Fluid therapy Fluid therapy in systemic disorders Fluid therapy in electrolyte disturbances

1. DR.RAHUL GARG
M.D.MEDICINE(Std.)
S.N.M.C.,AGRA
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2. DR.RAHUL GARG

3.  2/3
(65%) of TBW is intracellular (ICF)
 1/3 extracellular water
◦ 25 % interstitial fluid (ISF)
◦ 5- 8 % in plasma (IVF intravascular fluid)
◦ 1- 2 % in transcellular fluids – CSF,
intraocular fluids, serous membranes,
and in GI, respiratory and urinary tracts
(third space)
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4. DR.RAHUL GARG

5. COMPOSITION OF COMMON IV
FLUID(mEq/L
DEXT. Na+
K+
Cl-
mOsm
Ca++ HPO4 ACET. Lact. /L
50
-
-
-
-
-
-
-
278
NS
D5,.
45%NS 50
154
-
154
-
-
-
-
308
77
-
77
-
-
-
-
432
DNS
154
-
154
-
-
-
-
586
130
4
109
3
-
-
28
274
D5
50
RL
ISO-G
50
63
17
150
-
-
-
-
580
ISO-M
50
40
35
40
-
15
20
-
410
270
-
270
-
-
-
-
540
513
-
513
-
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-
-
1025
1.6%NS
3%NS
-

6. 


SODIUM BICARBONATE(NaHCO3):
-Commonly available as7.5%w/v,10ml inj
-each amp. contain 22.5 mEq Na+ and
HCO3- 22.5mEq
Amount of NaHCO3 req.(in mEq/l)= 0.5 * wt
in Kg * (desired HCO3 - Actual HCO3)
Approx 50% of calculated deficit is corrected
in 4hr and rest gradually over 24hrs.
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7.  Special
precaution with NaHCO3:
-should not be given as iv bolous
-in presence of renal failure it can cause
tetany or pulmonary edema,so safer Tt will be
dialysis if acidosis and renal failure are sever
-never correct acidosis without correcting
hypokalemia b/c this can aggravate K+
deficit.
- do not mix inj Ca with NaHCO3 b/c it can
ppt CaCO3 as white crystal
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8. 
POTASSIUM CHLORIDE:
-Inj KCl 15% 10 ml amp contain 20 mEq of
K+.
-Never give inj KCl as direct iv,always use in
diluted infusion.
-Never add more than 40mEq/l
-Never in fuse more than 10mEq/hr
-Never add KCl in ISOM.
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9. Fluid therapy in
hypovolemia
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10. 



Hypovolemia can be
Mild (<2lit in adult): symptom can be thirst,
conc. Urine
Moderate (2-3 lit in adult): symp. Above plus
dizziness ,weakness ,
oliguria(<400ml/day),postura hypotension,
low jvp
Severe(>3lit in adult): symp. Above plus
cnfusion , stupor, syst BP<100, tachycardia,
low vol pulse, cold extremities,reduced skin
turgor.
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11. 


Approx fluid deficit can be calculated by
ECF deficit(L)=0.2*lean body wt *(current
Hct/normal Hct - 1)
Effective rate of fluid replacement per hr
= 50 to 100 ml + U.O. per hr + ongoing
loss(such as diarrhoea or tube drain) per hr
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12. DR.RAHUL GARG

13. 


Isotonic saline is initial fluid of choice b/c 1
lit of NS will expend of intravascular vol. by
300ml ,sso rise in bp is much rapid.
Once renal output is established preferred
fluid is RL b/c its composition is almost
idetical to ECF so large vol. can be infused
without fear of electrolyte imbalance.
Lactate in RL converted to HCO3 and can
correct acidosis
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14. 

RL avoided in initial treatment shock b/c
-K+ in RL is unsafe till renal status is
uncertain
-In shock hepatic conversion of lactate to
bicarbonate is uncertain
Primary indication of use of albumin or other
colloid is in hypovolemia with hypotension in
protein losing state such burns.
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15. 

Hypovolemic pt who are bleeding or have
marked anemia require administration of
blood in addition to fluid
However with BT haematocrit should not be
raised over 35% b/c increase PCV increase
viscosity that can lead to stasis in already
impaired capillary circulation.
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16. DR.RAHUL GARG

17. Vomiting
Na loss
Dehydration
Aldosterone HCO3 absorption
In proximal tubules
Na absorpation
K secretion & urinary loss
Loss of Cl-
loss of h+
Hypochloremia
Metabolic alkalosis
Hypokalemia
When severe hypokalemia H+ secretion in DCT
For increased Na absorption
PARADOXICAL ACIDURIA
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18. 

