2. BURNS
• Wounds caused by exposure to:
• Excessive heat
• Chemicals
• Fire/steam
• Radiation
• Electricity
Ravishankar J et al. Int J Res Med Sci. 2016 Dec;4(12):5364-5371
3. Calculation of Burned Body Surface
Area
• Superficial burns are not involved in the calculation
• Lund and Browder Chart is the most accurate
because it adjusts for age
• Rule of nines divides the body – adequate for initial
assessment for adult burns
Ravishankar J et al. Int J Res Med Sci. 2016 Dec;4(12):5364-5371
5. Rules Of Nines
• Head & Neck = 9%
• Each upper extremity (Arms) = 9%
• Each lower extremity (Legs) = 18%
• Anterior trunk= 18%
• Posterior trunk = 18%
• Genitalia (perineum) = 1%
Ravishankar J et al. Int J Res Med Sci. 2016 Dec;4(12):5364-5371
6. Magnitude of the burns problem
• A severe burn will significantly alter haematologic
parameters.
• This manifests as anaemia, which is commonly found in
patients with greater than 10% total body surface area
(TBSA) involvement
• In India
• According to National Crime Records Bureau (NCRB)
reports, total accidental deaths in 2013 were 4,00,517 of
which total deaths due to accidental fires are 22,177
(6.6%)
• Burns are the second commonest cause of injuries after
road traffic accidents
Ravishankar J et al. Int J Res Med Sci. 2016 Dec;4(12):5364-5371
7. Magnitude of the burns problem
• Even though 90% of burns are preventable
• 10% of these burn injuries are life-threatening
• 50% of the hospitalized patients die of their injuries
• Nearly 70% of burn victims are in the 15 to 40 age
group
Ravishankar J et al. Int J Res Med Sci. 2016 Dec;4(12):5364-5371
8. Definition of Anaemia
• World Health Organization (WHO) defines anaemia
as a
• Adult male
• Haemoglobin value of <13 g/dl (haematocrit <39%)
• Adult non-pregnant female
• Haemoglobin value of <12 g/dl (haematocrit <36%)
Curinga G et al, b u r n s 3 7 ( 2 0 1 1 ) 7 4 2 – 7 5 2
9. Causes Of Anaemia In Burn Patients
• Decrease In Production
• Delayed decreased erythropoiesis
• Increase In Destruction
• Thermal injury
• Injury related coagulopathy
• Hypotermic coagulopathy
• Thrombocytopenia
• DIC
Curinga G et al, b u r n s 3 7 ( 2 0 1 1 ) 7 4 2 – 7 5 2
10. Causes Of Anaemia In Burn Patients
• Increase In External loss
• Wounds
• Iatrogenic
• Initial excision, multiple
• debridements
• Donor site bleeding
• Phlebotomy/lab draw
Curinga G et al, b u r n s 3 7 ( 2 0 1 1 ) 7 4 2 – 7 5 2
11. Management of anaemia in the burn
patient
• Criteria for the optimal management of anaemia in
trauma and burn patients are poorly defined
• Management of anaemia in burn patients must follow
a two-pronged approach:
• Treatment
• Prevention
Curinga G et al, b u r n s 3 7 ( 2 0 1 1 ) 7 4 2 – 7 5 2
12. Blood and blood products
• Whole Blood
• Obtained from human donors by venesection and is
collected into a sterile, disposable plastic pack
• Blood Components
1. Red Cell Concentrate (Packed Red Cells)
• Prepared by allowing the blood to separate under gravity
or by centrifuging
2. Red Cell Suspension
• Prepared by adding an additive diluent solution
formulated for the best preservation of red cells.
Madhusudan et al, Indian J. Anaesth. 2003; 47 (5) : 388-395
13. Blood and blood products
3. Leucocytes
• Removal of these cells from other blood products can
reduce the incidence of febrile reactions and the risk of
transmitting cytomegalovirus (CMV) and other
intracellular infectious agents by transfusion.
4. ‘Buffy Coat’ depleted red cells
• Leucocytes and most of the platelets remain in a layer
called the ‘buffy coat’ that forms the interface between red
cells and plasma.
