Transcript A 53kg woman with plasma Na concentration of 123 meq/L

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WORKSHOP CASE FOR FLUID
AND ELECTROLYTE DISORDERS
Saldana, E. * Sales, S. * Salonga, C. * San Diego, P.
San Pedro, R. * Sanez, E. * Sanidad, E. * Santos, E.
Santos, J. * Santos, J. * Santos, K. * Santos, E.
51 year old, female
CHIEF COMPLAINT:
Vomiting
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• Fever, dysuria and urgency
• Paracetamol and an antibiotic
1 week PTC
(relieved the fever)
• Headache, body malaise and
nausea
2 days PTC • Vomited thrice, 50cc per episode
Persistence of vomiting
CONSULTATION
PAST MEDICAL HISTORY
• Hypertensive for 10 years
• Medications:
• Telmisartan, 40mg
• Hydrochlorthiazide 12.5 daily
• Amlodipine was discontinued due to bipedal
edema
PERSONAL HISTORY
• No smoking
• No alcohol intake
REVIEW OF SYSTEMS
• Unremarkable
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Weight
Weak looking
• 50 kg
• Usual weight: 53 kg
Wheelchair-borne
Poor skin turgor
Blood pressure
• Supine: 120/80
• Sitting: 90/60
• Usual BP: 130/80
Dry mouth and tongue
Heart rate
• Supine: 90 bpm
• Sitting: 105 bpm
Dry axillae
JVP: < 5cm H2O at 45o
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Patient’s
Normal
Hgb
132 mg/dL
12 – 16 g/dL
Hct
0.35
0.36 – 0.46
WBC
Neut.
Lymph.
12.5
0.88
0.12
3.8 – 11 x 103
0.54 – 0.62
0.25 – 0.33
ARTERIAL BLOOD GAS
Patient’s
Normal
pH
7.3
7.35 – 7.45
CO2
35
33 – 35
HCO3
18
22 - 26
URINALYSIS
Patient’s
Normal
Patient’s
Normal
Plasma Na
123 mEq/L
135 – 147
Urine
Yellow, slightly
turbid
Straw
colored, clear
Plasma K
3.7 meq/L
3.5 - 5
pH
6.0
4.6 – 8
Chloride
71meq/L
95 - 105
S.G.
1.020
1.003 – 1.040
BUN
22mg/dl
6 – 23
Albumin
(-)
(-)
Serum
creatinine
0.9 mg/dl
0.6 – 1.2
Sugar
(-)
(-)
Glucose
98 mg/dl
65 - 99
Hyaline casts
5/hpf
Urine Na
100 mmol/L
30 – 280
Pus cells
10-15/hpf
Uosm
540 mosm/L
450 – 900
RBC
2-5/hpf
(not dysmorphic)
SALIENT FEATURES
• 51 year old, female (vomiting)
• Fever, dysuria, urgency
• Intake of paracetamol and
antibiotic
• Headache, body malaise,
nausea
• Vomiting: 50cc/episode
• Known hypertensive
• Telmisartan (40 mg)
• Hydrochlorthiazide (12.5
daily)
• Weak looking, wheelchairborne
• BP: 120/80 (supine), 90/60
(sitting), 130/80 (usual)
• HR: 90 bpm (supine), 105
bpm (sitting)
• Lost weight (53 kg  50 kg)
• Poor skin turgor
• Dry mouth, tongue and
axillae
• Normal JVP
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HYPOVOLEMIC HYPONATREMIA SECONDARY TO
THIAZIDE DIURETIC INTAKE
Source: Guyton and Hall. Textbook of Medical Physiology
20% of total
body weight
40% of total
body weight
Source: Guyton and Hall. Textbook of Medical Physiology
Source: Guyton and Hall. Textbook of Medical Physiology
PATIENT’S PROFILE
Body
malaise
Weakness
Poor skin
turgor
Dry mouth
and tongue
Dry axillae
Postural
hypotension
Postural
tachycardia
Decreased
JVP
a state of combined salt and water loss
exceeding intake
IMPORTANCE OF SODIUM
• Essential for regulation of body
fluids and blood.
