Burns

VBMC TRAUMA CARE SERVICES GUIDELINE

BURNS

Wound Care, Size Estimate, Escharotomy

Basic Burn Assessment

A. Assess for associated injuries

B. History - time and mechanism of the injury; enclosed fire, or if toxic chemicals involved

C. Assess burn

1. Superficial: (Sunburns): characterized by erythema, pain, and the absence of blisters – NOT COUNTED IN TBSA

2. Partial thickness: (Superficial Partial Thickness or Deep partial thickness): characterized by a red or mottled appearance with swelling and blister formation. The surface may have a weeping, wet appearance and is painfully hypersensitive

3. Full thickness: (full thickness): skin appears dark and leathery; may also appear translucent, mottled, or waxy white; the surface is painless and generally dry, but may also be moist

D. Circumferential extremity burns:

1. Remove rings and bracelets and Assess distal circulation

2. Check pulses with a Doppler (absent pulse may indicate inadequate fluid resuscitation)

d. Observe for cyanosis, impaired capillary refill, or progressive neurological signs (i.e., paresthesia and deep tissue pain)

E. Limb Escharotomy

Relieve compromised distal circulation in a circumferentially burned limb by escharotomy, which can be done without anesthesia, due to the insensitive full - thickness burn

1. The incision must extend across the entire length of the eschar in the lateral and/or medial line of the limb including the fingers and joints

2. The incision should be deep enough to allow the cut edges of the eschar to separate

F. Thoracic Escharotomy:

Circumferential burns of the thorax occasionally impair respiratory excursion. Bilateral, mid-axillary escharotomy incisions should be considered

Special Burn Requirements

A. Chemical burns

1. Flush burns for at least 20 to 30 minutes; alkali burns require longer irrigation

2. Brush dry powder off before irrigation

3. Alkali burns to the eye require continuous irrigation during the first eight hours

B. Electrical burns - frequently more serious than they appear on the surface

1. Initial care as above

2. Full spinal immobilization

3. EKG monitoring

4. Urinary catheter

a. Observe for myoglobinurea (due to rhabdomyolysis)

b. Increase IV rate fluid to ensure UO of at least 100 ml/hour

c. Consult Medical Control for Mannitol 25 GM IVP and IV infusion with 12.5 GMs of mannitol/1000 cc NS to maintain the diuresis

C. Explosive Injuries – Any patient involved in an explosion should be considered as having a mechanism for traumatic injuries. Even if the patient states they were NOT thrown a distance. The force of a flash flame explosion is enough energy to cause concussive type of injuries.

Patient Care:

Evaluate the Airway & Breathing: All patients receive 100% FIO2. If the patient has singed nasal hairs, suspect an inhalational injury and consider intubation vs close observation. Document the ETT size.

Evaluate the Circulation: Obtain a manual blood pressure and place monitors as able to the skin. The monitors may be stapled to the skin if necessary.

Evaluate the Burn Size: Notate the degree and location of all burn area preferably with a burn diagram. Turn the patient to evaluate the back and perineum. Look for areas of circumferential burn and assess distal pulses. Calculate the TBSA%; obtain the patient’s weight in kilograms, and the time of injury.

Wound Care: Cover the burns with sterile sheets and ensure that the burns are evaluated by the plastic surgery team. Do not cover the wound with any topical agents until ordered by the plastic surgery team.

Fluid Resuscitation: If >20% TBSA burn, recommendations from the American Burn Association are that referring facilities and EMS no longer need to calculate the Parkland Formula. A modified Brooks formula is used.

The current guideline for initial fluid resuscitation is 100ml/hr per 10% TBSA.

*Adjustment of the fluid regimen for pediatric patients*

Pain Control: If intubated and normotensive, consider fentanyl and propofol gtts. If intubated and hypotensive, consider fentanyl and versed or ketamine gtts.

Intubation RSI: Consider etomidate and rocuronium. Succinylcholine is acceptable if the burn is within 12 hrs.

