Background

Lipomas are the most common soft-tissue tumor. These slow-growing,

benign fatty tumors form soft, lobulated masses enclosed by a thin,
fibrous capsule. Although it has been hypothesized that lipomas may
rarely undergo sarcomatous change, this event has never been
convincingly documented. It is more probable that lipomas are at the
benign end of the spectrum of tumors, which, at the malignant end,
include liposarcomas (see Pathophysiology).
Because more than half of lipomas encountered by clinicians are
subcutaneous in location, most of this article will be devoted to that
subgroup. Additional information about other locations (eg,
intramuscular, retroperitoneal, gastrointestinal [GI]) will be included as
appropriate.
Pathophysiology
Lipomas are common benign mesenchymal tumors. They may develop
in virtually all organs throughout the body. The anatomy depends on the
tumor site. Subcutaneous lipomas are usually not fixed to the underlying
fascia. The fibrous capsule must be removed to prevent recurrence.
In the GI tract, lipomas present as submucosal fatty tumors. The most
common locations include the esophagus, stomach, and small intestine.
Symptoms occur from luminal obstruction or bleeding.
Duodenal lipomas are mostly small but may become pedunculated with
obstruction of the lumen. They may cause pain, obstructive jaundice, or
intussusception in younger patients.[1] Mucosal erosion over the lipoma
may lead to severe bleeding (see the image below). Small intestinal
lipomas occur mainly in elderly patients. They tend to be pedunculated
submucosal lesions. They are more common in the ileum than in the
duodenum or jejunum. As with duodenal lipomas, severe hemorrhage
or intussusception may occur.
Inline figure
Upper gastrointestinal series shows duodenal lipoma with central ulceration where
the overlying mucosa has thinned, ulcerated, and bled.
/Inline figure
Colonic lipomas are usually discovered on endoscopy. Gentle palpation
with a biopsy forceps reveals the soft nature of the submucosal mass. A
biopsy specimen of the mucosa may reveal underlying fat, the so-called
naked fat sign. As with lipomas in other locations, colonic lipomas may
cause pain with obstruction or intussusception.
As noted above, a fatty protrusion of preperitoneal fat termed a "lipoma
of the spermatic cord" is a common finding on groin exploration for
hernia repair.
Numerous case reports document the presence of lipomas in other, rare
locations, with these tumors having been found virtually everywhere in
the body.[2, 3, 4, 5, 6] Lipomatous involvement of endocrine organs, including
the thyroid, adrenal glands, pancreas, and parathyroid glands, has been
described. Maxillofacial lipomas, including intralingual, parotid,
orbitonasal, maxillary sinusoidal, and parapharyngeal space masses,
have also been documented.
In rare instances, intraosseous and intra-articular involvement occurs.
Involvement of the structural components of the mediastinum, including
the airways and pleura, has also been reported. Gynecologic lipomas
may occur in the uterus, ovaries, and broad ligament. Critical organ
involvement of the heart (causing ventricular tachycardia), superior
vena cava, brain, and spinal cord may pose a significant clinical
challenge.[7, 8]
Mixed histologies, such as angiolipomas and fibrolipomas, are often
encountered and are usually benign. Differentiation from liposarcoma
may be difficult.
Other fatty tumors include lipoblastomas, hibernomas, atypical
lipomatous tumors, and liposarcomas. Lipoblastomas occur almost
exclusively in infants and children. They have a benign clinical course
and a low recurrence rate after surgical excision. Hibernomas, also rare,
derive their name from the morphologic resemblance to the brown fat of
hibernating animals. They presumably arise from fat that may occur in
the back, hips, or neck in adults and infants. Atypical lipomatous tumors
are generally considered to be low-grade sarcomas, with a strong
propensity to recurrence but little metastatic potential. Liposarcomas are
true mesenchymal malignancies.
Etiology
Speculation exists regarding a potential link between trauma and
subsequent lipoma formation.[9] One theory suggests that trauma-related
fat herniation through tissue planes creates so-called pseudolipomas. It
has also been suggested that trauma-induced cytokine release triggers
pre-adipocyte differentiation and maturation. To date, no definitive link
between trauma and lipoma formation has been prospectively
demonstrated.
While the exact etiology of lipomas remains uncertain, an association
with gene rearrangements of chromosome 12 has been established in
cases of solitary lipomas, as has an abnormality in the HMGA2-LPP
fusion gene.[10]
Epidemiology
