S
Scalp Tenderness
The cause of scalp tenderness can best be recalled utilizing the mnemonic MINT.
M—Mental disorders such as pseudoneurosis can be associated with diffuse scalp tenderness.
I—Inflammation would bring to mind herpes zoster, pediculosis, tinea capitis, cellulitis, an infected sebaceous cyst, and impetigo.
N—Neurologic disorders associated with a tender scalp include temporal arteritis, occipital nerve entrapment, trigeminal neuralgia, and neoplasms that involve the cranium and meninges (i.e., meningioma).
T—Trauma would suggest scalp contusions, fractures, and hematomas.
Approach to the Diagnosis
Most skin conditions should be easily diagnosed by inspection. A Wood lamp inspection would assist in the diagnosis of tinea capitis. A potassium hydroxide (KOH) preparation of scraping may be necessary. Skin biopsy will diagnose other skin disorders. A sedimentation rate and biopsy of the superficial temporal artery will diagnose temporal arteritis. If occipital nerve entrapment is suspected, a nerve block should be done to confirm the diagnosis. X-rays of the skull and a magnetic resonance imaging (MRI) may be necessary, but a neurologist should be consulted before ordering expensive diagnostic tests.
Scoliosis
The many causes of this deformity of the spine can be recalled by applying the mnemonic MINTS.
M—Malformation prompts the recall of osteogenesis imperfecta, congenital hemivertebra, Marfan syndrome, and arthrogryposis. It should also suggest a short leg syndrome.
I—Inflammation suggests tuberculosis and fungal disease of the spine. The I should also remind one of idiopathic scoliosis, responsible for 80% of the cases.
N—Neurologic disorders that may cause scoliosis include syringomyelia, poliomyelitis, muscular dystrophy, and Friedreich ataxia.
T—Trauma should facilitate the recall of thoracolumbar sprain, compression, fracture, and herniated disk. It should also remind one of thoracoplasty and other surgical causes.
S—Systemic diseases associated with scoliosis include Paget disease, pulmonary fibrosis, and Ehlers–Danlos syndrome.
Unfortunately, rickets and osteoporosis will not be recalled with this mnemonic.
Approach to the Diagnosis
To diagnose scoliosis, have the patient bend over, and there will be asymmetry in the height of the scapulae (Adam test). Most causes of scoliosis will require only an x-ray of the spine to clarify the diagnosis. An orthopedic consult should be obtained before any further workup. Be sure to measure the leg length. If there are objective neurologic signs, a neurologist should be consulted. A bone scan, MRI, or computed tomography (CT) scan may be necessary in difficult diagnostic problems.
Other Useful Tests
Complete blood count (CBC) (osteomyelitis)
Sedimentation rate (osteomyelitis, tuberculosis)
Arthritis panel (rheumatoid spondylitis)
Human leukocyte antigen (HLA) B-27 (rheumatoid spondylitis)
Pulmonary function tests (pulmonary fibrosis)
Bone survey (Paget disease)
Electromyogram (EMG) (muscular dystrophy)
Sensory Loss
Anatomy is the key to developing a list of possible causes of sensory loss. Tracing the nerve endings in the face or extremities to the brain we have the peripheral nerves, nerve plexus, nerve roots, spinal cord, brain stem, and cerebrum. Now cross-index these structures with the various etiologies (vascular, inflammatory, neoplastic, etc.), and you have an excellent list of possibilities.
Peripheral nerve—This structure should prompt the recall of carpal tunnel syndrome, ulnar entrapment in the hand or elbow, and diffuse peripheral neuropathy (diabetes, nutritional disorders, etc.).
Nerve plexus—This structure should suggest brachial plexus neuritis, sciatic neuritis, brachial plexus compression by a Pancoast tumor or thoracic outlet syndrome, or lumbosacral plexus compression by a pelvic tumor.
Nerve roots—This would facilitate the recall of space-occupying lesions of the spinal cord (e.g., tumor, abscess) and fractures of the spine compressing the root. It would also help to recall tabes dorsalis, herniated disk disease, osteoarthritis, cervical spondylosis, spinal stenosis, and spondylolisthesis. Guillain–Barré syndrome affects the nerve causing sensory loss.
