Borchers Andrea Ann (ed.) Handbook of Signs & Symptoms 2015

patient’s level of consciousness, using the Glasgow Coma Scale. Note decerebrate or decorticate posture. Examine the pupils for size, equality, and response to light. Check for signs of increased ICP

— increased blood pressure, increasing pulse pressure, and bradycardia.

Medical Causes

Brain stem infarction. Brain stem infarction causes absent doll’s eye sign with coma. It also causes limb paralysis, cranial nerve palsies (facial weakness, diplopia, blindness or visual field deficits, and nystagmus), bilateral cerebellar ataxia, variable sensory loss, a positive Babinski’s reflex, decerebrate posture, and muscle flaccidity.

Brain stem tumor. Absent doll’s eye sign accompanies coma in a brain stem tumor. This sign may be preceded by hemiparesis, nystagmus, extraocular nerve palsies, facial pain or sensory loss, facial paralysis, a diminished corneal reflex, tinnitus, hearing loss, dysphagia, drooling, vertigo, dizziness, ataxia, and vomiting.

EXAMINATION TIP Testing for Absent Doll’s Eye Sign

To evaluate the patient’s oculocephalic reflex, with the patient lying supine, hold her upper eyelids open and quickly (but gently) turn her head from side to side, noting eye movements with each head turn.

With absent doll’s eye sign, the eyes remain fixed in midposition.

Central midbrain infarction. Accompanying absent doll’s eye sign are coma, Weber’s syndrome (oculomotor palsy with contralateral hemiplegia), contralateral ataxic tremor, nystagmus, and pupillary abnormalities.

Pontine hemorrhage. Absent doll’s eye sign and coma develop within minutes with pontine hemorrhage, a life-threatening disorder. Other ominous signs — such as complete paralysis, decerebrate posture, a positive Babinski’s reflex, and small, reactive pupils — may rapidly progress to death.

Posterior fossa hematoma. A subdural hematoma at the posterior fossa typically causes absent doll’s eye sign and coma. These signs may be preceded by characteristic signs and symptoms, such as a headache, vomiting, drowsiness, confusion, unequal pupils, dysphagia, cranial nerve palsies, a stiff neck, and cerebellar ataxia.

Other Causes

Drugs. Barbiturates may produce severe central nervous system depression, resulting in coma and absent doll’s eye sign.

Special Considerations

Don’t attempt to elicit doll’s eye sign in a comatose patient with suspected cervical spine injury; doing so risks spinal cord damage. Instead, evaluate the oculovestibular reflex with the cold caloric test. Normally, instilling cold water in the ear causes the eyes to move slowly toward the irrigated ear. Cold caloric testing may also be done to confirm an absent doll’s eye sign.

Continue to monitor vital signs and neurologic status in the patient with an absent doll’s eye sign.

Patient Counseling

Explain to the patient’s family the underlying cause of the patient’s condition, and encourage questions they may have about treatment options.

Pediatric Pointers

Normally, doll’s eye sign isn’t present for the first 10 days after birth, and it may be irregular until age 2. After that, this sign reliably indicates brain stem function.

An absent doll’s eye sign in children may accompany coma associated with a head injury, near

drowning or suffocation, or brain stem astrocytoma.

Drooling

Drooling — the flow of saliva from the mouth — results from a failure to swallow or retain saliva or from excess salivation. It may stem from facial muscle paralysis or weakness that prevents mouth closure, from neuromuscular disorders or local pain that causes dysphagia or, less commonly, from the effects of drugs or toxins that induce salivation. Drooling may be scant or copious (up to 1 L daily) and may cause circumoral irritation. Because it signals an inability to handle secretions, drooling warns of potential aspiration.

History and Physical Examination

If you observe the patient drooling, first determine the amount. Is it scant or copious? When did it begin? Ask the patient if his pillow is wet in the morning. Also, inspect for circumoral irritation.

Then, explore associated signs and symptoms. Ask about sore throat and difficulty swallowing, chewing, speaking, or breathing. Have the patient describe pain or stiffness in the face and neck and muscle weakness in the face and extremities. Has he noticed mental status changes, such as drowsiness or agitation? Ask about changes in vision, hearing, and sense of taste. Also, ask about anorexia, weight loss, fatigue, nausea, vomiting, and altered bowel or bladder habits. Has the patient recently had a cold or other infection? Was he recently bitten by an animal or exposed to pesticides? Finally, obtain a complete drug history.

