Clinical Analysis of Risk Factors for Mortality in Type A Acute Aortic Dissection: A Single Study From China

Objective: Acute type A aortic dissection (ATAAD) is a fatal condition that requires emergency surgery. The aim of the present study was to determine pre- and intra-operative risk factors for in-hospital mortality in patients with ATAAD.Methods: Consecutive 313 patients with ATAAD who underwent emergency surgery at our hospital from February 2012 to February 2017 were enrolled in our study. Univariate and multivariate logistic regression analysis were performed to identify the pre-operative and intra-operative risk factors for in-hospital mortality.Results: Of the 313 patients, 32 patients (10.2%) died. Compared with survivors, non-survivors had higher heart rate, serum potassium level and EuroSCORE II, and higher incidence of moderate to severe pericardial effusion, supra-aortic vessels involvement, myocardial ischemia and lower-extremity ischemia. As for surgery-related factors, the duration of surgery and cardiopulmonary bypass time were longer in non-survivors than survivors. In addition, non-survivors were more likely to undergo coronary-artery bypass graft compared with survivors. On multivariate analysis, elevated plasma potassium level (OR: 43.0, 95% CI: 3.8–51.5, p < 0.001), high incidence of supra-aortic vessels involvement (OR: 4.4, 95% CI: 1.5–7.0, p = 0.008) and lower-extremity ischemia (OR: 4.9, 95% CI: 1.6–6.9; p = 0.009), and longer duration of surgery (OR 6.0, 95% CI: 1.8–18.7, p = 0.000) and cardiopulmonary bypass time (OR: 3.7, 95% CI: 1.3–9.3, p = 0.001) were independently predictive of higher mortality in patients with ATAAD.Conclusions: Supra-aortic vessels involvement, lower-extremity ischemia and elevated plasma potassium level are independent predictors of mortality in patients with ATAAD. A significant decrease in duration of surgery and cardiopulmonary bypass time is helpful to improve survival of patients.

Abstract 16412: The Predictors of Hemodynamic Response to Phosphodiesterase-5a Inhibition in Advanced HFrEF

Introduction: In advanced HFpEF, acute phosphodiesterase 5 (PDE5) inhibition leads to favorable change in pulmonary vascular resistance (PVR) and to an increased cardiac output (CO) of variable degree. The determinants of the response are poorely understood. Methods: 47 HFrEF patients (85% males, 57±11 years, NYHA 2.9±0.5, 55% non-ischemic, PAmean 42±8 mmHg, 43% RV dysfunction) underwent clinical exam, echocardiography, biochemical tests and right heart catheterization (RHC) before and after I.V. administration of sildenafil (20 mg). Baseline predictors of absolute and relative (%diff) change of PVR and CO were studied. Results: PDE5i led to highly significant (p<0.001) reduction of pulmonary artery (PA) mean pressure (-11±9 mmHg), PVR (-2.2±1.6 WU;-42±24%), PA wedge pressure (-5.2±7.3 mmHg), CVP (-3.2±2.3 mmHg) and to increase in cardiac output (+0.6±0.7 l/min; +18±23%). PVR decreased more than systemic resistance (PVR/SVR -27±30%diff). Predictors of high CO response (COdiff%) were: low BMI, no diabetes, low baseline CO and severity of mitral or tricuspid regurgitation (r=0.53 or =0.43, both p<0.003). The strongest predictor of high PVR%diff was plasma potassium level. HF etiology, renal function, gender, RAAS inhibitor dose, renin or aldosterone levels were unelated to pulmonary vasoreactivity. Patients who dropped PVR<3 WU after PDE5i had higher plasma K+ (4.1±0.5 vs 4.5±0.3 mmol/L, p=0.01) than those who did not, similar relation was found for K+ and PDE5i-induced change of transpulmonary gradient. Conclusions: The largest increase in CO after PDE5i is observed in HFrEF patients with severe mitral (or tricuspid) regurgitation, probably due to chamber unloading and reduction of regurgitant SV. Pulmonary vasodilator response to PDE5i may be influenced by plasma potassium level. High-normal plasma potassium levels may preserve normal pulmonary vasoreactivity in HFrEF, perhaps by influencing K-channels in pulmonary vascular smooth muscle cells.

