Добавил:

Sekretar kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.

Вуз:

Ростовский Государственный Медицинский Университет

Предмет:

Медицина общая

Файл:

Книга_2617_Библиотеки_им_академика_М_И_Перельмана

.pdf

Скачиваний:

Добавлен:

30.08.2026

Размер:

59 Мб

Скачать

☆

<<< < Предыдущая 16 17 18 19 20 21 22 23 24 25 26 2728 / 5028 29 30 31 32 33 34 35 36 37 38 39 40 > Следующая >>>

Hydroelectrolytic Disorders

membrane

all

• Capillary walls (interstitium/plasma)

https://t.me/medicina_free

MarcelloCiaccio, AnnaMariaCiaccio, andLuisaAgnello

Introduction

Maintaining body uid and electrolyte balance is of paramount importance for normal functioning. Any alteration in this balance falls under the denition of “hydroelectrolytic disorders.”

This chapter describesthe pathophysiology of the regulation of the hydroelectrolytic balance and the main causes water balance, sodium balance, and potassium balancealterations.

Pathophysiology

The human organism consists of 50–60% water; this percentage is slightly higher in children than in adults and men than in women. Water is distributed in two compartments, intracellular and extracellular, which differ in solute composition. The intracellular compartment contains about twothirds of the total pool of water (intracellular uid, ICF). In contrast, the extracellular compartment contains the remain-

ing one-third of water (extracellular uid, ECF) and can be further distinguished into extravascular or interstitial (connective, bone, serous cavities, and secretions) and intravascular (plasma) (Fig. 20.1). The intra- and extracellular compartments, although separated by cell membranes and capillary walls, are in dynamic equilibrium. The concentration of solutes in a liquid is termed “osmolality” and is expressed in milliosmoles per kilogram of water (mOsm/kg). Sodium (Na+) and the anions Cl− and HCO

−

represent the

primary solutes of ECF, whereas potassium (K+) and organic phosphorus esters (adenosine triphosphate (ATP), creatine phosphate, and phospholipids) represent the primarysolutes of ICF.The solutes in each compartment determine the effective osmolality of the compartment. The cell membrane and capillary wall are highly permeable barriers to water, which pass from one compartment to another to maintain osmotic balance. In particular, the watermovement through the capillary wall depends on Starling’s forces (hydrostatic pressure and colloid osmotic pressure), whereas that through the cell membranes depends on the difference in osmolality between ICF and ECF.

M. Ciaccio (*) Department of Biomedicine, Neurosciences and Advanced Diagnostics, Institute of Clinical Biochemistry, Clinical Molecular Medicine and Clinical Laboratory Medicine, University Hospital “P.Giaccone”, Palermo, Italy

Department of Laboratory Medicine, University Hospital “P.Giaccone”, Palermo, Italy e-mail: marcello.ciaccio@unipa.it

A. M. Ciaccio Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties (ProMISE) “G.D’Alessandro”, University Hospital “P.Giaccone”, Palermo, Italy

L. Agnello Department of Biomedicine, Neurosciences and Advanced Diagnostics, Institute of Clinical Biochemistry, Clinical Molecular Medicine and Clinical Laboratory Medicine, University Hospital “P.Giaccone”, Palermo, Italy

50% water

1/3 intracellular

Cellular

2 interchange sites between components:

• Cellular membranes (ECF/ICF)

Fig. 20.1 Distribution of water in the body. (Copyright EDISES 2021. Reproduced with permission)

2/3 extracellular

PlasmaCell

Interstitial

space

60% water

Capillar

269

270

ater

https://t.me/medicina_free

M. Ciaccio et al.

The composition of extracellular liquids can vary within narrow limits; water and the solutes dissolved play an essential role in cellular metabolic reactions, so excessive variations inextracellular liquids compositionmaylead to severe cell function alterations. It is, therefore, essential that the body’s hydroelectrolytic content is kept constant according to the law of conservation of matter: everything that enters the body must leave it, if the body does not need it.

Daily, our organism acquires from the outside about 2 liters of water and food that contain NaCl, K+, H+, Ca

−

HCO

, and phosphate ions. The body has several ways to

excrete water and ions, mainly the kidneys; a small amount is also lost through stool, sweating, and respiration. In addition to physiological mechanisms, behavioral mechanisms, such as thirst and appetite for salt, also play an important role.

The maintenance of hydroelectrolytic balance is critical for the homeostasis. Water and Na+ are critical for the volume and osmolality of ECF.Consequently, their alterations can result in cell volumechanges, either shriveling or swelling, thus compromising cell function. Potassium (K+) is, on the other hand, important for the membrane potential of excitable cells, and, its alterations can, therefore, compromise cardiac, muscular, and nervous functions.

