Pathophysiology of Burn Shock and Review of Resuscitation

Liwei Ren

Anaesthetic Trainee

Concord Hospital 2014

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In this burn presentation

• Pathophysiology of burn shock• Adult fluid resuscitation• Monitoring of burn shock resuscitation

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Burn Shock

• Cutaneous thermal injury involving more than one-third (even 20-25%) of the total body surface area (TBSA) results in the severe and unique derangements of cardiovascular function known as burn shock.

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Pathophysiology of burn shock

• Intravascular volume depletion due to massive oedema formation:- Decreased (negative) interstitial pressure- Increased microvascular permeability- Increased capillary hydrostatic pressure- Decreased intravascular oncotic pressure- Relative increased interstitial oncotic pressure

• Myocardial depression - Circulating humoral factors eg TNF α, decreased coronary blood flow and an attenuated response to both endogenous and exogenous catecholamines

• Cellular changes -decrease in cell transmembrane potential, involving non-thermally injured cells as well

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Jackson’s Burn Wound Model zone of coagulation- irreversible tissue necrosis at the centre of the burn due to exposure to heat, chemicals or

electricity

intermediate zone — stasis of blood flow

peripheral zone - vasodilatation, increased blood flow and hyperaemia

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Estimation of Burn Size and Depth

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Fluid resuscitation by Parkland Formula in first 24 hours

4 ml/kg/ % TBSA burned(2nd and 3rd degree )50% of the volume during the first 8 hours, commence at the time of burn, not

from the time of presentation, 50% in the next 16 hours Example:70 kg man with 50% TBSA burn: 2h post burns

4 mL × 70 kg × 50% = 14,000 mL7 liters first 8 hours 7 liters over next 16 hours

so in the first 6h, 7000ml/6Hartmann’s

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• Resuscitation fluid - evidence still conflicting

• Crystalloid- CSL is most commonly used

• Slightly hypotonic compared with plasma, it effectively treats both hypovolemia and extracellular sodium deficits caused by thermal injury

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Crystalloid or Colloid

Many formulae used

• No evidence of improved outcome with early colloiduse - Cochrane Collaboration 2006

• No evidence of improved outcome with earlyhypertonic saline use - Cochrane Collaboration 2006

• No evidence of improved outcome with albumin inburns resuscitation - Cochrane Collaboration 2006

•Albumin not harmful, it actually conferred a mortality benefit in their study that confirmed on multivariate analysis -Cochran A 2007

Cochran A,Morris SE, Edelman LS, Saffle JR: Burn patient characteristicsand outcomes following resuscitation with albumin. Burns 2007, 33:25-30.

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Burn resuscitation review

Frederick

• Limit crystalloid administration with protocol-based use of vasoactive drugs and colloidsin patients failing to respond to the initial resuscitation

• Crystalloid administration is capped at 100mL of fluid/kg with second and third degree injury. When this physical limit is reached, a transition is made to colloids regardless of the time since injury.

Frederick W. Endorf, MD is Staff Surgeon at RegionsHospital, the Level I Trauma and Burn Center, in St.Paul, Minnesota, USA.

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FFP?

Frederick W. Endorf

Use fresh frozen plasma (FFP) as a part of our resuscitation strategy when crystalloid volumes exceed 100 mL/kg

FFP is administered at 0.5mL/kg/%TBSA, transfused over 8 hours.

controversial

Frederick W. Endorf, MD is Staff Surgeon at RegionsHospital, the Level I Trauma and Burn Center, in St.Paul, Minnesota, USA.

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In the second 24 hours

• colloid fluids can be used • 0.5ml of 5% albumin x kg x % burn

• recommended in 2013-2014 Emergency management of Severe Burns (EMSB) by Australian and New Zealand Burn Association

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ABA for Acute Burn Resuscitation 2008

• The addition of colloid-containing fluid following burn injury, especially after the first 12 to 24 hours post burn, may decrease overall fluid requirements

• Hypertonic saline should be reserved to providers experienced in this approach. Plasma sodium concentrations should be closely monitored to avoid excessive hypernatremia.

