Burns Flashcards
Different types of burns
Chemical
Electrical
Thermal/Heat (Flame or Scald)
Inhalational
Chemical
Commonly occur in laboratory or industrial setting
Noxious chemical contact the skin
Chemical must be removed or neutralized to stop injury
Remove contaminated clothing, neutralize or dilute with water
Chemical burns are uncommon in children
Electrical
Extent of injury depends on the voltage and duration of contact
Extent is difficult to predict by inspection
Dysrhythmias are common
Low voltage <1000V local contact burn
High voltage >1000V entrance and exit wound
Damage to bones, blood vessels, muscles, and nerves
Myoglobinuria can lead to renal failure, affects the renal tubular function
Thermal
Commonly occur in and around the home
70% of burns by children up to the age 4 are scald injuries
Flame burns are most common for children 5 years and older
Inhalational
Associated with thermal burns
Suspected and aggressively ruled out. Warning signs; singed nasal hair horse voice, productive (soot) cough, stridor, facial burns, breathed fire, and voice change.
Three types:
Upper airway injuries; thermal injury to the mouth larynx and oropharynx
Lower airway injuries; trachea lower bronchioles and alveoli
Metabolic Asphyxiation; carbon monoxide or hydrogen cyanide impair O2 delivery
Cyanide Poisoning
Hydrogen Cyanide (HCN) is produced by burning plastic, foam, paint, wool, and silk.
Cyanide poisoning blocks the intercellular use of oxygen causing hypoxia and lactic acidosis
SIGNS AND SYMPTOMS: LOC, dilated pupils, seizures, hypotension, and high lactate levels
Rx: Vitamin B12 binds cyanide and is directly excreted in the urine
Stabilization of cardiopulmonary status improves hepatic clearance
Nitroprusside and Cyanide Poisoning
Seen with chronic administration (more than 72 hours) particularly with faster than 2mcg/kg/min, cyanide is produced faster than can be eliminated
NTP is a direct acting vasodilator, that acts by releasing NO
Rapid onset (within seconds) and rapid duration (1-3 minutes)
Reduces afterload and preload
Contains 5 cyanide ions within its chemical structure and its metabolism by plasma hemoglobin causes the release of these cyanide ions
chemical structure of sodium nitroprusside
Tx for nitroprusside induced cyanide poisoning
Discontinue infusion
Administer oxygen, treat metabolic acidosis
Sodium nitrate 3%, 4-6mg/kg over 3-5 minutes: promotes the production of methemoglobin so that excess cyanide ions can be bound
Sodium thiosulphate 150-200mg/kg over 15 minutes (every 2 hours as needed)
Other drugs uses: Hydroxocobalamin and Methylene Blue 1-2mg/kg may be useful
CO binds with hemoglobin with an affinity _________
200 times that of O2
CO shifts the oxyhemoglobin curve to the ____
LEFT
Clinical findings and treatment for carbon monoxide poisoning
Metabolic acidosis is the result of poor O2 delivery and poor utilization
Blood becomes cherry red
SaO2 is not accurate (false high reading)
Treatment with 100% FIO2 or hyperbaric oxygen
Symptoms of CO poisoning related to percentage in the blood
< 10%: none
10-20%: slight headache
21-30%: headache, slight increase in RR, drowsiness
31-40%: headache, impaired judgment, SOB, increasing drowsiness, blurred vision
41-50%: Pounding HA, confusion, marked SOB, marked drowsiness, increased blurred vision
> 51%: Unconsciousness, eventual death if victim is not removed from source of CO
1st degree burn
Involves epidermis
Superficial partial thickness 2nd degree burn
Involves epidermis and superficial dermis
Deep partial thickness 2nd degree burn
Involves epidermis and deep reticular dermis
3rd degree burn AKA ___
Full thickness
Involves epidermis and entire dermis
4th degree burn
Involving underlying structure (subcutaneous fat, muscle, bone)
How do we assess burn percentage?
