01Approach to the Critical Patient/attcp60

Immediate threats and stabilization

›Life-threatening presentations

›Cardiac arrhythmia from systemic phenol absorption

›Ventricular tachycardia or fibrillation

›Supraventricular tachycardia

›PVCs as early warning sign

›Cardiovascular collapse

›Hypotension or shock physiology

›MAP < 65 mmHg triggers resuscitation

›Airway compromise from inhalation exposure

›Stridor or hoarseness

›Oropharyngeal burns with edema risk

›Altered mental status or seizures

›CNS toxicity from systemic absorption

›GCS < 13 warrants immediate airway control

›Decontamination as the critical intervention

›Don PPE before patient contact

›Level C minimum — phenol absorbs through rescuer skin

›Nitrile gloves inadequate; butyl rubber preferred

›Remove all contaminated clothing immediately

›Secondary exposure risk to healthcare providers

›Bag and seal contaminated garments

›Preferred decontaminant: polyethylene glycol 400

›Apply liberally, wipe repeatedly

›More effective than water for dermal phenol

›Alternative: 70% isopropyl alcohol

›Equally effective for burns < 5% TBSA

›More widely available than PEG 400

02History/hx71

Exposure characterization

›Exposure context

›Industrial sources

›Resins, plastics, explosives, fertilizers, paints

›Textiles, pharmaceuticals, wood preservatives

›Cosmetic procedures

›Phenol-based chemical face peels

›Deep peels at higher concentration and risk

›Household products at low concentrations

›Exposure details critical for severity

›Agent concentration

›Solutions > 5% phenol carry highest systemic risk

›Concentrated solutions cause more rapid dermal absorption

›Volume and body surface area involved

›> 5% TBSA significantly increases systemic toxicity risk

›Small burns can be fatal if decontamination is delayed

›Duration of skin contact before decontamination

›Decontamination within 10 minutes markedly reduces injury

›> 30 minutes dramatically increases systemic absorption

›Route of exposure

›Dermal most common

›Inhalation, ingestion, or ocular as alternatives

›Decontamination already performed

›Agent used: water, PEG, isopropyl alcohol

›Time to decontamination from exposure

Systemic symptom review

›Cardiovascular symptoms

›Palpitations

03Physical Exam/exam67

Vital signs and hemodynamics

›Cardiovascular stability

›Heart rate

›Tachycardia as earliest sign of systemic toxicity

›Arrhythmia type characterization

›Blood pressure

›Hypotension indicating cardiovascular collapse

›MAP < 65 mmHg threshold for intervention

›Respiratory rate

›Tachypnea from pain, inhalation, or acidosis

›Temperature

›Hypothermia from large area exposure and fluid shifts

›SpO2 on room air

Skin and burn assessment

›Burn characteristics

›Color progression

›Initially white or blanched coagulated area

›Progresses to brown/tan leathery eschar over hours

›May appear deceptively superficial early

›Characteristic sweet, acrid odor of phenol

›Painless or reduced sensation area

›Local anesthetic effect of phenol

›Leads to underestimation of burn severity

›Burn depth assessment

›Superficial partial-thickness

›Blistering, moist, painful

›Deep partial-thickness to full-thickness

›Typical result of phenol burns

04Differential Diagnosis/ddx46

Chemical burn agents

›Other chemical burns requiring differentiation

›Hydrofluoric acid burn

›ICD-10 T54.2

›Systemic hypocalcemia and QT prolongation

›Treatment with calcium gluconate not phenol protocol

›Strong acid burns (sulfuric, hydrochloric, nitric)

›Coagulative necrosis similar to phenol

›No local anesthetic effect; painful

›Water irrigation preferred; no PEG advantage

›Strong alkali burns (sodium hydroxide, lime)

›ICD-10 T54.3

›Liquefactive necrosis; deeper penetration than acids

›Chromic acid

›Systemic toxicity with hepatorenal damage

›Green-yellow coloration of wound

›Cresol or creosote exposure

›Phenol derivatives with similar systemic toxicity

›Wood preservative sources

Non-chemical burn mimics

›Thermal burn

›ICD-10 T30.0

›No systemic cardiotoxic or neurotoxic profile

›Distinguish by history of heat source vs chemical exposure

›Electrical burn

›ICD-10 T75.4

›Entry and exit wounds

›Deeper tissue injury with minimal skin surface involvement

05Laboratory Tests/lt56

Core metabolic and organ function labs

›Complete blood count

›Baseline leukocyte count

›Leukocytosis from burn stress response

›Leukopenia rare; suggests marrow toxicity

›Hemoglobin and hematocrit

›Hemolysis marker

›Hemoconcentration from fluid losses

›Comprehensive metabolic panel

›Renal function (creatinine, BUN)

