ACS: Abdominal compartment syndrome; APTT: Active partial thromboplastin time; BE: Base excess; CVP: Central venous pressure; DAP: Diastolic arterial pressure; EtCO2: End-tidal carbon dioxide; Hat: Hematoctit; Hb: Hemoglobin; HR: Heart rate; FFP: Fresh frozen plasma; FiO2: Fraction of inspirited oxygen; IAH: Intra-abdominal hypertension; IAP: Intra-abdominal pressure; INR: International normalized ratio; MAC: Minimum alveolar concentration; MAP: Mean arterial pressure; PLT: Plateles; PCV: Pressure controlled ventilation; PEEP: Positive end expiratory pressure; RBC: Red blood cells; SAP: Systolic arterial pressure; WBC: White blood cells

Intra-abdominal pressure (IAP) is defined as pressure in the abdominal cavity, which is determined by the abdominal contents and elasticity of the abdominal wall structures [1]. Under physiological conditions, IAP ranges from 3 to 7 mmHg and is markedly affected by body weight [2]. In obese patients, IAP can exceed 10 mmHg. Increased IAP, known as intra-abdominal hypertension (IAH) is likely to lead to multiorgan failure. The multiorgan failure resulted from acute increase in IAP is called the abdominal compartment syndrome (ACS) [1]. In 1996, Burch and colleagues [3] analyzed increases in IAP in relation to the severity of ASC symptoms and distinguished four grades of IAH. In 2006, their scale was modified by the World Society of Abdominal Compartment Syndrome (WSACS, www.wsacs.org). At present, the following grades of IAH are distinguished: I, IAP between 12 and 15 mmHg (1.56 – 1.95 kPa); II, IAP between 16 and 20 mmHg (1.98 and 2.6 kPa); III, IAP between 21 and 25 mmHg (2.73 – 3.25 kPa); and IV, IAP > 25 mmHg (< 3.25 kPa).

The most common causes of IAH include a massive hemorrhage to the abdominal cavity and/or extraperitoneal space, injuries to the intestines and abdominal organs, peritonitis and enteritis, rapidly increasing ascites, surgical “packing”, surgical procedures with extracorporeal circulation, septic shock and extensive burns [4,5]. Moreover, fluid resuscitation may be of importance [6-9]. The aim of the present report was to analyze IAP changes in a patient subjected to the surgical stabilization of lower limb crush fractures, complicated by massive intraoperative hemorrhage.

A 40-year-old patient was transported to the hospital by an ambulance because of injuries resulting in a displaced fracture of both crural bones, which was accompanied by soft-tissue crushing, and a displaced fracture of the femur (Figure 1). On admission, the patient was in moderately severe general condition, conscious, and responsive and had efficient respiration and circulation; he did not require massive fluid therapy. The external injuries included marked deformity of the entire lower extremity, marked edema of soft tissues of the crushed calf and a slight wound to the lower leg. Additional examinations did not reveal any abnormalities (Table 1). To exclude the possibility of serious injury to the crural arteries, CT and vascular examination of the crushed limb were performed (Figure 1). These techniques did not disclose any significant damage to arterial vessels of the lower extremity. The patient was qualified for emergent reposition of the lower limb fractured bones. During the diagnostic procedures performed in the hospital emergency department, the patient received 1000 ml of the crystalloid solution and 500 ml of the colloid solution. Diuresis was found to be 100 ml.

Figure 1: Computer tomography scans of injured leg. The computer tomography was performed using 64-multidetector row spiral MDCT (VCT, GE Healthcare, Milwaukee, Wi). First, routine examination was performed using 1.25 mm contiguous section (120 kV, 170 mA and 0,5 rotation). For lower limb arteries imagining, an intravenous injection of 120 ml Iopromidum (Visipaque 320, GE Healthcare) was administrated at the rate of 3 ml/sec. The CTangiography examination was performed using 0.6 mm contiguous section.
A – vascular visualization, B – general visualization of injured left leg, C – general view on legs (visible edema of soft tissues of the crushed lower leg), edema of the crushed lower leg and femoral bone with not swilling soft tissue.

Table 1: Laboratory results.

During the preoperative visit, subarachnoid anesthesia was suggested, but the patient did not initially consent and asked for continuous epidural anesthesia of the injured leg combined with general anesthesia. Once consent was obtained, the patient was assigned to the project overseeing IAP studies in patients undergoing orthopedic surgery, which had been approved by the Ethics Committee of the Medical University of Lublin.

