Nonoperative Management of Post-Traumatic Pulmonary Pseudocyst After Severe Thoracic Trauma and Hemorrhage by Coagulation Management, Kinetic Therapy, and Control of Secondary Infection: A Case Report

Case Report The Journal of TRAUMA威 Injury, Infection, and Critical Care Nonoperative Management of Post-Traumatic Pulmonary Pseudocyst After Severe Thoracic Trauma and Hemorrhage by Coagulation Management, Kinetic Therapy, and Control of Secondary Infection: A Case Report Eva Steinhausen, MD, Bertil Bouillon, MD, Nedim Yücel, MD, Thorsten Tjardes, MD, Dieter Rixen, MD, Thomas Paffrath, MD, Christian Simanski, MD, Dirk Knüttgen, MD, Volker Keppler, MD, and Marc Maegele, MD J Trauma. 2007;63:1391–1394. P ost-traumatic pulmonary pseudocyst (PPP) is a rare manifestation of blunt thoracic injury characterized by a cavitary lesion lacking an epithelial lining.1 Young adults and adolescents involved in high-speed motor vehicle crashes are predominantly affected.2– 4 While usually associated with a good prognosis5,6 serious morbidity and mortality may occur in cases of severe hemorrhage7 and secondary infection.6,8 –10 Treatment strategies include both surgical and nonsurgical approaches.1,3,5,7,8,10 –16 In cases of severe intrathoracic hemorrhage, i.e. intrathoracic blood loss ⬎1000 to 1500 mL/24 hours or continuos blood loss of 250 to 500 mL/ 3 hours7,16 –19 and disseminated intravascular coagulation,20 thoracotomy has been advocated. Here we report the successful outcome from PPP secondary to severe lung contusion with severe intrathoracal hemorrhage by aggressive coagulation management, kinetic therapy/postural drainage, and control of secondary infection. CASE REPORT A 28-year-old man was admitted to the emergency department (ED) after a motorcycle crash. At the scene he initially presented with a Glasgow Coma Scale (GCS) score of 14, blood pressure (BP) 110/80 mm Hg, unstable thoracic cage, hemorrhagic sputum, tachypnea, and SpO2 70%. He was intubated and mechanically ventilated with an FiO2 of 1.0 and a PEEP of 5 mbar. Ventilation of the lung was Submitted for publication December 4, 2004. Accepted for publication June 2, 2005. Copyright © 2007 by Lippincott Williams & Wilkins From the Department of Trauma and Orthopedic Surgery (E.S., B.B., N.Y., T.T., D.R., T.P., C.S., M.M.), and the Department of Anaesthesiology (D.K., V.K.), University of Witten/Herdecke, Hospital Cologne Merheim, Ostmerheimerstr. 200, D-51109 Cologne, Germany. Address for reprints: Marc Maegele, MD, Department of Trauma and Orthopedic Surgery, University of Witten/Herdecke, Merheim Medical Center, Ostmerheimerstr. 200, D-51109 Cologne, Germany; email: Marc.Maegele@tonline.de. DOI: 10.1097/01.ta.0000234656.93060.28 Volume 63 • Number 6 reduced on the right side on auscultation and a chest tube was inserted. During transportation cardiopulmonary function deteriorated and catecholamines were required. A total of 1500 mL blood was aspirated endotracheally. Upon arrival at the ED cardiopulmonary status was BP 80/50 mm Hg, tachycardia with 110 bpm, SpO2 78% while mechanically ventilated with an FiO2 of 1.0 and a PEEP of 5 mbar. A chest radiograph revealed a left tension pneumothorax that was immediately evacuated via insertion of a second chest tube, bronchoscopy showed massive hemorrhage in both lower lobes and in the right upper lobe. An additional 700 mL of blood was endotracheally aspirated. Laboratory findings: Hb 6.5 g/dL, platelets 188,000/nl, prothrombin time (PT) 39%, partial thromboplastin time (PTT) 61 seconds, base excess (BE) ⫺4.2 mmol/L, pH 7.22, pO2 102 mm Hg, pCO2 57 mm Hg under FiO2 of 1.0. Free intra-abdominal fluid was detected via ultrasonography and thus further diagnostic procedures were interrupted and immediate laparotomy was performed. A rupture of the spleen was identified as intra-abdominal bleeding source and a splenectomy was performed. Laboratory findings at that time point were Hb 4.8 g/dL, platelets 49,000/nl, PT 30%, PTT 80 seconds. The thrombelastogram indicated hyperfibrinolysis and subsequent fibrinogen(F1)-deficit. Coagulation was aggressively stabilized via administration of 12 units of packed red blood cells (pRBC), 11 units of fresh frozen plasma (FFP), 1 unit of platelet concentrate, 500.000 international units (IE) of aprotinin (Trasylol, Bayer Pharmaceuticals), and 2 g of fibrinogen. Respiratory dysfunction deteriorated intraoperatively (SaO2 61% under FiO2 1.0) while the patient continued to bleed intrathoracically and an additional 2500 mL of blood was aspirated from the lung. After surgical intervention the patient was transferred