(1)
Department of Fetal Medicine and Obstetric & Gynecological Ultrasound, Manipal Hospital, Bangalore, Karnataka, India
Arteriovenous malformations are seen infrequently and are difficult to differentiate from vascular retained products of conception (RPOC). Proper diagnosis is essential for appropriate management of these potentially life-threatening lesions. Perforation of the uterus is also a rare condition, and a few examples have been provided. Vesicouterine fistula, a rare complication most often following a caesarean section, is covered next. Retroflexed uterus, though a common normal variant, may be an indicator of pathology or may present with symptoms. Caesarean scar defect has become important due to the rising incidence of caesarean sections. Their evaluation is gaining importance because some of these patients may be symptomatic and because of its potential for rupture in a subsequent pregnancy. Intrauterine contraceptive devices can be evaluated on ultrasound to assess whether they are in the normal position. This is best studied by three-dimensional ultrasound and has been described in this chapter. The sonographic appearances vary with the type of device and its location. Images of patients with different types of IUCD in various locations (normal and otherwise) are shown. Practical aspects of follicular tracking (that is resorted to both in natural and induced cycles), have been briefly discussed. The last part of this chapter deals with ovarian hyperstimulation syndrome, a rare but potentially life-threatening complication that is usually the result of ovulation induction.
13.1 Uterine Vascular Abnormalities (Arteriovenous Malformations)
Uterine vascular malformations are rare but potentially life threatening. They are basically multiple arteriovenous fistulous communications within the uterus without an intervening capillary network. These can be congenital or acquired. Congenital ones are very rare and a result of defective embryonic development. These congenital lesions can penetrate surrounding tissues and grow as pregnancy progresses. Most, however, are believed to be acquired secondary to uterine damage by curettage, miscarriage or termination, trophoblastic disease, neoplasia and infection.
Uterine vascular abnormalities, most often reported in the literature as arteriovenous malformations (AVM), are used to describe uterine lesions showing a hypervascular appearance with turbulent flow. Uterine vascular abnormalities would be a better terminology to use for these malformations, as not all are true AVMs. True AVMs can be confirmed histopathologically and show early venous filling on angiography. All other lesions are really non-AVM vascular abnormalities.
Typical symptoms are menorrhagia and metrorrhagia. Some complain of lower abdominal pain. Most often, there is a history of a preceding pregnancy or, in rare cases, a gestational trophoblastic disease. Though these lesions grow slowly, the onset of symptoms could be sudden when the endothelial lining of the vessels gets disrupted during menstruation or curettage. If curettage is done without prior diagnosis of the vascular lesion, the patient could bleed torrentially.
It appears as a focal ill-defined heterogeneous mass in the myometrium formed by multiple irregular or tubular hypoechoic cystic structures that fill with colour. That is, the mass comprises of vascular channels only.
It is located in the area of the radial arteries of the uterus and is seen reaching up to the endometrium or even protruding into it.
The endomyometrial junction in the corresponding area is most often poorly defined.
On Doppler, the area shows turbulent flow which is seen as high colour filling with a mosaic pattern.
Flows show high velocity and low resistance, with average peak systolic velocity (PSV) of 63 cm/sec and RI of 0.38.
Vessels with a large diameter may be seen not only in the lesion but also in the related arcuate vessels and the parametrial vessels.
During a uterine contraction, flow to the area can decrease significantly, and therefore in case the suspected area (on greyscale) is not filling with colour on Doppler, it is important to wait for a short while.
Retained products of conception (typically seen as a heterogeneous mass in the endometrial cavity on greyscale with some flow)should be carefully looked for, because turbulent vascular flow may be seen not only in the endometrial cavity but also extending onto the adjoining myometrium in some cases with retained tissue.
The gold standard for definitive diagnosis for true AVMs is early venous filling on contrast angiography. The rest are termed non-AVM uterine vascular abnormalities. Presently, however, angiography (being invasive) is generally resorted to only for therapeutic embolisation.
The most important differential diagnoses for AVMs are retained products of conception (RPOC) and gestational trophoblastic disease (GTD).
Retained tissue may be clearly visualised in some cases, making the diagnosis simple. Greyscale ultrasound for RPOC is specific but not sensitive, and therefore ultrasound cannot rule out RPOC. Serum B hCG is useful in picking up RPOC and GTD and distinguishing them from true AVMs.
Once a uterine vascular abnormality is seen on ultrasound, if there is associated RPOC, curettage can be done. RPOC showing turbulent flow can be most often safely treated with curettage.
The rest of the AVMs (without confirming whether they are true AVMs or non-AVM vascular abnormalities) are treated based on clinical presentation. If bleeding is excessive or persistent, uterine artery embolisation or even hysterectomy may be resorted to.
