Fluid and electrolyte imbalance mec

FLUID AND
ELECTROLYTE
IMBALANCE
Meccar Moniem H. Elino
First Year Resident
Department of Internal Medicine
Southern Philippines Medical Center
October 14, 2019

OBJECTIVE
I – To present a clinical case in
correlation to the topic
II – To discuss key principles of fluid
balance, and electrolytes
III – To discuss the fluid derangement
and electrolyte imbalance with
their respective management

FLUID AND ELECTROLYTE IMBALANCE
C O N C E P T
M A P
Composition of Body
Fluids
Water Balance and
Circulation Integrity
Electrolyte Imbalance
Clinical
Scenario
Discussion
Key Principles
Hypovolemia
Disorders and
Management
Sodium Level
Disorders
Potassium Level
Disorders
Calcium Level
Disorders

REFERENCE
Jameson, J.L., Fauci, A., Kasper, D., Hauser, S., Longo, D. & Loscalzo, J. 2018. Harrison's
Principles of Internal Medicine 20th Edition. McGraw-Hill Education. ISBN: 978-1-
25-964404-7. Ch49

This is a case of
• D.G. Jr
• 52 year-old female
• Matina Pangi, Davao City
• Catholic
• Admitted last September 7, 2019 at our
institution due to shortness of breath
CASE SCENARIO

•Patient is a known hypertensive since
2014 with a poor compliance to
Amlodipine 10mg tab OD
•2 months PTA,
patient had an onset of on and off
dyspnea. No consult nor medication
taken.
CASE SCENARIO

•1 month PTA,
-Noted with easy fatiguability and
exertional dyspnea;
-Cannot tolerate anymore 2 flight of
stairs.
- Awakes at night due to Dyspnea.
- Still with no consult.
CASE SCENARIO

•2 weeks PTA,
Above symptoms were persistent.
Associated with non-productive
cough and bipedal edema
CASE SCENARIO

•4 days PTA,
Patient cannot tolerate to lie down.
Persistence of the dyspnea and loss
of appetite prompted the family to let
him be hospitalized.
CASE SCENARIO

Past Medical History
• Hypertension as prescribed
• PTB completed 6 month
treatment (2014)
• Family History: Unremarkable
• Personal Social: Nonsmoker,
Non Alcoholic Beverage
Drinker; Works as Tricycle 8-10
hrs/day
Review of System
• Paroxysmal Nocturnal Dyspnea
• 4-pillow Orthopnea
• Polyuria
• (-) Palpitation
Physical Findings
• 36.3C 114bpm 22cpm 140/80
• Awake Conversant In Mild
Respiratory Distress
• Anicteric Sclerae, Pink Palpebral
Conjunctivae
• Equal Chest Expansion, Fine
Crackles at Bilateral Middle
Lung fields
• Adynamic precordium, PMI at
Left 5th ICS Anterior Axillary;
Distinct S1 S2 (-) murmur;
• Globular, Nontender Abdomen
• (+) Bipedal Edema Grade 2
• Full and Equal pulses
CASE SCENARIO

Work up
Complete Blood Count
HGB 138.00 g/L(115-155)
HCT 0.35 % (0.36-0.48)
RBC 4.06 106/uL (4.2-6.1)
WBC 7.97 103/uL (5-10)
Neutrophil 94 % (55-75)
Lymphocyte 3 % (20-35)
Monocyte 4 % (2-10)
Eosinophil 0 % (1-8)
Basophil 0 % (0-1)
Platelet 301 109/L(150-450)
Urinalysis
Appearance Clear
Color Light Yellow
pH 6.5
Specific Gravity 1.010
Glucose Negative
Albumin Negative
Nitrite Negative
Esterase Negative
WBC 7.0 /uL (0-27)
RBC 2.0 /uL (0-28)
Epith Cell 0 /uL (0-7)
Bacteria 1.0 /uL (0-111)
Serum Chemistry
Sodium 117.0 mmol/L (136-144)
Potassium 4.4 mmol/L (3.6-5.1)
Calcium 2.11 mmol/L (2.23-2.58)
Magnesium 0.73 mmol/L (0.74-1.03)
Creatinine 62.0 umol/L (39-91)
BUN 5.9 mmol/L (2.9-7.1)
SGOT 24.4 U/L (15.0 – 41.0)
SGPT 13.6 U/L (14.0 – 54.0)
Alk Phos 68.86 Ul/L (38-126)
S Albumin 40.90 g/L
CXR
Pulmonary Congestion
ECG
Sinus Tachycardia

