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Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3860_Библиотеки_им_академика_М_И_Перельмана

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M. E. Rackson
Providing access for stone removal before PNL
Renal calculus disease requires the most specific ap­proach to PCN. The particular calyx that must be punc­tured varies with the size, location, and number of stones; more than one tract may be necessary. It is of paramount importance to discuss the case with the referring urologist to agree on the optimum approach as well as a backup plan. After the system has been accessed and the tract is dilated to 28 to 32 Fr, the urologist will insert a large-bore rigid working sheath into the tract. An endoscope will be placed through this sheath to visualize and extract the stones. If the angle between the endoscope and the stones is too acute or the tract is too long, the likely outcome is hours of operative frustration and an unsuccessful stone retrieval. Complications such as parenchymal damage due to overtorquing the kidney or renal pelvic lacerations and bleeding are also possible.
The other issue to decide at the initial consultation with the referring urologist is whether the urologist should place a retrograde ureteral occlusion balloon prior to PCN. This balloon can be used to distend the renal pelvis and calyces, facilitating PCN manipulations in nonobstructed systems or collecting systems with a large stone burden. Of course, this step entails an addi­tional procedure for the patient.
After the collecting system is accessed, a catheter should be manipulated down the ureter and into the bladder to ensure that access to the collecting system will not be lost during manipulations involving tract dilation, sheath, or endoscope insertion. Either a 5 Fr catheter that accepts a 0.038-inch guidewire can be placed into the bladder with an 8 Fr PCN left alongside it for drainage, or a nephroureteral stent can be inserted. If the radiolo­gist performs the tract dilation, preferably with a balloon catheter rather than serial dilators, a 28 Fr Foley is left in the collecting system and the patient is transferred to the operating room. In some institutions, the entire proce­dure, including stone extraction, is performed in the interventional suite, although to do so is usually imprac­tical because the second stage of the procedure ties up the suite for several hours and most interventional suites do not have the proper drainage systems to deal with the large amount of irrigation fluid used in nephrolithotomy procedures.
Access sites for various stones
Pelvic and posterior lower/midpole calculi are the sim­plest stones to access because the puncture is through a posterior or midpole calyx. For a pelvic stone, the punc­ture can be through any calyx that provides a good path to the stone. For a posterior or midpole calyx, direct punc­ture into the stone-bearing calyx should be performed.
The complex cases are those where staghorn calculi,
7,24–26
27
upper pole calculi, anterior calculi, or multiple calculi are present. Staghorn calculi are difficult because there may be branches into multiple calyces, which are difficult for the urologist to access from one puncture site. The larg­est stone containing posterior lower pole calyx should be punctured. Residual fragments may require a second puncture or a “Y” tract from the first puncture.
Upper pole stones are likely to be located above the costal margin, increasing the chances of pneumothorax or liver or spleen puncture with a puncture above the 12th rib. If no infundibular stenosis is present and the stone is small, a posterior lower pole calyx can be punc­tured and a flexible endoscope can be directed upward into the calyx. If the stone is large or there is an in­fundibular stenosis, a direct puncture into the upper pole calyx will be necessary.
Anterior calyceal stones, multiple calculi, and other complex situations require careful analysis and will be challenging even to experienced operators. Puncture into a posterior upper pole calyx generally provides ac­cess into all calyceal stone sites. Many other approaches are possible, however, and the access site must be tailored to the individual situation. The reader is referred to an advanced text for additional reading on this subject.
28
■ Troubleshooting
Most problems with nephrostomy tubes ultimately re­quire a tube change in the department and cannot be resolved at the bedside or over the telephone. The most common problems are occlusion of the tube, which re­quires a tube change, and inadvertent removal or dis­lodgement of the tube, which requires that the tube be reinserted or repositioned. At the least, the tube needs to be evaluated by a contrast nephrostogram or “tube check.” The following are commonly encountered prob­lems.
• The PCN tube is not draining: The tube is either occluded or dislodged. The tubes are made of kink­resistant material; so external kinking of the tube occurs infrequently. The tube may not even be a PCN but is an NU tube that is draining the urine antegrade (see next item).
