Signs and symptoms diseases

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Halitosis describes any breath odor that's unpleasant, disagreeable, or offensive. This common sign is usually easy to detect, but an embarrassed patient may take measures to hide it. The patient may be unaware that he has halitosis, even though he may complain of a bad taste in his mouth, or he may believe that he has halitosis but that no one else can detect it (psychogenic halitosis).
Certain types of halitosis characterize specific disorders—for example, a fruity breath odor typifies ketoacidosis. (See “Breath with ammonia odor,” page 120; “Breath with fecal odor,” page 121; “Breath with fruity odor,” page 123; and “Fetor hepaticus,” page 297.) Other types of halitosis include putrid, foul, fetid, and musty breath odors.
Halitosis may result from a disorder of the oral cavity, nasal passages, sinuses, respiratory tract, or esophageal diverticula. It may also stem from a GI disorder associated with belching, regurgitation, or vomiting, or it may be an adverse effect of an oral or inhaled drug.
Other causes of halitosis include cigarette smoking, ingestion of alcohol and certain foods (such as garlic and onions), and poor oral hygiene—especially in patients with an orthodontic device, dentures, or dental caries. In addition, offensive skin odors—for example, from foot perspiration—may be absorbed locally and later expelled by the lungs, resulting in halitosis.
If you detect halitosis, try to characterize the odor. Does it smell fruity, fecal, or musty? If the patient is aware of it, find out how long he has had it. Does he also have a bad taste in his mouth? Does he have difficulty swallowing or chewing? Does he have reflux or regurgitation? Does he have pain or tenderness? Ask the patient if he has a problem with flatus. Also ask him to describe the frequency of his bowel movements and the size and consistency of his stools.
Find out if the patient smokes or chews tobacco. Have him describe his diet and daily oral hygiene. Does he wear dentures? Complete the history by asking about chronic disorders and recent respiratory tract infection. If the patient reports a cough, find out if it's productive.
Begin the physical examination by examining the patient's mouth, throat, and nose. Look for lesions, bleeding, drainage, obstruction, and signs of infection, such as redness and swelling. Check for tenderness by percussing and palpating over the sinuses. Then auscultate the lungs for abnormal breath sounds. Auscultate the abdomen for bowel sounds, and percuss it, noting any tympany. Finally, take vital signs.
Bowel obstruction. Halitosis is a late sign in both small- and large-bowel obstructions, resulting from vomiting of bilious and later fecal material. Other findings in a small-bowel obstruction include constipation, abdominal

distention, and intermittent periumbilical cramping pain. In a large-bowel obstruction, abdominal pain is milder and more constant than that associated with a small-bowel obstruction and is usually located lower in the abdomen.
Bronchiectasis. Bronchiectasis usually produces foul or putrid halitosis, but some patients may have a sickeningly sweet breath odor. The patient typically also has a chronic productive cough with copious, foul-smelling, mucopurulent sputum. The cough is aggravated by lying down and is most productive in the morning. Associated findings commonly include exertional dyspnea, fatigue, malaise, weakness, and weight loss. Auscultation reveals coarse or moist crackles over the affected lung areas during inspiration. Digital clubbing is a late sign.
Common cold. A musty breath odor may accompany a common cold, which usually also causes a dry, hacking cough with sore throat, sneezing, nasal congestion, rhinorrhea, headache, malaise, fatigue, arthralgia, and myalgia.
Esophageal cancer. In esophageal cancer, halitosis may accompany classic findings of dysphagia, hoarseness, chest pain, and weight loss. Nocturnal regurgitation and cachexia are late signs.
Gastric cancer. Halitosis is a late sign in gastric cancer. Accompanying findings include chronic dyspepsia unrelieved by antacids, a vague feeling of fullness, nausea, anorexia, fatigue, pallor, weakness, altered bowel habits, weight loss, and muscle wasting. Hematemesis and melena are signs of associated gastric bleeding.
Gastrocolic fistula. In this disorder, fecal vomiting is responsible for fecal breath odor, which is typically preceded by intermittent diarrhea.
Gingivitis. Characterized by red, edematous gums, gingivitis may also cause halitosis. The gingivae between the teeth become bulbous and bleed easily with slight trauma.
Acute necrotizing ulcerative gingivitis also causes fetid breath, a bad taste in the mouth, and ulcers—especially between the teeth—that may become covered with a gray exudate. Severe ulceration may occur with fever, cervical adenopathy, headache, and malaise.
Hepatic encephalopathy. A characteristic late sign of hepatic encephalopathy is fetor hepaticus, a musty, sweet, or mousy (new-mown hay) breath odor. Other late effects include coma, asterixis (flapping tremor), and hyperactive deep tendon reflexes.
Ketoacidosis. Alcohol-induced, diabetic, and starvation forms of ketoacidosis produce a fruity breath odor. Alcohol-induced ketoacidosis is usually seen in poorly nourished alcoholics who have eaten very little over several days. Symptoms include sudden Kussmaul's respirations with vomiting for several days, light dehydration, abdominal pain and distention, and absent bowel sounds. The patient is alert and has a normal or slightly decreased blood glucose level.
Life-threatening diabetic ketoacidosis produces a rapid, thready pulse; marked hypovolemia; nausea and vomiting; and, in its early stages, the triad of polydipsia, polyphagia, and polyuria.
Also life-threatening, starvation ketoacidosis produces Kussmaul's respirations; weight loss; bradycardia; dry, scaly skin; sore tongue; muscle and tissue wasting; abdominal distention; and signs of dehydration, such as oliguria and poor skin turgor.
Other common effects of diabetic and starvation ketoacidosis include orthostatic hypotension, generalized weakness, anorexia, abdominal pain, and altered level of consciousness.
Lung abscess. Lung abscess typically causes putrid halitosis, but its cardinal sign is a productive cough with copious, purulent, often bloody sputum. Other findings include fever with chills, dyspnea, headache, anorexia, weight loss, malaise, pleuritic chest pain, asymmetrical chest movement, and temporary clubbing.
Necrotizing ulcerative mucositis (acute). A strong, putrid breath odor is characteristic of this uncommon disorder, which initially causes slight cheek inflammation that's rapidly followed by tooth loss and extensive bone sloughing in the mandible or maxilla.
Ozena. This severe, chronic form of rhinitis causes a musty or fetid breath odor as well as thick green mucus and progressive anosmia.
Periodontal disease. Periodontal disease causes halitosis and an unpleasant taste. Typically, the patient's gums bleed spontaneously or with slight trauma and are marked by pus-filled pockets around the teeth. Related findings include facial pain, headache, and loose teeth covered by calculi and plaque.
Pharyngitis (gangrenous). Halitosis is a chief sign of gangrenous pharyngitis. The patient also complains of a foul taste in the mouth, an extremely sore throat, and a choking sensation. Examination reveals a swollen, red, ulcerated pharynx, possibly with a grayish

membrane. Fever and cervical lymphadenopathy are also common.
Renal failure (chronic). Renal failure produces a urinous or ammonia breath odor. Among its widespread effects are anemia, emotional lability, lethargy, irritability, decreased mental acuity, coarse muscular twitching, peripheral neuropathies, muscle wasting, anorexia, signs of GI bleeding, ecchymosis, yellowbrown or bronze skin, pruritus, anuria, and increased blood pressure.
Sinusitis. Acute sinusitis causes a purulent nasal discharge that leads to halitosis. Besides a characteristic postnasal drip, the patient may exhibit nasal congestion, sore throat, cough, malaise, headache, facial pain and tenderness, and fever. Chronic sinusitis causes a continuous mucopurulent discharge that leads to a musty breath odor, postnasal drip, nasal congestion, and a chronic nonproductive cough.
Zenker's diverticulum. This esophageal disorder causes halitosis and a bad taste in the mouth associated with regurgitation. The patient may also report a chronic cough that's most pronounced at night, hoarseness, odynophagia, neck pain, and “gurgling” sounds in the throat when he swallows liquids.
Drugs. Drugs that can cause halitosis include triamterene, inhaled anesthetics, and any drugs known to cause metabolic acidosis such as nitroprusside.
image Some herbal medicines, such as garlic, may cause halitosis.
If examination of the mouth and sinuses doesn't reveal the cause of halitosis, prepare the patient for upper GI and chest X-rays or endoscopy.
In children, halitosis commonly results from physiologic causes, such as continual mouth breathing and thumb or blanket sucking. Phenylketonuria—a metabolic disorder that affects infants—may produce a musty or mousy breath odor.
Extensive dental caries, mouth dryness, and poor oral hygiene can cause halitosis in elderly patients.
To help control halitosis, encourage good oral hygiene. If halitosis is drug induced, reassure the patient that it will disappear as soon as his body completely eliminates the drug.
Halo vision
Halo vision refers to seeing rainbowlike colored rings around lights or bright objects. The rainbowlike effect can be explained by this physical principle: As light passes through water (in the eye, through tears or the cells of various anteretinal media), it breaks up into spectral colors.
Halo vision usually develops suddenly; its duration depends on the causative disorder. This symptom may occur in disorders associated with excessive tearing and corneal epithelial edema. Among these causes, the most common and significant is acute angle-closure glaucoma, which can lead to blindness. In this ophthalmic emergency, increased intraocular pressure (IOP) forces fluid into corneal tissues anterior to Bowman's membrane, causing edema. Halo vision is also an early symptom of cataracts, resulting from dispersion of light by abnormal lens opacity.
Nonpathologic causes of excessive tearing associated with halo vision include poorly fitted or overworn contact lenses, emotional extremes, and exposure to intense light, as in snow blindness.
First, ask the patient how long he has been seeing halos around lights and when he usually sees them. Patients with glaucoma usually see halos in the morning, when IOP is most elevated. Ask the patient if light bothers his eyes. Does he have eye pain? If so, have him describe it. Remember that halos associated with excruciating eye pain or a severe headache may point to acute angle-closure glaucoma, an ocular emergency. Note a history of glaucoma or cataracts.
Next, examine the patient's eyes, noting conjunctival injection, excessive tearing, and lens changes. Examine pupil size, shape, and response to light. Then test visual acuity by performing an ophthalmoscopic examination.
Cataract. Halo vision may be an early symptom of painless, progressive cataract formation.

The glare of headlights may blind the patient, making nighttime driving impossible. Other features include blurred vision, impaired visual acuity, and lens opacity, all of which develop gradually.
Corneal endothelial dystrophy. Typically, halo vision is a late symptom of this disorder, which may also cause impaired visual acuity.
Glaucoma. Halo vision characterizes all types of glaucoma. Acute angle-closure glaucoma —an ophthalmic emergency—also causes blurred vision, followed by a severe headache or excruciating pain in and around the affected eye. Examination reveals a moderately dilated fixed pupil that doesn't respond to light, conjunctival injection, a cloudy cornea, impaired visual acuity and, possibly, nausea and vomiting.
Chronic angle-closure glaucoma usually produces no symptoms until pain and blindness occur in advanced disease. Sometimes, halos and blurred vision develop slowly.
In chronic open-angle glaucoma, halo vision is a late symptom that's accompanied by mild eye ache, peripheral vision loss, and impaired visual acuity.
To help minimize halo vision, remind the patient not to look directly at bright lights.
Halo vision in a child usually results from congenital cataracts or glaucoma. In a young child, limited verbal ability may make halo vision difficult to assess.
Primary glaucoma, the most common cause of halo vision, is more common in older patients.
The most common neurologic symptom, headaches may be localized or generalized, producing mild to severe pain. About 90% of all headaches are benign and can be described as vascular, muscle-contraction, or a combination of both. (See Comparing benign headaches.) Occasionally, though, headaches indicate a severe neurologic disorder associated with intracranial inflammation, increased intracranial pressure (ICP), or meningeal irritation. They may also result from an ocular or sinus disorder, tests, drugs, or other treatments.
Other causes of headache include fever, eyestrain, dehydration, and systemic febrile illnesses. Headaches may occur in certain metabolic disturbances—such as hypoxemia, hypercapnia, hyperglycemia, and hypoglycemia—but they aren't a diagnostic or prominent symptom in these disorders. Some individuals get headaches after seizures or from coughing, sneezing, heavy lifting, or stooping.
If the patient reports a headache, ask him to describe its characteristics and location. How often does he get a headache? How long does a typical headache last? Try to identify precipitating factors, such as eating certain foods or exposure to bright lights. Ask what helps to relieve the headache. Is the patient under stress? Has he had trouble sleeping?
Take a drug and alcohol history, and ask about head trauma within the last 4 weeks. Has the patient recently experienced nausea, vomiting, photophobia, or visual changes? Does he feel drowsy, confused, or dizzy? Has he recently developed seizures, or does he have a history of seizures?
Begin the physical examination by evaluating the patient's level of consciousness (LOC). Then check his vital signs. Be alert for signs of increased ICP—widened pulse pressure, bradycardia, altered respiratory pattern, and increased blood pressure. Check pupil size and response to light, and note any neck stiffness. (See Differential diagnosis: Headache, pages 344 and 345.)
Anthrax, cutaneous. Along with a macular or papular lesion that develops into a vesicle and finally a painless ulcer, this disorder may produce a headache, lymphadenopathy, fever, and malaise.
Brain abscess. In this disorder, the headache is localized to the abscess site; it usually intensifies over a few days and is aggravated by straining. Accompanying the headache may be nausea, vomiting, and focal or generalized seizures. The patient's LOC varies from drowsiness to deep stupor. Depending on the abscess site, associated signs and symptoms may include aphasia, impaired visual acuity, hemiparesis, ataxia, tremors, and personality changes. Signs of infection, such as fever and pallor, usually develop late; however, if the


abscess remains encapsulated, these signs may not appear.
Brain tumor. Initially, a tumor causes a localized headache near the tumor site; as the tumor grows, the headache eventually becomes generalized. The pain is usually intermittent, deep seated, and dull and is most intense in the morning. It's aggravated by coughing, stooping, Valsalva's maneuver, and changes in head position, and it's relieved by sitting and rest.

Associated signs and symptoms include personality changes, altered LOC, motor and sensory dysfunction, and eventually signs of increased ICP, such as vomiting, increased systolic blood pressure, and widened pulse pressure.
Cerebral aneurysm (ruptured). Cerebral aneurysm is a life-threatening disorder that's characterized by a sudden excruciating headache, which may be unilateral and usually peaks within minutes of the rupture. The patient

may lose consciousness immediately or display a variably altered LOC. Depending on the severity and location of the bleeding, he may also exhibit nausea and vomiting; signs and symptoms of meningeal irritation, such as nuchal rigidity and blurred vision; hemiparesis; and other features.
Ebola virus. A sudden headache commonly occurs on the 5th day of this deadly illness. Additionally, the patient has a history of malaise, myalgia, high fever, diarrhea, abdominal pain, dehydration, and lethargy. A maculopapular rash develops between the 5th and 7th days of the illness. Other possible findings include pleuritic chest pain; a dry, hacking cough; pronounced pharyngitis; hematemesis; melena; and bleeding from the nose, gums, and vagina. Death usually occurs in the 2nd week of the illness, preceded by massive blood loss and shock.
Encephalitis. A severe, generalized headache is characteristic with this disorder. Within 48 hours, the patient's LOC typically deteriorates —perhaps from lethargy to coma. Associated signs and symptoms include fever, nuchal rigidity, irritability, seizures, nausea and vomiting, photophobia, cranial nerve palsies such as ptosis, and focal neurologic deficits, such as hemiparesis and hemiplegia.
Epidural hemorrhage (acute). Head trauma and a sudden, brief loss of consciousness usually precede this hemorrhage, which causes a progressively severe headache that's accompanied by nausea and vomiting, bladder distention, confusion, and then a rapid decrease in LOC. Other signs and symptoms include unilateral seizures, hemiparesis, hemiplegia, high fever, decreased pulse rate and bounding pulse, widened pulse pressure, increased blood pressure, a positive Babinski's reflex, and decerebrate posture.
If the patient slips into a coma, his respirations deepen and become stertorous, then shallow and irregular, and eventually cease. Pupil dilation may occur on the same side as the hemorrhage.
Glaucoma, acute angle-closure. This type of glaucoma is an ophthalmic emergency that may cause an excruciating headache as well as acute eye pain, blurred vision, halo vision, nausea, and vomiting. Assessment reveals conjunctival injection, a cloudy cornea, and a moderately dilated, fixed pupil.
Hantavirus pulmonary syndrome. Noncardiogenic pulmonary edema distinguishes this viral disease, which was first reported in the United States in 1993. Common reasons for seeking treatment include flulike signs and symptoms—headache, myalgia, fever, nausea, vomiting, and a cough—followed by respiratory distress. Fever, hypoxia, and (in some patients) serious hypotension typify the hospital course. Other signs and symptoms include a rising respiratory rate (28 breaths/minute or more) and an increased heart rate (120 beats/minute or more).
Hypertension. This disorder may cause a slightly throbbing occipital headache on awakening that decreases in severity during the day. However, if the patient's diastolic blood pressure exceeds 120 mm Hg, the headache remains constant. Associated signs and symptoms include an atrial gallop, restlessness, confusion, nausea and vomiting, blurred vision, seizures, and altered LOC.
Influenza. A severe generalized or frontal headache usually begins suddenly with the flu. Accompanying signs and symptoms may last for 3 to 5 days and include stabbing retro-orbital pain, weakness, diffuse myalgia, fever, chills, coughing, rhinorrhea and, occasionally, hoarseness.
Influenza type A H1N1 virus (swine flu). Influenza type A H1N1, or swine flu, is a respiratory disease of pigs caused by type A influenza virus. Swine flu viruses cause high levels of illness and low death rates in pigs. Swine flu viruses normally don't infect humans; however, sporadic human infections with swine flu have occurred. Most commonly, these cases occur in persons with direct exposure to pigs. The virus has changed slightly and is known as H1N1 flu. Recent outbreaks of H1N1 flu have shown that the virus can be transmitted from person to person, causing transmission across the globe. The H1N1 flu is similar to influenza, and causes illness and in some cases death. The symptoms of swine flu include headache, nonproductive cough, fatigue, myalgia, chills, fever, and vomiting. The use of antiviral drugs is recommended to treat H1N1 flu.
Intracerebral hemorrhage. In some patients, this hemorrhage produces a severe generalized headache. Other signs and symptoms vary with the size and location of the hemorrhage. A large hemorrhage may produce a rapid, steady decrease in LOC, perhaps resulting in a coma. Other common findings include hemiplegia, hemiparesis, abnormal pupil size and response, aphasia, dizziness, nausea,

