Borchers Andrea Ann (ed.) Handbook of Signs & Symptoms 2015
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fever, and local redness, warmth, induration, and tenderness.
Transfusion reaction. A hemolytic reaction may cause chills during the transfusion or immediately afterward. A nonhemolytic febrile reaction may also cause chills.
Special Considerations
Check the patient’s vital signs often, especially if his chills result from a known or suspected infection. Be alert for signs of progressive septic shock, such as hypotension, tachycardia, and tachypnea. If appropriate, obtain samples of blood, sputum, wound drainage, or urine for culture to determine the causative organism. Give the appropriate antibiotic. Radiographic studies may be required.
Because chills are an involuntary response to an increased body temperature set by the hypothalamic thermostat, blankets won’t stop a patient’s chills or shivering. Despite this, keep his room temperature as even as possible. Provide adequate hydration and nutrients, and give an antipyretic to help control a fever. The irregular use of an antipyretic can trigger compensatory chills.
Patient Counseling
Explain to the patient the following: the importance of documenting temperature to reveal patterns, the necessary treatment and antibiotics, the signs and symptoms of a worsening condition, and when to seek medical attention.
Pediatric Pointers
Infants don’t get chills because they have poorly developed shivering mechanisms. In addition, most classic febrile childhood infections, such as measles and mumps, don’t typically produce chills. However, older children and teenagers may have chills with mycoplasma pneumonia and acute pyogenic osteomyelitis.
Geriatric Pointers
Chills in an elderly patient usually indicate an underlying infection, such as a urinary tract infection, pneumonia (commonly associated with aspiration of gastric contents), diverticulitis, or skin breakdown in pressure areas. Also, consider an ischemic bowel in an elderly patient who comes into your facility with a fever, chills, and abdominal pain.
REFERENCES
Tang, Y. W. , Himmelfarb, E., Wills, M., & Stratton, C. W. (2010). Characterization of three staphylococcus aureus isolates from a 17- year-old female who died of tampon-related toxic shock syndrome. Journal of Clinical Microbiology. 48(5), 1974–1977.
Zaki, S. A., Shanbag, P., Chavan, V., & Shenoy, P. (2010). Staphylococcal toxic shock syndrome presenting as acute respiratory distress and cor pulmonale. Annals of Tropical Paediatrics. 30(1), 77–81.
Chvostek’s Sign
Chvostek’s sign is an abnormal spasm of the facial muscles elicited by lightly tapping the patient’s facial nerve near his lower jaw. (See Eliciting Chvostek’s Sign .) This sign usually suggests hypocalcemia, but can occur normally in about 25% of cases. Typically, it precedes other signs of
hypocalcemia and persists until the onset of tetany. It can’t be elicited during tetany because of strong muscle contractions.
Normally, eliciting Chvostek’s sign is attempted only in patients with suspected hypocalcemic disorders. However, because the parathyroid gland regulates calcium balance, Chvostek’s sign may also be tested in patients before neck surgery to obtain a baseline.
EMERGENCY INTERVENTIONS
Test for Trousseau’s sign, a reliable indicator of hypocalcemia. Closely monitor the patient for signs of tetany, such as carpopedal spasms or circumoral and extremity paresthesia.
Be prepared to act rapidly if a seizure occurs. Perform an electrocardiogram to check for changes associated with hypocalcemia that can predispose the patient to arrhythmias. Place the patient on a cardiac monitor.
History and Physical Examination
Obtain a brief history. Find out if the patient has had his parathyroid glands surgically removed or if he has a history of hypoparathyroidism, hypomagnesemia, or a malabsorption disorder. Ask him or his family if they have noticed any changes in the patient’s mental status, such as depression or slowed responses, which can accompany chronic hypocalcemia.
Eliciting Chvostek’s Sign
Begin by telling the patient to relax his facial muscles. Then, stand directly in front of him, and tap the facial nerve either just anterior to the earlobe and below the zygomatic arch or between the zygomatic arch and the corner of his mouth. A positive response varies from twitching of the lip at the corner of the mouth to spasm of all facial muscles, depending on the severity of hypocalcemia.
Medical Causes
Hypocalcemia. The degree of muscle spasm elicited reflects the patient’s serum calcium level.
Initially, hypocalcemia produces paresthesia in the fingers, toes, and circumoral area that progresses to muscle tension and carpopedal spasms. The patient may also complain of muscle weakness, fatigue, and palpitations. Muscle twitching, hyperactive deep tendon reflexes, choreiform movements, and muscle cramps may also occur. The patient with chronic hypocalcemia may have mental status changes; diplopia; difficulty swallowing; abdominal cramps; dry, scaly skin; brittle nails; and thin, patchy scalp and eyebrow hair.
