A CASE OF EFFECTIVE DIAGNOSIS AND TREATMENT OF A PATIENT WITH COMBINED SHOCKOGENIC TRAUMA Girsh A.O., Chumakov P.A., Maksimishin S.V., Korzhuk M.S., Malyuk A.I.
Kabanov City Clinical Hospital No.1,
Omsk State Medical University, Omsk, Russia
A clinical case was described on the basis of patient's written consent and approval from the ethical committee in compliance with Helsinki Declare − Ethical Principles for Medical Research with Human Subjects, 2000, and the Rules for Clinical Practice in the Russian Federation confirmed by the Order of Russian Health Ministry, June 19, 2003, No. 266.
A patient, age of 31, was admitted by a car of reformatory colony No. 3 of Federal Prisons Service of Omsk region to the admission unit of Kabanov City Clinical Hospital. After examination by the duty surgeon and the anesthesiologist-intensivist, he was admitted to the intensive care unit.
The anamnesis data showed a blunt thoracic and abdominal injury 4.5 hours ago. The condition was severe and was determined by traumatic shock of middle severity (arterial pressure (AP) = 80/60 mm Hg, heart rate (HR) = 120 per minute, shock index (SI) − 1.5. The patient was conscious, not obtunded (Glasgow Coma Scale (GCS) − 13). Pain was pale, body temperature − 36.1°C, respiratory rate (RR) − 24. SaO2 − not defined. There were complaints of abdominal pain to the right and pain in the chest to the left. The approximate blood loss was 1,500 ml (based on data of systemic hemodynamics and clinical symptoms).
The patient received catheterization for the right subclavian vein according to Seldinger (central venous pressure (CVP) ± 5 cm). Non-invasive monitoring of central hemodynamics parameters with MPR 6-03 (Triton Electronics, Russia) was initiated. It showed hemodynamic type of blood circulation (the table 1). Infusion therapy (isotonic sterofundin) and analgesia (i.v. promedol, 2 %, 1 ml) were prescribed. The test with fluid load (i.v., stream infusion of 200 ml 0f isotonic sterofundin) determined the increase in CVP to +8 and the decrease in stroke output (SO) to 25 ml.
Table 1
Values of central hemodynamics, hemostasis and laboratory data of the patient, age of 31
|
Values |
At admission to emergency unit |
At admission to ICU |
After 12 hours |
day 1 |
day 2 |
day 3 |
day 4 |
|
×ÑÑ,( ìèí-1) HR, (min-1) |
120 |
113 |
109 |
100 |
96 |
92 |
88 |
|
SV, (ml) |
28 |
36 |
41 |
48 |
65 |
76 |
85 |
|
MBV, (l/min) |
3.4 |
4.1 |
4.5 |
4.8 |
6.2 |
6.9 |
7.5 |
|
TPR, (dyn×s×cm-5) |
2953 |
2996 |
2869 |
2293 |
1975 |
1623 |
1472 |
|
Lactate, mmol/l |
3.6 |
3.8 |
3.3 |
2.8 |
2.1 |
1.9 |
1.6 |
|
APTT, (sec.) |
48 |
49 |
51 |
45 |
34 |
32 |
31 |
|
Platelets, (109/l) |
122 |
134 |
148 |
162 |
175 |
187 |
196 |
|
Total CPK, (U/l) |
891 |
635 |
429 |
253 |
197 |
188 |
183 |
|
CPK-MB, (U/l) |
112 |
97 |
76 |
52 |
34 |
22 |
21 |
|
Troponin test (+/-) |
+ |
+ |
+ |
+ |
+ |
- |
- |
Considering the above mentioned facts (basic positive CVP and its positive time course at the background of fluid load; low SO and its subsequent decrease at the background of infusion therapy), extremely high total peripheral vascular resistance (TPVR),which is not common for shock of middle severity, and anamnesis data (closed abdominal and thoracic injury), heart contusion was suspected. Echocardiography (MYLAB 20, ESAOT S.p.a. (Italy)) was carried out. Specific analyses (troponin test, plasma level of creatinine phosphokinase (CPC)) were made. The patient received ultrasonic examination of abdominal organs (free fluid was found in abdominal cavity) and chest X-ray examination (a fracture of 7th rib was found).