Spinal cord—Lesions in the spinal cord that cause sensory loss include space-occupying lesions, syringomyelia,
pernicious anemia, multiple sclerosis, and Friedreich ataxia, acute traumatic or viral transverse myelitis, and anterior spinal artery occlusion may also cause sensory loss.
Brain stem—This should prompt the recall of brain stem tumors, abscess and hematomas, multiple sclerosis, syringobulbia, encephalomyelitis, basilar artery, thrombosis, posterior inferior cerebellar artery occlusion, and neurosyphilis. Do not forget the thalamic syndrome.
Cerebrum—Space-occupying lesions of the cerebrum, cerebral hemorrhage, thrombosis, or embolism should be considered here. Encephalitis, toxic encephalopathy, and multiple sclerosis are less likely to cause significant sensory loss if the lesions are confined to the cerebral cortex.
Approach to the Diagnosis
The neurologic examination will help to determine the location of the lesion. Peripheral neuropathy presents with diffuse distal loss of sensation to all modalities. Nerve root involvement will present with sensory loss in a radicular distribution; spinal cord involvement will be associated with a sensory level. Sensory loss to pain and temperature on one side of the face and the opposite side of the body is typical of posterior inferior cerebellar artery occlusion. If there is only loss of vibratory and position sense, look for pernicious anemia or a cerebral tumor.
The workup for peripheral neuropathy and entrapment syndromes will include nerve conduction velocity (NCV) tests and EMGs. An MRI and CT scan can be done if brain and spinal cord pathology is suspected, but a neurologist should be consulted first. If a cerebrovascular disease is suspected, Doppler ultrasound and magnetic resonance angiography (MRA) may be necessary as well. Ultimately, four-vessel cerebral angiography may be indicated.
Other Useful Tests
CBC (pernicious anemia)
Chemistry panel (e.g., diabetic neuropathy)
Fluorescent treponemal antibody absorption (FTA–ABS) test (neurosyphilis)
Serum B12 (pernicious anemia)
Blood lead level (lead neuropathy)
Spinal tap (neurosyphilis, multiple sclerosis, Guillain–Barré syndrome)
Urine porphobilinogen (porphyria)
Antinuclear antibody (ANA) (collagen disorders)
Shoulder Pain
The differential diagnosis of shoulder pain, like other forms of pain, is best established by anatomy, working from the outside in Table 51. Beginning with the skin, one immediately thinks of cellulitis and herpes zoster. The muscles and tendons come next, and epidemic myalgia and the myalgias secondary to many infectious diseases lead the list. However, trichinosis, dermatomyositis, fibromyositis, and trauma must always be considered. Proceeding to the blood vessels, keep in mind thrombophlebitis, Buerger disease, vascular occlusion from periarteritis nodosa, and other forms of vasculitis.
Inflammation of the bursae is probably the most common cause of shoulder pain. This should be considered traumatic because in most cases the torn ligamentum teres rubs the bursa and causes the inflammation. Interestingly enough, aside from gout, the bursae are rarely involved in other conditions. Biceps tendonitis needs to be considered here as well. The shoulder joint itself is also a frequent site of pain. Osteoarthritis, rheumatoid arthritis, gout, lupus, and various bacteria all may involve this joint, but dislocation of the shoulder, fractures, and frozen shoulder should be considered. Inflammation of the acromioclavicular joint is usually traumatic in origin. If the bone is the site of pain, there is usually a fracture involved. Osteomyelitis and metastatic tumors, however, ought to be ruled out.
Neurologic causes are not the last to be considered just because anatomically they come last. The brachial plexus may be compressed by a cervical rib, a large scalenus anticus or pectoralis muscle, or the clavicle (costoclavicular syndrome). When the cervical sympathetics are irritated or disrupted, a shoulder–hand syndrome develops. The cervical spine is the site or origin of shoulder pain in cervical spondylosis, spinal cord tumors, tuberculosis and syphilitic osteomyelitis, ruptured disks, or fractured vertebrae.
It would be a grave error to omit the systemic causes of shoulder pain. Thus, coronary insufficiency, cholecystitis, Pancoast tumors, pleurisy, and subdiaphragmatic abscesses should be ruled out.
