Hypokalemia, or low potassium levels, can be caused by inadequate intake, excessive losses, or impaired renal excretion. Common symptoms include muscle weakness, constipation, and cardiac arrhythmias. Evaluation involves checking renal function tests and electrolyte levels. Management focuses on replacing potassium losses through oral or intravenous supplementation depending on the severity. Close monitoring is needed to prevent overcorrection.

1. Electrolyte Disturbances
Group 4

2. Outline
• Objectives
• Disturbances of sodium concentration
• Disturbances of Potassium concentration
• Disturbances of Calcium concentration
• Disturbances of Magnesium concentration
• References

3. Objectives
• To discuss the common presentations of electrolyte abnormalities
• To discuss the management of common electrolytes abnormalities

4. Kidan
Hyponatremia

5. Sodium – [L - Natrium]
• Body content
• 98% of body Na is found in ECF. Normal [Na+]= 135-145 mEq/L
• Principal determinant of extracellular osmolality
• Necessary for maintenance of intravascular volume
• >40% of total body sodium is in bone, the reminder interstitial and
intravascular spaces
10/8/2023 5

6. • Low intracellular sodium (10mEq/L) is maintained by Na+-K+ ATPase
• Sodium is unique among electrolytes because water balance
determines its concentration
• It is the amount of TBW relative to total body sodium that
determines sodium concentration.
10/8/2023 6

7. Hyponatremia
• Is the second most common electrolyte disorder.
• Can be a marker of underlying disorder, and usually caused by
inability to excrete water normally.
1. Due to dilution;
2. Due to depletion; or
3. Excess solute relative to free water
10/8/2023 7

8. Causes of Hyponatremia
Based on Tonicity
• Hypertonic Hyponatremia
• Hyperglycemia, DM, Manitol  increased osmolality
• Isotonic Hyponatremia
• Pseudohyponatremia  lab error due to Increased TAG, PTH
• Hypotonic Hyponatremia
• Most common form
• Further divided based on volume
10/8/2023 8

9. Cont’d
Based on Volume
Hypervolumic Euvolumic Hypovolumic
Heart Failure SIADH Volume depletion
Cirrhosis Renal failure Diuretics
Renal failure Hypothyroidism Addison’s disease
10/8/2023 9

10. Clinical Manifestations
• Depend on volume status, the rapidity of development and degree of
hypoosmolality
• Hypovolemic Hyponatremia  Symptoms of DHN
• Hyponatremia  decreases osmolality of ECF  water flows into ICF
• Rapid change results in brain edema  in severe cases Herniation
• Hyponatremia is the most common cause of afebrile seizure in children
<6months of age.
10/8/2023 10

11. Symptoms of hyponatremia
CNS
01
>Headache
>Bizarre
behavior
>Hallucinations
>Obtundation
>Incontinence
>Respiratory
insufficiency
>Decorticate or
decerebrate
posture
>Dilated pupils
>Seizure
>RF
>Coma
>altered T
regulation
02 Nausea
Vomiting
GI
Hemodynami
c/CVS
03
Brady-/tachycardia
Hyper-/hypotension
AKI due to
hypoperfusion
04
Muscle cramps
Weakness
MSK

12. Evaluation of the hyponatremic patient
● Psuedohyponatremia should be excluded. The causes are:
hyperglycemia, severe hypertriglyceridemia, and hyperproteinemia.
● Hyperglycemia can cause actual dilutional hyponatremia by
drawing water into vascular space.
● In true psedohyponatremia no water shift occurs and the serum
osmolality is normal.

13. History
● Patients with any of the following are likely to have isotonic or hypertonic
hyponatremia:
○ Recent surgery utilizing large volumes of electrolyte-poor irrigation
○ Treatment with mannitol, glycerol, or intravenous immune globulin
○ Lipemic serum
○ Obstructive jaundice
○ Plasma cell dyscrasia
● Otherwise, the patient is likely to have hypotonic hyponatremia, the causes
of which are listed on the next slide.

