5. Tetania
Estado de excitabilidad neuromuscular generalizada
Normo-Ca2+
y Normo-Mg2+
Alcalosis (> respiratoria)
Hipopotasemia
Hipernatremia
Tóxicos
Hipocalcémicas
Ca total < 8,5 mg/dL
Ca iónico < 1,1 mMol/L
Hipomagnesémicas
Mg total < 1,6 mg/dL
30/01/15 5
15. Causas de hipocalcemia
Recién
nacido
Lactantes y
Niños> 3 años
Precoz (< 72 h) Asfixia
Hijo de madre diabética
Hiperparatirodismo materno
Tardía (> 72 h) Aporte excesivo de P
Hipoparatiroidismo
Hipoparatiroidismo Congénito
Adquirido
Autoinmune
Resistencia a la PTH
Raquitismo Deficiencia de vit. D
Defectos del met. Vit D
Hiperfosfatemia Intoxicaciones
Insuficiencia renal
Enfermedad grave Shock séptico
30/01/15 15
17. Hipocalcemia. Tratamiento
Asintomática
–Suplementos orales
• Gluconato cálcico 10 % (Calcium Sandoz®)
–Vial 10 ml = 2,2 mmol de Ca ≈ 90 mg de Ca.
• Acetato cálcico (Royen®)
–Cápsulas 500 mg = 3,2 mmol de Ca ≈ 125 mg de Ca.
• Carbonato cálcico (Mastical®)
–Comprimidos 1,26 g = 12,5 mmol de Ca ≈ 500 mg de Ca.
• Pidolato cálcico (Ibercal®)
–Solución: 5 ml = 1,7 mmol de Ca ≈ 70 mg de Ca.
30/01/15 17
18. Hipocalcemia. Tratamiento
Sintomática:
–Gluconato cálcico 10 % (94 mg/ml de Ca elemental)
• Vía intravenosa lenta (< 1 ml/min). Auscultación continua de los
tonos cardiacos durante la administración.
• Añadido a fluidos i.v. (asegurar que no llevan HCO3Na).
• Dosis: 0,5-1,0 ml/kg cada 4-6 horas ≈ 200-500 mg/kg/día.
• Precauciones:
–Bradicardia/asistolia si administración i.v. rápida (> 1 ml/min).
–Vena bien canalizada: necrosis de partes blandas si hay extravasación.
–No administrar simultáneamente o inmediatamente antes o después de
HCO3Na, puede cristalizar (lavar vía con ClNa 0,9%)
30/01/15 18
19. 30/01/15 19
El factor IV de la cadena de coagulación es el Calcio
Recuerden también que el Citrato Trisódico (C6H5O7Na3) actúa
impidiendo que el calcio se ionice, evitando así la coagulación.
El citrato lo usan en Hemoterapia para evitar que la sangre de banco se
coagule por lo tanto tener presente que por cada 3 unidades
de sangre total transfundida, se debe administrar 1 g de cloruro cálcico o 4
g de gluconato de calcio. ...
31. Clínica de HiperMagnesemia
30/01/15 31
Clinical consequences related to serum concentration:
4.0 mEq/l hyporeflexia
>5.0 mEq/l Prolonged atrioventricular conduction
>10.0 mEq/l Complete heart block
>13.0 mEq/l Cardiac arrest
7.0-10.0 mEq/L - loss of patellar reflex
10.0-13.0 mEq/L - respiratory depression
15.0-25.0 mEq/L - altered atrioventricular conduction and (further)
complete heart block
>25.0 mEq/L - cardiac arrest
32. Causas de HiperMagnesemia
30/01/15 32
•Hemolysis, magnesium concentration in erythrocytes is
approximately three times greater than in serum, therefore hemolysis
can increase plasma magnesium. Hypermagnesemia is expected
only in massive hemolysis.
•Renal insufficiency, excretion of magnesium becomes impaired
when creatinine clearance falls below 30 ml/min. However,
hypermagnesemia is not a prominent feature of renal insufficiency
unless magnesium intake is increased.
•Other conditions that can predispose to mild hypermagnesemia are
diabetic ketoacidosis, adrenal insufficiency, hyperparathyroidism and
lithium intoxication.