5. Leucocyte depleted red cells
• Special leucocyte filters are used to remove virtually all
leucocytes at the time of transfusion
Madhusudan et al, Indian J. Anaesth. 2003; 47 (5) : 388-395
14. Blood and blood products
6. Plasma
7. Platelet Concentrates
• Platelets are generally separated from pooled plasma
8. Plasma Fractionation
• Albumin, coagulation factors and immunoglobulins are
obtained from plasma by fractionation
Madhusudan et al, Indian J. Anaesth. 2003; 47 (5) : 388-395
15. Transfusion Trigger in Burn
• Restrictive is giving less blood, at a lower Hb, lower
target Hb level, 7-8 g/dl
• Liberal is giving more blood at a higher Hb level, 9-
10 g/dl
Curinga G et al, b u r n s 3 7 ( 2 0 1 1 ) 7 4 2 – 7 5 2
16. Evidence Supporting Restrictive
Strategy
• TRICC
• Restrictive strategy is as safe as liberal in stable non-
bleeding critically ill patients.
• 30 day mortality was reduced in younger (age <55) P-0.03
and less sick patients (APACHE<20) P-0.02 with reverse
trend in IHD patients.
• 2 big observational studies
• ABC in Western Europe (146 units/ 3534 patients) and
CRIT in USA (284 units/ 4892 patients), increase mortality,
ITU and hospital LOS
• TRACS trial (JAMA 2010)
• Single Centre study in elective CABG patients showed
increase in 30 day mortality and risk of serious infection
by 20% after every unit of RBC (P=0.007)
Curinga G et al, b u r n s 3 7 ( 2 0 1 1 ) 7 4 2 – 7 5 2
17. Evidence Supporting Restrictive
Strategy
• Cochrane review (2012)
• 19 RCTs, 6264 patients across various clinical settings,
restrictive transfusion trigger is associated with fewer
transfusions without adverse association with mortality, cardiac
morbidity, functional recovery or hospital LOS
• (Rohde 2014)
• 18 RCTs, 7593 patients concluded that restrictive transfusion
strategy was associated with fewer health care associated
infections
Curinga G et al, b u r n s 3 7 ( 2 0 1 1 ) 7 4 2 – 7 5 2
19. Evidence Supporting Liberal Strategy
• Carson et al, 2013
• MINT trial, 110 patients with stable angina and ACS
undergoing cardiac catheterisation.
• Vincent et al, 2008
• SOAP investigators, observed improved survival in
critically ill septic patients with liberal strategy after
extended cox hazard analysis. (P-0.004)
• Park et al 2012
• Propensity matched analysis of CAP with septic shock, RBC
transfusion was associated with lower risk of 7 day
(P<0.001), 28 day (P=0.007) and in hospital mortality (P=
0.044).
Carson et al, Am Heart J. 2013 June ; 165(6): 964–971
Vincent et al, Anesthesiology, Clinical Science | January 2008
Park et al, Crit Care Med 2012 Vol. 40, No. 12
20. Others points to be considered before
transfusion
• Blood volume evaluation
• Serum lactate
• Mixed venous oxygen
Blood transfusion should be based on a comprehensive
assessment of the patient, including vital signs, estimation of
the amount of blood loss and evaluation of blood volume, as
well as clinical and laboratory evaluation of end-organ
perfusion.
Curinga G et al, b u r n s 3 7 ( 2 0 1 1 ) 7 4 2 – 7 5 2
21. Adverse events associated with RBC
transfusion
Estimated risks in transfusions per unit transfused
Curinga G et al, b u r n s 3 7 ( 2 0 1 1 ) 7 4 2 – 7 5 2
22. Allogenic Blood transfusion Hazards
• Transplantation of allogenic cells
• Risks modest but not negligible
• Haemolytic and Non-haemolytic febrile reactions
• TACO, TRALI, TRIM
• Citrate toxicity
• Hyperkalemia
• Hypothermia
• Infection- Hepatitis, HIV, Bacterial, Parasites, CJD
• Graft vs Host disease
Curinga G et al, b u r n s 3 7 ( 2 0 1 1 ) 7 4 2 – 7 5 2
23. Transfusion-related acute lung injury
(TRALI)
• Signs and symptoms of TRALI include
• Dyspnoea,
• Hypotension
• Fever
• Symptoms begin during, or shortly after transfusion,
• typically within 4 h after receiving blood.
