Books on the topic 'Hyperkalaemia'

The differential diagnosis and approach to patients with high or low serum potassium are described. Patients with either abnormality have an increased mortality in large population-based studies. Most have significant renal, cardiovascular, endocrine, liver, or gastrointestinal disease. They are frequently taking prescription or other drugs and the evaluation of their electrolyte disorder should not be conducted in isolation, but within the context of their disease or diseases. The presence of isolated hypokalaemia or hyperkalaemia in the absence of these other diseases or any apparent drug administration should prompt the clinician to re-consider the clinical history and the reported laboratory values.

Potassium is the major intracellular cation, and maintenance of potassium homeostasis is critical for normal cellular function. Serum potassium levels usually range from 3.5–4.5 mmol/l (compared with intracellular levels of ~150 mmol/l). Hypokalaemia is defined as a serum potassium level <3.5 mmol/l, and hyperkalaemia as a serum potassium level >4.5 mmol/l. Hyperkalaemia occurs in over 5% of hospitalized patients, and is most common in older age groups, where it is associated with renal impairment and medication use. Medications that block the renin–angiotensin system, such as angiotensin-converting-enzyme inhibitors and angiotensin receptor blockers, are often responsible. Hypokalaemia is also common, affecting over 15% of hospitalized patients, and is usually related to diuretic use, gastrointestinal losses, or inadequate potassium in the diet. This chapter reviews the causes and management of derangements of plasma potassium.

Plasma potassium levels are maintained in health between 3.5 and 5.0 mmol/L, and reflect total body potassium only in stable states at normal pH. Most true hyperkalaemia results from renal insufficiency. The goals of therapy are myocardial protection and return of plasma potassium to a safe level. Measures are commonly initiated above 5.5 mmol/L; above 6.5 mmol/L, aggressive measures should be adopted and calcium salts given if there are cardiac dysrhythmias or QRS-broadening. Glucose-insulin infusions and beta-2-agonists promote potassium shifts into cells. Diuretics and sodium bicarbonate may be helpful, but persistent hyperkalaemia is an indication for renal replacement therapy. Hypokalaemia may lead to dangerous arrhythmias, skeletal muscle weakness, ileus, and reduced vascular smooth muscle contractility. Rapid replacement should only be undertaken for severe hypokalaemia or in the context of arrhythmias. Once the extracellular deficit is corrected, there will usually be a continuing need for potassium supplementation to replenish intracellular stores.

Plasma potassium levels are maintained in health between 3.5 and 5.0 mmol/L, and reflect total body potassium only in stable states at normal pH. Most true hyperkalaemia results from renal insufficiency. The goals of therapy are myocardial protection and return of plasma potassium to a safe level. Measures are commonly initiated above 5.5 mmol/L; above 6.5 mmol/L, aggressive measures should be adopted and calcium salts given if there are cardiac dysrhythmias or QRS-broadening. Glucose-insulin infusions and beta-2-agonists promote potassium shifts into cells. Diuretics and sodium bicarbonate may be helpful, but persistent hyperkalaemia is an indication for renal replacement therapy. Hypokalaemia may lead to dangerous arrhythmias, skeletal muscle weakness, ileus, and reduced vascular smooth muscle contractility. Rapid replacement should only be undertaken for severe hypokalaemia or in the context of arrhythmias. Once the extracellular deficit is corrected, there will usually be a continuing need for potassium supplementation to replenish intracellular stores.

This chapter provides an overview of the background of fluid balance in the neonate, including the need to compensate for fluid loss (output), and the requirement to provide energy and nutrition. It also covers the management of common issues in fluid, electrolyte, and acid-base balance in the newborn period, including dehydration, sodium balance (hyponatraemia and hypernatraemia), hyperkalaemia, interpretation of blood gases (including pH, base excess, and anion gap), respiratory and metabolic acidosis, and hydrops fetalis.

Electrolyte disturbances are common in patients with acute kidney injury (AKI) and should be corrected. In particular, hyperkalaemia above 6–6.5 mmol/L (especially with electrocardiogram changes) constitutes a medical emergency and warrants immediate intervention. Both hypo- and hypernatraemia may occur during AKI. Chronic changes in serum sodium need to be corrected bearing in mind the underlying pathology; however, when severe and evolving rapidly they should be corrected faster, irrespective of the cause. Acid–base disorders are also common in AKI and need to be treated in the context of underlying problems and physiological compensatory mechanisms. In metabolic acidosis, a bicarbonate deficit may be corrected by sodium bicarbonate administration. Of note, whilst patients with AKI tend to retain electrolytes such as potassium and phosphate, this might be reversed during renal replacement therapy and even substitution of these losses may be required.

