Anaestthetic implications of hypo and hypercalcemia

1. HYPER AND HYPOCALCEMIA
ANAESTHETIC IMPLICATIONS
DR.SATHISH RAJA
DR.REENA

2. CALCIUM
One of the body’s most important intracellular
second messengers
It plays a key role in
muscular contraction
neuromuscular transmission
cell division and movement
oxidative pathways
coagulation

3. Normal serum calcium=4.5 to5mEq/L
[8.5 TO10.5 mg/dl]
Total body calcium
0.1% in ECF
1% in cells
rest all stored in bones.

5. Maintained by endocrine control system
1. vitamin D
2. PTH
3. Calcitonin
Ionized calcium –physiologically active[2 to2.5meq/l],depends on
arterial pH.
Sensed by extrcellular domain of GPCR on parathyroid cells –inhibits
PTH release.

6. Ca2+ homeostasis interlinked with magnesium but homeostasis of
phosphate is converse of ca2+.
The degree of albumin –protein binding is affected by pH.
Corrected total ca2+= 0.8mg/dl added per 1g/dl decrease in
albumin conc. Below 4g/dl.
Corrected ca2+=measured ca2++0.8 multiplied by [4-albumin]
Plasma albumin binds nonionized calcium.

7. Renal role in maintaining calcium:
only 10% is excreted in urine
Aproximately 90% - absorbed in PCT,LOH nd early distal tubules
10% - in late DCT and early CD depending on conc. In blood

9. Vitamin D
Has potentiating effect
 to increase ca2+ absorption from GI tract
 effect on bone deposition and absorption
 drcreases renal ca2+ excretion
It has to convert to its active form for producing these
effects.

11. If calcium falls below normal range
PTH promotes conversion of 25 to 1,25 [OH]2 cholecalciferol
In case of increased ca2+
PTH decreases and
converted to other form which is not active.
If values are too high formation is drastically reduced and
decreases its absorption from all sites .

12.  1,25[OH]2 cholecalciferol promotes intestinal absorption
of calcium by formation of calbindin.
Ca2+binding protein
Transport ca2+ into cell cytoplasm
Other ways through
formation of ca2+ stimulated ATPase in
brush bordr.
Alkaline phosphatase in epithelial cells.

13. PTH
 secreted by chief cells of parathyroid glands
They are located on posterior side of thyroid gland
Increases calcium
Increase calcium and phosphate absorption from
bone
Decreases excretion of calcium by kidneys.

14. Increases calcium by 2 phases:
RAPID PHASE: begins in minutes and increases
progressively for several hours
SLOW PHASE: several daysto weeks by proliferation
of osteoclasts
By increasing osteoclastic
reabsorption of bone itself.

16. MECHANISM
PTH on administration
increases cAMP in osteocytes
osteoclastic secretion of enzymes and acids
bone reabsorption and formation of 1,25[OH]2
cholecalciferol

18. Even slight decrease in ca++
PTH increases greatly within minutes and in
some it gets hypertrophied
Rickets
Pregnancy
Lactation
PTH is decreased in increased ca++ and vit D diet, disuse
of bones

19. Changes in ECF ion conc. detected by CaSR in parathyroid
cell membrane
activates phospholipase C
increases intracellular inositol 1,4,5 triphosphate and
diacylglycerol
stimulates ca2+ release from intracellular stores

21. CALCITONIN
Released from parafollicular c cells
It decreases ca2+
Action opposite to PTH
When serum ca2+ is high, it is stimulated to
decrease ca2+

22. HYPOCALCEMIA
 Serum calcium level less than 8.5 mg/dl
 Nerves are more excitable
 Neuronal membrane permeability to Na + ions increases which allows easy
initiation of action potentials
 If 50% below normal ,peripheral nerves also excitable
 If 35% below, carpopedal spasms occur
 Lethal if values are less than 4 mg/dl

23. CAUSES
Decreased PTH
Decreased vit D
Increased bone deposition
Calcium chelation
Changes in binding protein concentration

26. SYMPTOMS AND SIGNS
NM irritability
 circumoral and peripheral paraesthesia
 muscle cramps
 laryngospasm
 tetany
 seizures
SIGNS :
 CHOVSTEK SIGN
 TROUSSEAU SIGN

27. CARDIAC
 Impaired inotropy
 Prolonged QT
 Ventricular fibrillation
 Heart block

29. ANAESTHETIC IMPLICATIONS
 Hypocalcemia correction needed before surgery
 To give 10% of 10 ml calcium gluconate after massive transfusion
 To correct hypothermia and alkalosis
 Bronchospasm risk
 In thyroid and parathyroid resection –acute hypocalcemia postop can
occur – precipitates laryngospasm.
 If patient has metabolic or resp acidosis- correct calcium first
 NMB sensitivity – hypocalcemia prolongs NM blockade.
 Careful positioning – brittle bones due to chronic hypocalcemia
 Correct magnesium also.
 Muscle weakness may develop and precipitate resp failure.