• The NU tube is not draining: The tube is either occluded or the urine is draining antegrade into the bladder. If the tube check demonstrates that the tube is patent and the patient is urinating without difficulty, then the external portion of the tube can be capped off because the external drainage bag is unnecessary.
• The NU tube is draining externally, but the patient is not urinating: Either the internal ureteral portion of the stent is occluded while the PCN external por-
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tion is patent, or there is a bladder outlet obstruction with reflux or urine from the bladder up and out of the external portion of the tube. This situation could apply to a patient who has either one or two NU tubes. The tube also could be dislodged, but this is less likely to happen because long NU tubes are anchored more firmly than short PCN tubes.
• Urine is leaking around the tube: The tube is either occluded or dislodged, and urine is leaking along­side the tube through the tract to soak the dressing or clothing. The external portion of the tube also could be cracked or punctured. In this situation, the skin around the tube should be dry. Another possi­bility is that the pigtail retention suture on the Medi­tech tube was not cut short enough, thereby exiting the hub of the tube and getting caught in the Luer lock between the PCN tube and the connecting tube to the drainage bag, which will cause a urine leak.
• The tube is completely or partially dislodged: If the tube is partially dislodged, injecting the tube usually will opacify the tract and the collecting system. The tube should be removed carefully over a guidewire and replaced with a 5 Fr catheter. Further contrast injections should opacify the tract. Then the cathe­ter can be advanced back into the collecting system over a floppy-tipped guidewire (Bentson) or a hy­drophilic guidewire (Glidewire) and the tube re­placed. If the tube has been removed completely, the chance of reinserting it through the same tract is best if urine is still leaking out of the tract. Local anesthesia should not be administered because to do so will cause the soft tissue to swell and compress the tract. The key to recannulating the tract is to opacify it with a contrast injection at the dermatotomy site through a vessel dilator, short directional catheter, or Christmas tree adapter, followed by advancement of the catheter over a guidewire back into the collect­ing system. Failure will necessitate a new puncture, which may convert an outpatient to an inpatient or at least require a longer period of observation before discharge.
• Bloody drainage is extremely common. Even a single­stick atraumatic nephrostomy procedure can cause pink urine, which usually clears within hours. Grossly bloody urine often is seen after procedures requiring multiple punctures. If blood pulses out of the tract while the tract is being dilated, a large catheter should be inserted to tamponade the tract. The blood gener­ally clears in a few days, particularly with repeated flushing of the tube to ensure that it does not clot. If the urine fails to clear or the hematocrit drops, the tube should be exchanged for a larger tube to tam­ponade the tract. Larger tubes usually control the bleeding, although sometimes a segmental renal ar­tery needs to be embolized.
29,30
■ Outpatients
We routinely perform the following procedures on outpa­tients: PCN and NU tube changes and conversion of PCN to NU or double J stents. We also schedule initial PCN procedures on selected outpatients with the provision that the patient will be admitted if a complication occurs or if the patient is too drowsy to go home.
31
Routine tube changes can be performed every 3 months. The patient should be encouraged to drink a lot of fluids to dilute the urine, which will help prevent tube occlusion by urine sediment. Most nephrostomy tubes do not need to be flushed routinely.
All outpatients should have the phone number and names of the physicians and nurses in the interventional radiology department where the tube was placed. They should be encouraged to call if they experience any signs of blockage of the tube or infection such as fever, chills, flank pain, or leakage around the tube. Patients with capped tubes should reattach them to external drainage bags until they arrive in the department for a tube change and possible antibiotic therapy.
Patients with skin infections around the tube also should contact the department. Many skin infections will resolve within 48 hr with increased home care. Those that do not resolve will need formal evaluation and possible antibiotic therapy.