• Transmits nerve impulses and
controls heart activity.
• Assists in metabolic functions.
• Helps maintain BP levels.
HYPONATREMIA
• Plasma Na+ concentration <
135 mEq/L, and is considered
severe when the level is below
125 mEq/L.
• Most causes of hyponatremia
are associated with a low
plasma osmolality.
3 TYPES OF HYPONATREMIA
DIFFERENTIATED BY VOLUME STATUS
CLINICAL FEATURES OF
HYPONATREMIA
The clinical manifestations of hyponatremia are
related to osmotic water shift leading to increased
ICF volume, specifically cerebral edema.
CLINICAL FEATURES OF
HYPONATREMIA
SERUM SODIUM LEVELS:
• 125 mEq/L
Nausea and malaise
• 120 mEq/L
Headache, lethargy, obtundation
• 115 mEq/L
Seizure and coma
Patient profle:
Serum Na+: 123 mEq/L
Headache, body malaise, nausea,
weak looking, wheelchair-borne
FACTORS WHICH CONTRIBUTED TO THE
PATIENT’S HYPONATREMIA
Renal sodium
loss
• Medications
• Telmisartan
• HCTZ
Extra-renal
sodium loss
• Vomiting
• 3x
• 50cc/episode
FACTORS WHICH CONTRIBUTED TO THE
PATIENT’S HYPONATREMIA
HYDROCHLOROTHIAZIDE
TELMISARTAN
• Inhibits reabsorption of
sodium and chloride in the
distal convoluted tubule, thus
promoting water loss.
• Angiotensin II receptor
blocker
• Leads to Na+ and K+ depletion
and AVP-mediated water
retention.
Source: http://upload.wikimedia.org/wikipedia/commons/a/a2/Renin-angiotensin-aldosterone_system.png
3. Compute for the plasma
osmolality and effective plasma
osmolality. What is the
importance of computing for
such?
Plasma osmolality (mOsm/kg)
=
2 [ plasma Na ] + [ Glucose ] + [
BUN ]
18
2.8
http://www.merck.com/mmpe/print/sec12/ch156/ch156b.html
Plasma Osmolality
Plasma Na
123mEq/L
Glucose
98mg/dL
BUN
22mg/dL
Plasma osmolality (mOsm/kg) =
2 [ 123 mEq/L] + [ 98 mg/dL ] + [ 22 mg/dL ]
18
2.8
Plasma osmolality = 259.3
mOsm/kg
Effective Plasma
Osmolality
Plasma
Na
123mEq/
L
BUN
22mg/dL
Effective Plasma osmolality
= PlasmaOsmolality - BUN_
2.8
= 259.3 mOsm/kg – 22 mg/dL
2.8
= 251.44 mOsm/kg
http://cmbi.bjmu.edu.cn/uptodate/critical%20care/Fluid%20and%20electrolyte%20disorders/.ht
m
Significance of Plasma
Osmolality
• The osmolality of plasma is closely regulated by antidiuretic hormone (ADH).
• In response to even small increases in plasma
osmolality, ADH release from the pituitary is increased
causing water resorption in the distal tubules and
collecting ducts of the kidney and correction of the
increased osmolality.
• The opposite happens in response to a low plasma
osmolality with decreased ADH secretion and water loss
through the kidneys.
Significance of Plasma
Osmolality
• Plasma osmolality is used in two main
circumstances:
– Investigation of hyponatremia
– Identification of an osmolar gap
Significance of Plasma
Osmolality
• Serum osmolality is a useful preliminary
investigation for identifying the cause of
hyponatremia.
Significance of Effective Plasma
Osmolality
• Solutes that are restricted to the ECF or the ICF determine
the effective osmolality (or tonicity) of that compartment.
ECF
ICF
Na+
K+
Cl-
Organic phosphate esters
(ATP, creatinie phosphate,
phospholipids )
HCO3-
• In a patient with hyponatremia, normal or elevated effective
serum osmolality suggests the presence of either
pseudohyponatremia or increased concentrations of other
osmoles, such as glucose and mannitol.