14. ADH ←→ Impaired urine
dilution but normal
ADH suppression
Impaired urine
dilution due to
↑ADH
Abnormally low
osmostat: ↑ADH
• Primary
polydipsia
• Low dietary
intake
(potomania,
etc)
• Advanced renal
impairment
• Diuretic-induced
(eg: thiazides)
• True volume
depletion
• HF
• Cirrhosis
• Addison’s disease
• SIADH (euvolemic
hyponatremia)
• Nephrogenic
SIADH
• Reset osmostat of
chronic illness
• Genetic reset
osmostat
• Reset osmostat of
pregnancy (hCG)
• Exercise induced hyponatremia
• Cerebral salt wasting

15. History
● Loss of fluids with electrolytes
● High protein or high fluid intake
● HIV, MM, CNS or pulmonary disease, HF, CLD, recent surgery
● Medications, other drugs
● GBS/Edema
● Adrenal insufficiency, or S/Sx of hypothyroidism

16. 10/8/2023 16

17. Work UP
• Hyperosmolar causes should be excluded (eg, RBS)
• Dilutional are associated with hypervolemic circulation.
• Initial Ix: SCr, Se-, and bicarbonates, CBC, LFT
• Hyponatremia with decreased total body sodium  sodium loss >
water loss
• Renal [Urine Na > 20mEq/L]  Diuretic use [Thiazides], osmotic
diuresis[Mannitol or glucose], salt losing renal disease [Nephritis, obstructive
uropathy]
• Extrarenal  Vomiting and Diarrhoea, burn, peritonitis, pancreatitis [urine
Na < 20mEq/L]
• Normal volume status with hyponatremia SIADH
10/8/2023 17

18. Management
• Assess and treat the underlying causes + Determine the need for hospitalization.
• Assess the volume status and correct hypovolemic shock, if present, with NS.
• Prevent further decline in [Na]
• Decision to correct and rate of correction depend on the acuity, severity, and whether symptoms are
present.
• Severity:
• Severe: <120 mEq/L
• Moderate: 120-129 mEq/L
• Mild: 130-134 mEq/L
• Acuity. If hyponatremia develops over 48 hr, it is acute.
• Treatment of hyponatremia in areas where 3% HS is not available involves using enteral table salt.
10/8/2023 18

19. Hospitalization
● Acute hyponatremia
● Severe hyponatremia
● Symptomatic hyponatremia
● Those at risk for complications or overcorrection

20. ● If [Na]<130 AND Asx, 50 ml bolus of 3% saline UNLESS [Na] is autocorrecting
due to diuresis.
● If [Na]<130 AND +Sx, 100 ml bolus of 3% HS over 10’, up to 300 ml. This will
raise [Na] by 4-6 mEq/L & prevent herniation.
● Monitor patients who have mild hypoNa
Initial therapy of acute hypoNa

21. ● If mild, address causative conditions, fluid restriction.
● If moderate to severe AND +severe Sx or preexisting intracranial pathology, manage
as acute Sx hypoNa.
● If moderate AND +mild to moderate Sx, same management as mild chronic hypoNa
● If severe BUT no/mild Sx and no IC pathology, 3% HS @ 15-30ml/hr.
Initial therapy of chronic hypoNa

22. Subsequent management
● Monitoring of serum [Na]
● Deficit can be calculated as:
○ Dose (mEq) = TBW(140-[Na])
● The effect of a L of infusate on plasma [Na] can be estimated thus
○ ∆𝑃𝑙𝑎𝑠𝑚𝑎 𝑁𝑎 =
𝑓𝑙𝑢𝑖𝑑 𝑁𝑎 −𝑝𝑙𝑎𝑠𝑚𝑎 [𝑁𝑎]
𝑇𝐵𝑊+1
● [Na] should be corrected at a rate not greater than 10-12mEq/L if
acute and 8 mEq/L if chronic

24. Enteral table salt
● Each teaspoon of iodinated table salt contains 6 g of NaCl or 2400 mg of Na or 104
mEq of sodium.
● Enteral supplementation of sodium is safe and effective [].
● 3 teaspoons of table salt in 500 ml water will have 624 mEq/L of Na.
● Therefore, in a man weighing 70 kg and with initial [Na] of 125 mEq/L, each 10 ml
of this solution will raise serum [Na] by ~0.12mEq/L.
● 100 × ∆𝑃𝑙𝑎𝑠𝑚𝑎 𝑁𝑎 =
624−125
42+1