Work up
2D Echocardiography:
Ejection Fraction by Simpson: 27%,
No valvular and no wall motion
abnormalities
Whole Abdominal with Prostate
Ultrasound:
Incidental Finding of
Choledocholithiasis
Urine Chemistry
Urine Sodium:
11.13 mmol/L (40-220)
Urine Potassium:
27 mmol/L (25-125)
Serum Chemistry
HBA1c 5.9
CBG 132mg/dL (7.33 mmol/L)
Troponin 0.02 ng/mL
BUN 5.9 mmol/L
Derivational
• Serum Osmolality = 2 (Na + K) + RBS + BUN [if all units is mmol/L]
• Serum Osmolality of the Patient = 2 (117 +4.4) + 7.33 + 5.9 = 256.03
• Urine-to-plasma electrolyte ratio (urinary [Na+] + [K+]/plasma [Na+])
• Urine-to-Plasma Electrolyte Ratio = 0.37

Impression
Hypervolemic Hyponatremia and Pulmonary Congestion
secondary to Congestive Heart Failure secondary to
Hypertensive Cardiomyopathy (-) Left Ventricular
Enlargement (+) Left Ventricular Dysfunction 27% Ejection
Fraction, Sinus Rhythm, Functional Class III;
Choledocholithiasis.

Management
• PNSS 1L at KVO rate
• Low Fat Diet as Tolerated
• Medications:
Furosemide 40mg IV OD
Spironolactone 25 mg tab OD
Carvedilol 6.25mg tab OD
Sacubitril + Valsartan 50mg tab 1 tab BID
Tolvaptan 15mg tab OD
Berodual Nebulization 1 neb q8
Ursodeoxycholic Acid 300mg tab TID
Repeat Sodium every 6 hours

Management
Limit Oral Fluid Intake up to 1L/day only
O2 inhalation at 2LPM via Nasal Cannula as needed only

Summary of the Course in the
Wards
Day 1 Day2 Day3 Day4 Day 5
Serum Na: Na: 117.2
Na: 117.4
Na: 121.2
Na: 124.7
Na: 127.0
Na: 128.1
Na: 132.7
Na: 136.2
Na: 136.2
Auscultation: (+) Crackles (+) Crackles Relatively
Decreasing
Crackles
Clear Breath
Sound
Clear Breath
Sound
Position: Prefers
sitting tripod
position
Prefers
sitting tripod
position
High back rest Able to lie
with 3-pillow
Able to lie flat
and
decubitus
O2
Requirement
Requires O2 Requires O2 O2 PRN Room Air Room Air

Composition of Body Fluids
Water
The most abundant constituent in the body
~50% of total body weight in women
~60% of total body weight in men
Total-body water is distributed in
two major compartments:
55–75% is intracellular
25–45% is extracellular
Jameson, J.L., Fauci, A., Kasper, D., Hauser, S., Longo, D. & Loscalzo, J. 2018. Harrison's Principles of Internal Medicine 20th Edition. McGraw-Hill
Education. ISBN: 978-1-25-964404-7. Ch49

Composition of Body Fluids
Major ECF particles:
Na+ and its accompanying anions Cl– and HCO3–
Major ICF particles:
K+ and
organic phosphate esters
(ATP, creatine phosphate, and phospholipids)

Water Balance &
Circulatory Integrity
Normal Human Body Osmolality:
Between 280-295 mOsm/kg
Maintenance of Human Body Fluid Osmolality
1. Vasopressin
2. Water Ingestion
3. Renal Water Transport
• Countercurrent Mechanism
• Aldosterone

Water Balance &
Vasopressin
• Also known as Arginine-Vasopressin (AVP) or Antidiuretic
Hormone (ADH)
• Synthesized in magnocellular neurons within the
hypothalamus; the distal axons of these neurons project
to the posterior pituitary or neurohypophysis, from which
AVP is released into the circulation.