In most cases, the AVM lesion subsides in 6–8 weeks, but, in certain cases, it could take up to 6 months. Conservative management with serial B hCG and ultrasound is generally sufficient. Medical management with methotrexate is also an option.
In most cases of uterine vascular lesions, serum B hCG is elevated (though often only by a small amount), and as the B hCG values decline, so does the vascularity in the uterus, until it completely disappears. Increased vascularity of the myometrium of the placental bed following pregnancy (miscarriage or delivery) is common in the first few weeks following pregnancy even in the absence of retained placental tissue on ultrasound. On follow-up, the vascularity regresses gradually over the next few weeks.
One large study has suggested that patients can be triaged into high and low risk, based on peak systolic velocity (PSV) of flows in the AVM. Those with a PSV of 83 cm/sec or more are to be considered as ‘high risk’ cases, and those with a PSV of less than 39 cm/sec are considered as ‘low risk’ cases. The cases that are not ‘low risk’ should be monitored more closely.
Fig. 13.1
AV malformation of the uterus with normal levels of B hCG (0.1 mIU/mL) and LCB 3 yr and 8 months ago. No history of any pregnancy or surgical intervention following LCB. Last image taken at a repeat follow-up scan done 8 weeks later, showing persistence of the lesion. This is therefore likely to be a true AV malformation. (a) Ill-defined heterogeneous mass comprised of multiple cystic areas is seen in the posterior myometrium of the upper corpus reaching up to the endometrium. (b) The area is seen filling up with colour and shows turbulent flow (high filling with mosaic pattern). (c) High-velocity low-resistance flow is seen. (d) The arcuate and parametrial vessels are seen dilated and tortuous. (e) 3D HD Doppler glass body image showing the lesion with turbulent flow and dilated arcuate and parametrial vessels on the side of the lesion. This image was taken during a repeat scan after 8 weeks of the earlier images
Fig. 13.2
A small AV malformation in a patient whose last child birth with tubectomy was 25 years ago. (a) Shows a small lesion and prominent arcuate feeding vessels on Doppler. On greyscale the lesion is less well defined. (b) Prominent bilateral parametrial vessels are seen
Fig. 13.3
MTP with curettage was done 4 months ago. Patient presented with profuse bleeding for which this scan was done. B hCG on the day of scan was 35 mIU/mL. Patient was treated with methotrexate, and 2 months later B hCG came down to 0.22 mIU/mL and the lesion regressed on scan. (a) Heterogeneous ill-defined mass seen in the anterior myometrium extending into the endometrium. The endomyometrial junction in this area is poorly defined. On greyscale, margins of the lesion are difficult to define. (b) The lesion is seen filling up with colour and showing turbulent flow. (c) On TAS, the lesion with prominent arcuate feeder vessels is noted. (d) Flow showing high velocity and low resistance. (e) Repeat scan done 2 months later, when B hCG value was normal, showed that the lesion had regressed. A faint hyperechoic area is seen in the anterior myometrium which did not show any flow on Doppler
Summary of AV Malformation
May present with menorrhagia or metrorrhagia. History of recent pregnancy (including molar pregnancy) and instrumentation is common.
Ultrasound:
Ill-defined focal mass with cystic hypoechoic areas that fill with colour and show turbulent flow (high PSV and low RI).
Seen in the myometrium, extending up to or into the endometrial cavity.
Look for the presence of RPOC – which can also show turbulent flow at times.
Serum B hCG may help to differentiate true AVM from RPOC and GTD.
Most regress on follow-up – which includes serial scans and serum B hCG (if elevated). Those with excessive or persistent bleeding will require uterine artery embolisation or rarely hysterectomy.
13.2 Perforation of the Uterus
Perforation of the uterus refers to a through and through passage in the myometrium extending from the endometrium to the serosa. It may be iatrogenic or less often of spontaneous origin. Iatrogenic causes include: perforation during dilatation and curettage (particularly in a pregnant uterus), operative hysteroscopy, endometrial ablation, insertion of intrauterine contraceptive device (IUCD) and evacuation of retained placenta. Uterine perforation is most often seen in cases of abortion with suction and curettage. Ultrasound-guided procedures decrease the risk of perforation in these cases. Spontaneous perforation is usually due to trophoblastic invasion of the myometrium in cornual and interstitial pregnancies or GTD. Iatrogenic uterine perforation usually presents at the time of injury with a history of omental or bowel fat at suction or an inability to distend the uterine cavity on hysteroscopy due to extrauterine escape of fluid or as increased intrauterine or extrauterine haemorrhage. Most often, however, they are missed and may either be diagnosed at a later time or may heal on their own. An important problem of uterine perforation is uterine rupture in a subsequent pregnancy. Routine intraoperative transabdominal ultrasound-guided procedures increase safety and expedite the procedure.
