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

apical systolic murmur.

Mood disorder. Anxiety may be the patient’s chief complaint in the depressive or manic form of mood disorder. With the depressive form, chronic anxiety occurs with varying severity. Associated findings include dysphoria; anger; insomnia or hypersomnia; decreased libido, interest, energy, and concentration; appetite disturbance; multiple somatic complaints; and suicidal thoughts. With the manic form, the patient’s chief complaint may be a reduced need for sleep, hyperactivity, increased energy, rapid or pressured speech and, in severe cases, paranoid ideas and other psychotic symptoms.

Myocardial infarction (MI). With MI, a life-threatening disorder, acute anxiety commonly occurs with persistent, crushing substernal pain that may radiate to the left arm, jaw, neck, or shoulder blades. It can be accompanied by shortness of breath, nausea, vomiting, diaphoresis, and cool pale skin.

Obsessive-compulsive disorder. Chronic anxiety occurs with obsessive-compulsive disorder, along with recurrent, unshakable thoughts or impulses to perform ritualistic acts. The patient recognizes these acts as irrational, but is unable to control them. Anxiety builds if he can’t perform these acts and diminishes after he does.

Pheochromocytoma. Acute, severe anxiety accompanies pheochromocytoma’s cardinal sign: persistent or paroxysmal hypertension. Common associated signs and symptoms include tachycardia, diaphoresis, orthostatic hypotension, tachypnea, flushing, a severe headache, palpitations, nausea, vomiting, epigastric pain, and paresthesia.

Phobias. With phobias, chronic anxiety occurs along with a persistent fear of an object, activity, or situation that results in a compelling desire to avoid it. The patient recognizes the fear as irrational, but can’t suppress it.

Pneumonia. Acute anxiety may occur with pneumonia because of hypoxemia. Other findings include a productive cough, pleuritic chest pain, fever, chills, crackles, diminished breath sounds, and hyperresonant lung fields.

Pneumothorax. Acute anxiety occurs in moderate to severe pneumothorax associated with profound respiratory distress. It’s accompanied by sharp pleuritic pain, coughing, shortness of breath, cyanosis, asymmetrical chest expansion, pallor, jugular vein distention, and a weak, rapid pulse.

Postconcussion syndrome. Postconcussion syndrome may produce chronic anxiety or periodic attacks of acute anxiety. Associated signs and symptoms include irritability, insomnia, dizziness, and a mild headache. The anxiety is usually most pronounced in situations demanding attention, judgment, or comprehension.

Posttraumatic stress disorder. Posttraumatic stress disorder occurs in the patient who has experienced an extreme traumatic event. It produces chronic anxiety of varying severity and is accompanied by intrusive, vivid memories and thoughts of the traumatic event. The patient also relives the event in dreams and nightmares. Insomnia, depression, and feelings of numbness and detachment are common.

Pulmonary edema. With pulmonary edema, acute anxiety occurs with dyspnea, orthopnea, cough with frothy sputum, tachycardia, tachypnea, crackles, ventricular gallop, hypotension, and a thready pulse. The patient’s skin may be cool, clammy, and cyanotic.

Pulmonary embolism. With pulmonary embolism, acute anxiety is usually accompanied by dyspnea, tachypnea, chest pain, tachycardia, blood-tinged sputum, and a low-grade fever.

Rabies. Anxiety signals the beginning of the acute phase of rabies, a rare disorder, which is commonly accompanied by painful laryngeal spasms associated with difficulty swallowing and, as a result, hydrophobia.

Somatoform disorder. Somatoform disorder, which usually begins in young adulthood, is characterized by anxiety and multiple somatic complaints that can’t be explained physiologically. The symptoms aren’t produced intentionally, but are severe enough to significantly impair functioning. Pain disorder, conversion disorder, and hypochondriasis are examples of somatoform disorder.

Other Causes

Drugs. Many drugs cause anxiety, especially sympathomimetics and central nervous system stimulants. In addition, many antidepressants may cause paradoxical anxiety.

Special Considerations

Supportive care usually helps relieve anxiety. Provide a calm, quiet atmosphere, and make the patient comfortable. Encourage him to express his feelings and concerns freely. If it helps, take a short walk with him while you’re talking. Or, try anxiety-reducing measures, such as distraction, relaxation techniques, or biofeedback.

Patient Counseling

Instruct the patient on relaxation techniques, and help him to identify stressors and to understand more about coping mechanisms. Encourage the patient’s verbalization of anxiety.

