Analysis of the outcomes of cardiopulmonary resuscitation in an emergency department

OBJECTIVE: The aim of this study is to analyse the factors affecting emergency department (ED) cardiopulmonary resuscitation (CPR) outcome. METHODS: A standard CPR protocol was performed in all patients and certain pre and postresuscitation parameters including age, sex, initial arrest rhythm, primary underlying disease, initiation time of advanced cardiac life support, duration of return of spontaneous circulation were recorded. Patients were followed up to determine rates of successful CPR, survival and one-year survival. RESULTS: From December 1999 to May 2001, 80 consecutive adult patients in whom a standard CPR was performed in the ED were prospectively included in the study. The overall rate for successful CPR, survival and one-year survival were found to be 58.8% (47/80), 15% (12/80) and 10% (8/80), respectively. Survival and one-year survival rates were better in patients with an initial arrest rhythm of ventricular fibrillation or pulseless ventricular tachycardia (VF/pVT) than both pulseless electrical activity (pEA) and asystole; survival and one-year survival rates were better in patients with a primary underlying disease of cardiac origin than non-cardiac origin. Acute myocardial infarction had the best prognosis among conditions causing arrest. Presence of sudden death was found to have a better survival and one-year survival rate. CONCLUSION: Initial cardiac rhythm of VF/pVT, cardiac origin as the primary disease causing cardiopulmonary arrest and presence of sudden death were found to be good prognostic factors in CPR.     

Red blood cell rheological properties in various rat hypertension models

Red blood cell (RBC) properties were proposed to play role in the development of hypertension (HT). This study aimed at investigating the alterations of RBC deformability and aggregation, in various models of HT in rats. The following four models of HT were developed in rats: one kidney-one clip HT (1K-1C HT), two kidney-one clip HT (2K-1C HT), deoxycorticosterone acetate (DOCA) induced HT (15 mg/kg, 2 times/week, sc) and N-nitro L-arginine methyl ester (L-NAME) induced HT (50 mg/kg/day, 10 weeks, ip). The blood samples were obtained from abdominal aorta, under ether anesthesia, after a period of 10 weeks of increased blood pressure. RBC deformability was determined by ektacytometry. RBC aggregation was measured in autologous plasma and 0.5% dextran 500, using a photometric rheoscope. Plasma fibrinogen concentration was determined by Clauss method. The mean blood pressure in all four HT models were about 140 mmHg, on the day of sampling, compared to approximately 110 mmHg in the control group. RBC deformability was found to be significantly decreased in the L-NAME model of HT. RBC aggregation in autologous plasma was significantly higher than control in 2K-1C, L-NAME and DOCA models, DOCA HT model being the most effective in altering the RBC aggregation. Plasma fibrinogen values were found to be higher than control in 2K-1C and L-NAME HT models, but not in DOCA HT. These results confirm that RBC rheological properties might be altered in HT. It can also be suggested that these alternations may not simply be the result of the vascular effects of HT, but may play role in the development of HT, as the alterations in different HT models were not the same, although the length and magnitude of increased blood pressure were similar.     

Increased P wave dispersion: a new finding in patients with syndrome X

The present clinical study was undertaken in patients with syndrome X, namely angina with normal coronary arteries, to investigate the presence of increased P wave dispersion by comparing patients with coronary artery disease (CAD) and healthy control subjects. Three groups were studied - group A, 21 patients (48 6 years) with syndrome X; group B, 16 patients (56 9 years) with CAD; and group C, 16 healthy subjects (49 8 years). Patients with CAD were older than those in groups A and C (P=0.005 and P=0.035, respectively). All groups demonstrated similar PQ, QRS and RR intervals. Group B had a lower minimum P wave duration than group C (P=0.05). P wave dispersion in group A was found to be higher than that in groups B and C (P=0.018 and P=0.0001, respectively). Patients with syndrome X demonstrated increased P wave dispersion compared to patients with CAD and healthy subjects. High sympathetic tone or autonomic imbalance observed in patients with syndrome X may affect intra-atrial and interatrial conduction times, and leave them prone to develop atrial arrhythmias.     

