Pediatric Acute Paradoxical Cerebral Embolism with Pulmonary Embolism Caused by Extremely Small Patent Foramen Ovale.

Herein, we report a pediatric case of acute paradoxical cerebral embolism complicated by serious acute pulmonary embolism that was caused by an extremely small patent foramen ovale (PFO). The patient had no medical history suggestive of any other reason. Paradoxical cerebral embolism may occur even with an extremely small PFO because of the increased right-side pressure of the heart and a resulting right-to-left shunt from the acute pulmonary embolism. Although pediatric cases of pulmonary embolism are rare, when diagnosed, clinicians should consider the risk of a concurrent paradoxical cerebral embolism resulting from a latent PFO. The possibility of PFO should be assessed extremely carefully in pediatric critical care by checking for a thrombogenesis tendency and the existence of deep vein thrombosis in the patient.

High serum pentosidine in branch atheromatous disease among small vessels occlusion.

BACKGROUND: Cerebral branch atheromatous disease (BAD) are more likely to experience progressing stroke and neurological deterioration compared with lacunar infarction, although these small vessels occlusions are difficult to discriminate in acute phase of ischemic stroke. Advanced glycation end products including pentosidine have been implicated in atherosclerosis, and were associated with atheroma plaque progression. However, little is known about a relationship between serum pentosidine and small vessels occlusion. METHODS: Serum pentosidine levels were measured in 56 patients (BAD: N.=21; lacunar: N.=35) with small vessels occlusion among consecutive 208 patients with acute ischemic stroke at initial hospitalization as well as other risk factors of stroke. Univariate and multivariate logistic regression analyses were performed to analyze relationship between risk factors including pentosidine and small vessels occlusion. Sensitivity and selectivity of pentosidine to discriminate BAD from lacunar were calculated. RESULTS: Serum pentosidine was significantly higher in BAD group than lacunar group (0.081±0.081 µg/mL and 0.046±0.043 µg/mL, P<0.05). In the univariate logistic regression analyses, BAD was significantly related to high serum pentosidine (P=0.01), absence of dyslipidemia (P=0.04), and worse outcome measured by modified Rankin Scale (P=0.03). Multivariate logistic regression analysis showed that only high level of serum pentosidine was the independent risk factor for BAD (P=0.03). Sensitivity and specificity were 90% and 44%, respectively. CONCLUSIONS: High level of serum pentosidine in acute phase of stroke was associated with BAD, which led to worse outcome among patients with small vessels occlusion.

Serum pentosidine, an advanced glycation end product, indicates poor outcomes after acute ischemic stroke.

BACKGROUND: An advanced glycation end product has been implicated in a wide range of pathologic conditions, including diabetes mellitus, chronic kidney diseases, cardiovascular diseases, and arteriosclerosis. Little is known about its relationship with cerebral ischemia. The authors investigated serum levels of pentosidine and outcomes of patients with acute ischemic stroke METHODS: Serum pentosidine levels were measured in 83 patients with acute ischemic stroke at initial hospitalization and other risk factors of stroke. Outcomes of patients at 30 days from hospitalization were assessed by using modified Rankin Scale (mRS) score. Univariate and multivariate logistic regression analyses were performed to analyze the relationship between pentosidine and patient outcomes. RESULTS: In the univariate logistic regression analyses, poor outcomes, defined as mRS scores of >2, at 30 days were significantly related to high serum pentosidine (P = .001), type of stroke (P = .045), old age (P = .02), male sex (P = .042), and the absence of dyslipidemia (P = .02). Deterioration of mRS was significantly correlated with high serum pentosidine (P = .003) and creatinine (P = .02). Multivariate logistic regression analysis showed that a high level of serum pentosidine was the only independent risk factor for poor outcomes (P = .004) and deterioration of mRS (P = .01) at 30 days. CONCLUSIONS: A high level of serum pentosidine indicates poor and worse outcomes 30 days after acute ischemic stroke. This new biomarker is useful for risk stratification of patients with acute ischemic stroke.

Effects of bag-mask versus advanced airway ventilation for patients undergoing prolonged cardiopulmonary resuscitation in pre-hospital setting.

