FLUIDS AND ELECTROLYTES

Done by : Ahmad Jarrar Nour Al Khasieb

Supervised by : Dr . Raed Ennab.

ONE : Normal fluid and electrolytes balance in the body

FACTORS INFLUENCE TBW

1) AGE , more in infants , y ? 22) Gender3) Body weight , Fatty vs musculature 4) Temperature , every 1 c rise extra loss of 200

ml / day 5) Operation & Trauma , due to increased

aldosterone & ADH secretions in neuroendocrine response >> which will conserve water >> fluid collection in the third space .

Daily requirements:

• Water : 30-35 ml/kg

Electrolytes functions include: helping to maintain homeostasis, acid-base balance and water distribution, metabolic functions, cardiac and nerve conduction.,

• K : 1 mEq/kg

• Cl : 1.5 mEq/kg

• Na : 1-2mEq/kg.

(Hypovolemia)

Definition

Causes

Stages

HYPOVOLEMIA

Hypotonic fluid loss from extracellular space that results in decreased tissue perfusion

o Bleeding (trauma, GI, etc.)o Vomiting, diarrheao Neurogenic shocko Excessive fluid loss or third space fluid shift

Definition Causes

STAGES

Class IV Class III Class II Class I

>2000 1500-2000 750-1000 Up to 750 Blood loss ml

>40% 30-40% 15-30% Up to 10% Blood loss %BV

>140 >120 >100 <100 HR

Decreased Decreased Normal Normal BP

>35 30-40 20-30 14-20 RR

Negligible 5-15 20-30 >30 UO

Confused and

lethargic

Anxious and confused

Mild anxious Slightly anxious

CNS/mental status

AIM OF VOLUME RESUSCITATION

•Early, complete restoration of tissue oxygenation

•Minimal biochemical disturbance •Preservation of renal function

•Avoidance of transfusion complications

THREE : TYPES OF IV SOLUTIONS

1- Crystalloid

2- Colloid

3- Blood*

FLUID OF CHOICES

Fluid resembling ECF Rapid volume expansion of IVS Sustained expansion No sugar

CRYSTALLOIDS Lower cost Low molecular weight EC expander >> Replaces interstitial

fluid Greater urinary flow Transient haemodynamic improvement

(20 – 30 min) >> Large volume resuscitation needed (3-4:1)

S/E: 1) Peripheral oedema2) Pulmonary oedema

CRYSTALLOID

COLLOIDS Greater cost higher molecular weight IV expander . Smaller volume (1:1) Osmotic diuresis Longer duration of persistence (2 – 8 hours) S/E: 1) Less cerebral oedema2) Coagulopathy3) Pulm oedema (cap. leak state)4) GFR (hyperoncotic kidney failure syndrome) 5) Allergic risk (gelatin > dextran >

albumin>HES)

COLLOID (NO CAPILLARY LEAKAGE)

Colloids

CRYSTALLOIDS

Divided into: 1- Isotonic solutions

ex: 0.9% Normal saline, Ringer Lactate

2- Hypotonic solutionsex: 5% dextrose , .25% NS, .45% NS, 4%glucose + .18% NS

3- Hypertonic solutions (1.8 – 7.5% NaCl)

COMPONENTS

CrystalloidsNa+

mmol/LK+

mmol/LCa++

mmol/LCl-

mmol/LHCO3-

mmol/LpH Osmolarity

(mosmol/L)

Hartmann’s(Ringer’s lactate)

131 5 4 112 29 6.5 281

0.9% sodium chloride(Normal saline)

154 0 0 154 0 5.5 300

4% glucose +0.18 NaCl

31 0 0 31 0 4.5 284

5% Glucose(5% dextrose in water; D5W)

0 0 0 0 0 4.1 278

0.9% NORMAL SALINE If you need to restore the IV deficit using only

0.9NS, you need to give 3-4 times more than the deficit itself

Used as first line in resuscitation in ER

Used for electrolytes replacement (even from GI losses)

Could cause hyperchloremic metabolic acidosis 0.9% NaCl is preferred in the presence of

hyperkalemia, hypercalcemia, hyponatremia, hypochloremia, or metabolic alkalosis.

RINGER LACTATE (HARTMANN’S)

Same osmolality as ECF restore ECF volume For fluid resuscitation , but not for maintenance

May reduce iatrogenic hyperchloremic Metabolic acidosis associated with other higher chloride containing solutions .