vomiting, seizures, decreased sensation, irregular respirations, positive Babinski's reflex, decorticate or decerebrate posture, and increased blood pressure.
Listeriosis. If this infection spreads to the nervous system, it may cause meningitis, whose signs and symptoms include headache, nuchal rigidity, fever, and change in LOC. Earlier signs and symptoms of listeriosis include fever, myalgia, abdominal pain, nausea, vomiting, and diarrhea.
image Listeriosis during pregnancy may lead to premature delivery, infection of the neonate, or stillbirth.
Meningitis. This disorder is marked by the sudden onset of a severe, constant, generalized headache that worsens with movement. Fever and chills are other early signs. As meningitis progresses, it also causes nuchal rigidity, positive Kernig's and Brudzinski's signs, hyperreflexia, altered LOC, seizures, ocular palsies, facial weakness, hearing loss, vomiting and, possibly, opisthotonos and papilledema.
Plague. The pneumonic form of this lethal bacterial infection causes a sudden onset of headache, chills, fever, and myalgia. Pulmonary findings include a productive cough, chest pain, tachypnea, dyspnea, hemoptysis, respiratory distress, and cardiopulmonary insufficiency.
Postconcussion syndrome. A generalized or localized headache may develop 1 to 30 days after head trauma and last for 2 to 3 weeks. This characteristic symptom may be described as an aching, pounding, pressing, stabbing, or throbbing pain. The patient's neurologic examination is normal, but he may experience giddiness or dizziness, blurred vision, fatigue, insomnia, inability to concentrate, and noise and alcohol intolerance.
Q fever. Signs and symptoms of this disease include severe headaches, fever, chills, malaise, chest pain, nausea, vomiting, and diarrhea. The fever may last for up to 2 weeks, and in severe cases, the patient may develop hepatitis or pneumonia.
Severe acute respiratory syndrome (SARS). SARS is an acute infectious disease caused by a coronavirus. Although most cases have been reported in Asia (China, Vietnam, Singapore, Thailand), cases have cropped up in Europe and North America. After an incubation period of 2 to 7 days, the illness generally begins with a fever (usually greater than 100.4° F [38° C]). Other symptoms include headache, malaise, a nonproductive cough, and dyspnea. SARS may produce only mild symptoms, or it may progress to pneumonia and, in some cases, even respiratory failure and death.
Sinusitis (acute). This disorder is usually marked by a dull periorbital headache that's usually aggravated by bending over or touching the face and is relieved by sinus drainage. Fever, sinus tenderness, nasal turbinate edema, sore throat, malaise, cough, and nasal discharge may accompany the headache.
Smallpox (variola major). Initial signs and symptoms of this virus include a severe headache, backache, abdominal pain, high fever, malaise, prostration, and a maculopapular rash on the mucosa of the mouth, pharynx, face, and forearms and then on the trunk and legs. The rash becomes vesicular, then pustular. After 8 or 9 days, the pustules form a crust, which later separates from the skin, leaving a pitted scar. Death may result from encephalitis, extensive bleeding, or secondary infection.
Subarachnoid hemorrhage. This hemorrhage commonly produces a sudden, violent headache along with nuchal rigidity, nausea and vomiting, seizures, dizziness, ipsilateral pupil dilation, and altered LOC that may rapidly progress to coma. The patient also exhibits positive Kernig's and Brudzinski's signs, photophobia, blurred vision and, possibly, a fever. Focal signs and symptoms (such as hemiparesis, hemiplegia, sensory or vision disturbances, and aphasia) and signs of elevated ICP (such as bradycardia and increased blood pressure) may also occur.
Subdural hematoma. Typically associated with head trauma, both acute and chronic subdural hematomas may cause headache and decreased LOC. An acute subdural hematoma also produces drowsiness, confusion, and agitation that may progress to coma. Later findings include signs of increased ICP and focal neurologic deficits such as hemiparesis.
A chronic subdural hematoma produces a dull, pounding headache that fluctuates in severity and is located over the hematoma. Weeks or months after the initial head trauma, the patient may experience giddiness, personality changes, confusion, seizures, and progressively worsening LOC. Late signs may include unilateral pupil dilation, sluggish pupil reaction to light, and ptosis.
Temporal arteritis. A throbbing unilateral headache in the temporal or frontotemporal region may be accompanied by vision loss, hearing loss, confusion, and fever. The temporal

arteries are tender, swollen, nodular, and sometimes erythematous.
Tularemia. Signs and symptoms following inhalation of the bacterium Francisella tularensis include abrupt onset of headache, fever, chills, generalized myalgia, a nonproductive cough, dyspnea, pleuritic chest pain, and empyema.
Typhus. In typhus, initial symptoms of headache, myalgia, arthralgia, and malaise are followed by an abrupt onset of chills, fever, nausea, and vomiting. A maculopapular rash may also occur.
West Nile encephalitis. This brain infection is caused by West Nile virus, a mosquito-borne flavivirus commonly found in Africa, West Asia, the Middle East and, rarely, in North America. Most patients have mild signs and symptoms, including fever, headache, body aches, rash, and swollen lymph glands. More severe infection is marked by high fever, headache, neck stiffness, stupor, disorientation, coma, tremors, and paralysis.
Diagnostic tests. A lumbar puncture or myelogram may produce a throbbing frontal headache that worsens on standing.
Drugs. A wide variety of drugs can cause headaches. For example, indomethacin produces headaches—usually in the morning—in many patients. Vasodilators and drugs with a vasodilating effect, such as nitrates, typically cause a throbbing headache. Headaches may also follow withdrawal from vasopressors, such as caffeine, ergotamine, and sympathomimetics.
image Herbal remedies, such as St. John's wort, ginseng, and ephedra (ma huang), can cause various adverse reactions, including headaches. (Note: The FDA has banned the sale of dietary supplements containing ephedra because they pose an unreasonable risk of injury or illness.)
Traction. Cervical traction with pins commonly causes a headache, which may be generalized or localized to pin insertion sites.
Continue to monitor the patient's vital signs and LOC. Watch for any change in the headache's severity or location. To help ease the headache, administer an analgesic, darken the patient's room, and minimize other stimuli. Explain the rationale of these interventions to the patient.
Prepare the patient for diagnostic tests, such as skull X-rays, computed tomography scan, lumbar puncture, or cerebral arteriography.
If a child is too young to describe his symptom, suspect a headache if you see him banging or holding his head. In an infant, a shrill cry or bulging fontanels may indicate increased ICP and headache. In a school-age child, ask the parents about the child's recent scholastic performance and about any problems at home that may produce a tension headache.
Twice as many young boys have migraine headaches as girls. In children older than age 3, headache is the most common symptom of a brain tumor.
Hearing loss
Affecting nearly 16 million Americans, hearing loss may be temporary or permanent and partial or complete. This common symptom may involve reception of low-, middle-, or high-frequency tones. If the hearing loss doesn't affect speech frequencies, the patient may be unaware of it.
Normally, sound waves enter the external auditory canal and travel to the middle ear's tympanic membrane and ossicles (incus, malleus, and stapes) and then into the inner ear's cochlea. The cochlear division of the eighth cranial (auditory) nerve carries the sound impulse to the brain. This type of sound transmission, called air conduction, is normally better than bone conduction—sound transmission through bone to the inner ear.
Hearing loss can be classified as conductive, sensorineural, mixed, or functional. Conductive hearing loss results from external or middle ear disorders that block sound transmission. This type of hearing loss usually responds to medical or surgical intervention (or in some cases, both). Sensorineural hearing loss results from disorders of the inner ear or of the eighth cranial nerve. Mixed hearing loss combines aspects of conductive and sensorineural hearing loss. Functional hearing loss results from psychological factors rather than identifiable organic damage.
Hearing loss may also result from trauma, infection, allergy, tumors, certain systemic and hereditary disorders, and the effects of ototoxic drugs and treatments. In most cases, though, it results from presbycusis, a type of sensorineural hearing loss that usually affects people older

than age 50. Other physiologic causes of hearing loss include cerumen (earwax) impaction; barotitis media (unequal pressure on the eardrum) associated with descent in an airplane or elevator, diving, or close proximity to an explosion; and chronic exposure to noise over 90 decibels, which can occur on the job, with certain hobbies, or from listening to live or recorded music.
If the patient reports hearing loss, ask him to describe it fully. Is it unilateral or bilateral? Continuous or intermittent? Ask about a family history of hearing loss. Then obtain the patient's medical history, noting chronic ear infections, ear surgery, and ear or head trauma. Has the patient recently had an upper respiratory tract infection? After taking a drug history, have the patient describe his occupation and work environment.
Next, explore associated signs and symptoms. Does the patient have ear pain? If so, is it unilateral or bilateral? Continuous or intermittent? Ask the patient if he has noticed discharge from one or both ears. If so, have him describe its color and consistency, and note when it began. Does he hear ringing, buzzing, hissing, or other noises in one or both ears? If so, are the noises constant or intermittent? Does he experience any dizziness? If so, when did he first notice it?
Begin the physical examination by inspecting the external ear for inflammation, boils, foreign bodies, and discharge. Then apply pressure to the tragus and mastoid to elicit tenderness. If you detect tenderness or external ear abnormalities, ask the physician whether an otoscopic examination should be done. (See Using an otoscope correctly, page 255.) During the otoscopic examination, note any color change, perforation, bulging, or retraction of the tympanic membrane, which normally looks like a shiny, pearl gray cone.
Next, evaluate the patient's hearing acuity, using the ticking watch and whispered voice tests. Then perform the Weber and Rinne tests to obtain a preliminary evaluation of the type and degree of hearing loss. (See Differentiating conductive from sensorineural hearing loss, page 350.)
Acoustic neuroma. This eighth cranial nerve tumor causes unilateral, progressive, sensorineural hearing loss. The patient may also develop tinnitus, vertigo, and—with cranial nerve compression—facial paralysis.
Adenoid hypertrophy. Eustachian tube dysfunction gradually causes conductive hearing loss accompanied by intermittent ear discharge. The patient also tends to breathe through his mouth and may complain of a sensation of ear fullness.
Allergies. Conductive hearing loss may result when an allergy produces eustachian tube and middle ear congestion. Other features include ear pain or a feeling of fullness, nasal congestion, and conjunctivitis.
Aural polyps. If a polyp occludes the external auditory canal, partial hearing loss may occur. The polyp typically bleeds easily and is covered by a purulent discharge.
Cholesteatoma. Gradual hearing loss is characteristic in this disorder and may be accompanied by vertigo and, at times, facial paralysis. Examination reveals eardrum perforation, pearly white balls in the ear canal and, possibly, a discharge.
Cyst. Ear canal obstruction by a sebaceous or dermoid cyst causes progressive conductive hearing loss. On inspection, the cyst looks like a soft mass.
External ear canal tumor (malignant). Progressive conductive hearing loss is characteristic and is accompanied by deep, boring ear pain; a purulent discharge; and eventually facial paralysis. Examination may detect the granular, bleeding tumor.
Furuncle. Reversible conductive hearing loss may occur when one of these painful, hard nodules forms in the ear. The patient may report a sense of fullness in the ear and pain on palpation of the tragus or auricle. Rupture relieves the pain and produces a purulent, necrotic discharge.
Glomus jugulare tumor. Initially, this benign tumor causes mild, unilateral conductive hearing loss that becomes progressively more severe. The patient may report tinnitus that sounds like his heartbeat. Associated signs and symptoms include gradual congestion in the affected ear, throbbing or pulsating discomfort, bloody otorrhea, facial nerve paralysis, and vertigo. Although the tympanic membrane is normal, a reddened mass appears behind it.
Glomus tympanum tumor. This cancerous middle ear tumor causes slowly progressive hearing loss and throbbing or pulsating tinnitus.


It usually bleeds easily when manipulated. Late features include ear pain, dizziness, and total unilateral deafness.
Granuloma. A rare cause of conductive hearing loss, a granuloma may also produce fullness in the ear, deep-seated pain, and a bloody discharge.
Head trauma. Sudden conductive or sensorineural hearing loss may result from ossicle disruption, ear canal fracture, tympanic membrane perforation, or cochlear fracture associated with head trauma. Typically, the patient reports a headache and exhibits bleeding from his ear. Neurologic features vary and may include impaired vision and altered level of consciousness.
Herpes zoster oticus (Ramsay Hunt syndrome). This syndrome causes sudden severe, unilateral mixed hearing loss, which may be accompanied by vesicles in the external ear, tinnitus, vertigo, ear pain, malaise, and transient ipsilateral facial paralysis.
Hypothyroidism. This disorder may produce reversible sensorineural hearing loss. Other effects include bradycardia, weight gain despite anorexia, mental dullness, cold intolerance, facial edema, brittle hair, and dry skin that's pale, cool, and doughy.
Ménière's disease. Initially, this inner ear disorder produces intermittent, unilateral sensorineural hearing loss that involves only low tones. Later, hearing loss becomes constant and affects other tones. Associated signs and symptoms include intermittent severe vertigo, nausea and vomiting, a feeling of fullness in the ear, a roaring or hollow-seashell tinnitus, diaphoresis, and nystagmus.
Multiple sclerosis. Rarely, this disorder causes sensorineural hearing loss associated with myelin destruction of the central auditory pathways. The hearing loss may be sudden and unilateral or intermittent and bilateral. Among other characteristics are impaired vision, paresthesia, muscle weakness, gait ataxia, intention tremor, urinary disturbances, and emotional lability.
Myringitis. Rarely, acute infectious myringitis produces conductive hearing loss when fluid accumulates in the middle ear or a large bleb totally obstructs the ear canal. Small, reddened inflamed blebs may develop in the canal, on the tympanic membrane, or in the middle ear and may produce a bloody discharge if they rupture. Associated findings may include severe ear pain, mastoid tenderness, and fever.
Chronic granular myringitis produces gradual hearing loss accompanied by pruritus and a purulent discharge.
Nasopharyngeal cancer. This type of cancer causes mild unilateral conductive hearing loss when it compresses the eustachian tube. Bone conduction is normal, and inspection reveals a retracted tympanic membrane backed by fluid. When this tumor obstructs the nasal airway, the patient may exhibit nasal speech and a bloody nasal and postnasal discharge. Cranial nerve involvement produces other findings, such as diplopia and rectus muscle paralysis.
Osteoma. Commonly affecting women and swimmers, osteoma may cause sudden or intermittent conductive hearing loss. Typically, bony projections are visible in the ear canal, but the tympanic membrane appears normal.
Otitis externa. Conductive hearing loss resulting from debris in the ear canal characterizes both acute and malignant otitis externa. In acute otitis externa, ear canal inflammation produces pain, itching, and a foul-smelling, sticky yellow discharge. Severe tenderness is typically elicited by chewing, opening the mouth, and pressing on the tragus or mastoid. The patient may also develop a low-grade fever, regional lymphadenopathy, a headache on the affected side, and mild to moderate pain around the ear that may later intensify. Examination may reveal greenish white debris or edema in the canal.
In malignant otitis externa, debris is also visible in the canal. This life-threatening disorder, which most commonly occurs in diabetics, causes sensorineural hearing loss, pruritus, tinnitus, and severe ear pain.
Otitis media. This middle ear inflammation typically produces unilateral conductive hearing loss. In acute suppurative otitis media, the hearing loss develops gradually over a few hours and is usually accompanied by an upper respiratory tract infection with sore throat, cough, nasal discharge, and headache. Related signs and symptoms include dizziness, a sensation of fullness in the ear, intermittent or constant ear pain, fever, nausea, and vomiting. Rupture of the bulging, swollen tympanic membrane relieves the pain and produces a brief bloody and purulent discharge. Hearing returns after the infection subsides.
Hearing loss also develops gradually in patients with chronic otitis media. Assessment may reveal a perforated tympanic membrane, purulent ear drainage, earache, nausea, and vertigo.

Commonly associated with an upper respiratory tract infection or nasopharyngeal cancer, serous otitis media commonly produces a stuffy feeling in the ear and pain that worsens at night. Examination reveals a retracted—and perhaps discolored—tympanic membrane and possibly air bubbles behind the membrane.
Otosclerosis. In this hereditary disorder, unilateral conductive hearing loss usually begins when the patient is in his early twenties and may gradually progress to bilateral mixed hearing loss. The patient may report tinnitus and an ability to hear better in a noisy environment.
image Otosclerosis affects twice as many women as men and may worsen during pregnancy.
Skull fracture. Auditory nerve injury causes sudden unilateral sensorineural hearing loss. Accompanying signs and symptoms include ringing tinnitus, blood behind the tympanic membrane, scalp wounds, and other findings.
Syphilis. In tertiary syphilis, sensorineural hearing loss may develop suddenly or gradually and usually affects one ear more than the other. It's usually accompanied by a gumma lesion—a chronic, superficial nodule or a deep, granulomatous lesion on the skin or mucous membranes. The lesion is solitary, asymmetrical, painless, and indurated. The patient may also exhibit signs of liver, respiratory, cardiovascular, or neurologic dysfunction.
Temporal arteritis. This disorder may produce unilateral sensorineural hearing loss accompanied by throbbing unilateral facial pain, pain behind the eye, temporal or frontotemporal headache, and occasionally vision loss. The hearing loss is usually preceded by a prodrome of malaise, anorexia, weight loss, weakness, and myalgia that lasts for several days. Examination may reveal a nodular, swollen temporal artery. Low-grade fever, confusion, and disorientation may also occur.
Temporal bone fracture. This fracture can cause sudden unilateral sensorineural hearing loss accompanied by hissing tinnitus. The tympanic membrane may be perforated, depending on the fracture's location. Loss of consciousness, Battle's sign, and facial paralysis may also occur.
Tuberculosis. This pulmonary infection may spread to the ear, resulting in eardrum perforation, mild conductive hearing loss, and cervical lymphadenopathy.
Tympanic membrane perforation. Commonly caused by trauma from sharp objects or rapid pressure changes, perforation of the tympanic membrane causes abrupt hearing loss along with ear pain, tinnitus, vertigo, and a sensation of fullness in the ear.
Wegener's granulomatosis. Conductive hearing loss develops slowly in this rare necrotizing, granulomatous vasculitis. This multisystem disorder may also cause cough, pleuritic chest pain, epistaxis, hemorrhagic skin lesions, oliguria, and nasal discharge.
Drugs. Ototoxic drugs typically produce ringing or buzzing tinnitus and a feeling of fullness in the ear. Chloroquine, cisplatin, vancomycin, and aminoglycosides (especially neomycin, kanamycin, and amikacin) may cause irreversible hearing loss. Loop diuretics, such as furosemide, ethacrynic acid, and bumetanide, usually produce a brief, reversible hearing loss. Quinine, quinidine, and high doses of erythromycin or salicylates (such as aspirin) may also cause reversible hearing loss.
Radiation therapy. Irradiation of the middle ear, thyroid, face, skull, or nasopharynx may cause eustachian tube dysfunction, resulting in hearing loss.
Surgery. Myringotomy, myringoplasty, simple or radical mastoidectomy, or fenestrations may cause scarring that interferes with hearing.
When talking with the patient, remember to face him and speak slowly. Don't shout at the patient or smoke, eat, or chew gum when talking.
Prepare the patient for audiometry and auditory evoked-response testing. After testing, the patient may require a hearing aid or cochlear implant to improve his hearing.
About 3,000 profoundly deaf infants are born in the United States each year. In about half of these infants, hereditary disorders (such as Paget's disease and Alport's, Hurler's, and Klippel-Feil syndromes) cause the typically sensorineural hearing loss. Nonhereditary disorders associated with congenital sensorineural hearing loss include albinism, onychodystrophy, cochlear dysplasia, and Pendred's, Usher's, Waardenburg's, and Jervell and Lange-Nielsen syndromes. Sensorineural hearing loss may also result from maternal use of ototoxic drugs, birth trauma, and anoxia during or after birth.

