Renal Bruce L.
Artery
Dissections
Gewertz, MD; James C. Stanley, MD; William J. Fry,
MD
\s=b\ Renal artery dissections encountered in 15 patients, aged 3 to 75 years, were categorized as to pathogenesis (blunt abdominal trauma, catheter injury, and spontaneous). Blunt traumatic dissections (seven patients) were characterized by hypertension, gross hematuria, and pain. Catheter-induced dissections (four patients) were asymptomatic, although two exhibited accelerated hypertension. Spontaneous dissections (four patients) were all associated with preexistent arterial disease. Symptoms in these patients were uncommon, despite accelerated hypertension in three cases. Intravenous pyelography lacked specific diagnostic value for renal artery dissections. Early arteriographic examination proved essential in diagnosis and surgical treatment. Criteria for operative intervention included existence of technically correctable dissections causing (1) hemodynamically significant occlusions of the main or major segmental renal arteries, (2) documented renovascular hypertension, or (3) significant deterioration of renal function.
(Arch Surg 112:409-414, 1977)
renal artery dissections are rare. Severe hyper¬ or loss of a kidney often attend these lesions and justify continuing reappraisal of their cause and clinical importance. Many previous reports and collected series have detailed the pathologic process and difficult diagnostic problems associated with renal artery dissec¬ tion.1 --'' Unfortunately, uniformly poor results have been attributed to both expectant management and operative therapy of these lesions. Renal artery dissections affecting 15 patients encoun¬ tered at the University of Michigan Medical Center provide the basis for the present review. Categorization of dissections into subgroups according to cause proved important in defining the natural history of this disease entity. Specific subgroups identified included (1) dissec¬ tions subsequent to blunt abdominal trauma, (2) intralu¬ minal catheter-induced injuries, and (3) spontaneous dissections in arteriosclerotic or fibrodysplastic arteries. Aortic dissections involving renal vessels were excluded from study, as were macroaneurysms, pseudoaneurysms, minute intimai disruptions, and arterial thromboses not unequivocally associated with a dissecting process.
Isoltension ated
Accepted for publication Dec 8, 1976. From the Department of Surgery, University of Michigan Medical Center, Ann Arbor. Read before the 84th annual meeting of the Western Surgical Association, Coronado, Calif, Nov 15, 1976. Reprint requests to University Hospital, 1405 E Ann St, Ann Arbor MI 48109 (Dr Gewertz).
CLINICAL EXPERIENCE Renal artery dissections were documented among eight male and seven female patients, ranging in age from 3 to 75 years, treated at University Hospital from 1960 to 1976. Dissections were initially recognized by artériographie examination in all but one patient. In this latter case, arteriograms demonstrated an occluded renal artery that at the time of operation was discovered to be a typical dissection. The rarity of these lesions is emphasized in that only 15 patients harboring dissections were discovered during a time period when more than 11,000 abdominal arterio¬ grams were performed at our institution. Clinical characteristics of these patients are best defined in relation to underlying mechanisms responsible for the dissection.
Dissections
Secondary
to Blunt Abdominal Trauma
Four male and three female patients, with an average age of 24.4 years, exhibited renal artery dissections after sustaining severe abdominal trauma (Table 1). Motor vehicle accidents were responsible for five dissections, one followed a 20-foot fall, and another was the consequence of a boxing injury. Dissections affected right renal arteries in four patients, the left renal artery twice, and both vessels in one patient. Main renal arteries were the site of dissections in five instances; the remainder involved distal
branches.
Microscopic or gross hematuria and flank pain affected all patients with dissections due to abdominal trauma. Two patients had acute hypertension following injury, and in a third late blood pressure elevation developed. Three patients were initially hypotensive because of concomittant intra-abdominal injuries. Exclud¬ ing the boxing injury, dissections were recognized within 12 hours of hospitalization. Intravenous pyelograms were obtained in five patients. Absent, as well as delayed, nephrograms or evidence of renal contusions were observed in each instance. Artériographie studies confirmed the diagnosis of dissection in all patients. Immediate operative intervention was undertaken twice for traumatic lesions. Primary aortorenal bypass was successfully performed once. In the second case, a child with profound hypo¬ tension, nephrectomy was necessary. A third patient was treated by heminephrectomy for sustained hypertension secondary to segmental vessel occlusion four months after injury. A fourth patient underwent late operation for chronic hypertension. An unsuccessful attempt at reconstructing his severely injured renal artery eventuated in nephrectomy. This patient, who had bilateral disease with
a
limited dissection of the contralateral renal artery
(Fig 1, left), remains normotensive two years postoperatively. Three additional patients did not undergo surgical therapy. Two of these patients had clinically unimportant dissections. Multiple injuries of segmental vessels in a solitary kidney unamenable to conventional repair occurred in the third patient (Fig 1, right). Temporary hemodialysis was required for acute renal failure, with eventual return of normal renal function. Excluding the latter case, no patient with dissections caused by blunt trauma experi¬ enced compromise of renal function.
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Table 1.—Dissections
Patient/Age, yr/Sex 1/3/F
2/21/M
Mechanism of Injury Motor vehicle accident 20-foot fall
Secondary
Manifestations
Pain, hematuria,
hypotensive5 Pain, hematuria,
hypotensive
to Blunt Abdominal Trauma
Artériographie Findings Right main renal artery dissection Right main renal artery
Surgical Therapy Right nephrectomy
Normotensive, normal
None
Normotensive, normal
Results renal function
renal function
dissection
3/21/M
Motor vehicle accident
Pain, hematuria,
hypertensive (154/98 mm Hg),
Right segmental renal artery
None,
Left renal artery dissection
Left aortorenal
acute renal failure
4/21/F
Motor vehicle accident
Pain, hematuria,
hypotensive"
Normotensive, normal
hemodialysis (4 weeks)
dissection
branch of 2
Normotensive, normal renal function
saphenous vein graft
(cephalic
renal function
multiple renal arteries) 5/30/F
Motor vehicle accident
Pain, hematuria,
hypotensive"
Left main renal artery dissec¬
None
Right segmental renal artery
Right hemi¬ nephrectomy
Right segmental
Left
Normotensive, normal renal function
tion
6/35/M
Motor vehicle accident
Pain, hematuria,
hypertensive
dissection
7/40/M
Boxing
Pain, hematuria, hypertensive late (200/150 mm Hg)
dissection and left main renal
artery
nephrectomy
Normotensive with medication (130/90 mm Hg), normal renal function Normotensive, normal renal function
dissec¬
tion
"Hypotension
a
result of intra-abdominal
hemorrhage unrelated
to renal
artery dissection.
Fig 1 .—Dissections secondary to blunt abdominal trauma. Left, Limited, intramural dissection of proximal renal artery (arrow) attributed to boxing injury. Right, Infrarenal dissection (arrow) associated with severe parenchymal contusion in a solitary kidney. Both were treated nonoperatively. Dissections Secondary to Intraluminal Catheterizations In two male and two female patients, averaging 57.3 years in age, dissections developed following diagnostic catheter studies (Table 2). Severe antecedent renal artery disease affected each patient. Three exhibited arteriosclerotic renal artery disease, and the fourth had fibrodysplastic stenosis of this vessel. Préexistent hypertension became more severe after catheterization in two patients, resulting in early operative interventions. Successful aortorenal saphenous vein bypass was performed in one patient (Fig 2). Attempts to reconstruct the second patient's renal artery eventuated in nephrectomy. Renal function and blood pressure were normal in two patients treated nonoperatively. Pain and hematuria did not occur in any of these four patients.
