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BURNS

Caleb J. Mentzer, DO James R. Yon, MD

BASICS

DESCRIPTION

Tissue injuries caused by application of heat, chemicals, electricity, or irradiation

Extent of injury (depth of burn) is a result of intensity and duration of exposure.

1st degree involves superficial layers of epidermis.

2nd degree involves varying amounts of epidermis (with blister formation) and part of the dermis.

3rd degree involves destruction of all skin elements (full thickness) with

coagulation of subdermal plexus.

System(s) affected: endocrine/metabolic, pulmonary, skin/exocrine

Geriatric Considerations

Prognosis is worse for severe burns.

Patients >60 years of age account for 11% all of burns

Pediatric Considerations

Consider child abuse or neglect when dealing with hot water burns in children; abuse accounts for 15% of pediatric burns. Special concerns are sharply demarcated wounds, immersion injuries, and suspect stories. Involve child welfare services early.

EPIDEMIOLOGY

Predominant age: 30 years; 13% infants; 11% >60 years of age

Predominant gender: males account for 70%.

Incidence

Per year in the United States

1.2 to 2 million burns; 700,000 emergency room visits; 45,000 to 50,000 hospitalizations; 3,900 deaths owing to burn-related complications

In children: 250,000 burns; 15,000 hospitalizations; 1,100 deaths

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Estimated total cost of $2 billion annually for burn care

House fires cause 75% of deaths.

Burn deaths decreasing nationally due to improved prevention and treatment

Increase in burns from the illegal production of methamphetamines. Patients can present with a combination of chemical burn, thermal burn, and explosion injury.

ETIOLOGYAND PATHOPHYSIOLOGY

Open flame and hot liquid are the most common causes of burns (heat usually ≥45°C): flame burns more common in adults; scald burns are more common in children.

Caustic chemicals or acids (may show little signs or symptoms for the first few days)

Electricity (may have significant injury with very little damage to overlying skin)

Excess sun exposure

RISK FACTORS

Water heaters set too high

Workplace exposure to chemicals, electricity, or irradiation

Young children and older adults with thin skin are more susceptible to injury.

Carelessness with burning cigarettes: related to 18% of fatal fires in 2006

Inadequate or faulty electrical wiring

Lack of smoke detectors: Lacking or nonfunctioning smoke alarms are implicated in 63% of residential fires.

Arson: cause of 12.4% of fires that resulted in fatalities in 2012

GENERALPREVENTION

Home safety education should be a key mechanism for injury prevention.

Families educated on home safety were more likely to have safe hot water temperatures.

Safety education results in more families having functioning smoke alarms and increased use of fireguards.

COMMONLYASSOCIATED CONDITIONS

Smoke inhalation syndrome

May involve thermal burn to respiratory mucosa (e.g., trachea, bronchi) as well as carbon monoxide inhalation

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Occurs within 72 hours of burn

Should be suspected in all burns occurring in an enclosed space or exposure to explosions

DIAGNOSIS

HISTORY

History of source of burn

In children or elderly: Check for consistency between the history and the burn’s physical characteristics.

PHYSICALEXAM

1st degree: Erythema of involved tissue, skin blanches with pressure, skin may be tender.

2nd degree: Skin is red and blistered, skin is very tender.

3rd degree: Burned skin is tough and leathery; skin is nontender. Rule of 9s

Each upper extremity: adult and child 9%

Each lower extremity: adult 18%; child 14%

Anterior trunk: adult and child 18%

Posterior trunk: adult and child 18%

Head and neck: adult 10%; child 18%

Quick estimate: The surface area of the patient’s hand (palmar surface plus fingers) is 1% of the body surface area (BSA).

Careful documentation of extent of burn and the estimated depth of burn

Check for any signs suggestive of potential airway involvement: singed nasal hair, facial burns, carbonaceous sputum, progressive hoarseness, inflamed oropharynx, circumferential burns around the neck, tachypnea

DIAGNOSTIC TESTS & INTERPRETATION

Children: glucose (hypoglycemia may occur in children because of limited glycogen storage)

Smoke inhalation: arterial blood gas, carboxyhemoglobin

Electrical burns: ECG, urine myoglobin, creatine kinase isoenzymes

Initial Tests (lab, imaging)

Labs: hematocrit; type and crossmatching; electrolytes, including BUN and

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creatinine; urinalysis

Imaging: Chest radiograph; Xenon scan is useful in suspected smoke inhalation.

Diagnostic Procedures/Other

Bronchoscopy may be necessary in smoke inhalation to evaluate lower respiratory tract (1)[A].

TREATMENT

Prehospital care

Remove the patient from the source of burn.

Extinguish and remove all burning clothing.

Room-temperature water may be poured onto burn but only in the first 15 minutes following burn exposure.

Wrap patient to prevent hypothermia.

