Body Fluid & Electrolytes

An Overview

Human body is composed of 2/3rd fluid &1/3rd solid

Fluid is distributed as 2/3rd ICF & 1/3rd ECF Crystalloids are aqueous solutions of

mineral salts or water soluble molecules , weighing around 30kDa,can pass easily through pores of different body compartment

Crystalloids provides the tonicity of fluid name as osmolality

Normal plasma osmolality is 285-290 mmol/L

A fluid that is isotonic containing same no. of particles-the same osmolality of plasma

Osmolality can be calculated as (in mmol/L) Osmolality=2Na+2k+Glucose +Blood

Urea Colloids are larger insoluble particles,size

>30 kDa, standing mostly in vascular bed Blood itself is colloid

Ions (MEq/L) ICF Intravascular Interstitial

Na 10 145 142

K 140 4 4

Ca 1 3 2

Mg 50 2 2

Cl 4 105 110

HCO3 1o 24 28

PO4 75 2 2

Protein 16 7 2

Ionic Distribution

Na: 100mmol/day K : 75mmol/day Cl : 120mmol/day Mg: 8mmol/day Ca : 5-12 mg/day Protein: 30gm/day

Normal Requirements/Day

Input Output

Drink-1500ml Urine- 1500ml

Food- 800ml Insensible-800ml

Metabolism of Food - 200ml

Stool- 200ml

Total- 2500ml Total- 2500ml

Fluid Balance

Solution

Na(mmol/L)

K(mmol/L)

Cl(mmol/L)

Ca(mmol/L)

Glucose(g/L)

Lactate(mmol/L)

Acetate(mmol/L)

5%DA 0 0 0 0 50 0 0

½ NS 77 0 77 0 o 0 0

0.9%NS

154 0 154 0 0 0 0

Ringer’s Lactate

130 4 109 3 0 28 0

3%NaCl

512 0 512 0 0 0 0

5%DNS

154 0 154 0 50 0 0

Hartmann’s sol.

131 5 111 2 0 0 0

Cholera saline

133 13 98 0 o o 48

Composition of common crystalloids

Solution Change in ECF(ml) Change in ICF(ml)

5%DA 333 667

½ NS 667 333

NS 1000 0

Ringer’s Lactate 900 100

Change of adding 1LFluid

Primary disturbance

Altered physiology Clinical effect

Na ECF vol Circulatory changes

Water ECF osmolality Cerebral changes

K AP in excitable tissue N-M weakness,cardiac effect

H+ Acid-base balance Altered tissue function,respiratory compensation

Mg Cell membrane stability

N-M,vascular & cardiac effects

PO4 Cellular energetics Wide spread tissue effects

Manifestations of disordered water,electrolyte & acid-base status

Na intake & excretion imbalance is usually corrected by osmotic mechanism controlling water balance

Disorders of Na balance presents chiefly as alterations in ECF vol,resulting in Hypo or Hypervolemia

Disorders of Na balance

Hypovolaemia Symptoms Thirst Dizziness on standing Weakness Signs Low JVP Postural Hypotension Tachycardia,Dry mouth,reduced skin turgor Reduced urine output wt loss,confusion,stupor

C/F of Hypo &Hypervolaemia

Hypervolaemia Symptoms Ankle swelling,abdominal swelling Breathlessness Signs Peripheral edema raised JVP,Pulmonary creps Pleural effusion Ascites wt gain HTN (sometimes )

Contd.

