Sidelights
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| Clinical Sidelights to | |
Curvatures
At birth the entire vertebral column has a gentle curve that is concave on its ventral surface
(i.e., a kyphosis). This kyphosis persists in the thoracic region and in the sacrum. A lordosis
begins to form in the in the neck when the child learns to lift up its head, and becomes
accentuated as sitting develops. This lordosis is caused by the cervical intervertebral discs
becoming taller anteriorly than they are posteriorly. A second lordosis begins to form in the
lumbar region when the child learns to sit; it becomes accentuated as walking develops. The
lumbar lordosis is due to the fact that both the intervertebral discs and lumbar vertebral bodies
become taller anteriorly than posteriorly.
Herniated (Slipped) Intervertebral Disc (I wish to acknowledge the very great
contribution of Dr. Michael Egnor to this section.)
Protrusion of the nucleus pulposus covered by a thin layer of stretched anulus fibrosus, or
extrusion of nuclear material through a tear in the anulus, is called a slipped or herniated disc. It
occurs most commonly in the low lumbar region. No doubt this is due to the very much greater
stresses on the discs of this region. The second most frequent site is in the neck, usually as a
consequence of some trauma. A herniated nucleus pulposus will generally present to either the
right or left of the posterior longitudinal ligament. Central herniations (i.e., those that push out in
the midline) are uncommon but do occur, more frequently in the lumbar region than in the
cervical region because the posterior longitudinal ligament is weaker in the lumbar region.
When the herniation of the nucleus pulposus is to one side of the posterior longitudinal
ligament, a common consequence is compression of a spinal nerve as it is heading toward its
intervertebral foramen. Herniations of cervical discs affect the spinal nerve that exits at the
intervertebral foramen lying at the same level as the disc. Thus, herniation of the C5/6 disc may
compress the nerve that exits through the C5/C6 intervertebral foramen, which is the C6 spinal
nerve; herniation of the C7/T1 disc may compress the nerve heading toward the C7/T1
intervertebral foramen, which is the C8 spinal nerve.
The situation is different for lumbar disc herniations. Because lumbar pedicles attach to the upper
half of their vertebral body, lumbar intervertebral foramina are set high relative to the
intervertebral disc. As a lumbar spinal nerve exits its intervertebral foramen, it is related more to
the back surface of the vertebral body than to an intervertebral disc. For example, the L5 spinal
nerve exits the L5/S1 intervertebral foramen along the posterior surface of the lower half
of the L5 vertebral body, which places the nerve above and lateral to most herniations of the
L5/S1 disc. A herniation of the L5/S1
disc is far more likely to compress the S1 spinal nerve as it passes downward toward its exit
from the next lower intervertebral foramen. The general rule is that a slipped lumbar disc leads to
a radiculopathy (spinal nerve root disease) of the next lower spinal nerve. Therefore, whether you
are in the neck or in the lumbar region, herniation of a disc is most likely to affect the nerve with
the same name and number as the lower bounding vertebra, though the reasons for this are very
different in the two parts of the body.
In the more common case of a low lumbar slipped disc, the site of nuclear protrusion or
extrusion is
inferior to the spinal cord and only spinal nerve roots are in any danger of compression.
If the herniation occurs in the neck, the spinal cord may also be subjected to pressure. A central
herniation of the L4/L5 disc, while uncommon, may compress sacral nerves roots bilaterally,
producing what is called a "cauda equina syndrome", associated with difficulty urinating, fecal
incontinence, and pain or numbness in the perineum and lower limb. This requires immediate
surgery.
The most common symptoms of a slipped lumbar disc are pain in the back (possibly due to a
tear of the anulus) and pain in the body segment to which the affected spinal nerve distributes
(so-called radicular pain). Testing the skin supplied by the affected nerve reveals diminished or
lost sensation. Because acute compression of a peripheral nerve does not cause pain along that
nerve's area of distribution, but rather causes paresthesia (tingling, pins and needles) followed by
numbness, some authors believe that the radicular pain accompanying a slipped disc is caused
either by compression of the dorsal root ganglion and/or of the dorsal root that has been irritated
by an inflammatory process. Among the evidence for the latter viewpoint is that local injection of
corticosteroids, which reduce inflamation, will sometimes eliminate the radicular pain.
The most frequently herniated lumbar discs are L4/5 and L5/S1; thus the most
commonly affected nerves are L5 and S1. For this reason it is important that you the know the
rough distributions of these nerves. The pain resulting from L5 involvement spreads from the
outer aspect of the leg across the dorsum of the foot to its inner border. The pain of S1
involvement is down the
calf and into the sole and outer border of the foot. The numbness associated with L5 compression
is most marked over the dorsum of the big toe. The numbness associated with S1 compression is
most marked on the lateral part of the sole of the foot. The greatest degree of motor weakness
associated with L5 compression is that of dorsiflexion of the big toe, and to a lesser extent of the
other toes and ankle. The weakness associated with S1 compression is predominantly one of
plantarflexion of the foot. Compression of the L4 nerve roots is
less common than of either L5 or S1. Numbness is most marked over the medial malleolus; knee
extension (and to a lesser extent ankle dorsiflexion) is weak. Pain localized to the back, without
radiating along the distribution of a spinal nerve, is probably not due to a slipped disc, but rather
to strained ligaments or muscles of the back.
The physical exam procedure for a slipped disc is called the "straight leg raise". With the
patient lying on his/her back, you lift the lower limb on the same side as the pain has been
reported. If pain along the distribution path of a spinal nerve can be elicited before you have
flexed the hip through 70°, this suggests the presence a herniated disc. Since the nerve
roots don't even get stretched until you have flexed the hip through at least 30°, if the
patient complains of radicular pain early in the movement it is a sign of something other than a
slipped disc. A positive straight-leg raise (pain arising from 30-70°) is further confirmed if
the pain gets worse when you let the leg lie flat on the table but dorsiflex the ankle. You should
also try to raise the lower limb on the side opposite to that on which the patient has reported pain.
Although this contralateral straight leg raise usually will not reproduce the radicular pain even if
there is a slipped disc, if pain does occur it is even more diagnostic of a slipped disc than is a
positive ipsilateral straight leg test. When a contralateral straight test is positive, the herniated
nucleus pulposus is probably pressing into the acute angle between the spinal nerve and the dural
sac (the so-called axilla of the spinal nerve).
Spondylolysis and Spondylolisthesis
The superior surface of the S1 vertebral body is tilted to face partly forward. As a result,
body weight pushing down on the L5 vertebra should cause it to slip downward and forward off
of S1. While this is resisted by the two longitudinal ligaments, the IV disc, and the iliolumbar
ligaments (which run from the transverse processes of L5 to the ilia), the most important factor
preventing antero-inferior slippage of L5 is the orientation of the L5/S1 zygapophyseal joints.
This is revealed by cases in which trauma to the 5th lumbar vertebrae causes both the right and
left laminae to be fractured across their "pars interarticularis" regions, i.e., the region of the
lamina between the origins of the superior and inferior articular processes. Bilateral defects in the
partes interarticulares is called spondylolysis. A common consequence of L5
spondylolysis is a gradual yielding of the intact ligamentous structures that connect L5 to the ilia
and sacrum. This permits the body of L5 (with its attached pedicles and superior articular
processes) to slide downward and forward, a condition known as spondylolisthesis.
Because the laminae and inferior articular processes do not change position, there is no
compression of the contents of the vertebral canal. The symptoms of spondylolisthesis are
generally confined to the pain of ligamentous injury and/or muscle spasm.
Spinal Injuries
First, in order to predict the neurologic consequences of penetrating wounds to the back, one
must know where the different spinal cord segments lie in relation to the vertebral column. There
is a relatively simple guide to this information--only the digit 1 need be memorized:
The top of spinal cord segment C1 lies opposite top of vertebra C1. It is obvious that the cervical cord is virtually unshortened relative to the vertebral column.
The thoracic cord is shortened slightly. The lumbar segments of the cord run from the top of T11
to the top of L1 and are thus shortened considerably. The five sacral and one coccygeal segments
of the cord span only the distance occupied by the body of L1.
An injury to the spinal cord not only leads to paralysis of the muscles supplied by the
damaged region, it also leads to loss of cerebral control over muscles innervated by any intact
cord segments below the injury, and, of course, it prevents sensory information that enters such
intact segments from reaching consciousness. Intraspinal reflexes below the injury are unaffected
or, in the case of the stretch reflex of striated muscles, even accentuated. An injury to the spinal
cord above the L1 vertebra will remove descending influences on the sacral cord neurons
controlling striated muscles that regulate urination and defecation. However, such an injury will
not affect the intraspinal parasympathetic reflexes initiating these behaviors. Thus, the bladder
contracts when it is full, generating high intravesical pressure. However, the striated muscle that
normally is responsible for the voluntary control of urination, being deprived of descending
neural influences, becomes spastic and cannot properly relax. Urination is incomplete and a suite
of complications results. It may be necessary to cut the striated muscle, or its nerve, to enable
complete emptying of the bladder. I do not know if a similar problem characterizes defecation or
if it simply occurs automatically when visceral sensory neurons detect a full rectum. A man who
has suffered a spinal cord injury above the sacral levels of the cord can reflexly achieve an
erection (a result of parasympathetic discharge from S3 and S4) upon sensory stimulation of the
penis but cannot achieve erection when shown erotic pictures.
It should be obvious that injuries to the vertebral column below the L1/L2 intervertebral disc
have an impact only in so far as spinal nerve rootlets are damaged.
Lumbar Puncture
Because the subarachnoid space inferior to the L1/L2 disc is filled with dorsal and ventral
rootlets floating in a pool of cerebrospinal fluid, a needle inserted between spines of the lower
lumbar vertebrae through the dura/arachnoid into the subarachnoid space cannot injure the spinal
cord. Just as one would find it difficult to impale a piece of cooked spaghetti floating in water, so
a needle inserted between lumbar spines into the subarachnoid space will likely just push floating
rootlets aside. Such a procedure is called a lumbar puncture. The needle must pass
through the supraspinous ligament, interspinous ligament, ligamentum flavum (which is often
perceived as offering greater resistance), epidural space, dura, and arachnoid.
In the adult, the preferred site of a lumbar puncture is between the 3rd and 4th, or 4th and
5th, lumbar spines. This level is chosen because it is sufficiently low to avoid the spinal cord in
virtually every individual (there being some normal variation in how far down the spinal cord
goes). The 4th lumbar spine is palpable in posterior midline of the back at the site where it is
crossed by the supracristal plane. If the patient is asked to adopt a position with the lower back
flexed, the space for passage of the needle is widened.
In cases where there are signs of increased intracranial pressure (e.g., edema of the optic
disc--papilledema), lumbar puncture must be performed with great care because it entails the risk
of a rapid drop in spinal fluid pressure leading to a pressure differential between the fluid around
the brain and that around the spinal cord. This pressure differential may then push the brainstem
and cerebellar tonsils downward through the foramen magnum, causing death. If there are signs
of increased intracranial pressure, some physicians prefer to withdraw CSF from a site above the
foramen magnum. There is a substantial pool of CSF between the inferior surface cerebellum and
dorsal surface of the medulla. This pool is called the cisterna magna, and it can be approached by
a needle inserted upward and forward between the posterior arch of the atlas and the occipital
bone. Such a cisternal puncture should only be attempted by someone skilled in its practice, as
the risk to the brainstem is substantial.
Lumbar Epidural Anesthesia
Spinal anesthesia is no longer the preferred method for abdominopelvic procedures in which
general anesthesia is to be avoided. Instead, anesthetic is injected into the lumbar epidural space.
This entails essentially no risk of undesired spread of anesthetic to the higher regions (as can
occur if anesthetic is injected into the CSF), and it is compatible with insertion of a catheter that
allows continuous administration of anesthetic. The use of lumbar epidural anesthesia has
become very widespread in obstetrics.
The technique of lumbar epidural anesthesia is similar to that of lumbar puncture, with some
important distinctions. A needle is inserted between the L3/L4 or (unlike a lumbar puncture) the
L2/L3 vertebral spines. The trick in an epidural block is to pierce the ligamentum flavum but stop
before you pierce the dura, thus ending up in the epidural space. This is often done by using the
air-rebound technique. The needle is attached to a syringe filled with air. When you are
superficial to the ligamentum flavum, any attempt to inject the air will meet with resistance and
the plunger of the needle will rebound. When you have entered the epidural space, there is a
negative pressure and the air will be sucked in. You then exchange the air-filled syringe for one
with anesthetic, or pass a catheter through the needle. Depending on the volume of anesthetic
injected, or the direction of the catheter, one can control how many spinal nerves are
anesthetized.
Sacral Epidural Anesthesia (saddle block)
This is a method of anesthetizing sacral spinal nerves. It takes advantage of the fact that the
spinal arachnoid/dura is shorter than the vertebral column. Thus, one may introduce anesthetic
into the relatively wide epidural space of the sacral vertebral canal via a needle inserted through
the sacral hiatus. Saddle block was designed primarily for anesthetizing the perineum during
childbirth. It is no longer popular. One reason for its demise is because of the tendency of fecal
matter to leak from the anus and contaminate the site of entry of the catheter. The other reason is
the great success of lumbar epidural block for obstetrics. An approach to the epidural space
through the sacral hiatus is used by some physicians to inject anti-inflammatory drugs for the
treatment of spinal nerve compression caused by arthritic changes in the lumbar intervertebral
joints. The value of this treatment is not universally accepted.
Breast
The part of the glandular tissue of the breast that reaches the axilla is called its axillary tail of Spence. If
cystic, it will present as swellings in the armpit.
If breast cancer spreads to a Cooper's ligament, it will be shortened, causing the skin to
dimple.
Clinical Sidelights on Lymphatic Drainage of the Breast
Aortic Coarctation
Coarctation of the aorta is a congenital narrowing of this vessel, usually along the aortic arch
just distal to the origin of the left subclavian artery. Consequently, a greatly reduced amount of
blood reaches the descending aorta via the normal route. Alternate routes become dilated so that
enough blood reaches the descending aorta to keep the lower part of the body alive. As stated in
this chapter, one such alternate route exists by virtue of anastomoses between anterior and
posterior intercostal arteries. Blood is still able to pass normally from the aortic arch into the
subclavian, internal thoracic, and anterior intercostal arteries. It then travels through anastomotic
channels into posterior intercostal arteries, and can continue "backward" in these vessels to reach
the descending aorta. Whenever arteries are subjected to sustained increase in flow, they respond
by enlargement. (When flow is reduced in an artery for a sustained period, it responds by a
reduction in diameter.) In aortic coarctation, the intercostal arteries and the anastomotic channels
between them become greatly dilated. A pulse can then be felt in the intercostal spaces, and the
dilated tortuous intercostal arteries press on the inferior borders of the ribs, causing localized
areas of bone resorption that can be seen in Xrays as notching of the inferior borders of rib.
There are other anastomotic pathways that can bring blood from branches of the aortic arch
to the descending aorta. Two foremost among these are the epigastric and scapular anastomoses.
You will be able to deduce the participants of the former as you learn more anatomy. The latter is
described in Chapter 86.
Posterolateral Thoracotomy
One approach to lung surgery is a standard posterolateral thoracotomy. A giant incision is
made transversely along the lateral aspect of the chest. The latissimus dorsi and serratus anterior
are both transected. After these big muscles are cut, the intercostal space is opened. Most
surgeons prefer to enter the fifth intercostal space because the major
fissure lies here, and through it one can gain ready access to the vessels of the hilum. You can
determine which interspace is the fifth by running your hand up alongside the chest wall deep to
the serratus anterior until to you feel the first rib, identifiable because it lies more "inside" the
second rib than above it. If you can't feel that high, your next best guide is that the interspace
between the second and third ribs is wider than the more inferior interspaces. As always, the
incision through intercostal muscles is made just superior to
the lower bounding rib, so as to avoid the intercostal neurovascular bundle. The surgeon should
pay particular attention to this requirement as the incision progresses posteriorly, because the
intercostal neurovascular bundle lies closer to the center of the intercostal space near the
vertebral column. It is unwise to extend the incision medially
beyond articulation of the rib with the transverse process of the vertebra. As the incision is
extended anteriorly, the surgeon must be certain to stop
short of the internal thoracic vessels.
In the adult, a little pocket of parietal serous pericardium may bulge out through an acquired
defect in the fibrous pericardium to produce a so-called pericardial diverticulum. Although
uncommon and asymptomatic, pericardial diverticula do alter the cardiac shadow on Xray.
Inhaled Matter
As a result of the asymmetric position of the carina, inhaled foreign objects tend to pass into
the right bronchus more frequently than into the left. If a person is supine (as during surgery)
when foreign material enters the bronchial tree, such material will most likely flow into the
posteriorly placed segments of the lung, most often the posterior segment of the upper lobe, but
also the superior segment of the lower lobe, and the posterior basal segment of lower lobe.
Segmentectomy
While lacking the independence of lobes, bronchopulmonary segments are sufficiently
autonomous that infection, pneumonia, or atelectasis (collapse) may affect one segment while its
neighbors remain normal. It is even possible surgically to resect a single bronchopulmonary
segment. This is done by deflating the lung, tying off the bronchus and artery to the diseased
segment, reinflating the lung, and then removing the tissue that is unfilled by air. Obviously, it is
the veins between segments that are at greatest risk during such surgery. Segmentectomies are
not common procedures. They are done only if it is of paramount importance to preserve as much
lung tissue as is possible. A segmentectomy might be done in a patient with a solitary pulmonary
cancer nodule who has poor pulmonary function, but in this case the surgeon might opt for a
wedge resection, which is nonanatomic.