Used in losses rich in bicarbonate as , biliary , small bowel , and pancreatic

Limited usage in the cases of hyperkalemia and citrated blood, because of the K+ and Ca+2 components in the ringer lactate

It contain lactate that’s converted to bicarbonate in the liver , so avoided in pat with liver injury

5% DEXTROSE WATER

Hypotonic, after metabolism of Glucose only water remains and distribute to all body

Less than 10% remains IV no role for expansion

Treat dehydration from water loss

Excessive use hyponatremia

HYPERTONIC SALINE

High osmolality (2400 mOsmol/L) rise ECF osmolality

shift of fluid from ICF ECF, more expansion

Practical dose: 200mls 7.5% NaCl in 10 min Small Volume Resuscitation Reduced cerebral edema CI: dehydration, oliguric renal failure,

cardiogenic shock, DKA, coagulopathies or active hemorrhage

A randomized, double-blinded study of a 250-mL dose of hypertonic saline (7.5% NaCl, 6% dextran-70) compared to placebo (0.9% NaCl) given to patients in hemorrhagic shock after sustaining blunt trauma showed that the patients receiving the hypertonic saline bolus had significant blunting of neutrophil activation and alteration of the pattern of monocyte activation and cytokine secretionThis immunomodulatory effect of hypertonic saline plus dextran may help to prevent widespread tissue damage and multiorgan dysfunction seen after traumatic injury

HYPERTONIC SALINE

COLLOIDS

Derived from: 1- Gelatin (Haemaccel, Gelofusine) 2- dextrane 3- starch 4-Protein (albumin)

GELATINS

Short acting

No limit on total volume that can be administered (if Hb is maintained)

minimal effect on coagulation

Anaphylaxis could occur histamine release bronchospasm + urticarial + hypotension + tachycardia

DEXTRANS

Good duration of effect

Limited usage, 20ml/kg for the 1st 24 hours, then 10 ml/kg for the next 5 days only

Allergy risk

Significant coagulation effect (Associated with anti-coagulation, so it could be used in vascular surgeries to prevent thrombosis)

May interfere with cross-match

Dextran 40 can cause osmotic renal damage

HYDROXYETHYL STARCH (HES)

Limited usage (not like Gelatins) to 30-50 ml/kg

S/E: anaphylaxis, decrease Hb, bleeding (disturbance in coagulation), itching after usage

HUMAN ALBUMIN SOLUTION (HAS)

2 forms

1- 4.5% solution treat hypovolemia

2- 20% (salt-poor) solution treat hypoalbumenimia

SAFE (Saline versus Albumin Fluid Evaluation) study

found no significant difference in outcomes, including mortality and organ failure, between the two groups

FOUR : HOW SURGERY AFFECT FLUID AND ELECTROLYTES

BALANCE??

1) Fasting.2) Stimulating secretion of stress hormone

( ADH, aldosterone , Cortisol )3) Causing fluid and electrolytes loss from GIT(

laxative, IO, adynamic ileus , high output fistula , diarrhea)

4) Increase insensible loss5) Third spacing 6) Surgical drains7) Patient’s medication

PERIOPERATIVE FLUID REQUIREMENT .

1) Maintenance .2) NPO 3) Third space losses. 4) Replacement of blood loss5) Special additional losses .

1 )MAINTENANCE FLUID : Simply : 100-50-20 rule Or: “ 4-2-1 rule” >>

4ml/kg/hr for the 1st 10kg of TBW .2ml/kg/hr for the 2nd 10kg of TBW.1ml/kg/hr for the subsequent kg of TBW . * consider extra losses for fever , tracheotomy , denuded surfaces

ELECTROLYTES : Na: (1-2mEq/Kg/day)K: ( 0.5-1 mEq/Kg/day)

2 )NPO- NPO deficit = number of hours of NPO x

maintenance fluid requirment .

3 ) THIRD SPACE LOSSES loss phase, increased capillary permeability leads

to a loss of proteins and fluids from the intravascular space to the interstitial space. This phase lasts 24 to 72 hours after the initial insult that led to the increased capillary permeability (for example, surgery, trauma, burns, or sepsis). Signs and symptoms include weight gain, decreased urinary output, and signs of hypovolemia, such as tachycardia and hypotension.

reabsorption phase, tissues begin to heal and fluid is transported back into the intravascular space. Around POD#3 .Signs of hypovolemia resolve, urine output increases, the patient's weight stabilizes, and signs of shock (if any) begin to reverse.

