BURNS AND ANAESTHESIA

CHAIR PERSON: Dr. Shivakumar. G

MODERATOR: Dr. Diwakar.S.R
PRESENTER: Dr. Arpitha. R

16/3/2020
 DEFINITION

• Burns are tissue injury resulting from direct contact with flames, hot liquids, gases, caustic
chemicals ,electricity or radiation.
 ANATOMY OF SKIN

Epidermis
Dermis
Hypodermis
 FUNCTIONS OF SKIN

• It protects the body against invasion from microorganism

• Temperature regulation
• Fluid and electrolyte homeostasis
• Touch, pain and temperature sensations
• Vitamin D metabolism
• UV protection.
 TYPES OF BURNS

• Thermal ( heat ) burns

• Chemical burns
• Electrical burns
• Inhalational burns
 THERMAL BURNS

Classification
Depth
• Superficial
• Partial thickness –superficial , Deep
• Full thickness
Degree
First ,Second, Third, Fourth
 THERMAL BURNS

• Superficial burn :1st degree burn

Signs and symptoms
Erythema
Pain at burn site
Involves only epidermis
Absence of blisters.
Heals within 3-6 days. ( heals with dressing)
Ex : sunburn
 THERMAL BURNS

• Superficial partial thickness burn: Second degree burn.

Signs and symptoms
• Entire epidermal layer
• Part of underlying dermis
• Motteled and red ,painful swelling and blisters
• Healing in 10 -21 days
 THERMAL BURNS

Deep partial thickness burn

• 3rd Degree Burn
• Signs and symptoms
• Destruction of all epidemal and dermal elements.
• Burns into subcutaneous fat or deeper
• Skin is charred and leathery ( woody)
• Not painful (nerve endings are dead)
• Surgical intervention
 THERMAL BURNS

Fourth degree
• Full thickness
• Extending into muscle,tendon or bones
• Black and dry.
• No pain
• Eschar formation
 MAJOR BURNS
Based on body surface area burned and the area of the body burned:
• Third degree (full thickness) burn injuries involving > 10% of TBSA
• Second degree (partial thickness) burn injuries involving > 20% TBSA at extremes of age and > 25%
TBSA in adults
• Burns involving face, hands, feet, genitalia, perineum, major joints
• Inhalational injuries
• Chemical burn injuries
• Electrical burn injuries
• Burn injuries in patients with co-existing medical disease
• Burns associated with trauma.
 PATHOPHYSIOLOGICAL CHANGES

• Hemodynamic response
• Respiratory responses
• Metabolic responses
• Thermoregulation
• Immune system responses
• Hematologic system
• Renal and electrolytes
• Gastrointestinal tract
 ESTIMATION OF BURNT AREA

• Wallace rule of nine

 ESTIMATION OF BURNT AREA

• Lund and browder

 ESTIMATION OF BURNT AREA

• Palmar surface
 ELECTRICAL BURNS

• Low voltage causes local contact burn.

• Domestic supply is 50Hz A.C., 240V - cardiac arrest.
• High voltage (more than 500V) - flash burns or deep tissue damage due to current
transmission.
• The conversion of high voltage electric energy to thermal energy results in burns.
• The amount of thermal energy transferred -voltage of the electrical source, skin resistance
of the victim, duration of contact
 ELECTRICAL BURNS
Complications
• CVS : Continuous ECG monitoring - first 48 hours after burns - cardiac
dysrrhythmias,asystole.
• RS : Respiratory arrest - respiratory muscle paralysis - tetanic contractions or indirect trauma
post injury.
• CNS : acute and chronic
• Musculoskeletal : fractures and compartment syndrome
• Rhabdomyolysis → myoglobin → acute renal failure .
• Intravenous fluids - urine output of at least 1.5–2ml/kg/hour .
• ENT and head - Cataract - common
 ELECTRICAL BURNS
Criteria for High-risk for arrhythmias after electrical injury

• Abnormal ECG on presentation

• Loss of consciousness at time of electrical injury
• Exposure to high voltage (>240 volts)
• Past cardiac history
• Increased skin conduction, e.g. wet skin, high humidity
• Tetany at time of electrocution
 LIGHTNING ELECTRICAL BURN
• Extremely high voltage (approx.10–120 million volts).
• Lightning strikes inanimate objects like the ground, tree, or other objects .
• Type of injuries - 1/3 of injured people have signs of burns - superficial .
• Primarily neurological and affect all 3 components of the nervous system: central,
autonomic, and peripheral .
• Cardiac and respiratory arrest – can occur.
 CHEMICAL BURNS

• Acids , alkalies or petroleum products.