END RESULT :Hypokalemic Hypochlorimic
Matabolic Alkalosis.
Fluid use to correct deficit due to upper G.I.
loss:1-Isolyte-G: this is specific fluid used for
the replacement U.G.I. loss.
By its ammonia(70mEq/L),high Cl
(154mEq/L),K+(17mEq/L),& Na+ (63mEq/L)
it correct H+,Cl-,K+&Na+ losses
respectively.
2-Isotonic saline
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19. INFUSION OF ISOTINIC SALINE
Vol. correction
Renal HCO3- absorption
Na+supplementation
aldosterone
Correct
Hypochloremia
Urinary H+ loss and
K+ loss
Correct
metamolic acidosis
Cl- supplementation
Prevents Hypokalemia
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Favours HCO3secretion

20. 

Urinary pH is very imp. To assesss efficacy of
fluid therapy
Acidic pH suggest need for more vigerous Tt
and Alkaline urine suggests response to
therapy.
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21. DR.RAHUL GARG

22. 

In diarrhea stool usually contain large amount
of NaCl, K and HCO3 along with water.
Fluid and Electrolyte abnormality in
diarrhoea:Hypovolemia
Sodium deficit
Hypokalemia
Hypochloremia
Metabolic acidosis
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23. DIARRHOEA
Rich in K+ & HCO3-,contain water &Na+
K loss
Water loss
Na loss
Dehydration
Aldosterone
K seceretion&
Urinary loss
Na Absorption
Associated Renal
absorptio of Cl-
H ypokalemia
Hyperchloremia
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HCO3 loss
Intestinal lumina
Exchange of HCO
With Cl-
G.I Cl- absorption
Acidosis

24. 

Oral rehydration therapy:- it preferred
method of fluid replacement
ORS provide Na,K,Cl and HCO3 along with
glucose which effectively correct fluid and
electrolyte abnormalities and also provide
calories.
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25. 

I/v fluid therapy :- indicated when
-rapid correction of fluid required for
severe dehydration & shock
-inability of pt to take ORS due persistent
vomiting
-ORT fail to correct volume deletion due to
greater loss.
Preferred iv fluid in diarrhoea are RL & NS(but
iv fluid is ideal)
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26. Preferred iv fluid in diarrhoea are RL & NS(but
iv fluid is ideal)
 RL- preferred solution b /c it provide
adequate Na and also HCO3(by hepatic
conversion of lactate) for correction of
metabolic acidosis
-K conc. Is low (4 mEq/L) and RL provide no
glucose. so pt may require additional K and
glucose

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27.  NS-effectively correct hypovolemia and

provides Na along with water.
-pt may require additional supplementation
of K(10 to 20 mEq/L) and NaHCO3 (20-30
mEq/L)
-altthough NS lacks K+ ,but adequate
supply of Na & water prevent urinary loss of
K+ by suppressing aldosterone.
D5- not acceptable b/c it does not correct
acidosis,hypokalemia,and Na deficit.
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28. DR.RAHUL GARG

29. 

Avoid hypoglycemia:-pt are more prone to
hypoglycemia due to glycogenolysis and
gluconeogenesis. oral glucose
supplementation(200gm/day approx.) or 10% or
20% dextrose should be given by slow iv infusion
Avoid metabolic alkalosis:-overzealous use of
diuretics ,vigorous paracentesis or vomiting can
lead to metabolic alkalosis which can precipitate
or aggravate HE.
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30. 

Hypokalemia:- vomiting & diuretic therapy
causes hypokalemia, and can precipitate or
aggravate HE. It should be corrected by
oral/iv supplement of K+
Hyponatremia:- only dextrose containing
electrolyte free fluid can lead to
hyponatremia,which can aggravate cerebral
edema.
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31. Selection of iv fluid in HE:1-glucose containing fluid is preferred ,but
avoid 5% dextrose as it is hypotonic.
2-avoid islyte-G as it contains ammonium
chloride.
3-avoid RL as it contain lactate,which get
converted into HCO3 by liver and can cause
alkalosis,OR if lactate metabolism is
impaired,it can cause lactic acidosis.