K+, which is more concentrated within the cell, tends to leave by passive diffusion. In contrast, Na+ tends, by passive diffusion, to enterthe cell; the Na+/K+ATP-dependent pump actively extracts Na+ from the cell and reintroduces K+, thus allowing the maintenance of the different concentration of these solutes between the two compartments. The regulation of hydroelectrolytic balance is highly complex. It involves not only renal and behavioral responses but also the cardiovascular and respiratory systems, which are under the control of the nervous system.

Water Balance

The introduced amount of water must be equal to the excretedamount of water excretedto maintain homeostasis. Alterations in water balance cause hypo- or hypernatremia. On average, an adult introducesabout 2 liters of water daily through food and produces about 0.5 liters through cellular respiration (glucose + O2 ↔ CO2 + H2O), resulting in a total waterdaily intake of about 2.5L.Under physiological conditions, there is an obligatory loss of water of about

1.5Lthrough the urinary tract; a small quantity, about 0.1L, is lost through excretion, and, nally, a quota, corresponding to about 0.9 L, is eliminated by perspiratio insensibilis, which consists of skin and respiratory tract evaporation (Fig.20.2). In this way, the balance between the volume of incoming and outcoming water is maintained. Basically, body water volumeis controlled by its intake, through the stimulus of thirst, and by its excretion at the renal level.

Water outputWater entries

Skin and lungs:

Food and drink:

2 L/day

Metabolism:

0.5 L/day

Exogenous

water

(2 L/day)

Fig. 20.2 Water balance. (Copyright EDISES 2021. Reproduced with permission)

Endogenous

+– = 0

water

(0.5 L/day)

insensitive loss of w (0.9 L/day)

Kidneys: 1.5 L/day

Stool: 0.1 L/day

Outputs

(0.9 + 1.5

+ 0.1 L/day)

If total body Na+ is kept constant, a change in total body water alters osmolality. In other words, if there is an osmolalityincrease, the body’s response is to improvewater intake through the thirst sensation and the diuresis contraction. Viceversa, if there is an osmolalityreduction, the organism determines a reduction in the thirst sense and a diuresisincrease. The osmolalityalteration is detected by osmoreceptors in the hypothalamus. In case of increased plasma osmolality, even by 12%, the osmoreceptors stimulate vasopressin synthesis, also known as the antidiuretic hormone (ADH), in supraoptic and paraventricular nuclei of the hypothalamus. Then, it is secreted by the posterior pituitary gland. The ADH exerts its action at the collector duct, making it permeable to water. Following the interaction of ADH and its receptor on the cellularmembrane of the collector duct, the activation of a sequence of events leads to the insertion in the apical cellular membrane of channel proteins, known as aquaporins, allowingthe waterpassage. The effect is the passive reabsorption of water according to an osmotic gradient, from the lumen of the collecting tubule to the hypertonic medullary interstitium, and the production of concentrated urine. The ADH also acts on the ascending tract of Henle’s loop, increasing sodium transport into the medullary interstitium. The resulting increase in interstitial osmolality contribute to the osmotic gradient for water reabsorption. In the absence of the ADH, the collector duct is impermeable to water. The most powerful stimulus for ADH release is the increase ofplasma osmolality; however, other non-osmotic factors regulate ADH secretion, including blood pressurechanges and volemia, nausea, pain, stress, hypoglycemia, pregnancy, and various medications. Reductions in blood volume and blood pressure are detected, respectively, by voloreceptors, stretch receptors located in the cardiac

>280 mOsm/kg

Reduction of atrial

reabsorption

osmoreceptors

Liver

Angiotensinogen

Na reabsor

20 Hydroelectrolytic Disorders

https://t.me/medicina_free

271

Osmolality

Hypothalamic

Insertion of aquaporins into the membranes

Fig. 20.3 Factors inuencing ADH release. (Copyright EDISES 2021. Reproduced with permission)

stretch due to

reduction of

blood volume

Atrial

voloreceptors

Hypothalamic

neurons that

synthesize

ADH

ADH release from

posterior pituitary

of the collecting duct cells

Increased renal water

Blood pressure

reduction

Carotid and aortic

baroreceptors

atria, and baroreceptors in the carotid sinus, which stimulate hypothalamic ADH synthesis and release (Fig.20.3). While the osmoreceptors detect even small changes in plasma osmolality (1%), the voloreceptors and baroreceptors are less sensitive, detecting a reduction of no less than 10%.

