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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2593_Библиотеки_им_академика_М_И_Перельмана
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biologic sex, race, clinical presentation, medication history, and
lifestyle are factors that may influence reported laboratory results
and, therefore, must be taken into consideration. Statistical and
preanalytical variations are common, and must also be evaluated in
the context of the result obtained. Refer to Table 2-1 for examples of
common preanalytical variables.
Table 2-1
Preanalytical Variation: Factors Affecting the Test Result from
the Time the Test Is Ordered Until It Arrives at the Laboratory
Variable Example(s)
Incorrect test
ordered
Albumin ordered to assess the impact of recent dietary change
(prealbumin better marker for acute changes)
Sample
incorrectly
labeled
Sample obtained from one patient and labeled with another name
Improper
preparation
for test
Fasting indicated, but not followed: fasting glucose, complete lipid
panel
Pretest medications not administered in the appropriate manner
Pretest diet restrictions not met: rare meat ingested before guaiac
test
Medication Medication interfered with testing procedure or by pharmacologic
effect: β-agonist can reduce serum potassium concentrations,
thiazides can increase serum uric acid levels.
Improper
timing of
test
Vancomycin trough taken after first dose (rather than before the
fourth dose)
aPTT measured 2 hours after initial dose (rather than 6 hours
after start)
Fasting glucose test completed shortly after a meal, TSH
measured 2 weeks after dose change (rather than 4–6 weeks
after change)
Collection
incomplete
or
improper
Abnormal 24-hour urine collection secondary to patient forgetting
to void in provided container, blood specimen obtained from
extremity with IV infusion site resulting in dilutional effect of
glucose, BUN, and electrolytes, specimen collected in incorrect
container
Improper
handling or
Hyperkalemia because of hydrolysis of blood specimen
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storage
Poor
accuracy
or
precision
Faulty or outdated laboratory reagents in use
Technical Result incorrectly read, computer keying error
Biologic sex Many laboratory findings are sex dependent.
Age Neonatal, pediatric, adult, and geriatric populations have unique
reference ranges for numerous laboratory tests.
Pregnancy Gestational status impacts numerous laboratory findings: alkaline
phosphatase, cholesterol, iron, etc.
Posture Being in upright position during laboratory sampling can increase
albumin, calcium, iron, etc.
Exercise Strenuous exercise before testing can impact lactate, creatine
kinase, ALT, AST, uric acid, etc.
Normal
physiologic
fluctuations
Circadian rhythm can impact cortisol, serum iron, serum
creatinine, WBC count, etc.
Medical
procedures
Blood transfusion with red blood cells before hemoglobin A
1c
measured results in normal A1c for poorly controlled individual
with diabetes, creatine kinase elevated secondary to recent
cardioversion
A1c, hemoglobin A1c (also glycated hemoglobin); ALT, alanine aminotransferase;
aPTT, activated partial thromboplastin time; AST, aspartate aminotransferase;
BUN, blood urea nitrogen; IV, intravenous; TSH, thyroid-stimulating hormone;
WBC, white blood cell.
Test Reliability
As a result of probability, if the same test is completed multiple times
on the same sample, typically 1 of 20 results or 5% will be reported
outside of the provided reference range. Indicators of test reliability
include accuracy, precision, sensitivity, and specificity. Precision
refers to the repeatability of a laboratory test (ie, test results fall
within a similar value when repeated), whereas accuracy is the
ability of a test to provide a result that is reflective of the “true” value
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(ie, the test result matches the actual value). Quality control and
assurance practices at each laboratory are monitored regularly to
ensure reliability of results. Typically, if a result that is significantly
outside the reference range is obtained, the laboratory will repeat the
test to confirm or refute the finding.
