Electrolyte disorders in_critically_ill_patients__na

Electrolyte disorders in Critically ill patients

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“It is the internal environment (not the external world) that provides the physical need for life”

CLAUDE BERNARDCLAUDE BERNARD

Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India

BODY FLUID COMPARTMENTS Arrow represents fluid movement

Review of Medical Physiology, William F. Ganong


Electrolyte Composition of Body Fluid Compartments


Composition of body fluids losing continuously

Source Daily Loss Na+ K+ Cl- HCO3-

Saliva 1000 30-80 20 70 30

Gastric 1000-2000 60-80 15 100 0

Pancreas 1000 140 5-10 60-90 40-100Pancreas 1000 140 5-10 60-90 40-100

Bile 1000 140 5-10 100 40

Small Bowel 2000-5000 140 20 100 25-50

Large Bowel 200-1500 75 30 30 0

Sweat 200-1000 20-70 5-10 40-60 0

urine 1500-2000 <10

Frusemide diuresis 75


Composition of IV fluidsin comparison to Plasma

Fluid Na K Ca Mg Cl Buffers Glucose pH Osm

Plasma141 4.5 5 2 103

HCO3-26Prot-16

0.7-1.1 7.4 290

NS 154 154 6.0 308

1/2NS 77 77 5.0 154

RLRL 130 4 3 109 Lac-28 6.5 274

5%D 50 4.5 252

Plasmalyte140 5 3 98

Acet-27Gluc-23

7.4 294

Gel

3%Saline 513 513 4.5 1026

5%Alb

20%Alb


Sodium Water Sodium Water disturbances


Na is the most abundant molecule in ECFNa is the most osmotically active molecule in ECF

S. Osm ( mOsm/kg of water)(2*[Na] + [Glucose/18] + [BUN/2.8]

(Na in meq/L, Glucose in mg/dL, BUN in mg/dL)

Contribution of Gluc and BUN is 5 mOsm/L

(Na in meq/L, Glucose in mg/dL, BUN in mg/dL)

Osmotic pressure and osmolality determinesdistribution of fluid in body compartments


OSMOLALITY

280-295 mOsm/kg

Serum

Urine

24 hour urine sample-500-800 mOsm/kgExtreme range-50-1400mOsm/kg

Random urine sample- 300-900mOsm/kg

After overnight fluid restrictionUrine omolality > 3 times serum osmolality (>800)


Real story in critically ill patients

S. Osm = 2* (140) + 90/18 + 5/2.8= 280 + 5 + 1.7

= 286.7

S. Osm = 2* (145) + 180/18 + 60/2.8= 290 + 10 + 21

= 321


Na WATER


Na / water regulation

Thirst ADH RAA Kidney


Epidemiology of electrolyte disorder in ICUEpidemiology of electrolyte disorder in ICU


Intensive Care Medicine 2010, 36(2):304-11Incidence and prognosis of dysnatremias present on ICU admission

Funk GC, Lindner G, Druml W, Metnitz B, Schwarz C, Bauer P, Metnitz PG

retrospective study in 77 medical, surgical, and mixed ICUs in Austria, 151,486 adults patients admitted over a period of 10 years (1998-2007).

75% patients had normal sodium levels (Na:135-145) on ICU admission

Incidencehyponatremia-17.7%, Hypernatremia-6.9%

All types and grades of dysnatremia were associated with increased hospital mortality

independent mortality risk rising with increasing severity of both hyponatremia and hypernatremia


Critical Care 2008, 12:R162

The epidemiology of intensive care unit-acquired hyponatraemiaand hypernatraemia in medical-surgical intensive care units

Henry Thomas Stelfox, Sofia B Ahmed, Farah Khandwala, David Zygun, Reza Shahpori, Kevin Laupland

8142 adults admitted in 3 medical-surgical ICUs Over 6 yearsdocumented to have normal S. sodium levels (133 to 145 mmol/L) on

the first day of ICU admission

Incidence Hyponatremia- 11%, hypernatremia-26%

Median time to develop dysnatremia- 2 days

Median duration of dysnatremia-2 days

More than 1 distinct epi of dysnatremia- 25%(Hyponatremia-16%, hypernatremia-19%)

hospital mortality increased significantlyIndependent of SOI

( hypoNa-28%, hyperNa-34%, normoNa-16%)

Continued…..Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India




Continued…..Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India

Increased risk of hypernatremiaRaised S.creatinine

Mechanical ventilation

Increased risk of both hyper and hyponatremiaLength of stay in ICU




Length of stay in ICUIncreased APACHE II score

•Dysnatremias develop insidiously over 2 days

•Difficult to identify as clinicians preoccupied with more acute medical issues and other lab investigations


