1. CASE PRESENTATIONS
Rashid M.Khan
Reader
Department of Anaesthesiology
J.N.Medical College
Aligarh

2. CASES
 Burns: Acute & Late stages including
Contractures.
 Temporomandibular Joint Ankylosis.

3. Questions
Answers

4. STRUCTURED APPROACH
 Short Case Presentation with photographs.
 Relevant Anatomy & Physiology.
 Etiology.
 Classification.
 Diagnosis, Treatment.
 Anaesthetic Management with special
reference to airway management.

5. CASE – I
Burns

6. A 23 year-old female patient presented with severe
contractures of the face & neck following burns
sustained about 9 months back.

7. What is the normal structure of the skin?

8. What are the physiological functions of the skin?
 It is a sensory organ.
 It performs a major role in thermoregulation
for dissipation of metabolic heat.
 It acts as a barrier to protect the body
against microorganism in the environment

9. WE SHALL DISCUSS
BURNS
AS:
•ACUTE BURNS
* CHRONIC BURNS WITH CONTRACTURES

10. How are burns classified?
 1st degree burns = involves upper layer of epidermis, skin
is painful & red.
 2nd degree burns = Damage extends into the dermis,
develops blisters, has red or whitish areas, very painful.
Regenerates into new skin.
 3rd degree burns = Destruction of all layers of skin
including nerve endings, painless. No regeneration.
 4th degree burns = Destruction of all skin layers, muscle &
fascia, may even reach the bones.

11. How do you calculate the % of total body surface
burned?
Rule-of-nine for 2nd & 3rd degree burns
 Head & neck – 9%
 Upper extremities – 9% each.
 Chest [anterior & posterior] – 9% each.
 Abdomen – 9%.
 Lower back – 9%.
 Lower extremities – 18% each.
 Perineum – 1%.

12. What is the modified Rule-of-Nine for children?
Newborn 3 years 6 years
Head 18% 15% 12%
Trunk 40% 40% 40%
Arms 16% 16% 16%
Legs 26% 29% 32%

13. What is the definition of a MAJOR BURN?
The American Burn Association defines Major
Burns as:
 Full thickness burns > 10% TBSA.
 Partial thickness burns more > 25% in adults or 20%
at extremes of age.
 Burns involving face, hands, feet, or perineum.
 Inhalation, chemical, or electrical burns.
 Burns in patients with serious pre-existing medical
disorders.

14. If left unattended, why do patients with 3rd & 4th
grade burns develop Post-burn Fibrotic Deformity?
There are several causes which predispose a poorly
managed 3rd & 4th grade burnt patient to develop
post-burn fibrotic deformity. These include:
– Persistent edema.
– Wound infection.
– Poor post-burn positioning.
– Prolonged immobilization [lack of mobilization].
– Delayed or inadequate skin coverage.

15. Why do these patients usually develop a flexion
deformity?
The most common position of comfort that the patient
assumes in the post-burn period is usually flexion
(fetal posture)
[exception: hyperextension of intercarpo-phalyngeal
joints].
If this habitus is not quickly corrected, irrevocable
fibrosis develops even before full healing of the
burned area.

16. What systems are affected by burns?
Nearly all systems are affected by burns.
 Cardiovascular system.
 Respiratory system.
 Hepatic, Renal, and endocrine functions.
 G.I. System.
 Haempoiesis, coagulation, and immunologic
responses.

17. How is the CVS affected?
 ACUTE PHASE:[0 – 48Hrs]
Organ & tissue perfusion decreases due to 1. hypovolemia,
2. depressed myocardial function, 3. increased blood
viscosity, & 4. release of vasoactive substances.
 METABOLOIC PHASE: [48 Hrs onwards]
Increased blood flow to organs & tissues.
 NOTE: Geriatric patients may have a delayed or non-
existing metabolic phase.
Hypertension of unknown cause may develop.

18. How is the respiratory system affected?
THREE DISTNCT PHASES
1. Phase of early complications [0 – 24 hrs]: Includes CO
poisoning, direct inhalation injury leading to airway
obstruction & pulmonary edema.
2. Phase of delayed injury: [2 – 5 days]: ARDS.
3. Phase of late complications [>5 days]: Includes
pneumonia, atelectasis, pulmonary emboli.