Approach to the Diagnosis
The approach to ruling out various causes is most often clinical, provided x-rays of the shoulder and cervical spine have negative findings. If a torn rotator cuff is strongly suspected, an MRI or arthrogram should be done. In the classical case of subacromial bursitis (recently called impingement syndrome), in which passive movement is much less restricted than active movement and a point of maximum tenderness can easily be located, lidocaine and steroid injections into the bursa (at the point of maximum tenderness) may be done without x-rays. Cervical root blocks, stellate ganglion blocks for shoulder–hand syndrome, and aspiration and injection of the shoulder joint with lidocaine and steroids may also be useful in establishing the cause. Adson maneuvers will help to establish the diagnosis of scalenus anticus syndrome, but the clinician must bear in mind that there are many false positives for this test and the job is not finished until tests for pectoralis minor and costoclavicular compression are done. The history will help to diagnose systemic causes, but checking for dermatomal hyperalgesia or hypalgesia and other sensory changes will be most helpful in diagnosing disease of the cervical spine. Remember that a negative cervical spine x-ray does not rule out a herniated disk. If the pain is increased by pressure on the top of the head or by coughing and sneezing, then a herniated disk must be ruled out by an MRI.
Table 51 Shoulder Pain | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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|
 Shoulder pain, systemic causes. |
Other Useful Tests
CBC
Sedimentation rate (collagen disease, infection)
Chemistry panel (gout, pseudogout)
Arthritis panel
ANA analysis (collagen disease)
Exercise tolerance test (coronary insufficiency)
Nerve blocks (radiculopathy)
EMG (radiculopathy)
Bone scan (small fractures, osteomyelitis)
Arteriogram (thoracic outlet syndrome)
Chest x-ray (Pancoast tumor)
 Shoulder pain, local causes. |
Case Presentation #79
A 52-year-old white man complained of increasing stiffness and pain in his left shoulder for the past year. Physical examination revealed diffuse tenderness of the shoulder joint and limited abduction, extension, and rotation of the shoulder joint on both active and passive motion.
Question #1. Utilizing your knowledge of anatomy, what are the diagnostic possibilities at this point?
Further questioning revealed that he had a myocardial infarction 1 year ago.
Question #2. What is your diagnosis now?
(See Appendix B for the answers.)
Skin Discharge
The differential diagnosis of a weeping skin lesion is covered in the section on rash (see page 362), but certain conditions should be mentioned here. In all nonbloody discharges, infection (usually bacterial) is the most prominent etiology; Staphylococcus and Streptococcus organisms are the most common offenders in the skin. In working up from the smallest organism to the largest, however, one will not forget the weeping blisters of herpes zoster and simplex, smallpox, and chickenpox; the ulcers and bullae of syphilis; the draining sinuses and ulcers of actinomycosis, sporotrichosis, and other cutaneous mycosis; and the weeping ulcers of cutaneous leishmaniasis and amebiasis cutis. There are many more—but decidedly rare—infections in all these categories. By recalling the anatomy of the skin, the infected hair follicles and sebaceous cysts (furunculosis and carbuncles), infected apocrine glands (hidradenitis suppurativa), and inflamed sweat glands (miliariasis) come to mind. Finally, using the mnemonic VITAMIN one will recall the following:
V—Vascular conditions of the skin (e.g., postphlebitic ulcers) that cause a discharge
I—Inflammatory conditions of a noninfectious nature (e.g., erythema multiforme, pyoderma gangrenosum, and pemphigus) that produce weeping. Specific infections are listed above.
T—Traumatic conditions such as third-degree burns
A—Autoimmune and allergic disorders associated with weeping vesicles and ulcers, such as periarteritis nodosa and contact dermatitis
M—Malformations such as bronchial clefts and urachal sinus tracts
I—Intoxicating lesions such as a vesicular or bullous drug eruption
N—Neoplasms such as basal cell carcinoma and mycosis fungoides that produce weeping ulcers
Approach to the Diagnosis
Smear and culture of the lesion are most important, although a skin biopsy is sometimes necessary. Serologic tests or cultures on special media are necessary to diagnose fungi and parasites.
