Cardiac Output, Venous Return, and Their Regulation
Anaesthetic management in a patient of burns injury
1. J J M MEDICAL COLLEGE
DEPARTMENT OF ANAESTHESIOLOGY
A PRESENTATION BY
DR. KSHAMA BALAKRISHNA
POST GRADUATE
MODERATOR
DR. R. B. RAVISHANKAR MD, DA
PROFESSOR
ANAESTHETIC MANAGEMENT OF A PATIENT
OF BURNS
12.07.2019
2. INTRODUCTION
Definition:
A burn is an injury to the skin or other organic tissue
primarily caused by heat or due to radiation, radioactivity,
electricity, friction or contact with chemicals.
According to the WHO, an estimated of 1,80,000 deaths every
year are caused by burns.
Non- fatal burn injuries are a leading cause of loss of DALY
(disability adjusted life years).
A vast majority of these occur in low- income and middle- income
countries.
3. CLASSIFICATION:
Thermal burns- dry and wet
Electrical burns
1. Low tension (<1000V)- cellphone and charger related injury
2. High tension (>1000V)- flame, flash, current
3. Lightening (>2000V)– direct strike, side flash
Chemical burns- acid burns, alkali burns
Radiation burns- a, b, g, x-rays
4. PATHOPHYSIOLOGY
Inflammation and circulatory changes
Injury to airway and lungs
Immune system response
Gastrointestinal tract
Renal system
Haematological system
5. INFLAMMATORY AND CIRCULATORY
CHANGES
Massive release of inflammatory mediators increased capillary
permeability loss of water, electrolytes, proteins from
intravascular compartment severe hemoconcentration
Protein leakage hypoproteinemia increased oncotic pressure
in interstitial space tissue edema
Stimulation of pain fibres and alteration of proteins by heat
release of neuropeptides and activation of complement
Depressed cell membrane potential impaired function of Na+-
K+ ATPase Na+ and water accumulation cell swelling
7. EBB PHASE
(first 24hrs)
• Hypotension
• Low CO
• Metabolic acidosis
• Hypoventilation
• Hyperglycaemia
• Low O2
consumption
• Impaired
thermoregulation
FLOW PHASE
(catabolic)
Hypermetabolic
phase
• Increased CO
• Increased HR
• Better O2
consumption
• Supranormal
increases of
temperature
• Days to weeks
FLOW PHASE
(anabolic)
Healing and
rehabilitation
• Anabolism
• Normal function
restores
• Weeks to months
PATHOPHYSIOLOGY
8. Warning signs
Burns around neck and face
H/O being trapped in a burning room
Change in voice
Stridor
Soot in sputum
Respiratory Distress
If airway oedema suspected, immediate intubation must be
carried out. Mucosal oedema can ensue rapidly, particularly
with fluid resuscitation.
INJURY TO AIRWAY AND LUNG
9. ABOVE LARYNX
- Direct injury to nose,
mouth, tongue, palate,
larynx
- Saturated vapours
more injurious
- Upper airway oedema
peak at 24hrs, subside
<1st week
BELOW LARYNX
- Better heat exchange
mechanisms
- Steam can cause loss
of respiratory
epithelium and form
casts
10. INJURY TO AIRWAY AND LUNGS
Incomplete products of
combustion
Bronchospasm, mucosal
oedema ulceration
Impaired cilia,
mucosal damage
Inflammatory response
NH3, NO2, SO2,
Chlorine, Acrolein
Necrotic debris,
proteinaceous fluid,
cast formation
Pneumonitis- Alveolar injury,
impaired surfactant production
Atelectasis, V/Q
mismatch
Pneumonia,
sepsis, death
11. METABOLIC POISONING
CO POISONING
Manifestations - nausea and vomiting, headache, hypotension,
convulsions, coma
0.1% CO- 50% carboxyHb
240 times higher affinity to Hb, shift to left of ODC
Inhibits Cytochrome oxidase- tissue hypoxia, metabolic acidosis
Pulse oximetry - overestimate the true oxygen saturation. ABG
analysis recommended.
Treatment- 100% oxygen; if HbCO levels >25–30% should be
ventilated.
12. CYANIDE POISONING
Binds to Fe3+ in Cytochrome A3
Lactic acidosis persists despite adequate fluid resuscitation
MECHANICAL BLOCK OF RIB MOVEMENT
large full-thickness burn across the chest
Thick burned skin over the chest
Requires excision/ escharotomy
MECHANICAL VENTILATION
Lung protective ventilation (6mL/kg) and low plateau pressures
(<30cm of water)
Routine ventilator- associated pneumonia prevention strategies
should be implemented.