1.Inadequate Intake 2.GIT Na loss (vomiting , diarrhoea) 3.Skin Na loss (burn , excessive sweating) 4.renal Na loss (Diuretic Rx ,

tubulointerstitial disease) 5.Internal sequestration (bowel obstruction ,

peritonitis,crush injury) Rx---Appropriate IVF based on clinical

condition

Causes of Sodium & Water Depletion

1.Impaired renal function 2. Primary Hyperaldosteronism (Conn’s

Synd.) 3.Secondary Hyperaldosteronism (CCF,CLD

NS ,Protein losing enteopathy) Rx---Rational use of Diuretics

Causes of Na & water excess

Step-1>>>assess clinical volume status Step-2>>>review fluid balance chart Step-3>>>assess ongoing pathological

process Step-4>>>check plasma urea &

electrolytes Step-5>>>prescribe appropriate i.v.fluid Rx

Assessment of fluid & electrolyte balance in hospital

Disturbances in body water balance,in the absence of changes in Na balance,alter plasma Na concentration & hence plasma osmolality

When extra cellular osmolality changes abruptly, resulting cell swelling or shrinkage

Cerebral functions are very sensitive to such volume changes

Disorders of water balance

Hyponatraemia Often detected asymptomatically; may be associated with profound

disturbance of cerebral function manifesting as anorexia,nausea,vomiting,confusion,lethargy,seizure,coma

The degree of cerebral symptomology depends on the rapidity of electrolyte imbalace than it’s severity

Common Electrolyte Disturbancesin body water imbalance

Hypovolaemic (Na deficit with a relatively smaller water deficit)

Renal Na losses Diuretic Rx (specially thiazide) adrenocortical failure Gastrointestinal Na losses Vomiting Diarrhoea Skin Na losses Burns

Causes of Hyponatraemia

Euvolaemic(water retention) Primary polydipsia Excessive electrolyte free water

infusion SIADH Hypothyroidism

Hypervolaemic (Na retention with relatively greater water retention)

CCF Cirrhosis Nephrotic Synd CRF(during free water intake)

Causes >>Tumours e.g.lung or colon cancer >>CNS disorder:stroke,trauma,infection,psychosis >>Pulmonary

disorder:pneumonia,tuberculosis,obstructive lung disease >>Drugs Anticonvulsants e.g.carbamazepine Psychotropics e.g.heloperidol Antidepressants e.g.Amitriptyline,fluxetine Cytotoxics e.g.cyclophosphamide,vincristine Hypoglycemics e.g.chlorpropamide Opiates e.g. morphine >> Idiopathic

SIADH

Diagnosis of SIADH Low plasma sodium conc.(<130mmol/L) Low plasma osmolality (<270mmol/L) Urine osmolality not minimally low

(>150mmol/L) Urine sodium conc. Not minimally low

(>30mmol/L) Low-normal plasma urea,creatinine,uric acid Exclusion of other causes of hyponatraemia Appropriate clinical context

Rx is critically dependent on the rate of development,severity &underlying cause

In general,if hyponatraemia has developed rapidly & there is features of rapid obtundation of CNS function or convulsion ,rapid correction can be achieved with 3% NaCl in stead of .9% NaCl at the rate of 1-2 mmol/L/hr for 1st 3-4 hrs or until the seizure subsides

Rapid correction may cause myelinolysis,producing permanent structural & funtional damage to mid brain structures

Rx of Hyponatraemia

Na correction in asymptomatic pt should not be raised 0.5mmol/L/hr (10-12mmol/L/day) or even slower

Total Na deficit can be calculated as following formula= (Deficit)x0.6x Wt in Kg

During correction the normal daily requirement should be in mind

Hyponatraemia should be treated according to its type

Contd.

For Hypovolaemic Pt>>>controlling the source of Na loss &administering of Na supplement either orally or by I/V as warrented

Pt with Dilutional Hyponatraemia (Euvolemic) usually respond to fluid restriction 600-1000ml/day,accompanied where possible withdrawl of possible stimulus

If an inadequate response in Na rise >>Rx with Demeclocycline (600-900mg/day), enhance water excretion by interferring with ADH response in collecting duct

Oral Urea (30-45gm/day) or vasopressin receptor antagonist (Tolvaptan) may be alternative

Contd.

Hypervolaemic pt need optimal Rx of underlying condition , accompanying the cautious use of diuretics , in conjunction with fluid restriction;

K sparing diuretics are particularly useful in this context , as there is significant hyperaldosteronism

Contd.