Other Causes
Blood transfusion. A massive transfusion can lower serum calcium levels and allow Chvostek’s sign to be elicited.
Special Considerations
Collect blood samples for serial and ionized calcium studies to evaluate the severity of hypocalcemia and the effectiveness of therapy. Such therapy involves oral or I.V. calcium supplements. Also, look for Chvostek’s sign when evaluating a patient postoperatively.
Patient Counseling
Explain to the patient the early signs and symptoms of hypocalcemia; stress the importance of seeking immediate medical attention if they occur.
Pediatric Pointers
Because Chvostek’s sign may be observed in healthy infants, it isn’t elicited to detect neonatal tetany.
Geriatric Pointers
Always consider malabsorption and poor nutritional status in the elderly patient with Chvostek’s sign and hypocalcemia.
REFERENCES
McCormick, B. B., Davis, J., & Burns, K. D. (2012) . Severe hypocalcemia following denosumab injection in a hemodialysis patient.
American Journal of Kidney Diseases. 60(4), 626–628.
Recker, R. R., Lewiecki, E. M., Miller, P. D., & Reiffel, J. (2009). Safety of bisphosphonates in the treatment of osteoporosis. American Journal of Medicine. 122, S22–S32.
Clubbing
A nonspecific sign of pulmonary and cyanotic cardiovascular disorders, clubbing is the painless, usually bilateral increase in soft tissue around the terminal phalanges of the fingers or toes. (See Rare Causes of Clubbing, page 172.) It doesn’t involve changes in the underlying bone. With early clubbing, the normal 160-degree angle between the nail and the nail base approximates 180 degrees. As clubbing progresses, this angle widens and the base of the nail becomes visibly swollen. With late clubbing, the angle where the nail meets the now-convex nail base extends more than halfway up the nail.
History and Physical Examination
You’ll probably detect clubbing while evaluating other signs of known pulmonary or cardiovascular disease. Therefore, review the patient’s current plan of treatment because clubbing may resolve with correction of the underlying disorder. Also, evaluate the extent of clubbing in the fingers and toes. (See Checking for Clubbed Fingers.)
Rare Causes of Clubbing
Clubbing is typically a sign of pulmonary or cardiovascular disease, but it can also result from certain hepatic and GI disorders, such as cirrhosis, Crohn’s disease, and ulcerative colitis. Clubbing occurs only rarely in these disorders, however, so first check for more common signs and symptoms. For example, a patient with cirrhosis usually experiences right upper quadrant pain and hepatomegaly, a patient with Crohn’s disease typically has abdominal cramping and tenderness, and a patient with ulcerative colitis may develop diffuse abdominal pain and bloodstreaked diarrhea.
Medical Causes
Bronchiectasis. Clubbing commonly occurs in the late stage of bronchiectasis. Another classic sign is a cough that produces copious, foul-smelling, and mucopurulent sputum. Hemoptysis and coarse crackles over the affected area, heard during inspiration, are also characteristic. The patient may complain of weight loss, fatigue, weakness, and exertional dyspnea. He may also have rhonchi, fever, malaise, and halitosis.
Bronchitis. With chronic bronchitis, clubbing may occur as a late sign as the patient experiences inadequate ventilation-perfusion changes. The patient has a chronic productive cough and may display barrel chest, dyspnea, wheezing, increased use of accessory muscles, cyanosis, tachypnea, crackles, scattered rhonchi, and prolonged expiration.
Emphysema. Clubbing occurs late in emphysema. The patient may have anorexia, malaise, dyspnea, tachypnea, diminished breath sounds, peripheral cyanosis, and pursed-lip breathing. He may also display accessory muscle use, barrel chest, and a productive cough.
EXAMINATION TIP Checking for Clubbed Fingers
To assess the patient for chronic tissue hypoxia, check his fingers for clubbing. Normally, the angle between the fingernail and the point where the nail enters the skin is about 160 degrees. Clubbing occurs when that angle increases to 180 degrees or more, as shown below.
Endocarditis. With subacute infective endocarditis, clubbing may be accompanied by a fever, anorexia, pallor, weakness, night sweats, fatigue, tachycardia, and weight loss. The patient may also develop arthralgia, petechiae, Osler’s nodes, splinter hemorrhages, Janeway lesions, splenomegaly, and Roth’s spots. Cardiac murmurs are usually present.