Spontaneous
Dissections
Spontaneous dissections developed in two male patients with arteriosclerotic renal artery disease, and in two female patients with fibrodysplastic disease (Fig 3). All but one patient were hypertensive (Table 3). Gross or microscopic hematuria were not apparent in this group. One patient experienced flank pain. Arterial reconstructions were attempted twice; this was successful on one occasion and lead to a nephrectomy in the other. Primary nephrectomy was performed in an additional patient early in our experience. The remaining patient with a limited dissection, normal renal function, and blood pressure was treated conserva¬
tively.
COMMENT
Since the first
angiographie demonstration
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of
a
renal
Table 2.—Intraluminal Catheter-Induced Dissections* Associated Renal Manifestations
Patient/Age, yr/Sex 1/34/F
2/58/M
hypertension (200/130 mm Hg)
Accelerated
Accelerated
(220/120 3/62/F
hypertension Hg)
mm
None
Left main renal dissection
Arteriosclerosis
Left main renal
(bilateral) Arteriosclerosis
(unilateral) 4/75/M
None
Arteriosclerosis
(unilateral)
Surgical Therapy
Artériographie Findings
Artery Pathology Fibrodysplasia (bilateral)
Results
Left aortorenal
Normotensive.
saphenous vein graft Left nephrectomy
normal renal function Persistent
Right
hypertension Normotensive, Right nephrectomy normal renal for hypernephroma
Left main renal
None
Normotensive,
artery dissection main renal artery dissection, right hypernephroma
function
artery dissection
normal renal function
"Selective artériographie catheterizations.
Fig 2.—Left, Artériographie catheter-induced dissection (arrow) in fibrodysplastic renal artery. Right, postoperative appearance of arterial reconstruction using autogenous saphenous aortorenal vein graft.
artery dissection in 1956,' these lesions have been discov¬ ered with increasing frequency. Clinical reports continue to be anecdotal, with cumulative experiences from any one
institution exceeding ten patients being nonexistent. Criteria for radiologie diagnosis of renal artery dissections have been previously published,7 and include: (1) luminal irregularities with aneurysmal dilation or saccular dissec¬ tions associated with segmental stenoses, (2) predilection of dissection to extend distally to the first renal artery bifurcation, (3) "cuffing" at branchings, and (4) variable degrees of reversibility documented by subsequent artériographie studies. Common usage resulted in many dissections being referred to as dissecting aneurysms. This misnomer persists despite the occlusive nature of most renal artery dissections. Clinical manifestation of renal artery dissections are invariably associated with the consequences of renal ischemia. Renal infarction, compromised renal function, and renovascular hypertension are the most common
complications of dissections. These events are not inevitable. Certain dissections may be self-limited and of no functional importance. Contributing factors to dissections vary with different injuries or arterial diseases responsible for these lesions. The tendency for renal artery dissections to extend is less than that noted in dissections of the thoracic aorta. Blood viscosity, shearing forces, and flow turbulence are involved in the propagation of all dissections, but the single most important hemodynamic force relates to the first deriva¬ tive of aortic pressure curves (the slope of the pulse wave, dp/dt).-- -' As aortic pressure waves progress down the aorta to the renal artery level, dp/dt is diminished.-1 This natural damping phenomenon supports an assumption that hemodynamic forces implicated in proximal aortic dissec¬ tions are less important in renal artery dissections. Renal artery trauma or loss of structural integrity due to antesevere
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Table
3.—Spontaneous
Renal
Patient/Age, yr/Sex 1/34/F
2/35/M
Artery Pathology Fibrodysplasla (bilateral)
Manifestations Accelerated
Arteriosclerosis
Accelerated
(bilateral) 3/39/F
4/61/M
Flbrodysplasia (unilateral) Arteriosclerosis
Dissections
Left main renal dissection
Left aortorenal
Left
vein graft Left nephrectomy
hypertension (210/110 mm Hg)
hypertension
(210/120 mm Hg) Pain, accelerated
hypertension (200/100 mm Hg) None
(unilateral)
Surgical Therapy
Artériographie Findings
saphenous
segmental renal artery dissection
Results Normotensive with medications
(140/85
macroaneurysm) Right segmental renal
Hg)
with medications
(110/85 Left main renal artery dissection (associated
mm
Normotensive
Left
nephrectomy
mm
Hg)
Normotensive, normal renal function
None
artery dissection
Normotensive, normal renal function
Blunt Trauma and Dissections
Fig 3.—Spontaneous dissection (arrow) causing near total occlu¬ sion of distal main renal artery in patient exhibiting accelerated hypertension.
cèdent disease may influence propagation of dissections more than other variables. Conservation of renal parenchymal tissue is of utmost importance in patients exhibiting spontaneous dissections, or in those with préexistent renovascular disease and catheter-induced dissections. Renal artery disease involv¬ ing the contralateral kidney was noted among four of our eight patients having dissections unrelated to blunt abdominal trauma. Casual nephrectomies for dissections are unacceptable. Although certain dissections are not amenable to any form of operative treatment, recent advances in surgical technique17 -:> should improve dismal salvage rates described in the current literature. Arterial reconstruction utilizing autogenous saphenous vein is preferred, with ex vivo repairs being appropriate in selected cases.
