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actually have a normal or low blood pressure from systemic vasodilation, suggesting that the
association between pulmonary and systemic hypertension represents a generalized abnormality of vascular tone.
e presence of oxygen desaturation, elevated neck veins, ascites, or edema does not affect the
probability of pulmonary hypertension in these patients (EBM Box 8.4).
References may be accessed online at Elsevier eBooks for Practicing Clinicians.
3—GENERAL APPEARANCE OF THE PATIENT
References
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absence of anemia, fever, and jaundice. Acad Emerg Med. 2000;7(2):146–156.
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fibrosis and cirrhosis. Liver Int. 2008;28(5):659–666.
38. Romagnuolo J, Jhangri GS, Jewell LD, Bain VG. Predicting the liver histology in chronic hepatitis C:
how good is the clinician? Am J Gastroenterol. 2001;96(11):3165–3174.
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Tine F, Caltagirone M, Camma C, et al. Clinical indicants of compensated cirrhosis: a prospective study.
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patients with liver cirrhosis. J Gastroenterol Hepatol. 1999;14(8):785–790.
45. omopoulos KC, Labropoulou-Karatza C, Mimidis KP, Katsakoulis EC, Iconomou G, Nikolopoulou
VN. Non-invasive predictors of the presence of large oesophageal varices in patients with cirrhosis. Dig
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with a history of variceal hemorrhage. Arch Intern Med. 2001;161(21):2564–2570.
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using clinical, laboratory and imaging parameters. J Gastroenterol Hepatol. 2007;22(11):1909–1915.
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49. Arguedas MR, Singh H, Faulk DK, Fallon MB. Utility of pulse oximetry screening for hepatopulmonary
syndrome. Clin Gastroenterol Hepatol. 2007;5(6):749–759.
50. Lima BLG, Franca AVC, Pazin-Filho A, etal. Frequency, clinical characteristics, and respiratory param-
eters of hepatopulmonary syndrome. Mayo Clin Proc. 2004;79(1):42–48.
51. Martínez GP, Barberà JA, Visa J, etal. Hepatopulmonary syndrome in candidates for liver transplanta-
tion. J Hepatol. 2001;34(5):651–657.
52. Khoshbaten M, Rostami Nejad M, Ansarin K, etal. e association between clinical symptoms, labora-
tory findings and serum endothelin 1 concentrations, in cirrhotic patients with and without hepatopulmonary syndrome. Gastroenterol Hepatol N Y. 2012;5(suppl 1):S13–S19.
53. Abu El Makarem MA, Elakad A, Ali A, etal. Hepatopulmonary syndrome: prevalence and predictors in
Egyptian cirrhotic patients. Trop Gastroenterol. 2011;32(1):25–30.
54. Forde KA, Fallon MB, Krowka MJ, etal. Pulse oximetry is insensitive for detection of hepatopulmonary
syndrome in patients evaluated for liver transplantation. Hepatology. 2019;69(1):270–281.
55. Younis I, Sarwar S, Butt Z, Tanveer S, Qaadir A, Jadoon NA. Clinical characteristics, predictors, and
survival among patients with hepatopulmonary syndrome. Ann Hepatol. 2015;14(3):354–360.
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R, Mulcahy HE, Willner I, Reuben A. Prediction of esophageal varices in patients with
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56. Suceveanu AI, Mazilu L, Tomescu D, Ciufu N, Parepa IR, Suceveanu AP. Screening of hepatopulmonary
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syndrome (HPS) with CEUS and pulse-oximetry in liver cirrhosis patients eligible for liver transplant.
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survival in liver transplant candidates. Gastroenterology. 2008;135(4):1168–1175.
58. Tumgor G, Berdeli A, Arikan C, Levent E, Aydogdu S. Mcp-1, eNOS, tPA and PAI-1 gene poly-
morphism and correlation of genotypes and phenotypes in hepatopulmonary syndrome. Dig Dis Sci.
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59. Schenk P, Fuhrmann V, Madl C, etal. Hepatopulmonary syndrome: prevalence and predictive value of
various cut offs for arterial oxygenation and their clinical significance. Gut. 2002;51:853–859.
60. Pilatis ND, Jacobs LE, Rekpattanapipat P, etal. Clinical predictors of pulmonary hypertension in patients
undergoing liver transplant evaluation. Liver Transpl. 2000;6(1):85–91.
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CHAPTER
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Cyanosis
KEY TEACHING POINTS
• Cyanosis results from increased amounts of bluish-colored hemoglobin in the superficial
vessels of the skin. The usual cause is increased deoxyhemoglobin; rare causes are
increased methemoglobin or other abnormal hemoglobins.