Plasma Na>148mmol/L Presents with reduced cerebral function either

as a primary problem or as a consequence of the hypernatraemia itself , which results in dehydration of cerebral neurons & brain shrinkage>>> in presence of intact thirst mechanism & preserved capacity to obtain & ingest water , hypernatraemia may not progress very far

If adequate water is not obtained>>>dizziness>> confusion,weakness>>coma>>death

Hypernatraemia

Hypovolemic (sodium deficit with relatively greater water deficit)

Renal Na losses Diuretic Rx (specially osmotic diureticor

loop diuretic during water restriction) Glycosuria (HONK) Gastrointestinal Na losses Colonic diarrhoea Skin Na losses Excessive sweating

Causes of Hypernatraemia

Euvolaemic (water deficit alone) Diabetes insipidus (central or

nephrogenic)

Hypervolaemic (sodium retention with relatively less water retention)

Enteral or parenteral feeding I.V or oral salt administration CRF (during water restriction)

Rx depends on rate of development & underlying cause

If develop rapidly ,cerebral shrinkage may be acute >>>relatively rapid correction with appropriate volumes of IVF (5%DA or 0.45% NS) may be attempted

In older, institutionalized pts are more likely to be developed slowly >>so reduction of plasma Na should be cautious & slowly (to avoid the cerebral cerebral edema)

Where possible the underlying cause should be addressed

Rx of Hypernatraemia

Mild Hypokalaemia (3.0-3.5) is usually asymptomatic More severe fall of K leads to development of

muscular weakness & tiredness Cardiac effects include ventricular ectopics or more

serious arrhythmias & potentiaton of adverse effects of various drugs particularly Digoxin

Typical ECG affects the T wave,sometimes U wave

Functional bowel obstruction due to paralytic ileus Long standing hypokalaemia damages renal tubular

structures(hypokalaemic nephropathy)>>>Nephrogenic DI>>>resulting polyuria & polydipsia

Hypokalaemia

Hypokalaemia ?Redistribution into cells- <Alkalosis <Insulin excess <Catacholamine beta2 agonist <Hypokalaemic periodic paralysis Reduced K intake (dietary /IV therapy)

Excessive K losses ↓ ↓

Urine k Urine K <20-30 >20-30mmol/d mmol/d

Renal Gastrointestinal

Contd.

With HTN With normal- low BP

Hyperaldosteronism-1⁰(Conn’s Synd.),2⁰(with renal ischemia)

With Alkalosis Diuretic Rx(loop & thiazide) Bartter’s & Gitelman’s Synd.

Other forms of mineralocorticoid receptor activation- Cushing’s Synd./ectopic ACTH Corticosteroid Rx Apparent mineralocorticoid excess with Liquorice/carbenoxolone Rx

With Acidosis Renal tubular acidosis(type 1 &2) Carbonic anhydrase inhibitor Rx

Liddle’s Synd. With Variable Pᵸ Post obstructive diuresis Recovery after acute tubular necrosis Mg depletion

Renal

With Alkalosis With Acidosis

VomitingNasogastric aspiration

DiarrhoeaLaxative abuseVillous adenoma of rectumBowel obstruction/fistulaUreterosigmoidostomy

Gastrointestinal↓↓

A decrement of 1mmol/L in plasma k conc. (4.0 to 3.0 mmol/L) may represent total body K deficit 200-400 mmol & pt with Plasma level <3.0mmol/L require in excess of 600mmol of K to correct the deficit

Pts with severe Hypokalaemia <2.5mmol/L &/with dangerous symptoms & those who unable to taking anything by mouth, require IV replacement Rx with KCl

The maximum conc.of administered K should be no more than 40 mmol/L via peripheral line or 60mmol/L via a central venous line

Mx of Hypokalaemia

The rate of infusion should not exceed 20mmol/hr unless paralysis or malignant ventricular arrhythmia present

Ideally KCl should be mixed with Normal Saline or with 5% manitol solution

K>2.5 mmol/L >>>oral correction can be done,either with dietary(fruits juice,dub water), tablet or syrup (mixed with fruits juice, in full stomach)

Not more than 80-120 mmol/day should be corrected

Underlying treatable cause should be corrected

Contd.