Perforation is seen as a hyperechoic tract of varying thickness in the myometrium extending from the uterine cavity up to the serosa, in cases where there is some tissue in the myometrial tract (like omentum or placental tissue). In case there are bowels within the cavity, peristalsis may be noted. The myometrium in that area is therefore deficient.
Perforation that is recent and has no tissue within may not be visualised on ultrasound. On distension of the uterine cavity with fluid (as seen in hysteroscopy), it may show up transiently as an anechoic or hypoechoic, regular or irregular tract in the myometrium, extending from the endometrial cavity to the serosa.
At times (particularly if sometime has lapsed following the perforation), a perforation may only appear as a hyperechoic linear area extending between the endometrium and the serosa.
Often perforation itself is not noticed, but a diagnosis of a perforation having occurred may be implied as in finding of an intrauterine contraceptive device (IUCD) outside the uterus.
Fig. 13.4
Case of uterine perforation during surgical MTP. (a) Zoomed-in image of the sagittal section of the uterus. There is a hyperechoic tract (arrow) extending from the endometrial cavity to the serosa. (b) At laparoscopy, omentum is seen within the perforation (arrow). (c) Perforation is seen at the serosal surface of the uterine fundus (arrow) after the omentum was drawn out, which was bleeding
Fig. 13.5
Early trophoblastic perforation of non-communicating right-sided uterine horn (with a well-developed left horn). The placenta was seen within the endometrial cavity of the rudimentary horn. The placenta and umbilical cord were protruding out of the uterine perforation and extending up to the dead fetus. (a) Non-communicating right-sided horn with a hyperechoic complex tract (arrow) that extends from the cavity on to the serosal surface. (b) Post-operative specimen of the excised horn showing placental tissue extending out of the perforation (arrow). (c) Dead intra-abdominal fetus connected to the perforated uterine horn with the umbilical cord (arrow). (d) Diagrammatic representation of scan findings in the case. The uterine perforation due to invasion by trophoblastic tissue must have occurred early in pregnancy with the fetus escaping out of the rudimentary horn and continuing to grow intra-abdominally for a short period of time
Fig. 13.6
Case of IUCD (with missing thread) that had perforated the uterine wall and was lying in the uterovesical (UV) fold. (a) Long section of the uterus with the cross section of the shaft of the IUCD (arrow) seen in the UV fold. (b) Transverse section of the UV fold showing the shaft of the IUCD (arrow)
Summary of Perforation of the Uterus
Perforation is more often iatrogenic occurring during intrauterine procedures but it may be spontaneous due to invasion by trophoblastic tissue. Often it goes unnoticed, but those that are symptomatic present most often at the time of injury itself, commonly with haemorrhage and pain.
On ultrasound, they may be seen either as a hyperechoic thin linear area or a hyperechoic thick tract or a transiently filling anechoic tract through the myometrium.
13.3 Vesicouterine Fistula
Vesicouterine fistula is a communication between the bladder and the uterine cavity. This may result because of previous caesarean section, particularly when followed by vaginal delivery or as a complication of a perforating IUCD. Patients with vesicouterine fistula usually have urinary incontinence in the early post-operative period. Most often they complain of bleeding per urethra, with or without associated small clots, during menstruation.
Ultrasound Features of Vesicouterine Fistula (Fig. 13.7)
It appears as a fistulous anechoic tract extending between the endometrial cavity and the urinary bladder.
The length, breadth and thickness of the tract can be measured, including the opening in the endometrial cavity and the bladder mucosa.
A partially filled bladder helps in better delineation of the fistulous tract through the bladder wall.
The bladder is seen adherent to the anterior wall of the uterus at the site of the fistulous connection (most often the site of the LSCS scar). In other words, the bladder does not slide along the uterus/vagina on pressure by the TVS probe.
The rent in the bladder wall can be visualised well on 3D rendered images.
13.4 Retroflexed Uterus
A retroflexed uterus is one where the axis of the uterine cavity is bent backwards as compared to that of the cervical canal. This therefore causes an angulation (retroflexion) at the level of the internal os. A retroflexed uterus is a normal variant, and most often patients are asymptomatic. In some cases, however, the patients may be symptomatic, either because of acute retroflexion itself or because of pathology causing fixed retroflexion of the uterus as seen in endometriosis and PID. The common symptoms seen in women with retroflexion are pain (due to associated PID, endometriosis or incomplete drainage of menstrual blood), postmenstrual spotting (of collected menstrual blood) or occasionally urinary retention in a gravid retroflexed uterus.
