Frequency and predictors of hyperkalemia in patients ≥60 years of age with heart failure undergoing intense medical therapy

Hyperkalemia is a concern in heart failure (HF), especially in older patients with co-morbidities. Previous studies addressing this issue have focused mainly on younger patients. This study was aimed at determining the frequency and predictors of hyperkalemia in older patients with HF undergoing intense medical therapy. Frequency and predictors of hyperkalemia were defined in patients (n = 566) participating in the Trial of Intensified versus Standard Medical Therapy in Elderly Patients with Congestive Heart Failure, in which patients ≥60 years of age were randomized to a standard versus an intensified N-terminal brain natriuretic peptide-guided HF therapy. During an 18-month follow-up 76 patients (13.4%) had hyperkalemia (≥5.5 mmol/L) and 28 (4.9%) had severe hyperkalemia (≥6.0 mmol/L). Higher baseline serum potassium (odds ratio [OR] 2.92 per mmol/L), baseline creatinine (OR 1.11 per 10 μmol/L), gout (OR 2.56), New York Heart Association (NYHA) class (compared to NYHA class II, IV OR 3.08), higher dosage of spironolactone at baseline (OR 1.20 per 12.5 mg/day), and higher dose changes of spironolactone (compared to no dose change: 12.5 mg, OR 1.45; 25 mg, OR 2.52; >25 mg, OR 3.24) were independent predictors for development of hyperkalemia (p <0.05 for all comparisons). In conclusion, hyperkalemia is common in patients ≥60 years of age with HF undergoing intense medical therapy. Risk is increased in patients treated with spironolactone, in addition to patient-specific risk factors such as chronic kidney disease, higher serum potassium, advanced NYHA class, and gout. Careful surveillance of serum potassium and cautious use of spironolactone in patients at risk may help to decrease the incidence of potentially hazardous complications caused by hyperkalemia.

Ischemic muscle necrosis leading to life-threatening hyperkalemia. Case report and review of the literature

Objective: Description of a cat with ischemic muscle necrosis that suffered from cardiopulmonary arrest due to hyperkalemia. Pathogenesis, clinical signs and therapy of ischemic muscle necrosis are discussed and possible causes, symptoms and treatment of hyperkalemia are shown. Material and methods: case report of a four-year-old male castrated domestic shorthair cat. Results: The cat was successfully resuscitated and hyperkalemia was treated with different treatment modalities. Conclusion: Ischemic muscle necrosis can lead to severe live-threatening hyperkalemia which has to be anticipated, monitored and treated adequately. Aggressive fluid therapy might be responsible for a higher risk of hyperkalemia in predisposed cases. Clinical relevance: Potassium concentrations and acid-base disturbances must be closely monitored in patients with ischemic muscle necrosis

Lazy lips: hyperkalemia and acute tetraparesis-a case report from an urban emergency department.

A 58-year-old male patient was admitted to our emergency department at a large university hospital due to acute onset of general weakness. It was reported that the patient was bradycardic at 30/min and felt an increasing weakness of the limbs. At admission to the emergency department, the patient was not feeling any discomfort and denied dyspnoea or pain. The primary examination of the nervous system showed the cerebral nerves II-XII intact, muscle strength of the lower extremities was 4/5, and a minimal sensory loss of the left hemisphere was found. In addition, the patient complained about lazy lips. During ongoing examinations, the patient developed again symptomatic bradycardia, accompanied by complete tetraplegia. The following blood test showed severe hyperkalemia probably induced by use of aldosterone antagonists as the cause of the patient's neurologic symptoms. Hyperkalemia is a rare but treatable cause of acute paralysis that requires immediate treatment. Late diagnosis can delay appropriate treatment leading to cardiac arrhythmias and arrest.