Research studies generally establish the sensitivity and specificity
of laboratory tests. Clinically, these are essential to distinguish the
presence or absence of a disease or condition. Sensitivity is the
ability of the test to correctly identify the disease or condition. If a test
is 95% sensitive, then 95% of the individuals will be correctly
identified as having the disease or condition, but 5% will have a
negative test result even though they have the disease or condition
(false negative). Specificity is the ability of the test to rule out
individuals who do not have the disease or condition. If a test is 95%
specific, then 95% of the individuals without disease will have a
correct negative result, but 5% will be identified as having the
disease or condition even though they are negative (false positive).
Units of Measure
The International System of Units (SI) reports clinical laboratory
values using the metric system. The basic unit of mass for the SI
system is the mole, which is not influenced by the added weight of
salt or ester formulations. Therefore, the mole is technically and
pharmacologically more meaningful than is the gram because each
physiologic reaction occurs on a molecular level. Efforts to
implement the SI system internationally for laboratory test reports
have been resisted in the United States. Despite adopting SI
transition policies in the late 1980s, major American medical journals
have since reverted to the traditional units for laboratory test
reporting.
4,5
In this chapter, reference ranges for common laboratory
tests are presented in both conventional and SI units, along with
“conversion factors” to interchange traditional and SI units (Tables 2-
2 and 2-3).
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Table 2-2
Blood Chemistry Reference Values
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Homocysteine
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LDH
BNP
NT
proBNP
-
CRP
hs
CRP
-
Liver
Funaion
AST
ALT
ALP
GGT
Male
Female
Bllirubin
Bllirubin
Miscellaneous
Amylase
Lipase
PSA
TSH
Procalcitonin
Total
total
—
direct
—
cholesterol
LDL
HDL
Triglycerides
(
fasting
)
4
pmol
-
12
100-250
100
<
400
<
0-1.6
0-10
35
0
IU
-
0
IU
35
-
-
130
20
9
50
IU
-
8-40
IU
1
0.1
—
0-0.2
-
35
118
-
160
10
4
0
ng
-
-
0.5
4.7
ng
0.5
<
200
<
100
<
Female
Male
(
50
<
pg
pg
mg
mg
mg
mg
mg
mg
>
mg
/
/
/
/
/
mL
/
40
/
/
L
L
IU
L
L
IU
IU
plU
mL
>
IU
mL
mL
/
/
/
/
/
/
/
dL
dL
/
dL
dL
/
/
dL
dL
50
dL
L
/
/
L
L
L
/
mg
L
mL
mg
/
dL
4
pmol
-
12
L
/
17
1
4
67
-
ng
100
<
n
400
<
mg
-
16
0
^
L
pkat
/
L
/
L
L
/
1
0
01667
1
1
10
Damages
for
risk
eies
in
in
High
isoenzymes
mostly
nonspeclfic
are
renal
PE
.
BNP
>
Released
on
heart
proBNP
NI
failure
Nonspecific
tp
ESR
tlon
disease
lar
0-10
-
0
0
-
0.58
0
0
33
-
2
4
0
-
0
58
0
2
-
4
-
0
5
0
18
-
mg
58
2.17
-
pmol
pmol
1
-
67
pg
4.7
pkat
pkat
97
pkat
/
L
L
/
/
mlU
L
/
/
pkat
L
/
pkat
/
/
10
L
L
/
L
L
/
L
L
0.01667
0.01667
01667
0
I
17
1
17
001667
0.01667
1
1
More
sensitive
Large
amounis
amounts
Ml
and
From
heart
gibie
specidc
amounts
Large
bile
duet
rapid
Sensitive
helpful
in
high
Breakdown
bumin
dlrect
hemolysis
Pancreatie
obstruetion
Pancreatie
a
for
T
BPH
in
4
10
-
cancer
tate
TSH
T
ogenous
hyperthyroidism
pg
L
0.5
/
<
70
mmol
mmo
:
>
l
>
mmol
03
1
L
/
(
/
29
mmol
/
L
mmol
L
5.2
<
2.58
<
dL
Female
/
Male
1
<
1
02586
0
002586
0.02586
L
/
L
/
0.0113
T
Bacterial
;
mL
Consult
Current
to
high
Ification
Consult
by
alcohol
T
level
high
vessel
cardiac
folate
,
heart
liver
in
disease
500
ng
from
2000
>
.
indicatot
more
but
.