25. • Correction of Hyponatremia  loss of water in excess of Na.
• Aggressive correction may lead to the osmotic demyelination syndrome (ODS)
• Hyponatremia of acute onset [<48hrs]  safe to correct over 24 hrs
• Hyponatremia of gradual onset  Do not exceed rate of 0.5mEq/L/hr
• Start with isotonic crystalloids at rates determined by volume status

26. • In euvolemic and hypervolemic patients  At the rate of maintenance fluid.
• Fluid restriction to 2/3 of maintenance is the mainstay of therapy for SIADH
• Rise in serum Na of 5mEq/L can be achieved by IV infusion of 6ml/Kg of 3% NS
over 20-60minutes
• Single bolus is usually sufficient to reduce acute symptoms
• Loop diuretics: Furosemide  increases free water clearance
• Identify the underlying pathology and initiate appropriate treatment
10/8/2023 26

27. Hypernatremia
Phillipos

28. Hypernatremia
Sodium Excess
• Excess administration of
hypertonic saline
• Excessive sodium bicarbonate
• Inadequately diluted infant
formula
• Ingestion of sea water
Water Deficit - common
• Inadequate intake – infants,
mental illness, disabled – can’t
respond to thirst
• Excess loss
• GI loss - Vomiting and Diarrhea
• Urine - DM [Osmotic diuresis], DI
• Increased insensible water loss
10/8/2023 28

29. Clinical Manifestations
• Symptoms appear usually only with impaired thirst or restricted access
to fluid.
• Rare until >160mEq/L
• CNS effectscellular dehydration  possible hemorrhage
• Hypovolemic hypernatremia  classic signs of tachycardia,
orthostasis, hypotensionv
10/8/2023 29

30. Hypernatremia Evaluation
• Volume
• Serum sodium, osmolality, BUN/Creatinine
• Urine sodium, osmolality
10/8/2023 30

31. Management
• Initial therapy of hypovolemic hypernatremia is focused on correction of circulatory failure
• Water deficit = Body weight x 0.6 (1-145/[Current Na])
• Restoration of TBW should be gradually, over >48hrs
• Correction over 24hrs  Cerebral edema
• Start with isotonic crystalloids [NS better than RL], and complete with hypotonic crystalloid
[D5 0.45NaCl]
• Ongoing loss and maintenance fluid must be provided in addition to the deficit correction.
• Hypernatremia shouldn’t be corrected rapidly.
10/8/2023 31

32. • Goal:- To decrease serum Na by < 12mEq/L/d or 0.5-1 mEq/L/hr
• Frequent monitoring
• Suspected DI  Trial of vasopressin [Drug of choice is desmopressin]  initial
dose 0.05 – 0.1ml intranasaly BID.
• Primary sodium excess is treated by removal of sodium excess
• Restrict Na intake, if renal function is intact  Diuretics + Hypotonic fluid
• Patients with renal failure  Dialysis
10/8/2023 32

33. Hyperkalemia

34. Hyperkalemia > 5.5 mEq/L
1. Due to increased intake
- oral or IV intake
2. Increased release from cells hemolysis,
• Rhabdomyolysis
• Crash Injuries
• Acidosis
• Rapid rise in ECF osmolality
3. Impaired excretion by kidney:
• Drugs: ACEI, spironolactione, NSAIDS
• Acute and chronic renal insufficiency
10/8/2023 34

35. Clinical Manifestations
• Primarily GI, neuromuscular and CVS
abnormality.
• ECG changes:- Peaking of T waves 
increased PR interval, flattening of P wave,
widening of QRS complex  Ventricular
fibrillation
• However, the progression and severity of
ECG changes do not correlate well with
the serum potassium concentration.
10/8/2023 35

37. Diagnosis
• Often readily apparent
• Repeat potassium level is often appropriate, spurious hyperkalemia is
very common in children.
• If significant elevation of WBC or platelet  repeat sample from
plasma
• History:- Potassium intake, risk factors for transcellular shift,
medications, renal insufficiency [oliguria]
10/8/2023 37

38. • RFT [Creatinine, BUN], Acid base status
• Cell lysis:- Concomitant hyperphosphatemia & hyperuricemia and
hyperkalemia
• Hemolysis:- hemoglobinuria, decreased haematocrit, increased LDH and bilirubin
• Rhabdomyolysis:- elevated CPK, hypocalcemia
• Known T1DM  elevated glucose suggests transcellular shift of
potassium
10/8/2023 38