19. What is inhalation injury?
Causes:
Hot gases, toxic substance, reactive smoke particles in
tracheobronchial tree.
Results in :
Wheezing, bronchospasm, corrosion, and airway edema.
Implications of inhalational injury:
 Presence of carbonaceous sputum, perioral soot, burns to
face & neck, stridor, dyspnea,or wheezing are indications
for a low threshold for elective intubation.

20. What are the features of CO poisoning?
Causes
Incomplete combustion associated with fires, exhaust from internal
combustion engines, cooking stoves, and charcoal stoves.
Results in
COHb [CO affinity is 200 that of O2] that leads to 1.tissue hypoxia,
2. shift in O-Hb dissociation curve, 3. direct CVS depression, 4.
cytochrome enzyme inhibition, 5. overestimation of SaO2.
Treatment
1. Initiate 100% O2 therapy at atmospheric pressure [decreases half life
of COHb].
2. If COHb > 20%, comatose patient pregnancy, myocardial ischemia,
neonate, persistent symptoms after 4 hrs of 100% O2 therapy at
atmospheric, or lactic acidosis = Hyperbaric O2

21. How do burns affect the GI System?
 Adynamic ileus at any time after injury.
 Curling’s ulcer leading to GI bleeding.
 Small & large intestine may develop acute
necrotizing enterocolitis with abdominal distension,
hypotension, and bloody diarrhea.
 During 2nd & 3rd week – acalculous cholecystitis is
common

22. How is renal system affected?
ATN & ARF
Causes
Hemoglobinuria secondary to hemolysis.
Myoglobinuria secondary to muscle necrosis.
Incidence & mortality
ATN & ARF = 0.5% - 38%, Mortality = 77 – 100%.
Onset
Immediately: RBF & GFR is decreased. This activates RAA
system. Release of ADH leading to retention of Na & H2O and loss
of K, Ca, & Mg
Treatment
1. Vigorous fluid resuscitation [Formulae guided].
2. Maintain urine output , if needed with mannitol.
3. Administer bicarbonates to alkalinize urine to reduce pigment
associated renal failure.

23. How is hepatic system altered?
DECREASED HEPATIC FUNCTION
Causes
1. Acute reduction of Cardiac Output.
2. Increased viscosity of blood.
3. Splanchnic vasoconstriction leading to hepatic
hypoperfusion.
Effect
Reduced Phase I metabolism [oxidative]
Phase II reaction not effected [conjugative]
Treatment
Restore CO, decrease blood viscosity.

24. Are drug responses altered in patients with burns?
 1st 48 hrs = Decreased drug absorption [except IV route]
leads to slow, erratic action.
 After 48 hrs = Plasma albumin concentration decreases
leading to increase free drug fraction
SPECIFIC DRUGS
Diazepam – Effect prolonged.
Opioids – Requirement increased.
Ketamine – May cause hypotension.
Thiopental, propofol - May cause hypotension in the acute
hypovolemic stage.
Inhalational agent–Poorly tolerated in hypovolemics.
Muscle relaxants–Depolarizing: Sensitive/hyperkalemia
Non-depolarizing: Resistant

25. What is the cause of resistance to non-depolarizing
muscle relaxants?
 Patients with more than 30% burn area may manifest
resistance to non-depolarizing muscle relaxants.
 The cause is multi-factorial:
1. Proliferation of extra-junctional receptors,
2. Alterations in the number & affinity of junctional
receptors, and
3. Synthesis of α1 glycoproteins to which the muscle
relaxants binds leaving little free fraction to act.
 This is usually seen after one week of burns, lasting up to
3-6 months.

