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

Worsening hypoxia produces anxiety, tachycardia, and mental sluggishness.

Airway obstruction. Acute upper airway obstruction can be life threatening — fortunately, most obstructions are subacute or chronic. Typically, this disorder increases accessory muscle use. Its most telling sign, however, is inspiratory stridor. Associated signs and symptoms include dyspnea, tachypnea, gasping, wheezing, coughing, drooling, intercostal retractions, cyanosis, and tachycardia.

Amyotrophic lateral sclerosis. Typically, this progressive motor neuron disorder affects the diaphragm more than the accessory muscles. As a result, increased accessory muscle use is characteristic. Other signs and symptoms include fasciculations, muscle atrophy and weakness, spasticity, bilateral Babinski’s reflex, and hyperactive deep tendon reflexes. Incoordination makes carrying out routine activities difficult for the patient. Associated signs and symptoms include impaired speech, difficulty chewing or swallowing and breathing, urinary frequency and urgency and, occasionally, choking and excessive drooling. (Note: Other neuromuscular disorders may produce similar signs and symptoms.) Although the patient’s mental status remains intact, his poor prognosis may cause periodic depression.

Asthma. During acute asthma attacks, the patient usually displays increased accessory muscle use. Accompanying it are severe dyspnea, tachypnea, wheezing, a productive cough, nasal flaring, and cyanosis. Auscultation reveals faint or possibly absent breath sounds, musical crackles, and rhonchi. Other signs and symptoms include tachycardia, diaphoresis, and apprehension caused by air hunger. Chronic asthma may also cause barrel chest.

Chronic bronchitis. With chronic bronchitis, a form of COPD, increased accessory muscle use may be chronic and is preceded by a productive cough and exertional dyspnea. Chronic bronchitis is accompanied by wheezing, basal crackles, tachypnea, jugular vein distention, prolonged expiration, barrel chest, and clubbing. Cyanosis and weight gain from edema account for the characteristic label of “blue bloater.” A low-grade fever may occur with secondary infection.

Emphysema. Increased accessory muscle use occurs with progressive exertional dyspnea and a minimally productive cough in this form of COPD. Sometimes called a pink puffer, the patient will display pursed-lip breathing and tachypnea. Associated signs and symptoms include peripheral cyanosis, anorexia, weight loss, malaise, barrel chest, and clubbing. Auscultation reveals distant heart sounds; percussion detects hyperresonance.

Pneumonia. Bacterial pneumonia usually produces increased accessory muscle use. Initially, this infection produces a sudden high fever with chills. Its associated signs and symptoms include chest pain, a productive cough, dyspnea, tachypnea, tachycardia, expiratory grunting, cyanosis, diaphoresis, and fine crackles.

Pulmonary edema. With acute pulmonary edema, increased accessory muscle use is accompanied by dyspnea, tachypnea, orthopnea, crepitant crackles, wheezing, and a cough with pink, frothy sputum. Other findings include restlessness, tachycardia, ventricular gallop, and cool, clammy, cyanotic skin.

Pulmonary embolism. Although signs and symptoms vary with the size, number, and location of the emboli, pulmonary embolism is a life-threatening disorder that may cause increased accessory muscle use. Typically, it produces dyspnea and tachypnea that may be accompanied by pleuritic or substernal chest pain. Other signs and symptoms include restlessness, anxiety, tachycardia, a productive cough, a low-grade fever and, with a large embolus, hemoptysis, cyanosis, syncope, jugular vein distention, scattered crackles, and focal wheezing.

Spinal cord injury. Increased accessory muscle use may occur, depending on the location and severity of the injury. An injury below L1 typically doesn’t affect the diaphragm or accessory muscles, whereas an injury between C3 and C5 affects the upper respiratory muscles and diaphragm, causing increased accessory muscle use.

Associated signs and symptoms of spinal cord injury include unilateral or bilateral Babinski’s reflex, hyperactive deep tendon reflexes, spasticity, and variable or total loss of pain and temperature sensation, proprioception, and motor function. Horner’s syndrome (unilateral ptosis, pupillary constriction, facial anhidrosis) may occur with lower cervical cord injury.

