Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3706_Библиотеки_им_академика_М_И_Перельмана
.pdf
90
https://t.me/med1917
M. G. Hochman and C. Connolly
104. Sofka CM.Technical considerations: best practices for MR imaging of the foot and ankle. Magn Reson Imaging Clin N Am.
2017;25(1):1–10.
105. Chun CW, Jung JY, Baik JS, Jee WH, Kim SK, Shin SH.Detection
of soft tissue abscess: comparison of diffusion-weighted
imaging to contrast-enhanced MRI. J Magn Reson Imaging.
2018;47(1):60–8.
106. Liao D, Xie L, Han Y, Du S, Wang H, Zeng C, Li Y.Dynamic
contrast-enhanced magnetic resonance imaging for differentiating
osteomyelitis from acute neuropathic arthropathy in the complicated diabetic foot. Skeletal Radiol. 2018;47(10):1337–47.
107. Kotecha HM, Lo HS, Vendantham S, Shin H, Cerniglia
CA.Abbreviated MRI of the foot in patients with suspected osteomyelitis. Emerg Radiol. 2020;27(1):9–16.
108. Wertman R, Altun E, Martin DR, Mitchell DG, Leyendecker
JR, O’Malley RB, etal. Risk of nephrogenic systemic brosis:
evaluation of gadolinium chelate contrast agents at four American
Universities. Radiology. 2008;248(3):799–806.
109. Broome DR, Girguis MS, Baron PW, Cottrell AC, Kjellin I, Kirk
GA. Gadodiamide-associated nephrogenic systemic brosis:
why radiologists should be concerned. AJR Am J Roentgenol.
2007;188(2):586–92.
110. US Food and Drug Administration. FDA Drug Safety
Communication: New warnings for using gadolinium-based
contrast agents in patients with kidney dysfunction 09-09-
2010. https://www.fda.gov/Drugs/DrugSafety/ucm223966.htm.
Accessed 19 Feb 2017.
111. Sena BF, Stern JP, Pandharipande PV, Klemm B, Bulman J,
Pedrosa I, Rofsky NM.Screening patients to assess renal function before administering gadolinium chelates: assessment of the
Choyke questionnaire. AJR Am J Roentgenol. 2010;195(2):424–8.
112. Kanal E, Tweedle MF.Residual or retained gadolinium: practical implications for radiologists and our patients. Radiology.
2015;275(3):630–4.
113. Morrison WB, Schweitzer ME, Wapner KL, Hecht PJ, Gannon
FH, Behm WR.Osteomyelitis in feet of diabetics: clinical accuracy, surgical utility, and cost-effectiveness of MR imaging.
Radiology. 1995;196(2):557–64.
114. Miller TT, Randolph DA Jr, Staron RB, Feldman F, Cushin S.Fatsuppressed MRI of musculoskeletal infection: fast T2-weighted
techniques versus gadolinium-enhanced T1-weighted images.
Skeletal Radiol. 1997;26(11):654–8.
115. Collins MS, Schaar MM, Wenger DE, Mandrekar
JN. T1-weighted MNR characteristics of pedal osteomyelitis.
AJR. 2005;185:386–93.
116. Duryea D, Bernard S, Flemming D, Walker E, French C.Outcomes
in diabetic foot ulcer patients with isolated T2 marrow signal
abnormality in the underlying bone: should the diagnosis of
“osteitis” be changed to “early osteomyelitis”? Skeletal Radiol.
2017;46:1327–33. https://doi.org/10.1007/s00256- 017- 2666- x.
117. Sax AJ, Halpern EJ, Zoga AC, Roedl JB, Belair JA, Morrison
WB.Predicting osteomyelitis in patients whose initial MRI demonstrated bone marrow edema without corresponding T1 signal
marrow replacement. Skeletal Radiol. 2020;49(8):1239–47.
118. Jang YH, Park S, Park YU, Kwack K, Jeon SW, Lee HY.Multivariate
analysis of MRI ndings for predicting osteomyelitis of the foot in
diabetic patients. Acta Radiol. 2020;61(9):1205–121.
119. Morrison WB, Schweitzer ME, Batte WG, Radack DP, Russel
KM.Osteomyelitis of the foot: relative importance of primary and
secondary MR imaging signs. Radiology. 1998;207(3):625–32.
120. Horowitz SH. Diabetic neuropathy. Clin Orthop Relat Res.
1993;296:78–85.
121. Nigro ND, Bartynski WS, Grossman SJ, Kruljac S. Clinical
impact of magnetic resonance imaging in foot osteomyelitis. J Am
Podiatr Med Assoc. 1992;82(12):603–15.
122. Wang A, Weinstein D, Greeneld L, Chiu L, Chambers R, Stewart
C, etal. MRI and diabetic foot infections. Magn Reson Imaging.
1990;8(6):805–9.
123. Yu JS. Diabetic foot and neuroarthropathy: magnetic resonance imaging evaluation. Topics Magn Reson Imaging.
1998;9(5):295–310.
124. Weinstein D, Wang A, Chambers R, Stewart CA, Motz
HA. Evaluation of magnetic resonance imaging in the diagnosis of osteomyelitis in diabetic foot infections. Foot Ankle.
1993;14(1):18–22.
125. Berquist TH.Infection. In: Berquist TH, editor. Imaging of the
foot and ankle. Philadelphia, PA: Wolters Kluwer/Lippincott
Williams & Wilkins; 2011. p.436–86.
126. Ahmadi ME, Morrison WB, Carrino JA, Schweitzer ME, Raikin
SM, Ledermann HP.Neuropathic arthropathy of the foot with and
without superimposed osteomyelitis: MR imaging characteristics.
Radiology. 2006;238(2):622–31.
127. Donovan A, Schweitzer M. Use of MR imaging in diagnosisng
pedal osteomyelitis. Radiographics. 2010;30:723–36. https://doi.
org/10.1148/rg.303095111.
128. Bernstein B, Stouder M, Bronfenbrenner E, Chen S, Anderson
D. Correlating pre-operative MRI measurements of metatarsal
osteomyelitis with surgical clean margins reveals the need for a one
centimeter resection margin. J Foot Ankle Res. 2017;10:40–51.
129. Ledermann HP, Schweitzer ME, Morrison WB. Nonenhancing
tissue on MR imaging of pedal infection: characterization of
necrotic tissue and associated limitations for diagnosis of osteomyelitis and abscess. AJR Am J Roentgenol. 2002;178(1):215–22.