REPLACE 3RD SPACE LOSSES BY RINGER LACTATE ( SAME COMPOSITION FOR ECF)

Superficial surgical trauma 1-2 ml/kg/h

Minimal surgical trauma 3-4 ml/kg/hhead and neck, hernia, knee repair

Moderate surgical trauma 5-6 ml/kg/hhysterectomy , chest surgery

Severe surgical trauma 8-10 ml/kg/hAAA repair, Nephrectomy

4 )BLOOD LOSS

Replace 3cc of crystalloid solution per cc of blood loos ( bcz as we said crystalloid leaves rapidly )

When using blood products or colloids replace blood loss volume per volume

5) ADDITIONAL LOSS Bowel prep needs up to 1L . NGT , Stoma output …. Measurable Replace volume per volume with crystalloids

BUT HOW TO GIVE THE FLUID? A 70kg Patient went into a 5 hours elective

surgery, he was dynamically stable, he was NPO for 9 hours prior to surgery …..

Maintenance : given hourly Deficit : ½ in the first hour , the other ½

distributed equally to the rest .

ANSWER

Maintenance : Using the rule of 4-2-1 , (4*10) + (2*10) + (1*50) = 110 ml/h (must given every hour in the operation)

Deficit : NPO for 9 hours, so maintenance amount was deficit in the past 9 hours 110*9 = 990 ml.

FLUID REPLACEMENT IN CASES OF RESUSCITATION NOT INTRAOPERATIVE

1. Insert 2 large pour and short cannula , non dominant hand , most distally , not over a joint .

2. Start 1st NS bolus ( 1L/20min) and reassess then if not responding give 2nd one , if not responding start blood

CLINICAL ASSESSMENT The actual end point of fluid therapy is to optimize

tissue perfusion

1) Vital signs normal: specially the BP and HR 2) Urine out-put: at least 0.5 -1 ml/kg/h in adults (in children

more)

3) (ABGs )Metabolic acidosis hypoperfusion and hypovolemia4) Increase hematocrit, urea, nitrogen dehydration 5) Weights

6) Level of consciousness (changes in mental status)

7) Physically: no dryness in mucus membranes and no persistent thirst

8) Hemodynamic monitoring by CVP , normally is 2-8 mmhg

MONITORING

Central Venous Pressure (CVP), invasive monitoring normally 2-5 mmHg

Fluid challenge add 250 ml of fluid given rapidly to make change in CVP

In hypovolemia slight increase then rapid decrease

In adequate small sustained raise In over hydration high sustained raise

IMPORTANT NOTES

Priority is arrest of hemorrhage

Treatment with IV fluids before hemorrhage was controlled increased the mortality rate, especially if the BP was elevated.. Why ??

The optimal volume of IV fluid administered is a balance between improving tissue oxygen delivery against increasing the blood loss by raising SBP

OVER CORRECTION >> HYPERVOLEMIA VS WATER INTOXICATION

Hypervolemia : Excess isotonic fluid in extracellular spaces due to an increase in total body sodium content Can lead to heart failure and pulmonary edema, especially in prolonged or severe hypervolemia or In patients with poor heart function. Treatment diuretics and restriction of the intake of water, fluids, sodium, and salt.

Water intoxication : Excess fluid in the intracellular space from the extracellular space Causes increased intracranial pressure may lead to seizures and coma. Diuretics & Vasopressin receptor antagonists

Common Electrolyte Disorders

Nour Al-khasieb

effective osmoles

• extracellular fluid (e.g., Na+, glucose, mannitol, glycine)

• or intracellular fluid (e.g., K+, amino acids, organic acids)

• 1 mole = atomic wt in grams• 1 mmole = atomic weight in mg• mEq = (mg X valence)/atomic weight• mg= (mEq X atomic weight)/valence

Sodium

Sodium Balance- 44% in ECF- 9% in ICF and - 47% stored in bone- Normal Na+ concentration is 135 to 145 mmol/L- plasma osmolality (Posm) - 290 to 310 mOsm/L- normal individual consumes 3 to 5 g of NaCl daily- aldosterone.• Na excretion shutdown in trauma.