Two mechanisms have been alluded to in explaining renal artery injuries following blunt abdominal trauma. The first relates to a deceleration phenomenon of rela¬ tively mobile kidneys.-628 Sudden anterior displacement of the kidney may generate marked tension within the vascular pedicle. Subsequent fracture of the least elastic tissue, the intima, predisposes in subintimai dissection. A second mechanism involves direct vessel wall contusion against unyielding vertebral bodies.1" Intimai injury and hemorrhage within the media following rupture of vasa vasorum may initiate certain traumatic dissections. Trau¬ matic thromboses, often secondary to subintimai dissec¬ tions, have been reported to involve the left renal artery much more frequently than the right.'7·-"'10 Considering the lesser mobility of the left kidney and its shorter vascular pedicle, the predilection for left-sided thromboses is poorly explained by the aforementioned mechanisms. Data from the present experience and that of others11" does not support the tenet that left renal arteries are more favored sites for dissections.'" Hematuria is very common in patients with dissections secondary to blunt trauma. All of our patients exhibited this finding. Most instances of hematuria appear second¬ ary to renal parenchymal contusion, and not the arterial injury per se." Abnormal intravenous pyelograms are common in patients with traumatic renal artery dissec¬ tions.'- Pyelography is exceedingly nonspecific for renal trauma, and does not provide adequate information for assessing the presence or absence of traumatic renovascular lesions." Standard artériographie examinations in stable patients, or intraoperative studies in selected patients, provide the most reliable diagnostic information regarding dissections.2Si4",ä Emergent primary arterial reconstructions are recom¬ mended in patients having technically correctable dissec¬ tions secondary to blunt abdominal trauma if occlusion of the main renal artery or a major segmental branch is recognized, as well as when hypertension persists or renal function deteriorates following functionally significant injury. Early recognition of dissections and expeditious repair are often essential in preventing irreversible renal damage. Although ex vivo renal artery repair and autotransplantation has been employed for renal artery recon¬ struction at our institution, we have not had a recent
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opportunity
to utilize such a procedure for treatment of traumatic dissections. Ex vivo repair appears uniquely suited to the extensive pedicle injuries associated with arterial dissections.25-36-38
Angiographie Catheter-Induced
Dissections
The incidence of renal artery dissections occurring course of arteriography has been poorly docu¬ mented in the literature. Selective renal artery catheteri¬ zations are more likely to result in dissections than flush aortography. The rarity of this complication is confirmed by our experience, in which only four renal artery catheter dissections were encountered in more than 11,000 abdom¬ inal artériographie examinations, including approximately 2,200 selective renal arteriograms. Occurrence of these dissections is unquestionably related to underlying renovascular disease.7 Dissections are more likely to occur in vessels manifesting advanced arterioscle¬ rosis. Infrequent occurrence of catheter-induced dissec¬ tions in patients with fibrodysplasia suggests that medial alterations, even when associated with severe stenosis, do not predispose to such injuries. Most catheter-induced dissections are probably clinically covert. Pain and hematuria did not occur in our experience, and usually occurs only when extensive lesions cause near or complete occlusion of vessels and renal infarction. It is probable that many small dissections, such as intimai flaps, pass unrecognized. Greatest problems revolve around those instances where dissections cause ischemia severe enough to produce secondary hypertension or compromise renal function. These silent complications may persist until more serious sequelae ensue. Indications for operation in patients having renal artery dissections secondary to cath¬ eter injuries are identical to those of blunt traumatic dissections.
during the
Spontaneous
Dissections
Renal arteries are the most common site of primary dissections involving peripheral vessels.3 These lesions may be associated with coexisting macroaneurysms, arterial fibrodysplasia, arteriosclerosis, and medial necrosis.2·813·38 Nearly a 9% incidence of dissections in patients with fibrodysplastic renal arteries has been observed by others.8 Recent experience at our institution with more than 200 cases of renal artery fibrodysplasia in no way suggests these lesions to be so common. Differences in defining dissections and interpreting artériographie or histologie studies may account for discrepancies in these two experi¬ ences.4"
The pathogenesis of spontaneous renal artery dissec¬ tions is poorly understood. Necropsy studies usually demonstrate dissections extending within the outer media adjacent to the external elastic lamina, and less commonly within the more central media."·1"·-1 Only half these dissec-
tions may actually communicate with the vessel lumen.7 In obvious contradistinction are traumatic dissections, which usually originate from the lumen, extending along subintimal and inner medial tissue planes. Spontaneous renal artery dissections generally affect proximal vessels. Although intrinsic properties of an artery may account for this occurrence, physiologic mechanisms related to blood flow may predispose this site to dissec¬ tions. This may be of particular importance in arteries exhibiting multiple fibrodysplastic stenoses. Damping of steep systolic pressure waves has been documented in models of repetitive saccular dilations and stenoses com¬ parable to arterial fibrodysplasia.41 In another investiga¬ tion, diminutions of mean perfusion pressures have been documented beyond a series of subcriticai stenoses simula¬ ting fibrodysplastic disease.1- Both phenomena may account for limited distal propagation of mural dissec¬ tions. Spontaneous peripheral arterial dissections have been attributed to abnormalities involving vasa vasorum.,;l Hemorrhage may result from rupture of vasa vasorum. Subsequent intramural hematoma may increase medial ischemia and further compromise vessel wall integrity. Sustained arterial blood pressure elevations may contrib¬ ute to the development of renal artery dissections by potentiating arteriosclerosis and medial degeneration. It has not been proved that hypertension represents an initiating factor in dissecting aneurysms of muscular arteries." To the contrary, hypertension secondary to an occluding dissection causing renal ischemia is a more tenable explanation for coexisting elevations in blood pressure. Pain and hematuria have been described in patients with
spontaneous dissections,12'"·21 although they
were
not
observed in any of our patients. Without severe renal ischemia progressing to infarction, most spontaneous renal artery dissections are silent. In this respect, these lesions are similar to renal artery macroaneurysms unassociated with dissections." Acceleration of antecedent hypertension may occasionally herald a dissection involving a previouslydiseased renal artery. Reentry of dissections with resolu¬ tion of renal ischemia may occur."' It is unlikely that this event will prove as common as has been reported with spontaneous internal carotid artery dissections." Criteria for operative treatment of potentially correct¬ able spontaneous dissections include: (1) existence of hemodynamically significant acute occlusions accompanying dissections of main or major segmental renal arteries, and (2) documentation of severe renovascular hypertension or deteriorating renal function with arteriographically dem¬ onstrable dissections, regardless of their roentgenographic appearance. Expectant therapy in these situations may be catastrophic compared to results utilizing new techniques in arterial reconstructive surgery.
References 1. Boyd JF, Watson AF: Dissecting aneurysms due to trauma. Scott Med J 1:326-329, 1956. 2. Englund GW: Primary dissecting aneurysm of the renal artery: Report of a case and review of the literature. Am J Clin Pathol 45:472-479, 1966.
3. Foord
pulmonary 577, 1959.
AG, Lewis RD: Primary dissecting aneurysms of peripheral and arteries: Dissecting hemorrhage of media. Arch Pathol 68:553\x=req-\
4. Gilfillan RS, Smart
WR, Bostwick WL: Dissecting
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aneurysm of the
renal artery. Arch Surg 73:737-740, 1956. 5. Grablowsky OM, Weichert RF III, Goff JB, et al: Renal artery thrombosis following blunt trauma: Report of four cases. Surgery 67:895\x=req-\ 900, 1970. 6. Guthrie W, Maclean H: Dissecting aneurysms of arteries other than the aorta. J Pathol 108:219-235, 1972. 7. Hare WSC, Kincaid-Smith P: Dissecting aneurysm of the renal artery. Radiology 97:255-263, 1970. 8. Harrison EG Jr, Hunt JC, Bernatz PE: Morphology of fibromuscular dysplasis of the renal artery in renovascular hypertension. Am J Med 43:97\x=req-\ 117, 1967. 9. Henry L, Burke WD: Isolated dissecting aneurysms of the renal artery. Angiology 14:269-276, 1963. 10. Kauffman JJ, Coulson WF, Lecky JW, et al: Primary dissecting aneurysm of renal artery: Report of a case causing reversible renal hypertension. Ann Surg 177:259-263, 1973. 11. Khanna OP, Nedwick A, Gonick A: Accelerated hypertension due to intramural dissection of accessory renal artery. Urology 1:130-133, 1973. 12. Liebow IM, Cline T, Post RS, et al: Isolated bilateral simultaneous dissection of the renal arteries. Am J Med 21:151-156, 1956. 13. Meyers DS, Grim CE, Keitzer WF: Fibromuscular dysplasia of the renal artery with medial dissection: A case simulating polyarteritis nodosa. Am J Med56:412-416, 1974. 14. Neuman HW, Sakin AF: Unilateral dissecting aneurysm of the renal artery. Can J Surg 8:291-295, 1965. 15. Perry MO: Hypertension and dissecting aneurysms of the renal artery. Arch Surg 102:216-217, 1971. 16. Rosenblum WI: Isolated dissecting aneurysm of the renal artery. J Urol 95:135-138, 1966. 17. Skinner DG: Traumatic renal artery thrombosis: A successful thrombectomy and revascularization. Ann Surg 177:264-267, 1973. 18. Stables DP, Fouche RF, DeVilliers Van Neiker JP, et al: Traumatic renal artery occlusion: Twenty-one cases. J Urol 115:229-233, 1976. 19. Tuqan NA: Primary dissecting aneurysm of the renal artery. J Pathol Bacteriol 89:369-370, 1965. 20. Wadhwani IB, Johenning PW, Jawa PS: Unusual sequelae following blunt trauma to renal pedicle. Urology 3:79-81, 1974. 21. Watson AJ: Dissecting aneurysms of arteries other than the aorta.J Pathol Bacteriol 72:439-449, 1956. 22. Wheat MW Jr, Palmer RF: Dissecting aneurysms of the aorta. Curr Probl Surg, July, 1971. 23. Prokop EK, Wheat MW Jr, Palmer RF: Hydrodynamic forces in dissecting aneurysms. Circ Res 27:121-127, 1970. 24. Spencer MP, Dennison AB: Pulsatile blood flow in the vascular system, in Hamilton WR (ed): Handbook of Physiology. Washington, DC, American Physiological Society, 1963, vol 2, pp 839-864. 25. Lim RC Jr, Eastman AB, Blaisdell FW: Renal autotransplantation: Adjunct to repair of renal vascular lesions. Arch Surg 105:847-852, 1972. 26. Collins HA, Jacobs JK: Acute arterial injuries due to blunt trauma. J Bone Joint Surg 43A:193-196, 1961.
