WORKSHOP CASE FOR
FLUID AND ELECTROLYTE
DISORDERS
SUBSECTION D3
FACILITATOR: DRA. COMES-NATIVIDAD
RIVERE. ROBOSA. RODAS. RODRIGUEZ. ROGELIO.
ROQUE. RUANTO. SABALVARO. SALAC. SALAZAR,
J. SALAZAR, R. SALCEDO
Hyponatremia
51 year old, female
CC: vomiting
1 week
PTA
2 days PTA
• Fever, dysuria, urgency
• Took Paracetamol and antibiotic which relieved
fever
• Headache, body malaise, nausea, vomited 3x (50
cc/episode)
• Persistence of symptoms
Admission
History
ROS unremarkable
(-) for smoking and
alcohol history
Hypertensive for 10 yrs,
taking Telmisartan and
HCTZ daily for the past
month
Discontinued Amlodipine
due to bipedal edema
Physical Examination
Weak looking and
wheelchair borne, poor
skin turgor, dry mouth,
tongue and axilla
BP supine-120/80
sitting-90/60
usual-130/80
HR supine-90/min
sitting-105/min
Weighed 50 kg but usual
weight was 53 kg.
JVP <5cm H20 at 45
degrees
Laboratory Tests
Hb=132 mg/dL
Hct=0.35
WBC=12.5
Neutrophils=0.88
Lymphocytes=0.12
P Na=123 mEq/L
P K=3.7 mEq/L (N)
Cl=71 mEq/L
BUN=22 mg/dL
S Crea=0.9 mg/dL
Glucose=98 mg/dL
ABG:
pH=7.3
CO2=35
HCO3=18
U Na=100 mmol/L
U Osm=540 mosm/L
Urinalysis:
Yellow, sl.turbid
pH 6.0, SG 1.020
albumin and sugar (-)
hyaline casts 5/hpf
pus cells 10-15/hpf
RBC 2-5/hpf (not
dysmorphic)
Salient Features
 51 year old, female
• Vomiting
• Fever, dysuria, urgency
• Headache, body malaise, nausea
• Vomiting: 50cc/episode
• Known hypertensive
Telmisartan (40 mg)
• Hydrochlorthiazide (12.5 daily)
Weak looking, wheelchair-borne
BP: 120/80 (supine), 90/60 (sitting), 130/80 (usual)
HR: 90/min (supine), 105/min (sitting)
Lost weight, poor skin turgor, dry mouth, tongue and axillae
Normal JVP
•
•
•
•
•
•
1. What is the diagnosis? Basis?
Hypoosmolal hyponatremia secondary to
thiazide intake
Basis
Signs of ECF Volume Contraction
Body
malaise
Weakness
Poor skin
turgor
Dry mouth
and tongue
Dry axillae
Postural
tachycardia
Postural
hypotension
2. What factors contributed to the
development of hyponatremia in
the patient?
Factors in the Development of Hyponatremia
 Vomited 3x (50 cc/episode)
 Primary Sodium Loss (Secondary water gain): GastointestinaI
Losses

Due to vomiting predisposes the patient to hyponatremia since
there is a corresponding sodium loss associated with water loss
Factors in the Development of Hyponatremia
 Intake of hydrochlorothiazide
 Primary Sodium Loss (Secondary water gain): Renal Losses
It is important to note that diuretic-induced hyponatremia is
almost always due to thiazide diuretics  lead to Na+ and K+
depletion and AVP-mediated water retention.
 Inhibits reabsorption of sodium and chloride in the distal
convoluted tubule  promoting water loss.

Factors in the Development of Hyponatremia
 Intake of telmisartan
 ARB

Inhibits tubular Na and Cl reabsorption, K excretion, water
retention  promotes water loss.
3. Compute for the plasma osmolality and
the effective plasma osmolality. What is
the importance of computing for such?
Plasma Osmolality and Effective Plasma
Osmolality
 Osmolality (calc) = 2 x Na + glucose + urea
**if all measurements in mmol/L
 Osmolality (calc) = 2 x Na + glucose/18 + urea/2.8
**if measurements are in mg/dL
 Given:



Plasma Na = 123 mEq/L
Glucose = 98 mg/dL
Urea = 22 mg/dL
 Osmolality = 2(123) + (98/18) + (22/2.8)
 Osmolality = 259. 301
N = 275 – 295 milli-osmoles per kilogram
Reference: Becker, K. 2001. Principles and Practice of Endocrinology and Metabolism 3rd Ed.
Plasma Osmolality and Effective Plasma
Osmolality
 Effective Osmolality (calc) = 2 x Na + glucose
**if all measurements in mmol/L
 Osmolality (calc) = 2 x Na + glucose/18
**if measurements are in mg/dL
 Given:



Plasma Na = 123 mEq/L
Glucose = 98 mg/dL
Urea = 22 mg/dL
 Osmolality = 2(123) + (98/18)
 Osmolality = 251.44
< 275 = Hyponatremia
Reference: Becker, K. 2001. Principles and Practice of Endocrinology and Metabolism 3rd Ed.
Importance of computing for the plasma osmolality
and the effective plasma osmolality
 ECF tonicity is determined primarily by the Na+
concentration and patients who have hyponatremia
have a decreased plasma osmolality.
Reference: Becker, K. 2001. Principles and Practice of Endocrinology and Metabolism 3rd Ed.
4. What are the significance of
urine osmolality (Uosm) and urine
sodium (Una)?
Urine Osmolality (Uosm)
• A more exact measurement of urine concentration
than specific gravity
–
–
Patient with Uosm below 100 mOsm/kg are able to
appropriately suppress ADH release, leading to a maximally
dilute urine
Patients with a higher urine osmolality have an impairment in
water excretion due to the presence of ADH
• Indicated to evaluate the concentrating and diluting
ability of the kidney
•
•
Accurate test for decreased kidney function
Monitor course of renal disease/ electrolyte therapy
Reference: Rennke H., Denker, B. 2007. Renal Pathophysiology: The Essentials
Urine Sodium (UNa)
• Helps distinguish renal from non- renal causes of
hyponatremia
• Urine sodium exceeding 20 mEq/L is consistent with
renal salt wasting.
–
Diuretics, ACE inhibitors, mineralocorticoid deficiency, salt
losing nephropathy
• Urine sodium less than 10 mEq/L implies avid
sodium retention by the kidney.
–
Compensation for extra-renal fluid loss (vomiting, diarrhea,
sweating or third space wasting)
Reference: Rennke H., Denker, B. 2007. Renal Pathophysiology: The Essentials
Urine Sodium (UNa)
• Effective circulating volume depletion and SIADH are
the two major causes of true hyponatremia (with an
inappropriately high urine osmolality) and these disordes
can be distinguished by measuring the Una.
–
Patients with hypovolemia are sodium avid in an attempt to limit
further losses.
•
–
Urine sodium is generally below 25 mEq/L.
In comparison, patients with SIADH are normovolemic and sodium
excretion is in a steady state equal to intake.
•
Urine sodium concentration is typically above 40 mEq/L.
Reference: Rennke H., Denker, B. 2007. Renal Pathophysiology: The Essentials
5. Compute for the sodium (Na)
deficit.
Na deficit
 Sodium Deficit = Total Body Water * Normal Wt in
kg * (Pt's Na - Desired Na)
 (TBW = 0.6 if male and 0.5 if female)
Na deficit
 Sodium Deficit = (0.5)* (53kg)* (135mEq/L-
123mEq/L)
 Sodium Deficit= 318mmol/L
Principles of Therapy
 Raise plasma sodium concentration by restricting
water intake and promoting water loss.
 Correct underlying disorder.
6. What are the basic principles in
the treatment of hyponatremia?
Principles of Therapy
 Asymptomatic hyponatremia
 Sodium repletion (isotonic saline)
 Restoration of euvolemia removes the hemodynamic stimulus
for AVP release.
 Restriction of sodium and water intake, correction of
hypokalemia, and promotion of water loss in excess of
sodium.
 Dietary water restriction should be less than urine output.
Principles of Therapy
 Asymptomatic Hyponatremia
 Sodium concentration should be raised by no more than 0.5 –
1.0mmol/L over the first 24 hours.
 Acute or severe Hyponatremia
 Plasma sodium conc: < 110-115mmol/L
 Rapid correction
 Severe symptomatic
 Hypertonic saline
 1-2 mmol/l per hour for the first 3-4 hours
 Raised by no more than 12mmol/L during the first 24 hours
7. What is the complication of the
rapid correction of the
hyponatremia?
Complication of Rapid Correction of
Hyponatremia
 Rate of correction: depends on the absence or
presence of neurologic dysfunction