The most frequent clinical conditions complicated by bradyarrhythmias or atrioventricular blocks seen in an emergency setting are the degeneration of the conduction system, acute myocardial infarction, drug toxicity, and hyperkalaemia. Pacemaker malfunction is another cause of potentially life-threatening bradyarrhythmias. The presence of signs/symptoms of hypoperfusion and the localization of the block condition the therapeutic approach. Treatment of bradyarrhythmias and atrioventricular block in a critical care setting may be preventative or therapeutic. A preventative approach is necessary when the risk of a sudden block with an inadequate ventricular escape rhythm is present, but the patient is asymptomatic. Symptomatic patients require immediate treatment. If the block is located at His bundle level or at bundle branch level, atropine may be ineffective and may even worsen the degree of the block. If drug administration is ineffective, transvenous temporary pacing is indicated. Transcutaneous cardiac pacing is another temporary method of pacing indicated in various critical clinical settings.

Despite a gradual decline in the clinical use of digitalis glycosides, digitalis toxicity continues to be responsible for substantial morbidity and mortality, particularly among the elderly. Digitalis poisoning may occur acutely, after intentional overdose, but is more often seen as the result of chronic intoxication among patients receiving digitalis therapy. Clinical findings in chronic digitalis poisoning are often subtle. The astute clinician will enquire about digitalis use in older patients with vague complaints and will not be dissuaded from considering digitalis toxicity in the face of a ‘therapeutic’ digitalis blood concentration. Two digitalis preparations continue to be used with frequency, depending on geography. Digoxin is the digitalis glycoside of choice in the USA, while digitoxin prevails in some parts of Europe. While the methods and half-lives of elimination differ markedly for these two substances, the approach to poisoning by either is similar. Advanced age, underlying cardiovascular disease, and severe hyperkalaemia represent poor prognostic factors in digitalis poisoning. Early administration of digitalis Fab fragments should be undertaken when life-threatening symptoms are present. Prophylactic therapy with reduced doses of Fab fragments should be strongly considered for less serious toxicity.

Rhabdomyolysis is a potentially life-threatening syndrome characterized by the breakdown of skeletal muscle. It is associated with myalgia, muscle tenderness, swelling, and/or stiffness, accompanied by weakness and raised levels of creatine kinase (CK), myoglobin, phosphate and potassium, sometimes with acute kidney injury (AKI). There are multiple causes of this syndrome, traumatisms and myotoxic effect of drugs being the most frequent in developed countries. The pathophysiology involves direct trauma, as well as energy (ATP) depletion with disruption of sarcolemma integrity and muscle destruction. The sequestration of plasma water leads to hypovolaemic shock, while the release of muscle content, mainly myoglobin and potassium lead to the most severe complications of this syndrome, acute kidney injury/hyperkalaemia. The kidney injury is driven both by renal ischaemia due to vasoconstriction and to the toxic effects of myoglobin. The local oedema produced by the release of muscle content remains trapped within the fascia and can lead to compartment syndrome. Volume repletion with saline is essential to avoid hypovolaemic shock and acute kidney injury (AKI). With respect to compartment syndrome, close monitoring of clinical signs and compartment pressures is essential, since it can evolve to a surgical emergency. The prognosis of rhabdomyolysis is determined by age, baseline conditions and, most importantly, whether or not severe AKI develops.

The renal tubular acidoses are a collection of syndromes characterized by defective urinary acidification. These syndromes have classically caused some confusion, and many opine that the widely used numerical system (type 1, 2) should be abandoned. We consider distal renal tubular acidosis and proximal renal tubular acidosis separately, and briefly cover hypoaldosteronism. Distal (Type 1) renal tubular acidosis is a syndrome of hypokalaemia, metabolic acidosis, kidney stones, nephrocalcinosis, and osteomalacia or rickets. It is caused by failure of the acid secreting α‎‎‎-intercalated cells in the distal nephron. Proximal (Type 2) renal tubular acidosis is a syndrome of metabolic acidosis that is almost always accompanied by the Fanconi syndrome of glycosuria, phosphaturia, uricosuria, aminoaciduria, and low-molecular-weight proteinuria. It is caused by a failure of bicarbonate reabsorption by the proximal tubular cells. Type 3 or mixed renal tubular acidosis, as originally described, has vanished (or was originally incompletely described). It is sometimes used to describe a mutation of carbonic anhydrase II, which causes both proximal and distal renal tubular acidosis, as well as cerebral calcification and osteopetrosis. Type 4 or hypoaldosteronism is a syndrome of hyperkalaemia and mild metabolic acidosis. It is due to a lack of aldosterone or resistance to its action.

About one third of patients with type 1 diabetes develop diabetic nephropathy long-term (usually not before at least 10 years of diabetes), though this proportion is falling as standards of care have risen. Nephropathy is strongly associated with other microvascular complications of diabetes, so that some degree of retinopathy is to be expected, and evidence of neuropathy is common. Patients with type 2 diabetes are equally susceptible, but this is an older group in which vascular disease and other pathologies are also more likely. The rise in type 2 diabetes accounts for diabetes being the most common recorded cause of end stage renal disease (ESRD) in the developed world.Diabetic nephropathy is characterized by a progression through hyperfiltration, microalbuminuria, hypertension, overt proteinuria, nephrotic syndrome, loss of GFR, to ESRD. Risk factors for developing it include genetic factors (though no major single gene effects have been identified), and quality of glycaemic control.The risk of progression can at early stages be reduced by improved glycaemic control, and control of hypertension also slows progression. However angiotensin converting enzyme inhibitors or receptor blockers (ACEi, ARB) are the standard of care for patients with microalbuminuria or overt proteinuria, as they have been shown to reduce the risk of renal endpoints. Combination therapy with both ACEi and ARB together has been associated with a high risk of AKI, hyperkalaemia and other adverse effects so is not generally recommended. Other promising agents in combination are under investigation but none adequately proven at this stage.Patients who reach ESRD have reduced survival on all modalities compared to age-matched patients with other diagnoses. Best rehabilitation and survival for those who are suitable is through renal transplantation, though combined pancreas-renal transplantation may offer still better outcomes for selected patients.