27. Ross R, Ackerman E, Pierce JM: Traumatic subintimal hemorrhage of the renal artery. J Urol 104:11-13, 1970. 28. Caponegro PJ, Leadbetter GW: Traumatic renal artery thrombosis. J Urol 109:769-771, 1973. 29. Evans A, Mogg RA: Renal artery thrombosis due to closed trauma.J Urol 105:330-334, 1971. 30. Sturm JT, Perry JF, Cass AS: Renal artery and vein injury following blunt trauma. Ann Surg 182:696-698, 1975. 31. Itzchak Y, Adar R, Moses M, et al: Occlusion of renal and visceral arteries following blunt abdominal trauma: Angiographic observations. J Cardiovasc Surg 15:383-388, 1974. 32. Morse TS, Harris BH: Nonpenetrating renal vascular injuries. J Trauma 13:497-501, 1973. 33. Marks LS, Brosman SA, Lindstrom RR, et al: Arteriography in penetrating renal trauma. Urology 3:18-22, 1974. 34. Flaster SL, Bush IM: The use of intraoperative renal arteriography in evaluating renal injuries. J Urol 109:763-765, 1973. 35. Guerrier K, Albert DJ, Mahoney SA, et al: Delayed nephrectomy after trauma. J Trauma 9:465-469, 1969. 36. Jacdo ET, Reisin E, Golan M, et al: Ex situ renal artery angioplasty followed by heterotropic autotransplantation of kidney in renal arterial thrombosis. Vase Surg 7:238-246, 1973. 37. Fay R, Brosman S, Lindstrom R, et al: Renal artery thrombosis: A successful revascularization by autotransplantation. J Urol 111:572-576, 1974. 38. Bergentz SE, Faarup P, Hegedus V, et al: Diagnosis of hypertension due to occlusion of a supplemental renal artery; its localization, treatment by removal from the body, microsurgical repair and reimplantation: A case report. Ann Surg 178:643-647, 1973. 39. Stanley JC, Gewertz BL, Bove EL, et al: Arterial fibrodysplasia: Histopathologic character and current etiologic concepts. Arch Surg 110:561-566, 1975. 40. McCormack LJ, Poutasse EF, Meaney TF, et al: A pathologic\x=req-\ arteriographic correlation of renal arterial disease. Am Heart J 72:188, 1966. 41. Reich SB, Riley JC III, Christopher RA, et al: Changes in pulse wave form with flow through vessels with repetitive saccular dilatations and stenosis. Invest Radiol 10:622-626, 1975. 42. Flanigan DP, Tullis JP, Streeter VL, et al: Multiple subcritical arterial stenoses: Effect on poststenotic pressure and flow. Ann Surg. to be
published.
43. Nalbandian RM, Chason JL: Intramural (intramedial) dissecting hematomas in normal and otherwise unremarkable coronary arteries. Am J Clin Pathol 43:348-356, 1965. 44. Stanley JC, Rhodes EL, Gewertz BL, et al: Renal artery aneurysms: Significance of macroaneurysms exclusive of dissections and fibrodysplastic mural dilatations. Arch Surg 110:1327-1333, 1975. 45. Ehrenfeld WK, Wylie EJ: Spontaneous dissection of the internal carotid artery. Arch Surg 111:1294-1301, 1976.
Discussion Robert C. Lim, Jr, MD, San Francisco: In the past when this entity has been encountered, treatment has been with very little foreknowledge or experience. The authors appropriately group dissections by cause, the most common being trauma. At the San Francisco General Hospital we see approximately 5,000 trauma cases per year in our emergency department. We proceed with intravenous pyelograms in cases of hematuria secondary to blunt abdominal trauma. Patients whose conditions are unstable are operated on immediately. Those who are stable, and who have no indications for laparotomy, are followed up with a second intravenous pyelogram in one to two weeks. We have not routinely obtained arteriograms with all abnormal pyelograms. We agreed, in cases where in situ repair of the renal artery is difficult, that the kidney should be removed, repaired, and reimplanted. Do the authors have guidelines as to how one should interpret arterio¬ grams to predict which lesions are self-limiting, and which should be promptly operated on? Also, is there a time interval that is safe between obtaining an arteriogram and proceeding with surgical rare
repair? Dr Gewertz: Pertinent questions such as Dr Lim's usually elicit reasonable but speculative replies, rather than definitive responses backed by extensive experience. Urography is known to
a poor diagnostic screening test for renal artery dissections, although it is valuable in documenting the existence of a func¬ tioning contralateral kidney. It is important to realize that renal nonvisualization with intravenous pyelography may follow contu¬ sion alone, and not reflect major vascular injury. Similarly, normal urograms do not necessarily exclude dissections. Regardless of urographie findings, arteriography is indicated in nearly all cases of suspected renal trauma manifesting hypertension with hema¬ turia. Circumferential or deep mural dissections with intraluminal projection are more likely forerunners of thrombosis than small subintimai flaps. Unfortunately, the benign nature of any dissec¬ tion is never guaranteed, regardless of its artériographie appearance. Delays in surgical therapy longer than 12 hours certainly jeopardize beneficial results in instances of preexisting severe renal ischemia. However, presence or absence of irrepar¬ able renal ischemie injury is so influenced by other factors, such as existence of collaterals, prior renal diesase, and the like, that each case must be individualized. We wish to reemphasize that early operative intervention must be seriously considered in all instances of major vascular injury and those exhibiting secondary hypertension following renal artery dissections.
be
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Artery
Dissections
Gewertz, MD; James C. Stanley, MD; William J. Fry,
MD
\s=b\ Renal artery dissections encountered in 15 patients, aged 3 to 75 years, were categorized as to pathogenesis (blunt abdominal trauma, catheter injury, and spontaneous). Blunt traumatic dissections (seven patients) were characterized by hypertension, gross hematuria, and pain. Catheter-induced dissections (four patients) were asymptomatic, although two exhibited accelerated hypertension. Spontaneous dissections (four patients) were all associated with preexistent arterial disease. Symptoms in these patients were uncommon, despite accelerated hypertension in three cases. Intravenous pyelography lacked specific diagnostic value for renal artery dissections. Early arteriographic examination proved essential in diagnosis and surgical treatment. Criteria for operative intervention included existence of technically correctable dissections causing (1) hemodynamically significant occlusions of the main or major segmental renal arteries, (2) documented renovascular hypertension, or (3) significant deterioration of renal function.