Procedures: The following procedures should be performed by a resident or attending in the ED as part of the initial resuscitation if the patient is a red alert and intubated:

1. CVL in nonburn area (mandatory only if 20% TBSA or greater)

2. Arterial Line

3. NGT

4. Bronchoscopy to evaluate degree of inhalational injury if consideration of admission

6. CO level should be ordered on all burn patients.

Escharotomies: If the patient has circumferential extremity burns especially with diminished distal pulses, notify the plastics or critical care teams to consider escharotomies. If the patient has circumferential torso burns especially with difficult ventilation, notify the plastics or critical care teams to consider escharotomies.

Imaging: Burn patients should be evaluated for other traumatic injuries especially if involved in an explosion mechanism, MVC with fire or leapt from height. These patients should be given consideration for pan-scan.

Disposition:

The intubated and critically ill severely burned patient should be transferred.

All burn patients will be admitted by Trauma surgery

Inhalation

Thermal Inhalation Injury

Most thermal energy is dissipated upon the high surface area of the nasopharynx and oropharynx.

The least common but most deadly inhalation injury

Reflex closure of vocal cords to heat stimulus

Particle Inhalation Injury

Soot/dust/dirt is initially filtered by the nares.

Coughing up carbonaceous sputum & wheezing

The most common inhalation injury

Toxic Metabolic Byproducts from Combustion Inhalation

Carbon Monoxide and Cyanide Toxicity

Pulmonary Dysfuction Pathophysiology

Hypoxemia from V/Q Mismatch

Release of Pulmonary Smooth muscle Vasoconstrictors

Increased airway resistance

Increase in pulmonary neutrophil superoxide free radicals, conjugated dienes.

Pulmonary edema from increased alveolar capillary permeability

Mucociliary elevator impaired and unable to clear secretions, mucosal clumping.

Epithelial cells separated from basement membrane and secrete protein exudate fibrin casts

Fibrin casts can create “ball-valve” barotrauma.

Secondary bacterial pneumonia

Clinical Signs:

High index of suspicion (fire in an enclosed space)

Oropharyngeal burn

Carbonaceous deposits in oropharynx or nares

Patient with impaired sensorium or agitation

Coughing up carbonaceous sputum, wheezing

Initial “honeymoon period” ranging from 24-72 hours prior to respiratory difficulty.

Diagnosis:

Bronchoscopy:

Gold standard

Airway edema/erythema of mid-bronchioles

Secondary secretions

Tissue loss/deposits

Carbonaceous sputum

1^st degree: Erythema, Edema

2^nd degree: Mucosal disruption, Blistering, Exudates

3^rd degree: Hemorrhage, Ulceration

Treatment:

High-Flow Oxygen Therapy (100% NRB)

Humidified Air

Nebulized heparin and N-acetylcysteine alternating q4 for 5 days

· decreases formation of tracheobronchial casts

· decreases PIP

· decreased reintubation and mortality in children

Inhaled B-agonist to decrease bronchospasm.

Pulmonary Toilet

Consider Daily Bronchoscopy

Mechanical Ventilation: limit PIP to <40cmH20, permissive hypercapnia, pressure-limited modes

High frequency percussive ventilation (VDR) for severe inhalation injury or as a rescue modality

Enables recruitment of alveoli at lower airway pressures

Combines standard tidal volume of conventional mode with smaller high frequency respirations

Loosens inspissated secretions and improves pulmonary hygiene.

No role for steroids

No role for prophylactic antibiotics

Carbon Monoxide Poisoning

Mortality as high as 31%

Leading cause of CO poisoning is automobile fumes.

Smoke inhalation is 2^nd leading cause.

1. Inhibits ability to oxygenate

2. Deposits in CNS produce secondary potentially life-long dysfunction

CO Hb%	Symptoms
10%	Asymptomatic, Headache
20%	Dizziness, nausea, dyspnea
30%	Visual disturbance
40%	Confusion, syncope
50%	Seizures and coma
>60%	Cardiopulmonary dysfunction and death

CO affinity to Hb is 200X that of O2 = Decreased PaO2

Hb-O2 dissociation curve is shifted to the left.

PulseOx (O2sat) does not differentiate between CO and O2 and may have inaccurate normal reading.

Cyanide Toxicity is a byproduct of CO.