Mumps is the most common cause of unilateral sensorineural hearing loss in children. Other causes are meningitis, measles, influenza, and acute febrile illness.
Congenital conductive hearing loss may be caused by atresia, ossicle malformation, and other abnormalities. Serous otitis media commonly causes bilateral conductive hearing loss in children. Putting foreign objects in the ears can also cause conductive hearing loss.
Hearing disorders in children may lead to speech, language, and learning problems. Early identification and treatment of hearing loss is thus crucial to avoid incorrectly labeling the child as mentally retarded, brain damaged, or a slow learner.
When assessing an infant or a young child for hearing loss, remember that you can't use a tuning fork. Instead, test the startle reflex in infants younger than age 6 months, or have an audiologist test brain stem evoked response in neonates, infants, and young children. Also, obtain a gestational, perinatal, and family history from the parents.
In older patients, presbycusis may be aggravated by exposure to noise as well as other factors.
Instruct the patient to avoid exposure to loud noise and to use ear protection to arrest hearing loss. If the patient has an upper respiratory tract infection, tell him to avoid flying and driving.
Heat intolerance
Heat intolerance refers to the inability to withstand high temperatures or to maintain a comfortable body temperature. This symptom produces a continuous feeling of being overheated and, at times, profuse diaphoresis. It usually develops gradually and is chronic.
Most cases of heat intolerance result from thyrotoxicosis. In this disorder, excess thyroid hormone stimulates peripheral tissues, increasing basal metabolism and producing excess heat. Although rare, hypothalamic disease may also cause intolerance to heat and cold.
Ask the patient when he first noticed his heat intolerance. Did he gradually use fewer blankets at night? Does he have to turn up the air conditioning to keep cool? Is it hard for him to adjust to warm weather? Does he sweat a lot in a hot environment? Find out if his appetite or weight has changed. Also, ask about unusual nervousness or other personality changes. Then take a drug history, especially noting use of amphetamines or amphetamine-like drugs. Ask the patient if he takes a thyroid drug. If so, what is the daily dosage and when did he last take it?
As you begin the examination, notice how much clothing the patient is wearing. After taking vital signs, inspect the patient's skin for flushing and diaphoresis. Also, note tremors and lid lag.
Hypothalamic disease. In this rare disease, body temperature fluctuates dramatically, causing alternating heat and cold intolerance. Related features include amenorrhea, disturbed sleep patterns, increased thirst and urination, increased appetite with weight gain, impaired visual acuity, headache, and personality changes, such as bursts of rage or laughter. Common causes of hypothalamic disease are pituitary adenoma and hypothalamic and pineal tumors.
Thyrotoxicosis. A classic symptom of thyrotoxicosis, heat intolerance may be accompanied by an enlarged thyroid gland, nervousness, weight loss despite increased appetite, diaphoresis, diarrhea, tremor, and palpitations. Although exophthalmos is characteristic, many patients don't display this sign. Associated findings may affect virtually every body system. Some common findings include irritability, difficulty concentrating, mood swings, insomnia, muscle weakness, fatigue, lid lag, tachycardia, full and bounding pulse, widened pulse pressure, dyspnea, amenorrhea, and gynecomastia. Typically, the patient's skin is warm and flushed; premature graying and alopecia occur in both sexes.
Drugs. Amphetamines, amphetamine-like appetite suppressants, and excessive doses of thyroid hormone may cause heat intolerance. Anticholinergics may interfere with sweating, resulting in heat intolerance.
Adjust room temperature to make the patient comfortable. If the patient is diaphoretic,

change his clothing and bed linens as necessary, and encourage him to drink lots of fluids.
Rarely, maternal thyrotoxicosis may be passed to the neonate, resulting in heat intolerance. More commonly, acquired thyrotoxicosis appears between ages 12 and 14, although this too is infrequent. Dehydration may also make a child sensitive to heat.
Heberden's nodes
Heberden's nodes are painless, irregular, cartilaginous or bony enlargements of the distal interphalangeal joints of the fingers. They reflect degeneration of articular cartilage, which irritates the bone and stimulates osteoblasts, causing bony enlargement. Approximately 2 to 3 mm in diameter, Heberden's nodes develop on one or both sides of the dorsal midline. The dominant hand usually has larger nodes, which affect one or more fingers but not the thumb. (See Recognizing Heberden's nodes.)
Osteoarthritis is the most common cause of Heberden's nodes; in fact, more than one-half of all osteoarthritic patients have these nodes. Less commonly, repeated fingertip trauma may lead to node formation in only one joint (“baseball finger”). Because Heberden's nodes aren't associated with joint pain or loss of function, they aren't a primary indicator of osteoarthritis; however, they're a helpful adjunct to diagnosis.
Begin by asking the patient if anyone else in his family has had Heberden's nodes or osteoarthritis. Are the patient's joints stiff? Does stiffness disappear with movement? Ask him which hand is dominant. Also ask about repeated fingertip trauma associated with his job or sports.
Carefully palpate the nodes, noting any signs of inflammation, such as redness and tenderness. Then determine range of motion (ROM) in the fingers of each hand. As you do so, listen and feel for crepitation.
Osteoarthritis. This disorder commonly causes Heberden's nodes and may also cause nodes in the proximal interphalangeal joints (Bouchard's nodes). Its chief symptom, though, is joint pain that's aggravated by movement or weight bearing. Joints may also be tender and display restricted ROM. Typically, joint stiffness is triggered by disuse and relieved by brief exercise. Stiffness may be accompanied by bony enlargement and crepitus.
Remind the patient to take an anti-inflammatory drug and to exercise regularly. Encourage him to avoid joint strain, for example, by maintaining a healthy body weight.
Because children don't suffer from osteoarthritis, they don't develop Heberden's nodes.
Hematemesis, the vomiting of blood, usually indicates GI bleeding above the ligament of Treitz, which suspends the duodenum at its junction with the jejunum. Bright red or blood-streaked vomitus indicates fresh or recent bleeding. Dark red, brown, or black vomitus (the color and consistency of coffee grounds) indicates that blood has been retained in the stomach and partially digested.
Although hematemesis usually results from a GI disorder, it may stem from a coagulation disorder or from a treatment that irritates the GI tract. Swallowed blood from epistaxis or oropharyngeal erosion may also cause bloody vomitus. Hematemesis may be precipitated by straining, emotional stress, and the use of

anti-inflammatory drugs or alcohol. In a patient with esophageal varices, hematemesis may be due to trauma from swallowing hard or partially chewed food. (See Rare causes of hematemesis.)
Hematemesis is always an important sign, but its severity depends on the amount, source, and intensity of the bleeding. Massive hematemesis (vomiting of 500 to 1,000 ml of blood) may be life-threatening.
image If the patient has massive hematemesis, check his vital signs. If you detect signs of shock—such as tachypnea, hypotension, and tachycardia—place the patient in a supine position, and elevate his feet 20 to 30 degrees. Start a large-bore I.V. catheter for emergency fluid replacement. Also, obtain a blood sample for typing and crossmatching, hemoglobin level, and hematocrit, and administer oxygen. Emergency endoscopy may be necessary to locate the source of bleeding. Prepare to insert a nasogastric (NG) tube for suction or iced lavage. A Sengstaken-Blakemore tube may be used to compress esophageal varices. (See Managing hematemesis with intubation, page 356.)
If hematemesis isn't immediately life-threatening, begin with a thorough history. First, have the patient describe the amount, color, and consistency of the vomitus. When did he first notice this sign? Has he ever had hematemesis before? Find out if he also has bloody or black tarry stools. Note whether hematemesis is usually preceded by nausea, flatulence, diarrhea, or weakness. Has he recently had bouts of retching with or without vomiting?
Next, ask about a history of ulcers or of liver or coagulation disorders. Find out how much alcohol the patient drinks, if any. Does he regularly take aspirin or another nonsteroidal anti-inflammatory drug (NSAID), such as phenylbutazone or indomethacin? These drugs may cause erosive gastritis or ulcers.
Begin the physical examination by checking for orthostatic hypotension, an early warning sign of hypovolemia. Take blood pressure and pulse with the patient in the supine, sitting, and standing positions. A decrease of 10 mm Hg or more in systolic pressure or an increase of 10 beats/minute or more in pulse rate indicates volume depletion. After obtaining other vital signs, inspect the mucous membranes, nasopharynx, and skin for any signs of bleeding or other abnormalities. Finally, palpate the abdomen for tenderness, pain, or masses. Note lymphadenopathy.
Achalasia. Hematemesis is a rare effect of this disorder, which usually causes passive regurgitation and painless, progressive dysphagia. Regurgitation of undigested food may cause hoarseness, coughing, aspiration, and recurrent pulmonary infections.
Anthrax, GI. GI anthrax is caused by eating meat contaminated with the gram-positive, spore-forming bacterium Bacillus anthracis. Initial signs and symptoms of anorexia, nausea, vomiting, and fever may progress to hematemesis, abdominal pain, and severe bloody diarrhea.
Coagulation disorders. Any disorder that disrupts normal clotting, such as thrombocytopenia or hemophilia, may result in GI bleeding and moderate to severe hematemesis. Bleeding may occur in other body systems as well, resulting in such signs as epistaxis and ecchymosis. Associated effects depend on the specific coagulation disorder.
Esophageal cancer. A late sign of this cancer, hematemesis may be accompanied by steady chest pain that radiates to the back. Other features include substernal fullness, severe dysphagia, nausea, vomiting with nocturnal regurgitation and aspiration, hemoptysis, fever, hiccups, sore throat, melena, and halitosis.

Esophageal injury by caustic substances. Ingestion of corrosive acids or alkalies produces esophageal injury associated with grossly bloody or coffee-ground vomitus. Hematemesis is accompanied by epigastric and anterior or retrosternal chest pain that's intensified by swallowing. With ingestion of alkaline agents, the oral and pharyngeal mucosa may produce a soapy white film. The mucosa becomes brown and edematous with time. Dysphagia, marked salivation, and fever may develop in 3 to 4 weeks and worsen as strictures form.
Esophageal rupture. The severity of hematemesis depends on the cause of the rupture. When an instrument damages the esophagus, hematemesis is usually slight. However, rupture due to Boerhaave's syndrome (increased esophageal pressure from vomiting or retching) or other esophageal disorders typically causes more severe hematemesis. This life-threatening disorder may also produce severe retrosternal, epigastric, neck, or scapular pain accompanied by chest and neck edema. Examination reveals subcutaneous crepitation in the chest wall,

supraclavicular fossa, and neck. The patient may also show signs of respiratory distress, such as dyspnea and cyanosis.
Esophageal varices (ruptured). Life-threatening rupture of esophageal varices may produce coffee-ground or massive bright red vomitus. Signs of shock, such as hypotension and tachycardia, may follow or even precede hematemesis if the stomach fills with blood before vomiting occurs. Other symptoms may include abdominal distention and melena or painless hematochezia (ranging from slight oozing to massive rectal hemorrhage).
Gastric cancer. Painless bright red or dark brown vomitus is a late sign of this uncommon cancer, which usually begins insidiously with upper abdominal discomfort. The patient then develops anorexia, mild nausea, and chronic dyspepsia that's unrelieved by antacids and exacerbated by food. Later symptoms may include fatigue, weakness, weight loss, feelings of fullness, melena, altered bowel habits, and signs of malnutrition, such as muscle wasting and dry skin.
Gastritis (acute). Hematemesis and melena are the most common signs of acute gastritis. They may even be the only signs, although mild epigastric discomfort, nausea, fever, and malaise may also occur. Massive blood loss precipitates signs of shock. Typically, the patient has a history of alcohol abuse or has used aspirin or another NSAID. Gastritis may also occur secondary to Helicobacter pylori infection.
Gastroesophageal reflux disease. Although rare in this disorder, hematemesis may produce significant blood loss. It's accompanied by pyrosis, flatulence, dyspepsia, and postural regurgitation that can be aggravated by lying down or stooping over. Related effects include dysphagia, retrosternal angina-like chest pain, weight loss, halitosis, and signs of aspiration, such as dyspnea and recurrent pulmonary infections.
Leiomyoma. This benign tumor occasionally involves the GI tract, eroding the mucosa or vascular supply to produce hematemesis. Other features vary with the tumor's size and location. For example, esophageal involvement may cause dysphagia and weight loss.
Mallory-Weiss syndrome. Characterized by a mucosal tear of the mucous membrane at the junction of the esophagus and the stomach, this syndrome may produce hematemesis and melena. It's commonly triggered by severe vomiting, retching, or straining (as from coughing), usually in alcoholics or in people whose pylorus is obstructed. Severe bleeding may precipitate signs of shock, such as tachycardia, hypotension, dyspnea, and cool, clammy skin.
Peptic ulcer. Hematemesis may occur when a peptic ulcer penetrates an artery, vein, or highly vascular tissue. Massive—and possibly life-threatening—hematemesis is typical when an artery is penetrated. Other features include melena or hematochezia, chills, fever, and signs and symptoms of shock and dehydration, such as tachycardia, hypotension, poor skin turgor, and thirst. Most patients have a history of nausea, vomiting, epigastric tenderness, and epigastric pain that's relieved by foods or antacids. Some may also have a history of habitual use of tobacco, alcohol, or NSAIDs.
Treatments. Traumatic NG or endotracheal intubation may cause hematemesis associated with swallowed blood. Nose or throat surgery may also cause this sign in the same way.
Closely monitor the patient's vital signs, and watch for signs of shock. Check the patient's stools regularly for occult blood, and keep accurate intake and output records. Place the patient on bed rest in a low or semi-Fowler's position to prevent aspiration of vomitus. Keep suctioning equipment nearby, and use it as needed. Provide frequent oral hygiene and emotional support—the sight of bloody vomitus can be very frightening. Administer a histamine-2 blocker I.V.; vasopressin may be required for ruptured esophageal varices. As the bleeding tapers off, monitor the pH of gastric contents, and give hourly doses of antacids by NG tube as necessary.
Hematemesis is much less common in children than in adults and may be related to foreignbody ingestion. Occasionally, neonates develop hematemesis after swallowing maternal blood during delivery or breast-feeding from a cracked nipple. Hemorrhagic disease of the neonate and esophageal erosion may also cause hematemesis in infants; such cases require immediate fluid replacement.
In elderly patients, hematemesis may be caused by a vascular anomaly, an aortoenteric fistula, or upper GI cancer. In addition, chronic

obstructive pulmonary disease, chronic hepatic or renal failure, and chronic NSAID use all predispose elderly people to hemorrhage secondary to coexisting ulcerative disorders.
Explain diagnostic tests, such as endoscopy, barium swallow, and variceal banding. Explain laboratory tests, such as serum electrolyte levels, complete blood count, prothrombin time, partial thromboplastin time, and international normalized ratio.
[Rectal bleeding]
The passage of bloody stools, also known as hematochezia, usually indicates—and may be the first sign of—GI bleeding below the ligament of Treitz. However, this sign—usually preceded by hematemesis—may also accompany rapid hemorrhage of 1 L or more from the upper GI tract.
Hematochezia ranges from formed, bloodstreaked stools to liquid, bloody stools that may be bright red, dark mahogany, or maroon in color. This sign usually develops abruptly and is heralded by abdominal pain.
Although hematochezia is commonly associated with GI disorders, it may also result from a coagulation disorder, exposure to toxins, or certain diagnostic tests. Always a significant sign, hematochezia may precipitate life-threatening hypovolemia.
image If the patient has severe hematochezia, check his vital signs. If you detect signs of shock, such as hypotension and tachycardia, place the patient in a supine position and elevate his feet 20 to 30 degrees. Prepare to administer oxygen, and start a large-bore I.V. catheter for emergency fluid replacement. Next, obtain a blood sample for typing and crossmatching, hemoglobin level, and hematocrit. Insert a nasogastric tube. Iced lavage may be indicated to control bleeding. Endoscopy may be necessary to detect the source of the bleeding.
If the hematochezia isn't immediately life-threatening, ask the patient to fully describe the amount, color, and consistency of his bloody stools. (If possible, also inspect and characterize the stools yourself.) How long have the stools been bloody? Do they always look the same, or does the amount of blood seem to vary? Ask about associated signs and symptoms.
Next, explore the patient's medical history, focusing on GI and coagulation disorders. Ask about the use of GI irritants, such as alcohol, aspirin, and other nonsteroidal anti-inflammatory drugs.
Begin the physical examination by checking for orthostatic hypotension, an early sign of shock. Take the patient's blood pressure and pulse while he's lying down, sitting, and standing. If systolic pressure decreases by 10 mm Hg or more, or pulse rate increases by 10 beats/minute or more when he changes position, suspect volume depletion and impending shock.
Examine the skin for petechiae or spider angiomas. Palpate the abdomen for tenderness, pain, or masses. Also, note lymphadenopathy. Finally, a digital rectal examination must be done to rule out rectal masses or hemorrhoids.
Amyloidosis. Hematochezia occasionally occurs when this disorder affects the GI tract. Massive, rapid hematochezia may precipitate signs of shock, such as hypotension and tachycardia. Associated signs and symptoms include hypoactive or absent bowel sounds, abdominal pain, malabsorption, diarrhea, and renal disease. The patient may also have a stiff, enlarged tongue, resulting in dysarthria.
Anal fissure. Slight hematochezia characterizes this disorder; blood may streak the stools or appear on toilet tissue. Accompanying hematochezia is severe rectal pain that may make the patient reluctant to defecate, thereby causing constipation.
Angiodysplastic lesions. Most common in elderly patients, these arteriovenous lesions of the ascending colon typically cause chronic, bright red rectal bleeding. Occasionally, they may result in life-threatening blood loss and signs of shock, such as tachycardia and hypotension.
Anorectal fistula. Blood, pus, mucus, and occasionally stools may drain from this type of fistula. Other effects include rectal pain and pruritus.
Coagulation disorders. Patients with a coagulation disorder (such as thrombocytopenia or disseminated intravascular coagulation) may experience GI bleeding marked by moderate to severe hematochezia. Bleeding may also occur