39. Management
10/8/2023 39

40. Hypokalemia
Tigist

41. Potassium [L - Kalium]
Body Content
• Total Potassium in the body:-
• ICF – 98 % - The main intracellular
cation  135mEq/L
• Muscle, Liver, RBC
• ECF – 2 %  Bone [Majority],
Plasma
• Plasma Level  3.5 – 5 mEq/L
[Laboratory Result]
• The Na+ – K+ ATPase Pump
maintains this gradient
Physiologic Function
• The high potassium gradient
produces the resting membrane
potential of cells
• Neuromuscular responsiveness of
nerve and muscle cells 
Contractility of CARDIAC, Skeletal,
and SMOOTH MUSCLES.
• Intracellular potassium affects
cellular enzymes and intracellular
PH. [K+ - H+ antiport]
• Maintains cell volume  contributes
to intracellular osmolality
10/8/2023 41

42. Figure 24.4 1
The major factors involved in potassium balance
Factors Controlling Potassium Balance
Approximately 100
mEq (1.9–5.8 g) of
potassium ions are
absorbed by the
digestive tract each
day.
Roughly
98 percent of the
potassium
content of the
human body is in
the ICF, rather
than the ECF.
The K concentration in the
ECF is relatively low. The rate
of K entry from the ICF
through leak channels is
balanced by the rate of K
recovery by the Na/K
exchange pump.
When potassium
balance exists,
the rate of urinary
K excretion
matches the rate
of digestive tract
absorption.
The potassium ion
concentration in the
ECF is approximately
5 mEq/L.
KEY
 Absorption
 Secretion
 Diffusion through
leak channels
The potassium ion
concentration of the
ICF is approximately
135 mEq/L.
Renal K losses
are approximately
100 mEq per day

43. Hypokalemia
• Serum potassium (k+) level < 3.5 mEq/L
- Mild 3 - 3.4mEq/L
- Moderate 2.5 - 2.9mEq/L
- Severe < 2.5mEq/L

44. etiology
1. Intracellular shift/ Translocation
• Alkalosis
• Insulin
• elevated beta adrenergic activity
2. GI loss
- Upper Vs Lower GI tract

45. 3. Renal loss
• Diuretics
• Increased mineralocorticoid activity
• Excretion of non reabsorbable anions
4. Other causes
• Excessive sweating
• Patients undergoing dialysis or plasmapharesis

46. Clinical manifestations
• Severity is proportionate to the degree and duration of reduction in
serum level
- serum k+ < 3.0
- rapid fall
- predisposing factor to arrythmia due to use of digitalis

47. • Muscle weakness
• cardiac arrythmias & ECG abnormalities
-PAC, premature ventricular beats, sinus bradycardia, AV block,
ventricular tachycardia or fibrillation
- ST segment depression, decrease T wave or increased U wave
amplitude, prolonged QT interval
• kidney abnormality
• glucose intolerance

48. Diagnosis & Evaluation
• History - cause identification (diuretic use, diarrhea, vomiting)
• P/E - evaluation of muscle strength
• Lab - Sr electrolytes, RFT, Blood gas, urinary potassium

49. • ECG - T wave flattening or inversion
- ST depression
- prolonged PR interval
- presence of U waves, T & U wave fusion
- QT prolongation
- Dysrhythmias

50. • 2 major components to diagnostic evaluation
# assessment of urinary potassium excretion to distinguish renal
potassium losses(diuretic, 1*aldosteronism)from other causes
of hypokalemia
# assessment of acid base status

51. Treatment
• Goals - prevent or treat life threatening complications
- replace potassium deficit, mng of concurrent electrolyte abn.
- to diagnose and correct the underlying cause
• Main stay therapy - Potassium replacement*

52. • Mild hypokalemia (3.0 - 3.5mEq/L)
- prioritize treatment of underlying condition (eg- GI loss)
- increasing dietary potassium intake
- consider oral supplementation
• Moderate hypokalemia (2.5 - 2.9mEq/L)
- oral repletion (except in severe symptoms or ECG changes)

53. • Severe hypokalemia (<2.5mEq/L) &/or high risk of recurrent severe
hypokalemia
- IV KCL repletion - rate shouldnt exceed 10 - 20mEq/hr through a
peripheral IV (upto 40mEq/hr through central)
Potassium supplementation will be ineffective if concurrent
hypomagnesemia is left untreated.

