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ANESTHESIA and BURNS
Speaker: DR. Rajesh Choudhuri, PGT
Moderator: Dr. Biswajit Sutradhar, Asst. Prof.
DEPARTMENT OFANAESTHESIOLOGY
AGMC & GBP HOSPITAL,AGARTALA
Introduction
• Burns : are tissue injuries resulting from direct contact with
flames, hot liquids, gases, caustic chemicals; electricity; or
radiation.
• 3rd largest cause of accidental death
50% of adults <45 yr. survive 75% burns.
high risk groups for severe burn injuries:
• The very young
• The very old
• The very careless
Anatomy & Physiology of the Skin
• Largest body organ: 15% of body weight ,It is not a passive organ.
• Protects underlying tissues from injury
• Temperature regulation
• Acts as water tight seal, keeping body fluids in
• Sensory organ
• Two layers: Epidermis and Dermis
• Epidermis
• Outer cells are dead
• Act as protection and tight seal
• only the epidermis is capable of true regeneration
Types of Burns
•Thermal (heat) burns
•Chemical burns
•Electrical burns
•Inhalational burns
Thermal (heat) burns classification
• Superficial Burn/1st Degree Burn:
• Erythema ,pain at burn site , involves only epidermis,absence
of blisters , heals within 3 to 6 days
• Example – sunburn
• Partial-Thickness Burn/ 2nd Degree Burn:
• Entire epidermal layer , part of underlying dermis
• Mottled and red, painful, swelling and blisters
• Healing in 10 to 21 days
• Not enough to interfere with regeneration of the
epithelium
Thermal (heat) burns classification
• Full-Thickness Burn/ 3rd Degree Burn:
• Destruction of all epidermal and dermal elements
• Burn into subcutaneous fat or deeper
• Skin is charred and leathery (woody)
• Generally not painful (nerve endings are dead)
• Fourth-degree
• Full-thickness,Extending into muscle,
tendons or bones.
• Black and dry,No pain.
• Eschar formation.
Estimation of Burned Area
Electrical Burns
1.Burns are caused by heat generated by electrical energy as it passes through the
body.
2. Electrical burns result in internal tissue damage.
3. Cutaneous burns cause muscle and soft tissue damage that may be extensive,
particularly in high-voltage electric injuries .
4. The voltage, type of current, contact site, and duration of contact are important to
identify.
5. Alternating current is more dangerous than direct current because it is associated
with cardiopulmonary arrest, ventricular fibrillation, tetenic muscle contrations,
and long bone or vertebral fractures.
6. Subcutaneous (Fourth Degree).
Chemical burn
• Most acids produce a coagulation necrosis by denaturing proteins,
forming eschar that limits the penetration of the acid.
• Bases typically produce a more severe injury known as liquefaction
necrosis.
• Damage continues until the substance is removed or neutralized
Inhalational injury
• Its results from the airway inflammatory response to inhalation of the
products of incomplete combustion and is the leading cause of death (up to
77%) in burn patients .
•Effects of of Acute Smoke Inhalation Injury
Impairment of mucociliary function  infection
Mucus hypersecretion
Tissue inflammation with tracheobronchiolitis, bronchitis, laryngitis,
pneumonitis
Epithelial sloughing
Biochemical alteration with surfactant inactivation
Increases vascular permeability and lung edema
Bronchiconstriction
Initially large airway obstruction  late small and large airways
Carbon Monoxide (CO) poising
Signs of Carboxyhaemoglobinaemia
COHb levels Symptoms
0-10% Minimal (normal level in heavy smokers)
10-20% Nausea, headache
20-30% Drowsiness, lethargy
30-40% Confusion, agitation
40 -50% Coma, respiratory depression
>50% Death
Carbon Monoxide (CO) poising treatment
• Administration of 100% oxygen will shorten the half-life of COHb
from 4 h in room air to less than 1 h
• Mild poisoning (COHb<20%) --- 100% non-rebreathing mask until
level falls <5%
• Moderate poisoning (COHb 20 – 40%) without cardiac or
neurologic dysfunction --- monitoring of acid-base status and 100%
oxygen until level falls <5%
• Severe poisoning (COHb>40%) or with cardiac or neurologic
symptoms--- hyperbaric oxygen therapy
• Admission is required for all with level >25% or with cardiac and
neurologic symptoms.
Initial management
• History: time, extent and mechanism of burn , age and weight of the patient, brief medical history.
• Airway assessment: may require ET intubation and mechanical ventilation in case of acute
inhalational injury, upper airway oedema, chest wall restriction, CO poisoning.
• Breathing: administer 100% humidified oxygen via a non-re breathing mask.
• Circulation: establish two large bore IV cannula and commence fluid resuscitation.
• Assess neurological status.
• Analgesia: IV opiods .
• Formally assess burn area and re-evaluate fluid requirement.
• Monitoring: vital signs, urine output.
• Investigations: ABG, COHb, U & E, FBC, Clotting screen, cross-match, cross-match blood, ECG,
CXR.
• Secondary survey to exclude other injuries.
Fluid regimen for burn patients
• Proceed with regimen if > 15% burns in adults or > 10% in children.