to the intensive care unit (ICU) in stable condition without catecholamines. On ICU arrival coagulation had been successfully re-established: Hb 9.9 g/dL, PT 87%, PTT 40 seconds. However, repeated bronchoscopy revealed continuos 1391 The Journal of TRAUMA威 Injury, Infection, and Critical Care Fig. 1. Repeated chest CT scans 48 hours after admission (A), day 5 (B), 6 weeks (C), and 6 months (D) after injury. Note that pseudocysts initially enlarged (B), then resolved over time (C,D). The CT scan of the chest taken 6 months after injury reveals complete resolution (D). bleeding from both lower lobes and the right upper lobe. Within the first 24 hours upon ICU arrival another 5 pRBCs, 14 FFPs, and 1 platelet concentrate were administered. Low dose heparinization with 7500 IE/24 hours was initiated. Under these measures coagulation was further improved with PT consistently ⬎90%, PTT ⬍40 seconds. In parallel, mechanically assisted axial kinetic therapy (Rotorest, KCI Medizinprodukte, Walluf, Germany) was initiated; ventilatory support including PEEP, initially raised to 15 mbar, and FiO2 was progressively reduced. On the second day of ICU the patient was stabile enough to complete diagnostics. Computed tomography (CT) of the thorax demonstrated bilateral pulmonary contusions, laceration and a cavitary lesion with an air-fluid level in the right upper lobe (Fig. 1A). Axial kinetic therapy was continued while bronchoscopy still revealed intrapulmonary blood secretion; however, consistently decreasing in quantity and with a progressive change in aspect from “fresh” to “old.” Repeated CT of the thorax on ICU day 5 demonstrated the cavity to increase in size (Fig. 1B). Clinically, stabilization continued and ventilatory support was further reduced; on ICU day 8 the patient was transferred from the Rotorest-bed into a standard ICU bed followed by alternating postural drainage, i.e. alternating 135 degree prone position, for another 4 days. On ICU day 9 the patient’s temperature rose to 40.2°C together with laboratory signs of infection, i.e. white blood 1392 cell count (WBC) of 29.000/nl, c-reactive protein (CRP) 265 mg/L. A repeated chest CT revealed an infiltrate left with corresponding bronchoscopic findings. Gross pus was collected during repeated bronchoscopy that was sent in for microbiological evaluation. Cultures grew Klebsiella pneumonia, sensitive to piperacilline/sulbactam. Twenty-four hours after targeted antibiotics were initiated, the patient’s clinical course markedly improved. Body temperature dropped to normal after 3 days, laboratory and bronchoscopy findings improved in parallel. On ICU day 16 there was no pus observed in the tracheobronchial tree. The patient was successfully extubated free of fever and under stable cardiopulmonary conditions on ICU day 18. A repeated CT of the thorax showed a resolving cavity with a markedly reduced air-fluid level as compared with earlier scans (Fig. 1C). The patient was discharged from the hospital 45 days after injury. Six months after discharge, the patient was free of symptoms and a last control CT scan revealed complete resolution of the lesion (Fig. 1D). Functional pulmonary assessment using spirometry indicated absence of ventilatory dysfunction. DISCUSSION Pulmonary injuries because of chest trauma account for one-quarter of all motor vehicle crash related deaths;3 however, PPP formation after blunt chest trauma is an uncommon entity.20 As in the present case, young adults and adolescents December 2007 Nonoperative Management of Pulmonary Pseudocyst are mostly affected.3,4,8 Pathophysiologically, PPP is referred to as an air- or fluid-filled intraparenchymal cavity that occurs in the setting of blunt chest trauma.10 The major contributing factors associated with its formation are (1) centrifugal forces acting on surrounding parenchyma, (2) shear stress because of reduced compliance within the lesion, and (3) positive pressures within the cyst.1 A one direction valve mechanism producing air trapping is further discussed.1 Along with respiratory distress and impaired compliance negative pressure transfer from the pleura to the lesion may occur thus aggravating distress and cyst enlargement. As also observed in the present case, PPP may change size and shape, thus becoming larger within the first 2 weeks after impact.6,10 If equilibrium is achieved between compliance of contused parenchyma and cyst as well as between positive airway pressures during inspiration and the pseudocyst, lesion progression is stopped, and diminishment starts with repair of injured lung parechchyma including