Early critical cortical infarction by anti-angiotensin II type 1 receptor antibody: A case report and literature review.

RATIONALE: Anti-angiotensin II type 1 receptor antibodies (AT1R-Abs) have been demonstrated to increase the risk of antibody-mediated rejection. We report a case of AT1R-Ab mediated rejection which caused early critical cortical infarction. PATIENT CONCERNS: A 52-year-old man with end-stage kidney disease underwent preemptive kidney transplantation (KT) from his wife. He had no immunologic risk except ABO incompatibility. Proper desensitization treatment were applied prior to KT. On postoperative day 1, he showed stable clinical course with adequate urine output, but there was no decrease in serum creatinine level and imaging studies showed hypoperfusion in the transplanted kidney. DIAGNOSES: Allograft biopsy revealed total cortical infarction with severe necrotizing vasculitis, but the medullary area was preserved. Serum AT1R-Ab concentration was elevated from 10.9 U/mL before KT to 19.1 U/mL on 7 days after KT. INTERVENTIONS: He was treated with plasmapheresis, intravenous immunoglobulin, rituximab, high-dose methylprednisolone, and bortezomib. OUTCOMES: The treatment showed a partial response, and he was discharged with 7.3 mg/dL creatinine level. At 4 months, his creatinine plateaued at 5.5 mg/dL and AT1R-Ab decreased to 3.6 U/mL. LESSONS: This case highlights the risk of early active antibody-mediated rejection by preformed AT1R-Ab, suggesting its ability to exhibit atypical histopathologic findings, such as total cortical infarction.

Serum Neurofilament to Magnetic Resonance Imaging Lesion Area Ratio Differentiates Spinal Cord Infarction From Acute Myelitis.

BACKGROUND AND PURPOSE: The diagnosis of spontaneous spinal cord infarction (SCI) is limited by the lack of diagnostic biomarkers and MRI features that often overlap with those of other myelopathies, especially acute myelitis. We investigated whether the ratio between serum neurofilament light chain levels and MRI T2-lesion area (neurofilament light chain/area ratio-NAR) differentiates SCI from acute myelitis of similar severity. METHODS: We retrospectively identified Mayo Clinic patients (January 1, 2000-December 31, 2019) with (1) SCI, (2) AQP4 (aquaporin 4)-IgG or MOG (myelin oligodendrocyte glycoprotein)-IgG-associated myelitis at disease clinical presentation, or (3) idiopathic transverse myelitis from a previously identified population-based cohort of patients seronegative for AQP4-IgG and MOG-IgG. Serum neurofilament light chain levels (pg/mL) were assessed at the Verona University (SIMOA, Quanterix) in a blinded fashion on available stored samples obtained ≤3 months from myelopathy presentation. For each patient, the largest spinal cord lesion area (mm2) was manually outlined by 2 independent raters on sagittal T2-weighted MRI images, and the mean value was used to determine NAR (pg/[mL·mm2]). RESULTS: Forty-eight patients were included SCI, 20 (definite, 11; probable, 6; possible, 3); acute myelitis, 28 (AQP4-IgG-associated, 17; MOG-IgG-associated, 5; idiopathic transverse myelitis, 6). The median expanded disability status scale score (range) at myelopathy nadir were 7.75 (2-8.5) and 5.5 (2-8), respectively. Serum neurofilament light chain levels (median [range] pg/mL) in patients with SCI (188 [14.3-2793.4]) were significantly higher compared with patients with AQP4-IgG-associated myelitis (37 [0.8-6942.9]), MOG-IgG-associated myelitis (45.8 [4-283.8]), and idiopathic transverse myelitis (15.6 [0.9-217.8]); P=0.01. NAR showed the highest accuracy for identification of SCI versus acute myelitis with values ≥0.35 pg/(mL·mm2) yielding 86% specificity and 95% sensitivity (area under the curve=0.93). The positive and negative likelihood ratios were 6.67 and 0.06, respectively. NAR remained independently associated with SCI after adjusting for age, gender, immunotherapy before sampling, and days from myelopathy symptoms onset to sampling (P=0.0007). CONCLUSIONS: NAR is a novel and promising clinical biomarker for differentiation of SCI from acute myelitis.

Association Between Troponin Levels and Visceral Infarction in Patients with Acute Ischemic Stroke.