Sodium Balance

Sodium represents the primary electrolyte in extracellular uids. Approximately 90% of Na+ is in the extracellular compartment. Thus, the ECFvolume reects the body’s Na+ content. Na+ is critical for controllingosmolality and maintening ECF volume and blood pressure.

Under physiological conditions, natremia (or sodiemia) has a value between 135 and 145mmol/L.Our organism has regulatory mechanisms to maintain the balance betweenelimination and supply of Na+. Indeed, as already mentioned above, everything that is introduced in excess into the body must be excreted. Since the Na+daily introduction by diet (200mmol/L) exceeds our needs (20mmol/L), renal excretion is necessary to keep sodium homeostasis. Pathological conditions, such as excessive sweating, bleeding, diarrhea, and vomiting are associated with Na+ excretion through thekidneys.

Alterations in Na+ intake and elimination balance can result in either an excess, which determines an increase in ECF volume, manifesting clinically with edema and hypertension, or a decit, which results in ECF volumereduction, manifesting clinically with hypovolemia and hypotension. It

Adrenal gland

Kidney

and H2O

ption

Fig. 20.4 Renin–angiotensin–aldosterone system. (Copyright EDISES

2021. Reproduced with permission)

Renin

Angiotensin I

ACE

Angiotensin II

Aldosterone

is important to distinguish alterations between osmoregulation and volume regulation because osmolality and volemia are both independently regulated. Indeed, alterations in volume are perceived by detectors that stimulate compensatory mechanisms acting on the Na+ balanceregulation, whereas alterations in plasma osmolality are perceived by detectors that stimulate compensatory mechanisms acting on the water balanceregulation.

Renal Na+ excretion is fundamentally regulated by aldosterone, the primary mineralocorticoid hormone synthesized in the glomerular zone of the adrenal cortex, which controls Na+ reabsorption in the distal tubule and collector duct. Increased aldosterone levels result in increased renal Na+ reabsorption. Increased aldosterone-induced Na+ reabsorption does not affect ECFNa+ concentration because water reabsorption is simultaneously stimulated. The main stimulus for aldosterone secretion is angiotensin II, a protein of the renin–angiotensin–aldosterone system (RAAS) that is essential for the blood pressuremaintenance. The RAAS system is activated in response to stimuli related, either directly or indirectly, to a reduction in blood pressure. In particular, it is activated when the juxtaglomerular cells of the afferent arterioles of the nephron secrete renin. This enzyme converts angiotensinogen, an inactive plasma protein, into angiotensin I, which is converted by the angiotensin-converting enzyme (ACE) into angiotensin II.The latter stimulatesthe adrenal gland to synthesize and releasea ldosterone by(Fig.

20.4). Na+ reabsorption results in an arterial pressure

increasethrough indirect mechanisms, which include stimulation of water intake and expansion of blood volume.

272

https://t.me/medicina_free

M. Ciaccio et al.

Angiotensin II also plays acriticalrole in renal Na+ excretion regulation, independently of aldosterone secretion. It acts, indeed, directly at the level of proximal tubule cells, stimulating the Na+reabsorption of Na+.

As previousdescribed, renal Na+ reabsorption is also mediated by ADH at the Henle’s loop. Finally, renal Na+ reabsorption is regulated by atrial natriuretic peptide (ANP), a peptide hormone produced by specialized atrial myocardial cells. Following a volemia increase, atrial cells release ANP, which results in increased Na+ renal excretion+ through inhibition of renal renin secretion, a ldosterone production, and Na+ reabsorption at the collector duct.

Hyponatremia

Hyponatremia, dened as plasma Na+ concentration <135 mmol/L, represents the most common alteration of body uids and electrolyte balance. From a clinical point of view, hyponatremia is characterized by a broad spectrum of signs and symptoms, from subtle to severe, and is associated with increased mortality and morbidity.

Hyponatremia is characterized by water excess over sodium content in ECF, which may result from water accumulation or Na+depletion.

Hyponatremia can be classied according to several criteria, such as Na+ concentration (mild, moderate, severe),the timing of onset (acute or chronic), theseverity of symptoms (moderate or severe), and serum osmolality (hypotonic, isotonic, and hypertonic) (Table20.1).

Tonicity (or effective osmolality) is dened as the total osmolality capable of inducing the movement of water between compartments, and it is determined by all those solutes that cannot pass freely through cell membranes.

