WORKSHOP CASE FOR FLUID AND ELECTROLYTE DISORDERS

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.

HYPONATREMIA

51 year old, female

CHIEF COMPLAINT:Vomiting

H I S T O R Y

1 week PTC •Fever, dysuria and urgency•Paracetamol and an antibiotic

(relieved the fever)

2 days PTC •Headache, body malaise and nausea•Vomited thrice, 50cc per episode

CONSULTATION

Persistence of vomiting

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

PHYSICAL

EXAM

Weak looking

Wheelchair-borne

Blood pressure• Supine: 120/80• Sitting: 90/60• Usual BP: 130/80

Heart rate• Supine: 90 bpm• Sitting: 105 bpm

Weight• 50 kg• Usual weight: 53 kg

Poor skin turgor

Dry mouth and tongue

Dry axillae

JVP: < 5cm H2O at 45o

LABORATORY

Patient’s Normal

Hgb 132 mg/dL 12 – 16 g/dL

Hct 0.35 0.36 – 0.46

WBC Neut. Lymph.

12.50.880.12

3.8 – 11 x 103

0.54 – 0.620.25 – 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

Urine Yellow, slightly turbid

Straw colored, clear

pH 6.0 4.6 – 8

S.G. 1.020 1.003 – 1.040

Albumin (-) (-)

Sugar (-) (-)

Hyaline casts 5/hpf

Pus cells 10-15/hpf

RBC 2-5/hpf (not dysmorphic)

Patient’s Normal

Plasma Na 123 mEq/L 135 – 147

Plasma K 3.7 meq/L 3.5 - 5

Chloride 71meq/L 95 - 105

BUN 22mg/dl 6 – 23

Serum creatinine

0.9 mg/dl 0.6 – 1.2

Glucose 98 mg/dl 65 - 99

Urine Na 100 mmol/L 30 – 280

Uosm 540 mosm/L 450 – 900

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, wheelchair-borne

• 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

HYPOVOLEMIC HYPONATREMIA SECONDARY TO THIAZIDE DIURETIC INTAKE

IMPRESSION

Source: Guyton and Hall. Textbook of Medical Physiology


40% of total body weight

20% of total body weight


PATIENT’S PROFILE

Body malaise Weakness Poor skin

turgor

Dry mouth and tongue Dry axillae Postural

hypotension

Postural tachycardia

Decreased JVP

SIGNS OF ECF VOLUME CONTRACTION

ECF VOLUME CONTRACTION

Hypovolemia

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

• 120 mEq/L

• 115 mEq/L

Patient profle: Serum Na+: 123 mEq/LHeadache, body malaise, nausea,weak looking, wheelchair-borne

Nausea and malaise

Headache, lethargy, obtundation

Seizure and coma

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

• Inhibits reabsorption of sodium and chloride in the distal convoluted tubule, thus promoting water loss.

• Leads to Na+ and K+ depletion and AVP-mediated water retention.

TELMISARTAN

• Angiotensin II receptor blocker

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 (mOsm/kg) =2 [ 123 mEq/L] + [ 98 mg/dL ] + [ 22 mg/dL ]

18 2.8

Plasma osmolality = 259.3 mOsm/kg

Plasma OsmolalityPlasma Na 123mEq/L

Glucose 98mg/dL

BUN 22mg/dL

Effective Plasma osmolality = PlasmaOsmolality - BUN_

2.8 = 259.3 mOsm/kg – 22 mg/dL

2.8 = 251.44 mOsm/kg

Effective Plasma Osmolality

Plasma Na

123mEq/L

BUN 22mg/dL

http://cmbi.bjmu.edu.cn/uptodate/critical%20care/Fluid%20and%20electrolyte%20disorders/.htm

• The osmolality of plasma is closely regulated by anti-diuretic 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



• Serum osmolality is a useful preliminary investigation for identifying the cause of hyponatremia.

• Solutes that are restricted to the ECF or the ICF determine the effective osmolality (or tonicity) of that compartment.

• 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.

Significance of Effective Plasma Osmolality

ECF ICFNa+ K+

Cl- Organic phosphate esters (ATP, creatinie phosphate, phospholipids )

HCO3-

4. What are the significance of urine osmolality and urine sodium?

• 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 Osmolality

• In patients with hyponatremia and inappropriately concentrated urine, it is particularly important to assess the effective arterial blood volume.

Significance of Urine Sodium

5. Compute for the sodium deficit

.

Sodium Deficit

Sodium deficit = (desired serum Na – actual Na) x TBW = (140 mEq/L – 123 mEq/L) x (0.5 x [53]) = 450.5 mEq/L total needed

Plasma Na 123mEq/L

Weight 53 kg

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 Hyponatremia

Acute or severe hyponatremia

• Raised by no more than 0.5–1.0 mmol/L per h

• 1–2 mmol/L per hour for the first 3–4 h or until the seizures subside

• Less than 10–12 mmol/L over the first 24 h

• raised by no more than 12 mmol/L during the 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


• 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


• 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

• Sodium Deficit = 450.5 meq• O.9% NaCl = 154meq/L• Volume of 0.9% NaCl needed:• At 0.5 meq/L/hr, a correction of 17 meq (140-

123) should be done over 34 hours.• Rate of infusion:

2.9Lmeq/L 154meq 5.450

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

NaCl 0.9% ofmL/hr 85hrs 342,900mL

Reference: http://scalpel.stanford.edu/ICU/presentations/Fluid%2520and%2520Electrolyte%2520Physiology.ppt

Documents

WORKSHOP CASE FOR FLUID AND ELECTROLYTE DISORDERS