LETTERS TO THE EDITORS The Editors invite readers to submit letters commenting on the contents of articles that appear in the Journal. Also welcome are brief communications in letter form reporting investigative or clinical observations without extensive documentation and with brief bibliography (five tiles or less), not requiring peer review but open to critique by readers. Letters to the Editors should be no more than 500 words in length and they may have to be edited for publication.
Hematuria abdominal
is an indication aortic aneurysm
of rupture of an into the vena cava
To the Editors:
In a recent article in the JOURNAL, Salo et al.’ pointed out the importance of hematuria as a clinical sign indicating rupture of an abdominal aortic aneurysm into the vena cava. In discussingthe possiblemechanism of such hematuria, the authors speculated that it could be the result of renal damage,’ although venous congestion of the lower urinary tract had been suggested as the cause by earlier investigators.3 The authors based their opinion on the autopsy finding in their patients, asthey detected no dilated veins histologically, and bladder epithelium appeared normal. In 1976 after encountering similar casesin two patients we took this question to the research laboratory and attempted to elucidate the mechanism of hematuria associated with aortocaval fistula. In dogs we created large fistula by side-to-side anastomosis of infrarenal aorta to vena cava. Catheter pullthrough studies showed the vena cava pressure above fistula to remain near normal, whereas below the fistula it became equal to the aortic pressure.Ureteral catheter showed clearurine coming from the kidney, whereas bladder catheter urine turned hemorrhagic rapidly. Acute venous congestion can readily be identified visually in living subjects, but is difficult to document after the patient dies because the veins collapse back to the original sizewhen the high intraluminal pressureno longer exists. We believe the pressure gradient in the vena cava above and below the fistula, which existsat least in the acute phase, to be due to the transfer of high kinetic energy from aortic blood to the vena cava,which is directed toward the pelvis and the lower extremities. In fact, in one of our patients pulsation of superficial vein of the leg was noted, presumably because venous valve competence had been overcome by the high intraluminal pressure. Caval pressure above the fistula and pressure in the superior vena cavawill eventually rise with the onset of high-output cardiacfailure, which occurs later as a result of the presence of a large arteriovenous fistula. We thought these findings,4 which was not included in the reference list by the authors, may be of some interest to them and to the readers. Ray
C.-J. Chiu, MD, PhD, FRCSC
Professor of Surgery McGill University The Montreal General Hospital 1650 Cedar Ave. Montreal, Quebec H3G lA4 Canada
REFERENCES 1. Sale JA, Verkkala KA, Ala-Kulju KV, et al. Hematuria is an indication of rupture of an abdominal aortic aneurysm into the vena cava. J VASC SURC 1990;12:41-4. 2. Weber TR, Gewertz BL, Stanley JC, et al. Renal effects of acute infrarenal aorto-caval fistula. J Surg Res 1978;25:482-7. 3. Brewster DC, Ottinger LW, Darling RC, et al. Hematuria as a sign of aorto-cad fistula. Ann Surg 1977;186:766-71. 4. Livingstone AS, Chiu CJ, Mulder DS, et al. Spontaneous aortocaval fistula secondary to ruptured abdominal aortic aneurysm. Can J Surg 1977;20:33-6.
Substitution by adenosine for glucagon as a surgical diagnostic tool to detect mesenteric vascular adaptation To the Ed&s:
The recent article by Clark and Gewertz,’ “Glucagon potentiates intestinal repefision injury,” treats glucagon-induced adverse effects exclusively from the viewpoint of therapeutics and does not address the possibility of similar hazards that may be encountered when the agent is used as a diagnostic tool of adaptation potential as it has recently been proposed.’ However, by collating the important findings of Clark and Gewertz,’ with those of Lilly et al.* who advocated the widespread usage of glucagon to gauge vasodilator capacity in patients suspected of having mesenteric ischernia, the latter (hypothetical) conclusion also seemsinevitable. Gut segments of patients with diverse manifestations of mesenteric arterial insufficiency are constantly verging toward being submitted to irreversible necrosis. Repetitive but brief periods of intestinal ischemia, which characterize these syndromes, usually fail to elicit irreversible damages as long as postischemic reperf&ion is continued for hours, and, as Clark and Gewertz have convincingly shown, the ischemic (and probably the preischemic) phasesof such episodesare not associatedwith an unduly strong metabolic stress.At the same time, the whimsical time course of periodicity will locate each particular term of these cyclicpathologic events along a spectrum between the opposite ends of full recovery and ischemic nadir. The crucial point is that it is practically impossible to determine with a sufficient degree of certainty the exact timing of ischemic episodes, whereas the consequences become manifest only at later times. It follows that by testing his patients with glucagon, the surgeon may run unnecessaryand unwarranted risks. Although still unproven in details, these considerations should be taken into account in tailoring diagnostic measures- which are not necessarily uniform in every situation. In searchfor selecting vasoactiveagents that may 919
