|Year : 2020 | Volume
| Issue : 3 | Page : 193-196
Evaluation of burn sepsis with reference to platelet count as a prognostic indicator
Surya Prakash1, Chhaya Rani Shevra2, Dwijendra Nath2
1 Department of Surgery, Maharani Laxmi Bai Medical College, Jhansi, Uttar Pradesh, India
2 Department of Pathology, Maharani Laxmi Bai Medical College, Jhansi, Uttar Pradesh, India
|Date of Submission||22-May-2019|
|Date of Acceptance||17-Apr-2020|
|Date of Web Publication||25-Jan-2021|
Chhaya Rani Shevra
Department of Pathology, MLB, Medical College, Jhansi - 284 128, Uttar Pradesh
Source of Support: None, Conflict of Interest: None
Background: Burn is the oldest form of injury to inflict humankind, and infection is a major challenge in the management of burn patients and is a leading cause of morbidity and mortality. The onset of standard clinical indicators of sepsis is known to be delayed and is preceded by fall in platelet count. Thus, the declining platelet count in burn patients is useful prognostic indicator Aim: The following study is undertaken to examine the value of platelet count in predicting the development of sepsis and outcome. Settings and Designs: This was a retrospective study. Materials and Methods: The present study was conducted with eighty-four patients of burn. Routine investigation was done for all the patients. Total platelet count was calculated manually in 84 cases of burn patients. Results: A consistent correlation was noticed between the total platelet count, the presence of burn wound sepsis, and the final outcome. The Platelet count decreased initially in all cases of burn wound sepsis and later on got normal in those who survived while got more decreased in non survivors. Conclusion: Thus the declining platelet count in burn patients is useful prognostic indicator.
Keywords: Burn, platelet, sepsis
|How to cite this article:|
Prakash S, Shevra CR, Nath D. Evaluation of burn sepsis with reference to platelet count as a prognostic indicator. CHRISMED J Health Res 2020;7:193-6
|How to cite this URL:|
Prakash S, Shevra CR, Nath D. Evaluation of burn sepsis with reference to platelet count as a prognostic indicator. CHRISMED J Health Res [serial online] 2020 [cited 2022 Aug 17];7:193-6. Available from: https://www.cjhr.org/text.asp?2020/7/3/193/307824
| Introduction|| |
The problem of burns is as ancient as the time attempted to use fire. Burn has caused great suffering to humankind physically, socially as well as economically and remains a major health problem throughout the world. Thermal burns are caused by application of heat to the body. The degree of resulting burn injury is dependent on the intensity and duration of this heat application and conductivity of tissue involved congested living conditions and wearing loose garments cause burns from wood stores (Angithi), kerosene stoves, kerosene lamps, and leaking LPG cylinders.
A burning dress can produce a temperature of about 1000. In addition, thermal injury is frequently observed in patients who have been exposed to direct contact with hot liquid, hot metal, toxic chemicals, or high-voltage electric current. About 74% are domestic burns and 79% of all domestic burns involve women and children.
Infection is a major challenge in the management of burns patients and is a leading cause of morbidity and mortality., The thermal injury is not only a physical heat phenomenon, but it also starts an inflammatory reaction. The key cells in postburn inflammatory sequence are leukocyte platelets and mast cells. Together with endothelial cells, these cell types represent the prime target site responsible for the mediation, progression, and resolution of inflammatory process.,,
Although many physiological criteria are commonly claimed to reflect burn sepsis, they are mostly noninfectious manifestations. Postburn hypermetabolisms such as hypothermia, leukocytosis, and tachycardia are all nonspecific indicators of sepsis. While thrombocytopenia is caused by number of factors including infection and sepsis, normal-to-high platelet counts are observed in burn patients who are stable and have no evidence of sepsis. The most important observation is temporal relationship of these physiologic events. The onset of standard clinical indicators of sepsis is known to be delayed and is preceded by fall in platelet count.,,
| Materials and Methods|| |
The Institute Ethics Committee, MLB Medical College, Bundelkhand University, approved the study. All samples were coded and labeled properly.
A retrospective study was done in the Department of Surgery, Maharani Laxmi Bai Medical College, Jhansi, in the time between May 2017 and December 2018.
