Burn Patient

what is the major cause of death in burn patients $ what is the main cause of death <48hrs Major risk factors of death

The major causes of death are multiple organ failure and infection -Sepsis from open wounds Main cause of early death ( <48 hours) is shock and inhalation injury. The major risk factors for death are: Older age (> 60 years) Extreme youngness of age (higher surface area to body wt. ratio) Percentage of body burned Comorbidities

what is responsible for most fire deaths and and smoke inhalation deaths how much more affinity does CO have to Hb what happens to the oxyheme curve what results what does the abg look like

CO 200x left shift hypoxia and met. acidosis acidotic w/ 100%sat

what is the primary indicator for fluid resuscitation $

UO

UO goal for: aduls children infants what should fluids contain for children

Adult: > 0.5 ml/kg/h -If urine output is > 1 ml/kg/h, slow the infusion -Pts. with high-voltage electrical burns > 1-1.5 ml/hr. Children: > 1 ml/kg/h Infants < 1 y/o: > 1-2 ml/kg/h -dextrose

CO treatment

*100% oxygen (Face mask or ETT)* In ambient air (21% oxygen) the half-life of the COHgb complex is approximately 4-6 hours Compared with approximately 75 minutes using 100% oxygen at sea level pressure (1 atmosphere), also referred to as "normobaric oxygen" (NBO). Rx until HbCO level is <5% or 6 hrs. of 100% Ox High FiO2 accelerates the dissociation of HbCO by 50% every 30 min

ml of blood loss per 1% TBSA excised what should be ready before surg avg. of amount transfused for each % TBSA factors that increase or decrease blood loss: excission technique age of burn location

125-400ml T&C and blood 20ml decrease: fascial, fresh, torso increase: tangential, older, hands feet shoulders scalp

rule of 9s for adults

18% front of torso 18% back of torso 9% front of leg 9% back of leg Whole arm or head is 9% Used as a tool to calculate burn percentage and as a calculating factor in fluid replacement

when does the second phase of airway inhalation injury begin caused by what what increases mortality

24-96hrs after inj Results from pulmonary parenchymal damage caused by the chemical irritation and smoke inhalation pneumonias

%HbCO level and s/s

<15% Rarely any s/s 10-20% Headache, tinnitus, confusion 20-30% Nausea, fatigue, disorientation, visual changes 40-60% Hallucinations, combative, convulsion, coma, CVS instability, shock >60%Weak pulse, apneas, Death (>80% death in 1 hr.)

Phase 1 of burn

Burn Shock Decreased Cardiac Output -Occurs almost immediately -?? Cause—release of tissue factors from damage= decreased myocardium -A large TBSA burn often results in a rise in troponin independent of cardiac injury Intravascular fluid shift of plasma into the interstitial space ('relative' hypovolemia) -Onset of protein catabolism to meet this need Release of cytokines resulting in immunosuppression and inflammation Intravascular volume must be aggressively replaced to prevent end-organ damage and tissue hypo-perfusion Use of the Parkland or Brooke formula to guide fluid replacement needs

what happens to ACH receptors on muscles after burn when does this happen and how long does it last dose for NDMR

Burn injury cause Ach receptor proliferation -Develops within one week and persist for 18 mo. after burn heals Patients with burns > 25% TSBA are often resistant to non-depolarizers May take months to years to return to normal pre-burn response Marked resistance when burn is 30-40% TBSA -Require larger dose- 2-5 fold increase! -Duration of action is shorter -Monitor neuromuscular function

sux and burns

Burn injury🡪 denervation of tissue🡪 entire skeletal membrane develops excess Ach receptors -Succinylcholine🡪 exaggerated number of Ach receptors depolarize🡪 massive efflux of K from the cell into ECF -Defasciculating dose of NDMR does not prevent hyperkalemia -Hypersensitivity to succinylcholine: --Begins 24 hours after burn; Peaks 1-3 weeks --Succinylcholine is acceptable to use in the initial 24-48 hrs. post burn; should be avoided for 2 years after skin has completely healed. --Actual length of time for the risk of hyperkalemia is unknown. --Contraindicated in electrical burns since the pt. is already hyperkalemic from extensive muscle and tissue destruction

when do you change the CVC in burn pts non burn pts can you do a wire exchange?