Unusual case of severe late-onset cytomegalovirus-induced hemorrhagic cystitis and ureteritis in a renal transplant patient

Cytomegalovirus (CMV) infection is common in solid organ transplant recipients and accounts for the majority of graft compromise. Major risk factors include primary exposure to CMV infection at the time of transplantation and the use of antilymphocyte agents such as OKT3 (the monoclonal antibody muromonab-CD3) and antithymocyte globulin. It most often develops during the first 6 months after transplantation. Although current prophylactic strategies and antiviral agents have led to decreased occurrence of CMV disease in early posttransplant period, the incidence of late-onset CMV disease ranges from 2% to 7% even in the patients receiving prophylaxis with oral ganciclovir. The most common presentation of CMV disease in transplant patients is CMV pneumonitis followed by gastrointestinal disease. Hemorrhagic cystitis is a common complication following hematopoietic stem cell transplantation. The condition is usually due to cyclophosphamide-based myeloablative regimens and infectious agents. Even in these settings, CMV-induced cases occur only sporadically. Ureteritis and hemorrhagic cystitis due to CMV infection after kidney transplantation is reported very rarely on a case basis in the literature so far. We report here a case of late-onset CMV-induced hemorrhagic cystitis and ureteritis presenting with painful macroscopic hematuria and ureteral obstruction after 4 years of renal transplantation. The diagnosis is pathologically confirmed by the demonstration of immunohistochemical staining specific for CMV in a resected ureteral section. We draw attention to this very particular presentation of CMV hemorrhagic cystitis with ureteral obstruction in order to emphasize atypical presentation of tissue-invasive CMV disease far beyond the timetable for posttransplant CMV infection.     

Determination of etiology in patients admitted due to isolated leukopenia

Patients with isolated leukopenia pose difficulties in diagnosis because there is no related guideline in the literature. In this study, our aim was to evaluate the clinical and laboratory associations of isolated, nonspecific (not related to neutropenia) leukopenia.In this retrospective data review study, patients who were admitted to Hacettepe University Hematology Outpatient Clinic between 2014 and 2019 due to leukopenia were evaluated. The patients with anemia (other than iron deficiency) or thrombocytopenia were excluded. Clinical and laboratory data and the final diagnoses (if present) of the remaining cases and especially of those without neutropenia (the most difficult group to diagnose) were evaluated.One hundred sixty-nine patients were included in the study. One hundred forty-four (85.2%) patients were female and 25 (14.8%) were male. One hundred ten of them had 1500/µL or higher neutrophil count. In these nonneutropenic cases, the etiological factors contributing to leukopenia were as follows: iron deficiency anemia (21.8%), other autoimmune/autoinflammatory diseases (17.3%), autoimmune thyroid disease (21.8%), autoimmune laboratory tests (2.7%), drugs (12.7%), infection (5.5%), hematopoietic disorder (2.7%), hypersplenism (2.7%), radiotherapy sequel (1.8%), and B₁₂ deficiency (1.8%). No etiology was recognized in 44 patients. On the other hand, the etiological factors in patients with neutrophil count <1500/µL were as follows; iron deficiency anemia (10.2%), other autoimmune/autoinflammatory diseases (17%), autoimmune thyroid disease (5.1%), autoimmune laboratory tests (8.5%), drugs (8.5%), infection (6.8%), hematopoietic disorder (11.9%), hypersplenism (1.7%), radiotherapy sequel (1.7%), and B₁₂ deficiency (1.7%). No etiology was recognized in 25 patients. Physicians ordered bone marrow examination more frequently in patients with neutropenia. If isolated antinuclear antibody positivity was also considered in favor of autoimmunity, 91/169 (53.8%) cases had an autoimmune diagnosis or laboratory finding.In the present study, the most frequent reasons of isolated leukopenia in nonneutropenic patients are found as iron deficiency anemia, other autoimmune/autoinflammatory diseases, and autoimmune thyroid disease. In neutropenic patients, the most frequent reasons of isolated leukopenia are found as iron deficiency anemia, autoimmune/autoinflammatory diseases, and hematopoietic disorders. Therefore, autoimmunity is detected as an important factor leading to isolated leukopenia.     