Oxygen	Half-life of CO
Room Air	4-6 hrs
100% NRB	40-80 min
Hyperbaric O2 (3 ATM)	15-30 min

Delayed Sequelae (10% of patients with serious CO exposure):

Headaches, irritability, personality changes, confusion, memory loss, gross motor deficits

Will need speech therapy consult for cognitive evaluation and possible therapy

Cyanide Toxicity

Key points:

1. Confined space burn victims with autonomic instability should be treated early with CyanoKit. If still unstable can repeat dose at 30 minutes.

2. Thiosulfate as a second line agent.

3. Everyone needs a carboxyhemoglobin.

4. Caution against empiric administration of Cyanokit for simple for smoke inhalation. There's no proven benefit and increased risk of AKI.

General:

· The extent of poisoning caused by cyanide depends on concentration, route of exposure and length of exposure.

· Cyanide gas is less dense than air, so it will rise.

· Cyanide anion inhibits cytochrome c oxidase in the electron transport chain and thus disrupts ATP generation.

· Cyanide is more harmful to the heart and brain than to other organs because the heart and brain are more metabolically active.

Immediate signs and symptoms of exposure to cyanide:

Lab findings:

o Serum lactic acid > 10

o Arterialization of the venous blood gas (high PvO2, since oxygen extraction is impaired

· People exposed to a small amount of cyanide by breathing it, absorbing it through their skin, or eating foods that contain it may have some or all the following signs and symptoms within minutes:

o Dizziness

o Headache

o Nausea and vomiting

o Rapid breathing

o Rapid heart rate

o Restlessness

o Weakness

· Exposure to a large amount of cyanide by any route may cause these other health effects as well:

o Convulsions

o Loss of consciousness

o Low blood pressure

o Lung injury

o Respiratory failure leading to death

o Slow heart rate

All burn patients get a CO (carbon monoxide) level.

Cyanide poisoning screening and treatment:

Suspect cyanide toxicity in all patients with elevated CO level.

CyanoKit (hydroxocobalamin): These are stocked in the ER pyxis

Cyanide poisoning is treated with specific antidotes and supportive medical care in a hospital setting. Antidotes for cyanide poisoning are most useful if given as soon as possible after exposure. Clinicians should treat suspected cases accordingly and not wait for laboratory confirmation. The most important principle is for victims to seek medical treatment as soon as possible.

CDC Basic Cyanide facts. (2013). Retrieved from www.cdc.gov/agent/cyanide/basics/facts.asp

Want to know more?

Cyanide is a highly toxic chemical with a variety of uses, including chemical synthesis, laboratory analysis, and metal plating. Aliphatic nitriles (acrylonitrile and propionitrile) used in plastics manufacturing are metabolized to cyanide. The vasodilator drug nitroprusside releases cyanide upon exposure to light or through metabolism. Natural sources of cyanide (amygdalin and many other cyanogenic glycosides) are found in apricot pits, cassava, and many other plants and seeds, some of which may be important, depending on ethnobotanical practices. Acetonitrile, a solvent that was a component of some artificial nail glue removers, has caused several pediatric deaths.

Hydrogen cyanide is a gas easily generated by mixing acid with cyanide salts and is a common combustion by-product of burning plastics, wool, and many other natural and synthetic products. Hydrogen cyanide poisoning is an important cause of death from structural fires, and deliberate cyanide exposure (through cyanide salts) remains an important instrument of homicide and suicide. Hydrogen cyanamide, an agricultural chemical used as a plant regulator, is a potent toxin that inhibits aldehyde dehydrogenase but does not act as a cyanide analog.

Mechanism of toxicity

Cyanide is a chemical asphyxiant; binding to cellular cytochrome oxidase, it blocks the aerobic utilization of oxygen. Unbound cyanide is detoxified by metabolism to thiocyanate, a much less toxic compound that is excreted in the urine.

Toxic dose

Exposure to hydrogen cyanide gas (HCN), even at low levels (150–200 ppm), can be fatal. The air level considered immediately dangerous to life or health (IDLH) is 50 ppm. The Occupational Safety & Health Administration (OSHA) legal permissible exposure limit (PEL) for HCN is 10 ppm. The recommended workplace ceiling limit (ACGIH TLV-C) is 4.7 ppm (5mg/m3 for cyanide salts). Cyanide in solution is well absorbed across the skin. Adult ingestion of as little as 200mg of sodium or potassium salt may be fatal. Solutions of cyanide salts can be absorbed through intact skin.