Next, perform a physical examination. Take the patient’s vital signs. Inspect for signs of facial paralysis or abnormal expression. Examine the mouth and neck for swelling, the throat for edema and redness, and the tonsils for exudate. Note foul breath odor. Examine the tongue for bilateral furrowing (trident tongue). Look for pallor and skin lesions and for frontal baldness. Carefully assess any bite or puncture marks.

Assess cranial nerves II through VII, IX, and X. Then, check pupillary size and response to light. Assess the patient’s speech. Evaluate muscle strength, and palpate for tenderness or atrophy. Also, palpate for lymphadenopathy, especially in the cervical area. Observe the patient’s ability to swallow, and assess his gag reflex. Test for poor balance, hyperreflexia, and a positive Babinski’s reflex. Also, assess sensory function for paresthesia.

Medical Causes

Bell’s palsy. With Bell’s palsy, drooling accompanies the gradual onset of facial hemiplegia. The affected side of the face sags and is expressionless, the nasolabial fold flattens, and the palpebral fissure (the distance between the upper and lower eyelids) widens. The patient usually complains of pain in or behind the ear. Other cardinal signs and symptoms include unilateral diminished or absent corneal reflex, decreased lacrimation, Bell’s phenomenon (upward deviation of the eye with attempt at lid closure), and partial loss of taste or abnormal taste sensation.

Esophageal tumor. With an esophageal tumor, copious and persistent drooling is typically preceded by weight loss and progressively severe dysphagia. Other signs and symptoms include substernal, back, or neck pain and blood-flecked regurgitation.

Ludwig’s angina. With Ludwig’s angina, moderate to copious drooling stems from dysphagia and local swelling of the floor of the mouth, causing tongue displacement. Submandibular swelling of the neck and signs of respiratory distress may also occur.

Myotonic dystrophy. Facial weakness and a sagging jaw account for constant drooling in this disorder. Other characteristic findings include myotonia (inability to relax a muscle after its contraction), muscle wasting, cataracts, testicular atrophy, frontal baldness, ptosis, and a nasal, monotone voice.

Peritonsillar abscess. A severe sore throat causes dysphagia with moderate to copious drooling in this abscess. Accompanying signs and symptoms are a high fever, rancid breath, and enlarged, reddened, edematous tonsils that may be covered by a soft, gray exudate. Palpation may reveal cervical lymphadenopathy.

Pesticide poisoning. Toxic effects of pesticides may include excess salivation with drooling. Other effects are diaphoresis, nausea and vomiting, involuntary urination and defecation, blurred vision, miosis, increased lacrimation, fasciculations, weakness, flaccid paralysis, signs of respiratory distress, and coma.

Rabies. When this acute central nervous system infection advances to the brain stem, it produces drooling, or “foaming at the mouth.” Drooling stems from excessive salivation, facial palsy, or extremely painful pharyngeal spasms that prohibit swallowing. Rabies is accompanied by hydrophobia in about 50% of cases. Seizures and hyperactive deep tendon reflexes may also occur before the patient develops generalized flaccid paralysis and coma.

Seizures (generalized). Generalized seizures are tonic-clonic muscular reactions that cause excessive salivation and frothing at the mouth accompanied by loss of consciousness and cyanosis. In the unresponsive postictal state, the patient may also drool.

Special Considerations

Be alert for aspiration in the drooling patient. Position him upright or on his side. Provide frequent mouth care, and suction as necessary to control drooling. Be prepared to perform a tracheostomy and intubation, to administer oxygen, or to execute an abdominal thrust.

Help the patient cope with drooling by providing a covered, opaque collecting jar to decrease odor and prevent possible transmission of infection. Keep tissues handy, and drape a towel across his chest at mealtime. Encourage oral hygiene. Also, teach the patient exercises to help strengthen facial muscles, if appropriate. Assist him with meticulous skin care, especially around the mouth and in the neck area, to prevent skin breakdown. Cornstarch may be placed on the neck to reduce the risk of maceration.

