Dyselectrolytemias in Intensive Care Unit

Dr Vilas NaikDM (Nephrology)

Fellowship in Nephrology (University of Toronto)

Fluid and electrolyte disturbances

• Most common clinical problems encountered in ICU.

• Increased morbidity and mortality among critically ill

• Disturbances of monovalent ions (Na, K, Cl) and divalent ions (Ca, PO4 and Mg)

• K, Mg and PO4 are mostly intracellular cations. Cl exists in the extracellular space, at electrochemical equilibrium with Na.

Electrolyte blood pressV8 (2);dec 2010

Fluid and electrolyte disturbances

• An alteration in this ratio: significant effects on acid base balance

• Disorders like trauma, sepsis, brain damage, and heart failure cause disturbances in fluid and electrolyte homeostasis.

• Mechanisms:

– reduced perfusion to the kidney (hypovolemia or hypotension)

– – activation of hormonal systems such as RAAS and AVP

– Renal tubular damage.

Fluid and electrolyte disturbances

• Most important: inappropriate fluids

• Formulae to guide the therapy:

– All formulae regard the patient as a closed system

– none takes into account ongoing fluid losses that are highly variable between patients

– Therapy must be closely monitored with serial serum and urine electrolyte measurements.

Semin Dial. 2006 Nov-Dec;19(6):496-501.

Hyponatremia

Hyponatremia

• Commonest electrolyte disorder in hospitalized patients

• Mostly iatrogenic- wrong fluids, surgical wards and postoperative patients

• concept of “maintenance fluids”

Overview • Definition

• Physiology of Na and H2O

• Case

• Classify

• How urgent is the treatment and whom to treat?

• Treatment guideline.

Hyponatremia- Define it

• Relative water excessSr Na < 136 Meq/ L

– Low water and lower sodium content in the body

Hypovolemic hyponatremia

Extracellular fluid volume contraction (true volume depletion)

Syndrome of appropriate ADH secretion

always water excess

Hyponatremia- Define it

– Normal or excess Na, and still higher H2O content

CHF, Nephrotic syndrome, cirrhosis of Liver

Non osmotic release of ADH

“Effective” circulating volume contraction

Always relative excess of water

1L, 140 Na2L, 200 Na

140 Meq/L 100Meq/L

Don’t forget ADH…..

• Water surplus/ excess alone….

– Excess free water (electrolyte free water) ingestion alone – will result in large quantity of maximally diluted urine

– So only water surplus – cannot cause/ sustain hyponatremia

– ADH – almost always present

– What we want to know is why is the ADH present?

Symptoms and signsof hyponatremia

• None

• Headache

• Lethargy

• Dizziness and ataxia

• Mild confusion

• Psychosis

• Seizures

• Coma

Salt and water physiology

In an adult female and male- water content of the body (TBW) is approximate 50% and 60%

of body weight

2/3—1/3

ADH physiology

Water reabsorbtionOr

Water loss ADH

Painnausea

Osmoregulation Volume regulation

What is being sensed

osmolality Effective circulating volume

Sensors Hypothalamic

osmoreceptors

Carotid sinus,

Atria

Aff. Glomerular arteriole

Effectors ADH Sympathetic NS

RAAS

Natrauretic peptides

ADH

What is being effected

water excretion (ADH) Sodium excretion

H2O intake (thirst)

ADH and Sr Osmolality

Osmolality varies within 1%

282varies

ADH and blood volume

SNS

RAAS

ADH

5%

8%

12-15%

OSM or Volume….. ADH

The reverse is also true

ADH diorder

Na disorder

ADH acts on medullary collecting ducts (aquaporin type 2 receptors) - inserts Aquaporin (water) channels:

very rapid reabsorption of water

Filtrate/ water reabsorption

86 % water

H2Oimpermiable

CCD & MCDH2O permiable

Endocrine factors- remember

• Hypothyroidism

– commonest electrolyte derangement in hypothyroid

– Hyponatremia : 45% of hypothyroid patients

– Easily identified and correctable

• Addisons:

• hypersecretion of ADH

• Hyponatremia corrected by cortisol and volume repletion

• shuts off ADH release.

