Face Mass

To develop a list of possible causes of a face mass, let us turn to anatomy. The face is composed of skin, subcutaneous tissues, muscle, bone, teeth, the sinuses, salivary glands, arteries, veins, and nerves. Applying the mnemonic VINDICATE to each one of these structures, we can come up with an excellent list of possibilities.

  • Skin and subcutaneous tissues—Carbuncles, cellulitis, sebaceous cysts; lipomas, carcinomas, angioneurotic edema, and so forth.

  • Muscle—Myositis, myomas, hypertrophy

  • Bone—Osteomas, metastatic tumor, multiple myelomas, osteomyelitis

  • Teeth—Dental abscess, neoplasm

  • Sinuses—Wegener midline granuloma, mucormycosis, neoplasm

  • Salivary glands—Mumps, tumors, calculus, Mikulicz syndrome, Sjögren syndrome

  • Arteries and veins—Hemangiomas, arteriovenous fistula

  • Nerves—Neuroma, neurofibromatosis

Approach to the Diagnosis

If infection is suspected, smears and cultures of exudates should be done. X-rays of the skull, sinuses, and jaw may be helpful. A computed tomography (CT) scan will be more definitive. If neoplasm or granuloma is suspected, a biopsy or excision will be necessary. If there is still doubt about the etiology, an oral surgeon or otolaryngologist should be consulted.

Other Useful Tests

  • Complete blood count (CBC) (infection)

  • Sedimentation rate (abscess, osteomyelitis)

  • Chest x-ray (tuberculosis, Wegener granulomatosis)

  • Chemistry panel (multiple myeloma)

  • Blood cultures (osteomyelitis)

  • X-ray of the teeth (dental abscess)

  • Trial of epinephrine and antihistamines (angioneurotic edema)

  • Sialography (salivary gland duct calculus)

  • Cytoplasmic antineutrophil cytoplasmic antibody (C–ANCA) test (Wegener granulomatosis)

  • Rheumatoid arthritis (RA) test, anti-Ro (SSA)–antibodies (Sjögren syndrome)

Facial Pain

Visualize the structures of the face in a systematic fashion to develop a differential diagnosis of facial pain. With the skin, herpes zoster and carbuncles come to mind. Next, the internal maxillary artery suggests histamine cephalalgia and arteritis, just as the nerves suggest trigeminal neuralgia, herpes zoster, and the atypical facial neuralgias encountered in multiple sclerosis, Wallenberg syndrome, and other central nervous system conditions. These will almost invariably be associated with other neurologic findings. With reference to the bones, one should recall temporomandibular joint (TMJ) syndrome, sinusitis, and dental caries or abscesses. An elongated styloid process may cause facial pain (Eagle syndrome). Disorders of the eye that cause face pain are included in the section on eye pain (see page 164).

Of course, one could apply the mnemonic VINDICATE to the differential diagnosis and come up with an extensive list. Thus, V—Vascular conditions suggest histamine cephalalgia; I—Inflammatory conditions suggest herpes zoster, sinusitis, and dental abscesses; and N—Neoplasms suggest Schmincke tumors, carcinoma of the tongue, and so forth. This procedure, however, is more involved than is necessary.

Approach to the Diagnosis

The approach to the diagnosis of face pain includes a careful history and physical examination with a good neurologic examination. The sinuses are transilluminated, and x-rays may be performed. The teeth and occlusion are examined carefully and possibly x-rayed. A histamine test may be indicated to rule out histamine cephalalgia. The busy physician may want to refer the patient to a neurologist immediately, but this will obviously take away the challenge.

Other Useful Tests

  • Therapeutic trial of sumatriptan (migraine)

  • Therapeutic trial of carbamazepine (Tegretol) (trigeminal neuralgia)

  • Temporal artery compression (migraine)

  • Sedimentation rate (temporal arteritis)

  • X-rays of the TMJ (TMJ syndrome)

  • CT scan of the brain (tumors)

  • CT scan of the sinuses (sinusitis)

  • Nasopharyngoscopy

  • Magnetic resonance imaging (MRI) of the TMJ (TMJ syndrome)

  • Spinal fluid analysis (multiple sclerosis)

Facial pain.

Facial Paralysis

A facial palsy is usually considered to be Bell palsy and it frequently is. Nevertheless, the clinician who begins treatment without ruling out other possibilities will eventually get burned. Anatomy is the key to recalling these possibilities before the patient leaves the office. Follow the facial nerve from its origin along its pathway to its termination, and all the causes should come to mind.

