Shipitsyna I.V., Osipova E.V., Lyulin S.V., Sviridenko A.S.
Russian Ilizarov Scientific Center for Restorative Traumatology and Orthopaedics, Kurgan, Russia
PROCALCITONIN DIAGNOSTICAL VALUE IN THE POSTTRAUMATIC PERIOD IN PATIENTS WITH POLYTRAUMA
The
continuous increase in the injury rates after road traffic accidents (RTA)
causes the increasing proportion of patients with high energy trauma [1, 2].
The difficulties in treatment of polytrauma are determined by severe clinical
manifestations at the background of intense multiple organ dysfunction. The
patients with multiple trauma often suffer from infectious complications and
sepsis. Moreover, the clinical symptoms and the common markers are sometimes unreliable
for diagnostics.
Currently,
the prohormone of calcitonin – procalcitonin (PCT) – is widely used in the
clinical practice as the marker of bacterial infection. The advantage for
sepsis diagnosis is long term presence in the blood as compared to cytokines
[3]. The blood level pf PCT does not increase in viral infections, neoplastic
and autoimmune processes and in allergic responses [4]. The high levels of PCT
are observed in severe bacterial infections [5].
According
to the above-mentioned facts, the actuality of PCT monitoring in the blood in
patients with severe associated road traffic injury does not raise any doubts
for early identification of infectious complications.
Objective – to
study the posttraumatic time course of procalcitonin (PCT) level in blood of
the patients with polytrauma after road traffic accident.
MATERIALS AND METHODS
The
study object was the blood of 30 patients with severe high energy trauma after
RTA. The patients were admitted to the level 1 trauma center based on Kurgan
City Hospital No.2 within 1-2 hours after the injuries, which were accompanied
by traumatic shock of 1-3. The mean age of the patients was 37.4 ± 13.2. There
were 13 women and 17 men.
Depending
on ISS (Injury Severity Score) and SAPS (Original Simplified Physiology Score),
the patients were distributed into two groups: the group 1 – extremely severe
(n = 18) patients, the group 2 – severe (n = 12) patients (the table 1).
Table 1. Characteristics of patients
Values |
Extremely severe |
Severe |
Mean age, years |
39.2 ± 4.7 |
35.9 ± 8.6 |
Gender: male/female, abs. |
11/7 |
6/6 |
Injury severity estimated with ISS, points |
31 ± 3.6 |
20 ± 2.3 |
Condition severity according to SAPS, points |
13-14 |
7-8 |
Blood loss, l |
3.2 ± 0.4 |
1.9 ± 0.3 |
Dominating traumatic brain injury (TBI) |
14 |
8 |
Dominating spine and spinal cord injury |
1 |
- |
Dominating chest injury |
2 |
3 |
Dominating locomotor system injury |
1 |
1 |
Thecontrol group included 12 healthy volunteers: 6 women and 6 men, the age of
24-43. The PCT levels were within the reference values (0.05 (0.032; 0.053)
ng/ml) [6].
PCT
was measured with the enzymoimmunoassay and Procalcitonin-IFA-Best diagnostic
set of the reagents (Vector-Best, Novosibirsk).
The
statistical analysis of the data was conducted with AtteStat 13.0 and included the
formation of the null and alternative hypotheses, testing the hypothesis of compliance
between empiric distribution and the law of normal distribution with
Shapiro-Wilk’s test for small samples. Considering the fact that the
characteristics of distribution were different from the normal values in all
groups, the digital data was presented as the median (Me), 25 % and 75 %
quartiles (Q25-Q75). Mann-Whitney’s non-parametric test was used for decision
or rejection of the null hypothesis. The intergroup differences were considered
as statistically significant with p < 0.05.
The
ethical committee of Russian Ilizarov Scientific Center for Restorative
Traumatology and Orthopaedics gave the approval for the clinical study. The
study corresponded to the ethical standards of Helsinki Declare.
RESULTS
The posttraumatic plasma PCT levels were variable in the group 1, with the peaks on the days 1 and 7 (the table 2). After 14 days, the values were within the reference indices in 72 %, after 90 days – in all patients.
