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TABLE 17.5.2 Evaluation of the Patient with Acutely Elevated Creatinine
History Physical examination Testing Diagnosis
Prerenal
Diarrhea, vomiting,
decreased oral
intake, diuretic use,
fever
Dry mucous
membranes,
decreased urine
output, reduced
skinturgor
CBC, CMP, urine
electrolytes,
urinalysis
Hypoperfusion due
to gastrointestinal,
urinary, cutaneous
losses, bleeding, or
pancreatitis
Dyspnea, orthopnea,
tachycardia,
peripheral edema
Tachypnea,
tachycardia edema,
new murmur
on auscultation,
peripheral edema,
pulmonary rales
CBC, CMP, EKG,
cardiac enzymes,
echocardiogram,
D-Dimer, urinalysis,
urine electrolytes
Decreased cardiac
output due to heart
failure, pulmonary
embolus, acute
myocardial infarction,
severe valvular
disease, abdominal
compartment
syndrome
Fever, fatigue,
swelling, edema,
drug overdose
Tachycardia,
hypotension,
tachypnea, fever,
confusion
CBC, CMP, blood
cultures, urine drug
screen, urinalysis,
urine electrolytes
Systemic vasodilation:
sepsis, anaphy-
laxis, anesthetics,
drug overdose,
nephrotic syndrome,
cirrhosis, adrenocortic
insufciency
ACE inhibitor, ARB or
NSAID use
HTN CBC, CMP, blood
cultures, urine drug
screen, urinalysis,
urine electrolytes
Drug-induced impaired
renal blood flow
Intrinsic
Headaches, weight
loss, fatigue,
anorexia, rash,
preeclampsia
HTN, fever, rash,
peripheral edema
CBC, CMP, urinalysis,
urine sediment
and electrolytes,
erythrocyte
sedimentation rate
(ESR), C-reactive
protein (CRP),
ANA, anti-DNA,
RF, C3, C4, renal
ultrasound, renal
biopsy
VASCULAR
Microvascular disease:
atheroembolic disease
(cholesterol-plaque
microembolism),
thrombotic
thrombocytopenic
purpura, hemolytic
uremic syndrome,
HELLP syndrome, or
postpartum acute renal
failure
Macrovascular disease:
renal artery occlusion,
severe abdominal
aortic disease
(aneurysm)
(Continued)
378
Recent strep infection,
arthralgias, history
of rheumatologic
disease
Rash, joint swelling CBC, CMP, urinalysis,
urine sediment and
electrolytes, 24-h
urine protein, ESR,
CRP, ANA, anti-
DNA, ANCA, RF,
C3, C4, antibodies
to streptolysin O,
streptokinase, or
hyaluronidase, renal
ultrasound, renal
biopsy
GLOMERULAR
Inflammatory: anti-
glomerular basement
membrane disease
(Goodpasture
syndrome), anti-
neutrophil cytoplasmic
antibody-associated
glomerulonephritis
(Wegener
granulomatosis,
Churg-Strauss
syndrome, microscopic
polyangiitis), immune
complex GN (lupus,
postinfectious,
cryoglobulinemia,
primary
membranoproliferative
glomerulonephritis, IgA
nephropathy, Henoch-
Schönlein purpura,
polyarteritis nodosa)
Drugs: NSAIDs, gold,
penicillamine, captopril,
IVIG
Cancer, drug or
alcohol ingestion
history, seizure,
contrast use, recent
antibiotics
CBC, CMP, urinalysis,
urine sediment
and electrolytes,
CK, myoglobin,
appropriate drug
levels, renal
ultrasound,
renal biopsy,
serum protein
electrophoresis
Acute tubular
necrosis caused
by heme pigment
(rhabdomyolysis,
intravascular
hemolysis), crystals
(tumor lysis syndrome,
multiple myeloma,
seizures, ethylene
glycol poisoning,
megadose vitamin C,
acyclovir, indinavir,
methotrexate), drugs
(aminoglycosides,
lithium, amphotericin
B, pentamidine,
cisplatin, ifosfamide,
radiocontrast agents),
prolonged ischemia
(shock, surgery)
TABLE 17.5.2 Evaluation of the Patient with Acutely Elevated Creatinine
(Continued)
History Physical examination Testing Diagnosis
(Continued)
379
Antibiotic use, NSAID
use, fever
Rash CBC, CMP, urinalysis,
urine sediment and
electrolytes, WBC
casts, appropriate
drug levels, renal
ultrasound, renal
biopsy
Interstitial: drugs
(penicillins,
cephalosporins,
NSAIDs, proton
pump inhibitors,