Case 1

• 66 yrs old lady, HT since 5yrs

• 1 month ago: BP- 160/94, thiazide added to amlodep

• Progressive lethargy, fatigue, only taking liquids. decreased urine output.

• Confused since 1 day- GTCs 1 hr ago

• Hospitalized: 60 kg (previously recorded)

– HR- 100, BP 130/70, low JVP, post ictal state.– Appeared volume depleted

Case 1• Treatment:

– Catheterized- 200 ml immediately removed, blood tests sent, IV access, Ryles tube

– FPBS- 106, IV NS 1000 ml over 1/2 hr

– Noted urobag to be full- staff assumed

retention, everyone happy.

We got the blood tests…..and I was worried

Parameters Blood urineNa 125 8

K 3 10

Cl 62 12

Total protein 8.4

Hb / Hematocrit 17 gm/ 51%

HCO3 30

Urea 55

Creatinine 1.6

Ca 9.5

Case 1more worried when diuresis occurred

and Na changed rapidly

Repeat Sr Na, exactly 2 hours later135 Meq/L

Urine output was 2L in 2 hours

Case 1

• Why did this happen?

• Risks?

• What went wrong?

• What do we do next?

Case 1- why did this happen

• Lets calculate what went in and how much should have the Sr Na changed.

– TBW= 30 L (50% of weight in females)

– Given 150 Meq/ L of 0.9 % NS (ie 1 L of H2O + 150 Na)

– Na deficit (Na to be replaced to achieve a particular Sr Na Level) = TBW (desired Na- actual Na)

– 150 Meq/L = 31 L (x- 125 Meq/L).

– “X” is what the Na should be, if we replace 1 L of 0.9% NS

– X = 5 Meq/ L

Why did this happen ?

• ADH shut off- volume replacement

• Free water diuresis-

– Electrolyte free water is excreted

– So if H2O is removed from body, Na concentration rapidly increases

Risks

• Osmotic demyelination syndrome (ODS or CPM)

– Under estimated incidence

– Critically ill ICU patients, difficult to diagnose

– Brain shrinks with rapid correction of Na

– No treatment, prevention

pons

Non pontine areas

What went wrong?

• Classify hyponatremia

– Acute Vs Chronic is the only useful one for treatment

– Most chronics have an acute component

– In our case, even before we classified it, we corrected it inadvertently

– Lady definitely had and acute component, excessive water drinking….

• Why did the Na correct so rapidly even with 150 Meq/L of Na?

What went wrong?Why did the Na correct so rapidly?

Thinking beyond the algorithm for Na correction

• 1 L of 0.9 % NS (150 Meq/L of Na)- the Sr Na should by 5 Meq/ L

• Why did it go up so rapidly?

The concept of tonicity balance

What goes in and what comes out?

Tonicity balance

Input

1 L NS

i.e. 1 L of H2O+ 150 Meq (Mmols)Of Na

Body compartmentNa and water Content

Output2 L urine

U Na + K = 40

i.e. 2 L of water And 40 mol Na +K

30 L TBW in 60kg female

30 L of water3750 Mmols Na

Tonicity balance- new body content of Na and water

Body compartmentNew Na and water Content

30 L TBW in 60kg female

Water= 30+1-2=29L

Na: 3750+ 150-403910

Sr Na = 3910/ 29134.8

And that was Our Sr Na after 2 hours

Why GTCs at Na of 125??

• 1st- we check Venous Na, not arterial.

– Brain sees arterial Na, not venous.

– Arterial Na 3-5 Meq/L lower than venous Na

• 2nd and more important-

– Post GTCs: seizures increase Sr Na!!!

– During seizures: water shifts in muscle cell- Sr Na can rise by 10 to 15 Meq/L after seizures

Don’t forget the water in GI tract..