• Most acids produce a coagulation necrosis by denaturing proteins, forming eschar
that limits the penetration of acid.
• Base typically produce a more severe injury known as liquefaction necrosis.
• Damage continues until substance is removed or neutralized.
• Tratment - continuous irrigation with water.
 INHALATION INJURY

• Inhalation injury is the main cause of death in burn patients

• It results from airway inflammatory response to inhalation of products of
incomplete combustion and is the leading cause of death (up to 77 %)in burn
patients.
• Usually limited to upper airway
 INHALATION INJURY

Risk factors for significant smoke inhalation

• Exposure in closed spaces

• Unconsciousness or other neurologic alterations
• Facial or cervical burns
• Respiratory signs or symptoms .
 INHALATIONAL INJURY
• On examination there would be darkened or reddened oral and/or nasal mucosa, burns to the face, lips
or nares, singed eyebrows or nasal hairs.

• The presence of carbon or soot on teeth, tongue or throat, hoarse voice or productive cough would
indicate inhalational injury.

• Tracheal tug, inspiratory stridor or inability to clear secretions may indicate impending airway occlusion .

• Early intubation is indicated - swelling of tissues around the airway.

• ABG and CO level - degree of insult
 INHALATION INJURY
Effects of acute smoke inhalation injury
• Impairement of mucociliary function → infection
• Mucus hypersecretion .
• Tissue inflammation with tracheobronchitis, bronchitis, laryngitis, pneumonitis
• Epithelial sloughing
• Biochemical alteration with surfactant inactivation
• Increase vascular permiability and lung edema
• Bronchoconstriction
• Carbon monoxide poisoning
 PATHOPHYSIOLOGICAL CHANGES IN INHALATIONAL INJURY

• Airway injury above the larynx

• Airway injury below the larynx
• Chemical tracheobronchitis
• Systemic intoxication injuries
 OTHER COMPONENTS OF SMOKE

• Oxygen free radicals

• Ammonia
• Sulphur dioxide
• Nitrogen dioxide
• Chlorine
 CARBON MONOXIDE POISONING

• Colorless and odorless gas

• Carbon monoxide affinity for hemoglobin is 200 times greater than that of oxygen.
• Shift dissociation curve to left → tissue hypoxia.
• Normal COHb < 1.5 % in non smokers and < 10 % in smokers.
• Pulse oximeters using two wavelengths cannot detect COHb
Causes :
• Inhalation of combustible fumes produced by small gasoline engines, stoves, generators,
lanterns, gas ranges or by burning charcoal and wood in the household environment is the
largest source of CO poisoning
 CARBON MONOXIDE POISONING

Mechanisms of toxicity include:

• Decrease in the oxygen carrying capacity of blood.
• Leftward shift of the oxyhemoglobin dissociation curve, further decreases oxygen
delivery to the tissues.
• Binding with cytochrome A3 results in decrease in cellular respiration.
• Binding to myoglobin, potentially causing myocardial and skeletal muscle dysfunction
CARBON MONOXIDE POISONING
 TREATMENT OF CARBON MONOXIDE POISONING

• Acute CO poisoning is treated by terminating the exposure by removing the patient from the
exposed environment and by administering supportive care.
• The binding of CO with haemoglobin is competitive and reversible.
• Hence the mainstay of therapy for CO poisoning is supplemental O2, ventilatory support and
monitoring for cardiac arrhythmias .
• All patients should be given 15 L/min of oxygen via a non rebreather mask. The half-life of COHb
is 250 mins at atmospheric pressure, 40–80 minutes while breathing 100% O2 and 22 minutes in
a hyperbaric chamber at 2.5 atm.
 TREATMENT OF CARBON MONOXIDE POISONING