Critically ill patients prone to

electrolyte disturbanceselectrolyte disturbances


Disturbance in fluid and electrolyte homeostasissepsis, shock, cardiac failure, acute kidney injury, burn, surgery, C.N.S. disorders

Activation of neuro hormonal system- SNS, RAAS, Vasopressin

Non osmotic release of Vasopressinpain, nausea, medication, hypovolemia

Diuresisiotrogenic- renal and osmotic diuretics

Vasopressin deficiency in sepsis

Insensitivity to insensible losses

Impaired thirst mechanism

Inappropriate administration of fluid and electrolytes

iotrogenic- renal and osmotic diureticsUrea, glucose induced

Hypokalemia, hypercalcemiaDrug induced- aminoglycoside, ampho B


Am J Kidney Dis 2009 Oct, 54:674-679

tonicity balance in patients with Hypernatremia Acquired in the Intensive Care Unit

Gregor L, Nikolaus K, Ulrike Holzinger, Wilfred Druml, christiph schwartz

Solute balance= [Na+K]input – [Na+K]outputContinued…


osm

otic

Non

olig

uric

Urea/ glucose




Causes of ICU acquired hypernatremia

osm

otic

DI

Non

olig

uric

Addition of KCl to 0.9%saline led to positive solute balance in 27% patients

Hypertonic Osm>150

Continued…

•Positive solute balance contributed 56% cases

•Primary reason was inadequate substitution of hypotonic losseswith isotonic or hypertonic fluids

•Impaired sensorium and inability to express thirst leading to




•Impaired sensorium and inability to express thirst leading to inadequate intake of free water

Community acquired hypernatremia- hypovolemic hypernatria

ICU- euvolemic or hypervolemic hypernatremia

Continued…Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India




Characteristics of patients Continued…Ubaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India




Characteristics of patientsUbaidur Rahaman, Senior Resident, CCM, SGPGIMS, Lucknow, India

Patients admitted over 1 year medical, surgical or neurological ICU

Renal dysfunction, Hypokalaemia, hypercalcemia, mannitol, sodium bicarbonate•more common in cases

hypernatremia ≥150 mmol/l in the ICU

Nephrol Dial Transplant 2008,23:1562-1568Hypernatremia in critically ill patients: too little water and too much salt

Ewout J. Hoorn, Mecheil G.H.Betjes, Joachim Weigel, Robert Zietse

•more common in cases •independently associated with hypernatraemia.

• mortality was higher in case•Hypernatremia was independent predictor


•Approximately half of cases were polyuric, even when fluid balance was negative+

•Impaired thirst mechanism•Inappropriate iv fluid administration with isotonic fluids



•Aim of treatment- negative solute balance•Hypotonic fluid may aggravate fluid overload

•Diuretic may be considered: combination of loop diuretic and water or thiazide diuretic alone


Potential factors contributing to hypernatremia

Page 1566




Use of hypotonic fluid is avoided in ICU

Capillary leakiness in sepsis patientsCapillary leakiness in sepsis patients

Fear of hyponatremia as many patient show non osmotic release ofVasopressin


JUST ANJUST ANANALYSIS




•47-year-old male •(body weight 95 kg)

•cystectomy complicated byfaecal peritonitis.

•Hypernatraemia in1day

Tonicity balance illustrating mechanism of hypernatremia

•Hypernatraemia in1day

•large isotonic volume resuscitation,+ hypertonic fluids (NaHCO3)

•Water loss•Renal: renal insufficiency and

hyperglycaemia •non-renal: wound drains and

colostomy


Intensive Care Med 2001;27:921-924Tonicity balance, and not electrolyte free water calculations, more accurately

guide therapy for acute change in natremiaA.P.C.P. Carlotti, D. Bohn, J.P. Mallie, M.L. Halperin

14 year old male( weight 40 kg, total body water 24 L)

Operated for craniopharyngioma

During surgery• excreted 4L in 9 hours

TBW* ( [S.Na] /140 ) - 1

• excreted 4L in 9 hours

Over this period •P.[Na] rose from 140 to 157 meq/L

• received 3 L of isotonic saline

•His urine [Na+K] was 50 meq/L.