Patient Counseling

Explain to the patient his diagnosis and the treatment plan. Show the patient exercises to help strengthen facial muscles, if appropriate. Teach the patient good hygiene and skin care.

Pediatric Pointers

Normally, an infant can’t control saliva flow until about age 1, when muscular reflexes that initiate swallowing and lip closure mature. Salivation and drooling typically increase with teething, which begins at about the fifth month and continues until about age 2. Excessive salivation and drooling may

also occur in response to hunger or anticipation of feeding and in association with nausea.

Common causes of drooling include epiglottitis, retropharyngeal abscess, severe tonsillitis, stomatitis, herpetic lesions, esophageal atresia, cerebral palsy, mental deficiency, and drug withdrawal in neonates of addicted mothers. It may also result from a foreign body in the esophagus, causing dysphagia.

REFERENCES

Basic infection control and prevention plan for outpatient oncology settings. http://www.cdc.gov/hai/pdfs/guidelines/basic-infection- control-prevention-plan-2011.pdf. Atlanta, GA: Centers for Disease Control and Prevention, 2011.

Guide to infection prevention for outpatient settings: minimum expectations for safe care. http://www.cdc.gov/HAI/settings/outpatient/outpatient-care-guidelines.html. Updated July 2011. Atlanta, GA: Centers for Disease Control and Prevention, 2011.

Dysarthria

Dysarthria, poorly articulated speech, is characterized by slurring and labored, irregular rhythm. It may be accompanied by a nasal voice tone caused by palate weakness. Whether it occurs abruptly or gradually, dysarthria is usually evident in ordinary conversation. It’s confirmed by asking the patient to produce a few simple sounds and words, such as “ba,” “sh,” and “cat.” However, dysarthria is occasionally confused with aphasia, the loss of the ability to produce or comprehend speech.

Dysarthria results from damage to the brain stem that affects cranial nerves IX, X, or XII. Degenerative neurologic disorders and cerebellar disorders commonly cause dysarthria. In fact, dysarthria is a chief sign of olivopontocerebellar degeneration. It may also result from ill-fitting dentures.

EMERGENCY INTERVENTIONS

If the patient displays dysarthria, ask him about associated difficulty swallowing. Then, determine his respiratory rate and depth. Measure his vital capacity with a Wright respirometer, if available. Assess the patient’s blood pressure and heart rate. Usually, tachycardia, slightly increased blood pressure, and shortness of breath are early signs of respiratory muscle weakness.

Ensure a patent airway. Place the patient in Fowler’s position, and suction him if necessary. Administer oxygen, and keep emergency resuscitation equipment nearby. Anticipate intubation and mechanical ventilation in progressive respiratory muscle weakness. Withhold oral fluids in the patient with associated dysphagia.

If dysarthria isn’t accompanied by respiratory muscle weakness and dysphagia, continue to assess for other neurologic deficits. Compare muscle strength and tone in the limbs. Then, evaluate tactile sensation. Ask the patient about numbness or tingling. Test deep tendon reflexes (DTRs), and note gait ataxia. Assess cerebellar function by observing rapid alternating movement, which should be smooth and coordinated. Next, test visual fields, and ask about double vision. Check for signs of facial weakness such as ptosis. Finally, determine the patient’s level of consciousness (LOC) and mental status.

History and Physical Examination

Explore dysarthria completely. When did it begin? Has it gotten better? Speech improves with resolution of a transient ischemic attack, but not in a completed stroke. Ask if dysarthria worsens during the day. Then, obtain a drug and alcohol history. Also, ask about a history of seizures. Check dentures for a proper fit.

Medical Causes

Alcoholic cerebellar degeneration. Chronic alcohol intoxication can cause progressive degeneration of the cerebellum, the area of the brain that controls motor coordination. Alcoholic cerebellar degeneration commonly causes chronic, progressive dysarthria along with ataxia, diplopia, ophthalmoplegia, hypotension, and an altered mental status.

Amyotrophic lateral sclerosis (ALS). Dysarthria occurs when ALS affects the bulbar nuclei; it may worsen as the disease progresses. Other signs and symptoms include dysphagia; difficulty breathing; muscle atrophy and weakness, especially of the hands and feet; fasciculations; spasticity; hyperactive DTRs in the legs; and, occasionally, excessive drooling. Progressive bulbar palsy may cause crying spells or inappropriate laughter.