Sensation
The bronchi receive a rich parasympathetic (vagal) and sympathetic (T1-T5 or T6)
innervation. Also, visceral afferent fibers run alongside vagal autonomic fibers, but these don't
carry pain sensu stricto. They do carry information on stretch (which, however, does not seem to
reach consciousness) and they probably carry the sense of discomfort that one experiences after
mechanical or chemical irritation and asthmatic attacks.
Coronary Dominance
As stated in the chapter, coronary dominance is defined by the vessel that gives rise to the
posterior descending artery. While coronary angiographers routinely report which vessel is
dominant, it is not so obvious how this information is clinically useful. There is one report that
individuals undergoing bypass surgery for left main coronary artery stenosis have a higher
perioperative mortality if they are left coronary dominant. Also, the circumflex coronary artery
lies closer to the rim (anulus) of the mitral valve in left dominant hearts (maybe because the
vessel is bigger) and is more likely to be caught in a suture during mitral valve replacement than
if the heart were right coronary dominant.
Course of the Posterior Descending Artery in a Right
Coronary Dominant Heart
A common variation is an early origin of the posterior descending from the right coronary
artery. In this case, the PD comes off on the back surface of the heart prior to the junction of the
coronary sulcus with the posterior interventricular groove, then just meanders toward the
posterior interventricular sulcus. The surgeon must be aware of this possibility if it is necessary
to bypass a block in the PD.
Cardioplegia
In bypass surgery, cardioplegic solution (stuff that causes your heart to stop) is usually
administered through the coronary sinus and pumped backward (retrograde) into the capillary bed
of the coronary vessels. It leaves this bed via Thebesian veins, which are tiny veins that run from
the capillaries directly into the cavities of all the heart chambers.
False Heart Attack
Because the spinal cord segments receiving pain from the heart are the same as those
receiving pain from the thoracic esophagus, pain emanating from disease of the latter may be
confused with a heart attack. Maybe that's why 30% of persons who present with anginal pain
have normal coronary arteries (Garrison, DW et al., Pain 49:373-382).
An Uncommon Treatment for Cardiac
Angina
Because the pain arising from ischemia of the heart courses
along axons that follow the reverse route of sympathetic outflow to the heart, one method used to
treat intractable angina in patients who are not good candidates for coronary artery bypass grafts
or coronary angioplasty is to excise a portion of the upper thoracic sympathetic trunk. This is
done endoscopically and is essentially the same surgery as is used for treating combined palmar/axillary hyperhidrosis, except that the T5 ganglion may
also be destroyed. The surgery has the additional effect of increasing the time the patient can
exercise without experiencing anginal pain. Maybe there is reduced myocardial oxygen demand
during exercise because of the secondary effect of the sympathectomy to reduce heart rate and
blood pressure during exercise (Wettervik, C et al. 1995 in The Lancet 345:97-98).
During surgery in the superior mediastinum, it possible to nick one of the pulmonary arteries.
In order to control bleeding, it is far easier to open the pericardium and clamp the pulmonary
trunk within the pericardial sac than to try to clamp the damaged vessel in the superior
mediastinum.
Left Recurrent Laryngeal Nerve
The left recurrent laryngeal nerve is subject to compression by aortic arch aneurysm,
pulmonary trunk dilation (as can occur if the mitral valve is stenotic leading to pulmonary
hypertension), tumor of the esophagus, or tumor in tracheal lymph nodes. Thus, hoarseness (a
symptom of recurrent laryngeal nerve dysfunction - see Chapter 74) may arise from thoracic
disease. The nerve may be damaged during surgery in the superior
mediastinum, particularly for treating trauma to the aortic arch.
Broncho-aortic Constriction of Esophagus
Where the esophagus is crossed on its left side by the aortic arch and, below this, anteriorly
by the left mainstem bronchus, is the so-called broncho-aortic constriction. It can be visualized
on barium swallow and is one of the more common sites of esophageal cancer.
Left Atrial Hypertrophy and the Esophagus
If the left atrium is enlarged, as in mitral valve disease, it will displace the esophagus
posteriorly. This is easily recognized on Xrays of a barium swallow. Prior to CT, taking a lateral
chest Xray during a barium swallow was considered an excellent way of identifying left atrial
hypertrophy. It still is a cost-effective way, and is used if CT equipment is not available,
Size of the Heart
A heart whose apex is beyond the mammary line is clearly enlarged or displaced.
Heart Sounds
The sounds created by cardiac valves are best heard along the path of blood that has passed
through the valve, i.e., just distal to the valve itself. From a knowledge of valve position one may
deduce the following as good sites
Tricuspid Valve -
directly above the xiphisternal joint.
Mitral Valve - over
the apex of the heart.
Pulmonary Valve -
at the medial end of left 2nd intercostal space .
Aortic Valve - at
the medial end of right 2nd intercostal space.
Pericardiocentesis
The most important reasons for knowing the surface projections of the pleural cavities have
to do with choosing sites to introduce a needle for the purpose of withdrawing excess pericardial
or excess pleural fluid.
Withdrawing pericardial fluid is called pericardiocentesis. A prime objective is to avoid
penetrating the lung, which might lead to pneumothorax. When there is only a small
accumulation of fluid, blood, or pus in the pericardial cavity, the substernal paraxiphoid approach
(sometimes called subxiphoid approach) is used. The patient lies supine on a table tilted up at the
head so that the pericardial contents fall to the bottom of the sac. Then a needle is inserted in the
angle formed by the left border of the xiphoid process and the 7th costal cartilage. The needle is
angled 45° to the skin and directed toward the midpoint of the left clavicle. I have heard
some physicians say that they believe they must pierce the diaphragm before they reach the
pericardium, but I don't believe this. I believe the needle enters anterior to the diaphragm's origin
from the xiphoid process and ribs.
A second, far less common technique of pericardiocentesis is the left parasternal approach.
The needle is inserted through the 4th or 5th left intercostal space immediately adjacent to the
sternum. Because this coincides with the cardiac notch of the left lung, the latter structure is not
at risk. Also, if the lateral deviation of the left costomediastinal reflection is great enough in your
patient, penetration of the pleural cavity will be avoided. This cannot be done in everyone, but
the probability is maximized if the needle is inserted at the left margin of the sternum in the 5th
interspace. One wants to insert the needle as close to the sternal margin as possible, both because
this maximizes the probability of missing the pleural cavity and because this minimizes danger to
the internal thoracic vessels that lie about 1 fb lateral to the sternal margin.
Left parasternal pericardiocentesis may be attempted if the volume of pericardial effusion or
blood is large. It entails a greater risk of entering the pleural cavity and. more importantly, of
damaging the LAD artery.
Thoracentesis
Withdrawal of excess fluid from the pleural cavity is called thoracentesis. The fluid tends to
collect posteriorly and laterally in the most dependent portions of the cavity. Logic might suggest
that one tries to insert the needle into the costodiaphragmatic recess as close to the lower limit of
the pleural cavity as possible. This would be a mistake. Even in cases of pleural effusion, the
costodiaphragmatic recess is not very wide; the pressure of the abdominal organs pushes the
periphery of the diaphragm toward the inner surface of the rib cage and thus tends to keep the
costodiaphragmatic recess narrow. Inserting a needle too close to the lower limit of the pleural
cavity runs the risk of passing through the recess and diaphragm into the abdominal cavity.
Potential sites of insertion inferior to the 9th rib are to be avoided. (Indeed, needle biopsy of the
liver is often done by inserting the needle through the 9th intercostal space in the right
midaxillary line, with full knowledge that it will pass through the costodiaphragmatic recess and
diaphragm to reach the liver. The patient is asked to hold expiration so as to minimize any
chance of piercing the lung.) The most usual site of thoracentesis is just below the inferior angle
of the scapula with the arm abducted 90 degrees. This corresponds to the 6th or 7th interspace
near the posterior axillary line. Other routes may be chosen depending on radiologic findings.
Auscultation (Listening With a Stethoscope)
You can predict what part of a lung will be heard with a stethoscope if you know the surface
projections of the lobes and the position within a lobe of the bronchopulmonary segments.
It is most important to realize that you cannot hear the lower lobe along the front of the
chest, and you cannot hear the middle lobe in the midaxillary line.
Lumbocostal Trigone
For developmental reasons, the part of the diaphragm arising from the lateral arcuate
ligament and 12th rib may be deficient in actual muscle tissue (i.e., represented only by
epimysium). The deficient region is said to comprise a lumbocostal trigone and is a potential site
of herniation of abdominal contents into the thoracic cavity.
Superficial Epigastric Artery
Arising from the common femoral artery, the superficial
epigastric artery enters the subcutaneous layer and runs upward into Camper's fascia. This path
crosses that of an incision running from the anterior superior iliac spine to the pubic tubercle that
would be made during an external repair (as opposed to a laparoscopic repair) of an inguinal
hernia. The surgeon must identify and tie off the superficial epigastric artery or else the patient
will develop a bad hematoma.
Sympathetic innervation of the testis derives from T12-L1 of the spinal cord. Testicular pain
is referred to the T12-L1 body wall segments, predominantly along the distribution paths of the
iliohypogastric and ilioinguinal nerves.
Clinical Nomenclature
Clinicians often use different names for inguinal structures than do anatomists (although this
is becoming less frequent). The inguinal ligament may be called Poupart's ligament; the lacunar
ligament may be called Gimbernat's ligament. I don't like these eponyms, but sometimes I do
prefer clinical terminology. For example, I prefer to use the term Cooper's ligament for the
thickened periosteum behind the pecten pubis (see Chapter 94), whereas less ecumenical
anatomists call it the pectineal ligament.
Clinicians also define a space called Hesselbach's triangle. It is bounded by the inguinal
ligament (inferolaterally), the lateral edge of the rectus abdominis (medially), and the path of the
inferior epigastric artery (superolaterally). Direct hernias begin their push through the abdominal
wall in Hesselbach's triangle, as opposed to indirect hernias that do so through the deep ring lying
lateral to Hesselbach's triangle.
More About Direct Inguinal Hernias
Clinical texts describe a variety of ways in which direct inguinal hernias may present
differently than indirect hernias. First, in males direct hernias are less likely to pass into the
scrotum than are indirect hernias. A further difference can be deduced from the knowledge that
only indirect hernias pass through the deep ring. Often when a patient lies on his or her back, the
herniated structures fall back into the abdominal cavity. They can be made to herniate again if the
patient strains. In the case of small indirect hernias, this voluntary reherniation can be prevented
by the examiner pressing his or her thumb over the site of the deep ring. Such pressure will have
no effect on preventing direct reherniations.
Frequency of Hernias
As stated in the chapter, the frequencies of indirect inguinal
hernias, direct inguinal hernias, and femoral hernias are highly dependent on sex and age. This
topic has been reviewed by Rutkow (Surg. Clinics North Amer., 78:941-951, 1998). While
statistics vary from study to study, the following table is not far off the mark in presenting the
expected distribution of 100 hernias of the groin by sex. Not reflected in these
numbers
is the fact that the ratio of indirect to direct inguinal hernias in males is influenced by age, there
being a much higher proportion of indirect inguinal hernias in young boys because (a) so many
inguinal hernias in young males are due to partial persistence of processus vaginalis, and (2) as
one becomes older musculofascial weakness predisposes to direct inguinal hernias. Some persons
believe that indirect inguinal hernias in females can be traced to the abortive development of a
processus vaginalis. The abortive processus vaginalis of females is called the canal of Nuck.
Hepatic Blood Supply
The liver receives blood from two sources: the common hepatic artery and portal vein.
Because the volume of flow through the portal vein is so much greater than that through the
heaptic artery, some texts say that 50-55% of the liver's oxygen is actually provided by the
venous route even though venous blood is of much lower oxygen concentration. A
physiologically healthy liver with normal portal venous flow should survive inadvertent right or
left hepatic artery ligation. For example, if you tie off the right hepatic artery, although the
patient will experience an ischemic hepatitis (with pain and the release liver enzymes into the
blood), 80% of people will recover from this condition. Intrahepatic collateral circulation
between the right and left hepatic arteries no doubt contributes to the long-term survival of the
lobe whose artery was ligated (Mays ET, Wheeler, CS 1974 Demonstration of collateral arterial
flow after interruption of hepatic arteries in man. N Engl J Med 290:993-996).
Surgical Nomenclature for Liver Portions, Hepatic
Lobectomy and Segmentectomy
As stated in Core Concept 24, the right branches of the portal vein and hepatic artery
distribute to the right lobe of the liver, whereas the left branches of these vessels go the caudate,
quadrate, and left lobes (in truth, the caudate may get supplied by both the right and left branches
of the portal vein and hepatic artery). The right hepatic bile duct drains the right lobe of the liver;
the left duct drains the other three lobes. Surgeons recognize the physiological division of the
liver by using the term "left lobe" to include the caudate and quadrate lobes along with the
anatomist's' left lobe. The plane between the physiological right
and
left lobes is coincident with a line drawn from the left edge of the cystic fossa to the left edge of
the caval fossa. This is called Cantlie's line.
Surgeons also
place emphasis on the fact that the liver can be further
divided into segments based on the distribution of secondary and tertiary branches of the vascular
and biliary trees. (You will recall that a similar segmentation occurs in the lung.) Some
classifications refer to four major hepatic segments:
To perform a hepatic lobectomy, the surgeon goes to the porta hepatis and ties off the artery,
vein and duct of the portal triad going to the relevant lobe. The part of the liver that turns gray is
then resected. In cases of right lobectomy, the boundary between the red and gray parts will be
the main portal scissura (lying deep to the right sagittal fossa); the middle hepatic vein lies in this
boundary and must be preserved. One of the dangers of a left lateral segmentectomy is due to the
fact that deep to the fissure of the ligamentum teres (which surgeons call the umbilical fissure)
lies the only branch of the portal vein that does not follow arteries and bile ducts. This
"umbilical" part of the portal vein gives branches to both the left medial and left lateral segments.
During a left lateral segmentectomy this umbilical part of the portal vein must be preserved; only
its branches to the left lateral segment are tied off.
A method of hepatic resection that requires less knowledge of anatomy is the wedge
resection. The surgeon just places clamps between the tumor-bearing part of the liver and the
good part, then cuts out the former, clipping vessels and ducts along the way.
Gallbladder Pain
Most pain fibers from the gallbladder travel centrally in the same nerve bundles that bring
sympathetic innervation to that structure. Since the foregut receives its sympathetic innervation
from T5-T9, and the gallbladder is an outgrowth from the distal end of the foregut, you would be
correct to deduce that its pain fibers mainly return to T7 - T9 segments of the spinal cord.
Referred pain of cholecystitis or gallstones is usually felt along the right 7th - 9th intercostal
spaces, sweeping from back to front near the inferior angle of the scapula toward the epigastric
region.
Pain from the gallbladder may be referred to the right shoulder (C3,4). Some people believe
this is due to irritation of the peritoneum on the
undersurface of the diaphragm, which is innervated by the phrenic nerve (C3,4,5). I have also
read that the phrenic nerve, after it has pierced the
diaphragm to innervate that muscle's undersurface, gives a sensory twig that eventually reaches
the gallbladder.
Cholecystectomy
During cholecystectomy, if the surgeon identifies a cystic artery that seems to be too large, it
should be dissected out to make certain it is not a hepatic artery. If the cystic artery seems to
small, consideration must be given to the possibility that it is only an anterior branch of the cystic
artery, or that the patient has an anomalous double cystic artery. If the surgeon ties off only the
anterior branch, or only one of two cystic arteries, believing that it is the entire and only vessel,
there will be lots of bleeding when the gallbladder is pulled out.
A common anomaly of the biliary system is the existence of a small bile duct that leaves the
right lobe of the liver and runs in the gall bladder bed (i.e., in the subvesicular connective tissue
between the gall bladder and the liver) to reach the right hepatic or common hepatic bile duct.
This "duct of Luschka" can be injured in cholecystectomy. Also, there may be tiny bile ductuli
that leave the liver substance to end blindly in the subvesicular connective tissue. These are a
source of self-limiting bile leakage following a cholecystectomy.
Identifying Bowel Segments at Surgery
Upon entering the peritoneal cavity via an anterior abdominal incision, any mesenteric
portion of the bowel may be encountered first. Thus, the surgeon is confronted with deciding
whether a particular loop of bowel might be jejunum, ileum, transverse colon, or sigmoid colon.
First, decide if it is colon by looking for appendices epiploicae and taenia coli. If it is colon,
decide if it is transverse or sigmoid using the following criteria: (a) transverse colon is attached
to three mesenteries - gastrocolic ligament, apron of greater omentum, and transverse mesocolon,
whereas sigmoid colon is attached only to its mesocolon, and (b) transverse colon (like ascending
and descending) has three taenia coli whereas sigmoid colon has only two.
If you have determined that the loop of bowel isn't colon, decide if its jejunum or ileum using
the following criteria: (a) mesenteric fat does not uniformly reach the wall of the jejunum but
overlaps the wall of the ileum, and (b) the arterial supply to the jejunum is characterized by 1 or 2
arcades will long vasa recta (Chapter 26), whereas the arteries to the ileum form 3 or 4 arcades
with short vasa recta.
The Amazing Bloodless Fold of Treves
I help teach a surgical anatomy course to fourth-year medical students. During that course, one
my colleagues (Dr. Fidel Valea) made mention of a structure with which I was completely
unfamiliar. It is called the "bloodless fold of Treves". I quote from Morris' Human
Anatomy (pp. 1379-1380, 11th edition, eds. J. P. Schaeffer et al., McGraw-Hill,
NY):
"If the appendix is drawn caudally so as to put its mesentery on the
stretch, a peculiar fold will be found to join that mesentery. This
inferior ileocecal fold arises from the border of the ileum opposite the
attachment of the mesentery. It then passes across the iliocecal
junction on its caudal aspect and is adherent to the cecum., and finally
joins the surface of the mesentery of the appendix. This fold is
peculiar in that it scarcely has any visible vessels, and is often known
as the 'bloodless fold of Treves'."
