Vol. 220, No. 3, March 2015
by primary peritoneal drainage. With this in mind, we have embarked upon a stepwise series of ongoing studies, using prospectively collected data, with the aim to delineate the mortality of NEC overall and within clearly identifiable subgroups. Our initial study of NEC included very low birth weight (VLBW) neonates with either medical or surgical NEC.2 It showed that the incidence and mortality of NEC were most accurately predicted by birth weight. Our subsequent consideration of surgical NEC further demonstrated that birth weight, surgery, and primary peritoneal drainage (PPD) were all independent predictors of mortality.1 An interesting facet of this investigation was that although the highest mortality was associated with PPD, this was clearly a dichotomous group. Twenty-seven percent of the patients receiving PPD survived without needing another operation, so by inference, this set of patients was likely composed of neonates with relatively minimal NEC or SIP.1 In the Vermont Oxford Manual of Operations, a diagnosis of SIP is not imputed, but rather is determined by direct observation at laparotomy.3 Of note, two-thirds of all VLBW neonates who had surgery for either NEC or SIP in the United States had initial laparotomies, and further laparotomy was used more frequently than PPD even in the smallest of neonates.1 We prospectively garnered data to determine if SIP or standard NEC was present at the time of laparotomy. Our 5-year data collection allowed us to assess more than 6,000 neonates.3 The findings in this cohort included the following: the ratio of SIP to NEC was 1:2, SIP mortality was approximately half that of NEC, but in general, was significantly higher than baseline.3 This study also afforded birth-weight specific benchmark mortality rates for SIP.3 A further cohort of interest, both from a clinical and potentially mechanistic standpoint, is VLBW neonates with both severe congenital heart disease and NEC. In this group of patients, the mortality was 55%, which was significantly higher than in neonates with NEC alone or with congenital heart disease alone.4 Necrotizing enterocolitis is an umbrella diagnosis for a set of similarly presenting, largely idiopathic disease entities, and multiple further investigations are certainly required to more completely define outcomes in specific neonatal populations. REFERENCES 1. Hull MA, Fisher JG, Gutierrez IM, et al. Mortality and management of surgical necrotizing enterocolitis in very low birth weight neonates: a prospective cohort study. J Am Coll Surg 2014;218:1148e1155. 2. Fitzgibbons SC, Ching Y, Yu D, et al. Mortality of necrotizing enterocolitis expressed by birth weight categories. J Pediatr Surg 2009;44:1072e1075.
Letters
371
3. Fisher JG, Jones BA, Gutierrez IM, et al. Mortality associated with laparotomy-confirmed neonatal spontaneous intestinal perforation: a prospective 5-year multicenter analysis. J Pediatr Surg 2014;49:1215e1219. 4. Fisher JG, Bairdain S, Sparks EA, et al. Serious congenital heart disease and necrotizing enterocolitis in very low birth weight neonates: a prospective cohort analysis. J Am Coll Surg (In Press). doi: 10.1016/j.jamcollsurg.2014.11.026.
Disclosure Information: Nothing to disclose.
Assessment of Tumor Growth in von Hippel Lindau Syndrome Hamid Qazi, Hon. BSc, Hamza Ahmed, Saleem O Farooqui, MD, Steven C Cunningham, MD, FACS Baltimore, MD
MD,
We read with interest the recent study by Weisbrod and colleagues, “Assessment of tumor growth in pancreatic neuroendocrine tumors in von Hippel Lindau syndrome.”1 They conducted a prospective study of 87 patients with solid, hyper-enhancing pancreatic neuroendocrine tumors (PNET) associated with von Hippel Lindau (VHL) syndrome and concluded that tumor density may provide a specific indicator for malignancy. Given the difficulty in predicting behavior of PNET, and the ease of obtaining density measurements from pancreatic-protocol CT, these findings are interesting and provocative. We would like to congratulate the authors for taking advantage of a large volume of VHL patients to address an important question, the answer to which is potentially amenable to extrapolation to all PNET patients. However, we would like to raise 3 issues. First, the authors describe that arterial-phase imaging typically occurred 10 to 20 seconds after injection. Indeed, they cite exact timing of contrast administration as an uncontrollable factor, which occasions the question of whether bolus tracking2 or another technique was used to tailor the scan to the patient. Certainly the same lesion scanned 10 seconds earlier or later would have a vastly different density. Our institutional pancreatic-protocol CT scan uses a bolus-tracking method to initiate the scan only after IV contrast has reached a predetermined density threshold in the abdominal aorta, consistently capturing the desired phase, and controlling for variations in cardiac output. This technique is much more accurate than administering contrast strictly based on time elapsed because in hyperdynamic patients and patients with congestive heart failure, the intended arterial scan may occur too late or too early, respectively.