Mucolytics like N-acetylcysteine - airway clearance
13. IMMUNE SYSTEM RESPONSE
Global suppression of immune system, decreased opsonisation
Loss of skin (mechanical barrier )
Suppression of cell mediated response- susceptibility to
bacterial and fungal infections
Need for invasive lines- IV cannula, urinary catheter,
central lines, tracheostomies - portals of infection
Bacterial-colonized eschar overlying a wound full of
proteinaceous fluid- risk for infection
14. ANAEMIA
Loss from
wound site
RBC
survival
Reduced
production
Haemolysis
Hemoconcentration during 1st 48hrs
HCT- poor guide to assess need for transfusion
Platelet count and coagulation derangements- consumptive
coagulopathy with activation of thrombotic and fibrinolytic
system
HEMATOLOGY
15. RENAL SYSTEM
RAAS activation- Na+ and water retention with exaggerated
loss of K+, Mg2+, Ca2+
Drugs, myoglobin, sepsis related nephrotoxicity- kidney injury
Extensive tissue necrosis, haemolysis- hyperkalemia
Hypovolemia
Reduced
CO
Decreased
RBF
17. THERMOREGULATION
Loss of vasoactivity, pilorection, sweating and insulation,
which are chief thermoregulatory functions of the skin.
Daily loss from evaporation from the burn surface
accounts for 4000 mL/m2 in children and 2500 mL/m2 in
adults.
Strategies to prevent hypothermia- warmed room
(ambient temperature 28–32.8 C), warmed inspired air,
warming blankets, and warmed fluids
18. ATTENDING TO A PATIENT OF BURNS
PRE- HOSPITAL CARE
Rescuer safety
STOP, DROP and ROLL
CAB, rapid survey of other
injuries
Cool the wound
Oxygenation
Elevation
HOSPITAL CARE
A- Airway control
B- Breathing and ventilation
C- Circulation
D- Disability including assessment
of neurological status
E- Exposure in a controlled
environment
F- Fluid resuscitation
19. ASSESSMENT OF THE BURN WOUNDS
1. Measurement of the wound:
Wallace rule of nines
Total BSA is divided into multiples of 9
BACK FRONT
Head and neck 9%
Upper extremities 9% each
Chest ( anterior and
posterior)
9% each
Abdomen 9%
Lower back 9%
Lower extremities 18% each
Perineum 1%
20. Lund and Browder chart- TBSA according to sections of
anatomy and proportional to age of the patient
ASSESSMENT OF THE BURNS WOUND
Gluteal areas
2.5% each
21. Palmar surface
Patient’s palm = 1% of patient’s TBSA
Quick method, if burns upto 15% of TBSA
II. Depth of the wound:
ASSESSMENT OF THE BURNS WOUND
22. Superficial Superficial partial
thickness
Deep partial
thickness
Full thickness
Layers affected Epidermis Epidermis,
papillary dermis
Epidermis, upto
reticular dermis
Epidermis, dermis,
deeper structures
Adnexal skin
structures
Preserved Preserved Damaged Damaged
Appearance Erythemat
ous
Pink and moist,
mottled,
blistering+
Pale and dry Dark, leathery
Capillary return Blanching
+
Blanching+ Non- blanching, fixed
capillary staining
after 48hrs
Non- blanching+,
thrombosed vessels
under skin
Sensation Painful Painful No pain, only
pressure
Painless
Epithelialization Rapid Rapid Slow Slow and minimal
Healing <7days, no
scarring
10-14 days, no
scarring
Weeks to months,
hypertrophic scar
Severe scarring and
contracture
Treatment Non-
surgical
Non- surgical Excision and grafting Excision and grafting
25. WHAT IS A MAJOR BURN?
Full thickness burn injuries > 10% TBSA
Partial thickness burn injuries >20% TBSA in extremes of age,
>25% TBSA in adults
Burns involving- face, hands, feet, genitalia, perineum, major
joints
Inhalational injuries
Chemical burn injuries
Electrical burn injuries
Burn injuries in a patient with co-existing medical disease
Burns associated with trauma
26. ROLE OF AN ANAESTHESIOLOGIST
Initial resuscitation- securing airway, gaining vascular access
Intensive care management
“Perioperative- care consultant”
Surgical management of a burns patient
1. Excision of damaged tissues, wound debridement
2. Wound dressings
3. Reconstructive surgical procedures
Other surgical procedures in a case of post burns contracture
27. Initial Management of
Inhalational injury
Propped up position- 30-90
degrees
High flow humidified oxygen
Bronchodilators and
physiotherapy
Fiberoptic bronchoscopy in
intubated cases - better
diagnosis and enables
pulmonary toileting.
AIRWAY MANAGEMENT
28. AIRWAY MANAGEMENT
Early intubation considered if
Presence of stridor
GCS <8
Hypoxia or hypercapnia
Full-thickness neck burns
Deep facial burns
Oropharyngeal edema
TBSA >40% (massive edema likely to follow during fluid
resuscitation)
Use of direct laryngoscopes, LMAs, Bullard laryngoscopes
Choice of intubation technique depends on expertise of the operator
29. Succinylcholine can be safely used <24hrs , after which risk of release
of potassium from extrajunctional A-ch receptors persists upto a year.