BACKGROUND: Visceral infarctions appear to be more common in patients with embolic stroke subtypes, but their relation to troponin elevation remains uncertain. METHODS: Among patients with acute ischemic stroke enrolled in the Cornell AcutE Stroke Academic Registry (CAESAR) from 2011 to 2016, we included those with troponin measured within 24 hours from stroke onset and a contrast-enhanced abdominal computed tomographic scan within 1 year of admission. A troponin elevation was defined as a value exceeding our laboratory's upper limit of normal (.04 ng/ mL) in the absence of a clinically recognized acute ST-segment elevation myocardial infarction. Visceral infarction was defined as a renal or splenic infarction as ascertained by a single radiologist blinded to patients' other characteristics. Multivariable logistic regression was used to evaluate the association between elevated troponin and visceral infarction. RESULTS: Among 2116 patients registered in CAESAR from 2011 to 2016, 153 patients had both a troponin assay and a contrast-enhanced abdominal computed tomographic scan, of whom 33 (21%) had an elevated troponin and 22 (14%) had a visceral infarction. The prevalence of visceral infarction was higher among patients with an elevated troponin (30%; 95% confidence interval [CI], 16%-49%) than among patients without an elevated troponin (10%; 95% CI, 5%-17%) (P = .003). After adjustment for demographics and comorbidities, we found a significant association between elevated troponin and visceral infarction (odds ratio, 3.9; 95% CI, 1.5-10.4). CONCLUSIONS: Among patients with acute ischemic stroke, elevated troponin was associated with visceral infarction. Our results demonstrate that poststroke troponin elevation may indicate the presence of underlying embolic sources.

PR3 vasculitis presenting with symptomatic splenic and renal infarction: a case report and literature review.

BACKGROUND: ANCA-associated vasculitis is a life-threatening, systemic autoimmune disease. There is an increased risk of organ infarction but in many cases this is asymptomatic. We described here the first reported case of PR3 vasculitis presenting with symptomatic bilateral renal wedge infarction. CASE PRESENTATION: A 19-year old Caucasian woman with no past medical history presented on a number of occasions over a number of weeks with progressively more severe back pain, fevers and arthralgia. On the final presentation she was noted to have developed splinter haemorrhages and her blood tests revealed impaired renal function along with elevated inflammatory markers. She was subsequently found to have high titres of serum PR3 antibodies and focal necrotising glomerulonephritis on renal biopsy, consistent with a diagnosis of PR3 ANCA-associated vasculitis. Cross-sectional imaging revealed multiple wedge infarcts of her spleen and both kidneys, confirmed on contrast-enhanced ultrasound. Large vessel, cardiac and thrombophilic causes of thromboembolism were excluded. She was treated with high-dose corticosteroids and CD20 monoclonal antibodies (rituximab) and at time of writing, 4 months after initial presentation, has entered clinical remission. CONCLUSIONS: Here we describe the first reported case of PR3 vasculitis presenting with symptomatic renal wedge infarction. In patients with vasculitis who present with flank or back pain, infarction of abdominal organs should be considered in the differential. Both splenic and renal infarctions are likely underdiagnosed in the setting of ANCA-associated vasculitis but may have clinical impact in contributing to infection risk and the degree or renal recovery, respectively.

Serum Troponin Level in Acute Ischemic Stroke Identifies Patients with Visceral Infarcts.

BACKGROUND AND PURPOSE: Patients with ischemic stroke of cardioembolic origin are at risk of visceral (renal or splenic) infarction. We hypothesized that serum troponin level at time of ischemic stroke would be associated with presence of visceral infarction. METHODS: Data were abstracted from a single center prospective stroke database over 18 months and included all patients with ischemic stroke who underwent contrast-enhanced computerized tomography (CT) of the abdomen and pelvis for clinical purposes within 1 year of stroke. The primary predictor was troponin concentration ≥.1ng/mL. The primary outcome was visceral infarct (renal and/or splenic) on CT abdomen and pelvis. Univariate and multivariable logistic regression models were used to estimate the odds ratio and 95% confidence intervals (OR, 95% CI) for the association of troponin with visceral infarction. RESULTS: Of 1233 patients with ischemic stroke, 259 patients had a qualifying visceral CT. Serum troponin level on admission was measured in 237 of 259 patients (93.3%) and 41 of 237 (17.3%) had positive troponin. There were 25 patients with visceral infarcts: 16 renal, 7 splenic, and 2 both. In univariate models, patients with a positive troponin level (versus negative) were more likely to have visceral infarcts (39.1% [9/23] versus 15.0% [32/214], P = .008) and this association persisted in multivariable models (adjusted OR 3.83; 95% CI 1.42-10.31, P = .006). CONCLUSIONS: In ischemic stroke patients, elevated serum troponin levels may help identify patients with visceral infarcts. This suggests that troponin in the acute stroke setting is a biomarker of embolic risk. Larger studies with systematic visceral imaging are needed to confirm our findings.

