Clinical significance and risk factors for new onset and recurring atrial fibrillation following cardiac surgery - a retrospective data analysis.

BACKGROUND: Although mortality after cardiac surgery has significantly decreased in the last decade, patients still experience clinically relevant postoperative complications. Among others, atrial fibrillation (AF) is a common consequence of cardiac surgery, which is associated with prolonged hospitalization and increased mortality. METHODS: We retrospectively analyzed data from patients who underwent coronary artery bypass grafting, valve surgery or a combination of both at the University Hospital Muenster between April 2014 and July 2015. We evaluated the incidence of new onset and intermittent/permanent AF (patients with pre- and postoperative AF). Furthermore, we investigated the impact of postoperative AF on clinical outcomes and evaluated potential risk factors. RESULTS: In total, 999 patients were included in the analysis. New onset AF occurred in 24.9% of the patients and the incidence of intermittent/permanent AF was 59.5%. Both types of postoperative AF were associated with prolonged ICU length of stay (median increase approx. 2 days) and duration of mechanical ventilation (median increase 1 h). Additionally, new onset AF patients had a higher rate of dialysis and hospital mortality and more positive fluid balance on the day of surgery and postoperative days 1 and 2. In a multiple logistic regression model, advanced age (odds ratio (OR) = 1.448 per decade increase, p < 0.0001), a combination of CABG and valve surgery (OR = 1.711, p = 0.047), higher C-reactive protein (OR = 1.06 per unit increase, p < 0.0001) and creatinine plasma concentration (OR = 1.287 per unit increase, p = 0.032) significantly predicted new onset AF. Higher Horowitz index values were associated with a reduced risk (OR = 0.996 per unit increase, p = 0.012). In a separate model, higher plasma creatinine concentration (OR = 2.125 per unit increase, p = 0.022) was a significant risk factor for intermittent/permanent AF whereas higher plasma phosphate concentration (OR = 0.522 per unit increase, p = 0.003) indicated reduced occurrence of this arrhythmia. CONCLUSIONS: New onset and intermittent/permanent AF are associated with adverse clinical outcomes of elective cardiac surgery patients. Different risk factors implicated in postoperative AF suggest different mechanisms might be involved in its pathogenesis. Customized clinical management protocols seem to be warranted for a higher success rate of prevention and treatment of postoperative AF.

Base excess determined within one hour of admission predicts mortality in patients with severe pelvic fractures and severe hemorrhagic shock.

BACKGROUND: Unstable pelvic ring fractures with exsanguinating hemorrhages are rare but potentially lifethreatening injuries. The aim of this retrospective study was to evaluate whether early changes in acid- base parameters predict mortality of patients with severe pelvic trauma and hemorrhagic shock. METHODS: Data for 50 patients with pelvic ring disruption and severe hemorrhage were analyzed retrospectively. In all patients, the pelvic ring was temporarily stabilized by C-clamp. Patients with ongoing bleeding underwent laparotomy with extra and/or intraperitoneal pelvic packing, as required. Base excess, lactate, and pH were measured upon admission and at 1, 2, 3, 4, 6, 8, and 12 h postadmission. Patients were categorized as early survivors (surviving the first 12 h after admission) and nonsurvivors. Statistical analysis was performed by Mann-Whitney test; significance was assumed at p < 0.05. Receiver operating characteristic curves were generated for early mortality from each acid-base variable. RESULTS: Sixteen patients (32%) were nonsurvivors due to hemorrhagic shock (n = 13) or severe traumatic brain injury (n = 3). Thirty-four patients were early survivors. Base excess, lactate, and pH significantly discriminated between early survivors and nonsurvivors. Base excess determined 1 h after admission discriminated most strongly, with an area under the receiver operating characteristic curve of 0.915 (95% confidence interval, 0.836-0.993; p < 0.001). CONCLUSION: Base excess, lactate, and pH discriminate early survivors from nonsurvivors suffering from severe pelvic trauma and hemorrhagic shock. Base excess measured 1 h after admission best predicted early mortality following pelvic trauma with concomitant hemorrhage.

Prolonged superficial local cryotherapy attenuates microcirculatory impairment, regional inflammation, and muscle necrosis after closed soft tissue injury in rats.