BACKGROUND: There is no evidence that the advanced airway ventilation (AAV) method improves patient outcome in the pre-hospital cardiac arrest setting. OBJECTIVE: The aim of this study was to estimate the effectiveness of AAV vs. bag-mask ventilation (BMV) for cardiopulmonary arrest (CPA) patients, when administered by a licensed emergency medical technician in the pre-hospital setting. METHODS: The study used the database of patients who suffered out-of-hospital cardiogenic CPA from 2006 to 2007 in our hospital. Patient records were searched for the method of pre-hospital airway management (BMV or AAV) and the patient's outcomes were compared between groups. The primary endpoint was a favorable neurological outcome; the secondary endpoints were rate of return of spontaneous circulation (ROSC) and rate of admission to the intensive care unit (ICU). RESULTS: A total of 355 CPA patients (156 BMV and 199 AAV) were retrospectively enrolled. There was no significant difference in demographics between the two groups. The transportation time exceeded 30 min in both groups. The overall ROSC rate and ICU admission rate were significantly higher in the AAV group (p = 0.0352 and p = 0.0089, respectively). The data showed that AAV (odds ratio 1.960; 95% confidence interval 1.015-3.785) resulted in a higher overall ROSC rate than BMV, but there were no significant differences in either the rate of pre-hospital ROSC or in favorable neurological outcome. CONCLUSION: AAV may yield advantages over BMV in the overall rate of ROSC in CPA patients, but both approaches for airway management in this study resulted in a comparably favorable neurological outcome. Earlier ROSC would be required for improved overall outcome.

Change in brain glucose after enteral nutrition in subarachnoid hemorrhage.

BACKGROUND: The alteration of brain extracellular glucose after enteral nutrition (EN) remains unclear. In this study, we used brain microdialysis methods to estimate whether the physiologic elevation of plasma glucose following EN affects brain glucose metabolism of aneurysmal subarachnoid hemorrhage (SAH) patients. METHODS: Brain extracellular glucose, lactate, glycerol, glutamate, and pyruvate were measured with a brain microdialysis probe in 12 patients (mean age: 60.0 y+/-7.8 y) after SAH. The EN was initially administered a mean of 3.2 d after the onset of SAH. All of the measured parameters were estimated before and after EN. RESULTS: Cerebral perfusion pressure did not significantly change after SAH during the study period. Plasma glucose rose significantly after EN (141.4+/-11.6mg/dL before EN versus 183.8+/-26.2mg/dL immediately after EN (P=0.0006), 177.7+/-30.2mg/dL at 2h after EN (P=0.0033)). The brain extracellular glucose before EN (2.5+/-0.92mmol/L) was significantly lower than the levels measured just after (3.49+/-1.0mmol/L, P=0.0186) and 2h after the end of EN (3.70+/-1.0mmol/L, P=0.0053). Brain extracellular concentrations of lactate, glutamate, pyruvate, and glycerol showed no significant changes. CONCLUSIONS: Brain extracellular glucose increased after the transient elevation of plasma glucose following EN. These results suggest that brief, physiologic elevations in plasma glucose after EN produced no changes in brain extracellular glutamate concentration or lactate/pyruvate ratio. These data may help determine the plasma glucose levels most effective for avoiding brain metabolic acidosis in patients after SAH. It remains unclear, however, how SAH itself influences these findings.

Transient blockage of the CD11d/CD18 integrin reduces contusion volume and macrophage infiltration after traumatic brain injury in rats.

The early inflammatory response to traumatic brain injury (TBI) may result in secondary damage. The purpose of this study was to evaluate the effects of a transient treatment employing a blocking monoclonal antibody (mAb) to the CD11d/CD18 integrin on histopathological outcome and macrophage infiltration following TBI. A parasagittal fluid percussion (FP) brain injury (1.8-2.1 atm) was induced in male Sprague-Dawley rats. Rats were randomized into two trauma groups, treated (N=7) and nontreated (N=8) animals. In the treated group, a mAb to the CD11d subunit of the CD11d/CD18 integrin was administered 30 min, 24 and 48 h after brain injury. Control animals received an isotype-matched irrelevant mAb using the same dose and treatment regimen. At 3 days after TBI, animals were perfusion-fixed for histopathological and immunocytochemical analysis. The anti-CD11d mAb treatment reduced contusion areas as well as overall contusion volume compared to vehicle treated animals. For example, overall contusion volume was reduced from 2.7+/-0.5 mm(3) (mean+/-SEM) to 1.4+/-0.4 with treatment (p<0.05). Immunocytochemical studies identifying CD68 immunoreactive macrophages showed that treatment caused significant attenuation of leukocyte infiltration into the contused cortical areas. These data emphasize the beneficial effects of blocking inflammatory cell recruitment into the injured brain on histopathological outcome following traumatic brain injury.