Flash glucose monitoring system was applied to cortisol treatment for a patient with congenital adrenal hyperplasia and 17α-hydroxylase deficiency

Background Congenital adrenal hyperplasia (CAH) with 17α-hydroxylase deficiency is a rare disease; patients often require lifetime cortisol treatment. In this case report, we presented a patient with CAH and 17α-hydroxylase deficiency, who was previously misdiagnosed as having primary aldosteronism. Furthermore, the flash glucose monitoring system (FGMS) was used to ascertain a suitable cortisol therapeutic regimen for this patient. Case presentation A 29-year-old woman presented with sex dysgenesis, hypertension and hypokalaemia. She had been diagnosed with primary aldosteronism at a local hospital. The re-measured aldosterone level in our hospital was below the normal range after antihypertensive medication adjustment, suggesting that the primary aldosteronism was a misdiagnosis. The patient was finally diagnosed as having CAH with 17α-hydroxylase deficiency according to the endocrine profile, adrenocorticotropic hormone stimulation test, and genetic analysis. Then, the patient was recommended cortisol treatment, during which the endocrine profile, blood pressure, plasma potassium level, and blood glucose level were observed to ascertain a suitable dosage. The FGMS was used to monitor blood glucose level, which indicated that the patient’s glucose metabolism was maintained normally under the final treatment dosage. Conclusion The misdiagnosis might have been because of the effects of the antihypertension medications on aldosterone and renin levels. The final dosage of cortisol treatment achieved a normal endocrine profile, while maintaining the homeostasis of blood glucose level, plasma potassium level and blood pressure. FGMS may be an effective method to ascertain a suitable cortisol therapeutic regimen for patients with CAH and 17α-hydroxylase deficiency.

Tetraparesis with Major Hypokalaemia and Rhabdomyolysis Induced by Chronic Liquorice Ingestion

Chronic ingestion of liquorice induces a syndrome with findings similar to those for primary hyperaldosteronism. This is characterized by hypokalaemia, hypertension, metabolic alkalosis and suppression of the renin-aldosterone system. We describe a 30-year-old woman who, with a plasma potassium level of 1.5 mmol/l, presented with tetraparesis and severe rhabdomyolysis (CK up to 35,460 U/l). She admitted to a daily consumption of nearly 300 g of liquorice sweets during the previous 6 months. This case emphasizes the importance of a detailed anamnesis, which is essential for diagnosis, avoids unnecessary and expensive investigations and reduces the duration of hospitalization.

A physiology-based approach to a patient with hyperkalemic renal tubular acidosis

ABSTRACT Hyperkalemic renal tubular acidosis is a non-anion gap metabolic acidosis that invariably indicates an abnormality in potassium, ammonium, and hydrogen ion secretion. In clinical practice, it is usually attributed to real or apparent hypoaldosteronism caused by diseases or drug toxicity. We describe a 54-year-old liver transplant patient that was admitted with flaccid muscle weakness associated with plasma potassium level of 9.25 mEq/L. Additional investigation revealed type 4 renal tubular acidosis and marked hypomagnesemia with high fractional excretion of magnesium. Relevant past medical history included a recent diagnosis of Paracoccidioidomycosis, a systemic fungal infection that is endemic in some parts of South America, and his outpatient medications contained trimethoprim-sulfamethoxazole, tacrolimus, and propranolol. In the present acid-base and electrolyte case study, we discuss a clinical approach for the diagnosis of hyperkalemic renal tubular acidosis and review the pathophysiology of this disorder.

