DR. SUDHANSHU KOTHADIA

WATER & ELECTROLYTE

IMBALANCE

NORMAL WATER BALANCE

Total Body Water in 65 kg man

Intracellular Fluid Extracellular Fluid

(28L) (12L)

60-75% 25-40%

Plasma Water Interstitial Fluid

(3L) (9L)

1:3 Ratio

HYPOVOLEMIA

It is defined as a state of combined salt and water depletion exceeding intake leading to volume contraction.

Etiology :- I- ECF Volume Contracted

A) Extrarenal Na Loss

1) Gastrointestinal- Vomiting

Nasogastric Suction

Drainage

Fistula

Dairrhea

2) Skin/Respiratory- Insensible Loss Sweat Burns3) Hemorrhage

B) Renal Na and Water Loss 1) Diuretic 2) Osmotic Diuresis 3) Hypoaldosteronism 4) Salt and Water imbalance

C) Renal Water Loss

II) ECF Volume Normal or ExpandedA) Decreased Cardiac output1) Myocardial ,Valvular or Pericardial

diseaseB) Redistribution 1) Hypoalbunaemia - Hepatic Cirrhosis - Nephrotic Syndrome 2) Capillary Leak - Acute Pancreatitis - Ischemic Bowel - RhabdomyolysisC) Increased Venous Capicitance - Sepsis

PATHOPHYSIOLOGY

Cardiac Output Hypotension Stimulates barroreceptors in Carotid Sinus &

aortic arch

Stimulates Renin Angiotensin system

Na Reabsorption from tubule & GFR

Stimulation Of Angiotensin II

CLINICAL FEATURES

Symptoms - vomitting diarrhea polyurea abdominal and chest pain weakness muscle cramps thirst confusion

Signs - Cyanosis Oligourea Diminished Skin Turger Dry Oral mucus Membrane Decreased JVP Postural hypotension Postural tachycardia Cold and Clammy Extrimities Postural Disturbances

LAB DIAGNOSIS

1) Na Concentration - normal, or 2) Blood urea decreased is severe

depletion 3) Urinary sodium – a) In

Renal/Adrenal Causes › 20

mEq/L b) In

extrarenal Causes ‹ 10

mEq/L

TREATMENT

1) Mild Volume Contraction - Oral Route 2) Severe Hypovolemia a) Normonartemic or mild hyponatremic - Isotonic or normal saline (0.9%NaCl or

154 mmol/L Na)

b) Severe Hyponatremia - Hypertonic Saline(3%NaCl or 531

mmol/L) c) Hypernatremic - 0.5 Normal saline or 5% Dextrose (0.45%NaCl or 77 mmol/L Na)3) Patient With Haemorhage Or Anaemia – B.T

NORMAL Na BALANCE

Na is actively pumped out by Na-K- ATpase

Total Body Na

ECF ICF

(85-90%) (10-15%)

HYPONATREAMIA

It is defined as when serum Na is less than 135mEq/L

CAUSESI)PSUDOHYPONATREAMIAA)Normal plasma osmalality 1)Hyperlipidemia 2)Hyperproteinemia 3)Posttransurethral resection of prostate

or bladder tumorB)Increased plasma osmalality 1)Hyperglycemia 2)Mannitol

II) HYPOOSMOLAL HYPONATREMIA A)Primary Na loss(secondary water gain) 1)Intugumentary loss:sweating,burns 2)GI loss:vomitting,fistula,diarrhea 3)Renal loss:diuretics,osmotic diuretics, hypoaldosteronism, tubular necrosis B)Primary water gain(secondory Na loss) 1)Primary polydypsia 2)Decreased solute intake 3)AVP released due to pain,nausea,drugs 4)Syndrme of inappropriate secretion 5)Glucocorticoid deficiency 6)Hypothyroidism 7)Chronic renal insuficiency

PATHOPHYSIOLOGY

It is due to either retention of water or loss of Na Mechanism

Excessive ingestion SIADH

Of water

excretion of water slow urine flow

due to Kidney failure in kidney failure

CLINICAL FEATURES

Symptoms mainly depends on severity and rapidity of hyponatremia

1)Headache 2)Lythargy 3)Confusion 4)Stupor 5)Siezures 6)Coma-generaly if Na falls below

120mEq/L acutely

DIAGNOSISI)Plasma osmalality a)In primary hyponatreamia-decreased (If not decreased rule out psudohyponatremia)II)Urine osmalality a)Primary polydypsia -urine osmalality less than 100mmol/Kg -specific gravity less than 1.003 (If not then suspect impaired free water exceation)III)Urinary Na concentration-if more than 20mmol/L -a)salt wasting nephropathy b)diuretic therapy c)hypoaldosteronism d)occasionaly vomittingIV) Urinary K Low

