|Year : 2020 | Volume
| Issue : 1 | Page : 7-12
Understanding the role of serum lactate as an end point in burn resuscitation
Nita Trina D'souza, Abha Rani Kujur, D Rajeswari
Department of Plastic Surgery, St John's Medical College Hospital, Bengaluru, Karnataka, India
|Date of Submission||07-Jan-2020|
|Date of Decision||19-Nov-2020|
|Date of Acceptance||22-Jan-2021|
|Date of Web Publication||21-May-2021|
Dr. Abha Rani Kujur
Department of Plastic and Reconstructive Surgery, St John's Medical College Hospital, Bengaluru-34, Karnataka
Source of Support: None, Conflict of Interest: None
Context: Fluid resuscitation plays a significant role in burns treatment. Inappropriate resuscitation impacts morbidity and mortality. Urine output (UO), the current gold standard, alone, is not an adequate end point of fluid resuscitation in burns. Hence, we studied the utility of serum lactate levels as a reliable marker and end point of resuscitation.
Aims: (a) To understand the role of serum lactate levels in burns as end point in acute burn resuscitation and (b) To assess its sensitivity and specificity.
Settings and Design: Tertiary care hospital, urban setting, and cross-sectional study.
Subjects and Methods: The study was done from September 2015 to July 2017. Sixty-four patients with thermal burns were included. Serum lactate levels were recorded at arrival, 8 h, 16 h, 24 h, and 48 h interval postburn incident. Hourly UO heart rate and mean arterial pressure were recorded for the outcome measures.
Statistical Analysis Used: Chi-square test and nonparametric Mann–Whitney U-test. P ≤ 0.05 was considered statistically significant.
Results: (a) The initial serum lactate levels at presentation were directly proportional to:
- The total body surface area and percent deep component of burns sustained
- Delay in starting resuscitation.
b. Time taken for serum lactate levels to normalize is directly proportional to initial serum lactate level.
At 16 h, serum lactate showed (94%) specificity, (53%) sensitivity, and at 48 h (85%) sensitivity, (44%) specificity.
Conclusions: Serum lactate levels can help to monitor the adequacy of fluid resuscitation in burns. Serum lactate and UO, both, should be taken into consideration to determine the end point of resuscitation.
Keywords: Burns resuscitation, serum lactate, urine output
|How to cite this article:|
D'souza NT, Kujur AR, Rajeswari D. Understanding the role of serum lactate as an end point in burn resuscitation. Indian J Burns 2020;28:7-12
|How to cite this URL:|
D'souza NT, Kujur AR, Rajeswari D. Understanding the role of serum lactate as an end point in burn resuscitation. Indian J Burns [serial online] 2020 [cited 2021 Dec 8];28:7-12. Available from: https://www.ijburns.com/text.asp?2020/28/1/7/316563
| Introduction|| |
Urine output (UO) is used as end point of fluid resuscitation in burns. Studies indicate inadequacy of heart rate (HR), arterial pressure, and other invasive methods such as central venous pressure and cardiac output to monitor resuscitation.,,,,,, State of Science meeting in October 2006 in Washington DC concluded that, end points of resuscitation are not accurately defined. In the absence of universally accepted end point of resuscitation, burn patients can be under or over resuscitated increasing their overall morbidity and mortality.
We studied serum lactate levels and correlated it with UO to see if it can be used as a reliable maker to know the end point of resuscitation.
| Subjects and Methods|| |
The present study was approved by the Hospital Ethics Committee. Written informed consent was obtained from all patients involved in the study, including consent to participate in the study and consent to publish. The present study was conducted from September 2015 to July 2017.
- Adults with 15% and more total body surface area (TBSA) scald and flame burns
- Children with 10% and more TBSA scald and flame burns
- Patients reporting within 24 h from the burn incident.
- Patients having sustained electric burns
- Patients with inhalation injury
- Pregnant women with burns
- Patients with cardiac and renal failure.
The TBSA was calculated based on Lund and Browder Chart. Resuscitation fluid calculated using Modified Parkland formula. Half of this was administered over first 8 h, and the rest was administered over the next 16 h. Lactated Ringer's solution was the fluid administered for resuscitation. For children, half dextrose normal saline was also added as maintenance fluid.
Serum lactate level was recorded at admission, 8 h, 16 h, 24 h, and 48 h interval. UO and mean arterial pressure (MAP) were also recorded for monitoring purposes.