Free Water deficit: 24* [ (157/140) – 1 ] = 2.9 L

2.9L

2.9L


Intensive Care Med 2001;27:921-924

Tonicity balance, and not electrolyte free water calculations, more accurately guide therapy for acute change in natremia

A.P.C.P. Carlotti, D. Bohn, J.P. Mallie, M.L. Halperin

4 L urine with 200meq Na= 1.3 L isotonic saline + 2.7 L of EFW




Na 200 mmol

Tonicity balance




1

3 situations with hypernatremia and negative balance of 2.7 L of EFW

2

3


HYPERNATREMIAHYPERNATREMIA


HYPERNATREMIA

True/ Relative water deficit

S. Na > 145 meq/L

Clinical manifestation

ThirstThirstLethargy, irritability, restlessness

Spasticity, hyperreflexia, seizure, comaDeath

Cerebral Hemorrhage/ ischemiaInsulin resistance, impaired gluconeogenesis

Cardiac dysfunction

Severity of symptoms correlate with rate and magnitude of change in [Na]


APPROACHAPPROACH


Hypernatremia

Hypertonic saline loadNaHCO3, 3% salineHyperaldosteronismCushing’s syndrome

Primary Na gain

HYPERVOLEMIA

Hypotonicfluid loss

HYPOVOLEMIAISOVOLEMIA

Extra renal lossRenal loss

DiuresisOsmotic

glucose, urea, mannitol, high osmolar feeds

Diuretics- frusemide, thiazide

Insensible lossFever, burn

Diabetes insipidusCDI

NDIrenal disease

Drugs- amphoterecin, aminoglycosides, lithiumElectrolyte disorders- hypokalemia, hypercalcemia

Azotemia out of proportion to decrease in GFR

Catabolic patients withModerate renal

insuficiency on high protein diet and stress

dose steroid


Excretion of small volume (<800 ml)

Appropriate response to hypernatremia

Excretion of small volume (<800 ml)Of

concentrated urine (Osm U > 800 mOsm/L)


Hypernatremia

Urine volume

Hypotonicfluid loss

>1000 ml<800 ml

Urine osmolality

< 300300 - 800

HYPOVOLEMIA/ ISOVOLEMIA

Urine osmolality>800

Insensible lossesdiuretics

Response to dDAVP

Osmotic diuresis + complete CDI_ complete NDI

Inheritedlithium

Urine osmoleexcretion /day <900 mOsm/day

>900 mOsm/day

+ complete CDI with hypovolemia+ Partial CDI

- partial NDIRenal tubular disease

Drugselectrolyte disturbances

>800

Response to dDAVP

Solute diuresis

Water diuresis

MANAGEMENTMANAGEMENT

HYPERNATREMIACorrection

Risk : development of brain odema

Chronic hypernatramia- brain cells fully adaptedRisk is more

Rate of correction

Acute hypernatremia: 1-2 meq/L/h ( 10-12 meq/L/day)

Chronic hypernatremia: 0.5 meq/L/h ( 8-10 meq/L/day)

Rate of correction

GOALNa <145


HYPERNATREMIACorrection

TBW* ( [S.Na] /140 ) - 1

EFW deficit calculation (L)

Water deficit calculation (L)Water deficit calculation (L)Madias and Adrogue equation

Scan Page 74 JW LEE


Mind it

Ongoing lossMust be considered

along with calculated water deficit

Formulas assume a closed systemRequire separate account of ongoing losses

as


70 kg women Diarrhoea of volume 2 L/ day

S.[Na]= 160meq/L , S.[K]= 3.0meq/L

75 – 160 / (70*50) + 1 = - 2.3 meq/ L

Estimated change in S.[Na] with 1 L of N/2 saline

change of 10 meq/L = 4.3L of N/2 saline has to be given in 24 hours

But ongoing loss = 0.7 L + 2.0 L = 2.7 L / 24 hours

Total volume to be given

4.3 L + 2.7 L = 7.0 L / 24 hours


Hypernatremia

Hypotonic fluid ± diuretic

Urine output < water replacement

HYPERVOLEMIA Hypotonicfluid loss

HYPOVOLEMIAISOVOLEMIA

Insensible lossDiabetes insipidus

Osmotic diuresis

Insensible lossDiabetes insipidus

Hemodynamically unstableCorrect volume with isotonic saline

Switch over to hypotonic fluid toto correct Na

Remove / treat cause of DIReplace losses with hypotonic fluid

CDIDdavp

NDIlow Na diet + thiazide ± low protein diet ± NSAID


HYPERNATREMIAsummary of management

Hemodynamic unstable: resuscitate with isotonic fluid (0.9% saline or RL)

