fluids&e lectrolytes - nigel fong · 2019-10-23 · assessing volume status...

FLUIDS & ELECTROLYTES from basics Nigel Fong 2013

Dra1 not for circula6on

OUTLINE

•  Revision of physiology •  Disorders of extracellular volume & management •  Disorders of sodium & management •  Disorders of potassium & management •  Acid-‐base imbalances & management •  Disorders of calcium & management

THE KEY PLAYERS

Source: Guyton

INTRODUCTION

•  RAAS system •  ADH axis •  PTH/VitD axis •  Renal & Respi regula6on

NORMAL ELECTROLYTE BALANCE

PARAMETER NORMAL REGULATOR

Osmolarity 300 mOsm/L ADH

Na+ 140-‐145 mEq/L ADH

Volume 12L Aldosterone, Angiotensin II, ANP

K+ 4.2 ±0.3 mEq/L Aldosterone

Ca2+ 2.4 mEq/L PTH, Vitamin D (ac6vated)

pH 7.35-‐7.45 Respiratory and Renal

INTRODUCTION

RENAL PHYSIO - RECAP

Source: Guyton

INTRODUCTION

RENAL PHYSIO - RECAP INTRODUCTION

ASSESSING VOLUME STATUS VOLUME REGULATION

History Exam InvesBgaBons

Hypovolemia (early)

Low urine output Thirst Fluid loss e.g. d/v

↑ HR ↓ postural BP Dry mucous mem Capillary refill >2s

Dark urine Hyperosmolar urine ↑ Urea ↑ Hematocrit

Hypovolemia (late)

Drowsy Oliguria, anuria ↓ BP ↓ skin turgor

↑ crea6nine

Fluid overload Cardiac hx SOB, orthopnea Excess fluids

↑ RR ↑ JVP ↓ O2 sats Pifng edema Basal creps S3 heart sound

CXR pulm edema ↑ CVP

MONITORING FLUID BALANCE

•  I/O monitoring o1en rou6ne (pa6ent must be catheterized) –  Input: PO intake, IV fluids –  Output: Urine output, vomit, diarrhoea, drains

•  Allow 500-‐1000ml /24h insensible losses (e.g. swea6ng, breathing); more in burns pa6ents

•  When fluid enters the ‘third space’ (i.e. edema), pa6ent may have normal fluid balance but is hypovolemic – Beware!

•  Hypovolumic pa6ents do not always have tachycardia – especially if given beta-‐blockers etc.

VOLUME REGULATION

FLUID OVERLOAD: CAUSES

•  Heart failure : RAAS ac6va6on •  Hepa6c cirrhosis : hypoalbuminaemia, peripheral vasodila6on •  Nephro6c syndrome : hypoalbuminaemia •  Nephri6cs, CKD, ESRF : ↓ GFR •  Drugs : Mineralocor6coids, NSAIDs, Pioglitazone •  Iatrogenic : Excess fluid given

Normally NOT a cause •  ↑ salt intake: homeostasis ↑ excre6on •  Hyperaldosteronism (Conn’s syndrome): due to phenomenon of

aldosterone escape

VOLUME REGULATION

TREATMENT

•  Treat the cause •  Diure6cs

VOLUME REGULATION

TREATMENT

•  Treat the cause •  Diure6cs – See Pharmacology notes

VOLUME REGULATION

VOLUME REGULATION

But beware side effects

HYPOVOLEMIA: CAUSES

•  Dehydra6on •  Haemorrhage : open, concealed, intra-‐op losses •  Burns •  GIT losses : diarrhoea, vomi6ng, etc •  Renal loss : Renal disease e.g. nephro6c, DM •  Iatrogenic : Excessive diure6cs Also consider cardiogenic shock, anaphyla6c shock etc as the presenta6on is very similar to hypovolemia

VOLUME REGULATION

HYPOVOLEMIA: MANAGEMENT

•  Treat the cause •  Fluid challenge:

–  500ml (250ml if frail / CVS dx) 0.9% saline / 30 min –  If urine output ↑, implies hypovolemia was the cause of low urine output

VOLUME REGULATION

PRESCRIBING FLUIDS: INDICATIONS

•  Hypovolemia, dehydra6on •  ↑ loss: fluid losses, third space losses

–  E.g. Pre-‐op hydra6on •  ↓ intake: NBM, ↓ consciousness

–  Adults require 2-‐2.5L/day to cover urine output & losses

VOLUME REGULATION

PRESCRIBING FLUIDS: OPTIONS VOLUME REGULATION

Na (mmol/l) K (mmol/l) Cl (mmol/l) Normal plasma 140 2.4 110 5% Dextrose 0 You add it 0 Glucose saline 30 You add it 0 0.9% saline 150 You add it. 150 Hartmann 131 5 111