›Phenol directly nephrotoxic

›Trend every 6-12 hours in significant exposure

›Hepatic panel (AST, ALT, bilirubin)

›Phenol hepatically metabolized

›Elevation indicates hepatotoxicity

›Electrolytes

›Sodium for fluid management

›Potassium in hemolysis or rhabdomyolysis

›Glucose

›Stress hyperglycemia

›Hypoglycemia in severe hepatic failure

Toxicity-specific labs

›Urinalysis

›Urine color assessment

›Dark or smoky: phenol metabolite excretion (phenylsulfate, phenylglucuronide)

›Cola-colored: myoglobinuria or hemolysis

›Dipstick heme-positive without RBCs: myoglobin

›Urine phenol level if available

06Diagnostic Tests/dt83

Scoring Systems

›TBSA estimation tools

›Rule of Nines (adult)

›Head and neck 9%

›Each arm 9%

›Anterior trunk 18%, posterior trunk 18%

›Each leg 18%

›Perineum 1%

›Rapid field estimate; less accurate than Lund-Browder

›Lund-Browder chart

›Corrects for age-related body proportion differences

›Preferred method for accurate TBSA in burns

›Especially important in pediatric patients

›Palmar surface rule

›Patient's palm (fingers excluded) = approximately 0.5% TBSA

›Useful for scattered irregular burn pattern

›Burn severity scoring

›American Burn Association severity classification

›Major burn: > 25% TBSA adults or > 20% pediatric

›Moderate: 15-25% TBSA adults

›Minor: < 15% TBSA adults; < 10% pediatric

›Baux Score (mortality prediction)