Normal serum lactate level was taken to be 1 mmol/L. Normal UO was taken to be 1 ml/kg/h.
When hourly UO was <1 ml/kg/h and MAP is <65 mmHg and serum lactate levels was more than 1 mmol/L, then fluid administration was raised in gradual increments hourly till UO reached 1 ml/kg/h.
Time taken for serum lactate to reach 1 mmol/L was calculated. Correlations between the time required for serum lactate to reach 1 mmol/L and UO to reach 1 ml/kg/h was seen.
Statistical analysis was performed by the Chi-square test and nonparametric Mann–Whitney U-test. P ≤ 0.05 was considered statistically significant
| Results|| |
A total of 64 patients were enrolled in the study. 32 males and 32 females. Children were 22 in number with 42 being adults.
The initial serum lactate levels at presentation were directly proportional to
- The TBSA percentage of burns sustained [Figure 1]
- The percentage of deep component of burns [Figure 2]
- Delay in starting resuscitation from time of injury [Figure 3]
- Time taken for serum lactate levels to normalize.
|Figure 1: Shows greater the total burn surface area of burns, greater was the initial serum lactate levels, x axis-initial serum lactate values, y axis-TBSA|
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|Figure 2: Shows greater the percentage of deep component of burns, greater is the initial serum lactate levels, x axis-% of deep component burns, y axis-initial SL values|
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|Figure 3: Shows delay in resuscitation is directly proportional to the initial serum lactate levels, x axis-delay in resuscitation y- initial SL level|
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Standard error bars have been depicted by the bar lines.
Greater the percentage of burns, longer is the time taken for serum lactate to return to normal value of 1 mmol/l. In patients with 41%–50% TBSA burns, serum lactate took more than 48 h to normalize [Figure 4].
|Figure 4: Shows greater the percentage of burns, more is the time taken for serum lactate to normalize to one, x axis-TBSA, y axis- no of patient|
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More the deep component of burns, more time was required to normalize serum lactate levels. If patients had more than 31% TBSA deep burn component, it took more than 48 h for serum lactate values to normalize to one.
Longer the delay in starting fluid resuscitation more was the time required to normalize serum lactate [Figure 5]. Serum lactate reached normal levels of 1 by 16 h of starting resuscitation in patients with <30% TBSA while it took nearly 48 h for patients with 31%–40% TBSA.
|Figure 5: Shows greater the delay in starting resuscitation, greater time required to normalize serum lactate, x axis-time of starting resuscitation, y axis- number of patients|
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It took 48 h for 81% of the 64 patients serum lactate to reach value of 1 mmol/l. Serum lactate not reaching normal values even at 48 h was seen in eight patients (19% of the 64 patients). These eight patients either had extensive scald burns with deep component or had received resuscitation only after 12 h of burns.
In 80% of the children, serum lactate normalized by 24 h, indicating children responded better and quicker to fluid resuscitation.
At 48 h, serum lactate has sensitivity (85%) and specificity (44%), whereas it showed specificity (94%) and sensitivity (53%) at 16 h [Figure 6].
True positive is when UO is not 1 ml/kg/h and SL is not normalized to 1 which means patient is in shock
True negative is when UO is 1 ml/kg/h and SL is normalized to 1 which means patient is no longer in shock
Statistical analysis was performed by the Chi-square test and nonparametric Mann–Whitney U-test showed significant association between trend of serum lactate normalizing with TBSA involved, percentage of deep component and late resuscitation with P < 0.001 and significant association between serum lactate normalizing with type of burn (scald burn) with P < 0.0005.
Statistically, it was also shown that 1% raise in TBSA increased the serum lactate levels by 0.0679, whereas 1-h delay in resuscitation raised the serum lactate levels by 0.3022 indicating that inadequate tissue perfusion and burn shock mainly occurred due to delay in starting resuscitation.
| Discussion|| |
Burn patients require fluid to counter fluid leak, especially in the first 48–72 h., Extensive work has been done by many. Evans and Baxter derived formulas for fluid requirement of burn patients., Baxter's Parkland Formula suggested fluid replacement at 4 ml/kg body weight % TBSA., Moyer suggested using crystalloids because it is closest in physiology to the patient's serum. Monafo suggested the use of hypertonic saline solution, as it would cause fluid shift from intracellular to intravascular space and reduce edema.,
Various methods have been used to monitor fluid resuscitation in addition to UO. Transesophageal echocardiography, partial carbon dioxide rebreathing, intermittent transpulmonary thermodilution, impedance electrocardiography, and gastric tonometer have all been found to be unreliable to monitor resuscitation.,,,, Over resuscitation called “fluid creep”,,, causing pulmonary edema, compartment syndrome,,,, and progression of burn wound depth. Under resuscitation leads to tissue hypoperfusion and worsens the burn wound depth.
