GENERAL DATA
Name: F.H.S.
Age: 73
Sex: F
Address: Tondo, Manila
Occupation: None
Religion: Roman Catholic
CC: generalized body weakness
HISTORY OF PRESENT ILLNESS
3 days PTA:-generalized weakness (difficulty
getting up from bed, feeling of falling
when ambulating
-headache, nausea & vomiting
(3episodes)
-loss of appetite
-hospital: BP 190/100,
meds: Clonidine 75mg/tab sublingual
2 days PTA:- persistent generalized weakness
-1 episode of vomiting
-incoherence
Admission
REVIEW OF SYSTEMS
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Review of Systems
No weight loss
Wears glasses
(+) decreased hearing acuity, No ear pain, discharge or tinnitus
No sore throat, oral sores
No neck masses, no limitation of motion
No difficulty of breathing
(+) nocturia, frequency, (-) dysuria, (-) oliguria
(+) polyuria, polydipsia
No tremors, no heat or cold intolerance
No seizures, syncope
No joint pains, no joint stiffness, no swelling
No easy bruisability
PAST MEDICAL HISTORY
• (+) Hypertension (1987) medication:
Losartan+hydroclorothiazide 100mg/12.5mg
tab OD and Amlodipine 10mg/tab OD
• (+) 2007 – hospitalized for multiple electrolyte
imbalance secondary to GI losses secondary
to AGE
• (-) DM, CVA, Asthma, Allergy, CA, PTB
FAMILY HISTORY
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(+) Hypertension – father, siblings
(+) renal disease – sibling
(-) Diabetes Mellitus
(-) PTB
(-) Cancer
PERSONAL AND SOCIAL HISTORY
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Non Smoker
Non Alcoholic beverage drinker
No illicit drug use
Diet: prefers salty foods
PHYSICAL EXAMINATION
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Conscious, coherent, asthenic, well-kempt, ambulatory with assistance, not in
cardiopulmonary distress
VS: BP: 120/70 PR 69 bpm, RR 24 cpm, T 36.3 °C
Wt 56kg Ht 152.4 BMI 23.93
Warm moist skin with no active dermatoses
Pink palpebral conjunctiva, anicteric sclera, pupils 2-3 mm ERTL, (+) arcus senilis
OU
No tragal tenderness, no nasoaural discharge, nasal septum midline
Moist buccal mucosa, non-hyperemic posterior pharyngeal wall, tonsils not
enlarged
Supple neck, no palpable cervical lymph nodes, thyroid gland not enlarged
Symmetrical chest expansion, no lagging, no retractions, resonant on percussion,
clear breath sounds on both lung fields
Adynamic precordium, no heaves, lifts and thrills, AB at 6th LICS AAL, S1 > S2 at
apex, S2 > S1 at base, no murmurs
Abdomen flabby, NABS, no bruits, no masses, no guarding, nontender, tympanitic
on percussion, liver not enlarged, (-) CVA tenderness
Pulses full and equal, no edema, no cyanosis
Neurological Exam
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Conscious, coherent, can follow commands. GCS 15 E4V5M6
Cranial nerves:
CN I (-) anosmia
CN II intact papillary light reflex, and (+) ROR
CN III, IV, VI- EOMs full and equal
CN V- V1-V3 intact
CN VII- can raise eyebrows, can frown, can smile, can puff cheeks
CN VIII- decreased hearing acuity AU
CN IX, X- uvula midline on phonation
CN XI- can raise shoulders against resistance
CN XII- tongue midline uvula is in the midline on protrusion
MMT 5/5 on all extremities
No sensory deficits
Cerebellar function intact
(-) Babinski, (-) Nuchal rigidity, (-) Kernigs, (-) Brudzinski
ASSESSMENT
• Electrolyte imbalance secondary to 1.) GI loss
2. diuretic use 3. herbal use
• Hypertension St. II
• Urinary tract Infection
PLAN
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Plan:
Diagnostic
CBC c platelet,
CBG
Na, K
Plasma Osmolality
Urine Osmolality
Na Urine
K Urine
Urinalysis
CBC c Platelet