Sir Frederick Treves, who first described this structure, is nowadays more noted for having
treated the "Elephant Man". I am told by Matthew Ranzer (a medical student at Stony Brook) that
Treves was also well known for having performed an appendectomy on Edward VII, King of
England. According to Ranzer, the king desperately needed an appendicitis operation but
strongly opposed going into a hospital. 'I have a coronation on hand,' he protested. But Treves
was adamant: 'It will be a funeral, if you don't have the operation.' Treves won, the coronation
was postponed and the king lived.
In Treves' own textbook of anatomy he does not describe the significance of the bloodless
fold that now bears his name. Dr. Valea states that "it is, at times, a useful landmark when you
have limited exposure to identify the terminal ileum as it is the only place
on the small bowel that has antimesenteric fat." Another of my colleagues (Dr. Joseph Sorrento)
says that he follows it to a taenia that leads to the appendix. Personally, I find its history more
interesting that its clinical significance.
Pain
Derivatives of the midgut receive sympathetic innervation from T9-T12. The appendix is
innervated predominantly by T10. Referred pain from appendicitis is located in the T10 body
wall segment, thus in the vicinity of the umbilicus. When there is additional somatic pain located
in the abdominal wall over the appendix, this indicates spread of inflammation to the nearby
parietal peritoneum.
McBurney's Point
In 1889 the American surgeon Charles McBurney made the following observation:
"Whatever may be the position of the healthy appendix found in the dead-house and I am well
aware that its position when uninflamed varies greatly I have found in all of my operations that it
lay, either thickened, shortened, or adherent, very close to its point of attachment to the caecum.
This, of course, must, in early stages of the disease, determine the seat of greatest pain on
pressure. And I believe that in every case the seat of greatest pain, determined by the
pressure of one finger, has been very exactly between an inch and a half and two inches from
the anterior spinous process of the ilium on a straight line drawn from that process to the
umbilicus." (McBurney C 1889 Experience with early operative interference in cases of disease
of the vermiform appendix. New York Med Jour 50:676-684.)
Nowadays, McBurney's Point (of maximal tenderness in acute appendicitis) is said to be at the
junction of the lateral third and middle third of the line between the anterior superior iliac spine
and the umbilicus. Whereas McBurney thought this corresponded to the base of the appendix,
recent studies suggest that the latter is usually inferomedial to McBurney's point. Nonetheless,
physicians still consider maximal tenderness at McBurney's point to be a strong indicator of acute
appendicitis.
Portosystemic Venous Anastomoses
There is a fourth portacaval anastomosis not mentioned in Chapter 27. It occurs between
secondarily retroperitoneal mesenteric veins and the primarily retroperitoneal veins of the
posterior abdominal wall. Dilation of these anastomoses in portal hypertension is neither
observable nor symptomatic. However, their existence provides routes for spread of bowel cancer
to posterior body wall structures.
As stated in the chapter, bleeding from ruptured esophageal varices is the most serious
consequence of portal hypertension. Forty to fifty percent of those persons with cirrhosis of the
liver who actually experience esophageal variceal bleeds will die from their first such episode
within six weeks. There are nonsurgical methods of treating esophageal varices, most notably
sclerotherapy, in which fiberoptic endoscopy is used to guide injection of a
thrombosis-promoting solution into the dilated veins. The surgical
method is to relieve the portal hypertension via a shunt between the portal venous network and
the systemic (nonportal) veins.
While the preferred method of creating a portosystemic shunt used to be via a surgical
connection of the portal vein to the inferior vena cava because they were so close to another at
the epiploic foramen, this has fallen into disfavor because metabolic problems were caused by
diverting so much blood from the liver. Since the main goal of treating portal hypertension is to
eliminate the threat to life posed by esophageal varices, the currently preferred surgical procedure
is the splenorenal shunt, which consists of severing the splenic vein from its entry into the portal
vein and anastomosing it end-to-side to the left renal vein. You will recall that these two vessels
are in close proximity - the splenic vein lying on the posterior surface of the body of the pancreas
and the left renal vein being posterior to the lower border of the pancreatic body. At the same
time, the left gastric and right gastroepiploic veins are usually tied off so as to eliminate pathways
of venous return from the stomach that could circumvent the splenic vein.
There is also a new shunt technique that avoids abdominal surgery altogether. This entails
threading a tubular device down the right internal jugular vein and through the right
brachiocephalic vein, superior vena cava, right atrium, and inferior vena into an hepatic vein.
The device is then pushed through liver tissue into one of the large branches of the portal vein,
and left in place to create an intrahepatic shunt. This so-called Transjugular Intrahepatic
Portosystemic Shunt (TIPS) is performed under radiologic monitoring. The problem with TIPS is
that the shunt tends to become blocked over time. It may be the method of choice if the patient
will soon have a liver transplant, because TIPS doesn't leave intraabdominal adhesions that can
complicate the transplant surgery.
Anorectal varices are actually more common if portal hypertension has arisen from
obstruction of the portal vein outside the liver than from any hepatic disease, including cirrhosis.
In either case bleeding is an uncommon occurrence, but it may be serious if cirrhosis is the
underlying condition because that disease is often associated with a defect in blood clotting.
Hemorrhoids are distinct from anorectal varices. To understand
this, one needs to know a little bit of detail about anatomy of the anal canal. For two centimeters
above the anus the inner lining of the anal canal is composed of a modified squamous epidermis
devoid of hair and glands. This is sometimes called anoderm. Above this region the inner
lining of the anal canal is composed of columnar epithelium, like the rest of the rectum. The line
of demarcation is called the dentate or pectinate line. Both the anoderm and
columnar epithelium rest upon a layer of submucosal tissue (denser beneath the anoderm). Below
the dentate line the anal canal is highly sensitive, as is regular skin; above the dentate line the
innervation is visceral in nature. Normally there are dilated regions of veins in the submucosa of
the anal canal. If the submucosa, with its normal venous dilatations, becomes "loosened" from
deeper tissues and bulges into the lumen of the anal canal, sometimes prolapsing downward
through the anus, this is a hemorrhoid (or pile). It may occur below the dentate line - an external
hemorrhoid, above the dentate line - an internal hemorrhoid, or both. Because the covering of an
internal hemorrhoid is insensitive to somatic pain, it may be treated by ligation with a rubber
band.
The incidence of hemorrhoids in patients with portal hypertension is the same as in the
general population, illustrating the distinct nature of hemorrhoids from anorectal varices. The
latter can be distinguished from hemorrhoids because the swelling caused by varices collapses
when pressure is applied and reappears rapidly when the pressure is released.
Celiac lymph nodes can be palpated for detecting spread of cancer simply by poking one's
finger through the hepatogastric ligament. To palpate more widely in the floor of the lesser sac,
surgeons poke their fingers through the gastrocolic ligament.
Accessory Renal Arteries
Cognizance of the possibility of accessory renal arteries is important in renal transplant
surgery. All arteries feeding the donor kidney must linked together so that all will be fed when
joined to the artery of the recipient.
Renal Cell Carcinoma
Because of the short right renal vein, renal cell carcinoma of the right kidney may readily
enter the IVC and travel toward the heart. This tumor can usually be stripped out of the IVC
because it does not adhere to its wall, but if the tumor does reach the heart, cardiac bypass is
necessary to get it out.
Blood Supply to the Ureter
A ureter receives blood supply from several sources: a small twig from the renal artery, twigs
from the lumbar arteries, and small twigs from the internal iliac (or its branches, notably the
uterine in women, see Chapter 37). These vessels contribute to an arterial plexus embedded in
the fascial sheath of the ureter (Waldeyer's fascia). It is important not to interrupt this sheath and
its contained arterial plexus during abdominopelvic surgery.
Kidney Biopsy
Various diseases of the kidney are diagnosed by means of biopsy through the posterior
abdominal wall. Biopsy of the lower half of the kidney presents no special problems other than
the small risk of damage to the iliohypogastric and ilioinguinal nerves. The most direct approach
to the upper pole would involve inserting the needle opposite T12, either through the 11th
intercostal space or subcostally. Because such an approach will enter the pleural cavity, which
extends as far inferiorly as the tip of the 12th thoracic spine, it is generally advisable to insert the
needle below T12, on an oblique upward course that pierces the quadratus lumborum and
diaphragm below the inferior extent of the pleural cavity. Kocher Procedure (Maneuver)
At surgery, one may palpate the common bile to look for a stone by performing a Kocher
procedure, which consists of lifting the 2nd part of the duodenum and head of pancreas off the
posterior abdominal wall and toward the left. There is an avascular plane behind these structures
because that plane was originally (embryonically) parietal peritoneum. Kocher procedures are
also performed for determining of pancreatic cancer has involved the portal or superior
mesenteric veins.
Pancreatic Tumor
A tumor of the head of the pancreas will often compress the common bile duct embedded in
its posterior surface. This is revealed by jaundice and a distended gall bladder, which may be
palpable below the right costal margin where it is crossed by the transpyloric plane or linea
semilunaris. The jaundice caused by pancreatic tumor compression of the common duct is said to
be "painless". What is meant by this term is that the pain occurring in pancreatic cancer does not
emanate from the biliary system, nor will the gall bladder itself be tender. This clearly
distinguishes it from the pain associated with jaundice caused by gall stone obstruction of the
common bile duct.
Tumors of the body and tail of the pancreas are in some ways more insidious than those of
the head because they do not compress the common bile duct and can escape detection until they
have either metastasized or involved major arteries related the pancreas. Partial compression of
these arteries is sometimes revealed by a murmur detectable with a stethoscope placed on the
upper abdomen. Compression of the splenic vein may be revealed by splenomegaly.
An aberrant right hepatic artery (one arising from the superior mesenteric) can present a
problem in pancreatic resections because it passes posterior to the neck of the pancreas. It also
may get invaded by pancreatic tumor.
Superior Mesenteric Artery Syndrome
The superior mesenteric artery's descending course takes it across the anterior surface of the
third part of the duodenum. Normally there is sufficient fat in the root of the mesentery to form a
cushion between the artery and the duodenum. If a person undergoes dramatic loss of weight (or
growth in height without gain in weight) the arterial wall may come into direct contact with the
duodenum. Furthermore, in such a person the loss of mesenteric fat tends to allow the small
intestine to descend lower in the abdomen during erect posture. This descent pulls the superior
mesenteric artery taut across the third part of the duodenum and leads to compression of its
lumen. A similar phenomenon may occur in a person whose spine is held in hyperextension by a
cast. Afflicted persons may be unable to pass solid food through the third part of the duodenum.
Abdominal cramps and vomiting will follow attempts to eat solid food. The patient may have to
assume a prone position (which pulls the superior mesenteric artery away from the duodenum)
and eat soft foods in order to allow passage of food to the jejunum. If this fails gastrojejunostomy
(surgical connection of the stomach to the jejunum) or duodenojejunostomy (surgical connection
of a proximal part of the duodenum to the jejunum) may be required to allow food to bypass the
area of duodenal occlusion until weight is regained. Another option is to detach the root of the
mesentery and the superior mesenteric artery from the posterior abdominal wall and displace the
entire duodenum and jejunum to the right side of the abdomen.
Splenomegaly
Diseases that cause splenomegaly (expansion of the spleen) may reveal themselves because
the enlarged spleen displaces mobile structures to which it is related. As the spleen expands
anteriorly and to the right, the body of the stomach (related to the spleen's anteromedial surface)
is shoved in the same direction. This is detectable on xray as a displacement of the gastric air
lucency to the right. As the spleen expands inferiorly, the splenic flexure of the colon (related to
the inferior pole of the spleen) is pushed downward. Again , this is detectable on xray as an
inferior displacement of the air than usually resides in the splenic flexure.
Lesser Sac
Ulcers of the posterior wall of the stomach may erode into the lesser sac, spilling stomach
contents into that region of the peritoneal cavity, leading to a lesser sac abscess. It is also possible
for a posterior wall gastric ulcer to attach to and erode the pancreas and nearby vessels, the left
suprarenal gland, or the upper inner quadrant of the left kidney, all of which are said to lie in the
bed of the stomach.
Gallbladder
By virtue of the gallbladder's relationships, inflammatory disease of the gallbladder can
result in cholecystocolic or cholecystoduodenal fistulae.
Calot's triangle and its significance in gallbladder surgery is described on p. 57 of Core
Concepts. A small lymph node (Calot's node) lies in the triangle anterior to the cystic artery.
Indeed, my surgeon friends say that if you don't see this node in front of the artery, you should be
worried that the artery is not the cystic.
Truncal Vagotomy
There is a surgical operation (the Whipple procedure) that treats
patients with tumor of the head of the pancreas by removing this structure along with a segment
of the gut from the beginning of the pyloric antrum to just beyond the Ligament of Treitz. The
cut end of the remaining part of the pancreas (i.e., body + tail) is sutured into the cut end of the
jejunum; the cut end of the body of the stomach and the cut end of the bile duct are separately
anastomosed into the side of the jejunum. The Whipple procedure results in stomach acid
flowing directly into the jejunum, and over time this tends to causes jejunal ulcers at the site of
anastomosis. To avoid this, in days past some surgeons would cut the anterior and posterior vagal
trunks, thereby greatly reducing stomach acid production. The vagal trunks can be
identified by pulling down on the abdominal esophagus and feeling for taut cords on its anterior
and posterior surfaces. Interestingly, there were no obvious sequelae of this double vagotomy.
Nowadays, most surgeons do not perform truncal vagotomies along with the Whipple procedure.
This is so because the part of the stomach that has been removed is responsible for production of
the hormone gastrin, which stimulates acid production. What acid production persists can be
controlled by a drug like Prilosec.
A modified Whipple procedure that leaves the entire stomach and pylorus intact (i.e., a
pyloric-sparing Whipple) can be performed to treat cancer of the ampulla of Vater or the distal
common bile duct. Obviously one cannot combine this with a truncal vagotomy because vagal
firing is needed to relax the pyloric sphincter and allow normal stomach emptying.
The Pringle Maneuver
If the liver has been lacerated or otherwise traumatically damaged, one of the first things a
surgeon may do after entering the abdomen is an attempt to diagnose the source of the bleeding
(and maybe control it) by performing the Pringle maneuver. This maneuver consists of
compressing the structures of the hepatoduodenal ligament between the thumb and forefinger, or
between the prongs of a clamp that will not damage delicate tissue. By performing the Pringle
maneuver one stops the liver from receiving blood conveyed to it by the common hepatic artery
and portal vein. (If the right hepatic artery arises from the SMA, it too will be compressed by the
Pringle maneuver, but a left hepatic artery arising from the left gastric artery will escape such
compression.) If the Pringle maneuver stops the major bleeding, one has learned that the
damaged vessels are derived either from the portal vein or hepatic artery. If the bleeding
continues nearly unabated, then it is coming from torn tributaries of the hepatic vein. The Pringle
maneuver can be maintained for about half an hour without risk of damage to the liver. Warm ischemia time of the liver is an hour, but a little breathing
room is wise.
Spleen
The close relationship of the spleen to the posterior portions of left 9th - 11th ribs makes this
organ particularly susceptible to puncture by a rib fragment consequent upon traumatic injury to
the left posterior thorax.
Normally the spleen is not palpable. When it is greatly enlarged, it expands anteriorly to the
right and also inferiorly. Then it may be palpated (particularly on deep inspiration) emerging
under cover of the left costal margin, between this margin and the umbilicus.
Gall Bladder and Murphy's Sign
One clinical test for acute cholecystitis is the attempt to elicit Murphy's sign. You push down on
the abdomen at the right costal margin (where you expect the gall bladder to lie) and ask the
patient to make a deep inspiration. A positive Murphy's sign is defined as the abrupt and early
cessation of the patient's inspiratory effort. It is generally viewed as indicating acute
inflammation of the gall bladder.
Round Ligament
As the uterus enlarges during pregnancy its pull on the round ligament may cause inguinal
pain.
Culdocentesis
A physician may easily sample the contents of the posterior cul-de-sac by passing a needle
through the posterior fornix of the vagina and the peritoneum on its surface. This procedure,
called culdocentesis, is designed to look for depositions of free-floating abnormal contents of the
peritoneal cavity. There is no comparably easy way to enter the rectovesical pouch of males.
Pain of Labor and Delivery
The most severe labor pain arises from sustained contractions of the uterine body and is
carried centrally along the same nerves that bring sympathetic supply to the organ. Thus, it
reaches T10 - L1 of the spinal cord. A milder pain arises from cervical distension as the fetus
starts its descent. This pain travels centrally along nerve bundles that carry parasympathetic
innervation to the uterus. Thus, it reaches S3-4 of the spinal cord (and may be referred to the
region over the sacrum). The pain of delivery is a somatic pain due to perineal stretching and, if
performed, episiotomy. This pain is carried by the pudendal nerve (S2-4). It is possible to
eliminate all labor and delivery pain by anesthetizing spinal nerves T10 - S4. Nowadays, the most
popular means of producing anesthesia of T10 - S4 is via a lumbar epidural block (see above
comments for Chapter 7). One determines if the proper levels have been anesthetized by testing
the skin for its ability to respond to touch. The level of insensibility must rise as high as the
umbilicus (T10) and as low as the perineum.