54. Hypercalcemia
Samuel

55. Metabolism
• Absorption from GI tract
is by passive diffusion
and active transport
• Most of the calcium is
reabsorbed by the
kidney – net loss is
about 2%
• Calcium is controlled by
both PTH and calcitonin

56. • Total calcium
- Free (ionized) calcium (50%)
- Protein bound calcium (40%)
- Calcium complexed with
organic and inorganic
molecules (10%)
• High albumin states (volume depletion
or multiple myeloma) may lead to
pseudohypercalcemia.
• Low albumin states like malnutrition,
total serum calcium may appear low
while ionized calcium is again not very
affected.
• Ca2+= serum Ca2+ + 0.8 x [normal alb-
patient alb]

60. KIDNEY
SKELETON
GI
CNS
CVS
Signs and Symptoms

61. KIDNEY
SKELETON
GI
CNS
• Polyuria
• Renal insufficiency (rarely seen in mild
disease, in severe cases may cause a
reversible drop in GFR)
• Nephrolithiasis
• Nephrogenic DI
CVS
Signs and Symptoms

62. KIDNEY
SKELETON
GI
CNS
• Bone pains
• Arthritis
• Osteoporosis
• Osteitis fibrosa cystica
CVS
Signs and Symptoms

63. KIDNEY
SKELETON
GI
CNS
• Constipation
• Anorexia
• Nausea
• Pancreatitis
• Peptic Ulcers
CVS
Signs and Symptoms

64. KIDNEY
SKELETON
GI
CNS
• Depression or Anxiety
• Cognitive dysfunction
• Lethargy, confusion, stupor, and coma
may occur in patients with severe
hypercalcemia
• More likely to occur in the elderly and in
those with rapidly rising calcium
CVS
Signs and Symptoms

65. KIDNEY
SKELETON
GI
CNS
• Increases myocardial contractility
• Shortened QT interval/Prolonged
PR/Wide QRS complexes
• Calcium deposition in coronary arteries
and myocardial fibers
• Hypertension
CVS
Signs and Symptoms

66. KIDNEY
SKELETON
GI
CNS
CVS
Signs and Symptoms

67. KIDNEY
SKELETON
GI
CNS
CVS
Signs and Symptoms

68.  Ca++
PTH
Vitamin D
Malignancy
Medicines
Endocrine
Genetic
Causes

69. Hypo
calcemia
Normal
calcium
?
Suspect

Calcium
Medications
I-PTH
High/Normal PTH
Low
Vit D Toxicity
Milk-Alkali
Cancers/
Lymphoma
Low PTHrP
Hyper
calcemia
< 8.0
8.5 to 10.3
> 10.3

74. • Based on the Grade and Symptoms of Hypercalcemia:
• Grades/Classes:
• Mild – Ionized calcium 5.6 to 8 mg/dL (1.4 to 2 mmol/L)
• Moderate – Ionized calcium 8 to 10 mg/dL (2 to 2.5 mmol/L)
• Severe – Ionized calcium 10 to 12 mg/dL (2.5 to 3 mmol/L)
Management

75. General Approach:
• Patients with asymptomatic or mildly symptomatic (eg, constipation)
hypercalcemia (calcium <12 mg/dL [3 mmol/L]) do not require immediate
treatment.
• Patients with a serum calcium of 12 to 14 mg/dL (3 to 3.5 mmol/L) may not
require immediate treatment
• However, an acute rise to these concentrations may cause marked changes in
sensorium, which requires more aggressive measures.
• Patients with a serum calcium concentration >14 mg/dL (3.5 mmol/L) require
more aggressive treatment, regardless of symptoms.
Management

76. I.V. Saline
Hydration &
Diuresis
Gluco-
Corticoids
Anti-
resorptive
s
Calcitonin
I.M/S.C.
Fluid
• Depending on the clinical status
• 200-300 ml/hour to maintain UO of
100-150 ml/hour
• Dehydration can make
hypercalcemia worse by impairing
the renal excretion of calcium
Management

