(Continued) s l l i k s Table 3.11 (Continued) Tone: Look for hypotonia (flaccidity; a sign of LMN disease), spasticity (increased muscle tone with associated weakness, and flexor and exten- sor tone differ; a sign of UMN disease ), or rigidity (increased tone with no associated weakness, and flexor and extensor tone ar e the same; a sign of extrapyramidal disease, e.g., Parkinson \200\231s). Coordination: Loo k for ataxic movements that lack the speed, smooth- ness, and accuracy seen in normal perso ns (a sign of cerebellar disease). Tests include finger \200\223to-nose (must be done at fu ll arm \200\231s extension), heel-to-shin , and rapid alternating movements (if abnormal, t his is called dysdiadochokinesia). Gait: Observe patient walking normally, then on the toes , heels, and using tandem steps (heel-to-toe). Note whether any gait disturbance is sym- me tric or asymmetric. A positive Romberg \200\231s sign is inability to stand for 60 sec with feet together and eyes closed (signals a disturbance of pro- prioception, either from neur opathy or posterior column disease; not a sign of cerebellar disease). Reflexes Proper pati ent positioning and good technique are required to elicit muscle stretch reflexes. Grade as absent (0), 1+ (present with rein- forcement; e.g., when patient hooks fingers of both han ds and pulls them apart as strongly as possible), normal (2+), brisk (3+), or hyperactive ( 4+ including clonus ; i.e., rhythmic oscillations that continue as long as tension is appli ed to a hyperreflexic muscle). Enhanced reflexes are a sign of UMN disease, and reduced/abs ent reflexes are a sign of LMN disease (although these findings are nonspecific and may be seen in persons without neu- rologic disease). Associated nerve roots to memorize include C 6 (biceps and brachioradialis), C7 (triceps), L3 \200\2234 (patellar), and S1 (ankle). Also assess the Babinski reflex bilaterally (use a key or handle of reflex hammer to slowly scr atch a J-shaped stroke beginning at the lateral plantar surface up to the ball of the foot) . A normal response (i.e., Babinski is \200\234absent \200\235 or \200\234normal \200\235 ) is flexion of all toes, and a positive response is an upgoing (extension) of the great to e (with a fanning of the other four toes). Sensory exam Extent of testing depends on the cl inical setting but may include all four simple sensations: Light touch (cotton wool), pain (pin-prick), vibration (128 Hz tuning fork), and temperature (cold stem of tuning fork). Co mpare patient \200\231s perceptions to the contralateral side; note distribution and symmet ry of abnormality. Also assess proprioception (sensation of move- ment of great toe up or d own); proprioceptive loss is common in peripheral neuropathy, spinal cord disease, and seve re hemispheric disease. l a c i n i l C 63 Cranial nerve examination Approach to examining the cranial nerves In patients without neu- rologic complaints, a quick screening exam can include testing pupillary responses to ligh t, eye movements, visual field testing (in one eye), and facial strength. For clinical corr elations, see Table 3.12. I: Smell: Test ability of each nostril to differentiate familiar smells (rarely performed). II: Acuity: Test in each eye separately using a pocket Snellen card; have patients wear usu al corrective lenses. Visual fields: Compare during con- frontation with your own fields. P upils: (p. 81) Assess responses to the \200\234swinging flashlight test \200\235 (in relat ive afferent papillary defect, pupils con- strict with light into the normal eye and dilate with light into the abnor- mal eye). Funduscopic exam: Darken the room. Starting 12 \200 \22318 inches away from the patient \200\231s eye, look through the scope to find the red reflex. Slowly move in and bring a retinal vessel into focus; trace vessels medially toward the nose to find the optic disc, inspecting its shape, color, and clarity. III, IV, and VI: Assess for ptosis and test eye movements . III palsy: Ptosis, eye down and out, +/ \210\222 dilated pupil. May cause both vertical and hori- zontal diplopia. IV pals y: Vertical diplopia (often noticed on descending