Related to the rapidity of onset and magnitude of fall in plasma
Na+ concentration
 Rapid correction of hyponatremia leads to osmotic
demyelination syndrome (ODS).
Osmotic Demyelination Syndrome
 Neurologic disorder characterized by flaccid
paralysis, dysarthria and dysphagia
 Mechanism:
Patients with chronic
hyponatremia
(brain cell volume has
returned to near normal)
Hypokalemia
Malnutrition
secondary to
alcoholism
Prior
cerebral
anoxic injury
Administration
of hypertonic
saline
Sudden osmotic shrinkage of brain cells
References: Vellaichamy M. Hyponatremia. 2009. http://emedicine.medscape.com/article/907841-followup. Fauci et al. Harrison’s Principles of
Internal Medicine, 17th ed.
Subtype of osmotic
demyelination syndrome
occurring in the pons
Occurs when hypertonic
saline is given too rapidly in
a patient in whom
hyponatremia has been
present for >24-48 hours
Central
Pontine
Myelinolysis
Potentially fatal neurologic
syndrome characterized by
quadriparesis, ataxia,
abnormal extraocular
movements
May result in brain damage
and death
References: Vellaichamy M. Hyponatremia. 2009. http://emedicine.medscape.com/article/907841-followup. Fauci et al. Harrison’s Principles of
Internal Medicine, 17th ed. Schwartz’s Principles of Surgery, 8th ed.
Central Pontine Myelinolysis
 Predilection for pons:
Grid arrangement of the
oligodendrocytes in the base of
pons
Limits their mechanical
flexibility, thus capacity to swell
 During hyponatremia, these cells can adapt only by
losing ions instead of swelling. This limitation
makes them prone to damage when Na is replaced.
Reference: Vellaichamy M. Hyponatremia. 2009. <http://emedicine.medscape.com/article/907841-followup>
Central pontine myelinolysis,
MRI FLAIR
T2 weighted magnetic resonance scan
image showing bilaterally symmetrical
hyperintensities in caudate nucleus (small,
thin arrow), putamen (long arrow), with
sparing of globus pallidus (broad arrow),
suggestive of extrapontine myelinolysis.
8. What intravenous fluid would
you use? At what rate should it be
given?
Intravenous fluid to use and rate of infusion
 3% saline infused at a rate of ≤ 0.05 mL/kg body
weight per minute.
 Effect should be monitored continuously by STAT
measurements of serum sodium at least once every 2
hours.
Reference: Fauci et al. Harrison’s Principles of Internal Medicine, 17th ed.
Intravenous fluid to use and rate of infusion
 Infusion should be stopped as soon as serum sodium
increases by 12 mmol/L or to 130 mmol/L,
whichever comes first.
 Urine output should be monitored continuously.
 SIAD can remit spontaneously at any time, resulting in an
acute water diuresis that greatly accelerates the rate of rise in
serum sodium produced by fluid restriction and 3% saline.
Reference: Fauci et al. Harrison’s Principles of Internal Medicine, 17th ed.
Hyperkalemia
A 62 y/o M diabetic with chronic kidney
disease and a creatinine of 3.5 mg/dl and
an estimated GFR of 15 ml/min consults
due to the inability to lift himself from a
chair. He had been eating fruits with each
meal for the past two weeks. On PE there
is marked proximal weakness and
decreased skin turgor. The ECG revealed
peaked T waves and widening of the P
wave and QRS complex.
Salient Features
 62, M
 CKD
 Diabetic
 CC: inability to lift himself from a chair
 Creatinine of 3.5 mg/dl
 GFR of 15 ml/min – Low
 Decreased skin turgor and marked proximal
weakness
 ECG: Peaked T waves and widening of P wave and
QRS complex
Laboratory Results
Parameters
Patient
Normal Values
Plasma Na
130 meq/L
136-146 meq/L
K
8.5 meq/L
3.5-5.0 meq/L
Cl
98 meq/L
102-109 meq/L
HCO3
17 meq/L
22-30 meq/L
Creatinine
2.7 meq/L
0.6-1.2 meq/L
7.32
7.35-7.45
400 mmol/L
3.9-6.7 mmol
not more than 125 mg/dl
+
-
pH
Capillary Blood Glucose
Serum Acetone
1. What are the most likely factors
responsible for the elevation of the
plasma potassium?
Most likely causes of Hyperkalemia in the patient
1. ) The patient has chronic kidney disease and is in
renal failure – GFR 15 ml/min