allopurinol, rifampin,
indinavir, mesalamine,
sulfonamides), infection
(pyelonephritis,
viral nephritides),
systemic disease
(Sjögren syndrome,
sarcoid, lupus,
lymphoma, leukemia,
tubulonephritis)
Postrenal
Colicky ank pain,
hematuria
Flank pain, decreased
urine output
CBC, CMP, urinalysis,
urine electrolytes,
post-void residual,
abdominal/pelvis CT
or renal ultrasound
Nephrolithiasis
Male, weak stream,
nocturia
Enlarged prostate on
digital rectal exam,
distended bladder,
decreased urine
output
CBC, CMP, urinalysis,
post void residual,
urine electrolytes,
abdomen/pelvis
CT scan, prostate
biopsy
Benign prostatic
hypertrophy (BPH),
prostate cancer
Female, pelvic mass Pelvic mass,
decreased urine
output
CBC, CMP, urinalysis,
abdomen/pelvis CT
scan, biopsy
Malignancy
Painless hematuria,
weight loss, fever,
night sweats
Cachexia, distended
bladder, decreased
urine output
CBC, CMP, urinalysis,
urine electrolytes,
post void residual,
cystoscopy
Bladder cancer, clot,
fungus ball
History of diabetes,
multiple sclerosis,
stroke, decreased
sensation
Decreased sensation,
distended bladder,
decreased urine
output
CBC, CMP, urinalysis,
urine electrolytes,
post void residual
Neurogenic bladder
CBC, complete blood count; CMP, comprehensive metabolic panel; EKG, electrocardiogram; HTN,
hypertension; ANA, antinuclear antibody; RF, rheumatoid factor; C3, C4, complement factors; ANCA,
anti-neutrophil cytoplasmic antibody; WBC, white blood cell; NSAIDs, nonsteroidal anti-inammatory
drugs; CK, creatine kinase; IVIG, intravenous immunoglobulin
TABLE 17.5.2 Evaluation of the Patient with Acutely Elevated Creatinine
(Continued)
History Physical examination Testing Diagnosis
380
TABLE 17.5.3 Evaluation of the Patient with Chronically Elevated Creatinine
History Physical examination Testing Diagnosis
History of diabetes,
overweight
Overweight, retinopathy,
decreased sensation
in extremities, HTN
CBC, CMP, Mg, Ph,
Ca, urinalysis, 24-h
urine protein, renal
ultrasound, fasting
blood sugar, HbA1C
Diabetic nephropathy
Hypertension HTN, retinopathy,
leftventricular
hypertrophy
CBC, CMP, Mg, Ph,
Ca, urinalysis, 24-h
urine protein, renal
ultrasound, EKG
Hypertension
Rheumatologic
disease, recurrent
infections, arthritis,
patient older than
40 y
Rash, joint swelling CBC, CMP, urinalysis,
urine sediment and
electrolytes, 24-h urine,
renal biopsy, ESR,
CRP, ANA, anti-DNA,
RF, C3, C4, a ntibodies
to streptolysin O,
streptokinase, or
hyaluronidase, renal
ultrasound, renal biopsy
Glomerulonephritis
and vasculitis
Antibiotic use, NSAID
use, fever
Rash CBC, CMP, urinalysis,
urine sediment and
electrolytes, WBC casts,
appropriate drug levels,
SS-A, SS-B, renal
ultrasound, renal biopsy
Interstitial nephritis
Urinary frequency,
urgency, burning
with urination
Fever CBC, CMP, urinalysis,
urine culture, voiding
cystourethrography,
abdomen/pelvis CT
Chronic infection
Fever, weight loss,
night sweats,
anemia, patient
older than 40 y
CBC, CMP, urinalysis,
SPEP, UPEP, calcium
level, ESR
Neoplasm,
paraproteinemia
Family history of
polycystic kidney
disease, ank pain
Palpable kidneys CBC, CMP, urinalysis,
abdomen/pelvis CT
Polycystic kidney
disease
Refractory HTN,
sudden-onset
HTN, smoker
Abdominal bruit CBC, CMP, urinalysis,
renal Doppler
ultrasound or magnetic
resonance angiogram
(MRA)
Renal artery stenosis
CBC, complete blood count; CMP, comprehensive metabolic panel; EKG, electrocardiogram;
HTN, hypertension; HbA1C, hemoglobin A1C; ANA, antinuclear antibody; NSAIDs, nonsteroidal
anti-inammatory drugs; RF, rheumatoid factor; C3, C4, complement factors; SPEP, serum protein
electrophoresis; UPEP, urine protein electrophoresis; WBC, white blood cell.