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32. 4:-iv fluid preferred is D10,D25 & DNS.
KCl(1amp of 15% KCl contain 20mEq of K+)
may be added to iv fluid as per requirement. But
oral supplement is preferred.
5:- vol of fluid infused depends on hydration
status and urine output.
edematous pt may require fluid restriction along
with salt
In cirrhotic pt salt should be restricted to 13gm/day.(N req. is about 6gm(100mEq)per day)
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33. DR.RAHUL GARG

34.  CHF
-Edema in CHF is due to water and salt
retention. so total body water & Na is
more
in these pt , but water retention of water
is
more than salt .so hyponatremia is seen
usually dilutional
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35. DON’T
Don’t correct hyponatremia with salt
supplementation b/c it is dilutional and need
fluid restriction and loop diuretics for correction.
Don’t follow routine guidelines(i.e. total fluid
required per day=U.O.+700ml) replacement.aim
is to remove extra fluid from the body so restrict
fluid intake despite good U.O.
DON’T treat hypotension with Na rich fluid,

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36.  Dos
Give lrss fluid pt with severe anasarca require
restriction of fluid as low as 500-600ml/day
Restrict Na so avoid NS,DNS,&RL
K+ should be corrected adequately as required
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37. 
ESSENTIAL HYPERTENSION
-Restrict Na intake to roughlt 50mEq/day
-Avoid rapid correction of Na requirment
within shorter duration
-To deliver required Na use fluid with low
Na
conc.(ISOM ,ISOP)
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38. DR.RAHUL GARG

39. 


Maintain euvolemia: avoid hypovolemia and
hypotension. b/c hypovolemia can lead to
decrease in cerebral perfusion pressure.
Avoid hypotonic fluid (D5,RL) and
hypoosmolality b/c it can induce or aggravate
cerebral oedema
NS(0.9% NaCl) best fluid especially when large
volumes of fluid are to be infused.
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40. 


Avoid hyperglycemia: immediate period after
strok(i.e.for first 24 hr after a pt presents
with an anterior circulation infract and for 72
hr after post. Circulation event) avoid
dextrose containing fluid.
Avoid hypovolemia during mannitol therapy
Achive hypervolemia in vasospasm (like in
SAH)
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41. DR.RAHUL GARG

42. 

HEAT CRAMPS:
-oral saline solution (1 teaspoon of salt in
500 ml of water) is adequate to replace both
salt and water iv fluid rarely required
HEAT SYNCOPE:
- 1-2 lit of isotonic saline is given over 2-4
hr
-serum electrolyete replaced accordin to
need
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43. 
HEAT STROKE:
-Initially isotonic saline or RL is infused ,
subsequently 5%dextrose with 0-45%NS is
used
-Pt may need 1.2 to 1.4 lit or iv fluid during first
4
hr.
-Initially there is marked vasdilatation , so
vigorous fluid replacement is avoided b/c when
temp fall and vasoconstrication occur it may
lead to pulmonary oedema.
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44. DR.RAHUL GARG

45. DR.RAHUL GARG

46. • Definition:
– Commonly defined as a serum sodium
concentration <135 meq/L
– Hyponatremia represents a relative excess of
water in relation to sodium.
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47.  Hyponatremia is the most common
electrolyte disorder
 Acute hyponatremia (developing over 48 h
or less) are subject to more severe
degrees of cerebral edema
ocw.jhsph.edu
 sodium level is less than 105 mEq/L, the mortality is over
50%
 Chronic hyponatremia (developing over
more than 48 h) experience milder
degrees of cerebral edema
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48. 
Types
◦
◦
◦
◦
◦
Hypovolemic hyponatremia
Euvolemic hyponatremia
Hypervolemic hyponatremia
Redistributive hyponatremia
Pseudohyponatremia
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49. 

Develops as sodium and free water are lost
and/or replaced by inappropriately hypotonic
fluids
Sodium can be lost through renal or non-renal
routes
www.grouptrails.com/.../0-Beat-Dehydration.jpg
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50. 
Nonrenal loss
◦ GI losses
 Vomiting, Diarrhea, fistulas, pancreatitis
◦ Excessive sweating
◦ Third spacing of fluids
 ascites, peritonitis, pancreatitis, and burns
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◦ Cerebral salt-wasting syndrome
 traumatic brain injury, aneurysmal subarachnoid
hemorrhage, and intracranial surgery
 Must distinguish from SIADH
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51. 
Renal Loss
◦ Acute or chronic renal insufficiency
◦ Diuretics
www.ct-angiogram.com/images/renalCTangiogram2.jpg
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52. 
Normal sodium stores and a total body
excess of free water
◦ Psychogenic polydipsia, often in psychiatric patients
◦ Administration of hypotonic intravenous (5% DW) or
irrigation fluids ( sorbitol, glycerin) in the
immediate postoperative period
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53. ◦ administration of hypotonic maintenance
intravenous fluids
◦ Infants who may have been given inappropriate
amounts of free water
◦ bowel preparation before colonoscopy or colorectal
surgery
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54. 