130. Bus SA, Maas M, Cavanagh PR, Michels RP, Levi M. Plantar
fat-pad displacement in neuropathic diabetic patients with toe
deformity: a magnetic resonance imaging study. Diabetes Care.
2004;27(10):2376–81.
131. Andreassen CS, Jakobsen J, Ringgaard S, Ejskjaer N, Andersen
H.Accelerated atrophy of lower leg and foot muscles—a follow up study of long-term diabetic polyneuropathy using magnetic
resonance imaging (MRI). Diabetologia. 2009;52(6):1182–91.
132. Brash PD, Foster J, Vennart W, Anthony P, Tooke JE. Magnetic
resonance imaging techniques demonstrate soft tissue damage in
the diabetic foot. Diabet Med. 1999;16(1):55–61.
133. Dinh T, Doupis J, Lyons TE, Kuchibhotla S, Julliard W, Gnardellis
C, etal. Foot muscle energy reserves in diabetic patients without and with clinical peripheral neuropathy. Diabetes Care.
2009;32(8):1521–4. Pubmed Central PMCID: 2713635
134. Greenman RL, Panasyuk S, Wang X, Lyons TE, Dinh T, Longoria
L, etal. Early changes in the skin microcirculation and muscle
metabolism of the diabetic foot. Lancet. 2005;366(9498):1711–7.
135. Suzuki E, Kashiwagi A, Hidaka H, Maegawa H, Nishio Y, Kojima
H, etal. 1H- and 31P-magnetic resonance spectroscopy and imaging as a new diagnostic tool to evaluate neuropathic foot ulcers in
type II diabetic patients. Diabetologia. 2000;43(2):165–72.
136. Weaver JB, Doyley M, Cheung Y, Kennedy F, Madsen EL, Van
Houten EE, etal. Imaging the shear modulus of the heel fat pads.
Clin Biomech. 2005;20(3):312–9.
137. Tognarelli JM, Dawood M, Shariff MIF, Grover VPB, Crossey
MME, Cox IJ, Taylor-Robin SD, McPhail MJW.Magnetic resonance spectrsoscopy: principles and techniques: lessons for clinicians. J Clin Exp Hepatol. 2015;5:320–8.
138. Chance B, Eleff S, Leigh JS. Non-invasive, non-destructive
approaches to cell bioenergetics. Proc Natl Acad Sci USA.
1980;77(12):7430–4. [PMC free article] [PubMed] [Google
Scholar]
139. Bottomley PA, Charles HC, Roemer PB, Flamig D, Engeseth H,
Edelstein WA, Mueller OM.Human invivo phosphate metabolite
imaging with 31P NMR.Magn Reson Med. 1988;7(3):319–36.
[PubMed] [Google Schola

5 Imaging ofInfection intheDiabetic Foot
https://t.me/med1917
91
140. Ingwall JS. Phosphorus nuclear magnetic resonance spectroscopy of cardiac and skeletal muscles. Am J Physiol.
1982;242(5):H729–44.
141. Ingwall JS, Kramer MF, Fifer MA, Lorell BH, Shemin R,
Grossman W, Allen PD.The creatine kinase system in normal and
diseased human myocardium. N Engl J Med. 1985;313:1050–4.
142. Lin YC, Wu J, Baltzis D, Veves A, Greenman RL.MRI assessment
of regional difference in phosphorus-31 metabolism and morphological abnormalities of the foot muscles in diabetes. J Magn
Reson Imaging. 2016;44:1132–42.
143. Crowther GJ, Milstein JM, Jubrias SA, Kushmerick MJ, Gronka
RK, Conley KE.Altered energetic properties in skeletal muscle of
men with well-controlled insulin-dependent (type 1) diabetes. Am
J Physiol Endocrinol Metab. 2003;284(4):E655–62.
144. Isbell DC, Berr SS, Toledano AY, Epstein FH, Meyer CH,
Rogers WJ, Harthun NL, Hagspiel KD, Weltman A, Kramer
CM. Delayed calf muscle phosphocreatine recovery after exercise identies peripheral arterial disease. J Am Coll Cardiol.
2006;47(11):2289–95.
145. Schmid AI, Schrauwen-Hinderling VB, Andreas M, Wolzt M,
Moser E, Roden M.Comparison of measuring energy metabolism
by different P-31-magnetic resonance spectroscopy techniques
in resting, ischemic, and exercising muscle. Magn Reson Med.
2012;67(4):898–905.
146. Khegai O, Madelin G, Brown R, Parasoglou P.Dynamic phosphocreatine imaging with unlocalized pH assessment of the human
lower leg muscle following exercise at 3T. Magn Reson Med.
2018;79(2):974–80. https://doi.org/10.1002/mrm.26728.
147. Bolacchi F, Uccioli L, Masala S, Giurato L, Ruotolo V, Meloni
M, Baffari E, Cinelli E, Cadioli M, Squillaci E, Simonetti G,
Bergamini A.Proton magnetic resonance spectroscopy in the evaluation of patients with acute Charcot neuro-osteoarthropathy. Eur
Radiol. 2013;23(10):2807–13. https://doi.org/10.1007/s00330- -
013- 2894- y. Epub 2013 Jun 11
148. Ergen FB, Sanverdi SE, Oznur A.Charcot foot in diabetes and an
update on imaging. Diabet Foot Ankle. 2013;4(1):21884. Pubmed
Central PMCID: 3837304
149. Marmojelo VS, Arnold JF, Ponticello M, Andersen CA.Charcot
foot: clinical clues. Diagnostic strategies. And treatment principles. Am Fam Physician. 2018;97(9):594–9.
150. Beltran J. MR imaging of soft-tissue infection. Magn Reson
Imaging Clin N Am. 1995;3(4):743–51.
151. Sequeira W. The neuropathic joint. Clin Exp Rheumatol.
1994;12(3):325–37.
152. Zlatkin MB, Pathria M, Sartoris DJ, Resnick D.The diabetic foot.
Radiol Clin North Am. 1987;25(6):1095–105.
153. Brower AC, Allman RM. Pathogenesis of the neurotrophic joint: neurotraumatic vs. neurovascular. Radiology.
1981;139(2):349–54.
154. Yablon CM, Duggal N, Wu JS, Shetty SK, Dawson F, Hochman
MG.A review of Charcot neuroarthropathy of the midfoot and
hindfoot: what every radiologist needs to know. Curr Probl Diagn
Radiol. 2010;39(5):187–99.