The hyperthermic patient

Concepts used in this chapter include: Thermoregulation:- Thermoregulation refers to the body’s sophisticated, multi-system regulation of core body temperature. This hierarchical system extends from highly thermo-sensitive neurons in the preoptic region of the brain proximate to the rostral hypothalamus, down to the brain stem and spinal cord. Coupled with receptors in the skin and spine, both central and peripheral information on body temperature is integrated to inform and activate the homeostatic mechanisms which maintain our core temperature at 37oC1. Hyperthermia:- An imbalance between the metabolic and external heat accumulated in the body and the loss of heat from the body2. Exertional heat stroke:- A disorder of excessive heat production coupled with insufficient heat dissipation which occurs in un-acclimated individuals who are engaging in over-exertion in hot and humid conditions. This phenomenon includes central nervous system dysfunction and critical dysfunction to all organ systems including renal, cardiovascular, musculoskeletal and hepatic functions. Non-exertional heat stroke:- In contrast to exertional heatstroke as a consequence of high heat production during strenuous exercise, non-exertional heatstroke results from prolonged exposure to high ambient temperature. The elderly, those with chronic health conditions and children are particularly susceptible.3 Rhabdomylosis:- An acute, sometimes fatal disease characterised by destruction of skeletal muscle. In exertional heat stroke, rhabdomylosis occurs in the context of strenuous exercise when mechanical and/or metabolic stress damages the skeletal muscle, causing elevated serum creatine kinease. Associated with this is the potential development of hyperkalemia, myoglobinuria and renal failure. Malignant hyperthermia:- Malignant hyperthermia is “an inherited subclinical myopathy characterised by a hypermetabolic reaction during anaesthesia. The reaction is related to skeletal muscle calcium dysregulation triggered by volatile inhaled anaesthetics and/or succinylcholine.”4 Presentation includes skeletal muscle rigidity, mixed metabolic and respiratory acidosis, tachycardia, hyperpyrexia, rhabdomylosis, hyperkalaemia, elevated serum creatine kinease, multi-organ failure, disseminated intravascular coagulation and death.5

Biological impacts of enhanced alkalinity in Carcinus maenas

Further steps are needed to establish feasible alleviation strategies that are able to reduce the impacts of ocean acidification, whilst ensuring minimal biological side-effects in the process. Whilst there is a growing body of literature on the biological impacts of many other carbon dioxide reduction techniques, seemingly little is known about enhanced alkalinity. For this reason, we investigated the potential physiological impacts of using chemical sequestration as an alleviation strategy. In a controlled experiment, Carcinus maenas were acutely exposed to concentrations of Ca(OH)2 that would be required to reverse the decline in ocean surface pH and return it to pre-industrial levels. Acute exposure significantly affected all individuals' acid-base balance resulting in slight respiratory alkalosis and hyperkalemia, which was strongest in mature females. Although the trigger for both of these responses is currently unclear, this study has shown that alkalinity addition does alter acid-base balance in this comparatively robust crustacean species.

Management of hyperkalaemia

Hyperkalaemia, an elevated extracellular fluid potassium concentration, is a common electrolyte disorder and is present in 1-10% of hospitalised patients. Elevated serum potassium concentrations are usually asymptomatic but may be associated with electrocardiogram (ECG) changes. Hyperkalaemia occasionally leads to life-threatening cardiac arrhythmias. Prompt recognition of this disorder, patient risk management and administration of appropriate treatment can prevent serious cardiac complications of hyperkalaemia. Further assessment of the underlying basis for hyperkalaemia usually reveals a problem with renal potassium excretion (rather than transcellular shift of potassium or excess potassium intake). Reduced potassium excretion is typically associated with decreased potassium secretion in the aldosterone-sensitive distal nephron of the kidney. Common causes for hyperkalaemia include kidney failure, limited delivery of sodium and water to the distal nephron and drugs that inhibit the renin-angiotensin-aldosterone system. Treatment of life-threatening hyperkalaemia (particularly those patients with ECG changes) involves administration of intravenous calcium salts to stabilise the resting cardiac membrane potential. The potassium concentration can be lowered by administration of intravenous insulin combined with an infusion of glucose to stimulate intracellular uptake of potassium. Nebulised β-2 adrenoceptor agonists can augment the effects of intravenous insulin and glucose pending more definitive management of the recurrent hyperkalaemia risk. Additional management steps include stopping further potassium intake and careful review of prescribed drugs that may be adversely affecting potassium homeostasis. Changes to prescribing systems and an agreed institutional protocol for management of hyperkalaemia can improve patient safety for this frequently encountered electrolyte disorder.

Pseudohypoaldosteronisms, report on a 10-patient series.