stairs). Tilting the head toward the affe cted side aggravates the diplopia; many patients compensate by tilting their head away from the side of the lesion. VI nerve palsy: Esotropia (inward deviation) and an inability to a bduct the affected eye. Patient complains of horizontal diplopia on look- ing out at a dist ance. Nystagmus is involuntary, often jerky, eye oscilla- tions. Nystagmus lasting two beat s or less is normal, as is brief nystagmus at the extremes of gaze. Horizontal nystagmus is often due to cerebellar disease or peripheral vestibular disease (but may be due to other central nervous system disorders). Vertical nystagmus is often from a central etiology. V: Motor palsy: \200\234 Open your mouth \200\235: Jaw deviates to side of lesion. Sensory : Corneal reflex lost first; check light touch in all three divisions on the face. VII: Facial nerve lesions cause facial asymmetry (droop) and weakness of ipsilateral facial movements (except for lid movements). As the forehead has bilateral representation in the brain, only the lower two-thirds is affected in UMN lesions, but all of one side of the fac e in LMN lesions. Ask patient to \200\234raise your eyebrows \200\235 and \200\234show me your teeth. \200\235 64 VIII: Hearing: Rub your fingers together softly while holding them a few inches away from t he patient \200\231s ear. An alternative is the \200\234whispered voice test \200\235 (whi sper a combination of three letters or numbers while standing 2 feet behind the patient; th e examiner must occlude and rub the external auditory canal of the untested ear). The Weber and Rinne tests are not recommended for routine screening. IX and X: Ipsilateral palate elevation: Ask the patient to say \200\234aaah \200\235 and o bserve whether the two sides of the palate move fully and symmetrically. Can also use a swa b to assess pharyngeal sensation and gag reflex, although the gag reflex is often absent in normal persons, especially the elderly. XI : Trapezius: \200\234 Shrug your shoulders \200\235 against resistance. Sternocleidomas toid: \200\234 Turn your head to the left/right \200\235 against resistance. XII: Tongue protrus ion: Deviates to the side of the lesion. Table 3.12 Causes of cranial nerve lesions Any cranial nerve may be affected by diabetes mellitus, stroke, multiple sclerosis (MS), tu mors, sarcoidosis, vasculitis (e.g., polyarteritis nodosa [p. 416]), lupus, syphilis. Chron ic meningitis (malignant, TB, or fungal) tends to pick off the lower cranial nerves one-by- one. I: Trauma, respiratory tract infection, frontal lobe tumor, meningitis II: Field defec ts may start as small areas of visual loss ( scotomas ; e.g., in glaucoma). Monocular blind ness: Lesions of one eye or optic nerve (e.g., MS, giant cell arteritis, trauma) Bilateral blindness: Diabetes, glaucoma, infection, methanol Field defects: Bitemporal hemianopsia: O ptic chiasm compression (e.g., pituitary adenoma, craniopharyngioma, internal carotid arter y aneurysm) Homonymous hemianopsia: Affects half the visual field contralateral to the lesi on in each eye. Lesions lie beyond the chiasm in the tracts, radiation, or occipital cortex (e.g., stroke, abscess, tumor). (Continued) s l l i k s Table 3.12 (Continued) Papilledema (swollen disks): (1) \206\221 Intracranial pressure (ICP) (tumor, abscess, enc ephalitis, hydrocephalus, benign intracranial hypertension); (2) retro-orbital lesion (e.g. , cavernous sinus thrombosis, p. 368) Optic atrophy (pale optic disks and reduced acuity): MS, frontal tumors, Friedreich \200\231s ataxia, retinitis pigmentosa, syphilis, glaucoma, Leber \200\231s optic atrophy, optic nerve compression III alone: Diabetes, giant cell arte ritis, syphilis, posterior communicating artery aneurysm, idiopathic, \206\221 ICP (if unc al herniation through the ten- torium compresses the nerve); third nerve palsies without a dilated pupil are typically \200\234medical \200\235 (e.g., diabetes; \206\221 BP). Early dilatation of a pupil implies a compressive lesion, from a \200\234surgical \200\235 caus e (tumor, aneurysm). IV alone: Rare and usually due to trauma to the orbit. VI alone: M S, Wernicke \200\231s