155. Leone A, Cassar-Pullicino VN, Semprini A, Tonetti L, Magarelli
N, Colosimo C. Neuropathic osteoarthropathy with and without superimposed osteomyelitis in patients with a diabetic foot.
Skeletal Radiol. 2016;45(6):735–54.
156. Shibata T, Tada K, Hashizume C.The results of arthrodesis of
the ankle for leprotic neuroarthropathy. J Bone Joint Surg Am.
1990;72:749–56.
157. Rosenbaum AJ, DiPreta JA. Classications in brief:
Eichenholtz classication of Charcot arthropathy. Clin Orthop
Relat Res. 2015;473(3):1168–71. https://doi.org/10.1007/
s11999- 014- 4059- y.
158. Holmes C, Schmidt B, Munson M, Wrobel JS.Charcot stage 0: a
review and considerations for making the correct diagnosis early.
Clin Diabetes Endocrinol. 2015;1:18. https://doi.org/10.1186/
s40842- 015- 0018- 0.
159. Dardari D. An overview of Charcot’s neuroarthropathy. J Clin
Transl Endocrin. 2020;22:100239. https://doi.org/10.1016/j.
jcte.2020.100239.
160. Chantelau E. The perils of procrastination: effects of early vs.
delayed detection and treatment of incipient Charcot fracture.
Diabet Med. 2005;22:1707–12.
161. Wukich DK, Sung W, Wipf SA, Armstrong DG. The consequences of complacency: managing the effects of unrecognised
Charcot feet. Diabet Med. 2011;28:195–8.
162. Chantelau EA, Richter A.The acute diabetic Charcot foot managed on the basis of magnetic resonance imaging—a review of 71
cases. Swiss Med Wk. 2013;143(3132):w13831.
163. Short DJ, Zgonis T. Medical imaging in differentiating the diabetic Charcot foot from osteomyelitis. Clin Podiatr Med Surg.
2017;34(1):9–14. https://doi.org/10.1016/j.cpm.2016.07.002.
164. Yu GV, Hudson JR.Evaluation and treatment of stage 0 Charcot’s
neuroarthropathy of the foot and ankle. J Am Podiatr Med Assoc.
2002;92(4):210–20.
165. Ertugrul BM, Lipsky BA, Savk O. Osteomyelitis or Charcot
neuro-osteoarthropathy? Differentiating these disorders in diabetic patients with a foot problem. Diabet Foot Ankle. 2013;4.
Pubmed Central PMCID: 3819473
166. Jones EA, Manaster BJ, May DA, Disler DG.Neuropathic osteoarthropathy: diagnostic dilemmas and differential diagnosis.
Radiographics. 2000;20(suppl_1):S279–93.
167. Waibel FWA, Boni T.Nonoperative treatment of Charcot neuroosteoarthropathy. Foot Ankle Clin N Am. 2002;27:595–616.
168. van der Ven A, Chapman CB, Bowker JH. Charcot neuroarthropathy of the foot and ankle. J Am Acad Orthop Surg.
2009;17(9):562–71.
169. Bevan WP, Tomlinson MP.Radiographic measures as a predictor of ulcer formation in diabetic charcot midfoot. Foot Ankle Int.
2008;29(6):568–73.
170. Wukich DK, Raspovic KM, Hobizal KB, Rosario B.Radiographic
analysis of diabetic midfoot charcot neuroarthropathy with and
without midfoot ulceration. Foot Ankle Int. 2014;35(11):1108–15.
171. Rogers LC, Bevilacqua NJ.The diagnosis of Charcot foot. Clin
Podiatr Med Surg. 2008;25(1):43–51. vi
172. Rogers LC, Bevilacqua NJ. Imaging of the Charcot foot. Clin
Podiatr Med Surg. 2008;25(2):263–74. vii
173. Mortada M, Ezzeldin N, Hammad M.Ultrasonographic features
of acute Charcot neuroarthropathy of the foot: a pilot study. Clin
Rheumatol. 2020;39(12):3787–93.
174. McCarthy E, Morrison WB, Zoga AC.MR imaging of the diabetic
foot. Magn Reson Imaging Clin N Am. 2017;25(1):183–94.
175. Daneshvar K, Anwander H. Diagnostic imaging of diabetic
foot disorders. Foot Ankle Clin. 2022;27(3):513–27. https://doi.
org/10.1016/j.fcl.2022.01.002. Epub 2022 Aug 6
176. Chantelau EA, Grützner G. Is the Eichenholtz classication still valid for the diabetic Charcot foot? Swiss Med Wkly.
2014;144:w13948. https://doi.org/10.4414/smw.2014.13948.
177. Yansouni CP, Mak A, Libman MD. Limitations of magnetic
resonance imaging in the diagnosis of osteomyelitis underlying
diabetic foot ulcers. Clin Infect Dis. 2009;48(1):135. https://doi.
org/10.1086/595556.
178. Martín Noguerol TM, Luna Alcalá A, Beltrán LS, Gómez Cabrera
M, Broncano Cabrero J, Vilanova JC.Advanced MR imaging techniques for differentiation of neuropathic arthropathy and osteomyelitis in the diabetic foot. Radiographics. 2017;37(4):1161–80.
https://doi.org/10.1148/rg.2017160101.

92
https://t.me/med1917
M. G. Hochman and C. Connolly
179. Garcia Diez A, Fuster D, Morata L, Torres F, Garcia R, Poggio
D, Sotes S, Del Amo M, Isern Kebschull J, Pomes J, Soriano
A, Brugnara L, Tomas X. Comparison of diagnostic accuracy
of diffusion weighted and dynamic contrast-enhanced MRI
with 18F FDG PET/CT to differentiate osteomyelitis from
Charcot neuro- osteoarthropathy in diabetic foot. Eur J Radiol.
2020;132:109299.
180. Israel O, Sconenza LM, Lipsky BA.Diagnosing diabetic foot
infection: the role of imaging and a proposed ow chart for assessment. Q J Nucl Med Mol Imaging. 2014;58(1):33–45.
181. Basu S, Chryssikos T, Houseni M, Scot Malay D, Shah J, Zhuang
H, etal. Potential role of FDG PET in the setting of diabetic neuroosteoarthropathy: can it differentiate uncomplicated Charcot’s
neuroarthropathy from osteomyelitis and soft-tissue infection?
Nucl Med Commun. 2007;28(6):465–72.