Table 2. Changes in PCT plasma level in patients of groups 1 and 2
24 hours after trauma |
PCT level, ng/ml |
||
group 1 |
group 2 |
Statistical significance of differences between groups 1 and 2 (p) |
|
1 |
9.08 |
2.62 |
0.001 |
3 |
1.37 |
0.74 |
0.012 |
7 |
2.37 |
1.28 |
0.009 |
14 |
0.18 |
0.05 |
0.045 |
21 |
0.09 |
0.05 |
0.044 |
30 |
0.07 |
0.04 |
0.049 |
60 |
0.06 |
0.02 |
0.09 |
90 |
0.03 |
0.04 |
0.12 |
Note: the data is presented as median and 25-75 quartiles.
In
the group 2, the PCT levels were lower (despite of similar dynamics) as
compared to the group 1 (the table 1). The PCT levels were higher than the
reference values in all patients on the day 1, in 93 % on the day 3 and in 72 %
on the day 7. The levels were within the normal range in 93 % of the patients
on the day 14.
The
combination of severe high energy trauma and various complications of the
traumatic disease present the main cause of the death. The lethal outcomes were
registered in both groups.
The clinical case 1
The patient E., female, age of 22, was admitted with the diagnosis: “Severe associated injury. Closed traumatic brain injury. Brain concussion. Blunt chest injury. Bilateral pneumothorax. Thoracic subcutaneous emphysema. An opened displaced fragmented fracture of the sacrum. A lacerated wound near the sacrum. A fracture of pubic and ischial bones to the left. A fracture of the posterior acetabular rim to the left. A rupture of pubic symphysis. A closed dislocation of the right hip. A closed displaced fracture of the middle one-third of the left hip. Scratches on the face and the body. Traumatic shock of degree 3”. ISS was 27 points at the moment of admission, SAPS – 9-10 points. The death happened on the 14th day after the injury and was caused by renal insufficiency and bilateral pneumonia at the background of extensive injuries. The patient demonstrated the pathologic high level of PCT (35.6 ng/ml) on the first day after the trauma. PCT was slightly decreasing within two weeks. The level was 27.6 ng/ml on the 14th day (the day of death).
The clinical case 2
The patient A., female, age of 53, was admitted with the diagnosis: “Closed traumatic brain injury. Severe brain contusion with crushing injury to brain substance to the left. Small subdural hematoma to the left. Fractures of the left and right temporal and jugal bones, of both walls of orbits. A contused wound of the head. An opened displaced fracture of both bones of the right leg in the middle one-third. Non-displaced fractures of pubic and ischial bones to the right. A fracture of the lateral mass of the sacrum to the right. Fractures of L4-5 transverse processes to the right. A lacerated wound of the leg. Traumatic shock of degree 3”. ISS was 43, SAPS – 13-14. The death happened on the 31st day after trauma. The lethal outcome was caused by the injuries and an infectious complication (septic pneumonia). Blood PCT was changing in the wave form, with the peak values on the days 1 and 7 and gradual decrease by the day 14. On the 21st posttraumatic day, the recurrent peak value of PCT was observed that did not correspond to the general time course of the value in this group.
The clinical case 3
The
patient O., age of 28, female, was admitted with the diagnosis: “Severe
associated injury. Mild closed traumatic brain injury. Brain concussion. Blunt chest injury. A closed fracture
of the ribs 9-10 to the left and the ribs 6-8 to the right. Corpus sternum
dislocation. Ling contusion. Bilateral small hydrothorax. Multiple fractures of
the sacrum with displaced fragments. A fracture of the shaft of the right iliac
bone without displacement. Extensive hematoma of small pelvis. A closed
fracture of L4-5 transverse processes. A closed fragmentary intraarticular
fracture of both bones of the left leg in the lower one-third with
displacement. A closed dislocation of the 5th instep bone of the left foot.
Multiple fractures of the instep bones of the right foot. Soft tissue
contusion, facial scratches. DIC. Traumatic shock of degree 3”. ISS was 22 SAPS
– 7-8 at the moment of admission. The death happened as result of DIC and
bilateral posttraumatic pneumonia on the 8th day after trauma. Blood PCT was
2.98 ng/ml on the first posttraumatic day, 0.94 ng/ml on the 3rd day, with
four-fold increase (on the 7th day 11.5 ng/ml) as compared to the basic values.
The
absence of significant decrease in PCT or sharp increase in the posttraumatic
period in patients with polytrauma may indicate some possible infectious
complications and unfavorable outcome.
