Shipitsyna I.V., Osipova E.V., Lyulin S.V., Sviridenko A.S.

 Russian Ilizarov Scientific Center for Restorative Traumatology and Orthopaedics, Kurgan, Russia


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.


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


Extremely severe
(n = 18)

= 12)

Mean age, years

39.2 ± 4.7

35.9 ± 8.6

Gender: male/female, abs.



Injury severity estimated with ISS, points

31 ± 3.6

20 ± 2.3

Condition severity according to SAPS, points



Blood loss, l

3.2 ± 0.4

1.9 ± 0.3

Dominating traumatic brain injury (TBI)



Dominating spine and spinal cord injury



Dominating chest injury



Dominating locomotor system injury



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.


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
n = 18)

group 2
= 12)

Statistical significance of differences between groups 1 and 2 (p)


(2.670; 9.110)

(1.230; 6.350)



(0.960; 1.640)

(0.610; 0.960)



(1.150; 2.450)

(0.620; 1.540)



(0.060; 0.450)

(0.040; 0.060)



(0.050; 0.110)

(0.003; 0.058)



(0.040; 0.170)

(0.022; 0.050)



(0.040; 0.055)

(0.017; 0.026)



(0.022; 0.040)

(0.017; 0.038)


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.


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].


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.


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