381
IV. DIAGNOSIS. See Tables 17.5.1–17.5.3. Elevated creatinine is usually asymptomatic in the
early stages. Diagnosis is made by checking serum creatinine. Evaluation of the cause of
decreased renal function should be made and can include comparison with previous creatinine,
creatinine clearance (calculated with the Cockcroft-Gault formula or by 24-hour collection),
urinalysis, urinary sediment, measurement of diuresis over 24 hours (if anuria), 24-hour urine
collection to test for clearance of creatinine and proteins, urea, electrolytes, complete blood
count, glucose, bicarbonate, calcium and phosphorus, protein and albumin, renal ultrasonog-
raphy, or renal biopsy (4, 5, 6). The fractional excretion of sodium (FENa) can be used to dif-
ferentiate between prerenal, intrinsic, and postrenal causes. FENa is calculated by using serum
and urine sodium and creatinine. Prerenal causes will have a result of less than 1% and intrinsic
and postrenal causes will be greater than 2%. The FENa equation is given as
FENa = UNa × PCr × 100
Pna × UCr
REFERENCES
1. Donald DB, Richard LD, Richard FL. Chapter 18. Common laboratory tests. Degowin’s Diagnostic
Examination, 9th ed. New York, NY: McGraw-Hill, 2009.
2. Andrew L, Suren K. Acute kidney injury. Retrieved from Renal.org. March 8, 2011.
3. Richard T. Approach to managing elevated creatinine. Can Fam Physician 2004;50(5):735–740.
4. Brian A. Acute renal failure—differential diagnosis. Retrieved from Dynamed.ebscohost.com. Oct 17,
2011.
5. Malay A, Richard S. Acute renal failure. Am Fam Physician 2000;61(7):2077–2088.
6. Susan S, Bernadette P. Detection and evaluation of chronic kidney disease. Am Fam Physician
2005;72(9):1723–1732.
17.6
D-Dimer
Perry W. Sexton and Nicole Otto
I. BACKGROUND. D-dimer is a degradation product of cross-linked fibrin that has undergone
fibrinolysis in the final stages of the clotting cascade (1). Although the D-dimer test is useful
in the diagnosis of venous thromboembolism (VTE) (deep vein thrombosis and/or pulmonary
embolism), venogram, Doppler ultrasound, V/Q scan, arteriogram, and/or high-resolution
chest computed tomography (CT) scan are the definitive diagnostic tests for these conditions.
The challenge of some of these diagnostic tests is that the results are operator dependent and
can sometimes be “indeterminate.” The D-dimer test was developed to potentially eliminate the
need for further diagnostic testing in those who present with an unsure diagnosis of suspected
VTE (2,3).
II. EVALUATION
A.
The first step in approaching a patient with VTE is to establish the pretest probability on
the basis of clinical criteria such as the Wells Criteria (4–9) (see Tables 17.6.1 and 17.6.2).
Additional clinical risk factors include the use of hormonal contraception, smoking, obesity,
central venous catheters, thrombophilias, and inflammatory bowel disease (10).
1. In patients with a low clinical pretest probability of VTE, a D-dimer level can be
obtained to guide the diagnosis. A result of <500 ng/mL has a negative predictive value
of 95% (see Table 17.6.3) and eliminates the need for further testing. Patients with a
low pretest probability and a D-dimer of ≥500 ng/mL should go on to an appropriate
imaging study.
382
TABLE 17.6.2 Wells Criteria for Predicting Pulmonary Embolism
Criteria Number of points
Clinical signs and symptoms of DVT +3
An alternative diagnosis that is less likely than pulmonary embolism +3
Pulse rate >100 beats/min +1.5
Immobilization or surgery in the previous 4 wk +1.5
Previous DVT/pulmonary embolism +1.5
Hemoptysis +1
Malignancy +1
Risk score interpretation (probability of DVT): >6 points = high risk (78.4%); 2–6 points =
moderate risk (27.8%); < 2 points = low risk (3.4%).