Systemic inflammation exacerbates behavioral and histopathological consequences of isolated traumatic brain injury in rats.

The proinflammatory cytokine interleukin-1beta (IL-1beta) is induced rapidly after traumatic brain injury (TBI) and contributes to the inflammatory events that lead to neuronal loss. Although an important source of IL-1beta is from the injured brain itself, in patients with multiple organ trauma (polytrauma) IL-1beta is also released into the bloodstream which may potentially influence brain vulnerability. The purpose of this study was to determine the effects of systemic inflammation induced by peripheral administration of IL-1beta on histopathological and behavioral outcome after moderate fluid percussion (FP) brain injury in rats. At 30 min or 24 h after TBI, saline, 20 mug/kg or 40 mug/kg of IL-1beta was injected (n=4-9/group) intraperitoneally (IP). Sham operated animals (n=9) received either saline or IL-1beta (20 or 40 mug/kg) injections. The somatosensory tactile placing test was administered at 1, 2 and 3 days posttrauma. IL-1beta-treated animals showed significant placing deficits compared to vehicle-treated TBI animals. Three days after injection, contusion areas and volumes were significantly increased (p<0.05) with both IL-1beta doses and at both treatment times compared to vehicle-treated animals. IL-1beta-treated rats showed more contusion injury and hippocampal neuronal damage as well as enhanced perivascular neutrophil accumulation. Cortical IL-1r1 mRNA increased as early as 1 h following TBI, peaking at 24 h and remained elevated 3 days posttrauma. These data show that the posttraumatic administration of IL-1beta significantly aggravates behavioral outcome and increases overall contusion volume after TBI. Increased systemic inflammatory processes, including extravasation of activated leukocytes and proinflammatory cytokines could participate in this detrimental outcome. Because peripherally circulating cytokines and other neurotoxic factors may be increased following multi-organ trauma, these findings may be important in targeting therapeutic interventions in this patient population.

Interleukin-8 production from human umbilical vein endothelial cells during brief hyperglycemia: the effect of tumor necrotic factor-alpha.

BACKGROUND: This study evaluated the changes in chemokine interleukin (IL)-8 production from endothelial cells under various hyperglycemic conditions and investigated whether the hyperglycemia associated with the acute inflammatory response could enhance the IL-8 production from the endothelial cells. MATERIALS AND METHODS: Human umbilical endothelial cells (HUVECs) were seeded at a concentration of 1 x 10(5) cells/well and cultured. The culture medium was replaced with Medium 199 containing various concentrations of glucose (final glucose concentration of culture medium was 100, 200, 300, 400, 500 mg/dL; n = 7 each) with or without 100 ng of tumor necrosis factor-alpha (TNF-alpha). After 12 or 24 h at 37 degrees C, the supernatants were collected from the cultures and stored at -80 degrees C until cytokine assay. IL-8 levels of the samples from the supernatants were quantified using a commercially available enzyme-linked immunosorbent assay kit. RESULTS: The IL-8 production by the HUVECs was significantly higher in the high glucose culture than in the control culture (glucose concentration of 100 mg/dL) (P < 0.05). Moreover, the hyperglycemia associated with elevated TNF-alpha was found to enhance the level of IL-8 production by the HUVECs cultured at all glucose concentrations and over both time courses, compared to the control (P < 0.05). CONCLUSIONS: In this study we observed a significant augmentation of IL-8 production by endothelial cells during short-term hyperglycemia, and a similar but significantly stronger augmentation was obtained through TNF treatment. These findings suggest that the hyperglycemia associated with acute inflammatory response after trauma may put the patients at high risk for secondary tissue damage.

The expression of the inducible nitric oxide synthase messenger RNA on monocytes in severe acute pancreatitis.