Table 20.1 Hyponatremia classication

Classication criterion Description

serum

concentration

Serum osmolality <280mOsm/kg

Establishment times For less than

Symptoms Moderate

130–135mmol/L 125–129mmol/L <125mmol/L

280–295mOsm/kg >295mOsm/kg

48hours For at least 48hours

Severe

Denition of hyponatremia

Mild Moderate Severe Hypotonic Isotonic Hypertonic Acute Chronic

Moderate Severe

Hypotonic hyponatremia (or true hyponatremia), characterized by reduced plasma osmolality, is generally due to either a primitivewater increase (and a secondary loss of Na+) or a primitive Na+ loss (and a secondary increase in water) and can be further classied into (Table20.2):

• Hypovolemic: This is characterized by ECF depletion due

to a primitive Na+loss (and a relative increase of water)

that can be of renal or extrarenal origin. The contraction

of ECF volume stimulates thirst and ADH secretion.

Increased water intake and reduced renal excretion result

in hyponatremia.

• Euvolemic: This is characterized by a modest ECFexcess

due to a primitive waterincrease and relative Na+ de-

ciency. The syndrome of inappropriate ADH secretion

(SIADH) represents the most common cause of euvolemic

hyponatremia.

• Hypervolemic: This is characterized by an ECF excess

due to a primitive Na+increase in Na+ less than the sec-

ondarywater increase. It is usually associated with edema.

This form is due to pathologies, such as livercirrhosis,

which are associated with a reduction in effective circu-

lating arterial volume resulting in increased ADH levels

and a sense of thirst. Chronic and acute renal failure with

oliguria may be associated with hyponatremia if water

intake exceeds its elimination capacity.

Isotonic hyponatremia (or pseudohyponatremia), characterized by normal plasma osmolality, results from the accumulation of large amounts of isotonic substances lacking Na+ that can freely cross membranes, such as urea, non- hypertonic mannitol, and ethanol, causing pseudohyponatremia (laboratory artifact).

Hypertonic hyponatremia, characterized by increased plasma osmolality, is the result of watertransfer from cells to the extracellular compartment due to an excess of osmotic substances. It is usually due to hyperglycemia. In a patient with diabetes mellitus with poor metabolic control, glucose becomes an effective osmolyte capable of drawing water into the extracellular environment, resulting in hyponatremia; foreach excess of100mg/dL in plasma glucose concentration, there is a 1.4mmol/Lreduction in plasma Na+ concentration. In addition, intravenous administration of mannitol isanother cause of hypertonic hyponatremia.

The clinical manifestations of hyponatremia are related to the water osmotic displacement, which results in an increased ICF volume. Neurons are the mostsusceptible to this alteration due to the inability of the cranial box to expand. Consequently, the symptoms of hyponatremia are predominantly neurological (hyponatremic encephalopathy) and their severity depends on the absolute Na+reduc-

20 Hydroelectrolytic Disorders

https://t.me/medicina_free

273

Table 20.2

Hypovolemia Euvolemia Hypervolemia

Kidney losses

Diuretics Osmotic diuresis (glucose, mannitol) Hypoaldosteronism Sodium-dispersing nephropathy Post-obstructive diuresis Acute non-oliguric tubular necrosis

SIADH syndrome of inappropriate, ADH secretion

Table 20.3

Severity Symptom Mild Asymptomatic Moderate Headache

Serious Vomiting

Causes of hypotonic hyponatremia classied by volume

Extrarenal losses

Sweating Burns Vomiting Diarrhea Drainage Fistulas Small bowel occlusion Pancreatitis Peritonitis

Symptoms of hyponatremia

Nausea General malaise Mood alteration Difculty concentrating Mental confusion

Respiratory distress Lethargy Convulsions Coma (Glasgow Coma Scale ≤8)

SIADH Excessive water intake, e.g., primitive polydipsia Reduced food intake and urinary excretion of solutes (e.g., potomania or low protein diet) ADH secretion due to pain, nausea, drugs Glucocorticoid deciency Hypothyroidism Chronic renal failure

Heart failure Liver cirrhosis Nephrotic syndrome Chronic and acute renal failure

hyponatremia is rst based on history and objective examination that includes the assessment of the ECF status and circulating volume. Gathering the patient’s medical history may direct toward the cause of hyponatremia.