Question:
At what threshold osmolality AVP secretion is
stimulated?
a. 280
b. 285
c. 290
d. 295

Water Balance &
Vasopressin
For Circulatory Integrity:
Expression and activation of
1. Systemic V1A AVP receptors – vasoconstriction
and increase sympathetic nervous tone
2. V2 AVP receptors – Water Retention via
Aquaporin Channels

Question:
What abnormality of water homeostasis in the presence
normal circulating levels of AVP, there is a reduced or
absent insertion of active aquaporin-2 water channels into
the membrane of principal cells?
A. Syndrome of Inappropriate Antidiuretic Hormone
B. Nephrogenic Diabetic Insipidus
C. Central Diabetic Insipidus
D. Cerebral Salt Wasting

Water Balance &
Renal Water Transport
• Counter current mechanism
• Renin-Angiotensin-Aldosterone System

Hypovolemia
- True volume depletion
- Generally refers to a state of combined salt and
water loss, leading to contraction of the ECFV.
- May be renal or nonrenal in origin.

Hypovolemia
RENAL CAUSES EXTRARENAL CAUSES
• Osmotic Diuresis (eg Mannitol)
• Pharmacologic Diuresis/natriuresis
• Hereditary defects in Renal Transport
Proteins, Mineralocorticoid defects
• Tubulointerstitial injury (eg Interstitial
Nephritis, Acute Tubular Injury, Obstructive
Uropathy)
• Excessive Renal Water Excretion (e.g.,
diabetes insipidus)
• Fluid loss from GI tract (e.g. impaired GI
reabsorption, enhanced fluid secretion
• Insensible losses (evaporation of water
from skin and respiratory tract) : major
route for loss of solute-free water, typically
500-650 mL/day in healthy adults
• Accumulation of fluid within specific tissue
compartments (e.g., interstitium,
peritoneum, GI tract)

Hypovolemia
Management involves restoration of
normovolemia and replacement of ongoing losses
Mild Hypovolemia: oral hydration and
resumption of normal maintenance diet
Severe Hypovolemia: IV Hydration

Hypovolemia
Clinical Scenario Management
Normonatremic or Hyponatremic Patients Normal Saline (0.9% NaCl) is the most
appropriate resuscitation fluid
Hypernatremic Patiens Hypotonic Solutions
• 5% dextrose if water only (eg diabetes
insipidus)
Patients with Bicarbonate Loss and Metabolic
Acidosis
IV Bicarbonate (150meq of NaHCO3 in 5%
dextrose)
Patients with Severe Hemorrhage or anemia PRBC transfusion without increasing
hematocrit beyond 35%

DISCUSSION:
Electrolyte
Imbalance and
the Management

Question:
Which electrolyte imbalance is common among
hospitalized patients?
a. Hyponatremia
b. Hypokalemia
c. Hypocalcemia
d. Hyperkalemia

Question:
Which electrolyte imbalance is common among
hospitalized patients?
a. Hyponatremia – 22%
b. Hypokalemia – 20%
c. Hypocalcemia
d. Hyperkalemia – 10%

Hyponatremia
- Defined as plasma sodium <135 mmol/L
- Almost always due to increase circulating AVP
and/or increased renal sensitivity to AVP
combined with any intake of free water
(exception is hyponatremia due to low solute
intake e.g. beer potomania)
- Causes generalized cellular swelling

Hyponatremia
Manifestation
Early Symptoms: Nausea, Headache, Vomiting
Severe Cases: Seizures, Brainstem Herniation,
Coma and Death
Key complication: Normocapnic or Hypercapnic
Respiratory Failure (associated with hypoxemia
may amplify neurologic injury)

Hyponatremia
Three major considerations guide the therapy of
hyponatremia.
1. Severity of Symptoms
2. Chronicity
• Acute Hyponatremia: less than 48 hours
• Chronic Hyponatremia: more than 48 hours
3. Frequency Monitoring