BACKGROUND: Closed soft tissue injury induces progressive microvascular dysfunction and regional inflammation. The authors tested the hypothesis that adverse trauma-induced effects can be reduced by local cooling. While superficial cooling reduces swelling, pain, and cellular oxygen demand, the effects of cryotherapy on posttraumatic microcirculation are incompletely understood. STUDY DESIGN: Controlled laboratory study. METHODS: After a standardized closed soft tissue injury to the left tibial compartment, male rats were randomly subjected to percutaneous perfusion for 6 hours with 0.9% NaCL (controls; room temperature) or cold NaCL (cryotherapy; 8 degrees C) (n = 7 per group). Uninjured rats served as shams (n = 7). Microcirculatory changes and leukocyte adherence were determined by intravital microscopy. Intramuscular pressure was measured, and invasion of granulocytes and macrophages was assessed by immunohistochemistry. Edema and tissue damage was quantified by gravimetry and decreased desmin staining. RESULTS: Closed soft tissue injury significantly decreased functional capillary density (240 +/- 12 cm(-1)); increased microvascular permeability (0.75 +/- 0.03), endothelial leukocyte adherence (995 +/- 77/cm(2)), granulocyte (182.0 +/- 25.5/mm(2)) and macrophage infiltration, edema formation, and myonecrosis (ratio: 2.95 +/- 0.45) within the left extensor digitorum longus muscle. Cryotherapy for 6 hours significantly restored diminished functional capillary density (393 +/- 35), markedly decreased elevated intramuscular pressure, reduced the number of adhering (462 +/- 188/cm(2)) and invading granulocytes (119 +/- 28), and attenuated tissue damage (ratio: 1.7 +/- 0.17). CONCLUSION: The hypothesis that prolonged cooling reduces posttraumatic microvascular dysfunction, inflammation, and structural impairment was confirmed. CLINICAL RELEVANCE: These results may have therapeutic implications as cryotherapy after closed soft tissue injury is a valuable therapeutic approach to improve nutritive perfusion and attenuate leukocyte-mediated tissue destruction. The risk for evolving compartment syndrome may be reduced, thereby preventing further irreversible aggravation.

Local cooling restores microcirculatory hemodynamics after closed soft-tissue trauma in rats.

BACKGROUND: Severe closed soft-tissue injury (CSTI) results in progressively developing microvascular dysfunction and local inflammation. Cooling reduces swelling, pain, cellular oxygen demand, and metabolic activity. However, effects of cooling on posttraumatic microcirculation are not yet fully understood. Thus, we assessed effects of local cooling on microcirculation, regional inflammatory response including leukocyte-endothelial cell interaction, and edema formation after CSTI. METHODS: Standardized CSTI was induced by means of controlled impact injury in the left tibial compartment of 14 male Sprague-Dawley rats. Rats were assigned to four groups (n = 7 per group) as follows: group I, no trauma/no cooling; group II, no trauma/20 minutes of cooling; group III, 1.5 hours posttrauma/no cooling; and group IV, 1.5 hours posttrauma/20 minutes of cooling. RESULTS: CSTI resulted in a significant decrease in functional capillary density, a marked increase in microvascular permeability, and granulocyte infiltration (HIS48) as revealed by intravital microscopy and immunohistochemistry of the left extensor digitorum longus muscle. After 20 minutes of local cooling, these microvascular derangements were restored to the level of controls (group I). Edema (extensor digitorum longus muscle wet-to-dry weight ratio) was less pronounced compared with noncooling conditions (group III). Immunoreactivity for HIS48 (neutrophilic granulocytes) in injured rats subjected to local cooling (group IV) was markedly decreased compared with noncooling conditions (group III). CONCLUSION: These results provide in vivo evidence that cooling affords protection of posttraumatic microcirculation through sustained inhibition of microvascular and endothelial dysfunction leading to less granulocyte-dependent inflammation and skeletal muscle edema. Local cooling appears to reduce propagation of acute microvascular injury, preventing leukocyte-dependent tissue destruction and escalation of secondary tissue damage after musculoskeletal soft-tissue trauma.

Acute, transient hemorrhagic hypotension does not aggravate structural damage or neurologic motor deficits but delays the long-term cognitive recovery following mild to moderate traumatic brain injury.