escape of air from the pseudocyst to the airway.6 In contrast to perform early thoracotomy as commonly suggested in cases of severe hemorrhage with initial intrathoracic blood loss ⬎1,000 to 1,500 mL/24 hours or 250 to 500 mL/3 hours,7,16 –19 and although our patient sustained significant bleeding intrathoracically, primary management was directed toward aggressive stabilization of impaired coagulation as early as the patient entered our ED. This strategy was consistently followed throughout the operation phase and continued on the ICU. Thus, when the patient was transferred from the operation room to the ICU coagulation had already been sufficiently re-established (Hb 9.9 g/dL, PT 87% and PTT 40 seconds) and PT never dropped ⬍90% throughout the patient’s ICU stay. After 36 hours in the ICU and continued aggressive coagulation management repeated bronchoscopy revealed no further intrapulmonary bleeding. Bronchial isolation and embolization were considered however neglected as repeated airway toilet via bronchoscopy indicated bleeding from both lungs. This approach would have been reasonable if bleeding was restricted to one side only.21 Instead, PEEP was initially increased although at risk for air embolism but then progressively reduced as no further bleeding was detected. Complementary therapeutic strategies included mechanically assisted axial kinetic therapy (Rotorest) and postural drainage. Kinetic therapy and postural drainage, even used prophylactically in multiple trauma patients whose injuries and pattern predispose to acute respiratory distress syndrome (ARDS), has been shown to improve oxygenation in patients with impaired pulmonary function.22,23 To date, a series of studies in patients with thoracic trauma confirm these findings indicating better oxygenation/gaseous exchange, less atelectases, lower incidences of pneumonia and ARDS, and improved outcome with axial rotation.22,24 –30 The benefits attributable to kinetic therapy comprise mobilization and clearance of respiratory secretions thus improving ventilationperfusion ratios and pulmonary recruitment. As kinetic therapy is considered to substantially contribute toward improving negative outcome of patients with severe respiratory failure after Volume 63 • Number 6 major trauma, this strategy was integrated in our treatment regimen presented here.31 The costs to rent the bed may be offset by the potential cost reduction associated with kinetic therapy.30 Secondary infection of PPP occurs in some cases and has been reported to cause significant morbidity and mortality.6,8 –10 In the present case, delayed infection was suspected as clinical signs of infection were evident on ICU day 9. Microbiological analysis identified Klebsiella pneumonia and targeted antibiotics were administered. This approach was in concert with earlier reports5,9 and led to a profound clinical improvement within days. Despite initial enlargement, as known from earlier reports,5,6 the cavity progressively dissolved over time leaving the indications for further intervention absent. One may argue about the use of prophylactic antibiotics in the setting of acute thoracic trauma.32–36 However, pseudocyst infections usually occur late10 as also observed in the present case, and prologend antibiotic prophylaxis would most likely rather increase the selection of resistant strains thus promoting pathogen colonization than benefit. Although the nonoperative approach presently reported led to successful outcome, we cannot exclude operative strategies as therapeutical options in other cases. However, in cases of severe hemorrhage we emphasize the value of highly aggressive management of underlying coagulation disorders as routinely performed in the Cologne-Merheim trauma department. If coagulation is successfully restored and bleeding is controlled, this may prevent the patient from undergoing surgical procedures. Repeated bronchoscopy for airway toilet and consequent kinetic therapy/postural drainage were additional cornerstones of therapeutic initiatives, in particular within the early phase. Bronchial isolation and embolization may be considered if bleeding originates from one lobe only.21 Tight microbiological assessment of samples from the tracheo-broncho-pulmonary system is recommended to initiate targeted anti-infective therapy as early as possible to control secondary infection. Gincherman et al.9 proposed to send sputum cultures on all patients having sustained significant blunt chest trauma if radiologic findings of contusion or pseudocyst are present. 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