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312
M. Hunter and D. T. Harrington
Goals ofCare
Discussions about what to expect and overall prognosis should
begin when a patient is admitted to the ICU. Often, patients
are unable to participate in the discussions due to intubation or
burn shock. Providers should identify and involve the appropriate surrogate decision-makers [20]. In determining when to
withhold or withdraw life sustaining treatment, health care
providers should participate in shared decision-making taking
into account the patient’s advance directives or living will if
available. Factors related to burn mortality are the same that
correlate with withdrawal of care [21].
References
1. Pruitt BA, Wolf SE.An historical perspective on advances in burn
care over the past 100 years. Clin Plast Surg. 2009;36(4):527–45.
https://doi.org/10.1016/j.cps.2009.05.007.
2. Guzman EP, Oropello JM. Critical care of burn patients. In:
Oropello JM, Pastores SM, Kvetan V, editors. Critical care.
NewYork: McGraw-Hill Education; 2022. http://accessmedicine.
mhmedical.com/content.aspx?aid=1136417932.
3. Wurzer P, Culnan D, Cancio LC, etal. Pathophysiology of burn
shock and burn edema. In: Total burn care. 5th ed. Amsterdam:
Elsevier Inc.; 2018. p. 66–76.e3. https://doi.org/10.1016/
B978- 0- 323- 47661- 4.00008- 3.
4. Cancio LC, Bohanon FJ, Kramer GC.Burn resuscitation. In: Total
burn care. 5th ed. Amsterdam: Elsevier; 2018. p.77–86.e2. https://
doi.org/10.1016/B978- 0- 323- 47661- 4.00009- 5.
5. Latenser BA. Critical care of the burn patient. Crit
Care Med. 2010;38(4):1225–6. https://doi.org/10.1097/
ccm.0b013e3181d453fd.
6. Woodson LC, Sherwood ER, Kinsky MP, et al. Anesthesia
for burned patients. In: Total burn care. 5th ed. Amsterdam:
Elsevier Inc.; 2018. p. 131–157.e4. https://doi.org/10.1016/
B978- 0- 323- 47661- 4.00013- 7.
7. Walker PF, Buehner MF, Wood LA, et al. Diagnosis and man-
agement of inhalation injury: an updated review. Crit Care.
2015;19(1):1–12. https://doi.org/10.1186/s13054- 015- 1077- 4.
14 ICU Care ofBurn Patients
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313
8. Fan E, Brodie D, Slutsky AS.Acute respiratory distress syndrome
advances in diagnosis and treatment. JAMA J Am Med Assoc.
2018;319(7):698–710. https://doi.org/10.1001/jama.2017.21907.
9. Demling RH. Burns and other thermal injuries. In: Doherty
GM, editor. Current diagnosis and treatment: surgery. NewYork:
McGraw-Hill Education; 2015. http://accessmedicine.mhmedi-
cal.com/content.aspx?aid=1105485667.
10. Cambiaso-Daniel J, Gallagher JJ, Norbury WB, etal. Treatment
of infection in burn patients. In: Total burn care. 5th ed.
Amsterdam: Elsevier Inc.; 2018. p. 93–113.e4. https://doi.
org/10.1016/B978- 0- 323- 47661- 4.00011- 3.
11. Raes K, Blot K, Vogelaers D, et al. Protective isolation precautions for the prevention of nosocomial colonisation and infection in burn patients: a systematic review and meta-analysis.
Intensive Crit Care Nurs. 2017;42:22–9. https://doi.org/10.1016/j.
iccn.2017.03.005.
12. Rafla K, Tredget EE. Infection control in the burn unit. Burns.
2011;37(1):5–15. https://doi.org/10.1016/j.burns.2009.06.198.
13. Greenhalgh DG, Saffle JR, Holmes JH, et al. American burn
association consensus conference to define sepsis and infection in burns. J Burn Care Res. 2007;28(6):776–90. https://doi.
org/10.1097/BCR.0b013e3181599bc9.
