Correspondence

Ching-Hsing Lee MD

235

Post-computed tomography of the kidney, ureter, and

Department of Hyperbaric oxygen Therapy Center and Department of Emergency Medicine Chang Gung Memorial Hospital

and Chang Gung University College of Medicine

Taoyuan, Taiwan, ROC E-mail address: [email protected]

doi:10.1016/j.ajem.2010.10.002

Reference

[1] Lee SH, Ryu S, Lee JW, Kim SW, et al. Hyperthermia occurred after hyperbaric oxygen therapy for carbon monoxide poisoning. Am J Emerg Med. 2010;28:845.e5-6.

Hyperthermia occurred after hyperbaric oxygen therapy for carbon monoxide poisoning

To the Editor,

I want to thank the reader for his/her response to my article. I would like to point out the situation encountered that was described in this article. Hyperthermia occurred after Hyperbaric oxygen therapy was administered to a CO poisoning patient. We used the Ideal gas law to explain this case; however, this did not explain our findings entirely. However, the body temperature was normal after HBO therapy ceased without any interventions. I think if any causes were present, hyperthermia would have been steady until those causes were treated. Also, the temperature within the chamber (monochamber) itself might not reach above normal body temperature as the reader cited. No study cites a situation when a human is within the chamber. I think there would be some differences between the standard chamber and a human within the chamber in terms of hormones, metabolism, convection, and so on. Therefore, my colla- borators and I are currently investigating the relation of standard chamber and the body temperature within HBO

chamber (monochamber).

Seung Han Lee MD Seung Ryu MD

Jin Woong Lee MD Seung Whan Kim MD In Sool Yoo MD YeonHo You MD

Department of Emergency Medicine

College of Medicine Chungnam National University Hospital Daejeon 301-721, South Korea

E-mail address: [email protected] doi:10.1016/j.ajem.2010.10.001

bladder diagnosis of Urinary extravasation

To the Editor,

We read with great interest the paper by Lien et al who reported 3 cases of spontaneous urinary extravasation (SUE), secondary to ureteral rupture caused by impacted stones at ureterovesical junction (UVJ) [1]. All three of the authors’ cases well demonstrated contrast leakage from ureteropelvic junction (UPJ) on enhanced computed tomographic scans. In this article, we present a case of SUE due to an impacted UVJ stone. abdominal CT scans revealed perirenal fluid accumulation, hydronephrosis, and an impacted UVJ stone, but did not identify Contrast medium extravasation. However, the diagnosis was confirmed by a subsequent post- CT radiograph of kidney, ureter, and bladder . We suggest that a post-CT KUB radiograph might be a choice of imaging modality for the diagnosis of SUE.

A previously healthy, 51-year-old man presented to the emergency department with complaints of sudden onset of severe left upper quadrant pain concomitant flank pain. Physical examination revealed left flank knocking pain. Laboratory evaluation disclosed an elevated WBC count (10980 cells/mm³) with 94% segmented neutrophils and a normal urinalysis. abdominal radiography showed no calcifications. Ultrasound disclosed left hydronephrosis with perirenal fluid collection. An abdominal CT with and without enhancement was obtained to differentiate the cause of hydronephrosis and perirenal fluid accumulation. Unen- hanced CT scans demonstrated a small UVJ stone (Fig. 1A). Enhanced CT scans showed hydronephrosis of left kidney and perirenal fluid accumulation without excretion of contrast medium into the fluid (Fig. 2B). The KUB obtained 23 minutes subsequently after the enhanced CT scan was remarkable for contrast medium extravasation from UPJ and around left renal pelvis and ureter, consistent with ureteral rupture (Fig. 2). The patient was hospitalized and managed conservatively with analgesics, intravenous anti- biotics, and fluids. A follow-up ultrasonography performed on the fourth day revealed resolution of left hydronephrosis and disappearance of the fluid collection. He had an uneventful recovery.