Hyponatremia

Hyponatremia • Isotonic hyponatremia 1- isotonic infusion 2- isotonic expansion• Hypertonic hyponatremia 1- hypertonic infusion ( mannitol … ) 2- hyperglycemia ( 100 mg/dl : 1.3 mmol/l)• Hypotonic hyponatremia 1- hypovolemic 2- euvolemic 3- hypervolemic

• Hypovolemic hyponatremia : GI , lungs and skin loss of fluid And Replaced by hypotonic fluid in surgical patient

• Hypervolemic hyponatremia : Liver failure, CHF, Nephrotic syndrome

• Euvolemic hyponatremia : in the setting of trauma or other damage to the brain … SIADH , water intoxication (primary polydipsia , renal failure ) Reset osmostat ( TB , cirrhosis … ) , K loss • Transurethral resection syndrome

Clinical features

• < 120 meq/l • Nausea , vomiting , headache , weakness ,

confusion , seizures and coma .• Dehydration• Volume overload : dependent edema, ascites ,

rales .

Treatment

• restrict the patient to 1-2 L per day of maintenance fluid until diuresis has been established .

• HypoV. - isotonic saline .• hyperV - infusion of hypertonic sodium solution

maybe required . ++ loop diuretic , BNP … - Until 120 mmol/l

• Na+ deficit (mmol) = 0.60 × lean body weight (kg) × [120 - measured serum Na+ (mmol/L)].

• Correct no more than 12 mmol/l in 24h , risk of central pontine demyelination .

• Serum Na should be increased by no more than 0.5 mmol per hour over the first 24 hours

• For acute hyponatremia the serum Na may be corrected more rapidly 1-2 mmol per hour .

Hypernatremia

-ICP

Clinical features

• Thirst • Restless, agitation , Lethargy, seizures . • Weakness , Muscle twitching .• Dry tongue , Thirst Dry skin & mucus

membranes , sunken eyeballs .• Slight puffiness of the face is the only early sign .

• Pitting edema , pulmonary edema and polyuria

Treatment

By administration of water by mouth or IV 5% dextrose .

Water deficit (L) = 0.60 × total body weight (kg) × [(serum Na+ in mmol/L/140) - 1].

- Risk of cerebral edema in rapid correctionCDI – desmopressin acetateNDI - remove drugs , F. restriction , thiazide

Potassium

Potassium Balance

• Serum K is 3.3-4.9 mmol/L• 98% in I.C.F & 2% in ECF• 75% is found in skeletal muscles.• 50 to 100 mmol daily absorbed • Augmented –K- excretion of trauma due to

the effect of increased aldosterone secretion in trauma.

• K vs H

Hypokalemia

Hypokalemia

• Sudden in1-Diabetic ketoacidosis treated with insulin and

glucose2- Acute Alkalosis as an IV injection of HCO3 in

CPR

Hypokalemia

• Gradual- increased GI loss esp. vomiting, diarrhea, NG tube

• Metabolic alkalosis• Mg deficiency• Renal loss : Diuretic, Hyperaldosteronism• Burns • Refeeding syndrome

Clinical features

• < 3 mmol/l • Disturbances in muscular contractility, muscle

weakness, hypotonia, loss of reflexes and slow speech , muscle cramps and pain .

• Paralytic ileus leads to abdominal distension

ECG changes :

1. Hypokalemia potentiates a variety of arrhythmias .

2. Hypokalemia is associated with flat T wave , ST depression , prolonged QT , prominent U wave .

Treatment • Correct volume loss and acid-base disturbances • Oral- fruit, milk, meat and honey• Serum potassium level <4.0 mEq/L: if - Asymptomatic, tolerating enteral nutrition: KCl 40 mEq

per enteral access × 1 dose- Asymptomatic, not tolerating enteral nutrition: KCl 20

mEq IV q2h × 2 doses- Symptomatic: KCl 20 mEq IV q1h × 4 doses Recheck potassium level 2 h after end of infusion; if <3.5

mEq/L and asymptomatic, replace as per above protocol

Hyperkalemia

Hyperkalemia

• Causes:• Over dose “while treating cases of hypokalemia without proper monitioring “• Excessive intake• Crush injuries, Shock• Renal failure• Massive Blood transfusion• Metabolic acidosis• Tourniquet and ß blocking agents• Cell lysis …

Clinical features

• > 6.5 mmol/l• Paresthesia ( early sign ) • Nausea , abdominal cramping , diarrhea • Skeletal muscle weakness which may lead to

flaccid paralysis• Decreased deep tendon reflexes• Bradycardia, irregular pulse, hypotension

( may lead to cardiac arrest )

ECG changes :

1. Hyperkalemia is manifested by peaked T waves, prolongation of the PR segment, reduced P-wave voltage, and prolongation of the QRS complex.