(Arch Surg 112:409-414, 1977)
renal artery dissections are rare. Severe hyper¬ or loss of a kidney often attend these lesions and justify continuing reappraisal of their cause and clinical importance. Many previous reports and collected series have detailed the pathologic process and difficult diagnostic problems associated with renal artery dissec¬ tion.1 --'' Unfortunately, uniformly poor results have been attributed to both expectant management and operative therapy of these lesions. Renal artery dissections affecting 15 patients encoun¬ tered at the University of Michigan Medical Center provide the basis for the present review. Categorization of dissections into subgroups according to cause proved important in defining the natural history of this disease entity. Specific subgroups identified included (1) dissec¬ tions subsequent to blunt abdominal trauma, (2) intralu¬ minal catheter-induced injuries, and (3) spontaneous dissections in arteriosclerotic or fibrodysplastic arteries. Aortic dissections involving renal vessels were excluded from study, as were macroaneurysms, pseudoaneurysms, minute intimai disruptions, and arterial thromboses not unequivocally associated with a dissecting process.
Isoltension ated
Accepted for publication Dec 8, 1976. From the Department of Surgery, University of Michigan Medical Center, Ann Arbor. Read before the 84th annual meeting of the Western Surgical Association, Coronado, Calif, Nov 15, 1976. Reprint requests to University Hospital, 1405 E Ann St, Ann Arbor MI 48109 (Dr Gewertz).
CLINICAL EXPERIENCE Renal artery dissections were documented among eight male and seven female patients, ranging in age from 3 to 75 years, treated at University Hospital from 1960 to 1976. Dissections were initially recognized by artériographie examination in all but one patient. In this latter case, arteriograms demonstrated an occluded renal artery that at the time of operation was discovered to be a typical dissection. The rarity of these lesions is emphasized in that only 15 patients harboring dissections were discovered during a time period when more than 11,000 abdominal arterio¬ grams were performed at our institution. Clinical characteristics of these patients are best defined in relation to underlying mechanisms responsible for the dissection.
Dissections
Secondary
to Blunt Abdominal Trauma
Four male and three female patients, with an average age of 24.4 years, exhibited renal artery dissections after sustaining severe abdominal trauma (Table 1). Motor vehicle accidents were responsible for five dissections, one followed a 20-foot fall, and another was the consequence of a boxing injury. Dissections affected right renal arteries in four patients, the left renal artery twice, and both vessels in one patient. Main renal arteries were the site of dissections in five instances; the remainder involved distal
branches.
Microscopic or gross hematuria and flank pain affected all patients with dissections due to abdominal trauma. Two patients had acute hypertension following injury, and in a third late blood pressure elevation developed. Three patients were initially hypotensive because of concomittant intra-abdominal injuries. Exclud¬ ing the boxing injury, dissections were recognized within 12 hours of hospitalization. Intravenous pyelograms were obtained in five patients. Absent, as well as delayed, nephrograms or evidence of renal contusions were observed in each instance. Artériographie studies confirmed the diagnosis of dissection in all patients. Immediate operative intervention was undertaken twice for traumatic lesions. Primary aortorenal bypass was successfully performed once. In the second case, a child with profound hypo¬ tension, nephrectomy was necessary. A third patient was treated by heminephrectomy for sustained hypertension secondary to segmental vessel occlusion four months after injury. A fourth patient underwent late operation for chronic hypertension. An unsuccessful attempt at reconstructing his severely injured renal artery eventuated in nephrectomy. This patient, who had bilateral disease with
a
limited dissection of the contralateral renal artery
(Fig 1, left), remains normotensive two years postoperatively. Three additional patients did not undergo surgical therapy. Two of these patients had clinically unimportant dissections. Multiple injuries of segmental vessels in a solitary kidney unamenable to conventional repair occurred in the third patient (Fig 1, right). Temporary hemodialysis was required for acute renal failure, with eventual return of normal renal function. Excluding the latter case, no patient with dissections caused by blunt trauma experi¬ enced compromise of renal function.
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Table 1.—Dissections
Patient/Age, yr/Sex 1/3/F
2/21/M
Mechanism of Injury Motor vehicle accident 20-foot fall
Secondary
Manifestations
Pain, hematuria,
hypotensive5 Pain, hematuria,
hypotensive
to Blunt Abdominal Trauma
Artériographie Findings Right main renal artery dissection Right main renal artery
Surgical Therapy Right nephrectomy
Normotensive, normal
None
Normotensive, normal
Results renal function
renal function
dissection
3/21/M
Motor vehicle accident
Pain, hematuria,
hypertensive (154/98 mm Hg),
Right segmental renal artery
None,
Left renal artery dissection
Left aortorenal
acute renal failure
4/21/F
Motor vehicle accident
Pain, hematuria,
hypotensive"
Normotensive, normal
hemodialysis (4 weeks)
dissection
branch of 2
Normotensive, normal renal function
saphenous vein graft
(cephalic
renal function
multiple renal arteries) 5/30/F
Motor vehicle accident
Pain, hematuria,
hypotensive"
Left main renal artery dissec¬
None
Right segmental renal artery
Right hemi¬ nephrectomy
Right segmental
Left
Normotensive, normal renal function
tion
6/35/M
Motor vehicle accident
Pain, hematuria,
hypertensive
dissection
7/40/M
Boxing
Pain, hematuria, hypertensive late (200/150 mm Hg)
dissection and left main renal
artery
nephrectomy
Normotensive with medication (130/90 mm Hg), normal renal function Normotensive, normal renal function
dissec¬
tion
"Hypotension
a
result of intra-abdominal
hemorrhage unrelated
to renal
artery dissection.
Fig 1 .—Dissections secondary to blunt abdominal trauma. Left, Limited, intramural dissection of proximal renal artery (arrow) attributed to boxing injury. Right, Infrarenal dissection (arrow) associated with severe parenchymal contusion in a solitary kidney. Both were treated nonoperatively. Dissections Secondary to Intraluminal Catheterizations In two male and two female patients, averaging 57.3 years in age, dissections developed following diagnostic catheter studies (Table 2). Severe antecedent renal artery disease affected each patient. Three exhibited arteriosclerotic renal artery disease, and the fourth had fibrodysplastic stenosis of this vessel. Préexistent hypertension became more severe after catheterization in two patients, resulting in early operative interventions. Successful aortorenal saphenous vein bypass was performed in one patient (Fig 2). Attempts to reconstruct the second patient's renal artery eventuated in nephrectomy. Renal function and blood pressure were normal in two patients treated nonoperatively. Pain and hematuria did not occur in any of these four patients.