Direct surgical approach to airway
Needle cricothyroidotomy
Surgical cricothyroidotomy
Tracheostomy
High incidence of complications- hence, last resort
AIRWAY MANAGEMENT
30. VASCULAR ACCESS
Ideally, 2 large bore IV lines to be secured away from burned tissue
If other sites not available, securing in burned skin is justified
provided eschar is still sterile ( early post burn)
Priority- unburned tissue>> burned tissue>> central venous access
For rapid initiation of fluid resuscitation – large bore IV access
preferred over central venous catheter
Preferred sites- Subclavian vein > IJV > femoral vein
Groins are usually spared so femoral venous cannulation is often
possible
31. FLUID RESUSCITATION
Principle- Intravascular volume must be maintained following a burn,
in order to provide sufficient circulation to perfuse not only the vital
organs, but also the peripheral tissues and especially the damaged
skin.
Recommendation : In adults, if burns >15% TBSA or 10% with
smoke inhalation. In children, burns >10% TBSA
Oral resuscitation- oral fluids with added salt, to avoid
hyponatremia and water intoxication.
Parkland formula- fluid resuscitation for initial 24hrs
Percentage of burned surface area x weight (kg) x 4
half transfused over 1st 8hrs, remaining over next 16hrs
32. A 32-yr-old man weighing 80 kg with a 30% flame burn was
admitted at 23:00 h. His burn occurred at 22:00 h. He has already
received 1000 ml of crystalloid from the emergency services.
Total fluid requirement for first 24 h= 4 ml(30% TBSA)(80 kg)=
9600 ml
Will receive 4800 ml during 0–8 h and 4800 ml during 8–24 h
4800 (for first 8 h)–1000 (fluid already received)= 3800 ml
Burn occurred at 22:00 h, so 8 h point is 06:00 h. Patient arrived
at 23:00 h, so need 3800 ml over next 7 h.
3800/7= 543 ml/hr from 23:00 to 06:00 h
4800/16= 300 ml/hr from 06:00 to 22:00 h the next day.
CASE SCENARIO
33. Crystalloid resuscitation, fluid of choice- Ringer’s lactate
In children, maintenance fluids with Holliday Segar formula
(100ml/kg x 24hrs for 1st 10kg) + (50ml/kg x 24hrs for next 10kg)+ (20ml/kg x
24hrs for each kg above 20 kg body weight)
Hypertonic saline- produces hyperosmolarity and hypernatremia which
reduces fluid shift from intracellular to extracellular space.
Colloid resuscitation-recommended after 12hrs of burns, commonly used-
Human albumin solution
Muir and Barclay formula
0.5 x percentage of burned surface area x weight
Periods of 4/4/4, 6/6 and 12 hours respectively, one portion to be given in
each period
4hr 4hr 4hr 6hr 6hr 12hr
0 4 8 12 18 24 36
34. MONITORING OF RESUSCITATION
Urine output: Adult- 0.5-1ml/kg/hr; Child- 1-2ml/kg/hr
If not, then infusion rate increased by 50%
Inadequate U/O with signs of hypoperfusion, give a bolus of
10ml/kg
If U/O > 2ml/kg/hr – over-resuscitation, decrease infusion rate
However, in a case of electrical burns with massive rhabdomyosis,
U/O has to be maintained at 1.5-2ml/kg/hr as myoglobinuria can
cause ARF.
ABG analysis
CVP monitoring and TEE in patients with cardiac dysfunction
35. ANAESTHESIA FOR A PATIENT OF BURNS
Recent approach, early excision and wound
coverage
Risk reduced- wound infection and sepsis
Risk involved- physiological insult of surgery to a
patient who may well be deteriorating rapidly
from their initial injuries
The most important and difficult clinical
decisions are often made by the team at this
stage.
36. ESHCHAROTOMY AND FASCIOTOMY
A circumferential full thickness burn acts like a
tourniquet as the limb swells limb ischemia
Early signs- numbness and tingling
4 Ps- Pain, pallor, paraesthesia, pulselessness
Requires decompression of compartment making
radial incisions and blunt dissection with a
haemostat
4-14days post- burn after resuscitation done or
<5days before bacterial colonization under eschar
37. Incisions are made
at the anterior
axillary line from the
level of the 2nd rib to
the level of the 12th
rib. They are joined
transversely so the
chest wall can
expand
38.
39. CHALLENGES IN ANAESTHESIA
Airway maintenance, choice of anaesthesia, hemodynamic
stability, thermoregulation, pharmacological agents
Premedication: Antisialogogue- Inj. Glycopyrrolate 0.2mg IV,
narcotic analgesic Inj. Morphine 0.1mg/kg IV or Inj. Fentanyl
1mcg/kg IV, Inj. Midazolam 0.05mg/kg IV
Aspiration prophylaxis: H2 receptor antagonist, Prokinetics
Monitoring: Temp, SpO2, ECG (needle probes), ETCO2, CVP, U/O
Adequate preoxygenation- high metabolic rate, tachycardia,
increased oxygen demand
40. Induction agents:
Inhalational induction preferred to maintain airway
Thiopentone/ Propofol better avoided or use at titrated doses
to avoid hypotension
Ketamine- sole anaesthetic 1-2mg/kg, with oxygen (30-50%)
with nitrous oxide
During ongoing resuscitation, possible sepsis, potential full
stomach- GA with ETT intubation and controlled ventilation
with post-operative elective ventilation. Ketamine or Etomidate
preferred in such cases
Airway- ETT, LMA. Fiberoptic assisted awake intubation
Inj. Ketamine infusion at 4mg/kg/hr can be used for
maintenance of anaesthesia
41. Use of Relaxants:
Succinylcholine- significant transient increase in serum K+
levels (as high as 13 mEq/L), resulting in V Fib and cardiac
arrest.