182. Pickwell KM, van Kroonenburgh MJ, Weijers RE, van
Hirtum PV, Huijberts MS, Schaper NC. F-18 FDG PET/CT
scanning in Charcot disease: a brief report. Clin Nucl Med.
2011;36(1):8–10.
183. Rastogi A, Bhattacharya A, Prakash M, Sharma S, Mittal BR,
Khandelwal N, Bhansali A.Utility of PET/CT with uorine- 18uorodeoxyglucose-labeled autologous leukocytes for diagnosing
diabetic foot osteomyelitis in patients with Charcot’s neuroarthropathy. Nucl Med Commun. 2016;37(12):1253–9. https://doi.
org/10.1097/MNM.0000000000000603.
184. Tram NK, Chou TH, Patel S, Ettefagh LN, Go MR, Atway SA,
Stacy MR.Novel application of 18F-NaF PET/CT imaging for evaluation of active bone remodeling in diabetic patients with Charcot
neuropathy: a proof-of-concept report. Front Med (Lausanne).
2022;9:795925. https://doi.org/10.3389/fmed.2022.795925.
PMID: 35252240; PMCID: PMC8896741
185. Park HM, Wheat LJ, Siddiqui AR, Burt RW, Robb JA, Ransburg
RC, Kernek CB.Scintigraphic evaluation of diabetic osteomyelitis: concise communication. J Nucl Med. 1982;23(7):569–73.
186. Segall GM, Nino-Murcia M, Jacobs T, Chang K.The role of bone
scan and radiography in the diagnostic evaluation of suspected
pedal osteomyelitis. Clin Nucl Med. 1989;14(4):255–60. https://
doi.org/10.1097/00003072- 198904000- 00003.
187. Seldin DW, Heiken JP, Feldman F, Alderson PO.Effect of softtissue pathology on detection of pedal osteomyelitis in diabetics. J
Nucl Med. 1985;26(9):988–93.
188. Oyen WJ, Netten PM, Lemmens JA, Claessens RA, Lutterman
JA, van der Vliet JA, Goris RJ, van der Meer JW, Corstens
FH. Evaluation of infectious diabetic foot complications with
indium-111-labeled human nonspecic immunoglobulin G. J
Nucl Med. 1992;33(7):1330–6.
189. Palestro CJ, Love C.Nuclear medicine and diabetic foot infections. Semin Nucl Med. 2009;39(1):52–65.
190. Newman LG.Imaging techniques in the diabetic foot. Clin Podiatr
Med Surg. 1995;12(1):75–86.
191. Beltran J, Campanini DS, Knight C, McCalla M. The diabetic
foot: magnetic resonance imaging evaluation. Skeletal Radiol.
1990;19(1):37–41. https://doi.org/10.1007/BF00197927.
192. Lauri C, Glaudemans AWJM, Campagna G, Keidar Z, Muchnik
Kurash M, Georga S, Arsos G, Noriega-Álvarez E, Argento G,
Kwee TC, Slart RHJA, Signore A. Comparison of white blood
cell scintigraphy, FDG PET/CT and MRI in suspected diabetic
foot infection: results of a large retrospective multicenter study.
J Clin Med. 2020;9(6):1645. https://doi.org/10.3390/jcm9061645.
PMID: 32486304; PMCID: PMC7356770

Principles ofCare intheDiabetic
https://t.me/med1917
Surgical Patient
NatashaKhazai andOsamaHamdy
6
Abstract
Currently, around 37.3million Americans—about one in
ten—have diabetes, and about one in ve people with diabetes do not know they have it. It is also estimated that
96million are thought to have prediabetes. Diabetes is currently the eighth leading cause of death in the United
States, while health care spending on diabetes is soaring
with an estimate of $327billion, of which 43% is spent on
hospital care to treat diabetes and its complications.
Patients with diabetes are frequently admitted to the hospital for surgical interventions. Common surgical reasons in
relation to diabetes include diabetic foot problems, vascular surgeries, coronary artery bypass, kidney transplants,
and eye surgeries. Meanwhile, patients with diabetes are
frequently admitted for other surgical interventions unrelated to diabetes. During admission, diabetes management
may vary based on the location of the patient, whether in
surgical intensive care units (ICUs) or in regular wards. It
also varies based on nutrition, whether it is regular oral
feeding, enteral tube feeding, parenteral feeding, or just
clear intravenous (IV) uids. Good glycemic control
shortens the length of hospital stay, lessens complications,
reduces hospital mortality, and decreases hospitals’ 30and 90-day readmission rates. While oral medications and/
or insulin are commonly used to treat diabetes in outpatient settings, only insulin is recommended for treating
diabetes during surgical admission. Insulin method of
administration, insulin type, and dose vary signicantly
between patients. The use of steroids may complicate an
insulin regimen. Patients on insulin infusion pumps also
require specic consideration. The major risk of insulin
use is hypoglycemia, which is infrequently severe. This
chapter comprehensively covers the principles of diabetes
management during hospital admission.
Rationale
In hospitalized patients, both hyperglycemia and hypoglycemia have been associated with poor outcomes. During the
inpatient period, hyperglycemia has been associated with
increased risk of infection [1, 2], cardiovascular events [3–
5], and mortality [6, 7]. It is also associated with longer
length of hospital stay [3, 8, 9]. Hypoglycemia has been also
associated with an increased risk of mortality [10]. Therefore,
current evidence supports the avoidance of both conditions
among hospitalized patients, whether they are admitted to
critical care units or noncritical care units [5, 9, 11].
Glucose Targets inNoncritically Ill Patients
Unfortunately, due to a limited number of trials, optimal blood
glucose (BG) targets are still debated [12]. However, glucose
targets recommended by the consensus guidelines issued
jointly by the American Diabetes Association (ADA) and the
American Association of Clinical Endocrinologists (AACE)
[9] and separately by the Endocrine Society [5] are shown in
Table 6.1. Higher BG targets can be set for those who are
prone to hypoglycemia, have severe comorbidities, or are terminally ill [11]. However, even then, it is recommended that
BG be kept below 200mg/dL in order to avoid symptomatic
hyperglycemia [11]. Basal-bolus insulin doses should be
N. Khazai
University of Tahran, Tehran, Iran
O. Hamdy (*)
Joslin Diabetes Center, Harvard Medical School,
Boston, MA, USA
e-mail: Osama.Hamdy@joslin.harvard.edu
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024
A. Veves et al. (eds.), The Diabetic Foot, Contemporary Diabetes, https://doi.org/10.1007/978-3-031-55715-6_6
Table 6.1 Blood glucose targets in an inpatient setting for noncritically ill patients according to the joint consensus of the American
Diabetes Association (ADA) and the American Association of Clinical
Endocrinologists (AACE) [9]
Random or bedtime Fasting and premeal Hypoglycemia
<180mg/dL 100–140mg/dL <70mg/dL
93

94
https://t.me/med1917
N. Khazai and O. Hamdy
reduced if BG falls below 100 mg/dL unless the patient is
clinically stable and had tight control before admission [11].