Hgb
RBC
Hct
MCV
MCH
MCHC
RDW
MPV
Platelet
WBC
Neutrophils
Reference Range
120-170
4.0-6.0
0.37-0.54
87±5
29±2
34±2
11.6-14.6
7.4-10.4
150-450
4.5-10.0
7/21
124
4.36
0.37
84.10
28.40
33.70
14.10
5.60
295
11.00
0.65
Metamyelocytes
-
Bands
-
Segmented
0.65
Lymphocytes
0.34
Monocytes
-
Eosinophils
0.01
Basophils
-
7/20
BUN
Creatinine
Reference
Range
9-23
0.5-1.2
Sodium
137-147
119.84
124.00/131.79
135.00
Potassium
3.8-5
3.73
3.48/3.48
3.93
Plasma
Osmolality
280-295
275.00
Urine Sodium
40-220
13.00
Urine
Potassium
25-125
4.30
Urine
Osmolality
500-800
92.00
FBS
70.9-110
Chemistry
7/21
7/22
8.39
0.72
111.41
Urinalysis 7/21
Color light yellow,
Transparency
turbid, pH 7.0,
Specific gravity
1.005, Albumin (-),
Sugar (-), RBC 2030/hpf, Pus over
100/hpf,
Squamous cells
few, Bacteria
++++, Mucus
threads few
Chest X-ray
(Official) 7/21
The heart is
enlarged
Aorta is calcified
The pulmonary
vascularity is
normal
The diaphragm
and sinuses are
intact
The visualized
osseous structures
are unremarkable
IMPRESSION:
Cardiomegaly,
Atheromatous
aorta
Urine Gram stain
7/21
No
microorganisms
seen on both
centrifuged and
uncentrifuged
sample
Urine Culture
7/23/10
No growth after 2
days of incubation
Potassium Balance
Haziel dela Rosa
Potassium
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major intracellular cation
plasma K+ concentration is 3.5–5.0 mmol/L
intacellular: 150 mmol/L
extracellular: 30–70 mmol
– constitutes <2% of the total body K+ content (2500–
4500 mmol).
• ratio of ICF to ECF K+ concentration
– (normally 38:1) : due to resting membrane potential
• crucial for normal neuromuscular function
Potassium balance
– basolateral Na+, K+-ATPase pump actively
transports K+ in and Na+ out of the cell in a 2:3
ratio
– passive outward diffusion of K+
• quantitatively the most important factor that generates
the resting membrane potential
– Na+, K+-ATPase pump
• Stimulated by increased intracellular Na+ concentration
• Inhibited by:
– digoxin toxicity or chronic illness such as heart failure or renal
failure
Potassium balance
• Maintenance of the steady state necessitates matching
K+ ingestion with excretion
• extrarenal adaptive mechanisms, followed by urinary
excretion
– Prevents doubling of the plasma K+ concentration that
would occur if the dietary K+ load remained in the ECF
compartment
• following a meal, most of the absorbed K+ enters cells
– initial elevation in the plasma K+ concentration
– facilitated by insulin release and basal catecholamine
levels
Potassium balance
• excess K+ is excreted in the urine
• amount of K+ lost in the stool can increase
from 10 to 50% or 60% (of dietary intake) in
chronic renal insufficiency
• colonic secretion of K+ is stimulated in patients
with large volumes of diarrhea
– severe K+ depletion
Potassium Excretion
• Renal excretion
– major route of elimination of dietary and other
sources of excess K+
– filtered load of K+ (GFR x plasma K+ concentration
= 180 L/d x 4 mmol/L = 720 mmol/d) is ten- to
twentyfold greater than the ECF K+ content
Potassium Excretion
– 90% of filtered K+ is reabsorbed by the proximal
convoluted tubule and loop of Henle
– Proximally, K+ is reabsorbed passively with Na+ and
water
– luminal Na+-K+-2Cl– co-transporter mediates K+
uptake in the thick ascending limb of the loop of
Henle
Potassium Excretion
• K+ delivery to the distal nephron [distal
convoluted tubule and cortical collecting duct
(CCD)]
– approximates dietary intake
• Net distal K+ secretion or reabsorption occurs in
the setting of K+ excess or depletion, respectively.