32,33
REFERENCES
1. Lang EK, Price ET. Redefinitions of indications for percutaneous nephrostomy. Radiology 1983;147:419–426.
2. Barbaric ZL. Percutaneous nephrostomy for urinar y tract obstruc­tion. AJR, Am J Roentgenol 1984;143:803–809.
3. Reznek RK, Talner LB. Percutaneous nephrostomy. Radiol Clin North Am 1984;22:393–406.
4. Keidan RD, Greenberg RE, Hoffman JP, et al. Is PCN for hydro­nephrosis appropriate in patients with advanced cancer? Am J Surg 1988;156:206–208.
5. Watkinson AF, A’Hern RP, Jones A, et al. Role of percutaneous nephrostomy in malignant urinary tract obstruction. Clin Radiol 1993;47:32–35.
6. Yoder IC, Lindfors KK, Pfister RC. Diagnosis and treatment of pyonephrosis. Radiol Clin North Am 1984;2:407–414.
7. Castaneda-Zuniga WR, Clayman R, Smith A, et al. Nephrostoli­thotomy: percutaneous technique for urinary calculus removal. AJR Am J Roentgenol 1982;139:721–726.
8. Matalon TAS, Thompson MJ, Patel SK, et al. Percutaneous treat­ment of urine leaks in renal transplantation patients. Radiology 1990;174:1049–1051.
9. Bell DA, Rose SC, Starr NK, et al. Percutaneous nephrostomy for nonoperative management of fungal urinary tract infections. J Vasc Interv Radiol 1993;4:311–315.
10. Whitaker RH, Chir M. The Whitaker test. Urol Clin North Am 1979;6:529–539.
11. Naidich JB, Rackson ME, Mossey RT, et al. Non-dilated obstructive uropathy: percutaneous nephrostomy performed for severe renal failure. Radiology 1986;160:653–657.
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12. Lee WJ, Patel V, Patel S, et al. Emergency PCN: results and compli­cations. J Vasc Interv Radiol 1994;5:135–139.
13. Babel SG, Winterkorn KG. Retrograde catheterization of the ureter without cystoscopic assistance. Radiology 1993;187:547–549.
14. Clayman RV. Nephrolithotomy (nephrostolithotomy): concepts and rationale. Semin Intervent Radiol 1984;1:75–78.
15. Dunnick NR, Carson CC III, Moore AV, et al. Percutaneous ap­proach to nephrolithiasis. AJR Am J Roentgenol 1985;144:451–455.
16. Stables DP. Percutaneous nephrostomy: techniques, indications, and results. Urol Clin North Am 1982;9:15–29.
17. Papanicolaou N. Renal anatomy relevant to percutaneous interven­tions. Semin Intervent Radiol 1995;12:163–172.
18. Lang EK. Percutaneous management of ureteral strictures. Semin Interv Radiol 1987;4:79–89.
19. Cardella JF, Castaneda-Zuniga WR, Hunter DW. Long term ureteral stenting: techniques and effectiveness. Radiology 1986;161:313–318.
20. Salzman B. Ureteral stents: indications, variations and complica­tions. Urol Clin North Am 1988;15:481–491.
21. Rackson ME, Mitty HA, Dan SJ, et al. Elevated bladder pressure: a cause of apparent ureteral stent failure. AJR Am J Roentgenol 1988;151:335–336.
22. de Baerre T, Denys A, Pappas P, et al. Ureteral stents: exchange under fluoroscopic control as an effective alternative to cystoscopy. Radiology 1994;190;887–889.
23. Mitty HA, Train JS, Dan SJ. Placement of ureteral stents by ante­grade and retrograde techniques. Radiol Clin North Am 1986;24: 587–600.
24. Lee WJ, Smith AD, Cubelli V, et al. Percutaneous nephrolithotomy: analysis of 500 consecutive cases. Urol Radiol 1986;8:61–66.
25. LeRoy AJ, May GR, Bender CE, et al. Percutaneous nephrostomy for stone removal. Radiology 1984;151:607–612.
26. Clayman RV, Surya V, Miller RP, et al. Percutaneous nephroli­thotomy: extraction of renal and ureteral calculi from 100 patients. J Urol 1984;131:868–871.