3
CRP
>
in
muscle
liver
Injury
,
liver
untess
parenchymai
than
obstruetlon
growth
bone
test
reflecting
in
differentiating
chronlc
produet
,
conjugated
(
conjugated
cholestasis
.
enzyme
enzyme
period
longer
and
also
ngTnL
increased
in
primary
thyroid
Infectlons
risk
current
guldelines
intensity
-
consult
:
current
saturated
.
Consult
endothelial,which
disease
Associated
,
kidney
LD
L
/
measure
is
should
,
„
B
vitamin
,
liver
.
1
LD
and
and
skeletal
mallgnancy
T
in
indicates
ventricles
indicates
ng
L
/
of
acute
rapid
onser
dL
mg
increases
/
of
in
and
heart
kidney
.
liver
Less
,
muscle
.
AST
duets
bile
in
,
obstruetive
(
eg
Paget
.
hepatocellular
alcoholics
of
hemoglobin
liver
in
)
and
indirect
liver
.
T
pancreatitis
in
:
T
acute
.
than
In
prostate
be
worked
if
free
hypothyroidlsm
supplememation
low
—
sepsis
severe
of
guldelines
recommend
therapy
statin
current
guldelines
fats
current
guidellnes
may
with
vitamin
and
skeletal
and
mostly
2
In
LD
muscle
.
exrensive
.
congestive
T
workload
with
congestive
Inflammation
greater
and
risk
of
CRP
livet,moderate
pancreas
and
.
spedde
pancreas
kidney
.
liver
disease
.
placema
.
liver
disease
livet
disorders
,
bound
bllirubin
.
Total
bllirubin
injury
or
pancreatitis
amylase
Is
PSA
cancer
.
Risk
up
PS
/
Vtotal
requtres
i
.
risk
sepsis
of
If
2.0
>
.
starting
based
,
drugs
.
.
Obtain
guldelines
Increase
deficien
,
B
2
.
musete
heart
LD
.
3
LD
and
burns
failure
heart
placed
heart
.
Similar
eleva
cardiovascu
t
with
Is
than
ALT
T
negli
More
liver
bone
T
disease
)
pregnancy
.
not
injury
:
Usually
al
to
includes
T
with
duet
elevated
.
leveis
pros
of
0.25
PSA
<
-
ex
TSH
in
If
0.5
<
/
mL
ng
moderate
on
risk
fasting
Five
5
In
.
of
strat
the
4
.
-
-
ng
-
-
-
/
-
ALP, alkaline phosphatase; ALT, alanine aminotransferase; AST, aspartate
aminotransferase; BNP, brain natriuretic peptide; BPH, benign prostatic
hypertrophy; BUN, blood urea nitrogen; CHF, congestive heart failure; CK, creatine
kinase (formerly known as creatine phosphokinase); CrCl, creatinine clearance;
CRP, C-reactive protein; cTnI, cardiac troponin I; ESR, erythrocyte sedimentation
rate; GFR, glomerular filtration rate; GGT, γ-glutamyl transferase; GI,
gastrointestinal; HDL, high-density lipoprotein; IM, intramuscularly; LDH, lactate
dehydrogenase; LDL, low-density lipoprotein; MI, myocardial infarction; NG,
nasogastric; PE, pulmonary embolism; PSA, prostate-specific antigen; SI,
International System of Units; TPN, total parenteral nutrition; TSH, thyroidstimulating hormone.