in other body systems, producing such signs as epistaxis and purpura. Associated findings vary with the specific coagulation disorder.
Colitis. Ischemic colitis commonly causes bloody diarrhea, especially in elderly patients. Rectal bleeding may be slight or massive and is usually accompanied by severe, cramping lower abdominal pain and hypotension. Other effects include abdominal tenderness, distention, and absent bowel sounds. Severe colitis may cause life-threatening hypovolemic shock and peritonitis.
Ulcerative colitis typically causes bloody diarrhea that may also contain mucus. Blood loss may be slight or massive and is preceded by mild to severe abdominal cramps. Associated signs and symptoms include fever, tenesmus, anorexia, nausea, vomiting, hyperactive bowel sounds and, occasionally, tachycardia. Weight loss and weakness occur late.
Colon cancer. Bright red rectal bleeding with or without pain is a telling sign, especially in cancer of the left colon. This type of tumor usually causes early signs of obstruction, such as rectal pressure, bleeding, and intermittent fullness or cramping. As the disease progresses, the patient also develops obstipation, diarrhea or ribbon-shaped stools, and pain that's typically relieved by passage of stools or flatus. Stools are grossly bloody.
Cancer of the right colon may initially cause melena and abdominal aching, pressure, and dull cramps. As the disease progresses, the patient may also experience diarrhea, anorexia, weight loss, anemia, weakness and fatigue, vomiting, an abdominal mass, and signs of obstruction, such as abdominal distention and abnormal bowel sounds.
Colorectal polyps. These polyps are the most common cause of intermittent hematochezia in adults younger than age 60, but they don't always produce symptoms. When located high in the colon, polyps may cause bloodstreaked stools that yield a positive response when tested with guaiac. If the polyps are located closer to the rectum, they may bleed freely.
Crohn's disease. Hematochezia is not a common sign of this disorder unless the perineum is involved. If rectal bleeding does occur, it's likely to be massive. The chief clinical features of Crohn's disease include fever, abdominal distention and pain with guarding, diarrhea, hyperactive bowel sounds, anorexia, nausea, and fatigue. Palpation may reveal a mass in the colon.
Diverticulitis. Most common in elderly patients, this disorder can suddenly cause mild to moderate rectal bleeding after the patient feels the urge to defecate. The bleeding may end abruptly or may progress to life-threatening blood loss with signs of shock. Associated signs and symptoms may include left-lower-quadrant pain that's relieved by defecation, alternating episodes of constipation and diarrhea, anorexia, nausea and vomiting, rebound tenderness, and a distended tympanic abdomen.
Dysentery. Bloody diarrhea is common in infection with Shigella, Amoeba, and Campylobacter, but rare with Salmonella. Abdominal pain or cramps, tenesmus, fever, and nausea may also occur.
Esophageal varices (ruptured). In this life-threatening disorder, hematochezia may range from slight rectal oozing to grossly bloody stools and may be accompanied by mild to severe hematemesis or melena. Signs of shock, such as tachycardia and hypotension, may follow or occasionally precede overt signs of bleeding. Typically, the patient has a history of chronic liver disease.
Food poisoning (staphylococcal). The patient may have bloody diarrhea 1 to 6 hours after ingesting food toxins. Accompanying signs and symptoms, which last a few hours, include severe, cramping abdominal pain, nausea and vomiting, and prostration.
Hemorrhoids. Hematochezia may accompany external hemorrhoids, which typically cause painful defecation, resulting in constipation. Less painful internal hemorrhoids usually produce more chronic bleeding with bowel movements, which may eventually lead to signs of anemia, such as weakness and fatigue.
Leptospirosis. The severe form of this infection—Weil's syndrome—produces hematochezia or melena along with other signs of bleeding, such as epistaxis and hemoptysis. The bleeding is typically preceded by a sudden frontal headache, severe thigh and lumbar myalgia, cutaneous hyperesthesia, and conjunctival suffusion. Bleeding is followed by chills, a rapidly rising fever, and perhaps nausea and vomiting. Fever, headache, and myalgia usually intensify and persist for weeks. Other findings may include right-upper-quadrant tenderness, hepatomegaly, and jaundice.
Peptic ulcer. Upper GI bleeding is a common complication in this disorder. The patient may display hematochezia, hematemesis, or melena, depending on the intensity and amount of

bleeding. If the peptic ulcer penetrates an artery or vein, massive bleeding may precipitate signs of shock, such as hypotension and tachycardia. Other findings may include chills, fever, nausea and vomiting, and signs of dehydration, such as dry mucous membranes, poor skin turgor, and thirst. Most patients have a history of epigastric pain that's relieved by foods or antacids; some also have a history of habitual use of tobacco, alcohol, or nonsteroidal anti-inflammatory drugs.
Rectal melanoma (malignant). This rare form of rectal cancer typically causes recurrent rectal bleeding that arises from a painless, asymptomatic mass.
Small-intestine cancer. This disorder occasionally produces slight hematochezia or bloodstreaked stools. Its characteristic features include colicky pain and postprandial vomiting. Other common signs and symptoms include anorexia, weight loss, and fever. Palpation may reveal abdominal masses.
Typhoid fever. About 10% of patients with typhoid fever develop hematochezia, which is occasionally massive. However, melena is more common. Both signs of bleeding occur late and may be accompanied by marked abdominal distention, diarrhea, significant weight loss, mental dullness, and profound fatigue. Earlier signs and symptoms are pathognomonic rose spots, headache, chills, fever, constipation, dry cough, conjunctivitis, and epistaxis.
Ulcerative proctitis. In this disorder, the patient typically has an intense urge to defecate but passes only bright red blood, pus, or mucus. Other common findings include acute constipation and tenesmus.
Heavy metal poisoning. Bloody diarrhea is accompanied by cramping abdominal pain, nausea, and vomiting. Other signs may include tachycardia, hypotension, seizures, paresthesia, depressed or absent deep tendon reflexes, and an altered level of consciousness.
Tests. Certain procedures, especially colonoscopy, polypectomy, and proctosigmoidoscopy, may cause rectal bleeding. Bowel perforation is rare.
Place the patient on bed rest and check his vital signs frequently, watching for signs of shock, such as hypotension, tachycardia, weak pulse, and tachypnea. Monitor the patient's intake and output hourly. Remember to provide emotional support because hematochezia may frighten the patient.
Prepare the patient for blood tests and GI procedures, such as endoscopy and GI X-rays. Visually examine the patient's stools and test them for occult blood. If necessary, send a stool specimen to the laboratory to check for parasites.
Hematochezia is much less common in children than in adults. It may result from structural disorders, such as intussusception and Meckel's diverticulum, and from inflammatory disorders, such as peptic ulcer disease and ulcerative colitis.
In children, ulcerative colitis typically produces chronic, rather than acute, signs and symptoms and may also cause slow growth and maturation related to malnutrition. Suspect sexual abuse in all cases of rectal bleeding in children.
Because older people have an increased risk of colon cancer, hematochezia should be evaluated with colonoscopy after perirectal lesions have been ruled out as the cause of bleeding.
A cardinal sign of renal and urinary tract disorders, hematuria is the abnormal presence of blood in the urine. Strictly defined, it means three or more red blood cells (RBCs) per highpower microscopic field in the urine. Microscopic hematuria is confirmed by an occult blood test, whereas macroscopic hematuria is immediately visible. However, macroscopic hematuria must be distinguished from pseudohematuria. (See Confirming hematuria.) Macroscopic hematuria may be continuous or intermittent, is often accompanied by pain, and may be aggravated by prolonged standing or walking.
Hematuria may be classified by the stage of urination it predominantly affects. Bleeding at the start of urination—initial hematuria—usually indicates urethral pathology; bleeding at the end of urination—terminal hematuria—usually indicates pathology of the bladder neck, posterior urethra, or prostate; bleeding throughout urination —total hematuria—usually indicates pathology above the bladder neck.

Hematuria may result from one of two mechanisms: rupture or perforation of vessels in the renal system or urinary tract, or impaired glomerular filtration, which allows RBCs to seep into the urine. The color of the bloody urine provides a clue to the source of the bleeding. Generally, dark or brownish blood indicates renal or upper urinary tract bleeding, whereas bright red blood indicates lower urinary tract bleeding.
Although hematuria usually results from renal and urinary tract disorders, it may also result from certain GI, prostate, vaginal, or coagulation disorders or from the effects of certain drugs. Invasive therapy and diagnostic tests that involve manipulative instrumentation of the renal and urologic systems may also cause hematuria. Nonpathologic hematuria may result from fever and hypercatabolic states. Transient hematuria may follow strenuous exercise. (See Hematuria: Causes and associated findings, pages 362 to 365.)
After detecting hematuria, take a pertinent health history. If hematuria is macroscopic, ask the patient when he first noticed blood in his urine. Does it vary in severity between voidings? Is it worse at the beginning, middle, or end of urination? Has it occurred before? Is the patient passing any clots? To rule out artifactual hematuria, ask about bleeding hemorrhoids or the onset of menses, if appropriate. Ask if pain or burning accompanies the episodes of hematuria.
Ask about recent abdominal or flank trauma. Has the patient been exercising strenuously? Note a history of renal, urinary, prostatic, or coagulation disorders. Then obtain a drug history, noting the use of anticoagulants or aspirin.
Begin the physical examination by palpating and percussing the abdomen and flanks. Next, percuss the costovertebral angle (CVA) to elicit tenderness. Check the urinary meatus for bleeding or other abnormalities. Using a chemical reagent strip, test a urine specimen for protein. A vaginal or digital rectal examination may be necessary.
Appendicitis. About 15% of patients with appendicitis have either microscopic or macroscopic hematuria accompanied by bladder tenderness, dysuria, and urinary urgency. More typical findings include constant right-lowerquadrant pain (especially over McBurney's point), nausea and vomiting, anorexia, abdominal rigidity, rebound tenderness, constipation, tachycardia, and low-grade fever.
Bladder cancer. A primary cause of gross hematuria in men, bladder cancer may also produce pain in the bladder, rectum, pelvis, flank, back, or leg. Other common features are nocturia, dysuria, urinary frequency and urgency, vomiting, diarrhea, and insomnia.
Bladder trauma. A characteristic finding in traumatic rupture or perforation of the bladder, gross hematuria is typically accompanied by lower abdominal pain. The patient may also develop anuria despite a strong urge to void; swelling of the scrotum, buttocks, or perineum; and signs of shock, such as tachycardia and hypotension.
Calculi. Both bladder and renal calculi produce hematuria, which may be associated with signs of urinary tract infection, such as dysuria and urinary frequency and urgency. Bladder calculi may also cause gross hematuria, referred pain to the lower back or penile or vulvar area and, occasionally, bladder distention. Renal calculi may produce microscopic or gross hematuria. The cardinal symptom, though, is colicky pain that travels from the CVA to the flank, suprapubic region, and external





genitalia when a calculus is passed. The pain may be excruciating at its peak. Other signs and symptoms may include nausea and vomiting, restlessness, fever, chills, abdominal distention and, possibly, decreased bowel sounds.
Coagulation disorders. Macroscopic hematuria is commonly the first sign of hemorrhage in coagulation disorders, such as thrombocytopenia or disseminated intravascular coagulation. Among other features are epistaxis, purpura (petechiae and ecchymosis), and signs of GI bleeding.
Cortical necrosis (acute). Accompanying gross hematuria in this renal disorder are intense flank pain, anuria, leukocytosis, and fever.
Cystitis. Hematuria is a telling sign in all types of cystitis. Bacterial cystitis usually produces macroscopic hematuria with urinary urgency and frequency, dysuria, nocturia, and tenesmus. The patient complains of perineal and lumbar pain, suprapubic discomfort, and fatigue and occasionally has a low-grade fever.
More common in women, chronic interstitial cystitis occasionally causes gross hematuria. Associated features include urinary frequency, dysuria, nocturia, and tenesmus. Both microscopic and macroscopic hematuria may occur in tubercular cystitis, which may also cause urinary urgency and frequency, dysuria, tenesmus, flank pain, fatigue, and anorexia. Viral cystitis usually produces hematuria, urinary urgency and frequency, dysuria, nocturia, tenesmus, and fever.
Diverticulitis. When this disorder involves the bladder, it usually causes microscopic hematuria, urinary frequency and urgency, dysuria, and nocturia. Characteristic findings include left-lower-quadrant pain, abdominal tenderness, constipation or diarrhea and, occasionally, a palpable, firm, fixed, and tender abdominal mass. The patient may also develop mild nausea, flatulence, and a low-grade fever.
Endocarditis (subacute infective). Occasionally, this disorder produces embolization, resulting in renal infarction and microscopic or gross hematuria. Common related findings are constant fever, chills, night sweats, fatigue, pallor, anorexia, weight loss, polyarthralgia, petechiae, flank pain, severe back pain, stiff neck, cardiac murmurs, tachycardia, and splenomegaly.
Glomerulonephritis. Acute glomerulonephritis usually begins with gross hematuria that tapers off to microscopic hematuria and RBC casts, which may persist for months. It may also produce oliguria or anuria, proteinuria, mild fever, fatigue, flank and abdominal pain, generalized edema, increased blood pressure, nausea, vomiting, and signs of lung congestion, such as crackles and a productive cough.
Chronic glomerulonephritis usually causes microscopic hematuria accompanied by proteinuria, generalized edema, and increased blood pressure. Signs and symptoms of uremia may also occur in advanced disease.
Nephritis (interstitial). Typically, this infection causes microscopic hematuria. However, some patients with acute interstitial nephritis may develop gross hematuria. Other findings are fever, maculopapular rash, and oliguria or anuria. In chronic interstitial nephritis, the patient has dilute—almost colorless—urine that may be accompanied by polyuria and increased blood pressure.
Nephropathy (obstructive). This disorder may cause microscopic or macroscopic hematuria, but urine is rarely grossly bloody. The patient may report colicky flank and abdominal pain, CVA tenderness, and anuria or oliguria that alternates with polyuria.
Polycystic kidney disease. This hereditary disorder may cause recurrent microscopic or gross hematuria. It commonly produces no symptoms before age 40 but may cause increased blood pressure, polyuria, dull flank pain, and signs of urinary tract infection, such as dysuria and urinary frequency and urgency. Later, the patient develops a swollen, tender abdomen and lumbar pain that's aggravated by exertion and relieved by lying down. He may also have proteinuria and colicky abdominal pain from the ureteral passage of clots or calculi.
Prostatic hyperplasia (benign). About 20% of patients with an enlarged prostate have macroscopic hematuria, usually when a significant obstruction is present. The hematuria is usually preceded by diminished urinary stream, tenesmus, and a feeling of incomplete voiding. It may be accompanied by urinary hesitancy, frequency, and incontinence; nocturia; perineal pain; and constipation. Inspection reveals a midline mass representing the distended bladder; rectal palpation reveals an enlarged prostate.
Prostatitis. Whether acute or chronic, prostatitis may cause macroscopic hematuria, usually at the end of urination. It may also produce urinary frequency and urgency and dysuria followed by visible bladder distention.
Acute prostatitis also produces fatigue, malaise, myalgia, polyarthralgia, fever with

chills, nausea, vomiting, perineal and low back pain, and decreased libido. Rectal palpation reveals a tender, swollen, boggy, firm prostate.
Chronic prostatitis commonly follows an acute attack. It may cause persistent urethral discharge, dull perineal pain, ejaculatory pain, and decreased libido.
Pyelonephritis (acute). This infection typically produces microscopic or macroscopic hematuria that progresses to gross hematuria. After the infection resolves, microscopic hematuria may persist for a few months. Related signs and symptoms include persistent high fever, unilateral or bilateral flank pain, CVA tenderness, shaking chills, weakness, fatigue, dysuria, urinary frequency and urgency, nocturia, and tenesmus. The patient may also exhibit nausea, vomiting, anorexia, and signs of paralytic ileus, such as hypoactive or absent bowel sounds and abdominal distention.
Renal cancer. The classic triad of signs and symptoms includes gross hematuria; dull, aching flank pain; and a smooth, firm, palpable flank mass. Colicky pain may accompany the passage of clots. Other findings include fever, CVA tenderness, and increased blood pressure. In advanced disease, the patient may develop weight loss, nausea and vomiting, and leg edema with varicoceles.
Renal infarction. Typically, this disorder produces gross hematuria. The patient may complain of constant, severe flank and upper abdominal pain accompanied by CVA tenderness, anorexia, and nausea and vomiting. Other findings include oliguria or anuria, proteinuria, hypoactive bowel sounds and, a day or two after the infarction, fever and increased blood pressure.
Renal papillary necrosis (acute). This disorder usually produces gross hematuria, which may be accompanied by intense flank pain, CVA tenderness, abdominal rigidity and colicky pain, oliguria or anuria, pyuria, fever, chills, vomiting, and hypoactive bowel sounds. Arthralgia and hypertension are common.
Renal trauma. About 80% of patients with renal trauma have microscopic or gross hematuria. Accompanying signs and symptoms may include flank pain, a palpable flank mass, oliguria, hematoma or ecchymosis over the upper abdomen or flank, nausea and vomiting, and hypoactive bowel sounds. Severe trauma may precipitate signs of shock, such as tachycardia and hypotension.
Renal tuberculosis. Gross hematuria is often the first sign of this disorder. It may be accompanied by urinary frequency, dysuria, pyuria, tenesmus, colicky abdominal pain, lumbar pain, and proteinuria.
Renal vein thrombosis. Gross hematuria usually occurs in this type of thrombosis. In an abrupt venous obstruction, the patient experiences severe flank and lumbar pain as well as epigastric and CVA tenderness. Other features include fever, pallor, proteinuria, peripheral edema and, when the obstruction is bilateral, oliguria or anuria and other uremic signs. The kidneys are easily palpable. Gradual venous obstruction causes signs of nephrotic syndrome, proteinuria and, occasionally, peripheral edema.
Schistosomiasis. This infection usually causes intermittent hematuria at the end of urination. It may be accompanied by dysuria, colicky renal and bladder pain, and palpable lower abdominal masses.
Sickle cell anemia. In this hereditary disorder, gross hematuria may result from congestion of the renal papillae. Associated signs and symptoms may include pallor, dehydration, chronic fatigue, polyarthralgia, leg ulcers, dyspnea, chest pain, impaired growth and development, hepatomegaly and, possibly, jaundice. Auscultation reveals tachycardia and systolic and diastolic murmurs.
Systemic lupus erythematosus. Gross hematuria and proteinuria may occur when this disorder involves the kidneys. Cardinal features include nondeforming joint pain and stiffness, a butterfly rash, photosensitivity, Raynaud's phenomenon, seizures or psychoses, recurrent fever, lymphadenopathy, oral or nasopharyngeal ulcers, anorexia, and weight loss.
Urethral trauma. Hematuria may occur initially, possibly with blood at the urinary meatus, local pain, and penile or vulvar ecchymosis.
Vaginitis. When this infection spreads to the urinary tract, it may produce macroscopic hematuria. Related signs and symptoms may include urinary frequency and urgency, dysuria, nocturia, perineal pain, pruritus, and a malodorous vaginal discharge.
Vasculitis. Hematuria is usually microscopic in this disorder. Associated signs and symptoms include malaise, myalgia, polyarthralgia, fever, increased blood pressure, pallor and, occasionally, anuria. Other features, such as urticaria and purpura, may reflect the etiology of vasculitis.
Diagnostic tests. Renal biopsy is the diagnostic test most often associated with hematuria.