Switch over to hypotonic fluid once resuscitated

Hypovolemic hypernatremia: AIM- positive EFW and solute balance

isovolemic hypernatremia: AIM- positive EFW balance

Replace losses with Hypotonic fluidTreatment of cause: DI

Hypervolemic hypernatremia: AIM- negative EFW and solute balance

Na restriction + Hypotonic fluid + frusemide

CDI: ADH analoguedDAVP: 10-20 ug intranasal bd

or 1-2ug sc bd

NDIremove/ correct causative agent

Thiazide/ indomethacin


hypernatremia

Duration of hypernatremia

Absent/ mild neurologic signs

[Na] ≥155 meq/L

Severe neurologic compromise

Initial acute management of

[Na] <155 meq/L

Search for alternative cause of neurologic compromize

Duration of hypernatremia[Na] ≥155 meq/L

5% dextrose

Initial goalFall of [Na] by 1.5-2.0 meq/L/h

for 3-4 hours or until symptoms resolveChange in [Na] can occur rapildlyImmediate attainment to normal

Is not goal

[Na] <155 meq/L

< 2 days

> 2 days

Change in [Na] should not exceed 10 meq/L in first 24 hours


DIABETES INSIPIDUS

Hypotonic urine in face of hyperosmolar plasma

CDI- Osm U <200NDI- Osm U 200-500

Water restriction: failure of Osm U to rise by 50 mOsm/ L in first few hours

Vasopressin- CDI Osm U rise by atleast 50% immediately


HYPONATREMIAHYPONATREMIA

HYP0NATREMIA

True/ Relative water excess

S. Na < 135 meq/L

Clinical manifestation

headache, nausea lethargy, disorientation, restlessnesslethargy, disorientation, restlessness

Muscle cramp, weakness, depressed reflexes, seizures, comaDeath

Chronic hyponatremia: developing over >48 hours

Adaptative mechanism minimize symptoms

Severity of symptoms correlate with rate and magnitude of fall in [Na]


APPROACH APPROACH


hyponatremia

Hypertonic HypoNaHyperglycemia

Hypertonic sodium free sol(mannitol)

Hypotonic HypoNa

Isotonic HypoNaPseudohyponatremia

Hyperlipidemiahyperproteinemia

Normal serum osmolality

low serum osmolality

high serum osmolality

Assess serum osmolality

hypotonic Hypovolemichyponatremia

Assess volume status

isovolemichypovolemic hypervolemic

hypotonic isovolemic hyponatremia

hypotonic HypervolemicHyponatremia

CirrhosisCongestive heart failure

Nephrotic syndromeRenal falire

Discussed in next pages

DiuresisOsmotic- glucose, urea, mannitol

Diuretics- thiazide, frusemide

Electrolytes-Hypokalemia, hypercalcemiaDrugs- aminoglycoside, ampho B

hypotonic Hypovolemic Hyponatremia

Adrenal deficiencyMineralocorticoid deficiency

Renalloss

LOSS (both water and Na) = Negative water and Na balance

Salt wasting nephropathyCerebral salt wasting

GI lossnaso gastric aspirate,

abdominal Drains/ fistulathird space loss

(pancreatitis, ileus, obstruction)

Vomiting, diarrhea

Non renalloss

Skin lossfever

open wounds,burns

hemorrhage

Acute psychosisCNS disorders

Hypotonic Isovolemic Hyponatremia

Drug inducedOpiodsNSAIDS

Antipsychotics- haloperidolSSRI- fluoxetine, sertraline

Pain, nausea, stress

SIADH

Impaired free water loss in urine Normal Na loss in urine

hypothyroidism

TCACarbamezapineantineoplastics

Pulmonary diseaseInfections

malignancy

Cortisol deficiency

CORRECTION CORRECTION

PRECAUTION IN CORRECTION

Absolute magnitude of correction in 24 hoursmore important than rate

central pontine myelinosis

Initial rapid rate of correction tapering off after several hoursincurs less risk

thanslow steady correction that exceeds 12 meq/L in 24 hours

Increased riskHypoxemia, hypokalemia, malnutrition, alcoholism


HYPONATREMIA

1-2 meq/L/h ( 10-12 meq/L/day)

Rate of correction

Symptomaticor

Acute hyponatremia (change >0.5 meq/L/h or onset in < 48 hours)

0.5 meq/L/h ( 8-10 meq/L/day)Chronic hyponatremia

(Change over > 48 hours or unknown duration)Increased risk of CPM

as adaptive mechanism has occured

120-130 meq/LLower iin patients with s.Na<105GOAL of Correction


Any saline solution that is hyperosmolar to urine can increase [Na]when

oral water intake is restricted

Mind itRULE FOR CORRECTION

A crystalloid with an osmolarity less than urine osmolaritymay actually worsen hyponatremia,

even if the fluid [Na] is greater than serum [Na]

CONTINUED….