Thoracic injury. Increased accessory muscle use may occur, depending on the type and extent of injury. Associated signs and symptoms of this potentially life-threatening injury include an obvious chest wound or bruising, chest pain, dyspnea, cyanosis, and agitation. Signs of shock, such as tachycardia and hypotension, occur with significant blood loss.

Other Causes

Diagnostic tests and treatments. Pulmonary function tests (PFTs), incentive spirometry, and intermittent positive-pressure breathing can increase accessory muscle use.

Special Considerations

If the patient is alert, elevate the head of the bed to make his breathing as easy as possible. Encourage him to get plenty of rest and to drink plenty of fluids to liquefy secretions. Administer oxygen. Prepare him for such tests as PFTs, chest X-rays, lung scans, arterial blood gas analysis, complete blood count, and sputum culture.

If appropriate, stress how smoking endangers the patient’s health, and refer him to an organized program to stop smoking. Also, teach him how to prevent infection. Explain the purpose of prescribed drugs, such as bronchodilators and mucolytics, and make sure he knows their dosage and schedule.

Patient Counseling

Teach the patient relaxation techniques to reduce his apprehension, pursed-lip, diaphragmatic breathing to ease the work of breathing (for patients with chronic lung disorders) and coughing and deep breathing exercises to keep airways clear. Explain measures to prevent infection and how to take prescribed drugs, and provide resources for quitting smoking.

Pediatric Pointers

Because an infant or child tires sooner than an adult, respiratory distress can more rapidly precipitate respiratory failure. Upper airway obstruction — caused by edema, bronchospasm, or a foreign object

— usually produces respiratory distress and increased accessory muscle use. Disorders associated with airway obstruction include acute epiglottiditis, croup, pertussis, cystic fibrosis, and asthma. Supraventricular, intercostal, or abdominal retractions indicate accessory muscle use.

Geriatric Pointers

Because of age-related loss of elasticity in the rib cage, accessory muscle use may be part of the older person’s normal breathing pattern.

REFERENCES

Groth, S. S., & Andrade, R. S. (2010). Diaphragm plication for eventration or paralysis: A review of the literature , Annals of Thoracic Surgery, 89(6), S2146–S2150.

Weiss, C., Witt, T., Grau, S., & Tonn, J. C. (2011). Hemidiaphragmatic paralysis with recurrent lung infections due to degenerative motor root compression of C3 and C4. Acta Neurochirurgica, 153(3), 597–599.

Agitation

(See Also Anxiety)

Agitation refers to a state of hyperarousal, increased tension, and irritability that can lead to confusion, hyperactivity, and overt hostility. Agitation can result from a toxic (poisons), metabolic, or infectious cause; brain injury; or a psychiatric disorder. It can also result from pain, fever, anxiety, drug use and withdrawal, hypersensitivity reactions, and various disorders. It can arise gradually or suddenly and last for minutes or months. Whether it’s mild or severe, agitation worsens with increased fever, pain, stress, or external stimuli.

Agitation alone merely signals a change in the patient’s condition. However, it’s a useful indicator of a developing disorder. Obtaining a good history is critical to determining the underlying cause of agitation.

History and Physical Examination

Determine the severity of the patient’s agitation by examining the number and quality of agitationinduced behaviors, such as emotional lability, confusion, memory loss, hyperactivity, and hostility. Obtain a history from the patient or a family member, including diet, known allergies, and use of herbal medicine.

Ask if the patient is being treated for any illnesses. Has he had any recent infections, trauma, stress, or changes in sleep patterns? Ask the patient about prescribed or over-the-counter drug use, including supplements and herbal medicines. Check for signs of drug abuse, such as needle tracks and dilated pupils. Ask about alcohol intake. Obtain the patient’s baseline vital signs and neurologic status for future comparison.

