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Chapter 18. Anemia
387
• The Mentzer index may help hint towards an undiagnosed
thalassemia when the MCV is very low.
• Patients diagnosed with pernicious anemia should be
referred to a gastroenterologist for further evaluation and
endoscopy given the higher risk of gastric cancer in these
patients.
• All patients with sickle cell anemia or who have had a
splenectomy should receive appropriate pneumococcal
vaccinations to protect against encapsulated organisms, as
these patients are particularly susceptible to severe
infection.
• All patients with unexplained normocytic anemia should
undergo evaluation for hemolytic anemia.
References
1. World Health Organization. Haemoglobin concentrations for
the diagnosis of anaemia and assessment of severity. World
Health Organization; 2011.
2. Adamson JW, Longo DL.Anemia and polycythemia. In: Jameson
JL, etal., editors. Harrison’s principles of internal medicine, vol.
20e. New York: McGraw Hill; 2018. https://accessmedicine-
mhmedical- com.elibrary.einsteinmed.edu/content.aspx?bookid
=2129§ionid=192014145.
3. Powell DJ, Achebe MO.Anemia for the primary care physician.
Prim Care. 2016;43(4):527–42.
4. Warner MJ, Kamran MT. Iron deficiency anemia. StatPearls;
2021.
5. Adamson JW.Iron deficiency and other hypoproliferative anemias. In: Jameson JL, etal., editors. Harrison’s principles of internal medicine, vol. 20e. New York: McGraw Hill; 2018. https://
accessmedicine- mhmedical- com.elibrary.einsteinmed.edu/content.aspx?bookid=2129§ionid=192017034.
6. Means RJ, Brodsky RA. Diagnostic approach to anemia in
adults. UpToDate. 2021. https://www.uptodate.com/contents/
diagnostic- approach- to- anemia- in- adults?search=normocyti
c+anemia§ionRank=1&usage_type=default&anchor=H1146
51562&source=machineLearning&selectedTitle=1~95&disp
lay_rank=1#H114651562.
388
B. Cohen
7. Camaschella C, Weiss G. Anemia of chronic disease/anemia of
inflammation. UpToDate. 2022. https://www.uptodate.com/con-
tents/anemia- of- chronic- disease- anemia- of- inflammation?searc
h=anemia+of+chronic+disease&source=search_result&selected
Title=1~150&usage_type=default&display_rank=1#H15632436.
8. Weiss G, Goodnough LT.Anemia of chronic disease. N Engl J
Med. 2005;352(10):1011–23.
9. Hoffbrand AV. Megaloblastic anemias. In: Jameson JL,
et al., editors. Harrison’s principles of internal medicine, vol.
20e. New York: McGraw Hill; 2018. https://accessmedicine-
mhmedical- com.elibrary.einsteinmed.edu/content.aspx?bookid
=2129§ionid=192017242.
10. Stabler SP. Vitamin B12 deficiency. N Engl J Med.
2013;368(2):149–60.
11. Luzzatto L.Hemolytic anemias. In: Jameson JL, et al., editors.
Harrison’s principles of internal medicine, vol. 20e. NewYork:
McGraw Hill; 2018. https://accessmedicine- mhmedical- com.
elibrary.einsteinmed.edu/content.aspx?bookid=2129§io
nid=192017418.
12. Centers for Disease Control and Prevention. Data & statistics on sickle cell disease. Centers for Disease Control and
Prevention. 2020. https://www.cdc.gov/ncbddd/sicklecell/data.
html#:~:text=In%20the%20United%20States&text=It%20
is%20estimated%20that%3A,every%2016%2C300%20
Hispanic%2DAmerican%20births.
13. Benz J, Edward J. Disorders of hemoglobin. In: Jameson JL,
et al., editors. Harrison’s principles of internal medicine, vol.
20e. New York: McGraw Hill; 2018. https://accessmedicine-
mhmedical- com.elibrary.einsteinmed.edu/content.aspx?bookid
=2129§ionid=192017118.
14. Sundd P, Gladwin MT, Novelli EM. Pathophysiology of sickle
cell disease. Ann Rev Pathol. 2019;14:263–92.
15. National Heart, Lung, and Blood Institute. Evidence-based management of sickle cell disease–expert panel report, 2014: guide to
recommendations. 2014. www.nhlbi.nih.gov.
16. Li CK. New trend in the epidemiology of thalassaemia. Best
Pract Res Clin Obstet Gynaecol. 2017;39:16–26.
1 7. Zamora EA, Schaefer CA.Hereditary spherocytosis. StatPearls;
2021.
18. Bolton-Maggs PHB, et al. Guidelines for the diagnosis and management of hereditary spherocytosis. Br J Haematol. 2004;126(4):455–74. https://doi.
org/10.1111/j.1365- 2141.2004.05052.x.
