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 / @xirurgi_2025 / @xirurgi_2025 - 949 - файл
.pdf
24
B. T. Stewart
25. Allen CE, Figueroa J, Agarwal M, Little WK. Pediatric scald
injuries sustained from instant soup and noodle products. Clin
Pediatr (Phila). 2021;60:16–9.
26. Bentivegna K, McCollum S, Wu R, Hunter AA. A state-wide
analysis of pediatric scald burns by tap water, 2016-2018. Burns.
2020;46:1805–12.
2 7. Baggott K, Rabbitts A, Leahy NE, Bourke P, Yurt RW.Pediatric
sink-bathing: a risk for scald burns. J Burn Care Res.
2013;34:639–43.
28. Palmieri TL, Alderson TS, Ison D, etal. Pediatric soup scald burn
injury: etiology and prevention. J Burn Care Res. 2008;29:114–8.
29. Tyler MD, Richards DB, Reske-Nielsen C, etal. The epidemiology
of drowning in low- and middle-income countries: a systematic
review. BMC Public Health. 2017;17:413.
30. Ablewhite J, McDaid L, Hawkins A, etal. Approaches used by
parents to keep their children safe at home: a qualitative study
to explore the perspectives of parents with children aged under
five years. BMC Public Health. 2015;15:983.
31. Mashreky SR, Rahman A, Svanstrom L, Linnan MJ, Shafinaz
S, Rahman F. Experience from community based childhood
burn prevention programme in Bangladesh: implication for low
resource setting. Burns. 2011;37:770–5.
32. Peck M, Molnar J, Swart D.A global plan for burn prevention
and care. Bull World Health Organ. 2009;87:802–3.
33. Shields BJ, Comstock RD, Fernandez SA, Xiang H, Smith
GA. Healthcare resource utilization and epidemiology of
pediatric burn-associated hospitalizations, United States, 2000.
J Burn Care Res. 2010;31:506–7.
34. Potokar T, Bendell R, Chamania S, Falder S, Nnabuko R,
Price PE. A comprehensive, integrated approach to quality
improvement and capacity building in burn care and prevention
in low and middle-income countries: an overview. Burns.
2020;46:1756–67.
35. Hyder AA, Sugerman DE, Puvanachandra P, et al. Global
childhood unintentional injury surveillance in four cities in
developing countries: a pilot study. Bull World Health Organ.
2009;87:345–52.
36. Pham TN, Kramer CB, Wang J, etal. Epidemiology and outcomes
of older adults with burn injury: an analysis of the National Burn
Repository. J Burn Care Res. 2009;30:30–6.
Chapter 1. Epidemiology
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
25
3 7. Marshall SW, Runyan CW, Bangdiwala SI, Linzer MA, Sacks
JJ, Butts JD.Fatal residential fires: who dies and who survives?
JAMA. 1998;279:1633–7.
38. Romanowski K, Curtis E, Barsun A, Palmieri T, Greenhalgh
D, Sen S.The frailty tipping point: Determining which patients
are targets for intervention in a burn population. Burns.
2019;45:1051–6.
39. Maxwell D, Rhee P, Drake M, Hodge J, Ingram W, Williams
R. Development of the Burn Frailty Index: a prognostication
index for elderly patients sustaining burn injuries. Am J Surg.
2019;218:87–94.
40. Romanowski KS, Barsun A, Pamlieri TL, Greenhalgh DG, Sen
S.Frailty score on admission predicts outcomes in elderly burn
injury. J Burn Care Res. 2015;36:1–6.
41. Pham TN, Carrougher GJ, Martinez E, et al. Predictors of
discharge disposition in older adults with burns: a study of the
burn model systems. J Burn Care Res. 2015;36:607–12.
42. McGwin G Jr, Chapman V, Rousculp M, Robison J, Fine P.The
epidemiology of fire-related deaths in Alabama, 1992-1997. J
Burn Care Rehabil. 2000;21:75–3; discussion 4.
43. Peck MD.Epidemiology of burns throughout the World. Part II:
intentional burns in adults. Burns. 2012;38:630–7.