Basilar artery insufficiency. Basilar artery insufficiency causes random, brief episodes of bilateral brain stem dysfunction, resulting in dysarthria. Accompanying it are diplopia, vertigo, facial numbness, ataxia, paresis, and visual field loss, all of which last for minutes to hours.

Botulism. The hallmark of botulism is acute cranial nerve dysfunction causing dysarthria, dysphagia, diplopia, and ptosis. Early findings include a dry mouth, a sore throat, weakness, vomiting, and diarrhea. Later, descending weakness or paralysis of muscles in the extremities and trunk causes hyporeflexia and dyspnea.

Head trauma. Dysarthria can accompany a severe head trauma resulting from damage to the areas of the brain that control the muscles of speech and coordination. Associated signs and symptoms may include blurred or double vision, headache, loss of consciousness, severe headache that doesn’t go away, repeated nausea and vomiting, weakness in one side or area of the body, pallor, seizures or convulsions, or coma.

Mercury poisoning. Chronic mercury poisoning causes progressive dysarthria accompanied by weakness, fatigue, depression, lethargy, irritability, confusion, ataxia, and tremors.

Multiple sclerosis. When demyelination affects the brain stem and cerebellum, the patient displays dysarthria accompanied by nystagmus, blurred or double vision, dysphagia, ataxia, and intention tremor. Exacerbations and remissions of these signs and symptoms are common. Other findings include paresthesia, spasticity, intention tremor, hyperreflexia, muscle weakness or paralysis, constipation, emotional lability, and urinary frequency, urgency, and incontinence.

Myasthenia gravis. Myasthenia gravis is a neuromuscular disorder that causes dysarthria associated with a nasal voice tone. Typically, the dysarthria worsens during the day and may temporarily improve with short rest periods. Other findings include dysphagia, drooling, facial weakness, diplopia, ptosis, dyspnea, and muscle weakness.

Olivopontocerebellar degeneration. Dysarthria, a major sign, accompanies cerebellar ataxia and spasticity.

Parkinson’s disease. Parkinson’s disease produces dysarthria and a monotone voice. It also produces muscle rigidity, bradykinesia, involuntary tremor usually beginning in the fingers,

difficulty walking, muscle weakness, and a stooped posture. Other findings include masklike facies, dysphagia, and occasionally drooling.

Shy-Drager syndrome. Marked by chronic orthostatic hypotension, Shy-Drager syndrome eventually causes dysarthria as well as cerebellar ataxia, bradykinesia, masklike facies, dementia, impotence and, possibly, a stooped posture and incontinence.

Stroke (brain stem). A brain stem stroke is characterized by bulbar palsy, resulting in the triad of dysarthria, dysphonia, and dysphagia. Dysarthria is most severe at its onset; it may lessen or disappear with rehabilitation and training. Other findings include facial weakness, diplopia, hemiparesis, spasticity, drooling, dyspnea, and a decreased LOC.

Stroke (cerebral). A massive bilateral stroke causes pseudobulbar palsy. Bilateral weakness produces dysarthria that’s most severe at onset. This sign is accompanied by dysphagia, drooling, dysphonia, bilateral hemianopsia, and aphasia. Sensory loss, spasticity, and hyperreflexia may also occur.

Other Causes

Drugs. Dysarthria can occur when the anticonvulsant dosage is too high. Ingestion of large doses of barbiturates may also cause dysarthria.

Special Considerations

Encourage the patient with dysarthria to speak slowly so that he can be understood. Give him time to express himself, and encourage him to use gestures. Dysarthria usually requires consultation with a speech pathologist.

Patient Counseling

Explain different ways in which the patient can communicate. Encourage the patient to express his feelings.

Pediatric Pointers

Dysarthria in children usually results from brain stem glioma, a slow-growing tumor that primarily affects children. It may also result from cerebral palsy.

Dysarthria may be difficult to detect, especially in an infant or a young child who hasn’t perfected speech. Make sure to look for other neurologic deficits as well. Encourage speech in a child with dysarthria; a child’s potential for rehabilitation is typically greater than an adult’s.

REFERENCES

Fattal-Valevski, A., Nissan, N., Kramer, U., & Constantini, S. (2012). Seizures as the clinical presenting symptom in children with brain tumors. Journal of Child Neurology, 28(3), 292–296.