Spontaneous
Dissections
Spontaneous dissections developed in two male patients with arteriosclerotic renal artery disease, and in two female patients with fibrodysplastic disease (Fig 3). All but one patient were hypertensive (Table 3). Gross or microscopic hematuria were not apparent in this group. One patient experienced flank pain. Arterial reconstructions were attempted twice; this was successful on one occasion and lead to a nephrectomy in the other. Primary nephrectomy was performed in an additional patient early in our experience. The remaining patient with a limited dissection, normal renal function, and blood pressure was treated conserva¬
tively.
COMMENT
Since the first
angiographie demonstration
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of
a
renal
Table 2.—Intraluminal Catheter-Induced Dissections* Associated Renal Manifestations
Patient/Age, yr/Sex 1/34/F
2/58/M
hypertension (200/130 mm Hg)
Accelerated
Accelerated
(220/120 3/62/F
hypertension Hg)
mm
None
Left main renal dissection
Arteriosclerosis
Left main renal
(bilateral) Arteriosclerosis
(unilateral) 4/75/M
None
Arteriosclerosis
(unilateral)
Surgical Therapy
Artériographie Findings
Artery Pathology Fibrodysplasia (bilateral)
Results
Left aortorenal
Normotensive.
saphenous vein graft Left nephrectomy
normal renal function Persistent
Right
hypertension Normotensive, Right nephrectomy normal renal for hypernephroma
Left main renal
None
Normotensive,
artery dissection main renal artery dissection, right hypernephroma
function
artery dissection
normal renal function
"Selective artériographie catheterizations.
Fig 2.—Left, Artériographie catheter-induced dissection (arrow) in fibrodysplastic renal artery. Right, postoperative appearance of arterial reconstruction using autogenous saphenous aortorenal vein graft.
artery dissection in 1956,' these lesions have been discov¬ ered with increasing frequency. Clinical reports continue to be anecdotal, with cumulative experiences from any one
institution exceeding ten patients being nonexistent. Criteria for radiologie diagnosis of renal artery dissections have been previously published,7 and include: (1) luminal irregularities with aneurysmal dilation or saccular dissec¬ tions associated with segmental stenoses, (2) predilection of dissection to extend distally to the first renal artery bifurcation, (3) "cuffing" at branchings, and (4) variable degrees of reversibility documented by subsequent artériographie studies. Common usage resulted in many dissections being referred to as dissecting aneurysms. This misnomer persists despite the occlusive nature of most renal artery dissections. Clinical manifestation of renal artery dissections are invariably associated with the consequences of renal ischemia. Renal infarction, compromised renal function, and renovascular hypertension are the most common
complications of dissections. These events are not inevitable. Certain dissections may be self-limited and of no functional importance. Contributing factors to dissections vary with different injuries or arterial diseases responsible for these lesions. The tendency for renal artery dissections to extend is less than that noted in dissections of the thoracic aorta. Blood viscosity, shearing forces, and flow turbulence are involved in the propagation of all dissections, but the single most important hemodynamic force relates to the first deriva¬ tive of aortic pressure curves (the slope of the pulse wave, dp/dt).-- -' As aortic pressure waves progress down the aorta to the renal artery level, dp/dt is diminished.-1 This natural damping phenomenon supports an assumption that hemodynamic forces implicated in proximal aortic dissec¬ tions are less important in renal artery dissections. Renal artery trauma or loss of structural integrity due to antesevere
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Table
3.—Spontaneous
Renal
Patient/Age, yr/Sex 1/34/F
2/35/M
Artery Pathology Fibrodysplasla (bilateral)
Manifestations Accelerated
Arteriosclerosis
Accelerated
(bilateral) 3/39/F
4/61/M
Flbrodysplasia (unilateral) Arteriosclerosis
Dissections
Left main renal dissection
Left aortorenal
Left
vein graft Left nephrectomy
hypertension (210/110 mm Hg)
hypertension
(210/120 mm Hg) Pain, accelerated
hypertension (200/100 mm Hg) None
(unilateral)
Surgical Therapy
Artériographie Findings
saphenous
segmental renal artery dissection
Results Normotensive with medications
(140/85
macroaneurysm) Right segmental renal
Hg)
with medications
(110/85 Left main renal artery dissection (associated
mm
Normotensive
Left
nephrectomy
mm
Hg)
Normotensive, normal renal function
None
artery dissection
Normotensive, normal renal function
Blunt Trauma and Dissections
Fig 3.—Spontaneous dissection (arrow) causing near total occlu¬ sion of distal main renal artery in patient exhibiting accelerated hypertension.
cèdent disease may influence propagation of dissections more than other variables. Conservation of renal parenchymal tissue is of utmost importance in patients exhibiting spontaneous dissections, or in those with préexistent renovascular disease and catheter-induced dissections. Renal artery disease involv¬ ing the contralateral kidney was noted among four of our eight patients having dissections unrelated to blunt abdominal trauma. Casual nephrectomies for dissections are unacceptable. Although certain dissections are not amenable to any form of operative treatment, recent advances in surgical technique17 -:> should improve dismal salvage rates described in the current literature. Arterial reconstruction utilizing autogenous saphenous vein is preferred, with ex vivo repairs being appropriate in selected cases.
Two mechanisms have been alluded to in explaining renal artery injuries following blunt abdominal trauma. The first relates to a deceleration phenomenon of rela¬ tively mobile kidneys.-628 Sudden anterior displacement of the kidney may generate marked tension within the vascular pedicle. Subsequent fracture of the least elastic tissue, the intima, predisposes in subintimai dissection. A second mechanism involves direct vessel wall contusion against unyielding vertebral bodies.1" Intimai injury and hemorrhage within the media following rupture of vasa vasorum may initiate certain traumatic dissections. Trau¬ matic thromboses, often secondary to subintimai dissec¬ tions, have been reported to involve the left renal artery much more frequently than the right.'7·-"'10 Considering the lesser mobility of the left kidney and its shorter vascular pedicle, the predilection for left-sided thromboses is poorly explained by the aforementioned mechanisms. Data from the present experience and that of others11" does not support the tenet that left renal arteries are more favored sites for dissections.'" Hematuria is very common in patients with dissections secondary to blunt trauma. All of our patients exhibited this finding. Most instances of hematuria appear second¬ ary to renal parenchymal contusion, and not the arterial injury per se." Abnormal intravenous pyelograms are common in patients with traumatic renal artery dissec¬ tions.'- Pyelography is exceedingly nonspecific for renal trauma, and does not provide adequate information for assessing the presence or absence of traumatic renovascular lesions." Standard artériographie examinations in stable patients, or intraoperative studies in selected patients, provide the most reliable diagnostic information regarding dissections.2Si4",ä Emergent primary arterial reconstructions are recom¬ mended in patients having technically correctable dissec¬ tions secondary to blunt abdominal trauma if occlusion of the main renal artery or a major segmental branch is recognized, as well as when hypertension persists or renal function deteriorates following functionally significant injury. Early recognition of dissections and expeditious repair are often essential in preventing irreversible renal damage. Although ex vivo renal artery repair and autotransplantation has been employed for renal artery recon¬ struction at our institution, we have not had a recent
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opportunity
to utilize such a procedure for treatment of traumatic dissections. Ex vivo repair appears uniquely suited to the extensive pedicle injuries associated with arterial dissections.25-36-38
Angiographie Catheter-Induced
Dissections
The incidence of renal artery dissections occurring course of arteriography has been poorly docu¬ mented in the literature. Selective renal artery catheteri¬ zations are more likely to result in dissections than flush aortography. The rarity of this complication is confirmed by our experience, in which only four renal artery catheter dissections were encountered in more than 11,000 abdom¬ inal artériographie examinations, including approximately 2,200 selective renal arteriograms. Occurrence of these dissections is unquestionably related to underlying renovascular disease.7 Dissections are more likely to occur in vessels manifesting advanced arterioscle¬ rosis. Infrequent occurrence of catheter-induced dissec¬ tions in patients with fibrodysplasia suggests that medial alterations, even when associated with severe stenosis, do not predispose to such injuries. Most catheter-induced dissections are probably clinically covert. Pain and hematuria did not occur in our experience, and usually occurs only when extensive lesions cause near or complete occlusion of vessels and renal infarction. It is probable that many small dissections, such as intimai flaps, pass unrecognized. Greatest problems revolve around those instances where dissections cause ischemia severe enough to produce secondary hypertension or compromise renal function. These silent complications may persist until more serious sequelae ensue. Indications for operation in patients having renal artery dissections secondary to cath¬ eter injuries are identical to those of blunt traumatic dissections.
