The Diagnosis of and Therapy for Common Fluid and

Electrolyte Imbalances

Angela Heithaus, MD, PS

Internal Medicine
Seattle Healing Arts Center
 Leonardo da Vinci
 24 YO M comes to see you
complaining that after 2 days of
vomiting and diarrhea without fever
or abdominal pain or hematochezia
that he becomes light headed when
standing and thought at one point he
was going to pass out.
 On exam there is no abdominal
tenderness
 Questions
 What should you document/check?

 How should you treat?

Volume Depletion
 Volume Depletion
 Loss of isotonic fluid from the extracellular fluid at a
rate exceeding net intake.
 Can occur through:
 gastrointestinal tract (vomiting, diarrhea, bleeding)
 skin (sweat, burns)
 lungs (bronchorrhea, pleural effusion, evaporation)
 urine (diuretics, osmotic diuresis, salt wasting
nephropathies, and hypoaldosteronism)
 acute sequestration in the body in a "third space" that is not
in equilibrium with the extracellular fluid (GI obstruction,
crush injury, bleeding, acute pancreatitis)
History and Symptoms of
Volume Depletion
History
vomiting, diarrhea, diuretic use, or polyuria
(may identify the source of fluid loss)
Symptoms
 lethargy, easy fatiguability, thirst, muscle cramps,
and postural dizziness (volume depletion)
 Generalized weakness, irritability, maybe
twitching, seizures (if also severely hyponatremic)
 muscle weakness, polyuria, polydipsia, confusion

(from concomitant electrolyte and

acid-base disorders)
 PEx findings in

Hypovolemia
BP, HR, and JVD
 BP drops in upright position
 ‘orthostatic hypotension’ – after two to five minutes of quiet standing, one or
more of the following is present:
 At least a 20 mmHg fall in systolic pressure
 At least a 10 mmHg fall in diastolic pressure
 Symptoms of cerebral hypoperfusion (dizziness)
 HR increase by more than 10-20 bpm
 Decreased JVD
 Skin
 Increased pigmentation, decreased turgor, dry axilla
 Mucous membranes
 Tongue and oral mucosa dry
 Laboratory Studies
 Urine
 urinalysis can be normal
 sodium concentration < 25 meq/L and may be as low as
1 meq/L
 chloride concentration low
 osmolality >450 mosmol/kg
 specific gravity > 1.015
 oliguria
 Blood
 Elevated serum sodium = dehydration
 If [Na] WNL then pt not dehyrated but hypovolemic
 Elevated BUN/plasma creatinine level
 HCT (relative polycythemia) and plasma albumin level
increases
 Replacement Therapy
 IVF Bolus
 5cc/kg over 20 minutes
 Usually rounded to 500cc for adults and
extended to 30 minutes
 Normal Saline (isotonic) best
 Ringers lactate (has bicarb) if >4 liters will be
given
 This prevents development of metabolic acidosis
 IV Catheters
 18 gauge best
 Replacement Therapy
Precautions
 Excess NS can cause pulmonary
edema in some pts:
 Elderly pts with hx of CHF
 Pts with known severe VHD

 Renal failure pts

 In these pts use 3cc/kg over 30

minutes for boluses and listen to lungs
often, measure SaO2 if possible
 Answers
 What should you document?
 Orthostatic BP/HR- (pt still hypovolemic?)
 How much volume should you replete and
how fast?
 Bolus 500cc over 30 minutes
 Which type of fluid should you use?
 Normal Saline (isotonic) best
 Ringers lactate (has bicarb) if >4 liters anticipated
 This prevents development of metabolic acidosis
 Leonardo continued…
 When have you given enough IVF?
 Recheck orthostatic pressures and sx
 If still orthostatic?
 Rebolus, repeat cycle until
asymptomatic, making urine, mucous
membranes moist
 Sophia Loren
 70 YO F with H/O HTN on HCTZ
presents C/O nausea and malaise x 1
month
 PEx is WNL
 Labs: Na+ 121
 Clinical Manifestations of
Hyponatremia
Plasma Na+ 125-130 meq/L
nausea and malaise
Plasma Na+ <115-120 meq/L
headache, lethargy, and
obtundation and eventually
seizures, coma and respiratory
arrest
 Differential Diagnosis for
Hyponatremia
 In almost all cases, results from the
intake (either oral or intravenous)
and subsequent retention of water
 In almost all cases, occurs because
there is an impairment in renal water
excretion, due most often to an
inability to suppress ADH release
 ADH
 Elevated
 Effective circulating volume depletion
 Heart failure, cirrhosis, thiazide diurectics
 Syndrome of Inappropriate ADH
secretion
 Hormonal changes

