Calcium,magnesium,phosphate and chloride imbalances
Their treatment,my main reference is Eric strong's lectures in youtube,and some of the websites.Hope everyone finding Serum electrolytes find atleast some use of it .
Thank you
3. • Most of the calcium in the body is stored in the
bones as hydroxyapatite (Ca₁₀(PO₄)₆(OH)₂).
• Calcium in the plasma :
45% free ionized form
45% bound to proteins
(predominantly albumin)
10% complexed with anions
(eg: citrate ,sulfate,phosphate)
Normal serum Ca+29-11mg/dl.
Physiologically active
Typically
measured
in routine
blood tests
4.
5.
6.
7. In addition to its regulation by serum Ca+2,PTH is
also regulated by serum acid –base status.
↓SERUM
pH
↑PTH
↑urinary excretion of
Phosphate
↑buffering of
H+ions excreted
in the distal
tubule
↑serum
pH
10. PTH excess
Hormone
Independe
nt Bone
Resorption
Vitamin D
excess
Excessive
Dietary intake
of Ca+2
Thiaz
ides
Rare
Miscellaneous
Mechanisms
Hyperparathyroidi
sm
Osteolytic
bone
metastase
s
↑intake of
Vitamin D
Milk-Alkali
Syndrome
(↑intake of
CaCO3)
Adrenal Crisis
PTHrP –secreting
malignancy
Paget’s
disease
Ectopic
Calcitriol
Production
Severe
Rhabdo.
Complicated
by AKI
Lithium Hyperthyr
oidism
Theophylline
Toxicity
Familial
Hypocalciuric
hypercalcemia
Immobiliz
ation
11. Clinical manifestations
• Stones , bones,groans and psychiatric overtones
(moans).
• Other symptoms include : Constipation
Anorexia
Nausea
Weakness
lethargy
There are no reliable physical findings of
hypercalcemia.
12. • Short QT interval
• Additional findings are: Dehydration
Renal Insufficiency
Nephrogenic Diabetes
insipidus
Type 1 Renal tubular
acidosis
13. Diagnostic Evaluation
• Step1: correct calcium for low albumin
• Step2:Perform thorough Physical examination
and obtain Chest X-ray.
• Step3 : Measure PTH.
17. etiology
•Hypoparathyroidism:
• s/p thyroidectomy or other neck surgery
• s/p I131 therapy for graves disease or thyroid cancer
• Autoimmune hypoparathyroidism
• Infiltration of parathyroids
• Hypomagnesemia
• Genetic /congenital
19. Symptoms
• Perioral paresthesias
• Muscle stiffness ,spasms and cramps
• Shortness of breath (diaphragmatic spasms)
• Diaphoresis
• EKG finding –long QT interval
• Other severe symptoms –seizures, hypotension,
emotional lability , psychosis.
20. Signs
• Chvostek’s sign:Facial spasm elicited by
tapping on the ipsilateral facial nerve anterior
to the ear.
• Trousseau’s sign- Carpopedal spasm induced
by inflation of a BP cuff above SBP for 3
minutes.
21. Diagnostic evaluation
• Step1 :correct calcium for low albumin
• Step 2: Measure PTH , creatinine , phosphate ,
magnesium , calcidiol and calcitriol
22. Treatment
• Oral calcium(1500-2000mg elemental calcium
daily in divided doses)
• IV calcium
• Vitamin D
• Magnesium
Should be reserved for the pts with severe symptoms-
seizures ,tetany, prolonged QT ,abrupt decrease
<7.5mg/dl
Although common to
give as a slow bolus(ie.
over 10-20 min)this
improves calcium
levels only transiently.
Magnesium sulfate IV (1-
2gm)with frequent monitoring
Pts with moderate def. – 600-
800units/day
Pts with severe malabsorption- 10000-
50000units/day.