Role of hyperbaric oxygen therapy in CO poisoning:

Hyperbaric oxygen (HBO) therapy reduces the half life of COHb to 20–30 minutes.
• It also increases the amount of oxygen dissolved in the blood from 0.3 mL/dL with
isobaric therapy (FiO2 100%) to 5.5–6.4 mL/dL (2.4–2.8 atm)

• HBO induces cerebral vasoconstriction, which may reduce intracranial pressure and
cerebral edema, HBO result in more rapid dissociation of CO from respiratory
cytochromes
• HBO may antagonize the oxidative injury that occurs after CO poisoning.
 TREATMENT OF CARBON MONOXIDE
POISONING

Indications for considering hyperbaric oxygen therapy :

• Any neurological abnormality or cognitive impairment
• Seizure
• Hypotension
• Chest pain, abnormal ECG or elevated cardiac enzymes, arrhythmias
• COHb levels more than 40%
• Pregnancy with COHb level more than15%
• History of loss of consciousness or syncope
• Comatose patients.
 TREATMENT OF CARBON MONOXIDE
POISONING

Relative indications for HBO therapy include:

• Persistent neurologic symptoms (headache or dizziness) after 4 hours of high flow
oxygen therapy via non-rebreathing mask.
• Persistent acidosis
• Concurrent chemical or thermal burns
• Pregnancy with history of any CO exposure.
 PROGNOSIS

• Baux score
• Mortality = age + percent TBSA

• Other factors - inhalational injury, depth of burn , other injuries sustained

during burns and associated medical conditions.
 RESUSCITATION OF A PATIENT WITH BURNS

• Amaerican college of surgeons committee on trauma (evaluation of burn)

• Primary survey and secondary survey.
• Treat according to CPR protocol.
• Inhalational injury – endotracheal intubation . 100% oxygen.
• First aid
RESUSCITATION OF A PATIENT WITH BURNS

Primary Survey
• A. Airway maintenance with cervical spine control
• B. Breathing and Ventilation
• C. Circulation with Hemorrhage control
• D. Disability – neurological status
• E. Exposure and environmental control
• F. Fluid resuscitation proportional to burn size

Secondary survey
 PRIMARY SURVEY

Airway maintenance
• Identify inhalational injury in burns patient
• Trauma - cervical spine should be immobilized.
• After clearing the airway - administer 100% oxygen via a reservoir mask- this would also help to treat
CO poisoning.
• Elevate the head of bed to 30–90° to reduce the facial or airway edema provided there is no cervical
spine injury.
• Endotracheal intubation and mechanical ventilation is needed in patients who are unconscious from co-
existing trauma or from inhalation of toxic substances, patients who develop acute respiratory failure
due to smoke inhalation and in patients with major burns.
 PRIMARY SURVEY

Upper airway edema

• Most pronounced first 8 hrs .postburn.

• Signs and symptoms
• Stridor,horseness,facial burns,signed nasal hair or eyebrows,soot in sputum or oropharynx,respiratory
distress.

Treatment :
• Early intubation before edema makes it impossible
• Humidified O2 to help clear secretions

• Bronchodilators to manage bronchospasm

 PRIMARY SURVEY
• Breathing
• Chest wall restriction
• Found mostly with circumferential 3rd degree burns
• Loss of elasticity →work of breathing required to maintain FRC and TV
• Symptoms may increase 10- 12 hrs postburn secondary to maximum edema formation.
Treatment
• Mechanical ventilation
• Escharotomies
 PRIMARY SURVEY

Circulation
• Burn patients have increased capillary permiability in all burned areas resulting in
intravascular fluid shift into interstitial space.

• Rapid assessment of the volume status should be done.