• Mechanism of TRALI is not completely understood,
but it appears to involve
• localization of antibody-coated leucocytes to pulmonary
vasculature resulting in increased permeability and
oedema
• Estimated frequency is approximately 1 in 5000
transfusions, and it is fatal in 5–10% of cases
Caused by noncardiogenic pulmonary oedema
Curinga G et al, b u r n s 3 7 ( 2 0 1 1 ) 7 4 2 – 7 5 2
24. Transfusion errors
• Human errors are responsible for more than half of all
transfusion-related fatalities
• Mistransfusion, defined as an ABO-incompatible reaction
owing to an error
• Leading cause of morbidity and mortality from transfusion
because it can lead to a major haemolytic reaction
• Non-ABO acute haemolytic reactions and febrile
nonhaemolytic reactions
• Much more common but are generally mild and self-limiting in
nature
• Mistransfusion may lead to an acute haemolytic reaction,
characterised by
• fever, chills, pain, nausea, vomiting, hypotension, tachycardia,
Curinga G et al, b u r n s 3 7 ( 2 0 1 1 ) 7 4 2 – 7 5 2
26. Conclusion
• Blood transfusion is not a benign therapy
• Patients who receive PRBCs have an increased incidence
of complications
• The optimal transfusion strategy for burn patients has
not yet been definitively determined, and additional
clinical research is needed.
• The most important physiologic consequence of anaemia
is a reduction in the oxygen-carrying capacity of blood.
• Anaemia is well tolerated as long as intravascular volume
is maintained.
• Blood volume evaluation should be evaluated and
corrected based on the length and severity of the
anaemia.
Regardless, an important consideration for any decision to give blood is the acuity of the blood loss. Patients with acute, massive haemorrhage show signs of haemodynamic instability early in their presentation. The clinical picture depends on the amount of blood loss. Loss of about 20% of blood volume elicits compensatory increases in heart rate and cardiac output, as well as a rise in vasoactive hormones, redistribution.
of blood flow and influx of extravascular fluid to the
intravascular compartment [44–47].
Therefore, with anaemia, oxygen delivery is maintained through a series of complex interactions and compensatory mechanisms. Blood volume evaluation should be estimated to restore adequately the circulatory system, preventing complications of inadequate or overload fluid resuscitation, which can aggravate the anaemic status. Clinical signs at the bedside have been proven insensitive and nonspecific markers of hypoxia; blood pressure, heart rate, changes in mental status and urine output, suffer confounding factors in their interpretation, and may not accurately predict the clinical status [48,49]. Base deficit, a surrogate marker for lactic acidosis, reflects failing tissue oxygenation, is easily measured but is confounded by a range of conditions aswell as resuscitative efforts [48]. The measurement of serum lactate has also been proposed as a test to estimate andmonitor the extent of bleedingandshock [50]. In fact, the clearance of serumlactate to normal levels within 24 h is a powerful predictor of mortality in the critically ill patient. The amount of lactate produced by anaerobic glycolysis is an indirect marker of oxygen debt, tissue hypoperfusion and the severity of haemorrhagic shock [51–54]. Therefore, serum lactate adds another variable to decide when to transfuse. Mixed venous oxygen saturation should be the best guide to need transfusion, but is limited by the need for invasive monitoring using a pulmonary artery catheter or right atrial central line [55,56]. Central venous oxygen saturation, a more easily measured approximation of mixed venous saturation, and currently a marker used to guide early goal-directed therapy in the adult septic shock patients, can be misleading [56].
Tissue-specific markers of hypoxia are ST segment changes on electrocardiogram and P300 latency on electroencephalogram. Myocardial insufficient tissue oxygenation can be detected by continuous five-lead ECG monitoring as new ST-depression >0.1 mV or as new ST-segment elevation >0.2 mV for more than a minute [57]. Although authors reported that St segment change is a physiological transfusion trigger [58,59] it cannot be used to signal the need for transfusion. There are no evidence literature data to support these findings. Current monitoring techniques that assess the heart for development of myocardial ischaemia are electrocardiogram and transoesophageal echocardiography. Weiskopf et al. [60] have opened the ‘window to the brain’ with respect to monitoring the adequacy of cerebral oxygenation during acute
anaemia. The P300 latency above a certain threshold might serve as amonitor of inadequate cerebral oxygenation and as an
organ-specific transfusion trigger in the future [49,61