ACID-BASE-ELECTROLYTES DISORDERS | Study notes Physiology

Nelson Textbook of Pediatrics (21st ed) (Chap68)

HYPERNATREMIA

Hypernatremia is a [Na+ ] >145 mEq/L, although it is

sometimes defined as >150 mEq/L

iatrogenic caused by inadequate water

administration or, less often, by excessive Na+

administration

effects of hypernatremia on the brain by rapid

correction

sodium intoxication by sodium bicarbonate,

hyperaldosteronism

causes of hypernatremia from a water deficit are

nephrogenic and central diabetes insipidus

Adipsia, the absence of thirst, is usually secondary

to damage to the hypothalamus

Essential hypernatremia is rare in children and is

thought to occur with injury to the hypothalamic-

posterior pituitary axis

Patients are irritable, restless, weak, and lethargic.

Some infants have a high-pitched cry and

hyperpnea

Hypernatremia is associated with fever,

hyperglycemia and mild hypocalcemia

As the extracellular osmolality increases, water

moves out of brain cells, leading to a decrease in

brain volume = tearing intracerebral veins

(hemorrhage)

Salt poisoning is associated with an elevated

fractional excretion of Na+ , whereas

hypernatremic dehydration causes a low fractional

excretion of Na+

As hypernatremia develops, the brain generates

idiogenic osmoles to increase the intracellular

osmolality and prevent the loss of brain water THUS

IF the serum [Na+ ] is lowered rapidly , there is

movement of water from the serum into the brain

cells leading to brain swelling manifested as seizures

or coma

child with central diabetes insipidus should receive

desmopressin acetate because this treatment

reduces renal excretion of water

desmopressin acetate in children are for the

management of central diabetes insipidus and

nocturnal enuresis

HYPONATREMIA

a serum sodium level <135meq/l

Pseudohyponatremia measured osmolality is

normal like in hyperlipidemia, hyperproteinemia

Hyperosmolality like hyperglycemia causes a low

[Na+ ] because water moves down its osmotic

gradient from the ICS into the ECS diluting the Na+

(eg. SIADH)

hypovolemic hyponatremia the child has lost Na+

from the body; Na loss is higher than water loss

Diarrhea as a result of gastroenteritis is the most

common cause of hypovolemic hyponatremia in

children

if the patient receives hypotonic fluid this leads to

ADH production and water retention

thiazide diuretics can concentrate the urine and is

at higher risk for severe hyponatremia

Central Pontine Myelinolysis is classically

associated with overly rapid correction of

hyponatremia, both central pontine and

extrapontine myelinolysis can occur in children with

hypernatremia

causes of hypovolemic hyponatremia is usually a

high serum [K+ ] is associated with disorders in

which the Na+ wasting is caused by absence of or

ineffectiveness of aldosterone (hypoaldosteronism,

diuretics, vomiting)

Renal salt wasting occurs in hereditary kidney

diseases, such as juvenile nephronophthisis and

autosomal recessive polycystic kidney disease

type II renal tubular acidosis (RTA), usually

associated with Fanconi syndrome there is

increased excretion of Na+ and bicarbonate in the

urine

hypervolemic hyponatremia there is an excess of

TBW and Na+ , although the increase in water is

greater than the increase in Na

decrease in the effective blood volume, resulting

from third space fluid loss, vasodilation, or poor

cardiac output

water intake exceeds sodium intake

Children with hypervolemia are edematous on

physical examination. They may have ascites,

pulmonary edema, pleural effusion, or hypertension

euvolemic hyponatremia with no evidence of

volume overload or volume depletion

SIADH is unable to excrete water that results in

dilution of the serum Na+ and hyponatremia

Partial preview of the text

Download ACID-BASE-ELECTROLYTES DISORDERS and more Study notes Physiology in PDF only on Docsity!

Nelson Textbook of Pediatrics (21st ed) (Chap68) HYPERNATREMIA  Hypernatremia is a [Na+ ] >145 mEq/L , although it is sometimes defined as >150 mEq/L  iatrogenic caused by inadequate water administration or, less often, by excessive Na+ administration  effects of hypernatremia on the brain by rapid correction  sodium intoxication by sodium bicarbonate, hyperaldosteronism  causes of hypernatremia from a water deficit are nephrogenic and central diabetes insipidus  Adipsia , the absence of thirst, is usually secondary to damage to the hypothalamus  Essential hypernatremia is rare in children and is thought to occur with injury to the hypothalamic- posterior pituitary axis  Patients are irritable, restless, weak, and lethargic. Some infants have a high-pitched cry and hyperpnea  Hypernatremia is associated with fever, hyperglycemia and mild hypocalcemia  As the extracellular osmolality increases, water moves out of brain cells, leading to a decrease in brain volume = tearing intracerebral veins (hemorrhage)  Salt poisoning is associated with an elevated fractional excretion of Na+ , whereas hypernatremic dehydration causes a low fractional excretion of Na+  As hypernatremia develops, the brain generates idiogenic osmoles to increase the intracellular osmolality and prevent the loss of brain water THUS IF the serum [Na+ ] is lowered rapidly, there is movement of water from the serum into the brain cells leading to brain swelling manifested as seizures or coma  child with central diabetes insipidus should receive desmopressin acetate because this treatment reduces renal excretion of water  desmopressin acetate in children are for the management of central diabetes insipidus and nocturnal enuresis HYPONATREMIA  a serum sodium level <135meq/l  Pseudohyponatremia measured osmolality is normal like in hyperlipidemia, hyperproteinemia  Hyperosmolality like hyperglycemia causes a low [Na+ ] because water moves down its osmotic gradient from the ICS into the ECS diluting the Na+ (eg. SIADH)  hypovolemic hyponatremia the child has lost Na+ from the body; Na loss is higher than water loss  Diarrhea as a result of gastroenteritis is the most common cause of hypovolemic hyponatremia in children  if the patient receives hypotonic fluid this leads to ADH production and water retention  thiazide diuretics can concentrate the urine and is at higher risk for severe hyponatremia  Central Pontine Myelinolysis is classically associated with overly rapid correction of hyponatremia , both central pontine and extrapontine myelinolysis can occur in children with hypernatremia  causes of hypovolemic hyponatremia is usually a high serum [K+ ] is associated with disorders in which the Na+ wasting is caused by absence of or ineffectiveness of aldosterone (hypoaldosteronism, diuretics, vomiting)  Renal salt wasting occurs in hereditary kidney diseases, such as juvenile nephronophthisis and autosomal recessive polycystic kidney disease  type II renal tubular acidosis (RTA), usually associated with Fanconi syndrome there is increased excretion of Na+ and bicarbonate in the urine  hypervolemic hyponatremia there is an excess of TBW and Na+ , although the increase in water is greater than the increase in Na  decrease in the effective blood volume, resulting from third space fluid loss, vasodilation, or poor cardiac output  water intake exceeds sodium intake  Children with hypervolemia are edematous on physical examination. They may have ascites, pulmonary edema, pleural effusion, or hypertension  euvolemic hyponatremia with no evidence of volume overload or volume depletion  SIADH is unable to excrete water that results in dilution of the serum Na+ and hyponatremia