Clinical laboratory provides valuable information for the differential diagnosis of hyponatremia. In particular, the key tests include plasma and urinaryosmolality, and urinary Na+ concentration (Fig.20.5). In addition, blood glucose and hormonal patterns (including the hypothalamic–pituitary–thyroid and hypothalamic–pituitary– adrenal axes) provides essential support for differential

tion in Na+ and the developmentrapidity. Mild forms are generally asymptomatic. Nausea and general malaise are the rst symptoms of moderate forms. The symptoms of hyponatremia, especially when it is mild or moderate, are nonspecic and often lead to a failure to diagnose it, with consequent therapeutic delay (Table 20.3). Seizures occuratextremely low natremiavalues, witha high risk of permanent brain damage. The guidelines suggest a threshold of 48hours to distinguish acute from chronic hyponatremia because cerebral edema occurs more frequently when hyponatremia develops in less than 48hours. Indeed, the brain needs about 48hours to adapt to a hypotonic environment and, before adaptation, there is a high risk of edema. Adaptation involves the activation of compensatory mechanisms leading to the loss of Na+ and K+, followed by the loss of organic osmolytes, aimed at protecting cell volume through the displacement of water from ICF to ECF.However, once adaptation is complete, if Na+ concentration increases too rapidly, neurons may undergo further

diagnosis.

Recently, an algorithm for the differential diagnosis of the causes of hyponatremia has been proposed and it is based on the determination of copeptin (Fig.20.6).

SIADH is characterized by hypotonic hyponatremia with inappropriately concentrated urine (urinary osmolality >100mOsm/kg). Patients usuallyare euvolemic and have a normal Na+ balance.

The aim of hyponatremia therapy is, to correct the plasma Na+ concentration and resolve the primary disease underlying altered Na+ concentration. In an asymptomatic patient with mild hyponatremia, therapy consists of treating the underlying pathologies, removing the causal factors, such as the use of diuretics, the use of drugs that can cause SIADH, as well as stress, pain, and anxiety, which can stimulate the secretion of ADH.In a symptomatic patient, therapy is based on the correction of hyponatremia through the administration of 0.9% isotonic saline solution or 3% or 5% hypertonic saline solution by slow drip.

damage. One of the most serious complications associated with correcting hyponatremia is the demyelinating osmotic syndrome, characterized by the breakdown of the myelin

Hypernatremia

sheath that insulates neurons.

Hypernatremia is dened as a plasma Na+ concentration

Diagnosis andTherapy

Hyponatremia represents the manifestation of numerous diseases. Therefore, the diagnostic approach to a patient with

>145 mmol/L. Since Na+ is the main osmolyte of ECF, hypernatremia results in a state of hyperosmolality. Hypernatremia may be due to a primitive increase in Na+ but,

274

Hyponatriemia

Kidne

failure

Extra-renal leakage

https://t.me/medicina_free

M. Ciaccio et al.

([Na+] Serum <135 mmol/L)

Plasma osmolality

<280 mOsm/kg >295 mOsm/kg280–295 mOsm/kg

Isotonic hyponatremia Hypotonic hyponatremia Hyper tonic hyponatremia

Pseudohyponatremia • Hyperglycaemia

Increased

[Na+] urine [Na+] urineUrine osmolality

>20 mmol/L

y injury

Edematous disorders:

Heart failure

Cirrhosis

Nephrotic syndrome

and decreased fT4

>100 mOsm/kg >20 mmol/L

Thyroid

hormones

measurement

Increased TSH

Hypothyroidism

• Administration of hypertonic fluids

ECF Volume

ReducedNormal

Primary polydipsia Renal leakage

normal TSH

and fT4

Stimulation test

with ACTH

Normal Altered

IADHS Adrenal

Fig. 20.5 Diagnostic algorithm of hyponatremia. (Copyright EDISES 2021. Reproduced with permission)

in most cases, is the result of water loss. Water loss may consist of:

• Loss of body water (with an associated increase in Na+)

• Loss of hypotonic uid, which can be of renal or extrarenal origin (the loss of body water is accompanied by a loss of Na+, which is in lesser proportion and, therefore, there is a relative increase).

Table 20.4 shows the causes of hypernatremia. Hyperosmolality due to hypernatremia results in the

watermovement to the extracellular environment, thus leading tothe contraction of ICF volume. The cells of the central nervous system are the mostaffected. Therefore, the main symptoms of hypernatremia are neurological and include asthenia, neuromuscular irritability, confusion, coma, and

convulsions. Patients may also present with polyuria, intense thirst, nausea, and vomiting. The severity of clinical manifestations depends on the rate and magnitude of increase in plasma Na+ concentration. In chronic hypernatremia, brain cells activate an adaptive response consisting of initial electrolyte acquisition (early compensation) followed by production and accumulation of intracellular osmolytes, such as inositol. The patients at risk of developing hypernatremia are young children, elderly subjects, and neurological patients who have already been hospitalized.