DISCUSSION
Induction
and action of PCT presents the multifactorial process including some cellular
interactions, cell activation (time depending) and different cell behavior [7].
The cause of posttraumatic PCT induction has not been studied to the full
degree. The in vivo and in vitro experimental studies have shown
that PCT can be induced by bacterial endotoxins, as well as by various
proinflammatory mediators such as TNF-
α, IL-2, IL-6 and others [8, 9, 10].
According
to the literature data, the peak levels of PCT are common for the days 1 or 2
after trauma [7]. Usually in patients without infectious complications, the PCT
level quickly returns to the normal values [11]. The sepsis predictors are
non-decreasing high levels or secondary increase in PCT [12].
It
is known that multiple organ dysfunction develops in 84.5 % of patients with
polytrauma. There are two types of the clinical course: early or non-bacterial
(the days 1-2) and late or bacterial (from the day 3). Late syndrome is diagnosed
in 71.6 % of patients on the day 7 after trauma [13].
In our study, the PCT level had some
specific features in severe high energy associated injury after RTA. Both
groups of the patients demonstrated the wavy pattern of PCT with the peak
values on the day 1 and 7 after trauma. PCT decreased to the reference values
in different time points and depended on injury severity.
According to the literature data, the
patients with polytrauma show the similar time course of other biomarker -
lipopolysaccharide-binding protein (LPS-BP) [14]. It is considered that LPS-BP
can be considered as the marker for diagnostic interval between the decrease in
interleukins and increasing C-reactive protein (CRP) [15]. However after
surgery, LPS-BP and CRP often demonstrate non-specific increase to the levels,
which are observed in sepsis [16]. Surgical trauma and anesthesia do not make
statistically significant influence on PCT [15]. It testifies the necessity of
inclusion of this parameter into the diagnostic algorithm of posttraumatic
complications.
One has to agree that a combination
of several biomarkers in complex estimation of cytokine status allows receiving
or increasing the accuracy of prognosis of development of complications [14,
15].
CONCLUSION
Therefore, the examination of PCT in the blood of patients with severe associated injury can be used for monitoring of patients’ condition with severe associated injury. Absence of posttraumatic decrease in PCT is the unfavorable prediction sign.
Information about financing and conflict of interests
The
study was conducted without sponsorship.
The authors declare the absence of any
clear and potential conflicts of interests relating to publication of this
article.
REFERENCES:
1. Shchedrenok VV, Ladeyshchikov VM, Anikeev NV, Simonova IA,
Moguchaya OV. Clinical-statistical and organizational aspects of concomitant
craniocerebral injuries in towns with different population size. Perm Medical Journal. 2011; XXVIII(4): 131-139. Russian (Щедренок В.В., Ладейщиков В.М., Аникеев Н.В.,
Симонова И.А., Могучая О.В. Клинико-статистические и
организационные аспекты сочетанных черепно-мозговых повреждений в городах с
различной численностью населения //Пермский медицинский журнал. 2011. Т. XXVIII, № 4. С. 131-139)
2. Lyulin SV, Meshcheryagina IA, Samusenko
DV, Stefanovich SS. The tactics of traumatic disease treatment in patients with
polytrauma at the resuscitation stage. Genius
of Orthopedics. 2015; (3): 31-37. Russian (Люлин С.В., Мещерягина И.А.,
Самусенко Д.В., Стефанович С.С. Тактика лечения травматической болезни у
пациентов с политравмой на реанимационном этапе //Гений ортопедии. 2015. № 3. С. 31-37)
3. Cho
SY, Choi JH. Biomarkers of sepsis. Infect.