If one desires only to eliminate the pain of delivery, it is possible to perform a pudendal
nerve block. The most common method of pudendal block is the transvaginal approach, which
involves inserting a finger and a needle, protected by guard, into the vagina. The finger identifies
the ischial spine and the needle is pushed through the vaginal mucosa and sacrospinous ligament,
so that the tissue around the pudendal nerve (which lies on the dorsal surface of the ligament) can
be infiltrated with anesthesia. The position of the internal pudendal artery crossing the tip of the
ischial spine makes puts it out of the way of the needle, but one must always withdraw the
plunger of the syringe to verify that the needle has not entered this vessel or its accompanying
vein(s).
Connection Between Peritoneal Cavity and External
World
in Women
Because infections can travel from the vagina into the peritoneal cavity, gonorrhea may
spread to the peritoneal cavity in females in a way not possible in males. When a fertilized
ovum (zygote) turns around and exits the oviduct to enter the peritoneal cavity, the result may be
an abdominal ectopic pregnancy in which the embryo implants on the broad ligament, bowel
mesentery, loop of bowel, or parietal peritoneum. Uterine lining shed during menses may
travel into the peritoneal cavity, where (some people think) cells may attach to the parietal
peritoneal of the pelvis, causing a condition known as endometriosis.
Finally, the physician, may inject radio-opaque dye or radiolucent gas into the uterus, with
the full expectation that if oviducts are normal the injected material will reach the peritoneal
cavity. If it does not, there is an obstruction in the lumen of the oviduct.
The pelvic splanchnic nerves are sometimes called nervi erigentes (L. erigo, to raise),
because they carry the preganglionic parasympathetic axons that, upon stimulation, cause the
phallus to erect. These particular axons probably synapse in ganglia within the pelvic plexuses.
In males, the relevant postganglionic fibers emerge from the pelvic plexus and descend inferiorly
along the posterolateral aspect of the prostate gland. Surgeons refer to these as the cavernous
nerves. They run next to a prostatic artery and vein, forming a neurovascular bundle (see
Fig. 1 in Schlegel PN, Walsh PC. 1987 Neuroanatomical approach to radical cystoprostatectomy
with preservation of sexual function. J. Urol 138:1402-1406). At the apex of the prostate the
nerves pass onto the posterolateral aspect of the membranous urethra, which they follow through
the pelvic diaphragm and perineal membrane to reach the corpora cavernosa. Operations on the
rectum put the pelvic plexus at risk. Operations on the prostate put the cavernous nerves at risk.
Damage to either may lead to impotence - hence the development of "nerve sparing" prostatic
surgery described in several papers (such as the one cited above) by Dr. Patrick C. Walsh of
Johns Hopkins University School of Medicine.
More on Ruptured Urethra in Men
If the rupture of the urethra into the perineal cleft is unilateral, urine will first fill one side of
the perineum and one scrotal sac. However, because the anterosuperior edge of the scrotal
septum is free, urine always passes to the other side.
In addition to the possibility that a careless catheterization may rupture the exposed part of
the urethra between the perineal membrane and bulb, leading to urine accumulation in the
perineal cleft and confluent spaces, there are also cases in which the tip of the catheter may be
driven through the back wall of the bulbar urethra. If the rupture goes no further, urine will
simply spread throughout the blood-filled sinuses of the bulb and corpus spongiosum. If the
catheter also pierces the tunica albuginea of the bulb, bloody urine will enter the space between
external perineal fascia and the tunica albuginea of the bulb (ordinarily this space is occupied
only by the bulbospongiosus muscle) but will still be confined to the middle of the perineum and
ventral surface of the penis. Subsequent infection may then cause breakdown of the external
perineal fascia and entry of urine into the perineal cleft. This entire process may also result from
primary untreated infection of the penile urethra.
Rectal Examination in Women
Normally the posterior wall of the vagina is examined intravaginally. However, if a vaginal
examination cannot be performed (such as in a child) a rectal examination can give some
information about the back wall of the vagina. Rectal examination in adult women is done
primarily to provide information about posterior cul-de-sac, the uterine cervix, and the lower
uterine body.
Suprapubic Incision
The close relationship of the urinary bladder to the anterior pelvic brim is of significance.
When empty, the bladder does not rise out of the pelvis, but when full it may do so. As the
bladder roof rises, it takes parietal peritoneum with it. Thus, with the patient's bladder full, one
may make a surgical incision above the pubic symphysis and enter the subperitoneal area of the
pelvic cavity. If this is desired, the bladder is artificially inflated at the time of surgery by means
of a urethral catheter.
Surgeons view the parotid gland as being divided into superficial and deep lobes by the facial
nerve. The superficial lobe comprises 70% of the gland. This is purely descriptive, there being no
other anatomical or functional significance to this nomenclature. Depending on tumor location, it
may be possible to effect a cure by removal of only the superficial lobe, rather than performing a
total parotidectomy.
The distribution of the supraclavicular nerves has a particular relevance for clinical
diagnosis. It will be recalled that the bulk of the phrenic nerve derives from the same spinal
segments (C3 and C4) as do the supraclavicular nerves. Disease of the mediastinal or central
diaphragmatic pleura may give rise not only to pain perceived as being deep within the chest, but
also to a referred pain perceived as being located in the subcutaneous tissues supplied by the
supraclavicular nerves. It will be recalled that gallbladder disease sometimes leads to referred
pain in the shoulder. This is probably due to irritation of the diaphragmatic peritoneum, but I
have also read that some peculiar phrenic fibers reach the gallbladder.
The valleculae and piriform recesses are places where fish bones and the like may lodge.
Anesthesia of Airway for Orotracheal Intubation in a Conscious
Patient
Position of Larynx at Birth
It is interesting that the larynx actually sits higher in the newborn than in the adult. At birth,
the superior tip of the epiglottis lies just behind the palate. The oropharynx exists only as a small
region anterior to the epiglottis. An oropharynx of significant dimensions develops concomitantly
with descent of the larynx in early childhood. As a result of the high position of the larynx in the
newborn, the food and air passageways are separate, enabling liquid food to be swallowed at the
same time as breathing occurs. Newborns tend to breathe solely through their noses, although they
outgrow this habit before the larynx descends.
Intubation of Children
Long term intubation of children is prone to lead to a condition called subglottic stenosis,
which is a narrowing of the air passage at the level of the cricoid cartilage. It develops because
the cricoid is a complete ring and cannot yield around the tube. The result is the formation of scar
tissue at the site of tube-cricoid contact.
Subclavian Steal
If there should develop a block in one subclavian artery prior to the origin of its vertebral
branch, then blood cannot reach any branch of that subclavian by the normal route. What often
happens is that the body takes advantage of a normal right-left anastomosis between the two
subclavian arteries. Blood passing through the normal vessel and its vertebral branch will
obviously reach the beginning of the basilar artery. Some of this blood continues into the basilar,
but some also travels down the contralateral vertebral artery to reach the pathologic subclavian
distal to its occlusion. This is called the subclavian steal phenomenon. It may seem to
be useful, since it allows the upper limb on the pathologic side to get blood. However, the limb
gets this blood at the expense of the brain.
Most of the time the diminution of blood flow to the brain that occurs in a subclavian steal is
insufficient to cause neurologic symptoms. If neurologic symptoms do arise, they are said to
constitute a subclavian steal syndrome. The most common neurologic symptoms are
dizziness and a sense that one is about to faint. More rarely, the patient may experience visual
disturbances and/or problems with coordination. Sometimes, neurologic symptoms only appear
when the patient exercises the upper limb whose subclavian artery is blocked. Exercise draws
more blood to that limb and away from the brain. Furthermore, if the extra blood going to the
limb is insufficient to meet its increased demands for oxygen, the patient may experience
ischemic pain in the exercising limb (i.e., claudication).
Esophagus
Surgery on the cervical esophagus approaches it from the left side, where it is partly exposed.
Thoracic Duct
Surgery at the root of the neck on the left side runs the risk of nicking the thoracic duct. If
this occurs, the vessel must be ligated to prevent continuous discharge of lymph into the neck. To
avoid such a possibility, surgeons may first identify and tie off the thoracic duct. A similar
attempt to tie off smaller lymphatic ducts may be made during surgery at the root of the right
neck. When I first learned of this, I thought it was crazy, but there are apparently no
consequences of tying off major lymphatic vessels on one side of the body. Cranial Vault Size
Because the size of the cranial vault is not controlled genetically, but rather is a function of
what is going on inside the braincase, if the newborn's brain does not grow adequately, the
cranial vault stays small (microcephaly). If the cranial contents become excessively voluminous,
as in hydrocephalus, the cranial vault responds by excessive enlargement.
If the anterior fontanelle can be palpated well into the second year of postnatal life, the
physician must consider causes of decelerated maturation (e.g., malnutrition).
Sutural Fusion, Both Normal and Otherwise
After adulthood, the sutural connective tissue is no longer essential for growth of the
neurocranium. Nevertheless, this tissue usually persists well past puberty (except for the metopic
suture). In middle age the bones bordering any given suture may bridge across the connective
tissue and fuse. The suture is then said to be obliterated. This happens a lot in some people and
hardly at all in others. It is of no functional consequence.
In rare instances the metopic suture does not become closed in early childhood. It can then be
visualized in anteroposterior Xrays as a wavy radiolucency in the midline of the frontal "bone." It
is important to recognize this possibility so that such a wavy midline radiolucency is not
mistaken for a fracture (which, by the way, is hardly ever in the midline and never appears wavy).
More commonly a bit of the metopic suture just superior to the nasal bones persists well into
adult life.
If any suture closes significantly before its period of growth normally ends, expansion of the
cranial vault perpendicular to that suture is retarded. The remaining normal sutures will undergo
excessive growth in order to keep the size of the vault in pace with intracranial contents. This
leads to recognizable deformations of the skull. For example, if the metopic suture closes shortly
after birth, the forehead ceases growth in width, but the back of the skull compensates. The result
is a skull that, when viewed from the top, appears triangular, with the apex anteriorly. This is
called trigonocephaly. If the sagittal suture closes prematurely, growth in width of most of the
cranial vault will be retarded. Compensatory growth in the coronal suture will cause the
braincase to become longer than normal, and compensatory growth in the lambdoidal and
squamosal sutures will lead to excessive skull height. This condition is called scaphocephaly; it
is the most common deformation due to premature sutural closure.
Premature sutural fusion is known as craniosynostosis. It comes in two varieties: simple (one
suture fused) or compound (two or more fused sutures). Either may be primary (there are no
other recognizable physical abnormalities) or secondary (associated with other obvious
developmental defects). In simple primary craniosynostosis, the rate of mental retardation is
3-6% (somewhat higher when the coronal suture is fused than when the sagittal suture is fused).
This value is 2 to 3 times greater than would otherwise be expected. In compound primary
craniosynostosis, mental retardation occurs 35-50% of the time. Less severe learning disabilities
appear in about half the children with simple primary craniosynostoses. It has not been
determined whether the cognitive problems associated with craniosynostoses are caused by an
underlying brain malformation, by increased intracranial pressure, or by a distortion of the brain
due to the synostosis. Most people believe that the latter possibility is only reasonable when
multiple sutures are fused.
Premature sutural fusion is treated surgically. In the simplest case, a strip of bone on either
side of the fused suture is removed and some measure taken to prevent regrowth and closure. It
has not been possible to demonstrate that surgery to correct the synostosis alters the cognitive
development of the patient. One recent study on a small sample of children with simple
synostosis, some of whom had surgery to correct it and others of whom did not, found no effect
of surgical correction on rate of mental retardation or learning disability. The primary reason for
performing such surgery is cosmetic.
Scalp Wounds
In the case transverse scalp wounds that penetrate the galea, the wound margins are held
apart by the opposite pulls of frontalis and occipitalis on the epicranial aponeurosis, causing
extensive bleeding. Wounds to the scalp that penetrate the galea also present a risk of infectious
matter entering the subaponeurotic space and spreading over the entire surface of the cranial
vault. The infectious material may even spread through emissary foramina to reach the cranial
cavity.
Subdural Hematoma
The veins on the lateral and superior surfaces of the cerebral hemispheres pass to the superior
sagittal sinus. Cerebral veins that are destined for the posterior part of this sinus turn forward
while still in the subarachnoid space to approach the dural wall of the sinus at an acute angle.
These veins then travel obliquely forward through the dural wall before opening into the sinus.
To some degree the oblique course of cerebral veins into the superior sagittal sinus minimizes the
likelihood that forward and backward motion of the cerebrum will cause the veins to shear off
the sinus wall. However, apparently such a mechanism is imperfect, for occasionally a severe
blow to the front or back of the skull causes such large anteroposterior displacements of the brain
that some cerebral veins do shear off the superior sagittal sinus wall. Blood then spills into a
subdural space producing a subdural hematoma. The blood is under low pressure and
accumulation is usually gradual. Symptoms of cerebral compression may not occur until much
later, when the blood breaks down and forms a fluid of high osmotic pressure that draws in
further tissue fluid causing an increase in size.
Middle Ear Veins
Veins from the middle ear find their way to the superior petrosal sinus. This is of clinical
significance as a route of spread of infection from the middle ear to the superior petrosal and
transverse sinuses.
Cavernous Sinus Disease
The potential threats to life resulting from cavernous sinus infection are the same as those of
any other sinus. However, before these occur, existence of cavernous sinus thrombosis is
betrayed by a series of other symptoms. Many of these will not be understood until you learn
more anatomy, but they will all be described here.
First there occurs a swelling of the eyelids and neighboring tissues, owing to retardation of
venous flow through the superior and inferior ophthalmic veins. Second, there is dilatation of
retinal veins (which may be visualized ophthalmoscopically) and edema of orbital tissues (which
causes the eyeball to move forward--a condition known as exophthalmos). The optic nerve may
or may not become swollen.
Because important nerves run through the cavernous sinus, an inflammatory state within it
will soon produce symptoms related to axonal malfunctioning. Thus, pain or tingling over the
sensory distribution of the ophthalmic nerve will develop. This will be followed by anesthesia
over the same area. In the case that the maxillary nerve has a course through the lower part of the
sinus, its areas of sensory distribution may be subject to the same disturbances as those of the
ophthalmic nerve. Weakness (paresis) and then paralysis of the muscles supplied by the
oculomotor, trochlear, and abducens nerves becomes apparent. Usually, the abducens nerve is the
first to be affected because of its central location within the sinus. As if septic thrombosis of
one cavernous sinus were not bad enough, the existence of intercavernous sinuses permits spread
from one side to the other. Hopefully, long before this happens, the patient will have been treated
with antibiotics. Nerve symptoms will then disappear and collateral routes of venous drainage
will expand, or the thrombus will resolve.
Aneurysm of the internal carotid artery with the cavernous sinus may mimic some of the
symptoms of sinus thrombosis, especially those related to retardation of superior ophthalmic
venous return and compression of the abducens nerve. If the aneurysm ruptures to create an
arteriovenous fistula, the exophthalmotic eyeball will pulsate.
Spread of Infection
An example of how the state of superficial structures may provide information about dural
sinuses is the dilatation of veins and swelling of tissue over the mastoid process when there is
thrombosis at the junction of the transverse and sigmoid sinuses secondary to a middle ear
infection. The thrombus and infection may even spread to the tissue over the mastoid region.
Infections of the face pose the very serious threat of passage to the cavernous sinus. One
route is from the communication established between the facial vein and the cavernous sinus by
the superior ophthalmic vein. Another, more complicated, route starts out by passing from the
facial vein to the pterygoid plexus via the deep facial vein. Then, from the pterygoid plexus
infectious material may spread to the cavernous sinus via the emissary vein through the foramen
ovale, or via the emissary vein that runs through the inferior orbital fissure to the inferior
ophthalmic vein (see figure for Chapter 68).
Eye Color
The posterior (retinal) layer of the iris normally always contains pigment. If the anterior
(uveal) layer of the iris is unpigmented, one will have blue eyes. If the anterior layer of the iris
contains lots of pigment, the eyes will be brown. Variants between blue and brown depend on the
amount of pigment in the anterior layer.
Episcleral Space
Because Tenon's capsule intervenes between the bulbar conjunctiva and the visible part of
the sclera, blood or infectious matter that accumulates in the episcleral space (i.e., between the
sclera and Tenon's capsule) may reveal themselves by elevation of the bulbar conjunctiva.
Glaucoma
Glaucoma must be treated because the increased intraocular pressure presents a threat to the
optical retina. Some cases can be treated medically, others are treated by surgically creating a
path of egress of aqueous humor.
Cataract
Cataract is treated surgically, by incising the capsule, vacuuming out all the lens fibers, and
replacing them with an artificial lens.
Range of Ocular Motion
An eyeball can be abducted or adducted a maximum of 50 degrees in either direction. It can
be elevated or depressed a maximum of 45 degrees in either direction. However, in normal use
the eyeball rarely deviates from its primary position more than 15 degrees in any direction (von
Noorden, GK, 1990, Binocular Vision and Ocular Motility, 4th ed., CV Mosby, St.
Louis).
Cyclovertical Muscles
Each vertical rectus and each oblique muscle produces significant rotations of the eyeball
around two axes - optic and horizontal. For this reason, ophthalmologists group these four
muscles together under the rubric "cyclovertical muscles". As the eye abducts, the vertical recti
become increasingly better at producing vertical excursions and increasingly poor at producing
torsions; the obliques become better cyclorotators and worse at elevation/depression. In contrast,
during adduction of the eye the opposite changes occur - the vertical recti becoming increasingly
good at cycloductions and worse at producing vertical motions, while the obliques become
increasingly better at producing vertical excursions and worse at producing torsions. At
maximum adduction the obliques are almost pure elevator/depressors whereas the vertical recti
are primarily cyclorotators. However, in more commonly used states of adduction, the strong
vertical recti are able to make a very significant (some say even predominant) contribution to
vertical excursion. Indeed, persons with both obliques nonfunctioning can still elevate and
depress the adducted eye (von Noorden, pers. comm.).