Diagnosis andTherapy

A complete medical history, including a list of medications prior to and concurrent with the visit, and aphysical examination, with the assessment of mental and neurological status, are the rst investigations allowing the detection

iate ADH secretion syndrome

u-Na+, urinary sodium; u-Osm, urinary osmolality.

20 Hydroelectrolytic Disorders

https://t.me/medicina_free

Hypotonic urine

275

Hyponatremia

(Na+ <135 mmol/L)

Rule out pseudohyponatremia*

and non-hypotonic hyponatremia**

u-Osm <300 mOsm/L

and copeptin <3 pmol/L

Reduced effective

arterial volume

u-Na*<30 mmol/L u-Na*>30 mmol/L

Non-Euvolemic

Patient

Sodium depletion

(diarrhea, vomiting,

renal sodium loss)

Measure u-Osm and copeptin

u-Osm >300 mOsm/L

and/or copeptin >3 pmol/L

Measure u-Na

Assess copeptin/u-Na

Sodium expansion

(heart failure, cirrhosis,

nephrotic syndrome)

ratio ×100

Non-hypotonic urine

Preserved effective

arterial volume

Rule out kidney disease

and use of diuretics

<30>30

Secondary

Hypocorticosurrenalism

or IADHS

Euvolemic

patient

*Assess triglycerides, total cholesterol, total protein; **assess urea, blood glucose. Effective p-Osm = 2 × (s-Na+ + s-K+) + glycemia/18. K+,serum potassium; Na+, serum sodium; PP, primary polydipsia; IADHS, inappropr

Fig. 20.6 Algorithm for the differential diagnosis of hyponatremia based on copeptin. (Copyright EDISES 2021. Reproduced with permission)

Table 20.4 Causes of hypernatremia

Water loss alone –Perspiratio insensibilis (evaporation from the skin or respiratory tract)

–Hypodipsia/adipsia (reduction/absence of thirst by insufcient water intake) –

 Neurogenic diabetes insipidus (excessive excretion of water by the kidneys due to impaired ADH production)

–Nephrogenic diabetes insipidus (reduced sensitivity to ADH in the kidneys)

Hypotonic uid loss Kidney causes:

–Osmotic diuresis (glucose, mannitol) Urinary obstruction Extrarenal causes: Vomiting Diarrhea Fever Profuse sweating Burns Nasogastric drainage

(continued)

276

] >20 mmol/L

<20 mmol/L

leakage

insensibilis

hypodipsia

Hypernatremia

https://t.me/medicina_free

Table 20.4 (continued)

Primitive Na+ increase

M. Ciaccio et al.

Increased production: Infusion of hypertonic NaCl solution Introduction of sodium bicarbonate Emetics rich in sodium chloride Hypertonic saline enemas Enteral and parenteral nutrition Corticosteroid therapy Intake of improperly diluted infant formula Renal retention: Primitive hyperaldosteronism Cushing’s syndrome

Fig. 20.7 Diagnostic algorithm of hypernatremia. (Copyright EDISES 2021. Reproduced with permission)

Hypovolemia HypervolemiaEuvolemia

Urinary [Na+]

Extra-renal

Renal leakage Perspiratio

of hypernatremia cause. The clinical laboratory provide important support in this context. In particular, assessment of ECF volume, urinary osmolality, and urinary Na+ concentration are essential to assess hyperosmolality (Fig.20.7).

Therapy aimsto treat the underlying disease and correct the

water decit. Patients withhypernatremia inless than 24hours, natremia should be corrected rapidly, i.e.,about 1–2mmol/L per hour. Patients with hypernatremia for a more extended period, as early as a few days, the correction should be slower, i.e.,0.5mmol/L per hour, because the cerebraladaptation has been activated and, therefore, a rapid correction could lead to cerebral edema, coma, convulsions, and death.

Potassium Balance

Potassium is the primary ICFelectrolyte; only about 2% is found in ECF. The intracellular concentration is 140– 150 mmol/L, whereas the extracellular concentration is

3.5–5mmol/L. The difference in K+ concentration between

ICF and ECF is the primary determinant of the resting membrane potential, which, in turn, is critical for nerve impulse conduction and muscle cell contraction, including cardiac cells. K+ can passively diffuse from the inside to the outside of the cell.The Na+/K+ATP-dependent pump actively transports it from the outside to the inside.