The patients who are included in the study were broadly divided into two groups: Group I – those patients of burn in whom platelet counts increased gradually and final outcome and Group II – those patients of burn in whom platelet counts decreased gradually and who did not survive. The patients admitted with burn immediately resuscitated with intravenous fluids and sedation as per the requirement extent and depth of burn. Appropriate care was given to the wound. Patients were daily observed for clinical evidence of sepsis. The following investigations were carried out: hemoglobin, blood urea, serum creatinine, serum electrolyte, and fasting blood sugar. Blood samples were collected on the day of admission (day 1), day 3, day 7, day 14, and day 21 of burn and sent for total platelet count, total leukocyte count, culture, and sensitivity test. For total platelet count, 2 m1 of venous blood was taken in glass tube containing EDTA as an anticoagulant and mixed gently. Then, it was diluted with 10 mg/lt of ammonium oxalate solution into red blood cell (RBC) pipette in 100 times and mixed for 10–15 min. Then, the diluted fluid was discharged on RBC chamber, and platelets were counted in 10 small squares. If the number of platelets was <100, then some more small squares were counted until 100 platelets were recorded. Then, platelets were calculated as follows:
| Results|| |
Eighty-four patients of burn were studied in the Department of Surgery, Maharani Laxmi Bai Medical College, Jhansi, over a period of 1 and 1/2 years. Each patient was followed from the first day of admission till the final outcome of patients. Maximum cases were in the second (34.5%) and third (33.3%) decades of life with predominance of female patients, with a ratio of 3:1 (female: 73.9% and male: 26.1%). Majority of the patients (27.4%) of burn were of 40%–50%. The study group comprising 84 patients was admitted into two groups: Group I – those patients of burn in whom platelet count increased gradually and final outcome and Group II – those patients of burn in whom platelet counts decreased gradually and who did not survive [Table 1]. The most common microorganism complicating burns were Escherichia coli, Proteus, and Pseudomonas. In the survivor group, most of the cultures were positive [Table 2]. When various features (temperature, pulse rate, and platelet count) were compared in the survivor and nonsurvivor groups, there was no definite change in temperature and pulse rate in both the groups, but platelet count gradually increased in the survivor group, while in the nonsurvivor group, it gradually decreased [Table 3], [Table 4], [Table 5], [Table 6].
|Table 1: Distribution of patients into group1 (survivors) and group 2 (non survivors)|
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|Table 3: Feature in case of survivors in whom platelet count was normal to high|
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|Table 5: Features in cases of nonsurvivors in whom platelet count was low|
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|Table 6: Features in cases of nonsurvivors in whom platelet count was normal|
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When platelet count was estimated in both the groups, it was low in majority of the cases in the nonsurvivor group (28 out of 36), while platelet count was low in few patients of the survivor group (18 out of 48) [Figure 1] and [Figure 2].
|Figure 1: Mean platelet count in cases of non survivors in whom platelet count was low|
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|Figure 2: Mean platelet count in cases of survivors in whom platelet count normal to high|
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Total platelet count was observed in 84 cases of burn patients. A consistent correlation was noticed between the total platelet count, the presence of burn wound sepsis, and the final outcome. The platelet count decreased initially in all cases of burn wound sepsis. It, later on, got raised to normal in those who survived while maintaining the downward trend in nonsurvivors. Thus, the declining platelet count in burn patients is a useful prognostic indicator.
| Discussion|| |
Infection is one of the greatest threats to the survival of patients with major thermal injury. The thermal injury induces a dose-related sepsis. The resulting immunological alteration can be significantly correlated with the survival of patients and those who succumbed because of septic complications. Thrombocytopenia probably occurs more frequently in Gram-negative bacteremic infection. Granulocytopenia is an accepted laboratory finding in Gram-negative bacillary sepsis. Granulocytopenia or lack of brisk granulocytosis, in some cases, proved to be a reliable indicator of bacteremic episodes or as additional signs of continuing sepsis. The platelet count and granulocyte count response sometimes were parallel at the onset of sepsis. Housinger et al. have emphasized that platelet count is an independent predictor of sepsis and death.
Eurenius et al. found that thrombocytosis around day 7 might be because of associated infection. In sepsis, there is thrombocytopenia. Eurenius et al. have suggested that the initial thrombocytopenia is due to platelet destruction by extrinsic mechanism following which there is a marrow megakaryocytic response, which creates the secondary thrombocytosis.
Caprini et al. have suggested intravascular contamination in burn victims, early due to tissue damage and later possibly from sepsis for this type of platelet response.