OBJECTIVES: Posttraumatic hypotension is believed to increase morbidity and mortality in traumatically brain-injured patients. Using a clinically relevant model of combined traumatic brain injury with superimposed hemorrhagic hypotension in rats, the present study evaluated whether a reduction in mean arterial blood pressure aggravates regional brain edema formation, regional cell death, and neurologic motor/cognitive deficits associated with traumatic brain injury. DESIGN: Experimental prospective, randomized study in rodents. SETTING: Experimental laboratory at a university hospital. SUBJECTS: One hundred nineteen male Sprague-Dawley rats weighing 350-385 g. INTERVENTIONS: Experimental traumatic brain injury of mild to moderate severity was induced using the lateral fluid percussion brain injury model in anesthetized rats (n = 89). Following traumatic brain injury, in surviving animals one group of animals was subjected to pressure-controlled hemorrhagic hypotension, maintaining the mean arterial blood pressure at 50-60 mm Hg for 30 mins (n = 47). The animals were subsequently either resuscitated with lactated Ringer's solution (three times shed blood volume, n = 18) or left uncompensated (n = 29). Other groups of animals included those with isolated traumatic brain injury (n = 34), those with isolated hemorrhagic hypotension (n = 8), and sham-injured control animals receiving anesthesia and surgery alone (n = 22). MEASUREMENTS AND MAIN RESULTS: The withdrawal of 6-7 mL of arterial blood significantly reduced mean arterial blood pressure by 50% without decreasing arterial oxygen saturation or Pao2. Brain injury induced significant cerebral edema (p < .001) in vulnerable brain regions and cortical tissue loss (p < .01) compared with sham-injured animals. Neither regional brain edema formation at 24 hrs postinjury nor the extent of cortical tissue loss assessed at 7 days postinjury was significantly aggravated by superimposed hemorrhagic hypotension. Brain injury-induced neurologic deficits persisted up to 20 wks after injury and were also not aggravated by the hemorrhagic hypotension. Cognitive dysfunction persisted for up to 16 wks postinjury. The superimposition of hemorrhagic hypotension significantly delayed the time course of cognitive recovery. CONCLUSIONS: A single, acute hypotensive event lasting 30 mins did not aggravate the short- and long-term structural and motor deficits but delayed the speed of recovery of cognitive function associated with experimental traumatic brain injury.

The effect of N-acetylcysteine on posttraumatic changes after controlled cortical impact in rats.

OBJECTIVE: The antioxidant potential N-Acetylcysteine (NAC) and its improvement of posttraumatic mitrochondrial dysfunction have been reported. This study investigated the effect of NAC on posttraumatic changes after controlled cortical Impact (CCI) injury. DESIGN AND SETTING: Prospective randomized controlled animal study. METHODS: A moderate left focal cortical contusion was induced using CCI. Either NAC (163 mg/kg bw) or physiological saline was administered intraperitoneally immediately and 2 and 4 h after trauma. Blood gases, temperature, mean arterial blood pressure (MABP), and intracranial pressure (ICP) were monitored. Twenty-four hours after trauma brains were removed and either posttraumatic edema was quantified gravimetrically (n=24], or contusion volume was determined morphometrically using slices staining and computerized image analysis (n=24]. Laser Doppler flowmetry was used to assess pericontusional cortical perfusion before trauma, 30 min and 4 and 24 h after trauma (n=14]. MEASUREMENTS AND RESULTS: Physiological parameters remained within normal limits. ICP measurements and water content in traumatized hemispheres did not differ between the groups. Relative contusion volume of the left hemisphere was slightly but nonsignificantly diminished in NAC-treated animals (4.7+/-0.4% vs. 5.9+/-0.5% in controls). In both groups pericontusional perfusion was significantly reduced at 4 h followed by a state of hyperperfusion at 24 h with no differences between the groups. CONCLUSIONS: Despite previously reported neuroprotective abilities of NAC, no positive effect on posttraumatic perfusion, brain edema formation, or contusion volume after focal brain injury was observed in this study.

Acute effects of N-acetylcysteine on skeletal muscle microcirculation following closed soft tissue trauma in rats.