Other Useful Tests
CBC (systemic infection)
Sedimentation rate (systemic infection, collagen disease)
Tuberculin test
Venereal disease research laboratory (VDRL) test (primary or secondary syphilis)
X-ray of area involved (abscess, osteomyelitis)
ANA analysis (collagen disease)
Skin test and serology for fungi
Biopsy
Muscle biopsy (collagen disease, trichinosis)
Skin Mass
Masses of the skin may be better termed nodules if they are larger than 0.5 cm and are not just neoplastic in origin. The term VINDICATE serves as a useful mnemonic to recall the important skin masses. When the physician is considering the cause of a mass in any part of the body, he or she must include a possible skin mass in the differential. Therefore, although I have limited the discussion of skin lesions in other sections, the reader should turn to this section if the mass is thought to originate in the skin.
V—Vascular lesions include cavernous hemangiomas, varicose veins, hemorrhages from scurvy or coagulation disorders, and emboli from subacute bacterial endocarditis (SBE) (Osler nodules).
I—Inflammatory masses include caruncles, furuncles, warts, condyloma latum and acuminatum, molluscum contagiosum, tuberculomas, gummas, and granulomas from coccidioidomycosis, sporotrichosis, and other fungi.
N—Neoplasms constitute the largest group of skin masses. The important ones to remember are basal and squamous cell carcinomas, melanomas, nevi, sarcomas, metastatic nodules, Kaposi sarcomas, lipomas, neurofibromatosis, dermoid cysts, leiomyomas, lymphangiomas, and mycosis fungoides. Leukemic infiltration and Hodgkin disease may cause skin nodules or plaques.
D—Degenerative diseases do not produce any skin masses worthy of mention but do predispose to pressure sores. Heberden nodes of osteoarthritis should be considered here.
I—Intoxication suggests the lesions of bromism.
C—Cystic lesions of the skin include sebaceous cysts, epithelial cysts, and dermoid cysts. Congenital lesions such as eosinophilic granulomas of the skin, tuberous sclerosis, and neurofibromatosis should not be overlooked.
A—Autoimmune disease includes the aneurysms of periarteritis nodosa, rheumatoid and rheumatic nodules, localized lupus or amyloidosis, and Weber–Christian disease.
T—Trauma induces contusions and edema of the skin.
E—Endocrine and metabolic diseases that cause skin masses are diabetes mellitus (abscesses, necrobiosis lipoidica diabeticorum), hyperthyroidism (pretibial
myxedema, acromegaly [tufting of the distal phalanges]), gout (tophaceous deposits), hyperlipemia and hypercholesterolemia with multiple xanthomas, and calcinosis in hypercalcemic states.
Approach to the Diagnosis
A biopsy or excision is the best approach to the diagnosis. If a systemic disease is suspected because of a lesion, appropriate studies for these are listed below.
Other Useful Tests
CBC (abscess)
Sedimentation rate (infection)
Incision and drainage (I&D) and culture of exudate
Tuberculin test
Skin tests and serology for fungi
Kveim test (sarcoidosis)
ANA analysis (collagen diseases)
Frei test (lymphogranuloma venereum)
Muscle biopsy (collagen disease)
Skin Pigmentation and other Pigmentary Changes
To recall the causes of a diffuse pigmentation of the skin, one might simply visualize various organs of the body where a cause may originate. The adrenal gland brings to mind Addison disease, the liver suggests hemochromatosis, the thyroid suggests hyperthyroidism, the uterus suggests pregnancy (more likely to cause chloasma), and the ovaries suggest the chloasma of menopause and melasma of chronic birth control use. The liver is also the cause of jaundice (see page 271). The skin itself is the site of melanotic carcinoma, which in occasional cases causes a deeply pigmented skin, and tinea versicolor, which produces a patchy yellow-brown pigmented area over the trunk. Any dermatitis that takes a long time to heal may cause a patchy pigmentation. Cushing syndrome and ectopic adrenocorticotropic hormone (ACTH) production by a malignancy (especially a carcinoma of the lung) should be ruled out.
Other causes of patchy pigmentation are the café au lait spots of neurofibromatosis, stasis dermatitis from chronic thrombophlebitis and varicose veins, the pigmentation of the dorsal surfaces of the hands and face in pellagra, carcinoid syndrome, porphyria, and Gaucher disease. Ochronosis produces a bluish black or bluish brown pigment of the sclera, ears, skin, and nails. Vitiligo (idiopathic type) suggests a patchy pigmentation but is really a depigmentation. Acanthosis nigricans characterized by pigmented lesions of the skin flexures, neck, and nipples is often associated with malignancies.