A practical approach to infarction of the spleen as a rare manifestation of multiple common diseases.

INTRODUCTION: There are insufficient data on the aetiologic factors underlying splenic infarction (SI). Therefore, there is no consensus regarding the appropriate diagnostic approach. METHODS: We conducted a retrospective analysis of all patients admitted with SI from January 2004 to December 2014. Medical records were screened for the clinical presentation, underlying causes, associated medical conditions and methods of patient evaluation. RESULTS: We found 89 subjects with 90 episodes of SI. Presentation of SI was characterized by abdominal, flank and chest pain (82.2%, 18.9%, 7.8%, respectively); leukocytosis (in 67% of tested subjects); elevated LDH (72%), CRP (97.5%) and D-Dimer (100%). The main underlying mechanisms were cardioembolic (54.4%), vascular (20%), haematologic disorders (15.6%) and multiple causes (21.1%). Atrial fibrillation and atherosclerosis were common in older patients (age > 70 years) while antiphospholipid syndrome occurred exclusively in younger individuals. SI was the presentation of previously unknown medical conditions in 38% of patients. Abdominal CT, ECG, echocardiography and blood cultures demonstrated the highest diagnostic yield. CONCLUSIONS: Contributing factors are identified in the majority of SI patients. We recommend CT, ECG, echocardiography and blood cultures in all cases. Atrial fibrillation should be sought in older patients, while APLS and haematologic disorders should be suspected in younger ones. KEY MESSAGES There is no consensus regarding the diagnostic approach and management of splenic infarction. Cardiovascular disease and atrial fibrillation are the main causes for SI in elderly subjects while hematological, infectious and other causes are more prevalent in younger ones. Our data strongly suggests a high diagnostic yield for CT scan, ECG, blood culture and echocardiogram in every patient with SI.

Utility of Neutrophil-to-Lymphocyte Ratio (NLR) as a Predictor of Acute Infarction in New-Onset Acute Vertigo Patients Without Neurologic and Computed Tomography Abnormalities.

BACKGROUND: Neutrophil-to-lymphocyte ratio (NLR) has been used as a predictive marker for various conditions. However, there are no previous studies about NLR as a prognostic marker for acute infarction. OBJECTIVE: To evaluate the potential utility of NLR as a predictor of acute infarction in acute vertigo patients without neurologic and computed tomography (CT) abnormalities. METHODS: We conducted a prospective, observational study in the Emergency Department (ED) between January 2015 and December 2016. All patients underwent physical examination, laboratory tests, CT, and magnetic resonance imaging (MRI). Results of the initial and follow-up MRI with clinical progress note were considered as the reference standard. Statistically, multivariate logistic regression analysis and receiver operating characteristic (ROC) curve were used. RESULTS: Thirty-five (25.9%) patients were diagnosed with acute infarction and 100 (74.1%) patients were diagnosed with peripheral vertigo. Horizontal nystagmus (p = 0.03; odds ratio 0.22) and NLR (p = 0.03; odds ratio 5.4) were significant factors for the differential diagnosis of acute infarction and peripheral vertigo. NLR > 2.8 showed the greatest area under the ROC curve (AUC; 0.819), optimal sensitivity (85.7%), and specificity (78.0%). NLR > 1.4 showed the highest sensitivity (97.1%) and relatively low specificity (41%). The absence of horizontal nystagmus increased the specificity (81.0%) and AUC (0.844). CONCLUSIONS: A combination of NLR > 2.8 and the absence of horizontal nystagmus is sufficiently specific for acute infarction in an ED patient with acute vertigo; thus, further testing with MRI is indicated. NLR < 2.8 by itself or combined with the presence of horizontal nystagmus is not sufficiently sensitive to rule out the need for further testing.