Rule of 9s
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
Considerations for treating the burn patient
Resuscitation Phase
Airway
Fluid requirements
Abdominal Compartment Syndrome
Airway and burns
Fiberoptic bronchoscopy is the standard to evaluate airway injury
Tracheal intubation should occur early
Surgical airway increases the risk of pulmonary sepsis and late pulmonary complications and should be used as a last resort
Initial Airway Assessment
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 edema suspected, immediate intubation must be carried out. Mucosal edema can ensue rapidly, particularly with fluid resuscitation
Grading Scheme for Bronchoscopy Findings in Inhalation Injury
Grade 0: Findings = Normal (no injury) Mortality = 0%
Grade B: Findings = Positive based on biopsy only Mortality = 0%
Grade 1: Findings = Hyperemia Mortality = 2%
Grade 2: Severe edema and hyperemia Findings = Mortality = 15%
Grade 3: Findings = Severe Injury, Ulcerations, and Necrosis Mortality = 62%
Why do we intubate these patients early?
Glottis edema will worsen with fluid administration and over time
RSI with IV induction in the absence of airway abnormality
Succinylcholine safe in the first 24 hours not after
24hr-2years after injury – up regulation of acetylcholine receptors can lead to hyperkalemia and cardiac arrest
Non-depolarizing muscle relaxants Increased Dose
Up-regulation of acetylcholine receptors, fluid shifts significantly changing the volume of distribution and decreased receptor sensitivity
What is the pathophysiology behind burns and fluid loss?
Restoring blood volume after the airway has been secured improves chances of survival of burn victims
Burns lead to increase microvascular permeability which leads to capillary leak (becomes greater with major burn inhalational injury or a delay in resuscitation)
Capillary leak leads to edema
Protein rich fluid lost to interstitial space decreases plasma oncotic pressure
Loss of intravascular volume leads to hypovolemia and hemoconcentration
Fluid Management with Burns.. Dos and Donts
Edema and fluid shifts are greatest in the first 12 hours
No albumin in the first 24 hours
Hemolysis is common in the initial stage (hypovolemia and hemoconcentration)
An elevated HCT in the first 24 hours suggests inadequate fluid resuscitation
Transfuse < 20% if healthy, <30% if CV disease
Parkland Fluid Formula
First 24 hours:
4ml LR* X %TBSA burned X kg ½ in the first 8 hours ½ in the next 16 hours
No colloid
Second 24 hours: D5W maintenance and colloid
0.5ml* X %TBSA X kg
American Burn Association Fluid Formula
Adults: LR 2-4 ml * Kg weight * %TBSA burned
Children: LR 3-4 ml * Kg weight * TBSA burned
Formula for Minimum Urinary Output in Burn Patients
Adults: 0.5-1 ml/kg/hr.
Children (<30Kg): 1ml/kg/hr.
High voltage Electrical Injury: 1-1.5ml/kg/hr.
Fluid Creep
Excess fluid loading is termed fluid creep, common in burn patients
Can be the result of fluid miscalculation
Lack of vigilance
Increased use of sedation and analgesic agents
Excess crystalloid over colloid replacement
Associated with abdominal compartment syndrome
Abdominal Compartment Syndrome
Defined as an intraabdominal pressure > 20mmHg by transduction of bladder pressure and evidence of end organ dysfunction
Rx: NMBD, sedation, diuresis, abdominal decompression (ex. Lap)
Pathophysiologic Changes in the early phase of a burn (24-48 hours)
Pathophysiologic Changes in the hypermetabolic/late phase of a burn (>48 hours)
Hypermetabolic/Hyperhemodynamic Phase
Severe thermal injuries with burns over 40% of TBSA is followed by a pronounced hypermetabolic response that persists for up to 2 years
There is a 10-50 fold increase in catecholamine and corticosteroid levels that lasts for up to 9 months post burn
Increased metabolic rate, multi-organ dysfunction, blunted growth insulin resistance, and increased risk for infection
Pathophysiology of the Ebb phase
(first 24hrs)
Hypotension
Low CO
Metabolic acidosis
Hypoventilation
Hyperglycaemia
Low O2 consumption
Impaired thermoregulation
Pathophysiology of the Flow (catabolic) phase
Hypermetabolic phase
Increased CO
Increased HR
Better O2 consumption
Supranormal increases of temperature
Days to weeks
Pathophysiology of the Flow (anabolic) phase
Healing and rehabilitation
Anabolism
Normal function restores
Weeks to months
Transportation PEARLS for the burn patient
Bring transport bag and ambu bag (with all equipment for reintubation)
Transport Ventilator: If on high levels of PEEP, continue during transport and the OR
Clamp/occlude during disconnecting from circuit to minimize de-recruitment
Burn Patients are hypermetabolic for many reasons (e.g. sepsis, burn). Match minute ventilation from the ICU in the OR.