Origin: Diseases of the brain and brainstem are considered here. They are usually distinguished from Bell palsy by the presence of other neurologic findings. The mnemonic ANITA will help recall them in an organized fashion.

  • A—Arterial diseases include aneurysms, emboli, thromboses, and hemorrhages. Occlusion of the posterior inferior cerebellar artery will cause a peripheral facial palsy, but it can easily be distinguished from Bell palsy by the
    presence of a Horner syndrome, hoarseness, ataxia, and crossed hemianalgesia.

  • N—Neoplasms include gliomas and the cerebellopontine angle tumor or acoustic neuroma.

  • I—Inflammation suggests neurosyphilis, tuberculosis, brain abscess, and encephalitis.

  • T—Trauma helps recall skull fractures and epidural and subdural hematomas.

  • A—Autoimmune disease suggests multiple sclerosis, the collagen diseases, and early Guillain–Barré syndrome.

Facial paralysis.

Pathway: The facial nerve has a long pathway, and along that path, it can be destroyed by the following:

  • A—Arterial aneurysms

  • N—Neoplasms such as acoustic neuromas and parotid gland tumors

  • I—Inflammatory conditions like herpes zoster (Ramsey–Hunt syndrome), petrositis, mastoiditis, and cholesteatomas

  • T—Trauma such as basilar skull fractures and otologic surgery

  • A—Autoimmune disease such as Bell palsy, or uveoparotid fever

Termination: The site of termination of the facial nerve should suggest myasthenia gravis, muscular dystrophy, and facial hemiatrophy. These rarely present with an isolated facial palsy.

Approach to the Diagnosis

The clinical picture will frequently help to determine the cause of facial paralysis. Peripheral facial palsy as occurs in Bell palsy involves the forehead muscles and there is difficulty in closing the eyelid, whereas central facial palsy involves the face and lips and there is often associated hemiplegia or monoplegia. When there is exclusively a peripheral facial palsy without hearing loss or other neurologic signs, Bell palsy should be strongly suspected, although diabetes and myasthenia gravis need to be excluded. A bilateral peripheral nerve palsy should make one consider Guillain–Barré syndrome as well as Lyme disease; be on the lookout for paralysis of the extremities as well. Bilateral facial palsy is also seen in myotonic dystrophy and myasthenia gravis. A “Bell palsy” with hearing loss and an aural discharge should prompt consideration of mastoiditis and petrositis. If there is hearing loss without a discharge, the possibility of an acoustic neuroma or cholesteatoma must be entertained. The association of a central facial palsy with hemiplegia brings up a host of possibilities including subdural hematoma, brain abscess, brain tumor, and cerebrovascular accident. The workup of these conditions is considered on page 218.

If the patient has clinical Bell palsy, one could start a therapy without a workup, but it is wise to get an x-ray of the skull and mastoids to rule out mastoiditis and petrositis and a glucose tolerance test to rule out diabetes.

An acetylcholine receptor antibody titer or Tensilon test would only be ordered if the palsy were intermittent or there were other cranial nerve signs. If a middle ear infection or acoustic neuroma is suspected, the patient needs x-rays of the mastoids and petrous bones and a CT scan or MRI of the brain and auditory canal.

Other Useful Tests

  • CBC (ear infection)

  • Sedimentation rate (ear infection)

  • Venereal disease research laboratory (VDRL) test (neurosyphilis)

  • Cultures of ear discharge (otitis)

  • Audiogram and caloric tests (petrositis, acoustic neuroma)

  • Posterior fossa myelogram (acoustic neuroma)

  • Electromyogram (EMG) (Bell palsy)

  • Lyme disease antibody titer (Lyme disease)

  • Blood lead level (lead neuropathy)

  • Spinal tap (Guillain–Barré syndrome)

  • Serologic tests (enzyme-linked immunosorbent assay [ELISA]) for Lyme disease

Facies, Abnormal

A list of possible causes of abnormal facies can best be arrived at by thinking of the endocrine, cardiovascular, nervous, and skeletal systems.

  • Endocrine system: This would bring to mind the coarse facial features of myxedema and cretinism, the proptosis of hyperthyroidism, the moon face of Cushing syndrome, and the square protruding jaw of acromegaly. It would also suggest the Peter Pan face of hypopituitarism.