23. Phosphate
• Serum phosphate level
Reference range in adults,
2.5-4.5 mg/dL
• in children, 3-6 mg/dL
• hemolysis or hyperlipidemia of the
serum sample may lead to falsely
elevated phosphorus levels
24. • Most of the phosphate in the body is
also stored in the bones as
hydroxyapatite.
• Most of the remainder of the body’s
phosphate is intracellular ,as
component of phospholipids in cell
membranes ,DNA,RNA and ATP and
ADP.
25. • The small fraction of phosphate that is in the
serum exists as circulating phospholipids and
inorganic phosphate.
• Inorganic phosphate consists of HPO4
-2 and
H2PO4
-1 in a 4:1 ratio at pH 7.40 which is
physiologically active and what is typically
measured in routine blood tests.
30. MECHANISM
EARLY
MANIFESTATIONS
(serum phosphate 1-2
mg/dl)
LATE MANIFESTATIONS
(serum phosphate
<1mg/dl)
Dysfunctional
bone metabolism
↓bone
mineralization
Bone pain
Rickets(children)
Osteomalacia
(adults)
↓
Intracellular
ATP
↓Myocardial
contractility
Proximal muscle
weakness
↑RBC rigidity
Encephalopathy
Heart failure
Rhabdomyolysis
Hemolysis
Seizures , coma
↓RBC
2,3DPG
↑affinity of
Hb for O2
Systemic
ischemia
31. Diagnostic evaluation
• The first step is measurement of 24hr urine
phosphate excretion , and/ or fractional
excretion of phosphate.(FE PO4)
32. Patients with uncorrectable ,ongoing urinary loss of
phosphate will require ongoing oral phosphate repletion
even after serum phosphate is normalized
35. Hyperphosphatemia symptoms
• Altered mental status
• Delirium
• Obtundation
• Coma
• Convulsions and seizures
• Muscle cramping or tetany
• Neuromuscular hyperexcitability (ie, Chvostek
and Trousseau signs)
• Paresthesias (particularly perioral and distal
extremities)
36. Diagnostic evaluation
• The cause of the clinically relevant
hyperphosphatemia is rarely a diagnostic
mystery.
• Pseudohyperphosphatemia should be
identified
• When uncertain as to the etiology , it is best
to start by working up the likely concurrent
calcium disorder.
37. Acuity Renal
function Treatment
Acute
intact
For mild hyperphosphatemia
,therapy is unnecessary
Will usually resolve within 6-
12hrs.
IF degree is Life threatening
Consider normal saline +/-
acetazolamide
impaired
Consider
Hemodialysis
38. Acuity Renal
function Treatment
Chronic
Intact
For Vitamin D excess and
Hypoparathyroidism treatment
of the underlying condition is
usually sufficient
For Familial tumoral calcinosis
,treatment requires low
phosphate diet and phosphate
binders
impaired
low phosphate diet and
phosphate binders
39.
40. Magnesium
• needed for more than 300 biochemical
reactions in the body. It helps to maintain
– normal nerve and muscle function
– supports a healthy immune system,
– keeps the heart beat steady, and helps bones
remain strong.
– It also helps regulate blood glucose levels and
– aid in the production of energy and protein.
41. • ~50% of Mg is stored in bone
• ~49% is in the intracellular space
• Of the remaining 1%:
• ~20%bound to albumin
• ~10% complexed with anions
• ~70% Unbound(ie. Biologically
active)
• Serum Mg correlates poorly with total body Mg
content.
• Average daily intake: 360mg
47. Symptoms/Signs :
– Tetany (seizures in children/neonates)
– Hypokalemia
– Hypoparathyroidism hypocalcemia (<1.2mg/dL)
– Vitamin D deficiency (due to low calcitriol)
– EKG changes: widened QRS, peaked T-waves, PR
interval prolongation,
– Ventricular arrhythmias (especially during
ischemia or bypass), like TORSADE de POINTES.
48. Treatment
• Abrupt increases in serum Mg (as seen during IV
administration )inhibit Mg reabsorption in the loop
of henle and lead to transient Mg wasting ,limiting
the utility of the IV route.