If Hypokalaemia being associated with systemic acidosis (RTA),alkaline salts of K such as KHCO3 can be given

If Mg depletion is also present,replacement of Mg may be necessary to allow correction of K

Use of K sparing diuretics such as amiloride can assist the correction of hypokalemia,hypomagnesemia &metabolic alkalosis specially when these are due to loop or thiazide diuretic

Hypokalemic periodic paralysis treated with Acetazolamide

Contd.

A Ca channel disorder of muscle Common in Adolescence age group;male

predominant Episodic weakness with onset after the age

of 25 is almost never due to familial periodic paralysis (with exception of Thyrotoxic Periodic Paralysis)

Provoked by meals high in CHO or Na & may accompany rest following prolonged excersise

Hypokalaemic Periodic Paralysis

Weakness more in proximal muscle group than distal Ocular & bulbar muscles are less likely to be effected Respiratory muscles are usually spared,if involved it

is very fatal Weakness may take as long as 24 hrs to resolve Life threating Cardiac arrhythmia may occur;late

complication >>severe disabling proximal lower extremities weakness

Attack of Thyrotoxic Periodic Paralysis resembles primary hypokalaemic periodic paralysis---more in female, attacks abate Rx of underlying Thyroid condition

Contd.

Supplementation (oral/IV) Diet-low CHO,low salt No vigorous exercise Drug- acetazolamide (125-1000mg/day) Sometimes Triamterene/spirolactone

may be added

Rx of Periodic Hypokalaemic Paralysis

Significant Hyperkalaemia can be very dangerous , because of the risk of cardiac arrest caused by the marked slowing of the action potential conduction in the presence of K levels>7mmol/L

Presents with progressive muscular weakness , sometimes there’s no symptoms until cardiac arrest occurs

Hyperkalaemia

Typical ECG changes are tall,peaked T (early change) &widening of the QRS complex(presages a dangerous cardiac arrhythmia)

In all conditions of aldosterone deficiency or aldosterone resistance hyperkalaemia may be associated with acid retention,giving rise to RTA(distal-type 4)

Contd.

Hyperkalaemia ↓↓-----?Spurious(in vitro

hemolysis,very high WBC or Platelet count) ↓↓ ?Redistribution out of

cells(Acidosis,Insulin deficiency,Beta blockers,Hyperkalaemic periodic paralysis,Severe hyperglycemia)

↓↓ ?↑K intake(exogenous-

diet,IVF;endogenous-hemolysis,rhabdomyolysis) ↓↓

Renal retention of K plasma creatinine Plasma creatinine >500micromol/L <500micromol/L ↓↓ ↓↓ Renal Failure Tubular secretory Failure

Contd.

Renal Failure Tubular Secretory Failure

ARF(severe)-

Specially with acidosis/hemolysis/rhabdomyolysis

With Low Aldosterone-

Adrenocortical failure(Addison’s Disease)Adrenal enzyme defectsHyporeninaemic hypoaldosteronismDrugs(NSAIDs,ACEI,BBs,Ciclosporin ,prolonged Heparin Rx)

CRF(advanced)-

Specially with oliguria/K load

With Normal—High Aldosterone- Tubular transport defects(Pseudohypoaldosteronism)Tubulointerstitial Disease(SLE,Renal transplant,Amylodosis ,Obstruction/Infection)Drugs(amiloride,spironolactone)

Rx depends on severity & the rate of development

In the absence of neuromuscular symptoms or ECG changes,reduction of K intake & correction of underlying abnormalities may be sufficient

In acute &/or severe hyperkalaemia (plasma K>6.5-7.0mmol/L) more urgent measures must be taken

Mx of Hyperkalaemia

Mechanism Therapy

Stabilise cell membrane potential IV calcium gluconate(10 mlof 10% solution)

