Gordana Cavrić

The right atrial thrombus: the sword of Damocles with real risk of massive pulmonary embolism.

Cases of 6 patients admitted at the intensive care unit for massive pulmonary embolism are reported. All patients presented with dyspnea, tachypnea, and tachycardia, and 4 were hypotensive and had syncope. Lung ventilation/ perfusion scans revealed perfusion defects in 4 patients. Transthoracic echocardiography (TTE) demonstrated acute cor pulmonale. It also revealed mobile right atrial thrombi in 5 patients, adherent thrombus in the right atrium in 1 patient and patent foramen ovale in 4 patients. Thrombolytic therapy was initiated in 4 patients, and 2 patients received heparin infusion only. Effects of thrombolysis were monitored using bedside TTE during the first 24 hours and in follow-up. The outcome of 4 patients who received thrombolytic therapy was good whereas other 2 patients, who received only heparin, died. Thrombotic mass disappeared 8 to 12 hours after initiation of therapy, and 10 weeks after discharge TTE showed normalized right ventricle dimensions and function in all 4 patients.

Direct oral anticoagulant therapy and drug interactions in patients with atrial fibrillation

Background. Drug-drug interactions (DDIs) are one potential cause of adverse drug events. Very little has been done to study the relationship between potential DDIs in patients (p) with atrial fibrillation (AF) on direct oral anticoagulants (DOACs). Many anticoagulants are eliminated by the kidneys, so they can accumulate if their dose is not adapted to the kidney function. DDI is one particular type of drug error that can result in adverse drug events (ADEs) in exposed patients and was the aim of this study. Materials and Methods. A total of 50 patients with AF on DOACs (25 patients on dabigatran and 25 on rivaroxaban) with normal, mildly or moderately decreased (estimated GFR > 30 mlmin-11.73m2) renal function were included (age 69±7 years, 26M/24F, body mass index (BMI) 35.4±5.1 kg/m2, duration of hypertension 11±5 years, duration of AF 5±2 years, eGFR 58±23 mlmin-11.73m2 (was calculated using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formula). Results. The 12-month administration of DOACs caused a nonsignificant decrease of eGFR (declined from 58±23 mlmin-11.73m2 to 56±17 mlmin-11.73m2 (p=0.01). All patients have the right dose of DOACs according to eGFR. Patients with AF and DOACs on more than 3 different drugs (20%) such as statins, verapamil and amiodarone were more prone to AE. Conclusion. DDIs are one of the most important problems in every day practice. Coadministration of statins with dabigatran worsens clinical outcomes and a similar interaction might be seen with verapamil and amiodarone. Patients need to be on the right drug/right dose given the kidney function they have, with special care on DDIs.

Rhabdomyolysis in a patient with chronic uncontrolled diabetes mellitus and hypothyroidism

Rhabdomyolysis is a syndrome characterised by muscle necrosis and dispersing its intracellular content in the circulation. Clinical symptoms are usually presented by muscle pain and muscle weakness. Rhabdomyolysis could be produced, among other causes, by diabetic ketoacidosis and hypothyroidism. We report a case of a 36 years old female patient who was admitted to the medical intensive care unit (MICU) because of rhabdomyolysis. At her admission we found compensated diabetic ketoacidosis with normal serum osmolarity and mild hypothyroidism. The patient was treated by rehydration, urine alkalinisation, forced augmentation of diuresis, correction of blood glucose levels, and levothyroxine substitution therapy. After 17 days, she was completely recovered and discharged home. We believe that rhabdomyolysis in our patient developed as a summary of two important factors, uncontrolled diabetes mellitus and hypothyroidism. Hypothyroidism, possibly fueled by bad regulate diabetes, may amplify the symptoms. Each considered factor separately may not be cause a muscle breakdown, but their combination can lead to serious and severe clinical symptoms associated with high levels of creatine kinase (CK) enzyme.

Resistant Hypertension and Cardiorenovascular Risk

Abstract Studies have documented independent contribution of sympathetic activation to the cardiovascular disease continuum. Hypertension is one of the leading modifiable factors. Most if not all the benefit of antihypertensive treatment depends on blood pressure lowering, regardless how it is obtained. Resistant hypertension is defined as blood pressure that remains uncontrolled in spite of the concurrent use of three antihypertensive drugs of different classes. Ideally, one of the three drugs should be a diuretic, and all drugs should be prescribed at optimal dose amounts. Poor adherence to antihypertensive therapy, undiscovered secondary causes (e.g. obstructive sleep apnea, primary aldosteronism, renal artery stenosis), and lifestyle factors (e.g. obesity, excessive sodium intake, heavy alcohol intake, various drug interactions) are the most common causes of resistant hypertension. Cardio(reno)vascular morbidity and mortality are significantly higher in resistant hypertensive than in general hypertensive population, as such patients are typically presented with a long-standing history of poorly controlled hypertension. Early diagnosis and treatment is needed to avoid further end-organ damage to prevent cardiorenovascular remodeling. Treatment strategy includes lifestyle changes, adding a mineralocorticoid receptor antagonist, treatment adherence in cardiovascular prevention and, in case of failure to control blood pressure, renal sympathetic denervation or baroreceptor activation therapy. The comparative outcomes in resistant hypertension deserve better understanding. In this review, the most current approaches to resistant hypertension and cardiovascular risk based on the available literature evidence will be discussed.

Oral anticoagulants in patients with chronic kidney disease and atrial fibrillation

The aim of this study was to investigate the effects of new/direct oral anticoagulants (DOACs) on renal function parameters in chronic kidney disease patients with esti-mated glomerular filtration rate (eGFR) that therapy with new/direct oral antico-agulants (non-VKA oral anticoagulants) have a better bleeding risk profile and less decline in eGFR compared with vitamin K antagonists.

