CONFIRMING DIAGNOSIS Patient, family, and occupational histories and a complete audiologic examination usually provide ample evidence of hearing loss and suggest possible causes or predisposing factors.
The Weber, Rinne, and specialized audiologic tests differentiate between conductive and sensorineural hearing loss.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Introduction: Malignant Neoplasms:
Diagnostic methods
(Professional Guide to Diseases (Eighth Edition))
A thorough medical history and physical examination should precede sophisticated diagnostic procedures. Useful tests for the early detection and staging of tumors include X-ray, endoscopy, isotope scan, computed tomography scan, and magnetic resonance imaging, but the single most important diagnostic tool is a biopsy for direct histologic study of tumor tissue. Biopsy tissue samples can be taken by curettage, fluid aspiration (pleural effusion), fine-needle aspiration biopsy (breast), dermal punch (skin or mouth), endoscopy (rectal polyps), and surgical excision (visceral tumors and nodes).
An important tumor marker, carcinoembryonic antigen (CEA), although not diagnostic by itself, can signal malignancies of the large bowel, stomach, pancreas, lungs, and breasts. CEA titers range from normal (less than 5 ng) to suspicious (5 to 10 ng) to suspect (over 10 ng). CEA serves many valuable purposes:
❑as a baseline during chemotherapy to evaluate the extent of tumor spread
❑to regulate drug dosage
❑to prognosticate after surgery or radiation
❑to detect tumor recurrence.
Although no more specific than CEA, alpha-fetoprotein — a fetal antigen uncommon in adults — can suggest testicular, ovarian, gastric, and hepatocellular cancers. Beta human chorionic gonadotropin may point to testicular cancer or choriocarcinoma. Other commonly used tumor markers include prostate-specific antigen to detect and monitor prostatic cancer, and CA-125, useful for monitoring ovarian, colorectal, and gastric cancers.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Malignant spinal neoplasms:
Diagnosis
(Professional Guide to Diseases (Eighth Edition))
❑Spinal and lumbosacral magnetic resonance imaging confirm spinal tumor.
❑ X-rays show distortions of the intervertebral foramina; changes in the vertebrae or collapsed areas in the vertebral body; and localized enlargement of the spinal canal, indicating an adjacent block.
❑ Myelography identifies the level of the lesion by outlining it if the tumor is causing partial obstruction; it shows anatomic relationship to the cord and the dura. If obstruction is complete, the injected dye can't flow past the tumor. (This study is dangerous if cord compression is nearly complete because withdrawal or escape of cerebrospinal fluid (CSF) will allow the tumor to exert greater pressure against the cord.)
❑ Radioisotope bone scan demonstrates metastatic invasion of the vertebrae by showing a characteristic increase in osteoblastic activity.
❑ Computed tomography scan shows cord compression and tumor location.
❑ Frozen section biopsy at surgery identifies the tissue type.
❑ Lumbar puncture may be normal, abnormal, or nonspecific. It may show clear yellow CSF as a result of increased protein levels if the flow is completely blocked. If the flow is partially blocked, protein levels rise, but the fluid is only slightly yellow in proportion to the CSF protein level. Cytology of the CSF may show malignant cells of metastatic carcinoma.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Hearing loss:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
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 289.) 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.)
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Costovertebral angle tenderness:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
After detecting CVA tenderness, determine the possible extent of renal damage. First, find out if the patient has other symptoms of renal or urologic dysfunction. Ask about voiding habits: How frequently does he urinate and in what amounts? Has he noticed any change in intake or output? If so, when did he notice it? (Ask about fluid intake before judging his output as abnormal.) Does he have nocturia, pain or burning during urination, or difficulty starting a stream? Does the patient strain to urinate without being able to do so (tenesmus)? Ask about urine color; brown or bright red urine may contain blood.
Explore other signs and symptoms. For example, if the patient is experiencing pain in his flank, abdomen, or back, when did he first notice it? How severe is it, and where is it located? Find out if the patient or a family member has a history of urinary tract infections, congenital anomalies, calculi, or other obstructive nephropathies or uropathies. Also, ask about a history of renovascular disorders, such as occlusion of the renal arteries or veins.
