treatment of hyponatremia
High-risk groups for poor outcomes
Menstruant females
Children
Hypoxic patients
Hyponatremic encephalopathy with evidence of severe cerebral edema (active seizures, respiratory arrest)
–Bolus, 100 mL of 3% NaCl over 10 min
–Can repeat bolus 1–2 times with the goal of increasing serum sodium 2–4 mEq/L or until clinical improvement
–Begin infusion as for hyponatremic encephalopathy
Hyponatremicencephalopathy ( decreased mental status, headache, nausea, vomiting)
–Infuse 3% NaClat a rate of 1 mL/kg/h. ICU setting using infusion pump
–Check serum sodium every 2 hours until symptom-free
–Stop hypertonic saline when patient is symptom-free or serum sodium has increased by 15–20 mEq/L in the initial 48 hours of
therapy
Asymptomatic hyponatremia
–Fluid restriction unless hypovolemiais suspected
–Demeclocycline
–VasopressinV2 receptor antagonists(vaptons)
SGPGI PG ARC 20197
Hypernatremia
SGPGI PG ARC 20198
approach to hypernatremia
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:
Table 5: Etiology of hyperkalemia
Assess for increased potassium intake
Assess for shift of potassium intracellular fluid to extracellular fluid
Metabolic acidosis
Tissue necrosis (rhabdomyolysis, bowel infarction, tumor lysis) or depolarization
Insulin deficiency
β2-Blockade
Assess for reduced potassium excretion in urine
Renal failure
Low aldosteroneaction (Think drugs: especially heparin, cyclosporine, tacrolimus, ARB, ACE-I)
Decreased distal nephronflow rate
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Clinical Manifestations:
related to the neuromuscular transmission and
conduction in the heart
Other manifestations include ileus, muscular
cramps, augmented ammonia production in the
kidney (which can potentiate hepatic
encephalopathy), and rhabdomyolysis
SGPGI PG ARC 201915
SGPGI PG ARC 201916
Management of Hypokalemia:
Rate of replacement:
Standard method of K+ replacement is
to add 20 mEqof K+ to 100 ml of
isotonic saline and infuse over 1 hour.
Maximum infusion rate of intravenous
potassium replacement is set at 20
mEq/hr,butdose rate upto40 mEq/hr
may be needed in severe hypokalemia
associated with arrhythmia.
Infusion through large,centralvein is
preferred,ifpossible because of irritating
property of hyperosmolarKCL
solutions.However, delivery into the
superior vena cava is not recommended
if infusion rate of more than 20 mEq/hr
is required because there is a risk of an
abrupt rise in plasma K+ in the right
heart chamber severe enough to
produce asystole.
SGPGI PG ARC 201917
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Hypocalcemia:
Table 10: Etiology of Hypocalcemia
Hypoparathyroidism/pseudohypoparathyroidism
Hyperphosphatemia
Hypomagnesemia
Vitamin D deficiency
-Dietary deficit
-Reduced sun exposure
-Decreased 25-hydroxylation of vitamin D (liver disease, alcoholism)
-Decreased vitamin D–sensitive rickets type 1 (1-α hydroxylase deficiency) and type 2 (receptor deficiency)
Renal failure (reduced 1-hydroxylation of vitamin D)
Osteoblastic metastases (prostate, breast)
Saponification in severe pancreatitis
Citrate load (blood transfusion)
SGPGI PG ARC 201919
ClinicalManifestations:
The clinicalmanifestations includealteredmental
statusand tetany. (Chvostekand Trousseau signs).
Management of Hypocalcemia:
Hypocalcemiaiscommonin sepsisand treatment
isusuallynot necessaryunlesscardiovascular
collapse withionizedcalcium levelsof lessthan0.8
mmol/Lispresent.
For acute symptomatichypocalcemia, administer
intravenouscalcium chlorideor calcium gluconate
(preferredas lesscausticto veins.
Do not infuse more rapidlythan2.5 to 5 mmolin 20
minutes becauseof the riskof cardiacabnormalities
and asystole.
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Management of Hypercalcemia:
Table 12: Treatment of Severe Hypercalcemia
-Replete intravascular volume with normal saline.
-Use intravenous furosemideto increase calcium excretion (after volume repletion).
-In hypercalcemiaof malignancy, use bisphosphonatesto decrease calcium reabsorption from the bone.
-Adjunctive therapy includes calcitonin(effect is usually short term; tachyphylaxisdevelops).
-Start hemodialysis.
SGPGI PG ARC 201922