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Curriculum Vitae

Name : Hermina Novida


Place & date of birth : Madiun, November 12, 1977
Mailing address : Surabaya Diabetes and
Nutrition Centre
Division of Endocrinology,
Department of Internal
Medicine
Dr. Soetomo Teaching Hospital
- Faculty of Medicine Airlangga
University
Jl. Prof. Moestopo 6-8
Surabaya, Indonesia
Phone office : +62315023866
Mobile phone : +6281331526625
E-mail address : herminanovida@ymail.com
Facsimile : +62315012775
Education
2001 : General Medicine, Faculty of Medicine Airlangga University
2010 : Internal Medicine, Faculty of Medicine Airlangga University
2011 : Fellowship in Research of Diabetes and Nutrition, Kobe Womens
University, Kobe, Japan (Oct-Nov 2011)
2013 : Fellowship in Diabetes, Endocrinology and Metabolic, Royal Adelaide
Hospital, Adelaide, Australia (January-March 2013)
2014 : Fellowship in Molecular Pathogenesis of Diabetes, Kumamoto University
Japan (August 2014)
2016 : EndocrineMetabolic-Diabetes Consultant, Faculty of Medicine Airlangga
University

Employment
2006 - present : Lecturer, School of Medicine Faculty of Medicine, Airlangga
University, Majoring Subject in Internal Medicine
2010 present : Staff of Diabetes and Nutrition Centre Dr. Soetomo Teaching
Hospital Faculty of Medicine Airlangga University
2010 present : Staff of Internal Medicine Department Airlangga University
Hospital
Professional Society Membership :
Indonesian Medical Association (IDI)
Indonesian Internist Association (PAPDI)
Indonesian Endocrinologist Association (PERKENI)
Indonesian Diabetes Association (PERSADIA)
European Association for the Study of Diabetes
American Diabetes Association
Electrolyte Imbalance :
Evaluation and Management

Hermina Novida

Workshop FK UHT Surabaya, 14 Oktober 2017


Topics
Introduction
Sodium (Natrium) disorders
Hyponatremia
Hypernatremia
Potassium (Kalium) disorders
Hypokalemia
Hyperkalemia
Others electrolyte disorders
Topics
Introduction
Sodium (Natrium) disorders
Hyponatremia
Hypernatremia
Potassium (Kalium) disorders
Hypokalemia
Hyperkalemia
Others electrolyte disorders
Introduction
Electrolytes are minerals in body fluids that carry an electric
charge
Electrolytes affect the amount of water, the acidity of blood
(pH), muscle function, and other important processes in the
body
There are six major electrolytes
Sodium Na+ Major cation in extracellular fluid (ECF)
Potassium K+ Major cation in intracellular fluid (ICF)
Calcium Ca++ Major cation found in ECF and teeth and bones
Chloride Cl- Major anion found in ECF
Phosphate PO43 Major anion found in ICF
Magnesium Mg++ Major cation found in ICF (closely related
to Ca++ and PO4)
Topics
Introduction
Sodium (Natrium) disorders
Hyponatremia
Hypernatremia
Potassium (Kalium) disorders
Hypokalemia
Hyperkalemia
Others electrolyte disorders
Sodium Disorders
Hyponatremia and hypernatremia are common findings in the inpatient
and outpatient settings.
Sodium disorders are associated with an increased risk of morbidity and
mortality.
Plasma osmolality plays a critical role in the patho- physiology and
treatment of sodium disorders.
Hyponatremia and hypernatremia are classified based on volume status
(hypovolemia, euvolemia, and hypervolemia).
Sodium disorders are diagnosed by findings from the history, physical
examination, laboratory studies, and evaluation of volume status.
Treatment is based on symptoms and underlying causes.
Sign and Symptoms of Sodium Disorders

Hyponatremia Hypernatremia
Fatigue Thirst
Muscle weakness Fever
Muscle twitching Flushed skin
Decreased skin turgor Oliguria
Headache Disorientation
Tremor Dry sticky membranes
Seizures
Coma
Evaluation of Hyponatremia

Cleve Clin J Med 2006; 73(suppl3):S4-S12


True Hyponatremia
Common Treatment Options
Water restriction
Diuresis (with loop diuretic)
Volume infusion (with crystalloid)
Hypertonic saline
Demeclocycline
ADH antagonists
Complications of Treating Hyponatremia

Delayed treatment
Cerebral edema
Permanent neurological injury
Death
Inappropriately rapid treatment
Cerebral dehydration/demyelination
Permanent neurological injury
Death
Inappropriate treatment
Failure to improve morbidity
Delayed improvement morbidity
Further deterioration
What if he had cerebral edema?