4. What are the significance of
urine osmolality and urine
sodium?
Significance of Urine Osmolality
• Urine osmolality may vary between 50 and 1200
mmol/kg in a healthy individual depending on the state of
hydration.
• The urine osmolality is the best measure of urine
concentration with high values indicating maximally
concentrated urine and low values very dilute urine.
• The main factor determining urine concentration is the
amount of water which is resorbed in the distal tubules
and collecting ducts in response to ADH.
Significance of Urine Osmolality
• The test is useful in the following areas:
– For determining the differential diagnosis of hyper- or
hyponatraemia.
– For identifying SIADH
– For differentiating pre-renal from renal kidney failure (high
urine osmolality is consistent with pre-renal impairment, in
renal damage the urine osmolality is similar to plasma
osmolality).
– For identifying and diagnosing diabetes insipidus (low
urine osmolality not responding to water restriction).
Significance of Urine Sodium
• In patients with hyponatremia and inappropriately
concentrated urine, it is particularly important to assess
the effective arterial blood volume.
5. Compute for the sodium
deficit
.
Plasma Na
123mEq/L
Weight
53 kg
Sodium Deficit
Sodium deficit
= (desired serum Na – actual Na) x TBW
= (140 mEq/L – 123 mEq/L) x (0.6 x [53])
= 540.6 mEq/L total needed
6. What are the basic principles
in the treatment of
hyponatremia?
Hyponatremia
• Goals of therapy
– To raise the plasma Na+ concentration by
restricting water intake and promoting water
loss
– To correct the underlying disorder
Treatment
• Mild asymptomatic hyponatremia
– Generally of little clinical significance and
requires no treatment
• Asymptomatic hyponatremia associated
with ECF volume contraction
– Na+ repletion isotonic saline
– Restoration of euvolemia removes the
hemodynamic stimulus for AVP release
Treatment
• Hyponatremia associated with edematous
states
– Have increased total body water that exceeds
the increase in total body Na+ content
– Restriction of Na+ and water intake, correction
of hypokalemia, and promotion of water loss
in excess of Na+
Treatment
• Acute or severe hyponatremia (plasma Na+
concentration <110–115 mmol/L)
– Tends to present with altered mental status
and/or seizures
– Requires more rapid correction
– Treated with hypertonic saline
Rate of Correction
• depends on the absence or presence of
neurologic dysfunction
Asymptomatic
Acute or severe
Hyponatremia
hyponatremia
• Raised by no more than • 1–2 mmol/L per hour
0.5–1.0 mmol/L per h
for the first 3–4 h or until
the seizures subside
• Less than 10–12
• raised by no more than
mmol/L over the first 24
12 mmol/L during the
h
first 24 h
7. What is the complication of the
rapid correction of the
hyponatremia?
Osmotic demyelination syndrome
(ODS)
• Follows too-rapid correction of hyponatremia
• Neurologic disorder characterized by flaccid
paralysis, dysarthria, and dysphagia
• Diagnosis is usually suspected clinically and
can be confirmed by appropriate
neuroimaging studies
• No specific treatment for the disorder
• Associated with significant morbidity and
mortality
Osmotic demyelination syndrome
(ODS)
• Chronic hyponatremia
– Most susceptible to ODS, since their brain cell
volume has returned to near normal as a
result of the osmotic adaptive mechanisms
– Administration of hypertonic saline to these
individuals can cause sudden osmotic
shrinkage of brain cells
Osmotic demyelination syndrome
(ODS)
• Risk factors
– Prior cerebral anoxic injury
– Hypokalemia
– Malnutrition, especially secondary to
alcoholism
8. What intravenous fluid would
you use? At what rate should it be
given?
Correction of Sodium Deficit
A 53kg woman with plasma Na concentration of 123
meq/L
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318 meq
 2L
154 meq/L
Sodium Deficit = 318 meq
O.9% NaCl = 154meq/L
Volume of 0.9% NaCl needed:
At 0.5 meq/L/hr, a correction of 12 meq (135123) should be done over 24 hours.
• Rate of infusion:
2,000mL
 83 mL/hr of 0.9% Na
24 hrs