2. When potassium levels reach 8–9 mmol/l, the ECG may resemble a sine wave; further elevation may cause asystole.

Treatment• Mild – loop D. + reduce K • > 6.5 mmol/l• Shift :• 100 ml 20% dextrose +10 units insulin• IV 10% Ca. gluconate • Na₂HCO₃• Inhaled β-agonists • Excretion :• Sodium polystyrene sulfonate (Kayexalate) :an ion-exchange resin

can be given by enema and exchange potassium by sodium or calcium

• Hydration + loop diuretic • Peritoneal or hemodialysis

Calcium

Calcium Balance

2.23 to 2.57 mmol/l99% in bone It is present as : Ionized (45%) - 1.15 to 1.27 mmol/LNon-ionized Bound to proteins

Calcium

Ca balance depends on: - Renal and G.I. function - Vit. D, parathormone, calcitonin - PH changes - Plasma proteins

Calcium

Functions: - Neuromuscular transmission - Blood coagulation - enzyme regulation

Hypocalcaemia

Hypocalcaemia

Causes• Hypoparathyroidism “ after thyroid surgery “ IMP.• Calcium sequestration : acute pancreatitis,

rhabdomyolysis, or rapid administration of blood (citrate acting as a calcium chelator)

• Severe trauma , Crush injuries • Vitamin D deficiency• Malnutrition , Mal-absorption• alkalemia• Drugs : calcitonin and bisphosphonate .

Clinical features

• Peripheral and perioral numbness • Muscle cramps• Carpopedal spasm • Chovstek’s sign • Hyperreflexia , Tetany

Ecg changes :

• Hypocalcemia is manifested by prolongation of the QT interval; the ST segment is usually flat and the T wave is not distorted

• ventricular arrhythmias.

Treatment

• Correction of alkalosis • Symptoms such as overt tetany, laryngeal

spasm, or seizures are indications for parenteral calcium

• IV Calcium as gluconate or chloride may be needed in acute cases . 200mg for tetany

• Oral calcium , Vit-D and often aluminium hydroxide gel to bind phosphate in the intestine in chronic hypoparathyrodism .

Treatment from Schwartz

• Ionized calcium level <4.0 mg/dL:• With gastric access and tolerating enteral

nutrition: Calcium carbonate suspension 1250 mg/5 mL q6h per gastric access;

• recheck ionized calcium level in 3 d• Without gastric access or not tolerating enteral

nutrition: Calcium gluconate 2 g IV over 1 h × 1 dose; recheck ionized calcium

• level in 3 d

Hypercalcaemia

Hypercalcaemia

Causes:

• Malignancy with bony metastases .• Hyperparathyroidism , hyperthyrodism .• Prolonged immobilization .• Excess vit. D intake • Drugs : thiazide .

Clinical features

> 3 mmolFatigue ,anorexia , nausea, vomiting , abdominal

pain , constipation , muscle weakness , renal stones , altered mental status .

parathyroid bone disease and nephrolithiasis

• Hypercalcemia is associated with a short QT interval , arrhythmias.

Treatment

Mild – conservative TT

Sever • IV normal saline + Loop Diuretics• Salmon calcitonin• Pamidronate disodium• Plicamycin

Haemodialysis

Phosphorus

• 0.81 to 1.45 mmol/L• ECF – 1% • 800 to 1,000 mg of phosphorus daily

Hypophosphatemia

Hypophosphatemia

• Causes• Decreased intestinal phosphate absorption - vitamin D deficiency, - malabsorption, - phosphate binders (e.g., aluminum-, magnesium-, calcium-,

or iron-containing compounds).• Renal phosphate loss• Phosphorus redistribution : respiratory alkalosis , refeeding

syndrome• Burn

Clinical manifestations

• Severe hypophosphatemia ( 0.32 mmol/L)• respiratory muscle dysfunction, diffuse

weakness, and flaccid paralysis.