• The blue color of cyanosis requires a minimum absolute amount of abnormal hemoglobin
(i.e., >2.38 g/dL arterial deoxyhemoglobin). This explains why polycythemic patients
develop cyanosis more easily than do anemic patients.
• Cyanosis is either central or peripheral, a distinction made at the bedside. This
distinction, in turn, implies specific etiologies.
• In patients with chronic liver disease, the finding of cyanosis increases the probability of
hepatopulmonary syndrome.
• Pseudocyanosis, unlike cyanosis, does not blanch with pressure, a finding indicating that
the color is not from abnormally colored blood but instead from abnormal pigments in the
skin (e.g., silver, amiodarone).
9
Definitions
I.
Cyanosis is an abnormal bluish discoloration of the skin and mucous membranes, caused by bluecolored blood circulating in the superficial capillaries and venules. e blue color usually represents
excessive amounts of deoxygenated hemoglobin, although in some patients it results from increased
amounts of methemoglobin or sulfhemoglobin. Cyanosis may be central or peripheral. In central
cyanosis the blood leaving the heart is colored blue; in peripheral cyanosis, the blood leaving the
heart is red but becomes blue by time it reaches the fingers and toes. Pseudocyanosis, in contrast,
refers to a permanent bluish discoloration caused by deposition of blue pigments in the skin.
Cyanosis was first described in 1761 by Morgagni, who attributed it to pulmonary stenosis.
1869, Claude Bernard described the qualitative difference in blood gases between blue venous and
red arterial blood. e first person to quantify the amount of deoxygenated hemoglobin necessary
to produce the blue color was Lundsgaard in 1919.
II. Pathogenesis
A. THE BLUE COLOR
Blood becomes blue when an absolute amount of blue pigment (usually deoxyhemoglobin) accumulates, probably because only then is the blue color deep enough to be seen through the opaque
epidermis.
the amount of additional red blood (or oxyhemoglobin) matters little to the overall skin color.
1–4
Once this minimal amount of deoxyhemoglobin accumulates and cyanosis appears,
1
In
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3—GENERAL APPEARANCE OF THE PATIENT
e color of the skin depends on the color of blood flowing through the dermal capillaries and
subpapillary venous plexus, not the arteries and veins that lie too deep to contribute to skin color.
1,5
ere has been much confusion over the absolute concentration of deoxyhemoglobin required
for cyanosis, primarily because some investigators have mistakenly equated the arterial levels of
deoxyhemoglobin, which are easy to measure, with the capillary levels thereof, which impart the
blue color but must exceed the measured arterial levels. In patients with central cyanosis, the aver-
age amount of arterial deoxyhemoglobin is 3.48 ± 0.55 g/dL (or 5.35 g/dL in the capillaries and
small venules). e minimal amount of arterial deoxyhemoglobin causing cyanosis is 2.38 g/dL (or
4.25 g/dL in the capillaries and small venules).
*.4
Because cyanosis depends on the absolute quantity of deoxyhemoglobin, not the relative amount,
the appearance of cyanosis also depends on the patient’s total hemoglobin concentration (i.e., 5 g/dL
of capillary deoxyhemoglobin represents a higher percent of oxygen desaturation for an anemic
patient, who has less total hemoglobin, than it does for a polycythemic patient). Table 9.1 displays
this relationship: polycythemic patients (haemoglobin = 20 g/dL) may appear cyanotic with only
mild hypoxemia (i.e, oxygen saturation [SaO2] = 88% or pO2 = 56 mm Hg), yet anemic patients
(haemoglobin = 8 g/dL) do not develop the finding until the hypoxemia is severe (i.e., SaO2 = 70%
or pO2 = 36 mm Hg). ese figures are calculated as follows: for the polycythemic patient (haemoglo-
bin = 20 g/dL), 2.38 g/dL of arterial deoxyhemoglobin indicates that there is 20 − 2.38 or 17.62 g/dL
of arterial oxyhemoglobin. e oxygen saturation, therefore, is (17.62)/(20) = 0.88, or 88%. For the
anemic patient, the calculation is (8 − 2.38)/8 = 0.7, or 70% saturation.
B. PERIPHERAL CYANOSIS
In peripheral cyanosis, the blood leaving the heart is red; however, because of increased extraction
of oxygen by the peripheral tissues, enough deoxyhemoglobin accumulates to render it blue in the
subepidermal blood vessels of the feet and hands. e clinician can easily demonstrate peripheral
cyanosis by wrapping a rubber band around his or her own finger and watching the distal digit
turn blue as oxygen continues to be extracted from the stagnant blood.
TABLE 9.1 ■ Cyanosis and Hemoglobin Concentration.
Hemoglobin concentration (g/dL)
6 60 31
8 70 36
10 76 40
12 80 45
14 83 47
16 85 50
18 87 54
20 88 56
*These figures assume that central cyanosis begins to appear when 2.38 g/dL deoxygenated hemoglobin
accumulates in the arterial blood (see text for calculations). The corresponding pO2 was obtained from standard
hemoglobin dissociation curves for oxygen.