• Monitor the blood pressure, pulse and capillary refill in both burned and unburned limbs
• Stop any bleeding with direct pressure.
 PRIMARY SURVEY

• Disability
• Exposure and environmental control
 FLUID REPLACEMENT

• Tissue burns - increased capillary permeability - Large fluid shift

• Edema formation - particularly during first 36 hrs.
• Greatest in first few hours.
• Early resuscitation is essential -- to avoid ARF and hypovolemic shock.
• 15% TBSA adults and 10% TBSA children - needs resuscitation.
• Urine output - 0.5ml/kg in adults and 1ml/kg in children who way less than 30 kgs.
 FLUID REPLACEMENT

• 2 large bore iv cannulae - non burnt area

• Other options –
Saphenous cut down,femoral cut down and interaosseous needles in children .
• Consists of crystalloid ,usually Ringer’s lactate, with or without the addition of
colloid.
• Standard protocols for fluid replacement use body weight in kg and percent TBSA
burned
 FLUID REPLACEMENT

• Parkland formula (4 ml of Ringer’s lactate per kg %TBSA burn per 24 hours)

• Half the calculated fluid deficit is administered during the first 8 hours postburn
and the remainder is administered over the next 16 hours.
• The patient’ daily maintenance fluid requirements are given concurrently.
• In children - maintenance fluid containing glucose is administered in addition to
burn formula ( glycogen storage)
FLUID RESUSCITATION
 FLUID REPLACEMENT

• US army institute of surgical research - RULE of TEN

• Initial fluid rate in ml/hr = % TBSA × 10
• Every 10 kg above 80 kg 100ml is added this rate.
• The endpoints of fluid therapy are hemodynamic stability and maintenance of an adequate
urine output.
• In extensive burns,fluid management is adjusted according to invasive monitors and laboratory
studies.
 PRIMARY SURVEY

• Blood - BG,Cross matching,blood glucose ,serum electrolytes,RFT,COHb ,ABG

• Urine - myoglobin /hemoglobin.
• Chest x - ray
• Pain management
• Severely burned patients - restless and anxious - hypoxemia and hypovolemia
• Narcotic analgesics and sedatives should be administered in small frequent doses by
intravenous route only.
• Intramuscular and subcutaneous injections should be avoided as absorption will be
erratic and analgesia delayed
 SECONARY SURVEY

• examine for any concomitant injuries

• Insert nasogastric tube and decompress the stomach if nausea and vomiting are present, in patients
with burns more than 20% TBSA and all intubated patients
• Enteral feeding should be commenced as soon as possible after burn injury to promote normal gut
function and to decrease the potential for bacterial translocation across the gastric mucosa.
• Prophylactic antibiotics are not indicated in the early post burn period. Antibiotics should be reserved
for treatment of infection.
• Tetanus prophylaxis should be given.
• Early referral to a burns centre would be appropriate
 COMMON OPERATION FOR BURN PATIENT

• Decompression procedures - escharotomies and fasciotomies

• Burn excision and skin grafting
• Reconstructionoperations
• Supportive procedures
tracheostomy, gastrostomy, vascular access
 ANESTHETIC CONSIDERATIONS

Preoperative
• Burn injuries may result in a broad spectrum of physiologic impairements.
• These vary depending on the percent on the percent of TBSA burned,location of
burns,age of the patient, time elapsed since initial injury .
• Ideally,burn patients are fluid resuscitated and stabilized 48 hrs before being
brought to the OR
 ANESTHETIC CONSIDERATION

Physiologic impairements:
• Respiratory
• Upper airway : A patient with burns around the airway (signed nose hairs) should be
intubated as early as possible.
• Direct inhalational injury and fluid resuscitation may make delayed intubation more
difficult secondary to upper airway edema
 ANESTHETIC CONSIDERATIONS
Respiratory
• Lower airway : physiologic derangements may include pulmonary edema and ARDS
Additionally,burn patients can be severely hypermetabolic(eg : a patient with 40 % TBSA
burns may have twice the normal metabolic rate) with corresponding increased CO2
production.
• ↓lung and chest wall compliance ,↓FRC,↑ carboxyhemoglobinemia .
 ANESTHETIC CONSIDERATIONS

Cardiovascular :
• Alterations in microvascular permeability result in a trans – capillary fluid flux and tissue
edema 12 -24 hours after thermal injury
• Large amounts of water,electrolytes and protien are lost into the extravascular space
,leading to intravascular fluid depletion and hypovolemic shock. (burn shock)
• Elevated circulating levels of catecholamines → ↑HR and ↑ CO
• Major burns require 1.5 – 1.7 times the caloric need.
 ANESTHETIC CONSIDERATIONS