• Most cases of acute on chronic hyponatremia, occurring at home- solute free water intake/ fruit juices etc – water source

• Insert RT in hyponatremic convulsion- remove water in stomach if its there

Remember about K correction….

• Most body K – intracellular

• K replaced for correction of hypokalemia:

– Enters the cells, intracellular Na comes out

– So giving 80 Meq/L of K is equivalent to giving Na

– K replacement is equivalent to giving Na

Back to our Case

• Lower the Na: 1 L of 5D = will decrease Na by 5Meq/L– 3910/30= 130

• Stop further diuresis of free water: DDAVD (desmopressin)

– Ideally IV 2 to 10ug, till urine output < 100 ml/hr

– Used 20 ug intranasal- decreased diuresis

• 6 hrly monitoring of Sr and urine electrolytes

• Replace what comes out (urine)- volume + electrolytes

Replace what comes out (urine)

• Urine 100 ml/ hr, Urinary Na + K = 70

– Give half NS with Na content of 75 meq

– This will prevent further rise

• Free water restriction to < 1 L/ day

Summary of guidelines for therapy

• Classify acute Vs Chronic- history, change in medications

• Assess volume status

– Most reliable hematocrit and total Sr. proteins

– Urine electrolytes (UNa < 10)

– Hemodynamic and clinical: least reliable

• Therapeutic considerations in acute hyponatremia and diagnostic considerations in chronic hyponatremia

Summary of guidelines for therapy

• Acute component of Chronic:

– Raise Na by < 5 Meq/L, use 3% NS

– Later fluid restriction and find the cause

• Ask 2 questions in the patient with low Na

– Why is the ADH present?

– Will the release of ADH cease and cause rapid water diuresis?

Specific to ICUs

• Symptoms may not be apparent in ICUs

– ventilated and sedated patients in the ICU

– worsening of cerebral edema

– catastrophic consequences such as brainstem herniation and respiratory arrest.

Copyright ©2006 American College of Cardiology Foundation. Restrictions may apply.

deGoma, E. M. et al. J Am Coll Cardiol 2006;48:2397-2409

Vasopressin (AVP) stimulates synthesis of aquaporin-2 (AQP) water channel proteins and their transport to the apical surface of collecting duct principal cells

TOLVAPTANNOT in hypovolemicHyponatremia

Hyperkalemia

Hyperkalemia: Life threatening Emergency

Common

Treatable

K physiology

• Total body K stores are approximately 3000 meq

• K: primarily intracellular cation {98 % of body K}

• Ratio of the K concentrations in the cells and outside: major determinant of the resting membrane potential across the cell membrane

• Generation of the action potential: essential for normal neural and muscle function

• K abnormalities: Muscle weakness and arrythmia

Regulation of urinary potassium excretion Connecting segment & Cortical duct

Na comes here

Lumen Negative

ROMK

Electrical gradientFor K secretion

Na-K ATPaseElectrical and

chemical gradient for Na reasbsorption

Regulation of urinary potassium excretionStimulation of K secretion by principal cells 

• An increase in plasma potassium concentration and/or potassium intake

• An increase in aldosterone secretion

• Enhanced delivery of sodium and water to the distal potassium secretory site

An increase in plasma potassium concentration and/or potassium intake

An increase in aldosterone secretion

Hyperkalemia

Renin angiotensinAldosterone system

(RAAS)

Na channel

Aldosterone deficiency, blockade

Enhanced delivery of sodium and water to the distal potassium secretory site

We need Na and Water here.

No distal Na (decresed GFR),No K secretion e.g Renal failure

Increased distal flow,Increased Na delivary, Increased K secretionEg diuretics

Distribution of potassium between the cells and the extracellular fluid

98 % K intracellularMaintained by thispump

Pump block eg digitalis toxicityBeta blockers

Pump stimulationInsulin, beta2 stimulation

Distribution of potassium between the cells and the extracellular fluid

Distribution of potassium between the cells and the extracellular fluid

Hyperkalemia

• Increased intake: K adaptation, rapid

• Shift: intracellular to extracellular, alone again not enough to sustain hyper K.