Total body sodium increases, and TBW
increases to a greater extent.
Can be renal or non-renal
◦ acute or chronic renal failure
 dysfunctional kidneys are unable to excrete the
ingested sodium load
◦ cirrhosis, congestive heart failure, or nephrotic
syndrome
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55. ◦ Water shifts from the intracellular to the
extracellular compartment, with a resultant dilution
of sodium. The TBW and total body sodium are
unchanged.
 This condition occurs with hyperglycemia
 Administration of mannitol
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56. 
Pseudohyponatremia
◦ The aqueous phase is diluted by excessive proteins
or lipids. The TBW and total body sodium are
unchanged.
 hypertriglyceridemia
 multiple myeloma
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57. 
Clinical Manifestations
◦ most patients with a serum sodium concentration
exceeding 125 mEq/L are asymptomatic
◦ Patients with acutely developing hyponatremia are
typically symptomatic at a level of approximately
120 mEq/L
◦ Most abnormal findings on physical examination
are characteristically neurologic in origin
◦ patients may exhibit signs of hypovolemia or
hypervolemia
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58. 
Diagnosis
◦
◦
◦
◦
CT head, EKG, CXR if symptomatic
Repeat Na level
Correct for hyperglycemia
Laboratory tests provide important initial
information in the differential diagnosis of
hyponatremia




Plasma osmolality
Urine osmolality
Urine sodium concentration
Uric acid level
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59. 
Laboratory tests Cont.
◦ Plasma osmolality
 normally ranges from 275 to 290 mosmol/kg
 If >290 mosmol/kg :
 Hyperglycemia or administration of mannitol
 If 275 – 290 mosmol/kg :
 hyperlipidemia or hyperproteinemia
 If <275 mosmol/kg :
 Hypervolemic/ Euvolemic status/ hypovolemic
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60. 
Laboratory tests Cont.
◦ Plasma osmolality < 275 mosmol /kg
 Increased volume:
 CHF, cirrhosis, nephrotic syndrome
 Euvolemic
 SIADH, hypothyroidism, psychogenic polydipsia, beer
potomania, postoperative states
 Decreased volume
 GI loss, skin, 3rd spacing, diuretics
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61. 
Laboratory tests Cont.
◦ Urine osmolality
 Normal value is > 100 mosmol/kg
 Normal to high:
 Hyperlipidemia, hyperproteinemia, hyperglycemia, SIADH
 < 100 mosmol/kg
 hypoosmolar hyponatremia





Excessive sweating
Burns
Vomiting
Diarrhea
Urinary loss
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62. 
Laboratory tests Cont.
◦ Urine Sodium
 >20 mEq/L
 SIADH, diuretics
 <20 mEq/L
 cirrhosis, nephrosis, congestive heart failure, GI loss, skin,
3rd spacing, psychogenic polydipsya
◦ Uric Acid Level
 < 4 mg/dl consider SIADH
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63. 
Treatment
◦ four issues must be addressed




Asyptomatic vs. symptomatic
acute (within 48 hours)
chronic (>48 hours)
Volume status
◦ 1st step is to calculate the total body water
 total body water (TBW) = 0.6 × body weight
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64. 
Treatment Cont.
◦ next decide what our desired correction rate should
be
◦ Symptomatic
 immediate increase in serum Na level by 8 to 10
meq/L in 4 to 6 hours with hypertonic saline is
recommended
◦ acute hyponatremia
 more rapid correction may be possible
 8 to 10 meq/L in 4 to 8 hours
◦ chronic hyponatremia
 slower rates of correction
 12 meq/L in 24 hours
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65. 
Symptomatic or Acute
◦ Treatment Cont.  estimate SNa change on the basis of the amount of Na
in the infusate
 ΔSNa = {[Na + K]inf − SNa} ÷ (TBW + 1)
 ΔSNa is a change in SNa
 [Na + K]inf is infusate Na and K concentration in 1 liter of
solution
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66. 
Asypmtomatic or Chronic
◦ SIADH
 Water restriction
 0.5-1 liter/day
 Salt tablets
 Demeclocycline
 Inhibits the effects of ADH
 Onset of action may require up to one week
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67. PLASMA Na > 145mEq/L
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68. 
Hypernatremia is usually due to water deficit
Excess water loss :eg- heat exposure
diabetes insipidus
Impaired thirst:eg-primary hypodypsia,
comatose
Excessive Na retension
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69.  Clinical



feature-
Excessive thirst,polyuria,nausea
Muscular weakness, neuromuscular irritability
Altered mental status,focal neurological
deficit occasionally coma or seizures
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70. 