Lipomas occur in 1% of the population. Most of these are small
subcutaneous tumors that are removed for cosmetic reasons. These
subcutaneous lipomas will be considered separately from lipomas in
other locations in the discussion below. In the intestine, lipomas
constitute 16% of benign, small neoplasms; this percentage is lower
than that of leiomyomas (18%) and higher than that of adenomas
(14%).
Prognosis
The outcome and prognosis are excellent for benign lipomas.
Recurrence is uncommon but may develop if the excision was
incomplete.
Pang et al compared outcomes in 238 patients who underwent total or
near-total (T/NT) resection for dorsal, transitional, or chaotic spinal cord
lipomas (with 16-year follow-up), along with complete reconstruction of
the neural placode, with results from 116 patients who underwent partial
resection for spinal cord lipomas (with 11-year follow-up).[11, 12]
Although in the T/NT and partial resection groups the rate of immediate
symptom stabilization or improvement was similar (more than 95%), the
combined cerebrospinal fluid leakage and wound complication rate was
only 2.5% for T/NT resections, compared with 6.9% for partial
resections. Moreover, the overall progression-free survival probability
(Kaplan-Meier analysis) was 82.8% for T/NT resection patients at 16
years postoperative, compared with 34.6% for partial resection patients
at 10.5 years post operation. Evidence indicated that the superior
results in the T/NT resection patients were associated with the fact that
lower cord-sac ratios were achieved in these patients than in the partial-
resection group.[11, 12]
Background
Anatomy of the muscles of the hand
Normal positioning and movement of the digits depends on the
functional integrity of extrinsic and intrinsic muscles. The extrinsic
muscles originate in the forearm, and the intrinsic muscles originate
distal to the wrist. The intrinsic muscles are traditionally divided into 5
groups: thenar, hypothenar, palmar interossei,[1] dorsal interossei, and
lumbricals.
The 4 thenar muscles are the abductor pollicis brevis, flexor pollicis
brevis, opponens pollicis, and adductor pollicis. The abductor pollicis
brevis abducts the thumb away from the palm. The flexor pollicis brevis
flexes the thumb metacarpophalangeal (MCP) joint. The opponens
pollicis abducts, flexes, and pronates the first metacarpal. With these
muscles, the thumb is brought from lateral to medial position across the
palm in opposition to the 4 ulnar digits. The adductor pollicis adducts
the thumb toward the palm.
The hypothenar muscles are the abductor digiti minimi, the flexor digiti
minimi brevis, and the opponens digiti minimi. The abductor digiti minimi
abducts the little finger away from the fourth finger. The flexor digiti
minimi brevis flexes the little finger at the MCP joint. The opponens digiti
minimi abducts, flexes, and supinates the fifth metacarpal. With these
muscles, the little finger is brought into opposition to the thumb.
Most anatomists describe 3 palmar interossei and 4 dorsal interossei
muscles. The dorsal interosseous muscles flex the MCP joints and
extend the interphalangeal (IP) joints. The dorsal interossei also abduct
the 4 ulnar digits from one another; the volar interosseous muscles
adduct the 4 ulnar digits together toward the third finger. There are 4
lumbrical muscles. They function as a connection between the flexor
digitorum profundus (FDP) and the extensor mechanism. Their main
function is to facilitate extension of the IP joints. The lumbricals can
extend the IP joints in any position of the MCP joints.
An image depicting the Froment sign can be seen below.
Inline figure
Image in a patient with ulnar neuropathy demonstrates the Froment sign during
pinching. Loss of the ulnar-innervated adductor pollicis results in reliance on the
flexor pollicis longus and exaggerated interphalangeal (IP) joint flexion. Loss of the
metacarpophalangeal (MCP) joint flexor leads to MCP hyperextension over time.
/Inline figure
Anatomy of the nerves of the hand
The ulnar nerve innervates most of the intrinsic muscles in the hand: all
the interossei, the 3 hypothenar muscles, the adductor pollicis, the deep
head of flexor pollicis brevis, and the 2 ulnar lumbricals. All remaining
intrinsic musclesthat is, the 2 radial lumbricals, the abductor pollicis
brevis, the opponens pollicis, and the superficial head of the flexor
pollicis brevisare thus innervated by the median nerve.[2]
Inline table
Table. Muscles of the Forearm (Open Table in a new window)
Muscles of anterior fascial compartment
Name of Muscle Nerve Supply
Pronator teres Median nerve
Flexor carpi radialis Median nerve
Palmaris longus Median nerve
Flexor carpi ulnaris Ulnar nerve
Flexor digitorum superficialis Median nerve
Anterior interosseous