Hyponatremia
Overly rapid correction
• Defined as >8–10 mM in 24 h or 18 mM in 48 h
• Associated with a disruption in integrity of the blood-brain barrier
• Allowing the entry of immune mediators that may contribute to
Osmotic demyelination Sydrome.
The lesions of ODS classically affect the pons, a neuroanatomic
structure wherein the delay in the reaccumulation of osmotic
osmolytes is particularly pronounced;

Hyponatremia
The traditional approach is to calculate an Na+ deficit,
where the
Na+ deficit = 0.6 × body weight × (target plasma Na+
concentration – starting plasma Na+ concentration),
followed by a calculation of the required rate.
Plasma Na+ concentration should be monitored
every 2–4 h during treatment, with appropriate changes in
therapy based on the observed rate of change.

Hyponatremia
Maximum Rate Change of Sodium from the
Baseline:
Chronic: 8-10 mmol/L in any 24 hour period
Acute: 4-6 mmol/L within the first to 2-4 hours

Scenario:
30y/M; 60kg; 3 day History of diarrhea; Non diabetic
Na = 120, K=4.2, Ca=2.3, Mg =1.02
(Desired – Actual) x Body Weight x 0.6
(135-120) x 60 x 0.6 = 540
(15) X 60 x 0.6 =540
the required change should not exceed by 10mmol, thus
(10) X 60 x 0.6 = 340

IV Solution (1 Liter) Na
mmol/L
K
mmol/L
5% NaCl in H2O 855 mmol/L 0
3% NaCl in H2O 513 mmol/L 0
0.9% NaCl in H2O 154 mmol/L 0
Ringer’s Lactate 130 mmol/L 4
0.45% NaCl in H2O 77 mmol/L 0
5% Dextrose in H2O 0 mmol/L 0

Hyponatremia
Serum glucose should also be measured.
Plasma Na+ concentration falls by ~1.6–2.4 mM for every
100-mg/dL increase in glucose.
Corrected Na+ =
Corrected Na+ =
1.6 x (glucose in mg/dL – 100)
100
Actual Na+ +
1.6 x (glucose in mmol/L – 56)
56
Actual Na+ +

Hyponatremia
Hypervolemic Hyponatremia
AVP antagonists (vaptans) are highly effective in SIAD and
in hypervolemic hyponatremia due to heart failure or
cirrhosis, reliably increasing plasma Na+ concentration
due to their “aquaretic” effects (augmentation of free water
clearance).
Most of these agents specifically antagonize the V2 AVP
receptor; tolvaptan is currently the only oral V2 antagonist
to be approved by the U.S. Food and Drug Administration.
Conivaptan, the only available intravenous vaptan, is a
mixed V1A/V2 antagonist, with a modest risk of
hypotension due to V1A receptor inhibition.

Hyponatremia
Fluid Restriction
• The urine-to-plasma electrolyte ratio (urinary [Na+] +
[K+]/plasma [Na+]) can be exploited as a quick indicator
of electrolyte-free water excretion;
If the urine-to-plasma electrolyte has
• Ratio of >1: Fluid Restriction at <500 mL/d;
• Ratio of ~1: restricted to 500–700 mL/d
• Ratio <1 should be restricted to <1 L/d.

In correlation to the main case
2D Echocardiography:
Ejection Fraction by Simpson: 27%,
No valvular and no wall motion
abnormalities
Whole Abdominal with Prostate
Ultrasound:
Incidental Finding of
Choledocholithiasis
Urine Chemistry
Urine Sodium:
11.13 mmol/L (40-220)
Urine Potassium:
27 mmol/L (25-125)
Serum Chemistry
HBA1c 5.9
CBG 132mg/dL (7.33 mmol/L)
Troponin 0.02 ng/mL
Derivational
• Serum Osmolality = 2 (Na + K) + RBS + BUN [if all units is mmol/L]
• Serum Osmolality of the Patient = 2 (117 +4.4) + 7.33 + 5.9 = 256.03
• Urine-to-plasma electrolyte ratio (urinary [Na+] + [K+]/plasma [Na+])
• Urine-to-Plasma Electrolyte Ratio = 0.37