Pediatric Pointers

Anxiety in children usually results from painful physical illness or inadequate oxygenation. Its autonomic signs tend to be more common and dramatic than in adults.

Geriatric Pointers

In an elderly patient, distractions from ritual activity may provoke anxiety or agitation.

REFERENCES

Ferrari, A. J., Charlson, F. J., Norma, R. E., Patten, S. B., Freedman, G. , Murray, C. L., …Whiteford, H. A. (2013) . Burden of depressive disorders by country, sex, age, and year: Findings from the global burden of disease study 2010. PLOS Medicine, 10(11), e1001547.

Gulliver, A., Griffiths, K., & Christensen, H. (2010). Perceived barriers and facilitators to mental health help seeking in young people: A systematic review,. BMC Psychiatry, 10(1), 113.

Aphasia [Dysphasia]

Aphasia, impaired expression or comprehension of written or spoken language, reflects disease or injury of the brain’s language centers. (See Where Language Originates.) Depending on its severity, aphasia may slightly impede communication or may make it impossible. It can be classified as

Broca’s, Wernicke’s, anomic, or global aphasia. Anomic aphasia eventually resolves in more than 50% of patients, but global aphasia is usually irreversible. (See Identifying Types of Aphasia , page 60.)

Where Language Originates

Aphasia reflects damage to one or more of the brain’s primary language centers, which, in most persons, are located in the left hemisphere. Broca’s area lies next to the region of the motor cortex that controls the muscles necessary for speech. Wernicke’s area is the center of auditory, visual, and language comprehension. It lies between Heschl’s gyrus, the primary receiver of auditory stimuli, and the angular gyrus, a “way station” between the brain’s auditory and visual regions. Connecting Wernicke’s and Broca’s areas is a large nerve bundle, the arcuate fasciculus, which enables the repetition of speech.

EMERGENCY INTERVENTIONS

Quickly look for signs and symptoms of increased intracranial pressure (ICP), such as pupillary changes, a decreased level of consciousness (LOC), vomiting, seizures, bradycardia, widening pulse pressure, and irregular respirations. If you detect signs of increased ICP, administer mannitol I.V. to decrease cerebral edema. In addition, make sure that emergency resuscitation equipment is readily available to support respiratory and cardiac function, if necessary. You may have to prepare the patient for emergency surgery.

History and Physical Examination

If the patient doesn’t display signs of increased ICP or if his aphasia has developed gradually, perform a thorough neurologic examination, starting with the patient history. You’ll probably need to obtain this history from the patient’s family or companion because of the patient’s impairment. Ask if the patient has a history of headaches, hypertension, seizure disorders, or drug use. Also ask about the patient’s ability to communicate and to perform routine activities before aphasia began.

Identifying Types of Aphasia

Check for obvious signs of neurologic deficit, such as ptosis or fluid leakage from the nose and ears. Take the patient’s vital signs and assess his LOC. Be aware, however, that assessing LOC is usually difficult because the patient’s verbal responses may be unreliable. Also, recognize that dysarthria (impaired articulation due to weakness or paralysis of the muscles necessary for speech) or speech apraxia (inability to voluntarily control the muscles of speech) may accompany aphasia; therefore, speak slowly and distinctly, and allow the patient ample time to respond. Assess the patient’s pupillary response, eye movements, and motor function, especially his mouth and tongue movement, swallowing ability, and spontaneous movements and gestures. To best assess motor function, first demonstrate the motions and then have the patient imitate them.

Medical Causes

Alzheimer’s disease. With Alzheimer’s, a degenerative disease, anomic aphasia may begin

insidiously and then progress to severe global aphasia. Associated signs and symptoms include behavioral changes, loss of memory, poor judgment, restlessness, myoclonus, and muscle rigidity. Incontinence is usually a late sign.

Brain abscess. Any type of aphasia may occur with brain abscess. Usually, aphasia develops insidiously and may be accompanied by hemiparesis, ataxia, facial weakness, and signs of increased ICP.

Brain tumor. A brain tumor may cause any type of aphasia. As the tumor enlarges, other aphasias may occur along with behavioral changes, memory loss, motor weakness, seizures, auditory hallucinations, visual field deficits, and increased ICP.