Central hypovolemia occurs due to extravasation of fluid into third space in burns. This may not reflect in HR, MAP, or UO. It can be guided by serum lactate thus avoiding unnecessary fluid input. When there is normalization of the elevated serum lactate levels, it indicates adequate tissue perfusion, correction of the oxygen debt, and adequate oxygen extraction along with an intact lactate metabolism in the liver. The first 48 h is critical for the management of patient's physiology and to prevent the progression of depth of the burn wound.
The qualities of an optimal resuscitation marker include ease of measurement, accuracy, reproducibility, and rapid change in response to resuscitation. Broder and Weil noticed that patients with undifferentiated shock and lactate excess of >4 mmol/L had high morbidity and mortality. This prompted them to use serum lactate as a clinical indicator of patient outcome. Definition of elevated lactate levels is not well defined in the literature. Reviewed articles have taken a cutoff between 2 and 2.5 mmol/L. In our study, we have taken “normal lactate levels” as reaching to 1 mmol/L. Lactate levels from arterial or venous blood samples are similar as shown in a study by Kruse et al.
Greater the burn surface area involved and greater the depth of burn tissue, more is the fluid leak that occurs causing the patient to go into hypovolemic shock and tissue hypoperfusion. This is aptly reflected in the high serum lactate values of the patient on arrival in the emergency room. Similarly, delay in starting the fluid resuscitation meant no fluid replacement for a long period. This also resulted in the tissues being hypo-perfused reflected by high lactate levels.
In a patient with extensive burns and in frank shock, as determined by tachycardia, hypotension, and reduced UO, it is clear that they require urgent fluid resuscitation and require to be monitored in an intensive care unit. Hourly pulse rate, blood pressure, and UO are monitored to ensure patient remains adequately resuscitated with serum lactate levels done at 8 h, 16 h, 24 h, and 48 h interval.
However, in a burn patient who is not in shock and initial serum lactate level is >3 mmol/dl, it indicates that patient is having inadequate tissue perfusion and patient can go into frank shock if not adequately resuscitated and monitored. Hence, such patients would benefit from being monitored closely in an intensive care unit till serum lactate levels normalize to 1 mmol/dl. This can reduce the overall morbidity of the patient by reducing the progression of the deep component, thereby reducing the percentage of tangential excision required. Furthermore, close monitoring reduces chance of under or over hydration of the patient and prevents patient developing pulmonary edema and abdomen compartment syndrome. Thus, initial serum lactate levels can be used as a guide to determine the patients that need close monitoring in intensive care units.
When hourly UO is <1 ml/kg and MAP is <65 mmHg, but serum lactate levels are 1 or <1 mmol/L, then the rate of fluid being administered is not changed, thus avoiding over resuscitation. Whereas, if hourly UO is <1 ml/kg and MAP is <65 mmHg and serum lactate levels are more than 1 mmol/L, then fluid administration is raised in gradual increments. Thus, serum lactate can be used as a guide for the rate of fluid administration.
If patient is maintaining UO at 1 ml/kg/h and MAP is maintained at more than 65 mmHg, indicating the patient is well hydrated, but lactate levels continue to be more than 1 mmol/l, then the other causes of raised serum lactate levels have to be considered. Most common being occult inhalation injury detected by bronchoscopy.
Increased serum lactate level can be associated with many other coexisting conditions in patients which have been excluded in the study. Liver dysfunction can cause increased lactate production and decreased clearance. Liver function test should be considered for unexplained elevated serum lactate levels in well-resuscitated patients. Excess muscle activity can also cause raised serum lactate levels due to anaerobic metabolism. Patients can struggle against the restraints due to delirium as seen sometimes in major burns or in patients with seizure related burns. Samples collected soon after the struggle can lead to raised lactate levels and this could be erroneously interpretated. Diabetic ketoacidosis can also cause raised lactate levels due to metabolic dysfunction; hence, glucose levels should be regularly monitored in burn patients with diabetics and anti-hypoglycemic administered promptly. Thiamine deficiency is seen in nutritional deficiency like alcoholism and when there is thiamine deficiency, anaerobic metabolism predominates, and lactate production increases. This is a treatable cause, and in Indian scenario, flame burn in chronic alcoholics is well-known. In the pediatric population, elevated lactate can be caused by inborn errors of metabolism wherein there is metabolic dysfunction at various steps. Other confounding factors include mitochondrial dysfunction (including potential lack of key enzymatic cofactors) and the presence of a hyper metabolic state, causing persistent elevated lactate levels in initial 48 h.