First Scenario:
30y/M; 60kg; 3 day History of diarrhea; Non diabetic
Na = 120, K=4.2, Ca=2.3, Mg =1.02
1. (10) X 60 x 0.6 = 360 mmol
= 2.337 L
2. We will use 0.9% PNSS (154 mmol/L)
360 mmol
154 mmol/L
3. 2.337 L for 24 hours or 97cc/hour
4. Repeat Sodium 2- 4 hours

Case
Fluid Restriction
• The urine-to-plasma electrolyte ratio (urinary [Na+] +
[K+]/plasma [Na+]) can be exploited as a quick indicator
of electrolyte-free water excretion;
If the urine-to-plasma electrolyte has
• Ratio of >1: Fluid Restriction at <500 mL/d;
• Ratio of ~1: restricted to 500–700 mL/d
• Ratio <1 should be restricted to <1 L/d.

Hypernatremia
• defined as an increase in the plasma Na+
concentration to >145 mM.
• less common than hyponatremia, hypernatremia
is nonetheless associated with mortality rates of
as high as 40–60%
• usually the result of a combined water and
electrolyte deficit, with losses of H2O in excess
of Na+.

Hypernatremia
Maximum Rate Change of Sodium from the
Baseline:
Chronic: not more than 10mM/day or 10 mmol/L
per day
Acute: 1 mM/h or 1mmol/L/hour
Legend: 1mM = 1mmol/L
For solutes that are univalent like Na+, K+ (not Ca++ or Mg++)

Scenario:
40y/M; 60kg; Vehicular Accident; presented with
decreased sensorium at ER; Non diabetic
Na = 165, K=4.3, Ca=2.2, Mg =1.01
1. Maximum Desired Change: 10 mmol
Effect change of Sodium
of Chosen Solute to the
Patient
2. Choose Infusate. Determine its effect sodium change to the patient
(Sodium of Infusate – Actual Sodium)
Total Body Water + 1
=
“We will choose 5% Dextrose” It has Zero Sodium Content. We will
now determine its Effect change of Sodium

Scenario:
Na = 165, K=4.3, Ca=2.2, Mg =1.01
1. Desired Change: 10 mmol
Effect change of Sodium
of Chosen Solute to the
Patient
(Sodium of Infusate – Actual Sodium)
Total Body Water + 1
=
/ 0 – 165 /
( 60 x 0.6 )+ 1 Legend:
Total Body Water is 60% of Male
Weight and 50% of Female weight.
=
For D5Water
4.4 mmol

Scenario:
Na = 165, K=4.3, Ca=2.2, Mg =1.01
10mmol
4.4mmol/L
=
For D5Water
4.4 mmol / L
3. Determine how many liters is needed to have the desired change of
up to 10mmol.
/ 0 – 165 /
( 60 x 0.6 )+ 1
= 2.272 L for 24 hours
or 94cc/hour of D5W, then monitor Na 2-4 hours
=

Hypernatremia
Free Water Deficit
• It is imperative to correct hypernatremia slowly to avoid
cerebral edema, typically replacing the calculated free
water deficit over 48 h.
• Water should ideally be administered by mouth or by
nasogastric tube, as the most direct way to provide free
water, i.e., water without electrolytes.
• For Patients with Nephrogenic and Central Diabetes
Insipidus ,Calculation of urinary electrolyte-free water
clearance is required to estimate daily, ongoing loss of
free water which should be replenished daily.

Scenario:
Na = 165, K=4.3, Ca=2.2, Mg =1.01
1. Calculate Free Water Deficit:
Actual Sodium – 140
140
x TBW
165 – 140
140
x (60kg x 0.6)
=
=
Water Deficit
6.42 L
to be given in 72 hrs
= 89cc/hour
“or 360cc Free Water Flushing per NGT every 4 hours”

Hypokalemia
• Defined as a plasma K+ concentration of <3.5
mM, occurs in up to 20% of hospitalized
patients.
• Associated with a tenfold increase in in-hospital
mortality, due to adverse effects on cardiac
rhythm, blood pressure, and cardiovascular
morbidity.
• Mechanistically, hypokalemia can be caused by
redistribution of K+ between tissues and the
ECF or by renal and nonrenal loss of K+

Hypokalemia
• Systemic Hypomagnesemia – can cause
treatment-resistant hypokalemia, due to a
combination of reduced cellular uptake of K+
and exaggerated renal secretion.
• Spurious hypokalemia or “pseudohypokalemia”
can occasionally result from in vitro cellular
uptake of K+ after venipuncture, for example,
due to profound leukocytosis in acute leukemia.