Cyclovertical Muscles as
Adductors/Abductors
Cyclovertical muscles also have an effect around the vertical axis to produce either adduction
or abduction. However, it is known from experiments on monkeys that no combination of the
vertical recti and obliques is able to adduct an eye whose medial rectus is paralyzed but whose
lateral rectus is intact, nor to abduct one whose lateral rectus is paralyzed but medial rectus
intact. It is true that if both horizontal recti are eliminated, the vertical recti have the ability to
adduct the eye somewhat, and the obliques have the ability to abduct it somewhat. It has been
said that in the normal eye the vertical recti are important adductors once the eye has already
been brought to 35ø of adduction by the medial rectus, but such a position is uncommon.
Normal Cyclorotation
There is one behavior in which cyclorotation of the eyeball normally occurs. When a person
laterally flexes the neck so that his or her ear approaches the shoulder, the eyes cyclorotate in the
opposite direction by several degrees. For example, if you tilt your head so your right ear
approaches your right shoulder, your right eye will incycloduct (intort) and your left eye will
excycloduct (extort), in a seeming attempt to minimize your perception of environmental
spinning. The right eye's intorsion is brought about by the SR and SO, whose vertical effects
nullify; the left eye's extorsion is brought about by the IR and IO, whose vertical effects cancel.
This normal cyclorotation during head tilt is the basis of a very important diagnostic test
described below.
More About Strabismus
As stated in this chapter, strabismus is defined as divergence of the optic axes (more
precisely, the condition in which the optic axis of one eye is no longer directed at the object
fixated by the other eye). If one eye aims higher than its partner, this is called hypertropia.
Hypertropia of an eye may be due to pathology on either side. For example, a right hypertropia is
said to occur if either the right eye points higher than normal because its depressors are weak, or
because the left eye points lower than normal because its elevators are weak. An eye that is
abnormally deviated inward is said to be esotropic; one that is abnormally deviated outward is
said to be exotropic. Diplopia will occur during significant strabismus because the image of an
object falls on noncorresponding parts of the right and left retinae and, consequently, cannot be
fused by the brain.
With complete paralysis of an extraocular muscle, strabismus and diplopia will often occur
even when the patient attempts to look forward. For example, paralysis of the SO usually causes
the affected eye to point slightly upward when the patient looks straight ahead. Strabismus
worsens when the eye is placed into a position that requires greater participation of the affected
muscle, and will diminish when the eye is placed in a position that requires little or no
participation by the affected muscle. Since the superior and inferior oblique muscles play a
significant role in determining the vertical position of an adducted eye, but almost no role in
determining the vertical position of an abducted eye, any observable strabismus caused by a weak
oblique muscle will get worse when the affected eye is adducted and is likely to go away when
the affected eye is abducted. In our example of a paralyzed SO, any hypertropia will become
worse when the affected eye looks medially, whereas it may virtually disappear when the affected
eye abducts. By similar reasoning, since the superior and inferior recti play a dominant role in
determining the vertical position of an abducted eye, but a much smaller role in determining the
vertical position of an adducted eye, any observable strabismus caused by a weak vertical rectus
muscle will get worse when the affected eye is abducted and will diminish or go away when the
affected eye is adducted.
With only weakness (paresis) of a muscle, strabismus and diplopia may not be noticeable
until the patient actually attempts to move the affected eye in a direction that requires extra effort
by the weak muscle. For example, weakness of the SO may lead to a noticeable strabismus only
upon looking downward, or downward and inward. The chart on page 111 indicates the motions
of the eye that should be elicited in order to look for strabismus resulting from a paretic
extraocular muscle.
Bielschowsky Head-Tilt Test
Because the vertical recti still contribute in a major way to elevation/depression of an eye
that is moderately adducted (and for reasons relating to changes in the intact extraocular muscles
after one of their colleagues has been paralyzed for a long time), testing the obliques by eliciting
elevation and depression of the adducted eye may sometimes be unrevealing. A second way to
examine the strength of the superior and inferior oblique muscles relies on understanding the
cyclorotation that normally occurs when someone laterally flexes his/her neck. If you ask a
patient to tilt the head to the right, you know that he or she will increase effort in both the right
SO and SR to effect a counter incycloduction of the right eye, and there will occur a similar
increase in the effort of both the left IO and IR to effect a counter excycloduction of the left eye.
If the right SO is weakened, its depressor action will be unable to counteract the elevating action
of the right SR, and the right eye will deviate upwards during the head tilt. If the left IO is
paretic, it will be unable to overcome the depressor action of the left IR, and the left eye will
deviate downward during the head tilt. A head-tilt to the left serves to test the left SO and right
IO.
The attempt to observe abnormal vertical deviation of an eye during head-tilts is called the
Bielschowsky Head-Tilt Test. Although logic would suggest that weakness of a vertical rectus
muscle could be revealed by this test (e.g., if the right SR is weak, the right eye should depress
upon a head-tilt to the right), it has been observed that strabismus upon head-tilt is a consistent
observation when an oblique muscle is weak, but inconsistently present in the case of weak
vertical recti. This is probably related to the fact that the obliques are predominantly cyclorotators
when the eye is the primary position.
Head Posture With Strabismus
Strabismus is defined as deviation of the optic axes, but in some cases it may be possible for
the patient to get the two optic axes to point in the same direction by adopting a head position
that calls upon the good eye to point in the same direction as the affected eye. One example is
illustrated in Chapter 70: if a lateral rectus is paralyzed, the patient can get both optic axes to
point in the same direction by adopting a head position that requires the normal eye to abduct.
Paralysis of one or the other oblique muscles is frequently associated with abnormal head
positions. Since, in the primary position of the eye, these muscles are mainly cyclorotators, the
paralysis of either one causes a cyclodeviation (torsion) of the affected eye producing a peculiar
kind of strabismus called cyclotropia. Paralysis of the SO leads to an excyclodeviation
(excyclotropia) of the affected eye; paralysis of the IO leads to an incyclodeviation
(incyclotropia). Take the case of a patient who has an excyclotropia of the right eye due to SO
paralysis; he or she can avoid diplopia by adopting a head position in which excycloduction of
the right eye is normal, i.e., one in which the head is tilted to the left. Such a position
induces the normal left eye to incycloduct, resulting in comparable torsions of the two eyes and
corresponding positions of their retinal images. (By the way, this head-tilt to the left will also
cause any right hypertropia associated with right SO paralysis to diminish since it is a position in
which use of the SO is minimal.) In general, persons with an SO paralysis frequently carry their
heads tilted toward the contralateral side. You should be able to deduce that persons with an IO
paralysis will use an ipsilateral head tilt to avoid diplopia. Such head-tilts used to avoid diplopia
are referred to as ocular torticollis.
Check Ligaments
In the words of von Noorden (1990, Binocular Vision and Ocular Motility, 4th ed.,
CV Mosby, St. Louis), "there are numerous extensions from all the sheaths of the extraocular
muscles, which form an intricate system of fibrous attachments interconnecting the muscles,
attaching them to the orbit, supporting the globe, and checking the ocular movements." This
intricate system is thought to prevent certain muscles from overshortening, to support the eyeball
against the pull of gravity, and to keep the eyeball from being pulled backward into the depth of
the orbit by contraction of the rectus muscles. It is said that developmental anomalies of the
fascial system are more common than those of the extraocular muscles and are clinically more
significant. Thus, ophthalmologists put a lot of effort into naming and describing various parts of
the fascial system. If that becomes your chosen field, be forewarned.
Because the ostia (i.e., openings) of the paranasal sinuses into the nasal cavities are small and
surrounded by easily swollen mucous membrane, the flow of air between the paranasal sinuses
and nasal cavities is highly restricted. Mucous secreted by the epithelium lining each sinus
normally flows into the nasal cavities unless the mucous membrane lining its ostium becomes
swollen to the point of occlusion. Then the patient will want to take decongestants to reduce this
swelling, open the ostium, and thereby "decompress" the sinus. Infectious organisms may pass
from the nasal cavities into the sinuses, leading to the well-known condition of sinusitis.
Genioglossus and Sleep
It has been suggested that some persons are subject to respiratory distress during sleep
because they have periods of inactivity of the genioglossus, with the result that the tongue falls
backward into the oropharynx. Certainly during general anesthesia, one must guard against the
tongue falling backward and obstructing the air passageway.
Lingual Frenulum
One cause of speech impediments is a short lingual frenulum, which may then be incised.
The dilator tubae portion of the tensor veli palatini is often called into action by the same
behaviors that require the rest of the muscle to tighten the soft palate. Thus, during the descent of
an airplane passengers are advised to swallow or yawn in order to equalize pressure between the
external environment and middle ear cavity. These maneuvers often fail to work, indicating that
it is possible to contract the bulk of the tensor veli palatini without simultaneous recruitment of
dilator tubae. Eventually, however, a reflex swallow or yawn occurs in which the auditory tube is
opened.
It is branches of the central artery of the retina that are seen when looking into the eye with
an ophthalmoscope.
Olfactory Nerve
Bilateral loss of smell is usually of no significance. Many common nasal infections greatly
impair the sense of smell bilaterally. Also, some persons are simply born with a very poor sense
of smell. On the other hand, tumors or fractures often involve damage to only one side.
The sense of smell is rarely tested unless one suspects traumatic damage to the olfactory
nerve or a tumor in the anterior cranial fossa. If one wishes to test for smell, each olfactory nerve
must be tested separately in order to detect asymmetry in the response. A nonirritating
odoriferous substance is placed beneath one nostril while the other nostril is compressed. Coffee,
oil of
peppermint, wintergreen, cloves, or camphor are commonly used.
Testing the Optic Nerve
Neuro-ophthalmologists have ways of accurately assessing visual field defects. In the more
typical physical exam, the exploration of visual fields is usually done simply by bringing a
wiggling finger into view of the patient from the sides, from above, and from below. The patient
looks straight ahead and is requested to state when the finger can first be seen.
Routine testing of extraocular muscles involves asking the patient to look at your finger as
you move it in directions that should elicit adduction and abduction of the eye, elevation and
depression of the eye when it is adducted, and elevation and depression of the eye when it is
abducted. Chapter 62 discusses which muscles (and therefore which nerves) are required for
these motions. The clinical comments for Chapter 62 (above) provide additional information on
testing extraocular muscles. Test of the levator palpebrae superioris is as simple as asking the
patient to look upward so you can observe if elevation of the eyelid accompanies this effort.
Testing the parasympathetic pathway to the constrictor pupillae done by shining a light in the
patients' eye. The pupil should constrict. Note that this pupillary light reflex is consensual, which
means that shining a light into only one eye causes both pupils to constrict. Testing the
sympathetic pathway to the dilator pupillae is done by shielding an eye from light; its pupil
should dilate. This reflex is also consensual.
A second test for the parasympathetic pathway to the constrictor pupillae relies on the reflex
that causes the pupil to constrict when one attempts to focus on an object very close to the eye.
Normally this involves convergence of the eyes, i.e., rotation so that their optical axes converge
on the nearby point. The test is performed by asking the patient to follow your finger as you bring
it toward the bridge of his/her nose. One assumes that the ciliary muscle is also contracting, but
there is no easy way of determining this. Paralysis of the ciliary muscle should cause focusing
problems, but these may be unnoticed by the patient.
While damage to the oculomotor nerve affects both the pupillary light and pupillary
accommodation reflexes, some central nervous system diseases (e.g., neurosyphilis) produce a
pupil that constricts on accommodation but not in response to light. This is called an
Argyll-Robertson pupil (mnemonic: the initials AR correspond to Accommodation Reactive).
Isolated lesions of the trochlear nerve are uncommon. The abducens is the most frequently
damaged of all nerves feeding extraocular muscles. It is the first nerve to be affected by septic
thrombosis of the cavernous sinus. Aneurysm of the internal carotid artery within the cavernous
sinus may put pressure on the abducens. A variety of tumors at the base of the brain will tend to
compress the nerve against the clivus.
Chapter 71 lists some symptoms of trigeminal palsy. No mention was made of problems
arising from paralysis of nonmasticatory muscles innervated by the trigeminal. Extirpation of the
tensor veli palatini in experimental animals leads to severe middle ear pressure dysfunction. Yet I
have not encountered a description of similar problems arising from trigeminal nerve damage in
humans. Neither have I discovered reports of difficulties in swallowing resulting from paralysis
of the mylohyoid.
Testing the Trigeminal Nerve
Damage to the ophthalmic nerve is tested by determining the responsiveness of the skin of
the forehead (frontal nerve) to touch and prick with a sharp object (like a broken Q-tip). A
second test involves the corneal reflex. When the cornea is touched, the sensation travels via
V¹ back to the trigeminal nerve and thence to the brain. Here fibers synapse with facial
neurons innervating the palpebral portion of orbicularis oculi, which is caused to contract,
producing a blink. Like the pupillary light reflex, the corneal reflex is consensual, i.e., both
eyelids blink when either cornea is touched. Obviously, disturbances of the corneal reflex will
occur if either the sensory or motor limb is damaged. If the sensory limb is damaged, neither
eyelid will blink when the affected cornea is touched. On the other hand, if touching the cornea
of one eye produces a blink in the opposite eye, the examiner knows that V¹ is working
and that the defect is in the facial nerve.
Damage to the maxillary nerve is usually tested only by assessing the responsiveness of the
skin over the front of the cheek (infraorbital nerve) to touch and pain. Nasal, palatal, and upper
dental sensation are affected by damage to maxillary nerve, but these are not tested for routinely.
During a routine exam, the test for sensory fibers that run in V³ is usually confined to
the skin over the chin (mental nerve) and side of the cheek (buccal nerve). General sensation to
the front of the tongue (lingual nerve) may also be tested. Obviously, a thorough neurological
exam can involve tests over other regions (e.g., temple, ear).
Tests for strength of the masseter and pterygoids are often made in routine physical
examinations. The examiner places one hand over the left masseter and the other hand over the
right masseter and then asks the patient to clench his or her teeth. As assessment is made about
the degree to which one side may be contracting less strongly than the other. (The test can also be
done with the hands placed over the temporalis muscles, but these are less easily palpable.) The
lateral pterygoid, medial pterygoid, and superficial masseter, when acting together on one side,
protract that side and cause the jaw to deviate toward the opposite side. The left protractors push
the chin toward the right; the right protractors push the chin to the left. If the examiner places a
hand on the right side of the chin and attempts to push the jaw to the left, the patient must use the
left protractors to resist this. If the examiner places a hand on the left side of the chin and
attempts to push the jaw to the right, the right muscles must be used to resist this. By asking the
patient to resist such pushes on the jaw, an assessment of strength of the jaw protractors on one
side compared with those on the other may be made. The symptoms of damage to the facial nerve within the posterior wall of the tympanic cavity
are summarized in Chapter 72. Additionally, some patients with damage to the chorda tympani
also complain of partial numbness of the tongue on the ipsilateral side. It is not known whether
this is simply the way persons perceive disruption of sensory input from the tongue, or if some of
the sensory axons within the chorda tympani of humans are connected to mechanoreceptors, as
occurs in cats.
Surgery on the middle ear may damage the facial nerve within the labyrinthine wall of the
tympanic cavity, leading to all the symptoms mentioned in Chapter 72. Tumors within the
petrous temporal may affect the facial nerve at the site of the geniculate ganglion. This leads to
the above-mentioned symptoms plus loss of tearing on the affected side. Lesions of the facial
nerve between the brain and the facial canal may affect one root and not the other because the
two roots are actually separate during this part of their courses.
There is a peculiarity about the cortical input to the facial nuclei of the brainstem that is
useful in diagnostics. The facial motoneurons projecting to the upper third of the face receive
cortical control from both the right and left cerebral hemispheres, whereas the facial
motoneurons to the lower two thirds of the face receive cortical control only from the opposite
cerebral hemisphere. Thus, if a facial paralysis is due to unilateral interruption in the pathway
from the cerebral cortex to the brainstem, the symptoms due to paralysis of the mouth and cheek
on the opposite side are full-blown, but the orbicularis oculi and frontalis of that side are not
nearly as weakened as in Bell's palsy.
Testing the Facial Nerve
Testing the facial nerve during a routine physical examination begins with observing the
appearance of the face to assess the normality of skin creases, width of palpebral fissure, and
position of the corner of the mouth. Then, the patient is asked to raise the eyebrows or wrinkle
the forehead (frontalis) and the examiner looks to see if this is done symmetrically. The patient
may be asked to close the eyes very tightly (orbicularis oculi) and the examiner tries to pry them
open by pushing up on the eyebrows. A broad smile is requested (several muscles) and assessed
for symmetry. The patient is asked to puff out the cheeks. Puffing out one's cheeks is made
possible by the action of orbicularis oris in preventing escape of air between the lips. If one side
is very weak, air escapes on that side. If air does not escape, the examiner may apply a test of
strength by pushing in on both cheeks to see if the orbicularis oris on one side can be
overwhelmed.
Only if these tests of facial muscles reveal deficit does the examination progress to a test of
taste or lacrimation. Taste on the anterior two thirds of the tongue can be evaluated by applying a
strong tasting solution (e.g., salt, sugar, citric acid, quinine) to its right and left edges, where most
of the taste buds are concentrated. There exist special absorbent paper strips that can be applied
to the surface of the eye for assessing tear production. Vestibulocochlear Nerve
The assessment of sense of equilibrium, or of frequency of auditory sensitivity, is left to
specialists. However, a routine physical examination may attempt to judge general hearing
acuity, particularly as it depends on adequate operation of the middle ear mechanism.