•  Giving pure water causes RBC lysis! •  K replacement o1en necessary too •  IV 5% glucose distributed equally into extracellular & intracellular

compartments; IV 0.9% saline remains in extracellular compartment – this is the correct treatment for water deple6on

•  However 1L 0.9% saline exceeds daily Na requirements, large volumes can cause hypernatremia

PRESCRIBING FLUIDS: OPTIONS

•  PO fluids if possible! –  Oral rehydra6on salts –  PO NaHCO3 tablets also in chronic mild sodium deple6on with acidosis e.g. CKD.

•  Maintenance fluids typically 1L/8h –  0.9% saline + 20mmol/L KCl, alterna6ng with 5% glucose –  Or Hartmann’s (crystalloid isotonic with blood)

•  Be careful in pt with CHF, cirrhosis, kidney failure –  There is no logic to giving fluid + furosemide –  Fluid restric6on may be required

VOLUME REGULATION

HYPONATREMIA SODIUM

With hypovolemia Euvolemia With hypervolemia

Extrarenal •  Vomi6ng •  Diarrhoea •  Haemorrhage •  Burns •  Pancrea66s

Renal •  Osmo6c diuresis (e.g. DM) •  Diure6cs •  Recovery from acute kidney failure •  Adrenocor6cal insuficiency •  Others

Urinary Na >20mmol/L?

Yes No

Edema Signs of

hypovolemia

HYPONATREMIA SODIUM


Edema Signs of

hypovolemia

•  Heart failure •  Liver failure •  Renal failure •  Nephro6c syn

What is the pathogenesis of hyponatremia in heart failure? •  Severe ↓ cardiac output sensed by baroreceptors •  ↑ ADH secre6on in defence of cardiac output •  ADH and osmolarity delinked; ↑ ADH regardless of osmolarity

Extrarenal losses

Renal losses


Yes No

HYPONATREMIA SODIUM


Extrarenal losses

Renal losses


Yes No

Edema Signs of

hypovolemia


↑ H2O intake

↓ H2O output

Excess fluids (e.g. IV postop)

S6mula6on of ADH release by osmo6cally ac6ve solutes •  Glucose •  Mannitol

Abnormal ADH release •  Hypothyroidism •  Addison’s disease •  K, Mg deple6on

(e.g. due to diure6cs)

SIADH (dx of exclusion) •  Malignancy •  Medica6ons •  CNS disorders •  Pulmonary disorders •  Idiopathic

HYPONATREMIA: FEATURES

Consequences of hyponatremia with hypo or hyper volemia is usually similar to that of the underlying cause

Euvolumic (diluBonal) hyponatremia •  Principally neurological symptoms due to osmo6c shi1s,

cerebral edema •  Headache, confusion, restlessness •  Drowsiness, myoclonic jerks, coma

SODIUM

HYPONATREMIA: WORKUP

•  Exclude pseudohyponatremia: blood collec6on from arm with IV fluids, lipaemic sample, hyperglycemia

•  Determine if pt is symptoma6c •  Determine acute vs chronic hyponatremia * •  Determine ECF volume status •  Check meds •  Ix: U/E/Cr, glucose, osmolarity, urine osmolarity, urine

sodium, thyroid func6on, cor6sol evalua6on

SODIUM

HYPONATREMIA: MANAGEMENT

Chronic hyponatremia cannot be rapidly corrected due to OsmoBc DemyelinaBon Syndrome •  Brain loses osmolytes quickly to adapt to hyponatremia •  However with rapid replacement of sodium, brain gains

osmolytes slowly •  Hypoosmolar intracellular compartment shrinks BBB

endothelium, allowing immune cells to enter and cause demyelina6on

Maximum correc6on rate: 8 mmol/day

SODIUM

HYPONATREMIA: MANAGEMENT SODIUM

CONDITION GOAL MX Mild Review diure6cs

Restrict water intake 0.9% saline slowly

Acute symptoma6c Avoid cerebral edema ↑ Na 4-‐6mmol in 1st 4h ↑ Na 18 mmol in 48h