1. Correct [Na+] to 125-130mEq/L to temporarily


relieve edema
2. [Na+] should NOT increase by more than 8-12
mEq/L in 1st 24 hours ~ .33 mEq/L/hr
3. Slow/Stop infusion as soon as symptoms improve
3% NaCl Calculation
[Na+] = 116 mEq/L
Goal [Na+] = 125 mEq/L at 24 hours
Amount of [Na+] to be given as 3% infusion:
= [Serum Na(desired) Serum Na(measured) ]
(TBW) = [125 116] [(0.5)(60kg)]= 270 mEq Na
NaCl 3% saline = 513 mEq sodium/L
Amount of NaCl 3% saline: 270/513 = 0.5 L =
500 ml over 24 hrs.
Evaluation of Hypernatremia
Treatment
Establish documented onset (acute, < 24 h; chronic, >24h)
In acute hypernatremia, correct the serum sodium at an initial
rate of 2-3 mEq/L/h (for 2-3 h) (maximum total, 12 mEq/L/d).
Measure serum and urine electrolytes every 1-2 hours
Chronic hypernatremia with no or mild symptoms should be
corrected at a rate not to exceed 0.5 mEq/L/h and a total of 8-10
mEq/d (eg, 160 mEq/L to 152 mEq/L in 24 h).
If a volume deficit and hypernatremia are present, intravascular
volume should be restored with isotonic sodium chloride prior to
free-water administration.
Estimation of the replacement fluid
Water deficit:
TBW deficit = correction factor x BW x (1 - 140/Na+)
However, the conventional equation for water deficit is not
useful in situations in which sodium and potassium must be
used in the infusate. Formulas used to manage hypernatremia
are
TBW = weight (kg) x correction factor
Correction factor
- Children: 0.6
- Nonelderly men: 0.6
- Nonelderly women: 0.5
- Elderly men: 0.5
- Elderly women: 0.45
NEJM, 2000, vol 342, 1497
Example
80-year-old man has sodium concentration is 165 mmol/L.
BW 70 kg. This man is found to have hypernatremia due to
insensible water loss. The man's TBW is calculated by the
following: (0.5 x 70) = 35 L

To reduce the man's serum sodium, D5 W will be used.


Thus, the retention of 1 L of D5 W will reduce his serum
sodium by (0 - 165) (35 + 1) = -4.6 mmol. The goal is to
reduce his serum sodium by no more than 10 mmol/L in a
24-hour period. Thus, (10 4.6) = 2.17 L of solution is
required. About 1-1.5 L will be added for obligatory water
loss to make a total of up to 3.67 L of D5 W over 24 hours,
or 153 cc/h.
Topics
Introduction
Sodium (Natrium) disorders
Hyponatremia
Hypernatremia
Potassium (Kalium) disorders
Hypokalemia
Hyperkalemia
Others electrolyte disorders
Potassium (Kalium) Disorders
Normal value in serum is 3.5-5mEq/L
Potassium is a major intracellular electrolyte
Influence both cardiac and skeletal muscle activity
Potassium is very sensitive to change in serum level
Kidney is the primary regulator of serum potassium
with 80% excretion through kidney while the other
20% is excreted via bowle and sweat
Potassium Deficit (Hypokalemia)
Decrease in serum potassium less than 3.5mEq/L
Causes include diuretics, gastrointestinal loss as in vomiting
and diarrhea, illeostomy, increase aldosteron secretion,
diabetes.
Clinical manifestation : Fatigue, anorexia, nausea, muscle
weakness, paresthesia, decrease bowel motility
Inability of kidney to excrete urine
Increase sensitivity to digitalis( digoxin)
Electrocardiogram (ECG) changes flat T wave, inverted T wave,
depressed ST segment elevated U wave

11/21/2017 25
Evaluation of Hypokalemia
Management of Hypokalemia

Potassium supplement: usually 40-80mEq/L


High potassium diet as most fruits, legume, whole grain, milk.
IV potassium should be reserved for patients with severe
hypokalemia, hypokalemic ECG changes, or physical signs or
symp- toms of hypokalemia, or for those unable to tolerate
the oral form.
When intravenous potassium is used, standard administration
is 20 to 40 mEq of potassium in 1 L of normal saline.
Correction typically should not exceed 20 mEq/h, although
higher rates using central venous catheters have been
successful in emergency situations. Continuous cardiac
monitoring is indicated if the rate exceeds 10 mEq/h.

11/21/2017 27
Potassium Excess (Hyperkalemia)

Potassium increase more than 5 mEq/L


Mainly is caused by decrease renal excretion ( renal failure),
decrease aldosteron secretion, side effect of medications such
as heparin, ACE inhibitor, NSAID, potassium sparing diuretic
such as spironalacton.
ECG changes: Peaked narrow T wave, St segment depression,
Shortened QT interval, PR interval prolonged followed by
disappearance of P wave, Prolongation of QRS complex that
entails cardiac arrhythmia and cardiac arrest
Muscle weakness may be paralysis related to depolarization
block ( speech muscle and respiratory muscle)

11/21/2017 28
Evaluation of Hyperkalemia

American Family Physician Vol 92, Number 6


Management of Hyperkalemia
Restriction of potassium
Cation exchange resin ( Kayexalate): bind with potassium in
the intestine and removed through stool.
Administration of calcium gluconate ( to protect the heart but
has no effect on the potassium level)
Administration of sodium bicarbonate
Administration of hypertonic dextrose solution with insulin:
insulin bind potassium and sugare and move it to the cells

11/21/2017 30
Medication to Treat Hyperkalemia
Topics
Introduction
Sodium (Natrium) disorders
Hyponatremia
Hypernatremia
Potassium (Kalium) disorders
Hypokalemia
Hyperkalemia
Others electrolyte disorders
Calcium (Ca++)
Normal Serum Level 2.15-2.55 mmol/L
Chloride (Cl-)
Normal Serum Level 95-110 mmol/L
Phosphate (PO4)
Normal Serum Level 0.8-1.5 mmol/L
Magnesium (Mg++)
Normal Serum Level 0.70-1.05 mmol/L
Thank You

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