SUBJECT SEMINAR

ELECTROLYTE IMBALANCE IN GERIATRIC

PATIENTS
Chairperson:- Dr.Raveendra K R (Professor & HOD)
Associate Professor:- Dr. B C Prakash
Assistant Professor:- Dr. Yogananda M N
Senior Resident:- Dr. Pooja A G
Dr. Deepak
Dr. Geetu Krishna P
Time-02:15 to 04:00pm
Venue-Medicine Seminar Hall
Date:-23.08.2023
Presenter-Dr. Rohit K L
1st Year Post Graduate
Department of Geriatric Medicine
BMCRI
 Introduction
• Aging is associated with extensive changes in body composition that alter water &
electrolyte distribution & predispose older adults to the development of fluid &
electrolyte imbalance.

• Kidney is the primary organ responsible for salt, water and mineral homeostasis
through selective reabsorption & secretion of these substances.

• The wide range of capacity of kidney to handle electrolytes & fluids takes a
downward turn in geriatric age group.
 Effect of Aging on Body
Composition
• Percentage of body weight occupied by water progressively decreases.
• Total body water in geriatric patients decreases from 60%50% due to increase
fat mass & decrease in muscle mass.
• Loss/Gain of same amount of body water will have greater impact on
• blood pressure
• Cardiovascular status
• Osmolality
• Decreased muscle mass↓ Potassium stores
• Older individual will require lesser amounts of potassium to replete potassium
stores & will be unable to handle a large K⁺ load.
 Effect of Aging on Kidney
• 2/3rd of adult patients will undergo a significant decline in their kidney fuctions as they age.
• Usually electrolyte imbalance in hospital setting is usually treated with impaired kidney
function already set in.

• In the absence of overt structural or urinary abnormalities, an estimated glomerular filtration

rate (eGFR) <60 mL/min has been defined as the cutoff for declaring a state of chronic kidney
disease (CKD).

• Clinically manifests as ↓ ability to handle solutes & water excess load.

• E.g., While a young individual may be able to excrete a 20 mL/kg water load easily within 2
hours, an older individual may take considerably longer.
• Glomerulosclerosis & Interstitial nephritis is commonly seen in aging kidney
1. Proteinuria
2. Architecture distortion for normal homeostatic kidney function.
a) Tubuloglomerular feedback
b) Urinary concentration
c) Dilution.
• Graded corticomedullary hypertonic interstitiumNa⁺/Cl ⁻/UreaEnsure horizontal
transfer of urea, K⁺, NH ₃ for urinary concentration, Na⁺ reabsorption, net acid excretion.
 Disorder of Water balance
• Water balance determines body fluid osmolalitythe solute to water ratiogoverned by
serum sodium concentration.
• CNS osmoreceptors innervating the posterior hypophysis (ADH) keep a tight control over
the intraindividual variation of Na⁺ concentration in serum.
↑ in osmolality
ADH production and secretion
collecting tubule of the nephron,
expression of aquaporin water channels and urea transporters
concentrated urine.
• Maximal urine concentration capacity-1200mOsm/kg
• Maximal dilution capacity-40 to 50mOsm/kg
• ADH is a small peptide hormone with a short half-life, serum osmolality is sensed and
regulated on a minute-to-minute basis.
• Aging is accompanied by curtailment of all steps in the process of regulation of water
homeostasis.
• Osmoreceptionimpaired.
• ADH release sluggish
• Effect of ADH on the collecting tubulesustained.
 Hyponatriemia
• Most common electrolyte abnormality in clinical medicine.
• Inability to excrete a water load due to excessive ADH presence or due to lack of
sufficient solute excretion.
• 10% of ambulatory older individuals
• Hospitalized or institutionalized patients with estimates ranging from 25% to 50%.
• Common associated conditionswith hyponatriemia
• congestive heart failure,
• cirrhosis,
• cancers,
• chronic kidney disease.
• chronic central nervous system disorders
• chronic pulmonary disease
• Most common cause of hyponatriemia in elderly is SIADH.
• Common symptoms associated with hyponatriemia even with mild changes:-
• fatigue,
• inanition,
• weakness
• nausea
• As the [Na⁺] falls more serious symptoms arise
• Clouded sensoriumInability to concentrate on tasks
• Falls
• Seizures
• Coma
• More than the value of [Na⁺] it’s the rate of fall of osmolality.
• If the fall is gradual, then the overt symptoms are unlikely to precipitate.
• [Na⁺] less than 115mEq/L is bound to present with symptoms.
• Approach to hyponatriemia in elderly is determined
• Clinical context
• Severity
• Chronicity
• True hyponatriemia & pseudohyponatriemia should be differentiated.
• Hyperglycemia, leads to intracellular shift of free water leading to hemodilution &
consequently ↓ [Na⁺] .
• Corrected [Na⁺] in view of hyperglycemia.
[(Measured Glucose-100/100)]X1.5+Measured [Na⁺]=Corrected [Na⁺]
• If corrected Sodium falls within normal range then it is pseudohyponatriemia.
• Even hyperlipidemia can cause hyponatriemiaHypertriglyceridemia.
• HyperproteinemiaMultiple myeloma, paraproteinemias
• Serum osmolality will be normal in above scenarios.