Fig. 13.7
Long-standing (13 years) uterovesical fistula following LSCS, with a history of blood-stained urine during menstruation. Patient presented with recent onset of menorrhagia with passage of clots in urine and painful micturition. (a) Narrow anechoic/hypoechoic tract (arrow) extending from the bladder into the lower corpus of the uterus. (b) The tract is seen communicating with the endometrial cavity (arrow) of the lower corpus. (c) 3D rendering of the bladder end of the fistula that measured about 1.3 cm transversely
In a midsagittal section, the endometrial cavity is seen bent backwards as compared to that of the cervical canal.
The retroflexion typically occurs at the internal os between the cervix and the lower corpus.
Hematometra – In an acutely retroflexed uterus at times, there may be some amount of menstrual blood seen in the uterine cavity which is believed to be because of the effect of gravity and acute angulation, impairing the drainage of normal menstrual flow.
In patients with PID and endometriosis, the uterus is usually fixed in flexion, i.e. the posterior wall of the uterus is adherent to the bowels and or the diseased adnexa.
Uteri that are fixed in flexion due to PID and endometriosis usually show angulation above the level of the internal os, often between the lower corpus and the midcorpus, giving the uterus a ‘question mark’ – or ‘ear’ – shaped appearance.
In patients with endometriosis, the posterior wall of the uterus may show coarse echoes secondary to diffuse adenomyosis.
Fig. 13.8
Retroflexed uterus with hematometra showing the fluid–fluid level with the denser fluid in the dependent upper uterine cavity. Here, flexion is seen at the junction of the cervix with the uterine body (i.e. level of internal os) (arrow)
Fig. 13.9
Retroflexed uterus in a patient with DIE. (a) TVS – the flexion is more pronounced at the midcorpus (arrow). The posterior wall is thick and shows slightly coarse echoes suggestive of adenomyosis. (b) TAS – flexion at midcorpus (arrow) with an ‘ear’- or ‘question mark’- shaped uterus
13.5 Caesarean Scar Defect (LSCS Scar Defect)
With increasing caesarean section (CS) rates worldwide and its associated complications of late, there has been an increased interest in evaluation of the caesarean section scar defects (CSDs) and their relation to complications. Though the evaluation of a scar can be accurately done on ultrasound (TVS), the analysis of its association with complications requires in-depth studies. CSD is seen in about 70 % (on TVS) to 84 % (on SHG) of women with a previous history of cesarean section (Osser.V., UOG 2010, UOG 2011).
Multiple caesarean sections, single-layer myometrial closure and retroflexed uteri are reported in the literature to increase the risk of scar defects and are accordingly more often associated with larger scar defects. Caesarean scar defects are associated with symptoms of postmenstrual spotting (a commonly seen symptom, with typically darkish altered blood), dysmenorrhoea and chronic pelvic pain. Scar defects have also been studied with the idea to evaluate the potential risk for obstetric complications in future pregnancies like scar ectopic pregnancy, placenta previa, adherent placenta and scar dehiscence.
A caesarean scar defect is diagnosed by the presence of a hypoechoic (or anechoic) cystic area within the anterior myometrium of the lower uterine segment at the site of the previous LSCS. The collection in the defect is basically retained menstrual blood. It is seen somewhere between the level of the internal os below (identified by the level of entry of the uterine arteries and the apical upper end of cervical mucosa) and the uterovesical fold of peritoneum above.
Most often, the defect is triangular or wedge shaped with its base towards the endometrial cavity and its apex pointing towards the serosa. Some defects, however, may be ‘U’ shaped or irregular and are most often seen with larger defects.
The evaluation is done on TVS, and the image should be magnified to include the cervical canal, the bladder and the lower uterine cavity. Care must be taken not to apply too much pressure with the TVS probe as that may alter the shape and measurements of the scar defect.
The current recommendation to measure the scar is to take four measurements (Fig. 13.15):
Scar width (W) – is its distance along the cervico-endometrial canal taken in the sagittal section of the uterus. Increasing scar width has been found to be associated with postmenstrual spotting, dysmenorrhoea and chronic pelvic pain.
Scar depth (D) – is the vertical distance between the base (facing the uterine cavity) and the apex of the defect (towards the uterine serosa) taken in the sagittal section of the uterus.
Scar length (L) – is the length of the defect in the transverse section (this may be assessed in transverse or coronal views).
Residual myometrial thickness (RMT) – is the thickness of the myometrium between the apex of the scar and the overlying serosa taken in the sagittal section of the uterus.
There is no uniform definition for a large scar. Some consider a large scar to be one where there is a loss of more than 50 % of the myometrial thickness at the scar (RMT/thickness of adjacent myometrium) or an RMT of less than or equal to 2.2 mm on TVS (Osser UOG 2010). The thinner the residual myometrium, the higher is the chance of scar dehiscence; however, no cut-off has been established yet.
The axis of the cervical canal to the axis of the uterine cavity should also be noted, as patients with retroflexed uterus are more likely to be symptomatic with postmenstrual spotting.
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