kept at bed rest with the leg straight to allow the femoral puncture site to seal and to avoid bleeding. Vital signs must be monitored for several hours post-angiogram to look for hypotension or tachycardia which might indicate bleeding. The groin and peripheral pulses must be checked with each vital sign check to make sure there are no puncture site complications. Monitoring to see if the intervention successfully stopped the bleeding is of utmost importance. This includes following the hemoglobin and hematocrit, transfusion requirements, and output of blood (hematemesis or melena). The later can be difcult for lower GI bleeds since the colon is a large reservoir and the patient can continue to have bloody bowel movements long after embolization has actually stopped the bleeding. If the patient has any preexisting renal dysfunction, a serum creatinine should be checked a day or two after the angiogram to look for contrast nephropathy.
27 GI Bleeding
309
Fig. 27.3 (a) Celiac arteriogram in a patient with bleeding from a duo-
denal ulcer. The GDA (arrow) is faintly seen, because of poor penetra­tion of the x-rays due to the patient’s obesity, but no extravasation is seen. (b) Selective catheterization and arteriogram in the GDA now clearly show the extravasation (arrow). (c) Coils (large arrow) were
The How To
1. Prior to starting make sure there is adequate IV
medication infusion (such as vasopressors).
2. Arterial access is most often from a femoral artery approach via the Seldinger technique (refer to Chap. 8 for further information).
3. A sheath is placed to allow easy introduction of catheters but also to maintain access in case the angiographic catheter should become occluded by the embolic material.
4. Initial selective arteriography is done with a 5 Fr catheter positioned in the trunk of the visceral ves­sels. Which vessel to start with depends on your suspicion of what part of the GI tract the bleeding
placed in the GDA distal to the site of bleeding to avoid back-bleeding from collaterals. Extravasation of contrast (small arrow) is still seen because the bleeding originates proximal to the coils and close to the origin of the GDA. (d) Arteriogram after embolizing more proximally up to the GDA origin (arrow) shows bleeding has stopped
27.3a
suspected small bowel or right colon bleeding.
to arise distal to the transverse colon.
5. arteriograms should be performed. Which vessel is selected depends on the suspected site. For example, the gastroduodenal artery would be sub­selected for a suspected duodenal bleed (see
27.3b).
6. into the target vessel that is bleeding. With gastro­duodenal or left gastric bleeds, this may be done with the 5 Fr angiographic catheters, but usually a
(continued)
310
micro-catheter is advanced through the 5 Fr cath­eter in order to super-select the bleeding vessel. Micro-catheters are essential for LGIB because here the catheter has to be advanced as close to the vasa recta as possible to avoid bowel ischemia.
7. After selecting the bleeding vessel, the vessel is occluded with the embolic material of choice. In some vessels it is important to start beyond (distal
27.3c).
8. After embolization, repeat angiography is done
27.3d).
9. Other vessels that might provide collateral blood supply to the bleed then need to be angiographi­cally interrogated. For example, after a GDA embolization via the celiac trunk, the SMA needs to be injected because the inferior pancreaticoduo­denal artery arising from the SMA can provide collateral supply to a GDA bleed.
10. that vessel is catheterized and also embolized.
11. stopped, catheters are removed and the arterial access is closed with a closure device or by man­ual compression. If there is concern that the patient may acutely rebleed (in patients with non-focal diffuse blood supply or patients with coagulopa­thy), a sheath may be left in place to allow rapid access back into the arterial system for repeat arteriography.
M. Darcy
Complications
Complications common to any angiographic procedure include occlusion, bleeding or hematoma at the access site, and contrast-induced nephropathy or allergic reactions. The main embolization-related complications include bowel ischemia or infarction and nontarget embolization.
Bowel ischemia is rare after embolization for UGIB because of the robust collateral supply to the stomach and duodenum. The risk of ischemia is increased if the patient has had any prior surgery on these organs since surgery may have disrupted some of the potential collateral pathways. For LGIB, the rate of signicant ischemia is around 5% or lower [4, 19, 22]. Although the collateral supply is less robust, modern micro-catheter techniques allow for very focal embolization with emboli being deposited often as far as the vasa recta. However while a focal bleeding source like a diverticular bleed might be controlled by embolizing a single vasa recta, more diffuse bleeding may require embolizing several branches increasing the risk for bowel ischemia. Animal studies have shown that the chance of ischemia sig­nicantly increases if four or more vasa recta are embolized [30]. Ischemic changes can range from asymptomatic muco­sal abnormalities identied only at endoscopy all the way to complete infarction of the affected bowel which requires surgical resection if death is to be avoided.
Nontarget embolization refers to migration of the embolic device or material from the intended target artery into an undesired artery that you don’t want to occlude. This can be the result of reux of injected particles or a mechanical device backing out during placement (Fig.27.4). If the non­target emboli are in a non-critical vessel, they can be left in place, but if occlusion would lead to organ ischemia, then retrieval of the errant embolic device should be attempted.
Key Point
Which vessel to select rst on angiography:
• Celiac rst for suspected UGIB
• SMA rst for suspected bleed of the small bowel or right colon
• IMA rst for suspected bleed distal to the transverse colon
Key Point
Risk factors for embolization:
• Bowel ischemia
• Bowel infarction
• Nontarget embolization
27 GI Bleeding
Fig. 27.4 (a) Celiac
arteriogram demonstrating massive extravasation (arrows) from the GDA. (b) Common hepatic arteriogram showing persistent extravasation (arrow) from the GDA proximal to the coils. (c) After attempting to pack coils all the way to the GDA origin, the last coil backed out and is sitting in the proper hepatic artery (arrow)
311