Medical Causes

Alcohol withdrawal syndrome. Mild to severe agitation occurs in alcohol withdrawal syndrome, along with hyperactivity, tremors, and anxiety. With delirium, the potentially lifethreatening stage of alcohol withdrawal, severe agitation accompanies hallucinations, insomnia, diaphoresis, and a depressed mood. The patient’s pulse rate and temperature rise as withdrawal progresses; status epilepticus, cardiac exhaustion, and shock can occur.

Anxiety. Anxiety produces varying degrees of agitation. The patient may be unaware of his anxiety or may complain of it without knowing its cause. Other findings include nausea, vomiting, diarrhea, cool and clammy skin, frontal headache, back pain, insomnia, depression, and tremors.

Dementia. Mild to severe agitation can result from many common syndromes, such as Alzheimer’s and Huntington’s diseases. The patient may display a decrease in memory, attention

span, problem-solving ability, and alertness. Hypoactivity, wandering behavior, hallucinations, aphasia, and insomnia may also occur.

Drug withdrawal syndrome. Mild to severe agitation occurs in drug withdrawal syndrome. Related findings vary with the drug, but include anxiety, abdominal cramps, diaphoresis, and anorexia. With opioid or barbiturate withdrawal, a decreased level of consciousness (LOC), seizures, and elevated blood pressure, heart rate, and respiratory rate can also occur.

Hepatic encephalopathy. Agitation occurs only with fulminating encephalopathy. Other findings include drowsiness, stupor, fetor hepaticus, asterixis, and hyperreflexia.

Hypersensitivity reaction. Moderate to severe agitation appears, possibly as the first sign of a reaction. Depending on the severity of the reaction, agitation may be accompanied by urticaria, pruritus, and facial and dependent edema.

With anaphylactic shock, a potentially life-threatening reaction, agitation occurs rapidly along with apprehension, urticaria or diffuse erythema, warm and moist skin, paresthesia, pruritus, edema, dyspnea, wheezing, stridor, hypotension, and tachycardia. Abdominal cramps, vomiting, and diarrhea can also occur.

Hypoxemia. Beginning as restlessness, agitation rapidly worsens. The patient may be confused and have impaired judgment and motor coordination. He may also have headaches, tachycardia, tachypnea, dyspnea, and cyanosis.

Increased intracranial pressure (ICP). Agitation usually precedes other early signs and symptoms, such as headache, nausea, and vomiting. Increased ICP produces respiratory changes, such as Cheyne-Stokes, cluster, ataxic, or apneustic breathing; sluggish, nonreactive, or unequal pupils; widening pulse pressure; tachycardia; a decreased LOC; seizures; and motor changes such as decerebrate or decorticate posture.

Post-head trauma syndrome. Shortly after, or even years after injury, mild to severe agitation develops, characterized by disorientation, loss of concentration, angry outbursts, and emotional lability. Other findings include fatigue, wandering behavior, and poor judgment.

Vitamin B6 deficiency. Agitation can range from mild to severe. Other effects include seizures, peripheral paresthesia, and dermatitis. Oculogyric crisis may also occur.

Other Causes

Drugs. Mild to moderate agitation, which is commonly dose related, develops as an adverse reaction to central nervous system stimulants — especially appetite suppressants, such as amphetamines and amphetamine-like drugs, and sympathomimetics, such as ephedrine, caffeine, and theophylline.

Radiographic contrast media. Reaction to the contrast medium injected during various diagnostic tests produces moderate to severe agitation along with other signs of hypersensitivity.

Special Considerations

Because agitation can be an early sign of many different disorders, continue to monitor the patient’s vital signs and neurologic status while the cause is being determined. Eliminate stressors, which can increase agitation. Provide adequate lighting, maintain a calm environment, and allow the patient ample time to sleep. Ensure a balanced diet, and provide vitamin supplements and hydration.

Remain calm, nonjudgmental, and nonargumentative. Use restraints sparingly because they tend to

increase agitation. If appropriate, prepare the patient for diagnostic tests, such as a computed tomography scan, skull X-rays, magnetic resonance imaging, and blood studies.