A first test - the Weber test - can be done to determine if there is unilateral hearing
diminution due either to sensorineural (cochlea or nerve) or conductive (eardrum and ossicular
chain) problems. Although the Weber test is described in most physical diagnosis and neurology
texts, there is evidence that it has a high risk both of giving false positive and false negative
results (Miltenburg, DM, J. Otolaryngology, 23:254-259, 1994). Nonetheless, I shall
describe how it is performed. The stem of a vibrating tuning fork (256 or 512 Hz) is placed in
contact with the vertex of the skull so that sound is sent directly through the bone to reach both
the right and left cochleae. If hearing is normal, the sound will be reported as being equally loud
in both ears. As you might expect, if a cochlea or its nerve is damaged on one side, the sound of
the tuning fork will be heard as louder on the opposite, normal side. On the other hand, you
might be surprised to learn that if there is a problem on one side with the conductive mechanism,
the tuning fork will actually be heard as louder on this abnormal side. This is because the sound
of the tuning fork transmitted through the bone of the skull competes with room noise
transmitted through the eardrum and ossicular chain. Such room noise becomes a poorer
competitor if the conductive mechanism that brings it to the cochlea is defective, with the
consequence that the tuning fork sounds louder in that ear. To summarize, in a Weber test,
lateralization of the tuning fork's sound to a particular side occurs if there is a problem either
with that side's conductive mechanism or the opposite side's sensorineural mechanism. The
inherent ambiguity of this result should be resolved by the application of the Rinne test,
described next.
The Rinne test is considered a pretty good (though not perfect) method for
determining if a suspected hearing loss is due to a conductive or sensorineural problem. The
Rinne test is applied to each side separately. Various neurology and physical diagnosis texts
describe it as consisting of three steps: (1) apply the stem of a vibrating tuning fork to the
patient's mastoid process so that the vibrations reach the cochlea via bone conduction, (2) ask the
patient to report when the sound is no longer heard, (3) then place the tines of the tuning fork
near the external auditory meatus and inquire if the sound can once again be heard. If the patient's
middle ear on the tested side is operating normally, the sound will once again be heard, usually
for an additional period of time that equals the duration of the audible bone conduction through
the mastoid process.
Otolaryngologists seem to agree that the accuracy of the Rinne test can be improved by
performing it somewhat differently than just described. They recommend the following
method: Glossopharyngeal Nerve
The routine test of glossopharyngeal function is the gag reflex. This reflex consists of
pharyngeal constriction when the back wall of oropharynx is touched. The glossopharyngeal
nerve is supposed to be the sensory limb of the gag reflex; the vagus is the motor limb. However,
since some authors state that the gag reflex is not lost after glossopharyngeal section, the vagus
may participate in conducting pharyngeal sensation. If this is true, then the standard test for
glossopharyngeal function is not informative.
Taste on the posterior third of the tongue can be assessed by applying a small electrical
current between copper electrodes placed on the back of the tongue. An acid or metallic taste is
elicited. This is not a common procedure. Applying solutions of strong taste to the back of the
tongue is not a good method because of the rapid spread to the other side. However, since some
authors report that intracranial transection of the glossopharyngeal nerve does not lead to loss of
taste or general sensation from the tongue, it would seem that more remains to be learned about
the complete pathway of such modalities.
Vagus Nerve
The discussion presented in Core Concept 74 regarding differences in vocal fold position
following injury to the recurrent laryngeal nerve (RLN) versus injury to the vagus proximal to its
superior laryngeal (SL) branch is based on the Wagner-Grossman hypothesis, which had nearly
universal acceptance prior to 1993. Since that time (and largely initiated by the research of Dr.
Gayle E. Woodson, Southern Illinois University School of Medicine) evidence has accumulated
that no such difference exists. First and foremost, it seems that except under the experimental
circumstance of electrically induced maximum contraction, the cricothyroid muscle does not
produce vocal fold adduction. Consequently, immediately after complete injury to a RLN, the
ipsilateral vocal fold usually does not assume a taut paramedian position, but instead is flaccid
and only slightly more adducted than in quiet respiration (illustrated in Core Concept 74 as the
cadaveric position, but more properly called the intermediate position). The symptoms associated
with such a paralyzed vocal fold are (1) hoarse and breathy voice, (2) weak cough, (3) risk of
aspiration of fluids (which risk arises not only because the folds cannot be tightly approximated
but also because sensation is diminished on one side of the glottis), and (4) exertional dyspnea
(breathing during normal activities is not a problem since the intact cord can compensate for the
mildly narrowed glottis by wider abduction; only during exertion is there likely to be any
difficulty breathing). If the vagus is injured proximal to its SL branch, the
ipsilateral vocal fold appears the same as just described for a RLN injury. In other words, one
cannot diagnose the site of nerve injury based on vocal fold position.
Regardless of the site of nerve injury, after several months the paralyzed vocal fold may
move
medially, sometimes actually reaching the paramedian position.. One explanation offered for why
a paralyzed vocal fold might move medially is reinnervation by axonal regrowth from the part of
the nerve proximal to the injury. Animal experiments have demonstrated a remarkable ability of
RLN axons to cross surgically created gaps in the nerve and eventually reach the internal
laryngeal muscles on the affected side. The axons do not end up going to the same muscles they
had originally innervated, so useful control of vocal fold position is not regained. However, since
there are four times as many adductor muscle motor units as posterior cricoarytenoid motor units,
the statistically favored effect is to cause a more adducted position of the cord. Additionally,
reinnervation of the thyroarytenoid muscle reverses atrophy of this muscle and leads to increased
bulk of the paralyzed fold. I emphasize that these changes do not always happen - some patients
with longstanding vocal fold paralysis (due either to RLN or high vagal injury) have intermediate
folds, some have paramedian folds. If the paralyzed fold does move medially, there is a
diminution of symptoms because the intact fold is now better able to make firm contact with the
fuller, tauter paralyzed fold. If the paralyzed fold stays in the intermediate position, surgical
treatment to "medialize" it is often attempted. Finally, bilateral RLN injury does usually result in
an unacceptably narrow glottis sooner or later.
Testing the Vagus Nerve
If there are no symptoms attributable to vagal damage, routine testing of the vagus nerve
consists of (1) observation of the soft palate at rest and while the patient says "Ah," and (2)
elicitation of the gag reflex. If the soft palate droops on one side or does not rise on that side
when the patient says "Ah," damage to the ipsilateral vagus must be suspected. Failure of the
paralyzed half of the palate to rise when the patient says "Ah" may cause the uvula to deviate to
the intact side. If the contraction of the pharynx that is elicited by touching its back wall is absent
on the same side as the drooping soft palate, this is further indication of vagal malfunction.
Anesthesia of the Airway for
Orotracheal Intubation in a Conscious Patient (I want to
acknowledge Dr. Michael M. Todd, Professor of Anesthesiology, University of Iowa, for
assistance with this topic.)
Whereas many patients are given intravenous anesthesia prior to airway intubation, selected
patients (e.g., those with cervical spine fractures) are intubated while awake. It is then necessary
to anesthetize the oropharynx and larynx to provide comfort and eliminate the risk of injury
associated with coughing and gagging. A solution of lidocaine sprayed into the back of the mouth
is often sufficient for oropharyngeal anesthesia, but this may be supplemented with an injection
of lidocaine into the middle of the palatopharyngeal fold (posterior faucial pillar), where it will
block the glossopharyngeal nerve prior to its branches to the tongue and adjacent region of the
pharynx. Anesthesia of the larynx is accomplished using two approaches. Sensation from the
supraglottic larynx is eliminated by administering lidocaine adjacent to the internal laryngeal
nerve (although this technique is usually referred to as "superior laryngeal nerve block"). It will
be recalled that the internal laryngeal nerve enters the larynx by piercing the posterior portion of
the thyrohyoid membrane. Thus, one may either aim the needle to hit the greater cornu of the
hyoid bone just anterior to its tip, then inject anesthesia as you walk the needle downward, or one
may aim for the superior border of the thyroid lamina in front of its superior horn and inject
anesthesia as you walk the needle upward. In either case, the needle is also pushed through the
thyrohyoid membrane (which offers a palpable resistance) and anesthetic solution injected
around the nerve deep to this structure. The lower part of the larynx is made insensate by
spraying lidocaine through a catheter that has been inserted either through the median
cricothyroid ligament or transtracheally, above or below the first tracheal ring.
Testing the Accessory Nerve
Assessing the strength of the sternocleidomastoids and trapezius are done as a part of any
routine test for the integrity of the accessory nerve. The patient is asked to turn the head to one
side against resistance from the examiner. A resisted turn to the right tests the left
sternocleidomastoid,
and vice versa. Again, the examiner is trying to discover weakness of one side relative to the
other. Another way to judge strength of the sternocleidomastoids is to have the patient attempt to
flex the neck against resistance applied to the forehead. In this case, the examiner compares
strength of the right and left muscles by palpating the rigidity of each tendon that comes from the
manubrium.
To test for strength of the trapezius, the patient is asked to shrug the shoulders against
resistance by the examiner. Both sides are tested simultaneously so that a weakness of one side
relative to the other can be detected. Clearly this test informs one only about strength of the upper
fibers of the muscle, but these are the ones that receive most of their innervation from the
accessory nerve.
Cerebral control of the sternocleidomastoids is unusual. Whereas the general rule is that one
side of the cerebral cortex controls muscles on the opposite side of the body (but see discussion
of superior facial muscles above), the sternocleidomastoids get cortical input from both cerebral
hemispheres. As would be predicted from the general rule, the contralateral hemisphere
stimulates the sternocleidomastoid when you use it to flex or laterally flex your neck. For
example, a right hemisphere lesion causes weakness in the left sternocleidomastoid when you try
to touch your left ear to your left shoulder. Unexpectedly, the ipsilateral hemisphere stimulates
the sternocleidomastoid when you turn your head. For example, when you want to turn your head
to the right, use of your left sternocleidomastoid is initiated by the ipsilateral left cerebral cortex.
Since the left cortex also causes your eyes to turn to the right, deviation from the normal pattern
for sternocleidomastoid during head turning behaviors is functionally sound.
Testing the Hypoglossal Nerve
Routine examination of the hypoglossal nerve consists of a request that the patient stick out
the tongue and wiggle it from side to side. If it can only be wiggled to one side, the muscles of
that side are paralyzed. The patient may also be asked to push first one and then the other cheek
out with the tongue while the examiner resists the movement. In theory the left genioglossus is
primarily responsible for pushing out the right cheek while the right genioglossus is chiefly
responsible for pushing out the left cheek. This test is entirely analogous to resisting sideways
deviations of the chin in order to assess mandibular protractors.
Parotid Gland
In surgery on the parotid gland, it is important to see the facial nerve so that it be preserved.
Surgeons locate it by finding the posterior belly of the digastric and tracing this upward; the
facial nerve is anterior to it near the base of the skull. If you haven't seen the facial nerve, and
your patient has postoperative facial palsy, you must go back in and look for the nerve. If you
have cut it, you must reanastomose the ends. If you saw the nerve but the patient has
postoperative facial palsy, you can reassure him/her that recovery will occur.
The skin incision for parotid surgery usually sacrifices the anterior branch of the great
auricular nerve.
Epistaxis
Nosebleeds (epistaxis) are classified as anterior or posterior. Anterior bleeds usually stop by
themselves; if not, packing is usually successful. Posterior bleeds are harder to control. If all
conservative measures fail, the surgeon enters the pterygopalatine fossa through the maxillary
sinus and ties off the inner division of the maxillary artery. A newer approach entails
catheterization and embolization of the sphenopalatine and descending palatine arteries under
radiographic guidance. However, regardless of the technique used to occlude the branches of the
maxillary artery to the nose, many surgeons recommend simultaneous ligation of the anterior
ethmoidal artery because it anastomoses with such branches. Even this procedure may fail and
posterior ethmoidal artery ligation also be necessary.
More on Horner's Syndrome
The mild ptosis of Horner's syndrome can be easily distinguished from the more marked
ptosis due to levator palpebrae superioris paralysis simply by asking the patient to direct the gaze
upward, which will elicit elevation of the upper lid if the LPS is intact.
One anatomically interesting phenomenon is the occurrence of a reversible Horner's
syndrome in some persons who experience migraine headaches. Such headaches are believed to
be caused by vasodilation of meningeal branches of the external carotid artery. However, in some
persons the vasodilation may involve the internal carotid artery. Since this vessel passes through
the inexpansible carotid canal of the petrous temporal, expansion of the artery can compress and
temporarily damage the sympathetic nerves that surround it. The result is a Horner's syndrome
that resolves itself over the course of the next few months.
Excessive Frequency and
Extent of Facial Blushing (I wish to thank Peter Yoo for
drawing
my attention to this Clinical Sidelight.)
Some persons blush intensely at the slightest provocation, and
this can lead to dread of social situations and be psychologically debilitating. Since emotional
vasodilation of facial vessels is controlled by preganglionic sympathetic cells lying
predominantly in the T2 level of the spinal cord, interrupting the course of their axons can cure
the condition. Surgeons use the same endoscopic upper thoracic sympathectomy (or
sympathicotomy) procedure that was developed to control excess
sweating in the palm. This procedure has also been used to treat complaints of excessive
facial sweating.
Parotid Duct
The rule of thumb is that a vertical laceration of the face below the zygomatic arch and
posterior to the lateral canthus of the eye threatens the parotid duct. This is so because the duct
lies on the relatively unyielding masseter here.
Erb-Duchenne Syndrome
Falls that cause the head and shoulder to be pushed apart may result in tearing, or actual
avulsion from the spinal cord, of the upper roots (C5 and C6) of the brachial plexus. The same
damage may occur in a newborn if the person "assisting" a normal head-first delivery tries to
promote passage of the shoulders by laterally flexing the child's neck and pulling. The motor
symptoms of brachial plexus upper root damage are said to constitute the Erb-Duchenne
syndrome. Since these roots innervate predominantly muscles proximal to the elbow, motions at
the shoulder and elbow joints are most affected. There occurs paralysis of abduction and lateral
rotation of the shoulder, paralysis of elbow flexion, and weakness of supination of the forearm.
The upper limb hangs limply at the side with the arm in medial rotation and the forearm pronated
(the waiter's tip position discussed in lecture). There is also a characteristic sensory deficit
associated with injury to the C5 and C6. As might be expected, the skin over the pre-axial side of
the limb is without feeling.
To a certain extent one can predict which muscles will be paralyzed in Erb-Duchenne
syndrome from a knowledge of brachial plexus formation and the distribution of specific nerves.
The upper roots form the superior trunk, which is the sole source of axons to the suprascapular
nerve. The superior and middle trunks (C5, C6, C7) are the sole source of axons to the lateral
cord, from which the musculocutaneous nerve is derived. Unfortunately, there are other paralyses
that cannot be deduced in this way.
Avulsion of C5 and C6 leads to paralysis of some trunk muscles attaching to the shoulder
girdle (e.g., subclavius, rhomboids, and most of serratus anterior). However, Erb-Duchenne
syndrome is defined by the consequences of limb muscle denervation and can occur by damage
to the superior trunk of the brachial plexus, which will not affect trunk muscles innervated by C5
and C6.
Klumpke Syndrome
Damage to the lower roots (C8 and T1) of the brachial plexus can occur during strong
upward traction on the upper limb. This might occur if a person attempts to stop a fall by
grabbing onto an overhead support. It also may occur during delivery of a neonate if an attempt is
made to facilitate passage of the trunk by pulling on the upper limb. The motor deficits that result
from damage to the lower roots of the brachial plexus constitute the Klumpke syndrome. Since
these roots innervate predominantly muscles distal to the elbow, motions of the wrist and hand
are most affected.
We can predict certain of the deficits in Klumpke syndrome by realizing that C8 and T1 are
the sole source of axons to the medial cord and ulnar nerve. Thus, all the ulnar innervated
muscles of the forearm and hand will be paralyzed. It just so happens that those fibers of the
median nerve destined for intrinsic hand muscles and for the deep extrinsic digital flexors are
also derived from C8 and T1. The sensory deficit in Klumpke's syndrome is characterized by loss
of sensation in the skin along the postaxial aspect of the upper limb.
Anastomoses Between Median and Ulnar
Nerves
The ventral division axons for muscles distal to the elbow are carried by either the median or
ulnar nerve. Interestingly, nerve fibers that normally run with the ulnar nerve may sometimes
leave the brachial plexus in the median nerve, and vice versa. Such fibers may stay with their
abnormal carrier all the way to the muscle for which they are destined, in which case that muscle
has an anomalous innervation from the "wrong" nerve. More frequently, these fibers cross from
the abnormal carrier to their proper carrier somewhere below the elbow. The most common form
of such a median/ulnar communication is called the Martin-Gruber anastomosis, which occurs in
about 15% of limbs. It arises when motor axons that should have left the brachial plexus with the
ulnar nerve to innervate certain muscles of the hand, instead leave with the median nerve. Then
in the forearm, these misdirected axons correct their mistake by crossing from the median nerve
to join the ulnar nerve, thereby creating the anastomosis.
The significance of Martin-Gruber anastomosis is that injury to the median nerve proximal to
the anastomosis will lead to specific hand muscle paralyses expected from ulnar nerve damage,
and damage to the ulnar nerve proximal to the anastomosis fails to yield these expected
symptoms.