›Age + % TBSA = Baux score

›Score > 100 associated with > 50% mortality

›Revised Baux adds 17 for inhalation injury

›Chemical-specific risk stratification

›Phenol exposure risk tier

›High risk: > 5% TBSA or any systemic symptoms

›Moderate risk: 2-5% TBSA with adequate early decontamination

›Lower risk: < 2% TBSA superficial with decontamination within 10 minutes

MRI

›MRI role in phenol burns

›Generally not indicated acutely for dermal phenol burns

›CT and clinical exam sufficient for acute management

›MRI time requirements incompatible with monitoring needs

›Late complications assessment

›MRI for compartment syndrome sequelae if clinically indicated

›Neurologic sequelae from CNS phenol toxicity

›Not first-line; only if CT inconclusive

›MRI brain

›Consideration for persistent neurologic deficits post-exposure

›Phenol-induced leukoencephalopathy rarely reported

›Indication: altered mental status not resolving after decontamination

CT

›CT chest for inhalation exposure

›Indications

›Facial burns with suspected airway involvement

›Persistent respiratory symptoms after decontamination

›Abnormal chest radiograph

›Findings

›Airway edema or mucosal injury pattern

›Pulmonary infiltrates from chemical pneumonitis

›Pneumothorax if barotrauma from aggressive ventilation

›CT abdomen and pelvis for ingestion exposure

›Indications

›Suspected oral/GI phenol ingestion

›Abdominal pain, guarding, or peritoneal signs

›Findings

›Visceral perforation pattern

›Free air or free fluid

›Mucosal edema of esophagus or stomach

›CT extremities

›Compartment syndrome evaluation from circumferential burns

›Clinical diagnosis takes precedence

›CT shows fascial compartment edema

›Emergent surgical consultation triggers if pressures > 30 mmHg

Ultrasound

›Bedside POCUS in phenol burns

›Cardiac POCUS

›Ventricular function assessment during arrhythmia

›Pericardial effusion from systemic toxicity

›Volume status via IVC collapsibility

›IVC assessment

›Collapsibility index > 50%: fluid responsive

›Flat IVC: severe hypovolemia, aggressive resuscitation

›Lung ultrasound

›B-lines: pulmonary edema from fluid resuscitation

›Consolidation: chemical pneumonitis from inhalation

›Pleural effusion from inflammatory response

›Vascular access ultrasound

›Guided central venous access for large bore access

›Burn-involved extremities may limit peripheral access

›Wound assessment adjuncts

›Laser Doppler imaging if available

›Indeterminate burn depth assessment

›Reduces unnecessary surgical intervention

›Not standard at most emergency departments

07Disposition/dispo41

Admission criteria

›ICU or Burn Unit admission indications

›Cardiac arrhythmia or ECG abnormality of any type

›Burns > 5% TBSA

›Dramatically increases systemic absorption risk

›Requires continuous monitoring and resuscitation

›Full-thickness burns of any size

›Hemodynamic instability

›MAP < 65 mmHg or persistent tachycardia

›Altered mental status, seizures, or coma

›Elevated serum phenol levels

›Hepatic or renal laboratory abnormalities

›Inhalation exposure

›Even without immediate symptoms; edema can be delayed

›Burns to high-risk areas

›Face, hands, feet, genitalia, perineum, over major joints

Burn center transfer criteria

›American Burn Association referral criteria

›Partial-thickness burns > 10% TBSA

›Full-thickness burns of any size

›Burns involving face, hands, feet, genitalia, perineum, major joints

›Chemical burns (all phenol burns qualify for consideration)

›Inhalation injury

›Circumferential limb or chest burns

›Patients with pre-existing medical disorders complicating management

›Burns with concomitant trauma

›Transfer timing

›Stabilize airway, breathing, circulation before transfer

08Treatment/t92

Decontamination protocol

›PPE and scene safety first

›Butyl rubber or neoprene gloves

›Nitrile gloves have inadequate phenol protection

›Face shield and impermeable gown

›Level C protection minimum for significant exposures

›Decontamination agent selection

›Polyethylene glycol 400 (preferred)

›Apply liberally and wipe off repeatedly

›Continue until odor dissipates and skin color normalizes

›Low-molecular-weight PEG (300-400) most effective in studies

›High-molecular-weight PEG 3350 or water acceptable alternatives

›70% isopropyl alcohol (equally effective alternative)

›Swab affected area repeatedly

›Change swabs frequently to avoid re-exposure

›Preferred when PEG unavailable for < 5% TBSA

›Water irrigation

›Copious irrigation >= 15-30 minutes

›Use immediately if PEG or IPA unavailable

›Do not delay decontamination to obtain preferred agent

›Some animal data suggest water may increase absorption vs IPA, but real-world data do not confirm harm

›Agents to avoid

›Neutralizing agents contraindicated

›Occlusive dressings that trap phenol against skin

Cardiac management

›Continuous telemetry mandatory for >= 24 hours in significant exposures

›Prophylactic lidocaine

›Consider for large BSA phenol exposures (> 5% TBSA)

›1-1.5 mg/kg IV bolus then 1-4 mg/min infusion

›Titrate to arrhythmia suppression

›Monitor for lidocaine toxicity

›Arrhythmia treatment per ACLS protocols

›Ventricular fibrillation

›Defibrillation 200 J biphasic immediately

›Epinephrine 1 mg IV every 3-5 minutes

›Amiodarone 300 mg IV after third shock

›Ventricular tachycardia with pulse

›Cardioversion 100 J synchronized if hemodynamically unstable

›Amiodarone 150 mg IV over 10 minutes if stable

›Supraventricular tachycardia

›Adenosine 6 mg IV rapid push; repeat 12 mg if no response

›Rate control with beta-blocker if hemodynamically stable

›Avoid class IA antiarrhythmics (quinidine, procainamide)