26. Is there any non-depolarizing muscle relaxant which is
not affected by burns?
 Mivacurium is a muscle relaxant, degraded by plasma
cholinesterase, whose enzyme activity is decreased in
burns.
 The decreased metabolism of mivacurium, resulting from
depressed plasma cholinesterase activity, probably
counteracts the receptor-mediated potential for resistance.
 Martyn et al have shown that a normal mivacurium dosage
(0.2 mg/kg) effects good relaxation conditions in burned
patients, with an onset time similar to that in controls
[Anesthesiology 2000; 92: 31-7]

27. What is the endocrine response to a burn?
MASSIVE RELEASE OF:
 Catecholamines.
 Glucagon.
 ACTH.
 ADH.
 RAA.
1. Hyperglycemia [non-ketotic hyperosmolar coma]
2. Adrenal necrosis [should be suspected in hypotensive
patients unresponsive to volume infusion].

28. What are the hematologic complications of
burns?
ANEMIA
 Early Anemia due to RBC damage, dilutional due to
fluid resuscitation.
 Decreased erythropoiesis.
 Ongoing infection.
 Various degrees of coagulopathy.
PLATELET FUNCTIONS
Qualitatively & quantitatively depressed

29. What are the 3 Phases of burn management?
 I- Resuscitative phase
 2. Stabilization phase.
 3. Reconstructive phase.

30. What are your priorities in the resuscitative phase?
A,B,C,D,E,F,G,H
 A-Airway management.
 B-Breathing.
 C-Circulation/CVS stabilization.
 D-Drugs [Analgesics, Antibiotics, Vasoactive
drugs].
 E-Escharectomy.
 F-Fluid management.
 G-Gen. Supp. Care [Nutritional,
Physiotherapy,Psychological support]

31. How will you manage the Airway in the resuscitative
phase?
 Secure the airway early before airway edema progresses to
obstruction [1. difficulty in swallowing, 2. stridor, and
3.use of accessory muscle].
 Administer humidified O2 by mask to all patients
immediately.

32. Why does airway edema occur in acute burn patients?
 Exposure of the epiglottis or larynx to either dry air
at 3000C or steam at 1000C.
 Chemical products of combustion such as ammonia,
nitrogen dioxide, sulfur dioxide, and chlorine
dissolves in the upper airway & produce edema.

33. What are the indications for ETI in the resuscitative
phase?
 Airway obstruction.
 Depressed level of consciousness.
 Posterior pharyngeal wall swelling.
 Circumferential nasolabial burns [full
thickness]
 Hypoxia uncontrolled with mask & O2

34. What are the modes of securing the airway?
 Nasal/oral intubation [FOI, Fastrach aided Anesth Analg 2002; 95: 1454-
8, Trachlight aided, Blind].
 LMA [Anesthesiology 1997; 86:1011-2], Combitube [J Clin Anesth 2003; 15: 463-6],
Cobra PLA [Can J Anesth 2005; 52: 340] or any suitable supraglottic
device till you can arrange alternative intubation
technique.
 Needle cricothyroidotomy
 Surgical cricothyroidotomy.
 Tracheostomy ?

35. What will be your ventilation strategy [Breathing]
 If carboxyhemoglobin [COHB] is < 20%, ventilate
with titrated O2 to achieve SaO2 > 95%.
 If COHB is >20%, ventilate with 100% O2.
 If COHB is >20% and is unresponsive to ventilation
with 100% O2, consider hyperbaric oxygenation.

36. How would you resuscitate the Circulation?
REASON FOR RESUSCITATION
To correct hypovolemia secondary to increased capillary
permeability leading to fluid & protein loss in interstitial
tissue.
DIFFERENT FORMULA FOR FLUID
RESUSCITATION
 Parkland Formula.
 Brooke Formula.
 Evan’s Formula
 Muir & Barclay Formula.
END POINT OF RESUSCITATION
1. Hemodynamic stability.
2. Urine output > 1 ml/lkg/hr.

37. Parkland formula for fluid administration
 For the first 24 h is: Lactated Ringer 4 ml / kg / %
burn / 24h, of which 50% should be administered
over the first 8 h. Remaining 50% over the next 16 h
 Over the next 24 h, D5W should be administered at
the rate of 2ml / kg / % burn, plus plasma calculated
as 0.3-0.5ml / kg / % burn.

38. Brooke Formula for fluid resuscitation
 For the first 24 h is: Lactated Ringer 2 ml / kg / %
burn / 24 h.
 This is to be followed with D5W 1-2ml / kg / %
burn, plus plasma calculated as 0.3-0.5ml / kg / %
burn over the second 24 h.