27. Bjarnason H, Ferral H, Stackhouse DJ, et al. Complications related to percutaneous nephrolithotomy. Semin Interv Radiol 1994;11: 213–225.
28. Castaneda-Zuniga WR, Tadavarthy SM, Hunter DW, et al. Interven­tional uroradiology. In: Castaneda-Zuniga WR, Tadavarthy SM, eds. Interventional radiology, 2nd ed, vol 2. Baltimore: Williams & Wilkins, 1992:777–989.
29. Ferral H, Stackhaus DJ, Bjarnason H, et al. Complications of percu­taneous nephrostomy tube placement. Semin Interv Radiol 1994; 11:198–206.
30. Cope C. Zeit RM. Pseudoaneurvsms after nephrostomy. AJR Am J Roentgenol 1982;139:255–261.
31. Cochran ST, Barbaric ZL, Lee JJ, et al. Percutaneous nephrostomy tube placement: an outpatient procedure? Radiology 1991:179: 843–847.
32. Cronan JJ, Horn DL, Marcello A, et al. Antibiotics and nephrostomy tube care: preliminary observations. Part II. Bacteriuria. Radiology 1989;172:1043–1045.
33. Nephrostomy catheter care. Informational pamphlet for patients dis­tributed by SCVIR, Fairfax, VA, 1992.
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Pelvic and Obstetric Hemorrhage
ANDREW KERR
Life-threatening pelvic hemorrhage may result from blunt or penetrating trauma, pregnancy, malignancy, or arterial venous malformation. The pelvis is supplied by an extensive network of collateral vessels. Consequently, surgical ligation of the hypogastric artery origins has minimal effect on bleeding. Operative exposure and li­gation of the bleeding distal hypogastric artery branches are a technical nightmare. toneum to find the hypogastric artery origins at laparo­tomy often exacerbates bleeding by removing compres­sion of the bleeding site provided by adjacent anatomic structures. Because of technical difficulties posed by the surgical approach, angiographic embolization is the treatment of choice for pelvic arterial hemorrhage. Em­bolic materials released into the internal iliac artery are carried by the bloodstream to occlude the artery beyond the larger collaterals. The arterial pressure at the bleeding site then decreases sufficiently to permit hemo­stasis.
■ Trauma
1
Dissection of the retroperi-
Approach to the patient with pelvic fractures and shock: Stop the bleeding!
The patient with life-threatening pelvic hemorrhage may be in florid shock or may not appear to be seriously injured at all when he or she is brought to the emer­gency department. Sometimes, flank and buttock hema­tomas are present. Displaced pelvic fractures may cause obvious leg-length discrepancies, visible. Blood pressure may be normal; baseline blood
2
or no injuries may be
pressure varies from individual to individual. An adult can lose 30% of the blood volume acutely before systolic pressure begins to drop (although it then drops rapidly). Initially, the hematocrit is likely to be normal because it takes hours of equilibration with extravascular fluids be­fore the serum hematocrit reflects an acute blood loss. Initially, the only abnormalities that may be observed are tachycardia (pulse ⬎ 100/min), tachypnea, coolness of the skin caused by peripheral vasoconstriction, a nar­rowed pulse pressure (actually an elevated diastolic pres­sure caused by catecholamine release), and low urine output. If the trauma patient has signs of shock after intravenous infusion of 2 L of fluid, it is most likely the consequence of active internal bleeding. mortality from pelvic fractures is 6 to 19%, and half of these deaths are from hemorrhage and the others from associated injuries. If tachycardia is attributed to pain from pelvic fractures, the diagnosis of shock may not be made until systolic blood pressure falls. The mortality rate rises to 50% when hypotension is present. tensive patients are treated with large volumes of intra­venous crystalloid solution and packed red blood cells. If platelets and plasma are not infused as well, a dilu­tional coagulopathy develops. If the intravenous solu­tions are not warmed, the patient may become hypother­mic. Hypothermia interferes with normal coagulation. Consequently, fluid resuscitation for hypotension may worsen the bleeding. Patients who are hypotensive for prolonged periods often develop multiple organ-system failure and sepsis. site of bleeding and to stop it before the patient’s con­dition deteriorates.