BACKGROUND/AIMS: Although there have been numerous studies that nitric oxide (NO) is produced in monocytes and macrophages in animal models, it still remains controversial whether NO is produced by human monocytes and macrophages. To clarify whether NO is produced by human monocytes in patients with systemic inflammatory response syndrome (SIRS), we examined the expression of inducible nitric oxide synthase (iNOS) messenger RNA (mRNA) and constitutive nitric oxide synthase (cNOS) mRNA in cultured monocytes derived from severe acute pancreatitis patients complicated with SIRS. METHODOLOGY: Monocytes were harvested from peripheral blood of nine severe acute pancreatitis patients with SIRS (group S) and five mild acute pancreatitis patients with no SIRS (group M). Then we examined the expression of iNOS mRNA and cNOS mRNA in cultured monocytes using the reverse transcription PCR (RT-PCR) method. RESULTS: iNOS mRNA was expressed in the cultured monocytes derived from eight of the nine patients in group S, but not in any of the five patients in group M, while cNOS mRNA was not found in cultured monocytes derived from any patient in either group. CONCLUSIONS: Although it is still not clear whether NO is produced in human monocytes or not, these findings indicate that iNOS is induced in monocytes in severe acute pancreatitis patients with SIRS, but not in mild pancreatitis patients.

Reduced effectiveness of hypothermia in patients lacking the wave V in auditory brainstem responses immediately following resuscitation from cardiac arrest.

AIMS: Therapeutic hypothermia appears to improve the outcome of pre-hospital cardio-pulmonary arrest (CPA) in patients with an initial cardiac rhythm of ventricular fibrillation or nonperfusing ventricular tachycardia (VF/VT). Notwithstanding, the outcome of this procedure is certainly difficult to predict based solely on the initial rhythm. The aim of the present study was to predict the outcome using auditory brainstem responses (ABRs) in CPA patients treated with therapeutic hypothermia. DESIGN AND SETTING: A prospective observational study in the intensive care unit of a university hospital. PATIENTS: The study included 26 patients resuscitated from out-of-hospital CPA. INTERVENTIONS: Basic and advanced cardiac life support, intensive care and post-resuscitative hypothermia. MEASUREMENT AND RESULTS: ABRs were recorded immediately after the return of spontaneous circulation (ROSC). An ABR wave V was recorded in 16 patients. Among 8 patients with a favourable outcome, the initial rhythms were VF/VT in 6 patients and other rhythms in 2. All 10 patients without a detectable ABR wave V had an unfavourable outcome. The VF/VT as the initial arrest rhythm and the presence of wave V were significantly (p = 0.0095) correlated with a favourable outcome. The presence of wave V had a 100% sensitivity to a favourable outcome. CONCLUSION: The absence of the ABR wave V in the early phase after ROSC wave indicated a reduced effect of therapeutic hypothermia, even in cases that underwent hypothermia promptly after out-of-hospital CPA. Measurement of ABRs appears to be useful as a predictor of effectiveness and as a criterion for determining the indication for therapeutic hypothermia.

Risk factors for intraoperative hypotension in traumatic intracranial hematoma.

Patients suffering from traumatic intracranial hemorrhage (TICH) may experience an episode of catastrophic intraoperative hypotension (IHT), after decompression of the brain. The aim of this study was to investigate the risk factors for IHT during emergency craniotomy A total of 67 patients, who underwent emergency craniotomy due to TICH, were divided into two groups: IHT ( n=31 ) or without IHT ( n=36 ). Data concerning (1) age; (2) gender; (3) mechanism of injury; (4) Glasgow Coma Scale (GCS) on admission; (5) abnormality of the pupils (anisocoria or mydriasis); (6) mean arterial blood pressure; (7) heart rate; (8) time elapsed before craniotomy from injury; (9) initial brain CT scans; (10) duration of craniotomy; and (11) total infusion or urine volume until craniotomy were collected prospectively as IHT risk factors. Low GCS score (<5), tachycardia (heart rate >112min(-1)) and hypertension (mean blood pressure >131mmHg) before emergency craniotomy were strongly ( P<0.05 ) associated with IHT. Delayed surgery (>173min until craniotomy) also had a significant ( P<0.005 ) effect on IHT. The risk factors for IHT were considered as a low GCS score on admission, tachycardia, hypertension before emergency craniotomy and delayed surgery. These results suggested the patients with IHT had a high sympathetic tone before emergency craniotomy A sudden reduction in sympathetic tone after surgical decompression of the brain might cause IHT. We concluded that an important factor in the occurrence of IHT was not only the injury severity, but also the balance between sympathetic and parasympathetic activity before decompression surgery.