Acute cyanide poisoning is relatively rare with nitroprusside infusion (at normal infusion rates) or after ingestion of amygdalin-containing seeds (unless they have been pulverized).

Clinical Presentation

Abrupt onset of profound toxic effects shortly after exposure is the hallmark of cyanide poisoning. Symptoms include headache, nausea, dyspnea, and confusion. Syncope, seizures, coma, agonal respirations, and cardiovascular collapse ensue rapidly after heavy exposure.

A brief delay may occur if the cyanide is ingested as a salt, especially if it is in a capsule or if there is food in the stomach.

Delayed onset (minutes to hours) also may occur after ingestion of nitriles and plant-derived cyanogenic glycosides because metabolism to cyanide is required.

Chronic neurologic sequelae may follow severe cyanide poisoning, consistent with anoxic injury.

Diagnosis

Diagnosis is based on a history of exposure or the presence of rapidly progressive symptoms and signs. Severe lactic acidosis is usually present with significant exposure. The measured venous oxygen saturation may be elevated owing to blocked cellular oxygen consumption. The classic "bitter almond" odor of hydrogen cyanide may or may not be noted, in part because of genetic variability in the ability to detect the smell.

Labs

Cyanide determinations are rarely of use in emergency management because they cannot be performed rapidly enough to influence initial treatment. In addition, they must be interpreted with caution because of a variety of complicating technical factors.

Whole-blood levels higher than 0.5–1 mg/L are considered toxic. Cigarette smokers may have levels of up to 0.1 mg/L. Rapid nitroprusside infusion may produce levels as high as 1 mg/L, accompanied by metabolic acidosis.

Other useful laboratory studies include electrolytes, glucose, lactate, arterial blood gases, mixed venous oxygen saturation, and carboxyhemoglobin (via co-oximetry, if the patient experienced smoke inhalation exposure).

Treatment

Emergency and supportive measures. Treat all cyanide exposures as potentially lethal.

1. Maintain an open airway and assist ventilation if necessary. Administer supplemental oxygen.

2. Treat coma, hypotension, and seizures if they occur.

3. Start an IV line and monitor the patient's vital signs and ECG closely.

Specific drugs and antidotes

1. The conventional cyanide antidote package consists of amyl and sodium nitrites, which produce cyanide-scavenging methemoglobinemia, and sodium thiosulfate, which accelerates the conversion of cyanide to thiocyanate.

a. Break a pearl of amyl nitrite under the nose of the victim and administer sodium nitrite, 300 mg IV (6 mg/kg for children, not to exceed 300 mg). Adjust the dose downward if anemia is present. Caution: Nitrite-induced methemoglobinemia can be extremely dangerous and even lethal. Nitrite should not be given if the symptoms are mild or if the diagnosis is uncertain, especially if concomitant carbon monoxide poisoning is suspected.

b. Administer sodium thiosulfate, 12.5 g IV. Thiosulfate is relatively benign and may be given empirically even if the diagnosis is uncertain. It also may be useful in mitigating nitroprusside toxicity.

2. The most promising alternative antidote is hydroxocobalamin. Long available in Europe, more recently it has become available in the United States as Cyanokit.

a. In acute poisoning, give 5 g of hydroxocobalamin (children: 70 mg/kg) by IV infusion over 15 minutes.

b. In severe cases, a second administration may be considered.

c. For prophylaxis of cyanide toxicity from nitroprusside, recommended hydroxocabalamin dosing is 25 mg/h by IV infusion.

3. Dicobalt edentate is also used outside the United States.

4. Hyperbaric oxygen has no proven role in cyanide poisoning treatment.

Decontamination

Caution: Avoid contact with cyanide-containing salts or solutions and avoid inhaling vapors from vomitus (which may give off hydrogen cyanide gas).

1. Inhalation. Remove victims from hydrogen cyanide exposure and give supplemental oxygen if available. Each rescuer should wear a positive-pressure, self-contained breathing apparatus and, if possible, chemical-protective clothing.