Chapter 18. Anemia
19. Richardson SR, O’Malley GF.Glucose 6 phosphate dehydrogenase deficiency. In: StatPearls. 2021.
20. Glader, Bertil. Diagnosis and management of Glucose6- phosphate dehydrogenase (G6PD) deficiency. UpToDate.
https://www.uptodate.com/contents/diagnosis- and- managementof- glucose- 6- phosphate- dehydrogenase- g6pd- deficiency?sea
rch=g6pd&source=search_result&selectedTitle=1~150&usa
ge_type=default&display_rank=1#H151883311.
21. NORD.Warm autoimmune hemolytic anemia. NORD (National
Organization for Rare Disorders); 2020. https://rarediseases.org/
rare- diseases/warm- autoimmune- hemolytic- anemia/.
22. Gabbard AP, Booth GS. Cold agglutinin disease. Clin Hematol
Int. 2020;2(3):95.
389
Chapter 19
Edema
ValerieJorgeCabrera
Introduction
Edema is defined as palpable swelling caused by accumulation of fluid in the interstitial space. Edema can be a localized
phenomenon, or when generalized throughout the body, it is
called anasarca. Different clinical conditions, including localized conditions (e.g., venous and lymphatic disease) and systemic conditions, such as cardiac, liver, and renal disease, can
cause edema. The etiology of edema can usually be determined by a careful history and a physical examination.
Routine labs can help rule out common conditions that cause
edema.
The Starling forces are involved in maintaining the balance between the intravascular space and the interstitial
space. Changes to this homeostasis can result in edema [1].
These physiologic forces include the gradient between the
intravascular and extravascular hydrostatic pressures and the
differences in oncotic pressure between the interstitial space
and plasma. The hydrostatic pressure within the capillaries
tends to drive fluid out of the capillaries, whereas the oncotic
V. J. Cabrera (*)
Northeast Ohio Nephrology Associates, Akron, OH, USA
e-mail: vjcabrera@northeastohionephrology.com
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2022
E. Sydney et al. (eds.), Handbook of Outpatient Medicine,
https://doi.org/10.1007/978-3-031-15353-2_19
391
392
V. J. Cabrera
pressure exerted within the capillaries tends to draw fluid
back. If the hydrostatic capillary pressure is increased or the
capillary oncotic pressure is diminished, a condition favoring
edema results. Conditions causing increased capillary permeability, those affecting the electrolyte balance of the body
with sodium and chloride retention and decreased lymphatic
drainage, can also lead to edema.
Differential Diagnosis
Peripheral edema is a nonspecific finding common to a host
of diseases [2, 3]. The acute edema of a single limb (usually
defined as occurring for less than 72h) should raise suspicion
for deep vein thrombosis (DVT), cellulitis, or a ruptured popliteal cyst (Fig.19.1). In those patients with history of recent
trauma or surgery, compartment syndrome should be considered. Complex regional pain syndrome, an entity that can
occur weeks after limb trauma, manifests with pain, edema,
and changes in skin color and temperature.
Edema
Systemic causes
• Cardiac disease
• Liver disease
• Kidney disease
• Thyroid disease
• Malabsorption/
protein malnutrition
• Allergic reactions
• Others: medications,
pregnancy/
premenstrual,
idiopathic
Localized causes
• Deep vein
thrombosis (DVT)
• Cellulitis
• Chronic venous
insufficiency
• Lymphedema
• Compartment
syndrome
• Ruptured popliteal
cyst
F . Systemic and localized causes of edema
Chapter 19. Edema
There are two types of lower extremity edema, venous
edema and lymphedema. Chronic venous insufficiency is
associated with other chronic skin changes such as hyperpigmentation and prominent veins. Some patients with underlying unilateral chronic venous disease might have asymmetric
edema. Lymphedema is usually non-pitting, and the skin has
a verrucous aspect. Lymphedema can be the result of lymph
node dissection. Lastly, obstruction by a tumor or lymphadenopathy can lead to unilateral edema. Also consider in your
differential lipedema, a condition in which there is deposition
of excess fat in the lower extremities and can be mistaken for
edema.
Edema related to systemic conditions is often subacute or
chronic and bilateral, affects the lower extremities, and on
occasion becomes generalized (Fig. 19.1). Certain clues can
orient to the etiology of edema. The presence of jugular
venous distention, positive hepatojugular reflux, an S3 gallop,
rales, and ascites are features of cardiac disease (e.g., congestive heart failure and pulmonary hypertension). Jaundice,
ascites, and asterixis are seen with liver disease, and a frothy
urine could be a manifestation of underlying kidney disease.
Generalized edema can be seen in a diet deficient in protein
or in patients with malabsorption. Thyroid disease can result
in generalized myxedema as seen in hypothyroidism or pretibial myxedema as seen in hyperthyroidism. Idiopathic
edema is a diagnosis of exclusion and may occur in a cyclical
fashion.