Shift K into cells Inhaled beta-2 agonist,e.g.salbutamol, IV glucose(50 ml of 50% solution) &Insulin (5u Actrapid)Intravenous NaHCO3

Remove K from body IV frusemide & normal salineIon exchange resin(e.g resonium) orally or rectallyDialysis

Rx of sever hyperkalaemia

Na channel disorder AD Pts are often normokalaemic during attack;the fact that

the attacks are precipitated by K administration best defines the disease

Onset is in 1st decade Attacks are brief,mild,30mints-4 hrs Weakness affects proximal muscle sparing bulbar

muscle Attacks precipitated by rest following exercise,& fasting A variant of myotonia without weakness Rx----Acetazolamide

Hyperkalaemic Periodic Paralysis

A Plasma conc.<the normal range (0.75-1.0mmol/L) is usually the reflection of the condition

Hypomagnesaemia is frequently associated with hypocalcaemia(probably because Mg is required for the normal secretion of PTH in response to a fall Serum Ca & because hypomagnesaemia induces resistance to PTH in bone)

Hypomagnesaemia

C/F of hypomagnesaemia resembles that of hypocalcaemia

There may be ---tetany , cardiac arrhythmia(notably Torsades de Pointes),CNS excitation & seizure as well as vasoconstriction & HTN

Mg depletion is also associated with hyponatraemia & hypokalaemia

Mechanism Examples

Inadequate intake Starvation,malnutrition (alcoholism),parenteral alimentation

Excessive losses

GIT

Urinary

Prolonged vomiting/N-G aspiration,chronic diarrhoea/laxative abuse,malabsorption,small bowel bypass surgery,fistulaDiuretic Rx(loop,thiazide),alcohol,tubulotoxic drugs(gentamicin,cisplatin),volume expansion(e.g.primary hyperaldosteronism),DKA,post obstructive diuresis,recovery from ATN Bartter’s & Gitelmen’s synd.,primary renal Mg wasting

Miscellaneous Acute pancreatitis,foscarnet Tx, hungry bone synd.,DM

Aetiology of Mg Depletion

Rx involves>>> identification & correction of underlying cause where possible

Oral Mg salt has little effect as poorly absorbed & may cause diarrhoea

When symptoms present----Rx with IV MgCl2 at a rate not exceeding 0.5mmol/kg in the first 24 hrs (if IV access not feasible,MgSO4 can be given I/M

If Mg depletion due to diuretic Rx,adjunctive use of K sparing agent will reduce Mg loss into urine

Rx of Hypomagnesaemia

Phosphate may redistribute into cells during periods of increased energy utilization(as in refeeding after a period of starvation) & during systemic alkalosis

P04 depletion reflects the widespread involment of tissue metabolism

Defects appear in the>>>a. blood as impaired function & survivality of all cell lines

>>>b.Skeletal muscle(weakness, respiratory failure)

>>>c. Cardiac muscle(CCF) >>>d.Smooth muscle(ileus) >>>e. CNS(decreased

consciousness,seizure & coma) >>>f. Bone(osteomalacia)

Hypophosphataemia

Mechanism Examples

Redistribution into cells Refeeding after starvation,respiratory alkalosis,Rx for DKA

Inadequate intake or absorption Malnutrition,malabsorption,chronic diarrhoea,PO4 binders(antacids),Vit D deficiency or resistance

Increased renal excretion Hyperparathyroidism,ECF vol expansion with diuresis,osmotic diuresis,proximal tubular transport defect(Fanconi’s syndrome),familial hypophosphataemic rickets,cancer indced hypophosphataemia

Causes of Hypophosphaetaemia

Oral PO4 supplementation And high protein/high dairy dietary

supplements (rich in naturally occurring PO4 IV Rx with Na or K phosphate salts can be

used in critical condition ( there is risk of precipitating hypocalcaemia & metastatic calcification)

Rx of Hypophosphataemia

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