Before the anesthetic procedure was performed by the indirect method, the arterial pressure was measured, and a standard continuous measurement of heart rate was initiated using a MINDRAY PM-9000 express monitor (BioMedical Electronics, D). Before anaesthesia, the intra-abdominal pressure was measured using Kron’s technique (Figure 2). Considering the patient’s preoperative request and the extent of trauma, the epidural anaesthesia was performed using 5 ml 2% xylocaine injected between the third and fourth spinous process (L3 - L4). The BALTON epidural catheter was inserted for postoperative analgesia. Additionally, the ventilated induced and maintained anesthesia was used with sevoflurane (Sevorane, ABBOTT UK) at the doses of 1.5 – 2.0 minimum alveolar concentration (MAC). Before intubation, a single dose of fentanyl was administered (0.2 mg), and muscle relaxation was obtained using succinylcholine at a dose of 1 mg/kg b.w.

Figure 2: Changes in intra-abdominal pressure (IAP), abdominal perfusion pressure (APP) and mean artery pressure (MAP) in study stages: 1 – before surgery and anesthesia (since admission to the hospital), 2 – two hours after surgery, 3 – morning hours of postoperative day 1 (8 hours after surgery and anesthesia), 4 – 14 hours after surgery, 5 – 20 hours after surgery (in the evening of postoperative day 1), 6 – in the morning of postoperative day 2, 7 – in the morning of postoperative day 3.

The patient’s condition did not markedly change immediately after incision of the integuments. The crural bone fractures were repositioned by inserting the external stabilizer. In consideration of the acute compartment syndrome, decompression fasciotomy was elected. After cutting the fascia of the calf bicep muscle medially, significant outflow of blood was observed, which increased during tissue preparation. A vascular surgeon found massive damage to the lower leg deep veins with multisite arterial hemorrhage. Anticipating the necessity of administering intensive fluid therapy, the central vascular access and additional peripheral vascular access routes were prepared. Arterial pressure monitoring was widened by continuous direct measurement of the radial artery. During the preparation of injured vessels, massive hemorrhage developed, requiring 13000 ml of crystalloid solution, 3000 of colloid solution, 19 units of red blood cells and 14 units of fresh frozen plasma. Despite rapid supplementation of the volume of circulating blood, arterial pressure dropped to undetectable values (Figure 3). Therefore, the infusion of dobutamine and norepinephrine at doses of 9 μg/kg b.w./min and 1 μg/kg b.w./min was initiated. Because of the problems with providing hemostasis, the popliteal artery was temporarily closed. The intraoperative morphology confirmed lifethreatening blood loss (Table 1). Gasometry demonstrated significant metabolic acidosis (Table 1). Since the injured vessels could not be secured, it was decided to amputate the affected limb at the level of the lower leg. Before commencing the next stage of surgery, the intravascular volume was supplemented with 3000 ml of crystalloids, 1000 ml of colloids, 4 units of concentrated red blood cells and 12 units of platelet concentrates. The treatment was supplemented with a single dose of methylprednisolone (1000 mg, Solu-Medrol, Pharmacia Upjohn). The therapy allowed us to discontinue the infusion of noradrenaline and to markedly reduce the dose of dobutamine. After completing the surgery, the patient was not woken up and was transferred to the Department of Intensive Therapy for further treatment.

Figure 3: Changes in mean arterial pressure (MAP) during surgery and anesthesia (measurements every 10 min). Time point 1 – MAP before induction of anaesthesia. The induction of anaesthesia slightly decreased MAP. During the external crural reposition, MAP didn’t change significantly. From 110 min after induction of anaesthesia (during decompression fasciotomy), MAP decreased successively till 150 min of surgery, when its value dropped drastically and the infusion of dobutamine and norepinephrine was initiated. From this time point, the level of MAP was corrected by norepinephrine infusion.

On admission, the patient’s general condition was severe, and his respiration was inefficient; he required artificial ventilation using fraction of inspirited oxygen (FiO₂) - 0.6 and positive end expiratory pressure (PEEP) +5 cmH₂O. The circulatory parameters were maintained with the infusion of dobutamine at a dose of 5 μg/ kg b.w./min. Immediately after admission, the patient received 1000 ml of crystalloids, 2 units of concentrated red blood cells and 12 units of platelet concentrates. The repeated blood tests did not reveal any relevant abnormalities (Table 1).

During the ICU treatment, the patient’s general condition improved. At postoperative hour 8, the infusion of dobutamine was discontinued; at postoperative hour 14, artificial lung ventilation was discontinued, and the endotracheal tube was removed. On treatment day 3, the patient was transferred to the Department of Orthopaedics for further treatment.