This sign may also result from biopsy or manipulative instrumentation of the urinary tract, as in cystoscopy.
Drugs. Drugs that commonly cause hematuria are anticoagulants, aspirin (toxicity), analgesics, cyclophosphamide, metyrosine, penicillin, rifampin, and thiabendazole.
image When taken with an anticoagulant, herbal medicines such as garlic and ginkgo biloba can cause excessive bleeding and hematuria.
Treatments. Any therapy that involves manipulative instrumentation of the urinary tract, such as transurethral prostatectomy, may cause microscopic or macroscopic hematuria. After a kidney transplant, a patient may experience hematuria with or without clots, which may require indwelling urinary catheter irrigation.
Because hematuria may frighten and upset the patient, be sure to provide emotional support. Check his vital signs at least every 4 hours and monitor intake and output, including the amount and pattern of hematuria. If the patient has an indwelling urinary catheter in place, ensure its patency and irrigate it if necessary to remove clots and tissue that may impede urine drainage. Administer prescribed analgesics, and enforce bed rest as indicated. Prepare the patient for diagnostic tests, such as blood and urine studies, cystoscopy, and renal X-rays or biopsy.
Many of the causes described above also produce hematuria in children. However, cyclophosphamide is more likely to cause hematuria in children than in adults.
Common causes of hematuria that chiefly affect children include congenital anomalies, such as obstructive uropathy and renal dysplasia; birth trauma; hematologic disorders, such as vitamin K deficiency, hemophilia, and hemolyticuremic syndrome; certain neoplasms, such as Wilms' tumor, bladder cancer, and rhabdomyosarcoma; allergies; and foreign bodies in the urinary tract. Artifactual hematuria may result from recent circumcision.
Evaluation of hematuria in elderly patients should include a urine culture, excretory urography or sonography, and consultation with a urologist.
Teach the patient how to collect serial urine specimens using the three-glass technique. This technique helps determine whether hematuria marks the beginning, end, or entire course of urination.
Hemianopsia is loss of vision in one-half the normal visual field (usually the right or left half ) of one or both eyes. However, if the visual field defects are identical in both eyes but affect less than half the field of vision in each eye (incomplete homonymous hemianopsia), the lesion may be in the occipital lobe; otherwise, it probably involves the parietal or temporal lobe. (See Recognizing types of hemianopsia.)
Hemianopsia is caused by a lesion affecting the optic chiasm, the optic tract, or the optic radiation. Defects in visual perception due to cerebral lesions are usually associated with impaired color vision.
Suspect a visual field defect if the patient seems startled when you approach him from one side or if he fails to see objects placed directly in front of him. To help determine the type of defect, compare the patient's visual fields with your own—assuming that yours are normal. First, ask the patient to cover his right eye while you cover your left eye. Then move a pen or similarly shaped object from the periphery of his (and your) uncovered eye into his field of vision. Ask the patient to indicate when he first sees the object. Does he see it at the same time you do? After you do? Repeat this test in each quadrant of both eyes. Then, for each eye, plot the defect by shading the area of a circle that corresponds to the area of vision loss.
Next, evaluate the patient's level of consciousness (LOC), take his vital signs, and check his pupillary reaction and motor response. Ask if he has recently experienced headache, dysarthria, or seizures. Does he have ptosis or facial or extremity weakness? Hallucinations or loss of color vision? When did his neurologic symptoms start? Obtain a medical history, noting especially eye disorders, hypertension, diabetes mellitus, and recent head trauma.


Carotid artery aneurysm. An aneurysm in the internal carotid artery can cause contralateral or bilateral defects in the visual fields. It can also cause hemiplegia, decreased LOC, headache, aphasia, behavior disturbances, and unilateral hypoesthesia.
Occipital lobe lesion. The most common symptoms arising from a lesion of one occipital lobe are incomplete homonymous hemianopsia, scotomas, and impaired color vision. The patient may also experience visual hallucinations: flashes of light or color, or visions of objects, people, animals, or geometric forms. These may appear in the defective field or may move toward it from the intact field.
Parietal lobe lesion. This disorder produces homonymous hemianopsia and sensory deficits, such as an inability to perceive body position or passive movement or to localize tactile, thermal, or vibratory stimuli. It may also cause apraxia and visual or tactile agnosia.
Pituitary tumor. A tumor that compresses nerve fibers supplying the nasal half of both retinas causes complete or partial bitemporal hemianopsia that first occurs in the upper visual fields but later can progress to blindness. Related findings include blurred vision, diplopia, headache, and (rarely) somnolence, hypothermia, and seizures.
Stroke. Hemianopsia can result when a hemorrhagic, thrombotic, or embolic stroke affects any part of the optic pathway. Associated signs and symptoms vary according to the location and size of the stroke but may include decreased LOC; intellectual deficits, such as memory loss and poor judgment; personality changes; emotional lability; headache; and seizures. The patient may also develop contralateral hemiplegia, dysarthria, dysphagia, ataxia, unilateral sensory loss, apraxia, agnosia, aphasia, blurred vision, decreased visual acuity, and diplopia as well as urine retention or incontinence, constipation, and vomiting.
If the patient's visual field defect is significant, further visual field testing, such as perimetry or a tangent screen examination, may be indicated.
To avoid startling the patient, approach from the unaffected side and position his bed so that his unaffected side faces the door. If he's ambulatory, remove objects that could cause falls, and alert him to other possible hazards. Place his clock and other objects within his field of vision, and avoid putting dangerous objects (such as hot dishes) where he can't see them.
A brain tumor is the most common cause of hemianopsia in children. To help detect this sign, look for nonverbal clues, such as the child reaching for a toy but missing it. To help the child compensate for hemianopsia, place objects within his visual field; teach his parents to do this as well.
Explain to the patient the extent of his defect so that he can learn to compensate for it. Advise him to scan his surroundings frequently, turning his head in the direction of the defective visual field so that he can directly view objects he would normally notice only peripherally.
Frightening to the patient and often ominous, hemoptysis is the expectoration of blood or bloody sputum from the lungs or tracheobronchial tree. It's sometimes confused with bleeding from the mouth, throat, nasopharynx, or GI tract. (See Identifying hemoptysis.) Expectoration of 200 ml of blood in a single episode suggests severe bleeding; expectoration of 400 ml in 3 hours or more than 600 ml in 16 hours signals a life-threatening crisis.
Hemoptysis usually results from chronic bronchitis, lung cancer, or bronchiectasis. However, it may also result from inflammatory, infectious, cardiovascular, or coagulation disorders and, rarely, from a ruptured aortic aneurysm. In up to 15% of patients, the cause is unknown. The most common causes of massive hemoptysis are lung cancer, bronchiectasis, active tuberculosis, and cavitary pulmonary disease from necrotic infections or tuberculosis.
A number of pathophysiologic processes can cause hemoptysis. (See What happens in hemoptysis, page 372.)
image If the patient coughs up copious amounts of blood, endotracheal intubation may be required. Suction frequently to remove blood. Lavage may be necessary to loosen tenacious secretions or clots. Massive hemoptysis can cause airway obstruction and asphyxiation. Insert an I.V. catheter to allow fluid replacement, drug administration, and blood transfusions if needed. An emergency bronchoscopy

should be performed to identify the bleeding site. Monitor blood pressure and pulse to detect hypotension and tachycardia, and draw an arterial blood sample for laboratory analysis to monitor respiratory status.
If the hemoptysis is mild, ask the patient when it began. Has he ever coughed up blood before? How much blood is he coughing up now and how often? Ask about a history of cardiac, pulmonary, or bleeding disorders. If he's receiving anticoagulant therapy, find out which drug, its dosage and schedule, and the duration of therapy. Is he taking other prescription drugs? Does he smoke? Ask the patient if he has recently had any infections or been exposed to tuberculosis. When was his last tine test and what were the results?
Take the patient's vital signs and examine his nose, mouth, and pharynx for sources of bleeding. Inspect the configuration of his chest and look for abnormal movement during breathing, use of accessory muscles, and retractions. Observe his respiratory rate, depth, and rhythm. Finally, examine his skin for lesions.
Next, palpate the patient's chest for diaphragm level and for tenderness, respiratory excursion, fremitus, and abnormal pulsations; then percuss for flatness, dullness, resonance, hyperresonance, and tympany. Finally, auscultate the lungs, noting especially the quality and intensity of breath sounds. Also auscultate for heart murmurs, bruits, and pleural friction rubs.
Obtain a sputum specimen and examine it for overall quantity, for the amount of blood it contains, and for its color, odor, and consistency.
Aortic aneurysm (ruptured). Rarely, an aortic aneurysm ruptures into the tracheobronchial tree, causing hemoptysis and sudden death.
Blast lung injury. Although individuals with this type of injury may not have obvious external chest injuries, they sometimes show other indications of internal damage, such as hemoptysis. Health care providers should evaluate survivors of explosive detonations for other classic signs and symptoms of a blast lung injury, such as chest pain, cyanosis, dyspnea, and wheezing. Treatment includes careful administration of fluids and oxygen to ensure tissue perfusion.
Bronchial adenoma. This insidious disorder causes recurring hemoptysis in up to 30% of patients along with a chronic cough and local wheezing.
Bronchiectasis. Inflamed bronchial surfaces and eroded bronchial blood vessels cause hemoptysis, which can vary from blood-tinged sputum to blood (in about 20% of patients). The patient typically has a chronic cough producing copious amounts of foul-smelling, purulent sputum. He may also exhibit coarse crackles, clubbing (a late sign), fever, weight loss, fatigue, weakness, malaise, and dyspnea on exertion.
Bronchitis (chronic). The first sign of this disorder is typically a productive cough that

lasts at least 3 months. Eventually this leads to production of blood-streaked sputum; massive hemorrhage is unusual. Other respiratory effects include dyspnea, prolonged expirations, wheezing, scattered rhonchi, accessory muscle use, barrel chest, tachypnea, and clubbing (a late sign).
Coagulation disorders. Such disorders as thrombocytopenia and disseminated intravascular coagulation can cause hemoptysis, multisystem hemorrhaging (for example, GI bleeding or epistaxis), and purpuric lesions.
Laryngeal cancer. Hemoptysis occurs in this cancer, but hoarseness is usually the initial sign. Other findings may include dysphagia, dyspnea, stridor, cervical lymphadenopathy, and neck pain.
Lung abscess. In about 50% of patients, this disorder produces blood-streaked sputum resulting from bronchial ulceration, necrosis, and granulation tissue. Common associated findings include a cough producing large amounts of purulent, foul-smelling sputum; fever with chills; diaphoresis; anorexia; weight loss; headache; weakness; dyspnea; pleuritic or dull chest pain; and clubbing. Auscultation reveals tubular or cavernous breath sounds and crackles. Percussion reveals dullness on the affected side.
Lung cancer. Ulceration of the bronchus commonly causes recurring hemoptysis (an early sign), which can vary from blood-streaked sputum to blood. Related findings include a productive cough, dyspnea, fever, anorexia, weight loss, wheezing, and chest pain (a late symptom).
Plague. The pneumonic form of this acute bacterial infection, caused by Yersinia pestis, can produce hemoptysis, a productive cough, chest pain, tachypnea, dyspnea, increasing respiratory distress, and cardiopulmonary insufficiency. Pneumonic plague begins abruptly with chills, fever, headache, and myalgia.
Pneumonia. In up to 50% of patients, Klebsiella pneumonia produces dark brown or red (currant-jelly) sputum, which is so tenacious that the patient has difficulty expelling it from his mouth. This type of pneumonia begins abruptly with chills, fever, dyspnea, a productive cough, and severe pleuritic chest pain. Associated findings may include cyanosis, prostration, tachycardia, decreased breath sounds, and crackles.
Pneumococcal pneumonia causes pinkish or rusty mucoid sputum. It begins with sudden shaking chills; a rapidly rising temperature; and, in over 80% of patients, tachycardia and tachypnea. Within a few hours, the patient typically experiences a productive cough along with severe, stabbing, pleuritic pain that leads to rapid, shallow, grunting respirations with splinting. Examination reveals respiratory distress with dyspnea and accessory muscle use, crackles, and dullness on percussion over the affected lung. Malaise, weakness, myalgia, and prostration accompany a high fever.
Pulmonary arteriovenous fistula. Occurring in young adults, this genetic disorder causes intermittent hemoptysis along with cyanosis, clubbing, mild dyspnea, fatigue, vertigo, syncope, confusion, and speech and visual impairments. The patient may bleed from the nose, mouth, or lips. Ruby red patches appear on the face, tongue, skin, mucous membranes, or nail beds.
Pulmonary contusion. Blunt chest trauma commonly causes a cough with hemoptysis. Other signs and symptoms that appear over several hours include dyspnea, tachypnea, chest pain, tachycardia, hypotension, crackles, and decreased or absent breath sounds over the affected area. Severe respiratory distress—with oppressive dyspnea, nasal flaring, use of

accessory muscles, extreme anxiety, cyanosis, and diaphoresis—may develop at any time.
Pulmonary edema. Severe cardiogenic or noncardiogenic pulmonary edema commonly causes frothy, blood-tinged pink sputum, which accompanies severe dyspnea, orthopnea, gasping, anxiety, cyanosis, diffuse crackles, a ventricular gallop, and cold, clammy skin. This life-threatening condition may also cause tachycardia, lethargy, cardiac arrhythmias, tachypnea, hypotension, and a thready pulse.
Pulmonary embolism with infarction. Hemoptysis is a common finding in this life-threatening disorder, although massive hemoptysis is rare. Typical initial symptoms are dyspnea and anginal or pleuritic chest pain. Other common clinical features include tachycardia, tachypnea, low-grade fever, and diaphoresis. Less common features include splinting of the chest, leg edema, and—with a large embolus—cyanosis, syncope, and jugular vein distention. Examination reveals decreased breath sounds, pleural friction rub, crackles, diffuse wheezing, dullness on percussion, and signs of circulatory collapse (weak, rapid pulse and hypotension), cerebral ischemia (transient loss of consciousness and seizures), and hypoxemia (restlessness and, particularly in elderly patients, hemiplegia and other focal neurologic deficits).
Pulmonary hypertension (primary). Hemoptysis, exertional dyspnea, and fatigue generally develop late in this disorder. Angina-like pain usually occurs with exertion and may radiate to the neck but not to the arms. Other findings include arrhythmias, syncope, cough, and hoarseness.
Pulmonary tuberculosis. Blood-streaked or blood-tinged sputum commonly occurs in this disorder; massive hemoptysis may occur in advanced cavitary tuberculosis. Accompanying respiratory findings include a chronic productive cough, fine crackles after coughing, dyspnea, dullness on percussion, increased tactile fremitus and, possibly, amphoric breath sounds. The patient may also develop night sweats, malaise, fatigue, fever, anorexia, weight loss, and pleuritic chest pain.
Silicosis. This chronic disorder causes a productive cough with mucopurulent sputum that later becomes blood streaked. Occasionally, massive hemoptysis may occur. Other findings include fine end-inspiratory crackles at lung bases, exertional dyspnea, tachypnea, weight loss, fatigue, and weakness.
Systemic lupus erythematosus. In 50% of patients with this disorder, pleuritis and pneumonitis cause hemoptysis, a cough, dyspnea, pleuritic chest pain, and crackles. Related findings are a butterfly rash in the acute phase, nondeforming joint pain and stiffness, photosensitivity, Raynaud's phenomenon, seizures or psychoses, anorexia with weight loss, and lymphadenopathy.
Tracheal trauma. Torn tracheal mucosa may cause hemoptysis, hoarseness, dysphagia, neck pain, airway occlusion, and respiratory distress.
Wegener's granulomatosis. Necrotizing, granulomatous vasculitis characterizes this multisystem disorder. Findings include hemoptysis, chest pain, cough, wheezing, dyspnea, epistaxis, severe sinusitis, and hemorrhagic skin lesions.
Diagnostic tests. Lung or airway injury from bronchoscopy, laryngoscopy, mediastinoscopy, or lung biopsy can cause bleeding and hemoptysis.
Comfort and reassure the patient, who may react to this alarming sign with anxiety and apprehension. If necessary, to protect the nonbleeding lung, place him in the lateral decubitus position, with the suspected bleeding lung facing down. Perform this maneuver with caution because hypoxemia may worsen with the healthy lung facing up.
Prepare the patient for diagnostic tests to determine the cause of bleeding. These may include a complete blood count, a sputum culture and smear, chest X-rays, coagulation studies, bronchoscopy, lung biopsy, pulmonary arteriography, and a lung scan.
Hemoptysis in children may stem from Goodpasture's syndrome, cystic fibrosis, or (rarely) idiopathic primary pulmonary hemosiderosis. Sometimes no cause can be found for pulmonary hemorrhage occurring within the first 2 weeks of life; in such cases, the prognosis is poor.
If the patient is receiving anticoagulants, determine any changes that need to be made in his diet or medications (including over-the-counter