For SIDAH – hyposmotic hyponatremia - urinary Na › 40 mmol/L

TREATMENT

A) Main Points we have to remember dur ing T/t 1) Rapid correction leads to vascular

overload & brain shrinkage 2) Rate of correction should be around 0.6

MEq/L 3) It requires either addition of Na or

removal of water or 4) when slow correction of hyponatremia in

volume expanded subject is desired,best to restrict fluids- if not possible then use Loop Diuretics

B) Hypertonic Saline a) For Symptomatic – 3%

hypertonic saline b) For chronic – rate should not

exceed 0.5 mEq/L c) For A.C. – 1-2 mEq/L d) Na level check after 2,3,6 hrsC) Vasopressin V₂ receptor Antagonist a) Tolvaptan – orally useful in

chronic hyponatremia b) S/E - urine flow,thirst and dry

mouth

HYPERNATREMIA

An elevation in the serum Na concentration above 145 mEq/L is Hypernatremia.

CAUSES - 1) Decreased Intake –

coma,depression,inability to swallow

2) Loss From Skin – fever,hyperthyroidism,hot environment

3) Respiratory Loss – Hyperventilation

4) Loss In Urine – Diabetes Insipidus,medullary

cystic disease

PATHOPHYSIIOLOGYHypernatremia is much less common than Hyponatremia because even a

small increase in the serum Na concn.is a potent stimulus to thirst.

Elevated Na conc.develops only in those patients who are unable to experience thirst or are unable to gain access to water.

EFFECTS OF HYPERNATREMIA ON BRAIN :

Within minutes after the development of hypertonicity,brain cells loss water causing shrinkage of the brain and an incerase in osmorality.

Rapid adaptation occurs within a few hours as elecrolyte enter the brain cells causing partial increase in brain volume.

Over several days,the brain volume becomes normal due to intracellular accumulation of organic compounds.

Slow correction of the hypertonic state does not induce cerebral oedema as the accumulated solutes are gradually shifted out of the brain cells.

In contrast,rapid correction may result in cerebral oedema as brain uptakes water from the relatively hypotonic extracellular fluid.

CLINICAL FEATURES

1) Altered mental state2) Weakness3) Neuromuscular irritability4) Focal neurological deficit5) Occasionally coma and seizures6) Exessive sweating7) Diarrhoea8) Osmotic diuresis9) Polyurea and thirst

Morality rate associated with Na conc › 180 mmol/L

LAB DIAGNOSIS

1) Haematocrit usually ›50%2) Blood urea levels3) Plasma Na4) Urine specific gravity ›1.010

Water deficit – plasma Na conc – 140

140

Total Body Water

MANANGMENT

In patients with gradual onset of depletion of water over more than 2 days,correction should be done slowly as rapid lowering of Na produces shift of water from ECF into brain cells.The rate of correction should not exceed 0.7 mEq/L/hr

When hypernatremia is associated with hypotension due to volume depletion,the initial solution should be isotonic saline so as to increase the ECF volume.However,if neurological features are also present,therapy should be started with N/2 saline.

As a rough guide,the box on next slide shows the requirment of fluids in 65-kg person.

Severity Fluid and route Quantity

of administration & time for

replacmnt

1) Mild depletion water by mouth or 5% glucose IV 2L,over 6-12 hrs

(1-2 L deficit)

2) Moderate 5% glucose IV 2-4L,over 24hrs

(2-4 L deficit)

3) Severe 0.9% NaCl IV 1 L,over 1 hour

(4-10 L deficit) 5% Dextrose IV 3 L,over 2 hours

5% Dextrose IV 4 L,ovr 24-48 hrs

Relief of thirst,urine output more than 1500 mL/24 hrs and normal plasma Na levels indicate adequate correction.

NORMAL POTTASIUM BALANCE

Normal K⁺ - 3.5 – 5 mmol/L

Almost 98% of it is present in ICF.

Abundent in meat,oranges,lemon,grapes,bananas

and dry fruits.

PHYSIOLOGY

1) Mainly intracellular cation & maintained by Na-K stimulated ATP ase system.

2) Greatly influences neuromuscular function as latter depends upon ratio of ICF: ECF

3) For loss or gain of 100-200 mEq, the plasma K reduces or increases by 1 mEq/L

4) Renal Excretion mainly by secretion at the levels of collecting ducts.