Hyperkalemic response begins 24- 48hrs post-burn and can
persist as long as 1- 2yrs, irrespective of degree and size of
burn injury.
Gronert and Theye postulated that the abrupt release of K+ is
from the hypersensitive muscle membranes. Stimulation of
extrajunctional A-ch receptors on the muscle membranes of
burned patients mediate potentially lethal efflux of K+.
42. What are extra-junctional
receptors ?
They differ from junctional receptors
Upregulation due to deficient stimulation of
the skeletal muscle
Shorter half-life (<24 hours)
Highly sensitive to A-Ch and suxamethonium
Open for longer duration but ion
conductance is smaller
Concentrated around the end plates, but can
also be found anywhere on the
(postjunctional) muscle membrane
Similar pentameric structure, but have the
foetal d subunit increased of the normal
adult e subunit
Foetal
(postjunctional)
Mature
(junctional)
43. POST BURNS CONTRACTURE NECK
PROBLEMS FACED
Grossly restricted neck movements
Patients are likely to be malnourished, anaemic and
hypoproteinemic
Restricted mouth opening and narrowed nasal passages.
Difficult laryngoscopy and endotracheal intubation
Compromised airway
Poor oral hygiene in patients
44. Mild- Scar apparent during neck extension
with the loss of the cervico-mental angle; neck
extension- 95 to 110
Moderate- Scar apparent in resting position,
which hinders neck extension; neck
extension- 85 to 95°
Severe- Neck in flexed position and limiting
any neck movement; neck extension is <85°
CLASSIFICATION- Based On Severity
45. BASED ON SCAR
Linear scar- scar tissue is a fibrous tissue line.
Band scar- scar width forms <50% of the anterior surface of the
neck.
Broad scar- scar width forms >50% of the anterior surface of the
neck.
46. RELEVANT EXAMINATION
1. Contracture- location, duration,
consistency, extent
2. Mouth opening, mandibular movement
3. Patency of nasal passage
4. Difficulty in breathing
5. Can he blow air through mouth and
nose?
PREPARATION OF THE PATIENT
1. Improve oral hygiene
2. Correct anaemia and hypoproteinemia
3. H2 receptor antagonists, prokinetics
4. Anti emetics
5. Aggressive treatment of upper and
lower respiratory tract infections
PRE-OP WORKUP
1. CBC, Blood grouping
2. RFT, Sugars, S. electrolytes
3. Chest X-Ray, ECG
4. Serology
47. ANAESTHETIC CONSIDERATIONS
Goal - total control of the airway
Preserve spontaneous respiration till trachea is intubated
Consider using nasopharyngeal airway, oro-pharyngeal
airway, and laryngeal mask airway where ever feasible
Consider superficial cervical plexus block if contracture is
situated in between sternomastoids
I.M Ketamine is a more useful option than I.V. Ketamine
in a dose of 2-5 mg/kg
48. AIRWAY MANAGEMENT OPTIONS
TIVA - maintenance with combination of IV
Ketamine 0.4mg/kg, Propofol 1mg/kg
Blind nasal intubation
LMA insertion ( difficult in microstomia)
Awake intubation with topical anaesthesia/ regional
anaesthesia
Awake Fiberoptic intubation ( patency of external nares-
necessary)
Patient can be maintained with volatile anaesthetic and
preferably muscle relaxants are avoided
49. AWAKE ENDOTRACHEAL INTUBATION
1. Topical anaesthesia
Lidocaine- 4% solution and 10% spray
higher doses can be used than the recommended 2 mg/kg (lesser
systemic absorption)
Along with vasoconstrictor agents such as xylometazoline and
phenylephrine
Application techniques
i. Spray from container
ii. Local anaesthetic soaked in ribbon gauze
iii.McKenzie technique
iv.Inhalation of nebulized lidocaine
v. Spray as you go” via epidural catheter
50. AWAKE ENDOTRACHEAL INTUBATION
2. Regional anaesthesia techniques
i. Glossopharyngeal Nerve Block
ii. Superior Laryngeal Nerve Block
iii. Recurrent Laryngeal Nerve Block
51. TUMESCENT TECHNIQUE
Solution- Lignocaine, adrenaline, hyaluronidase and saline/water.