Porter, K., McCathy, B., Freels, S., Kim, Y., & Davies, F. (2010). Prevalence estimates for primary brain tumors in the United States by age, gender, behavior, and histology. Journal of Neurology and Oncology, 12, 520–570.

Dysmenorrhea

Dysmenorrhea — painful menstruation — affects more than 50% of menstruating women; in fact, it’s the leading cause of lost time from school and work among women of childbearing age. Dysmenorrhea may involve sharp, intermittent pain or dull, aching pain. It’s usually characterized by mild to severe cramping or colicky pain in the pelvis or lower abdomen that may radiate to the thighs and lower sacrum. This pain may precede menstruation by several days or may accompany it. The pain gradually subsides as bleeding tapers off.

Dysmenorrhea may be idiopathic, as in premenstrual syndrome (PMS) and primary dysmenorrhea. It commonly results from endometriosis and other pelvic disorders. It may also result from structural abnormalities such as an imperforate hymen. Stress and poor health may aggravate dysmenorrhea; rest and mild exercise may relieve it.

History and Physical Examination

If the patient complains of dysmenorrhea, have her describe it fully. Is it intermittent or continuous? Sharp, cramping, or aching? Ask where the pain is located and whether it’s bilateral. When does the pain begin and end, and when is it severe? Does it radiate to the back? How long has she been experiencing the pain? If it’s a recent complaint, obtain a human chorionic gonadotropin level to determine if the patient is or was pregnant, because miscarriage can cause painful bleeding. Explore associated signs and symptoms, such as nausea and vomiting, altered bowel or urinary habits, bloating, water retention, pelvic or rectal pressure, and unusual fatigue, irritability, or depression.

Then, obtain a menstrual and sexual history. Ask the patient if her menstrual flow is heavy or scant. Have her describe vaginal discharge between menses. Does she experience pain during sexual intercourse? Does it occur with menses? Find out what relieves her cramps. Does she take pain medication? Is it effective? Note her method of contraception, and ask about a history of pelvic infection. Does she have signs and symptoms of urinary system obstruction, such as pyuria, urine retention, or incontinence? Determine how she copes with stress. Determine her risk of sexually transmitted diseases.

Next, perform a focused physical examination. Take the patient’s vital signs, noting fever and accompanying chills. Inspect the abdomen for distention, and palpate for tenderness and masses. Note costovertebral angle tenderness.

Medical Causes

Adenomyosis. In adenomyosis, endometrial tissue invades the myometrium, resulting in severe dysmenorrhea with pain radiating to the back or rectum, menorrhagia, and a symmetrically enlarged, globular uterus that’s usually softer on palpation than a uterine myoma.

Cervical stenosis. Cervical stenosis is a structural disorder that causes dysmenorrhea and scant or absent menstrual flow.

Endometriosis. Endometriosis typically produces steady, aching pain that begins before menses and peaks at the height of menstrual flow; however, the pain may also occur between menstrual periods. The pain may arise at the endometrial deposit site or may radiate to the perineum or rectum. Associated signs and symptoms include premenstrual spotting, dyspareunia, infertility, nausea and vomiting, painful defecation, and rectal bleeding and hematuria during menses. A tender, fixed adnexal mass is usually palpable on bimanual examination.

Pelvic inflammatory disease. Chronic infection produces dysmenorrhea accompanied by a fever; malaise; foul-smelling, purulent vaginal discharge; menorrhagia; dyspareunia; severe

abdominal pain; nausea and vomiting; and diarrhea. A pelvic examination may reveal cervical motion tenderness and bilateral adnexal tenderness.

PMS. The cramping pain of PMS usually begins with menstrual flow and persists for several hours or days, diminishing with decreasing flow. Common associated effects precede menses by several days to 2 weeks: abdominal bloating, breast tenderness, palpitations, diaphoresis, flushing, depression, and irritability. Other findings include nausea, vomiting, diarrhea, and a headache. Because PMS usually follows an ovulatory cycle, it rarely occurs during the first 12 months of menses, which may be anovulatory.