• Decrease excretion: almost always present

– Aldosterone

– Decreased distal delivery of Na/ water

– Renal dysfunction

Case 1

• 52/ male, DM and HT- 15 yrs

• Uncontrolled HT, Edema 3+

• Recent change in medications

• Adm: rapid onset quadriparesis over last 24 hours

Case1: examination

• ECG: HR of 30, broad QRS, CHB like pattern

• Rest vitals stable

• Higher functions normal

• Quadriparesis (grade 2 power, absent reflexes)

Case 1: Labs

• Na 129

• K 8.7

• Cl 96

• HCO3 16

• AG 17

• Creat 4.4

• Glucose 600

• CBC leucocytosis

• Urine• Sugar- 4+

• Ketones- nil

• Plenty pus cells

Hyperkalemia appraoch

• Intake

• Shift

• Impaired excretion

Case: analysis

• Intake: propably reduced (UTI, blood sugars)

• Shift:

– Severe hyperglycemia

– Insulin deficiency

– Acidosis

Case analysis

• Decreased renal excretion (almost always)

• Was started on ramipril (ACEI) for HT

– RAAS blockade (decreased aldosterone)

Decreased GFR

so decreased distal delivery of Na and water,

no Na reabsorption, no electronegative potential in lumen

No secretion of K

Na+

--

----

--

--

K+

Case analysis

• The patient was also started on spironolactone which blocked aldosterone action

• NSAIDS for fever

– Deceased GFR

– Renal failure

More mechanisms

• K loading increases ROMK expression and insertion into CCD luminal membrane

• ? May be gut signal to kidney to change ROMK

• Another K channel in CCD

– High capacity K channels (big K or Maxi K)

– Activated of high flow (water and Na delivery)

– Activated by K depletion

– Aldosterone independent action

Another K channel: intercalated cells

• H-K exchanger in IC cells of CCD

• Activated in K depletion

• Absorbs K+ and secretion of H+

Evaluation of hyperkalemia

• Exclude Pseudohyperkalemia

– potassium movement out of the cells during or after the blood collection

– Torniquet

– Thrombocytosis, high WBC counts (leukemias)

Assessing K excretion

• Kidneys can vary K excretion from < 5 Meq/L to 400 Meq/L, with decreased or increased intake

• Urine K/ Creatinine ratio

– < 15 mmol/gm in K depletion

– >200 mmol/gm in hyperkalemia–

Case 1

• Urine Na- 120 Meq/L

• Urine K- 15 Meq/L

• SO distal delivery of Na is adequate

• Severely impaired K excretion

• Aldosterone deficiency: hyporeninemic hypoaldosteronism in DM

• Drugs blocking aldosterone production and action

• Decreased GFR

Case 1

• NSAIDS: worsening of RFT (GFR)

• PG synthesis inhibited– PG inhibit renin –reduce aldosterone

• So in this patients, almost all things to increase his K has been done– ACEI, aldosterone blockade– NSAIDS

Treatment of severe hyperkalemia

• Calcium: if hypocalcemia or ECG changes

• Shift inside the cells:

– Insulin alone (hyperglycemia) or with 25 % Dextrose

– B2 agonist

– Bicarbonate if acidosis

Treatment

• Excretion

– Saline, especially if depleted

– Thiazide and loop diuretic

– K binding resins, small effect, increasing GI excretion, given with lactulose

• Dialysis- the most rapid and effective means in the presence of renal dysfuction and fluid overload

Case 1

• We started the patient on dialysis, normal sinus rhythem in 45 minutes

• Stopped implicated drugs, treated UTI

• Baseline creatinine of 2 mg % on follow up.

• K normal

The message..

