a case of burn with post burn contracture posted for surgery
ZikrullahMallick
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69 slides
Aug 28, 2020
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About This Presentation
a case of burn with post burn contracture posted for surgery
Size: 298.4 KB
Language: en
Added: Aug 28, 2020
Slides: 69 pages
Slide Content
POST BURN CONTRACTURE NECK Dr. ZIKRULLAH
Define burn and its cause???
Damage to body tissues caused by heat, chemicals, electricity, sunlight, or radiation. Scalds from hot liquids & steam, building fires &, flammable liquids & gases are the most common causes.
Burn Classifications Superficial (1 st degree) Least destruction Only epidermis injured Partial-thickness ( 2 nd degree ) Epidermis destroyed Varying depths of dermis damaged/destroyed Superficial partial-thickness Erythematous and moist with vesicles painful 6
Deep partial-thickness Red and waxy without blisters Moderate edema, lesser degree of pain Hypoxia and ischemia can cause extension of wound Full-thickness (3 rd degree) Entire epidermis and dermis involved No viable epithelial cells, grafts required Hard, dry leathery eschar 7
8 Deep full-thickness (4 th degree) Extend beyond skin into underlying fascia and tissues Muscle, bone and tendon damage with exposure to surface Blackened and depressed, little or no sensation Early excision and grafting beneficial
How would you Estimate burn size??
Estimation of burn size Rule of nines 9 Head 9 Each upper limb 18 Front trunk 18 Back trunk 18 Each lower limb 1 perineum 10 % burns
Rule of fives ( child ) 20 Head 10 Each upper limb 20 Front trunk 20 Back trunk 10 Each lower limb 11 % burns
Anaesthetic considerations peculiar to Postburn Contracture patients ?
1.Difficult airway 2.Use of muscle relaxants 3. Patient positioning 4. IV access 5. Application of monitors 6. Hypothermia
what is important in pre operative history before anaesthesia in burn patients?
Time of burn and its duration Types of burn Loss of consciousness with burn injury
What preoperative test are required before anaesthesia??
Serum electrolytes-sodium, potassium Haemogram RFT Chest X ray ECG ABG
What Problems associated with facial / neck contractures ??
1.Reduced mouth opening 2. Restricted neck movements 3. Stiff submandibular space 4. Scar and contractures in suprasternal area obviates the use of lightwand / cricothyrotomy / emergency tracheostomy 5. Larynx may be shifted from midline 6. Ineffective cricoid pressure 7. Application of OELM/ BURP during difficult laryngoscopy and intubation are not possible
How do you assess airway in this patient??
Examination of head and neck flexion- extention movement Head and neck lateral ratation MP grade Perioral wound or contracture patency of the nasal passages and for any history of epistaxis . Mouth opening
MANDIBULAR SPACE COMPLIANCE LENGTH OF NECK THICKNESS OF NECK
What are option available for airway management in this patients?
Awake intubation (nasal/ oral) ILMA + ETI (if MO> 2 finger) LMA classic / Combitube ( if tracheal stenosis suspected secondary to inhalation burns) Pre-induction neck contracture release under tumescent local anesthesia / ketamine anaesthesia Elective tracheostomy /PCT
How will you prepare this patient for awake intubation??
Make sure that you have all the appropriate resuscitation equipment to hand. The patient should be fully monitored throughout the procedure (blood pressure, pulse oximetry , ECG). Ideally, capnography should be available. Calculation of your local anaesthetic dose beforehand is essential.
Xylometazoline or Oxymetazoline nasal spray (or any other available topical vasoconstrictors) Obtain intravenous access and administer Glycopyrronium 3-4mcg/kg IV to minimise the airway secretions (alternatively, Atropine can be given). Communication with your patient throughout the procedure is of vital importance
1. Position the patient on the trolley for administration of local anaesthetic, followed by a semi-recumbent or supine position, depending on operator’s preference/patient convenience, for the endoscopy and intubation. 2. Identify the patient’s most patent nasal passage. 3. Spray nasal mucosal with vasoconstrictor ( oxymetazoline / xylometazoline ) 4. Nebulise 2ml 4% Lignocaine (80mg, of which 25% is typically absorbed = 20mg)
5. Nose and nasopharynx : Soak cotton bud (cotton applicators mounted on sticks)/pus swab sticks/ribbon gauze leaving it in situ for around 3 minutes. 6. Tongue and oropharynx : 4 puffs 10% Lignocaine to throat . 7.Cricothyroid (trans-tracheal) injection, to anaesthetise subglottic region, vocal cords and trachea. 8.glossopharyngeal, superior laryngeal and recurrent laryngeal nerve blocks .