393
Key History andPhysical Exam
The history should include details about the onset of edema
(acute or chronic), if unilateral or bilateral, if it involves the
upper extremities or lower extremities or is generalized, and
if it is positional (Fig.19.2) [4]. Associated symptoms should
also be assessed, with emphasis on local skin changes and
presence or absence of pain. The clinician should also inquire
about the presence of other systemic symptoms such as fever,
394
V. J. Cabrera
Edema: Key H&P
Key history
• Onset: acute ( <72 hours)
vs chronic ( ≥72 hours)
• Symmetry: unilateral vs
bilateral
• Location: upper/lopwer
extermities vs generalized
• Medication history
• Associated symptoms:
skin changes, pain, fever,
chills, dyspnea, orthopnea,
paroxysmal nocturnal
dyspnea
• Distribution: unilateral,
bilateral vs generalized
(anasarca)
• Pitting
• Tenderness
• Skin changes: temperature
(warm, cold), color
(discoloration, erythema,
cyanosis)
• Presence of ulcers or
palpable vein cords
• Associated signs: jugular
venous distention,
crackles, frothy urine,
oliguria, jaundice,
asterixis, ascites
Key physical
F . Key history and physical in the evaluation of edema
chills, or weight loss as well as those suggestive of hypervolemia. The medication list, including over-the-counter remedies, should be thoroughly reviewed given that commonly
used medications can be associated with edema (Table19.1).
Physical examination should focus on evaluating the distribution and severity of edema (Fig.19.2) [4]. The physician
should evaluate for the presence or absence of pitting by
pressing with his or her finger continuously for 5 s. Pitting
refers to the movement of fluid in the interstitial space when
pressure is applied. The categorization of edema is based on
a scale of 1–4+, and it is useful to describe the distribution of
the pitting (e.g., pedal or pretibial). Edema can be found in
the lower extremities in ambulatory patients and in dependent areas in those who are confined to a bed (e.g., sacrum).
Non-pitting edema is suggestive of lymphedema or thyroid
disease (pretibial myxedema).The Kaposi-Stemmer sign
refers to the inability to form a fold on the skin at the base of
the second toe and is suggestive of lymphedema [2, 8].
Chapter 19. Edema
T . Commonly used medications associated with edema [1,
5–7]
Category Examples
Antihypertensives Amlodipine, minoxidil
Corticosteroids Prednisone, fludrocortisone
Nonsteroidal anti-inflammatory
drugs (NSAIDs)
Antidiabetic drugs Pioglitazone
Others Estrogen/progesterone,
Ibuprofen
testosterone
395
The skin should be thoroughly evaluated describing its
color, temperature, and presence of ulcers or palpable vein
cords. In patients with deep vein thrombosis, a larger calf
circumference is a useful finding. Homan’s sign, which consists of calf pain elicited by foot dorsiflexion, is not reliable.
The systemic evaluation should include the evaluation for
jugular venous distention, hepatojugular reflux, rales on lung
examination, sacral edema, and ascites.
Decision-Making/Treatment
Edema is a common manifestation of many disease states. In
those patients with findings of acute-onset, painful unilateral
edema with risks for hypercoagulability concerning for DVT
(Fig.19.3), a -dimer and venous ultrasound can be part of
the initial evaluation depending on the level of clinical suspicion [9]. In patients presenting with acute bilateral leg edema,
the possibility of DVT must still be considered. The presence
of bilateral DVT can be associated with malignancy. If the
clinical probability of DVT is high, proceed with further testing. Tests evaluating serum creatinine, liver function, and
serum albumin level along with urinalysis for proteinuria,
presence of white blood cells, red blood cells, and casts are
useful initial labs in patients with bilateral or generalized
edema (Fig.19.4). Thyroid-stimulating hormone can also be
included if there is suspicion for thyroid disease. Duplex
396
V. J. Cabrera
Chronic ≥72 hours
History of
malignancy,
Skin thickenning,
positive Stemmer
trauma, or surgery
lymphedema
sign consider
Proceed with
or thrombosis
pelvic imaging to
evaluate for tumor
Diagnose clinically.
venous
insufficiency
Venous ulcers,
palpable venous
cords suggesting
Unilateral edema
for DVT
Acute <72 hours
Clinical suspicion
Check venous
yes
No: consider other
etiologies (cellulitis,
ruptured popliteal cyst)
compartment syndrome,
ultrasound
Low
check venous
Intermediate/high
Check D-dimer
ultrasound
If positive check
venous ultrasound
etiologies
If negative:
consider other
If negative for
DVT: consider
other etiologies
DVT: treat
If positive for
etiologies
consider other
Negative for DVT:
treat
Positive for DVT:
F . Clinical approach for the patient presenting with unilateral edema
Diagnosis
inical
is cl
lymphedema.
eat
tr
insufficiency:
397
Chapter 19. Edema
der
consi
ve
i
gat
ne
If
insufficiency
Ye s: discontinue
Check venous US
ous
for ven
sitive
Po
No: consider venous
No
medications
Any potential culprit
Edema
Bilateral or generalized
systemic disease
H&P suggestive of
estricition
r
FTs,
L
umin
ry,
Ye s
Evaluate for heart
failure, liver cirrhosis,
st
chemi
k
renal or thyroid disease
Chec
um alb
A, ser
U
TSH, echocardiogram
suspicion
based on clinical
Diagnose/Treat
sease
lying di
under
Emphasize salt
iate
retics if
appropr
se diu
U
F . Clinical approach for the patient presenting with bilateral or generalized edema