MORPHOFUNCTIONAL CHANGES IN KIDNEYS OF RATS WITH GENTAMICIN-INDUCED ACUTE KIDNEY INJURY AND USE OF MELATONIN

Aminoglycosides are effective antibiotics, but their accumulation in kidney cortex causes nephrotoxic effects in 20-30% of patients, which significantly limits their use. For this reason, search for the new therapies aimed at prevention of gentamicin-induced acute kidney injury (AKI) is highly relevant. Thus, the objective of our research was to study the functional and histopathological changes in kidneys of rats with gentamicin-induced AKI, and estimate the renoprotective potential of pineal hormone melatonin, which possesses antioxidant, anti-inflammatory and immunomodulatory effects. The study was conducted on 24 non-linear male rats. Gentamicin-induced AKI was modeled by daily administration of 4% gentamicin sulphate (80 mg/kg) for 6 days. Melatonin (Sigma Aldrich, USA) was injected daily at a dose of 5 mg/kg. Functional state of kidneys was assessed by diuresis, creatinine clearance, urine protein excretion, fractional excretion of sodium, and plasma potassium level. Documentation of the pathological processes was performed by the computer morphometry of objects in histological preparations. Statistical analysis of the data was performed using SPSS 17.0 software. Administration of gentamicin resulted in a significant impairment of renal function of experimental animals. A decrease in creatinine clearance by 3.1 times along with a reduction of diuresis by 1.9 times, and an increase in plasma creatinine concentration by 2.6 times was observed. There also was an increase in urine protein level by 5.2 times, an elevation of fractional sodium excretion and a reduction of plasma potassium level. Use of melatonin caused a significant improvement of renal function comparing to model pathology group. Functional disturbances were accompanied with the significant histopathological changes in kidney tissue: necrosis of the 27±5.2% epithelial cells of proximal tubules with the signs of hydropic vacuolization (7±2.1%) or reversible hydropic swelling (76±1.5%) in the rest of cells; swelling or deformation of some glomeruli. In the medulla tubular lumen were dilated and partially filled with hyaline casts, tubular cells had signs of dystrophy. Use of melatonin contributed to the restraint of the histopathological changes, confirmed by the decrease of the prevalence and severity of tubular necrosis (1.2%), dystrophy (64±2.3%), and injury of glomeruli. Obtained results verify the significant nephroprotective effect of pineal hormone melatonin, providing a background for the further in-depth study of its renal effects as well as its prospects as a nephroprotector.

Pseudohyperkalemia in a patient with chronic lymphoblastic leukemia and tumor lysis syndrome

Purpose: Recognition of pseudohyperkalemia is essential to prevent medical mismanagement of erroneous hyperkalemia. The purpose of this case is to describe pseudohyperkalemia attributed to malignant leucocytosis in a patient with chronic lymphoblastic leukemia and tumor lysis syndrome. Methods for determination of pseudohyperkalemia are discussed. Summary: A 75-year-old male with progressive chronic lymphoblastic leukemia was hospitalized for medical evaluation and chemotherapy administration. Notable laboratory findings included white blood cell count of 479 × 103 cells/µL (4.00 × 103 cells/µL–10.80 × 103 cells/µL) with 95% lymphocytes (20%–50%) and 5% blasts (zero) present in the differential, serum potassium 9.8 mM/L (3.4 mM/L–5.0 mM/L), uric acid of 11.8 mg/dL (3.5 mg/dL–8.0 mg/dL), serum creatinine 1.47 mg/dL (0.60 mg/dL–1.30 mg/dL), and lactate dehydrogenase of 2529 IU/L (100 IU/L–220 IU/L). The patient was anemic (Hb 7.6 g/dL (14.0 g/dL–18.0 g/dL)) and thrombocytopenic (17 × 103 platelets/μL (140 × 103 platelets/μL–400 × 103 platelets/μL)). There were no electrocardiographic findings indicating systemic hyperkalemia. Repeat analysis of the blood potassium level using a heparinized tube assayed immediately after specimen collection demonstrated a plasma potassium level 4.1 mM/L. Subsequent analysis of specimens using similar methodology demonstrated potassium results within the normal limits despite continued laboratory evidence of pseudohyperkalemia. Based on the patient’s conscious and interactive condition, ECG findings, and normal plasma potassium level following immediate analysis, the diagnosis of pseudohyperkalemia was made. Laboratory findings of pseudohyperkalemia persisted throughout the period of leukocytosis. Conclusion: This case describes pseudohyperkalemia attributed to malignant leucocytosis in a patient with chronic lymphoblastic leukemia (CLL). Practitioners should consider pseudohyperkalemia as the underlying cause of elevated potassium levels in patients with malignant leucocytosis who do not have signs or symptoms of systemic hyperkalemia.