Flexor pollicis longus

branch of median nerve

Flexor digitorum profundus Ulnar and median nerves

Median nerve supplies index and middle fingers in 75% of patients. Ulnar nerve supplies middle, ring, and little
fingers in 75% of patients (therefore, the middle finger has dual innervation in 75% of patients)
Pronator quadratus Anterior interosseous branch of median nerve
Muscles of lateral fascial compartment
Brachioradialis Radial nerve
Extensor carpi radialis longus Radial nerve
Muscles of posterior fascial compartment
Extensor carpi radialis brevis Deep branch of radial nerve
Extensor digitorum Deep branch of radial Nerve
Extensor digiti minimi Deep branch of radial Nerve
Extensor carpi ulnaris Deep branch of radial Nerve
Anconeus Radial nerve
Supinator Deep branch of radial Nerve
Abductor pollicis longus Deep branch of radial Nerve
Extensor pollicis brevis Deep branch of radial Nerve
Extensor pollicis longus Deep branch of radial Nerve
Extensor indicis Deep branch of radial Nerve
Muscles of the hand lumbricals
Two radial lumbricals Median nerve
Two ulnar lumbricals Ulnar nerve
Interossei Ulnar nerve
Abductor pollicis brevis Median nerve
Flexor pollicis brevis Median nerve
Opponens pollicis Median nerve
Adductor pollicis Ulnar nerve
Abductor digiti minimi Ulnar nerve
Flexor digiti minimi Ulnar nerve
Opponens digiti minimi Ulnar nerve
/Inline table
Median nerve injury
Median nerve injuries are commonly referred to as high (ie, at or above
the elbow) or low (ie, distal to mid forearm). While a high injury affects
both intrinsic and intrinsic motor function, a low injury affects only
intrinsic motor function.
A high median nerve division paralyzes the extrinsic muscles: pronator
teres, flexor carpi radialis, palmaris longus, flexor digitorum superficialis
(FDS), flexor pollicis longus, radial half of the FDP, and pronator
quadratus. As a result, the forearm tends to rest in supination with the
wrist in ulnar deviation. The median-innervated intrinsic muscles are
also paralyzed. The lumbricals to the index and long fingers are
paralyzed. Therefore, only weak flexion of the MCP joints is possible
with the ulnar-innervated interosseous muscles.[3, 4, 5]
The IP joints of the thumb and the index and middle fingers cannot flex
as a result of paralysis of the FDP and FDS motor units. If the ulnar
nerve supplies the FDP to the ring finger, the ring finger IP joints can
then flex. The ulnar nerve supplies the FDP motor units to the ring and
little fingers, so the fourth and fifth fingers can flex. The abductor pollicis
brevis, and opponens pollicis muscles are paralyzed. The thumb rests
in the plane of the palm and cannot be positioned for a pulp-to-pulp
pinch between the thumb and fingers. The thumb IP joint is extended
due to paralysis of the flexor pollicis longus.
Median nerve injury at the wrist preserves extrinsic muscle function.
The pronator teres, FDS, FDP, and flexor pollicis longus motor units are
intact. The first 2 lumbricals, the abductor pollicis brevis, and the
opponens pollicis are paralyzed. When the patient slowly makes a fist,
the index and middle fingers clearly lag behind the fourth and fifth
fingers because of a lack of initiation of flexion at the MCP joints by the
lumbricals. The thumb rests in the plane of the palm and cannot oppose
the fingers (see image below). The patient can flex the thumb terminal
phalanx because the flexor pollicis longus is not paralyzed.
Inline figure

The intrinsic muscles innervated by the median nerve (abductor pollicis brevis and
opponens pollicis) are checked by resisting palmar abduction of the thumb.
/Inline figure
Ulnar nerve injury
Ulnar nerve lacerations are commonly referred to as high or low to
reflect whether the injury affects extrinsic and intrinsic muscles.[4, 6, 7, 8]

