Transport considerations when caring for the severely burned patient.

2. Transport Considerations of
the Burned Patient
Gustavo E. Flores, MD EMT-P

3. Objectives
• Classification of burns
• Initial resuscitation
• Transport considerations

4. Etiologies
• Based on the mechanism of injury:
• scalds,
• contact burns,
• fire,
• chemical,
• electrical, and
• radiation.

5. Classification
• 1st Degree (superficial)
• 2nd Degree (partial thickness)
• 3rd Degree (full thickness)
• 4th Degree (subdermal)
• Routinely underestimated during the initial examination.
• Devitalized tissue may appear viable for some time after injury
• Some degree of progressive microvascular thrombosis is observed on the
wound periphery.

6. 1st Degree / Superficial
• Usually red, dry, and painful.
• Burns initially termed first-degree are often actually superficial
second-degree burns, with sloughing occurring the next day.

7. 2nd Degree / Partial Thickness
• Second-degree burns are often red, wet, and very painful.

8. 3rd Degree / Full Thickness

9. 4th Degree / Subcutaneous
• Fourth-degree burns involve underlying subcutaneous tissue, tendon,
or bone.

10. Estimating Burn Size
• Accurate estimate is important.
• (Size does matter.)
• Lund-Browder diagram (age-specific)
• Rule of 9
• Palm of patient’s hand

11. Initial Burn Size and Depth
• Outside reports are notoriously unreliable.
• Correctly estimated only 1/3 of times.
• Leads to over-resuscitation.

12. Systemic inflammatory response (1/4)
• When TBSA > 30%, cytokines and other mediators are released into
the systemic circulation, causing a systemic inflammatory response.
• Because vessels in burned tissue exhibit increased vascular
permeability, an extravasation of fluids into the burned tissues occurs.
• Hypovolemia is the immediate consequence of this fluid loss, which
accounts for decreased perfusion and oxygen delivery.
• In patients with serious burns, release of catecholamines,
vasopressin, and angiotensin causes peripheral and splanchnic bed
vasoconstriction that can compromise in-organ perfusion.
• Myocardial contractility also may be reduced by the release of
inflammatory cytokine tumor necrosis factor-alpha.

13. Edema Formation (2/4)
• At the peak of edema formation, essentially all whole blood elements up to the
size of RBCs are able to transmigrate through the vessel wall in burned tissue.
• As a result of this capillary leak, replacing the intravascular
deficits drives the continued accumulation of edema.
• Nearly 50% of infused crystalloid volume lost to the interstitium.
• As the burn size approaches 15-20% total body surface area (TBSA), shock sets in
if the patient does not undergo appropriate fluid resuscitation.

14. Edema Formation (3/4)
• The peak of this third-spacing occurs at some point 6-12 hours postburn as
the capillary barrier begins to regain its integrity.
• Hence the reduction in fluid requirements observed in resuscitation formulas around
this point.
• At this point, the theoretic benefits of adjuvant colloid therapy during the
resuscitation allow the careful downward titration of fluid administration to
reduce the obligatory edema.

15. Systemic inflammatory response (4/4)
• Hemolysis may occur in deep 3rd deg burns.
• PRBC to HCT of 30-35
• Decrease in pulmonary function can occur in severely burned patients
without evidence of inhalation injury from the bronchoconstriction
caused by humoral actors, such as histamine, serotonin, and
thromboxane A2.
• Burned skin  increased evaporative water loss  heat loss 
hypothermia.

16. Patient Evaluation
• Primary Survey: ABCDE
• Secondary Survey: Hx and Physical Exam (burn-
specific)
• Determination of mechanism of injury,
• Presence or absence of inhalation injury and carbon
monoxide intoxication,
• Examination for corneal burns,
• Consideration of the possibility of abuse, and
• Detailed assessment of the burn wound
• Imaging studies
• Laboratory studies

17. Vital Signs
• Very difficult to interpret in patients with large burns.
• BP ok due to catecholamine release despite extensive intravascular
depletion.
• Edema limits usefulness of NIBP.
• Arterial line measurements limited by peripheral vasospasm from
high-cathecolamine state.
• Tachycardic due to pain and high adrenergic state, not just
hypovolemia.
• Following a trend is much more useful than any single reading.

18. Fluid Resuscitation
Parkland Formula
mL in 24 hrs

19. Caution
• Not all burns require use of the Parkland formula for resuscitation.
• Adult with < 15-20% TBSA without inhalation injury does not require
Parkland Formula.
• Not enough to initiate the systemic inflammatory response.
• These patients can be rehydrated successfully primarily via the oral route with
modest IV fluid supplementation.

20. Parkland Formula
4 mL x BSA x kg
• 50% in first 8 hrs
• 50% in remaining 16 hrs
• Example: 4 x 45 BSA x 100 kg = 18,000 mL (24 hrs)
• 9,000 mL in 1st 8 hrs
• 1,125 mL per hour (1st 8 hrs)

21. Adequate Fluid Resuscitation
• Urine output
• Adults 0.5 – 1 mL / kg / hr
• Peds 1 mL / kg / hr
• If myoglobinuria and/or rhabdomyolysis
suspected?
• 1 – 1.5 mL / kg / hr

22. Ringer Lactate
• NaCl
• Ringer Lactate 130 mEq/L
• Normal Saline 154 mEq/L
• pH
• Ringer Lactate 6.5
• Normal Saline 5.0
• Plasmalyte?