Perform a brief physical examination. Begin by taking the patient’s vital signs. Fever and chills in a patient with CVA tenderness may indicate acute pyelonephritis. If the patient has hypertension and bradycardia, be alert for other autonomic effects of renal pain, such as diaphoresis and pallor. Inspect, auscultate, and gently palpate the abdomen for clues to the underlying cause of CVA tenderness. Be alert for abdominal distention, hypoactive bowel sounds, and palpable masses.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Hearing Loss:
History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
Proactive detection of minor hearing alterations is necessary because most patients with hearing loss do not present with a hearing complaint. Many elderly patients, in particular, accept hearing loss as an expected part of aging.
A. Presentation. A small number of patients will present with a complaint of decreased hearing, a few more will admit to abnormal hearing, but most will have no specific hearing concern. A patient’s depression, confusion, social isolation, or poor job performance can be caused or complicated by hearing impairment. Family members may describe abnormal, slow, or overly loud answers. A sudden tendency to monopolize or disrupt conversation, or to tilt the head in conversation, may suggest hearing loss.
B. Duration. CHL is often of sudden onset but of a mild degree. Complete occlusion or rapid collection of fluid in middle ear causes abrupt change in hearing. SNHL can be abrupt and severe (stroke, idiopathic, trauma) or gradual (Ménière’s syndrome, acoustic neuroma, hypothyroidism). Some forms may be intermittent (such as Ménière’s syndrome.)
C. Quality of hearing. CHL often affects quality of hearing first. Described as muffled “like a head in a drum,” the patient may lose high frequency and voice discrimination, yet still be able to detect subtle sounds. SNHL, when not associated with tinnitus, can have good quality but diminished hearing that is usually more profound than CHL.
D. Associated symptoms. Tinnitus is classically associated with Ménière’s syndrome or disease, but may be seen with other causes of SNHL. Vertigo is associated with inner ear disorders, and is often self-limited (Chapter 6.9). Associated fluctuating neurologic defects of many sites suggest MS, whereas focal deficits suggest CNS tumors or vascular insufficiency.
E. Family history. This may be positive in presbycusis, Ménière’s, otosclerosis, and acoustic neuroma.
F. Social and work history. Recreational history (loud music or target shooting) or work history (pilots, factory workers, firefighters) can implicate excessive noise exposure. Inquire about use of protective equipment and chronicity of exposure.
Physical examination
Gross tests of hearing are only helpful to confirm significant hearing asymmetry or to detect profound hearing loss. With one ear covered, the patient tries to hear soft sounds such as the tick of a watch, scratching of two fingers rubbed together, or a softly whispered voice.
A. Visual examination of ears. Inspect the canal and TM to rule out obvious causes of CHL. Cerumen impaction is a remarkably common and easily corrected cause of hearing loss. Pneumoscopy to check for normal movement of the TM helps rule out perforation, atelectasis, eustachian tube dysfunction, stiffened TM, ossicular disruption, and middle ear effusion.
B. Weber test. With a vibrating tuning fork placed on the top of the head, the patient is asked to describe the sound heard. The patient will perceive the sound to be louder in the affected ear in CHL, because the background noise will be absent on that side. The unaffected ear will be perceived as louder in SNHL.
C. Rinne test. With the vibrating tuning fork placed on the mastoid, the patient detects bone conduction (BC). The tuning fork is removed when the patient can no longer hear the sound. Then the tuning fork is held next to the ear to test for air conduction (AC). In an individual with normal hearing, AC is significantly better than BC. CHL will reduce AC, with little effect on BC.
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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Hearing Loss:
Differential Overview
(Field Guide to Bedside Diagnosis)
Sensorineural
❑ Presbyacusis
❑ Noise-induced loss
❑ Drugs
❑ Ménière disease
❑ Eighth nerve injury
❑ Acoustic neuroma
❑ Multiple sclerosis
Conductive
❑ Impacted cerumen
❑ Otitis media
❑ Middle ear effusion
❑ Perforation of tympanic membrane
❑ Otosclerosis
❑ Exostoses
❑ Developmental defect
❑ Glomus tumor
Diagnostic Approach
Conductive hearing loss presents with loss of low tones and vowels. Sensorineural hearing loss produces impaired high tone perception, with diminished speech discrimination—especially for female voices—and hearing ringing sounds (tinnitus). Hyperacusis (the sensation that sounds are overly loud to the point of discomfort) is associated with sensorineural cochlear hearing loss. Paracusis (words perceived more clearly in a noisy environment) is associated with conductive middle ear hearing loss.