Primary (idiopathic) dysmenorrhea. Increased prostaglandin secretion intensifies uterine contractions, apparently causing mild to severe spasmodic cramping pain in the lower abdomen, which radiates to the sacrum and inner thighs. The cramping abdominal pain peaks a few hours before menses. Patients may also experience nausea and vomiting, fatigue, diarrhea, and a headache.

Uterine leiomyomas. If these tumors twist or degenerate after circulatory occlusion or infection or if the uterus contracts in an attempt to expel them, the tumors may cause constant or intermittent lower abdominal pain that worsens with menses. Associated signs and symptoms include backache, constipation, menorrhagia, and urinary frequency or retention. Palpation may reveal the tumor mass and an enlarged uterus. The tumors are almost always nontender.

Other Causes

Intrauterine devices (IUDs). IUDs may cause severe cramping and heavy menstrual flow.

Special Considerations

In the past, a woman with dysmenorrhea was considered neurotic. Although current research suggests that prostaglandins contribute to this symptom, old attitudes persist. Encourage the patient to view dysmenorrhea as a medical problem — not as a sign of maladjustment. (See Relief for Dysmenorrhea.)

Relief for Dysmenorrhea

To relieve cramping and other symptoms caused by primary dysmenorrhea or an intrauterine device, the patient may receive a prostaglandin inhibitor, such as aspirin, ibuprofen, indomethacin, or naproxen. These nonsteroidal anti-inflammatory drugs block prostaglandin synthesis early in the inflammatory reaction, thereby inhibiting prostaglandin action at receptor sites. These drugs also have analgesic and antipyretic effects.

Make sure that you and the patient are informed about the adverse effects and cautions associated with these drugs.

ADVERSE EFFECTS

Alert the patient to possible adverse effects of prostaglandin inhibitors. Central nervous system effects include dizziness, a headache, and vision disturbances. GI effects include nausea, vomiting, heartburn, and diarrhea. Advise the patient to take the drug with milk or after meals to

reduce gastric irritation.

CONTRAINDICATIONS

Because prostaglandin inhibitors are potentially teratogenic, make sure to rule out the possibility of pregnancy before starting therapy. Advise the patient who suspects she’s pregnant to delay therapy until menses begins.

OTHER CAUTIONS

If the patient has cardiac decompensation, hypertension, renal dysfunction, an ulcer, or a coagulation defect (and is receiving ongoing anticoagulant therapy), use caution when administering a prostaglandin inhibitor. Because a patient who’s hypersensitive to aspirin may also be hypersensitive to other prostaglandin inhibitors, watch for signs of gastric ulceration and bleeding.

Patient Counseling

Once a diagnosis is established, explain the cause of the patient’s dysmenorrhea and her treatment options.

Pediatric Pointers

Dysmenorrhea is rare during the first year of menstruation, before the menstrual cycle becomes ovulatory. However, the incidence of dysmenorrhea is generally higher among adolescents than older women. Teach the adolescent about dysmenorrhea. Dispel myths about it, and inform her that it’s a common medical problem. Encourage good hygiene, nutrition, and exercise.

REFERENCES

Acién, P., & Acién, M. I. (2011). The history of female genital tract malformation classifications and proposal of an updated system.

Human Reproduction Update, 17, 693–705.

Acién, P., Acién, M., Fernández, F., Mayol, M. J., & Aranda I. (2010). The cavitated accessory uterine mass. A Mullerian anomaly in women with an otherwise normal uterus. Obstetrics and Gynecology, 116, 1101–1109.

Dyspepsia

Dyspepsia, also called indigestion, refers to an uncomfortable fullness after meals that’s associated with nausea, belching, heartburn and, possibly, cramping and abdominal distention. Frequently aggravated by spicy, fatty, or high-fiber foods and by excess caffeine intake, dyspepsia without other pathology indicates impaired digestive function.

Dyspepsia is caused by GI disorders and, to a lesser extent, by cardiac, pulmonary, and renal disorders and the effects of drugs. It apparently results when altered gastric secretions lead to excess stomach acidity. This symptom may also result from emotional upset, eating too much or too fast, or improper chewing. It usually occurs a few hours after eating and lasts for a variable period. Its severity depends on the amount and type of food eaten and on GI motility. Additional food or an antacid may relieve the discomfort. (See Dyspepsia: Common Causes and Associated Findings, page 256.)