0.5% Lignocaine solution with 1 in 1, 00,000 adrenaline
{25 ml 2 % lignocaine + hyalase 1 to 2 ml + 1ml of 1 in 1, 00,000
adrenaline + distilled water to a total volume of 100ml }
Advantage:
1. Release of contracture without much blood loss.
2. Hydrostatic cleavage of operative field and better dissection.
3. Poor vascularity of scar tissue and use of adrenaline- decreased
risk of toxicity
52. Substance Initial
Concentration
Quantity Final
Concentration
Lidocaine 2% 4mL 0.2%
Adrenaline 1:1,000 44 drops or 0.2mL 1:200,000
NaHCO3 8.4% 4 mL 0.84%
Saline 0.9% 40.0 mL 0.71%
TUMESCENT TECHNIQUE
Rule of four for anaesthetic solution
The concentrations of each component is given by:
Final concentration of the substance (FCS) = concentration of the
substance (CS) x volume of the substance (VS) / volume of solution
(VSOL)
Lidocaine 2% 10.0 mL
Adrenaline 1:1,000 0.4 mL
NaHCO3 8.4% 4.0 mL
Saline 40.0 mL
53. SKIN BANK
Skin banks are facilities that stockpile skin and its derivatives
and provide them on request
This skin bank is essential for the treatment of seriously
burned patients because it provides the Burns Centre with
homologous skin
Both autologous and homologous skin are cool-treated and to
be used within a period of not more than 3 weeks.
In deep and extensive burns, there is often a lack of suitable
autologous donor areas. In such cases, the best possible
coverage continues to be homologous skin, despite its
limitations (immunogenicity and the risk of the transmission
of infectious disease).
54. CONCLUSION
Anaesthesia providers play a key role in overcoming the
hurdles in the management of such cases by securing airway
and maintenance of respiration, gaining vascular access for fluid
resuscitation and providing anaesthesia/ analgesia in early
surgical procedures and wound dressings. Hence, it is
important to understand the physiological and pathological
changes related to it.
Anaesthesiologists must also be familiar with the various
techniques to deal with patients with post burns contracture
neck who may come for reconstructive surgeries or other
surgical procedures.
55. REFERENCES
Bailey and Love’s Short Practice of Surgery- 27th edition
Wylie Churchill-Davidson’s a Practice of Anaesthesia- 7th edition
Paul G. Barash Textbook of Clinical Anaesthesiology- 8th edition
Tintinalli’s Emergency Medicine- 9th edition
Stoelting’s Anaesthesia and Coexisting Diseases- 2nd South Asian
Edition
http://dx.doi.org/10.1016/j.ccc.2016.06.001 criticalcare.theclinics.com
Curr Anesthesiol Rep (2016) 6:16–21
Continuing Education in Anaesthesia, Critical Care & Pain j Volume 12
Number 3 2012
Annals of Burns and Fire Disasters Vol. XVI n. 4 December 2003
RACE- 2016 and 2007
https://anaesthesianews.wordpress.com
Notas del editor
Thermal burns- inflicted by flame, contact with a hot substance or scald burns from steam. Flame burns- high mortality rate
Electrical burns- Main concerns -cardiac arrhythmias and compartment syndromes with concurrent rhabdomyolysis.
Low- voltage injuries -small, localised wound, caused by domestic appliances. Main danger- alternating current can cause tetany in muscles; interfere with normal cardiac pacing.
High-tension lines arc over the patient and cause flash burn, cause heating of surrounding air and cause explosion- flame burn. Accompanied by entry and exit wounds, damage to underlying subcutaneous tissue and muscles causing compartment syndrome and myoglobinuria.
Chemical- acid burns- coagulation necrosis and eschar formation, alkali liquefactive necrosis with continuous penetration into deeper tissues. Formic acid- hemolysis, Hburia, hydrofluoric acid- hypocalcemia
Radiation injury- through skin penetration, ingestion or inhalation. Signs of major radiation injuries acute desquamation of skin. Non- lethal radiation has number of other side effects related to gut mucosa and immune system dysfunction.
alpha- min penetration, beta- high energy, high penetration, gamma high penetration, extensive internal damage
The damage caused by burn injuries mostly affects the skin and subcutaneous tissues. However, it can also damage the airway and lungs with life- threatening complications.
Severe burn is a systemic disease that stimulates the realease of inflammatory mediators into the circulation- like interleulins, TNF- locally and into the circulation.
Stimulation of pain fibres and alteration of proteins by heat causes a release of neuropeptides and activation of complement. The activation of Hageman factor initiates a number of protease-driven cascades, altering the arachidonic acid, thrombin and kallikrein pathways. Various inflammatory mediators include oxygen radicals, histamine, prostaglandin, bradykinin, nitric oxide, serotonin, substance P and complement.
At cellular level, complement activates degranulation of mast cells and coats the proteins altered by burn. This in turn attracts neutrophils, which also degranulate with an immense amount of release of free radicals and proteases. As a result of which, there is further damage to the cell.