A reliable qualitative screen for high frequency hearing loss is the ability to hear whispered speech. Stand behind the patient at arm’s length and test one ear at a time. Whisper a combination of 3 letters and numbers (e.g., 4-K-2), and ask the patient to repeat it. The screen is passed when 3/6 are correctly identified. The 256 Hz tuning fork tests 10 to 15 dB, and the 512 Hz 20 to 30 dB. The Rinne test (bone conduction . air conduction) is sensitive to a 20 dB hearing loss. The Weber test is sensitive to 5 dB of hearing loss. A tuning fork is placed in the midline. With conductive loss, it lateralizes to the affected ear, and with sensorineural loss, to the unaffected ear.
Pneumoscopy is performed by first insufflating the ear then releasing. A nonmobile TM may be due to fluid or a mass in the middle ear cavity, or a stiff or sclerotic TM. A hypermobile TM may indicate ossicular chain disruption. A TM that moves only with negative pressure can be due to a retracted TM or a middle ear with a blocked eustacian tube, with resulting negative ear pressure.
Acute hearing loss occurs with infection, traumatic tympanic membrane rupture, or acute vascular event. Unilateral sensorineural loss suggests an inner ear disorder such as Meniere disease or an acoustic neuroma.
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Source: Field Guide to Bedside Diagnosis, 2007
Hearing loss:
Diagnosis
(Handbook of Diseases)
Patient, family, and occupational histories and a complete audiologic examination usually provide ample evidence of hearing loss and suggest possible causes or predisposing factors. The Weber and Rinne tests and other specialized audiologic tests differentiate between conductive and sensorineural hearing loss.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Hearing loss:
History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
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, or 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?
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Costovertebral angle tenderness:
History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
After detecting CVA tenderness, determine the possible extent of renal damage. First, find out if the patient has other symptoms of renal or urologic dysfunction. Ask about voiding habits: How frequently does he urinate, and in what amounts? Has he noticed any change in intake or output? If so, when did he notice the change? (Ask about fluid intake before judging his output as abnormal.) Does he have nocturia? Ask about pain or burning during urination or difficulty starting a stream. Does the patient strain to urinate without being able to do so (tenesmus)? Ask about urine color; brown or bright-red urine may contain blood.
Explore other signs and symptoms. For example, if the patient is experiencing pain in his flank, abdomen, or back, when did he first notice the pain? How severe is it, and where is it located? Find out if the patient or a family member has a history of urinary tract infections, congenital anomalies, calculi, or other obstructive nephropathies or uropathies. Also, ask about a history of renovascular disorders, such as occlusion of the renal arteries or veins.
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Hearing Loss and Deafness:
Clinical Features and Diagnosis
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
Conductive Hearing Loss
External Auditory Canal Disorders
Atresia of External Auditory Canal
Absenceof meatus under tragus signifies presence of external auditory canalatresia. External ear is usually small and deformed.CT should be performed to identifyother abnormalities, especially in middle ear, and to help in evaluationof possible surgical repair. Impacted Cerumen
Impacted cerumen (earwax) in external canalis common cause of conductive hearing loss. Hearing returns to normalafter its removal. Otitis Externa
Inflammationof external auditory canal with discharge and swelling causes obstructionand diminished sound transmission. Hearing returns to normal afterinflammation subsides.See Chap.16, Earache. Exostosis
Exostoses(bone overgrowths) may be found in external auditory canal or middleear but are uncommon in pediatric population.Usually bilateral and close to tympanicmembrane.Although diagnosis is usually clinical,CT may be useful in defining their extent. Masses
Foreignbodies (e.g., cotton balls, erasers, beads, and other small objects)that obstruct external canal can cause decreased hearing. Readilyseen by otoscopy.Polyps are reddish or purplish massesthat bleed easily. Can arise from external canal and tympanic membraneor protrude from middle ear into canal through perforation in membrane.Often associated with cholesteatoma. Excisional biopsy is diagnostic.Neoplasms arising from external auditorycanal are rare in pediatric population but include neurofibromas,eosinophilic granulomas, and rhabdomyosarcomas. CT shows locationand extent of lesion. Histologic diagnosis is definitive. Middle Ear Disorders