The trauma patient with active hemorrhage usually
6
Therefore, it is essential to find the
3
The overall
4
Hypo-
5
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arrives in the emergency department with little clinical history but with many injuries. Complete evaluation of the patient requires numerous diagnostic tests. If the patient is to be saved, the sequence of tests must be prioritized so that potentially lethal injuries are ad­dressed first and less dangerous (although frequently more obvious) injuries are evaluated later. The workup must proceed rapidly despite the fact that the patient may be hemodynamically unstable. Resuscitation and evaluation must take place simultaneously. Suspending the workup so that the patient can be “tuned-up” first will delay the time when a surgical or interventional pro­cedure can be performed to stop the bleeding. Often, it is necessary to institute therapeutic procedures based on a probable diagnosis before a complete clinical picture is available.
7,8
Diagnostic peritoneal lavage
The pelvic fracture patient with a patent airway in whom hemothorax, pneumothorax, cardiac contusion, and pericardial tamponade have been ruled out who shows signs of shock after vigorous intravenous fluid infusion is presumed to be actively bleeding. Supraumbilical diag­nostic peritoneal lavage then is performed. If gross blood is found at lavage, it is likely that the bleeding emanates from a ruptured intraperitoneal organ (usually spleen or liver). The patient is taken for laparotomy. If the lavage does not reveal gross blood or if the patient remains unstable after laparotomy, ongoing retroperi­toneal hemorrhage is probable. The patient then under­goes diagnostic pelvic angiography and possible emboli-
9
zation.
bones and is more fragile than the pelvic arteries (Fig. 25-2). The venous bed is a low-pressure, but high-capac­ity, structure. The pelvic veins are valveless and are there­fore in open communication with the inferior vena cava, and they are also in open communication with the portal vein via the superior rectal vein. In dogs simultaneous ligation of the lumbar arteries, inferior mesenteric ar­tery, medial sacral artery, right and left hypogastric, ex­ternal iliac, and profunda femoral arteries had no effect on pelvic venous pressure.
14
Pelvic venous bleeding is stopped by the tamponade (compression) effect of sur­rounding structures. An unstable pelvic fracture (par­ticularly of the open-book type) can greatly increase the potential volume of venous hemorrhage. A 3-cm diastasis of the pubic symphysis will increase the potential volume of the pelvis from the normal 4 L to 8 L.
15
Realigning the fractured and displaced bones by placement of ex­ternal fixators is an orthopedic procedure performed to control venous bleeding. External fixation is helpful when there is a diastasis of the pubic symphysis. It de­creases the potential space in which bleeding can take place and aids coagulation by preventing the fracture fragments from moving in relation to each other. Angiographic embolization and external fixation treat different types of bleeding. External fixation controls osseous and venous bleeding but not arterial bleeding. Angiographic embolization controls arterial but not ve­nous bleeding. At present, it is not possible to know initially whether a pelvic fracture patient is bleeding pri­marily from an arterial or a venous source; thus, which procedure should be performed first is a subject of con­troversy.
2
Angiography and embolization
Hemorrhage from branches of the internal iliac artery requiring embolization occurs in 7 to 11% of patients with pelvic fractures.
10
The most commonly injured ar­teries are the superior gluteal, iliolumbar, and lateral sacral (associated with sacral fracture and sacroiliac joint disruption), and the internal pudendal and the obtura­tor arteries (associated with pubic ramus and acetabular fractures) (Fig. 25-1).
11
Transcatheter embolization is successful in treating pelvic arterial hemorrhage in 85 to 90% of cases.
6,12,13
There is great potential for cross-pel­vic collateralization via anterior and posterior division branches of the internal iliac arteries. Therefore, selective injections of both internal iliac arteries should be performed, and bilateral embolization is often nec­essary.