Chemother. 2014; 46: 1-12
4. Puchkova MS, Dzeboeva TA, Kaminskaya LA. Procalcitonin
functional role for different diseases. The analysis of laboratory data based
on Central City Hospital of Ekaterinburg. Herald
of Science and Education. 2015; 3(5): 163-168. Russian (Пучкова М.С., Дзебоева Т.А., Каминская Л.А. Функциональная
роль прокальцитонина при различных заболеваниях. Анализ лабораторных данных на
базе ЦГБ г. Екатеринбурга //Вестник науки и
образования. 2015. № 3(5). С. 163-168)
5. Dudina KR, Kutateladze MM, Znoyko OO, Bokova NO, Shutko SA,
Filina LD et al. Clinical significance of acute inflammation markers for
infection pathology. Kazan Medical
Journal. 2014; 95(6): 909-915. Russian (Дудина К.Р., Кутателадзе М.М., Знойко О.О., Бокова Н.О., Шутько С.А., Филина Л.Д. и др. Клиническая
значимость маркёров острого воспаления при инфекционной патологии //Казанский
медицинский журнал. 2014. Т. 95, № 6. С. 909-915)
6. Velkov VV. Procalcitonin and C-reactive protein in modern
laboratory diagnosing. Clinico-laboratory
Concilium. 2008; (6): 46-52. Russian (Вельков
В.В. Прокальцитонин и С-реактивный белок в современной лабораторной диагностике
//Клинико-лабораторный консилиум.
2008.
№ 6. С. 46-52)
7. Meisner
M, Adina H, Schmidt J.
Correlation of procalcitonin and C-reactive protein to inflammation,
complications, and outcome during the intensive care unit course of
multiple-trauma patients. Crit. Care. 2006; 10(1): R1
8. Cho SY, Choi JH. Biomarkers of sepsis. Infect Chemother. 2014; 46(1): 1-12
9. Pierrakos C, Vincent JL. Sepsis biomarkers: a review. Crit. Care. 2010; 14(1): R15
10. Dahaba
AA, Metzler H. Procalcitonin’s role in the sepsis cascade. Is procalcitonin a
sepsis marker or mediator? Minerva Anestesiol. 2009; 75: 447-452
11. Ciriello
V, Gudipati S, Stavrou PZ, Kanakaris NK, Bellamy MC, Giannoudis PV. Biomarkers
predicting sepsis in polytrauma patients: Current evidence. Injury. 2013; 44(12): 1680-1692
12. Sakran
JV, Michetti CP, Sheridan MJ, Richmond R, Waked T, Aldaghlas T et al. The
utility of procalcitonin in critically ill trauma patients. J. Trauma Acute Care Surg. 2012; 73(2): 413-418
13. Samokhvalov
IM, Boyarintsev VV, Nemchenko NS, Gavrilin SV, Suvorov VV, Gayduk SV, et al.
Prediction of functional disorders in the systems of immunity and hemostasis
using clinical condition scoring (Field Surgery-SS) in injured persons with
polytrauma. Herald of Anesthesiology and
Critical Care Medicine. 2010; 7(1): 10-15. Russian (Самохвалов И.М., Бояринцев В.В., Немченко Н.С., Гаврилин С.В., Суворов В.В., Гайдук С.В. и др. Прогнозирование функциональных
нарушений в системах иммунитета и гемостаза с использованием балльной оценки
клинического состояния (ВПХ–СС) у пострадавших с политравмой //Вестник
анестезиологии и реаниматологии 2010. Т. 7, №
1. С. 10-15)
14. Ustyantseva IM, Khokhlova OI, Petukhova
OV, Zhevlakova YuA. Time Course of Changes in
Lipopolysaccharide-Binding Protein and Lactate in the Blood of Patients with
Polytrauma. General Critical Care
Medicine. 2014; 10(5): 18-26. Russian (Устьянцева И.М., Хохлова О.И., Петухова О.В.,
Жевлакова Ю.А. Динамика липополисахаридсвязывающего протеина и лактата в крови
пациентов с политравмой //Общая реаниматология. 2014. Т. 10, № 5. С. 18-26)
15. Pavlushkina LV, Chemevsky EA, Dmitrieva IB,
Beloborodova NV. Biomarkers in clinical practice. Laboratory. 2013; 3: 11-14. Russian (Павлушкина Л.В., Черневская Е.А., Дмитриева
И.Б., Белобородова Н.В. Биомаркеры в клинической практике //Лаборатория. 2013. № 3. С. 11-14)
16. Tschaikowsky K, Hedwig–Geissing
M, Schmidt J, Braun GG. Lipopolysaccharide-Binding
Protein for Monitoring of Postoperative Sepsis: Complemental to C-Reactive
Protein or Redundant? PLoS ONE. 2011; 6(8): e23615
Статистика просмотров
Ссылки
- На текущий момент ссылки отсутствуют.