Echocardiography confirmed the hemodynamic type of blood circulation, the sharp decrease in SO (to 25 ml), as well as the decrease in ejection fraction (EF) to 38 %,which is a pathognomonic sign of heart contusion [1, 2]. Moreover, positive troponin test and a high plasma level of CPC were found, indicating the presence of heart contusion (the table 1). Inotropic support with dobutamine (5 µg/kg of body mass per minute) with use of perfusor compact C (B. Braun, Germany) was prescribed. It favored the decrease in CVP (to + 5 cm) at the background of infusion therapy (isotonic sterofundin (500 ml) + 4 % modified starch (MS) (250 ml) in ratio 2:1), promoted an increase in SO (to 33 ml) and arterial pressure (to 90/60 mm Hg), and a decrease in HR (to 115 per minute).
Presence of shock was confirmed by lactate in venous blood [3], APTT (the table 1) and absence of hourly urine output. The blood analysis showed a decrease in hematocrit (to 24 %), red blood count (to 1.96 × 109) and hemoglobin (to 61 g/l).
Based on the clinical, laboratory and instrumental data, the diagnosis was made after case conference: "Closed abdominal injury. Intraabdominal bleeding. Closed chest injury. A fracture of 7th rib to the left. Heart contusion. Left lung contusion. Traumatic shock of degree 2". Surgical treatment was required. At 9:50 p.m., the patient was admitted to the surgical room. At the background of total intravenous (fentanyl + ketamine) anesthesia with myorelaxants in conditions of artificial lung ventilation (ALV) with air-oxygen mixture, and CVP monitoring, the surgery (65 minutes) was conducted: laparotomy; liver rupture suturing; abdominal cavity sanitation and draining.
During surgery, the patients' condition was severe: skin was pale and cold, body temperature − 36.1 °C, no SaO2, CVP +7 cm, AP = 95/65-90/60 mm Hg, HR − 115-113 per min. Parameters of central hemodynamics (SO − 3.9 l/min., SO − 34 ml, TPVR − 2,784 dyn×cm×c-5) were without dynamic worsening at the background of infusion therapy (isotonic sterofundin − 500 ml + 4 % MS − 250 ml) and inotropic support (dobutamine − 5 µ/kg of body mass per min.). On the basis of systemic hemodynamics, clinical symptoms, hemoglobin and hematocrit, the total blood loss was 1,800 ml.
After admission to ICU, ALV with Chirolog Aura (Chirana, Slovakia) in CMV mode (Vt – 480 ml, MV – 7.2 l, FiÎ2 – 0.35 %) was initiated. Infusion (isotonic sterofundin, 500 ml) and transfusion (fresh frozen single group plasma, 770 ml / single group packed red blood cells, 410 ml, 2:1) therapy was initiated (total volume of 1,680 ml). Antibacterial therapy was initiated: monotherapy with augmentin (4 days) at the beginning; later − according to results of microbiological studies, cefoperazonum/sulbactamum (8 days). Symptomatic treatment (analgetic agents, sedative drugs, anticoagulants, proton pump inhibitors) was initiated. Due to persistent hemodynamic disorders, inotropic support was continued (dobutamine − 5 µg/kg of body mass per minute) for maintenance of CVP at the level of +7 cm and positive influence on SO, resulting in increasing AP (to 100/70 mm Hg) (the table 1). At the same time, circulatory disorders were persistent. It was shown by lactate (the table 1), cold and pale skin, low body temperature (to 36.2 °C), absent urine output and SaO2.
By the end of the first day, the intensive therapy promoted the positive changes in central hemodynamics, correction of anemia and coagulopathy, and improvement in tissue perfusion (the table 1) and body temperature (to 36.5 °C), and initiation of urination (350 ml). The patient showed positive time trends of plasma CPC, but with positive troponin test (the table 1). Echocardiography (with similar data of central hemodynamics monitoring) confirmed persistent hemodynamic type of blood circulation, and identified an increase in EF to 43 %. The daily fluid balance (without perspiration) was +1,030 ml.