Although many factors may influence prognosis, the severity of the burn, the presence of inhalation injury, associated injuries, the patient’s age, comorbid conditions, and acute organ system failure are most important
EBB phase- Initial period of hypofunction
During the first 24 hours of burns, there is release of catecholamines, vasopressin and angiotensin which causes peripheral and splanchnic vasoconstriction and decreased cardiac contractility and further result in organ hypoperfusion. This phase is known as burn shock.
Burn shock is a combination of hypovolemic, cardiogenic and distributive element. Excessive resuscitation at this stage, may result in generalized oedema, further compromising tissue oxygenation. Resuscitation also results in reperfusion injury from free radicals causing cell membrane damage and immune response.
Hypermetabolic hyperdynamic response
peaks in 10-14 days post-injury
Recedes with wound healing or surgical wound grafting
Airway injuries most commonly offer in burs involving the face and neck. Meanwhile, the respiratory system is involved in a scenario where a person is trapped in a burning vehicle or room and is exposed to inhale hot and poisonous gases.
Inhalational injury occurs as a direct thermal injury to the mucosa of the respiratory tract or from chemical tracheobronchitis as a result of inhalation of incomplete products of combustion.
Singeing of nasal hair
Red and oedematous posterior pharynx and larynx
Direct thermal primarily occurs in the upper respiratory tract. This is attributable to the reflex glottis closure and heat dissipation from the tracheobronchial tree. Hot gases can physically burn the nose, mouth, tongue, palate and larynx causing oedema and may lead to complete blockade of the airway if not secured immediately.
Upper airway oedema peaks at 24 hours following injury and usually resolves within the first week.
Heat exchange mechanisms are usually able to safely absorb the heat from hot air. However, steam contains a large amount of latent heat of evaporation which can cause loss of respiratory epithelium forming casts, which can ultimately block the airway.
Below larynx- Clinical signs include dyspnoea, coughing wheezing, and the production of copious secretions. Findings at bronchoscopy include carbonaceous deposits, oedema, bronchial mucosal erythema, haemorrhage, and ulceration. Bronchial lavage with 1.4% bicarbonate solution has been used to neutralize acidic deposits and remove soot contamination.
Inhalation of incomplete products of combustion produce pulmonary inflammatory response similar to that of aspiration pneumonitis.
.Ammonia, NO2, SO2 and chlorine combine with water in the respiratory tract to form strong acids and alkalis.
Acrolein, which is produced by combustion of cotton, wood and synthetic fibres, damage mucosal surface and causes impaired ciliary action. They also directly irritate the mucosa causing bronchospasm, oedema and ulceration.
Necrotic cell debris, particulate matter and proteinaceous fluid accumulate to form casts and cause atelectasis. With evolution of alveolar injury, surfactant production is impaired and leads to ventilation/ perfusion mismatch.
Lung injury develops in 24- 48 hours resulting in delayed hypoxemia. This coincides with period of maximum tissue oedema. The combination of low capillary oxygen tension and reduced tissue oxygen diffusion will enhance tissue hypoxia and subsequent reperfusion may worsen the situation.
CO, a product of incomplete combustion ,fires in enclosed spaces, history of a person being found with altered consciousness at the scene of a fire.
The amount of carboxyhaemoglobin (HbCO) formed depends on inspired CO concentration and duration of exposure. Conc of carboxyHb above 10% are dangerous, 20-30% throbbing headache and. Conc above 60% may lead to coma and death. Hypoxic encephalopathy secondary to CO poisoning is thought to result from reperfusion injury in which products of lipid peroxidation and free radicals increase mortality and morbidity. Pulse oximetry cannot differentiate between HbO2 and HbCO and will overestimate the true oxygen saturation. Arterial blood gas analysis using a co-oximeter is required.
Treatment is with 100% oxygen which will decrease the elimination half-life of CO from 4 h to under 1 h—it is reduced further to under 30 min with hyperbaric O2 at 3 atm.treatment with 100% oxygen for more than 24 hours
Other toxins include hydrogen cyanide, ammonia, hydrofluoric acid and phosgene, which can reach the systemic circulation. Cyanide causes lactic acidosis by interfering with mitochondrial respiration by binding to ferric ion in cytochrome A3.
Other toxins include ammonia, hydrofluoric acid and phosgene, which can reach the systemic circulation.
Cell- mediated response is suppressed in a patient of burns, leaving them highly susceptible to bacterial and fungal infections. There is loss of skin barrier and suppression of immune system following extensive burns injury. Need for invasive lines, for example venous cannulation, urinary catheterisation, central lines, tracheostomies become portals of infection.
Diminished production of macrophages
These changes, together with a non-perfused, bacterially-colonized eschar overlying a wound full of proteinaceous fluid, put the patient in a significant risk for infection
Anaemia in burns patients can be due to loss of erythrocytes from wound site, haemolysis due to thermal injury or due to loss during surgery. Following major burns injury, there is suppression of erythrocyte production and reduced RBC survival (increased fragility).