drugs and natural supplements) because these factors may affect clotting.
Hemoptysis usually ceases gradually during treatment of the causative disorder. Many chronic disorders, however, cause recurrent hemoptysis. Instruct the patient to report recurring episodes and to bring a sputum specimen containing blood if he returns for treatment or reevaluation.
Hepatomegaly, an enlarged liver, indicates potentially reversible primary or secondary liver disease. This sign may stem from diverse pathophysiologic mechanisms, including dilated hepatic sinusoids (in heart failure), persistently high venous pressure leading to liver congestion (in chronic constrictive pericarditis), dysfunction and engorgement of hepatocytes (in hepatitis), fatty infiltration of parenchymal cells causing fibrous tissue (in cirrhosis), distention of liver cells with glycogen (in diabetes), and infiltration of amyloid (in amyloidosis).
Hepatomegaly may be confirmed by palpation, percussion, or radiologic tests. It may be mistaken for displacement of the liver by the diaphragm (in a respiratory disorder), by an abdominal tumor, by a spinal deformity such as kyphosis, by the gallbladder, or by fecal material or a tumor in the colon.
Hepatomegaly is seldom a patient's reason for seeking care. It usually comes to light during palpation and percussion of the abdomen.
If you suspect hepatomegaly, ask the patient about his use of alcohol and exposure to hepatitis. Also ask if he's currently ill or taking any prescribed drugs. If he complains of abdominal pain, ask him to locate and describe it.
Inspect the patient's skin and sclerae for jaundice, dilated veins (suggesting generalized congestion), scars from previous surgery, and spider angiomas (common in cirrhosis). Next, inspect the contour of his abdomen. Is it protuberant over the liver or distended (possibly from ascites)? Measure his abdominal girth.
Percuss the liver, being careful to identify structures and conditions that can obscure dull percussion notes, such as the sternum, ribs, breast tissue, pleural effusions, and gas in the colon. (See Percussing for liver size and position.) Next, palpate the liver's edge during deep inspiration; it's tender and rounded in hepatitis and cardiac decompensation, rocklike in carcinoma, and firm in cirrhosis.
Take the patient's baseline vital signs, and assess his nutritional status. An enlarged liver that's functioning poorly causes muscle wasting, exaggerated skeletal prominences, weight loss, thin hair, and edema.
Evaluate the patient's level of consciousness. When an enlarged liver loses its ability to detoxify waste products, metabolic substances toxic to brain cells accumulate. As a result, watch for personality changes, irritability, agitation, memory loss, inability to concentrate, poor mentation, and—in a severely ill patient—a coma.
Amyloidosis. This rare disorder can cause hepatomegaly and mild jaundice as well as renal, cardiac, and other GI effects.
Cirrhosis. Late in this disorder, the liver becomes enlarged, nodular, and hard. Other late signs and symptoms affect all body systems. Respiratory findings include limited thoracic expansion due to abdominal ascites, leading to hypoxia. Central nervous system findings include signs and symptoms of hepatic encephalopathy, such as lethargy, slurred speech, asterixis, peripheral neuritis, paranoia, hallucinations, extreme obtundation, and coma. Hematologic signs include epistaxis, easy bruising, and bleeding gums. Endocrine findings include testicular atrophy, gynecomastia, loss of chest and axillary hair, and menstrual irregularities. Integumentary effects include abnormal pigmentation, jaundice, severe pruritus and dryness, poor tissue turgor, spider angiomas, and palmar erythema.
The patient may also develop fetor hepaticus, enlarged superficial abdominal veins, muscle atrophy, right-upper-quadrant pain that worsens when he sits up or leans forward, and a palpable spleen. Portal hypertension—elevated pressure in the portal vein—causes bleeding from esophageal varices.
Diabetes mellitus. Poorly controlled diabetes in overweight patients commonly produces fatty infiltration of the liver, hepatomegaly, and right-upper-quadrant tenderness along with polydipsia, polyphagia, and polyuria. These features are more common in type 2 than in type 1 diabetes. A chronically enlarged fatty liver typically produces no symptoms except for slight tenderness.

Granulomatous disorders. Sarcoidosis, histoplasmosis, and other granulomatous disorders commonly produce a slightly enlarged, firm liver.
Heart failure. This disorder produces hepatomegaly along with jugular vein distention, cyanosis, nocturia, dependent edema of the legs and sacrum, steady weight gain, confusion and, possibly, nausea, vomiting, abdominal discomfort, and anorexia due to visceral edema. Ascites is a late sign. Massive right-sided heart failure may cause anasarca, oliguria, severe weakness, and anxiety. If left-sided heart failure precedes right-sided heart failure, the patient exhibits dyspnea, paroxysmal nocturnal dyspnea, orthopnea, tachypnea, arrhythmias, tachycardia, and fatigue.
Hemochromatosis. This rare disease of iron metabolism causes hepatomegaly, altered skin pigmentation and, possibly, cardiac failure.
Hepatic abscess. Hepatomegaly may accompany fever (a primary sign), nausea, vomiting, chills, weakness, diarrhea, anorexia, elevated right hemidiaphragm, and right-upper-quadrant pain and tenderness.
Hepatitis. In viral hepatitis, early signs and symptoms include nausea, anorexia, vomiting, fatigue, malaise, photophobia, sore throat, cough, and headache. Hepatomegaly occurs in the icteric phase and continues during the recovery phase. Also, during the icteric phase, the early signs and symptoms diminish and others appear: liver tenderness, slight weight loss, dark urine, clay-colored stools, jaundice, pruritus, right-upper-quadrant pain, and splenomegaly.
Leukemia and lymphomas. These proliferative blood cell disorders commonly cause moderate to massive hepatomegaly and splenomegaly as well as abdominal discomfort. General signs and symptoms include malaise, low-grade fever, fatigue, weakness, tachycardia, anorexia, weight loss, and bleeding disorders.
Liver cancer. Primary tumors commonly cause an enlarged, irregular, nodular, firm liver with pain or tenderness in the right upper quadrant and a friction rub or bruit over the liver. Common related findings are anorexia, weight loss, cachexia, nausea, and vomiting. Peripheral edema, ascites, jaundice, and a palpable rightupper-quadrant mass may also develop. When metastatic liver tumors cause hepatomegaly, the patient's signs and symptoms reflect his primary cancer.
Mononucleosis (infectious). Occasionally, this disorder causes hepatomegaly. Prodromal symptoms include headache, malaise, and fatigue. After 3 to 5 days, the patient typically develops a sore throat, cervical lymphadenopathy, and temperature fluctuations. He may also develop stomatitis, palatal petechiae, periorbital edema, splenomegaly, exudative tonsillitis, pharyngitis and, possibly, a maculopapular rash.
Obesity. Hepatomegaly can result from fatty infiltration of the liver. Weight loss reduces the liver's size.
Pancreatic cancer. In this disease, hepatomegaly accompanies such classic signs and

symptoms as anorexia, weight loss, abdominal or back pain, and jaundice. Other findings include nausea, vomiting, fever, fatigue, weakness, pruritus, and skin lesions (usually on the legs).
Pericarditis. In chronic constrictive pericarditis, an increase in systemic venous pressure produces marked congestive hepatomegaly. Distended jugular veins (more prominent on inspiration) are a common finding. The usual signs of heart disease typically are absent; other features include peripheral edema, ascites, fatigue, and decreased muscle mass.
Drugs. Hepatomegaly is a rare but serious side effect of drugs used to treat HIV-positive hepatitis, such as tenofovir and lamivudine.
Prepare the patient for hepatic enzyme, alkaline phosphatase, bilirubin, albumin, and globulin studies to evaluate liver function, and for X-rays, liver scan, celiac arteriography, computed tomography scan, and ultrasonography to confirm hepatomegaly.
Bed rest, relief from stress, and adequate nutrition are important for the patient with hepatomegaly to help protect liver cells from further damage and to allow the liver to regenerate functioning cells. Dietary protein intake may need to be monitored and possibly restricted. Ammonia, a major cause of hepatic encephalopathy, is a byproduct of protein metabolism. Hepatotoxic drugs or drugs metabolized by the liver should be given in very small doses, if at all. Expalin these treatment measures to the patient.
Assess hepatomegaly in children the same way you do in adults. Childhood hepatomegaly may stem from Reye's syndrome; biliary atresia; rare disorders, such as Wilson's disease, Gaucher's disease, and Niemann-Pick disease; or poorly controlled type 1 diabetes mellitus.
Hiccups occur as a two-stage process: an involuntary, spasmodic contraction of the diaphragm followed by sudden closure of the glottis. Their characteristic sound reflects the vibration of closed vocal cords as air suddenly rushes into the lungs. (See How hiccups occur.)
Usually benign and transient, hiccups are common and usually subside spontaneously or with simple treatment. However, in a patient with a neurologic disorder, they may indicate increasing intracranial pressure or extension of a brain stem lesion. They may also occur after ingestion of hot or cold liquids or other irritants, after exposure to cold, or with irritation from a drainage tube. Persistent hiccups cause considerable distress and may lead to vomiting. Increased serum levels of carbon dioxide may inhibit hiccups; decreased levels may accentuate them.
Find out when the patient's hiccups began. If he's also vomiting and unconscious, turn him on his side to prevent aspiration.
If the patient is conscious, find out if the hiccups are tiring him. Ask if he has had hiccups before, what caused them, and what made them stop. Also, note whether he has a history of abdominal or thoracic disorders.
Abdominal distention. The most common cause of hiccups, abdominal distention also causes a feeling of fullness and, depending on the cause, abdominal pain, nausea, and vomiting.
Brain stem lesion. Producing persistent hiccups, this type of lesion causes decreased level of consciousness, dysphagia, dysarthria, an absent corneal reflex on the side opposite the lesion, altered respiratory pattern, abnormal pupillary response, and ocular deviation.
Gastric cancer. Persistent hiccups can be the presenting sign of this disease, which may be accompanied by dyspepsia, abdominal pain, anorexia, early satiety, and weight loss.
Gastric dilation. Besides hiccups, possible signs and symptoms include a sense of fullness, epigastric pain, and regurgitation or persistent vomiting.
Gastritis. This disorder can cause hiccups along with mild epigastric discomfort (sometimes the only symptom). The patient may develop upper abdominal pain, eructation, fever, malaise, nausea, vomiting, hematemesis, and melena.
Increased intracranial pressure. Early findings may include hiccups, drowsiness, and


headache. Classic later signs include changes in pupillary reactions and respiratory pattern, increased systolic pressure, and bradycardia.
Pancreatitis. Hiccups, vomiting, and sudden and steady epigastric pain (often radiating to the back) may occur in this disorder. A severe attack may cause persistent vomiting, extreme restlessness, fever, and abdominal tenderness and rigidity.
Pleural irritation. Besides hiccups, this condition may cause cough, dyspnea, or chest pain.
Renal failure. Hiccups may occur in the late stages of both chronic and acute renal failure. Associated signs and symptoms affect every body system and include fatigue, oliguria or anuria, nausea, vomiting, confusion, yellowbrown or bronze skin, uremic frost, ammonia breath odor, bleeding tendencies, gum ulcerations, asterixis, and Kussmaul's respirations.
Surgery. Mild and transient attacks of hiccups occasionally follow abdominal surgery.
Teach the patient simple methods of relieving hiccups, such as holding his breath repeatedly or rebreathing into a paper bag (both of which increase his serum carbon dioxide level). Other treatments for hiccups include gastric lavage or applying finger pressure on the eyeballs (through closed lids). Hiccups may also be relieved by briefly applying ice cubes to both sides of the neck at the level of the larynx. If hiccups persist, a phenothiazine (especially chlorpromazine), metoclopramide, or nasogastric intubation may provide relief. (Caution: The tube may cause vomiting.) If simpler methods fail, treatment may include a phrenic nerve block.
In an infant, hiccups usually result from rapid ingestion of liquids without adequate burping. Tell parents to hold the infant upright during feedings.
If abdominal distention is the probable cause of hiccups, teach the patient lifestyle changes, such as eating smaller, more frequent meals and avoiding large meals before bedtime. Also, advise the patient to increase fiber and fluid intake to avoid constipation.
Warn the patient with chronic renal failure that persistent hiccups, usually accompanied by nausea and vomiting, can indicate worsening or acute decompensation of renal function.
Hirsutism is the excessive growth of coarse body hair in females. Excessive production of androgens (male hormones) stimulates hair growth on the pubic region, axillae, chin, upper lip, cheeks, anterior neck, sternum, linea alba, forearms, upper arms, abdomen, and back. This condition may also occur in a patient with normal levels of androgens whose skin is more sensitive to the hormones. In mild hirsutism, fine and pigmented hair appears on the sides of the face and the chin (but doesn't form a complete beard) and on the extremities, chest, abdomen, and perineum. In moderate hirsutism, coarse and pigmented hair appears on the same areas. In severe hirsutism, coarse hair also covers the whole beard area, the proximal interphalangeal joints, and the ears and nose.
Depending on the degree of excess androgen production, hirsutism may be associated with acne and increased skin oiliness, increased libido, and menstrual irregularities (including anovulation and amenorrhea). Extremely high androgen levels cause further virilization, including such signs as breast atrophy, loss of female body contour, frontal balding, and deepening of the voice. (See Recognizing signs of virilization.)
Hirsutism may result from endocrine abnormalities and idiopathic causes. It may also occur in pregnancy from transient androgen production by the placenta or corpus luteum, and in menopause from increased androgen and decreased estrogen production. Some patients have a strong familial predisposition to hirsutism, which may be considered normal for their genetic background, culture, and race. Although hirsutism is a female characteristic, excessive hair growth may also be present in male family members.
Begin by asking the patient where on her body she first noticed excessive hair. How old was she then? Where and how quickly did other hirsute areas develop? Does she use any hair removal technique? If so, how often does she use it, and when did she use it last? Next, obtain a menstrual history: the patient's age at menarche,

the duration of her periods, the usual amount of blood flow, and the number of days between periods.
Ask about medications, too. If the patient is taking a drug containing an androgen or progestin compound, or another drug that can cause hirsutism, find out its name, dosage, schedule, and therapeutic aim. Does she sometimes miss doses or take extra ones?
Next, examine the hirsute areas. Does excessive hair appear only on the upper lip or on other body parts as well? Is the hair fine and pigmented, or dense and coarse? Is the patient obese? Observe her for other signs of virilization.
Acromegaly. About 15% of patients with this chronic, progressive disorder display hirsutism. Acromegaly also causes enlarged hands and feet, coarsened facial features, prognathism, increased diaphoresis and need for sleep, oily skin, fatigue, weight gain, heat intolerance, and lethargy.

Adrenocortical carcinoma. This disorder produces rapidly progressive hirsutism along with truncal obesity, buffalo hump, moon face, oligomenorrhea, amenorrhea, muscle wasting, and thin skin with purple striae. The patient also exhibits muscle weakness, excessive diaphoresis, poor wound healing, weakness, fatigue, hypertension, hyperpigmentation, and personality changes.
Androgen overproduction by ovaries. The most common cause of hirsutism, this condition is associated with anovulation that progresses slowly over several years.
Cushing's syndrome (hypercortisolism). This disorder commonly causes increased hair growth on the face, abdomen, breasts, chest, or upper thighs. Other findings include truncal obesity, buffalo hump, moon face, thin skin with purple striae, ecchymosis, petechiae, muscle wasting and weakness, poor wound healing, hypertension, weakness, fatigue, excessive diaphoresis, hyperpigmentation, menstrual irregularities, and personality changes.
Hyperprolactinemia. This disorder produces hirsutism, hypogonadism, galactorrhea, amenorrhea, and acne.
Idiopathic hirsutism. In patients with normal-sized ovaries, normal menses, and no evidence of adrenal hyperplasia or adrenal or ovarian tumors, excess hair appears at puberty and increases into early adulthood. It's accompanied by acne, obesity, infrequent menses or anovulation, and thick, oily skin. Idiopathic hirsutism with regular ovulation and no menstrual abnormalities may be hereditary or related to certain ethnic groups who are hypersensitive to androgens.
Ovarian tumor. An ovarian tumor may produce no symptoms, or it can cause rapidly progressing hirsutism (only if the tumor produces androgens) as well as amenorrhea and rapidly developing virilization.
Polycystic ovary disease. Ovarian cysts, particularly chronic ones, can cause hirsutism. This hirsutism usually occurs after the onset of menstrual irregularities, which may begin at puberty. The patient may also be obese and have amenorrhea, oligomenorrhea, menometrorrhagia, infertility, insulin resistance and diabetes, and acne.
Drugs. Hirsutism can result from drugs containing androgens or progestins or from aminoglutethimide, glucocorticoids, metoclopramide, cyclosporine, and minoxidil.
Prepare the patient for tests to determine blood levels of luteinizing hormone, folliclestimulating hormone, prolactin, and other hormones. Other tests may include computed tomography scan and ultrasonography.
At the patient's request, provide information on hair removal methods, such as bleaching, tweezing, hot wax treatments, chemical depilatories, shaving, and electrolysis. Inform the patient that electrolysis should be done only by a licensed professional.
Childhood hirsutism can stem from congenital adrenal hyperplasia. This disorder is usually detected at birth because affected infants have ambiguous genitalia. Rarely, a mild form becomes apparent after puberty when hirsutism, irregular bleeding or amenorrhea, and signs of virilization appear. Hirsutism that occurs at or after puberty often results from polycystic ovary disease.
Give the parents as well as the child emotional support and clear explanations about the cause of hirsutism. Allow the parents and child to express their concerns separately.
Hirsutism can occur after menopause if peripheral conversion of estrogen is poor.
Help relieve the patient's anxiety by explaining the cause of excessive hair growth and by encouraging her to talk about her self-image problems or fears. Involve the family in your discussions.
Tell the patient that hormonal treatment stops further hair growth but doesn't always reverse hair growth that has already occurred. Treatment requires at least 6 to 24 months and may be lifelong.
Hoarseness—a rough or harsh sound to the voice—can result from infections, inflammatory lesions, or exudates of the larynx; from laryngeal edema; and from compression or disruption of the vocal cords or recurrent laryngeal nerve. This common sign can also result from a thoracic aortic aneurysm, vocal cord paralysis, and systemic disorders, such as Sjögren's syndrome