• Increase intake- not sufficient

• Hyperkalemia is always a kidney problem

• Consider shift

• Drug history very important

• Assess excretion– Urine electrolytes- distal Na delivery– Aldosterone deficiency/ block– Urine K/ Creatinine is important

Hypokalemia

Severe KEmergency

ArrythmiasMuscular weakness

In ICUs….

• Upto 20% of patients

• Symptoms: mainly neuromuscular

• Risks:

– Respiratory muscle weakness, difficult to wean

– Life threatening cardiac arrthymias

– Paralytic ileus, risk of transmigration, nutrition

hypokalemia

• Low intake: possible, if prolonged, critically ill

– Kidneys can decrease excretion < 20 Meq/ day

– Low intake alone, not be sufficient unless severe

• Shift very important in this settings, drugs

• Excretion: diuretics

– Drugs like amphoterecin B

– Non absorbable anions- penicillins

Case 1

• 62/F, diabetic- 10 yrs, HT

• Admitted with fever, cough, SOB: 8 days

• Pneumonia

• Anorexia, severe nausea

• Meds- insulin, amlodepine, thiazides

• HR- 130, BP- 766/50, volume depleted

Case 1

• Hb- 14, TLC- 26000

• Creatinine- 1.2 mg%

• Na- 130, K- 4.6, Cl- 96

• HCO3- 23, pH- 7.3

• BS- 600

Case 1

• CAP: levofloxacin, pipericillin- Tazobactum

• IV insulin 20 units bolus, Insulin drip

• IV NS 1 L bolus, another 1 L after an hour

• BP 80/50

• Dopamine drip

• 6 am, inablility to move limbs

• Intubated because of hypoventilation, hypoxia

Case 1

• Na- 134, K- 1.8, Cl-102

• Urine output- 1200 ml

• Urine K- 20 Meq/L, Na - 12

Where did the K go?

Case analysis

• Intake- poor, nausea

– Likely lower body content: thiazides

– Hyperglycemia (sepsis)- osmotic diuresis

• Initial K normal: shift out of cells

– Hyperglycemia

– Insulin deficiency

Case analysis

Shift

insulin

Beta stimulationEndogenousSalbutamolDopamine/dobut

AlkalosisBicarb infusion

Shift

• Increased RBC production:

– treatment of megaloblastic anemia with B12 or folic

– GMCSF for neutropenia

• Hypokalemic periordic paralysis: Ca channel mutation

• Thyrotoxic paralysis

– B2 receptor stimulation

– Insulin resistence hyperinsulinemia

Shift

• Chloroquin intoxication

• Anti phychotic drugs: quitiapine and resperidone

Case analysis: Renal excretion

• Distal delivery of Na and K: NS infusion

• Diuretics: increase distal delivery of Na and Water

• Hyperglycemia: Osmotic diuresis

Excretion: Distal delivery of Na

Na comes here

Lumen Negative

ROMK

Electrical gradientFor K secretion

Renal excretion: aldosterone

• Aldosterone: Stimulate ENAC, Na-K- ATPase

– Malignant Hypertension: RAAS, Symp Nervous system stimulation

– Primary aldosteronism

– Endogenous and exogenous Steroids : Action on mineralocorticoid receptors

Renal excretion: aldosterone

Renal excretion: non-reabsorbable anions

• Like β-hydroxybutyrate in DKA,

– penicillin derivative in high dose penicillin therapy

• Accompanying Na ions, increased distal delivery, more Na reabsorption, more lumen negative

• Final pathway here is increased distal Na delivery

Renal losses

• Renal tubular acidosis

• Hypomagnesemia

• Barrters and Gietelmanns syndrome

Extra renal loses

• Loss of gastric secretions (vomiting, aspiration)

– Little K in gastric juice

– Loss of H+ met alkalosis increased HCO3 + Na

– Na exchanged with K

• Diarrhea: K content in intestinal juices (30- 50 meq)

•

Case analysis

• Decreased intake- yes, low stores (thiazides)

• Shift: definitely– Insulin– Beta stimulation

• Excretion: NO. Urine Na and K, appropriately low

Thanks for your patience