Hypokalemia
• History: medications, diet and/or symptoms pointing
to a probable cause such as diarrhea and periodic
weakness
• Manifestation: Presents as cardiac (major risk factor
for both ventricular and atrial arrhythmias), skeletal
(weakness, paralysis) and intestinal disturbances
(paralytic ileus)
• Predisposes to Digoxin Toxicity (reduced
competition between K and Digoxin for shared
binding sites on cardiac Na/K/ATPase channel

Hypokalemia
• Predisposes to acute kidney injury and can lead to
end-stage renal disease (ESRD) in patients with
long-standing hypokalemia due to eating disorders
and/or laxative abuse

Hypokalemia
• An important precipitant of arrhythmia in patients with
additional genetic or acquired causes of QT
prolongation.
• Results in hyperpolarization of skeletal muscle, thus
impairing the capacity to depolarize and contract;
weakness and even paralysis may ensue.
• Electrocardiographic changes (marked when < 2.7
mmol/L):
• Broad Flat T waves
• ST Depression
• QT prolongation

Magnesium Deficiency an
Hypokalemia
• Magnesium depletion has inhibitory effects on muscle
Na+/K+-ATPase activity, reducing influx into muscle
cells and causing a secondary kaliuresis.
• In addition, magnesium depletion causes exaggerated
K+ secretion by the distal nephron; this effect is
attributed to a reduction in the magnesium-dependent,
intracellular block of K+ efflux through the secretory K+
channel of principal cells (ROMK)
• In consequence, hypomagnesemic patients are
clinically refractory to K+ replacement in the absence
of Mg2+ repletion.

Hypokalemia
Management:
Oral replacement with K+-Cl– is the mainstay of therapy in
hypokalemia.
Urgent but cautious K+ replacement should be considered
in patients with severe redistributive hypokalemia (plasma
K+ concentration <2.5 mM) and/or when serious
complications ensue.
The use of intravenous administration should be limited to
patients unable to use the enteral route or in the setting of
severe complications (e.g., paralysis, arrhythmia).

Hypokalemia
Correction: 24-48 hours
Peripheral intravenous dose:
• Maximum of 20–40 mmol of KCl per saline solution liter
Central Intravenous dose:
• Absolute amount to 20 mmol in 100 mL of saline solution
• For severe (<2.5 mmol/L) and/or critically symptomatic
• Central vein, preferably femoral vein with cardiac
monitoring in an intensive care setting, at rates of 10–20
mmol/h

Scenario:
32y/M; presented with bilateral lower extremity weakness
after a sumptuous meal during fiesta; Non diabetic
Na = 136, K=2.9, Ca=2.4, Mg =1.2
1. Calculate Potassium Deficit
Desired K – Actual K
0.27
x 100
3.5 – 2.9
0.27
x 100
=
=
Potassium Deficit
222 mEqs

Scenario:
32y/M; presented with bilateral lower extremity weakness
after a sumptuous meal during fiesta;
Na = 136, K=2.9, Ca=2.4, Mg =1.2
1. Calculated Potassium Deficit: 222 mEqs
2. Available preparation in our setting: KCl 40mEqs per Ampule
A. PNSS 1L + 40 mEqs KCl to run for 8 hours (120cc/hour)
Repeat for 3 cycles = 120 mEqs
B. KCl tablets 2 tablets 3x daily (1 tablet ~ 10mEqs) = 60 mEqs
C. 2 Banana per meal ( 1 serving ~12 meqs) = 48 mEqs
228 mEqs
Repeat S. Potassium every 6 hours until it is corrected
There’s no Hard and Fast Rule in correcting Hypokalemia

Hypokalemia
Goals of Therapy
1. Prevent life-threatening and/or chronic
consequences
2. Replace the potassium
3. Correct the underlying cause and/or mitigate
future hypokalemia