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Factors that increase resuscitation fluid requirements

• Inhalation injury•Delay in resuscitation•Electrical injury•Deep burns•Associated soft tissue injuries

- dehydration firefighter, intoxicated patients - escharotomy or fasciotomy - patients on home diuretic therapy preexisting free-water

deficits

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Danger of Fluid Creep

• Abdominal compartment syndrome

• Pleural effusions, pulmonary edema, ARDS

• Tissue oedema will decrease tissue oxygen delivery, loss of viable tissue in zone of stasis and thus increased TBSA of burn

• Extremity compartment syndrome - escharotomies

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Physiological endpoints for adequate fluid resuscitation- HUO

• Adequate urine output 0.5 mL/kg/h= 30-50ml/h

- if UO is not adequate, give boluses of 5-10ml/kg or increase the next hour’s fluid to 150% of planned volume

- if haemoglobinuria, increase UO to 2ml/kg/h, consider Mannitol 12.5g over 1 hour

• Complicating factors exist with monitoring urine output

- glycosuria can result in an osmotic diuresis ,performing a urinalysis at some point during the first 8 hours

- older patients with long-standing diuretic use may be dependent on diuretics and may not be able to maintain a desired urine output despite what appears to be an adequate resuscitation volume.

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Endpoints for adequate fluid resuscitation

• MAP>70 NIBP, Art line

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Endpoints for adequate fluid resuscitation

• ABG PH<7.35• Base deficit <5

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Endpoints for adequate fluid resuscitation

• Blood lactate <2 mmol/L

Cochran A, 2007 found that the non-survivors had higherlactates at admission, 12, 18, and 24 hours than thegroup of survivors. Elevation of lactate in the first 48hours was an independent predictor of mortality, butthey were unable to demonstrate a specific threshold forclinical use.

The relationship between serum lactate and base deficit in burn patients to mortality. J Burn care Res 2007, 28:231-240.

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Endpoints for adequate fluid resuscitation

• Cardiac index (4.5 L/min per m2)

• Oxygen delivery index (DO2I) (600 mL/min per m2)

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Physiological endpoints for adequate fluid resuscitation- debatable

• Central venous pressure or pulmonary capillary wedge pressure

- correlate poorly with circulating blood volume, especially during positive-pressure ventilation

- factors as pulmonary vasoconstriction, the same interpretive problems are true for central venous pressure measurements

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Who needs invasive cardiovascular monitoring?

• not used routinely in burned patients to guide volume resuscitation

• underlying cardiovascular disease

• non-responders

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Endpoints for adequate fluid resuscitation

Arlati S 2007 resuscitation to ITBV end points using the PiCCO rather than to urine output could actually lead to less fluid administration, less oedema formation and less organ dysfunction. This was termed ‘permissive hypovolaemia’.

Arlati S, Storti E, Pradella V, Bucci L, Vitolo A, Pulici M. Decreased fluid volumeto reduce organ damage: a new approach to burn shock resuscitation? Apreliminary study. R . esuscitation 2007;72:371–8. 25

TPTD by PiCCO system (Pulsion Medical Systems, Munich, Germany)

• Holm and colleagues observed that ITBV, but not central venous and pulmonary capillary occlusive pressure, correlated with cardiac index and oxygen delivery during fluid resuscitation of burn patients.

• The use of ITBV to successfully restore cardiac index in this series was associated with significantly larger volumes than predicted by the Parkland formula.

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PiCCO

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Consequence of the use ofITBVI as an endpoint

• Increased fluid volumes, most of which are deliveredduring the first 8 h

• The total increase in fluid volume (ITBVI guided) compared with the Parkland strategy in their control group was 4.7–5.7 ml/kg/TBSA%.

• Most of the extra fluid (58%) was given during the first 8 h

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Summary

• Burn shock

- Intravascular volume depletion

- Interstitial oedema

- Myocardial depression

• Parkland formula – only a guide

• Colloid and crystalloid are both used

• Monitoring adequate resuscitation – historical and current tools

Thank you

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reference 1. Csontos C, Foldi V, Fischer T, Bogar L. Arterial thermodilutionin burn patients suggests a more rapid fluidadministration during early rescitation. Acta AnaesthesiolScand 2008; 52: 742–749.

1. Csontos C, Foldi V, Fischer T, Bogar L. Arterial thermodilutionin burn patients suggests a more rapid fluidadministration during early rescitation. Acta AnaesthesiolScand 2008; 52: 742–749.

1. Csontos C, Foldi V, Fischer T, Bogar L. Arterial thermodilutionin burn patients suggests a more rapid fluidadministration during early rescitation. Acta AnaesthesiolScand 2008; 52: 742–749.

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16 Holm C, Mayr M, Tegeler J, et al. A clinical randomized study on the effects of invasive monitoring on burn shock resuscitation. Burns. Dec 2004;30(8):798-807. [Medline].

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