In the present study, out of 84 cases, maximum cases belonged to the second (29 cases [34.5%]) and third decades of life (28 cases [33.3%]). The male-to-female ratio is 1:3. Flame was the most common causative agent. The highest number of cases (23, 27.4%) had burn area of 40%–50% of total body surface area. Seventeen patients (20.2%) had 30%–40%. Sixteen patients (19%) had 60%–70%. Twelve patients (14.3%) had 20%–30%.
On day 1, there was no definite relationship between the extent of injury and platelet count. Compared to day 1, on day 3, there was a decrease in platelet count.
The initial thrombocytopenia was related to severity of injury. As the extent of injury increases, there is an increase in the degree of thrombocytopenia.
[Table 3], [Table 4], [Table 5], [Table 6] correlate different features of sepsis against platelet count in cases of survivors and nonsurvivors. The temperature and pulse rate have got no definite relationship in both the groups.
In this series, when the survivors and nonsurvivors were compared, it was observed that platelet count rises to the initial normal level in cases of survivors but further falls in cases of nonsurvivors [Figure 1] and [Figure 2].
In [Table 2], surface culture report in the two groups is shown. In Group 1, out of 48 patients, only 25 patients had a positive culture, while in Group II, out of 36 patients, 31 patients had a positive culture. E. coli was the most common organism in both the groups. The next common organism was Proteus. In [Table 7], the relationship of survival (outcome) and platelet count is shown, where a significantly large number of patients who died had low platelet count. In the survivor group, out of 48 patients, only 18 patients had low platelet counts, while in the nonsurvivor group, out of 36 patients, 28 patients had low platelet count. Thus, low platelet count is suggestive of the outcome of the patient.
Thrombocytopenia is related to the presence of septic complication, as suggested by many authors. The counts decreased with septic complications at times even before their actual clinical manifestation.
| Conclusion|| |
The result of this study showed that there was no relationship between the initial platelet count and the degree of injury. There was early thrombocytopenia in most of the cases, which increases with consistent relationship to septic complication. The low platelet count indicates a poor prognosis. Thus, the platelet count has a prognostic significance.
Financial support and sponsorship
We are thankful to our technical staff for technical support and thankful to both pathology and surgery departments.
Conflicts of interest
There are no conflicts of interest.
| References|| |
Luterman A, Dacso CC, Curreri PW. Infection in burn patients. Am J Med 1986;81:45-52.
Liedberg NC, Reiss E, Artz CP. Infection in burns: Ill. Septicaemia, a common cause of death. Surg Gynecol Obstet 1954;99:151-8.
D'Alessandro MM, Gruber DF. Quantitative and functional alteration of the peripheral blood neutrophils after 10% and 30% of thermal injury. J Burn Care Rehabil 1990;11:295-300.
Macdonald AH, Levenson SM, Davidson CS, Tagnon HJ, Taylor FH. Studies on the peripheral blood in patients with thermal burns. 1. Thrombocytopenia. Science 1944;99:519.
Pepper H, Lindsay S. Response of platelets, eosinophils and total leucocytes during and following surgical procedures. Surg Gynecol Obstet 1960;110:319-28.
Takashima Y. Blood platelets in severely injured burned patients. Burns 1997;23:591-5.
Maduli IC, Patil A, Pardhan NR, Panigraphy PK, Mukherjee LM. Evaluation of burn sepsis with reference to platelet count as a prognostic indicator. Int J Surg 1999;61:235-38.
Sarda DK, Dagwade AM, Lohiya S, Kamble AT. Evauation of platelet count as a prognostic indicator in early detection of post burn septicaemia. Bombay Hosp J 2005;47:3-6.
Ninnemann JL. Immunological defenses against infection: Alterations following thermal injuries. J Burn Care Rehabil 1982;3:355-66.
Cohen P, Gardner FH. Thrombocytopenia as a laboratory sign and complication of gram negative bacteraemic infection. Arch Intern Med 1966;117:113-23.
Housinger TA, Brinkerhoff C, Warden GD. The relationship between platelet count, sepsis, and survival in pediatric burn patients. Arch Surg 1993;128:65-6.
Eurenius K, Mortensen RF, Meserol PM, Curreri PW. Platelet and megakaryocyte kinetics following thermal injury. J Lab Clin Med 1972;79:247-57.
Caprini JA, Lipp V, Zuckerman L, Vagher JP, Winchester DP. Hematologic changes following burns. J Surg Res 1977;22:626-35.
[Figure 1], [Figure 2]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7]