Patient Counseling

Reassure the patient, and orient him to the procedures and routines of the unit. Provide emotional support and a quiet environment. Explain stress reduction measures.

Pediatric Pointers

A common sign in children, agitation accompanies the expected childhood diseases as well as more severe disorders that can lead to brain damage: hyperbilirubinemia, phenylketonuria, vitamin A deficiency, hepatitis, frontal lobe syndrome, increased ICP, and lead poisoning. In neonates, agitation can stem from alcohol or drug withdrawal if the mother abused these substances.

When evaluating an agitated child, remember to use words that he can understand and to look for nonverbal clues. For instance, if you suspect that pain is causing agitation, ask him to tell you where it hurts, but make sure to watch for other indicators, such as wincing, crying, or moving away.

Geriatric Pointers

Any deviation from an older person’s usual activities or rituals may provoke anxiety or agitation. Any environmental change, such as a transfer to a nursing home or a visit from a stranger in the patient’s home, may trigger a need for treatment.

REFERENCES

Altshuler, J., & Spoelhof, B. (2013). Pain, agitation, delirium, and neuromuscular blockade: A review of basic pharmacology, assessment, and monitoring. Critical Care Nursing Quarterly, 36(4), 356–369.

Baker, S., & Weant, K. (2012). Management of acute agitation in the emergency department, Advanced Emergency Nursing Journal, 34(4), 306–318.

Amenorrhea

The absence of menstrual flow, amenorrhea can be classified as primary or secondary. With primary amenorrhea, menstruation fails to begin before age 16. With secondary amenorrhea, it begins at an appropriate age, but later ceases for 3 or more months in the absence of normal physiologic causes, such as pregnancy, lactation, or menopause.

Pathologic amenorrhea results from anovulation or physical obstruction to menstrual outflow, such as from an imperforate hymen, cervical stenosis, or intrauterine adhesions. Anovulation itself may result from hormonal imbalance, debilitating disease, stress or emotional disturbances, strenuous exercise, malnutrition, obesity, or anatomic abnormalities, such as a congenital absence of the ovaries or uterus. Amenorrhea may also result from drug or hormonal treatments. (See Understanding Disruptions in Menstruation, pages 36 and 37.)

Understanding Disruptions in Menstruation

A disruption at any point in the menstrual cycle can produce amenorrhea, as illustrated in the

flowchart below.

History and Physical Examination

Begin by determining whether the amenorrhea is primary or secondary. If it’s primary, ask the patient at what age her mother first menstruated because age of menarche is fairly consistent in families. Form an overall impression of the patient’s physical, mental, and emotional development because these factors as well as heredity and climate may delay menarche until after age 16.

If menstruation began at an appropriate age but has since ceased, determine the frequency and duration of the patient’s previous menses. Ask her about the onset and nature of any changes in her normal menstrual pattern, and determine the date of her last period. Find out if she has noticed any related signs, such as breast swelling or weight changes.

Determine when the patient last had a physical examination. Review her health history, noting especially any long-term illnesses, such as anemia, or use of hormonal contraceptives. Ask about exercise habits, especially running, and whether she experiences stress on the job or at home. Probe the patient’s eating habits, including the number and size of daily meals and snacks, and ask if she has gained weight recently.

Observe her appearance for secondary sex characteristics or signs of virilization. If you’re responsible for performing a pelvic examination, check for anatomic aberrations of the outflow tract, such as cervical adhesions, fibroids, or an imperforate hymen.

Medical Causes

Adrenal tumor. Amenorrhea may be accompanied by acne, thinning scalp hair, hirsutism, increased blood pressure, truncal obesity, and psychotic changes. Asymmetrical ovarian enlargement in conjunction with the rapid onset of virilizing signs is usually indicative of an adrenal tumor.

Adrenocortical hyperplasia. Amenorrhea precedes characteristic cushingoid signs, such as truncal obesity, moon face, buffalo hump, bruises, purple striae, hypertension, renal calculi, psychiatric disturbances, and widened pulse pressure. Acne, thinning scalp hair, and hirsutism typically appear.