Extravasation of urine secondary to Ureter rupture may be responsible for some of the acute abdomen-like cases in ED that can be managed with conservative treatment and careful monitoring [1,2]. The major clinical manifestation of SUE is sudden-onset abdominal and concomitant flank pain on the ruptured side. In previous reports, Ureteral stone disease was the most common etiologic cause associated with ureteral rupture [1-4]. Ultrasound is an essential screening modality to detect perinephric fluid in patients with features of renal colic and is easily accessible for serial evaluation. Enhanced CT scans may play a role in determining the site of rupture, although intravenous urography (IVU) is considered as the radiologic method of choice [1,2]. In our case, contrast-

236 Correspondence

Fig. 1 A, Unenhanced CT scan showed a tiny calcification impacted at the left ureterovesical junction (arrow). B, Enhanced CT showed hydronephrosis of left kidney and perirenal fluid accumulation without active contrast extravasatoin.

enhanced CT scans could not identify the site of rupture. However, a post-enhanced-CT KUB allowed for reliable detection of extravasation from the ureter in this patient. Patients with ureteral rupture and urinary extravasation will be diagnosed, if appropriate imaging modalities are chosen to investigate ED patients with acute flank pain. Ultrasound may be used in immediate detecting the presence of hydronephrosis and perirenal fluid accumulation and subse- quent enhanced CT scans in determining the site of rupture.

Fig. 2 Post-contrast-enhanced CT abdominal radiograph showed contrast medium extravasation from ureteropelvic junction and around left renal pelvis and ureter.

We suggest that a post-enhanced-CT KUB might be valuable in determining the site of rupture as traditional IVU.

Chung-Pang Wang Department of Emergency Medicine Taichung Veterans General Hospital Taichung 40705, Taiwan, R.O.C.

E-mail address: [email protected]

Yao-Tien Chang Department of Emergency Medicine Taichung Veterans General Hospital Taichung 40705, Taiwan, R.O.C. National Taichung Nursing College Taichung 40343, Taiwan, R.O.C.

Yu-Tse Tsan Department of Emergency Medicine Taichung Veterans General Hospital Taichung 40705, Taiwan, R.O.C.

School of Medicine Chung-Shan Medical University Taichung 40201, Taiwan, R.O.C.

Jin-An Huang Department of Emergency Medicine Taichung Veterans General Hospital Taichung 40705, Taiwan, R.O.C.

Department of Health Services Administration

China Medical University Taichung 40402, Taiwan, R.O.C.

doi:10.1016/j.ajem.2010.09.037

References

1. Lien W, Chen W, Wang H, et al. Spontaneous urinary extravasation: an overlooked cause of acute abdomen in ED. Am J Emerg Med 2006;24: 347-9.

Correspondence 237

1. Akpinar H, Kural AR, Tufek I, et al. Spontaneous ureteral rupture: is immediate surgical intervention always necessary? Presentation of four cases and review of the literature. J Endourol 2002;16:179-83.
2. Cooke GM, Bartucz JP. Spontaneous extravasation of contrast medium during intravenous urography: report of fourteen cases and a review of the literature. Clin Radiol 1974;25:87-93.
3. Diamond DA, Marshall FF. The diagnosis and management of Spontaneous rupture of the ureter. J Urol 1982;128:808-10.

Diagnostic and Therapeutic implications in post- myocardial infarct patients with raised brain natriuretic peptide levels

To the Editor,

Despite the fact that survivors of ST-segment elevation myocardial infarct with diastolic dysfunction had signifi- cantly (P = .01) higher median levels of Brain natriuretic peptide , compared with counterparts without diastolic dysfunction, subjects with BNP greater than 500 pg/mL, nevertheless had significantly (P = .003) lower left ventricular ejection fraction (LVEF; mean value 37%) than counterparts with BNP less than 500 pg/mL (in whom the mean value was 48%) [1]. This was probably a reflection of the fact that in some post-myocardial infarction (post-MI) subjects, exemplified, in one study, by a subgroup of 18 subjects with mean LVEF as low as 36.9%, severe left ventricular diastolic dysfunction may coexist with systolic dysfunction and, hence, subnormal LVEF [2]. That this should be the case is consistent with the observation that in the animal model of post-MI, survival myocardial fibrosis in the noninfarcted region is the histologic correlate of systolic as well as diastolic dysfunction [3].