Treatment
correct water deficit
water deficit =
(plasma Na-140)/140*0.6*body wt in kg
Rate of correction :
-Acute hypernatremia- 1mEq/L/hr
-Chronic hypernatremia-1mEq/L/hr or
10mEq/L over 24hr
-rapid correction may lead to cerebral oedema
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71. Plasma K < 3.5 mmol/L
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72. Neuromuscular effects :
- weakness, myalgia, fatigue
- hypo/areflexia
- paralyis, rhabodmyolysis, dyspnea
Cardiac effects : delay in ventricular repolarization
- ECG (T flat, depressed ST, U wave)
- arrhythmia (reentry currents during prolonged repolarization)
- ↑ sensibility to toxic drugs (digoxin)
Renal effects : nephrogenic diabetes insipidus, Interstitial nephritis, ↑
ammoniagenesis
Glucose intolerance : ↓ insulin secretion β-cell
Blood pressure : ↑ (low K+ diet) or ↓ (Gitelmann)
Growth defect : impaired protein metabolism – GH release
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73. Approx. K deficit ,normal plasma pH
Serum K+ >3.5
(mEq/l)
3
2
Total K
deficit
(mEq)
300
450-600
0
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<2
>600

74. Serum K:Tt guidelines



3.5 to 4 mEq/L
-no K+ supplement
-Increase oral intake of K rich food
-Add K sparing diuretics or decrease dose
of
diuretics
3 to 3.5 mEq/L:
-Tt in selected high risk pt eg: CHF,
DIGITALIS
therapy ,IHD etc.
<3 mEq/L
-Need definativ Tt
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75. Oral supplementation
: safer mode than iv
 Avg dose of KCl is 60 to 80 mEq/day in divided
doses
 Iv therapy: reserved for severe symptomatic
hypokaemia (<3mEq/l)
-Never give inj. KCl as direct iv,always use in
diluted infusion.
-Never add more than 40mEq/l
-Never in fuse more than 10mEq/hr
-Never add KCl in ISOM.

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76. Plasma K > 5 mmol/L
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77. 
Cardiac

Neuromuscular

Renal electrolyte

Endocrine
◦ Abnormal electrocardiogram
◦ Atrial /ventricular arrhythmias
◦ Pacemaker dysfunction
◦ Paresthesias
◦ Weakness
◦ Paralysis
◦ Decreased renal NH4+ production
◦ Natriuresis
◦ Increased aldosterone secretion
◦ Increased insulin secretion
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78.  ECG
changes
-Tall peaked t wave
- loss of p wave ,widening ofQRS complex
-QRS merges with T wave forming sine waves
- A-V dissociation
-Ventricular tachycardia
-fibrillation
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79. 

Antagonize the cardiac effect of hyperkalemia
◦ 10% Calcium gluconate 10 cc over 5-10 min
◦ Can be repeated after 5 min if EKG changes
persist
◦ Except if the patient on digoxin
◦ Onset 1-3 min, duration 30-60 min
Induce intracellular K+ shift;
◦ Insulin 10-20 IU IV 25-50 cc D50%
 Onset 30 min, duration 4-6 hrs
◦ Nebulized albuterol 10-20 mg or 0.5 mg IV
 Onset 30 min, duration 2-4 hrs
◦ Na Bicarb IV if acidotic 50 mEq over 2 min
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80. 
External removal;
◦ Renal
 IVF + diuretics
 Fludrocortisone 0.05 – 0.1 mg
◦ GI
 Na or Ca resonium
with tap water)
sorbitol (15 gm PO or 50 gm rectal
 Onset 1-2 hrs, duration 4-6 hrs
◦ Dialysis: immediate onset
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81. DR.RAHUL GARG

82. 

Most common causes include primary
hyperparathyroidism and malignancies ( more than
90% patients )
REMEMBER: as a general rule, primary
hyperparathyroidism is the etiology in OPD patients
who are asymptomatic and with a serum calcium level
of <=11 mg/dl. Malignancy is often the cause in
symptomatic patients with an abrupt onset of disease
and serum calcium >=14 mg/dl
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83. 