Change line q 72 hrs. if line is placed through burned tissue Change line q 7 days if line is placed in a site remote from burn tissue No wire changes are performed

UO for children and adults what causes Coagulopathy and Thrombocytopenia in burns $

Children adequate urine output is 1 ml/kg/hr Adults adequate urine output is 0.5 ml/kg/hr dilutional effect from fluid admin

what can happen to children after 24hrs onset effects cause how long does it last

Children with extensive burns can become hypertensive requiring medication (around 30% of them) Onset is usually within the first 2 weeks Untreated may develop hypertensive encephalopathy (seizures, irritability) Cause is unknown May persist for up to 2 years

effects on albumin and alpha1-acid glycoprotein effects what drugs when is fluid loss the greatest $

Decreased albumin (benzos dilantin) Increased alpha1-acid glycoprotein (AAG) lidocaine, Demerol, propranolol *first 12hrs and stabalizes after 24hrs*

layers of skin which on is avascular which regulates body temp

Epidermis Outer most, thin, avascular Water proof barrier (keeps fluids in) Keratin, melanocytes 2. Dermis Beneath the epidermis Tough connective tissue, hair follicles, nerves, blood vessels, sweat glands 3. Hypodermis (Subcutaneous) Deeper Fat, lymphatics, connective tissue Regulates body temperature

5 types of burns

Heat/Thermal (house fires, scalding, fireworks) *Chemicals (strong acids or bases, bleach, cleaners) *Electricity (voltage, lightning) Radiation (UV light, sun, tanning booths, microwave, arc welding, nuclear) Friction (drag, rub, wind)

Phase 2 of burn

Hypermetabolism Massive catecholamine/corticosteroid surge (50x > nonburn levels)🡪 Hypermetabolic response develops 48-72 hrs. post-burn -Increased myocardial O2 consumption -Increased cardiac work -Persistent tachycardia (110-120) -Hypertension -Increased muscle protein degradation -Insulin resistance/hyperglycemia -Hyperthermia -Liver dysfunction Cardiac Output can increase by 150% and can stay up for 2 years!! Proteins and amino acids are metabolized from muscle to meet metabolic demands🡪 loss of lean body mass, week immune function, decrease wound healing

indications for immediate intubation

Inhalational injury with airway obstruction or impending airway obstruction Cardiovascular instability CNS depression *Massive burns >60% TBSA*

GI effects caloric requirements how should pt get nutrients what can they develop and how to prevent

Injury induced GI mucosal atrophy (occurs within 12 hrs.) -Alteration in digestive absorption—ileus is common -Decreased intestinal blood flow -Increased intestinal permeability Pts. with burns are very catabolic Caloric requirements for a patient with a 40% thermal injury are estimated to be 132% higher than basal energy expenditure; compared with a 70% increase for sepsis and a 25% increase for major elective surgery -*Require intensive nutritional support* -*Should enteral feed on day one and continue pre-op* Development of Cushing's ulcer from stress is common Prophylactic treatment with H2 blockers

abdominal compartment syndrome def who's at risk treatment

Intra-abdominal pressure >20mmHg AND evidence of organ dysfunction -Hemodynamic instability, oliguria, increased PIP Who's at Risk: Pediatrics with burns Adults with circumferential abdominal burns Patient receiving IV fluids >6 ml/kg/%TBSA Any big deep burn escharotomy fasciotomy laparotomy

classification of a major burn

Is a second-degree burn involving more than 20% of the TBSA in adults or 10% in extremes of age (elderly and babies/toddlers) A third degree burn involving more than 10% of the TBSA in adults ANY electrical burn A burn complicated by smoke inhalation significant burn to face, hands, feet, and/or joints

fluid resuscitation: preferred solution colloids? what are acceptable hcts

LR unless kidney failure avoid in first 24- increased cap. permiability will cause to leak out Death is higher when used; blood is not usually given unless HCT is <20% in healthy pts. requiring limited surgeries HCT is ~25% in healthy pts. but need extensive procedures HCT is 30% in pts. with preexisting cardiovascular diseas

acute fluid resuscitation 24-48hrs is more better? primary goal? When do fluid requirements start do you usually give blood what is a rising Hgb a sign of