High ulnar nerve injury results in paralysis of the flexor carpi ulnaris and
the ulnar half of the flexor FDP muscles, generally FDP III-V. The distal
phalanges of the fourth and fifth fingers cannot flex. Because the FDP
motor units have a common origin, some weak flexion of the fourth and
fifth fingers may be possible, even if the ulnar half is supplied by the
ulnar nerve. An attempt to flex the wrist results in radial deviation due to
paralysis of the flexor carpi ulnaris.
All 7 interosseous muscles, the third and fourth lumbrical muscles, the
adductor pollicis muscle, generally also one head of FPB, and all 3
hypothenar muscles (flexor digiti minimi brevis, abductor digiti minimi,
and opponens digiti minimi) are paralyzed. The patient cannot adduct or
abduct the fingers. If the examiner places a piece of paper between the
patient's fingers he or she cannot hold it when the examiner pulls the
paper away.
The MCP joints are hyperextended, and the IP joints are flexed. These
changes are more obvious at the ring and little fingers, because the first
and second lumbrical muscles are not paralyzed. This condition is
called a claw-hand deformity . The thumb can weakly adduct through
the extensor pollicis longus. The patient can pinch and hold a paper
between the thumb and index finger by strongly flexing the IP joint with
the flexor pollicis longus. The combination of strong IP and weak MCP
flexion called the Froment sign.

Ulnar nerve injury at the wrist spares the flexor carpi ulnaris and the
medial half of the FDP muscles. The patient can flex the wrist and all
the distal IP (DIP) joints. However, all intrinsic muscles innervated by
the ulnar nerve are paralyzed, and both the clawhand deformity and the
Froment sign are prominent (see image below).
Inline figure

Image in a patient with ulnar neuropathy demonstrates the Froment sign during
pinching. Loss of the ulnar-innervated adductor pollicis results in reliance on the
flexor pollicis longus and exaggerated interphalangeal (IP) joint flexion. Loss of the
metacarpophalangeal (MCP) joint flexor leads to MCP hyperextension over time.
/Inline figure
Epidemiology
Open or closed trauma is the most frequent cause of intrinsic hand
deformities. Although sensory loss contributes to the overall impairment,
it does not contribute to the deformity. Ulnar nerve compression can
occur at the elbow (the cubital tunnel) or at the wrist (in the Guyon
canal). Median nerve compression associated with intrinsic loss can
occur with pronator syndrome or carpal tunnel syndrome. Anterior
interosseous nerve compression does not result in intrinsic loss
because this nerve innervates only the extrinsic motor units.
One third of all patients with rheumatoid disease (RA) develop some
degree of intrinsic contracture during the course of their disease, Hand
deformities tend to progress in RA.[9] Peripheral nerve palsy, most
commonly afflicting the ulnar nerve at the elbow, occurs in 20-25% of
patients with leprosy. Claw hand due to ulnar nerve paresis is therefore
the most common presentation in this group of patients.
Etiology
Intrinsic muscle contracture can be caused by trauma,[10] inflammation,
tumor, central nervous system disease, joint destruction, leprosy
(Hansen disease), compartment syndrome, or rheumatoid disease.
Pathophysiology
Fixed contractures of the intrinsic muscles may severely impair the
function of the hand. A mild contracture may inhibit certain hand
functions without any gross deformity. The patient may complain of a
weak grip when using, for example, a screwdriver or a hammer. Severe
contractures cause MCP joint flexion and IP joint extension, resulting in
an intrinsic-plus deformity. The patient experiences difficulty in grasping,
pinching, and abducting the fingers. In combination with sensory loss,
the hand is severely disabled.
Individual involvement of intrinsic muscles results in characteristic
deformities. Lumbrical contracture causes finger extension while the
patient is trying to flex the finger. The origin of the lumbrical is pulled
proximally with extrinsic flexion, and the IP joints are extended.
Contraction of the abductor digiti minimi presents as small-finger
abduction and causes MCP joint flexion and IP joint extension. Thenar
intrinsic muscle contracture can cause thumb adduction, MCP joint
flexion, and IP joint hyperextension. The patient loses effective pinch,
large-volume grip, and hand dexterity.
Presentation
History
The patient may present with a history of trauma, inflammation, tumor,
leprosy disease, compartment syndrome, or rheumatoid disease.
Physical examination
The first dorsal interosseous muscle is tested by having the patient
place the ulnar side of the hand on the examination table. The radial
side of the index finger is facing up. The patient is asked to raise the
index finger toward the ceiling. The examiner applies resistance and
observes the patient's strength. Muscle strength testing is likely to be
more sensitive if the right and left sides are tested simultaneously rather
than one after the other.[11]
The second, third, and fourth dorsal interosseous muscles are tested by
having the patient place the palm on the examination table. The patient
spreads all of the fingers against resistance (see image below). The
volar interosseous muscles are examined by placing a piece of paper
between the digits and by having the patient hold his or her fingers
tightly together as the examiner tries to withdraw the paper. The test is
repeated between each of the adjacent fingers.
Inline figure