23. Hypoperfused?
• Failure to meet these goals should be addressed with gentle upward
corrections in the rate of fluid administration by approximately 25%.
• Frequent boluses result in transient elevations in hydrostatic pressure
gradients that further increase the shift of fluids to the interstitium and
worsen the edema.
• However, do not hesitate to administer a bolus to patients as appropriate early
in the resuscitation for hypotensive shock.

24. Hyperperfused?
• Avoid urine output at rates > 0.5 - 1 mL / kg / h.
• Fluid overload in the critical hours of early burn management leads to unnecessary
edema and pulmonary dysfunction.
• It can necessitate morbid escharotomies and extend the time required for ventilator
support.

25. Even More Fluids
• Inhalation injuries sometimes as much as 30-40% higher (close to 5.7 mL/kg
x BSA)
• Delays in initiating resuscitation promptly have also been shown to increase
fluid requirements by as much as 30%, presumably by permitting the
occurrence of an increased inflammatory cascade.
• Home diuretic therapy frequently have preexisting free-water deficits in
addition to burn shock.
• Escharotomy or fasciotomy can substantially increase free water loss from
the wound.
• Electrical burns, associated with large and underappreciated tissue insult

26. Formula Fluid in First 24 Hours Crystalloid in Second 24-Hours Colloid in Second 24-Hours
Parkland RL at 4 mL/kg per percentage burn 20-60% estimated plasma volume Titrated to urinary output of 30 mL/h
Evans[2]
NS at 1 mL/kg per percentage burn, 2000 mL
D5W*, and colloid at 1 mL/kg per percentage
burn
50% of first 24-hour volume plus 2000 mL D5W 50% of first 24-hour volume
Slater[2] RL at 2 L/24 h plus fresh frozen plasma at 75
mL/kg/24 h
Brooke[2]
RL at 1.5 mL/kg per percentage burn, colloid at
0.5 mL/kg per percentage burn, and 2000 mL
D5W
50% of first 24-hour volume plus 2000 mL D5W 50% of first 24-hour volume
Modified Brooke RL at 2 mL/kg per percentage burn
MetroHealth
(Cleveland)
RL solution with 50 mEq sodium bicarbonate per
liter at 4 mL/kg per percentage burn
Half NS titrated to urine output
1 U fresh frozen plasma for each liter of half NS
used plus D5W as needed for hypoglycemia
Monafo hypertonic
Demling[22, 23]
250 mEq/L saline titrated to urine output at 30
mL/h, dextran 40 in NS at 2 mL/kg/h for 8 hours,
RL titrated to urine output at 30 mL/h, and fresh
frozen plasma 0.5 mL/h for 18 hours beginning 8
hours postburn
One-third NS titrated to urine output
*D5W is dextrose 5% in water solution
Table 2. Resuscitation Formulas

27. Pediatrics
• Burns < 15% BSA are not associated with an
extensive capillary leak.
• Fluid resuscitation = 150% maintenance rate
• And continuous monitoring of fluid status.
• In smaller children, low hepatic glycogen reserves
can be exhausted quickly:
• Hypoglycemia is a threat. Monitor every 4-6 hrs.
• Ringer lactate solution with 5% dextrose should be
added at a maintenance rate.

28. Pain Control
1. Morphine @ 2mg increments up to 20 mg max;
2. Ativan @ 1-2 mg increments up to 4 mg max.;
3. Fentanyl @ 1-3mcg/kg or 50-200 mcg IV q 30-40 minutes;
4. Propofol (Diprivan) @ 5 mcg/kg/min
• Increase 5-10 mcg/kg/min to max of 80 mcg/kg/min.
• Maintenance rate @ minimum 25-50 mcg/kg/min;
5. If patient is wheezing administer: Albuterol 2.5/3 cc with repeat
prn and if pt. is intubated administer in-line;

29. Circunferential Burns
• Neck = INTUBATE NOW.
• Chest
• Interferes with ventilation.
• Extremity
• Progressive edema leads to poor chest wall compliance.
• Extremity escharotomies
• As soon as peripheral perfusion is threatened.
• Do not wait until the extremity is overtly ischemic.
• Torso escharotomies
• As soon as ventilation appears compromised.

30. Monitor Electrolytes
• Hyponatremia can lead to cerebral edema and seizures.
• Rapid correction of hyponatremia may result in central pontine
demyelinating lesions.

31. Take-home
•Airway deteriorates over time. Consider early intubation.
•Breathing may become difficult if patient is awake and has low
chest wall compliance. Manage pain aggressively.
•Circulation is very labile. 4 mL x BSA x kg. Keep an eye on BP and
urine output if using multiple analgesics and sedation.
•Disability is due to low perfusion unless TBI is also suspected.
•Exposure is critical to re-evaluate extent. Prevent hypothermia.

32. References
• Initial Evaluation and Management of the Burn Patient
• http://emedicine.medscape.com/article/435402-overview#showall
• Burn Resuscitation and Early Management
• http://emedicine.medscape.com/article/1277360-overview#showall

34. Thank you!