  • Cardiovascular system: This should prompt the recall of the malar flush in mitral stenosis and the cyanosis of congenital heart disease. Facial edema is seen in superior vena cava syndrome and nephritis.

  • Nervous system: This should suggest the masked face of Parkinsonism, the hatchet-shaped face of myotonic dystrophy, the snarl of myasthenia gravis, and the drawing of the face to one side in Bell palsy with flattening of the nasolabial fold. It should also suggest the expressionless face and often drooling mouth of bulbar and pseudobulbar palsy and sarcastic smile of patients with tetanus.

  • Skeletal system: This would bring to mind the protruding forehead of Paget disease and the wide separation of the eyes in hypertelorism.

Aside from these disorders it is well to recall the flushing of the face in alcoholism, Cushing syndrome, carcinoid syndrome, and menopause as well as the waxy nonwrinkled face of scleroderma and the oriental appearance of the face in mongolism.

Approach to the Diagnosis

Obviously, the workup of abnormal facies will depend on what disease is suggested by the facial appearance combined with other abnormalities of the physical and neurologic examination. A careful history will be helpful in many cases.

Failure to Thrive

Failure to thrive is germane to the pediatric patient who is not growing adequately or fails to gain weight and appears emaciated. The physiologic model of intake, absorption, transport, and utilization will help develop a differential diagnosis.

  • Intake: Intake of food may be impaired by social conditions of poverty, malnutrition, and child abuse. It may also be impaired by chronic anxiety and depression or other psychiatric disorders. Finally, the patient may not eat because of a neurologic disorder such as microcephaly, hydrocephalus, cerebral palsy, or other disorders associated with mental retardation.

  • Absorption: Absorption of food may be impaired by malabsorption syndrome and fibrocystic disease.

  • Transport: This topic brings to mind chronic anemia and congenital heart disease especially when associated with hypoxemia.

  • Utilization: Utilization of food is impaired in diabetes mellitus, hypothyroidism, pituitary insufficiency, galactosemia, and uremia.

Several chronic infectious diseases are associated with failure to thrive. The child may also come from an abnormal gestation where the mother suffered alcoholism, drug abuse, or chronic illness.

Approach to the Diagnosis

Routine diagnostic workup should include a CBC, sedimentation rate, urinalysis, urine culture, chemistry panel, sweat test, stool for quantitative fat, chest x-ray, and electrocardiogram (ECG). Bone age x-rays are helpful in determining growth retardation. At this point, it is helpful to consult a pediatrician before ordering expensive diagnostic tests. When studies are negative, consider constitutional growth delay as the cause.

Failure to thrive.

Other Useful Tests

  • D-xylose absorption test (malabsorption syndrome)

  • Stool for ova and parasites (intestinal parasites)

  • Serum growth hormone (pituitary insufficiency)

  • Somatomedin-C level (pituitary insufficiency)

  • Overnight dexamethasone suppression test (adrenogenital syndrome)

  • Thyroid profile (myxedema)

  • CT scan of the brain (hydrocephalus, etc.)

  • MRI of the brain (hydrocephalus)

  • Neurology consult

  • Orthopedic consult

  • Endocrinology consult

  • Buccal smear for Barr bodies (Turner syndrome)

  • Karyotyping (Turner syndrome)


This sign is generally considered pathognomonic for anterior horn cell or root disease. It may occur, however, in certain cases of peripheral neuropathy, in electrolyte disturbances, and in myasthenia gravis, especially under treatment. It is also found in healthy states, most commonly in the twitching of the orbicularis oculi muscle from nervous tension or eyestrain. Fasciculations must be distinguished from fibrillations that are not visible, are detected only with EMG, and are caused by muscle disease. The causes can easily be recalled by visualizing the anterior horn cells and nerves and applying the mnemonic VINDICATE to this area.

  • V—Vascular conditions include anterior spinal artery occlusion and intermittent claudication from peripheral vascular disease.

  • I—Inflammatory diseases include poliomyelitis, viral encephalomyelitis, tetanus, syphilis, and diphtheria.

  • N—Neoplasm suggests intramedullary tumors of the cord such as ependymomas, and extramedullary tumors such as meningioma, Hodgkin lymphoma, metastatic carcinoma, and multiple myeloma must be considered.

  • D—Degenerative diseases are the most important causes of fasciculations. They include progressive spinal muscular atrophy, amyotrophic lateral sclerosis, Werdnig–Hoffmann disease, and syringomyelia.