*
Capillary
deoxyhemoglobin is 1.87g/dL more than arterial levels, based on three assumptions: (1) the
difference in oxygen content between the arteries and veins is 5
of deoxyhemoglobin in the capillaries is midway between that of the arteries and vein; and (3) 1.34
oxygen binds to 1g of saturated hemoglobin. erefore, 5/(2 × 1.34) = 1.87.
Cyanosis appears at:*
Oxygen saturation (%)
below:
Arterial pO2 (mm Hg)
below:
mL of oxygen/dL blood; (2) the amount
mL of
9—CYANOSIS
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73
III. The Finding
Cyanosis is best appreciated in areas where the overlying epidermis is thin and subepidermal
vessels are abundant, such as the lips, nose, cheeks, ears, hands, feet, and the mucous membranes of
the oral cavity.
lighting or daylight.
A. CENTRAL CYANOSIS
Patients with central cyanosis have blue discoloration of the lips, tongue, and sublingual tissues, as
well as the hands and feet. e correlation between severity of oxygen desaturation and the depth
of the cyanotic color is best appreciated by examining the patient’s lips and buccal mucosa.
Some patients with longstanding central cyanosis have associated clubbing (see Chapter 28).
When central cyanosis is suspected yet administration of oxygen fails to diminish the blue color,
the clinician should consider methemoglobinemia or sulfhemoglobinemia. e color of patients
with methemoglobinemia often has a characteristic brownish hue (so-called chocolate cyanosis).
Because cyanosis depends on blue blood being present in the underlying blood vessels, maneuvers that express blood out of the vessels (e.g., pressure on the skin) make the blue color temporarily
disappear.
B. PERIPHERAL CYANOSIS
Peripheral cyanosis causes blue hands and feet, although the mucous membranes of the mouth are
pink. Warming the patient’s limb skin often diminishes peripheral cyanosis because blood flow
to the involved area improves, whereas the color of central cyanosis is unchanged or deepens after
warming of the skin.
1,6
Cyanosis is detected more easily with fluorescent lighting than with incandescent
4
7,8
9
C. PSEUDOCYANOSIS
In patients with pseudocyanosis, the mucous membranes of the mouth are pink, and pressure on
the skin fails to blanch the abnormal color.
D. CYANOSIS AND OXIMETRY
Cyanosis affects co-oximetry (i.e., blood gas analysis in the laboratory) differently from how it affects
pulse oximetry (i.e., equipment used at the bedside; see Chapter 20). Because co-oximetry can distinguish deoxyhemoglobin from other abnormal hemoglobins, it indicates hypoxemia only in patients
with central cyanosis (i.e., it samples arterial blood and therefore indicates normal oxygen levels in
peripheral cyanosis). Pulse oximetry, in contrast, detects the color of the pulsatile waveform in the digit.
Although it also indicates hypoxemia in patients with central cyanosis, pulse oximetry may falsely
indicate arterial hypoxemia in patients with peripheral cyanosis or with abnormal hemoglobin (see
Chapter 20). Both co-oximetry and pulse oximetry indicate normal oxygen levels in pseudocyanosis.
IV. Clinical Significance
A. CENTRAL CYANOSIS
Any disorder causing hypoxemia may generate sufficient deoxyhemoglobin in the blood leaving
the heart to produce central cyanosis. e typical etiologies are pulmonary edema, pneumonia,
and intracardiac right-to-left shunts. e finding of central cyanosis increases the probability of
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3—GENERAL APPEARANCE OF THE PATIENT
EBM BOX 9.1 Central Cyanosis, Detecting Arterial Deoxyhemoglobin
≥2.38 g/dL*
Finding (Reference)
Central cyanosis
*Corresponding to O2 saturation of 80% and pO2 of 45 mm Hg if hemoglobin concentration is 12 g/dL
(see Table 9.1).
†
Likelihood ratio (LR) if finding present = positive LR; LR if finding absent = negative LR.
against arterial deoxyhemoglobin
2,4
LRs
Absence of cyanosis, arguing
Sensitivity
(%)
79–95 72–95 7.4 0.2
Decrease Increase
0.1 0.2 0.5 12510
>2.38 g/dL
Specificity
(%)
CYANOSIS
Probability
Likelihood Ratio† if Finding Is
Present Absent
+45%+30%+15%–15%–30%–45%
LRs
Presence of cyanosis, detecting
arterial deoxyhemoglobin >2.38
g/dL
hypoxemia greatly (likelihood ratio [LR] = 7.4, see EBM Box 9.1). In these studies, hypoxemia
is defined as arterial deoxyhemoglobin level ≥2.38 g/dL, corresponding to SaO2 ≤80% and pO2
≤45 mm Hg in patients with normal amounts of hemoglobin (see Table 9.1). e absence of
central cyanosis decreases the likelihood of such severe hypoxemia (LR = 0.2, EBM Box 9.1).