• Kidney response can be assessed by urine osmolality

• Specific gravity
• 1.010Isothenuric (300mOsm/kg)
• 1.006 Urinary dilution
• .1.010 in absence of glycosuriaUrinary concentration.
• Urine osmolality ↓ to 100-150mOsm/kg in case of hypo-osmolar condition.
• Inability to dilute urine Excessive ADH secretionInability to excrete free water load.
• Volume status assessment like in hypovolemia
• Low blood pressure
• Orthostatic hypotension
• Weight loss
• Low urine Sodium (<20-40 mEq/L)
• Hypervolemic hyponatriemia
• Hypertension
• Peripheral/Pulmonary edema.

• Edema forming condtionsCCF, Cirrhosis, Nephrotic Syndromeassociated with

Hyponatriemia
• SIADH is not an end diagnosis but a sign of underlying disease.
• Head trauma,
• CNS disorder,
• Medication
• Cancer
• In hypovolemiaUrine sodium is lower and Fractional Sodium Excretion (FeNa)
• Serum uric acid tends to remain higher in hypovolemia/Thiazide diuretic induced ↓ [Na⁺].
• ↑Aldosterone levelsHypovolemia
• Aldosterone is also frequently suppressed in SIADH.
• Cerebral salt wasting syndrome & Renal salt wasting syndrome.
• Presenting feature ↓[S. Na⁺] & ↑ [U. Na⁺] >40mEg/L
• Cerebral salt wasting syndrome-Neurosurgical setting.
• Renal salt wasting syndromeCisplatin (Neoplasm treatment).
• In renal wasting Severe hypovolemia is also observed.
• Uric acid can be low in them & hence can be mistaken for SIADH.
• Low urine osmolality in the setting of hyponatremia, <100 mOsm/kg,
• low solute ingestion state, either subsistence on the so-called tea and toast diet or beer
potomania
• not possible to excrete water in the absence of any solute, failure to ingest salts or proteins
will limit water excretion by limiting solute delivery in the nephron.
• hyponatremic with true psychogenic polydipsiaexcrete a very dilute urine as with the
low solute ingesters, high volume urine.
• Mild degree of ↓[S. Na⁺] is associated with
• Falls
• Bone loss
• Cognitive impairment.
Correction necessary, in that case.Correctable causes
Diet
Medication Mild fluid restriction
Forced fluid ingestion
Severe symptomatic hyponatriemiaMedical Emergency.
To raise [S. Na⁺] to such a level where life threatening symptoms abate.
Correction8mEq/L in 1st 24 hours.
SIADH, High urine osmolality responds appropriately to Hypertonic saline+/- Loop diuretic for free water
loss.
• Hypovolemic patientNormal saline correction.
• Patients in hyervolemic state like congestive heart failure can be treated with high dose
high ceiling diuretics & fluid restriction.
• Within 1st 24 hours serial monitoring is required with emphasis of not overcorrecting.
 Hypernatriemia
• Occurs far less frequently than hyponatremia and tends to occur at the extremes of ages-
neonates and the very old.
• Hyperosmolar condition loss of water through
• renal or
• extrarenal mechanisms and/or
• inability to sense or respond to thirst by increasing fluid intake
• Older individualsreduced thirst sensation,
• Critical mechanism to prevent the development of hypernatremia-Lost in elderly.
• Unable to concentrate the urine maximallymore water losses through renal excretion.
 Causes
• Stroke/limitation to mobilityunable to obtain fluids,
• severe diarrheaintestinal fluid losses,
• Advanced chronic kidney disease, or
• Uncontrolled diabetes mellitus with severe polyuria
• Development of partial or complete central diabetes insipidushead trauma after a fall or
surgery.
• High mortality associatedwith hypernatriemia due to the underlying causes than the
effect.
• normal renal response to hypernatremia will be
• elaboration of a low-volume,
• highly concentrated urine,
• urine output of less than 20 mL/h and a
• urine osmolality of greater than 600 mOsm/kg.
• extrarenal water losses such as diarrhea or inability to obtain water to drink due to
immobility can be though of with such a renal response.
• Hypernatremic person shows
• polyuria with a urine output greater than 50 to 100 mL/h and/or a
• urine osmolality of 300 mOsm/kg or less,
• suggests renal losses of water osmotic diuresis
Uncontrolled diabetes mellitus or
Nephrogenic or central diabetes insipidus.
• Gold standard for diagnosing the cause of polyuria/polydipsia syndromes has been 18- to
24-hour water deprivation with
• measurement of serum and urine osmolality and
• serum ADH levels followed by an assessment of the response to exogenous ADH, .
• Interpretation of polyuria/polydipsia syndromes is also complicated by the fact that
• High urine volume state medullary “washout” of the interstitialurinary concentration
decreased
• downregulation of aquaporin channels required for water reabsorption from the tubule.