The values of intra-abdominal pressure were determined immediately before the surgery and anesthesia and during the subsequent postoperative hours (Figure 2). The analysis involved systolic, diastolic and mean arterial blood pressure, central venous pressure, heart rate and laboratory results, i.e. arterial blood, clotting parameters and arterial blood gasometry (Table 1, 2).

Table 2: Changes in intra-abdominal pressure (IAP), systolic artery pressure (SAP), diastolic arterial pressure (DA) and central venous pressure (CVP) as well as volume of infused fluids and fluid balance at successive stages of therapy.

Hemorrhagic shock causes 40% of deaths in patients treated for multiorgan trauma [8]. In the majority of cases (80%), the cause of death is uncontrollable intraoperative hemorrhage, which is particularly common after thoracic and abdominal trauma [9]. Many post-transfusion complications are also relevant, including ACS. The report discussed IAP changes after the surgical stabilization of lower limb fractures complicated by massive hemorrhage. The highest (over threefold) increase in IAP was noted during the immediate postoperative period whereas IAP decreased to the baseline value on day 3.

Massive therapy with crystalloids is considered to be a common cause of IAP increase [6,7,10,11]. It is believed that relationship between the volume of crystalloids administered and IAP is linear; the largest increases are observed on postoperative day 3 [7]. According to some authors, IAP increases in patients with burns are noticed after 3500 ml of crystalloids have been administered over the course of 24 h. [6]. Others suggest that the administration of 0.35 L/kg b.w./24 h of crystalloid solution results in grade III IAH whereas 0.475 L/kg b.w./24 h leads to grade IV IAH [7]. Moreover, IAP increases significantly after 10 units of red blood cells are administered to patients with severe hemorrhagic shock [11]. In our case, the patient (in the Emergency Department and during anesthesia) received 236.11 ml/kg b.w. of crystalloids, 62.5 ml/kg b.w. of colloids and 23 units of concentrated red blood cells; the highest IAP value (15 mmHg) was noted on postoperative day 2. Therefore, it is not easy to explain a relatively slight IAP elevation after such massive fluid therapy. The degree of inflammatory response appears to be essential, as burns are considered the most stressogenic injuries. This response could have been also impaired by a single dose of methylprednisolone; however, the down-regulating effects of steroid therapy on inflammatory response-induced IAP increases require further study. Furthermore, the effects of anesthesia are relevant. Both epidural block and muscle relaxants limit IAP increases [5,12]. This effect was likely to modulate the IAP changes during the immediate postoperative period.

A slight (≤15 mmHg) increase in intra-abdominal pressure does not result in significant organ dysfunction and is of no clinical relevance. Therefore, intensive treatment is not recommended but, rather, frequent observation of IAP changes. When the IAP values exceed 15 mmHg, appropriate therapy should be instituted. IAP in excess of 15 mmHg can limit haemodynamic functions of the myocardium by reducing the amount of blood returning to the right ventricle, increasing the pulmonary pressure and hindering blood ejection to the periphery. These changes are likely to be accompanied by a compensatory heart rate acceleration and reduced blood flow through the coronary vessels [1,4,13]. Such cardiovascular destabilization requires the infusion of positive ionotropic agents. In our case, a fourfold IAP increase compared with the baseline values was observed, reaching 15 mmHg at postoperative hour 2. During this period, the noradrenaline infusion was terminated, and the dose of dobutamine was low.

Moreover, increased IAP has adverse effects on the respiratory system. Respiratory changes are observed even during slight IA increases. During laparoscopic procedures, IAP is routinely increased to 11-12 mmHg, which limits the movement of the diaphragm, dislocating it cephally by approximately 1.9 cm and reducing the total lung capacity by 300 ml [14]. The values of IAP above 15 mmHg significantly reduce the vital lung capacity, functional residual capacity, and residual capacity and increase the airway pressure and intrapulmonary shunting, leading to clinically relevant hypoxia and hypercapnia [14,15]. In many cases, such significantly increased changes require artificial lung ventilation. However, it is difficult to determine the extent to which the observed IAP increase impaired respiratory efficiency in the case presented here. After surgery, the patient was purposefully not woken up, and the relatively rapid discontinuation of artificial lung ventilation excluded the possibility of severe respiratory insufficiency induced by IAH. Thus, it can be concluded that neither massive fluid therapy nor IAP increase affected the ventilation parameters of our patient.

Our case, in which the patient underwent surgery due to the crushed lower limb, complicated by hemorrhage requiring intensive fluid resuscitation, does not confirm the relationship between the volume of fluids administered and IAP increases as described in the literature. A relatively slight IAP increase was of no clinical importance and did not result in severe multiorgan failure. Therefore, it can be concluded that intensive crystalloid resuscitation of patients without systemic conditions does not induce significant dysfunction of vital organs.