39. Role of colloid during resuscitation ?
 In the United States, The American College of
Surgeons Committee on Trauma advocates only
crystalloids for resuscitation of all burn patient
because of its simplicity, reduced cost, and nearly
identical outcome with that wherein colloid regimes
are used.
 In Europe, some institutions use resuscitation
regimens which include a combination of
crystalloid and colloid. However, this simply adds
to the expense without demonstrable benefit.

40. End point of successful resuscitation.
 Hemodynamic stability: In a young patient HR of 100/min
or lower and systolic blood pressure of 100mmHg or more.
 -Correction of base deficit.
 -Mixed or central venous oxygen saturation exceeding 60%.
 -Urine output > 1 ml/kg/hr.
 Approximately 20% of the patients will be over-hydrated,
particularly with the Parkland Formula. If urine output
exceeds 2 ml/kg/h, then the rate of infusion should be
reduced in steps of 25%.
 Approximately 10% of the burned patients shall not respond
to fluid therapy as outlined above. These are generally older
patients, having underlying medical conditions, had a delay
in initiating resuscitation, and may be having concomitant
inhalation injury.

41. What is important in the preoperative history before
anaesthesia?
 Time of burn: For fluid replacement.
 Type of burn: [Thermal or electrical]
 Associated injuries.
 Past & current medical conditions.
 Past & current medications.
 Allergies.
 Anaesthetic history.

42. What should the anaesthesiologist look for on the
preoperative physical examination?
 Status of patient’s airway: Complete Airway
Assessment.
 Excessive sputum & decreased breath sounds
may suggest inhalation injuries.
 CVS: HR, Rhythm, BP,Cardiac filling pressures
[if available].
 Urine output.
 CNS: Level of consciousness & orientation.

43. What preoperative Lab tests are required before
induction of anaesthesia?
 ABG for correcting acid-base & electrolyte
imbalance.
 Blood Chemistry.
 Chest radiograph.
 COHb level estimation.
 Coagulation tests.

44. What monitors are needed to give a safe anaesthetic?
 Access for monitoring may be difficult.
 Needle electrodes for EKG & PNS.
 NIBP cuff or arterial catheter for IBP/ABG.
 ETCO2
 Temperature probe.
 CVP: If large blood loss is anticipated.
 PA catheter, if severe myocardial
dysfunction.

45. What induction agents will you use in patients with
acute burns?
 Ketamine.
 Propofol/thiopentone–safe if adequately resuscitated.
 Etomidate – If patient is still hemodynamically
unstable.
Role of narcotics, muscle relaxants & inhalational
agents has already been discussed.

46. What are the Surgical Objective During Reconstructive Stage?
Severe anterior neck burn scar contracture issues in
serious functional embarrassment.
Reconstruction is based on three principles:
1. Releasing shrinked area.
2. Restoring contour of the mento-collical angle, &
3. Preventing recurrence.

47. What are the problems of airway management for elective
anaesthesia during the Reconstructive Phase, like the present
case?
 Difficulty in securing airway [ETI] especially in
facial & neck contractures.
 Use of muscle relaxants [Dep/Non-dep].
 Patient positioning.
 Securing IV lines.
 Applying monitoring devices.

48. What are the problems associated with facial/neck
contractures during airway management?
 Reduced mouth opening.
 Restricted neck movement.
 Stiff submandibular space [Anterior larynx]
 Scar & contracture in suprasternal area obviates the
use of lightwand assisted ETI / cricothyrotomy /
emergency tracheostomy.
 Larynx may be shifted from the midline.
 Ineffective cricoid pressure.
 Applying OELM during difficult laryngoscopy
/intubation is not possible.
 Applying BURP on the larynx may not be possible

49. What are the implications of a non-compliant
submandibular space?
During laryngoscopy the tongue is
depressed into the submandibular space. A
non-compliant space will not accept the base
of the tongue and patient will exhibit the
appearance of an anterior/superior larynx.