44. Fagenholz PJ, Sheridan RL, Harris NS, Pelletier AJ, Camargo
CA Jr. National study of Emergency Department visits for burn
injuries, 1993 to 2004. J Burn Care Res. 2007;28:681–90.
45. Sengoelge M, El-Khatib Z, Laflamme L. The global burden of
child burn injuries in light of country level economic development
and income inequality. Prev Med Rep. 2017;6:115–20.
46. Gupta S, Mahmood U, Gurung S, et al. Burns in Nepal: a
population based national assessment. Burns. 2015;41:1126–32.
4 7. Peden M, Oyegbite K, Ozanne-Smith J, et al. World report on
child injury prevention. Geneva, Switzerland: World Health
Organization; 2008.
48. Mehta K, Thrikutam N, Nakarmi KK, Hoyte-Williams PE, Peck
M, Stewart BT. Epidemiology and outcomes of cooking and
cookstove-related burn injuries: a World Health Organization
(WHO) Global Burn Registry (GBR) report. J Burn Care Res.
2021;42:51–2.
49. Rosenthal J, Quinn A, Grieshop AP, Pillarisetti A, Glass RI.Clean
cooking and the SDGs: Integrated analytical approaches to
guide energy interventions for health and environment goals.
Energy Sustain Dev. 2018;42:152–9.
26
B. T. Stewart
50. Gallagher M, Beard M, Clifford MJ, Craig M, Watson. An
evaluation of a biomass stove safety protocol used for testing
household cookstoves, in low and middle-income countries.
Energy Sustain Dev. 2016;33:14–25.
51. Carrougher GJ, Bamer AM, Mandell SP, etal. Factors affecting
employment after burn injury in the united states: a burn model
system national database investigation. Arch Phys Med Rehabil.
2020;101:S71–85.
52. Carrougher GJ, Brych SB, Pham TN, Mandell SP, Gibran NS.An
intervention bundle to facilitate return to work for burn-injured
workers: report from a burn model system investigation. J Burn
Care Res. 2017;38:e70–e8.
53. Gupta S, Groen TA, Stewart BT, etal. The spatial distribution
of injuries in need of surgical intervention in Nepal. Geospat
Health. 2016;11:359.
54. Sandvall BK, Jacobson L, Miller EA, etal. Fireworks type, injury
pattern, and permanent impairment following severe fireworksrelated injuries. Am J Emerg Med. 2017;35:1469–73.
55. Boschini LP, Tyson AF, Samuel JC, et al. The role of seizure
disorders in burn injury and outcome in Sub-Saharan Africa. J
Burn Care Res. 2014;35:e406–12.
56. Al-Qattan MM, Al-Zahrani K. A review of burns related
to traditions, social habits, religious activities, festivals and
traditional medical practices. Burns. 2009;35:476–81.
5 7. Livingston G, Huntley J, Sommerlad A, et al. Dementia
prevention, intervention, and care: 2020 report of the Lancet
Commission. Lancet. 2020;396:413–46.
58. Forjuoh SN. The mechanisms, intensity of treatment, and
outcomes of hospitalized burns: issues for prevention. J Burn
Care Rehabil. 1998;19:456–60.
59. Tung KY, Chen ML, Wang HJ, etal. A seven-year epidemiology
study of 12,381 admitted burn patients in Taiwan—using the
Internet registration system of the Childhood Burn Foundation.
Burns. 2005;31(Suppl 1):S12–7.
60. Mannan A, Ghani S, Clarke A, Butler PE. Cases of chemical
assault worldwide: a literature review. Burns. 2007;33:149–54.
61. Ahmed F, Maroof H, Ahmed N, Sheridan R.Acid attacks: a new
public health pandemic in the west? Int J Surg. 2017;48:32–3.
62. Bagcchi S.Private hospitals are told to treat acid attack victims
free of charge. BMJ. 2015;350:h2224.
63. Kay M. Indian court restricts the sale of acid to try to curb
attacks on women. BMJ. 2013;347:f4762.