Hyperkalemia
• Hyperkalemia is defined as a plasma potassium
level of 5.5 mM, occurring in up to 10% of
hospitalized patients;
• Severe hyperkalemia (>6.0 mM) occurs in ~1%, with
a significantly increased risk of mortality.
• A decrease in renal K+ excretion is the most
frequent underlying cause

Hyperkalemia
• Medical emergency due to its effects on the
heart.
• Cardiac arrhythmias associated with
hyperkalemia include sinus bradycardia, sinus
arrest, slow idioventricular rhythms, ventricular
tachycardia, ventricular fibrillation, and asystole.

Hyperkalemia
ECG Serum Potassium Levels
Tall Peaked T waves 5.5 – 6.5 mmol/L
Loss of P waves 6.5 – 7.5 mmol/L
Widened QRS Complex 7-8 mmol/L
Sinusoidal Pattern ≥ 8 mmol/L

Transtubular
Potassium
Gradient (TTKG)
If TTKG >7-8,
indicative of reduced
tubular flow such as
in reduced ECFV or
in advanced renal
failure
Hyperkalemia
If TTKG < 3, can be
due to reduced distal
K secretion such as
during tubular
resistance to
mineralocorticoids
Hypokalemia

Hyperkalemia
Management
• Electrocardiographic manifestations of
hyperkalemia should be considered a medical
emergency and treated urgently.
• However, patients with significant hyperkalemia
(plasma K+ concentration ≥6.5 mM) in the
absence of ECG changes should also be
aggressively managed, given the limitations of
ECG changes as a predictor of cardiac toxicity

Hyperkalemia
Three Stages:
1. Immediate antagonism of the cardiac effects of
hyperkalemia
2. Rapid reduction in plasma K+ concentration
redistribution into cells.
3. Removal of potassium

Hyperkalemia
2. Rapid reduction in plasma K+ concentration
redistribution into cells.
Treatment Dosing Pharmacokinetics Others
Insulin
10 units RI + 50mL d50
Water
Effect in 10-20 min
Peaks at 30-60 min
Last for 4-6 hours
Hypoglycemia as Side
Effect;
May give insulin without
glucose if CBG 200-
250mg/dL
Beta Agonists
10-20mg nebulized
Salbutamol in 4 mL
PNSS
Effect in 30 min
Peaks at 90
Last 2 to 6 hours
Inhaled over 10 minutes
Bicarbonate IV 150mEqs + 1L D5W
Reserved for hyperkalemia
and Concomitant Acidosis

Hyperkalemia
3. Removal of Potassium
Treatment Key Points
Cation Exchange
Resins
• Sodium Polyestyrene Sulfonate (SPS) exchanges for Na for K in
the GI tract and increases fecal K secretion
• Given as 15-30g pre made suspension with 33% Sorbitol
Full Effect only after 24 hours
• Usually requires dosing every 4-6 hours
Diuretics
Loop and thiazide diuretics can be utilized to reduce K+ in volume
replete or hypervolemic patient with sufficient renal function
Dialysis
Hemodialysis: most effective & reliable method to reduce plasma
K+

Calcium Levels
The first step in the diagnostic evaluation of
hyper- or hypocalcemia is to ensure that the
alteration in serum calcium levels is not due to
abnormal albumin concentrations. About 50% of
total calcium is ionized, and the rest is bound
principally to albumin.
It is generally preferable to measure total calcium
and albumin to “correct” the serum calcium.

Calcium Levels
• Corrected Calcium
= Actual Calcium + 0.02 (4.1g/dL – Albumin g/dL)
There is 0.2 mM (0.8 mg/dL) increment to the total
calcium level for every decrement in serum albumin of 1.0
g/dL below the reference value of 4.1 g/dL for albumin

Hypercalcemia
Physiologic range: 8.9–10.1 mg/dL (2.2– 2.5 mM)
Mild hypercalcemia
• 11–11.5 mg/dL or
• 2.75 to 3.5 mmol/L
Severe hypercalcemia
• >12–13 mg/dL
• >3.5 mmol/L

Hypercalcemia
Mild hypercalcemia (up to 11–11.5 mg/dL)
• Usually asymptomatic and recognized only on
routine calcium measurements.
• If symptomatic: may complain of vague
neuropsychiatric symptoms, including trouble
concentrating, personality changes, or
depression.
• Other presenting symptoms may include peptic
ulcer disease or nephrolithiasis, and fracture risk
may be increased.

