diabetestalk.net

Aldosterone In Dka

Hyperkalaemia

Hyperkalaemia

Clinical Cases Causes of HYPERkalaemia Serum potassium levels above the normal range (3.5-5.0 mmol/L) 1) Increased potassium intake (rare) Oral (potassium supplements) IV (transfusion of stored blood, supplement infusions) 2) Increased production Tissue injury Rhabdomyolysis, tumour lysis syndrome Burns, ischaemia, haemolysis Intense physical activity 3) Decreased renal excretion Renal failure (ARF and CRF) Aldosterone (Mineralocorticoid acting on collecting duct to reabsorb Na and excrete K and maintain intravascular volume) Hypoaldosteronism, Addison’s, Chronic active hepatitis Obstructive uropathy 4) Transcellular shift Acidosis: Metabolic acidosis (DKA, mineral acid overdose) HYPERglycaemia Respiratory acidosis 5) Fictitious (Pseudohyperkalaemia) Laboratory error Haemolysis of sample, clenched fist, ischaemic tourniquet Leucocytosis, thrombocytosis 6) Drugs causing hyperkalaemia Transcellular Suxamethonium, Beta blockers, phenylephrine Aldosterone inhibition ACE inhibitors, Angiotensin II blockers Heparin, spironolactone, Beta blockers Increased aldosterone resistance (Trimethoprim, amiloride) Inhibition Na/K/ATPase (Digoxin) Potassium supplements and IV additives (Increase exogenous potassium) Clinical Muscle weakness Lethargy Ascending paralysis Respiratory failure Complications Cardiac Arrhythmia Correction Membrane stabilization Calcium chloride/gluconate ECF – ICF shift Sodium bicarbonate Insulin/dextrose Beta agonists (Salbutamol) Removal of K from body Urine – Frusemide Faeces – Resonium Blood – Dialysis Correction principles for hyperkalaemia MILD (5-6mEq/L) Diuretic-Frusemide Calcium resonium- sodium polystyrene sulphate 100/gram. PO or PR 6 hourly Exchange resin with 1mmol K for every gram used. MODERATE (6-7) Glucose-insulin (10U insulin 50G dex Continue reading >>

Hyperkalemia (high Blood Potassium)

Hyperkalemia (high Blood Potassium)

How does hyperkalemia affect the body? Potassium is critical for the normal functioning of the muscles, heart, and nerves. It plays an important role in controlling activity of smooth muscle (such as the muscle found in the digestive tract) and skeletal muscle (muscles of the extremities and torso), as well as the muscles of the heart. It is also important for normal transmission of electrical signals throughout the nervous system within the body. Normal blood levels of potassium are critical for maintaining normal heart electrical rhythm. Both low blood potassium levels (hypokalemia) and high blood potassium levels (hyperkalemia) can lead to abnormal heart rhythms. The most important clinical effect of hyperkalemia is related to electrical rhythm of the heart. While mild hyperkalemia probably has a limited effect on the heart, moderate hyperkalemia can produce EKG changes (EKG is a reading of theelectrical activity of the heart muscles), and severe hyperkalemia can cause suppression of electrical activity of the heart and can cause the heart to stop beating. Another important effect of hyperkalemia is interference with functioning of the skeletal muscles. Hyperkalemic periodic paralysis is a rare inherited disorder in which patients can develop sudden onset of hyperkalemia which in turn causes muscle paralysis. The reason for the muscle paralysis is not clearly understood, but it is probably due to hyperkalemia suppressing the electrical activity of the muscle. Common electrolytes that are measured by doctors with blood testing include sodium, potassium, chloride, and bicarbonate. The functions and normal range values for these electrolytes are described below. Hypokalemia, or decreased potassium, can arise due to kidney diseases; excessive losses due to heavy sweating Continue reading >>

Hyperaldosteronism

Hyperaldosteronism

Primary aldosteronism (PA) is a clinical syndrome of hypertension, suppressed renin activity and increased aldosterone secretion. The two most common causes of PA are aldosterone producing adrenal adenoma (APA), seen in ~35% of cases, a unilateral adrenal cortical tumour resulting in autonomous secretion of aldosterone, or bilateral adrenal hyperplasia (IHA), seen in ~60% of cases, where both adrenal glands secrete excessive amounts of aldosterone in response to angiotensin-II. Less common causes include primary unilateral adrenal hyperplasia (PAH), glucocorticoid remediable aldosteronism (GRA), and very rarely adrenal carcinoma. Some 15-25% of patients with PA have glucose intolerance, and diabetes is twice as common as in control populations. The prevalence of PA is increased in people with resistant hypertension associated with diabetes, with rates of 13% and 14% in two separate studies.Early detection and treatment can prevent long-term micro- and macrovascular complications in a significant proportion of patients. Impaired glucose metabolism is a frequent finding in patients with PA but the mechanism that leads to dysglycaemia requires further study. Continue reading >>