Sympathectomy (or
Sympathicotomy) for Palmar Hyperhidrosis
The upper limb receives its sympathetic innervation through
gray rami that join the ventral rami of the brachial plexus. These gray rami derive from cells in
the middle and inferior cervical sympathetic ganglia and the first thoracic ganglion. More
importantly, these postganglionic cells are controlled by preganglionic axons that arise in the
T2-3 spinal cord segments, travel in the 2nd and 3rd white rami communicantes to the T2 and T3
paravertebral ganglia, then ascend in the sympathetic chain to the ganglia of synapse. Endoscopic
surgical removal or destruction of the T2 and T3 sympathetic ganglia , or even cutting the
sympathetic trunk (i.e., sympathicotomy) at one or more sites just below the T1 ganglion, is now
a common procedure to treat a distressing condition in which the patient is plagued by excessive
sweating (hyperhidrosis) of the palm. As long as the T1 ganglion and its white ramus are left
unscathed, no ocular symptoms characteristic of a Horner's syndrome are produced. (However,
since the sweat glands and vasculature of the face are innervated by the T2 level of the spinal
cord, functions of these structures are affected by the surgery. Indeed, such surgery may be done
primarily to treat excessive facial sweating or blushing .)
Following treatment the most frequently voiced complaint is excessive compensatory sweating
elsewhere in the body, often including a greater propensity to gustatory sweating in the face.
If the hyperhidrosis also involves the armpit, the T4 ganglion must be additionally destroyed.
However, since the axillary apocrine glands (which produce the odiferous secretion) are not
controlled by sympathetic innervation, and it is possible to surgically remove the glands of the
armpit without major disfigurement, sympathectomy is not recommended if axillary
hyperhidrosis is the sole complaint.
There is variation in anatomy that is relevant to the conduct of sympathectomy or
sympathicotomy for treatment of palmar hyperhidrosis. In a small percentage of persons some of
the sympathetic preganglionic axons running in the T2 ventral ramus fail to enter its white ramus
communicans. Instead, they leave the ventral ramus as a separate bundle (the nerve of Kuntz) that
runs just posterior the sympathetic chain and joins the T1 ventral ramus. Here the axons
backtrack to get to the T1 white ramus and thus to the chain. Sometimes the nerve of Kuntz
connects the T3 and T2 ventral rami, carrying preganglionic axons from the T3 ventral ramus to
reach the chain at the T2 level. Regardless, failure to destroy the nerve of Kuntz may leave the
upper limb with enough sympathetic innervation to negate the beneficial effects of surgery to
treat palmar hyperhidrosis (Drott, C et al. 1993 in Arch. Surgery 128:237-241).
Pancoast (Superior Sulcus) Tumor and
Syndrome
You will recall that the apex of the lung rises as high as the neck of the first rib. The ventral
ramus of T1 crosses in front of the neck of the first rib (hence behind the apex of the lung) to
reach the superior surface of the rib just posterior to the subclavian artery. At this site the ventral
ramus of T1 is joined by the ventral ramus of C8 to form the inferior trunk of the brachial plexus.
You should also recall that lying on the head of the first rib is the first thoracic sympathetic
ganglion (called stellate ganglion if it is joined to the inferior cervical ganglion). From these
relationships you can deduce that tumors of the apex of the lung, particularly those located
posteriorly in the apex, may compress or involve the lower trunk of the brachial plexus and the
first thoracic sympathetic ganglion. Such tumors often produce pain (and later numbness and
weakness) in those regions of the upper limb served by C8 and T1. About 20% of the time a
Horner's syndrome is also produced [Detterbeck FC 1997 Pancoast (Superior Sulcus) Tumors.
Ann Thor Surg 63:1810-1818]. Tumors in the apex of the lung producing these symptoms are
called Pancoast tumors (after a radiologist named Henry Pancoast), and the suite of symptoms
due to nerve involvement are said to constitute a Pancoast syndrome. Although other diseases
involving the apex of the lung can produce a Pancoast syndrome, they are rare compared to
Pancoast tumor.
Repeated strenuous movements of the shoulder may lead to painful inflammation of the
subacromial bursa.
In older persons with arthritis of the shoulder, the intracapsular part of the biceps long head
tendon may erode, so that the biceps long head then arises from the intertubercular sulcus of the
humerus.
Winging of the Scapula
When the serratus anterior is paralyzed, the inferior angle of the scapula moves posteriorly
away from the chest wall to make a noticeable ridge beneath the skin of the back, a condition
known as winging of the scapula. Paralysis of the trapezius yields a similar change in appearance
of the back. At first look, the examiner may be unable to decide whether winging of the scapula
is due to a serratus anterior or a trapezius paralysis. The determination is then made by requiring
the patient to perform a motion for which one of the muscles is significantly more important than
the other. If that important muscle is damaged, the winging will become worse; if that muscle is
intact, the winging will become less noticeable. For example, when the patient abducts the arm, a
trapezius-winging will become more prominent but a serratus-winging will lessen (or remain
unchanged). When the patient flexes the arm, a serratus-winging will worsen but any winging
caused by a paralyzed trapezius will diminish.
Winging due to a paralyzed serratus anterior is also accentuated by applying a dorsally
directed force to the scapula that the paralyzed serratus is unable to resist. In diagnosis, this is
accomplished by asking the patient to hold his or her hands stretched out in front of the body and
then lean against a wall supported by the outstretched hands. This maneuver stresses the
protracting ability of the serratus and causes a serratus-winging to become even worse. Had the
appearance of winging at rest been due to a weak trapezius, the winging would virtually
disappear when the patient performed such a test.
Posterolateral Thoracotomy
In the standard posterolateral thoracotomy, the serratus anterior is divided transversely. Many
surgeons prefer to make this cut lower than the intercostal space to be entered so as to preserve as
much as possible of the nerve to serratus anterior.
Extension of Fingers
Since each of the two methods for stable extension of the fingers involves an active
contribution by some intrinsic hand muscles, it will be obvious that if these muscles are
paralyzed, the finger cannot be completely extended. Under the influence of only the extrinsic
muscles, all the fingers assume a clawed position. A hand in which all the fingers are clawed is
said to be intrinsic-minus.
Synovial Sheaths
The synovial digital flexor sheaths provide a passageway for infectious material that is
introduced into them by a penetrating wound of the finger to travel proximally into the palm.
Because such sheaths do not extend to the tips of the fingers, wounds here run less risk of
proximal spread of infection. Because the synovial sheath of the little finger is connected to the
synovial bursa in the carpal tunnel, an infection of the former can spread to the latter. Similarly,
an infection of the thumb's synovial digital flexor sheath can spread into the carpal tunnel.
Superficial Ulnar Artery
The reason that injections meant for the median cubital vein may have dire consequences if
put in a superficial ulnar artery is that solutions of drugs meant for intravenous injection are
usually highly concentrated in anticipation of the fact that they will become diluted with venous
blood from other parts of the body when they reach the heart. If such a solution is injected into an
artery by mistake, it reaches the capillary bed of that artery without significant dilution. The
result may be serious injury to capillary walls and to the tissues supplied by these capillaries.
Arterial Anastomoses in the Hand and the Allen
Test (I wish to thank Scott McGovern for drawing my
attention to this Clinical Sidelight.)
In the hand there are two major anastomotic routes between the radial and ulnar arteries:
This issue has come to fore for three main reasons: (a) the radial artery is becoming an
increasingly popular substitute for the great saphenous vein during coronary artery bypass
grafting, (b) the radial artery may become occluded as a complication of cannulating it for the
purpose of monitoring blood pressure and oxygen levels, and (c) hemodialysis usually involves
establishing an arteriovenous fistula between the radial artery and a vein at the wrist. Before
one removes the radial artery, or risks occluding it, or diverts its blood, it would be nice to know
if the patient's ulnar supply to the hand is intact.
There are some very sophisticated ways of assessing flow within the distribution of the ulnar
artery to the hand, but many physicians recommend performing a very simple test called the
Allen test. The essence of the Allen test is to get most of the blood out of the hand, then
compress the radial artery, and finally observe if the ulnar artery can refill the hand with blood
while the radial artery remains compressed. There are a few different ways to do the Allen test.
One way you can perform on yourself is to clear your hand of blood by holding it above heart
level and tightly clenching your fist for about a minute. Next, while your fist is still clenched,
compress your radial artery at the site where you would take its pulse (i.e., just proximal to the
wrist). Then look at your palm and fingers as you open your fist. If the palm and fingers turn
from pale to red within 7 seconds, your ulnar artery is working fine. If they take longer than 15
sec to become red, your ulnar artery supply to the hand is probably not sufficient to sustain
removal or occlusion of the radial artery. When you do the test don't overextend your wrist or
completely straighten your fingers. To do so places tension on the skin and palmar aponeurosis
that may compress the cutaneous vessels and give you a false positive result (i.e., continued
pallor of the palm and fingers even though everything is OK). Though not particularly relevant to
the clinical scenarios described, one can also judge the contribution of the radial artery supply to
the hand by performing an Allen test with compression of the ulnar artery. In this case, if the
palm and fingers turn red upon release of the compression, you are genuinely seeing the result of
collateral circulation, since the main distribution of the radial artery is to the thumb and radial
side of the index finger.
Some papers I have read suggest that, even when carefully done, Allen tests tend to give a lot
of false positive results. That is, a vessel judged inadequate by an Allen test can be shown by
more sophisticated studies to be capable of supplying blood to the whole hand. However, a
negative Allen test (i.e., the hand turns red within 7 seconds) is a pretty good indication that you
have nothing to worry about.
Warm Ischemia Time
An organ or structure deprived of its blood supply will die. The length of time it can remain alive
at room temperature without lasting damage is called its "warm ischemia time". The warm
ischemia time of limb segments containing muscle is about 6 hours. Major causes of limb
ischemia are arterial occlusion and, more dramatically, accidental amputation. After 6 hours of
warm ischemia, 10% of patients will have irreversible damage; by 12 hours, 90% (Marx: Rosen's
Emergency Medicine: Concepts and Clinical Practice, 5th ed.,
Copyright © 2002 Mosby, Inc.). Limb segments with no muscle, like digits, have a warm
ischemia time of approximately 8 hours. In either case, if the affected segment is cooled to 4
°C the ischemic lifetime can be greatly extended (doubled or more).
Suprascapular Nerve
The suprascapular nerve is not often injured by itself, although trauma to posterior triangle of
the neck, or falls on the shoulder, may do so. In addition to the symptoms mentioned in the
chapter, right-handed persons usually experience difficulty in writing, since movement of the
hand across the page involves lateral rotation of the humerus. Although a test of abduction
strength would reveal weakness of supraspinatus in the case of suprascapular nerve injury, the
examiner would be unable to distinguish this from weakness of deltoid due to axillary nerve
injury without further observations. Thus, the least ambiguous test for the suprascapular nerve is
for strength of lateral rotation of the arm. The patient is instructed to hold the arms at the sides
with the elbows flexed. The examiner attempts to push the hand inward against resistance by the
patient. The teres minor is too weak a lateral rotator to confound results of this test.
Subscapular Nerves
The subscapular nerves are rarely injured. One can theorize that such injury would greatly
affect medial rotation of the arm and also affect combined extension/adduction of the arm. The
test for strength of medial rotation is to ask the patient to hold the arms at the side, with the
elbows flexed, and then resist the attempt of the examiner to push the hands apart. If the patient
is able to offer only weak resistance to this movement, and palpation of the pectoralis major
indicates it is working, one can suspect injury to subscapular nerves. The test for strength of
combined extension/adduction of the arm consists of asking the patient to hold the arm straight
out to the side and resist the examiner's attempt to lift it upward and forward.
Axillary Nerve
The test
for the axillary nerve consists of asking a patient to hold the arms straight out to the side while
the examiner attempts to push them down. In this way, weakness of one deltoid relative to the
other may be easily assessed. The motion will be weak if the supraspinatus is paralyzed, so one
must use his/her powers of observation or palpation to determine that the weakness is due to a
paralyzed deltoid.
Radial Nerve
Tests for motor function of the radial nerve consist of assessing strength of elbow extension,
wrist extension, and finger extension. Sensory examination involves choosing a spot of skin
whose innervation by the radial nerve is rarely, if ever, altered by variations in nerve distribution.
Such a spot is the web of skin overlying the 1st dorsal interosseous muscle on the back of the
hand. This is stimulated by soft and sharp objects to determine the patient's response.
Pectoral Nerves
Specific injuries to the pectoral nerves are rare. To assess function of the pectoral nerves, one
asks the patient to hold the arms out in front of the body, and the examiner attempts to push the
elbows apart against the patient's resistance.
Musculocutaneous Nerve
The musculocutaneous nerve is rarely injured alone. Fractures of the humerus, direct wounds
to the axilla, or even axillary artery aneurysm may affect it. It must be watched out for in an
anterior approach to surgery on the shoulder. This is done by staying on the lateral side of the
conjoint tendon of origin of coracobrachialis and short head of biceps brachii. The motor test for
function of the musculocutaneous nerve is no more complicated than asking the patient to flex
the elbow against resistance by the examiner.
Ulnar Nerve
In routine physical examinations, assessment of the ulnar nerve is usually confined to one
sensory and one motor test. The skin over the tip of the little finger is chosen for the sensory test,
because its innervation by the ulnar nerve is rarely, if ever, altered by variations in nerve
distribution. To assess ulnar-innervated muscles the patient is asked to spread his or her fingers
while the examiner tries to squeeze the index and little fingers together. This tests the strength of
the first dorsal interosseous and abductor digiti minimi (with flexor carpi ulnaris used as a
synergist to prevent pisiform displacement).
Median Nerve
In routine physical examinations, one motor and one sensory test for the median nerve are
performed. The motor test consists of asking the patient to make a circle by opposing the pads of
the thumb and little finger, whereupon the examiner attempts to pull the thumb away by applying
a force to its proximal phalanx. This is a test of strength for the thenar eminence muscles. The
sensory test consists of assessing cutaneous sensation at the tip of the index finger. This is the
part of the median's distribution area least susceptible to variation in nerve supply. Obviously,
other tests can be performed (e.g., of wrist flexion and finger flexion) if these two standard tests
produce suspicious results.
Quadrangular Space
During surgery on the shoulder from the anterior approach, one eventually reaches a point
where the subscapularis must be transected. In so doing, the surgeon must take care not to extend
the incision into the quadrangular space, wherein reside some important things.
Snuffbox
It is significant that the scaphoid is in the floor of the snuffbox since fractures of the
scaphoid are indicated by tenderness or swelling in the snuffbox.
Carpal Tunnel Syndrome
Carpal tunnel syndrome is treated by surgical transection of the transverse carpal ligament.
The initial skin incision starts just proximal to the projected position of the superficial palmar
arch and extends to the distal carpal flexor crease. It lies along a line corresponding to the radial
edge of the ring finger because this maximizes the chance of missing the palmar cutaneous
branch of the median nerve. If this nerve is cut, the patient will likely develop a painful neuroma.
The incision in the transverse carpal ligament is made near its ulnar attachment, so as to
minimize the possibility of damaging the median nerve.
A human who sustains a minor fracture of the fibula will not generally require a cast because
the bone is subject to such minimal stresses.
Isolated injuries of the anterior cruciate ligament do occur, but there is no consensus on what
motion produces them. Excessive axial rotation, which involves injury to one of the collateral
ligaments, is often accompanied by an anterior cruciate tear. One
clinical test for the anterior cruciate ligament involves the examiner placing the knee of a supine
patient in 90° of flexion, then attempting to the pull the tibia forward off the
undersurface of the femur. A more sensitive test for anterior cruciate injury is the Lachman test, but it requires
greater skill to
interpret. The difference is that the knee is placed is placed in only 20-30° of flexion. Now
when
the examiner tries to pull the tibia forward he or she will normally be able to elicit a few
millimeters of
movement, but this movement should have a firm stopping point. If the stopping point is
"mushy", this is a
sign of anterior cruciate ligament damage.
Isolated injuries of the posterior cruciate are usually the result of blows to the front of the
tibia or hyperflexion of the knee. The clinical test for the posterior cruciate ligament involves the
examiner attempting to the push the flexed tibia backward off the undersurface of the femur.
Virtually no motion is allowed in a normal knee; if significant movement does occur because of
an injured posterior cruciate ligament, this constitutes a positive posterior drawer sign.
A blow to the lateral aspect of the knee (not uncommon in football) may very well rupture
both the superficial and deep fibers of the medial collateral ligament. Because the latter are
adherent to the capsule, it and the attached medial meniscus may also be torn.
The lateral ligaments of the ankle are more frequently sprained than is the deltoid ligament.
A physician tests for the integrity of these ligaments by manually trying to move the foot in a way
that the intact ligament would resist. For example, the test for the anterior talofibular ligament is
for the examiner to place one hand on the front of the leg and then attempt to pull the foot
forward by pressure applied to the heel. If the foot can be pulled forward relative to the leg, this
is said to be a positive anterior drawer sign of the ankle, indicating a torn anterior talofibular
ligament. Q Angle
In clinical practice, the Q angle is estimated by angle between two lines: one between the
anterior superior iliac spine and the center of the patella, the other between the center of the
patella and the tibial tuberosity. So estimated, the Q angle averages 13ø in males and 16ø in
females. Lateral patellar dislocation occurs more often in women than men because of this
difference, a reflection of women's higher femoral bicondylar angles.
Plantaris
The very small plantaris muscle gives rise to a long thin tendon that is separate from the
Achilles tendon. It is a clinically significant structure for two reasons: (a) rupture of the plantaris
tendon is a highly painful condition, (2) the plantaris tendon may be removed to be used as a
graft for repair of badly damaged tendons in the hand.