On the second day, the patient showed the normodynamic type of blood circulation (by means of increase in SO and decrease in HR) (the table 1) at the background of infusion (isotonic sterofundin, 1,500 ml, and 4 % MS, 1,000 ml) and inotropic (decreasing dose of dobutamine to 4 µg/kg of body mass per minute) therapy. Echocardiography (with data of central hemodynamics monitoring) confirmed the presence of circulation of normodynamic type and determined the positive time course of EF (48 %). Also positive time course of plasma CPC was noted, but, again, with positive troponin test (the table 1). Lactate level [3], TPVR and appearance of sings of SaO2 (98 %) [4, 5] testified efficient correction of perfusion disorders. Therefore, ALV for the patient in medication sleep (i.v. morphine + sibazon) was continued with the same modes. It was also confirmed by oxygenation index (OI = ÐàÎ2/FiÎ2 – 300). Diuresis was 950 ml. Daily fluid balance (with consideration of perspiration) was +1,150 ml.
On the third day, the patient showed the positive time trends of parameters of heart function, and further regression of circulatory disorders (the table 1). Negative troponin test was registered. Plasma CPC was normal (the table 1). Moreover, echocardiography showed an increase in EF (to 54 %). It allowed decreasing the inotropic support with dobutamine to 3 µg/kg of body mass per min. AP was 120/80 mm Hg, CVP − +7 cm. The skin was pale, SaO2 − 94 %, hourly urination − 0.7 ml/kg of body mass. Infusion therapy volume was 2,500 ml (isotonic sterofundin − 2,000 ml, 4 % MS − 500 ml), daily fluid balance (with consideration of perspiration) − +800 ml. The time trends of OI (265) was the cause for correction of ALV (PEEP mode, +5 cm of H2O, increasing FiO2 to 0.45 %). Further estimation of OI (255) did not find any efficient correction of pulmonary dysfunction. As result, PEEP ad FiO2 were increased (to + 8 cm of H2O and to 0.5 %, correspondingly).
Acute respiratory distress syndrome (ARDS) was also confirmed by X-ray examination of the lungs (bilateral infiltrates to the right and to the left), presence of the indirect risk factor (traumatic shock of middle severity), acute onset (within the first 72 hours) and regression of insufficiency of myocardial contractility. Also X-ray examination showed the left-sided posttraumatic exudative pleuritis. The thoracic surgeon carried out pleural puncture and removed 550 ml of light exudate.
Inotropic support with dobutamine was cancelled by the end of the fourth day owing to improvement in central hemodynamics, normalization of specific markers of myocardial injury and hypoperfusion (the table 1), and increasing EF (to 62 %). AP was 120/80 mm Hg, CVP − +8 cm. The skin was pale and warm. The hourly urine output was 0.6 ml/kg. Infusion therapy included 2,500 ml of isotonic sterofundin. The daily fluid balance (with consideration of perspiration) was +850 ml. In its turn, an increase in pulmonary dysfunction was noted (OI − 227). It required for increase in PEEP (to +10 mm H2O) and FiO2 (to 0.6 %). OI increased to 252.
Certainly, development of ARDS at the background of acute cardiovascular failure was the main factor [6] for estimation of intensity of multiple organ dysfunction syndrome (MODS) [7], which determined development of hypermetabolism (the table 2). Actually, metabolic monitoring (indirect calorimetry) found high energy requirements, which are common for MODS (the table 2) [8]. It was confirmed by laboratory predictors of hypermetabolism and systemic inflammation (the table 2). Therefore, beginning from 5th day, antibacterial therapy was changed, and enteral nutrition was initiated, which included isocaloric (1kcal per 1 ml) polysubstrate mixture with Nutricomp Fiber (1,000 ml per day) with the infusion pump FmS (B. Braun, Germany) with the rate of 40 ml per hour, with subsequent decrease of infusion therapy to 1,500 ml (isotonic sterofundin). Next day, the volume of enteral nutrition was increased to 1,000 ml (isotonic sterofundin). At the same time, tracheostomy was performed for continuation of ALV with previous modes.