Tube fixation in burn??
Tube fixation The fixation of the ET is a challenge in the burned patient. The ideal fixation secures the tube safely without additional injury to the tissue of the face and is flexible enough to adjust to edema formation. Suturing the tube to the gums, wiring the tube around a tooth, and circumferential fixation or devices that allow frequent adjustment are examples. 31
The usual forms of adhesive tape are not effective in the burned patient because they do not adhere adequately even to nonburned skin. Usually, a soft sling ribbon is used. It is tied at the back of the head (not the neck), and gauze padding should be added to avoid constriction of soft tissues. 32
What is impact of burn on muscle relaxants??
Patients are resistant to non depolarizing muscle relaxants and increased sensitivity to depolarising muscle relaxants due to extra junctional proliferation of acetylcholine receptors .Marked resistance only occur when burn is>30%of TBSA.
Higher than usual doses Larger the burn area – larger the dose and faster the recovery time. Not seen in first postburn week. Not relavant in burns < 10 % Normal doses of reversal agent can be used Atracurium (1 mg/kg)/ vecuronium (.15 mg /kg) may be used.
Unlike other NDMR Mivacurium , it is degraded by plasma cholinesterase whose activity is decreased in burn. Normal doses (.25 mg/kg) of Mivacurium will be sufficient with similar onset of action.
Why is Succinylcholine contraindicated in burned patients? For how long should be avoided?
Succinylcholine is contraindicated in burned patients because it causes significant transient increase in serum potassium levels as high as 13mEq perL , resulting in ventricular fibrillation and cardiac arrest. This hyperkalemic response begins approximately 5 to 15 days after the burn and persists for 2 to 3 months or longer Most authors recommend the avoidance of succinylcholine from 24 to 48 hours after the burn injury and the recommended limit now is extended to approximately 2 years after the burned skin has healed.
Why are you concerned about the patient's body temperature ?
Massively burned patients with loss of skin have constant evaporation from open surface. Tend to develop severe intraoperative hypothermia and it is exaggerated by the effects of general anaesthesia on the temperature-regulating centers , by vasodilation , and by the cool relatively dry environment of the operating room. Normothermia for a burned patient is approximately 38.5°C because the burned patient develops a resetting of the centrally mediated thermostat.
Temperature probe Maintenance of normothermia is of paramount importance for survival of flap Hypothermia : hypoxia, bleeding & haematoma Active warming starts before the patient is asleep. The ambient temperature in theatre is raised to about 22–24 degree C. Heat loses from fresh gas flows and inhalation agents should be taken in to consideration
Monitoring in burn patient??
Applying monitors may be difficult in pt with limb and chest wall burns.( Needle ECG electrodes & invasive arterial BP) In addition to basic monitoring Invasive blood pressure monitoring to enable safe manipulation of the perfusion pressure. provides access to blood gas analysis and haematocrit estimations. (at the start of the operation and repeated every 2 hours)
Urine output is another indicator of volume status. A urine output of 1–2 ml/kg/hour should be maintained intraoperatively and postoperatively Temperature probe
The patient is ventilated to normocapnia . Hypocapnia increases peripheral vascular resistance and reduces cardiac output, while hypercapnia causes sympathetic stimulation. If the surgeon uses the microscope for vessel preparation or anastomosis on the chest or abdomen, the tidal volume is reduced to minimize movement in and out of the surgeon’s field of vision. The respiratory rate is then increased to maintain minute ventilation.
What precaution you will take prior to & after extubation in the post operative period??