The dietary intake of K+ is approximately 1–2mmol/day

per kg of body weight, of which 90% is absorbed in the gas-

([Na+] serum >145 mmol/L)

ECF volume

Urinary osmolality

<700 mOsm/kg

Diabetes insipidus or

Urinary [Na

Primitive Na

increase

trointestinal tract. An equal amount must be excreted to maintain K+ balance. K+ excretion is regulated by renal and extrarenal mechanisms. Extrarenal mechanisms regulatepotassium distribution (intra- and extracellular) by acting directly or indirectly on the Na+/K+ATP-dependent pump. The activity of this pump is inuenced by various factors, such as insulin, catecholamines, aldosterone, acid–base balance, osmolality, and adrenergic drugs. In particular, beta-agonists promote the entry of K+ into the cell, whereas beta-blockers and alpha-agonists promote the movement of K+ into the extracellular environment. Insulin promotes the entry of K+ inside the cells (especially at the hepatic and muscular level); insulin deciency induces a shift of potassium from the intracellular to the extracellular compartment. Potassium balance is closely related to the acid–base balance. In particular, potassium and pH vary in opposite directions: a decrease in pH of 0.1units results in an increase in potassium of 0.5mmol/L and vice versa. In metabolic acidosis, there is the movement of K+ toward the outside of the cell in exchange with protons, whose blood concentrations are reduced; vice versa, in metabolic alkalosis, there is the passage of K+ inside the cell in exchange with protons, whose blood concentrations increase.

However, the main route of eliminating potassiumexcess is renal excretion at the distal nephron. The most important regulator of renal potassium excretion is aldosterone, which stimulates tubular potassium secretion by increasing the number of Na+/K+ATP-dependent pumps and sodium chan-

20 Hydroelectrolytic Disorders

https://t.me/medicina_free

277

nels. Filtered potassium is almost completely reabsorbed in the proximal tubule and secreted into the distal convoluted tubule and the collector tubule. Net excretion is, therefore, the result of reabsorption and concomitant secretion.

Hyperpotassemia determines an increase in potassium excretion through basically two mechanisms: aldosterone secretion and tubular potassium secretion through the increase of the same in the tubular cell. Indeed, the Na+/ K+ATP-dependent pump increases the K+intracellular concentration, which will be released into the tubular lumen. During hypokalemia, however, the renal excretion of potassium is decreased or absent.

Due to the important action of potassium on excitable tissues, it is essential to keep potassium values within the normal range; an alteration can lead to impaired functionality of the nervous and muscular tissues. In particular, low blood levels of potassium (hypokalemia) are associated with muscular weakness due to the greater difculty of hyperpolarized neurons and muscles to trigger action potentials; hyperkalemia, on the other hand, is a more dangerous condition because the tissuesdepolarization initially makes them more excitable but subsequently, the cells are unable to repolarize entirely and, therefore, become less excitable. In this condition, they present action potentials smaller than normal or absent. Hyperkalemia can cause severecardiac arrhythmias.

Hypokalemia

Hypokalemia is dened as a plasma potassium concentration <3.5mmol/L. It is mild when serum potassium values are between 3 and 3.4mmol/L; it is severe when serum potassium values are less than 3mmol/L.

The causes of hypokalemia can be distinguished into three classes:

• Reduced dietary intake

• Passage of potassium into the intracellular compartment

• Increased renal or extrarenal leakage

Table 20.5 summarizes the main causes of hypokalemia.

Reduced dietary potassium intake is a rare cause because it can be compensated by reduced renal potassium excretion. Commonly, dietary potassium intake exceeds the amount excreted in the urine. Several causes of hypokalemia due to renal potassium lossleadto excess aldosterone (primary and secondary hyperaldosteronism) or, in general, excess mineralocorticoid and glucocorticoid hormones.

From a clinical point of view, the symptoms of hypokalemia rarely appear unless the potassium concentration is less than 3mmol/L.Symptoms are related to alterations in muscular system (muscular asthenia, myalgia, muscle cramps), the cardiovascular system (palpitations, tachycar-

Table 20.5 Causes of hypokalemia

Food intake reduction

Potassium passage into the intracellular compartment

Increased lost Renal Potassium-sparing diuretic therapy

Malnutrition due to: – Neoplasms – Nervous anorexia – Acquired immunodeciency syndrome (AIDS) – Abuse of ethanol – Poverty Parenteral nutrition not integrated with potassium supplements Alterations of acid–base balance: – Metabolic or respiratory alkalosis Hormonal causes: – Insulin – Beta-2 adrenergic agonists (endogenous or

exogenous) – Alpha-adrenergic antagonists Anabolic conditions: – Increased hematopoiesis following vitamin

B12, folate, and erythropoietin administration Other causes: – Accidental or induced hypothermia – Barium intoxication – Periodic hypokalemic paralysis