• In the absence of symptoms ,arrhythmias ,or
concurrent hypokalemia oral repletion is usually
preserved.
• Treat underlying disease (PPI, diuretics, alcohol,
uncontrolled diabetes)
49. • In the presence of symptoms ,arrhythmias ,
and/or hypokalemia , IV Mg can be given ,usually
1-2gms at a time .
• Although it is common practice to give IV Mg
relatively quickly (ie.,<15min/gram),this speed is
usually not necessary.
• Avoid replacement in patients with reduced GFR
55. • Chloride - the major anion of extracellular
fluid
• Chloride accounts for two-thirds of all serum anions.
–Chloride moves passively with Na+ or against
HCO3
- to maintain neutral electrical charge
–Chloride usually follows Na (if one is
abnormal, so is the other)
56. Functions
–- not completely known,
–it maintains cellular integrity by:
•hydration
•osmotic pressure
•electrical neutrality & other functions
• Chloride is secreted by the stomach's
mucosa as hydrochloric acid.
57. • Normal range: 98-106 mmol/L
• Critical values: < 70 or >120 mmol/L
• Chloride daily requirements for
adults are 80-120 mEq/d as NaCL
• CSF – 120-132 mEq/L
61. Symptoms
• Excess fluid loss or dehydration (diarrhea,
vomiting)
• Muscle hypertonicity (Spasticity)
• Tetany
• Shallow, depressed breathing
• Muscle weakness
• Sweating
• High fever
• Weight loss
62. diagnosis
• Serum chloride levels < 98 mEq/L confirm the
diagnosis.
• Serum pH is above 7.45
• Serum carbon dioxide levels > 32 mEq/L.
• Serum osmolarity < 280mOsm/L
• Arterial blood gas analysis for identifying any acid
base imbalance.
• Sometimes, a chloride test can be done.This finds
out how much chloride is excreted in the urine.
63. Treatment
• Electrolyte replacement therapy
• IV administration of normal (0.9 NaCl) or half
strength saline (0.45 NaCl).
• Ammonium chloride (an acidifying agent) – This is
for treating the metabolic alkalosis. Dosage
depends up on the serum chloride level and weight
of the patient. This is contraindicated in cases of
impaired renal or liver functions.
64. • Oral or intravenous KCl (10-
40mEq PO). IV should not exceed
20 mEq/hr.
• Dietary modifications
–Consume sodium and potassium rich
diet, as hypochloremia causes
deficiency of these nutrients.
66. Causes of hyperchloremia may include
• Loss of body fluids from prolonged vomiting,
diarrhea, sweating or high fever (dehydration).
• High levels of blood sodium.
• Kidney failure, or kidney disorders
• Diabetes insipidus or diabetic coma
• Drugs such as: androgens, corticosteroids,
estrogens, and certain diuretics.
67. Symptoms/signs
• Excess fluid loss or dehydration (diarrhea, vomiting)
• High blood sugar
• Kussmaul’s breathing (deep and rapid breathing)
• Dyspnea
• Intense thirst
• Weakness
• Tachypnea
• Hypertension
• Pitting edema
• Diminished cognitive ability
• Possible coma
68. Hyperchloremia Diagnosis
• Serum chloride levels > 106 mEq/L confirm the
diagnosis.
• Serum pH is under 7.35
• Serum carbon dioxide levels < 22 mEq/L.
• Sometimes, a chloride test can be done .
69. Treatment
• Sodium bicarbonate I.V infusion
– This is to raise the bicarbonate level in blood
and for permitting renal excretion of chloride
anion, as chloride and bicarbonate compete to
combine with sodium.
• Lactated Ringer’s solution
– This is administered in cases of hyperchloremia.
In liver, this gets converted to bicarbonate,
thereby increasing the base bicarbonate for
correcting the acidosis caused.
• Low sodium diet
– The excess chloride ions may combine with
sodium to form hypernatremia.