Adrenal insufficiency,
hypothyroidism, pregnancy
Evaluation of Patients with
Hyponatremia
 Assess volume status of patient
 Hypovolemia: orthostatic, dry mucous membranes
 Hypervolemia: peripheral edema, pulmonary
edema, JVD, ascites
 For Euvolemic pt:
 Check TSH
 Check urine osmolarity for SIADH (inappropriately
concentrated urine- should be dilute in this setting)
 Treatment of
Hyponatremia
 Initial treatment in such patients typically
consists of gradual correction of the
hyponatremia via water restriction or the
administration of isotonic saline (or oral salt)
 More aggressive therapy is indicated in
patients who have symptomatic or severe
hyponatremia (plasma sodium concentration
below 110 to 115 meq/L).
 Gabriele Falloppio
 60 yo male with diarrhea x 1 wk, no
vomiting; good PO intake, comes to
see you because of mild intermittent
leg cramps
 PEx is unremarkable, there is no
abdominal tenderness or
neurological deficit
 Labs reveal K of 2.9, otherwise WNL
 Hypokalemia
 GI, urinary losses
 Mild loss, K+ between 3.0 and 3.5 meq/L
 usually produces no symptoms
 replace lost K+ and treat underlying disorder (such as
vomiting, diarrhea)
 treatment is usually started with 10 to 20 meq of
potassium chloride given two to four times per day (20
to 80 meq per day), depending on the severity of
hypokalemia and on whether hypokalemia developed
acutely or is chronic
 sequential monitoring of plasma K+ is essential to
determine continued requirements, with frequency of
monitoring dependent on the severity of hypokalemia
 Severe Hypokalemia
 Symptoms generally do not become manifest until the
serum K+ is below 3.0 meq/L
 Muscular abnormalities
 muscle cramps, rhabdomyolysis, and myoglobinuria
 Cardiac arrhythmias and ECG abnormalities
 PAC, PAT, PVC, AVB, VT
 Renal abnormalities
 impaired urinary concentrating ability (which may be symptomatic
with nocturia, polyuria and polydipsia
 Enrico Fermi
 60 YO M comes in for physical exam
which is WNL; labs reveal Ca 12.6
 Is further evaluation indicated and if
so, what?
 Calcium
 Range 8.5-10.6 mg/dL
 Plasma Ca2+ concentration includes all the Ca2+ in the
plasma, of which only about 45 percent circulates in the
physiologically important ionized or unbound state.
 Common exception occurs in patients with hypoalbuminemia
in whom the concomitant decrease in ion binding leads to a
reduction in the total plasma Ca2+ concentration without
change in the ionized form
 if albumin <2.0 g/dL (roughly 2.0 g/L less than normal), then the
corrected plasma Ca2+ concentration would be 7.5 + (2 x 0.8) or 9.1
mg/dL, which is normal
 Differential Diagnosis of
Hypercalcemia
 Hyperparathyroidism
 >90% of ambulatory cases
 Primary hyperparathyroidism is most often due to a
parathyroid adenoma
 Cancer
 solid tumors and leukemias
 Local resorption of bone induced by metastases
(mediated by local release of cytokines such as
tumor necrosis factor and interleukin-1) or the
production of humoral osteoclast activators,
particularly PTH-related protein
 Hyperthyroidism
 15-20% of patients can develop mild hypercalcemia
 Evaluation of
Hypercalcemia
 Correct diagnosis in 95% of cases by evaluating:
 History
 PEx
 CXR (r/o malignancy or sarcoidosis) and
 Lab data: PTH (serum intact), PTHRP related peptide,
serum protein electrophoresis (r/o multiple myeloma),
creatinine

 Primary hyperparathyroidism is often associated

with borderline or mild hypercalcemia with the
serum calcium concentration often being below 11
mg/dL (2.75 mmol/L)
 Treatment Goals in
Hypercalcemia
 Lowering serum Ca++ level
 Saline administration to produce volume
expansion and increase urinary Ca++
excretion (oral hydration + high salt diet)
 Concurrent tx with biphosphonates) +/-
calcitonin (decrease bone resorption)
 Oral phosphate 250-500 mg QID (decrease
absorption in gut)

 Correcting or decreasing underlying

disease
 Hyperparathyroidism