50. What are the options available for airway
management in the present case undergoing elective
anaesthesia?
 Awake FOI [nasal or oral] especially if mouth opening is <
2 fingers.
 Mouth opening >2 finger ILMA + ETI in awake patient.
 Mouth opening >2 finger breadth – LMA in awake patient.
 Release of contracture partially under ketamine anaesthesia
or L.A + hyaluronidase infiltration & then try to intubate by
conventional laryngoscope [Acta Chir Plast. 1997;39(2):56-9]. .
 Successful Combitube placement has been described in
burned patients with limited mouth opening .
REMEMBER= Release of contracture in the front of neck
does not guarantee a lax, pliable submandibular space. ETI
may be still difficult.

51. What about conventional rigid laryngoscopy &
intubation?
 In this patients with fixed flexion deformity
of the head & neck [as in the present case], it
is not possible to align the 3 airway axes and
this would most likely lead to failed
laryngoscopy & intubation.
 Non compliant submandibular space will not
allow the tongue to be compressed by the
laryngoscope : Anterior larynx.
 Persisting with this technique may produce
trauma and subsequent edema leading to
failure of other methods [FOI].

52. What about Trachlight Intubation, Blind Intubation,
Retrograde Intubation and Surgical Tracheostomy?
 Trachlight would fail in the presence of the neck scar.
 Experienced person may give a trial of awake blind
intubation techniques.
 Retrograde method is also not recommended due to loss of
landmarks over front of the neck.
 Surgical tracheostomy should be reserved as the last option.
Its presence makes skin grafting difficult and it may run the
risk of infection.

53. How will you prepare this patient for awake
intubation?
 Premedicate with mild sedation + drying agent.
 Instill vasoconstrictor in the nose.
 Topicalization of the airway using 4% xylocaine
spray & 4% xylocaine gargle or “spray-as-you-
go” using 4% xylocaine through suction channel
of the bronchoscope.

54. How will you conduct GA in such patient if patient is
not feasible or refuses awake intubation?
 It is prudent to gradually induce the patient with inhalational agent in
100% O2, after adequate depth attempt gentle laryngoscopy to assess
laryngeal view and then decide to intubate with or without muscle
relaxants. Keep FO/ LMA/ Combitube ready as alternative devices.
 Release of contracture partially under ketamine anaesthesia or L.A +
hyaluronidase infiltration & then intubate.
 Vasilious et al have successfully induced patients with propofol and
fentanyl after preoxygenation. They ventilated the lungs manually
with oxygen and halothane by a size 4 face mask. If regular
laryngoscopy failed, they passed LMA.
Anesthesiology 86:1011-2, 1997

60. What are special features of electric burns?
 Extent of injury is misleading resulting in under initial
fluid resuscitation.
 Myoglobinuria is common [ATN].
 Neurologic complications are more common such as
peripheral neuropathies or spinal cord deficits.
 Cardiac arrhythmias, VF, or asystole may occur upto 48
hrs.
 Apnea from tetanic contraction or cerebral medullary
injury.
 Cataract formation as a late sequele.
END OF CASE – II

61. CASE – II
Temporomandibular
Joint Ankylosis

62. A 14-year-old female patient has come with
complaints of limited mouth opening [< I cm] and
poorly developed lower jaw. She had sustained lower
jaw injury during fall from stairs when she was 4
years old.

63. What is your working dignosis?
Post Traumatic Temporo-mandibular Joint
Dysfunction

64. What is the gross anatomy of TMJ?
It is a diarthrodial synovial joint like most other joints with
three important exceptions:
 Both TMJ’s function as a single unit i.e. craniomandibular
articulation.
 Articular surfaces are lined with fibrocartilage instead of
the usual hyaline cartilage.
 Articular disc [ dense fibrous connective tissue –
biconcave] separates the joint into 2 spaces, each with a
different function.

65. What is the physiological function of the TMJ?
 Chewing
 Speech

66. During maximum jaw opening what motions can be
observed?
2 separates motions can be observed in 2 distinct joint
spaces:
*Hinge like movement
*Sliding movement

67. What history would you like to elicit in addition to
what patient has already complained off?
Classic Triad
 H/O pain in the preauricular area.
 Noises emanating from the region of TMJ.
 Limited mandibular movement

68. What physical examination would you conduct?
 Joint movement in all directions [Maximum
opening - inter-incisor = 4-5 cms, Lateral
jaw excursions – 1cm]
 Pay attention to the face for any signs of
facial asymmetry.
 Occlusion defects.
 Dentitions problems.