›May worsen phenol-induced QT prolongation

Fluid resuscitation

›IV fluid resuscitation goals

›Parkland formula for burns > 20% TBSA

›4 mL/kg/% TBSA of lactated Ringer's in first 24 hours

›Half in first 8 hours from time of burn

›Half over next 16 hours

›Modified Brooke formula alternative

›2 mL/kg/% TBSA lactated Ringer's in first 24 hours

›Urine output target

›0.5-1 mL/kg/hour in adults

›1 mL/kg/hour in children

›Increase target if myoglobinuria or hemoglobinuria

›Forced diuresis for phenol metabolite clearance

›Furosemide 20-40 mg IV if adequate fluid resuscitation confirmed

›Maintain urine output 1-2 mL/kg/hour

›Alkalinize urine with sodium bicarbonate if myoglobinuria

Wound care

›Post-decontamination wound management

›Standard burn wound dressings

›Silver sulfadiazine 1% cream to burn wound

›Modern alternatives: silver-containing dressings, mafenide acetate

›Change every 24-48 hours

›Tetanus prophylaxis

›Tetanus toxoid 0.5 mL IM if last booster > 5 years

›Tetanus immunoglobulin 250 units IM if unvaccinated or unknown

›No prophylactic systemic antibiotics

›Antibiotics reserved for clinical infection

›Wound swab culture if infection develops

›Escharotomy for circumferential burns

›Compartment pressure > 30 mmHg is indication

›Distal ischemia is clinical indication

›Burn surgery consultation

Analgesia and supportive care

›Pain management

›Opioids for moderate-severe pain

›Morphine 0.05-0.1 mg/kg IV every 2-4 hours titrated

›Fentanyl 1-2 mcg/kg IV for procedural pain

›NSAIDs as adjunct if no contraindication

›Avoid if renal toxicity developing

›Note: phenol local anesthetic effect may mask pain

›Do not undertreat based on reported comfort

›Seizure management

›Lorazepam 0.05-0.1 mg/kg IV for active seizures

›Levetiracetam 20-30 mg/kg IV for refractory seizures

›Treat underlying cause: correct hypoxia, metabolic derangements

›Airway management for inhalation injury

›Early intubation before edema progresses

›Video laryngoscope preferred for anticipated difficult airway

›RSI with ketamine 1.5 mg/kg IV and succinylcholine 1.5 mg/kg IV

›Ventilator settings

›Tidal volume 6-8 mL/kg ideal body weight

›PEEP 5-8 cmH2O initial

›SpO2 target 95-98%

09Special Populations/sp77

Pregnancy

›Physiologic considerations

›Increased skin absorption surface area with dermal edema of pregnancy

›Hypervolemia of pregnancy may dilute toxin initially

›Fetal cardiac sensitivity to phenol metabolites

›Phenol crosses placenta; direct fetal cardiotoxicity risk

›Uterine blood flow compromise during maternal arrhythmia

›Fetal monitoring mandatory after significant exposure

›Management modifications

›Immediate obstetric consultation for any significant exposure

›Continuous fetal heart monitoring if >= 24 weeks gestation

›Decontamination protocol unchanged

›PEG 400 or IPA decontamination safe in pregnancy

›Copious water irrigation if preferred agents unavailable

›Fluid resuscitation

›Standard Parkland formula applies

›Higher baseline cardiac output requires higher fluid targets

›Medication safety

›Lidocaine Class B in pregnancy; acceptable for arrhythmia prophylaxis

›Amiodarone Class D; avoid if possible; use only for life-threatening arrhythmia

›Furosemide Category C; use with caution; avoid in first trimester

›Left lateral decubitus positioning to relieve aortocaval compression

›TBSA estimation may be affected by abdominal enlargement

›Modify Rule of Nines for fundal height

Geriatric

›Physiologic vulnerabilities

›Thinner skin with decreased barrier function

›More rapid dermal phenol absorption

›Burns more likely to be full-thickness

›Reduced cardiac reserve

›Lower threshold for arrhythmia from phenol toxicity

›Reduced ability to tolerate tachyarrhythmias

›Impaired renal and hepatic clearance

›Slower phenol metabolism prolongs toxicity

›Higher serum phenol levels with equivalent exposure

›Polypharmacy

›QT-prolonging medications increase arrhythmia risk

›Anticoagulants increase bleeding risk in escharotomy

›Management modifications

›Lower threshold for ICU admission

›Any systemic symptom warrants admission

›Fluid resuscitation caution

›Risk of fluid overload with aggressive Parkland formula

›Target lower end of urine output goals

›Monitor for pulmonary edema

›Medication dose adjustment

›Lidocaine dose reduction by 30-50% for reduced hepatic clearance

›Opioid dosing start low; 0.025 mg/kg morphine IV

›Skin fragility

›Wound care with non-adhesive dressings

›Higher rate of wound complications

Pediatrics

›Physiologic differences

›Thinner skin increases dermal absorption rate

›Systemic toxicity with smaller TBSA burns

›Higher body surface area to weight ratio

›Greater systemic phenol burden per unit mass

›More significant fluid losses per kg

›Immature hepatic metabolism

›Slower conjugation of phenol metabolites

›Prolonged and more severe toxicity in neonates and infants

›Burn center referral recommended for all significant pediatric chemical burns

›JAMA Network Open 2026: adherence to pediatric burn center referral criteria improves outcomes

›Weight-based dosing

›IV fluid resuscitation

›Parkland formula: 3-4 mL/kg/% TBSA lactated Ringer's in first 24 hours

›Plus maintenance fluids (4 mL/kg/hour for first 10 kg, etc.)

