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