372
Letters
J Am Coll Surg
Second, tumor density strongly and inversely correlated with larger tumors, and decreasing density was associated with increased aggressiveness. But they suggest that high tumor density may be specific for malignancy. How do the authors reconcile these observations? Third, the authors note that a density cut-off of 200 (presumably Hounsfield units?) was 75% specific for malignant tumors. We would like to respectfully raise the question, “Is 75% a clinically useful specificity?” Many, if not most, tests currently in clinical use have vastly higher specificities (eg PCR for C diff, 99%3; CT for pulmonary embolism (PE), >90% to 95%4,5; CT for appendicitis,
by primary peritoneal drainage. With this in mind, we have embarked upon a stepwise series of ongoing studies, using prospectively collected data, with the aim to delineate the mortality of NEC overall and within clearly identifiable subgroups. Our initial study of NEC included very low birth weight (VLBW) neonates with either medical or surgical NEC.2 It showed that the incidence and mortality of NEC were most accurately predicted by birth weight. Our subsequent consideration of surgical NEC further demonstrated that birth weight, surgery, and primary peritoneal drainage (PPD) were all independent predictors of mortality.1 An interesting facet of this investigation was that although the highest mortality was associated with PPD, this was clearly a dichotomous group. Twenty-seven percent of the patients receiving PPD survived without needing another operation, so by inference, this set of patients was likely composed of neonates with relatively minimal NEC or SIP.1 In the Vermont Oxford Manual of Operations, a diagnosis of SIP is not imputed, but rather is determined by direct observation at laparotomy.3 Of note, two-thirds of all VLBW neonates who had surgery for either NEC or SIP in the United States had initial laparotomies, and further laparotomy was used more frequently than PPD even in the smallest of neonates.1 We prospectively garnered data to determine if SIP or standard NEC was present at the time of laparotomy. Our 5-year data collection allowed us to assess more than 6,000 neonates.3 The findings in this cohort included the following: the ratio of SIP to NEC was 1:2, SIP mortality was approximately half that of NEC, but in general, was significantly higher than baseline.3 This study also afforded birth-weight specific benchmark mortality rates for SIP.3 A further cohort of interest, both from a clinical and potentially mechanistic standpoint, is VLBW neonates with both severe congenital heart disease and NEC. In this group of patients, the mortality was 55%, which was significantly higher than in neonates with NEC alone or with congenital heart disease alone.4 Necrotizing enterocolitis is an umbrella diagnosis for a set of similarly presenting, largely idiopathic disease entities, and multiple further investigations are certainly required to more completely define outcomes in specific neonatal populations. REFERENCES 1. Hull MA, Fisher JG, Gutierrez IM, et al. Mortality and management of surgical necrotizing enterocolitis in very low birth weight neonates: a prospective cohort study. J Am Coll Surg 2014;218:1148e1155. 2. Fitzgibbons SC, Ching Y, Yu D, et al. Mortality of necrotizing enterocolitis expressed by birth weight categories. J Pediatr Surg 2009;44:1072e1075.
Letters
371
3. Fisher JG, Jones BA, Gutierrez IM, et al. Mortality associated with laparotomy-confirmed neonatal spontaneous intestinal perforation: a prospective 5-year multicenter analysis. J Pediatr Surg 2014;49:1215e1219. 4. Fisher JG, Bairdain S, Sparks EA, et al. Serious congenital heart disease and necrotizing enterocolitis in very low birth weight neonates: a prospective cohort analysis. J Am Coll Surg (In Press). doi: 10.1016/j.jamcollsurg.2014.11.026.
Disclosure Information: Nothing to disclose.
Assessment of Tumor Growth in von Hippel Lindau Syndrome Hamid Qazi, Hon. BSc, Hamza Ahmed, Saleem O Farooqui, MD, Steven C Cunningham, MD, FACS Baltimore, MD
MD,
We read with interest the recent study by Weisbrod and colleagues, “Assessment of tumor growth in pancreatic neuroendocrine tumors in von Hippel Lindau syndrome.”1 They conducted a prospective study of 87 patients with solid, hyper-enhancing pancreatic neuroendocrine tumors (PNET) associated with von Hippel Lindau (VHL) syndrome and concluded that tumor density may provide a specific indicator for malignancy. Given the difficulty in predicting behavior of PNET, and the ease of obtaining density measurements from pancreatic-protocol CT, these findings are interesting and provocative. We would like to congratulate the authors for taking advantage of a large volume of VHL patients to address an important question, the answer to which is potentially amenable to extrapolation to all PNET patients. However, we would like to raise 3 issues. First, the authors describe that arterial-phase imaging typically occurred 10 to 20 seconds after injection. Indeed, they cite exact timing of contrast administration as an uncontrollable factor, which occasions the question of whether bolus tracking2 or another technique was used to tailor the scan to the patient. Certainly the same lesion scanned 10 seconds earlier or later would have a vastly different density. Our institutional pancreatic-protocol CT scan uses a bolus-tracking method to initiate the scan only after IV contrast has reached a predetermined density threshold in the abdominal aorta, consistently capturing the desired phase, and controlling for variations in cardiac output. This technique is much more accurate than administering contrast strictly based on time elapsed because in hyperdynamic patients and patients with congestive heart failure, the intended arterial scan may occur too late or too early, respectively.
372
Letters
J Am Coll Surg
Second, tumor density strongly and inversely correlated with larger tumors, and decreasing density was associated with increased aggressiveness. But they suggest that high tumor density may be specific for malignancy. How do the authors reconcile these observations? Third, the authors note that a density cut-off of 200 (presumably Hounsfield units?) was 75% specific for malignant tumors. We would like to respectfully raise the question, “Is 75% a clinically useful specificity?” Many, if not most, tests currently in clinical use have vastly higher specificities (eg PCR for C diff, 99%3; CT for pulmonary embolism (PE), >90% to 95%4,5; CT for appendicitis,
![[Von Hippel-Lindau syndrome].](/assets/img/hold.png)