2. Skin. Remove and isolate all contaminated clothing and wash affected areas with copious soap and water.

3. Ingestion. Even though charcoal has a relatively low affinity for cyanide, it will effectively bind the doses typically ingested (eg, 100–500 mg).

a. Prehospital. Immediately administer activated charcoal if it is available and the patient is alert. Do not induce vomiting unless the victim is more than 30 minutes from a medical facility and charcoal is not available.

b. Hospital. Immediately place a gastric tube and administer activated charcoal, then perform gastric lavage. Give additional activated charcoal and a cathartic after the lavage.

Enhanced elimination.

There is no role for hemodialysis or hemoperfusion in cyanide poisoning treatment. Hemodialysis may be indicated in patients with renal insufficiency who develop high thiocyanate levels while on extended nitroprusside therapy.

Electrical Injury Management Guideline

Overall Standards: An electrocardiogram (ECG) should be performed on all patients who sustain electrical injuries (high and low voltage) (ABA Practice Guidelines; J Burn care Res 2006; 27).

Overall Guidelines:

1. Children and adults who sustain low-voltage electrical injuries, have no ECG abnormalities, no history of loss of consciousness, and no other indications for admission (ie, soft-tissue injury), can be discharged from the emergency room.

2. All patients with history of loss of consciousness or documented dysrhythmia either before or after admission to the emergency room should be admitted for telemetry monitoring. Patients with ECG evidence of ischemia should be admitted and placed on cardiac monitors (monitoring for 24 hours has been reported in several studies).

3. Creatine kinase enzyme levels, including MB fraction, are not reliable indicators of cardiac injury after electrical burns and should not be used in decisions regarding patient disposition. Insufficient data exists on troponin levels to formulate a guideline.

4. Alkalinization of the urine is not necessary in all patients.

5. Maintain UOP.

Overall Options: Electrical injuries can result in potentially fatal cardiac dysrhythmias. The need for cardiac evaluation and subsequent cardiac monitoring are critical components in electrical burn management. Most patients who sustain electrical injuries undergo ECG evaluation, and patients with documented dysrhythmias, cardiac ischemia, or history of loss of consciousness will be admitted to the hospital for further evaluation and monitoring. However, the appropriate cardiac diagnostic tests and the indications for hospital admission, necessity of cardiac monitoring, and appropriate duration of cardiac monitoring have not been well established.

Upper Extremity Standards: Insufficient data exist to support a treatment standard for this topic.

Upper Extremity Guidelines:

1. Patients with high-voltage electrical injury to the upper extremity should be referred to specialized burn centers experienced with these injuries as per American Burn Association referral criteria.

2. Indications for surgical decompression include progressive neurologic dysfunction, vascular compromise, increased compartment pressure, and systemic clinical deterioration from suspected ongoing myonecrosis. Decompression includes forearm fasciotomy and assessment of muscle compartments. The decision to include a carpal tunnel release should be made on a case-by-case basis.

Upper Extremity Options: There are several methods to evaluate the injured extremity. Compartment pressures may be measured as an adjunct to clinical examination. Pressures greater than 30 mm Hg, or tissue pressure reaching within 10 to 20 mm Hg of diastolic pressure, may be used as evidence of increased compartment pressure and potential deep-tissue injury, indicating the need for surgical decompression in the appropriate clinical setting. Technetium-99m pyrophosphate scan may be used as an adjunct to clinical examination at centers experienced with this technology. Doppler flow meter can be used as an adjunct to assess extremity perfusion. It should not be relied on as the sole indicator of deep-tissue viability and adequate perfusion.

PT/OT/Mobility in Burns

PT/OT consults should be performed upon patient admission.

PT evaluation of burn patients is a high priority and patients are generally seen within 24 hours or sooner. Inhalational burns can benefit from PT/OTas well for pulmonary mobility.

PT focuses on lower extremities while OT focuses on upper extremities though they work very closely with each other.

Splints should be used as indicated and will be determined by PT/OT depending on the type of burn and area involved. Avoid sending splints to OR with patients unless specifically requested by the surgeon. They tend to get thrown away and then have to be remade and the patient is recharged for additional splints.

PT/OT should be invited to be present on rounds with the team whenever possible to help determine patient needs.