3% saline 100ml Q1-‐2h Monitor frequently Beware of overcorrec6on

Chronic symptoma6c Slow correc6on to avoid osmo6c demyelina6on

Must calculate Monitor frequently

Chronic asymptoma6c Treat underlying cause Rapid correc6on not nec

3% saline not warranted

Correc6on of volume takes precedence over correc6on of Na

HYPERNATREMIA: CAUSES

•  Fluid loss •  Inadequate water intake

Others: fluid loss / inadequate intake PLUS •  Nephrogenic diabetes insipidus •  Neurogenic diabetes insipidus •  Osmo6c diuresis •  Hyperosmolar hyperglycemia state •  Iatrogenic

SODIUM

HYPERNATREMIA: MANAGEMENT

•  Symptoms usually nonspecific; worrying if ↓ GCS, ↑ HR, ↓ BP •  Assess volume status •  Look for cause

Treatment •  Treat the cause •  Withdraw nephrotoxic drugs •  Hypotonic fluids (PO or NG preferable to IV): Slow correc6on to

prevent cerebral edema •  Normal saline only if significant hypotension from dehydra6on

SODIUM

HYPERKALEMIA

POTASSIUM

↓ excreBon ↑ release from cells

Spurious •  Hemolysed bld •  Transient a1

exercise

Drugs •  ACE-‐I •  K-‐sparing diure6cs

-‐ Amiloride -‐ Spironolactone

•  NSAIDs

Renal & Endocrine •  AKI & CKD •  Addison’s •  Hypoaldosteronism •  Other rare causes

Excess K input •  Large transfusion •  Iatrogenic

•  Acidosis •  Diabe6c ketoacidosis •  Tumor lysis •  Rhabdomyolysis

HYPERKALEMIA: COMPLICATIONS

K > 7 is a emergency •  Depolariza6on of cell membranes •  Muscle weakness o1en only symptom •  Decreased cardiac excitability -‐-‐> ECG changes, hypotension, bradycardia, sudden asystole

POTASSIUM

HYPERKALEMIA: WORKUP

•  Repeat bloods if K <7 AND sample hemolysed AND no ECG changes, else treat immediately.

•  Assess hemodynamic stability, vitals •  Enquire symptoms: palpita6ons, dizziness, chest pain •  Do ECG – look for tented T waves, later flat P waves, ul6mately VF

•  Look for cause: drugs, CBG, ABG, renal failure

POTASSIUM

HYPERKALEMIA: MANAGEMENT

•  Stop offending drugs •  Insulin + Dextrose : Shi1 K into cells (monitor CBG) •  Ca gluconate : Protect heart •  Resonium : K-‐binding resin •  ?Salbutamol •  Repeat bloods, para, ECG •  If persistent, dialysis.

POTASSIUM

HYPERKALEMIA

POTASSIUM

↓ K output ↑ release from cells

Excess K input HYPO

↑ K output ↑ uptake into cells

Reduced

HYPOKALEMIA

POTASSIUM

↑ K output ↑ uptake into cells

GI loss •  D/V •  Ileostomy •  Etc

↑ Aldosterone •  Heart failure •  Liver failure •  Nephro6c syn •  Cushing’s syn •  Conn’s syn •  Exogenous

Renal •  Diure6cs (most) •  Nephrotoxic drugs •  Post-‐AKI diuresis •  Renal disease •  Mg deple6on

↓ K input •  IV fluids without K •  Dietary deficiency

•  Alkalosis •  Adrenaline

(AMI, beta-‐agonists) •  Insulin

HYPOKALEMIA: CONSEQUENCES

Usually asymptoma6c •  Muscle weakness, cramps, hypotonia, cons6pa6on •  Arrhythmias – but unlikely in pt without cardiac disease

•  ↑ Risk of digoxin toxicity: ↑ digoxin binding to cardiac cells, poten6a6ng ac6on

POTASSIUM

HYPOKALEMIA: WORKUP

•  Assess volume status •  Check for symptoms & complica6ons (watch for ↓ RR) –  Do ECG: look for U waves, ST depression, T inversion, arrhythmias etc

•  Check meds: beware digoxin toxicity •  Check for cause: ? Loss ? Intracellular shi1 –  Take BP: consider endocrine causes –  Bloods: ABG if alkalosis suspected –  Bloods: Crea6ne kinase if myolysis suspected –  Bloods: Mg for ↓ Mg & coexis6ng electrolyte imbalances

POTASSIUM

HYPOKALEMIA: MANAGEMENT

Asymptoma6c, K >2.5 •  Stop offending drugs •  Span K tablet or add 20-‐40mmol KCl to IV fluids •  Correct ↓ Mg Symptoma6c, K<2.5 or ECG changes •  As above, and •  Replace K slowly (max 10mmol/h)

POTASSIUM

NEVER GIVE KCl BOLUS

APPROACH TO ABG

Please learn how to read ABG! •  Is there acidosis or alkalosis? •  Is it respiratory or metabolic? •  Is there appropriate compensa6on? (Inappropriate compensa6on – mixed acid/base disorder)

•  What is the cause? •  Is PO2 affected?