Approach to the Diagnosis
The workup for diffuse pigmentation involves ruling out hemochromatosis, hepatobiliary disease, and Addison disease with appropriate tests for these disorders (see Appendix A) and using the expertise of a dermatologist in the cases of patchy pigmentation.
Other Useful Tests
Wood lamp (tinea versicolor)
Serum electrolytes (Addison disease)
Serum cortisol (Addison disease)
Serum iron and iron-binding capacity (hemochromatosis)
Urine porphyrins and porphobilinogen (porphyria)
Urine melanin (melanoma)
Urine for homogentisic acid (ochronosis)
Free thyroxine (FT4) level (hyperthyroidism)
Serum follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels (menopause)
Skin biopsy
Serum ACTH (ectopic ACTH production)
Skin Thickening
Diffuse thickening of the skin is typical of myxedema, whereas thickening of the skin of the hands and face is also found in scleroderma and hereditary osteoarthropathy. Thickening of the skin of the lower legs is found in lymphedema and carcinoid syndrome. If the thickening is primarily localized to the face, consider the possibility of Chagas disease and porphyria cutanea tarda.
Approach to the Diagnosis
If myxedema is suspected, a thyroid-stimulating hormone (TSH) test and FT4 test can be ordered. If scleroderma is suspected, order an ANA, anticentromere antibody titer, or a skin biopsy. Urine for porphyrins will help to identify porphyria. Carcinoid syndrome can be identified by a urine test for 5-hydroxyindole acetic acid (HIAA).
Skin Ulcers
The differential diagnosis of skin ulcers may be approached with anatomy as the basic science, particularly if the ulcer is on one of the legs. Beginning with the skin itself and applying the mnemonic MINT, one can recall the following:
M—Malformations suggest sickle cell anemia.
I—Infection suggests syphilis, chancroid, lymphogranuloma, actinomycosis, tularemia, and other infections.
N—Neoplasms suggest basal cell and squamous cell carcinomas.
T—Trauma suggests third-degree burns, unsutured lacerations, and pressure sores (bedsores).
Now visualize the structure beneath the skin. The arteries suggest arteriosclerosis and diabetic ulcers; the veins prompt the recall of varicose ulcers or postphlebitic ulcers; the nerves suggest trophic ulcers of tabes dorsalis, syringomyelia, and peripheral neuropathy; and the bone suggests osteomyelitis (e.g., staphylococcal, tuberculosis) that penetrates the skin.
 Skin mass. |
 Skin pigmentation and other pigmentary changes. |
In contrast to the method described above, a somewhat more complete differential diagnosis may be developed with the mnemonic VINDICATE.
V—Vascular disorders suggest peripheral arteriosclerosis, diabetic ulcers, and varicose ulcers.
I—Infections suggest syphilis, chancroid, yaws, and tularemia.
N—Neoplasm suggests carcinomas, sarcomas, and mycosis fungoides.
D—Degenerative disorders suggest ulcers associated with degenerative and deficiency diseases, such as peripheral neuropathy, syringomyelia, muscle atrophy, and peroneal muscular atrophy.
I—Intoxication suggests the ulcer of chronic dermatitis.
C—Congenital recalls the ulcers of sickle cell anemias.
A—Autoimmune brings to mind the ulcers of periarteritis nodosa, pyoderma gangrenosum (associated with ulcerative colitis and Crohn disease), and Stevens–Johnson syndrome.
T—Trauma identifies ulcers of burns and radiation secondary to unhealed lacerations and decubitus ulcers.
E—Endocrine disorders suggest diabetic ulcers.
Infections can be further elucidated by working from the smallest organism to the largest. Beginning with viruses, herpes simplex, and lymphogranuloma is suggested. Bacteria remind one of tuberculosis, tularemia, leprosy, and cutaneous diphtheria. Spirochetes suggest syphilis and yaws. Parasites identify leishmaniasis and amebiasis cutis. The rest are fungal and include actinomycosis, blastomycosis, sporotrichosis, and cryptococcosis.