›Urine output target 1 mL/kg/hour

›Analgesia

›Morphine 0.05-0.1 mg/kg IV per dose

›Fentanyl 1 mcg/kg IV for procedural pain

›Seizure prophylaxis and treatment

›Lorazepam 0.05-0.1 mg/kg IV (max 4 mg)

›Levetiracetam 20 mg/kg IV

›Decontamination

›Same agents as adults; avoid hypothermia from prolonged irrigation

›Warm water for decontamination in infants

›Safeguarding consideration

›Unexplained chemical burns in children warrant child protection evaluation

›Non-accidental injury pattern if history inconsistent with burn distribution

10Background/b76

Epidemiology

›Incidence and exposure sources

›Phenol is a widely used industrial chemical

›Production: approximately 10 million metric tons annually worldwide

›Industrial exposure most common cause of significant burns

›Cosmetic chemical peels increasingly reported cause of iatrogenic burns

›Cosmetic exposure data

›13% of plastic surgeons performing phenol peels reported cardiac complications

›Tachycardia most frequent cardiac complication reported

›Complications include arrhythmia, laryngospasm, hypersensitivity

›Approximately 50% of reported phenol intoxication cases have fatal outcome

›High lethality due to rapid systemic absorption

›Fatal cases often involve delayed decontamination

›ICD-10 codes

›T65.891: Toxic effects of phenol, accidental

›T54.1: Toxic effects of other corrosives

›Chemical burns coded by body site T20-T32

Pathophysiology

›Local tissue injury mechanism

›Coagulative necrosis of skin proteins

›Phenol denatures proteins at cell surface

›Creates eschar barrier that may limit further penetration

›However, coagulum also can trap phenol against skin

›Dermal absorption

›Highly lipophilic molecule; penetrates intact skin rapidly

›Absorption begins within minutes of contact

›Warm skin, abraded skin, and higher concentrations accelerate absorption

›Systemic toxicity mechanisms

›Cardiotoxicity

›Direct membrane destabilization of cardiac myocytes

›Prolongation of action potential duration

›Increased automaticity triggering ventricular arrhythmias

›QTc prolongation predisposes to torsades de pointes

›Neurotoxicity

›CNS depression from direct neural membrane effects

›Seizures from cortical irritation

›Local anesthetic effect via sodium channel blockade

›Hepatotoxicity

›Phenol oxidatively metabolized by CYP2E1 to catechol and hydroquinone

›Reactive intermediates cause oxidative hepatocellular injury

›Conjugation to sulfate and glucuronide in liver before renal excretion

›Nephrotoxicity

›Direct tubular toxicity from phenol and metabolites

›Hemolysis and myoglobinuria cause secondary tubular obstruction

›Renal failure rare with adequate decontamination and hydration

›Decontaminant mechanism of action

›PEG and IPA dissolve phenol from skin without saponification

›Remove phenol faster than water alone

›Critical window: decontamination within 10 minutes markedly reduces injury

Therapeutic Considerations

›Decontamination evidence base

›Hunter DM et al. Ann Emerg Med 1992

›IPA and PEG significantly reduce full-thickness burn area vs water

›Animal (pig skin) models show IPA reduces phenol absorption by 75%

›IPA and PEG equivalent in efficacy; both superior to water in formal study

›Monteiro-Riviere NA et al. Toxicol Ind Health 2001

›PEG reduces dermal absorption and burn severity in pig skin model

›IPA shows equivalent penetration reduction

›2024 AHA/Red Cross First Aid Guidelines

›Water irrigation remains acceptable and available option

›Do not delay decontamination to obtain PEG or IPA

›Testa J et al. JOEM 2025

›Low molecular weight PEG (300-400) preferred over high MW forms

›LMW-PEG rarely stocked in emergency departments

›High MW alternatives acceptable when LMW unavailable

›Cardiac management evidence

›Horch R et al. Burns 1994

›Cardiac arrhythmias primary cause of death from phenol burns

›Prophylactic lidocaine considered for large TBSA exposures

›Continuous telemetry essential for >= 24 hours

›Rubinstein J et al. Environ Health 2024

›Urinary phenol levels associated with cardiac electrical alterations

›QT interval prolongation correlates with phenol burden

›Wound care evidence base