Hematuria abdominal
is an indication aortic aneurysm
of rupture of an into the vena cava
To the Editors:
In a recent article in the JOURNAL, Salo et al.’ pointed out the importance of hematuria as a clinical sign indicating rupture of an abdominal aortic aneurysm into the vena cava. In discussingthe possiblemechanism of such hematuria, the authors speculated that it could be the result of renal damage,’ although venous congestion of the lower urinary tract had been suggested as the cause by earlier investigators.3 The authors based their opinion on the autopsy finding in their patients, asthey detected no dilated veins histologically, and bladder epithelium appeared normal. In 1976 after encountering similar casesin two patients we took this question to the research laboratory and attempted to elucidate the mechanism of hematuria associated with aortocaval fistula. In dogs we created large fistula by side-to-side anastomosis of infrarenal aorta to vena cava. Catheter pullthrough studies showed the vena cava pressure above fistula to remain near normal, whereas below the fistula it became equal to the aortic pressure.Ureteral catheter showed clearurine coming from the kidney, whereas bladder catheter urine turned hemorrhagic rapidly. Acute venous congestion can readily be identified visually in living subjects, but is difficult to document after the patient dies because the veins collapse back to the original sizewhen the high intraluminal pressureno longer exists. We believe the pressure gradient in the vena cava above and below the fistula, which existsat least in the acute phase, to be due to the transfer of high kinetic energy from aortic blood to the vena cava,which is directed toward the pelvis and the lower extremities. In fact, in one of our patients pulsation of superficial vein of the leg was noted, presumably because venous valve competence had been overcome by the high intraluminal pressure. Caval pressure above the fistula and pressure in the superior vena cavawill eventually rise with the onset of high-output cardiacfailure, which occurs later as a result of the presence of a large arteriovenous fistula. We thought these findings,4 which was not included in the reference list by the authors, may be of some interest to them and to the readers. Ray
C.-J. Chiu, MD, PhD, FRCSC
Professor of Surgery McGill University The Montreal General Hospital 1650 Cedar Ave. Montreal, Quebec H3G lA4 Canada
REFERENCES 1. Sale JA, Verkkala KA, Ala-Kulju KV, et al. Hematuria is an indication of rupture of an abdominal aortic aneurysm into the vena cava. J VASC SURC 1990;12:41-4. 2. Weber TR, Gewertz BL, Stanley JC, et al. Renal effects of acute infrarenal aorto-caval fistula. J Surg Res 1978;25:482-7. 3. Brewster DC, Ottinger LW, Darling RC, et al. Hematuria as a sign of aorto-cad fistula. Ann Surg 1977;186:766-71. 4. Livingstone AS, Chiu CJ, Mulder DS, et al. Spontaneous aortocaval fistula secondary to ruptured abdominal aortic aneurysm. Can J Surg 1977;20:33-6.
Substitution by adenosine for glucagon as a surgical diagnostic tool to detect mesenteric vascular adaptation To the Ed&s:
The recent article by Clark and Gewertz,’ “Glucagon potentiates intestinal repefision injury,” treats glucagon-induced adverse effects exclusively from the viewpoint of therapeutics and does not address the possibility of similar hazards that may be encountered when the agent is used as a diagnostic tool of adaptation potential as it has recently been proposed.’ However, by collating the important findings of Clark and Gewertz,’ with those of Lilly et al.* who advocated the widespread usage of glucagon to gauge vasodilator capacity in patients suspected of having mesenteric ischernia, the latter (hypothetical) conclusion also seemsinevitable. Gut segments of patients with diverse manifestations of mesenteric arterial insufficiency are constantly verging toward being submitted to irreversible necrosis. Repetitive but brief periods of intestinal ischemia, which characterize these syndromes, usually fail to elicit irreversible damages as long as postischemic reperf&ion is continued for hours, and, as Clark and Gewertz have convincingly shown, the ischemic (and probably the preischemic) phasesof such episodesare not associatedwith an unduly strong metabolic stress.At the same time, the whimsical time course of periodicity will locate each particular term of these cyclicpathologic events along a spectrum between the opposite ends of full recovery and ischemic nadir. The crucial point is that it is practically impossible to determine with a sufficient degree of certainty the exact timing of ischemic episodes, whereas the consequences become manifest only at later times. It follows that by testing his patients with glucagon, the surgeon may run unnecessaryand unwarranted risks. Although still unproven in details, these considerations should be taken into account in tailoring diagnostic measures- which are not necessarily uniform in every situation. In searchfor selecting vasoactiveagents that may 919