Compartment Syndromes
The anterior tibial, peroneal, and deep posterior compartments of the calf are inexpansible.
Buildup of pressure within any of these compartments is a potentially serious problem because
the small veins in that compartment become compressed.
When this happens, the diminished capillary flow results in ischemia of the contained structures.
Nerves are most sensitive to such ischemia, and the first sign that compartmental pressure has
reached dangerous levels is tingling or diminished sensation in the areas of skin supplied by
intracompartmental nerves. Pain upon passive stretching of the involved muscles is also a sign
for concern. The compartmental ischemia leads to increased capillary permeability and further
swelling, so that the pressure buildup becomes increasingly worse, with resultant occlusion of
capillaries and, finally, arteries. If untreated all the compartmental contents will die. Muscles
killed in this way become fibrotic and shortened. Not only are they nonfunctional, but the
shortening results in deformities.
Muscles become swollen and tender after an unaccustomed period of strenuous use. If the
overuse involves muscles within inexpansible compartments, the pressure buildup may resolve
itself without damage to compartmental structures, or an exertional compartment syndrome may
develop. One example of this is anterior tibial syndrome, which may occur after a long walk by
an otherwise sedentary person. Anterior tibial syndrome (like any other compartment syndrome)
is accompanied by pain in the compartment. However, the first sign that intervention may be
necessary is malfunctioning of the deep peroneal nerve, revealed by tingling or diminished
sensation in the dorsal web of skin between the first and second toes.
Compartment syndromes may also arise following trauma (like a broken bone) that causes
bleeding into the compartment. A third cause of compartment syndrome is reperfusion injury.
When a structure is deprived of blood, the capillaries become more permeable. If blood flow is
suddenly returned, the structure so reperfused will swell. One must be on the lookout for
reperfusion compartment syndromes of the leg following surgical procedures that improve
circulation, or those that restrict circulation during the procedure itself. The general rule is that if
a limb has been ischemic for 6 hours, you should do a prophylactic fasciotomy prior to restoring
circulation. Obviously, if a limb has been ischemic for significantly more than six hours, it must
be amputated (see Warm Ischemia Time).
Medial Tibial Stress Syndrome (Shin
Splints)
The term "shin splints" has been applied to so many different conditions (incipient anterior
tibial syndrome, incipient deep posterior compartment syndrome, and stress fractures, among
others) that most clinicians now advise against its use. However, it seems that the majority of
persons who present with what they believe to be shin splints are actually suffering from a
condition more properly called medial tibial stress syndrome. This condition is characterized by
pain along the posteromedial border of the distal tibial shaft caused by running or other athletic
endeavor. Evidence is accumulating that it is caused by a periostitis in the vicinity of the
lowermost tibial attachment of the soleus and its fascia. This might explain why shin splints have
been associated with excessive subtalar pronation, since the soleus would be recruited more
strongly in an attempt to prevent this motion.
Varicose Veins
Varicose superficial veins of the lower limb are not an uncommon result of pregnancy, since
the enlarged uterus compresses the common iliac veins and thereby elevates venous pressure
within the lower limb.
Great Saphenous Vein
Probably everyone knows that the great saphenous vein has particular clinical significance
for coronary bypass surgery. Being long and easily located, it is resected so that segments of it
may be used as grafts extending from the ascending aorta to various coronary arteries beyond the
site of their occlusion. It also used for femoropopliteal bypass surgery (connecting the common
femoral artery to the popliteal artery so that blockage on the superficial femoral artery may be
bypassed). During femoropopliteal bypass, the great saphenous may be excised and turned
around so that the valves permit distal flow of blood, or it may be left in situ and all the valves
stripped out. If left in situ, its tributaries must be sutured so that arteriovenous fistulae do not
develop.
NOTE: For information on causes of injury to these nerves I
have relied heavily on the text Focal Peripheral Neuropathies by JD Stewart, 1993, Raven Press,
NY.
Femoral Nerve
The femoral nerve may be inadvertently cut during pelvic,
groin,
or hip surgeries. It may be stretched by a retractor during pelvic surgery. It may be compressed
against
the inguinal ligament during prolonged lithotomy position. Pelvic tumors, pelvic fractures,
anterior hip
dislocations, and penetrating injuries to the groin also place the nerve at risk. Motor tests require
the
patient to
extend the lower leg against resistance and, for the purpose of testing the rectus femoris and
iliopsoas, to flex the thigh against resistance.
Obturator Nerve
The anterior division of the obturator nerve is of particular clinical significance in the
symptomatic treatment of cerebral palsy. Children with this disorder may experience a severe
impairment of gait due to spastic medial rotation and adduction of the thigh. Transection of the
anterior division of the obturator nerve will paralyze gracilis, adductor longus, and adductor
brevis; such paralysis actually has a salutatory effect on locomotion. Elimination of spasticity in
the gracilis has the additional positive result of reducing the tendency of the knee to be held in a
partly flexed posture.
Like the femoral nerve, the obturator is not often injured. Intrapelvic tumors may compress
the obturator nerve. Sometimes the pressure exerted by the fetal head during parturition may
damage the maternal obturator nerve. Fracture of the superior pubic ramus, or hernia of bowel
through the obturator canal are other potential sources of injury. One tests for damage to the
obturator nerve by requiring the patient to adduct the thigh against resistance.
Superior Gluteal Nerve
The Trendelenburg test is described in Chapter 104. Another test for damage to the superior
gluteal nerve requires the patient to lie on his/her side and attempt to elevate the lower limb
against resistance.
Inferior Gluteal Nerve
The inferior gluteal nerve is tested by requiring the prone patient to flex the knee and then
raise the thigh off the examining table against resistance. The muscle should be palpated as the
test is performed. Flexion of the knee is necessary because it causes the hamstring muscles to
operate in unfavorable regions of their length-tension curves and, therefore, enables a purer test
of gluteus maximus strength.
Sciatic Nerve
Damage to the entire sciatic nerve may occur in major
traumatic injury to the buttock or thigh, fractures or dislocations of the hip, and during hip
surgery. Intrapelvic tumors and very poorly placed injections in the buttock can produce partial
injuries. Compression of the nerve can arise from sitting for a long time wedged in a toilet seat
(usually associated with inebriation), or in emaciated patients that lie supine on an operating table
for a long time, or during bicycling, or from prolonged sitting on one's thick wallet (usually
associated with being a professor). Paralysis of lower leg muscles supplied by both the common
peroneal and tibial nerves should cause one to think of damage to the sciatic, rather than separate
damage to its branches. Paralysis of the hamstrings is a sign of damage above the proximal thigh.
Some tests for motor function of the sciatic nerve are the same as those for its common
peroneal and tibial branches (see further on). However, assessing strength of knee flexion can
give an indication of the integrity of its supply to the hamstrings and short head of biceps
femoris. So that the examiner can distinguish weakness of knee flexion due to sartorius or
gracilis paralysis from that due to muscles innervated by the sciatic nerve, palpation of the
hamstrings is essential.
Tibial Nerve
The tibial nerve may be injured by wounds to the popliteal
fossa or back of the leg, fractures at the knee, or dislocations of the knee. It can be compressed by
a Baker's cyst, which is a fluid-filled pouch derived either from one of the bursae at the back of
the knee or from an outpocketing of synovial membrane through the posterior capsule of the
joint. Testing the motor functions of the tibial nerve is done by
requiring the patient to plantarflex the foot, invert the foot, and flex the toes against resistance.
Asking the patient to walk on his/her toes is another good test for the strength of the triceps
surae. Some physicians ask the patient to spread the toes apart in an attempt to assess the intrinsic
muscles of the foot, however, many of us perfect persons cannot perform this maneuver.
As stated in Chapter 108, the common peroneal nerve is the most frequently injured nerve of
the lower limb. In addition to the listed causes of injury, plaster
casts, or the supports used to hold up the legs in the lithotomy position, can also compress the
nerve. Signs of injury are a combination of those resulting from
malfunctioning of both the deep and superficial peroneal nerves.
Specific motor test of the superficial peroneal nerve requires the patient to evert the foot
against resistance; the strength of this motion is due far more to lateral compartment muscles
than to peroneus tertius.
Specific test of the deep peroneal requires the patient to dorsiflex the foot and toes against
resistance. Another test is to ask patient to walk on his or her heels; this requires strong anterior
tibial compartment muscles.
Common Femoral Artery
The ability to compress the common femoral artery against the head of the femur has
significance beyond taking the pulse of this vessel. Radiologists frequently use the common
femoral artery as a site to gain entry into the arterial system. Typically, a hypodermic needle is
inserted through the anterior and posterior walls of the vessel where it lies anterior to head of the
femur. The needle is partly withdrawn so its opening lies in the arterial lumen, then a guide wire
followed by a catheter are introduced into the vessel. Catheters inserted in this manner may be
passed superiorly into the aorta or its branches for the purpose of angiography or selective arterial
embolization. At the end of the procedure, when the catheter is withdrawn, bleeding from the
common femoral artery may be controlled by compressing it against the femoral head. If, by
mistake, the puncture needle is directed too obliquely upward, with the result that it enters the
common femoral artery proximal to the femoral head or, worse, enters the external iliac
artery, one is left with a hole in a vessel that has no posterior structure against which it can be
compressed. The result may a considerable hematoma in the proximal thigh and/or pelvis. On the
other hand, if the puncture is placed too far below the level of the femoral head, it may occur at a
site in the superficial femoral artery where this vessel lies anterior, not lateral, to the superficial
femoral vein. Then, because the standard procedure involves piercing the posterior wall of the
artery, the needle may be pushed into the vein, creating the risk that an arteriovenous fistula will
develop.
Sural Nerve
The location of the sural nerve posterior to the small saphenous vein behind the lateral
malleolus is a guide to its harvesting. It can be traced upward from this point and removed
virtually in its entirety to supply bridging segments during attempts to repair damage to more
important nerves of the body.
Uterine Cancer
It is generally true that pelvic organs drain to internal iliac nodes, but lymph from the fundus
of the uterus and uterine tubes may drain via channels that accompany ovarian vessels back to
lumbar nodes. As mentioned in Table 98, when the normal routes of uterine lymphatic drainage
become blocked, lymph may drain through channels that accompany the round ligament through
inguinal canal, and then to the superficial inguinal nodes. If the latter are sites of metastatic
uterine cancer, this is a bad sign because almost certainly intrapelvic nodes are also involved.
Tongue Cancer
Any region of the tongue near its midline will also send some lymph to the contralateral side.
The tip of the tongue drains to both right and left submental nodes, as well as directly to both
right and left jugulo-omohyoid nodes. Regions of the lower lip near the midline send lymph to
both ipsilateral and contralateral submental nodes. Consequently, paramedian cancer of the
tongue or lower lip is far more serious than cancer of their lateral edges, because of the potential
for metastases to both deep cervical chains.
Sampling Axillary Nodes for
Spread of Breast Cancer
Surgeons use a different terminology for naming groups of axillary nodes than do anatomists.
Surgeons use the term "central nodes" to refer to those in the vicinity of part 2 of the axillary
vein. More importantly, they often simply speak of level 1 nodes (pectoral, subscapular, lateral
axillary), level 2 nodes ("central"), and level 3 nodes (apical axillary). The lower the level, the
more likely is the node group to be a recipient of tumor spread (but spread to level 2 can occur
with negative level 1 nodes and, although unlikely, there can be positive level 3 nodes without
tumor detected in either levels 1 or 2).
Most surgeons accept that 75% of the lymph from the breast goes to the axillary nodes, while
25% goes to the parasternal nodes. Nonetheless, because studies have shown that only 5 - 8% of
the time is tumor found in the parasternal nodes but not the axillary nodes, the former are not
usually sampled.
Crossing near the floor of the axilla is the intercostobrachial nerve. It is often sacrificed
during dissections of axillary lymph nodes for sampling. This leaves the patient with numbness
on the posteromedial aspect of the upper arm. Also, in an axillary dissection, the surgeon should
look out for the thoracodorsal nerve, the nerve to serratus anterior, and the thoracodorsal artery.
Preservation of the latter is especially important because the latissimus dorsi may be used later
for breast reconstruction.
When sampling nodes along the axillary vein, those in the concavity are taken, but those on
the convexity are preserved. This is because breast lymph rarely goes to nodes on the convexity,
which mainly receive lymph from the upper limb. By preserving them, you minimize problems
with lymphatic drainage from the upper limb.
To reach apical axillary nodes (level 3), which are usually only removed if there is to be a
mastectomy, the surgeon will cut ("take down") the pectoralis minor at its origin in order to
improve exposure of the relevant region. Effort should be made to preserve the medial pectoral
nerve, which often pierces the pectoralis minor. If this nerve is cut, the sternocostal pectoralis
major becomes atrophic.
Surgical Nomenclature for Nodes Draining the
Lungs
Surgeons tend to use a nomenclature for lymph nodes draining the lungs that differs from
what you will find in most anatomy texts. The surgical nomenclature is as follows:
peribronchial nodes - lie along bronchi within the substance of a lung Iliac Node Dissection
When removing external iliac lymph nodes, the surgeon must be careful not to damage to the
genitofemoral nerve lying lateral to these nodes. When removing internal iliac nodes, it is the
obturator nerve that is in danger.
The
top of spinal cord segment T1 lies opposite top of vertebra T1.
The top of
spinal cord segment L1 lies opposite top of vertebra T11.
The top of
spinal cord segment S1 lies opposite top of vertebra L1.
(1) A
stethoscope placed in the supraclavicular fossa (i.e., just superior to medial third of the clavicle)
will hear the apical segment of upper lobe
.(2) A stethoscope placed on the back not far from the
vertebral column will hear (a) the upper lobe (posterior segment)
superior to the site where the spine of the scapula meets its vertebral border; (b) the superior segment of the lower lobe just
inferior to where the scapular spine meets its vertebral border; (c) the posterior basal segment of the lower lobe
medial to the inferior angle of the scapula. (3) A
stethoscope placed in the midaxillary line will hear (a) the upper
lobe above the 5th rib; (b) the lower
lobe (lateral basal segment) from the 5th to 8th ribs. (4) A
stethoscope placed on the front of the chest between the midclavicular line and the sternum will
hear (a) the upper lobe (anterior segment)
above the 4th costal cartilage (b) on
the right side, the middle lobe (medial segment) from the 4th to 6th costal cartilages.
Inguinal Femoral
MALES 58 indirect
29 direct
87 total 2
FEMALES 6.6 indirect
0.4 direct
7 total 4
A more detailed classification divides each of these four
segments into two, creating eight segments in total. If the patient has a tumor nodule confined to
one segment of the liver, that segment alone may be removed. However, the most common types
of partial liver resections are
1) left lateral, which is the
anatomist's left lobe
2) left medial, which
comprises the anatomist's quadrate and caudate lobes
3) right anterior, the anterior
part of the right lobe
4) right posterior, the posterior
part of the right lobe.
1) right lobectomy - removal of both
major segments of the right lobe
2) left lobectomy - removal of the left
medial and left lateral segments (i.e., caudate lobe, quadrate lobe, and the anatomist's left
lobe)
3) left lateral segmentectomy - removal
of the anatomist's left lobe
4) right trisegmentectomy - removal of
the right lobe (which has two major segments) and the left medial segment (caudate and quadrate
lobes)
1) strike a 256 or 512 Hz tuning fork and hold its tines about one inch from the
external auditory meatus for a few seconds;
2) move the stem of the tuning fork onto the
patients mastoid process for a few seconds;
3) ask the patient whether the sound was
louder in the front or the back.
If the patient reports that the front (i.e., air conduction)
sounded louder than the back (i.e., bone conduction), the test indicates that nothing is wrong with
the conductive mechanism - any hearing loss probably being sensorineural in origin. If the bone
conduction sounded louder than the air conduction, there is a significant likelihood of a problem
with the conductive mechanism.
As a result of these
anastomotic routes, if either the ulnar or radial artery is injured at the wrist, patients tolerate
ligation of the injured vessel very well. Does this mean you need not worry about damaging one
of these arteries during the course of another procedure?
(1) the superficial palmar arch, which is grossly visible as a
complete arch
less than 50% of the time (but some say is physiologically complete in a much higher percentage
of individuals); (2) the deep palmar arch,
which is grossly visible as a complete arch in almost everybody.
Very little motion is allowed in a normal knee. Some books say that more than 3 mm is
abnormal. If significant movement does occur because of an injured anterior cruciate ligament,
this constitutes a positive
anterior drawer sign. (Before using this test to gain information on the anterior cruciate
ligament, you should be sure that the tibia has not fallen posteriorly relative to the femoral
condyles
because of a torn posterior cruciate ligament. If it had, you would be able to pull it forward into
its normal position, but this would tell you nothing about the ACL.)
hilar nodes - lie around the mainstem bronchus within the root of a lung
subcarinal nodes - lie in the inferior angle of the tracheal bifurcation
paratracheal nodes - lie alongside the trachea
pretracheal nodes - lie in
front of the trachea
The standard route of lymphatic drainage from a lung
is then peribronchial —> hilar —> subcarinal —> paratracheal nodes. The right
lung drains almost entirely to right paratracheal nodes. The left upper lobe drains almost entirely
to left paratracheal nodes. The left lower lobe drains to both right and left sides. If there is
evidence of left lower lobe cancer, surgeons want to know if the
cancer has spread to the right paratracheal nodes, because such spread is a counterindication for
surgical treatment of the cancer. One way to get the necessary information is to perform a
mediastinoscopy. Some facilities have supplanted this with a PET (Positron Emission
Tomography) scan of the superior mediastinum, which is as sensitive, or more so, in revealing
tumor involvement of relevant nodes.
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