DVT, deep vein thrombosis.
TABLE 17.6.1 Wells Criteria for Predicting Deep Vein Thrombosis (DVT)
Criteria Number of points
Active cancer (treatment within 6 mo or palliation)
+1
Paralysis, paresis, or immobilization of lower extremity
+1
Bedridden for more than 3 d or major surgery (within 12 wk)
+1
Localized tenderness along distribution of deep veins
+1
Entire leg swollen
+1
Unilateral calf swelling of >3 cm (measured 10 cm below tibial tuberosity) +1
Unilateral pitting edema
Collateral supercial veins (non-varicose)
Previously documented DVT
Alternative diagnosis as likely as or more likely than DVT
+1
+1
+1
−2
Risk score interpretation (probability of DVT): 3 points = high risk (75%); 1–2 points = moderate
risk (17%); <1 point = low risk (3%).
DVT, deep vein thrombosis.
2. Patients with a high pretest probability of VTE should be evaluated first by an imaging
study; D-dimer is used only when the imaging results are “indeterminate.”
B. It is important to note that a low D-dimer test is able to rule out VTE. By contrast,
an elevated D-dimer level is not able to establish a diagnosis of VTE—this test is not
sufficiently specific.
383
C. There are many other systemic causes of an elevated D-dimer (see Table 17.6.4). D-dimer
is primarily cleared via the kidneys and partially cleared through the liver, so dysfunction in
either system can lead to decreased clearance and falsely elevated levels (11).
D. The laboratory-based quantitative enzyme-linked immunosorbent assay provides quantita-
tive values for interpretation, whereas the bedside immunochromatographic point of care
assay provides a rapid qualitative value, with similar accuracy for low-risk patients (12,13).
E. The D-dimer test is being investigated for potential use in other clinical settings, including
1. Determination of the duration of anticoagulation for VTE patients (14)
2. Diagnosis of acute aortic dissection (though a potentially delayed D-dimer measurement
should not preclude imaging of this life-threatening condition) (15)
3. Utilization of an age-adjusted D-dimer cutoff (patient’s age × 10 μg/L) to increase the
number of patients above 50 years in whom PE can be excluded (16–18)
4. Inclusion of D-dimer in the laboratory evaluation of disseminated intravascular coagula-
tion (19)
III. DIAGNOSIS. The D-dimer test is a quick, noninvasive, and non-operator-dependent labora-
tory test that can exclude the diagnosis of VTE when negative in patients with low pretest
probability but does not have sufficient specificity to rule in VTE with certainty when positive
(see Table 17.6.4 for other systemic causes of an elevated D-dimer) (11).
TABLE 17.6.3 Interpreting D-dimer Results
D-dimer value
Pretest probability for
VTE (DVT or PE) Interpretation Diagnostic decision
<500 μg/mL
Low pretest probability Normal Can safely exclude the
diagnosis of VTE
(Any value) High pretest probability VTE cannot be
excluded
Need further imaging
>500 μg/mL
Any clinical probability VTE cannot be
excluded
Need further imaging
DVT, deep vein thrombosis; PE, pulmonary embolism; VTE, venous thromboembolism.
Table 17.6.4 Factors that Affect the Predictability of the D-dimer Test
Increased false-positive results Increased risk of false-negative results
Cancer (20)
Inammatory states
Cancer (21)
Recent surgery
Infection Pregnancy
Sepsis (18) Hypercoagulable state
Supercial thrombophlebitis (22)
Trauma
Hospitalization (23)
Advanced age (16–18)
Renal disease (10)
384
REFERENCES
1. Adam S, Key N, Greenberg C. D-dimer antigen: current concepts and future prospects. Blood
2009;113:2878–2887.
2. Ramzi D, Leeper K. DVT and pulmonary embolism: part I. Diagnosis. Am Fam Physician
2004;90:2829–2836.
3. Qaseem A, Snow V, Barry P, et al. Current diagnosis of venous thromboembolism in primary care:
a clinical practice guideline form the American Academy of Family Physicians and the American
College of Physicians. Ann Intern Med 2007;146:454–458.
4. Wells PS, Anderson DR, Bormanis J, Guy F, Mitchell M, Gray L, et al. Value of assessment of pretest
probability of the deep-vein thrombosis in clinical management. Lancet 1997;350:1795–1798.