External fixation
Venous bleeding is common after pelvic fractures. An extensive venous plexus exists adjacent to the pelvic
■ Indications for Other Radiographic
Studies in the Pelvic Fracture Patient
Plain films
The only radiographs that an unstable blunt trauma pa­tient should have are cervical spine, anteroposterior (AP) chest, and AP abdomen. of the potentially lethal injuries that can be visualized by plain films. The patient may well have obvious extremity fractures and facial lacerations. Evaluation and treatment of these must wait until life-threatening injuries have been treated or ruled out. Foley et al. trauma patients who bled to death of ruptured spleens while plain films were being obtained in the emergency department.
Computed tomography scanning
Trauma patients with neurosurgical emergencies requir­ing immediate evacuation of intracranial hematomas usually present with one or more of the following: hy-
3
These studies will identify most
16
reported on four
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Superior Gluteal
FIGURE 25-1. Internal iliac artery branches vulnerable to pelvic fractures. The superior gluteal and internal pudendal arteries
are most commonly affected.
Internal Pudendal
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thoracic aortography and pelvic angiography should be performed.
10
Uroradiographic studies
A patient in shock must have a catheter to drain the bladder and to measure urine output. Urethral injury in females is rare. If a male with pelvic trauma is unable to void, has blood at the meatus, has a prostate that is high riding or is not palpable, or has a scrotal hematoma, he may have sustained a urethral injury. To avoid converting a partial urethral tear to a complete transection, ure­thrography should be performed before a Foley catheter is placed. thrography, cystography, or intravenous urography for two reasons: First, time is better spent stopping the bleed­ing than performing studies to evaluate injuries that are not life threatening; second, contrast that extravasates from an injured bladder may render pelvic angiography uninterpretable. Patients in shock who may have urethral injury and have an easily palpable bladder should have a suprapubic cystostomy placed at the bedside, which can be performed quickly and without contrast and is thera­peutic. Many of these patients will require elective repair of urethral strictures after the urethral injury has healed.
17
A patient in shock should not undergo ure-
18
FIGURE 25-2. Pelvic venous plexus and collateral pathways.
pertension (not shock), bradycardia (not tachycardia), altered mental status (Glasgow coma scale of 8 or less), a dilated pupil on the side of the intracranial bleeding, and a peripheral neurological deficit on the side oppo­site the injury. For these patients, immediate computed tomography (CT) scan of the head is indicated.
3
Chest and body CT scanning is appropriate for evalu­ation of the hemodynamically stable trauma patient but in general should not be performed on the patient in shock. Oral contrast should not be used when there is a possibility that angiography may follow CT scanning. In the unstable patient with pelvic fractures and when find­ings on the chest film suggest great vessel injury, both
■ Obstetric Hemorrhage
Bleeding in excess of 1 L occurs in 1 to 2% of deliver-
19
ies;
11 to 13% of pregnancy-related maternal deaths in the United States are caused directly by hemorrhage, averaging 53 maternal deaths from bleeding each year. The pregnant uterus is extremely vascular. It is perfused by the uterine branches of the internal iliac arteries as well as by the ovarian arteries, which in most cases origi­nate from the abdominal aorta (Fig. 25-3). The ovarian arteries may arise from the renal, iliac, lumbar, or adre­nal arteries.
21
The collateral blood supply to the uterus is excellent. Fatal obstetric hemorrhage can take place within minutes. Bilateral hypogastric artery ligation is successful in curtailing hemorrhage only 50% of the time. Bilateral uterine artery ligation is successful 95% of the time.
19
Packing the uterus with gauze when co­agulopathy is present and even hysterectomy occasion­ally fails to stop uterine hemorrhage. When medical management fails, angiographic embolization in many cases can obviate laparotomy and may preser ve fertility by making hysterectomy unnecessary.
22–26
When a pa­tient is considered at high risk for postpartum bleeding, an angiographic catheter can be placed into the aorta through a left axillary approach while a lead apron shields the pelvis before the patient is taken to the op­erating room for cesarian section. Then intraoperative
20
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FIGURE 25-3. Arterial anatomy of the female reproductive organs.
embolization can be performed using C-arm fluoroscopy if hemorrhage is severe. the full-term uterus are extremely vascular structures, embolization to stop bleeding from a postpartum uterus or from an ectopic placenta frequently requires far larger quantities of Gelfoam than needed to control posttraumatic hemorrhage. Obstetric hemorrhage may be caused by bleeding from the placental implantation site, by trauma during delivery, or by the HELLP (hemolysis, elevated liver enzymes, and low platelet count) syndrome.