  • I—Intoxication includes lead poisoning and alcoholism.

  • C—Congenital disorders suggest Werdnig–Hoffmann disease, spondylolisthesis, and other anomalies of the spinal cord that may compress the anterior horn and roots.

  • A—Autoimmune disorders recall transverse myelitis, myasthenia gravis (under treatment), periarteritis nodosa, and Guillain–Barré syndrome.

  • T—Trauma suggests herniated discs and fractures that compress the anterior horn or roots.

  • E—Endocrine and metabolic diseases include hypoparathyroidism and other causes of tetany, magnesium deficiency and other electrolyte disturbances, diabetic myelopathy, and hypothyroid myopathy (more commonly the cause of fibrillations which can only be detected by EMG).

Approach to the Diagnosis

Deciding on the cause of fasciculations will usually be based on other neurologic symptoms and signs. Muscular atrophy without sensory changes suggests progressive muscular atrophy, whereas atrophy and fasciculations with sensory changes suggest syringomyelia, peripheral neuropathy, and root compression (e.g., a herniated disc). Treatable neurologic disorders should be considered first. Thus, x-rays of the spine, spinal fluid analysis, and MRI should be performed to rule out a space-occupying lesion. EMG is useful in detecting which level is involved and in following the progress of the disease. Serum electrolytes, calcium, phosphorus, and magnesium levels are useful in selected disorders.

Other Useful Tests

  • Blood lead level (lead poisoning)

  • Glucose tolerance test (diabetes mellitus)

  • Serum protein electrophoresis (polyclonal gammopathy)

  • Antinuclear antibody (ANA) analysis (collagen disease)

  • Nerve conduction velocity (NCV) test (peripheral neuropathy)

  • Free thyroxine and sensitive thyroid-stimulating hormone (S-TSH) levels (hypothyroid myopathy)

  • Acetylcholine receptor antibody titer (myasthenia gravis)

  • CT scan of the thoracic or lumbar spine (space-occupying lesion)

  • MRI of the cervical, thoracic, or lumbar spine (space-occupying lesion)

  • Neurology consult

  • Muscle biopsy


The differential diagnosis of fever is best developed using physiology first and anatomy second.

  • Physiology: Increased heat in the body is caused by increased production or decreased elimination or dysfunction of the thermoregulatory system in the brain. Increased production of heat occurs in conditions with increased metabolic rate such as hyperthyroidism, pheochromocytomas, and malignant neoplasms. Poor elimination of heat may occur in congestive heart failure (CHF) (poor circulation through the skin) and conditions where the sweat glands are absent (congenital) or poorly functioning (heat stroke). Most cases of fever are caused by the effect of toxins on the thermoregulatory centers in the brain. These toxins may be exogenous from drugs, bacteria (endotoxins), parasites, fungi, rickettsiae, and virus particles, or they may be endogenous from tissue injury (trauma) and breakdown (carcinomas, leukemia, infarctions, and autoimmune disease).

  • Anatomy: With the etiologies suggested by the mnemonic VINDICATE, one can apply anatomy and the various organ systems and make a useful chart (see Table 28). The infections should be divided into the systemic diseases that affect more than one organ, such as typhoid, brucellosis, tuberculosis, syphilis, acquired immunodeficiency syndrome (AIDS), leptospirosis, Lyme disease, and bacterial endocarditis, and the localized diseases that usually affect the same specific organ, such as infectious hepatitis, subacute thyroiditis, pneumococcal pneumonia, and cholera. It is wise to divide the localized infectious diseases into the “itises” (e.g., pneumonitis, hepatitis, and prostatitis) and the abscesses (dental abscess, empyema, perinephric abscess, liver abscess, and subdiaphragmatic abscess).

Also, when the physician attempts to recall the specific infections, he or she can group them into six categories beginning with the smallest organism and working up to the largest as follows: viruses, rickettsiae, bacteria, spirochetes, fungi, and parasites. Endogenous toxins released by infarctions of various organs form another convenient group. Finally, the most common neoplasms to cause fever (by tissue breakdown) are illustrated on page 172.

Table 28 Fever

Only gold members can continue reading. Log In or Register to continue

You may also need

Sep 23, 2018 | Posted by in CRITICAL CARE | Comments Off on F
Premium Wordpress Themes by UFO Themes