Table 2-3
Hematologic Laboratory Values
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ANC, absolute neutrophil count; ESR, erythrocyte sedimentation rate; Hct,
hematocrit; Hgb, hemoglobin; MCH, mean corpuscular hemoglobin; MCHC, mean
cell hemoglobin concentration; MCV, mean cell volume; RBC, red blood cell; SI,
International System of Units; TIBC, total iron-binding capacity; WBC, white blood
cell.
a
fL, femtoliter; femto, 10
−15
; pico, 10
−12
; nano, 10−9; micro, 10−6; milli, 10−3.
FLUIDS AND ELECTROLYTES
Refer to Chapter 27, Fluid and Electrolyte Disorders, for more
detailed information.
Sodium
Reference Range: 135–147 mEq/L or mmol/L
Sodium is the predominant cation of the extracellular fluid (ECF),
and human cells reside in salt water. Along with chloride, potassium,
and water, sodium is important in establishing serum osmolarity and
osmotic pressure relationships between intracellular fluid (ICF) and
ECF. Osmoregulatory system regulates the plasma sodium
concentrations to remain in a normal range by controlling water
intake and excretion.6 An increase in the serum sodium
concentration could suggest either impaired sodium excretion or
volume contraction. On the contrary, a decrease in the serum
sodium concentration to less-than-normal values could reflect
hypervolemia, abnormal sodium losses, or sodium starvation.
Although healthy individuals are able to maintain sodium
%
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Eosinophils
Basophils
Ratelets
Iron
a
Male
Female
TIBC
%
0
8
-
%
%
-
3
0
150-450
05-160
-
30
160
220-420
Mg
pg
x
/
/
pg
lOVpL
dL
dL
/
dL
0-0.08
03
0-0
150-450x10
-
31.3
8.1
5.4
39.0
-
31.3
75.2
—
pmol
pmol
pmol
CJ
.
I
/
L
/
L
/
/
L
Eosinophils
neoplasms
x
lOVpL
100
<
20x10
<
Body
stores
;
only
liver
deficiency
of
T
in
needs
T
capacity
T
allergies
with
thrombocytopenia
T
iL
risk
|
V
two
thirds
-
small
amount
pregnancy
bind
iron
to
of
in
and
with
parasitic
.
severe
Hgb
present
lactation
iron
bleeding
;
one
-
in
deficiency
infections
third
in
plasma
bone
Blood
.
and
.
marrow
certain
loss
spleen
.
major
,
cause
homeostasis without difficulty, patients with kidney failure, heart
failure (HF), or lung disease often encounter sodium and water
imbalances. In adults, changes in serum sodium concentrations
most often represent water rather than sodium imbalance. Therefore,
serum sodium concentrations are more reflective of a patient’s fluid
status rather than of sodium balance. Clinical manifestations of
hyponatremia or hypernatremia are mostly neurologic, and rapid
changes in serum sodium concentrations can lead to severe and
sometimes fatal brain injury.
6
HYPONATREMIA
Hyponatremia can result from dilution of the sodium concentration in
serum or from a total body depletion of sodium. The finding of
hyponatremia implies that sodium has been diluted throughout all
body fluids because water moves freely across cell membranes in
response to oncotic pressures. Hyponatremia can denote low, high,
or normal tonicity. Dilutional hyponatremia is the most common form
and results from water retention.7 Some clinical conditions such as
cirrhosis, congestive heart failure (CHF), the syndrome of
inappropriate antidiuretic hormone secretion (SIADH), and renal
impairment, as well as the administration of osmotically active
solutes (eg, albumin and mannitol) are commonly associated with
dilutional hyponatremia. Drugs that can induce SIADH, thereby
causing a reversible hyponatremia (especially in the elderly), include
cyclophosphamide, carbamazepine, desmopressin, oxcarbazepine,
oxytocin, serotonin selective reuptake inhibitors, and vincristine.