• principal cell
– responsible for K+ secretion in the late distal
convoluted tubule (or connecting tubule) and CCD
• Virtually all regulation of renal K+ excretion and
total body K+ balance occurs in the distal nephron
Potassium Excretion
• secretion is regulated by two physiologic
stimuli
– aldosterone and hyperkalemia
• Aldosterone
– secreted by the zona glomerulosa cells of the
adrenal cortex in response to high renin and
angiotensin II or hyperkalemia
– plasma K+ concentration, independent of
aldosterone, can directly affect K+ secretion
Potassium Excretion
Aldosterone
– K+ concentration in the lumen of the CCD, renal K+
loss depends on the urine flow rate, a function of
daily solute excretion
– increased distal flow rate can significantly enhance
urinary K+ output
– severe K+ depletion
• secretion is reduced and reabsorption in the cortical
and medullary collecting ducts is upregulated.
Estimation of Potassium Deficit
• For a fall in serum potassium from 4.0 to 3.0
meq/L, body potassium deficit is 200-300
meq/70 kg BW
• For a serum potassium at 2.5 meq/L, body
deficit is 500 meq/70 kg BW
• For a serum potassium at 2.0 meq/L, body
deficit is 700 meq/70 kg BW
In the patient....
Reference
value
7/20
7/21
7/22
Serum
Potassium
3.8-5
3.73 LOW
3.48/3.48
LOW
3.93
Urine
Potassium
Plasma
Osmolality
Urine
Osmolality
25-125
4.30 LOW
280-295
275.00
LOW
92.00 LOW
500-800
Potassium
Deficit
200-300
meq/70 kg
BW
Clinical Features of Hypokalemia
Hypokalemia
• Symptoms seldom occur unless the plasma K+
concentration is <3 mmol/L.
• Fatigue, myalgia, and muscular weakness of
the lower extremitieslower (more negative)
resting membrane potential.
• More severe hypokalemia :
– progressive weakness,
– hypoventilation (due to respiratory muscle
involvement),
– complete paralysis.
• Increase risk of rhabdomyolysis
Electrographic changes of hypokalemia
• Early changes:
– flattening or inversion of the
T wave,
– a prominent U wave
– ST-segment depression,
– a prolonged QU interval.
• Severe K+ depletion:
– prolonged PR interval
– decreased voltage and
widening of the QRS complex,
– increased risk of ventricular
arrhythmias, especially in
patients with myocardial
ischemia or left ventricular
hypertrophy.
Etiology of Hypokalemia
CAUSES OF HYPOKALEMIA
I. Decreased Intake
A) starvation
B) clay ingestion
II. Redistribution into the cells
A) Acid-Base
1) Metabolic Alkalosis
B) Hormonal
1) Insulin
2) B2-Adrenergic agonists
3) Alpha-Adrenergic antagonists
C)Anabolic state
1) Vitamin B12 or folic acid
2) Granulocyte-macrophage colony stimulating factor
3) Total parenteral nutrition
D) Others
1)Pseudohypokalemia
2)Hypothermia
3)Hypokalemic periodic paralysis
4)Barium toxicity
CAUSES OF HYPOKALEMIA
III. Increased loss
A) Nonrenal
1. Gastrointestinal loss (diarrhea)
2. Integumentary loss (sweat)
B) Renal
1. Increased distal flow: diuretics,
osmotic diuresis, salt-wasting
nephropathies
2. Increased secretion of potassium
2) Increased secretion of potassium
A. Mineralocorticoid excess: primary hyperaldosteronism,
secondary hyperaldosteronism (malignant hypertension,
renin-secreting tumors, renal artery stenosis,
hypovolemia), apparent mineralocorticoid excess (licorice,
chewing tobacco, carbenoxolone), congenital adrenal
hyperplasia, Cushing's syndrome, Bartter's syndrome
B. Distal delivery of non-reabsorbed anions: vomiting,
nasogastric suction, proximal (type 2) renal tubular
acidosis, diabetic ketoacidosis, glue-sniffing (toluene
abuse), penicillin derivatives
C. Other: amphotericin B, Liddle's syndrome,
hypomagnesemia
Hyponatremia
Causes of Hyponatremia
I. Pseudohyponatremia
A. Normal plasma osmolality
1.
2.
3.
Hyperlipidemia
Hyperproteinemia
Posttransurethral resection of prostate/bladder
B. Increased plasma osmolality
1.
2.
Hyperglycemia
Mannitol
Causes of Hyponatremia
II. Hypoosmolal hyponatremia
A.