Diabetic Ketoacidosis In The Pediatric Population With Type 1 Diabetes

Diabetic Ketoacidosis In The Pediatric Population With Type 1 Diabetes

Diabetic Ketoacidosis in the Pediatric Population with Type 1 Diabetes Abstract: Diabetic ketoacidosis (DKA) is a leading cause of morbidity and mortality in patients with type 1 diabetes (T1DM). Individuals familiar with this complication of diabetes should be able to identify the earliest signs and symptoms and act promptly to prevent further deterioration. However, even in patients with established diabetes, the rates of DKA are considerable. This chapter discusses in detail the various aspects of DKA in the pediatric population with T1DM. The prevalence and regional effects on the prevalence of DKA as well as the specific risk factors, whether disease, patient, or physician related, are reviewed. Patients with DKA experience a condition of starvation despite the abundance of metabolic substrate (i.e., glucose); the pathophysiological mechanisms responsible for the development of DKA are outlined. Next, a detailed discussion of the clinical aspects of DKA is provided. This includes the clinical findings at presentation, the approach to treatment, and potential complications. Prevention is the best method for reducing rates of DKA. Somewhat different factors apply in patients with new-onset diabetes when compared with those with established diabetes and these are reviewed. Continue reading >>

Severe Hyperkalaemia In Association With Diabetic Ketoacidosis In A Patient Presenting With Severe Generalized Muscle Weakness

Severe Hyperkalaemia In Association With Diabetic Ketoacidosis In A Patient Presenting With Severe Generalized Muscle Weakness

Diabetic ketoacidosis (DKA) is an acute, life‐threatening metabolic complication of diabetes mellitus. Hyperglycaemia, ketosis (ketonaemia or ketonuria) and acidosis are the cardinal features of DKA [1]. Other features that indicate the severity of DKA include volume depletion, acidosis and concurrent electrolyte disturbances, especially abnormalities of potassium homeostasis [1,2]. We describe a type 2 diabetic patient presenting with severe generalized muscle weakness and electrocardiographic evidence of severe hyperkalaemia in association with DKA and discuss the related pathophysiology. A 65‐year‐old male was admitted because of impaired mental status. He was a known insulin‐treated diabetic on quinapril (20 mg once daily) and was taking oral ampicillin 500 mg/day because of dysuria which had started 5 days prior to admission. He was disoriented in place and time with severe generalized muscle weakness; he was apyrexial (temperature 36.4°C), tachycardic (120 beats/min) and tachypneic (25 respirations/min) with cold extremities (supine blood pressure was 100/60 mmHg). An electrocardiogram (ECG) showed absent P waves, widening of QRS (‘sine wave’ in leads I, II, V5 and V6), depression of ST segments and tall peaked symmetrical T waves in leads V3–V6 (Figure 1). Blood glucose was 485 mg/dl, plasma creatinine 5.1 mg/dl (reference range (r.r.) 0.6–1.2 mg/dl, measured by the Jaffe method), urea 270 mg/dl (r.r. 11–54 mg/dl), albumin 4.2 g/dl (r.r. 3.4–4.7 g/dl), sodium 136 mmol/l (r.r. 135–145 mmol/l), chloride 102 mmol/l (r.r. 98–107 mmol/l), potassium 8.3 mmol/l (r.r. 3.5–5.4 mmol/l), phosphorus 1.6 mmol/l (r.r. 0.8–1.45 mmol/l) and magnesium 0.62 mmol/l (r.r. 0.75–1.25 mmol/l). A complete blood count revealed leukocytosis (12 090/µl with Continue reading >>