encephalopathy, false localizing sign in \206\221 ICP, pontine stroke ( presents with fixed small pupils quadriparesis). V: Sensory: Trigeminal neuralgia (pain but no sensory loss), herpes zoster, nasopharyngeal cancer, acoustic neuroma (p. 356) Motor : Rare VII: LMN: Bell \200\231s palsy (p. 389), polio, otitis media, skull fracture, cerebe llo-pontine angle tumors (e.g., acoustic neuroma, parotid tumors, herpes zoster [Ramsay Hun t syndrome]). UMN: (spares the forehead \200\224 bilateral innervation) stroke, tumor VIII: Noise, Paget \200\231s disease, M ni re \200\231s disease, herpes zoster, acoustic n euroma, brainstem CVA, drugs (e.g., aminoglycosides) IX, X, XII: Trauma, brainstem lesions, neck tumors XI: Rare; polio, syringomyelia, tumors near jugular foramen, stroke, bul- bar palsy, trauma, TB Groups of cranial nerves VIII, then V VI: Cerebellopontine angle tumor s; e.g., acoustic neuroma (p. 356; facial weakness is, surprisingly, not a prominent sign). V, VI: Gradenigo \200\231s syndrome: Lesions within the petrous temporal bone III, IV, VI: Stroke, tumors, Wernicke \200\231s encephalop- athy, aneurysms, MS III, IV, V a , VI: Cave rnous sinus thrombosis, superior orbital fissure lesions (Tolosa \200\223Hunt syndrome) IX, X, XI: Jugular foramen lesion Other differential diagnoses: Myasthenia gravis, muscular dy strophy, myotonic dystrophy, mononeuritis multiplex (p. 385) l a c i n i l C 65 Speech and higher mental function Aphasia (Impairment of language caused by brain damage) A ssessment: 1 If speech is fluent, grammatical, and meaningful, aphasia is unlikely. 2 Compr ehension: Can the patient follow one, two, and multistep com- mands ( \200\234Touch your ear, stand up, then close the door \200\235)? 3 Repetition: Can the patient repeat a sentence? 4 Naming: Can the patient name common and uncommon things (e.g., parts of a watch)? 5 Reading and writing: Normal? They can be affected like speech in dyspha- sia. (See Table 3.13.) Classification: Broca \200\231s (expressive) aphasia: Nonfluent speech produced with effort and frustration with malformed words 356 (e.g., \200\234spoot \200\235 for \200\234spoon , \200\235 or \200\234that thing \200\235). Reading and writing are impaired but comprehen sion is relatively intact. Patients understand questions and attempt to convey meaningful a nswers. Site of lesion : Inferolateral dominant frontal lobe Wernicke \200\231s (receptive) aphasia: Empty, fluent speech, like talking ragtime with pho nemic ( flush for brush ) and semantic ( comb for brush ) paraphasias/ neologisms (may be m istaken for psychotic speech). The patient is oblivious of errors. Reading, writing, and co mprehension are impaired (replies are inappropriate). Site of lesion : Posterior superior t emporal lobe (dominant) Conduction aphasia: Traffic between Broca \200\231s and Wernicke \200\231s area is inter- rupted. Fluent aphasia with impaired repetition and frequent parap hasic errors but relatively preserved comprehension. Anomic aphasias: Naming is affected in all aphasias, but in anomic aphasia, objects cannot be named but other aspects of speech a re normal. This occurs with dominant posterior temporoparietal lesions. Mixed aphasias are common. Discriminating features take time to emerge after an acute brain injury. Consider s peech therapy (of variable use). Dysarthria Difficulty with articulation due to incoordinat ion or weakness of the musculature of speech. Language is normal (see above). Assessment: A sk to repeat \200\234baby hippopotamus. \200\235 Cerebellar disease: Ataxic speech muscles cause slurring (as if drunk) and speech that is irregular in volume and rhythm. Extrapyram idal disease: Soft, indistinct, and monotonous speech. Pseudobulbar palsy: Spastic dysarthr ia ( upper motor neuron ; speech is slow, indistinct, and effortful ( \200\234Donald Duck \200\235 or \200\234hot potato \200\235 voice) from bilat- eral hemispheric lesions or sev ere MS. Bulbar palsy: Lower motor neuron (e.g., facial nerve palsy, Guillain \200\223Barr ) \200\224 any associated palatal paralysis gives speech a nasal character. Dysphonia Dif ficulty with speech volume due to weakness of