Na=118

Gain of 154 mOsm will be lost in 300 ml urineGain of 700 ml of EFW

(154* 1000/500= 300 ml, OsmU > 500)

60 years male, febrile encephalopathyBody weight: 60 kg, TBW: 36 L

Develops SIADH

S.[Na]= 118, urine Osm > 500 mOsm/L

Given 1 L of 0.9% saline

ONE RULE FOR CORRECTION

Na=154

Water=1000

Na=0

water= 700 Water= 300

Na=154

Na=115

Na=118

Simultaneous IV loop diuretic can counteract this phenomenon By promoting free water excretion


HYPONATREMIACALCULATION OF [Na] deficit

TBW* ( 140 – s.Na)

Na deficit (meq)

Anticipated change in s.Na with 1L of fluidAnticipated change in s.Na with 1L of fluid(Madias and Adrogue equation)

Scan Page 74 JW LEE


HYPONATREMIA

Remove or treat cause of hypertonicity

Hypertonic HypoNaHyperglycemia

Hypertonic sodium free sol(mannitol)

Repeat labUse newer method of lab

Isotonic HypoNaPseudohyponatremia

Hyperlipidemiahyperproteinemia

Fluid shift to ICF compartment does not take placeNeuronal cell swelling does not occur


hypotonic hyponatremia

Primary polydypsiaBeer potomania

Post TURP

urine osmolality <100 mOsm/L

Assess urine osmolality

Assess volume statusEFW restriction± loop diuretic

Correct hypokalemia

hypovolemic

urine osmolality > 100 mOsm/L

Urine [Na]<10meq/L

Urine [Na]>20meq/L

Renal loss Non renal loss

hypovolemic

TreatmentcIsotonic saline to correct hypovolemia

Correct hypokalemia if present

hypervolemic

IsovolemicContinued

on next page

Continued….


hypotonic hyponatremia

Assess volume status

Urine [Na]<10meq/L

Urine [Na]>20meq/L

hypervolemic

urine osmolality > 100 mOsm/L

Urine [Na]>20meq/L

Isovolemic

<10meq/L>20meq/L

Renal failureCirrhosis

Congestive heart failureNephrotic syndrome

EFW restriction(restriction less than urine output)

>20meq/L

SIADHHypothyroidism

Cortisol deficiency,

Administer saline with osmolality more than urine osmolality

Loop diureticADH antagonist

Treat underlying diseaseStop drug causing increased ADHsecretion

Correct hypokalemia if present

TREATMENT


HYPONATREMIAsummary of management

Replace calculated Na deficit with isotonic saline or RL

hypotonic Hypovolemic hyponatremiaAIM- positive water and Na balance

hypotonic isovolemic hyponatremiaAIM- negative EFW and positive Na balance

Symptomaticfrusemide ivi + 3% saline

AsymptomaticWater restriction ± Intermittent frusemide ± enteral salt

hypotonic Hypervolemic hyponatremiaAIM- negative EFW and Na balance

Na and EFW restriction + frusemide

ADH antagonist( for chronic SIADH as delayed onset of action)

demeclocycline HCL: 600-1200mg PO dailyPhenytoin sod: 200-300mg PO daily

Lithium: 600-1200mg PO daily


hyponatremia

Duration of hyponatremia

Absent/ mild neurologic signs

[Na] < 125 meq/L

Severe neurologic compromise

Initial acute management of

[Na] >125 meq/L

Search for alternative cause of neurologic compromize

Duration of hyponatremia[Na] < 125 meq/L

3% saline ivi

Initial goalincrease [Na] by 1.5-2.0 meq/L/h

for 3-4 hours or until symptoms resolveChange in [Na] can occur rapildlyImmediate attainment to normal

Is not goal

[Na] >125 meq/L

< 2 days

> 2 days

Change in [Na] should not exceed 10 meq/L in first 24 hours and

18 meq/L in first 48 hours


SOLUTION= SOLUTE+ SOLVENT

Molality: number of moles of a solute per kilogram of solventMolarity: number of moles of solute per litre of solution

Osmolality: number of osmoles of solute per kilogram of solventOsmolarity: number of osmoles of solute per litre of solutionOsmolarity: number of osmoles of solute per litre of solution

Tonicity = effective osmolality sum of the concentrations of the solutes which have the capacity to exert an

osmotic force across the membrane.


Free water (FW)Calculated base on osmolality

(Na, Glucose, BUN)

As urea is freely permeable across all cell membraneDoes not contribute to effective osmolality ie tonicity

Electrolyte free water (EFW)Calculation based on S.[Na}

Modified Electrolyte free water (MEFW)Calculation takes into consideration Glucose along with s.[Na]


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Electrolyte disorders in_critically_ill_patients__na