Diabetes Management forNoncritically ill
Hospitalized Patients
In all patients with diabetes, hemoglobin HbA1c (A1C) should
be checked upon admission unless the patient had a value
within one month of admission [5, 9, 11]. For patients without
diabetes, who have random blood glucose levels exceeding
140mg/dL, whether in the emergency room or during hospitalization, A1C should be checked. If A1C is ≥6.5%, it
strongly suggests that diabetes preceded hospitalization [11].
If random blood glucose is >140mg/dL but A1C is ≤6.4, a
diabetes diagnosis cannot be totally excluded and an oral glucose tolerance test should be ordered after discharge.
The involvement of a diabetes educator early in the course
of admission may help newly diagnosed patients learn several
essential skills that may help them upon discharge, including
glucose monitoring, prevention and management of hypoglycemia, and proper intake of oral antihyperglycemic medications [9, 11]. The same is true for patients starting insulin for
the rst time, where the involvement of a diabetes educator not
only ensures they receive instructions and have hands-on practice on proper insulin injection technique but also may identify
barriers to self-management, such as poor patient dexterity,
which precludes insulin self- administration. This may allow
for the early involvement and teaching of the patient’s caregiver or, if needed, a change in the patient’s diabetes discharge
plan to one that either the patient or their caregiver is able to
execute. The early identication and management of these
issues ensure a safe and timely discharge [13].
Medical Nutrition Therapy
Medical nutrition therapy is important for both outpatient and
inpatient diabetes management. All patients with diabetes should
be on a balanced, hypocaloric, and carbohydrate- consistent diet.
If enteral nutrition is used, a diabetes-specic formula is preferred over a standard formula. Carbohydrate consistency helps
in the proper matching of prandial insulin with the carbohydrate
content of meals [8]. Carbohydrate should be from whole grains,
vegetables, fruits, and low-fat dairy with restricted amounts of
added sugar and sucrose- containing food [14].
Oral Antihyperglycemic Medications
andGlucagon-like Peptide-1 Receptor
Agonists (GLP1-RA)
Guidelines from ADA, AACE, and the Endocrine Society
recommend against the inpatient use of oral antihypergly-
cemic medications or GLP-1-RA, due to a lack of efcacy
studies and because of safety issues [5, 9, 11]. Metformin
use in hospitalized patients may potentially lead to lactic
acidosis in the event of continued use during renal insufciency, sepsis, hypotension, or a hypoxic state such as heart
failure. Sulfonylureas are associated with an increased risk
of hypoglycemia, especially upon unpredicted discontinuation of a patient’s oral feeding (NPO). In case of declining
renal function, hypoglycemia due to sulfonylureas may
become severe and protracted. A few studies investigating
the use of GLP- 1RA among hospitalized patients with type
2 diabetes showed noninferior glycemic control and hypoglycemic event rates when compared with basal-bolus insulin. [15] However, these therapies often need additional
basal insulin therapy to maintain optimal glycemic control.
Furthermore, GLP-1RA therapies are associated with early
gastrointestinal side effects, such as nausea and vomiting,
in up to 66% of patients. These side events are specically
undesirable in already anorexic patients or in patients who
are sedated as they put them at a higher risk for aspiration
pneumonia [16]. Hospitalized patients may continue their
oral medications and/or GLP-1RA only if they meet all the
criteria listed in Box 6.1 while taking into consideration all
the precautions listed in Box 6.2. There are some indications that well tolerated nonhypoglycemic agents; for
example, a DPP-4 inhibitor may be used in an inpatient setting. Sodium-glucose cotransporter 2 (SGLT2) inhibitors
should be avoided in cases of severe illness, in patients with
ketonemia or ketonuria, and during prolonged fasting and
surgical procedures. Until safety and effectiveness are
established, SGLT2 inhibitors are not recommended for
routine in-hospital use. Furthermore, the Food and Drug
Administration (FDA) has recently warned that SGLT2
inhibitors should be stopped 3days before the scheduled
surgery (4 days in the case of ertugliozin). All other
patients should be treated with insulin. It needs to be noted
that if oral agents are held, the treating physician should
have a plan to resume them 1–2days before discharge to
ensure their efcacy and safety [11].
Box 6.1: Criteria for Continuing Oral Antihyperglycemic
Medications and GLP-1 RA during Hospital Admission
• Low risk, stable patient and
• Hemoglobin A1C <8% and
• Eating >50% of diet and
• Expected discharge within 24–48h and
• No plans for contrast studies and
• No acute renal failure and
• No steroid therapy and
• No infection

6 Principles ofCare intheDiabetic Surgical Patient
https://t.me/med1917
Box 6.2: Cautions for the Use of Oral Antihyperglycemic
Medications and GLP-1 RA during Hospital Admission
Metformin
• Discontinue if Cr is >1.4 mg/dL and/or eGFR is
<60mL/min per 1.73m2.
• Hold for 48 h after IV contrast study and check
renal function daily for 2days [17].
• Discontinue in hypoxic states (CHF, COPD exacerbation, sepsis).
• Discontinue if the patient has liver disease.
Sulfonylurea
• Discontinue if the patient has renal acute or chronic
insufciency.
• Discontinue if the patient is made NPO.
Pioglitazone
• Discontinue if the patient has congestive heart failure or lower extremity edema.
GLP1-RA
• Discontinue if the patient develops pancreatitis,
nausea, or vomiting.
SGLT2 inhibitors
• Discontinue 3 days before scheduled surgeries
(4days in the case of ertugliozin).