Chapter 1. Epidemiology
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
27
64. Sugrue R, Reilly F, Kelly J, Clover J.The discordant relationship
between acid attack incidence and advances in management.
Burns. 2018;44:236–7.
65. Justice? What Justice?: tackling acid violence and ensuring
justice for survivors. J.Sagar Associates, India: Acid Survivors
Trust International and TrustLaw; 2017.
66. Alishahi Tabriz A, Dabbagh H, Koenig HG. Medical ethics
in qisas (eye-for-an-eye) punishment: an islamic view; an
examination of acid throwing. J Relig Health. 2016;55:1426–32.
6 7. Bagcchi S.Acid attack victims should have same rights as disabled
people, Indian Supreme Court rules. BMJ. 2015;351:h6787.
68. Kazerooni Y, Mishra B, Gibran N, et al. A systematic review
and comprehensive legislative framework to address chemical
assault globally. Health Policy Plan. 2020;35:1188–207.
69. Nagarajan M, Mohamed S, Asmar O, Stubbington Y, George S,
Shokrollahi K.Data from national media reports of ‘Acid attacks’
in England: a new piece in the Jigsaw. Burns. 2020;46:949–58.
70. Stewart BT, Lafta R, Esa Al Shatari SA, Cherewick M, Burnham
G, Hagopian A, Galway LP, Kushner AL. Burns in Baghdad
from 2003 to 2014: Results of a randomized household cluster
survey. Burns. 2016;42(1):48–55. https://doi.org/10.1016/j.
burns.2015.10.002. Epub 2015 Oct 31.
71. Stewart BT, Trelles M, Dominguez L, etal. Surgical burn care by
Medecins Sans Frontieres-Operations Center Brussels: 2008 to
2014. J Burn Care Res. 2016;37:e519–e24.
72. Peck M, Falk H, Meddings D, Sugerman D, Mehta S, Sage M.The
design and evaluation of a system for improved surveillance and
prevention programmes in resource-limited settings using a
hospital-based burn injury questionnaire. Inj Prev. 2016;22(Suppl
1):i56–62.
73. Mashreky SR, Rahman A, Chowdhury SM, etal. Consequences
of childhood burn: findings from the largest community-based
injury survey in Bangladesh. Burns. 2008;34:912–8.
74. Dave DR, Nagarjan N, Canner JK, Kushner AL, Stewart BT,
Group SR.Rethinking burns for low & middle-income countries:
differing patterns of burn epidemiology, care seeking behavior,
and outcomes across four countries. Burns. 2018;44:1228–34.
75. Runyan CW. Using the Haddon matrix: introducing the third
dimension. Inj Prev. 1998;4:302–7.
Chapter 2
Pathophysiology
andHypermetabolic
Response toBurn
RoohiVinaik, DaliaBarayan, andMarcG.Jeschke
Introduction
Burn injuries represent one of the most severe forms of
trauma affecting more than two million people in North
America each year [1]. According to the World Health
Organization, there are an estimated 300,000 deaths per
year worldwide related to thermal injury [2]. In Canada,
there are approximately 43,000 emergency visits and over
2000 hospitalization per annum due to burn injuries [3].
R. Vinaik · D. Barayan
Sunnybrook Research Institute, Toronto, Canada
e-mail: roohi.vinaik@mail.utoronto.ca;
dalia.barayan@sri.utoronto.ca
M. G. Jeschke (*)
Hamilton Health Sciences, Hamilton, ON, Canada
McMaster University Hamilton, ON, Canada
e-mail: marc.jeschke@hhsc.ca
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
J. O. Lee (ed.), Essential Burn Care for Non-Burn Specialists,
https://doi.org/10.1007/978-3-031-28898-2_2
29
30
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
R. Vinaik et al.
Outcomes have improved over the years due to establishment of specialized burn centers and improvements in resuscitation, dedicated burn-specific protocols, improved wound
coverage and infection control, and improved management
of inhalation injury [4]. However, burn patients still experience unacceptably high rates of morbidity and mortality
despite improved clinical care.