Excess of steroids: – Primary aldosteronism – Secondary aldosteronism – Cushing’s syndrome – Adrenogenital syndromes – Steroid therapy – Apparent excess of

mineralocorticoids due toabuse of licorice and chewing tobacco, containing

glycyrrhizic acid Metabolic alkalosis Osmotic diuresis Abuse of ethanol, due to its diuretic effect Drugs (amphotericin B, cyclosporine, nonsteroidal anti-inammatory drugs (NSAIDs)) Hypomagnesemia Renal tubular acidosis

Extrarenal Vomiting

Nasogastric drainage Malabsorption Diarrhea Profuse sweating Extensive burns

dia, electrocardiographic changes), nervous system (mental confusion, depression), urinary system (polyuria, renal morphological damage), gastrointestinal system (dysphagia, constipation, nausea, vomiting), and metabolism (reduced protidosynthesis, reduced glucose tolerance, metabolic alkalosis).

Diagnosis andTherapy

Hypokalemia is often asymptomatic. Evaluation begins by looking for signs and symptoms that require urgent treatment, such as asthenia or palpitations, electrocardiogram

278

Hypokalemia

Metabolic acidosis

amphotericin B)

https://t.me/medicina_free

M. Ciaccio et al.

Fig. 20.8 Diagnostic algorithm of hypokalemia. (Copyright EDISES 2021. Reproduced with permission)

Measure magnesium and supplement if it is low

Urinary excretion of potassium

<15 mmol/day

Extra-renal

leakage

([K+] serum <3.5 mmol/L)

Evaluation of severe signs

Assessment of reduced dietary intake

Renal

leakage

and symptoms

Pseudohypokalemia

assessment

or transcellular shift

YES

Tr eat

according

to etiology

Urgent therapy

No further

investigation

(e.g. renal

tubular acidosis,

(ECG) changes, severe hypokalemia, rapid onset of hypokalemia, underlying heart disease, or cirrhosis. Identication and treatment of concurrent hypomagnesemia is critical because magnesium depletion often prevents potassium correction and may exacerbate hypokalemia-induced heart rhythm alterations.

In most cases, an accurate history allows to identify the K+ depletionetiology. Diuretic or laxative abuse as well as induced vomiting, although difcult to ascertain, should be excluded. In patients with marked leukocytosis (e.g., in acute myeloid leukemia) and normokalemia, plasma potassium concentration may be reduced due to a laboratory artifact related to the ability of leukocytes to capture K+ at room temperature. This pseudohypokalemia can be avoided by separating plasma (or serum) from cells immediately after collection.

High blood pressure

and

hypervolemia

Evaluate acid-base

balance

Variable

(e.g. hypomagnesemia)

YES

vomiting, use of diuretics)

Assess conditions

associated

with mineralocorticoid

excess (hyperaldosteronism

I and II, Cushing's syndrome, etc.)

Metabolic

alkalosis (e.g.,

A history of paralysis, hyperthyroidism, or the use of insulin or beta-agonists suggests a possible transcellular shift leading to redistribution-related hypokalemia (passage of K+ within cells).

After ruling out reduced dietary intake or transcellular displacement of K+, the evaluation of renal response can helpdetectthe hypokalemiacause. Hypokalemia with minimal urinary potassium excretion <15mmol/day suggests that potassium loss is due to extrarenal causes (through the skin or gastrointestinal tract). Assessment of acid–base balance by hemogasanalysis may provide helpful information about the potassium losssite. However, an increased urinary potassium excretion (>15mmol/day) suggests the renalpotassium loss. ECF volume status, blood pressure, and acid–base balance alterations may identify the cause of excessive renal potassium loss (Fig.20.8).

<<< < Предыдущая 16 17 18 19 20 21 22 23 24 25 26 2728 / 5028 29 30 31 32 33 34 35 36 37 38 39 40 > Следующая >>>

Соседние файлы в папке Библиотека им академика М.И. Перельмана

#
30.08.202661 Мб0Книга_2609_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202660 Мб0Книга_2610_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202660 Мб0Книга_2611_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202660 Мб0Книга_2612_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202659 Мб0Книга_2616_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202659 Мб0Книга_2617_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202659 Мб0Книга_2618_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202658 Мб0Книга_2619_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202658 Мб0Книга_2620_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202657 Мб0Книга_2621_Библиотеки_им_академика_М_И_Перельмана.pdf
#
30.08.202657 Мб0Книга_2622_Библиотеки_им_академика_М_И_Перельмана.pdf