MCQs in Fluid And Electrolyte Therapy

Q1 :

A 5 kg infant with bronchiolitis is transferred to the pediatric intensive care unit actively seizing and is found to have a serum sodium of 123 mmol/L. Which of the following is the MOST appropriate therapy?

A. 0.9% normal saline bolus (10 mL/kg).

B. 3% normal saline bolus of 10 mL over 10 min.

C. 3% normal saline infusion at 5 mL/h.

D. intravenous lorazepam (0.5 mg).

E. intravenous mannitol (5 g) over 15 min.

Correct Answer : 

B

Explanation :

Hyponatremic Encephalopathy

Clinical Symptoms

A major consequence of hyponatremia is the infl ux of water into the intracellular space

resulting in cellular swelling, leading to cerebral edema and encephalopathy. The symptoms

of hyponatremic encephalopathy can be quite variable, with the only consistent symptoms

being headache, nausea, vomiting, emesis, and weakness. As cerebral edema worsens,

patients develop behavioral changes, with impaired response to verbal and tactile stimuli.

Advanced symptoms are consequences of cerebral herniation, with seizures, respiratory

arrest, dilated pupils and decorticate posturing. Not all patients have the usual progression of

symptoms such that advanced symptoms can present with sudden onset.

Age

Children under 16 years of age are at increased risk for developing hyponatremic encephalopathy

due to their relatively larger brain to intracranial volume ratio as compared to adults.

A child’s brain reaches adult size by 6 years of age, whereas the skull does not reach adult

size until 16 years of age. Consequently, children have less room available in their rigid

skulls for brain expansion and are likely to develop brain herniation from hyponatremia at

higher serum sodium concentrations than adults. Immediate initiation of appropriate therapy

is crucial to prevent signifi cant morbidity.

Treatment of Hyponatremic Encephalopathy :

Regarding the treatment of hyponatremic encephalopathy, there are two aspects generally

accepted by experts in the fi eld: (1) treatment should be directed based on the neurological

involvement and not the absolute serum sodium, (2) hypertonic saline is not indicated in the

asymptomatic patient who is neurologically intact, regardless of the serum sodium.

 In general, rapid correction with hypertonic saline is unnecessary and potentially harmful if there are no

neurological symptoms. Symptomatic hyponatremia, on the other hand, is a medical emergency.

Treatment of hyponatremic encephalopathy should precede any neuroimaging studies to

confi rm cerebral edema and should occur in a monitored setting where the airway can be secured

and serum sodium level measured frequently. 

Fluid restriction alone has no place in the treatment of symptomatic hyponatremia. If symptomatic hyponatremia is recognized and treated promptly, prior to the development of a hypoxic event, the neurological outcome is good.

Patients with symptomatic hyponatremia need aggressive management with 3% NaCl

(513 mmol/L). Children with severe symptoms such as seizures, respiratory arrest or neurogenic

pulmonary edema should receive 2 mL/kg of 3% NaCl, with a maximum of 100 mL,

as a bolus over 10 min in order to rapidly reverse brain edema. This dose might need to be

repeated once or twice until symptoms subside, with the remainder of therapy delivered via

continuous infusion. Patients with less-severe symptoms, such as headache, nausea, vomiting

or lethargy, can be treated via an infusion pump to achieve a correction of 4–8 mmol/L

in the fi rst 4 h. To prevent complications arising from excessive therapy, 3% NaCl should be

discontinued when symptoms subside, the rate of correction should not exceed 20 mmol/L

in the fi rst 48 h, and correction should be to mildly hyponatremic values, avoiding normalization

of serum sodium or hypernatremia in the fi rst 48 h. In general, 1 mL/kg of 3% NaCl

will increase the serum sodium level by about 1 mmol/L. A continuous infusion of 3% NaCl

at a rate of 1–2 mL/kg/h administered over 4 h is usually suffi cient to reverse symptoms.