High-dose immunoglobulin therapy in renal transplant recipients with hemophagocytic histiocytic syndrome

BACKGROUND: Hemophagocytic histiocytic syndrome (HHS) generally occurs in immunocompromised patients and often has a rapidly fatal course. HHS may be cured by treatment of the underlying disorder, especially when it is triggered by an infection. If no cause has been found, no therapy is known and outcome is poor. The aim of this study was to investigate the clinical course and response to intravenous immunoglobulin treatment in renal transplant patients diagnosed with HHS. METHODS: Thirteen patients who were diagnosed with HHS between 1995 and 2003 were retrospectively assessed. The mean age of HHS patients was 38.6 +/- 10 years (5 women, 8 men). RESULTS: Median time to onset of symptoms after renal transplantation was 15.1 +/- 12.1 months (range 0.5-30 months). The first 2 patients in whom no etiologic factor was found were seen before 1998 and died due to multiorgan failure. HHS was related to an infectious etiology in 6 of 13 patients: tuberculosis (n=3), cytomegalovirus (CMV) infection (n=2), Escherichia coli (E. coli)-associated septicemia (n=1), but HHS was cured by antimicrobial therapy in only 2 of them (1 with tuberculosis, the other with E. coli-associated septicemia). After June 1998, high-dose immunoglobulin (IVIg) therapy was used in 6 patients. HHS was related to an infectious etiology in 2 patients unresponsive to antimicrobial treatment, and of unknown etiology in 4 patients. All of them completely recovered. Before 1998, 2 patients unresponsive to antimicrobial therapy (1 with tuberculosis, the other with CMV) died. They were not given IVIg. CONCLUSIONS: We concluded that when HHS does not respond to treatment of the underlying infection, or is of unknown etiology in immunocompromised patients, high-dose IVIg therapy should be administered.     

Results of 4-year analysis of conversion from calcineurin inhibitors to mTOR inhibitors in renal transplant patients: single-center experience

In this retrospective study, 83 patients were accepted. Mammalian target of rapamycin (mTOR) group consisting of 37 patients were converted from calcineurin inhibitors (CNI), and the control group included 46 patients (initially CNI-receiving patients). As a control-match of each mTOR inhibitor patient, the succeeding patient with transplantation who continued CNI therapy was chosen. All patients received CNI, MMF, and prednisolone as an immunosuppressive therapy initially. In comparison of two groups, there was no significant difference between sex, donor organ source, donor organ ischemia time, or mismatches. However, mean age between groups was significantly different (mTOR group: 48.3 ± 12, CNI group: 38.6 ± 11, p < 0.001). Decision of conversion to mTOR inhibitors in 30 patients was made by biopsy. The reasons for conversion were determined as CNI nephrotoxicity in 15 patients, chronic allograft nephropathy in 15 patients, malignancy in 6 patients, and renal artery stenosis in 1 patient. Basal glomerular filtration rates (GFRs) were markedly lower in mTOR group than in CNI group (38.8 mL/min vs. 72.7 mL/min). At the end of 48-month follow-ups, GFR increased from 38 mL/min to 54 mL/min in mTOR group; however, it decreased to 53 mL/min from 72 mL/min in CNI group. There was no difference left between the two groups in GFR after 4-year follow-up. Hyperlipidemia was higher in mTOR group. Acute rejection rates were similar. Cytomegalovirus (CMV) disease was more prevalent in CNI group. Graft failure developed due to secondary reasons, causing mortality in both groups. We suggest that conversion to mTOR inhibitors maintains and improves graft functions well.     

Familial primary carpal tunnel syndrome with possible skipped generation

Carpal tunnel syndrome, an entrapment neuropathy of the median nerve, is rarely seen in childhood. Familial carpal tunnel syndrome, an even more exceptional entity, is frequently associated with inherited systemic disorders. Rarely it can be presented as a primary familial form with Mendelian autosomal dominant inheritance. We report the occurrence of carpal tunnel syndrome in two generations of a family in which the index case was a 6-year-old boy with bilateral hand pain and paresthesias. Our report demonstrates an interesting inheritance pattern of carpal tunnel syndrome in a family transmitted by an autosomal dominant gene with variable expressivity and reduced penetrance. To our knowledge, it is the first report of familial bilateral carpal tunnel syndrome in a family with possible skipped generation.