• response to exogenous or endogenous ADH may be impaired, leading to the mistaken

diagnosis of nephrogenic diabetes insipidus
• measurement of serum copeptin, a small peptide secreted along with ADH, hold promise
as more sensitive and specific diagnostic tools, particularly for chronic hypernatremia.
• Nephrogenic diabetes insipidus
• chronic kidney diseases,
• chronic urinary tract obstruction-prostatic hypertrophy,
• Medications-lithium.
• The polyuria in these conditions may be extreme—6 to 7 L/day—closer to 3 to 4 L/day
and can be managed conservatively.
• Thiazide diuretic can be used as adjunct.
• True ADH deficiencyOral Vasopressin 0.1mg uptil 0.4mg.
• TREATMENT
• Water replacement
• Correction of hypernatremia should be judicious, limiting the decrease serum sodium to
approximately 8 to 10 mEq/L/24 h,
• Some have suggested that 50% of the water deficit can be safely corrected in the first 24
hours.
• Water deficit= %body water X mass X [(measured-ideal [Na⁺])/(ideal [Na⁺])].
• water deficit is less than 3 Loral water repletion is reasonable.
• intravenous administration of 5% dextrose in water
• Cardiovascular status is in jeopardy, then the initial fluid of choice is 0.9% saline to
ensure adequate intravascular volume
• Degree of volume depletion is felt to be moderate, then initial therapy with 5% dextrose
in 0.45% saline would be a reasonable choice.
 Potassium homeostasis
• Serum potassium is influenced by two separate sets of factors: those related to kidney
function and those related to the transmembrane movement of potassium in and out of
cells.
• well-preserved kidney function, older individuals have a normal serum potassium under
unstressed conditions.
• As GFR declines, the fractional excretion of potassium does not rise as much as in young
individuals.
• Kaliuretic response to furosemide is blunted in older adults relative to younger
individuals.
• Lower aldosterone levels and/or aldosterone resistance in older adults
• glucoregulatory hormones insulin and glucagon,
• adrenergic stimulation of either α- or β-receptors, Alter potassium concentration intra
• acid-base balance, and & extracellularly
• alterations in serum osmolality
• Sodium-potassium ATPase in muscle cells of older adults differs in pattern of isoform
expression and phosphorylation status
 Hypokalemia
• serum potassium less than 3.5 mEq/L,
• Prevalence in community setting-5%
• Hospitalized setup-20%
• hypokalemia clinical features
• muscle weakness including
• proximal muscle weakness and
• intestinal ileus,
• cardiac arrhythmias-atrial tachyarrhythmias
• polyuria,
• fatigue.
• accompanied by multiple electrolyte abnormalities including
• hyper- or hyponatremia,
• metabolic acidosis or alkalosis, and
• Hypomagnesemia
• Hypokalemia can result from
• poor intake (eating disorders, alcoholism),
• increased losses (diuretics, mineralocorticoid excess, diarrhea), or
• shift of potassium from the extracellular to the intracellular compartment (insulin therapy).
isolated urine potassium of greater than 4 mEq/L suggests excessive renal losses,
• TTKG = (Kurine × osmolalityserum)/(Kserum × osmolalityurine)
• TTKG >7 urinary loss
• TTKG <3 urine losses are not a major contributor.
• potassium replacement is orally, through potassium-rich foods or potassium supplements,
as overdose is unlikely.
• Determining the amount of potassium needed to replace losses is inexact at best due to
confounding factors such as
• ongoing losses,
• acid-base status,
• differences in muscle mass, and
• underlying medical conditions
• relatively small doses such as 10 or 20 mEq at a time with frequent repeat measures safest
approach, especially among kidney disease patients,
• who are on potassium-sparing medications, or who are very emaciated.