The ulnar-innervated intrinsic muscles can be checked by resisting abduction of the

index (first dorsal interosseous muscle) and small fingers (abductor digiti quinti
muscle).
/Inline figure
Adhesions and contractures of the intrinsic and extrinsic extensor
muscles can limit flexion of the digits. The intrinsic tightness test can be
used to differentiate extrinsic pathology from intrinsic pathology. During
a test for intrinsic tightness, the examiner usually attempts to fully flex
the proximal interphalangeal (PIP) joint of an examined finger while the
MCP joint is kept in full extension and flexion, respectively. In the case
of intrinsic tightness, (passive) flexion of the IP joint is more restricted
when the MCP joint is in extension than when the MCP joint is in flexion
(see image below).
Inline figure
The gloved examiner checks for intrinsic tightness. With the metacarpophalangeal
(MCP) joint hyperextended, the proximal interphalangeal (PIP) joint is passively
flexed. The intrinsic muscles are volar to the axis of rotation of the MCP joint and
dorsal to the axis of the PIP joint. MCP joint hyperextension tightens the intrinsics.
Results of this test are compared with those in the contralateral, normal hand. Note
intrinsic atrophy in the first dorsal web space.
/Inline figure
If the intrinsic muscles are scarred, passive MCP joint extension
increases PIP joint extension and makes passive PIP joint flexion more
difficult (see images below).
Inline figure
Image in a patient with a partial ulnar nerve paralysis is asked to extend the digits.
Hyperextension of the metacarpophalangeal (MCP) joints of the ring and small
fingers occurs with the loss of intrinsic ulnar-innervated MCP flexors. The index and
middle fingers have median innervated intrinsics (lumbricals) that allow the extrinsics
to extend the interphalangeal (IP) joints.
/Inline figure Inline figure

When the examiner prevents metacarpophalangeal hyperextension of the ring and

fifth fingers, the patient can completely extend the interphalangeal joints with the
extrinsic tendons.
/Inline figure
The abductor pollicis brevis is tested as the patient pushes against
resistance while the thumb is in the abducted position. The opponens
pollicis is similarly tested with the thumb more circumducted. The
adductor pollicis is evaluated as the patient pinches a piece of paper
between the thumb and index finger while the examiner pulls on the
paper. The flexor pollicis brevis is assessed with the thumb MCP joint in
flexion and with resistance applied volarly.
The abductor digiti minimi is tested by having the patient place the back
of the hand on the examining table while the little finger is abducted
against resistance. The flexor digiti quinti is examined by flexing the
MCP joint while the finger is adducted. The IP joints must be kept in
extension. To test the opponens digiti minimi, the patient performs a
pulp-to-pulp pinch by moving the little finger to the thumb.
Intrinsic tightness can result in a swan-neck deformity, which is
characterized by PIP joint hyperextension and DIP joint flexion. The
tight intrinsic muscles pull the PIP joints into extension, which allows
passive DIP joint flexion. Over time, the PIP joint volar plate stretches
as the extensor mechanism pulls the proximal phalanx into
hyperextension. As PIP joint hyperextension increases, DIP joint flexion
increases.
Intrinsic contracture disturbs fine hand-muscle balance. The fingers
become stiff, function deteriorates, and the hand becomes disabled.
Boutonniere deformity
The boutonniere deformity involves PIP joint flexion and hyperextension
of DIP and MP joints. Attenuation of the central slip with separation from
the transverse retinacular ligaments cause migration of the lateral
bands volar to the PIP joint rotational axis. Thus the lateral bands act as
flexors of the PIP joint. As a result, the FDS meets less resistance and
flexes the PIP joint. Contraction of the lateral bands and oblique
retinacular ligaments prevents extension of the PIP joint. The lateral
bands extend the DIP joint. The MCP joint hyperextends as the sagittal
band applies traction on the extensor tendon.[12, 13, 14]
Physical examination involves evaluation of the range of motion, both
active and passive, of both DIP and PIP joints. The examiner tries to
passively flex the DIP joint while passively extending the PIP joint. In
the presence of boutonniere deformity, both lateral bands and oblique
retinacular ligaments are contracted and the DIP joint will not flex. The
examiner flexes the PIP joint, and the DIP joint can then actively and
passively flex because both the lateral bands and the oblique
retinacular ligaments are now relaxed.
Indications
Intrinsic and extrinsic tightness may coexist in the same patient. Intrinsic
contracture may not be clinically apparent until associated extrinsic
changes are corrected.
In cases of extrinsic tightness, PIP joint flexion increases when the MCP
joint is extended and decreases when the MCP joint is flexed.