30.  Coagulopathy occurs if level less than 1.2 meq/l
supplemental ca2+ given to support cardiac inotropy and NM
function
calcium given during cardiac surgery to optimize ventricular
function.
Calcium levels should be checked frequently after
parthyroidectomy

31. Adequate calcium and vit d in diet
adequate sunlight exposure
treat the cause
oral formulations are available [calcium carbonate
,citrate,gluconate and lactate]
calcium carbonate is cost effective and taken with a meal to ensure
optimal absorption .
given prophylactically in pregnancy ,lactation and in
postmenopausal women.

32. MANAGEMENT
Calcium gluconate
 10% of 10 ml contains 9mg /ml of
elemental calcium
 Is preferred
 Given in peripheral line
 Tissue injury from extravasation is
less severe
Calcium chloride
 10% contains 27 mg /ml of elemental
calcium
 Causes local irritation and necrosis on
peripheral administration
 Should be given in central line

33. HYPERCALCEMIA
Occurs when ECF ca2+influx from GIT and bone outweighs
efflux to bone or excretion via kidneys
Depresses nervous system and reflex activity of cns gets
sluggished
Symptoms are more marked above 15mg/dl
If more than 17mg/dl ,calcium phosphate crystals
precipitate throughout the body.
Precipitate in degenerative tissues and in old blood clots
and in arteriosclerosis.

34. CAUSES
 Primary hyperparathyroidism –sporadic or associated with MEN
 Malignancy
 Sarcoidosis
 TB
 Familial hypocalciuric hypocalcemia
 Pagets disease
 Tertiary hyperparathyroidism
 Endocrine [hyperthyroidism,acromegaly,pheochromocytoma]
 Drug induced[thiazide diuretics,vit A and D excess,lithium,milk alkali
syndrome with calcium containing antacids

36. SYMPTOMS
 Neurologic symptoms
 drowsiness
 weakness,muscle pain
 depression
 lethargy,confusion
 coma
 GI symptoms
 constipation ,abdominal pain
 nausea,vomiting
 anorexia,peptic ulcers

37. Renal manifestations
Nephrogenic DI[polyuria]
renal stones[renal angle tenderness and
hematuria]
oliguria[in AKI]
ECG changes
short QT interval [arrythmias]
prolonged PR interval
potentiation of digoxin toxicity

39. Investigations
CBC
Serum calcium
RFT, TFT,alkaline phosphatase
Serum electrolytes including serum phosphorus
Urinary calcium
PTH, vitamin D levels
PTHrP
Chest x ray ,ecg,IGF-1,pituitary MRI

41. TREATMENT
 Treat underlying cause
 Isotonic saline to increase renal calcium excretion
 Loop diuretics
 This both will reduce ca2+by 1 to 3 mg /dl in 1 to 2 days
 Bisphosphonates enhance osteoclastic bone deposition
 PAMIDRONATE 60 mg or 90 mg single dose iv
 ZOLEDRONIC ACID more effective ,given iv at 4 mg
 Glucocoticoids may be given
 Calcitonin increases renal excretion and reduces bone resorption.
 Surgical parathyroidectomy

43. ANAESTHETIC IMPLICATIONS
 Hypercalcemia should be treated if more than 13 mg/dl or if patient is
symptomatic.
 Hydrate-rehydrate prior to induction, usually associated with
hypovolemia due to polyuria.
 Fluid replacement helps to lower ca2+ levels
 Loop diuretics given to increase excretion only after adequate fluid
resuscitation.

44. • Avoid lactated ringers – contains calcium
Administration of calcitonin and bisphosphonates- will inhibit
bone resorption
NO thiazide diuretics[it increases ca2+reabsorption]
watch hemodynamics
careful positioning
judicious paralytics-due to hypotonia and regular TOF
monitoring

45. Hypercalcemia can cause hypokalemia due to transcellular
shifts
watch urine output- renal vasoconstriction and nephrogenic
DI.
Avoid drugs causing hypercalcemia
steroids may be considered if not contraindicated ,it helps
in renal excretion and decrease intestinal absorption.

46. Inhalational agents –nonspecific ca2+ antagonists and by altering
ca2+ influx resulting in
myocardial depression
vasodilation.
Benzodiazepines inhibit voltage gated ca2+ channel –inhibits ca2+
entry in vascular smooth muscles and bronchial muscles leading to
relaxation
iv agents exert cardiodepressant and vasodilatory agents.
Iv succinylcholine – decreases ca2+ due to cellular migration in
fasciculations.
Increased ionized ca2+ decreases sensitivity of NMBA
decreased ca2+ potentiates action of NMBA.