In our study, serum lactate normalized by 24 h in 41% adults and 80% children indicating that children showed better response to fluid resuscitation. In four children with <15% scald burns and <4% deep component and who were started on resuscitation within 4 h, serum lactate normalized in 8 h. Patients who received resuscitation by 4 h and/or with <30% TBSA serum lactate normalized by 16 h. Patients who received resuscitation after 4 h and/or with 30%–40% TBSA serum lactate normalized by 48 h. This shows the importance of early resuscitation.
At 48 h, serum lactate has better sensitivity (85%) and poor specificity (44%), whereas it showed better specificity (94%) and poor sensitivity (53%) at 16 h. Better sensitivity at 48 h means if serum lactate levels normalized despite UO being low then we can safely stop resuscitation, thus avoiding over resuscitation of patients. Serum lactate having better specificity at 16 h means if serum lactate levels are high then the patient would benefit from a raise in fluid being administered, thus preventing underperfusion of the tissues and progression of deep burn component.
| Conclusions|| |
If burn patients are given fluid without adequate monitoring it results in progression of the burn wound depth and pulmonary edema. By titrating fluid administration based on serum lactate and UO levels, burn wound progression and pulmonary edema can be prevented. Thus, the percentage TBSA to be tangential excised is reduced. This is a major change in the line of treatment for the patient for fluid resuscitation to be more accurate if serum lactate is considered with UO rather than UO alone.
Serum lactate levels and UO should be considered together for end point of fluid resuscitation in burns.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Greenhalgh D. Burn resuscitation. J Burn Care Res 2007;28:555-6.
Baxter CR. Fluid volume and electrolyte changes in the early post burn period. Clin Plast Surg1974;1:693-703.
Pruitt BA Jr. Protection from excessive resuscitation: “Pushing the pendulum back”. J Trauma 2000;49:567-8.
Engrav LH, Colescott PL, Kemalyan N, Heimbach DM, Gibran NS, Solem LD, et al
. A biopsy of the use of the Baxter formula to resuscitate burns or do we do it like Charlie did it? J Burn Care Rehabil 2000;21:91-5.
Dries DJ, Waxman K. Adequate resuscitation of burn patients may not be measured by urine output and vital signs. Crit Care Med 1991;19:327-9.
Mitra B, Fitzgerald M, Cameron P, Cleland H. Fluid resuscitation in major burns. ANZ J Surg 2006;76:35-8.
Shah MR, Hasselblad V, Stevenson LW, Binanay C, O'Connor CM, Sopko G, et al
. Impact of the pulmonary artery catheter in critically ill patients: Meta-analysis of randomized clinical trials. JAMA 2005;294:1664-70.
Martin RS, Norris PR, Kilgo PD, Miller PR, Hoth JJ, Meredith JW, et al. Validation of stroke work and ventricular arterial coupling as markers of cardio vascular performance during resuscitation. J Trauma 2006; 60:930–5.
Della Rocca G, Costa MG, Pompei L, Coccia C, Pietropaoli P. Continuous and intermittent cardiac output measurement: Pulmonary artery catheter versus aortic transpulmonary technique. Br J Anaesth 2002;88:350-6.
Holm C, Mayr M, Tegeler J, Hörbrand F, Henckel von Donnersmarck G, Mühlbauer W, et al
. A clinical randomized study on the effects of invasive monitoring on burn shock resuscitation. Burns 2004;30:798-807.
Underhill FP. The significance of anhydremia in extensive surface burn. JAMA 1930;95:852-7.
Moore FD. The body-weight burn budget. Basic fluid therapy for the early burn. Surg Clin North Am 1970;50:1249-65.
Artz CP, Moncrief JA. The burn problem. In: Artz CP, Moncrief JA, editors. The Treatment of Burns. Philadelphia: WB Saunders Co.; 1969. p. 1-22.