and rheumatoid arthritis. It's characteristically worsened by excessive alcohol intake, smoking, inhalation of noxious fumes, excessive talking, and shouting.
Hoarseness can be acute or chronic. For example, chronic hoarseness and laryngitis result when irritating polyps or nodules develop on the vocal cords. Gastroesophageal reflux into the larynx should also be considered as a possible cause of chronic hoarseness. Hoarseness may also result from progressive atrophy of the laryngeal muscles and mucosa caused by aging, which leads to diminished control of the vocal cords.
Obtain a patient history. First, consider the patient's age and sex; laryngeal cancer is most common in men between ages 50 and 70. Be sure to ask about the onset of hoarseness. Has the patient been overusing his voice? Has he experienced shortness of breath, a sore throat, dry mouth, a cough, or difficulty swallowing dry food? In addition, ask if he has been in or near a fire within the past 48 hours. Be aware that inhalation injury can cause sudden airway obstruction.
Next, explore associated symptoms. Does the patient have a history of cancer, rheumatoid arthritis, or aortic aneurysm? Does he regularly drink alcohol or smoke?
Inspect the oral cavity and pharynx for redness or exudate, possibly indicating an upper respiratory tract infection. Palpate the neck for masses and the cervical lymph nodes and the thyroid gland for enlargement. Palpate the trachea to determine if it's midline. Ask the patient to stick out his tongue; if he can't, he may have paralysis from cranial nerve involvement. Examine the eyes for corneal ulcers and enlarged lacrimal ducts (signs of Sjögren's syndrome). Dilated neck and chest veins may indicate compression by an aortic aneurysm.
Take the patient's vital signs, noting especially fever and bradycardia. Examine him for asymmetrical chest expansion or signs of respiratory distress—nasal flaring, stridor, and intercostal retractions. Then auscultate for crackles, rhonchi, wheezing, and tubular sounds, and percuss for dullness.
Gastroesophageal reflux. In this disorder, retrograde flow of gastric juices into the esophagus may then spill into the hypopharynx. This, in turn, irritates the larynx, resulting in hoarseness as well as a sore throat, a cough, throat clearing, and a sensation of a lump in the throat. The arytenoids and the vocal cords may appear red and swollen.
Hypothyroidism. Hoarseness may be an early sign of hypothyroidism. Others include fatigue, cold intolerance, weight gain despite anorexia, and menorrhagia.
Laryngeal cancer. Hoarseness is an early sign of vocal cord cancer, but it may not occur until later in cancer of other laryngeal areas. The patient usually has a long history of smoking. Other common findings include a mild, dry cough; minor throat discomfort; otalgia; and, sometimes, hemoptysis.
Laryngeal leukoplakia. Leukoplakia is a common cause of hoarseness, especially in smokers. Histologic examination by direct laryngoscopy usually reveals mild, moderate, or severe dysphagia.
Laryngitis. Persistent hoarseness may be the only sign of chronic laryngitis. In acute laryngitis, hoarseness or a complete loss of voice develops suddenly. Related findings include pain (especially during swallowing or speaking), a cough, fever, profuse diaphoresis, sore throat, and rhinorrhea.
Rheumatoid arthritis. Hoarseness may signal laryngeal involvement. Other findings include pain, dysphagia, a sensation of fullness or tension in the throat, dyspnea on exertion, and stridor.
Sjögren's syndrome. This rheumatic disorder produces hoarseness, but its cardinal signs are dry eyes, nose, and mouth. Initially, the patient complains of gritty, burning pain around the eyes and under the lids. Ocular dryness also leads to redness, photosensitivity, impaired vision, itching, and eye fatigue. Examination reveals enlarged lacrimal glands and corneal ulcers.
The patient may complain of a dry, sore mouth and difficulty chewing, talking, or swallowing. He may also exhibit nasal crusting, epistaxis, enlarged parotid and submaxillary glands, dry and scaly skin, a nonproductive cough, abdominal discomfort, and polyuria.
Thoracic aortic aneurysm. Depending on the size and exact location of the aneurysm, patients may remain asymptomatic. When the aneurysm exerts pressure on surrounding structures, however, patients may experience a variety of symptoms. Hoarseness occurs when the

aneurysm compresses nerves associated with the larynx. Other clinical features may include a brassy cough; dyspnea; wheezing; a substernal aching in the shoulders, lower back, or abdomen; a tracheal tug; facial and neck edema; jugular vein distention; dysphagia; prominent chest veins; stridor; penetrating pain that's especially severe when the patient is supine; and, possibly, paresthesia or neuralgia.
Tracheal trauma. Torn tracheal mucosa may cause hoarseness, hemoptysis, dysphagia, neck pain, airway occlusion, and respiratory distress.
Vocal cord nodules or polyps. Raspy hoarseness, the chief complaint, accompanies a chronic cough and a crackling voice.
Vocal cord paralysis. Unilateral vocal cord paralysis causes hoarseness and vocal weakness. Paralysis may accompany signs of trauma, such as pain and swelling of the head and neck.
Inhalation injury. An inhalation injury from a fire or an explosion produces hoarseness and coughing, singed nasal hairs, orofacial burns, and soot-stained sputum. Subsequent signs and symptoms include crackles, rhonchi, and wheezing, which rapidly lead to respiratory distress.
Treatments. Occasionally, surgical trauma to the recurrent laryngeal nerve results in temporary or permanent unilateral vocal cord paralysis, leading to hoarseness. Prolonged intubation may cause temporary hoarseness.
Carefully observe the patient for stridor, which may indicate bilateral vocal cord paralysis. When hoarseness lasts for longer than 2 weeks, indirect or fiber-optic laryngoscopy is indicated to observe the larynx at rest and during phonation.
In children, hoarseness may result from congenital anomalies, such as laryngocele and dysphonia plicae ventricularis. In prepubescent boys, it can stem from juvenile papillomatosis of the upper respiratory tract.
In infants and young children, hoarseness often stems from acute laryngotracheobronchitis (croup). Acute laryngitis in children younger than age 5 may cause respiratory distress because the larynx is small and prone to spasm if irritated or infected. This may cause partial or total obstruction of the larynx. Temporary hoarseness often results from laryngeal irritation due to aspiration of liquids, foreign bodies, or stomach contents. Hoarseness may also stem from diphtheria, although immunization has made this disease rare.
Help the child with hoarseness rest his voice. Comfort an infant to minimize crying, play quiet games with him, and humidify his environment.
Stress to the patient the importance of resting his voice because talking—even whispering— further traumatizes the vocal cords. Suggest other ways to communicate, such as writing or using body language. Urge the patient to avoid alcohol, smoking, and the company of smokers. If he has laryngitis, advise him to use a humidifier.
Homans' sign
Homans' sign is positive when deep calf pain results from strong and abrupt dorsiflexion of the ankle. This pain results from venous thrombosis or inflammation of the calf muscles. However, because a positive Homans' sign appears in only 35% of patients with these conditions, it's an unreliable indicator. (See Eliciting Homans' sign.) Even when accurate, a positive Homans' sign doesn't indicate the extent of the venous disorder.
This elicited sign may be confused with continuous calf pain, which can result from strains, contusions, cellulitis, or arterial occlusion, or with pain in the posterior ankle or Achilles tendon (for example, in a woman with Achilles tendons shortened from wearing high heels).
When you detect a positive Homans' sign, focus your patient history on signs and symptoms that can accompany deep vein thrombosis or thrombophlebitis. These include throbbing, aching, heavy, or tight sensations in the calf and leg pain during or after exercise or routine activity. Also, ask about any shortness of breath or chest pain, which may indicate pulmonary embolism. Be sure to ask about predisposing events, such as leg injury, recent surgery, childbirth, use of hormonal contraceptives, associated diseases (cancer, nephrosis, hypercoagulable states), and prolonged inactivity or bed rest.

Next, inspect and palpate the patient's calf for warmth, tenderness, redness, swelling, and a palpable vein. If you strongly suspect deep vein thrombosis, elicit Homans' sign very carefully to avoid dislodging the clot, which could cause a life-threatening pulmonary embolism.
In addition, measure the circumference of both the patient's calves. The calf with the positive Homans' sign may be larger because of edema and swelling.
Cellulitis (superficial). This disorder typically affects the legs but can also affect the arms, producing pain, redness, tenderness, and edema. Some patients also experience fever, chills, tachycardia, headache, and hypotension.
Deep vein thrombophlebitis. A positive Homans' sign and calf tenderness may be the only clinical features of this disorder. However, the patient may also have severe pain, heaviness, warmth, and swelling of the affected leg; visible, engorged superficial veins or palpable, cordlike veins; and fever, chills, and malaise.
Deep vein thrombosis (DVT). DVT causes a positive Homans' sign along with tenderness over the deep calf veins, slight edema of the calves and thighs, a low-grade fever, and tachycardia. If DVT affects the femoral and iliac veins, you'll notice marked local swelling and tenderness. If DVT causes venous obstruction, you'll notice cyanosis and possibly cool skin in the affected leg.
Popliteal cyst (ruptured). Rupture of this synovial cyst may produce a positive Homans' sign as well as sudden onset of calf tenderness, swelling, and redness.

Place the patient on bed rest, with the affected leg elevated above the heart level. Apply warm, moist compresses to the affected area, and administer mild oral analgesics. In addition, prepare the patient for further diagnostic tests, such as Doppler studies and venograms.
Once the patient is ambulatory, advise him to wear elastic support stockings after his discomfort decreases (usually in 5 to 10 days) and to continue wearing them for at least 3 months. In addition, instruct the patient to keep the affected leg elevated while sitting and to avoid crossing his legs at the knees because this may impair circulation to the popliteal area. (Crossing at the ankles is acceptable.)
Homans' sign is seldom assessed in children, who rarely have DVT or thrombophlebitis.
If the patient is prescribed long-term anticoagulant therapy, instruct him to report any signs of prolonged clotting time. These include black, tarry stools; brown or red urine; bleeding gums; and bruises. Also, stress the importance of keeping follow-up appointments so that prothrombin time can be monitored.
Instruct the patient to avoid alcohol and restrict his intake of green leafy vegetables (spinach and parsley), which are high in vitamin K. Also instruct him to review all medications he's taking with his physician because some drugs may enhance or inhibit the effects of the anticoagulant. The patient should also verify with his physician that any future prescription and over-the-counter medications are safe to take.
Hyperpigmentation, or excessive skin coloring, usually reflects overproduction, abnormal location, or maldistribution of melanin—the dominant brown or black pigment found in skin, hair, mucous membranes, nails, brain tissue, cardiac muscle, and parts of the eye. This sign can also reflect abnormalities of other skin pigments: carotenoids (yellow), oxyhemoglobin (red), and hemoglobin (blue).
Hyperpigmentation most commonly results from exposure to sunlight. However, it can also result from metabolic, endocrine, neoplastic, and inflammatory disorders; chemical poisoning; drugs; genetic defects; thermal burns; ionizing radiation; and localized activation by sunlight of certain photosensitizing chemicals on the skin.
Many types of benign hyperpigmented lesions occur normally. Some, such as acanthosis nigricans and carotenemia, may also accompany certain disorders, but their significance is unproven. Chronic nutritional insufficiency may lead to dyspigmentation—increased pigmentation in some areas and decreased pigmentation in others.
Typically asymptomatic and chronic, hyperpigmentation is a common problem that can have distressing psychological and social implications. It varies in location and intensity and may fade over time.
Hyperpigmentation isn't an acute process, but an end result of another process, which should be the main target of your examination. Begin with a detailed patient history. Do any other family members have the same problem? Was the patient's hyperpigmentation present at birth? Did other signs or symptoms, such as a rash, accompany or precede it? Obtain a history of medical disorders (especially endocrine) as well as contact with or ingestion of chemicals, metals, plants, vegetables, citrus fruits, or perfumes. Is the hyperpigmentation related to exposure to sunlight or a change of season? Is the patient pregnant or taking prescription or overthe-counter drugs?
Explore other signs and symptoms, too. Ask about fatigue, weakness, muscle aches, chills, irritability, fainting, and pruritus. Does the patient have any cardiopulmonary signs or symptoms, such as cough, shortness of breath, or swelling of the ankles, hands, or other areas? Any GI complaints, such as anorexia, nausea, vomiting, weight loss, abdominal pain, diarrhea, constipation, or epigastric fullness? Also, ask about genitourinary signs and symptoms, such as dark or pink urine, increased or decreased urination, menstrual irregularities, and loss of libido.
Next, examine the patient's skin. Note the color of hyperpigmented areas: Brown suggests excess melanin in the epidermis; slate gray or a bluish tone suggests excess pigment in the dermis. Inspect for other skin changes,

too—thickening and leatherlike texture as well as changes in hair distribution. Check the patient's skin and sclerae for jaundice, and note any spider angiomas, palmar erythema, or purpura.
Take the patient's vital signs, noting fever, hypotension, or pulse irregularities. Evaluate his general appearance. Does he have exophthalmos or an enlarged jaw, nose, or hands? Palpate for an enlarged thyroid gland, and auscultate for a bruit over the gland. Palpate the muscles for atrophy and the joints for swelling and tenderness. Assess the abdomen for ascites and edema, and palpate and percuss the liver and spleen to evaluate their size and position. Check the male patient for testicular atrophy and gynecomastia.
Acanthosis nigricans. This soft velvetybrown verrucous pigmentation is found most commonly in the skin folds and may have associated skin tags. It typically occurs in individuals younger than age 40, may be genetically inherited, and is associated with obesity or endocrinopathies, such as hypothyroidism or hyperthyroidism, acromegaly, polycystic ovary disease, insulin-resistant diabetes, or Cushing's disease.
When seen in individuals older than age 40, this disorder is commonly associated with an internal malignancy, usually adenocarcinoma, and most commonly of the GI tract or uterus; less commonly of the lung, prostate, breast, or ovary. Acanthosis nigricans of the oral mucosa or tongue is highly suggestive of a neoplasm, especially of the GI tract. This skin condition commonly regresses with successful treatment of the neoplasm and may recur with reoccurrence of the disease.
Acromegaly. This disorder results from a pituitary tumor that secretes excessive amounts of growth hormone after puberty. Hyperpigmentation (possibly acanthosis nigricans) may affect the face, neck, genitalia, axillae, palmar creases, and new scars. Skin appears oily, sweaty, thick, and leathery, with furrows and ridges formed over the face, neck, and scalp. The tongue is enlarged and furrowed; lips are thick; and the nose is large. Body hair is markedly increased. The hands are broad and spadelike. Marked prognathism interferes with chewing.
Adrenocortical insufficiency (Addison's disease). This disorder produces diffuse tan, brown, or bronze-to-black hyperpigmentation of both exposed and unexposed areas of the face, knees, knuckles, elbows, antecubital areas, beltline, palmar creases, lips, gums, tongue, and buccal mucosa (where hyperpigmentation may be bluish black). Normally pigmented areas, moles, and scars become darker. Early in the disorder, hyperpigmentation occurs as persistent tanning after exposure to the sun. Some patients (usually female) lose axillary and pubic hair; about 15% have vitiligo. Patients may develop slowly progressive fatigue, weakness, anorexia, nausea, vomiting, weight loss, orthostatic hypotension, abdominal pain, irritability, weak and irregular pulse, diarrhea or constipation, decreased libido, amenorrhea, syncope and, sometimes, an enhanced sense of taste, smell, and hearing.
Cirrhosis, biliary. Hyperpigmentation is a classic feature of this disorder, which primarily affects women between ages 40 and 60. A widespread and accentuated brown hyperpigmentation appears on areas exposed to sunlight, but not on the mucosa. Pruritus that worsens at bedtime may be the earliest symptom. Fatigue, weight loss, and vague abdominal pain may appear years before the onset of jaundice. Malabsorption may cause nocturnal diarrhea, frothy and bulky stools, weight loss, purpura, and osteomalacia with bone and back pain. The patient may also have hematemesis from esophageal varices, xanthomas and xanthelasmas, hepatosplenomegaly, ascites, edema, spider angiomas, and palmar erythema.
Cirrhosis, Laënnec's. After about 10 years of excessive alcohol ingestion, progressive liver dysfunction causes diffuse, generalized hyperpigmentation on sun-exposed areas. Early in the disorder, the patient may complain of increasing weakness, fatigue, anorexia, slight weight loss, nausea and vomiting, indigestion, constipation or diarrhea, and a dull abdominal ache. As the disorder progresses, the patient may display major signs and symptoms in every body system resulting from hepatic insufficiency and portal hypertension.
Cushing's syndrome (hypercortisolism). Most common in females, this syndrome is caused by excessive levels of adrenocortical hormones or related corticosteroids. In addition to hyperpigmentation, findings include diabetes mellitus, hypertension, left ventricular hypertrophy, capillary fragility, increased susceptibility to infection, decreased resistance to stress, suppressed inflammatory response, muscle weakness, pathologic changes from bone demineralization, gynecomastia in males, and mild virilism and amenorrhea or oligomenorrhea in females.