ACID-‐BASE

ACIDOSIS ACID-‐BASE

Metabolic Respiratory Mainly CO2 reten6on Type 2 respi failure: ↓O2 ↑CO2

Central causes •  Drugs (seda6ve, opiate) •  Head injury •  CNS lesions •  Chronic type 2 resp failure

over treated with O2

Peripheral causes •  Lung – Asthma, COPD, CA, pneumothorax •  Ribs – Trauma, etc •  Neuromuscular – Myasthenia gravis,

Gullian Barre, C-‐spine injury

↓ HCO3-‐ ↑ CO2


Metabolic Respiratory Mainly CO2 reten6on Type 2 respi failure: ↓O2 ↑CO2

Central Peripheral

Measure anion gap

Normal High

The Anion Gap Ca6ons -‐ Anions = Unmeasured anions [ Na + K] -‐ [ HCO3

-‐ + Cl-‐ ] = Albumin, phosphate, lactate, sulphate etc Adjustment necessary for ↓ albumin Normal anion gap: < 12 (check with lab) ↑ anion gap implies unmeasured anion produc6on e.g. lactate, exogenous acid

↓ HCO3-‐ ↑ CO2


Metabolic Respiratory CO2 reten6on

Central

Peripheral

Measure anion gap

Normal

↓ HCO3-‐ ↑ CO2

High AG met acidosis High

Normal AG met acidosis

H -‐ Hyperalimenta6on A -‐ Acetazolamide R -‐ Renal tubular acidosis D -‐ Diarrhoea U -‐ Uretosigmoid fistula P -‐ Pancrea6c fistula

M -‐ Methanol U -‐ Uremia D -‐ Diabe6c ketoacidosis P -‐ Propylene glycol I -‐ Isoniazid L -‐ Lac6c acidosis E -‐ Ethylene glycol S -‐ Salicylates

Be\er to understand the pathophysiology than memorise the acronym!



Central

Peripheral

Measure anion gap

Normal

↓ HCO3-‐ ↑ CO2

High AG met acidosis

Kidney failure (uremic acidosis)

LacBc acidosis •  Anaerobic metab

e.g. hypoxia, shock •  Me~ormin •  Others

DiabeBc ketoacidosis •  Starva6on •  Insulin ↓ •  New dx

Exogenous acid •  Salicylate •  Poisoning

High




Central

Peripheral

Measure anion gap

Normal

↓ HCO3-‐ ↑ CO2

High AG met acidosis

Uremic acidosis

Lac6c acidosis

Diabe6c ketoacidosis

Exogenous

High


↓ HCO3-‐ ↑ H+

•  Renal tubular acidosis

GIT -‐ Diarrhoea -‐ Ileostomy -‐ Uretosigmoid fistula

Renal -‐ Acetazolamide -‐ HyperPTH -‐ Tubular damage (drugs, heavy metals) -‐ Hyperkalemia

ACIDOSIS: PRESENTATION

•  SOB •  Kussmaul respira6on: deep, laboured, gasping •  CVS dysfunc6on •  CNS: headache, dysfunc6on

Look for hyperkalemia: Acidosis is associated with hyperkalemia, alkalosis with kypokalemia •  Exchange of K+/H+ between extracellular fluid & cells •  Subs6tutes in renal secre6on

ACID-‐BASE

ACIDOSIS: MANAGEMENT

Find the underlying cause •  Respiratory acidosis: Supp O2, ven6latory support (but do not suppress hypoxic drive)

•  Lac6c acidosis: maximise O2 delivery •  Diabe6c ketoacidosis: Insulin •  Treat methanol & ethylene glycol poisoning (ethanol) •  Dialyse salicylate

Tx of severe acidosis with bicarbonate is controversial

ACID-‐BASE

ALKALOSIS ACID-‐BASE

Metabolic Respiratory

↑ HCO3-‐ ↓ CO2

HCl depleBon Hypokalemia •  GIT loss: vomi6ng •  Diure6cs •  Cys6c fibrosis (sweat Cl)