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Uterine Artery Embolization

NicoleA.Keefe andZivJHaskal

Pathophysiology

Fibroids
Uterine broids, also known as leiomyomas or myomas, are tumors that arise from the uterine smooth muscle. Historically, references of broids date back to the time of Hippocrates, when they were referred to as “uterine stones.” Furthermore, ancient Egyptian female mummies show evi­dence of calcied pelvic masses suggestive of broids [1].
Fibroids affect up to 80% of women of reproductive age with the majority of cases diagnosed in their 30s and 40s [2]. Fibroids are benign however rarely (0.1%) undergo sarcoma­tous degeneration [3]. They can become problematic as they grow and cause both pressure and bleeding problems. They can range from 1 cm up to 20 cm [4]. Fibroids can cause heavy or prolonged menstrual bleeding, leading to anemia (Table28.1). In postmenopausal women, vaginal bleeding is atypical and should prompt further evaluation for endome­trial cancer before attributing it to broids. Fibroids also lead to “bulk” symptoms due to pressure on various structures.
Reproductive and environmental factors inuence a woman’s risk of developing broids. Nulliparity is associ­ated with an increased risk [5]. Both early menarche before the age of 10 and the use of combined oral contraceptive pills before the age of 16 increase risk [6]. Fibroids tend to regress after menopause, emphasizing the hormonal relationship. The risk of broids is also genetic, with rst-degree relatives having a 2.5 times increased risk of developing broids [7].
Fibroids can be classied into four types based on the location: submucosal, subserosal, intramural, and peduncu-
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Table 28.1 Symptoms of uterine broids
Abnormal uterine bleeding, metrorrhagia Pelvic pressure Constipation, bloating Back pain Infertility Increased thromboembolic disease Sciatica pain Dyspareunia
Key Point
Fibroids grow with hormonal inuences and shrink with menopause.
lated (Figs. 28.1 and 28.2) [2]. Diffuse broids within the uterus are referred to as uterine leiomyomatosis.
• Submucosal broids are located beneath the endometrium.
• Subserosal broids are located beneath the serosal surface.
• Intramural broids are located within the thick myometrium.
• Pedunculated broids grow on a stalk connecting them to either the outer wall of the uterus in which they project into the peritoneal cavity or to the inner wall of the uterus in which they project into the endometrial canal.
Adenomyosis
Urinary frequency, difculty urinating or retention
Increased rate of miscarriage
N. A. Keefe (*) · Z. J Haskal University of Virginia School of Medicine, Department of Radiology and Medical Imaging, Interventional Radiology Division, Charlottesville, VA, USA
© Springer International Publishing AG, part of Springer Nature 2018 N. A. Keefe et al. (eds.), IR Playbook, https://doi.org/10.1007/978-3-319-71300-7_28
Another uterine pathology that causes menorrhagia is adeno­myosis (Fig.28.3). This is characterized by endometrial glands and stroma arising aberrantly in the uterine musculature. Instead of having a “bumpy” uterine shape characteristic of
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