›Treat phenol burn wounds as standard chemical burns after decontamination

›No evidence for specific wound care products unique to phenol

›Depth reassessment at 24-48 and 72 hours mandatory

›Burns commonly convert from partial to full thickness

›Early surgical planning for full-thickness areas

11Patient Discharge Instructions/pdi41

copy discharge instructions

›Discharge instructions for phenol burn patients

›Your injury

›You were treated for a chemical burn caused by phenol (carbolic acid)

›Phenol burns can initially appear less severe than they are

›Your burn may appear worse over the next 2-3 days as the injury fully declares itself

›You received decontamination treatment to remove the chemical from your skin

›Wound care at home

›Keep the burn area clean and covered with the dressing provided

›Change your dressing as instructed, typically every 24-48 hours

›Do not apply ice, butter, oil, or home remedies to the burn

›Wash hands before touching the burn or dressing

›Pain management

›Take pain medication as prescribed

›Over-the-counter ibuprofen or acetaminophen for mild discomfort

›Note that the burned area may feel numb initially — this is normal and does not mean healing is complete

›Monitoring for complications

›Drink plenty of fluids and monitor your urine

›Urine should be clear to light yellow; dark or cola-colored urine requires immediate return

›Follow-up appointment

›Return to burn clinic or your doctor within 24-48 hours for wound reassessment

›Burn depth can change over the first 72 hours

›You may need further treatment including skin grafting depending on how the wound heals

›If this was a workplace exposure

›Report the incident to your occupational health department

›Obtain the Safety Data Sheet for the chemical involved

›Your employer may be required to file an OSHA report

›Return to emergency department immediately for

12References/r28

Guidelines and key sources

›Decontamination guidelines

›Hewett Brumberg EK et al. 2024 AHA and American Red Cross Guidelines for First Aid. Circulation 2024

›Recommends water irrigation; acknowledges PEG and IPA superiority when available

›Do not delay decontamination to obtain preferred agent

›Hunter DM, Timerding BL, Leonard RB et al. Effects of isopropyl alcohol, ethanol, and PEG in treatment of acute phenol burns. Ann Emerg Med 1992

›Landmark comparison study of decontamination agents

›IPA and PEG superior to water for dermal phenol exposure

›Monteiro-Riviere NA et al. Efficacy of topical phenol decontamination strategies. Toxicol Ind Health 2001

›Pig skin model confirming PEG and IPA efficacy

›Testa J, Chambers A, Cumpston K. Is low molecular weight polyethylene glycol used for decontamination of dermal phenol exposures? JOEM 2025

›Cardiotoxicity and systemic toxicity references

›Horch R, Spilker G, Stark GB. Phenol burns and intoxications. Burns 1994

›Arrhythmia as primary cause of death; prophylactic lidocaine discussion

›Rubinstein J et al. Association of urinary phenol levels and cardiac electrical alterations. Environ Health 2024

›QT prolongation correlation with urinary phenol burden

›Gaudy JH et al. Serious heart rate disorders following perioperative splanchnic nerve phenol block. Can J Anaesth 1993

›de Oliveira Ciaramicolo N et al. Adverse effects of irresponsible use of phenol peeling. Oral Surg Oral Med Oral Pathol 2025

›Burn center referral criteria

›Bettencourt AP et al. Updating the burn center referral criteria: 2018 eDelphi consensus. J Burn Care Res 2020

›Updated ABA referral criteria supporting chemical burn transfer

›Chai H et al. Chemical burn to the skin: systematic review of first aid impacts on clinical outcomes. Burns 2022

›Gus E et al. Adherence to burn center referral criteria for pediatric burns. JAMA Netw Open 2026

›Toxicology and general references

›Bruce RM, Santodonato J, Neal MW. Summary review of health effects associated with phenol. Toxicol Ind Health 1987

›Henretig FM, Kirk MA, McKay CA. Hazardous chemical emergencies and poisonings. NEJM 2019

›Comprehensive hazardous chemical management including phenol

›Lanham JS et al. Outpatient burn care: prevention and treatment. Am Fam Physician 2020

Evidence & Review