Nonocclusive mesenteric infarction after cardiac surgery: potential biomarkers.

BACKGROUND: Nonocclusive mesenteric ischemia can cause intestinal infarction but the diagnosis is challenging. This prospective study evaluated three plasma biomarkers of intestinal infarction after cardiac surgery. MATERIALS AND METHODS: Patients were recruited after cardiac surgery if they required laparotomy (with or without intestinal resection) for suspected nonocclusive mesenteric ischemia. Plasma levels of D-lactate, intestinal fatty acid-binding protein (i-FABP), and smooth muscle actin (SMA) before laparotomy were measured. RESULTS: Twenty patients were recruited (68 ± 9 y, EuroSCORE: 8.7 ± 2.8, mortality 70%). A positive laparotomy (n = 13) was associated with no change in D-lactate (P = 0.95), decreased i-FABP (P = 0.007), and increased SMA (P = 0.01). All patients with high SMA had a positive laparotomy. A subgroup analysis was undertaken in the eight patients who required multiple laparotomies. D-lactate increased between the two laparotomies in nonsurvivors (n = 4). Plasma i-FABP (P = 0.008) and SMA (P = 0.036) significantly decreased after the bowel resection, regardless of survival outcome. CONCLUSIONS: None of the biomarkers were accurate enough to reliably diagnose intestinal infarction. However, all patients with high values of SMA developed intestinal infarction, thus warranting further investigation. An increasing D-lactate after intestinal resection suggests impending death.

Predictive Factors of Intestinal Necrosis in Acute Mesenteric Ischemia: Prospective Study from an Intestinal Stroke Center.

OBJECTIVES: To identify predictive factors for irreversible transmural intestinal necrosis (ITIN) in acute mesenteric ischemia (AMI) and establish a risk score for ITIN. METHODS: This single-center prospective cohort study was performed between 2009 and 2015 in patients with AMI. The primary outcome was the occurrence of ITIN, confirmed by specimen analysis in patients who underwent surgery. Patients who recovered from AMI with no need for intestinal resection were considered not to have ITIN. Clinical, biological and radiological data were compared in a Cox regression model. RESULTS: A total of 67 patients were included. The origin of AMI was arterial, venous, or non-occlusive in 61%, 37%, 2% of cases, respectively. Intestinal resection and ITIN concerned 42% and 34% of patients, respectively. Factors associated with ITIN in multivariate analysis were: organ failure (hazard ratio (HR): 3.1 (95% confidence interval (CI): 1.1-8.5); P=0.03), serum lactate levels >2 mmol/l (HR: 4.1 (95% CI: 1.4-11.5); P=0.01), and bowel loop dilation on computerized tomography scan (HR: 2.6 (95% CI: 1.2-5.7); P=0.02). ITIN rate increased from 3% to 38%, 89%, and 100% in patients with 0, 1, 2, and 3 factors, respectively. Area under the receiver operating characteristics curve for the diagnosis of ITIN was 0.936 (95% CI: 0.866-0.997) depending on the number of predictive factors. CONCLUSIONS: We identified three predictive factors for irreversible intestinal ischemic injury requiring resection in the setting of AMI. Close monitoring of these factors could help avoid unnecessary laparotomy, prevent resection, as well as complications due to unresected necrosis, and possibly lower the overall mortality.

A case series of acute renal infarction at a single center in Japan.