 Excess water ingestion can produce dilutional hyponatremia, suppresses ADH secretion, and there is a marked water diuresis by the kidney = intake of water exceeds the kidney’s ability to eliminate water  Hyponatremia may result in transient seizures, hypothermia, and poor tone  the water intoxication causes acute hyponatremia and is caused by a massive acute water load  Exercise-induced hyponatremia, reported frequently during marathons, is caused by excessive water intake, salt losses from sweat, and secretion of ADH  Can cause brain swelling = dangerous  Acute, severe hyponatremia can cause brainstem herniation and apnea; respiratory support is often necessary  Neurologic symptoms of hyponatremia include anorexia, nausea, emesis, malaise, lethargy, confusion, agitation, headache, seizures, coma, and decreased reflexes  rhabdomyolysis can occur with water intoxication  The presence of a low osmolality indicates “true” hyponatremia  Hypoxia worsens cerebral edema, and hyponatremia may exacerbate hypoxic cell swelling. Therefore, pulse oximetry should be monitored and hypoxia aggressively corrected.  avoid overly rapid correction, which may cause central pontine myelinolysis (CPM)  CPM is more common in patients who are treated for chronic hyponatremia  seizures associated with hyponatremia generally are poorly responsive to anticonvulsants  hypovolemic hyponatremia to restore the intravascular volume with isotonic saline  hypervolemic hyponatremia manage with therapy by water and Na+ restriction, because patients have volume overload , use DIURETICS  isovolumic hyponatremia there is usually an excess of water and a mild Na+ deficit. Therapy is directed at eliminating the excess water  Furosemide and NaCl supplementation are effective in the patient with SIADH and severe hyponatremia  Vaptans which block the action of ADH and cause a water diuresis, are effective at correcting euvolemic hyponatremia

HYPERKALEMIA

 potential for lethal arrhythmias  Spurious hyperkalemia or pseudohyperkalemia DUE TO difficulties in obtaining blood specimens  Elevated WBC counts , typically >200,000/m3 , can cause a dramatic elevation in the serum [K+ ].  Cell destruction , as seen with rhabdomyolysis, tumor lysis syndrome, tissue necrosis, or hemolysis, releases K+ into the extracellular milieu  increase in insulin causes K+ to move intracellularly  diabetic ketoacidosis (DKA), the absence of insulin causes potassium to leave the ICS  Gordon syndrome , is an autosomal dominant disorder characterized by hypertension caused by salt retention and impaired excretion of K  Potassium-sparing diuretics may easily cause hyperkalemia, especially because they are often used in patients receiving oral K+ supplements  paresthesias, fasciculations, weakness, and even an ascending paralysis  Chronic hyperkalemia is generally better tolerated than acute hyperkalemia.  Genetic diseases, such as congenital adrenal hyperplasia and pseudohypoaldosteronism  High serum [K+ ] and the presence of ECG changes require vigorous treatment  Peak T waves are the first sign of hyperkalemia, followed by a prolonged PR interval  The treatment of hyperkalemia has 2 basic goals: (1) to stabilize the heart to prevent life-threatening arrhythmias and (2) to remove K+ from the body  Calcium stabilizes the cell membrane of heart cells, preventing arrhythmias; it is given intravenously over a few minutes, and its action is almost immediate  Bicarbonate causes potassium to move intracellularly , lowering the plasma [K+ ]  Insulin causes K+ to move intracellularly but must be given with glucose to avoid hypoglycemia.  Nebulized albuterol , by stimulation of β1- adrenergic receptors, leads to rapid intracellular movement of K+  loop diuretic increases renal excretion of K+ HYPOKALEMIA  Hypokalemia is common in children, with most cases related to gastroenteritis

ACID-BASE-ELECTROLYTES DISORDERS, Study notes of Physiology

Related documents

Partial preview of the text

Download ACID-BASE-ELECTROLYTES DISORDERS and more Study notes Physiology in PDF only on Docsity!

HYPERKALEMIA