• Individuals with chronic kidney disease or those who are already taking a medication that
blunts renal potassium excretion such as
• trimethoprim-sulfamethoxazole,
• a calcineurin inhibitor (cyclosporine or tacrolimus),
• an angiotensin-converting enzyme (ACE) inhibitor,
• angiotensin receptor blocker.
 Hyperkalemia
• Older patients are more susceptible to hyperkalemia because of the
• loss of kidney function,
• the loss of muscle mass,
• the changes in regulation of muscle ion content,
• lower levels of renin and aldosterone,
• medications for chronic conditions which are associated with hyperkalemia
• ACE inhibitors,
• angiotensin receptor blockers, and
• potassium-sparing diuretics
• Older individuals glucose intolerance blunt the ability of K+ to be translocated to the
intracellular compartment
• Type IV renal tubular acidosis which will diminish renal potassium excretion even in the
presence of relatively normal kidney function.
• Hyperkalemia is seen in up to 10% of hospitalized patients
• ACE inhibitors & ARB can’t be held as the sole culprit of hyperkalemia in elderly
patients have been proven the same in various studies like Seyed et al., published in
Theraupetics & Clinical risk management journal
• Potassium of greater than 5.3 mEq/L is accepted as hyperkalemia.
• Spurious hyperkalemia, where the measured potassium is elevated but the ambient serum
potassium is normal,
• hemolysis of the blood sample associated with difficult phlebotomy
• deterioration of the sample,
• severe thrombocytosis,
• severe leukocytosis, or
• red cell disorders.
• Hyperkalemia is frequently asymptomatic.
• Muscle weakness and fatigue are the most common symptoms.
• [K⁺] greater than 7 mEq/L, including
• sinus bradycardia,
• complete heart block,
• wide QRS tachycardia, or the
• classic sine wave pattern
• The widely taught progression of the ECG manifestations of hyperkalemia such as
• peaked T waves,
• prolonged PR interval,
• absence of P wave, and
• QRS prolongation is
seldom seen
• Absence of ECG findings in the presence of a high [K⁺] should not lead the clinician to
conclude that the hyperkalemia is erroneous or insignificant.

• Physical examination
• muscle weakness,
• a reduction in deep tendon reflexes, and
• bradycardia.
• Severe hyperkalemia in older adults
• trimethoprim/sulfamethoxazole in patients on spironolactone,
• the use of two inhibitors of the renin-angiotensin-aldosterone axis,
• the use of nonsteroidal anti-inflammatory drugs, and the
• presence of type 2 diabetes
• non–life-threatening hyperkalemia outpatient setting
• elimination of medications that cause hyperkalemia,
• improving hydration status, and
• reversible causes of reduction in kidney function such as medications and
• volume depletion
• Intravenous calcium gluconate will stabilize the myocardial cell membrane, decreasing
the potential for cardiac arrest but does not lower potassium levels.
• Intravenous insulin (works fastest, within 15 minutes, but is more transient than the β-
agonists.)
• Inhaled β-agonists
• Intravenous bicarbonate,
• Forced diuresis with loop diuretics, (preserved eGFR)
• Exchange resins such as sodium polystyrene sulfonate, or Aggressive [K⁺] reduction
• Dialysis (reduced eGFR)
Mineral Homeostasis
1. Calcium
2. Phosphate
• References:-
• 1. Hazzards textbook of Geriatric Medicine & gerontology
• 2. Brocklehurst textbook of Geriatric Medicine & Gerontology
• 3. Harrison’s Principle of Internal Medicine
• 4. Washington Manual of Medical Theraupetics