Table 2
Energy requirements, SOFA data and laboratory values of the patient, age of 31
|
Values |
day 5 |
day 7 |
day 9 |
day 11 |
day 12 |
|
Energy requirements, (kcal per day) |
2841 |
2621 |
2143 |
1828 |
1734 |
|
SOFA, (points) |
3 |
2 |
1 |
0 |
0 |
|
Leukocytes, (109/l) |
14.6 |
13.7 |
12.6 |
11.5 |
10.1 |
|
Bilirubun, (mmol/l) |
18.9 |
17.4 |
15.3 |
12.1 |
12.7 |
|
Glucose, (mmol/l) |
6.2 |
5.9 |
4.7 |
4.3 |
3.9 |
|
Urea, (mmol/l) |
10.5 |
9.6 |
8.4 |
6.9 |
6.3 |
|
Creatinine, (mmol/l) |
119.4 |
110.5 |
97.6 |
92.7 |
86.1 |
|
Albumin, (g/l) |
23 |
22 |
25 |
27 |
26 |
On the seventh day, the volume of enteral nutrition was increased to 2,000 ml, and infusion therapy volume was decreased to 500 ml (isotonic sterofundin). Also, considering the positive time trends of OI (258), PEEP was decreased (to 5 cm of H2O), as well as FiO2 was decreased (to 0.5 %). Moreover, on the eighth day, ALV was performed with CRAP mode (FiO2 − 0.45 %) due to increasing OI. Decreasing pulmonary dysfunction determined the decrease in intensity of MODS, reducing systemic inflammation and determined the decrease in energy requirements [6]. Therefore, infusion therapy was discontinued, and enteral nutrition volume was increased to 2,500 ml. In its turn, it favored further degradation of hypermetabolism and organ-system disorders (the table 2).
On the ninth day, the patient was in consciousness (GCS − 14-15 at the moment of cancellation of sedative and narcotic agents) and was adequate. It allowed exclusion of neurovegetative blocking from the treatment program. ALV was in PS mode (FiO2 − 0.4 %). It favored further increase in OI (300) and, as result, decreasing systemic inflammation and less energy requirements (the table 2).
On the tenth day, the patient was awake. ALV was in PS mode (OI − 315). Echocardiography, which was conducted along with central hemodynamics monitoring, did not find any significant changes in indices of cardiovascular system, but it found increasing EF (to 74 %). On the day 11, the patient was switched to independent breathing (HR − 16-18 per min, OI − 350, SaO2 − 99 %, body temperature − 37.3 °C, AP − 120/80 mm Hg, HR − 86 per min., CP − +6 cm; the skin was pale and warm; diuresis − 1,250 ml) with moistened oxygen (FiO2 − 0.3 %) through the nasal catheter. Moreover, the patient showed absent MODS, a decrease in plasma urea and reducing energy requirements that supposed relief of hypermetabolism at the background of increasing serum albumin, and normoglycemia (the table 2) [8]. From 12th day, the patient could breath independently (HR − 14-16 per min., OI − 345, SaO2 − 98 %, body temperature − 37.1 °C, AP − 120/80 mm Hg, HR − 88 per min., CVP − +6 cm, pale and warm skin, diuresis − 1,100 ml) without oxygen; on 13th day, in condition of middle severity, the patient was transferred to the profile surgery unit.
CONCLUSION
Therefore, the above mentioned findings show the characteristics and subsequence of diagnostic and curative processes for patients with traumatic shock and heart contusion. Therefore, timely identification and targeted treatment require: 1) consideration of clinical and anamnestic data; 2) realization of all medicodiagnostic procedures in the intensive care unit from the moment of hospital admission; 3) from admission to ICU, it is advisable to use non-invasive monitoring of central hemodynamics parameters with their detalization and interpretation in relation to severity of traumatic shock and possible (according to anamnesis and clinical examination data) heart contusion; 4) estimation of CVP after catheterization of the subclavian vein before initiation and during infusion therapy; 5) verification of hemodynamically significant heart contusion with use of echocardiography in combination in troponin test and creatinine phosphokinase in blood plasma, and their dynamic control up to stabilization of systemic hemodynamics; 6) prescription of selective β2 adrenoceptor agonist dobutamine with cardiotropic dose (3-5 µg/kg per minute in dependence on SO, HR and EF) is pathogenetically required after verification of hemodynamically significant heart contusion; 7) realization of infusion-transfusion therapy requires for monitoring of central hemodynamics, hematocrit, hemoglobin, CVP, hourly diuresis and daily fluid balance in the period of hemodynamic disorders; 8) qualitative and quantitative composition of infusion-transfusion therapy in the period of hemodynamic disorders should be individualized and goal-oriented according to the above-mentioned monitored parameters, a clinical situation, and patient's individual response to treatment; 9) after stabilization of systemic hemodynamics, infusion therapy should be carried out only with balanced crystalloids, and its volume is minimized by means of early initiation of enteral nutrition, especially for patients with ARDS.
Information on financing and conflict of interest
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.