HYPOKALEMIAIt is defined as plasma K⁺ conc. ‹ 3.5 mmol/L CAUSES – 1) Decreased Intake

a) starvation

b) clay ingestion

2) Redistribution Into Cells

a) Acid Base

1) Metabolic alkalosis

b) Hormonal

1) Insulin

2) β₂ Adrenergic agonists

3) α Adrenergic antagonists

c) Anabolic State

1) Vitamin B₁₂ or Folic Acid

2) Granulocyte-macrophase colony stimulating factor

3) Total parental nutrition

d) Other

1) Psuedohypokalemia

2) Hypothermia

3) Hypokalemic Periodic Paralysis

4) Barium Toxicity

3) Increased Loss

A) Nonrenal

1) Gastrointestinal loss(diarrhea)

2) Integumentary Loss(Sweat)

B) Renal

1) Increased distal flow : diuretics,osmotic diuresis

2) Increased secreation of pottasium

a) minaralocorticoid excess:primary & secondary hyperaldosteronism,renin-screting tumors,renal artery stenosis

b) Distal delivery of non-reabsorbed anions : vomitting,nasogastric suction,diabetic ketoacidosis

c) Other : amphotericin B,hypomagnesemia

CLINICAL FEATURES

1) Generalised muscle weakness & depression of tendon reflexes

2) Paraesthesiae,apathy,confusion & coma3) Paralytic ileus4) Rhabdomyolysis 5) ECG changes of hypokalemia include flattening

& inversion of T waves,satgging of the ST segment,and appearance of U wave

6) Atrial & ventricular arrythmias may occur,especially in patients receiving digitalis

7) Death may occur due to respiratory paralysis or cardiac arrest

MANAGEMENT1) T/t must be directed at correcting hypokalemia & eliminating

the cause of K loss.K supplimentation can be given orally or IV in the form of KCL.2) Patients with mild hypokalemia with K bet. 3-3.5 mEq/L are

usually asymptomatic & don’t need urgent treatment.these patients should be advised to take a diet rich in potassium.

3) Patients with mild hypokalemia with K bet. 2.5-3 mEq/L should receive oral pottasium in a dose of 60-80 mEq/day in divided doses(20 mL of KCL oral solution contains 15 mEq of K)

4) If patient cant tolerate oral pottasium or GI losses are massive,IV K supplimentation is required.patients with symptomatic moderate or severe hypokalemia with K below 2.5 require IV K.

5) Isotonic saline (500 mL) containing 20 mEq of K(as chloride) should be given over 2-3 hrs.Repeted measurments of plasma K are necessary to determine whether further KCL is required.It is also preferable to monitor the patient using cardiac monitor.

HYPERKALEMIAHyperkalemia is defined as a plasma K⁺ conc. › 5 mmol/L.

CAUSES :

1) Renal Failure2) Decreased distal flow(i.e;decreased effective circulating

arterial volume3) Decreased K⁺ secretion A) Impaired Na⁺ reabsorption a) primary hypoaldosteronism : adrenal

insufficiency,adrenal enzyme deficiency b) Secondary hypoaldosteronism :

hyponatremia,drugs(NSAIDs,heparin,ACE inhibitors c) Resistance to aldosterone : pseudohypoaldosteronism B) Enhanced Cl⁻ reabsorption(chloride shunt) a) Gordon syndrome b) Cyclosporine

CLINICAL FEATURES

1) The common clinical features include cardiac arrythmias,muscular weakness progressing to flaccid paralysis & respiratory embarrassment.

2) ECG manifistations : a) Tall,peaked T waves b) Prolongation of PR interval c) Reduced height of P waves d) Prolongation of QRS complex e) ‘Sine wave’ pattern3) Terminally ventricular fibrillation and

standstill may occur.

MANAGEMENT

1) Identification and elimination of underlying cause.2) When there are marked ECG changes,10 mL of 10% calcium

gluconate solution is given IV slowly over 2-5 min. It stabilises the myocardial cells.

3) IV administration of glucose along with insulin encourages shift of pottasium from extracellular compartment to intracellular compartment.

a) 50 mL of 50% glucose plus 10 units of soluble insulin(plain) may be given IV as a bolus.

b) Alternatively,500 mL of 20% glucose plus 10 units of soluble insulin may be given as an infusion over 6-12 hrs.

4) IV administration of 50-100 mL of 8.4% sodium bicarbonate is useful in renal failure patients with hyperkalemia & acidosis.

5) Nebulisation of β-agonists also can reduce pottasium levels by producing shift of pottasium to intracellular compartment.Dose of salbutamol is 10-20 mg over 10 min & can be repeted every 2-6 hrs.

6) Cation exchange resins such as sodium polystyrene sulphonate are helpful in the removal of K⁺. The resins can be given orally or as enema.

7) If these measures fails then haemodialysis is done.

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