The Renin Angiotensin Aldosterone Reflex

The Renin Angiotensin Aldosterone Reflex

We are going to talk about the homeostatic reflex mentioned as the following things in a textbook: renin-angiotensin system (RAS) renin-angiotensin-aldosterone system (RAAS) renin-angiotensin-aldosterone pathway (RAA pathway) Don’t let these words scare you! We’re going to follow a pattern here. Renin leads to Angiotensin being released which eventually leads to Aldosterone being released. We’re going to explain all that in detail. We begin with the kidney. The kidney is an endocrine gland (since it secretes several hormones) and it excretes two hormones we are going to learn about: renin (renal means kidney) and erythropoietin (brand name Procrit). The cells that secrete renin are called Juxtaglomerular (J-G) cells. Three triggers that cause JG cells to secrete Renin into the blood stream: A drop in blood pressure, A decrease in blood sodium levels, An increase in blood potassium levels. That triggers this hormonal homeostatic reflex. A homeostatic reflex is there to compensate or correct for a stress. Examples of homeostatic reflexes: The RAA pathway ensures that it will correct for all three of these triggers. It makes this a very important reflex because it controls your blood pressure and your two most important minerals in your body: sodium and potassium. When Renin is secreted, it stimulates a protein in your blood stream called angiotensinogen. The liver makes most of these plasma proteins (such as albumin). This angiotensinogen is always circulating in the blood stream. Renin activates it and turns it into angiotensin-1. (There are many proteins that have to be “activated.” The inactivated form usually it ends with -gen. Then when it’s activated, you drop that ending so it becomes angiotensinogen to angiotensin 1. For example: Your stomach cells sec Continue reading >>

Renin-angiotensin-aldosterone System In Diabetes Mellitus.

Renin-angiotensin-aldosterone System In Diabetes Mellitus.

Abstract The renin-angiotensin-aldosterone system appears to function normally in uncomplicated diabetes mellitus. Alterations in this system, however, have been observed in several of the microvascular and electrolyte complications associated with this disease. Plasma renin activity (PRA) and aldosterone are decreased in diabetic with nephropathy and hypertension, in those with neuropathy including orthostatic hypotension, and in those with hypoaldosteronism. PRA is low in rats with uncontrolled, nonketotic diabetes, and pressor responsiveness to angiotension II is increased in patients with diabetic retinopathy. Potential mechanisms responsible for the decreased PRA include plasma volume expansion, hyalin destruction of the juxtaglomerular cells, defective synthesis of renin, and inadequate catecholamine stimulation of renin, and inadequant cathecholamine stimulation of renin release. In diabetic ketoacidosis, PRA and aldosterone are stimulated secondary to the associated dehydration with hypovolemia. This report reviews the current status of the function of the renin-angiotensin-aldosterone system in diabetes mellitus and proposes a possible role for the altered function of this system in the pathophysiology of several diabetic complications. Continue reading >>

Prevalence And Potential Risk Factors Of Hypokalemia In Pediatric Patients With Diabetic Ketoacidosis

Prevalence And Potential Risk Factors Of Hypokalemia In Pediatric Patients With Diabetic Ketoacidosis

Aims To examine the local prevalence of hypokalemia in patients with diabetic ketoacidosis (DKA), both at presentation and during treatment, and to investigate the potential risk factors leading to significant hypokalemia during treatment of DKA. Methods Retrospective review of 114 consecutive patient-episodes. Univariate analyses were performed to study any difference in mean between the group with nadir of potassium (Kn) >= 3.0mmol/L from group with Kn < 3.0mmol/L for predictors concerning patients’ demographics, the baseline characteristics, the therapies for DKA (including average insulin infusion rate before Kn), and the pace of recovery from DKA. Predictors deemed statistical significant in univariate analyses were subjected to multivariate analysis. Results The period prevalence of hypokalemia at presentation and during treatment of DKA were 13.8% and 92.5% respectively. Univariate analysis showed patients who were younger, with lower mean body weight, lower mean plasma bicarbonate at presentation, lower mean serum potassium level at presentation, higher urine output per unit body weight (in the first 24 hours of admission), higher amount of potassium supplement given before Kn, shorter time lag of starting potassium supplements (as reference to time of start of insulin) and longer duration of metabolic acidosis were independently associated with risk of developing Kn < 3.0mmol/L. Multivariate analysis showed that duration of metabolic acidosis was the sole risk factor for having Kn < 3.0mmol/L. Conclusions In our cohort, the longer duration of metabolic acidosis predicts significant hypokalemia during DKA treatment, which could have represented a persistent accumulation of free fatty acid and an on-going stimulus for aldosterone secretion, hence kaliuresis-rel Continue reading >>

A Renal Mechanism Limiting The Degree Of Potassium Loss In Severely Hyperglycemic Patients

A Renal Mechanism Limiting The Degree Of Potassium Loss In Severely Hyperglycemic Patients