Adrenocortical hypofunction. In addition to amenorrhea, adrenocortical hypofunction may cause fatigue, irritability, weight loss, increased pigmentation (including bluish black discoloration of the areolas and mucous membranes of the lips, mouth, rectum, and vagina), vitiligo, nausea, vomiting, and orthostatic hypotension.

Amenorrhea-lactation disorders. Amenorrhea-lactation disorders, such as Forbes-Albright and Chiari-Frommel syndromes, produce secondary amenorrhea accompanied by lactation in the absence of breast-feeding. Associated features include hot flashes, dyspareunia, vaginal atrophy, and large, engorged breasts.

Anorexia nervosa. Anorexia nervosa is a psychological disorder that can cause either primary or secondary amenorrhea. Related findings include significant weight loss, a thin or emaciated appearance, compulsive behavior patterns, a blotchy or sallow complexion, constipation, reduced libido, decreased pleasure in once-enjoyable activities, dry skin, loss of scalp hair, lanugo on the face and arms, skeletal muscle atrophy, and sleep disturbances.

Congenital absence of the ovaries. Congenital absence of the ovaries results in primary amenorrhea and the absence of secondary sex characteristics.

Congenital absence of the uterus. Primary amenorrhea occurs with congenital absence of the uterus. The patient may develop breasts.

Corpus luteum cysts. Corpus luteum cysts may cause sudden amenorrhea as well as acute abdominal pain and breast swelling. Examination may reveal a tender adnexal mass and vaginal and cervical hyperemia.

Hypothalamic tumor. In addition to amenorrhea, a hypothalamic tumor can cause endocrine and visual field defects, gonadal underdevelopment or dysfunction, and short stature. Hypothyroidism. Deficient thyroid hormone levels can cause primary or secondary amenorrhea. Typically vague, early findings include fatigue, forgetfulness, cold intolerance, unexplained weight gain, and constipation. Subsequent signs include bradycardia; decreased mental acuity; dry, flaky, inelastic skin; puffy face, hands, and feet; hoarseness; periorbital edema; ptosis; dry, sparse hair; and thick, brittle nails. Other common findings include anorexia, abdominal distention, decreased libido, ataxia, intention tremor, nystagmus, and delayed reflex relaxation time, especially in the Achilles tendon.

Mosaicism. Mosaicism results in primary amenorrhea and the absence of secondary sex characteristics.

Ovarian insensitivity to gonadotropins. A hormonal disturbance, ovarian insensitivity to gonadotropins leads to amenorrhea and an absence of secondary sex characteristics.

Pituitary tumor. Amenorrhea may be the first sign of a pituitary tumor. Associated findings include headache; visual disturbances, such as bitemporal hemianopsia; and acromegaly. Cushingoid signs include moon face, buffalo hump, hirsutism, hypertension, truncal obesity, bruises, purple striae, widened pulse pressure, and psychiatric disturbances.

Polycystic ovary syndrome. Typically, menarche occurs at a normal age, followed by irregular menstrual cycles, oligomenorrhea, and secondary amenorrhea. Or periods of profuse bleeding may alternate with periods of amenorrhea. Obesity, hirsutism, slight deepening of the voice, and enlarged, “oyster-like” ovaries may also accompany this disorder.

Pseudoamenorrhea. An anatomic anomaly, such as imperforate hymen, obstructs menstrual flow, causing primary amenorrhea and, possibly, cyclic episodes of abdominal pain. Examination may reveal a pink or blue bulging hymen.

Pseudocyesis. With pseudocyesis, amenorrhea may be accompanied by lordosis, abdominal distention, nausea, and breast enlargement.

Testicular feminization. Primary amenorrhea may signal this form of male pseudohermaphroditism. The patient, outwardly female but genetically male, shows breast and external genital development but scant or absent pubic hair.

Thyrotoxicosis. Thyroid hormone overproduction may result in amenorrhea. Classic signs and symptoms include an enlarged thyroid (goiter), nervousness, heat intolerance, diaphoresis, tremors, palpitations, tachycardia, dyspnea, weakness, and weight loss despite increased appetite.