Insulin
Patients with established or newly diagnosed diabetes who
have a good nutrition plan should be started on long-acting
basal insulin plus rapid-acting bolus (nutritional) insulin for
meals plus a corrective dose of the same rapid-acting insulin
while in the hospital [5, 9]. Those who have poor nutritional
intake or are on NPO should receive basal insulin, along with
corrective doses of short-acting insulin. [9, 15] Once they
resume nutritional intake, a safe step can be administering
nutritional (bolus) insulin right after the patient eats in order
to allow for better matching of insulin with actual carbohydrate intake [11]. Patients who are well trained and use carbohydrate counting should have the option to continue using
the same outpatient insulin-to-carbohydrate ratio to calculate
their nutritional insulin needs for each meal. The use of a
“sliding scale” (corrective) insulin alone without basal and
95
Table 6.2 Calculation of total daily dose (TDD) of insulin
Patient and glycemic prole TDD units/kg of body weight
Oral agents or lifestyle therapy as
outpatient, A1C<7%
Newly diagnosed patients,
A1C<7%
Oral agents as outpatient, A1C
7–7.9%
Any treatment and age≥70years
and/or eGFR <60mL/min per
1.73m2 [21]
Any DM with blood glucose
140–200mg/dL or admission
A1C<10%
Any DM with blood glucose
200–400mg/dL or admission
A1C≥10%
Consider corrective insulin only.
If BG is consistently >140mg/
dL, add basal insulin (0.1 unit/
kg body weight)
0.2–0.3unit/kg body weight
0.4unit/kg body weight
0.5unit/kg body weight
nutritional insulin is strongly discouraged (except in select
cases; see Table6.2), with strong evidence showing its inferior performance compared to a basal-nutritional-corrective
regimen [18]. The basal, bolus, and corrective insulin dose
for each patient depends on a number of factors. These factors include the presence or absence of diabetes, the type of
diabetes, the admission A1C level, and how diabetes was
managed prior to admission. It is expected that patients with
type 2 diabetes who are well controlled on oral medications
as outpatients will need a smaller total daily dose (TDD) of
insulin compared to patients with type 2 diabetes who are
poorly controlled on insulin as outpatients. Suggested guidelines for calculating the TDD of insulin are summarized in
Table6.2 [5, 9, 19, 20]. It needs to be stressed that similar to
an outpatient setting, inpatient diabetes management also
needs to be individualized and that the suggested calculations should only serve as starting points. Of note, for patients
who are inadequately controlled (A1C>10%) on oral antihyperglycemic medications with or without GLP-1 RA as
outpatients, basal insulin will likely be added to their outpatient diabetes regimen upon discharge. The early involvement of a diabetes educator in insulin teaching is strongly
advised for those patients. Patients who were well controlled
on basal and nutritional insulin as outpatients can be continued on their home dose of basal insulin. It is recommended
to reduce home doses of their nutritional insulin by 25–50%
initially to avoid hypoglycemia in case the carbohydrate content in their hospital meals is signicantly less than their diet
at home. On the other hand, patients who were adherent to
their insulin regimen at home but were poorly controlled
(A1C > 10%) should have their TDD calculated based on
Table 6.2. If the calculated TDD is lower than what they
were using at home, they should be started on their outpatient regimen with daily up-titration of their TDD based on
BG response in the hospital. Frequently, poor outpatient con-

96
https://t.me/med1917
N. Khazai and O. Hamdy
trol among those patients is related to poor dietary adherence. This poor dietary adherence is mostly eliminated in the
hospital with the institution of a calorie-restricted,
carbohydrate- consistent diet. The calculation of basal, nutri-
adjustment, therefore, is a highly individualized process.
Some guidelines that are commonly used for adjusting basal
and nutritional insulin, along with examples to help highlight
these guidelines, are shown in Table6.4.
tional, and corrective insulin doses based on TDD are outlined in Table 6.3. It was shown that patients with renal
insufciency (eGFR <60mL/min per 1.73 m2) who started
Computerized Provider Insulin Order Entry
on glargine or detemir insulin using a lower multiplier of 0.2
(instead of 0.5) multiplied by the patient’s body weight (in
kg) had reduced the incidence of hypoglycemia by around
50% [21].
Computerized provider order entry (CPOE) for insulin has
been shown to signicantly improve the percentage of time
in which a patient’s BG is within the target range and lower
mean BG without an increase in hypoglycemic events [22,
23]. The institution of a CPOE is a core requirement under
Adjusting Basal andBolus (Nutritional) Insulin
the Health Information Technology and Clinical Health Act
(HITECH) and is also recommended by the Institute of
When adjusting insulin doses, one has to take into account
the patient’s clinical status, concomitant medications (see the
Glucocorticoid section), blood glucose values, individualized glucose targets, and nutritional status (see the Enteral
and Parenteral section), among other factors [9]. Insulin
Table 6.3 Basal-bolus (nutritional) and corrective insulin dose calculation
Basal insulin Starting dose=TDDa×0.5
– Glargine insulin: One dose at bedtime or
– Detemir insulin: One dose at bedtime (type 2) or split into two equal doses AM and bedtime (type 1) or
– NPH insulin: 2/3AM and 1/3 bedtime
– Premixed insulin: 70/30, 75/25, or 50/50 is not generally recommended in the hospital unless the patient
needs to be discharged on this regimen
Note 1: Glargine and detemir are preferred over NPH in a hospital setting (lower risk of hypoglycemia as NPH
peak may seriously decrease blood glucose when patients are fasting for a procedure or any other reason)
Note 2: Use NPH if a short hospital stay is anticipated and the patient is unable to afford/switch to glargine/
detemir as an outpatient. NPH is also preferred in patients on oral steroid therapy
Nutritional (bolus) insulin Starting dose=TDDa×0.5 divided equally before each meal
– Lispro, aspart, and glulisine are preferred over regular insulin for hospitalized patients (less risk of
hypoglycemia)
Note 3: Inject 50% or less of calculated nutritional insulin if the patient has reduced intake
Note 4: Hold nutritional insulin if the patient is not able to eat
Corrective insulin CF (correction factor)=1700 ÷ TDD
This means that 1unit of insulin will lower BG by CF mg/dL; therefore:
Corrective insulin dose or STAT dose=(current BG–100)÷CF
– Build the scale by increasing insulin dose by 1 unit for every CF
– Give nutritional and correction doses as 1 injection with meals
Example: An 80kg patient with type 2 diabetes and A1C of 11% needs:
TDD=80kg×0.5=40units
Basal insulin = TDD×50%=20units of glargine or detemir insulin qhs
Nutritional insulin = 20÷3=~7units rapid-acting insulin with each meal
Correction factor=1700÷40=42mg/dL
This means that 1 unit of insulin is expected to lower BG by ~40mg/dL
Corrective insulin dose=(BS-100)/CF
A scale can be made as follows:
Premeal corrective insulin scale (BG goal<140mg/dL)
Scale: 140–180mg/dL=1unit
181–220mg/dL=2units
221–260mg/dL=3units etc.