14. Shan J, Chen HL, Zhu JH.Diagnostic accuracy of clinical pulmonary infection score for ventilator-associated pneumonia:
a meta-analysis. Respir Care. 2011;56(8):1087–94. https://doi.
org/10.4187/respcare.01097.
15. Clark A, Imran J, Madni T, et al. Nutrition and metabolism in burn patients. Burn Trauma. 2017;5(1):1–12. https://doi.
org/10.1186/s41038- 017- 0076- x.
16. Porter C, Tompkins RG, Finnerty CC, etal. The metabolic stress
response to burn trauma: current understanding and therapies. Lancet. 2016;388(10052):1417–26. https://doi.org/10.1016/
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1 7. Carson JS, Goverman J, Fagan SP.Acute renal failure in associa-
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M. Hunter and D. T. Harrington
19. Williams DJ, Walker JD. A nomogram for calculation of
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org/10.1016/j.burns.2014.05.001.
20. Pham TN, Otto A, Young SR, etal. Early withdrawal of life support in severe burn injury. J Burn Care Res. 2012;33(1):130–5.
https://doi.org/10.1097/BCR.0b013e31823e598d.
21. Bartley CN, Atwell K, Cairns B, etal. Predictors of withdrawal of
life support after burn injury. Burns. 2019;45(2):322–7. https://doi.
org/10.1016/j.burns.2018.10.015.
Chapter 15
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Pain Management
inBurn Patients
JordanB.Starr, PaulI.Bhalla, andSamR.Sharar
Introduction
Pain management is a critical component of burn care. Pain
control acutely after a burn injury mitigates the physiologic stress
response. In the long term, reduced pain intensity and interference are associated with improved mobility, psychosocial outcomes, quality of life, and chronic pain severity [1–3]. Despite the
importance of pain control after burns, pain in this population is
difficult to treat and vulnerable to under- treatment [4–7].
This is partly due to the multiple sources of pain from burns.
After a burn injury, patients have background pain from the
trauma. This can be exacerbated with breakthrough pain from
physical therapy or even smaller tasks, such as turning in bed. In
addition to these constant threats, burn patients are subjected to
procedure related pain from dressing changes and post-operative pain from more significant debridements and grafting.
Pain mechanisms in burn patients are also diverse,
complicating which therapies are best to choose for any given
patient. Because full-thickness burns destroy afferent nerves,
there is primary pain from the initial injury and secondary
J. B. Starr (*) · P. I. Bhalla · S. R. Sharar
Department of Anesthesiology and Pain Medicine, University of
Washington, Seattle, WA, USA
e-mail: starrj@uw.edu; pbhalla@uw.edu; sharar@uw.edu
© 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_15
315
316
J. B. Starr et al.
pain from healing and reinnervation of previously destroyed
tissues. These different stages lead to nociceptive pain from
tissue damage and inflammation as well as neuropathic pain
from damage to neurologic structures [8].
Further complicating pain management in burn patients is
that pre-injury psychiatric disorders and substance use disorders are risk factors for burn injuries [9–11]. Patients are also
at risk for developing mood disorders, anxiety, post-traumatic
stress disorder (PTSD), and addiction after their burns, all of
which can affect pain and engagement with care [11, 12].
Pain Assessment
The first step in the management of pain is regular, adequate
assessment of pain intensity and its interference with function.
Multiple tools measuring pain intensity exist, with the simplest being the 10-point numeric rating scale (NRS) and visual
analog scale (VAS) in patients who can communicate. Though
simple to use, interpretation of patient-reported scores can be
difficult in patients with comorbid psychiatric or substance
abuse disorders. For this reason, pain score trends combined
with behavioral cues are often more clinically informative
than absolute cut-offs (e.g., NRS greater than 4/10 indicating
moderate pain) for altering treatment strategies. In non-communicating adults, the critical-care pain observation tool
(CPOT) is a validated measure to assess pain that relies on
observable physiological and behavioral indicators [13]. Scores
greater than two suggest the presence of pain [14].