Anaesthesia induces changes in many organ systems within the body, though clearly none more so than the central nervous system. The physiology of the normal central nervous system is complex and the addition of chronic pathology and polypharmacy creates a significant challenge for the anaesthetist. This chapter demonstrates a common approach for the anaesthetist and specific considerations for a wide range of neurological conditions. Detailed preoperative assessment is essential to gain understanding of the current symptomatology and neurological deficit, including at times restrictions on movement and position. Some conditions may pose challenges relating to communication, capacity, and consent. As part of the consent process, patients may worry that an anaesthetic may aggravate or worsen their neurological disease. There is little evidence to support this understandable concern; however, the risks and benefits must be considered on an individual patient basis. The conduct of anaesthesia may involve a preference for general or regional anaesthesia and requires careful consideration of the pharmacological and physiological impact on the patient and their disease. Interactions between regular medications and anaesthetic drugs are common. Chronically denervated muscle may induce hyperkalaemia after administration of succinylcholine. Other patients may have an altered response to non-depolarizing agents, such as those suffering from myasthenia gravis. The most common neurological condition encountered is epilepsy. This requires consideration of the patient’s antiepileptic drugs, often relating to hepatic enzyme induction or less commonly inhibition and competition for protein binding, and the effect of the anaesthetic technique and drugs on the patient’s seizure risk. Postoperative care may need to take place in a high dependency unit, especially in those with limited preoperative reserve or markers of frailty, and where the gastrointestinal tract has been compromised, alternative routes of drug delivery need to be considered. Overall, patients with chronic neurological conditions require careful assessment and preparation, a considered technique with attention to detail, and often higher levels of care during their immediate postoperative period.

The term ‘polytrauma’ refers to blunt (or crush) trauma that involves multiple body regions or cavities, and compromises physiology to potentially cause dysfunction of uninjured organs. Polytrauma frequently affects muscles resulting in rhabdomyolysis. In daily life, it mostly occurs after motor vehicle accidents, influencing a limited number of patients; after mass disasters, however, thousands of polytrauma victims may present at once with only surgical features or with additional medical complications (crush syndrome). Among the medical complications, acute kidney injury (AKI) deserves special mention, since it is frequent and has a substantial impact on the ultimate outcome.Several factors play a role in the pathogenesis of polytrauma (or crush)-induced AKI: (1) hypoperfusion of the kidneys, (2) myoglobin-induced direct nephrotoxicity, and intratubular obstruction, and also (3) several other mechanisms (i.e. iron and free radical-induced damage, disseminated intravascular coagulation, and ischaemia reperfusion injury). Crush-related AKI is prerenal at the beginning; however, acute tubular necrosis may develop eventually. In patients with crush syndrome, apart from findings of trauma, clinical features may include (but are not limited to) hypotension, oliguria, brownish discoloration of urine, and other symptoms and findings, such as sepsis, acute respiratory distress syndrome, disseminated intravascular coagulation, bleeding, cardiac failure, arrhythmias, electrolyte disturbances, and also psychological trauma.In the biochemical evaluation, life-threatening hyperkalaemia, retention of uraemic toxins, high anion gap metabolic acidosis, elevated serum levels of myoglobin, and muscle enzymes are noted; creatine phosphokinase is very useful for diagnosing rhabdomyolysis.Early fluid administration is vital to prevent crush-related AKI; the rate of initial fluid volume should be 1000 mL/hour. Overall, 3–6 L are administered within a 6-hour period considering environmental, demographic and clinical features, and urinary response to fluids. In disaster circumstances, the preferred fluid formulation is isotonic saline because of its ready availability. Alkaline (bicarbonate-added) hypotonic saline may be more useful, especially in isolated cases not related to disaster, as it may prevent intratubular myoglobin, and uric acid plugs, metabolic acidosis, and also life-threatening hyperkalaemia.In the case of established acute tubular necrosis, dialysis support is life-saving. Although all types of dialysis techniques may be used, intermittent haemodialysis is the preferred modality because of medical and logistic advantages. Close follow-up and appropriate treatment improve mortality rates, which may be as low as 15–20% even in disaster circumstances. Polytrauma victims after mass disasters deserve special mention, because crush syndrome is the second most frequent cause of death after trauma. Chaos, overwhelming number of patients, and logistical drawbacks often result in delayed, and sometimes incorrect treatment. Medical and logistical disaster preparedness is useful to improve the ultimate outcome of disaster victims.