Poor outcomes in severe burns, or burns encompassing
more that 20% of the total body surface area (TBSA), are
attributable in part to the debilitating hypermetabolic stress
response, which is unrivaled in terms of its magnitude and
persistence [5]. Post-burn hypermetabolism is associated with
negative sequelae, including sepsis and multi-organ failure—
leading causes of death in burn patients [4]. Essentially, metabolic dysfunction in burns is characterized by two distinct
phases, an initial “ebb phase” during which metabolism and
tissue perfusion are decreased, and a following “flow phase”
defined by elevated resting energy expenditure (REE)
>110% of predicted REE [6]. The flow phase is accompanied
by pronounced muscle catabolism and lipolysis, loss of total
and lean body mass, and stress-induced diabetes, which eventually lead to physiologic exhaustion. However, although the
phenomenon of hypermetabolism has been well documented,
the mechanisms underlying this response are still not completely elucidated. An improved understanding of post-burn
hypermetabolism, accompanying changes, and management
are necessary to optimize patient care.
In this chapter, we define the hypermetabolic response
after burns, highlighting the key metabolic consequences. In
particular, we focus on glucose, lipid, and protein metabolism.
Then, we discuss the various organ systems affected by postburn hypermetabolism including the cardiac, renal, gastrointestinal, and immune systems. We conclude with a discussion
of management of hypermetabolism in the clinical setting,
namely focusing on how to calculate energy expenditure,
conservative measures such as nutritional supplementation
and early mobilization, and pertinent pharmacological
intervention.
Chapter 2. Pathophysiology andHypermetabolic…
31
What Is Hypermetabolism?
Several reports demonstrated that post-burn metabolic
changes occur in a biphasic fashion. Two distinct patterns of
metabolic regulation can be observed following injury [7].
The first phase is early shock hypometabolism (ebb phase),
which usually occurs within 48h post-burn. This response is
characterized by decreased cardiac output, oxygen consumption, and metabolic rate as well as impaired glucose
tolerance associated with the hyperglycemic state [8].
Within the first five days post-injury, however, these metabolic variables gradually increase to a plateau phase. This
second hypermetabolic phase (flow phase) is characterized
by a hyperdynamic circulation and increased metabolic rate
with resulting increases in body temperature, oxygen and
glucose consumption, CO2 production, and futile substrate
cycling [8]. Typically, patients are considered hypermetabolic when their REE is increased 10% or more above
normal [5]. This hypermetabolic stress response is initiated
to provide sufficient energy for maintaining organ function
and whole-body homeostasis under demanding trauma
conditions [4, 7–9].
While initially ubiquitous and essential, prolonged postburn hypermetabolism has negative consequences that are a
byproduct of pronounced metabolic derangements. For
example, elevated circulating levels of catecholamines, glucagon, and cortisol after injury stimulate excess release of free
fatty acids (FFAs) and glycerol from fat (450% increase in
triglyceride-fatty acid cycling), eventually resulting in organ
alterations associated with organ damage and dysfunction.
Increased lipolysis is further accompanied by increased glucose production by the liver (250% increase in glycolyticgluconeogenic cycling) and insulin release that is twice that of
controls in response to glucose load, indicative of profound
insulin resistance [10–14]. Stress hormones induce proteolysis
to increase availability of amino acids leading to cachexia (all
summarized in Fig. 2.1). The extent and duration of this
altered metabolic demand (discussed below) are directly
32
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
R. Vinaik et al.
F . Schematic depicting key post-burn hypermetabolic
alterations
related to the degree of burn injury quantified based on total
body surface area (TBSA) with partial- and full-thickness
burns [15–17].
Magnitude andDuration
A recent comparison of genomic alterations in white blood
cells (WBCs) following acute lipopolysaccharide (LPS) exposure, blunt trauma, and severe burns demonstrated that gene
expression returns to normal within 24 h of LPS exposure
[18] and one month after blunt trauma [19]. However, the
WBC genome of burn patients uniquely remains altered for
up to one-year post-injury—the furthest time point studied.