Potassium (K) secretion in the cortical ‘distal nephron’ was assessed in vivo in 29 consecutive patients presenting with diabetic ketoacidosis (DKA) or the hyperglycemic hyperosmolar syndrome (HHS). The only selection criteria applied were that the electrolytes and osmolality be measured in the urine on admission. Five patients with DKA and 3 patients with HHS were reported in detail as plasma aldosterone levels were also measured in these patients on admission. K secretion in the ‘cortical distal nephron’ was assessed by a semiquantitative index, the transtubular K concentration gradient (TTKG). TTKG values less than 6.0, consistent with less than maximal renal K secretion, were found in 28 of 29 patients despite the presence of hyperkalemia and/or stimuli for renin and aldosterone release. Plasma aldosterone levels on admission were very elevated in 4 patients, at the upper end of the usual normal range in 3 and in the low part of the normal range in 1 patient. Treatment with intravenous saline, KC1 and insulin corrected the fluid and electrolyte abnormalities in the plasma over 24–48 h. Concurrently, plasma aldosterone levels fell, but the TTKG rose; this suggests that there was an increased renal tubular response to aldosterone after initial therapy. The mechanism responsible for this reversible impairment of renal K secretion is unknown. It may limit total body K depletion in patients presenting with DKA and HHS by diminishing renal K excretion. © 1988 S. Karger AG, Basel Article / Publication Details Continue reading >>

Hyperosmolar Hyperglycemic State

Hyperosmolar Hyperglycemic State

Background Hyperosmolar hyperglycemic state (HHS) is one of two serious metabolic derangements that occurs in patients with diabetes mellitus (DM). [1] It is a life-threatening emergency that, although less common than its counterpart, diabetic ketoacidosis (DKA), has a much higher mortality rate, reaching up to 5-10%. (See Epidemiology.) HHS was previously termed hyperosmolar hyperglycemic nonketotic coma (HHNC); however, the terminology was changed because coma is found in fewer than 20% of patients with HHS. [2] HHS is most commonly seen in patients with type 2 DM who have some concomitant illness that leads to reduced fluid intake, as seen, for example, in elderly institutionalized persons with decreased thirst perception and reduced ability to drink water. [3] Infection is the most common preceding illness, but many other conditions, such as stroke or myocardial infarction, can cause this state. [3] Once HHS has developed, it may be difficult to identify or differentiate it from the antecedent illness. (See Etiology.) HHS is characterized by hyperglycemia, hyperosmolarity, and dehydration without significant ketoacidosis. Most patients present with severe dehydration and focal or global neurologic deficits. [2, 4, 5] The clinical features of HHS and DKA overlap and are observed simultaneously (overlap cases) in up to one third of cases. According to the consensus statement published by the American Diabetes Association, diagnostic features of HHS may include the following (see Workup) [4, 6] : Effective serum osmolality of 320 mOsm/kg or greater Profound dehydration, up to an average of 9L Detection and treatment of an underlying illness are critical. Standard care for dehydration and altered mental status is appropriate, including airway management, intravenous (I Continue reading >>

Hypokalemia During Treatment Of Diabetic Ketoacidosis: Clinical Evidence For An Aldosterone-like Action Of Insulin

Hypokalemia During Treatment Of Diabetic Ketoacidosis: Clinical Evidence For An Aldosterone-like Action Of Insulin

Abstract Objectives: To investigate whether the development of hypokalemia in patients with diabetic ketoacidosis (DKA) treated in the pediatric critical care unit (PCCU) could be caused by increased potassium (K(+)) excretion and its association with insulin treatment. Study design: In this prospective observational study of patients with DKA admitted to the PCCU, blood and timed urine samples were collected for measurement of sodium (Na(+)), K(+), and creatinine concentrations and for calculations of Na(+) and K(+) balances. K(+) excretion rate was expressed as urine K(+)-to-creatinine ratio and fractional excretion of K(+). Results: Of 31 patients, 25 (81%) developed hypokalemia (plasma K(+) concentration <3.5 mmol/L) in the PCCU at a median time of 24 hours after therapy began. At nadir plasma K(+) concentration, urine K(+)-to-creatinine ratio and fractional excretion of K(+) were greater in patients who developed hypokalemia compared with those without hypokalemia (19.8 vs 6.7, P = .04; and 31.3% vs 9.4%, P = .004, respectively). Patients in the hypokalemia group received a continuous infusion of intravenous insulin for a longer time (36.5 vs 20 hours, P = .015) and greater amount of Na(+) (19.4 vs 12.8 mmol/kg, P = .02). At peak kaliuresis, insulin dose was higher in the hypokalemia group (median 0.07, range 0-0.24 vs median 0.025, range 0-0.05 IU/kg; P = .01), and there was a significant correlation between K(+) and Na(+) excretion (r = 0.67, P < .0001). Conclusions: Hypokalemia was a delayed complication of DKA treatment in the PCCU, associated with high K(+) and Na(+) excretion rates and a prolonged infusion of high doses of insulin. Continue reading >>