• PARKLAND FORMULA:
Requirement in first 24 hours ( ml)= BW ×% Burn ×4 ml.
Fluid given as R/L alone, 50 % within first 8 hr, 25% in second 8 hr, 25 % in last 8 hr.
Colloids administered only after first 24 hr, 5 % dextrose is required at 1-2
ml/kg/hr after first 24 hr.
• Brooke formula:
1.5 mL of R/L per kg per % TBSA burn per 24 hours plus 0.5 mL of colloid per kg per
% TBSA burn per 24 hours plus 2,000 mL of 5% dextrose in water 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.
• Daily maintenance fluid after 24th hour: “ 4-2-1” rule.
Special considerations during resuscitation
• Central venous access is usually required with burns > 20% BSA.
• A high index of suspicion for airway burns should be maintained in all cases and
prophylactic tracheal intubation is often justified, particularly in children and if
inter hospital transfer is required.
• Indication for ICU admission include: potential airway problems, burns involving
> 20 % BSA and the presence of other injuries.
• Volume replacement titrated to achieve a urine output of 0.5-1 ml/kg/hr in aduits
and 1.0-1.5 ml/ kg/hr in children.
• bladder pressure monitoring ( to detect intra abdominal hypertension ) for all
patients with major burns of > 30% BSA.
Challenges in Burn anaesthetic management
Compromised airway.
Pulmonary insufficiency.
Altered mental status.
Associated injuries.
Difficult vascular access.
Rapid blood loss.
Impaired tissue perfusion.
Positioning.
• Edema.
• Dysarhythmias.
• Impaired temperature regulation.
• Altered drug responses.
• Renal insufficiency.
• Immunosuppression.
• Infection/ sepsis.
Anesthetic Management
• Preop Meds
Provide adequate analgesia
Fluids
• Establish Adequate Vascular Access
Consider Invasive Monitoring
• Airway Management
Consider Alternatives to Direct
Laryngoscopy
Awake FOB
RSI
• Ventilation
Increased minute ventilation
increased metabolic rate
• Fluids & Blood
Anticipate rapid, large blood loss
Parkland Formula
• Temperature Regulation
Increase ambient temperature
Warm IV fluids
• Anesthetic Drugs
Include opioids.
Consider effects of increased
circulating catecholamines.
Induction with Propofol/ Thiopental (if
adequate volume resuscitation)
Etomidate/ ketamine( if volume depleted)
• Muscle Relaxants
Avoid Succinylcholine after
24th postburn and for at least 1 year.
Anticipate resistance to
nondepolarizing muscle relaxants
• Postoperative
Anticipate increased analgesic
requirements
Burn and anaesthesia

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Burn and anaesthesia

  • 1. ANESTHESIA and BURNS Speaker: DR. Rajesh Choudhuri, PGT Moderator: Dr. Biswajit Sutradhar, Asst. Prof. DEPARTMENT OFANAESTHESIOLOGY AGMC & GBP HOSPITAL,AGARTALA
  • 2. Introduction • Burns : are tissue injuries resulting from direct contact with flames, hot liquids, gases, caustic chemicals; electricity; or radiation. • 3rd largest cause of accidental death 50% of adults <45 yr. survive 75% burns. high risk groups for severe burn injuries: • The very young • The very old • The very careless
  • 3. Anatomy & Physiology of the Skin • Largest body organ: 15% of body weight ,It is not a passive organ. • Protects underlying tissues from injury • Temperature regulation • Acts as water tight seal, keeping body fluids in • Sensory organ • Two layers: Epidermis and Dermis • Epidermis • Outer cells are dead • Act as protection and tight seal • only the epidermis is capable of true regeneration
  • 4. Types of Burns •Thermal (heat) burns •Chemical burns •Electrical burns •Inhalational burns
  • 5. Thermal (heat) burns classification • Superficial Burn/1st Degree Burn: • Erythema ,pain at burn site , involves only epidermis,absence of blisters , heals within 3 to 6 days • Example – sunburn • Partial-Thickness Burn/ 2nd Degree Burn: • Entire epidermal layer , part of underlying dermis • Mottled and red, painful, swelling and blisters • Healing in 10 to 21 days • Not enough to interfere with regeneration of the epithelium
  • 6. Thermal (heat) burns classification • Full-Thickness Burn/ 3rd Degree Burn: • Destruction of all epidermal and dermal elements • Burn into subcutaneous fat or deeper • Skin is charred and leathery (woody) • Generally not painful (nerve endings are dead) • Fourth-degree • Full-thickness,Extending into muscle, tendons or bones. • Black and dry,No pain. • Eschar formation.
  • 8. Electrical Burns 1.Burns are caused by heat generated by electrical energy as it passes through the body. 2. Electrical burns result in internal tissue damage. 3. Cutaneous burns cause muscle and soft tissue damage that may be extensive, particularly in high-voltage electric injuries . 4. The voltage, type of current, contact site, and duration of contact are important to identify. 5. Alternating current is more dangerous than direct current because it is associated with cardiopulmonary arrest, ventricular fibrillation, tetenic muscle contrations, and long bone or vertebral fractures. 6. Subcutaneous (Fourth Degree).