33. Tratamiento
30/01/15 33
Prevention of hypermagnesemia usually is possible. In mild cases,
withdrawing magnesium suppletion is often sufficient. In more severe
cases the following treatments are used:
Intravenous calcium gluconate, because the actions of magnesium in
neuromuscular and cardiac function are antagonized by calcium.
Definitive treatment of hypermagnesemia requires increasing renal
magnesium excretion through:
Intravenous diuretics, in the presence of normal renal function
Dialysis, when kidney function is impaired and the patient is
symptomatic from hypermagnesemia
35. HipoFosfatemia Causas
30/01/15 35
Refeeding syndrome This causes a demand for phosphate in cells due to the action of
phosphofructokinase, an enzyme that attaches phosphate to glucose to begin metabolism of
this. Also, production of ATP when cells are fed and recharge their energy supplies, requires
phosphate.
Respiratory alkalosis Any alkalemic condition moves phosphate out of the blood into cells. This
includes most common respiratory alkalemia (a higher than normal blood pH from low carbon
dioxide levels in the blood), which in turn is caused by any hyperventilation (such as may result
from sepsis, fever, pain, anxiety, drug withdrawal, and many other causes).
Alcohol abuse Alcohol impairs phosphate absorption. Alcoholics are usually also malnourished
with regard to minerals. In addition, alcohol treatment is associated with refeeding, and the
stress of alcohol withdrawal may create respiratory alkalosis, which exacerbates
hypophosphatemia (see above).
Malabsorption This includes GI damage, and also failure to absorb phosphate due to lack of
vitamin D, or chronic use of phosphate binders such as sucralfate, aluminum-containing
antacids, and (more rarely) calcium-containing antacids.
Phosphaturia or hyperexcretion of phosphate in the urine. This condition is divided into primary
and secondary types. Primary hypophosphatemia is characterized by direct excess excretion of
phosphate by the kidneys, as from primary renal dysfunction, and also the direct action of many
classes of diuretics on the kidneys. Additionally, secondary causes, including both types of
hyperparathyroidism cause hyperexcretion of phosphate in the urine.
36. HipoFosfatemia Síntomas
30/01/15 36
Muscle dysfunction and weakness. This occurs in major muscles, but also may
manifest as: diplopia, low cardiac output, dysphagia, and respiratory depression
due to respiratory muscle weakness.
Mental status changes. This may range from irritability to gross confusion, delirium,
and coma.
White cell dysfunction, causing worsening of infections
Instability of cell membranes due to low ATP levels: this may cause
rhabdomyolysis with increased CPK, and also hemolytic anemia.
37. Tratamiento de HipoFosfatemia
30/01/15 37
Standard intravenous preparations of potassium
phosphate are available and are routinely used in
malnourished patients and alcoholics. Oral
supplementation also is useful where no
intravenous treatment is available. Historically one
of the first demonstrations of this was in
concentration camp victims who died soon after
being re-fed: it was observed that those given milk
(high in phosphate) had a higher survival rate than
those who did not get milk.
39. Causas de HiperFosfatemia
30/01/15 39
Hypoparathyroidism: In this situation, there are low
levels of Parathyroid hormone (PTH). PTH normally
inhibits renal reabsorption of phosphate, and so
without enough PTH there is more reabsorption of
the phosphate.
Chronic renal failure: When the kidneys aren't
working well, there will be increased phosphate
retention.
Drugs: hyperphosphatemia can also be caused by
taking oral sodium phosphate solutions prescribed
for bowel preparation for colonoscopy in children
41. Tratamiento de la Hiperfosfatemia
30/01/15 41
High phosphate levels can be avoided with phosphate binders and dietary
restriction of phosphate.
42. Fin
La presentación la pueden bajar de
http://f1.grp.yahoofs.com/v1/MM15TJbeDibsLxgCSRNBpobQiHG58C5oLjcSOfCldb7PP8EPtbSlbM
TX15Srxl2cltaJh1x9vACzlXTIsbqzkQ/Presentaciones%20en%20PPT/04%20Calcio
%20Magnecio%20%20Fosforo.pdf
30/01/15 42