Transcript Fluids, Electrolyte Imbalance, IV Therapies

The Diagnosis of and Therapy for Common Fluid
and Electrolyte Imbalances
Angela Heithaus, MD, PS
Internal Medicine
Seattle Healing Arts Center
Leonardo da Vinci
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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
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What should you document/check?
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How should you treat?
Volume Depletion
Volume Depletion
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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)
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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)
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PEx findings in Hypovolemia
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BP, HR, and JVD
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Skin
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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
Increased pigmentation, decreased turgor, dry axilla
Mucous membranes
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Tongue and oral mucosa dry
Laboratory Studies
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Urine
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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
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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
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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
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This prevents development of metabolic acidosis
IV Catheters
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18 gauge best
Replacement Therapy Precautions
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Excess NS can cause pulmonary edema in some
pts:
Elderly pts with hx of CHF
 Pts with known severe VHD
 Renal failure pts
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In these pts use 3cc/kg over 30 minutes for
boluses and listen to lungs often, measure SaO2
if possible
Answers
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What should you document?
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How much volume should you replete and how
fast?
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Orthostatic BP/HR- (pt still hypovolemic?)
Bolus 500cc over 30 minutes
Which type of fluid should you use?
Normal Saline (isotonic) best
 Ringers lactate (has bicarb) if >4 liters anticipated
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This prevents development of metabolic acidosis
Leonardo continued…
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When have you given enough IVF?
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Recheck orthostatic pressures and sx
If still orthostatic?
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Rebolus, repeat cycle until asymptomatic, making
urine, mucous membranes moist
Sophia Loren
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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
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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
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Elevated
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Effective circulating volume depletion
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Heart failure, cirrhosis, thiazide diurectics
Syndrome of Inappropriate ADH secretion
 Hormonal changes
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Adrenal insufficiency, hypothyroidism, pregnancy
Evaluation of Patients with
Hyponatremia
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Assess volume status of patient
Hypovolemia: orthostatic, dry mucous membranes
 Hypervolemia: peripheral edema, pulmonary edema,
JVD, ascites
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For Euvolemic pt:
Check TSH
 Check urine osmolarity for SIADH (inappropriately
concentrated urine- should be dilute in this setting)
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Treatment of Hyponatremia
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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
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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
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GI, urinary losses
Mild loss, K+ between 3.0 and 3.5 meq/L
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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
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Symptoms generally do not become manifest until the
serum K+ is below 3.0 meq/L
Muscular abnormalities
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Cardiac arrhythmias and ECG abnormalities
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muscle cramps, rhabdomyolysis, and myoglobinuria
PAC, PAT, PVC, AVB, VT
Renal abnormalities
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impaired urinary concentrating ability (which may be
symptomatic with nocturia, polyuria and polydipsia
Enrico Fermi
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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
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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
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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
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Hyperparathyroidism
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Cancer
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>90% of ambulatory cases
Primary hyperparathyroidism is most often due to a
parathyroid adenoma
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
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15-20% of patients can develop mild hypercalcemia
Evaluation of Hypercalcemia
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Correct diagnosis in 95% of cases by evaluating:
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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
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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)
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Correcting or decreasing underlying disease
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Hyperparathyroidism