77. I.V. Saline
Hydration &
Diuresis
Gluco-
Corticoids
Anti-
resorptive
s
Calcitonin
I.M/S.C.
Glucocorticoids
• Vitamin D intoxication or endogenous
production of calcitriol (sarcoidosis,
TB)
• Prednisone 20-40 mg
• Lowers calcium in 2-5 days
Management

78. I.V. Saline
Hydration &
Diuresis
Gluco-
Corticoids
Anti-
resorptive
s
Calcitonin
I.M/S.C.
Bisphosphonates
• Inhibit release of calcium by interfering
with osteoclast mediated bone resorption
• More potent than saline and calcitonin
• Can be used for hypercalcemia of any
cause
• Max effect seen in 2-4 days
• Also used to prevent hypercalcemia and
skeletal events in malignancy
Management

79. I.V. Saline
Hydration &
Diuresis
Gluco-
Corticoids
Anti-
resorptive
s
Calcitonin
I.M/S.C.
Bisphosphonates
• Pamidronate 60 or 90 mg IV over 2-4
hours
• Zoledronic acid (ZA) 4 mg over 15
minutes
• ZA preferred due to quicker infusion time
• Side effects (low grade fever, myalgias,
osteonecrosis of the jaw, atypical
fractures)
Management

80. I.V. Saline
Hydration &
Diuresis
Gluco-
Corticoids
Anti-
resorptive
s
Calcitonin
I.M/S.C.
Calcitonin
• IM or SQ injections at dose of 4 IU/kg
• At 6-12 hour intervals
• Modest reductions and low toxicity profile
• Vitamin D intoxication and immobilization
• Acts quickly
• Escape phenomenon may develop in 48
hours
Management

81. I.V. Saline
Hydration &
Diuresis
Gluco-
Corticoids
Anti-
resorptive
s
Calcitonin
I.M/S.C.
Others
• Dialysis
• Loop Diuretics
• Newer therapy:
• DENOSUMAB monoclonal
antibody
• RANKL inhibitor
• Humoral hypercalcemia of
malignancy
• Bisphosphonate refractory
hypercalcemia
Management

83. Hypocalcemia

84. • Ionized calcium < 4.5 mg/dL; total calcium < 8.5 mg/Dl
• Effects of albumin and Ph
• The fraction of ionized calcium is inversely related to plasma pH; alkalosis can
precipitate hypocalcemia by lowering ionized calcium without changing total
serum calcium
• Hypoproteinemia may lead to a false suggestion of hypocalcemia because the
serum total calcium level is low even though the ionized Ca2+ remains normal.
• It is best to measure serum ionized calcium if hypocalcemia or hypercalcemia
is suspected.

85. Causes
• Decreased entry of calcium into blood
• Vit d deficiency, hypoparathyroidism, bisphosphonate, denosumab,
pseudohypoparathyroidism, hypomagnesumia
• Increased exit of calcium out of blood
• Kidney failure, tissue injury, pancreatitis, blood transfusions, sepsis,
hyperphosphatemia
• Pseudohypocalcemia
• Hypoalbuminemia

86. • The clinical manifestations of hypocalcemia result from increased neuromuscular
irritability and include
• Muscle cramps
• Carpopedal spasm (tetany)
• Perioral tingling
• Weakness
• Paresthesia
• Laryngospasm
• Increase in DTR
• Seizure-like activity

87. • Tetany can be detected by:
• The Chvostek sign (facial
spasms produced by lightly
tapping over the facial nerve
just in front of the ear) or
• The Trousseau sign (carpal
spasms exhibited when
arterial blood flow to the
hand is occluded for 3 to 5
minutes with a blood
pressure cuff inflated to 15
mm Hg above systolic blood
pressure).

88. • Heart
• Hypotension
• Arrhythmias
• HF

91. • For Severe Tetany or seizures resulting from hypocalcemia consists of
intravenous calcium gluconate (1-2 mL/kg of a 10% solution) given slowly
over 10 minutes, while cardiac status is monitored by electrocardiogram
(ECG) for bradycardia, which can be fatal.
• Long-term treatment of hypoparathyroidism involves administering vitamin
D, preferably as 1,25-dihydroxyvitamin D, and calcium.
• Therapy is adjusted to keep the serum calcium in the lower half of the
normal range to avoid episodes of hypercalcemia that might produce
nephrocalcinosis and to avoid pancreatitis.

93. References
• Up-to-Date
•
•