All patients to receive 100% oxygen via face mask

Hospitalization for all serious burns

2nd-degree burns >10% of BSA

Any 3rd-degree burn

Burns of hands, feet, face, or perineum

Electrical or lightning burns

Inhalation injury

Chemical burns

Circumferential burn

Transfer to burn center for (2)[C]

2ndand 3rd-degree burns >10% of BSAin patients <10 years and >50 years of age

2nd-degree burns >20% of BSAand full-thickness burns >5% BSAin any age range

3rd-degree burns in any age group

Burns of hands, feet, face, or perineum

Electrical or lightning burns

Inhalation injury

Chemical burns

Circumferential burn

Burns in patients with additional trauma (fractures, etc.) in which the burn is the more severe injury; otherwise, send to trauma center for stabilization.

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Burn injuries in patients with preexisting medical conditions that could affect management, mortality, or recovery

GENERALMEASURES

Based on depth of burns and accurate estimate of total BSAinvolved (rule of 9s)

Tetanus prophylaxis (if not current)

Remove all rings, watches, and other items from injured extremities to avoid tourniquet effect.

Remove clothing and cover all burned areas with dry sheets.

Flush area of chemical burn (for ~2 hours).

For all major burns, use 100% oxygen administration; consider early intubation.

Do not apply ice to burn site.

Nasogastric tube (high risk of paralytic ileus)

Foley catheter

Analgesia

ECG monitoring in first 24 hours following electrical burn

Whirlpool hydrotherapy followed by silver sulfadiazine (Silvadene) occlusive dressings in severe burns

Daily or BID cleansing with dressing changes Burn fluid resuscitation

Calculate fluid resuscitation from time of burn, not from time treatment begins.

2 to 4 mLlactated Ringer × body weight (kg) × % BSAburn (1/2 given in first 8 hours, in second 8 hours, and in third 8 hours); in children, this is given in addition to maintenance fluids and is adjusted according to urine output and vital signs. Protocol-based resuscitation leads to superior outcomes.

Colloid solutions are not recommended during the first 12 to 24 hours of resuscitation (3)[A].

Other: Use of biologic membranes or skin substitutes may be indicated for burn coverage.

Inhalation injury

Intubation, ventilation with positive end-expiratory pressure assistance

Hyperbaric oxygen treatment may be useful in patients with carbon monoxide levels >25%, patients with coma, focal neurologic deficit, ischemic ECG changes, and pregnant patients.

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MEDICATION

First Line

IV morphine or hydromorphone (Dilaudid) for severe pain

Oral analgesics, such as acetaminophen (Tylenol) with codeine, acetaminophen with oxycodone (Percocet), or acetaminophen with hydrocodone (Lortab) for moderate pain

Silver sulfadiazine (Silvadene): Apply topically to burn site (can cause leukopenia). Do not use in sulfa-allergic patients, women who are pregnant/breastfeeding, or infants (<2 months).

Neosporin or bacitracin ointment: Apply to facial burns.

Mupirocin: has potent inhibitory activity against methicillin-resistant

Staphylococcus aureus (MRSA)

Acticoat A.B. (a dressing consisting of two sheets of high-density polyethylene mesh coated with nanocrystalline silver) has a more controlled, prolonged release of silver, allowing less frequent dressing changes.

Electrical burn with myoglobinuria will require alkalinization of urine and mannitol.

Consider H2 blockers (e.g., famotidine) or proton pump inhibitors (e.g.,

lansoprazole, pantoprazole) for stress ulcer prophylaxis in severely burned patients.

Tetanus toxoid/tetanus immunoglobulin

There is no clear indication for prophylactic systemic antibiotics.

Use of negative pressure wound therapy may result in a low-protease environment with higher levels of angiogenic factor (vascular endothelial growth factor [VEGF]) during wound healing, leading to more chaotic, hyperkeratinized, thickened epidermis when compared with a standard hydrocolloid dressing.

Second Line

Mafenide (Sulfamylon) for full-thickness burn, best against Pseudomonas (Caution: metabolic acidosis, painful)

Silver nitrate 0.5% (messy, leeches electrolytes from burn, causes water toxicity)

Povidone–iodine (Betadine) may result in iodine absorption from burn and “tan eschar,” makes débridement more difficult.

Travase (enzymatic débridement)

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SURGERY/OTHER PROCEDURES

Escharotomy may be necessary in constricting circumferential burns of extremities or chest due to compartment syndrome.

Tangential excision with split-thickness skin grafts: Early excision of burns results in a significant reduction in mortality (excluding patients with inhalational injury) and a significant decrease in hospital length of stay (4)[B]. Various dressings (e.g., biosynthetic, biologic) are available to help reduce the number of dressing changes and promote healing.

ONGOING CARE

FOLLOW-UPRECOMMENDATIONS

Early mobilization is the goal.

DIET

High-protein, high-calorie diet when bowel function resumes

Nasogastric tube feedings may be required in early postburn period.

