STRUCTURED APPROACH Short Case Presentation with photographs. Relevant Anatomy & Physiology. Etiology. Classification. Diagnosis, Treatment. Anaesthetic Management with special reference to airway management.
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
WE SHALL DISCUSS BURNS AS: •ACUTE BURNS* CHRONIC BURNS WITH CONTRACTURES
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.
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%.
What is the modified Rule-of-Nine for children? Newborn 3 years 6 yearsHead 18% 15% 12%Trunk 40% 40% 40%Arms 16% 16% 16%Legs 26% 29% 32%
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.
If left unattended, why do patients with 3rd & 4thgrade 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.
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.
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.
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.
How is the respiratory system affected? THREE DISTNCT PHASES1. 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.
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.
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. Treatment1. 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
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
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 Treatment1. 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.
How is hepatic system altered? DECREASED HEPATIC FUNCTION Causes1. 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.
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 DRUGSDiazepam – 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
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, and3. 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.
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]
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].
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
What are the 3 Phases of burn management? I- Resuscitative phase 2. Stabilization phase. 3. Reconstructive phase.
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]
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.
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.
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
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 ?
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.
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 RESUSCITATION1. Hemodynamic stability.2. Urine output > 1 ml/lkg/hr.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
What are the problems of airway management for electiveanaesthesia 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.
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
What are the implications of a non-compliant submandibular space? During laryngoscopy the tongue is depressed into the submandibular space. Anon-compliant space will not accept the base of the tongue and patient will exhibit the appearance of an anterior/superior larynx.
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.
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].
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.
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.
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
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
A 14-year-old female patient has come with complaints of limited mouth opening [< I cm] andpoorly developed lower jaw. She had sustained lower jaw injury during fall from stairs when she was 4 years old.
What is your working dignosis?Post Traumatic Temporo-mandibular Joint Dysfunction
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.
What is the physiological function of the TMJ? Chewing Speech
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
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
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.
What other associated problems secondary to TMJA you will look for? Nutrition problems. Oral hygiene leading to dental decay / abscess
What is the aetiopathogenesis in this case? Trauma Infection. Rheumatoid arthritis Congenital deformity
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.
What surgical interventions are possible in cases of TMJ dysfunction? TMJ Arthroscopy. TMJ Arthrotomy. TMJ Implants
What specific surgical interventions are reserved for TMJA? Condylectomy. Gap arthroplasty. Autogenous replacement of resected condyle with 5-6th rib graft
What airway assessment shall you perform? BONES LEMON
Anesthetists Concerns This relatively rare problem becomes even more difficult to manage in children because of theirsmaller mouth opening with near total trismus, andthe need for general anaesthesia before making any attempts to secure the airway.
What are your airway management options in this case? Nasotracheal intubation. PCT / tracheostomy.
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
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.
What will be your anaesthetic technique in this patient?AWAKE FO/LW AINTUBATION, AFTER CONSENT Psychological preparation. Antisialogogue. Sedation. LA-Topical & N. Block
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.
A simple and safe technique of intubation with minimal discomfort to the patient using anasopharyngeal airway, fibreoptic bronchoscope and guide wire in a three-year-old is presented Paediatric Anaesthesia 1999; 3: 260
In the absence of FiberscopeRecently BJA published report of 2 cases of TMJ Ankylosis where retrograde nasal intubation wasachieved 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]
What are your options for tracheostomy? Percutaneous dilatational tracheostomy. Surgical tracheostomy.
If while trying NTI suddenly your patient goes into CVCI situation, what will be your next step? CRICOTHYROTOMY• Needle cricothyrotomy.• Percutaneous cricothyrotomy.• Surgical cricothyrotomy.
What monitors you will apply to patient while attempting NTI? Pulse oximeter. Cardioscope. NIBP. PNS. Capnograph ready.
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