BACKGROUND: Type 1 pseudohypoaldosteronism (PHA1) is a salt-wasting syndrome caused by mineralocorticoid resistance. Autosomal recessive and dominant hereditary forms are caused by Epithelial Na Channel and Mineralocorticoid Receptor mutation respectively, while secondary PHA1 is usually associated with urological problems. METHODS: Ten patients were studied in four French pediatric units in order to characterize PHA1 spectrum in infants. Patients were selected by chart review. Genetic, clinical and biochemistry data were collected and analyzed. RESULTS: Autosomal recessive PHA1 (n = 3) was diagnosed at 6 and 7 days of life in three patients presenting with severe hyperkalaemia and weight loss. After 8 months, 3 and 5 years on follow-up, neurological development and longitudinal growth was normal with high sodium supplementation. Autosomal dominant PHA1 (n = 4) was revealed at 15, 19, 22 and 30 days of life because of failure to thrive. At 8 months, 3 and 21 years of age, longitudinal growth was normal in three patients who were given salt supplementation; no significant catch-up growth was obtained in the last patient at 20 months of age. Secondary PHA1 (n = 3) was diagnosed at 11, 26 days and 5 months of life concomitantly with acute pyelonephritis in three children with either renal hypoplasia, urinary duplication or bilateral megaureter. The outcome was favourable and salt supplementation was discontinued after 3, 11 and 13 months. CONCLUSIONS: PHA1 should be suspected in case of severe hyperkalemia and weight loss in infants and need careful management. Pathogenesis of secondary PHA1 is still challenging and further studies are mandatory to highlight the link between infection, developing urinary tract and pseudohypoaldosteronism.

Renal tubular NEDD4-2 deficiency causes NCC-mediated salt-dependent hypertension.

The E3 ubiquitin ligase NEDD4-2 (encoded by the Nedd4L gene) regulates the amiloride-sensitive epithelial Na+ channel (ENaC/SCNN1) to mediate Na+ homeostasis. Mutations in the human β/γENaC subunits that block NEDD4-2 binding or constitutive ablation of exons 6-8 of Nedd4L in mice both result in salt-sensitive hypertension and elevated ENaC activity (Liddle syndrome). To determine the role of renal tubular NEDD4-2 in adult mice, we generated tetracycline-inducible, nephron-specific Nedd4L KO mice. Under standard and high-Na+ diets, conditional KO mice displayed decreased plasma aldosterone but normal Na+/K+ balance. Under a high-Na+ diet, KO mice exhibited hypercalciuria and increased blood pressure, which were reversed by thiazide treatment. Protein expression of βENaC, γENaC, the renal outer medullary K+ channel (ROMK), and total and phosphorylated thiazide-sensitive Na+Cl- cotransporter (NCC) levels were increased in KO kidneys. Unexpectedly, Scnn1a mRNA, which encodes the αENaC subunit, was reduced and proteolytic cleavage of αENaC decreased. Taken together, these results demonstrate that loss of NEDD4-2 in adult renal tubules causes a new form of mild, salt-sensitive hypertension without hyperkalemia that is characterized by upregulation of NCC, elevation of β/γENaC, but not αENaC, and a normal Na+/K+ balance maintained by downregulation of ENaC activity and upregulation of ROMK.

Sodium and potassium balance depends on αENaC expression in connecting tubule.

Mutations in α, β, or γ subunits of the epithelial sodium channel (ENaC) can downregulate ENaC activity and cause a severe salt-losing syndrome with hyperkalemia and metabolic acidosis, designated pseudohypoaldosteronism type 1 in humans. In contrast, mice with selective inactivation of αENaC in the collecting duct (CD) maintain sodium and potassium balance, suggesting that the late distal convoluted tubule (DCT2) and/or the connecting tubule (CNT) participates in sodium homeostasis. To investigate the relative importance of ENaC-mediated sodium absorption in the CNT, we used Cre-lox technology to generate mice lacking αENaC in the aquaporin 2-expressing CNT and CD. Western blot analysis of microdissected cortical CD (CCD) and CNT revealed absence of αENaC in the CCD and weak αENaC expression in the CNT. These mice exhibited a significantly higher urinary sodium excretion, a lower urine osmolality, and an increased urine volume compared with control mice. Furthermore, serum sodium was lower and potassium levels were higher in the genetically modified mice. With dietary sodium restriction, these mice experienced significant weight loss, increased urinary sodium excretion, and hyperkalemia. Plasma aldosterone levels were significantly elevated under both standard and sodium-restricted diets. In summary, αENaC expression within the CNT/CD is crucial for sodium and potassium homeostasis and causes signs and symptoms of pseudohypoaldosteronism type 1 if missing.