Hypercalcemia
Severe hypercalcemia (>12–13 mg/dL)
• Result in lethargy, stupor, or coma, as well as
gastrointestinal symptoms (nausea, anorexia,
constipation, or pancreatitis).

Hypercalcemia
Severe hypercalcemia (>12–13 mg/dL)
• Decreases renal concentrating ability, which may
cause polyuria and polydipsia.
• With long-standing hyperparathyroidism, patients
may present with bone pain or pathologic
fractures.
• Result in significant electrocardiographic
changes, including bradycardia, AV block, and
short QT interval; changes in serum calcium can
be monitored by following the QT interval.

Hypercalcemia
Management
• Mild, asymptomatic hypercalcemia does not
require immediate therapy, and management
should be dictated by the underlying diagnosis.

Hypercalcemia
Management
• Significant, symptomatic hypercalcemia usually
requires therapeutic intervention independent of
the etiology of hypercalcemia.

Hypercalcemia
Management:
Symptomatic hypercalcemia
Initial therapy:
• 4–6 L of intravenous saline over the first 24 h,
• May require the use of loop diuretics to enhance
sodium and calcium excretion.
• For Hypercalcemia of Malignancy
• Zoledronic acid (4 mg intravenously over ~30 min),
Pamidronate (60–90 mg intravenously over 2–4 h),
Ibandronate (2 mg intravenously over 2 h)
• Denosumab – if refractory to bisphosphonates

Hypercalcemia
Management:
Symptomatic hypercalcemia
Initial therapy:
• 4–6 L of intravenous saline over the first 24 h,
• May require the use of loop diuretics to enhance
sodium and calcium excretion.
• For 1,25 (OH)2 D-mediated hypercalcemia
• IV Hydrocortisone 100-300mg daily or
• Oral prednisone 40-60mg daily for 3-7 days

Hypocalcemia
Physiologic range: 8.9–10.1 mg/dL (2.2– 2.5 mM)
Mild hypercalcemia
• 11–11.5 mg/dL or
• 2.75 to 3.5 mmol/L
Severe hypercalcemia
• >12–13 mg/dL
• >3.5 mmol/L

Hypocalcemia
Patients may be asymptomatic if the decreases in
serum calcium are relatively mild and chronic.

Hypocalcemia
Moderate to severe hypocalcemia
• Associated with paresthesias, usually of the fingers,
toes, and circumoral regions, and is caused by increased
neuromuscular irritability.
• Physical Examination:
Chvostek’s sign
Carpal spasm or Trousseau’s sign

Hypocalcemia
Severe hypocalcemia
• Can induce seizures, carpopedal spasm,
bronchospasm, laryngospasm, and prolongation
of the QT interval.

Hypocalcemia
Management:
• The approach to treatment depends on the
severity of the hypocalcemia, the rapidity with
which it develops, and the accompanying
complications (e.g., seizures, laryngospasm).
• Accompanying hypomagnesemia, if present,
should be treated with appropriate magnesium
supplementation.

Hypocalcemia
Management:
Acute, Symptomatic Hypocalcemia
• Calcium gluconate, 10 mL 10% diluted in 50 mL
of 5% dextrose or 0.9% sodium chloride, given
intravenously over 5 min.
• Continuing hypocalcemia: IV infusion
• 10 ampules of calcium gluconate or 900 mg of
calcium in 1 L of 5% dextrose or 0.9% sodium
chloride administered over 24 h.

Hypocalcemia
Management:
Chronic hypocalcemia due to hypoparathyroidism
• Treated with
Calcium supplements (1000–1500 mg/d elemental
calcium in divided doses); and either
Vitamin D2 or D3 (25,000–100,000 U daily) or
Calcitriol [1,25(OH)2D, 0.25–2 μg/d].

Fluid and electrolyte imbalance mec

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