Total parenteral nutrition if NPO is expected for >5 days

Early initiation of enteral nutrition in the first 24 hours of admission results in shorter intensive care unit (ICU) stay and lower wound infection rates

PATIENT EDUCATION

Use of sunscreen: Skin grafts or newly epithelialized skin is highly sensitive to sun exposure and thermal extremes.

Prevent access to electrical cords/outlets.

Isolate household chemicals.

Use low-temperature setting for water heater (<54°C).

Household smoke detectors with special emphasis on maintenance

Family/household evacuation plan

Proper storage and use of flammable substances

Burn management: http://www.aafp.org/afp/2000/1101/p2029.html

Burn prevention: http://www.aafp.org/afp/2000/1101/p2032.html

PROGNOSIS

1st-degree burn: complete resolution

2nd-degree burn: epithelialization in 10 to 14 days (deep 2nd-degree burns probably will require skin graft)

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3rd-degree burn: no potential for reepithelialization; skin graft is required.

Baux score (sum of age and TBSAburned) and Denver 2 score (pulmonary score ranging 0 to 3, using PaO2/FiO2 cutoffs of 100, 175, and 250), renal

score (0 to 3, using creatinine cutoffs of 1.8, 2.5, and 5.0 mg/dL), hepatic score (0 to 3, using bilirubin cutoffs of 2, 4, and 8 mg/dL), and cardiac score (0 to 3, based on number and dosage of inotropes) can be used to estimate mortality (5)[B].

Length of hospital stay and need for ICU care depend on extent of burn, smoke inhalation, comorbidities, and age.

Burn size is correlated to complications; >60% TBSAburned in children and >40% in adults are at increased risk for mortality and morbidity (5)[B].

A50% survival rate can be expected with a 62% burn in patients aged 0 to 14 years, 63% burn in patients aged 15 to 40 years, 38% burn in patients aged 40 to 65 years, and 25% burn in patients >65 years of age.

90% of survivors can be expected to return to an occupation comparable to their preburn employment.

COMPLICATIONS

Gastroduodenal ulceration (Curling ulcer)

Marjolin ulcer: malignant squamous cell carcinoma developing in old burn site

Signs of infection: discoloration, green fat, edema, eschar separation, and conversion of 2nd-degree to 3rd-degree wound

Biopsy is the best way to diagnose wound infection.

Burn wound sepsis: most commonly S. aureus (including MRSA), vancomycin-resistant enterococci, and gram-negative organisms

Pneumonia

Decreased mobility with possibility of future flexion contractures

Hypertrophic scarring common with burns

REFERENCES

1.Dries DJ, Endorf FW. Inhalation injury: epidemiology, pathology, treatment strategies. Scand J Trauma Resusc Emerg Med. 2013;21:31.

2.Bezuhly M, Fish JS. Acute burn care. Plast Reconstr Surg. 2012;130(2):349e–358e.

3.Perel P, Roberts I, Ker K. Colloids versus crystalloids for fluid resuscitation in critically ill patients. Cochrane Database Syst Rev. 2013;(2):CD000567.

4.Ong YS, Samuel M, Song C. Meta-analysis of early excision of burns. Burns.

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2006;32(2):145–150.

5.Jeschke MG, Pinto R, Kraft R, et al; and Inflammation and the Host Response to Injury Collaborative Research Program. Morbidity and survival probability in burn patients in modern burn care. Crit Care Med. 2015;43(4):808–815.

CODES

ICD10

T30.0 Burn of unspecified body region, unspecified degree T30.4 Corrosion of unspecified body region, unspecified degree

CLINICALPEARLS

1st degree: erythema of involved tissue; skin blanches with pressure. Skin may be tender.

2nd degree: Skin is red and blistered. Skin is very tender.

3rd degree: Burned skin is tough and leathery. Skin is not tender.

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BURSITIS, PES ANSERINE (PES ANSERINE SYNDROME)

Jennifer B. Schwartz, MD

BASICS

DESCRIPTION

The pes anserinus (“goosefoot”) is the combined insertion of the sartorius, gracilis, and semitendinosus (SGT) tendons on the anteromedial tibia.

The pes anserine muscles help flex the knee and resist valgus stress.

The pes anserine bursa lies deep to the SGT tendons and superficial to the tibial attachment of the medial collateral ligament.

Pes anserine syndrome is due to irritation of the bursa and/or tendons in this area.

EPIDEMIOLOGY

Incidence

Inflammation of the pes anserine bursa is detected in up to 2.5% of MRI studies of patients with knee pain. The overall incidence is likely higher.

ETIOLOGYAND PATHOPHYSIOLOGY

Pes anserine bursitis occurs due to:

Overuse injury

Excessive valgus and rotary stresses

Mechanical forces and degenerative changes

Direct trauma

RISK FACTORS

Obesity

Age, female gender

Pes planus; genu valgum

Knee joint laxity/ligamentous injury

Long distance running, hill running; change in mileage

Swimming (“breaststroker’s knee”); cycling

Sports with side-to-side (cutting) activity (soccer, basketball, racquet sports)

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