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Q 2:

A patient with nephrotic syndrome is found to have a total serum calcium level of 6.8 mg/dL with a serum albumin of 2.0 g/ dL. What is the corrected total serum calcium?

A. 6.0

B. 7.8

C. 8.4

D. 9.4

E. 10.0

The Answer :

C

Explanation :

The total serum calcium will fall by 0.8 mg/dL  for every 1 g/dL fall in serum albumin without affecting the ionized calcium.

Here :

4- current Albumen = 4-2= 2

2 X 0.8 = 1.6

1.6 + 6.8 = 8.4

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Q 3:

A 6-year-old girl presents with fever, abdominal pain, and diarrhea. Her oral intake of fluids

(water and fruit juice) has been fair, with occasional emesis. On physical examination, she has

mildly tacky mucous membranes, a capillary refill of 2 to 3 seconds, and no edema. Her

temperature is 38.6°C, heart rate is 120 beats/min, respiratory rate is 18 breaths/min, and blood

pressure is 102/56 mm Hg. Laboratory tests reveal:

· Sodium, 126 mEq/L (126 mmol/L)

· Potassium, 3.7 mEq/L (3.7 mmol/L)

· Chloride, 100 mEq/L (100 mmol/L)

· Bicarbonate, 16 mEq/L (16 mmol/L)

· Blood urea nitrogen, 25 mg/dL (8.9 mmol/L)

· Creatinine, 0.6 mg/dL (53.0 mcmol/L)

Urinalysis documents a specific gravity of 1.025, pH of 6, and trace ketones.

Of the following, the MOST likely additional laboratory finding is

A. elevated brain natriuretic peptide

B. fractional excretion of sodium greater than 1%

C. urine osmolality less than 300 mOsm/kg

D. urine potassium less than 10 mEq/L

E. urine sodium less than 10 mEq/L

Answer :

E


The girl described in the vignette has had gastroenteritis of a few days’ duration. Her physical examination shows features of mild-to-moderate dehydration, with tachycardia, tacky mucous membranes, and delayed capillary refill. Her laboratory findings are most notable for hyponatremia, a normal anion gap metabolic acidosis, and mild azotemia.

Hyponatremia is defined as an abnormally low serum sodium concentration, which can result from solute (sodium) loss or water retention.

In general, hyponatremia most commonly is due to abnormalities in water balance, not sodium balance. 

To excrete free water, a person must have normal renal function, normal renal blood flow, and inhibition of antidiuretic hormone (ADH) release by the posterior pituitary.

For the patient suffering from an illness that results in volume depletion, such as gastroenteritis, ADH release is physiologically appropriate.

The appropriate medical management is to replenish the patient’s extracellular fluid depletion with isotonic fluids.

The patient in the vignette was managing her own volume depletion by oral repletion with hypotonic fluids, which yielded hyponatremia. Thus, her gastroenteritis resulted in extracellular volume depletion with increased ADH release and impaired water excretion.

 Her consumption of hypotonic fluids led to relative water loading and hyponatremia.

In addition to high ADH concentrations, patients who have intravascular volume depletion can be expected to have activation of the renin-angiotensin-aldosterone system (RAAS) and renal sympathetic nerves, thereby resulting in avid sodium and water retention by the kidneys.

Results of the laboratory evaluation for the patient in the vignette would include:

                           -  A low urinary sodium concentration (<10 mEq/L)
                           -  A low fractional excretion of sodium (<1%)
                           - High urine osmolality (>500 mOsm/kg).

Because of the high activity of the RAAS, the high aldosterone effect would lead to sodium retention in exchange for potassium in the urine, thereby raising the urine potassium excretion.

Brain natriuretic peptide (BNP), like atrial natriuretic peptide, is released in the clinical setting of increased cardiac filling volume resulting in mild natriuresis.

The patient in the vignette is volume depleted and, thus, would not be expected to have elevated BNP concentrations in the blood.