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a LANGE medical book. CURRENT. Medical Diagnosis. & Treatment New table summarizing Revised Jones Criteria for rheumatic fever. CURRENT Medical Diagnosis and Treatment Study Guide, 2E (Lange Current): Publisher: McGraw-Hill Education / Medical; 2 edition (December 7, ). placeholder for MarKeTING paGe 1 7/29/14 PM This page intentionally left blank CURRENT Medical Diagnosis.

Serum osmolality is measured in an undiluted sample and the result will be within the normal range in case of pseudohyponatraemia. If the measurement of serum osmolality is not available, direct potentiometry using a blood gas analyser will yield the true sodium concentration, as this measures the sodium concentration in an undiluted sample too.

Download figure as PowerPoint slide Figure 5 Pseudohyponatraemia. In order to reduce the volume of blood needed for analysis, serum is frequently diluted before the actual measurement is obtained. When the fraction of solid-phase particles is increased, the same amount of diluent results in a greater dilution, unbeknownst to the laboratory personnel right side of figure. Consequently, the calculation of an ion level with the use of a degree of dilution that is based on the incorrect fraction of solid-phase particles will lead to an underestimate.

Clinical problem-solving. Mind the gap. Reset osmostat In reset osmostat, there is a change in the set point as well as in the slope of the osmoregulation curve The response to changes in osmolality remains intact.

Non-hypotonic hyponatraemia 5. Isotonic hyponatraemia In the majority of patients that present with hyponatraemia, the serum is hypotonic, i. Sometimes, the serum contains additional osmoles that increase effective osmolality and reduce the serum sodium concentration by attracting water from the intracellular compartment.

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Examples of such osmoles include glucose hyperglycaemia due to uncontrolled diabetes mellitus , mannitol and glycine absorption of irrigation fluids during urological or gynaecological surgery 31 , 32 , However, as described earlier, in pseudohyponatraemia, serum osmolality is normal and no shifts of water occur.

Hypertonic hyponatraemia In hyperglycaemia-induced hyponatraemia, hyponatraemia is caused by dilution due to hyperosmolality. It is important to make the distinction between measured osmolality and effective osmolality As water returns to the intracellular space during treatment of hyperglycaemia, serum sodium concentration should increase, thus resulting in a constant effective osmolality. If it does not, brain oedema may ensue due to an overly rapid drop in effective osmolality Ineffective osmoles High urea concentrations in kidney disease may also increase measured osmolality.

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However, urea is not an effective osmole because it readily passes across the cellular membrane. It does not change effective osmolality, does not attract water to the extracellular fluid compartment and does not cause hyponatraemia Hypotonic hyponatraemia with decreased extracellular fluid volume Depletion of circulating volume, with or without deficit of total body sodium, can markedly increase the secretion of vasopressin leading to water retention despite hypotonicity.

Although the vasopressin release in this case is inappropriate from an osmoregulatory point of view, it happens in order to preserve intravascular volume and can be considered appropriate from a circulatory point of view.

Non-renal sodium loss 5. Gastrointestinal sodium loss Volume depletion can occur if the body loses sodium through its gastrointestinal tract. In case of severe diarrhoea, the kidneys respond by preserving sodium and urine sodium concentrations are very low.

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In case of vomiting, metabolic alkalosis causes renal sodium loss as sodium accompanies bicarbonate in the urine despite activation of the renin—angiotensin system. By contrast, in patients with diarrhoea, chloride accompanies ammonium excreted by the kidneys in an effort to prevent metabolic acidosis. Transdermal sodium loss The body can lose substantial amounts of sodium transdermally due to heavy sweating.

This may be caused by impaired re-absorption of sodium in the sweat duct as in cystic fibrosis or by an impaired natural barrier function due to extensive skin burns.

It results in increased vulnerability to sodium depletion and volume depletion. The amount of sodium that is lost in sweat varies markedly between healthy individuals, but to date, no link has been found between the sodium concentration in sweat and cystic fibrosis-causing mutations of the cystic fibrosis transmembrane conductance regulator gene Renal sodium loss 5. Diuretics Urinary sodium loss can cause volume depletion and, if sufficiently severe, trigger vasopressin release.

Diuretics and especially thiazides are frequently implicated as a cause of hyponatraemia. The traditional explanation is that renal sodium loss leads to volume contraction with subsequent release of vasopressin.