Primary Na loss (secondary water gain)
1.
2.
B.
Integumentary loss: sweating, burns
GI loss: vomiting, tube drainage, fistula, obstruction, diarrhea
Primary water gain (secondary Na loss)
1.
2.
3.
4.
5.
6.
7.
Primary polydipsia
Decreased solute intake
AVP release d/t pain, nausea, drugs
SIADH
Glucocorticoid deficiency
Hypothyroidism
Chronic renal insufficiency
Cause of Hyponatremia
C. Primary Na gain (exceeded by secondary water
gain)
1. Heart failure
2. Hepatic cirrhosis
3. Nephrotic syndrome
Approach to the diagnosis of patients
with hyponatremia
Four laboratory findings often provide useful
information and can narrow the differential
diagnosis of hyponatremia:
(1) the plasma osmolality
(2) the urine osmolality
(3) the urine Na+ concentration
(4) the urine K+ concentration
Approach to a Patient with
Hyponatremia
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• (-) urine osmolality and specific gravity of
<100 mosmol/kg and 1.003- it suggests
impaired free-water excretion due to the
action of AVP on the kidney
• The secretion of AVP may be a physiologic
response to hemodynamic stimuli or it may be
inappropriate in the presence of
hyponatremia and euvolemia
Hypokalemia: Treatment
• Kalium durule (750 mg/tab)
1 durule TID x 4 doses
• Increase K in the diet
SIADH
• hypoosmotic hyponatremia in the setting of an
inappropriately concentrated urine (urine
osmolality >100 mosmol/kg).
• normovolemic and have normal Na+ balance.
• urine Na+ excretion rate equal to intake (urine Na+
concentration usually >40 mmol/L).
• normal renal, adrenal, and thyroid function and
usually have normal K+ and acid-base balance.
• associated with hypouricemia due to the
uricosuric state induced by volume expansion.
SIADH
• Most common causes: neuropsychiatric and
pulmonary diseases, malignant tumors, major
surgery (postoperative pain), and
pharmacologic agents
• Adrenal insufficiency and hypothyroidism may
present with hyponatremia and should not be
confused with SIADH
ADRENAL INSUFFICIENCY
• Decreased mineralocorticoids contribute to the
hyponatremia of adrenal insufficiency
• Cortisol deficiency hypersecretion of AVP both
indirectly (secondary to volume depletion) and
directly (cosecreted with corticotropin-releasing
factor)
HYPOTHYROIDISM
• The mechanisms that lead to hyponatremia:
– decreased cardiac output and GFR
– increased AVP secretion in response to
hemodynamic stimuli
Basic Principles in the Treatment
of Hyponatremia
Goals of Therapy
• (1) to raise the plasma Na+ concentration by restricting
water intake and promoting water loss
• (2) to correct the underlying disorder.
• Mild asymptomatic hyponatremia  no treatment
• Asymptomatic hyponatremia associated with ECF
volume contraction
– Na+ repletion with isotonic saline
– Restoration of euvolemia removes the hemodynamic
stimulus for AVP release, allowing the excess free water to
be excreted
Goals of Therapy
• Hyponatremia associated with edematous states
– Reflect severity of the underlying disease, usually
asymptomatic
– Restriction of Na+ and water intake
• hyponatremia associated with primary polydipsia, renal
failure, and SIADH
– Correction of hypokalemia
• Correction of the K+ deficit may raise the plasma Na+
concentration by favoring a shift of Na+ out of cells as K+
moves in
– Non-peptide vasopressin antagonists  new selective
treatment for euvolemic and hypervolemic
hyponatremia
Rate of Correction of Hyponatremia
• Depends on the absence or presence of
neurologic dysfunction
• Asymptomatic patients
– no more than 0.5–1.0 mmol/L per h and by less
than 10–12 mmol/L over the first 24 h
• Acute or severe hyponatremia (plasma Na+
concentration <110–115 mmol/L)
– altered mental status and/or seizures
– requires more rapid correction.
Rate of Correction of Hyponatremia
• Severe symptomatic hyponatremia
– Hypertonic saline
– 1–2 mmol/L per hour for the first 3–4 h or until the seizures
subside
– no more than 12 mmol/L during the first 24 h
– quantity of Na+ required to increase the plasma Na+
concentration by a given amount can be estimated by
multiplying the deficit in plasma Na+ concentration by the total
body water
– Amount of mmol of Na+ needed to raise the plasma Na
concentration from actual to desired = [(135 – actual) x BW x
0.5].