respiratory muscles or vocal cords (myastheni a, p. 390; Guillain \200\223Barr syndrome, p. 387). Parkinson \200\231s disease gives a mixed picture of dysarthria and dysphonia. Apraxia Loss of the ability to perform complex m ovements despite ability to perform each individual component. Test by asking the patient t o copy unfamiliar hand positions or mime an object \200\231s use (e.g., a comb). Can they m ake familiar gestures (e.g., a salute)? The term \200\234apraxia \200\235 is used in three other ways: \212Dressing apraxia: The patient is unsure of the orientation of clothes on his body. Test by pulling one sleeve of a sweater inside out before asking the patient to p ut it back on (mostly nondominant hemisphere lesions). \212Constructional apraxia: Difficu lty in assembling objects or draw- lesions, hepatic 66 ing a 5-pointed star (nondominant hemisphere encephalopathy). \212Gait apraxia: Inability to initiate the process of walking; the gait is broad-based wi th short steps, with a tendency to fall backward. Seen with bilateral frontal lesions, lesi ons in the posterior temporal region, and hydrocephalus. s l l i k s Table 3.13 The Mini-Mental Status Exami nation (MMSE) ( Kafka \200\231s law : \200\234In youth we take examinations to get into institutions. In old age to keep out of them. \200\235) The MMSE is a quick screening test for dementia (al though it is sometimes used to serially examine hospitalized patients with delirium). On lo ngitudinal follow-up, only changes of \211 4 points indicate a significant change of cogn ition. An important limita- tion of the MMSE is that performance is affected by the patient \200\231s level of education. Orientation \212What is the year? Season? Date? Day? Month? [1 point for each correct l a c i n i l C answer] \212Where are we now? (e.g., specific hospital, doctor \200\231s office) State? County? City? Floor? [1 point each] Registration \212I am going to name three objects. After I have finished saying all three, I want you to repeat them. Remember what they are because I am going to ask you to name th em again in a few minutes . The first repetition determines the score [1 point each, e.g., APPLE, PENNY, AIRPLANE]; repeat until all are learned. Attention and Calculation \212Begin with the number 100 and count backward by 7s (so you \200\231re sub- tracting 7 each time) . [1 point for each correct; stop after 5 answers] Alternative: Spell \200\234world \200 \235 backward. [1 point for each letter in correct order] 67 Recall \212What were the three objects I asked you to remember a little while ago? [1 point each] Language \212Show and ask patient to name a pencil and wristwatch . [1 point each] \212Pl ease repeat this sentence: \200\234No ifs, ands, or buts . \200\235 [1 point if exactly correct; 1 trial only] \212I am going to give you a piece of paper. When I do, take the paper in your right hand. Fold the paper in half. Put the paper on the floor. [ \200\2343-stage command \200\235; 1 point for each correct task] \212Please read what is written here and do what it says. Show card with \200\234CLOSE YOUR EYES \200\235 written on it. [1 point] \212Please write a complete sentence on this sheet of paper. [1 point if sen- tence contains a noun and verb and makes sense] Here is a drawing. Please copy the drawing. (See Figure 3.8) Give 1 point if the two figure s intersect to form a four-sided figure and if all angles are preserved. Interpreting the s core The maximum is 30; assuming there is no evi- dence of delirium, scores of 23 or lower strongly suggest dementia (and scores of 26 \200\22330 rule it out). Figure 3.8 Close your eyes Psychiatric assessment Introduce yourself, ask a few factual questions (full name, age, mar ital sta- tus, job, and who is at home). These will help your patient to relax. Presenting problem Ask for the main problems that led to this consulta- tion. Sit back and listen for 3 \200\2235 min. Don \200\231t worry whether the information is in a convenient form or not \200\224this is an opportunity for the patient to come out with his or her worries unsulli ed by your expectations. History of presenting problem For each problem, obtain