Although, hemoconcentration may occur in the first 48 hours, this is attributable to fluid shifts and dehydration, hence, haematocrit must not be considered a guide for need for transfusion. Platelet count and coagulation derangements can be due to dilution or due to consumptive coagulopathy with the activation of thrombotic and fibrinolytic system.
Oliguria and antidiuresis develops 1st 12-24hrs
With modest diuresis, as the capillaries seal, plasma volume normalizes and CO improves after prompt resuscitation, coinding with post burn hypermetabolic state and hyperdynamic circulation
Ileus is common in a burns patient, The reduced gut motility and can prevent the absorption of food. hence it requires early decompression of stomach with nasogastric tube. Failure of enteral feeding in a burns patient is a life threatening complication. This can lead to translocation of gut bacteria into the circulation, which is an important source of infection in a burns patient. Septicemia <12hrs
Curling’s ulcer- these are acute gastric and duodenal ulcerations that are seen in patients with extensive burns injuries and sepsis, the aetiology is not clear.
Gut mucosal swelling, gastric stasis and peritoneal oedema can cause abdominal compartment syndrome, henceforth causing splinting of diaphragm and respiratory distress.
These will respond with hemodynamic resuscitation and antacids and H2 receptor blockers for symptomatic treatment.
Following thermal injury, there is
Cool the wound- must be done for a minimum for 10 minutes and is effective even upto 1 hour after sustaining the injury. This provides analgesia and delays microvascular damage.
Elevation- to reduce swelling in the burned limbs, propped up position in a patient with burns to the airway may be life-saving.
The history of a burn injury -valuable information about the nature and extent of the burn, the likelihood of inhalation injury, the depth of burn, and the probability of other injuries.
Obtain an ABG, carboxyhemoglobin
level, and CXR. Monitor vital signs and oxygen saturation
Assessment of the burn injuries must be carried out in a controlled environment, allowing the areas to be exposed and wash off any soot or debris. Care must be taken against hypothermia.
Wallace rule of nines is used to assess the percentage of the body surface area affected by burns. This is used as a rule of thumb to quickly assess total BSA burnt. Though this method overestimates the area burnt, it is a suitable method for measuring medium to large burns.
This chart maps out percentage of TBSA of sections of our anatomy. It takes into account the different proportional BSA in children according to age.
It is not an accurate method for moderate burns. If burns more than 85%, then it can be used to measure unburnt areas.
Burn wounds are described as having three zones: the zone of coagulation, in which tissue is irreversibly destroyed with thrombosis of blood vessels; the zone of stasis, in which there is stagnation of the
Microcirculation, can become progressively more hypoxemic and ischemic if resuscitation is not adequate; and the zone of hyperemia, in which there is increased blood flow, there is minimal damage to the cells and spontaneous recovery is likely.
Propped up position provided no spine injury
An assessment must be made as to whether the airway is compromised or is at risk of compromise.
Airway can be supported with simple techniques or use of basic airway adjuncts
Maintaining head up position may delay airway oedema.
With abnormal airway or upper airway obstruction, the safest way to secure airway is with the patient awake. Prerequisites include proper positioning, effective topical anaesthesia (may not be effective in presence of airway oedema and inflammation) and supplemental oxygen.
Awake patients can be given IV opioids for pain relief, however use of sedatives must be carried out cautiously as it may worse airway obstruction.
Fiberoptic intubation techniques may not be useful as it may not be possible to anaesthetize the airway and airway instrumentation can cause further trauma and increase oedema.
Once intubated, tube must be secured well to avoid accidental extubation that may occur with increasing edema
If intubation is required at this early stage, it is usually technically easy as swelling of the airway has not yet occurred.
If upper airway has been badly damaged and endotracheal intubation is not possible direct surgical approach to the airway is indicated
Succinylcholine is safe in the first 24 h after a burn—after this time, its use is contraindicated due to the risk of hyperkalaemia leading to cardiac arrest, thought to be due to release of potassium from extrajunctional acetylcholine receptors. This can persist up to 1 year post-burn.
burnt tissue - difficult to isolate and secure veins, more chance of dislodgement from oedema, more chance of infection
Two large-bore i.v. cannulae should be inserted through the unburnt skin if possible and baseline bloods sent. The groins are usually spared so femoral venous cannulation is often possible
Parkland formula is calculated and fluid for resuscitation for 24hrs from the time of burns is calculated when patient arrives in the casualty. The volume already infused must be corrected according;ly
Fluid of choice- RL
Urine output- guide for resuscitation- 0.5ml/kg/hr.
Subtract any fluid already received and calculate hourly infusion rate for first 8 h
RL commonly used crystalloid, crystalloids are said to be as effective as colloids in maintaining intravascular volume and are significantly less expensive. Crystalloids are preferred over colloids, as large protein molecules move out of leaky capillaries and exacerbate interstitial edema and they can also cause AKI or ALI.
In children, preferable solution is dextrose-saline, 5D and half NOR.. Not both together, oral nutritious solution can be given like milk.