Compensatory mechanism for increasing distal flow rate and
K secretion per nephron is decreased because there is
decreased renal mass in chronic renal insufficiency
2.) The patient has diabetes
- Insulin deficiency and hypertonicity promote K shift from
the ICF to the ECF.
3. Intake of fruits does not necessarily cause
hyperkalemia.
- Huge amount of parenteral K can elicit
hyperkalemia.
4. Acidosis causes shift of potassium from
intracellular space into extracellular space.
2. Is this pseudohyperkalemia?
Why or why not?
PSEUDOHYPERKALEMIA
 Artificially elevated plasma K+ concentration due to
K + movement out of cells immediately prior to or
following venipuncture
 Contributing factors: prolonged use of tourniquet
with or without repeated fist clenching, hemolysis,
and marked leukocytosis or thrombocytosis
 marked leukocytosis or thrombocytosis  results in
an elevated serum K + concentration due to release of
intracellular K + following clot formation
References: Harrison’s Principles of Internal Medicine 17th ed. Onyekachi Ifudu, Mariana S. Markell, Eli A. Friedman. Unrecognized
Pseudohyperkalemia as a Cause of Elevated Potassium in Patients with Renal Disease.
PSEUDOHYPERKALEMIA
 Serum to plasma potassium difference of more than
0.4 mmol/l
 Occurs when platelets, leukocytes or erythrocytes
release intracellular potassium in vitrofalsely
elevated serum values.
 Observed in:
Myeloproliferative disorders including leukemia
 Infectious mononucleosis
 Rheumatoid arthritis

2. Is this pseudohyperkalemia?
Why or why not?
NO… THIS IS NOT PSEUDOHYPERKALEMIA SINCE THERE
ARE NO ENOUGH EVIDENCE OF BLOOD COUNT
DIFFERENTIALS AS WELL AS NO HISTORY PREDISPOSING
THE PATIENT TO DEVELOP SUCH.
ALSO, THE PRESENCE OF ECG ABNORMALITIES WHICH
REQUIRE EMERGENCY THERAPY IS NOT A COMMON
INDICATION IN PSEUDOHYPERKALEMIA.
3. What are the clinical manifestations of
hyperkalemia in this patient? Explain the
pathophysiology.
HYPERKALEMIA
 Excessive intake
 Uncommon cause of hyperkalemia
 Most often, hyperkalemia is caused by a relatively high
potassium intake in a patient with impaired mechanisms for
the intracellular shift of potassium or for renal potassium
excretion
 Decreased excretion
 Most common cause of hyperkalemia


Decreased excretion of potassium, especially coupled with
excessive intake
Decreased renal potassium excretion
Renal failure
 Ingestion of drugs that interfere with potassium excretion
 Potassium-sparing diuretics, angiotensin-convening enzyme
inhibitors, nonsteroidal anti-inflammatory drugs
 Impaired responsiveness of the distal tubule to aldosterone
 Type IV renal tubular acidosis observed with diabetes mellitus,
sickle cell disease, or chronic partial urinary tract obstruction

 Shift from intracellular to extracellular space
 Uncommon cause of hyperkalemia
 Exacerbate hyperkalemia produced by a high intake or
impaired renal excretion of potassium.
 Clinical situations in which this mechanism is the major cause
of hyperkalemia includes
Hyperosmolality
 Rhabdomyolysis
 Tumor lysis
 Succinylcholine administration
 Depolarizes the cell membrane and thus permits potassium to
leave the cells

CLINICAL MANIFESTATIONS
 Weakness
 Prolonged depolarization impairs membrane excitability


Since the resting membrane potential is related to the ratio of the
ICF to ECF K+ concentration, hyperkalemia partially depolarizes
the cell membrane
It may progress to flaccid paralysis and hypoventilation if the
respiratory muscles are involved
 Metabolic acidosis
 Net acid excretion is impaired


Inhibition of renal ammoniagenesis and reabsorption of NH4+ in
the TALH
It may exacerbate the hyperkalemia due to K+ movement out
of cells
 Cardiac toxicity
 Increased T-wave amplitude, or peaked T waves
 Prolonged PR interval and QRS duration, atrioventricular
conduction delay, and loss of P waves


Sine wave pattern


More severe degrees of hyperkalemia
Progressive widening of the QRS complex and merging with the T
wave
The terminal event is usually ventricular fibrillation or
asystole
How would you manage this
case?
Management
 Most important consequence of Hyper K is altered
Cardiac Conductance

With the risk of bradycardia and cardiac arrest
 The patient should be treated as an emergency case
and warrants emergency treatment