Bedtime corrective insulin scale (BG goal<180mg/dL)
Scale: 141–180mg/dL=0unit
181–220mg/dL=1unit
221–260mg/dL=2units etc.
a
TDD is calculated using the instructions in Table6.2
Medicine [11]. Routine structured order sets for basal, nutritional, and corrective insulin should be made part of CPOE.
Ordering individualized corrective insulin scales using the
patient’s calculated correction factor can be made possible in
such computerized order sets.
a

6 Principles ofCare intheDiabetic Surgical Patient
https://t.me/med1917
Table 6.4 General guidelines for adjusting basal and nutritional insulin
Fasting BG>140mg/dL – Increase bedtime long-acting insulin. If NPH or detemir are used q12h,
increase HS dose:
10% if FBG is 140–199mg/dL
20% if FBG is 200–299mg/dL
30% if FBG is 300–399mg/dL
Example: FBG—190mg/dL, prelunch—135mg/dL, predinner—120mg/dL,
bedtime—140mg/dL.The patient is on 40units of glargine insulin at bedtime
→ Increase basal glargine insulin by 10% from 40units to 44units
Premeal BG>140mg/dL or bedtime BG>180mg/dL and
Fasting BG<140mg/dL
Fasting and premeal
BG>140mg/dL and
Bedtime BG>180mg/dL
– Increase nutritional rapid-acting insulin:
10% if BG is 140–199mg/dL
20% if BG is 200–299mg/dL
30% if BG is 300–399mg/dL
Example: FBG—120mg/dL, prelunch—200mg/dL, predinner—230mg/dL,
bedtime—280mg/dL.The total nutritional insulin is 20units
→ Increase nutritional insulin by 20% from 20units to 24units
→ Increase both prandial and basal insulin as shown above
97
Glucose Monitoring
Blood glucose should be checked before meals and at bedtime.
For patients who are on NPO, the frequency may be increased
to every 4h while awake. For patients who are at risk of hypoglycemia, a 3a.m. blood glucose check is recommended. [11]
Glucometers that connect wirelessly to the hospital’s electronic
health record system can greatly facilitate and expedite needed
changes in the patient’s insulin orders and prevent recurrent
hypo- or hyperglycemia. Real- time continuous glucose monitoring (CGM) provides frequent measurements of interstitial
glucose levels as well as the direction and magnitude of glucose
trends. Even though CGM has theoretical advantages over POC
glucose testing in detecting and reducing the incidence of hypoglycemia, it has not been approved by the FDA for inpatient use
[11]. Some hospitals with established glucose management
teams allow the use of CGM in selected patients on an individual basis, provided both the patients and the glucose management team are well educated in the use of this technology. CGM
is not approved for intensive care unit use.
During the COVID-19 pandemic, several institutions
used CGM to minimize contact between health care providers and patients, especially those in the intensive care unit.
This approach seems to be helpful in that regard, as well as
in minimizing the use of personal protective equipment.
Unfortunately, data regarding the use of CGM to improve
either glycemic control or hospitalization outcomes are not
yet available. Preliminary data that are already at hand suggest that CGM can offer a signicant improvement to both
glycemic control and outcomes of hospitalization.
Corticosteroids
Glucocorticoid-induced hyperglycemia, dened as blood
glucose levels >180mg/dL after the initiation of glucocorti-
coids, has been reported in 32% [24]–52% [25] of inpatients.
Of these, 18% [24]–25% [25] were diagnosed with diabetes.
Hyperglycemia in these patients has been shown to be associated with an increase in mortality [26], infections [27], and
length of stay [28]. Despite the importance of controlling
hyperglycemia in these patients, not enough head-to-head
randomized controlled trials exist to recommend a specic
type or a starting dose of insulin for a certain type of steroid.
Since hyperglycemia in response to morning oral steroids is
predominately seen from noontime till evening, an additional
single dose of NPH given in the morning should be most
effective [11] compared to adjusting basal-bolus (even when
the noon and presupper bolus doses are increased) [29]. In
the only single randomized controlled trial done to date [19],
when NPH was added onto the patient’s basal-boluscorrective regimen, there was a trend toward improved glycemic control without an increased risk of hypoglycemia,
compared to adjusting the patient’s basal-bolus-corrective
insulin alone. This seems intuitive because NPH insulin
peaks 4–10h postinjection, around the same time prednisone
exerts its hyperglycemic effects (4–8 h). In addition, NPH
has a duration of action of approximately 12–18h, similar to
the duration of hyperglycemic effects of prednisone [30]. A
simplied version by Grommesh etal [19] of an insulin protocol for patients on glucocorticoids is shown in Table6.5. In
this protocol, the starting dose of NPH depends on the
patient’s prednisone dose and the absence or presence of diabetes. It needs to be emphasized that the NPH dose has to be
added to the patient’s existing basal-bolus and corrective
dose. Instead of using a xed NPH dose, the NPH dose can
be calculated as 0.27units/kg [31].
Multiple daily doses of glucocorticoids, such as hydrocortisone and methylprednisolone, and longer-acting glucocorticoids, such as dexamethasone, may be better controlled
with longer-acting insulin like glargine and detemir insulin.
[11] A retrospective study by Gosmanov etal. [32] assessing

98
https://t.me/med1917
N. Khazai and O. Hamdy
Table 6.5 NPH insulin dose administered at the time of glucocorticoid administration
Prednisone <40mg/day as a single morning
dose
Hyperglycemia but no history of diabetes 10units 15units
Established diabetes 15units 25units
– Increase NPH by 25% if BG>180mg/dL and increase by 50% if BG >300mg/dL
– Taper NPH by the same percentage as prednisone is tapered
– NPH can be stopped when the prednisone dose is reduced to <10mg/day
a
It is recommended that a mechanism be implemented in the CPOE that links the prednisone order to the NPH order, such that it is given at the
same time and signals a need for a change or hold in NPH if glucocorticoids are changed or held
the glycemic control of patients with diabetes and hematologic malignancies who were receiving dexamethasone
found that a daily-adjusted basal-bolus regimen achieved
lower-average blood glucose levels compared to a xed
sliding- scale insulin. For patients starting dexamethasone
therapy, a TDD is somewhere between 0.66 and 1.2units/kg.