Creutzfeldt-Jakob disease. Creutzfeldt-Jakob disease is a rapidly progressive dementia accompanied by neurologic signs and symptoms, such as myoclonic jerking, ataxia, aphasia, visual disturbances, and paralysis. It generally affects adults ages 40 to 65.

Encephalitis. Encephalitis usually produces transient aphasia. Its early signs and symptoms include fever, headache, and vomiting. Seizures, confusion, stupor or coma, hemiparesis, asymmetrical deep tendon reflexes, positive Babinski’s reflex, ataxia, myoclonus, nystagmus, ocular palsies, and facial weakness may accompany aphasia.

Head trauma. Any type of aphasia may accompany severe head trauma; typically, it occurs suddenly and may be transient or permanent, depending on the extent of brain damage. Associated signs and symptoms include blurred or double vision, headache, pallor, diaphoresis, numbness and paresis, cerebrospinal otorrhea or rhinorrhea, altered respirations, tachycardia, disorientation, behavioral changes, and signs of increased ICP.

Seizures. Seizures and the postictal state may cause transient aphasia if the seizures involve the language centers.

Stroke. The most common cause of aphasia, stroke may produce Wernicke’s, Broca’s, or global aphasia. Associated findings include decreased LOC, right-sided hemiparesis, homonymous hemianopsia, paresthesia, and loss of sensation. (These signs and symptoms may appear on the left side if the right hemisphere contains the language centers.)

Transient ischemic attack. Transient ischemic attacks can produce any type of aphasia, which occurs suddenly and resolves within 24 hours of the attack. Associated signs and symptoms include transient hemiparesis, hemianopsia, and paresthesia (all usually right-sided), dizziness, and confusion.

Special Considerations

Immediately after aphasia develops, the patient may become confused or disoriented. Help to restore a sense of reality by frequently telling him what has happened, where he is and why, and what the date is. Carefully explain diagnostic tests, such as skull X-rays, computed tomography scan or magnetic resonance imaging, angiography, and EEG. Later, expect periods of depression as the patient recognizes his disability. Help him to communicate by providing a relaxed, accepting environment with a minimum of distracting stimuli.

Be alert for sudden outbursts of profanity by the patient. This common behavior usually reflects intense frustration with his impairment. Deal with such outbursts as gently as possible to ease embarrassment.

When you speak to the patient, don’t assume that he understands you. He may simply be interpreting subtle clues to meaning, such as social context, facial expressions, and gestures. To help

avoid misunderstanding, use nonverbal techniques, speak to him in simple phrases, and use demonstration to clarify your verbal directions.

Remember that aphasia is a language disorder, not an emotional or auditory one, so speak to the patient in a normal tone of voice. Make sure that he has necessary aids, such as eyeglasses or dentures, to facilitate communication. Printed communication cards can assist him to communicate his basic needs. Refer the patient to a speech pathologist early to help him cope with his aphasia.

Patient Counseling

Discuss alternate means of communication and ways to reduce the risk factors for stroke.

Pediatric Pointers

Recognize that the term childhood aphasia is sometimes mistakenly applied to children who fail to develop normal language skills but who aren’t considered mentally retarded or developmentally delayed. Aphasia refers solely to a loss of previously developed communication skills.

Brain damage associated with aphasia in children most commonly follows anoxia — the result of near drowning or airway obstruction.

REFERENCES

Balasa, M., Gelpi, E., Antonell, A., Rey, M. J., Sanchez-Valle, R ., Molinuevo, J. L., & Llado, A. (2011) . Clinical features and APOE genotype of pathologically proven early-onset Alzheimer’s disease. Neurology, 76(20), 1720–1725.

Koedam, E. L., Lauffer, V., van der Vlies, A. E., van der Flier, W. M. , Scheltens, P., & Pijnenburg, Y. A. (2010) . Early-versus lateonset Alzheimer’s disease: More than age alone. Journal of Alzheimers Disease, 19(4), 1401–1408.

Apnea

Apnea, the cessation of spontaneous respiration, is occasionally temporary and self-limiting, as occurs during Cheyne-Stokes and Biot’s respirations. More commonly, however, it’s a lifethreatening emergency that requires immediate intervention to prevent death.

Apnea usually results from one or more of six pathophysiologic mechanisms, each of which has numerous causes. Its most common causes include trauma, cardiac arrest, neurologic disease, aspiration of foreign objects, bronchospasm, and drug overdose. (See Causes of Apnea.)