The duration of the genomic response to burn trauma parallels that of the metabolic perturbations induced by the injury
[1, 20, 21]. Within the first few months after burn, metabolic
rate increases ~40–80% above normal and remains elevated
for up to one-year post-injury [22]. Although both polytrauma [23] and sepsis [24] also trigger a similar metabolic
Chapter 2. Pathophysiology andHypermetabolic…
response, the degree of this hypermetabolic state is less than
that of burns and resolves more promptly. For patients with
>40% TBSA full-thickness burns, resting metabolic rate at
thermal neutral temperature (30°C) has been shown to surpass 140% of normal at admission and is reduced to 130%
once wounds are fully healed, to 120% at 6 months, and then
to 110% at 12 months post-injury [25]. While this hypermetabolic response decays significantly in the first 6 months after
burn, more recent studies have revealed that severely burned
patients can remain hypermetabolic for up to 3years postinjury [22, 26, 27].
The magnitude and persistence of this stress response
depend not only on burn size, age, and body composition but
also the patient’s preprogrammed genetic response to an
insult. Inhalation injury or another insult such as an infection
can further accentuate and prolong the increased metabolic
rate after injury [15]. Unfortunately, persistent hypermetabolism after burn trauma is a major concern as it is associated
with a profound catabolic state in almost every organ system
of the body [22, 28] (Fig.2.1). To date the cellular and molecular mechanisms underlying burn-induced hypermetabolism
have not been fully identified and despite improved clinical
care, the detrimental sequelae of this complex response are
major contributor to post-burn morbidity and mortality.
33
Biomarkers andMediators
As discussed above, marked and sustained increases in catecholamine, glucocorticoid, glucagon, and dopamine secretion
are involved in initiating the acute hypermetabolic response
and its ensuing catabolic state after injury [1, 29–37] The rise
in these catabolic hormones is accompanied by a decrease in
the normal endogenous activity of anabolic agents, primarily
human growth hormone and testosterone, which together
combine to result in a large net protein loss [38, 39]. Cytokines
such as interleukin 6 (IL-6) and tumor necrosis factor (TNF),
endotoxin, neutrophil-adherence complexes, reactive oxygen
34
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
R. Vinaik et al.
species, nitric oxide, and coagulation as well as complement cascades have also been implicated in mediating and
maintaining the post-burn hypermetabolic state [28]. Once
these cascades of events are initiated, their mediators and byproducts further drive the persistent and increased metabolic
rate accompanied by alterations in glucose, lipid, and amino
acid metabolism [40]. This self-perpetuating process is speculated to drive an entire spectrum of metabolic abnormalities
that are observed after severe burn injury. Thus, management
of burn-induced hypermetabolism remains a clinical priority.
If left untreated, this protective stress response becomes auto
destructive, ultimately causing vast cachexia, multi-organ failure, and even death [1–11, 13, 14]. In the ensuing section, we
will discuss some of the key metabolic sequelae after burns
in detail, along with the specific organ systems targeted in
thermal injuries.
Metabolic Consequences: Glucose, Lipids,
Amino Acids
Glucose Metabolism
Glucose homeostasis in healthy subjects is tightly regulated.
Under normal circumstances, post-prandial elevations in circulating glucose levels stimulate pancreatic β-cells to release
insulin—a potent anabolic hormone. Insulin release promotes peripheral glucose uptake into skeletal muscle and
adipose tissue and suppresses glucose production (i.e., gluconeogenesis) in the liver, thereby restoring blood glucose concentrations [41, 42]. However, post-burn metabolic alterations
cause significant shifts in energy substrate metabolism in
order to provide glucose—a major fuel source to vital organs.
In order to satisfy the high energy demands of the post-burn
hypermetabolic state, glucose levels are markedly increased
by (1) releasing the above-mentioned stress mediators, primarily glucagon and cortisol, to oppose the anabolic actions
of insulin, (2) activating hepatic gluconeogenesis to increase
Соседние файлы в папке @xirurgi_2025