Treatment

• Once the serum phosphorus level exceeds 2 mg/dL (0.65 mmol/L), the patient can be switched to oral therapy

• sodium-potassium phosphate salt

Treatment from Schwartz• Phosphate level 1.0–2.5 mg/dL:• Tolerating enteral nutrition: Neutra-Phos 2 packets q6h per gastric tube or

feeding tube• No enteral nutrition: KPHO4 or NaPO4 0.15 mmol/kg IV over 6 h × 1 dose• Recheck phosphate level in 3 d• Phosphate level <1.0 mg/dL:• Tolerating enteral nutrition: KPHO4 or NaPO4 0.25 mmol/kg over 6 h × 1

dose• Recheck phosphate level 4 h after end of infusion; if <2.5 mg/dL, begin

Neutra-Phos 2 packets q6h• Not tolerating enteral nutrition: KPHO4 or NaPO4 0.25 mmol/kg (LBW) over

6 h × 1 dose; recheck phosphate level 4 h after• end of infusion; if <2.5 mg/dL, then KPHO4 or NaPO4 0.15 mmol/kg (LBW)

IV over 6 h × 1 dose

Hyperphosphatemia

Hyperphosphatemia

• impaired renal excretion and transcellular shifts of phosphorus

• tissue trauma ,tumor lysis, insulin deficiency, or acidosis

• postoperative hypoparathyroidism

Clinical manifestations

• hypocalcemia and tetany

Treatment of hyperphosphatemia

• eliminate the phosphorus source - Phosphate binders (aluminum hydroxide)• remove phosphorus from the circulation - hydration (0.9% NaCl ) - diuresis (acetazolamide)• correct any coexisting hypocalcemia

Magnesium

Magnesium

o Mainly intracellularo 0.65 to 1.10 mmol/Lo Largely present in bone , and has an important

role in cellular energy metabolism .

Hypomagnesemia

It may occur in:• GI losses “massive small bowel resection ,small bowel /biliary

fistula , severe diarrhea , prolonged nasogastric suctionig “• Prolonged parenteral nutrition without Mg supplement.• Liver cirrhosis • primary hyperaldosteronism, • renal tubular dysfunction (e.g., renal tubular acidosis)• chronic alcoholism • drug side effect (e.g., loop diuretics, cyclosporine,

amphotericin B, aminoglycosides, cisplatin).

Clinical features

• Neuromuscular disturbances : altered mental status, tremors, hyperreflexia, and tetany

• cardiovascular effects - similar to those of hypokalemia

• Vomiting• Tachycardia , Low BP• Reduced protein formation

Treatment

• Acute : < 0.5 mmol/l• IV Mg sulphate or chloride .

• Chronic :• Oral replacement “2 g oral MgSO4 “

• remains the initial therapy of choice for torsades de pointes (polymorphologic ventricular tachycardia).

• Furthermore, it is used to achieve hypermagnesemia that is therapeutic for eclampsia and pre-eclampsia

Treatment from Schwartz

Magnesium level 1.0–1.8 mEq/L: then • Magnesium sulfate 0.5 mEq/kg in normal saline 250 mL infused IV

over 24 h × 3 d• Recheck magnesium level in 3 d• Magnesium level <1.0 mEq/L:• Magnesium sulfate 1 mEq/kg in normal saline 250 mL infused IV

over 24 h × 1 d, then 0.5 mEq/kg in normal saline 250 mL• infused IV over 24 h × 2 d• Recheck magnesium level in 3 d• If patient has gastric access and needs a bowel regimen:• Milk of magnesia 15 mL (approximately 49 mEq magnesium) q24h

per gastric tube; hold for diarrhea

Hypermagnesemia

Causes : • Burn and severe acidosis • chronic renal failure• iatrogenic

Clinical features • Nausea and vomiting• Hyporeflexia ,Generalized weakness • Facial parasthesia , Flushed appearance and

diaphoresis• Slow, shallow, depressed respirations , Respiratory

arrest• Hypotension, vasodilation• Arrhythmias and bradycardia• prolongation of PR, QRS, and QT intervals

Treatment

• Cessation of magnesium ingestion (orally or parenterally)

• Calcium salt administration• Volume replacement + loop diuretic • Dialysis in patients with severe renal

dysfunction

Thank you