Heart failure. Clubbing occurs as a late sign in heart failure along with wheezing, dyspnea, and fatigue. Other findings include jugular vein distention, hepatomegaly, tachypnea, palpitations, dependent edema, unexplained weight gain, nausea, anorexia, chest tightness, a slowed mental response, hypotension, diaphoresis, narrow pulse pressure, pallor, oliguria, a gallop rhythm (a third heart sound), and crackles on inspiration.
Interstitial fibrosis. Clubbing usually occurs in the patient with advanced interstitial fibrosis. Typically, he also develops intermittent chest pain, dyspnea, crackles, fatigue, weight loss, and possible cyanosis.
Lung abscess. Initially, lung abscess produces clubbing, which may reverse with resolution of the abscess. It can also cause pleuritic chest pain; dyspnea; crackles; a productive cough with a lot of purulent, foul-smelling, usually bloody sputum; and halitosis. The patient may also experience weakness, fatigue, anorexia, a headache, malaise, weight loss, and a fever with chills. You may hear decreased breath sounds.
Lung and pleural cancer. Clubbing occurs commonly in lung and pleural cancers. Associated findings include hemoptysis, dyspnea, wheezing, chest pain, weight loss, anorexia, fatigue, and a fever.
Special Considerations
Don’t mistake curved nails — a normal variation — for clubbing. Simply remember that the angle between the nail and its base remains normal in curved nails, but not in clubbed nails.
Patient Counseling
Teach the patient about the cause of clubbing and explain that clubbing may not disappear even if the cause has been resolved.
Pediatric Pointers
In children, clubbing usually occurs in those with cyanotic congenital heart disease or cystic fibrosis. Surgical correction of heart defects may reverse clubbing.
Geriatric Pointers
Arthritic deformities of the fingers or toes may disguise the presence of clubbing.
REFERENCES
Seifert, W., Kühnisch, J., Tüysüz, B., Specker, C., Brouwers, A., & Horn, D. (2012). Mutations in the prostaglandin transporter encoding gene SLCO2A1 cause primary hypertrophic osteoarthropathy and isolated digital clubbing. Human Mutations, 33, 660–664.
Tariq, M. , Azeem, Z. , Ali, G. , Chishti, M. S., & Ahmad, W. (2009) . Mutation in the HPGD gene encoding NAD+ dependent 15hydroxyprostaglandin dehydrogenase underlies isolated congenital nail clubbing (ICNC). Journal of Medical Genetics, 46(1), 14–20.
Cogwheel Rigidity
Cogwheel rigidity is a cardinal sign of Parkinson’s disease, marked by muscle rigidity that reacts with superimposed ratchet-like movements when the muscle is passively stretched. This sign can be elicited by stabilizing the patient’s forearm and then moving his wrist through the range of motion. (Cogwheel rigidity usually appears in the arms but can sometimes be elicited in the ankle.) The patient and examiner can see and feel these characteristic movements, thought to be a combination of rigidity and tremor.
History and Physical Examination
After you have elicited cogwheel rigidity, take the patient’s history to determine when he first noticed associated signs of Parkinson’s disease. For example, has he experienced tremors? Did he notice tremors of his hands first? Does he have “pill-rolling” hand movements? When did he first notice that his movements were becoming slower? How long has he been experiencing stiffness in his arms and legs? Has his handwriting gotten smaller? While taking the history, observe him for signs of pronounced parkinsonism, such as drooling, masklike facies, dysphagia, monotone speech, and an altered gait.
Find out which medications the patient is taking, and ask if they have helped relieve some of his symptoms. If he’s taking levodopa and his symptoms have worsened, find out if he has exceeded the prescribed dosage. If you suspect an overdose, withhold the drug. If the patient has been taking a phenothiazine or another antipsychotic drug and has no history of Parkinson’s disease, he may be having an adverse reaction. Withhold the drug, as appropriate.
Medical Causes
Parkinson’s disease. With Parkinson’s disease, cogwheel rigidity occurs together with an insidious tremor, which usually begins in the fingers (unilateral pill-rolling tremor), increases during stress or anxiety, and decreases with purposeful movement and sleep.
Bradykinesia (slowness of voluntary movements and speech) also occurs. The patient walks with short, shuffling steps; his gait lacks normal parallel motion and may be retropulsive or propulsive. He has a monotone way of speaking and a masklike facial expression. He may also experience drooling,
dysphagia, dysarthria, and the loss of posture control, causing him to walk with his body bent forward. An oculogyric crisis (eyes fixed upward and involuntary tonic movements) or blepharospasm (complete eyelid closure) may also occur.