In children, there are many age and developmental-level
appropriate pain scales. One of the most well studied is the
FLACC (Face, Legs, Activity, Cry, Consolability) scale for nonverbal children up to age seven [15]. Scores greater than three
are indicative of at least moderate pain [15]. In children 3years
and older who can communicate, but who cannot reliably report
on the NRS or VAS, the Wong-Baker FACES pain rating scale
is another validated metric. On the Wong-Baker FACES scale,
a score of six or “hurts even more” is consistent with a VAS
greater than four [16]. After determining a patient is in pain, the
primary interventions involve pharmacological (Table15.1) and
Chapter 15. Pain Management inBurn Patients
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Hypotension,
Hypotension,
Alpha-2
blockade
bradycardia
sedation, withdrawal
agonism
Contraindications
Hepatotoxicity Acute or chronic liver
Central COX
Primary
mechanism Side effects
Renal dysfunction,
injury
Bleeding, GI ulcers,
COX
inhibition
CNS hemorrhage
Sedation Dosed renally
renal injury
Calcium
inhibition
channel
Other serotonergic
meds, arrythmias
Sedation None
(TCAs)
CNS
SNRI Nausea, sedation
317
(continued)
depressant
dosing
agents
Acetaminophen Acetaminophen 1000mg
Class
PO q6h
Typical
Prototypical
T . Summary of medications for pain after burns
PRN
PO q6h
NSAIDs Ibuprofen 600mg
PRN
600mg
Gabapentinoids Gabapentin 300–
PO TID
Tizanidine 4mg PO
Alpha-2
TID
TCAs/SNRIs Duloxetine 60mg
agonists
daily
PO q6h
Methocarbamol 1000mg
Muscle
relaxants
318
Contraindications
J. B. Starr et al.
Respiratory
depression
Constipation,
pruritus, nausea,
sedation, tolerance,
Schizophrenia, hepatic
injury
Nightmares,
hallucinations
addiction
Respiratory
Local anesthetic
allergy, hypotension,
Nausea, CNS and
cardiac toxicity
compromise, delirium
arrhythmia
Respiratory
depression, delirium,
addiction
Primary
mechanism Side effects
Typical
dosing
Prototypical
agents
Class
T . (continued)
mu-opioid
agonism
q4h PRN
Opioids Oxycodone 5mg PO
NMDA
antagonism
kg/min IV
Ketamine 1–3mcg/
NMDA
antagonists
Sodium
channel
blockade
IV
Lidocaine 1mg/kg/h
Local
anesthetics
GABA
agonism
PRN
Anxiolytics Midazolam 2mg IV
Unknown Nausea, dysphoria Hypoxia, cytopenia
inhaled
gas
Anesthetics Nitrous oxide 50%
tor, TCA tricyclic antidepressant
CNS central nervous system, COX cyclooxygenase, GABA gamma aminobutyric acid, GI gastrointestinal, NMDA
N-methyl-D-aspartate, NSAID nonsteroidal anti-inflammatory drug, SNRI serotonin-norepinephrine reuptake inhibi-
Chapter 15. Pain Management inBurn Patients
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non-pharmacological treatment to reduce its intensity, along
with strategies to restore the function and well-being of burn
injured patients.
319
Medications
Acetaminophen
Acetaminophen is a mainstay of multimodal analgesia. It acts
centrally via COX enzyme inhibition, cannabinoid agonism,
and inhibition of nitric oxide pathways [17]. It can be given
orally (PO), rectally (PR), or intravenously (IV), with differences in time to efficacy but not potency. In adults, the maximum daily dose is 4 g, with reductions in the elderly and
patients with hepatic disease.