Baxter CR, Shires T. Physiological response to crystalloid resuscitation of severe burns. Ann N Y Acad Sci 1968;150:874-94.
Moyer CA, Margraf HW, Monafo WW Jr. Burn shock and extravascular sodium deficiency-treatment with Ringer's solution with lactate. Arch Surg 1965;90:799-811.
Monafo WW. The treatment of burn shock by the intravenous and oral administration of hypertonic lactated saline solution. J Trauma 1970;10:575-86.
Monafo WW, Halverson JD, Schechtman K. The role of concentrated sodium solutions in the resuscitation of patients with severe burns. Surgery 1984;95:129-35.
Bajorat J, Hofmockel R, Vagts DA, Janda M, Pohl B, Beck C, et al
. Comparison of invasive and less-invasive techniques of cardiac output measurement under different haemodynamic conditions in a pig model. Eur J Anaesthesiol 2006;23:23-30.
Wynne JL, Ovadje LO, Akridge CM, Sheppard SW, Vogel RL, Van de Water JM. Impedance cardiography: A potential monitor for hemodialysis. J Surg Res 2006;133:55-60.
Holm C, Hörbrand F, Mayr M, Henckel von Donnersmarck G, Mühlbauer W. Assessment of splanchnic perfusion by gastric tonometry in patients with acute hypovolemic burn shock. Burns 2006;32:689-94.
Venkatesh B, Meacher R, Muller MJ, Morgan TJ, Fraser J. Monitoring tissue oxygenation during resuscitation of major burns. J Trauma 2001;50:485-94.
Friedrich JB, Sullivan SR, Engrav LH, Round KA, Blayney CB, Carrougher GJ, et al. Is supra-Baxter resuscitation in burn patients a new phenomenon? Burns 2004;30:464-6.
Greenhalgh DG, Warden GD. The importance of intraabdominal pressure measurements in burned children. J Trauma 1994;36:685-90.
Latenser BA, Kowal-VernA, Kimball D, ChakrinA, Dujovny N. A pilot study comparing percutaneous decompression with decompressive laparotomy for acute abdominal compartment syndrome in thermal injury. J Burn Care Rehabil 2002;23:190-5.
Hobson KG, Young KM, Ciraulo A, Palmieri TL, Greenhalgh DG. Release of abdominal compartment syndrome improves survival in patients with burn injury. J Trauma 2002;53:1129-33.
Oda J, Yamashita K, Inoue T, Harunari N, Ode Y, Mega K, et al. Resuscitation fluid volume and abdominal compartment syndrome in patients with major burns. Burns 2006;32:151-4.
Wo CC, Shoemaker WC, Appel PL, Bishop MH, Kram HB, Hardin E. Unreliability of blood pressure and heart rate to evaluate cardiac output in emergency resuscitation and critical illness. Crit Care Med 1993;21:218-23.
Broder G, Weil MH. Excess lactate: An index of reversibility of shock AQ11 AQ12 in human patients. Science 1964;143:1457-9.
MoklineA, AbdennejiA, Rahmani I, Gharsallah L, Tlaili S, Harzallah I, et al. Lactate: Prognostic biomarker in severely burned patients. Ann Burns Fire Disasters 2017;30:35-8.
Kruse O, Grunnet N, BarfodC. Blood lactate as a predictor for in-hospital mortality in patients admitted acutely to hospital: A systematic review. Scand J Trauma Resusc Emerg Med 2011;19:74.
Andersen LW, Mackenhauer J, Roberts JC, Berg KM, Cocchi MN, Donnino MW. Etiology and therapeutic approach to elevated lactate levels. Mayo Clin Proc 2013;88:1127-40.
Mizock BA. The hepatosplanchnic area and hyperlactatemia: A tale of two lactates. Crit Care Med 2001;29:447-9.
Alshayeb H, ShowkatA, Wall BM. Lactic acidosis in restrained cocaine intoxicated patients. Tenn Med 2010;103:37-9.
Cox K, Cocchi MN, SalciccioliJD, Carney E, Howell M, Donnino MW. Prevalence and significance of lactic acidosis in diabetic ketoacidosis. J Crit Care 2012;27:132-7.
Butterworth RF. Thiamine deficiency-related brain dysfunction in chronic liver failure. Metab Brain Dis 2009;24:189-96.
Goldberg GR, Greene CL. Update on inborn errors of metabolism: Primary lactic acidemia. J Pediatr Health Care 1992;6:176-81.
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