Clinical features are due to
the underlying disorder causing hypercalcemia
hypercalcemia per se
CNS: weakness, fatigue, depression, confusion, stupor or
coma
GI: constipation, anorexia, nausea and vomiting.
Abdominal pain, if present, is a result of the induced
peptic ulcer or pancreatitis
Renal: polyuria, nocturia and stone formation
CVS: increased risk of digoxin toxicity, shortened QT
interval
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84. A.



Measures to increase urinary excretion
volume restoration, expansion and saline
diuresis: the most useful and effective methods
(the pt may need 4-6 L of fluid for the same,
therefore to be used cautiously in the elderly
and pts with heart disease)
Furosemide: effective but avoid dehydration,
hypokalemia and hypomagnesemia during
treatment
Hemodialysis: reserved for patients with severe
hypercalcemia and little or no renal function
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85. B.



Measures to inhibit bone resorption
Bisphosphonates: Pamidronate
Calcitonin: also increases urinary calcium
excretion. Has a rapid action and therefore
mainly used as urgent therapy in life
threatening hypercalcemia. Not useful for
long term therapy
Gallium Nitrate: not often used as it requires
5 days duration of infusion, has a potential
for nephrotoxicity and the availability of
better and safer alternatives
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86. C.



Measures to decrease intestinal absorption
Glucorticoids: decreases intestinal absorption along
with increasing urinary excretion in pharmacological
doses. They are mainly used in the cases caused due
to malignancies, sarcoidosis and vit d intoxication.
Not useful in primary hyperparathyroidism or in a
normal person
Oral phosphate: promotes calcium deposition in the
bone and soft tissue. Should only be used if serum
phosphate is <3 mg/dl and renal function is normal
Ketoconazole and hydroxychloroquine can also be
used
DR.RAHUL GARG

87. D.



Specific treatment
Discontinue the drugs responsible
Surgical removal of primary
hyperparathyroidism
Specific treatment for malignancy,
thyroxicosis, etc
DR.RAHUL GARG

88. DR.RAHUL GARG

89. 

Hypoalbuminemia is the most common cause
of hypocalcemia with normal ionised calcium.
True hypocalcemia is caused due to
decreased calcium absorption from the GI
tract or decreased reabsorption from the
bone, abnormalities of either PTH or Vit D
DR.RAHUL GARG

90. 




They vary with the degree and rate of onset and are
caused due to increased neuromuscular excitability
Pt usually complains of weakness, circumoral and
distal extremity parasthesia, muscle spasm,
carpopedal spasm, tetany and mental changes like
irritability, psychosis and depression
Chvostek’s sign and Trosseau’s sign positive
ECG may show prolonged QT interval. Digitalis effect
is reduced
Severe forms may cause lethargy, confusion,
laryngeal spasms, seizures or reversible heart failure
DR.RAHUL GARG

91. ETIOLOGY
SERUM
CA
TOTAL
LCIUM
SERUM
PHOSPHATE
SERUM PTH
IONIZED
Hypoalbuminemia
Low
Normal
Normal
normal
Alkalosis
Normal
Low
Normal
Normal-high
Vit-D
deficiency
Low
Low
Low
high
Chronic renal
failure
Low
Low
High
high
Hypoparathyroidis
m
Low
Low
High
low
DR.RAHUL GARG

92. Acute management
Emergency treatment required with 10% calcium
gluconate (90 mg elemental calcium/10 ml) 1020 ml i.v. slowly over 10 mins. Severe
symptomatic hypocalcemia may require infusion
of 60 ml of calcium gluconate in 500 ml of 5%
dextrose. Calcium concentration of the drip is 1
mg/ml and its requirement is 0.5- 2 mg/kg/hour

If i.v. calcium does not relieve the tetany, rule out
(and correct) hypomagnesemia
DR.RAHUL GARG

93. Long term management:
- Treat the underlying etiology
- Calcium supplementation: an aymptomatic
hypocalcemic pt needs 1-3 gm of calcium per day.
Calcium is best absorbed when taken b/w meals
 Vit D supplementation
Calcitriol is the most potent of the vit D preparations
and has the fastest onset and shortest duration of
action. C
Ergocalciferol requires several weeks to achieve full
effect. Although cost is low, its long half life and
storage in fat carry a high risk of vit D intoxication

DR.RAHUL GARG

94. THANK YOU
DR.RAHUL GARG