In patients with chronic liver disease, the finding of cyanosis increases the probability of hepa-
topulmonary syndrome (LR = 4.4; see Chapter 8).
B. PERIPHERAL CYANOSIS
In clinical practice, the common causes of peripheral cyanosis are low cardiac output, arterial
disease or obstruction (e.g., Raynaud disease), and venous disease.
C. PSEUDOCYANOSIS
Pseudocyanosis may occur after exposure to metals (argyria f rom topical silver compounds;
chrysiasis of gold therapy) or drugs (amiodarone, minocycline, chloroquine, or phenothiazines).
References may be accessed online at Elsevier eBooks for Practicing Clinicians.
10,11
References
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1. Lundsgaard C, Van Slyke DD. Cyanosis. Medicine. 1923;2:1–76.
2. Goss GA, Hayes JA, Burdon JGW. Deoxyhaemoglobin concentrations in the detection of central
cyanosis. orax. 1988;43(3):212–213.
3. Martin L, Khalil H. How much reduced hemoglobin in necessary to generate central cyanosis? Chest.
1990;97(1):182–185.
4. Barnett HB, Holland JG, Josenhans WT. When does central cyanosis become detectable? Clin Invest
Med. 1982;5(1):39–43.
5. Lewis T. e Blood Vessels of the Human Skin and eir Responses. London: Shaw & Sons; 1927.
6. Carpenter KD. A comprehensive review of cyanosis. Crit Care Nurse. 1993;13(4):66–72.
7. Kelman GR, Nunn JF. Clinical recognition of hypoxaemia under fluorescent lamps. Lancet.
1966;1(7452):1400–1403.
8. Medd WE, French EB, Wyllie VM. Cyanosis as a guide to arterial oxygen desaturation. orax.
1959;14(3):247–250.
9. Wright RO, Lewander WJ, Woolf AD. Methemoglobinemia: etiology, pharmacology, and clinical
management. Ann Emerg Med. 1999;34(5):646–656.
10. Baernstein A, Smith KM, Elmore JG. Singing the blues: is it really cyanosis? Respir Care. 2008;53(8):
1081–1084.
11. Weatherald J, Marrie TJ. Pseudocyanosis: drug-induced skin hyperpigmentation can mimic cyanosis. Am
J Med. 2008;121(5):385–386.
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CHAPTER
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10
Anemia
KEY TEACHING POINTS
• Examination for pallor focuses on those parts of the body that present large numbers
of superficial blood vessels with minimal natural skin pigments, such as the conjunctiva,
tongue, oral mucosa, and palmar creases.
• The most compelling argument for anemia is conjunctival rim pallor (see Fig. 10.1).
• No single physical finding convincingly excludes the diagnosis of anemia.
I. Introduction
Anemia refers to an abnormally low number of circulating red cells, caused by blood loss, hemolysis,
or underproduction of cells by the bone marrow. In patients with acute blood loss, the abnormal
vital signs of hypovolemia are the most prominent physical findings (see Chapter 17), but in
chronic anemia (the subject of this chapter) physical findings reflect instead changes in color of
the skin and conjunctiva.
II. The Findings
Chronic anemia causes the skin and conjunctiva to appear abnormally pale because of reduced
amounts of red-colored oxyhemoglobin that circulate in the dermal and subconjunctival capillaries and venules.1 Nonetheless, pallor does not always indicate anemia, because skin color
also depends on the diameter of these minute vessels, the amount of circulating deoxyhemoglobin, and the patient’s natural skin pigments.1 Vasoconstriction from cold exposure or sympathetic stimulation also may cause pallor, and the pallor of anemia may be obscured by the
red color of vasodilation (inflammation or permanent vascular injury from ischemia, cold, or
radiation), the blue color of cyanosis (see Chapter 9), or the brown pigments of dark-skinned
persons. eoretically, examination of the conjunctiva, nailbeds, and palms avoids the effects of
the patient’s natural skin pigments.
Most clinicians assess for pallor subjectively, by comparing the patient’s skin color with
their own color or their recollection of normal skin color. One definition of pallor, however,
is more objective: conjunctival rim pallor is present if examination of the lower lid’s conjunctiva reveals the color of the anterior rim to have the same pale fleshy color of the deeper
posterior aspect of the palpebral conjunctiva (see Fig. 10.1).2 In persons without anemia, the
normal bright red color of the anterior rim contrasts markedly with the fleshy color of the
posterior portion.
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