5. Wells PS, Anderson DR, Rodger M, et al. Evaluation of D-dimer in the diagnosis of suspected deep
vein thrombosis. N Engl J Med 2003;349:1227–1235.
6. Fancher TL, White RH, Kravitz RL. Combined use of rapid D-dimer testing and estimation of clini-
cal probability in the diagnosis of deep vein thrombosis: systematic review. BMJ 2004;329:821–824.
7. Bates SM, Jaescheke R, Stevens SM, et al. Diagnosis of DVT: antithrombotic therapy and preven-
tion of yhrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice
Guidelines. Chest 2012;141(2 Suppl):e35is–e418s.
8. Wells PS, Anderson DR, Rodger M, Ginsberg JS, Kearon C, Gent M, et al. Derivation of a simple
clinical model to categorize patients’ probability of pulmonary embolism: increasing the model’s util-
ity with the SimpliREDD-dimer. Thromb Haemost 2000;83:416–420.
9. Stein P, Woodward P, Weg J, et al. Diagnostic pathways in acute pulmonary embolism: recommenda-
tions of the PIOPED II investigators. Am J Med 2006;119:1048–1055.
10. Caprini J. Update on risk factors for venous thromboembolism. Am J Med 2005;118:3–10.
11. Karami-Djurabi R, Klok FA, Kooiman J, Velthuis SI, Nijkeuter M, Huisman MV. D-dimer
testing in patients with suspected pulmonary embolism and impaired renal function. Am J Med
2009;122:1050–1053.
12. Runyon MS, Beam DM, King MC, Lipford EH, Kline JA. Comparison of the simplify D-dimer
assay performed at the bedside with a laboratory-based quantitative D-dimer assay for the diagno-
sis of pulmonary embolism in a low prevalence emergency department population. Emerg Med J
2008;25:70–75.
13. Wells PS, Anderson DR, Rodger M, Stiell I, Dreyer JF, Barnes D, et al. Excluding pulmonary embo-
lism presenting to the emergency department by using a simple clinical model and D-dimer. Ann
Intern Med 2001;135:98–107.
14. Palareti G, Cosmi B, Legnani C, et al. D-dimer testing to determine the duration of anticoagulation
therapy. N Engl J Med 2006;355:1780–1789.
15. Sutherland A, Escano J, Coon TP. D-dimer as the sole screening test for acute aortic dissection: a
review of the literature. Ann Emerg Med 2008;52:339–343.
16. Van Es J, Mos I, Douma R, et al. The combination of four different clinical decision rules and an
age-adjusted D-dimer cut-off increases the number of patients in whom acute pulmonary embolism
can safely be excluded. Thromb Haemost 2012;107:167–171.
17. Douma R, le Gal G, et al. Potential of an age adjusted D-dimer cut-off value to improve the exclu-
sion of pulmonary embolism in older patients: a retrospective analysis of three large cohorts. BMJ
2010;340:1475–1481.
18. Tita-Nwa F, Bos A, Adjei A, Eshle WEB, Longo DL, Ferrucci L. Correlates of D-dimer in older
persons. Aging Clin Exp Res 2010;22:20–23.
19. Taylor FB Jr, Toh CH, Hoots WK, et al. Towards definition, clinical and laboratory criteria, and a
scoring system for disseminated intravascular coagulation. Thromb Haemost 2001;86:1327–1330.
20. Righini M, Le Gal G, De Lucia S, et al. Clinical usefulness of D-dimer testing in cancer patients with
suspected pulmonary embolism. Thromb Haemost 2006;95:715–719.
21. Carrier M, Lee AY, Bates SM, Anderson DR, Well PS. Accuracy and usefulness of a clinical predic-
tion rule and D-dimer testing in excluding deep vein thrombosis in cancer patients. Thromb Res
2008;123:177–183.
22. Gillet JL, FFrench P, Hanss M, et al. Predictive value of d-dimer assay in superficial thrombophlebitis
of the lower limbs. J Mal Vasc 2007;32:90–95.
23. Brotman DJ, Segal JB, Jani JT, et al. Limitations of D-dimer testing in unselected inpatients with
suspected venous thromboembolism. Am J Med 2003;114:276.
385
Hypercalcemia
Peter F. Cronholm, Mario P. DeMarco, and
Alexis M. Atwater
I. BACKGROUND. The normal range of serum calcium is 8.5–10.5 mg/dL. Hypercalcemia,
defined as serum calcium concentrations above 10.5 mg/dL, occurs when the calcium enters
the circulatory system more rapidly than it is excreted in the urine or deposited in bones. An
initial elevated calcium level should be repeated to confirm the abnormality (1).