Acute and Chronic Otitis Media and Otitis Media with Effusion
Most commoncauses of conductive hearing loss in children are acute and chronicotitis media and otitis media with effusion.See Chap.16, Earache. Tympanic Membrane Perforation
Most common causes of tympanic membrane perforationare acute otitis media and head trauma. The latter causes conductivehearing loss by accumulation of blood in external canal or middleear or by disruption of ossicular chain. Perforation is seen byotoscopy. Hemotympanum
Direct blowto ear or basilar skull fracture may cause hemotympanum.Tympanic membrane appears red or purplebecause of blood in middle ear space. Other findings that may beseen with basilar skull fracture include ecchymoses behind ear oraround eyes, and CSF drainage from nose or ears.CT helps determine extent of injury. Tympanosclerosis
Characterizedby whitish plaques in tympanic membrane and nodular deposits insubmucosal layers of middle ear. If deposits of calcium and phosphatecrystals involve ossicles, conductive loss can occur.Predisposing factors are chronic otitismedia and tympanostomy tube placement. Ossicular Chain Defect, Disruption, or Fixation
Should besuspected in cases of conductive hearing loss when external auditorycanal and middle ear appear normal on exam.History of head trauma suggests ossiculardisruption.CT of temporal bone shows ossicularchain and any abnormalities of otic capsule. Cholesteatoma and Other Middle Ear Masses
Cholesteatomausually appears as whitish mass in middle ear. Other middle earmasses are discussed by Bellet et al. (1992).Conductive hearing loss, tinnitus,ear fullness, or facial nerve palsy can indicate presence of middleear mass, regardless of whether it is visible by otoscopy.CT is initial imaging exam for middleear masses. Sensorineural Hearing Loss
Sensorineural Hearing Loss without Associated Abnormalities
In the past these disorders were usuallydistinguished from each other by mode of genetic transmission, ageof onset, severity of hearing loss, and type of audiogram (Gorlinet al., 1995). Recently, several genes for hearing loss have beenmapped to different chromosomes, permitting specific diagnosis (Willems,2000). Sensorineural Hearing Loss with Associated Abnormalities
Several syndromes may be associated withsensorineural hearing loss: Hurler, Hunter, Cockayne, Alport, Klippel-Feil,Wildervanck, Waardenburg, Usher, Pendred, Jervell and Lange-Nielsen,and branchio-oto-renal. Chromosomal Disorders
Although trisomies 13, 18, 21, and 22 maybe associated with sensorineural hearing loss, conductive loss dueto otitis media with effusion is more common. Inner Ear Malformations
The following malformations can usually bediagnosed by CT, although sometimes MRI may be necessary. Labyrinthine Aplasia
Michel malformation consists of aplasia ofcochlea, vestibule, and semicircular canals. Common Cavity Malformation
Exists when there is single labyrinthinecavity without cochlea or semicircular canals. Cochlear Malformations
Most commoncochlear malformation observed with imaging studies is Mondini malformation.Axial CT shows single cochlear cavitywith normal cochlear basal turn.Has been reported in many syndromes:DiGeorge, Goldenhar, Pendred, Waardenburg, and CHARGE association.Pseudo-Mondini malformation is presenceof a cochlear vestige that communicates directly with vestibulewithout intervening bony cochlear basal turn.With cochlear aplasia, nidus of scleroticbone replaces cochlea. Large Vestibular Aqueduct
Both the vestibular aqueduct and endolymphsac are enlarged in this malformation Although hearing loss is progressive,it is often fluctuating. Head trauma may result in sudden, irreversible,profound sensorineural hearing loss. Prematurity
Mechanism of hearing loss in premature infantswithout any other predisposing factor is unknown. Hypoxic-Ischemic Encephalopathy
Perinatal asphyxia, including birth trauma,may result in hypoxic-ischemic encephalopathy and hearing loss. Bilirubin Encephalopathy (Kernicterus)
Usuallycauses bilateral high-frequency hearing loss. Possible mechanismsinclude damage to cochlear nuclei and auditory pathways in brain.See Chap.3, Alteration in Consciousness. Infection
Congenitalinfection with rubella, cytomegalovirus, herpes simplex virus, toxoplasmosis,or syphilis (see Chap. 36, Jaundice)sometimes produces hearing loss and deafness.Although acute and chronic otitis mediacause conductive hearing loss, it is postulated that inflammatorymediators or toxins pass from middle ear to inner ear through roundwindow membrane to cause sensorineural hearing loss.Bacterial meningitis and encephalitiscan cause sensorineural hearing loss that can range from mild toprofound. Trauma
Loud noiseof sufficient duration and intensity can destroy organ of Cortiand its associated neural connections in base of cochlea.Tinnitus almost always occurs in noise-inducedhearing loss.Direct trauma including temporal bonefractures and penetrating wounds may disrupt bony and membranouslabyrinth to cause sensorineural hearing loss. CT is imaging procedureof choice. Drugs