Diagnósticos de enfermagem em pacientes submetidos à hemodiálise: semelhanças entre o modelo de adaptação e a NANDA internacional

The nurses in the hemodialysis has an important role in the nursing process implementation, in the context of a theoretical referential. Among the nursing theories, highlights the Roy´s adaptations model, who considers a person as an holistic adaptive system that aims to adapt customers to different living conditions. Thus, it is believed that the Roy´s nursing process will guide nursing care to patients on dialysis. Therefore, the study aimed to analyze the nursing diagnosis present in patients with chronic kidney disease on hemodialysis based on the theoretical model of Roy and NANDA-International. Descriptive and cros-sectional study, performed at a dialysis center in a city in northeastern Brazil. Sample of 178 patients and consecutive sampling by convenience. Data collection ocurred from October/2011 until February/2012, through interview and physical examination forms. Data analysis was initiated by clinical reasoning, diagnosis judgment and similarity relation. Then, the data were entered into SPSS program, 16.0 version, generating descriptive statistics. The project was approved by the Ethics Research Committee (protocol nº 115/11) with a Presentation Certificate for Ethics Appreciation (in 0139.0.051.000-111) and was funded by the Universal edict MCT / CNPq 14/2010. The results revealed that most patients were male (52.2%), married (62.9%) and residents in the Natal´s metropolitan region (54.5%). The mean age was 46.6 years and the years of study, 8,5. Regarding nursing diagnosis obtained an average of 6.6, especially: Risk of Infection (100%), excessive fluid volume (99.4%) and hypothermia (61.8%). On the other hand the adaptive problems average was 6.4, and the most common: intracellular fluid retention (99.4%); Hyperkalemia (64.6%); Hypothermia (61.8%) and edema (53.9%). Were established 20 similarity relations between the NANDA-International nursing diagnosis and adaptive problems of Roy, namely: risk of falls / injury risk and potential for injury, impaired physical mobility and walking mobility and / or restricted coordination, dressing self-care deficit and loss of self-care ability; hypothermia and hypothermia; impaired skin integrity and impaired skin integrity; excessive fluid volume and intracellular fluid retention / Hyperkalemia / Hypocalcemia / edema; imbalanced nutrition: less than body requirements and Nutrition less than the body's needs; constipation and constipation, acute pain and acute pain, chronic pain and chronic pain, sensorial perception disturbed: visual, tactile and auditory disabilities and a primary sense: sight, hearing and tactile; sleep deprivation and insomnia, fatigue and intolerance to activities; ineffective self health and fails in the role; sexual dysfunction and sexual dysfunction; situational low self-esteem and low self-esteem, and diarrhea and diarrhea. We conclude that there is similarity between the typologies and was required a model´s analysis, because they present different ways to establish the nursing diagnosis. Moreover, the nursing process use, under the context of a theory and a classification system, subsidizes the care and contributes to the strengthening of nursing science

Efeitos do fentanil, droperidol e inoval sobre função renal e eletrólitos (sódio e potássio)

The influence of Fentanyl, Droperidol and Innovar on renal function and electrolytes (sodium and potassium) were studied on 18 dogs. Fentanyl disturbs kidney function and decreases plasmatic potassium. Droperidol and Innovar do not disturb the main renal function but decrease plasmatic potassium. The results obtained point out the importance of associate employment of Fentamyl and Droperidol, since the latter seems to establish the renal disorders occasioned by Fentanyl, probably owing to its adrenergic α blocking action.

Insuficiência renal aguda. Estudo do quadro clínico e prognóstico.

Acute renal failure (ARF) is a frequent complication in hospitalized patients, and is strongly related to increase of mortality. PURPOSE: To analyze the clinical outcome and the prognostic factors in hospital acquired AFR. METHOD: A prospective study was performed. Data from 200 patients with established ARF admitted during the period of January, 1987 and July, 1990 were collected. RESULTS: The incidence of ARF was 4.9/1000 admissions. Renal ischemia (50%) and nephrotoxic drugs (21%) were the main etiologic factors. The histologic study done in 43 patients showed: acute tubular necrosis (53%), tubular hydrophic degeneration (16%), glomerulopathies (16%) and other lesions (15%). Dialysis therapy was performed in 101 patients and the main indications were: uremia (67%), hypervolemia (22%) and hyperkalemia (9%). The mortality rate was 46.5% and the most important causes of death were: sepsis (38%), respiratory failure (19%) and multiple organs failure (11%). Treatment withdraw was the cause of death in 2 patients. Higher mortality was observed in oliguric patients (62.9%) than non-oliguric (34.5%) (p < 0.05) and in ischemic renal failure (56.7%) when compared to nephrotoxic renal failure (14.7%) (p < 0.05). This difference was maintained when the comparison was done only between dialyzed patients. CONCLUSION: As primary cause of death was not associated to the acute renal failure, we conclude that acute renal failure is an important marker of the gravity of the underlying disease and not the cause of death.