Ensure that mobility orders in Cerner are current/accurate.

Most burn patients need frequent range of motion to prevent complications from immobility. PT/OT can generally only see each burn patient on a daily basis so bedside staff need to be diligent about performing range of motion. This can be taught to family members as well.

Specific activity/mobility/range orders, approved by Plastics, are needed for PT/OT to optimize care for all burn patients, especially after grafting.

Severe burns should prompt Rehabilitation Medicine Consultation for consideration of inpatient rehab or possibly support of home health and an outpatient program. Burn victims from rural areas are particularly prone to contractures because burn rehab (home health PT/OT) expertise is more limited.

Pain Management for Burns

BACKGROUND

Although pain is a well-recognized component of appropriate burn management, the available data suggests that burn pain is undertreated and is one of the most difficult types of pain to manage. In the short term, uncontrolled pain is associated with an increased risk of wound infection, longer hospitalization, poor compliance with rehabilitation therapy, and increased psychological stress. Acute uncontrolled pain also increases the risk of depression, PTSD, and attempted suicide after hospital discharge. Up to 52% of patients with uncontrolled acute pain develop chronic pain syndromes which can persist for up to 11 years post injury.

The pathophysiology of burn pain is complex and involves multiple neurotransmitters, meaning appropriate management must be comprehensive and multi-modal. Appropriate pain management is further complicated by development of opioid-induced hyperalgesia (OIH) and NMDA-mediated central sensitization which, if unaddressed, may lead to chronic pain syndromes. Additionally, acute decreases in renal and hepatic perfusion during the first 48 hours after burn injury may decrease drug clearance; after the first 48 hours, hypermetabolism likely increases drug clearance, and changes in plasma protein concentrations may increase the unbound drug fraction leading to hyperresponsiveness to various medications.

Burn pain is generally divided into three subtypes.

Background pain is a consistent, dull pain that is related to tissue injury and may be complicated by anxiety related to patient illness and immobility.

Procedural pain is high-intensity, short-lasting pain associated with wound cleaning, dressing changes, debridements, line insertions, and PT/OT.

Breakthrough pain is an unpredictable surge in pain that may happen at any time throughout the day. Intense tingling and itching as well as neuropathic pain may also occur as tissue regenerates.

PHARMACOLOGY

For typical dosing and titration parameters, see Tables 1 and 2 and Figure 1. The information below is intended to help guide selection of adjunctive medications using patient information.

Acetaminophen (APAP) is a mild analgesic that becomes more effective when added to baseline opioids. For small burns, monotherapy with APAP may provide adequate analgesia. In more severe burns, the addition of APAP to baseline opioids has been shown to be as effective as higher doses of opioids. Unless there are known contraindications such as cirrhosis, all patients with burn pain should receive APAP.

Alpha-2 Agonists such as clonidine and dexmedetomidine work through central modulation of pain perception and inhibition of substance P. Adjunctive clonidine has been shown to decrease opioid requirements, improves analgesia, and prolongs anesthetic action. Dexmedetomidine is generally a more effective sedative and analgesic than clonidine owing to its increased specificity for the A2 subtype of the alpha-2 receptor. Single-dose dexmedetomidine, when added to opioids and ketamine, has been shown to improve procedural analgesia. In the acute phase of burn (1^st 48 hours), cardiac depression with dexmedetomidine may preclude use in unstable patients, however when administered with ketamine the drug appears to have minimal cardiac depressive effects.

Benzodiazepines have no analgesic properties, but may improve associated anxiety and distress in patients with severe burns. The addition of low-dose benzodiazepines to both opioids and ketamine has been shown to improve procedural pain, and intermittent administration of low-dose lorazepam has been shown to improve opioid responsiveness in patients with severe breakthrough pain. In patients with mild pain, benzodiazepines are unlikely to be of benefit and should generally not be used given their side effect profile.

Gabapentinoids such as gabapentin and pregabalin work through inhibition of voltage-gated calcium channels to decrease release of excitatory neurotransmitters and increase inhibitory GABA release. Available data has shown an inconsistent opioid-sparing effect of gabapentin in the management of burn pain, however the drug has been successfully used to manage itching and neuropathic pain. Further, multimodal analgesia likely decreases the incidence of OIH, therefore gabapentin adjunctive therapy is recommended for patients with severe burns. Pregabalin is similar to gabapentin, however as it is a newer drug use is generally limited to neuropathic pain.

