Fluid

DR.RAHUL GARG

FLUID AND ELECTROLYTES

DR.RAHUL GARGM.D.MEDICINE(Std.)

S.N.M.C.,AGRA

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DR.RAHUL GARG

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)

Body Fluid Compartments

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Introduction of common iv fluids

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DEXT. Na+ K+ Cl- Ca++ HPO4 ACET. Lact.mOsm/L

D5 50 - - - - - - - 278

NS 154 - 154 - - - - 308D5,. 45%NS 50 77 - 77 - - - - 432

DNS 50 154 - 154 - - - - 586

RL 130 4 109 3 - - 28 274

ISO-G 50 63 17 150 - - - - 580

ISO-M 50 40 35 40 - 15 20 - 410

1.6%NS 270 - 270 - - - - 540

3%NS - 513 - 513 - - - - 1025

COMPOSITION OF COMMON IV FLUID(mEq/L)

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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.

Special fluid

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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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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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Fluid therapy in hypovolemia

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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.

Fluid therapy in hypovolemia

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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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Fluid therapy in hypovolemic shock

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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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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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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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Fluid therapy in vomiting

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Vomiting

Na loss Dehydration loss of h+Loss of Cl-

Aldosterone HCO3 absorption In proximal tubules Hypochloremia

Na absorpationK secretion & urinary loss Metabolic alkalosis

Hypokalemia

When severe hypokalemiaFor increased Na absorption

H+ secretion in DCT PARADOXICAL ACIDURIA

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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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INFUSION OF ISOTINIC SALINE

Cl- supplementationVol. correction Na+supplementation

Renal HCO3- absorption aldosterone Correct Hypochloremia

Urinary H+ loss and K+ loss

Favours HCO3-secretion

Correct metamolic acidosis

Prevents Hypokalemia

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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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Fluid therapy in Diarrhea

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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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DIARRHOEA

K loss Water loss Na loss HCO3 loss

Rich in K+ & HCO3-,contain water &Na+

Dehydration Aldosterone Intestinal luminalExchange of HCO3 With Cl-

K seceretion& Urinary loss

Na Absorption

Associated Renal absorptio of Cl-

G.I Cl- absorption

H ypokalemia AcidosisHyperchloremia

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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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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)


DR.RAHUL GARG

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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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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Fluid and electrolyte Mn in HEPATIC ENCEPHOPATHY

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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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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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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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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 1-3gm/day.(N req. is about 6gm(100mEq)per day)


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Fluid therapy in CVS disorders

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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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DON’TDon’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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DosGive lrss fluid pt with severe anasarca require

restriction of fluid as low as 500-600ml/dayRestrict Na so avoid NS,DNS,&RLK+ should be corrected adequately as

required


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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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Fluid therapy in neurological disorder

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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.


DR.RAHUL GARG

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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Fluid therapy in heat illness

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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


DR.RAHUL GARG

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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ELECTROLTTE DISTERBANCES

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Hyponatremia

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Hyponatremia

• 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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Hyponatremia is the most common electrolyte disorder

Acute hyponatremia (developing over 48 h or less) are subject to more severe degrees of cerebral edema 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

Hyponatremia

ocw.jhsph.edu

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Types◦ Hypovolemic hyponatremia◦ Euvolemic hyponatremia◦ Hypervolemic hyponatremia◦ Redistributive hyponatremia◦ Pseudohyponatremia

Hyponatremia

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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

Hypovolemic hyponatremia

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Nonrenal loss◦ GI losses

Vomiting, Diarrhea, fistulas, pancreatitis◦ Excessive sweating◦ Third spacing of fluids

ascites, peritonitis, pancreatitis, and burns ◦ Cerebral salt-wasting syndrome

traumatic brain injury, aneurysmal subarachnoid hemorrhage, and intracranial surgery

Must distinguish from SIADH


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Renal Loss◦ Acute or chronic renal insufficiency◦ Diuretics


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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

Euvolemic hyponatremia

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◦ administration of hypotonic maintenance intravenous fluids

◦ Infants who may have been given inappropriate amounts of free water

◦ bowel preparation before colonoscopy or colorectal surgery

Euvolemic hyponatremia

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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

Hypervolemic hyponatremia

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◦ 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

Redistributive hyponatremia

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Pseudohyponatremia◦ The aqueous phase is diluted by excessive

proteins or lipids. The TBW and total body sodium are unchanged. hypertriglyceridemia multiple myeloma

Hyponatremia

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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

Hyponatremia

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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

Hyponatremia

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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

Hyponatremia

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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

Hyponatremia

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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

Hyponatremia

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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

Hyponatremia

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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

Hyponatremia

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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

Hyponatremia

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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

Hyponatremia

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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

Hyponatremia

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HYPERNATREMIAPLASMA Na > 145mEq/L

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Hypernatremia is usually due to water deficit

Excess water loss :eg- heat exposure diabetes insipidus Impaired thirst:eg-primary hypodypsia, comatose Excessive Na retension

HYPERNATREMIA

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Clinical feature- Excessive thirst,polyuria,nausea Muscular weakness, neuromuscular

irritability Altered mental status,focal neurological

deficit occasionally coma or seizures

HYPERNATREMIA

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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

HYPERNATREMIA

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Hypokalemia Plasma K < 3.5 mmol/L

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Hypokalemia- Clinical Manifestations

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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Approx. K deficit ,normal plasma pH

Hypokalemia

Serum K+(mEq/l)

>3.5 3 2 <2

Total K deficit(mEq)

0 300 450-600 >600

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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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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.

Hypokalemia

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Hyperkalemia Plasma K > 5 mmol/L

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Cardiac◦ Abnormal electrocardiogram◦ Atrial /ventricular arrhythmias◦ Pacemaker dysfunction

Neuromuscular◦ Paresthesias◦ Weakness◦ Paralysis

Renal electrolyte◦ Decreased renal NH4+ production◦ Natriuresis

Endocrine◦ Increased aldosterone secretion◦ Increased insulin secretion

HyperkalemiaClinical Manifestations

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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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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

Management of Hyperkalemia

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External removal;

◦ Renal IVF + diuretics Fludrocortisone 0.05 – 0.1 mg

◦ GI Na or Ca resonium ± sorbitol (15 gm PO or 50 gm rectal

with tap water) Onset 1-2 hrs, duration 4-6 hrs

◦ Dialysis: immediate onset

Management of Hyperkalemia

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Hypercalcemia

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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

HYPERCALCEMIA

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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

Clinical Features

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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

Treatment

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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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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

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D. Specific treatment Discontinue the drugs responsible Surgical removal of primary

hyperparathyroidism Specific treatment for malignancy,

thyroxicosis, etc

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HYPOCALCEMIA

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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

Hypocalcemia

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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

Clinical Features

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ETIOLOGY SERUM CA

TOTAL

LCIUM

IONIZED

SERUM PHOSPHATE

SERUM PTH

Hypo-albuminemia

Low Normal Normal normal

Alkalosis Normal Low Normal Normal-high

Vit-D deficiency

Low Low Low high

Chronic renal failure

Low Low High high

Hypo-parathyroidism

Low Low High low

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Acute managementEmergency treatment required with 10% calcium

gluconate (90 mg elemental calcium/10 ml) 10-20 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

Treatment

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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 supplementationCalcitriol 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

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