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The management of pain related to burns presents a clinical challenge for providers given the complex physiology of injury, chronicity of pain, and the related psychological effects. Despite the variability in etiology, pathophysiology, and severity of burn injuries, treatment options for pain remain largely uniform despite the type of injury. So called traditional analgesic agents, including opioids, have been and remain a mainstay for the treatment of different types of burn pain. However, adjuvant agents and nonpharmacologic techniques also play important roles in the management of burn pain. Ideal management of patients with burn related pain involves a comprehensive and multi-disciplinary approach that involves pain management, psychological support, and nonpharmacologic therapy.
Chronic pain related to burn injury is highly relevant and is a significant challenge for burn survivors. In a survey of 336 burn patients, 52% reported ongoing pain with an average duration of 11 years after their injury. Of these respondents, 66% reported pain so severe that it interfered with rehabilitation, and 45% reported interference in their daily life. Although past attempts have been made to manage the complex pain associated with burn injuries, evidence-based treatment regimens and algorithms for burn pain management remain limited. Current practice standards for burn pain management are inadequate, inconsistent, and mostly unchanged in many centers for over two decades, with opioid- and benzodiazepine-based regimens as the mainstay of therapy in the acute setting. This chapter will highlight the epidemiology of burns, the pathophysiology of burn injuries and phases of recovery, and options for pain management, including pharmacologic and nonpharmacologic options.
Burn injuries represent a major public health concern. They represent the fourth most common type of trauma after traffic injuries, falls, and interpersonal violence worldwide. In 2004, approximately 11 million people sought medical care for burn related injuries globally. In the United States alone, 486,000 people sought care for burn injuries in 2016. The majority of burns are minor, involving less than 10% of the total body surface area. In 2016, the American Burn Association (ABA) documented that 40,000 patients were hospitalized with a burn injury.
The ABA 2019 National Burn Repository of patients admitted to burn centers in the United States (approximately 220,000 burn cases from 2009–2018) revealed that 60% of patients were Caucasian, 20.6% were Black, 9.5% were Hispanic, and 2.5% were Asian. Men constitute most burn patients, accounting for 62% of cases treated at burn centers in the United States. The distribution of burn injury is bimodal, with high prevalence in the adult (16 years of age and older) and pediatric (0 to 15.9 years old) groups. Though, the majority of burns (56%) occur between ages 20 and 60 years. The two most common causes of burns, fire/flame (37%) and scald (29%), make up 66% of all burn etiologies, followed by contact with hot objects (9.1%), electrical (3.6%), and chemical (3.5%) burns. The age of the person correlates with the type of injury, with scald burns occurring more frequently in children and flame-related burns more common in adults.
Significant advances have been made in public health efforts to mitigate burn related injury in high-income nations, such as smoke detector systems, flame-retardant children’s sleepwear, industrial innovations to avoid fire, and improvements in clinical care. However, low- and middle-income countries have yet to fully benefit from such advances. The World Health Organization estimates that over 300,000 people die from fire-related burn injuries each year. Over 95% of fire-related burns are in low- and middle-income nations. Deaths related to fire are highest in South-East Asia (11.6 per 100,000 population per year), the Eastern Mediterranean (6.4 per 100,000 population per year), and Africa (6.1 deaths per 100,000 population per year). With only one death per 100,000 population per year in high-income nations, fire-related mortality represents one of the largest discrepancies for any injury etiology. Moreover, burns are a major contributor to disability and disfigurement across the world, with fire-related burns accounting for ten million disability adjusted life years lost globally each year.
Based on the location and extent of the insult, burn injury is a traumatic event that may result in a systematic inflammatory response affecting all organ systems. At the molecular level, there is a massive activation of inflammatory mediators, including histamine, prostaglandins, thromboxane, bradykinin, serotonin, catecholamines, platelet aggregation factor, angiotensin II, vasopressin, oxygen radicals (superoxide, hydrogen peroxide, hydroxyl ion), and corticotrophin-releasing factor. At the cellular-level protein denaturation and coagulation, surrounding tissue hypoperfusion, capillary vasoconstriction occurs, where there may be disruption to structures deep to the skin (e.g. dermal tissue, muscle). Local responses to burn trauma can develop into a systemic response that manifests as myocardial dysfunction, increased systemic vascular resistance, increased pulmonary vascular resistance, increased pulmonary capillary wedge pressure, organ ischemia, peripheral capillary leak (causing interstitial and pulmonary edema secondary to hypoproteinemia), and temperature dysregulation (from loss of body heat and increased evaporative water loss). In severe cases, the result may be fatal as a consequence of infection, respiratory distress, shock, or multiple organ failure.