NMDA Antagonists such as ketamine and methadone have gained popularity as adjunctive therapy for the management of severe burns. As NMDA is postulated to be involved in the development of OIH, addition of antagonists at this receptor may improve responsiveness to opioids. A restrospective study of 70 patients with severe burns showed early initiation of methadone therapy (within 4 days of admission) was associated with increased ventilator-free days as compared to standard opioid monotherapy. Additionally, published protocols suggest methadone can be effectively used to decrease opioid requirements in patients receiving high-dose opioid therapy. Ketamine has been used both for procedural and background pain, but the majority of data supports use in the procedural setting. Generally, intravenous doses of 0.6-1.3mg/kg are required for an anesthetic response (absence of nociception). Ketamine is associated with an emergence phenomenon as well as an increase in cardiac activity. Co-administration with benzodiazepines may ameliorate the emergence phenomenon, and dexmedetomidine may improve both emergence and cardiac response.

NSAIDs such as ibuprofen are quite useful adjunctive therapies in minor (<15-20% TBSA) burns as they are opioid sparing and may alleviate OIH. However, routine use is not recommended in severe burns given the increased risk of renal failure, platelet dysfunction, and gastrointestinal ulceration/irritation.

Opioids such as morphine, fentanyl, oxycodone, and hydromorphone generally constitute the backbone of successful pain management, especially for large (>20% TBSA burns). Although their use is complicated by adverse reactions including constipation, respiratory depression, dependence, and possibly immunosuppression, opioids are advantageous in that they have no ceiling effect for analgesia. Of importance is the development of OIH and tolerance, both of which may decrease effectiveness of opioids. To minimize development of OIH, daily sedation holidays are strongly encouraged for patients receiving continuous infusion opioids. Further, mixed opioid analgesia (e.g., scheduled oral morphine with as needed oral oxycodone) may decrease the incidence of OIH, as will including the adjunctive therapies mentioned. In patients who develop OIH, decreasing the dose of opioid may improve analgesia. Alternatively, changing to an alternative opioid at a lower dose may prove efficacious, as will adding an NMDA antagonist (e.g., methadone) while decreasing the opioid dose. It is likely that semi- or fully synthetic opioids may induce less histamine release than morphine, which is of importance in patients who complain of itching.

Miscellaneous therapies such as synthetic cannabinoids and anesthetics may be of benefit as well. Although reports of successful use are limited, addition of dronabinol may moderately improve analgesia in patients with a history of THC use. Systemic lidocaine may also be of benefit, however use is limited at this time. Transdermal lidocaine should not be used as changes in absorption when applied to non-intact skin may cause life-threatening toxicity.

Nonpharmacologic therapies such as hypnosis, avoidance techniques, and preparatory/behavioral interventions may also be useful adjuncts to therapy and may be considered in appropriate patients. When combined with pharmacologic analgesia, hypnosis has been shown to reduce grafting needs and decrease hospital length of stay.

NOTABLE REFERENCES

1. Faucher L, Furukawa K. Practice guidelines for the management of pain. J Burn Care Res 2006; 27: 659-68.

2. Fry C, Edelman LS, Cochran A. Response to a nursing-driven protocol for sedation and analgesia in a burn-trauma ICU. J Burn Care Res 2009; 30: 112-8.

3. Jones GM, Porter K, Coffey R, et al. Impact of early methadone initiation in critically injured burn patients: a pilot study. J Burn Care Res 2013; 34: 342-8.

4. MacPherson R, Woods D, Pengold J. Ketamine and midazolam delivered by patient-controlled analgesia in relieving pain associated with burns dressings. Clin J Pain 2008; 24: 568-71.

5. Richardson P, Mustard L. The management of pain in the burns unit. Burns 2009; 35: 921-36.

6. *Retrouvey H, Shahrokhi S. Pain and the thermally injured patient – a review of current therapies. J Burn Care Res 2015; 36: 315-23.