Utilize lung protective ventilation when appropriate
Confirm adequate pressors available for transport/starting the case. If not enough obtain prior to leaving or have pharmacy prepare and bring to the room.
Fluid resuscitation should continue during transport
Patients should have a free running IV line to administer medications
If on dialysis review electrolytes, pH, and volume status
Continue TPN during transport and intra-op
Confirm blood glucose prior to surgery
What are some reasons burn patients need blood?
loss from wound site
anemia (hemolysis or decreased RBC survival)
Reduced production of RBCs
How do we plan for transfusions for the burn patient?
Call for blood on arrival into the room
Begin transfusions ahead of blood loss
Blood loss can be rapid and be hidden in drapes and sponges
NEVER rely on the canisters
Labs may not reflect acute blood loss, so resuscitation has to be based on visual cues
Transfusion triggers HGB <7, INR>1.6 etc do not apply in acute blood loss
Transfusions should follow a 4:2:1 RBC:FFP:Plt ratio
OK to replace RBC and FFP in 1:1 ratio. Do not forget platelets in massive transfusion
Calculation for expected blood loss
You must know the # of days since the burn to calculate this
< 1 day = 0.45 ml/cm2 burn area
1-3 days: 0.65 ml/cm2 burn area
2-16 days: 0.75 ml/cm2 burn area
> 16 days: 0.5-0.75 ml/cm2 burn area
Infected Wounds: 1-1.25 ml/cm2 burn area
Ischemia of gut mucosa in burn patients can be caused by _____
an inflammatory stimulus or microvascular damage
GI issues that occur with burns
Acute gastric dilatation within 2-4days
Paralytic ileus – decompression with NG tube
Failure of enteral feeding and translocation of gut bacteria
Curling’s ulcer: stress-induced ulcer of the stomach or duodenum that occurs in relation to extreme physical stress (massively burned patients)
Abdominal compartment syndrome
Acute pancreatitis, acute acalculous cholecystitis
Pain Management for Burn Patients
Do NOT rely on inhalational anesthetics drips alone to provide pain relief
Multi-modal therapy:
Ketamine
Methadone (if QTc appropriate)
Lidocaine
IV Tylenol
Magnesium
Dexmedetomidine
Regional anesthesia
Post Burn Neck Contracture
Grossly restricted neck movements
Patients are likely to be malnourished, anemic and hypoproteinemia
Restricted mouth opening and narrowed nasal passages.
Difficult laryngoscopy and endotracheal intubation
Compromised airway
Poor oral hygiene in patients
Post Burn Neck Contracture Classification
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°
Up Regulation of extrajunctional receptors begins 24 hours after injury which is why we avoid _____
succinylcholine and NDNMB’s
Patients will most likely require multiple surgical procedures; avoid etomidate due to _____
adrenocortical suppression
Burn patients have impaired temperature regulation and are at high risk for _____
perioperative hypothermia
What is the primary mechanism of heat loss for burn pts?
evaporation
Hypermetabolic state from burns causes ____
increases catabolism O2 consumption HR and RR