details, bo th current state and history of onset, precipitating factors, and effects on life. Ask what treatments have already been tried, including prescriptions and over-the-counter meds. Che ck of major psychiatric symptoms Check those that have not yet been covered: Depression (lo w mood), anhedonia (inability to feel pleasure), thoughts of worthlessness/hopelessness, sl eep and appetite disturbance. Ask specifically about suicidal ideation (and plans, if posit ive response) \200\234Have you ever been so low that you thought of harming yourself? \200 \235, \200\234Do you feel you \200\231d be better off dead? \200\235( passive death wish ) ; mania (periods of excessive energy and activity, euphoria, little need for sleep, reckles s behavior); hal- lucinations ( \200\234Have you ever heard voices when there hasn \200\231 t been anyone there, or seen visions? \200\235); delusions ( \200\234Have you ever had any thoughts or beliefs that have struck you afterward as bizarre? \200\235, \200\234Do you be lieve you are being monitored or that others want to harm you? \200\235); anxiety and avoid ance behavior (e.g., avoiding shopping because of anxiety or phobias); obsessive thoughts a nd compulsive behavior (e.g., handwashing); and eating disorders . Past psychiatric history Note prior hospitalizations and outpatient treatment (e.g., from therapists, psychiatrists , and primary docs). \200\234Do you know what you were diagnosed with? \200\235 History of response to medications and side effects. Alcohol and illicit drug use See Table 3.14. Ask how often they use or ever used (e.g., alcohol, cocaine, marijuana, amphetamines, heroin, pain pills, benzodiazepines, etc.). Ask about past and current drug treatment. Social Histo ry Housing, finance, work, relationship status, sexual ori- entation, children, friends, re ligion, education level, who raised them and where. Family history Note psychiatric and sub stance abuse history in parents, sibs, grandparents, aunts/uncles. Abuse history Ask about past and present sexual, physical, and verbal abuse. Mental status examination This is the state now , at the time of interview. \212Nonverbal behavior: Dress and grooming, eye cont act, affect, tears, laugh- ter, pauses (while listening to voices?), attitude (e.g., withdr awn), psycho- motor slowing or agitation, and abnormal movements (e.g., lip smacking, hand tremor) 68 \212Speech: Include rate of speech (e.g., pressured) and organization (e.g., circumstantial) \212Mood: Sad, euthymic, anxious, irritable, euphoric? Note thoughts about harming self or others. \212Beliefs: E.g., about one \200\231s self, one \200\231s own body, about other people, a nd the future; note persecutory, grandiose, or bizarre ideas. \212Hallucinations: Visual, auditory, tactile \212Orientation: In time, place, and person \212Memory: Ask patient if she has concerns about her memory. Give exam- ples. Test short- term (see MMSE p. 67) and remote memory (e.g., \200\234Where did you get married? \200\235 ). s l l i k s \212Attention/Concentration: Ask patient to recite days of the week, then ask l a c i n for them backward . Note the patient \200\231s \212 insight and the degree of your rapport . i l C Table 3.14 Screening for unhealthy alcohol use There is more than one way to screen for unhealthy alcohol use. The National Institute on A lcohol Abuse and Alcoholism (NIAAA) recom- mends a single-item screening test for people wh o drink alcoholic bever- ages at least sometimes. The question is: \200\234How many times in the past year have you had five or more drinks in a day (for men) or four or more drinks in a day (for women) ? \200\235 The test is positive if the answer is one or more times. N ote that one \200\234standard drink \200\235 is equivalent to 12 ounces of beer, 5 ounces of wine, or 1.5 ounces of 80-proof spirits. It is also a good idea to define alcohol as bee r, wine, or liquor. Other screening tests are available, but a practical approach is to ask directly about \200\234risky drinking \200\235 1 amounts (amounts associated with adverse consequences; for men, >14 drinks/week or >4/occasion; for women, >7/week or >3/ occasion) , plus the familiar CAGE questionnaire: \212 \212 \212 \212 69 Have you ever felt you should Have people Have you ever felt bad or Have you ever taken a d rink first thing in the morning ( to steady your nerves or get rid of a hangover? Cut down on your drinking? Annoyed you by criticizing your drinking? Guilty about your drinking? Eye-opener ) The CAGE questionnaire alone, using one affirmative response as a positive test, is about 8 0 \200\22390% sensitive and specific for an alcohol use disorder (using two as a cutoff is less sensitive). These questions can be asked verbatim as part of the routine medical histo ry, or can be asked only when patients report drinking risky amounts. Asking everyone will identify more patients with past problems or patients with current heavy drinking who did n ot understand the prior questions or accurately report their drinking amounts . 1 Risky drinking is much more common than alcohol dependence (also referred to as alcoholis m or addiction): Almost one-third of drinkers in the United States drink risky amounts, and nearly one in four of these individuals have alcohol dependence. Symptoms and signs April S. Fitzgerald , M.D. s n g i s d n a Symptoms are the features of a disease that a patient reports. Signs are the objective find ings elicited by a physician, often at the bedside. Together, symptoms and signs constitute the features of a disease. Their evolution over time, and interaction with the physical, p sychological, and social set- ting, comprise the natural history of a patient \200\231s dis ease. In this chapter, we discuss symptoms and signs in isolation. Although this is an arti ficial construct, it is the necessary step in learning the art of diagnosis. Abdominal dist ension Causes : The famous five \200\234 F \200\231 s \200\235 are F at , F luid , F ece s , F etus , or F latus . Also F ood (e.g., in malabsorption)can cause distension. Specific groups include: Air Gastrointestinal obstruction (incl. fecal) s m o t p m y S Ascites Malignancy Hypoproteinemia (e.g., nephrotic) Solid masses Malignancy Lymph nodes Aortic Pelvic masses Bladder: Full or cancer Fibroids; fetus Ovarian cyst Ovarian cancer 4 aneurysm Cysts : Renal, pancreatic Aerophagia (air swallowing) Right heart failure Portal 70 hypertension Uterine cancer Air is resonant on percussion. Ascites (free fluid in peritoneal cavity): Signs: Shifting d ullness (p. 61); fluid wave (place patient \200\231s hand firmly on his abdomen in sagittal plane and tap one flank with your finger while your other hand feels on the other flank fo r a fluid wave). The characteristic feature of pelvic masses is that you cannot palpate bel ow them (i.e., their lower border cannot be defined). Causes of right iliac fossa masses: A ppendix mass or abscess (p. 467), kidney mass, cecal cancer, a Crohn \200\231s or tubercula r (TB) mass, intussusception, amoebic abscess or any pelvic mass (above). Causes of ascites with portal hypertension (p. 220): See causes of hepato- megaly (p. 77), splenomegaly . Ab dominal pain varies greatly depending on the underlying cause. Examples include irritation of the mucosa (acute gastritis), smooth muscle spasm (acute enterocolitis), capsular stretc hing (liver congestion in conges- tive heart failure [CHF]), peritoneal inflammation (acute appendicitis), and direct splanchnic nerve stimulation (retroperitoneal extension of tumor ). The character (constant or intermittent, sharp or dull) , duration , and frequency depen d on the mechanism of production. The location and distribution of referred pain depend on the anatomical site. Time of occurrence and aggra- vating or relieving factors , such as me als, defecation, and sleep, also have special significance related to the underlying diseas e process. The site of the pain may provide a clue as to its cause. Amaurosis fugax ( see p . 