The appearance, presence of pain, and healing times of the different burn depths are shown in Table 78.1 . Recovery from burn injuries can be broadly divided into four phases. The first phase is the initial evaluation and resuscitation that occurs over one to three days post-injury. This is when the patient often requires large volume fluid resuscitation. The second phase is when the burn wounds are excised and temporarily closed with autografting or allografting of skin to accelerate the natural healing process. This generally occurs over weeks to months, depending on the size of the burn injury. The third phase occurs with definitive wound closure and reconstruction. Finally, the final stage of recovery is rehabilitation and reconstruction, which eventually leads to discharge and reintegration into society.
Burn Depth | Appearance | Blistering | Sensation | Healing Time | |
Epidermal |
|
None | Painful | Seven days | |
Partial Thickness | Superficial |
|
(+) | Painful | 14 days |
Deep |
|
(+/–) | Painful or painless | 21 days (+/–) burn excision & skin grafting |
|
Full Thickness |
|
None | None in the burned area (+/–) Pain at edges |
Usually requires burn excision & skin grafting |
Acute post-burn injury pain can be extremely challenging to treat, often necessitating aggressive use of opioids for analgesia. Burn depth, total body surface area affected, mechanism of injury, and various patient factors play a significant role in acute burn pain. Differences in the mechanism of burn injury may also alter the severity and complexity of pain experienced. For example, pain from a partial thickness (second degree) burn results from loss of dermis and epidermis exposing raw nerve fibers. In contrast, nerves are also burned with the upper skin layers in full thickness (third degree) burns, resulting in lower levels of acute pain. Pain from burns maybe both nociceptive and neuropathic in origin. Pain in burn patients can be divided into four different categories, which may intensify as tissues heal:
Rest pain - constant lower grade background pain
Breakthrough pain - intermittent, short duration, rapid onset/ offset, sometimes excruciating pain in those with already established baseline pain control
Procedural pain - short duration, greatest intensity, occurring with certain activities (i.e. wound cleaning, debridement, dressing changes, joint range of motion exercises)
Psychogenic pain - anticipatory pain in the absence of mechanical stimulation
Current treatment of burn pain necessitates a multimodal approach to improve the likelihood of effective post-burn pain management, using both pharmacologic and nonpharmacologic methods. Many pharmacologic agents ( Table 78.2 ) are available to manage the various types of pain related to burn injuries. Because these have been presented in greater detail elsewhere in this text, we will only provide a cursory review of the various agents in a context appropriate for burn pain management.
Agents | Examples | Mechanism of Action | Administration |
Opioids | Fentanyl, morphine, hydromorphone, buprenorphine, methadone, levorphanol |
µ -R agonist | IV, PO, IM, TD |
NMDA antagonists | Ketamine Dextromethorphan |
Non-competitive NMDA-R antagonist | IV, |
NSAIDs | Ketorolac Ibuprofen Meloxicam (available IV) APAP- this is not accurate- Acetaminophen is not an NSAID, nor does it derive its action via Cox 1 and Cox 2 inhibition- please place this in a separate agent box and review the appropriate mechanism of action/available routes of administration |
Cyclooxygenase (COX-1 and 2) inhibition | IV, PO, PR; intrathecal/local (experimental) |
Gabapentinoids | Gabapentin Pregabalin |
Ca 2+ channel blockade (α2δ-1 subunit-containing channels) | PO |
Local anesthetics | Lidocaine Bupivacaine Ropivacaine |
Na + -channel blockade | IV (lidocaine), epidural/intrathecal, perineural, TD |
α2 Adrenergic agonists | Clonidine Dexmedetomidine |
Central and peripheral α2-adrenergic blockade/sympatholysis | IV (dexmedetomidine), PO |
SNRI agonists | Tapentadol, tramadol, duloxetine | Serotonin and norepinephrine reuptake inhibitor activity |
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