26,27
Because the placenta and
Bleeding from the site of placental implantation
The arterial flow to the placenta at term is approximately 600 mL/min. the vessels connecting the uterus to the placenta are torn. Approximately 500 mL of blood is usually lost at this time. Contractions of the uterus occlude the disrupted vessels. If part of the placenta remains adherent to the uterus, bleeding will continue until the residual placenta is re­moved. If the uterus does not contract after delivery
20
When the placenta is expelled at delivery,
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(atonic uterus), bleeding will persist. Atonic uterus usually responds to administration of oxytocin or, if this fails, to prostaglandin (15-methyl prostaglandin F
).19If the pla-
2a
centa attaches to the myometrium instead of to the en­dometrial decidua, it is called placenta accreta; if it invades deeply into the myometrium, placenta increta; and if it extends through the uterus and sometimes into adjacent organs, termed placenta percreta. Massive postpartum hem­orrhage is probable in these situations because the abnor­mal placenta will not separate from the uterus at delivery. If the placenta separates from the uterus before labor begins (placental abruption), severe bleeding may occur and frequently is exacerbated by a coagulopathy caused by substances released by the placenta. Placental abrup­tion associated with fetal distress or with continuing hem­orrhage is treated by delivery of the fetus. If the placenta is near or covers the cervix (placenta previa), massive bleeding is likely to occur when labor begins. Placenta previa is detected by prenatal ultrasound. The patient is then delivered by cesarean section before labor begins.
In ectopic pregnancy, the placenta attaches and devel­ops outside the uterus. Most commonly, the fetus devel­ops in a fallopian tube (tubal pregnancy). Less commonly, the fetus may develop in the peritoneal cavity (abdominal pregnancy) or in the uterine cervix (cer vical pregnancy). The ectopicgestation will establish bloodvessels to nearby structures. These abnormal placental attachments may separate partially, causing massive hemorrhage. When an advanced abdominal or cervical pregnancy is removed at laparotomy, massive hemorrhage frequently occurs when the placenta is dissected from its abnormal insertion site. When preoperative embolization of the placenta is per­formed, operative blood loss is usually minimal. Gelfoam embolization should be performed less than 24 h before surgery because the vessels perfusing the ectopic gesta­tion recanalize rapidly.
27,28
oping during pregnancy. When seizures are also present, the condition is termed eclampsia. Approximately 10% of severely preeclamptic patients and 30 to 50% of eclamp­tic patients develop the HELLP syndrome. The cause of these disorders is unknown, but current research suggests that it may be an as yet unidentified toxic substance produced by the placenta. The placental toxin theory is supported by the fact that the disease resolves only after delivery of the fetus and placenta. Further, recovery has been more rapid in some patients treated with postpar­tum uterine curettage, plasma exchange, or steroids. Patients with the HELLP syndrome develop disseminated intravascular coagulation (DIC). Liver infarction and in­trahepatic hematoma formation are also common. After infarction, the affected portions of the liver sometimes rupture following minimal trauma or during labor. Liver rupture in the presence of coagulopathy is associated with massive intraperitoneal hemorrhage. If hepatic in­farction or subcapsular hemorrhage is not associated with rupture of the liver capsule, the patient may be treated without surgery. Patients with intraperitoneal hemor­rhage from liver rupture are treated with surgical packing at the rupture site and drainage of the intraperitoneal hemorrhage; this controls the bleeding in most cases. One study reported an 82% survival rate following this procedure.
31
Transcatheter hepatic artery embolization is an alternative to laparotomy for treatment of intraperi­toneal hemorrhage from liver rupture in postpartum pa­tients who have the HELLP syndrome. Arteriography usually demonstrates an avascular area with stretching of adjacent hepatic artery branches and small pseudoaneu-
32,33
rysms.