Musculoskeletal
• Damaged muscle - ↑postsynaptic Acetylcholine receptor density,resulting in ↓
sensitivity to nondepolarizing muscle relaxant
• potentially fatal elevations of potassium in response to succinylcholine.
• Avoid succinylcholine after 24 hrs and for atleast 2 years thereafter.
 ANESTHETIC CONSIDERATIONS

• Hematologic : coagulopathies may result directly from the burn injury,as well as
from rapid replacement of blood loss during operative procedures
• IV access : may be difficult ,assessed in preoperative period.(2 large bore iv
canula)
• Consider central line placement with a large bore catheter.
• Premedication : patients are commonly placed on high dose narcotics after the
initial injury ,additional narcotics are frequently required to provide adequate
analgesia for transport and movement to the OR table.
 ANESTHETIC CONSIDERATIONS
Transport :
• For patients with severe ARDS,transportation from burn unit to OR may face
challenges with regard to ventilation.
• Cardiopulmonary monitoring must be continued during transport,the ventilation system
used in transport must be capable of delivering high minute volumes,PEEP,and
inspiratory pressures.
• These requirements may not be satisfied by standard bag valve systems and may
require a high – quality transport ventilator.
 ANESTHETIC CONSIDERATIONS

Intraoperative :
• Anesthetic technique : GA (opioid,muscle relaxant,volatile agent)
• Regional techniques prefered for minor burns.
• LMA are not recommended due to frequent repositioning of patient intraop.
• If the face is burned , - Difficult mask ventilation
• awake FOI may be necessary.(difficult airway)
• Securing the ETT maybe difficult .
• Alternatives to taping the ETT is required.
 ANESTHETIC CONSIDERATIONS

Induction :
• If the patient is adequately volume resuscitated:
• propofol(1.5- 2.5 mg/kg) or thiopental (3-5mg/kg) may be used.
• If the patient is intravascularly volume depleted
• Etomidate (0.3mg/kg) or ketamine (1-3mg/kg)is recommended
 ANESTHETIC CONSIDERATIONS

• Use of muscle relaxant

• Rapid sequence induction and intubation – indicated for full stomach
• Succinylcholine – C/I 24 hrs to 2 yrs after major burns , S/E profoud hyperkelemia
and cardiac arrest
• Rocuronium - 0.9 mg/kg
• Large dose of NDMR may be required due to increase in extrajunctional
acetylcholine receptors which bind non depolarizing drug without causing
neuromuscular effect
 ANESTHETIC CONSIDERATIONS

Emergence
• Estimation of an adequate dose of narcotic to provide postop analgesia should be
considered.
• If large volume resuscitation has occurred intraop ,the possibility of clinically significant
airway edema considered., use caution before extubating to ensure a patent airway.
• Blood and fluid requirements : eschar – major blood loss – blood must be in OR before
induction.
• Application of bandages soaked in 1:10,000 adrenaline after excision of burned skin is
effective in producing a bloodless surface for placement of skin grafts
 ANESTHETIC CONSIDERATIONS

• Thermal considerations:
• Tempearture monitered throughout the case.
• Warm all fluids
• Humidify gases.
• Warming blankets.
• Head cover.
• Monitoring
• Standard monitors: ECG may require needle electrodes if there is no skin availability to
apply adhesive electrodes.
 ANESTHETIC CONSIDERATIONS

• Positioning
• The burn patient may be uniquely susceptible to laryngeal or upper airway edema in the prone
position,therfore examination of the upper airway before extubation is recommended to avoid
emergent reintubation.
• Postoperative
• Complications
• Hypothermia – use radiant heater or warming blankets.
• Cogulopathy – may occur as the result of massive blood loss and replacement
• Pain management : PCA – fentanyl or morphine
 REFERENCES

• Millers Anesthesia 8th edition

• Morgan Clinical anaesthesiology 6th edition
• Barash 8th edition
THANK YOU