  • 9. Chemical burn • Most acids produce a coagulation necrosis by denaturing proteins, forming eschar that limits the penetration of the acid. • Bases typically produce a more severe injury known as liquefaction necrosis. • Damage continues until the substance is removed or neutralized
  • 10. Inhalational injury • Its results from the airway inflammatory response to inhalation of the products of incomplete combustion and is the leading cause of death (up to 77%) in burn patients . •Effects of of Acute Smoke Inhalation Injury Impairment of mucociliary function  infection Mucus hypersecretion Tissue inflammation with tracheobronchiolitis, bronchitis, laryngitis, pneumonitis Epithelial sloughing Biochemical alteration with surfactant inactivation Increases vascular permeability and lung edema Bronchiconstriction Initially large airway obstruction  late small and large airways Carbon Monoxide (CO) poising
  • 11. Signs of Carboxyhaemoglobinaemia COHb levels Symptoms 0-10% Minimal (normal level in heavy smokers) 10-20% Nausea, headache 20-30% Drowsiness, lethargy 30-40% Confusion, agitation 40 -50% Coma, respiratory depression >50% Death
  • 12. Carbon Monoxide (CO) poising treatment • Administration of 100% oxygen will shorten the half-life of COHb from 4 h in room air to less than 1 h • Mild poisoning (COHb<20%) --- 100% non-rebreathing mask until level falls <5% • Moderate poisoning (COHb 20 – 40%) without cardiac or neurologic dysfunction --- monitoring of acid-base status and 100% oxygen until level falls <5% • Severe poisoning (COHb>40%) or with cardiac or neurologic symptoms--- hyperbaric oxygen therapy • Admission is required for all with level >25% or with cardiac and neurologic symptoms.
  • 13. Initial management • History: time, extent and mechanism of burn , age and weight of the patient, brief medical history. • Airway assessment: may require ET intubation and mechanical ventilation in case of acute inhalational injury, upper airway oedema, chest wall restriction, CO poisoning. • Breathing: administer 100% humidified oxygen via a non-re breathing mask. • Circulation: establish two large bore IV cannula and commence fluid resuscitation. • Assess neurological status. • Analgesia: IV opiods . • Formally assess burn area and re-evaluate fluid requirement. • Monitoring: vital signs, urine output. • Investigations: ABG, COHb, U & E, FBC, Clotting screen, cross-match, cross-match blood, ECG, CXR. • Secondary survey to exclude other injuries.
  • 14. Fluid regimen for burn patients • Proceed with regimen if > 15% burns in adults or > 10% in children. • PARKLAND FORMULA: Requirement in first 24 hours ( ml)= BW ×% Burn ×4 ml. Fluid given as R/L alone, 50 % within first 8 hr, 25% in second 8 hr, 25 % in last 8 hr. Colloids administered only after first 24 hr, 5 % dextrose is required at 1-2 ml/kg/hr after first 24 hr. • Brooke formula: 1.5 mL of R/L per kg per % TBSA burn per 24 hours plus 0.5 mL of colloid per kg per % TBSA burn per 24 hours plus 2,000 mL of 5% dextrose in water 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. • Daily maintenance fluid after 24th hour: “ 4-2-1” rule.
  • 15. Special considerations during resuscitation • Central venous access is usually required with burns > 20% BSA. • A high index of suspicion for airway burns should be maintained in all cases and prophylactic tracheal intubation is often justified, particularly in children and if inter hospital transfer is required. • Indication for ICU admission include: potential airway problems, burns involving > 20 % BSA and the presence of other injuries. • Volume replacement titrated to achieve a urine output of 0.5-1 ml/kg/hr in aduits and 1.0-1.5 ml/ kg/hr in children. • bladder pressure monitoring ( to detect intra abdominal hypertension ) for all patients with major burns of > 30% BSA.
  • 16.
  • 17. Challenges in Burn anaesthetic management Compromised airway. Pulmonary insufficiency. Altered mental status. Associated injuries. Difficult vascular access. Rapid blood loss. Impaired tissue perfusion. Positioning. • Edema. • Dysarhythmias. • Impaired temperature regulation. • Altered drug responses. • Renal insufficiency. • Immunosuppression. • Infection/ sepsis.
  • 18. Anesthetic Management • Preop Meds Provide adequate analgesia Fluids • Establish Adequate Vascular Access Consider Invasive Monitoring • Airway Management Consider Alternatives to Direct Laryngoscopy Awake FOB RSI • Ventilation Increased minute ventilation increased metabolic rate • Fluids & Blood Anticipate rapid, large blood loss Parkland Formula • Temperature Regulation Increase ambient temperature Warm IV fluids • Anesthetic Drugs Include opioids. Consider effects of increased circulating catecholamines. Induction with Propofol/ Thiopental (if adequate volume resuscitation) Etomidate/ ketamine( if volume depleted) • Muscle Relaxants Avoid Succinylcholine after 24th postburn and for at least 1 year. Anticipate resistance to nondepolarizing muscle relaxants • Postoperative Anticipate increased analgesic requirements