BACKGROUND: The prevalence of acute renal infarction (ARI) in Japan remains unclear. We describe the clinical features and renal prognosis of ARI in Japanese patients. METHODS: This single-center, retrospective, observational study included 33 patients with newly diagnosed ARI (2009-2013). Their clinical features and long-term renal outcomes were evaluated. RESULTS: The prevalence of ARI among emergency room patients was 0.013 %. The incidence of ARI among in-patients was 0.003 % (mean age 71.9 ± 13.4 years; men 63 %). Enhanced computed tomography or renal isotope scans were obtained to diagnose ARI. ARI involved the left kidney in 70 %, right kidney in 18 %, and both kidneys in 12 % of patients. Four cases had splenic infarction, and 70 % of patients had atrial fibrillation. We noted abdominal or flank pain in 66 %, fever (>37.6 °C) in 36 %, and nausea/vomiting in 6 % of patients. The white blood cell count, and levels of lactate dehydrogenase and C-reactive protein peaked at 2-4 days after onset. Acute kidney injury due to ARI occurred in 76 % of patients. The estimated glomerular filtration rate decreased to ~70 % and recovered to ~80 % of the original value after 1 year. The mortality rates were 9 and 15 % at 1 month and 1 year, respectively. CONCLUSIONS: We determined the prevalence of ARI among emergency room patients, its incidence among in-patients, and short-term and long-term mortality. The majority of ARI cases were of cardiac origin, and the others were due to trauma or systemic thrombotic disease. Clinicians should recognize ARI as a fatal arterial thrombotic disease.

[Clinical analysis of syndrome-relative biological indices in acute lacuna encephalon infarction patients of upper hyperactivity of Gan Yang syndrome].

OBJECTIVE: To analyze and summarize changes of syndrome-related biological indices in acute lacuna encephalon infarction patients of upper hyperactivity of Gan yang syndrome (UHGYS), thus providing objective evidence for syndrome typing and disease identification. METHODS: Recruited were 50 patients at Department of Encephalopathy, Xiyuan Hospital, China Academy of Chinese Medical Sciences, who were in line with diagnostic criteria of UHGYS as the experimental group in this study. Another 40 healthy volunteers were recruited as the control group from May 2010 to July 2012. Blood routines (including WBC, RBC, Hb, NEUT%, and LY%), hepatic and renal functions tests (including ALT, AST, TBIL, TP, ALB, Cr, and BUN) were performed by automatic whole blood analyzer and colorimetric technique. The levels of fasting blood glucose, HbAlc, blood lipids (including TC, TG, HDL-C, LDL-C, and VLDL-C), and coagulation functions (including AT-III, PT, PTA, INR, TT, APTT, and FBG, reaction time), renin, angiotensin II, hs-CRP, and Hcy were also measured. The thyroid functions (including FT3, FT4, T3, T4, and TSH) were detected by electrochemiluminescence immunoassay. The levels of tumor necrosis factor alpha (TNF-alpha), IL-6 and IL-1 in serum were measured by ELISA and radioimmunoassay respectively. RESULTS: Compared with the control group, RBC, LY%, ALT, TP, ALB, HDL-C, AT-III activities, contents of PTA and FT4 obviously decreased, TBIL, BUN, Glu, HbAlc, TSH, hs-CRP, renin, Ang II, TNF-alpha, IL-1 and IL-6 significantly increased in the experimental group (P < 0.05, P < 0.01). CONCLUSION: The pathological process of acute lacuna encephalon infarction patients of UHGYS was closely correlated with thyroid functions, the renin-angiotensin-aldosterone system, the extrinsic and intrinsic coagulation systems, as well as inflammation reaction.

Acute renal infarction: a case series.

BACKGROUND AND OBJECTIVES: Renal infarction is an arterial vascular event that may cause irreversible damage to kidney tissues. This study describes the clinical characteristics of patients with renal infarction according to underlying mechanism of vascular injury. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: This study retrospectively identified 94 patients with renal infarction diagnosed between 1989 and 2011 with the aim of highlighting potential correlations between demographic, clinical, and biologic characteristics and the etiology of renal infarction. Four groups were identified: renal infarction of cardiac origin (cardiac group, n=23), renal infarction associated with renal artery injury (renal injury group, n=29), renal infarction associated with hypercoagulability disorders (hypercoagulable group, n=15), and apparently idiopathic renal infarction (idiopathic group, n=27). RESULTS: Clinical symptoms included abdominal and/or flank pain in 96.8% of cases; 46 patients had uncontrolled hypertension at diagnosis. Laboratory findings included increase of lactate dehydrogenase level (90.5%), increase in C-reactive protein level (77.6%), and renal impairment (40.4%). Compared with renal injury group patients, this study found that cardiac group patients were older (relative risk for 1 year increase=1.21, P=0.001) and displayed a lower diastolic BP (relative risk per 1 mmHg=0.94, P=0.05). Patients in the hypercoagulable group had a significantly lower diastolic BP (relative risk=0.86, P=0.005). Patients in the idiopathic group were older (relative risk=1.13, P=0.01) and less frequently men (relative risk=0.11, P=0.02). Seven patients required hemodialysis at the first evaluation, and zero patients died during the first 30 days. CONCLUSIONS: This study suggests that the clinical and biologic characteristics of patients can provide valuable information about the causal mechanism involved in renal infarction occurrence.