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However, this would require a substantial loss of sodium and body weight, while patients with thiazide-induced hyponatraemia often have increased body weight It might be reasonable to assume that thiazides directly induce the release of vasopressin or increase the response of the collecting duct to circulatory vasopressin. In any case, there appears to be an individual susceptibility to these effects, as hyponatraemia only occurs in certain patients and usually reoccurs if thiazides are reintroduced Despite the potential for causing more urinary sodium loss, loop diuretics only rarely cause hyponatraemia because they reduce osmolality in the renal medulla and thus limit the kidney's ability to concentrate urine Primary adrenal insufficiency In primary adrenal insufficiency, hypoaldosteronism causes renal sodium loss, contracted extracellular fluid volume and hyponatraemia.

Although primary adrenal insufficiency usually presents in combination with other clinical symptoms and biochemical abnormalities, hyponatraemia can be its first and only sign Cerebral salt wasting Renal sodium loss has been documented in patients with intracranial disorders such as subarachnoid bleeding.

Because diagnosis may be difficult, and both inappropriate antidiuresis and secondary adrenal insufficiency are actually more common in this clinical setting, cerebral salt wasting may be over diagnosed Nevertheless, the recognition of cerebral salt wasting is important because its treatment requires volume resuscitation rather than water restriction. Kidney disease Renal salt wasting can also occur in kidney dysfunction.

The so-called salt-losing nephropathies, such as tubulopathy after chemotherapy or in analgesic nephropathy, medullary cystic kidney disease and certain pharmacological compounds can inhibit the kidney's ability to re-absorb appropriate amounts of sodium Third spacing Bowel obstruction, pancreatitis, sepsis or muscle trauma may markedly reduce effective circulating blood volume through fluid leakage from blood vessels.

This causes baroreceptor activation and vasopressin release, which may result in hyponatraemia.

Infusion of hypotonic fluids in this case may worsen hyponatraemia. Hypotonic hyponatraemia with normal extracellular fluid volume Euvolaemic hyponatraemia is caused by an absolute increase in body water, which results from an excessive fluid intake in the presence of an impaired free water excretion, either due to inappropriate release of vasopressin or due to a low intake of solutes.

Syndrome of inappropriate antidiuresis The vasopressin secretion in SIADH is inappropriate because it occurs independently from effective serum osmolality or circulating volume. It may result from increased release by the pituitary gland or from ectopic production. Inappropriate antidiuresis may also result from increased activity of vasopressin in the collecting duct or from a gain-of-function mutation in its type 2 receptor Table 6 Diagnostic criteria for the syndrome of inappropriate antidiuresis.

A syndrome of renal sodium loss and hyponatremia probably resulting from inappropriate secretion of antidiuretic hormone. You'll find concise, evidence-based answers to questions about hosp This streamlined clinical companion is the fastest and easiest way to keep abreast of the latest diagnostic advances, prevention strategies, and cost-effective treatments.

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The Current Medical Diagnosis and Treatment 2009

Visitor Posts. Hussaini Julde. Current Medical Diagnosis and Treatment Written by clinicians renowned in their respective fields, CMDT offers the most current insight into epidemiology, symptoms, signs, and treatment for more than 1, diseases and disorders.

Download PDF https: March 16 at 7: Medical Textbooks free read online March 16 at 7: Answer this. Online Access http:Pseudohyponatraemia Pseudohyponatraemia is a laboratory artefact that occurs when abnormally high concentrations of lipids or proteins in the blood interfere with the accurate measurement of sodium.

It also has useful online access. Up-to-date references provide peer-reviewed, evidence-based information. CMDT Online is updated quarterly www.

Download PDF https: Update on the evaluation of chest pain New algorithms for the treatment of heart failure and NSTEMI New sections on pulmonary hypertension; treatment of pleural mesothelioma; diagnosis and treatment of subacute, postpartum, and silent thyroiditis and amiodarone- and iodine-induced thyrotoxicosis; and treatment of cryoglobulinemic vasculitis New tables on preferred initial antiretroviral regimen and fixed dose antiretroviral combinations for HIV infection, and on medications for management of diabetes Updated tables on cancer chemotherapeutic and supportive care agents.

Regulation of body water serves to minimise osmotically induced disruptions in cell volume with adverse effects on multiple cellular functions. Baroregulation of vasopressin release Stretch-sensitive receptors in the left atrium, carotid sinus and aortic arch sense circulating volume.