In those patients who remain uncontrolled with BG levels
>400 mg/dL on a subcutaneous regimen, an intravenous
insulin infusion should be considered.
[35–39] In standard enteral formulas, 55–60% of the calories
are provided by carbohydrates, whereas diabetic-specic
formulas reduce the carbohydrate contribution to a maximum of 40% of total caloric content. This is made possible
by substituting some of the carbohydrate content with monounsaturated fatty acids and dietary ber [40, 41]. A variety of
insulin regimens are used to manage hyperglycemia for
patients on parenteral nutrition. The superiority of one regimen over the other remains to be established. To date, there
a
Prednisone ≥40mg/day as a single morning
dose
have been several retrospective [42] and only one randomized controlled trial (RCT) examining this question [40].
Enteral andParenteral Nutrition
This RCT [43] showed that one dose of glargine insulin with
corrective regular insulin performed just as well as NPH
It is recommended that patients be started on nutritional support within 24–48h if they are critically ill or after 7–14days
if they are not critically ill [33] but unable to meet >60% of
twice daily with corrective regular insulin, with no difference
in target blood glucose achieved or hypoglycemic events
[44] (see Method 1, Table6.6 [45]).
nutritional needs by mouth. The recommended glycemic
goal is less than 180mg/dL (Table6.1); however, observational studies suggest that a lower BG target of <150mg/dL
Total Parenteral Nutrition
improves clinical outcomes for those receiving nutritional
support without increasing hypoglycemia risk [34].
Administering insulin directly into the TPN solution is asso-
ciated with lower hypoglycemia risk in the event of abrupt
TPN discontinuation. For patients with diabetes, start with
Enteral Nutrition
0.1 unit of regular insulin per 1g of dextrose with daily titra-
tion by 0.05units per 1g dextrose if blood glucose remains
Multiple randomized controlled trials support the use of
lower carbohydrate content (diabetes-specic) enteral formulas due to their association with reduced hyperglycemia.
above 150mg/dL [46]. For patients without diabetes, the unit
per dextrose grams ratio has been shown to be lower at 0.1
unit per 2g of dextrose [47].

6 Principles ofCare intheDiabetic Surgical Patient
https://t.me/med1917
Table 6.6 Diabetes management for patients on enteral and parenteral nutrition
Continuous enteral nutrition Method 1
Initial TDD=0.3–0.6u/kg body weight
• ½ TDD as basal: Glargine insulin q24h
• ½ TDD as “prandial”: NPH q8–12a or regular q6h
• Corrective insulin: Regular q6h
• BG checked q6h
• “Prandial” insulin is to be held if parenteral nutrition stopped
• “Prandial” insulin is adjusted by adding 80% of the previous day’s correctional insulin to the current
prandial dose
Method 2
TDD given as just basal:
2 doses of NPH or detemir
1 dose of glargine
Corrective insulin: Regular insulin q6h
• Basal insulin is adjusted by adding 50% of the previous day’s correctional insulin to the current basal
dose
• If parenteral nutrition is stopped, give only 0.3u/kg basal insulin, along with corrective insulin
Cyclic enteral nutrition • Continue existing basal, bolus, and corrective insulin
• In addition, give an extra insulin dose for cyclic EN=60% of (0.3–0.6) unit/kg body weight
• Given as NPH/regular or premixed 70/30 (or 75/25) at the time of TF initiation
• Titrate based on midnight, 3a.m., and 6a.m. BG
Bolus enteral nutrition • Continue existing basal, bolus, and corrective insulin
• Add additional rapid-acting insulin for each bolus feeding
• BG checked before meals and bedtime
Total parenteral nutrition (TPN) • Continue existing basal, bolus, and corrective insulin
• Add insulin to the TPN bag (0.1unit per 1g of dextrose)
• Titrate 0.05units per 1g of dextrose daily if BG>150mg/dL
• BG checked q6h
Interruption of enteral feedings • Adjust insulin appropriately with planned withholding of enteral nutrition
• Standing orders for “prandial” insulin are to be held and the MD to be notied if enteral feeds are to
be stopped at any point
• In the event of an unexpected and abrupt interruption of enteral feedings exceeding 2h, start D10W
intravenously at the same rate as the enteral feedings were given to prevent hypoglycemia and
dehydration
a
This decreases injection frequency while remaining a good option for lowering the risk of hypoglycemia if enteral nutrition is abruptly stopped
b
Please see Table6.3 for how to calculate this dose
c
If the previous day’s correctional insulin is added to basal insulin, a higher risk of hypoglycemia ensues upon an abrupt or planned discontinuation
of enteral nutrition. In the former case, providers might overestimate the true basal insulin needs
d
There would be a high risk of hypoglycemia with this regimen if enteral nutrition is abruptly stopped
c
d
c
b
b
99
Insulin Pump Management intheHospital
Approximately 63% of type 1 diabetes patients and an
increasing number of insulin- requiring type 2 patients are
using insulin pumps [48]. Most of them are currently using
hybrid closed-loop insulin pumps with CGM.The majority
of insulin pump users are well trained in diabetes selfmanagement and frequently get frustrated when they are
asked to stop using their insulin pump during hospitalization.
Adding to this frustration is the nonintentional delay in
administering their bolus or corrective insulin by hospital
staff. It is recommended that insulin pump users be allowed
to self-manage their diabetes during hospitalization, provided they are able to demonstrate adequate skill and ability
to manage their pumps and are able to procure their pump
supplies [11, 49]. An “insulin pump agreement” helps outline expectations that the patient needs to collaborate and
communicate with the hospital team by reporting blood glu-
cose and basal levels and any boluses given for meals or correction. These values need to be documented on a special
“insulin pump record sheet.” A hospital-wide insulin pump
policy can help in smoothing the transition to SC insulin in
the event of pump failure or a change in the patient’s cognition that prevents continued self-management. This policy
should delineate responsibilities for hospital team members
and ensure ultimate patient safety. The involvement of a diabetologist, either on-site or by phone, is highly recommended
to assist in recommending changes in basal, bolus, or corrective settings while the patient is in the hospital [48, 50].
In theEvent ofSurgery
Patients who are on an insulin pump can continue their usual
basal rate during minor surgeries and major noncardiac surgeries lasting less than 6h, providing that their ongoing basal
Соседние файлы в папке Библиотека им академика М.И. Перельмана