during the
Spontaneous
Dissections
Renal arteries are the most common site of primary dissections involving peripheral vessels.3 These lesions may be associated with coexisting macroaneurysms, arterial fibrodysplasia, arteriosclerosis, and medial necrosis.2·813·38 Nearly a 9% incidence of dissections in patients with fibrodysplastic renal arteries has been observed by others.8 Recent experience at our institution with more than 200 cases of renal artery fibrodysplasia in no way suggests these lesions to be so common. Differences in defining dissections and interpreting artériographie or histologie studies may account for discrepancies in these two experi¬ ences.4"
The pathogenesis of spontaneous renal artery dissec¬ tions is poorly understood. Necropsy studies usually demonstrate dissections extending within the outer media adjacent to the external elastic lamina, and less commonly within the more central media."·1"·-1 Only half these dissec-
tions may actually communicate with the vessel lumen.7 In obvious contradistinction are traumatic dissections, which usually originate from the lumen, extending along subintimal and inner medial tissue planes. Spontaneous renal artery dissections generally affect proximal vessels. Although intrinsic properties of an artery may account for this occurrence, physiologic mechanisms related to blood flow may predispose this site to dissec¬ tions. This may be of particular importance in arteries exhibiting multiple fibrodysplastic stenoses. Damping of steep systolic pressure waves has been documented in models of repetitive saccular dilations and stenoses com¬ parable to arterial fibrodysplasia.41 In another investiga¬ tion, diminutions of mean perfusion pressures have been documented beyond a series of subcriticai stenoses simula¬ ting fibrodysplastic disease.1- Both phenomena may account for limited distal propagation of mural dissec¬ tions. Spontaneous peripheral arterial dissections have been attributed to abnormalities involving vasa vasorum.,;l Hemorrhage may result from rupture of vasa vasorum. Subsequent intramural hematoma may increase medial ischemia and further compromise vessel wall integrity. Sustained arterial blood pressure elevations may contrib¬ ute to the development of renal artery dissections by potentiating arteriosclerosis and medial degeneration. It has not been proved that hypertension represents an initiating factor in dissecting aneurysms of muscular arteries." To the contrary, hypertension secondary to an occluding dissection causing renal ischemia is a more tenable explanation for coexisting elevations in blood pressure. Pain and hematuria have been described in patients with
spontaneous dissections,12'"·21 although they
were
not
observed in any of our patients. Without severe renal ischemia progressing to infarction, most spontaneous renal artery dissections are silent. In this respect, these lesions are similar to renal artery macroaneurysms unassociated with dissections." Acceleration of antecedent hypertension may occasionally herald a dissection involving a previouslydiseased renal artery. Reentry of dissections with resolu¬ tion of renal ischemia may occur."' It is unlikely that this event will prove as common as has been reported with spontaneous internal carotid artery dissections." Criteria for operative treatment of potentially correct¬ able spontaneous dissections include: (1) existence of hemodynamically significant acute occlusions accompanying dissections of main or major segmental renal arteries, and (2) documentation of severe renovascular hypertension or deteriorating renal function with arteriographically dem¬ onstrable dissections, regardless of their roentgenographic appearance. Expectant therapy in these situations may be catastrophic compared to results utilizing new techniques in arterial reconstructive surgery.
References 1. Boyd JF, Watson AF: Dissecting aneurysms due to trauma. Scott Med J 1:326-329, 1956. 2. Englund GW: Primary dissecting aneurysm of the renal artery: Report of a case and review of the literature. Am J Clin Pathol 45:472-479, 1966.
3. Foord
pulmonary 577, 1959.
AG, Lewis RD: Primary dissecting aneurysms of peripheral and arteries: Dissecting hemorrhage of media. Arch Pathol 68:553\x=req-\
4. Gilfillan RS, Smart
WR, Bostwick WL: Dissecting
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aneurysm of the
renal artery. Arch Surg 73:737-740, 1956. 5. Grablowsky OM, Weichert RF III, Goff JB, et al: Renal artery thrombosis following blunt trauma: Report of four cases. Surgery 67:895\x=req-\ 900, 1970. 6. Guthrie W, Maclean H: Dissecting aneurysms of arteries other than the aorta. J Pathol 108:219-235, 1972. 7. Hare WSC, Kincaid-Smith P: Dissecting aneurysm of the renal artery. Radiology 97:255-263, 1970. 8. Harrison EG Jr, Hunt JC, Bernatz PE: Morphology of fibromuscular dysplasis of the renal artery in renovascular hypertension. Am J Med 43:97\x=req-\ 117, 1967. 9. Henry L, Burke WD: Isolated dissecting aneurysms of the renal artery. Angiology 14:269-276, 1963. 10. Kauffman JJ, Coulson WF, Lecky JW, et al: Primary dissecting aneurysm of renal artery: Report of a case causing reversible renal hypertension. Ann Surg 177:259-263, 1973. 11. Khanna OP, Nedwick A, Gonick A: Accelerated hypertension due to intramural dissection of accessory renal artery. Urology 1:130-133, 1973. 12. Liebow IM, Cline T, Post RS, et al: Isolated bilateral simultaneous dissection of the renal arteries. Am J Med 21:151-156, 1956. 13. Meyers DS, Grim CE, Keitzer WF: Fibromuscular dysplasia of the renal artery with medial dissection: A case simulating polyarteritis nodosa. Am J Med56:412-416, 1974. 14. Neuman HW, Sakin AF: Unilateral dissecting aneurysm of the renal artery. Can J Surg 8:291-295, 1965. 15. Perry MO: Hypertension and dissecting aneurysms of the renal artery. Arch Surg 102:216-217, 1971. 16. Rosenblum WI: Isolated dissecting aneurysm of the renal artery. J Urol 95:135-138, 1966. 17. Skinner DG: Traumatic renal artery thrombosis: A successful thrombectomy and revascularization. Ann Surg 177:264-267, 1973. 18. Stables DP, Fouche RF, DeVilliers Van Neiker JP, et al: Traumatic renal artery occlusion: Twenty-one cases. J Urol 115:229-233, 1976. 19. Tuqan NA: Primary dissecting aneurysm of the renal artery. J Pathol Bacteriol 89:369-370, 1965. 20. Wadhwani IB, Johenning PW, Jawa PS: Unusual sequelae following blunt trauma to renal pedicle. Urology 3:79-81, 1974. 21. Watson AJ: Dissecting aneurysms of arteries other than the aorta.J Pathol Bacteriol 72:439-449, 1956. 22. Wheat MW Jr, Palmer RF: Dissecting aneurysms of the aorta. Curr Probl Surg, July, 1971. 23. Prokop EK, Wheat MW Jr, Palmer RF: Hydrodynamic forces in dissecting aneurysms. Circ Res 27:121-127, 1970. 24. Spencer MP, Dennison AB: Pulsatile blood flow in the vascular system, in Hamilton WR (ed): Handbook of Physiology. Washington, DC, American Physiological Society, 1963, vol 2, pp 839-864. 25. Lim RC Jr, Eastman AB, Blaisdell FW: Renal autotransplantation: Adjunct to repair of renal vascular lesions. Arch Surg 105:847-852, 1972. 26. Collins HA, Jacobs JK: Acute arterial injuries due to blunt trauma. J Bone Joint Surg 43A:193-196, 1961.