Unexpected Extremely High Level of Creatinine in Non-dialysed Female Patient

There are only a few published studies confirming the ability of either urea or creatinine to induce adverse biochemical and physiological effects and there is not a defined level of serum creatinine that is lethal itself. Given the fact that by consulting the literature we did not find the highest level of creatinine in a surviving patient published in Croatia, we want to present the highest recorded level in our practice and probably in Croatia. A sixty-two year old woman presented to the Merkur Clinical Hospital Emergency Department in Zagreb with the serum creatinine 2316 μmol/L (26.2 mg/dl) and a one week history of uremic symptoms. Her previous medical history was negative; she has not been taking any medications. Renal failure in this patient occurred due to bilateral hydronephrosis developed as the result of advanced cervical malignancy and was accompanied by severe microcytic anemia (hemoglobin 35 g/l, hematocrit 0.120, MCV 71.4 fL), compensated metabolic acidosis (arterial pH 7.230) and hyperkalemia (serum potassium 6.4 mmol/l). An acute hemodialysis was made on the day of admission. About one month later at the time of the discharge the serum creatinine was 490 μmol/L. During hospitalization the patient was conscious, oriented and cardiorespiratory compensated. Creatinine is the endogenous marker most commonly used to measure kidney function [1]. The proximal tubules secrete creatinine, which accounts for 10-20% of the excreted load [2]. The normal reference range for serum creatinine is 0.7 to 1.3 mg/dL (62-115 umol/L) for men and 0.6 to 1.1 mg/dL (53-97 umol/L) for women [3]. Progressive obstructive uropathy may lead to uremia, electrolyte imbalances and persistent urinary tract infections, if obstruction is not bypassed [4], as we report in this case. Although it is a marker of uremic toxicity, the actual effect of creatinine on homeostasis in humans is unresolved [3]. One of the most disabling features of kidney failure is encephalopathy that is caused by the accumulation of uremic toxins [5]. The patient we report on presented the highest creatinine level (2316 μmol/L) we experienced in our twenty-eight years long practice and presented with symptoms of uremia including nausea, vomiting, fatigue and slowed cognitive functions. Searching through literature and available data we could not find written evidence on the highest creatinine level in practice in Croatia in non-dialysed patients. A literature search indicates that the surviving uremic male patient (BMI 28) with creatinine 53 mg/dl (4685.2μmol/L) reported by A.C. Storm et al. in Open Journal of Nephrology (2013) could be the highest creatinine in the literature [3]. A renal failure and increased creatinine level in the patient we reported occurred due to bilateral hydronephrosis that had been developed due to advanced stage of cervical carcinoma. The finding of ureteral obstruction due to malignancy carries a poor prognosis with a resulting median survival of 3 to 7 months, and confers a worse overall prognosis [4,6]. Relief of obstruction is usually achieved by placement of a percutaneous nephrostomy tube, an internalized double J nephroureteral stent, or an internal/external nephroureteral stent (NUS) [7]. Our patient had rejected suggested bilateral percutaneous nephrostomy as modality of decompression and accepted life saving dialysis. This patient with the highest recorded serum creatinine in our practice and according to available data in Croatia has survived uremic symptoms and has been discharged with a program of hemodialysis three times per week. The highest level of creatinine (2316 μmol/L) we registered manifested through early symptoms of uremia and minimal changes in mental status suggest that creatinine as a potential uremic toxin has a minor pathophysiologic role in causing uremic syndrome and encephalopathy.

MicroRNA in kidney disease

Abstract Clinical and laboratory findings of kidney disease in an adult may find an explanation in kidney functional and/or structural abnormalities that already existed during infancy and childhood, but that may have been missed or underdiagnosed. All the cardiovascular abnormalities that occur in adults with chronic kidney disease are also present in children with chronic kidney disease. Complications in childhood chronic kidney disease will have consequences well beyond pediatric age and influence outcomes of affected young adults with disease. Kidney dysfunction appears early in the course of kidney disease and has been observed in children and adults with chronic kidney disease, condition characterised with kidney fibrosis. Transforming growth factor beta is recognized as a major mediator of kidney fibrosis. New evidence illustrates the relationship between transforming growth factor beta signaling and microRNAs expression during kidney diseases development. MicroRNAs play important roles in kidney development and kidney diseases; they are naturally occurring, 22-nucleotide, noncoding RNAs that mediate posttranscriptional gene regulation. Dysregulation of miRNA expression is an indicator of several diseases including chronic kidney disease. Targeting microRNAs should be a therapeutic potential to ameliorate the disease related to fibrosis. The discovery that circulating miRNAs are detectable in serum and plasma, and that their expression varies as a result of disease, presents great potential to be used as biomarkers in kidney disease prevention and diagnosis.

Asymptomatic pneumopericardium after blunt chest trauma

A 49-year-old man was admitted to the emergency room after a fall from a height of 4 m. He was conscious with intact neurological status and stabile vital function. Blunt chest trauma was presented with left side rib fractures (3-6), ipsilateral lung base contusion, pneumo-liqidothorax, pneumomediastinum and subcutaneus emphysema. A computed tomographic scan also confirmed pneumopericardium. Negative Hamman’s sign were presented. Although the patient had no symptoms, the presence of pneumopericardium might be a sign of severe injury and indicates the potential risk of cardiac tamponade and a lifethreatening condition. In the presence of pneumopericardium, cardiac tamponade could be triggered secondary by mechanical ventilation support. In our case report, we would like to stress the importance of early diagnostic of asympthomatic pneumopericardium after blunt chest trauma, which may be decisive in choosing the optimal therapeutic procedure.