7. Zor F, Ozturk S, Bilgin F, et al. Pain relief during dressing changes of major adult burns: ideal analgesic combination with ketamine. Burns 2010; 36: 501-5.

*of particular interest

Figure 1. Suggested initial background/breakthrough pain management in large burn.

Table 1. Suggested Oral Background/Breakthrough Pain Regimens
Regimen	Drugs Involved	Starting Dose	Titration	Maximum Dose
Large Burn (>15-20% TBSA), Prior fentanyl requirement ≤50mcg/hr	Morphine IR¹	15mg q4h	15mg per dose, titrate daily	N/A²
	Oxycodone/APAP	5/325mg, 1-2 tabs q4h PRN	N/A	2 tabs q4h
	Gabapentin	300mg TID	100mg per dose, titrate daily	2400mg per day
	Clonidine	0.1mg BID	0.1mg per dose, titrate daily	0.5mg q6h
	Lorazepam³	1mg q4h PRN	N/A	1mg q4h PRN
Large Burn (>15-20% TBSA), Prior fentanyl requirement >50mcg/hr	Morphine IR¹	30mg q4h	15mg per dose, titrate daily	N/A²
	Oxycodone/APAP	5/325mg, 1-2 tabs q4h PRN	N/A	2 tabs q4h
	Gabapentin	300mg TID	100mg per dose, titrate daily	2400mg per day
	Clonidine	0.1mg BID	0.1mg per dose, titrate daily	0.5mg q6h
	Lorazepam³	1mg q4h PRN	N/A	1mg q4h PRN
Small Burn (<15-20% TBSA)	APAP	975mg q6h	N/A	975mg q6h
	Ibuprofen	400mg q6h	200mg per dose	800mg q6h
	Oxycodone	5mg q4h PRN	5mg per dose	N/A

Note: attempt to wean pain medications daily as appropriate.

¹For patients with documented morphine allergy, consider hydromorphone 2-4mg PO q4h starting dose.

²For doses > 60mg q4h, consider addition of methadone 5mg PO TID with concomitant 50% reduction in morphine dose.

³Only consider for high pain scores

Table 2. Potential Procedural Pain Regimens
Regimen	Drugs Involved	Starting Dose	Timing of First Dose	Repeat Dosing	Maximum Dose
Large Procedure, 1^st 48 hours	Ketamine	1mg/kg IV	Beginning of procedure	0.5-1mg/kg IV q15min PRN	4mg/kg
	Midazolam	0.05mg/kg IV	Beginning of procedure	N/A	N/A
	Tramadol	1.5mg/kg PO	30min before procedure	N/A	N/A
	Fentanyl	N/A	N/A	50-100mcg IV q15min PRN	N/A
Large Procedure, After 1^st 48 hours	Ketamine	1mg/kg IV	Beginning of procedure	0.5-1mg/kg IV q15min PRN	4mg/kg
	Dexmedetomidine¹	1mcg/kg IV	Beginning of procedure	N/A	N/A
	Tramadol	1.5mg/kg PO	30min before procedure	N/A	N/A
	Fentanyl	N/A	N/A	50-100mcg IV q15min PRN	N/A
Large Procedure, After 1^st 48 hours (alternate)	Ketamine 10mg/mL + Midazolam 0.5mg/mL IV PCA (20mL)	1mL bolus with 3min lockout, no basal rate
Small Procedure	Tramadol	1.5mg/kg PO	30min before procedure	N/A	N/A
	Lorazepam	1-2mg PO	30min before procedure	N/A	N/A
	Morphine²	N/A	N/A	2-4mg IV q30min	N/A
Small Procedure (alternate)	Morphine²	2-4mg IV	Beginning of procedure	2-4mg IV q30min	N/A
Small Procedure (alternate)	Lorazepam	1-2mg IV	Beginning of procedure	N/A	N/A

Note: continue background pain medications throughout procedure.

¹Give slow IV push over 5-10 minutes. May consider continuous IV infusion of 0.5-1mcg/kg/hour for duration of procedure at attending discretion.

²In patients with documented morphine allergy, consider hydromorphone 0.3-0.6mg IV starting dose, followed by 0.3-0.6mg IV q30min PRN