EMERGENCY INTERVENTIONS

If you detect apnea, first establish and maintain a patent airway. Position the patient in a supine position, and open his airway using the head-tilt, chin-lift technique. (Caution: If the patient has an obvious or suspected head or neck injury, use the jaw-thrust technique to prevent hyperextending the neck.) Next, quickly look, listen, and feel for spontaneous respiration; if it’s absent, begin artificial ventilation until it occurs or until mechanical ventilation can be initiated.

Because apnea may result from cardiac arrest (or may cause it), assess the patient’s carotid pulse immediately after you’ve established a patent airway. Or, if the patient is an infant or small child, assess the brachial pulse instead. If you can’t palpate a pulse, begin

cardiac compression.

History and Physical Examination

When the patient’s respiratory and cardiac status is stable, investigate the underlying cause of apnea. Ask him (or, if he’s unable to answer, anyone who witnessed the episode) about the onset of apnea and events immediately preceding it. The cause may become readily apparent, as in trauma.

Take a patient history, noting especially reports of headache, chest pain, muscle weakness, sore throat, or dyspnea. Ask about a history of respiratory, cardiac, or neurologic disease and about allergies and drug use.

Inspect the head, face, neck, and trunk for soft tissue injury, hemorrhage, or skeletal deformity. Don’t overlook obvious clues, such as oral and nasal secretions reflecting fluid-filled airways and alveoli or facial soot and singed nasal hair suggesting thermal injury to the tracheobronchial tree.

Auscultate over all lung lobes for adventitious breath sounds, particularly crackles and rhonchi, and percuss the lung fields for increased dullness or hyperresonance. Move on to the heart, auscultating for murmurs, pericardial friction rub, and arrhythmia. Check for cyanosis, pallor, jugular vein distention, and edema. If appropriate, perform a neurologic assessment. Evaluate the patient’s level of consciousness (LOC), orientation, and mental status; test cranial nerve function and motor function, sensation, and reflexes in all extremities.

Causes of Apnea

AIRWAY OBSTRUCTION

Asthma

Bronchospasm

Chronic bronchitis

Chronic obstructive pulmonary disease

Foreign body aspiration

Hemothorax or pneumothorax

Mucus plug

Obstruction by tongue or tumor

Obstructive sleep apnea

Respiratory syncytial virus (RSV)

Secretion retention

Tracheal or bronchial rupture

BRAIN STEM DYSFUNCTION

Brain abscess

Brain stem injury

Brain tumor

Central nervous system depressants

Central sleep apnea

Cerebral hemorrhage Cerebral infarction Encephalitis

Head trauma

Increased intracranial pressure

Medullary or pontine hemorrhage or infarction Meningitis

Transtentorial herniation

NEUROMUSCULAR FAILURE

Amyotrophic lateral sclerosis

Botulism

Diphtheria

Guillain-Barré syndrome

Myasthenia gravis

Phrenic nerve paralysis

Rupture of the diaphragm

Spinal cord injury

PARENCHYMATOUS DISEASE

Acute respiratory distress syndrome

Diffuse pneumonia

Emphysema

Near drowning

Pulmonary edema

Pulmonary fibrosis

Secretion retention

PLEURAL PRESSURE GRADIENT DISRUPTION

Flail chest

Open chest wounds

PULMONARY CAPILLARY PERFUSION DECREASE

Arrhythmias

Cardiac arrest

Myocardial infarction

Pulmonary embolism

Pulmonary hypertension

Shock

Medical Causes

Airway obstruction. Occlusion or compression of the trachea, central airways, or smaller airways can cause sudden apnea by blocking the patient’s airflow and producing acute respiratory failure.

Brain stem dysfunction. Primary or secondary brain stem dysfunction can cause apnea by destroying the brain stem’s ability to initiate respirations. Apnea may arise suddenly (as in trauma, hemorrhage, or infarction) or gradually (as in degenerative disease or tumor). Apnea may be preceded by a decreased LOC and by various motor and sensory deficits.

Neuromuscular failure. Trauma or disease can disrupt the mechanics of respiration, causing sudden or gradual apnea. Associated findings include diaphragmatic or intercostal muscle paralysis from injury or respiratory weakness or paralysis from acute or degenerative disease.

Parenchymatous lung disease. An accumulation of fluid within the alveoli produces apnea by interfering with pulmonary gas exchange and producing acute respiratory failure. Apnea may arise suddenly, as in near drowning and acute pulmonary edema, or gradually, as in emphysema. Apnea may also be preceded by crackles and labored respirations with accessory muscle use.