Chloride Responsive Physiologic compensa6on of

alkalosis impaired in Cl deple6on. To allow↓ HCO3-‐ reabsorp6on, must have ↑ Cl-‐ reabsorp6on to

maintain electroneutrality

•  Hyperaldosteronism •  Other causes (see earlier)

Excess IV HCO3 fluids

•  Type 1 resp failure •  Hysteria

Chloride Resistant

ALKALOSIS: MANAGEMENT

•  Symptoms are difficult to separate from chloride, volume, or potassium deple6on

•  Cl responsive –  Isotonic saline to replace Cl & volume –  Fluid overload: IV HCl or acetazolamide (if renal func6on OK)

•  Cl resistant –  Correct underlying cause.

ACID-‐BASE

HYPERCALCEMIA

CALCIUM

↑Bone resorpBon

Others

Corrected Ca

Corrected Ca = Measured Ca + 0.02 (40-‐Albumin)

•  Only free (ionized) Ca is measured BUT 40% of Ca is protein bound •  Each 1g/L decrease in albumin will decrease measured Ca by 0.02 mmol/L

BUT you want to es6mate what calcium would be if albumin were normal

↑ Calcium absorpBon

HYPERCALCEMIA

CALCIUM

↑Bone resorpBon ↑ Calcium absorpBon

1˚ ↑PTH 3˚ ↑PTH Cancer

↑ PTH due to -‐ ↑ PO4: CKD -‐ ↓ Ca: vit D deficiency Ini6ally 2˚ ↑ PTH and ↓ Ca, but when longstanding can become 3˚ ↑ PTH (PTH secre6on independent of Ca)

(Adenoma)

•  Bone mets •  Produce osteoclast

ac6va6ng factors •  Produce PTHrP: PTH

related hormone

•  Excess CaCO3 e.g. iatrogenic (milk alkali syndrome)

•  Hypervitaminosis D, usually iatrogenic

Others •  Dehydra6on •  Lithium •  Thyrotoxicosis •  Thiazides

Most common

Common

HYPERCALCEMIA: PRESENTATION

“Stones, bones, abdominal groans and psychiatric moans” •  Stones : Nephrolithiasis, renal colic

: polyuria & polydipsia (↓ conc ability) •  Bones : Bone pain •  Groans : Cons6pa6on, indiges6on, n/v, abdo pain •  Moans : Depression, lethargy, fa6gue, etc

Pathophysiology: •  Ca & PO4 exceeding solubility -‐-‐> precipitate •  Depress muscle & nerve ac6vity (also ECG changes)

CALCIUM

HYPERCALCEMIA: WORKUP

•  Assess ABC, fluid & neuro status •  U/E/Cr + Ca + Mg + FBC + Glucose •  iPTH (intact PTH) –  High: Hyperparathyroidism –  Undetectable: ?? Malignancy -‐-‐> Inves6gate

•  Alkaline phosphatase (?parathyroid bone dx) •  ECG: look for short QT, arrhythmias •  Imaging workup: CXR, bone scan, US parathyroid

CALCIUM

HYPERCALCEMIA: MANAGEMENT

•  Treat underlying condi6on •  IV fluid hydra6on is primary tx (beware fluid overload)

Severe / symptoma6c – consider: •  IV bisphosphanate (do not ini6ate in dehydrated pt with renal

impairment) •  Calcitonin •  Steroids for bone mets, sarcoidosis, excess vit D

CALCIUM

HYPOCALCEMIA CALCIUM

↓ PTH

↑ PO43-‐

Chronic kidney disease

(↓ excre6on)

Others -‐ Thyroidectomy -‐ Congenital -‐ Idiopathic -‐ Severe ↓ Mg

MalabsorpBon Other causes •  ↓ Vitamin D •  Vit D resistance •  Celiac disease

•  Acute pancrea66s •  ↑ Transfusion of

citrated blood •  Hypoalbuminaemia •  Bisphosphonates •  Calcitonin •  PTH resistance

(pseudohypoPTH)

Corrected Ca

Corrected Ca = Measured Ca + 0.02 (40-‐Albumin)

HYPOCALCEMIA: PRESENTATION

Hypocalcemia presents as neuromuscular irritability

CALCIUM

Symptoms •  Cramps, Carpopedal spasm •  Twitching, parasthesia •  Anxiety •  Convulsions, dystonia •  Psychosis May cause arrythmias

Signs •  Hyperreflexia, tetany •  Trosseau sign (spasm of hand from 3min inflated BP cuff)