Turner’s syndrome. Primary amenorrhea and failure to develop secondary sex characteristics may signal this syndrome of genetic ovarian dysgenesis. Typical features include short stature, webbing of the neck, low nuchal hairline, a broad chest with widely spaced nipples and poor breast development, underdeveloped genitalia, and edema of the legs and feet.

Uterine hypoplasia. Primary amenorrhea results from underdevelopment of the uterus, which is detectable on physical examination.

Other Causes

Drugs. Busulfan, chlorambucil, injectable or implanted contraceptives, cyclophosphamide, and phenothiazines may cause amenorrhea. Hormonal contraceptives may cause anovulation and amenorrhea after they’re discontinued.

Radiation therapy. Irradiation of the abdomen may destroy the endometrium or ovaries, causing amenorrhea.

Surgery. Surgical removal of both ovaries or the uterus produces amenorrhea.

Special Considerations

In patients with secondary amenorrhea, physical and pelvic examinations must rule out pregnancy before diagnostic testing begins. Typical tests include progestin withdrawal, serum hormone and thyroid function studies, and endometrial biopsy.

Patient Counseling

Explain the treatment and expected outcomes, encourage the patient to discuss her fears, and refer her for psychological counseling if needed.

Pediatric Pointers

Adolescent girls are especially prone to amenorrhea caused by emotional upsets, typically stemming from school, social, or family problems.

Geriatric Pointers

In women older than age 50, amenorrhea usually represents the onset of menopause.

REFERENCES

Kelly-Weeder, S . (2012). Helping patients through the pain of infertility. The Nurse Practitioner: The American Journal of Primary Health Care, 37(2), 47–52.

McCormack, A. (2010) . Individuals with eating disorders and the use of online support groups as a form of social support. CIN: Computers, Informatics, Nursing, 28(1), 12–19.

Amnesia

Amnesia — a disturbance in, or loss of, memory — may be classified as partial or complete and as anterograde or retrograde. Anterograde amnesia denotes memory loss of events that occurred after the onset of the causative trauma or disease; retrograde amnesia, memory loss of events that occurred before the onset. Depending on the cause, amnesia may arise suddenly or slowly and may be temporary or permanent.

Organic (or true) amnesia results from temporal lobe dysfunction, and it characteristically spares patches of memory. A common symptom in patients with seizures or head trauma, organic amnesia can also be an early indicator of Alzheimer’s disease. Hysterical amnesia has a psychogenic origin and characteristically causes complete memory loss. Treatment-induced amnesia is usually transient.

Amnesia: Common Causes and Associated Findings

History and Physical Examination

Because the patient typically isn’t aware of his amnesia, you’ll usually need help in gathering information from his family or friends. Throughout your assessment, notice the patient’s general appearance, behavior, mood, and train of thought. Ask when the amnesia first appeared and what types of things the patient is unable to remember. Can he learn new information? How long does he remember it? Does the amnesia encompass a recent or remote period?

Test the patient’s recent memory by asking him to identify and repeat three items. Retest after 3 minutes. Test his intermediate memory by asking, “Who was the president before this one?” and “What was the last type of car you bought?” Test remote memory with such questions as “How old are you?” and “Where were you born?”

Take the patient’s vital signs and assess his level of consciousness (LOC). Check his pupils: They should be equal in size and should constrict quickly when exposed to direct light. Also, assess his extraocular movements. Test motor function by having the patient move his arms and legs through their range of motion. Evaluate sensory function with pinpricks on the patient’s skin. (See Amnesia: Common Causes and Associated Findings.)

Medical Causes

Alzheimer’s disease. Alzheimer’s disease usually begins with retrograde amnesia, which progresses slowly over many months or years to include anterograde amnesia, producing severe and permanent memory loss. Associated findings include agitation, inability to concentrate, disregard for personal hygiene, confusion, irritability, and emotional lability. Later signs include aphasia, dementia, incontinence, and muscle rigidity.