Other Causes
Drugs. Phenothiazines and other antipsychotics (such as haloperidol, thiothixene, and loxapine) can cause cogwheel rigidity. Metoclopramide infrequently causes it.
Special Considerations
If the patient has associated muscular dysfunction, assist him with ambulation, bathing, feeding, and other activities of daily living, as needed. Provide symptomatic care as appropriate. For example, if the patient develops constipation, administer a stool softener; if he experiences dysphagia, offer a soft diet with small, frequent feedings. Refer the patient to the National Parkinson Foundation or the American Parkinson Disease Association, both of which provide educational materials and support.
Patient Counseling
Teach the patient about Parkinson’s disease and its treatments. Refer the patient to the National Parkinson Foundation or the American Parkinson Disease Association for educational materials and support.
Pediatric Pointers
Cogwheel rigidity doesn’t occur in children.
REFERENCES
Brooks, M. Amantadine has lasting benefit on levodopa-induced dyskinesia. Medscape Medical News [serial online]. January 8, 2014; Accessed January 13, 2014. Available at http://Medscape Medical News.
Ory-Magne, F., Corvol, J. C., Azulay, J. P. , et al., (2014). Withdrawing amantadine in dyskinetic patients with Parkinson disease: The AMANDYSK trial. Neurology, 82(4), 300–307.
Confusion
An umbrella term for puzzling or inappropriate behavior or responses, confusion is the inability to think quickly and coherently. Depending on the cause, it may arise suddenly or gradually and may be temporary or irreversible. Aggravated by stress and sensory deprivation, confusion commonly occurs in hospitalized patients — especially the elderly, in whom it may be mistaken for senility.
When severe confusion arises suddenly and the patient also has hallucinations and psychomotor hyperactivity, his condition is classified as delirium. Long-term, progressive confusion with deterioration of all cognitive functions is classified as dementia.
Confusion can result from fluid and electrolyte imbalance or hypoxemia due to pulmonary disorders. It can also have a metabolic, neurologic, cardiovascular, cerebrovascular, or nutritional origin, or it can result from a severe systemic infection or the effects of toxins, drugs, or alcohol. Confusion may signal worsening of an underlying and perhaps irreversible disease.
History and Physical Examination
When you take his history, ask the patient to describe what’s bothering him. He may not report confusion as his chief complaint, but may suffer from memory loss, persistent apprehension, or the inability to concentrate. He may be unable to respond logically to direct questions. Check with a family member or friend about its onset and frequency. Find out, too, if the patient has a history of recent head trauma or a cardiopulmonary, metabolic, cerebrovascular, or neurologic disorder. Which medications is he taking, if any? Ask about any changes in eating or sleeping habits and in drug or alcohol use.
Perform an assessment to determine the presence of systemic disorders. Check the patient’s vital signs, and assess him for changes in blood pressure, temperature, and pulse.
Next, perform a neurologic assessment to establish the patient’s level of consciousness.
Medical Causes
Brain tumor. In the early stages of a brain tumor, confusion is usually mild and difficult to detect. As the tumor impinges on cerebral structures, however, confusion worsens and the patient may exhibit personality changes, bizarre behavior, sensory and motor deficits, visual field deficits, and aphasia.
Cerebrovascular disorders. Cerebrovascular disorders produce confusion due to tissue hypoxia and ischemia. Confusion may be insidious and fleeting, as in a transient ischemic attack, or acute and permanent, as in a stroke.
Decreased cerebral perfusion. Mild confusion is an early symptom of decreased cerebral perfusion. Associated findings usually include hypotension, tachycardia or bradycardia, an irregular pulse, ventricular gallop, edema, and cyanosis.
Fluid and electrolyte imbalance. The extent of imbalance determines the severity of the patient’s confusion. Typically, he’ll show signs of dehydration, such as lassitude, poor skin turgor, dry skin and mucous membranes, and oliguria. He may also develop hypotension and a low-grade fever.
Head trauma. Concussion, contusion, and brain hemorrhage may produce confusion at the time of injury, shortly afterward, or months or even years afterward. The patient may be delirious, with periodic loss of consciousness. Vomiting, a severe headache, pupillary changes, and sensory and motor deficits are also common.
Heatstroke. Heatstroke causes pronounced confusion that gradually worsens as the patient’s body temperature rises. Initially, he may be irritable and dizzy; later, he may become delirious, have seizures, and lose consciousness.