Before hepatic artery embolization, arterial portography should be performed to show that there is adequate perfusion of the liver by the portal vein. Care must be taken during embolization to place the catheter distal to the cystic artery origin to avoid gallbladder in­farction.
30
Traumatic obstetric hemorrhage
Significant bleeding may occur from lacerations of the vagina caused by forceps delivery or by episiotomy. The uterus may bleed after spontaneous rupture during de­livery or after cesarean section. The hemorrhage may be per the vagina, or it may be into the retroperitoneum and consequently not visible. Intractable bleeding usu­ally is treated by hypogastric artery ligation, uterine ar­tery ligation, or hysterectomy. Successful treatment of these injuries by angiographic embolization has been reported.
29
Intraperitoneal hemorrhage associated with the HELLP syndrome
Preeclampsia, which occurs in 7% of pregnancies, is de­fined as hypertension associated with proteinuria devel-
■ Pelvic Malignancy
Successful control of pelvic hemorrhage has been re­ported in patients with intractable bleeding from pri­mary carcinoma of the cervix, uterus, and bladder as well as invasion of these organs by metastases. Bleeding from pelvic malignancy can be fatal; however, the rate of bleeding is often too slow to be demonstrated angiog­raphically. The tumor usually can be well delineated angiographically, by CT scan, or magnetic resonance im­aging. If continuing pelvic hemorrhage is clinically evi­dent from a known pelvic tumor, angiographic demon­stration of the bleeding site is not required before embolization.
Embolization of pelvic malignancy is a palliative proce-
dure that does not eradicate the tumor. Bilateral emboli-
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zation of the anterior divisions of the internal iliac arter­ies is necessary to minimize the risk of rebleeding. When an appropriate embolic agent is used, infarction of nor­mal structures is unlikely because the collateral blood supply remains from the superior hemorrhoidal, iliac circumflex, gonadal, and profunda femoral arteries.
When embolization is performed for traumatic or ob­stetrical bleeding, a temporar y occluding agent such as Gelfoam can be used because rapid healing is to be ex­pected at the bleeding site. Unfortunately, pelvic malig­nancy will persist after embolization. Consequently, a per­manent embolic agent must be used. Polyvinyl alcohol (PVA) 250-590 micron is the embolic agent of choice because it is permanent, it will occlude distal vessels, and yet it is not so small as to block the precapillary collateral
34,35
plexus.
■ Uterine Fibroids
Uterine fibroids are present in 20 to 40% of women older than 35 years of age. The standard treatment for sympto-
matic patients (bleeding, pain) is hysterectomy or myomectomy. Since 1995 interventional radiologists have reported successful treatment of fibroid related symp­toms by transcatheter embolization of the uterine arteries
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bilaterally (Fig. 25-4).
This causes infarction of fibroids
but not of normal uterine tissue.
The procedure is performed using particulate polyvi­nyl alcohol, (500–710 microns). Technical success is achieved in over 95% of patients. Early and midtern follow up demonstrates that 80–94% of patients have moderate or marked improvement in symptoms, and over 90% of these patients have significant reduction in fibroid and uterine size.
37–39
Complication rates appear
low. The effect on fertility is not yet known.
■ Pelvic Vascular Malformations
Vascular malformations are abnormal communications between arteries and veins. They are low-resistance path­ways for arterial blood (high pressure) to enter the ve­nous system (low pressure) without first perfusing nor-
A
D
B
FIGURE 25-4. Bilateral uterine artery embolization. A: Pelvic arteriogram demonstrates bilateral large tor-
tuous uterine arteries feeding hypervascular uterine fibroid. B: The left uterine artery has been selectively catheterized from the contralateral femoral approach. C: Superselective catheterization of the left uterine artery using a coaxial microcatheter system, prior to particulate PVA embolization. D: The right uterine ar­tery has been catheterized. Note the marked hyper­vascularity of the uterine fibroid. E: Following emboli- zation, there is marked decreased vascularity and
E
marked arterial stasis.
C