Massive Fluid Resuscitation Pts. should receive the least amt. of fluid necessary to maintain adequate organ perfusion, cardiac output, and urine output *Primary goal- maintain U.O. rather than restoring* *intravascular euvolemia* Continual assessment and fluid titration to avoid over or under resuscitation *Fluid requirements start at the time of injury, including* *the amounts given pre-hospital* Blood products typically not required in this phase Hemolysis is common during the initial stage, but hypovolemia🡪 hemoconcentration *A rising Hgb in the first few days suggest inadequate* *volume resuscitation*

formulas to calculate fluid resuscitation 2 who dont these work for? timeframe for fluid admin where should base defecit be

Modified Brooke Formula 2 ml/kg (body wt.) / % TBSA burned i.e. 2 ml x 70 kg x 50 = 7,000 ml (first 24 hr. period) Parkland Formula 4 ml/kg (body wt..) /% TBSA burned i.e. 4 ml x 70 kg x 50 = 14,000 ml (first 24 hr. period) Formulas work best in adults. Especially poor with children <10 kg. used in first 24hrs -1/2 over 8hrs -1/2 over 16hrs Base def <2

rule of 9s babies/toddlers

The infant/toddler head is 18% Thorax/abdomen is 18% on each side whole arm 9% each leg 14% The skin to visceral component ratio is greater in small children

silver sulfadiazine and mafenide acetate characteristics

Silver sulfadiazine ? -less painful to apply but does not penetrate intact burn eschar -may also cause significant leukopenia, typically in the first few days of use Bacitracin, neomycin, polymyxin Mafenide acetate penetrates burn eschar but can be painful to apply patients with large burns or renal failure, a hyperchloremic metabolic acidosis is occasionally seen that may be attributable to the mafenide acetate cream and may not resolve until the drug use is discontinued

characteristics of electrical burns what should you monitor for what should you avoid $

Similar to thermal injuries, with a few distinctions Often little damage on the skin, but may have extensive underlying tissue destruction, resulting in extensive muscle necrosis🡪 Myoglobinemia 🡪 risk ARF Potassium, creatine phosphokinase, blood urea, and creatinine levels must be monitored Myoglobin is nephrotoxic; needs to be flushed out of the body No matter how small the injury, monitor pts. for cardiac arrhythmias for 24 h, even though significant arrhythmias are rare *Avoid succinylcholine even in the immediate injury* *phase*

what is fluid creep adverse outcomes

Too much IV fluid volume given beyond what's needed -Calculation errors (overestimation) -Hemodynamics changes related to sedation and not volume Adverse outcomes of Fluid creep -Intra-abdominal compartment syndrome 🡪 -Pulmonary complications 🡪 -Organ dysfunction 🡪 -Increased morbidity and mortality

Systemic Inflammatory Response Syndrome (SIRS) what when hormones involved how long does it last treatment

Systemic inflammatory syndrome is noted after a burn victim survives the initial 48 hours Burn injury induces a catabolic and hypermetabolic state: -Significant elevated levels of catecholamines -Hyperglycemia and insulin resistance -Glugogon, glucocorticoids -ADH, renin, angiotensin Can persists for several weeks-months, gradually receding to normal when the wound healing is well underway Insulin infusion: *Titrated to BS 130-150 mg/dl decreases M&M*, reserves muscle, decrease infection, and length of stay Treat to reduce the metabolic rate not over sedation Beta blocker

why should you use NSAIDs with caution

bleeding and renal failure inhibit synthesis of thromboxane A, resulting in failure of platelet aggregation, with potentially disastrous effects on hemostasis

what is a late sign of CO exposure What SaO2 would correlate to HbCO 20%

cherry red skin (doesnt always happen) 80%

cyanide toxicity s/s treatment half life

confused/comatose lactic acidosis blood level>.2mg/l 100%O2 1hr

what can soot in mouth be an indicator of how long can inhalation injury take to show up on xray are prophylactic antibiotics beneficial

edema and obstruction 24hrs no

myoglobinuria is most common in what burn $ When does hyper and hypokalemia happen

electrical Hyperkalemia early from tissue necrosis in the first 2 days Hypokalemia later in the course from diuresis

when is hyperbaric O2 used

history of loss of consciousness metabolic acidosis COHgb >25% age >50 years Or the presence of cerebral abnormalities on neurologic examination if burn >40% dont use if it will delay fluid resuscitation

what happens to svr in burns

massive vasoconstriction

can you continue tube feedings through surg? $

only in the secured airway