•  Chvostek sign (tap facial nerve causes ipsilateral facial twitch)

HYPOCALCEMIA: WORKUP

•  Bloods : U/E, Ca, Albumin – ↓ PTH? : PTH, PO4, Cr, Mg – Malabs? : Vitamin D

•  ECG: look for prolonged QT, arrhythmias, ST changes

CALCIUM

HYPOCALCEMIA: MANAGEMENT

•  Treat arrhythmias •  Treat the cause –  E.g. Vitamin D replacement, Ca supplementa6on –  Correct Mg

•  Severe tetany: calcium gluconate

CALCIUM

OUTLINE

•  Revision of physiology •  Disorders of extracellular volume & management •  Disorders of sodium & management •  Disorders of potassium & management •  Acid-‐base imbalances & management •  Disorders of calcium & management

HYPONATREMIA SODIUM


Extrarenal loss

•  Vomi6ng •  Diarrhoea •  Blood loss •  Burns •  Pancrea66s

Renal Losses

•  Osmo6c diuresis •  Diure6cs •  Recovery from AKI •  Adrenocor6cal

insuficiency •  Others


Yes No

Edema Signs of

hypovolemia


Excess intake

↓ H2O output

•  Osmo6c solutes s6mula6ng ADH release (e.g. glucose, mannitol)

•  Abnormal ADH release: addison’s dx, hypothyroid, K / Mg deple6on

•  SIADH

HYPERKALEMIA

POTASSIUM

↓ excreBon ↑ release from cells

Spurious •  Hemolysed

blood •  Transient a1

exercise

Drugs •  ACE-‐I •  K-‐sparing diure6cs

-‐ Amiloride -‐ Spironolactone

•  NSAIDs

Renal & Endocrine •  AKI & CKD •  Addison’s •  Hypoaldosteronism •  Other rare causes

Iatrogenic •  IV fluid •  Transfusion

•  Acidosis •  Diabe6c ketoacidosis •  Tumor lysis •  Rhabdomyolysis

HYPOKALEMIA

POTASSIUM

↑ K output

↑ uptake into cells

GI loss •  Diarrhoea •  Vomi6ng •  Ileostomy

↑ Aldosterone •  Heart failure •  Liver failure •  Nephro6c syn •  Cushing’s syn •  Conn’s syn •  Exogenous

Renal •  Diure6cs (most) •  Nephrotoxic drugs •  Post-‐AKI diuresis •  Renal disease •  Mg deple6on

↓ K input •  IV fluids without K •  Dietary deficiency

•  Alkalosis •  Adrenaline

(AMI, beta-‐agonists) •  Insulin



Central

Peripheral Measure anion gap

↓ HCO3-‐ ↑ CO2

High AG met acidosis •  Uremic acidosis: AKI, CKD •  Lac6c acidosis: hypoxia,

shock, me~ormin •  Diabe6c ketoacidosis •  Exogenous acid: salicylate,

poisoning


GIT -‐ Diarrhoea -‐ Ileostomy -‐ Uretosigmoid fistula

Renal -‐ Renal tubular acidosis -‐ Acetazolamide -‐ HyperPTH -‐ Tubular damage (drugs, heavy metals) -‐ Hyperkalemia

ALKALOSIS ACID-‐BASE

Metabolic Respiratory

↑ HCO3-‐ ↓ CO2

HCl depleBon Hypokalemia •  GIT loss: vomi6ng •  Diure6cs •  Cys6c fibrosis

Excess IV HCO3 fluids •  Type 1 resp failure

•  Hysteria

HYPERCALCEMIA

CALCIUM

↑Bone resorpBon ↑ Ca2+ absorpBon

1˚ ↑PTH (Adenoma)

3˚ ↑PTH Cancer •  Excess CaCO3 •  Excess vitamin D

Others •  Dehydra6on •  Lithium •  Thyrotoxicosis •  Thiazides

HYPOCALCEMIA CALCIUM

↓ PTH

↑ PO43-‐

Chronic kidney disease

Others -‐ Thyroidectomy -‐ Congenital -‐ Idiopathic -‐ Severe ↓ Mg

MalabsorpBon Other causes •  ↓ Vitamin D •  Vit D resistance •  Celiac disease

•  Acute pancrea66s •  ↑ Transfusion of citrated blood

•  ↓ Albumin •  Bisphosphonates •  Calcitonin •  PTH resistance (pseudohypoPTH)

fluids&e lectrolytes - nigel fong · 2019-10-23 · assessing volume status...

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