Hemochromatosis. In this inherited disorder (also called bronzed diabetes), most common in men between ages 40 and 60, early and progressive hyperpigmentation results from melanin (and possibly iron) deposits in the skin. Hyperpigmentation develops as generalized bronzing and metallic gray areas accentuated over sun-exposed areas, genitalia, and scars. Early related effects include weakness, lassitude, weight loss, abdominal pain, loss of libido, and signs of diabetes, such as polydipsia and polyuria. Later, signs of liver and cardiac involvement become prominent.
Malignant melanoma. This form of cancer causes malignant lesions of pigmented skin, commonly moles. Common sites include the head and neck in men, the legs in women, and the back in both men and women exposed to excessive sunlight. Up to 70% of these lesions arise from a preexisting nevus. Metastatic melanoma may produce generalized hyperpigmentation.
The cardinal sign of malignant melanoma is a skin lesion or nevus that enlarges, changes color, becomes inflamed, itches, ulcerates, bleeds, changes texture, or develops an associated halo nevus or vitiligo.
Melasma. This light or dark brown hyperpigmentation occurs on areas exposed to sunlight, most notably on the face, and is associated with use of hormonal contraceptives or pregnancy. Some cases are idiopathic. Lesions are symmetrical and usually involve the cheeks, forehead, and upper lip. When related to pregnancy, the pigmentation may decrease after delivery. Melasma has cosmetic significance only.
Porphyria cutanea tarda. Primarily affecting men between ages 40 and 60, this disorder produces generalized brownish hyperpigmentation on sun-exposed areas and extreme skin fragility (particularly on a bald scalp and on the face and hands). It also causes pink or brownish urine (from porphyrin excretion), anorexia, jaundice, and hepatomegaly.
Scleroderma (progressive systemic sclerosis). Both localized and systemic scleroderma produce generalized dark brown hyperpigmentation that's unrelated to sun exposure. Other skin findings include areas of depigmentation and spider angiomas. The patient initially experiences signs and symptoms of Raynaud's phenomenon —blanching, cyanosis, and erythema of the fingers and toes when exposed to cold or stress, and possible finger shortening, fingertip ulcerations, and gangrene of the fingers and toes. Later findings include pain, stiffness, and swelling of the fingers and joints; skin thickening that progresses to taut, shiny, leathery skin over the entire hands and forearms and then over the upper arms, chest, abdomen, and back; masklike facial skin and a pinched mouth; and, possibly, contractures. Systemic scleroderma also involves the GI, cardiovascular, and other body systems.
Thyrotoxicosis. This disorder can cause hyperpigmentation on the face, neck, genitalia, axillae, and palmar creases as well as in new scars. Other findings include vitiligo; warm, moist skin; erythematous palms; fine scalp hair with premature graying; and Plummer's nails.
Classic findings of Graves' disease, the most common form of thyrotoxicosis, include an enlarged thyroid gland, nervousness, heat intolerance, weight loss despite increased appetite, profuse diaphoresis, diarrhea, tremor, and palpitations. Exophthalmos, although characteristic, is absent in many patients.
Tinea versicolor. This benign fungal skin infection produces raised or macular scaly lesions, usually on the upper trunk, neck, and arms, which range from hyperpigmented patches in fair-skinned patients to hypopigmented patches in dark-skinned patients.
Arsenic poisoning. Chronic arsenic poisoning can cause diffuse hyperpigmentation with scattered freckle-size areas of normal or depigmented skin. Other features may include weakness, muscle aches, peripheral neuropathy, headache, drowsiness, confusion, seizures, and mucous membrane involvement (conjunctivitis, photophobia, pharyngitis, or an irritating cough).
Drugs. Hyperpigmentation can stem from use of barbiturates; salicylates; chemotherapeutic drugs, such as busulfan, cyclophosphamide, procarbazine, and nitrogen mustard; chlorpromazine; antimalarial drugs, such as hydroxychloroquine; hydantoin; minocycline; metals, such as silver (in argyria) and gold (in chrysiasis); corticotropin; and phenothiazines.
Wood's lamp, a special ultraviolet light, helps enhance the contrast between normal and hyperpigmented epidermis. A skin biopsy can help confirm the cause of hyperpigmentation.
Hyperpigmentation may persist even after treatment of the underlying disorder or with-drawal

of the causative drug. Bleaching creams may not be effective if most of the excess melanin lies in subepidermal skin layers. Overthe-counter bleaching creams tend to be ineffective because they contain less than 2% hydroquinone.
Most moles that are found in children are junctional nevi—flat, well demarcated, brown to black—that can appear anywhere on the skin. Although these lesions are considered benign, recent evidence suggests that some of them may become malignant in later life. Some physicians recommend removal of junctional nevi; others advise regular inspection. Congenital melanocytic nevi present at birth should be removed, especially if large (greater than 20 cm), because they become malignant in about 20% of cases. Some of these lesions may have an increased amount of hair.
Bizarre arrangements of linear or streaky hyperpigmented lesions on a child's sun-exposed lower legs suggest phytophotodermatitis. Advise parents to protect the child's skin with long pants and socks. Congenital hyperpigmented lesions include benign mongolian spots and sharply defined or diffuse lesions occurring in such disorders as neurofibromatosis, xeroderma pigmentosum, Albright's syndrome, Fanconi's syndrome, Gaucher's disease, Niemann-Pick disease, Peutz-Jeghers syndrome, phenylketonuria, and Wilson's disease.
Advise the patient to use corrective cosmetics, to avoid excessive sun exposure, and to apply a sunscreen or sun blocker such as zinc oxide cream. Advise patients who stop using bleaching agents to continue using sun blockers because rebound hyperpigmentation can occur.
Warn every patient with a benign hyperpigmented area to consult his physician if the lesion's size, shape, or color changes; this may signal a developing skin cancer.
Hyperpnea indicates increased respiratory effort for a sustained period—a normal rate (at least 12 breaths/minute) with increased depth (a tidal volume greater than 7.5 ml/kg), an increased rate (more than 20 breaths/minute) with normal depth, or increased rate and depth. This sign differs from sighing (intermittent deep inspirations) and may or may not be associated with tachypnea (increased respiratory rate).
The typical patient with hyperpnea breathes at a normal or increased rate and inhales deeply, displaying marked chest expansion. He may complain of shortness of breath if a respiratory disorder is causing hypoxemia, or he may not be aware of his breathing if a metabolic, psychiatric, or neurologic disorder is causing involuntary hyperpnea. Other causes of hyperpnea include profuse diarrhea or dehydration, loss of pancreatic juice or bile from GI drainage, and ureterosigmoidostomy. All these conditions and procedures cause a loss of bicarbonate ions, resulting in metabolic acidosis. Hyperpnea may also accompany strenuous exercise, and voluntary hyperpnea can promote relaxation in patients experiencing stress or pain—for example, women in labor.
Hyperventilation, a consequence of hyperpnea, is characterized by alkalosis (arterial pH above 7.45 and partial pressure of carbon dioxide [PCO2] below 35 mm Hg). In central neurogenic hyperventilation, brain stem dysfunction (as results from a severe cranial injury) increases the rate and depth of respirations. In acute intermittent hyperventilation, the respiratory pattern may be a response to hypoxemia, anxiety, fear, pain, or excitement. Hyperpnea may also be a compensatory mechanism in metabolic acidosis. Under these conditions, it's known as Kussmaul's respirations. (See Kussmaul's respirations: A compensatory mechanism, page 388.)
If you observe hyperpnea in a patient whose other signs and symptoms signal a life-threatening emergency, you must intervene quickly and effectively. (See Managing hyperpnea, page 389.) However, if the patient's condition isn't grave, first determine his level of consciousness (LOC). If he's alert (and if his hyperpnea isn't interfering with speaking), ask about recent illnesses or infections; ingestion of aspirin or other drugs or chemicals; or inhalation of drugs or chemicals. Find out if the patient has diabetes mellitus, renal disease, or any pulmonary conditions. Is he excessively thirsty or hungry? Has he recently had severe diarrhea or an upper respiratory tract infection?
Next, observe the patient for clues to his abnormal breathing pattern. Is he unable to speak, or does he speak only in brief, choppy phrases?

Is his breathing abnormally rapid? Examine the patient for cyanosis (especially of the mouth, lips, mucous membranes, and earlobes), anxiety, and restlessness—all signs of decreased tissue oxygenation, as occurs in shock. In addition, observe the patient for intercostal and abdominal retractions, use of accessory muscles, and diaphoresis, all of which may indicate deep breathing related to an insufficient supply of oxygen. Next, inspect for draining wounds or signs of infection, and ask about nausea and vomiting. Take the patient's vital signs, including oxygen saturation, noting fever. Also, examine his skin and mucous membranes for turgor, possibly indicating dehydration. Auscultate the patient's heart and lungs.
Head injury. Hyperpnea that results from a severe head injury is called central neurogenic hyperventilation. Whether its onset is acute or gradual, this type of hyperpnea indicates damage to the lower midbrain or upper pons. Accompanying signs reflect the site and extent of injury and can include loss of consciousness; soft-tissue injury or bony deformity of the face, head, or neck; facial edema; clear or bloody drainage from the mouth, nose, or ears; raccoon eyes; Battle's sign; an absent doll's eye sign; and motor and sensory disturbances.
Signs of increased intracranial pressure include decreased response to painful stimulation, loss of pupillary reaction, bradycardia, increased systolic pressure, and widening pulse pressure.
Hyperventilation syndrome. Acute anxiety triggers episodic hyperpnea, resulting in respiratory alkalosis. Other findings may include agitation, vertigo, syncope, pallor, circumoral and peripheral paresthesia, muscle twitching, carpopedal spasm, weakness, and arrhythmias.
Hypoxemia. Many pulmonary disorders that cause hypoxemia—for example, pneumonia, pulmonary edema, chronic obstructive pulmonary disease, and pneumothorax—may cause hyperpnea and episodes of hyperventilation with chest pain, dizziness, and paresthesia. Other effects include dyspnea, cough, crackles, rhonchi, wheezing, and decreased breath sounds.
Ketoacidosis. Alcoholic ketoacidosis (occurring most often in females with a history of alcohol abuse) typically follows cessation of drinking after a marked increase in alcohol consumption has caused severe vomiting. Kussmaul's respirations begin abruptly and are accompanied by vomiting for several days, fruity breath odor, slight dehydration, abdominal pain and distention, and absent bowel sounds. The patient is alert and has a normal blood glucose level, unlike the patient with diabetic ketoacidosis.
Diabetic ketoacidosis is potentially life-threatening and typically produces Kussmaul's respirations. The patient usually experiences polydipsia, polyphagia, and polyuria before the onset of acidosis; he may have a history of diabetes mellitus. Other clinical features include fruity breath odor; orthostatic hypotension; rapid, thready pulse; generalized weakness;


decreased LOC (lethargy to coma); nausea; vomiting; anorexia; and abdominal pain.
Starvation ketoacidosis is also potentially life-threatening and can cause Kussmaul's respirations. Its onset is gradual; typical findings include signs of cachexia and dehydration, decreased LOC, bradycardia, and a history of severely limited food intake.
Renal failure. Acute or chronic renal failure can cause life-threatening acidosis with Kussmaul's respirations. Signs and symptoms of severe renal failure include oliguria or anuria, uremic fetor, and yellow, dry, scaly skin. Other cutaneous signs include severe pruritus, uremic frost, purpura, and ecchymosis. The patient may complain of nausea and vomiting, weakness, burning pain in the legs and feet, and diarrhea or constipation.
As acidosis progresses, corresponding clinical features include frothy sputum, pleuritic chest pain, and signs of heart failure and pleural or pericardial effusion. Neurologic signs include altered LOC (lethargy to coma), twitching, and seizures. Hyperkalemia and hypertension, if present, require rapid intervention to prevent cardiovascular collapse.
Sepsis. A severe infection may cause lactic acidosis, resulting in Kussmaul's respirations. Other findings include tachycardia, fever or a low temperature, chills, headache, lethargy, profuse diaphoresis, anorexia, cough, wound drainage, burning on urination, confusion or change in mental status, and other signs of local infection.
Shock. Potentially life-threatening metabolic acidosis produces Kussmaul's respirations, hypotension, tachycardia, narrowed pulse pressure, weak pulse, dyspnea, oliguria, anxiety, restlessness, stupor that can progress to coma, and cool, clammy skin. Other clinical features may include external or internal bleeding (in hypovolemic shock); chest pain, arrhythmias, and signs of heart failure (in cardiogenic shock); high fever, chills and, rarely, hypothermia (in septic shock); or stridor due to laryngeal edema (in anaphylactic shock). Onset is usually acute in hypovolemic, cardiogenic, or anaphylactic shock, but it may be gradual in septic shock.
Drugs. Toxic levels of salicylates, ammonium chloride, acetazolamide, and other carbonic anhydrase inhibitors can cause Kussmaul's respirations. So can ingestion of methanol or ethylene glycol, found in antifreeze solutions.
Monitor vital signs, including oxygen saturation, in all patients with hyperpnea, and observe for increasing respiratory distress or an irregular respiratory pattern signaling deterioration. Prepare for immediate intervention to prevent cardiovascular collapse: Start an I.V. line for administration of fluids, blood transfusions, and vasopressors for hemodynamic stabilization, as ordered, and prepare to give ventilatory support. Prepare the patient for arterial blood gas analysis and blood chemistry studies.
Hyperpnea in children indicates the same metabolic or neurologic causes as in adults and requires the same prompt intervention. The most common cause of metabolic acidosis in children is diarrhea, which can cause a life-threatening crisis. In infants, Kussmaul's respirations may accompany acidosis due to inborn errors of metabolism.
Hypopigmentation is a decrease in normal skin, hair, mucous membrane, or nail color resulting from deficiency, absence, or abnormal degradation of the pigment melanin. This sign may be congenital or acquired, asymptomatic or associated with other findings. Its causes include genetic disorders, nutritional deficiency, chemicals and drugs, inflammation, infection, and physical trauma. Typically chronic, hypopigmentation can be difficult to identify if the patient is lightskinned or has only slightly decreased coloring.
Begin with a detailed patient history. Ask if any other family member has the same problem and if it was present from birth or developed after skin lesions or a rash. Were the lesions painful? Does the patient have any medical problems or a history of burns, physical injury, or physical contact with chemicals? Is he taking prescription or over-the-counter drugs? Find out if he

has noticed other skin changes—such as erythema, scaling, ulceration, or hyperpigmentation— or if sun exposure causes unusually severe burning.
Next, examine the patient's skin, noting erythema, scaling, ulceration, areas of hyperpigmentation, and other findings.
Albinism. This genetically inherited disease involves alterations of the melanin pigment system that affects skin, hair, and eyes. There are various forms of albinism, all of which are present at birth. Skin and hair color vary from snow white to brown, but the universal finding of iris translucency confirms the diagnosis. Associated eye findings include nystagmus, decreased visual acuity, decreased pigmentation of the retina, and strabismus.
Lifelong diligence is needed to protect the skin from sun exposure, including using sunblock with an SPF greater than 30; wearing protective clothing, hats, and sunglasses (even for infants); avoiding the sun during high solar intensity; and obtaining routine skin examinations for the development of skin cancers.
Suggest referral to a support group to assist patients with problems occurring in daily life. One such organization is the National Organization for Albinism and Hypomelanosis.
Burns. Thermal and radiation burns can cause transient or permanent hypopigmentation.
Discoid lupus erythematosus. This form of lupus erythematosus may produce hypopigmentation after inflammatory skin eruptions. Lesions are sharply defined, separate or fused macules, papules, or plaques; they vary from pink to purple, with a yellowish or brown crust and scaly, enlarged hair follicles. Although they may occur on other parts of the body, the lesions are typically distributed in a butterfly pattern over the cheeks and bridge of the nose. Telangiectasia may occur. After the inflammatory eruptive stage, noncontractile scarring and atrophy commonly affect the face and may also involve sun-exposed areas of the neck, ears, scalp (with possible alopecia), lips, and oral mucosa.
Hypomelanosis (idiopathic guttate). Common in lightly pigmented people older than age 30, this skin disorder produces sharply marginated, angular white spots on sun-exposed extremities. In blacks, hypopigmentation occurs mainly on the upper arms.
Inflammatory and infectious disorders. Skin disorders, such as psoriasis, and infectious disorders, such as viral exanthemas or syphilis, can cause transient or permanent hypopigmentation.
Tinea versicolor. This benign fungal skin infection produces scaly, sharply defined lesions that usually appear on the upper trunk, neck, and arms. The lesions range from hypopigmented patches in dark-skinned patients to hyperpigmented patches in fair-skinned patients.
Tuberculoid leprosy. This chronic disorder affects the skin and peripheral nervous system. Erythematous or hypopigmented macules have decreased or absent sensation for light, touch, and warmth. Because the lesions don't sweat, the skin feels dry and rough; it may be scaly. Associated effects may include very painful, palpable peripheral nerves; muscle atrophy and contractures; and ulcers of the fingers and toes.
Vitiligo. This common skin disorder produces sharply defined, flat white macules and patches ranging in diameter from 1 to over 20 cm. The hypopigmented areas commonly have hyperpigmented borders. Usually bilaterally symmetrical, lesions appear on sun-exposed areas; in body folds; around the eyes, nose, mouth, and rectum; and over bony prominences. Patches of vitiligo may coalesce to form universal lack of pigment and may involve the hair, eyebrows, and eyelashes. Spontaneous repigmentation can occur. Hypopigmented patches (halo nevi) may surround pigmented moles.
Chemicals. Most phenolic compounds—for example, amylphenol (a dye) and paratertiary butylphenol, which are used in plastics and glues, and germicides used in many household and industrial products—can cause hypopigmentation.
Drugs. Topical or intralesional administration of corticosteroids causes hypopigmentation at the treatment site. Chloroquine, an antimalarial drug, may cause depigmentation of hair (including eyebrows and lashes) and poor tanning 2 to 5 months after therapy begins.

In fair-skinned patients, a special ultraviolet (UV) light (Wood's lamp) can help differentiate hypopigmented lesions, which appear pale, from depigmented lesions, which appear white.
Advise patients to use corrective cosmetics to help hide skin lesions, and to use a sunblock because hypopigmented areas may sunburn easily. Encourage regular examinations for early detection and treatment of lesions that may become premalignant or malignant. Repigmentation therapy may be prescribed, combining a photosensitizing drug (psoralen) and UV light, wavelength A. Advise patients with associated eye problems, such as albinism, to avoid the midday sun and to wear sunglasses. Refer patients for counseling if lesions cause stress.
In children, hypopigmentation results from genetic or acquired disorders, including albinism, phenylketonuria, and tuberous sclerosis. In neonates, hypopigmentation may indicate a metabolic or nervous system disorder.
In elderly people, hypopigmentation is usually the result of cumulative exposure to UV light, which may also cause hyperpigmentation, telangiectasia, and purpura. These changes are known as dermatoheliosis.

Index: Foreword|A|B|C|D|E|F|G|H|I|J|K|L|M|N|O|PQ|R|S|T|U|V|QXYZ|Selected References|Appendices

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