Even in the early stages of post-MI heart failure [4], despite background prevalence of 78.8% for hypertension (a recognized risk factor for diastolic dysfunction) [5] and background prevalence of 49.6% for diabetes mellitus (also a risk factor for diastolic dysfunction) [6], mean LVEF may be as low as 39.11% [4], again probably reflecting the fact that LVEF may not be truly representative of the coexistence of diastolic dysfunction and its severity in subjects with subnormal LVEF. In the latter study, despite early initiation of angiotensin-converting enzyme (ACE) inhibitor therapy, there was only a modest (P b .05) “protective short term effect on mortality” [4], which, arguably, might have been considerably enhanced, had an aldosterone antagonist been coprescribed with the ACE inhibitor, as in the EPHESUS study (Eplerenone Post-acute myocardial infarction Heart failure Efficacy and Survival Study), which enrolled subjects with LVEF less than 40% [7]. It has been already shown that outside the post-MI context, the substitution of torasemide, a Loop diuretic with anti- aldosterone properties, for frusemide as an addition to existing ACE inhibitor or angiotensin receptor blocker therapy significantly (P b .01) reduces the collagen volume fraction (the fraction of myocardial volume occupied by collagen) on

an 8-month follow up, not only in patients with Diastolic heart failure but also in those with systolic heart failure [8]. In the latter study [8], as well as in a study exclusively enrolling heart failure subjects with intact LVEF, the success of antialdoster- one therapy in significantly (P = .006) attenuating the progressive increase in markers of collagen turnover (which reflect myocardial fibrosis) might, arguably, have been attributable to its coprescription with either ACE inhibitors or angiotensin receptor blockers [9], given the fact that in the animal model of post-MI survival, the severity of myocardial fibrosis can be significantly (P b .01) attenuated either by ACE inhibitor therapy or by aldosterone blockade [3]. Accordingly, in subjects such as the ones reported in the recent study, the advocacy for the use of “agents that antagonize the renin angiotensin aldosterone system” for the purpose of conferring clinical benefit in patients with ST-segment elevation myocardial infarction who have increased BNP levels [1] should comprise coprescription of ACE inhibitors and aldosterone antagonists regardless of baseline LVEF, so as to optimize the opportunity to mitigate the severity of post-MI myocardial fibrosis. Other benefits of coprescription of ACE inhibitors and aldosterone antagonists include a loop diuretic- sparing effect [10], which, in the context of loop diuretic- related activation of the Renin-angiotensin-aldosterone system [11], might mitigate the risk of renin-angiotensin- aldosterone system-related myocardial fibrosis, a phenome- non in which the role of diuretics has not been explored even in studies that report the occurrence of myocardial fibrosis in heart failure patients on background diuretic therapy [8,9].

Oscar M.P. Jolobe MB, ChB, DPhil

Manchester Medical Society C/o John Rylands University Library Manchester M13 9PP, UK

E-mail address: [email protected] doi:10.1016/j.ajem.2010.10.004

References

1. Neyou A, O’Neill B, Berman AD, Boura JA, McCullough PA. Determinants of markedly increased B-type natriuretic peptide in patients with ST-segment elevation myocardial infarction. Am J Emerg Med 2010. doi:10:1016/j.ajem 2009.08.003.
2. Khumri TM, reid KJ, Kosiborod M, Spertus JA, Main ML. Usefulness of left ventricular diastolic dysfunction as a predictor of one-year rehospitalization in survivors of acute myocardial infarction. Am J Cardiol 2009;103:17-21.
3. Zhang Y-L, Zhou S-X, Lei J, Yuan G-Y, Wang J-F. Blockades of angiotensin and aldosterone reduce osteopontin expression and interstitial fibrosis infiltration in rats with myocardial infarction. Chin Med J 2008;121:2192-6.
4. Nunez-Gil IJ, Garcia-Rubira J, Luaces M, et al. Mild heart failure is a mortality marker after non-ST-segment acute myocardial infarction. Eur J Intern Med 2010;21:439-43.
5. Mcmurray JJ, Carson PE, Komajda M, et al. heart failure with preserved ejection fraction: clinical characteristics of 4113 patients enrolled in I-PRESERVED trial. Eur J Heart Fail 2008;10:149-56.