7–9
Hyponatremia that results from sodium depletion presents as a low
serum sodium concentration in the absence of edema. Sodiumdepletion hyponatremia can be caused by mineralocorticoid
deficiencies, sodium-wasting renal disease, or replacement of
sodium-containing fluid losses with nonsaline solutions.7 Therapy
with thiazide diuretics may also lead to the development of severe
hyponatremia. Hyponatremia is frequently seen in hospitalized
patients; however, morbidity varies significantly in severity, and
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serious complications can be due to the disorder itself or due to the
inappropriate management and rapid correction of the sodium levels.
HYPERNATREMIA
Hypernatremia represents a state of relative water deficiency in
relation to the body’s sodium stores. Because sodium contributes to
the cell’s tonicity, hypernatremia denotes hypertonicity and at least
transient cellular dehydration.10 Some of the causes of
hypernatremia are loss of free water, loss of hypotonic fluid, or
excessive sodium intake. Free water loss is uncommon, except in
the presence of diabetes insipidus. Diarrhea is the most common
cause of hypotonic fluid loss in infants and the elderly. Increased
retention of sodium in patients with hyperaldosteronism can also
increase serum sodium concentrations. Excessive salt intoxication is
usually accidental or iatrogenic, and most commonly results from
inappropriate intravenous (IV) administration of hypertonic salt
solutions. Some β-lactam antibiotics (eg, ticarcillin) contain a modest
sodium load and can cause fluid overload when high dosages are
administered.
The primary defense against hypertonicity is thirst and subsequent
fluid intake. Hypernatremic syndromes, therefore, usually occur in
patients who are unable to drink sufficient fluids. For example,
demented elderly patients are at increased risk because they
depend on others for their water requirements. Similarly, patients
who are vomiting, comatose, or not allowed oral fluids are at risk for
hypernatremia.
Potassium
Reference Range: 3.5–5.0 mEq/L or mmol/L
Potassium is the most abundant intracellular cation in the body
responsible for regulating enzymatic function and neuromuscular
tissue excitability. Approximately 90% of the total body potassium is
found in the ICF, with the majority in skeletal muscle, and only about
10% available in the ECF. The intracellular and extracellular
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potassium concentrations are regulated by the sodium–potassium
adenosine triphosphatase (Na+-K+-ATPase) pump. The potassium
ion in the ECF is filtered freely at the glomerulus of the kidney,
reabsorbed in the proximal tubule, and secreted into the distal
segments of the nephron. Because the majority of potassium is
sequestered within cells, a serum potassium concentration is not a
good measure of total body potassium. Intracellular potassium,
however, cannot be measured easily. Fortunately, the clinical
manifestations of potassium deficiency (eg, fatigue, drowsiness,
dizziness, confusion, electrocardiographic changes, muscle
weakness, and muscle pain) correlate well with serum
concentrations. The serum potassium concentration is buffered and
can be within normal limits despite abnormalities in total body
potassium. During potassium depletion, potassium moves from the
ICF into the ECF to maintain the serum concentration. When the
serum concentration decreases by a mere 0.3 mEq/L, the total body
potassium deficit is ~100 mEq. Serum potassium concentrations,
therefore, can be misleading when interpreted in isolation from other
considerations, and assumptions should not be made as to the
status of total body potassium concentration based solely on a
serum concentration measurement. Disorders of potassium are
commonly the result of (a) alterations in intake, (b) alterations with
excretion, and/or (c) unbalanced transcellular shifting of potassium
(eg, metabolic acidosis/alkalosis).
HYPOKALEMIA
The kidneys are responsible for about 90% of daily potassium loss
(∼40–90 mEq/day), and the remaining 10% of potassium is excreted
in the stool and a negligible amount in sweat. The kidneys, however,
have only a limited ability to conserve potassium. Even when
potassium intake has ceased, the urine will contain at least 5 to 20
mEq of potassium per 24 hours. Therefore, prolonged IV therapy
with potassium-free solutions in a patient unable to obtain potassium
in foods (eg, nothing by mouth) can result in hypokalemia.
Hypokalemia can also be induced by osmotic diuresis (eg, mannitol
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