69. What other associated problems secondary to TMJA
you will look for?
 Nutrition problems.
 Oral hygiene leading to dental decay /
abscess

70. What is the aetiopathogenesis in this case?
Trauma
 Infection.
 Rheumatoid arthritis
 Congenital deformity

71. What are the investigations needed to confirm the
diagnosis?
 MRI : Investigation of choice.
 Conventional radiography [Transcranial view]
 CAT scanning with mouth open & closed position.
 Arthrography using contrast media into joint
spaces.
 ESR, Autoantibodies, Uric acid level may uncover
inflammatory TMJ.

72. What surgical interventions are possible in cases of
TMJ dysfunction?
 TMJ Arthroscopy.
 TMJ Arthrotomy.
 TMJ Implants

73. What specific surgical interventions are reserved for
TMJA?
 Condylectomy.
 Gap arthroplasty.
 Autogenous replacement of resected
condyle with 5-6th rib graft

74. What airway assessment shall you perform?
 BONES
 LEMON

75. Anesthetist's Concerns
This relatively rare problem becomes even more
difficult to manage in children because of their
smaller mouth opening with near total trismus, and
the need for general anaesthesia before making any
attempts to secure the airway.

76. What are your airway management options in this
case?
 Nasotracheal intubation.
 PCT / tracheostomy.

77. How will you achieve nasotracheal intubation in this
case?
 Fiberoptic nasotracheal intubation[FOI].
 Seeing optic stylet system [SOS] aided.
 Flexible airway scope tool [FAST] aided.
 Trachlight aided.
 Retrograde NTI
 Blind NTI

78. What are your anaesthetic options for achieving
NTI?
 Awake, under topical / nerve block
anaesthesia using mild sedation + drying
agent.
 Under inhalational anaesthesia L.A..
 Under inhalational muscle relaxant.

79. What will be your anaesthetic technique in this
patient?
AWAKE FO/LW AINTUBATION, AFTER
CONSENT
 Psychological preparation.
 Antisialogogue.
 Sedation.
 LA-Topical & N. Block

80. Alternative Anaesthetic Technique
A technique for securing the airway that combines
LA/GA:
 local blocks for nerves of larynx,
 topical anaesthesia of upper airways for
placement of these blocks,
 and minimal general anaesthesia
[halothane/sevoflurane] for airway manoeuvres.
Paediatr Anaesth. 2001; 11: 237-44.

81. A simple and safe technique of intubation with
minimal discomfort to the patient using a
nasopharyngeal airway, fibreoptic bronchoscope and
guide wire in a three-year-old is presented
Paediatric Anaesthesia 1999; 3: 260

82. In the absence of Fiberscope
Recently BJA published report of 2 cases of TMJ
Ankylosis where retrograde nasal intubation was
achieved using fluoroscopy-assisted nasal retrieval
of the guide wire [50 cm guide wire from a 16 G
central venous catheter] passed through a
cricothyroid puncture and up via nasal airways
placed in both the nostrils.
[ British Journal of Anaesthesia 2005 94:128-131]

85. What are your options for tracheostomy?
 Percutaneous dilatational tracheostomy.
 Surgical tracheostomy.

86. If while trying NTI suddenly your patient goes into
CVCI situation, what will be your next step?
CRICOTHYROTOMY
• Needle cricothyrotomy.
• Percutaneous cricothyrotomy.
• Surgical cricothyrotomy.

87. What monitors you will apply to patient while
attempting NTI?
 Pulse oximeter.
 Cardioscope.
 NIBP.
 PNS.
 Capnograph ready.

88. What precautions you will take prior to extubation of
this patient?
 Extubate when the patient is fully awake.
 Wait for complete reversal of the residual
NMB.
 Extubate over a ventilating stylet.
END OF CASE - II

89. Wish you all a grand success in the
exam