Pleural pressure gradient disruption. Conversion of normal negative pleural air pressure to positive pressure by chest wall injuries (such as flail chest) causes lung collapse, producing respiratory distress and, if untreated, apnea. Associated signs include an asymmetrical chest wall and asymmetrical or paradoxical respirations.

Pulmonary capillary perfusion decrease. Apnea can stem from obstructed pulmonary circulation, most commonly due to heart failure or lack of circulatory patency. It occurs suddenly in cardiac arrest, massive pulmonary embolism, and most cases of severe shock. In contrast, it occurs progressively in septic shock and pulmonary hypertension. Related findings include hypotension, tachycardia, and edema.

Respiratory syncytial virus (RSV). Apnea, coughing, rapid breathing, wheezing, nasal flaring, fever, chest retractions, and upper respiratory symptoms may occur with RSV bronchiolitis, an infection of the lower respiratory tract commonly seen in children younger than 1 year old. RSV infection results in edema that causes narrowing of the airway and inadequate oxygenation. Some children lose interest in eating and drinking and may need to be hydrated. Most children recover from RSV infection within 8 to 15 days without sequelae. Premature infants and those with underlying respiratory, cardiac, neuromuscular, and immunological conditions require special consideration.

Other Causes

Drugs. Central nervous system (CNS) depressants may cause hypoventilation and apnea. Benzodiazepines may cause respiratory depression and apnea when given I.V. along with other CNS depressants to elderly or acutely ill patients.

Neuromuscular blockers — such as curariform drugs and anticholinesterases — may produce sudden apnea because of respiratory muscle paralysis.

Sleep-related apneas. These repetitive apneas occur during sleep from airflow obstruction or brain stem dysfunction.

Special Considerations

Closely monitor the patient’s cardiac and respiratory status to prevent further episodes of apnea.

Patient Counseling

Explain the underlying cause and treatment plan, and teach safety measures to reduce the risk of aspiration and ways to avoid episodes of apnea, based on its cause. Encourage the patient’s family to learn cardiopulmonary resuscitation (CPR).

Pediatric Pointers

Premature neonates are especially susceptible to periodic episodes of apnea because of CNS immaturity. Other common causes include sepsis, intraventricular and subarachnoid hemorrhage, seizures, bronchiolitis, RSV, and sudden infant death syndrome.

In toddlers and older children, the primary cause of apnea is acute airway obstruction from aspiration of foreign objects. Other causes include acute epiglottiditis, croup, asthma, and systemic disorders, such as muscular dystrophy and cystic fibrosis.

Geriatric Pointers

In elderly patients, increased sensitivity to analgesics, sedative-hypnotics, or a combination of these drugs may produce apnea, even with normal dosage ranges.

REFERENCES

Leger, D., Bayon, V., Laaban, J. P., & Philip, P. (2012). Impact of sleep apnea on economics. Sleep Medicine Review, 16, 455–462. Philip, P., Sagaspe, P., Lagarde, E., Leger, D., Ohayon, M. M., Bioulac, B., … Taillard, J. (2010). Sleep disorders and accidental risk in a

large group of regular registered highway drivers. Sleep Medicine, 11, 973–979.

Apneustic Respirations

Apneustic respirations are characterized by prolonged, gasping inspiration, with a pause at full inspiration. This irregular breathing pattern is an important localizing sign of severe brain stem damage.

Involuntary breathing is primarily regulated by groups of neurons located in respiratory centers in the medulla oblongata and pons. In the medulla, neurons react to impulses from the pons and other areas to regulate respiratory rate and depth. In the pons, two respiratory centers regulate respiratory rhythm by interacting with the medullary respiratory center to smooth the transition from inspiration to expiration and back. The apneustic center in the pons stimulates inspiratory neurons in the medulla to precipitate inspiration. These inspiratory neurons, in turn, stimulate the pneumotaxic center in the pons to precipitate expiration. Destruction of neural pathways by pontine lesions disrupts normal regulation of respiratory rhythm, causing apneustic respirations.

Apneustic respirations must be differentiated from bradypnea and hyperpnea (disturbances in rate and depth, but not in rhythm), Cheyne-Stokes respirations (rhythmic alterations in rate and depth, followed by periods of apnea), and Biot’s respirations (irregularly alternating periods of hyperpnea and apnea).