Diabetic Ketoacidosis And Fluid Refractory Hypotension

Diabetic Ketoacidosis And Fluid Refractory Hypotension

SAGE Video Streaming video collections SAGE Knowledge The ultimate social sciences library SAGE Research Methods The ultimate methods library SAGE Stats Data on Demand CQ Library American political resources About Privacy Policy Terms of Use Contact Us Help Health Sciences Life Sciences Materials Science & Engineering Social Sciences & Humanities Journals A-Z Authors Editors Reviewers Librarians Researchers Societies Advertising Reprints Content Sponsorships Permissions ISSN: 0009-9228 Online ISSN: 1938-2707 Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus.[1] Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion, and occasionally loss of consciousness.[1] A person's breath may develop a specific smell.[1] Onset of symptoms is usually rapid.[1] In some cases people may not realize they previously had diabetes.[1] DKA happens most often in those with type 1 diabetes, but can also occur in those with other types of diabetes under certain circumstances.[1] Triggers may include infection, not taking insulin correctly, stroke, and certain medications such as steroids.[1] DKA results from a shortage of insulin; in response the body switches to burning fatty acids which produces acidic ketone bodies.[3] DKA is typically diagnosed when testing finds high blood sugar, low blood pH, and ketoacids in either the blood or urine.[1] The primary treatment of DKA is with intravenous fluids and insulin.[1] Depending on the severity, insulin may be given intravenously or by injection under the skin.[3] Usually potassium is also needed to prevent the development of low blood potassium.[1] Throughout treatment blood sugar and potassium levels should be regularly checked.[1] Antibiotics may be required in those with an underlying infection.[6] In those with severely low blood pH, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended.[1][6] Rates of DKA vary around the world.[5] In the United Kingdom, about 4% of people with type 1 diabetes develop DKA each year, while in Malaysia the condition affects about 25% a year.[1][5] DKA was first described in 1886 and, until the introduction of insulin therapy in the 1920s, it was almost univ Continue reading >>

Hyperaldosteronism In Ketoacidosis And In Poorly Controlled Non-ketotic Diabetes

Hyperaldosteronism In Ketoacidosis And In Poorly Controlled Non-ketotic Diabetes

Summary PLASMA aldosterone concentrations were measured in 14 patients in diabetic ketoacidosis and in 20 patients with poorly controlled non-ketotic diabetes, both before treatment and again when metabolic control was achieved. Plasma aldosterone was above normal in 12 of 14 patients in ketoacidosis and there was a highly significant fall in mean plasma aldosterone concentration when metabolic control improved. Plasma aldosterone concentration in ketoacidosis was significantly related to plasma angiotensin //, arterial pH and indirect indices of dehydration. Plasma aldosterone was also above normal before treatment in 7 of 20 patients with poorly controlled non-ketotic diabetes. When metabolic control improved there was a small but significant reduction in mean plasma aldosterone concentration. However, plasma aldosterone and angiotensin were not significantly related in these patients. It is concluded that ketoacidosis is usually associated with marked hyper-aldosteronism. Poorly controlled nonketotic diabetes is sometimes associated with mild aldosterone excess, which may contribute to the potassium wasting associated with poorly controlled diabetes. Continue reading >>

Pitfalls In The Management Of Diabetic Ketoacidosis In A Hospital In Ghana

Pitfalls In The Management Of Diabetic Ketoacidosis In A Hospital In Ghana

Diabetic Ketoacidosis (DKA) is a common acute complication among children and adolescents with type 1 diabetes in Africa. This is due to the fact that awareness about diabetes among children and adolescents is very poor in low income countries and in many cases there is little or no support for these patients. Ghana has no clinical guidelines for management of DKA and so mismanagement is likely very common. Misdiagnosis and mismanagement of DKA are worrying causes of morbidity and mortality among children with diabetes in Ghana and other resource constrained countries. Keywords:Diabetic Ketoacidosis; High Mortality; Hypokalaemia; Type 1 Diabetes. Continue reading >>

More in ketosis