[Renal infarction in two patients with acute abdominal pain]. / Nierinfarct bij 2 patiënten met acute buikpijn.

BACKGROUND: Renal infarction is a condition not known to every physician, with often non-specific symptoms. The diagnosis is therefore often not considered initially in patients with acute abdominal pain. CASE DESCRIPTIONS: In a 77-year-old man a renal infarction was found by chance on a CT-scan performed performed for the evaluation of dyspnoea. Previously he had visited the emergency unit with abdominal pain, in retrospect attributable to renal infarction. A 61-year-old man initially labelled as suffering from gastro-enteritis was diagnosed correctly with renal infarction after his renal function deteriorated and the lactate dehydrogenase (LDH) activity increased. CONCLUSION: A raised serum creatinine level and LDH activity are classic indicators of renal infarction. In addition, most patients have haematuria. Typical wedge-shaped perfusion defects are visible on a CT-scan with intravenous contrast. Timely diagnosis of renal infarction is important both for the prevention of recurrence of thromboembolic complications and for potential revascularisation. The diagnosis of renal infarction should be included in the differential diagnosis in patients with acute abdominal pain.

A case of renal infarction associated with elevated factor VIII level.

Elevated factor VIII level has recently been shown to be associated with increased risk of thrombosis. We report here a case of renal infarction in association with elevated factor VIII level. The patient presented with a three-day history of flank pain. Laboratory studies on presentation showed an elevated serum creatinine concentration and microscopic hematuria. He was found to have bilateral pulmonary emboli and left common femoral vein thrombosis; imaging studies showed evidence of renal arterial thrombosis with infarction. Hypercoagulability assessment showed an elevated factor VIII level. He was treated with heparin and warfarin with significant improvement in his renal function. Consideration should be given to measurement of factor VIII level as a part of the workup of unexplained thrombo-embolic events.

[Early diagnosis in acute mesenteric ischemia. Case series and clinical review]. / Diagnosi precoce nell'ischemia mesenterica acuta. Casistica e revisione clinica.

The AA report on 12 cases of intestinal infarction for acute mesenteric ischemia (IMA) in critical patients observed in the last 2 years. In this work some clinical data, blood tests and strumental considerations are described. IMA is a vascular emergency with severe prognosis and high rate morbidity and mortality, often correlated to a diagnostic delay. The discrepancy between symptoms and clinical objectivity must suggest the suspect, especially in patients with cardiac pathology, short lasting diarrhoea, bowel hemorrhage or only abdominal pain rebel to the analgesics; with the laboratory indexes and strumental data it can be carried out an early diagnosis and then begin the more opportune therapeutical treatment. The increase of blood sugar together to the triad leucocytosis--haemoconcentration and metabolic acidosis, in previously non diabetic patients, confirm the suspect of IMA in the very initial phases of this pathology.

Comparison of clinical characteristics and neutrophil values in omental infarction and acute appendicitis in children.

BACKGROUND: Omental infarction is a rare occurrence in children. It is often diagnosed during surgery for suspected appendicitis. This study investigated the use of clinical and laboratory data for distinguishing between omental infarction and acute appendicitis. METHODS: Seven patients with surgically and pathologically proven omental infarction and 28 age- and sex-matched patients with acute appendicitis were included in this study. The clinical characteristics, imaging study results and laboratory data were analyzed. RESULTS: All 35 patients had right lower quadrant abdominal pain at presentation. The frequency of nausea and fever were significantly lower in the omental infarction group compared with the acute appendicitis group (p< 0.001 and p= 0.018, respectively). In laboratory studies, the white blood cell count, C-reactive protein value and neutrophil percentage were all higher in the acute appendicitis group compared with the omental infarction group (p= 0.001, p< 0.001, and p= 0.008, respectively). It was possible to separate patients with omental infarction from those with acute appendicitis based on a neutrophil percentage of less than 77% (sensitivity 100%, specificity 100%). CONCLUSIONS: Results of the current study suggest that omental infarction should be considered as a possible diagnosis in patients presenting with right lower quadrant abdominal pain without nausea or fever, and with a neutrophil percentage below 77%.