Use of intraoperative dexamethasone 0.10-0.20 mg/kg iv to reduced airway edema formation Fully awaken the patients prior to extubation Wait for complete reversal of NMB Extubate over a jet stylet Nurse the patients post opp. In head up position for 12-24 hr Keep tracheostomy and TTJV kit ready
What is Indications for intubation in burn patients??
Airway obstruction Depressed level of consciousness Circumferential nasolabial burns Hypoxia CO poisoning Upper airway edema Subglottic thermal and chemical burns Chest wall restriction
What Fluid/Electrolyte Changes take place in burn patient?
Fluid Shift Period of inflammatory response Vessels adjacent to burn injury dilate → ↑ capillary hydrostatic pressure and ↑ capillary permeability Continuous leak of plasma from intravascular space into interstitial space Associated imbalances of fluids, electrolytes and acid-base occur
Hemoconcentration Lasts 24-36 hours Fluid remobilization Capillary leak ceases and fluid shifts back into the circulation Restores fluid balance and renal perfusion Increased urine formation & diuresis Continued electrolyte imbalances Hyponatremia Hypokalemia Hemodilution
Cardiac Decreased CO, decreased BP Due to decreased blood volume, & myocardial depressant factor Need fluid resuscitation and support with O 2 Pulmonary FRC reduced, Both lung compliance & chest wall compliance reduced Need aggressive pulmonary toilet & oxygenation Other System Changes 55
Gastrointestinal Decreased or absent motility (may need NG tube) Curling’s ulcer formation H 2 histamine blockers, mucoprotectants & enteral nutrition Metabolic Hypermetabolic state Increased oxygen and calorie requirements Increase in core body temperature 56
Immunologic Loss of protective barrier Increased risk of infection Suppression of humoral & cell-mediated immune responses Other System Changes 57
Drug metabolism in burn??
First 48 hr.-decreased drug absorption(except iv route) leads to slow erratic action due to organ blood flow is reduced because of hypovolemia and decreased C.O. After 48 hr.-plasma albumin concentration decreases leading to increase free drug fraction,plasma protein binding of drugs(BZD) is decreased,resulting in increased fraction of drug Fluid loss due to burn wound and oedema elsewhere can decrease plasma concentration of many drugs
Dizepam - prolonged Opioids-req.is increased due to burn patient experience intense pain and require larger doses of opioids Ketamine –used during burn dressing Thiopental,propofol,etomidate - causes hypotension in acute hypovolemia stage. Inhalational agent-poorly tolerated in hypovolemic patients. Muscle relaxants- pt.with thermal injury are resistant to the action of NDMR,this effect takes upto a week to as long as 18 month Resistance to NDMR will require larger doses than normal doses to achieve a desired effect
Fluid resuscitation ??
To correct hypovolaemia secondary to increased capillary permeability leading to fluid and protein loss in interstitial tissue. Formula for resuscitation:- Parkland formula Brooke formula Evan formula Muir & Barclay formula
Parkland formula for 24 hrs.is :- lactated ringer 4ml/kg/% burn/24hrs 50% administered over 8hrs. Next 24hrs,D5W should be administered @ rate of 2ml/kg/% burn,plus plasma calculated as 0.3-0.5 ml/kg/% burn Brooke formula for the 1 st 24 hrs is:- lactated ringer 2ml/kg/%burn/24hrs. Followed with D5W 1-2ml/kg/% burn,plus plasma calculated as 0.3-0.5ml/kg/% burn over next 24 hrs.
CO POISONING??
Carbon monoxide (CO) is a gas produced by the combustion of carbon-containing fuels or the Inadequate ventilation of natural gas. Once in the bloodstream, co prevents oxygen from reaching tissues. Exposure to co is the leading cause of death by poisoning in industrialized countries. Half of all co-poisoned patients may be misdiagnosed.
Treatment
Hyperbaric Oxygen Therapy (HBO) can decrease the half-life of CO to 22 minutes, induce cerebral vasoconstriction to reducing intracranial pressure and cerebral edema , and reduce the risk of long-term disability. In particular, HBO treatment is appropriate for patients who experience unconsciousness, neurological signs, cardiovascular dysfunction or severe metabolic acidosis, irrespective of their COHb levels.