II. PATHOPHYSIOLOGY. Nine out of ten cases of hypercalcemia in adults are caused by either
hyperparathyroidism or malignancy. Hyperparathyroidism causes most of the hypercalcemia in the
outpatient setting. Malignancy causes most of the hypercalcemia found in hospitalized patients.
Clinical features including presence of symptoms can help differentiate between these two main
causes. Less common causes of hypercalcemia are chronic renal failure, hyperthyroidism, hypervi-
taminosis A, hypervitaminosis D, immobilization, Paget’s disease, and granulomatous diseases (2).
Pseudohypercalcemia occurs when patients have increased serum calcium-binding proteins. For
example, dehydration severe enough to cause hyperalbuminemia may result in high serum calcium
levels. Such pseudohypercalcemia should resolve after the hemoconcentration is corrected.
III. EVALUATION
A. History.
Patients are often asymptomatic until the calcium level rises above 12 mg/dL, and
the symptoms are often nonspecific: generalized muscle weakness, muscle aches, decreased
coordination, decreased level of consciousness, headache, loss of appetite, nausea, vomiting,
constipation, increased salivation, dysphagia, and abdominal pain or distension. A review of
systems may turn up a history of a renal calculus or a history of a malignancy (3).
B. Physical Examination. Depending on the severity of hypercalcemia, physical examination
may reveal mental confusion, poor memory, slurred speech, acute psychotic behavior, lethargy
or coma, ataxia, poor overall muscle strength, hypotonia, hyperextensible joints, increased deep
tendon reflexes, positive Babinski reflexes, incoordination, decreased pain or vibration sense, cal-
cium deposits on the conjunctiva near the palpebral fissure or on the cornea around the iris, or
an acute abdomen or an ileus. A short QT interval may also be noted on the electrocardiogram.
C. Testing. See Table 17.7.1.
TABLE 17.7.1 Evaluation of the Patient with Hypercalcemia
History Physical examination Testing Diagnosis
A. Spurious
• Excessive thirst
• Vomiting or diarrhea
with poor oral intake
• Dry mucous
membranes
• Decreased skin turgor
• Confusion/lethargy
• Repeat calcium
after rehydration
• Pseudohypercalcemia
due to dehydration
B. Endocrine disorders
• Female
• >60 y old
• Aches and pains
• Neck mass (unlikely)
• No clinical evidence of
malignancy
• Serum calcium
<14.5 mg/dL
• Parathyroid
hormone
(elevated)
• Hyperparathyroidism
(4) primary or
secondary
(pheochromocytoma,
multiple endocrine
neoplasia I, IIa)
17.7
(Continued)
386
• Vague abdominal
pain
• Depressive symp-
toms
• Renal calculi
• Serum chloride
>102 mg/dL
• Alkaline
phosphatase (nor-
mal)
• Serum phosphate
• Bicarbonate
• X-ray hands and
clavicles
• Anxiety/tremor
• Weight loss
• Family history
• Heat intolerance
• Vision problems
• Exophthalmos
• Eyelid tremor
• Tachycardia
• Perspiration
• Hyperreexia
• Thyroid-stimulating
hormone, free T4
• Thyrotoxicosis
• Fatigue
• Weight loss
• Family history
• Nausea/vomiting
• Hypotension
• Lethargy
• Increased mucosal or
skin pigmentation
• Elevated potassium
• Decreased sodium
• Decreased blood
glucose
• Abnormal adrenal
cortical hormone
stimulation test
• Addison’s disease
C. Malignancy (5)
• >50 y old
• Weight loss
• Smoker
• Family history
• Other symptoms
specic to particular
tumor site
• Weight loss
• Signs specic to
particular tumor site
• Serum calcium
>14 mg/dL
• Serum chloride
<100 mg/dL
• Alkaline
phosphatase >2
times normal
• Parathyroid
hormone <2 times
normal
• CBC (anemia
frequent)
• Further workup
according to the
suspected site of
primary tumor
• Bone scan
Malignancy with or
without metastasis
• Lung cancer
• Renal cell carcinoma
• Squamous cell
carcinoma
TABLE 17.7.1 Evaluation of the Patient with Hypercalcemia (Continued)
History Physical examination Testing Diagnosis
(Continued)
387