Nonsteroidal Anti-inflammatory Drugs
Nonsteroidal anti-inflammatory drugs (NSAIDs) are useful
analgesics with opioid sparing effects. They inhibit COX-1
and COX-2, except for celecoxib, which is a selective COX-2
inhibitor. Ibuprofen is the prototypical NSAID with a maximum dose of 600mg every 6h or 800mg every 8h. Ketorolac
is useful as an IV agent that can be given for up to 5days. All
NSAIDs can cause renal injury. COX-1 inhibition more
strongly inhibits platelet aggregation and gastric mucosal
protection. COX-2 inhibition has a stronger association with
thrombosis [17].
Gabapentinoids
Gabapentin and pregabalin are also adjuncts with evidence
for efficacy in burn pain [18]. They both act via blockade of
nerve calcium channels. Gabapentin is typically the first-line
agent, with a therapeutic dose around 600 mg every 8 h in
320
J. B. Starr et al.
healthy adults. Because gabapentin has high variability in
gastric absorption, it is recommended to start at a lower dose
and increase every few days either to effect or sedation.
Pregabalin is usually reserved for patients with inadequate
pain relief or excessive sedation from gabapentin, with a
therapeutic dose around 150mg every 12h.
Alpha-2 Receptor Agonists
Clonidine, tizanidine, and dexmedetomidine are alpha-2
receptor agonists, which reduce norepinephrine release and
sympathetic outflow [18]. These medications have an opioid
sparing effect, reduce delirium, and have even been associated with a survival benefit in sepsis [19, 20]. Clonidine and
tizanidine can be given orally, while dexmedetomidine is an
infusion useful for sedation during mechanical ventilation or
procedures. If clonidine or tizanidine is used as scheduled
medications, they should be tapered off to prevent withdrawal symptoms. Tizanidine 2–4mg every 8h is useful as a
first-line agent given its reduced side-effect profile compared
to clonidine.
Tricyclic Antidepressants andSerotoninNorepinephrine Reuptake Inhibitors
These classes of medications have excellent evidence in
chronic, neuropathic pain conditions [21, 22]. Their evidence
in acute pain and burns specifically is weaker [22, 23].
Nevertheless, they can be considered in patients with poorly
controlled pain, predominantly neuropathic pain from burns
or another injury, or concomitant depression. Both medication classes increase serotonin and norepinephrine in the
synaptic cleft, while tricyclic antidepressants (TCAs) are also
antagonists on cholinergic, muscarinic, and histaminergic
receptors [21, 22]. Given its improved side-effect profile,
duloxetine is often started at 30 mg daily. This can be
Chapter 15. Pain Management inBurn Patients
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321
increased weekly to a goal dose of 60mg daily for pain or
120mg daily for pain and depression. The primary adverse
effect is nausea during the initial week of treatment. If a TCA
is selected, desipramine tends to have the fewest anticholinergic side effects.
Muscle Relaxants
Muscle relaxants are a diverse group of medications used in
chronic and acute pain conditions, though evidence in burn
pain is lacking. Benzodiazepines, tizanidine, and cyclobenzaprine, essentially a TCA, are discussed elsewhere. Carisoprodol
and metaxalone are usually avoided due to their addictive
properties and sedation. Though it is a general CNS depressant, methocarbamol is included in this class, as well as
baclofen, which is a centrally acting GABA-B receptor agonist. Methocarbamol is typically first line as its only common
side effect is mild sedation. Doses range from 500 to 1500mg
every 6 h as tolerated. Baclofen is usually reserved for
patients with upper motor neuron lesions causing spasticity,
and it can cause potentially lethal withdrawals if abruptly
discontinued.
Opioids
Opioids play a critical role in burn care. They act primarily via
mu-opioid receptor agonism, with contributions via kappaopioid and delta-opioid receptor agonism [18]. The most
commonly employed oral opioids include morphine, oxycodone, hydrocodone, and hydromorphone prescribed as
needed for background pain. Morphine or hydromorphone
IV is often added for breakthrough pain. For patients with
unknown opioid requirements or who have rapid changes in
their opioid needs, such as after surgery, utilizing patientcontrolled analgesia (PCA) can improve patient satisfaction
and care.
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