Trauma-induced microcirculatory dysfunction, formation of free radicals and decreased endothelial release of nitric oxide (NO) contribute to evolving tissue damage following skeletal muscle injury. Administration of N-acetylcysteine (NAC) known to scavenge free radicals and generate NO is considered a valuable therapeutic approach. Thus, the objective of this study was to quantitatively analyze the acute effects of NAC on skeletal muscle microcirculation and leukocyte-endothelial cell interaction following severe standardized closed soft tissue injury (CSTI). Severe CSTI was induced in the hindlimbs of 14 male anesthetized Sprague-Dawley rats using the controlled impact injury technique. Rats were randomly assigned (n = 7) to high-dose intravenous infusion of NAC (400 mg/kg body weight) or isovolemic normal saline (NS). Non-injured, sham-operated animals (n = 7) were subjected to the same surgical procedures but did not receive any additional fluid. Creatin kinase (CK) activity was assessed at baseline, 1 h before and 2 h following posttraumatic NAC or NS infusion. Microcirculation of the extensor digitorum longus (EDL) muscle was analyzed using intravital microscopy and Laser-Doppler flowmetry (LDF). Edema index (EI) was calculated by measuring the EDL wet-to-dry weight ratio (EI=injured/contralateral limb). EDL-muscles were analyzed for desmin immunoreactivity and granulocyte infiltration. Microvascular deteriorations observed following NS-infusion were effectively reversed by NAC: Functional capillary density was restored to levels found in sham-operated animals and leukocyte adherence was significantly (p < 0.05) reduced compared to the NS group. NAC significantly (p < 0.05) increased erythrocyte flux determined by Laser-Doppler flowmetry. Posttraumatic serum CK levels and EI were significantly (p < 0.05) decreased by NAC. During the posttraumatic acute phase, single infusion of NAC markedly reduced posttraumatic microvascular dysfunction, attenuated both leukocyte adherence and tissue infiltration. NAC also decreased CSTI-induced edema formation and myonecrosis as reflected by attenuated serum CK levels and attenuated loss of desmin immunoreactivity. NAC may serve as an effective therapeutic strategy by supporting microvascular blood supply and tissue viability in the early posttraumatic period. Additional studies aimed at long-term analysis and investigation of injury severity--or dosage dependency are needed.

Norepinephrine infusion increases interleukin-6 in plasma and cerebrospinal fluid of brain-injured rats.

BACKGROUND: Significantly increased plasma and CSF IL-6 levels reflect underlying tissue damage following clinical and experimental traumatic brain injury (TBI). Catecholamines, used under clinical conditions to maintain adequate cerebral perfusion pressure, induce a sustained IL-6 release. Thus an additional elevation in IL-6 could aggravate brain edema in the acute posttraumatic phase. We studied the changes in plasma and cerebrospinal fluid (CSF) IL-6 levels 4 and 24 hours after experimental TBI and assessed possible time-dependent effects of norepinephrine infusion on IL-6 and brain edema. MATERIAL/METHODS: Paired plasma and CSF IL-6 measured at 4 and 24 hours following TBI (n=10) were compared to levels in non-traumatized rats (n=5). In a placebo-controlled trial, 20 brain-injured male Sprague-Dawley rats were randomized to receive norepinephrine or NaCl for 90 minutes at 4 or 24 hours after TBI. Plasma IL-6 was measured before, during, and after the infusion period. One hour after stopping the infusion, CSF IL-6 and hemispheric swelling were determined. RESULTS: During the first posttraumatic day, plasma and CSF IL-6 levels were significantly increased compared to non-traumatized rats, reaching the highest values at 24 hours (p<0.05). Norepinephrine infusion significantly increased plasma IL-6 at 7 and 27 hours after TBI; IL-6 was significantly elevated in CSF only at 7 hours (p<0.05). Brain edema was not aggravated. CONCLUSIONS: The norepinephrine-induced increase in plasma and CSF IL-6 suggests that concomitant norepinephrine administration needs to be considered when interpreting systemic and local changes in IL-6 levels in TBI patients.

Mild cervical spine trauma showing symptomatic calcified cervical disc herniation in a child: a case report.

STUDY DESIGN: A case study was conducted. OBJECTIVE: A child with a previously unknown calcified cervical disc herniation experienced acute myelopathy after minor cervical trauma. SUMMARY AND BACKGROUND DATA: Calcified cervical intervertebral disc herniations are rare in children. Although these herniations typically pursue a benign course and respond to conservative treatment, surgical removal of the disc may become necessary if spinal cord compression becomes symptomatic. METHODS: After a minor traumatic event, a 12-year-old boy with an underlying calcified cervical disc herniation at C3-C4 experienced progressive myelopathy requiring anterior discectomy and intervertebral fusion. RESULTS: After the progression of myelopathy over a 3-week period, an anterior discectomy and fusion with autologous tricortical iliac bone graft was performed at C3-C4. Histologic analysis showed a calcified disc herniation. CONCLUSION: In the presence of a large, calcified cervical disc herniation, mild cervical trauma may result in the onset of severe spastic myelopathy warranting surgical correction.