+ ECG changes and K > 6.0 mM (Px= 8.5 mM)
Urgent Management
 12- lead ECG
 Admission to the hospital
 Continuous cardiac monitoring
 Immediate treatment
Treatment
 Antagonism of the cardiac effect of hyperkalemia
 Stabilize membrane potential
Calcium Therapy 10% Ca gluconate, 10 mL over 10 mins or
Calcium chloride 5 mL of 10% sol IV over 2 min
 Stop infusion if bradycardia develops

 Rapid reduction in K+ by redistribution into cells
 Cellular K+ uptake
Insulin 10 U R (CBG= 400 mmol/L)
 B2-agonist nebulize albuterol, 10-20 mg in 4mL saline

Treatment
 Removal of K+ from the body
 Furosemide 20-250 mg IV
 Kayexalate 30-60 g mixed with 100 mL of 20% sorbitol PO
 Hemodialysis (if necessary)
Intractable Acidosis
 Uncontrollable Hyperkalemia

 Sodium Bicarbonate
 1 mEq/kg slow IV push or continuous IV drip
Hypokalemia
History
A 55 year old man presents with diarrhea that has
lasted for several weeks. He works as a farmer in La
Trinidad, Benguet. He has become progressively
weak during the past week.
Laboratory Examination
Laboratory examination reveals the following
results:
Na = 140 mEq/L
Cl = 110 mEq/L
K = 2.0 mEq/L
An arterial blood gas determination shows:
pH = 7.28
pCO2 = 39 mmHg
HCO3 = 16
The urine potassium is 15 mEq/L.
1. Discuss the diagnostic approach
to hypokalemia. What is the cause
of hypokalemia in this patient?
HYPOKALEMIA
Decreased
Intake
Redistribution
into cells
Increased Loss
Nonrenal
Gastrointestinal
Loss
(Diarrhea)
Renal
Integumentary
Loss
(Sweat)
Hypokalemia Secondary to Profuse Diarrhea
 Increased gastrointestinal loss
 Loss of gastric secretions does not account for the moderate to




severe K+ depletion.
The hypokalemia is primarily due to increased renal K+
excretion.
Loss of gastric contents  volume depletion and metabolic
alkalosis  kaliuresis
Hypovolemia  Aldosterone release  Augmentation of K+
secretion by principal cells
The filtered load of HCO3– exceeds the reabsorptive capacity
of the proximal convoluted tubule, thereby increasing distal
delivery of NaHCO3, which enhances the electrochemical
gradient favoring K+ loss in the urine.
2. What are the signs and
symptoms of hypokalemia?
Symptoms
• Seldom occur unless the plasma K+ conc is <3mmol/L
• Fatigue, myalgia, and muscular weakness of the lower
extremities
• Palpitations, constipation, nausea or vomiting,
abdominal cramping, polyuria, nocturia, or polydipsia,
psychosis, delirium, or hallucinations, depression
• Severe hypokalemia may lead to progressive weakness,
hypoventilation and eventually complete paralysis.
• Hypokalemic periodic paralysis
Signs
•
•
•
•
•
•
•
•
•
•
•
•
Signs of ileus
Hypotension
Ventricular arrhythmias
Cardiac arrest
Bradycardia or tachycardia
Premature atrial or ventricular beats
Hypoventilation, respiratory distress
Respiratory failure
Lethargy or other mental status changes
Decreased muscle strength, fasciculations, or tetany
Decreased tendon reflexes
Cushingoid appearance (eg, edema)
3. What are the adverse medical
implications of this condition?
Hypokalemia
 Impaired muscle metabolism and blunted hyperemic
response to exercise associated with profound K+ depletion
increase the risk of rhabdomyolysis
 Smooth muscle function may also be affected and manifest
as paralytic ileus
 ECG changes:


Early changes: T wave flattening or inversion, prominent U wave, ST
segment depression, prolonged QU interval
Severe K+ depletion: prolonged PR interval, decreased voltage and
widening of QRS complex, and an increased risk of ventricular
arrythmias (px with Myocardial Ischemia or left ventricular
hypertrophy)
Hypokalemia
 Predispose to digitalis toxicity
 Associated with acid-base disturbances related to the
underlying disorder
 Intracellular acidification and an increase in net acid
excretion or new HCO3- production: consequence of
enhanced proximal HCO3- reabsorption, increased renal
ammoniagenesis, and increased distal H + secretion →
generation of metabolic alkalosis
 Glucose intolerance attributed to either impaired insulin
secretion or peripheral insulin resistance.
4. What is the significance of
the urinary K levels?
• Normal
–
Urine Potassium:25 to 120 mEq/L/day
• Increased
–
–
–
–
–
Primary or Secondary Aldosteronism
Glucocorticoids
Alkalosis
Renal Tubular Necrosis
Excess Potassium intake
• Decreased
–
–
–
–
Acute Renal failure
Potassium sparing diuretics
Diarrhea
hypokalemia
Decreased urine K levels (15mEq/L)
• Diarrhea for several weeks
• Hypokalemia secondary to increased GI loss
• 90% of K is reabosrbed by the PCT and loop of Henle
• Luminal Na K Cl co transporter mediated K uptake
in thick ascending loop
• K delivery to the distal nephron (DCT and CCD)
approximates dietary intake
• Net distal K secretion or reabsorption occurs in the
setting of K excess or depletion respectively
5. What is the treatment?
Emergency Department Care
 Patients in whom severe hypokalemia is suspected should be
placed on a cardiac monitor; establish intravenous access and
assess respiratory status.
 Direct potassium replacement therapy by the symptomatology
and the potassium level. Begin therapy after laboratory
confirmation of the diagnosis.
 Patients who have mild or moderate hypokalemia (potassium
level of 2.5-3.5 mEq/L) are usually asymptomatic; if these
patients have only minor symptoms, they may need only oral
potassium replacement therapy.
 Patients with mild hypokalemia whose underlying cause of
hypokalemia can be corrected may not need any potassium
replacement, such as those with vomiting successfully treated
with antiemetics.
Reference: http://emedicine.medscape.com/article/767448-treatment
 In severe hypokalemia, cardiac arrhythmias or
significant symptoms are present, then more
aggressive therapy is warranted.
 If the potassium level is less than 2.5 mEq/L,
intravenous potassium should be given. Admission
or ED observation is indicated; replacement therapy
takes more than a few hours.
 The serum potassium level is difficult to replenish if
the serum magnesium level is also low. Look to
replace both.
Reference: http://emedicine.medscape.com/article/767448-treatment
Emergency Treatment
According to, August 2009 Journal:
Emergency Treatment of Hypokalemia
A. Estimated Potassium Deficit
1. At a serum K <3 mEq/L, there is a K deficit of more than 300 mEq
2. At a serum K <2 mEq/L, there is a K deficit of more than 700 mEq
B. Indications for Urgent Replacement.

Electrocardiographic abnormalities consistent with severe K
depletion, myocardial infarction, hypoxia, digitalis intoxication,
marked muscle weakness, or respiratory muscle paralysis.
Reference: http://www.ccspublishing.com/journals2a/hypokalemia.htm
Emergency Treatment
C. Intravenous Potassium Therapy
1. Intravenous KCL is usually used unless
concomitant hypophosphatemia is present (diabetic
ketoacidosis), where potassium phosphate is
indicated.
2. The maximal rate of intravenous K
replacement is 30 mEq/hour. The K concentration of
IV fluids should be 40 mEq/L or less if given via a
peripheral vein. Frequent monitoring of serum K and
constant electrocardiographic monitoring are
required.
Reference: http://www.ccspublishing.com/journals2a/hypokalemia.htm
Non-Emergent Treatment of Hypokalemia
 Attempts should be made to normalize K levels if <3.5
mEq/L.
 Oral supplementation is significantly safer than IV. Micro-
encapsulated and sustained-release forms of KCL are less
likely to induce gastrointestinal disturbances than are waxmatrix tablets or liquid preparations.
1. KCL elixir, 1-3 tablespoon every day.
Reference: http://www.ccspublishing.com/journals2a/hypokalemia.htm
References
 Becker, K. 2001. Principles and Practice of Endocrinology and Metabolism 3rd










Ed.
Harrison’s Principle of Internal Medicine, 17th ed.
Onyekachi Ifudu, Mariana S. Markell, Eli A. Friedman. Unrecognized
Pseudohyperkalemia as a Cause of Elevated Potassium in Patients with Renal
Disease.
Rennke H., Denker, B. 2007. Renal Pathophysiology: The Essentials
Schwartz’s Principles of Surgery, 8th ed.
Vellaichamy M. Hyponatremia. 2009.
<http://emedicine.medscape.com/article/907841-followup>
http://www.benhhoc.com/post/1816/
http://en.wikipedia.org/wiki/Orthostatic_hypotension
http://www.mt911.com/site/lab/normal_lab_values.asp
http://www.ccspublishing.com/journals2a/hypokalemia.htm
http://emedicine.medscape.com/article/767448-treatment