Advantage of hypertonic saline- less tissue edema, resultant decrease in escharotomies and intubations
Colloids- HAS more expensive. Plasma proteins exert capillary oncotic pressure and counteract outward hydrostatic pressure. Recommended 12hrs post-burns as initially presence of leaky capillaries can exacerbate already existing tissue edema as the proteins can leak out of them.
ECG- needle electrodes sutured into appropriate sites for monitoring
PR<120bpm adequate resuscitation; >130bpm – inadequate
Pulse ox- may get false readings with associated carboxyHb and methHB
If urine output is less than 0.5ml/kg/hr, infusion rate has to be increased by 50%.
S]igns of hypoperfusion- tachycardia, restlessness, clammy hands, hypotension, high haematocrit
CVP monitoring and TEE in patients with cardiac dysfunction to know the exact measurement of filling pressure
early excision and wound coverage, aiming to remove the full-thickness injury and get biological closure.
In full thickness burns, the collagen fibres are coagulated. The normal elasticity of the skin is lost. This can lead to limb ischemia if not treated immediately.
Burns dressings- analgesia with ketamine, regional techniques, epidural/ peripheral blocks
If there are circumferential burns of the chest and neck, eschar may restrict ventilation. An escharotomy of the chest wall should be performed to allow adequate ventilation.
Anatomy – distorted: Difficult mask ventilation (raw areas of burns), Difficult airway, Difficult IV access
Psychological- Anxiety, Depression
Pharmacological- Altered volume distribution, Hypoalbuminemia, Altered metabolism, Concomitant drug therapy,Sensitivity to muscle relaxants, High requirement of analgesics
Adequate preoxygenation-
Anatomy – distorted: Difficult mask ventilation (raw areas of burns), Difficult airway, Difficult IV access
Psychological- Anxiety, Depression
Pharmacological- Altered volume distribution, Hypoalbuminemia, Altered metabolism, Concomitant drug therapy,Sensitivity to muscle relaxants, High requirement of analgesics
Adequate preoxygenation- high metabolic rate, tachycardia, increased oxygen demand
Burn patients show great resistance to the nondepolarizing relaxants. Although these patients have altered pharmacokinetics and increased plasma protein binding of the relaxants, most of the increased requirement appears to be due to alterations in the number and affinity of the junctional receptors. This alteration is quite variable.
* e.g. after denervation injury, burn, or CVA * Not found in normal active muscles
* c.f. Normal junctional ACh receptors is about 14 days
Where there is a large number of extrajunctional receptors
• Resistance to non-depolarising muscle relaxants
• Increased sensitivity to depolarising muscle relaxants --> Hyperkalaemic response can be exaggerated
RELEVANT ASPECTS IN HISTORY
Duration of contractures
History of convulsions
Difficulty in breathing and swallowing
H/O motion sickness
H/O snoring
H/O epistaxis and bleeding from oral cavity
H/O psychiatric problems
H/O acid peptic disease and reflux
Analgesia lasts longer upto 30-45 mins .By which time the contracture release will mostly be released.
➢ Less risk of resp. depression
➢ Stable hemodynamics
➢ Provides an ideal environment along with tumescent or regional technique.
➢ Patient can be smoothly transitioned into an inhalational technique
➢ If using LMA , fix the LMA to the maxilla /upperlip .Never to the mandible.
➢ Consider using a muscle relaxant only if mask/LMA ventilation is possible . Otherwise avoid them
➢ Try endotracheal intubation in deep planes of inhalational anaesthesia.In spontaneous respiration as far as possible.
➢ Consider bougies ,tube exchangers where ever laryngoscopy and endotracheal intubation obscures visibility.
➢ Fix E.T tubes always to the maxilla .Fixing them to mandible can soak them and soil them with blood and secretions from the operative field and can also interfere with field of surgery .
➢ Use narcotics like fentanyl etc ., only after securing access to trachea.
To successfully perform awake endotracheal intubation, one should be familiar with the following:
• Sensory innervation of the upper airway
• Agents available for topicalization
• Application techniques available to topicalize the airway
• Regional anesthesia techniques, landmark or ultrasound-guided
• Safe sedation techniques
Vasoconstrictors should be used when the nasal mucosa is being anesthetized; this is because the mucosa is highly vascular, and bleeding can readily occur on instrumentation, which can obscure the view seen on the fiberscope.
Solution for tumescent contains lignocaine, adrenaline, hyaluronidase and saline/water.
In the formula above, the final concentration of lidocaine would be: 2x10/54, 4 = 0.367%,
and the FCS of adrenaline: 1/1,000x0.4/54.4 = 0.735/100,000.
The skin is removed after the donor’s heart has ceased to beat, as part of a multi-organic transplant in an operating theatre; this procedure can however be performed in the morgue up to 12 h after death. If the body is refrigerated, the possible time for re moval of the skin extends up to 24 h. Serology- HIV 1-2, HTLV 1-2, HBV, HCV, syphilis, cytomegalo virus, and toxoplasma. Search for presence of neoplasias and neurological and autoimmune diseases; microbiological tests are conducted for aerobes, anaerobes, fungi, and yeasts.