Rate of correction and Fluids
Cruz, Karen
What IV fluids should be used?
At what rate should it be given?
• Asymptomatic patients:
– Isotonic saline
– Concentration should be raised by no more
than 0.5 to 1.0 mmol/L per hour and by less
than 10 to 12 mmol/L over 1st 24 hr
• Acute/severe hyponatremia
– Plasma Na concentration <110-115 mmol/L
– Tends to present with altered mental status
and/or seizures
– Requires more rapid correction
• severe symptomatic patients:
– Hypertonic saline (3%)
– Raised by 1 to 2 mmol/L per hr for the 1st 34 hr or until seizure subsides
– Raised by no more than 12mmol/L during
the first 24 hours
Different IV fluids and Na content
IV Fluids
Na Content (mEq/L)
PNSS
154
LRS
130
0.9% NaCl
154
D5 0.45% NaCL
77
D5 3% NaCl
513
D5 5% NaCl
855
FLUIDS
• LRS and normal saline
– Isotonic
– useful in replacing gastrointestinal losses and
extracellular volume deficits
• Lactated Ringer's is slightly hypotonic
– 130 mEq of sodium, which is balanced by 109 mEq
of chloride and 28 mEq of lactate
FLUIDS
• Sodium chloride
– mildly hypertonic  154 mEq of Na+ balanced by
154 mEq of Cl– an ideal solution for correcting volume deficits
associated with hyponatremia, hypochloremia,
and metabolic alkalosis
FLUIDS
• 0.45% sodium chloride
– useful to replace ongoing gastrointestinal losses as
well as for maintenance fluid therapy in the
postoperative period
– provides sufficient free water for insensible losses
and enough sodium to aid the kidneys in adjustment
of serum sodium levels
– 5% dextrose supplies 200 kcal/L, always added to
solutions containing less than 0.45% sodium chloride
to maintain osmolality  prevent lysis of RBCs that
may occur with rapid infusion of hypotonic fluids
FLUIDS
• Hypertonic saline solutions (3.5% and 5%)
– used for correction of severe sodium deficits
Sodium Deficit
Na Deficit = (Desired Na – Actual Na) x TBW x weight (kg)
– Actual Na: 119.84
– Weight: 56 kg
Total body weight (in Liters)
Children
0.6 x weight
Women
0.5 x weight
Men
0.6 x weight
Elderly Women
0.45 x weight
Elderly
Men
=
0.5 x weight
= 0.45 x 56kg x (130-119.84)
= (25.2) (10.16)
Sodium deficit = 256.03 mEq/L
Adrogue, HJ; and Madias, NE. Primary Care: Hypernatremia. New England Journal of Medicine 2000; 342(20):1493-1499. 342(21):1581-1589. .
Sodium Correction
Different IV fluids and Na content
IV Fluids
Na Content (mEq/L)
PNSS
154
LRS
130
0.9% NaCl
154
D5 0.45% NaCL
77
D5 3% NaCl
513
Na
Deficit
256.03 mEq/L
Maintenance
3 x BW
3 x 56
= 168
Losses
-
Total
424.03 meq/L
PNSS
__424.03 meq/L__ = 4.24 L
100 meq NaCl
__4240mL
= 176.7 cc/hr
24 hrs
__176.7 cc/hr__ = 44.16  45gtts/min
4
Osmotic Demyelinating
Syndrome
Osmotic Demyelination Syndrome
• Cause:
– rapid correction of hyponatremia
• Characterized by:
– flaccid paralysis
– dysarthria
– dysphagia
• At risk:
– prior cerebral anoxic injury
– hypokalemia
– malnutrition, especially secondary to alcoholism
Osmotic Demyelination Syndrome
• Diagnosis:
– suspected clinically
– confirmed by appropriate neuroimaging studies
• Treatment:
– no specific treatment
– supportive only
• Prevention:
– hyponatremia should be corrected at a rate not in
excess of 10mmol/L/24hr or 0.5 mEq/L/Hr
– diligently avoid hypernatremia