Hypothermia. Confusion may be an early sign of hypothermia. Typically, the patient displays slurred speech, cold and pale skin, hyperactive deep tendon reflexes, a rapid pulse, and decreased blood pressure and respirations. As his body temperature continues to drop, his confusion progresses to stupor and coma, his muscles become rigid, and his respiratory rate decreases.
Hypoxemia. Acute pulmonary disorders that result in hypoxemia produce confusion that can range from mild disorientation to delirium. Chronic pulmonary disorders produce persistent confusion.
Infection. Severe generalized infection, such as sepsis, typically produces delirium. Central
nervous system (CNS) infections, such as meningitis, cause varying degrees of confusion along with a headache and nuchal rigidity.
Metabolic encephalopathy. Hyperglycemia and hypoglycemia can produce sudden confusion. A patient with hypoglycemia may also experience transient delirium and seizures. Uremic and hepatic encephalopathies produce gradual confusion that may progress to seizures and coma. Usually, the patient also experiences tremors and restlessness.
Nutritional deficiencies. Inadequate dietary intake of thiamine, niacin, or vitamin B12 produces insidious, progressive confusion and possible mental deterioration.
Seizure disorders. Mild to moderate confusion may immediately follow any type of seizure. The confusion usually disappears within several hours.
Other Causes
Alcohol. Intoxication causes confusion and stupor, and alcohol withdrawal may cause delirium and seizures.
Drugs. Large doses of CNS depressants produce confusion that can persist for several days after the drug is discontinued. Opioid and barbiturate withdrawal also causes acute confusion, possibly with delirium. Other drugs that commonly cause confusion include lidocaine, a cardiac glycoside, indomethacin, cycloserine, chloroquine, atropine, and cimetidine.
HERB ALERT
Herbal remedies, such as St. John’s wort, can cause confusion, especially when taken in conjunction with an antidepressant or other serotonergic drug.
Special Considerations
Never leave a confused patient unattended, to prevent injury to himself and others. (Apply restraints only if necessary to ensure his safety.) Keep the patient calm and quiet, and plan uninterrupted rest periods. To help him stay oriented, keep a large calendar and a clock visible, and make a list of his activities with specific dates and times. Always reintroduce yourself to the patient each time you enter his room.
Patient Counseling
If possible, explain to the patient and his family the underlying cause of his confusion. Offer ways to help orient the patient by meeting in surroundings familiar to the patient or consider having a family member or other familiar person assist the patient.
Pediatric Pointers
Confusion can’t be determined in infants and very young children. However, older children with acute febrile illnesses commonly experience transient delirium or acute confusion.
REFERENCES
National Institute on Aging. (2013). 2011–2012 Alzheimer’s disease progress report: intensifying the research effort . Bethesda, MD: U.S. Department of Health and Human Services, National Institutes of Health; Available at http://www.nia.nih.gov/alzheimers/publication/2011-2012-alzheimers-disease-progress-report.
Wagster, M. V. , King, J. W. , Resnick, S. M., & Rapp, P. R. (2012). The 87%. Journal Gerontological and Biological Science and Medical Science, 67, 739–740.
Constipation
Constipation is defined as small, infrequent, or difficult bowel movements. Because normal bowel movements can vary in frequency and from individual to individual, constipation is relative and must be determined in relation to the patient’s normal elimination pattern. Constipation may be a minor annoyance or, uncommonly, a sign of a life-threatening disorder such as an acute intestinal obstruction. Untreated, constipation can lead to headache, anorexia, and abdominal discomfort and can adversely affect the patient’s lifestyle and well-being.
Constipation usually occurs when the urge to defecate is suppressed and the muscles associated with bowel movements remain contracted. Because the autonomic nervous system controls bowel movements — by sensing rectal distention from fecal contents and by stimulating the external sphincter — any factor that influences this system may cause bowel dysfunction. (See How Habits and Stress Cause Constipation, page 178.)
History and Physical Examination
Ask the patient to describe the frequency of his bowel movements and the size and consistency of his stools. How long has he had constipation? Acute constipation usually has a physiological cause such as an anal or rectal disorder. In a patient older than age 45, a recent onset of constipation may be an early sign of colorectal cancer. Conversely, chronic constipation typically has a functional cause and may be related to stress.
Does the patient have pain related to constipation? If so, when did he first notice the pain, and where is it located? Cramping abdominal pain and distention suggest obstipation — extreme, persistent constipation due to intestinal tract obstruction. Ask the patient if defecation worsens or helps relieve the pain. Defecation usually worsens pain, but with such disorders as irritable bowel syndrome, it may relieve it.
How Habits and Stress Cause Constipation