Drugs takenduring pregnancy that may cause hearing loss in neonates includequinine, chloroquine, and isotretinoin.Aminoglycosides (streptomycin, kanamycin,gentamicin, amikacin, neomycin), loop diuretics (furosemide, ethacrynicacid), and cisplatin can cause sensorineural loss in infants andchildren. Perilymph Fistula
Abnormalleak of perilymph (cerebrospinal fluid) into middle ear or mastoidair cell system is caused by defects in temporal bone, particularlyin region of stapes footplate or round window.Defects may be congenital or acquired(secondary to trauma of the temporal bone). They are associatedwith sudden fluctuating or progressive sensorineural hearing lossand can predispose to recurrent meningitis. Vertigo also may occurbut is rare.Injection of intrathecal radioisotopeor dye with subsequent nuclear scintigraphy or CT, respectively,often identifies site of leak. See Chap.41, Nasal Discharge. Neoplasm
Some neoplasticdiseases (e.g., leukemia and neuroblastoma) can invade temporal boneand damage cochlea or auditory pathways.Acoustic neuroma, a benign tumor ofeighth cranial nerve, can cause sensorineural hearing loss, tinnitus,vertigo, and facial nerve paralysis. Presence of bilateral tumorssignifies neurofibromatosis.Posterior fossa tumors in area of cerebellopontineangle (e.g., meningioma) can cause hearing loss, tinnitus and ataxia.CT and MRI can locate and define extent of tumor. Histologic diagnosisis definitive. Ménière Disease
Sensorineural fluctuating hearing loss, tinnitus,and vertigo characterize Ménière disease. Unknown
There are a number of cases of hearing lossin which the etiology is unknown. Mixed Hearing Loss
In children with sensorineural hearing loss,presence of acute otitis media or otitis with effusion may produceconductive hearing loss. Diagnostic Approach
Auditoryand language findings listed in Table26.1 are indications for possible hearing loss or deafness.Suspected hearing loss should be investigatedto determine the type, severity, and cause.Any child with suspected hearing lossshould be referred for audiologic evaluation. Speech and languageassessment is often necessary. Neurologic and otolaryngologic consultationmay be required, depending on suspected problem.
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Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
Hearing loss:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
If the patient reports hearing loss, ask him to describe it. 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, or 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 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, notify the physician to discuss whether an otoscopic examination should be done. (See Using an otoscope correctly, page 223.) During the otoscopic examination, note 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 Weber's and the Rinne tests to obtain a preliminary evaluation of the type and degree of hearing loss. (See Differentiating conductive from sensorineural hearing loss, page 304.)
» READ BOOK EXCERPT ONLINE »
Source: Nursing: Interpreting Signs and Symptoms, 2007
Costovertebral angle tenderness:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
After detecting CVA tenderness, determine the possible extent of renal damage. First, find out if the patient has other symptoms of renal or urologic dysfunction. Ask about voiding habits: How frequently does he urinate, and in what amounts? Has he noticed any change in intake or output? If so, when did he notice the change? (Ask about fluid intake before judging his output as abnormal.) Does he have nocturia? Ask about pain or burning during urination or difficulty starting a stream. Does the patient strain to urinate without being able to do so (tenesmus)? Ask about urine color; brown or bright red urine may contain blood.
Explore other signs and symptoms. For example, if the patient is experiencing pain in his flank, abdomen, or back, when did he first notice the pain? How severe is it, and where is it located? Find out if the patient or a family member has a history of urinary tract infections, congenital anomalies, calculi, or other obstructive nephropathies or uropathies. Also, ask about a history of renovascular disorders such as occlusion of the renal arteries or veins.
Perform a brief physical examination. Begin by taking the patient's vital signs. A fever and chills in a patient with CVA tenderness may indicate acute pyelonephritis. If the patient has hypertension and bradycardia, be alert for other autonomic effects of renal pain, such as diaphoresis and pallor. Inspect, auscultate, and gently palpate the abdomen for clues to the underlying cause of CVA tenderness. Be alert for abdominal distention, hypoactive bowel sounds, and palpable masses.
» READ BOOK EXCERPT ONLINE »
Source: Nursing: Interpreting Signs and Symptoms, 2007
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