27. Ross R, Ackerman E, Pierce JM: Traumatic subintimal hemorrhage of the renal artery. J Urol 104:11-13, 1970. 28. Caponegro PJ, Leadbetter GW: Traumatic renal artery thrombosis. J Urol 109:769-771, 1973. 29. Evans A, Mogg RA: Renal artery thrombosis due to closed trauma.J Urol 105:330-334, 1971. 30. Sturm JT, Perry JF, Cass AS: Renal artery and vein injury following blunt trauma. Ann Surg 182:696-698, 1975. 31. Itzchak Y, Adar R, Moses M, et al: Occlusion of renal and visceral arteries following blunt abdominal trauma: Angiographic observations. J Cardiovasc Surg 15:383-388, 1974. 32. Morse TS, Harris BH: Nonpenetrating renal vascular injuries. J Trauma 13:497-501, 1973. 33. Marks LS, Brosman SA, Lindstrom RR, et al: Arteriography in penetrating renal trauma. Urology 3:18-22, 1974. 34. Flaster SL, Bush IM: The use of intraoperative renal arteriography in evaluating renal injuries. J Urol 109:763-765, 1973. 35. Guerrier K, Albert DJ, Mahoney SA, et al: Delayed nephrectomy after trauma. J Trauma 9:465-469, 1969. 36. Jacdo ET, Reisin E, Golan M, et al: Ex situ renal artery angioplasty followed by heterotropic autotransplantation of kidney in renal arterial thrombosis. Vase Surg 7:238-246, 1973. 37. Fay R, Brosman S, Lindstrom R, et al: Renal artery thrombosis: A successful revascularization by autotransplantation. J Urol 111:572-576, 1974. 38. Bergentz SE, Faarup P, Hegedus V, et al: Diagnosis of hypertension due to occlusion of a supplemental renal artery; its localization, treatment by removal from the body, microsurgical repair and reimplantation: A case report. Ann Surg 178:643-647, 1973. 39. Stanley JC, Gewertz BL, Bove EL, et al: Arterial fibrodysplasia: Histopathologic character and current etiologic concepts. Arch Surg 110:561-566, 1975. 40. McCormack LJ, Poutasse EF, Meaney TF, et al: A pathologic\x=req-\ arteriographic correlation of renal arterial disease. Am Heart J 72:188, 1966. 41. Reich SB, Riley JC III, Christopher RA, et al: Changes in pulse wave form with flow through vessels with repetitive saccular dilatations and stenosis. Invest Radiol 10:622-626, 1975. 42. Flanigan DP, Tullis JP, Streeter VL, et al: Multiple subcritical arterial stenoses: Effect on poststenotic pressure and flow. Ann Surg. to be
published.
43. Nalbandian RM, Chason JL: Intramural (intramedial) dissecting hematomas in normal and otherwise unremarkable coronary arteries. Am J Clin Pathol 43:348-356, 1965. 44. Stanley JC, Rhodes EL, Gewertz BL, et al: Renal artery aneurysms: Significance of macroaneurysms exclusive of dissections and fibrodysplastic mural dilatations. Arch Surg 110:1327-1333, 1975. 45. Ehrenfeld WK, Wylie EJ: Spontaneous dissection of the internal carotid artery. Arch Surg 111:1294-1301, 1976.
Discussion Robert C. Lim, Jr, MD, San Francisco: In the past when this entity has been encountered, treatment has been with very little foreknowledge or experience. The authors appropriately group dissections by cause, the most common being trauma. At the San Francisco General Hospital we see approximately 5,000 trauma cases per year in our emergency department. We proceed with intravenous pyelograms in cases of hematuria secondary to blunt abdominal trauma. Patients whose conditions are unstable are operated on immediately. Those who are stable, and who have no indications for laparotomy, are followed up with a second intravenous pyelogram in one to two weeks. We have not routinely obtained arteriograms with all abnormal pyelograms. We agreed, in cases where in situ repair of the renal artery is difficult, that the kidney should be removed, repaired, and reimplanted. Do the authors have guidelines as to how one should interpret arterio¬ grams to predict which lesions are self-limiting, and which should be promptly operated on? Also, is there a time interval that is safe between obtaining an arteriogram and proceeding with surgical rare
repair? Dr Gewertz: Pertinent questions such as Dr Lim's usually elicit reasonable but speculative replies, rather than definitive responses backed by extensive experience. Urography is known to
a poor diagnostic screening test for renal artery dissections, although it is valuable in documenting the existence of a func¬ tioning contralateral kidney. It is important to realize that renal nonvisualization with intravenous pyelography may follow contu¬ sion alone, and not reflect major vascular injury. Similarly, normal urograms do not necessarily exclude dissections. Regardless of urographie findings, arteriography is indicated in nearly all cases of suspected renal trauma manifesting hypertension with hema¬ turia. Circumferential or deep mural dissections with intraluminal projection are more likely forerunners of thrombosis than small subintimai flaps. Unfortunately, the benign nature of any dissec¬ tion is never guaranteed, regardless of its artériographie appearance. Delays in surgical therapy longer than 12 hours certainly jeopardize beneficial results in instances of preexisting severe renal ischemia. However, presence or absence of irrepar¬ able renal ischemie injury is so influenced by other factors, such as existence of collaterals, prior renal diesase, and the like, that each case must be individualized. We wish to reemphasize that early operative intervention must be seriously considered in all instances of major vascular injury and those exhibiting secondary hypertension following renal artery dissections.
be
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