Elevation of serum creatine phosphokinase in hospitalized patients.

BACKGROUND: The clinical characteristics and outcomes of patients with significant noncardiac and cardiac serum creatine phosphokinase (CPK) elevations are not well described. METHODS: One hundred fifty-eight inpatients who had CPK elevation of >1000 IU/L were identified. One hundred thirty-seven patients whose CPK elevations could be attributed to either noncardiac or cardiac etiologies were included and analyzed for clinical characteristics, 30-day, 3-month, and 1-year all-cause mortality rates. Twenty-one patients were excluded, in whom noncardiac and cardiac CPK (CCPK) elevations coexisted, or etiologies were unclear. RESULTS: Of the 137 patients, 43 (31%) patients had CCPK elevation and 94 (69%) patients had noncardiac CPK (NCCPK) elevation. One-year mortality rate was 26.6% (25 of 94 patients) in NCCPK elevation group. Decedents were older (P < 0.05), had higher blood urea nitrogen (P < 0.01) and creatinine (P < 0.05) levels, and had higher white blood cell counts (P < 0.05) compared with survivors. In CCPK elevation group, 37.2% (16 of 43 patients) died within 1 year after admission. Decedents were also older (P < 0.01) and had higher blood urea nitrogen (P < 0.01) and creatinine (P < 0.01) levels. CONCLUSION: The incidence of NCCPK elevation is greater than that of CCPK elevation in a veteran, mostly male, population. One-year mortality rate in patients with NCCPK elevation is comparable to that in patients with CCPK elevation (26.6% versus 37.2%, P = 0.290). Age and renal insufficiency are 2 major predictors for increased mortality in both groups.

Acute bone crises in sickle cell disease: the T1 fat-saturated sequence in differentiation of acute bone infarcts from acute osteomyelitis.

AIM: To prove the hypothesis that acute bone infarcts in sickle cell disease are caused by sequestration of red blood cells (RBCs) in bone marrow, and to evaluate the unenhanced T1 fat-saturated (fs) sequence in the differentiation of acute bone infarction from acute osteomyelitis in patients with sickle-cell disease. MATERIALS AND METHODS: Two studies were undertaken: an experimental study using in-vitro packed red blood cells and normal volunteers, and a retrospective clinical study of 86 magnetic resonance imaging (MRI) studies. For the experimental study containers of packed RBCs were placed between the knees of four healthy volunteers with a saline bag under the containers as an additional control, and were scanned with the pre-contrast T1-fs sequence. Signal intensity (SI) ratios were obtained for packed RBCs:skeletal muscle and packed RBCs:saline. For the clinical study, the SIs of normal bone marrow, packed RBCs, bone and/or soft-tissue lesions, and normal skeletal muscle of 74 patients (86 MRI studies) were measured using unenhanced, T1 fat-saturated MRI. The ratios of the above SIs to normal skeletal muscle were calculated and subjected to statistical analysis. RESULTS: Fifty-one of 86 MRI studies were included in the final analysis. The ratios of SIs for normal bone marrow, packed red cells, bone infarction, acute osteomyelitis, and soft-tissue lesions associated with bone infarct, compared with normal skeletal muscle were (mean+/-SD) 0.9+/-0.2, 2.1+/-0.7, 1.7+/-0.5, 1.0+/-0.3, and 2.2+/-0.7, respectively. The difference in the ratio of SIs of bone infarcts and osteomyelitis was significant (p=0.003). The final diagnoses were bone infarction (n=50), acute osteomyelitis (n=1), and co-existent bone infarction and osteomyelitis (n=2). Seven patients who had suspected osteomyelitis underwent image-guided aspiration. CONCLUSION: Acute bone infarcts in sickle cell disease are caused by sequestration of red blood cells in the bone marrow. The unenhanced, T1-fat-saturated sequence alone is diagnostic for acute bone infarcts. Contrast enhancement aids in the diagnosis of acute osteomyelitis. MRI can thus help in early diagnosis, specific treatment, and preventing empirical antibiotic therapy.