363 ) Anemia may be assessed from the skin creases and conjunctivae (pale if Hb is <9 g/d L). Koilonychia and stomatitis (p. ) suggest iron deficiency. Anemia with jaundice suggests malignancy or hemolysis (p. 609). Apex beat \200\223Cheyne \200\223Stokes respiration Apex beat (aka apical impulse or point of maximum impulse [PMI]). This is the point furthest from the manubrium where the heart ca n be felt beating \200\224normally the fifth intercostal space in the mid-clavicular line ( fifth ICS MCL). Lateral displacement may be from cardiomegaly or mediastinal shift. Assess character using your palm or fingertips: A pressure loaded apex is a forceful, sustained un displaced impulse (blood pressure (BP) ^ or aortic stenosis causing LV hypertrophy with une nlarged cavity). A volume over- loaded (hyperdynamic) apex is forceful, nonsustained, and d isplaced down and laterally (e.g., cavity enlargement from aortic or mitral regurgitation). It is tapping in mitral Apex beat \200\223Chvostek \200\231s sign stenosis (palpable 1st h eart sound), dyskinetic after anterior myocardial infarction (MI) or with left ven- tricula r (LV) aneurysm, double or triple impulse in hypertrophic obstructive cardiomyopathy (HOCM) (p. 53). Athetosis is due to a lesion in the putamen, which causes slow sinuous writhing m ovements in the hands, which are present at rest. Pseudoathetosis refers to athetoid moveme nts in patients with severe proprioceptive loss. Backache (p. 401) Breathlessness (dyspnea) (p. 74) Breast pain Most common cause is hormonal fluctuations \200\231 effect on breast t issue ( cyclical mastalgia, but patients sometimes worry that breast cancer is causing the symptom. Perform a careful examination (p. 497) and refer for ultrasound or mammography as appropriate. If there is no sign of breast pathology, and it is not cyclical, think of: Gal lstones \212 s n g i s d n a s m o t p m y S Tietze \200\231s syndrome \212 \212 Angina Estrogens (hormone replacement therapy [HRT]) Cervical radiculopathy \212 71 \212 Bornholm \200\231s disease \212 Pulmonary embolus \212 If none of the above, wearing a supportive bra may help, as may NSAIDs. Cachexia Severe gen eralized muscle wasting implying malnutrition, neo- plasia, CHF, Alzheimer \200\231s diseas e, hyperthyroidism, prolonged inanition, or infection (e.g., TB, AIDS, intestinal parasites , such as from Cryptosporidium , p. 545). Carotid bruits indicate atheroma. A bruit is a po or predictor of carotid stenosis or stroke risk but is a predictor of ischemic cardiac dise ase; con- sider risk factor management. The key question for carotid disease is whether the patient is symptomatic. Stroke or transient ischemic attack (TIA) from carotid stenosis ar e considered symptomatic and often benefit from carotid revascularization. Asymptomatic pat ients usually benefit from medical management without surgery, but a select subset may also benefit from endarterectomy. Chest deformity Barrel chest: ^ AP diameter, tracheal descent and expansion reduced; seen in chronic hyperinflation (e.g., asthma/chronic obstructive pu lmonary disease [COPD]). Pigeon chest (pectus carinatum): Prominent sternum with a flat che st, seen in chronic childhood asthma and rickets. Funnel chest (pectus excavatum) (PLATE 10 ) : Developmental defect involving local sternum depression (lower end). Kyphosis: \200 \234Humpback \200\235 from increased thoracic spine curvature. Scoliosis: Lateral curvature ; both may cause restrictive ventilatory defect. Chest pains (see p. 90) Cheyne \200\223Sto kes respiration Breathing becomes progressively deeper and then shallower ( episodic apne a) in cycles. Causes: Brainstem lesions or compression (stroke, ^ intracerebral pressure [I CP]); if the cycle is long (e.g., 3 min), the cause may be a long lung-to-brain circulation time Cheyne \200\223Stokes respiration \200\223Cyanosis (e.g., in chronic pulmonary edema, poor cardiac output). It is enhanced by narcotics. Chorea means dance \200\224a continuous flow of jerky movements, flitting from one limb or part to another. Each movement looks like a f ragment of a normal movement. Cause : Basal ganglia lesion: Huntington \200\231s, Sydenham \200\231s (p. 137), systemic lupus erythematosus (SLE) (p. 410), Wilson \200\231s (p. 233), kernicterus, polycythemia vera (p. 633), neuroacanthocytosis (a familial association of ac anthocytes in peripheral blood with chorea, orofacial dys- kinesia, and axonal neuropathy), thyrotoxicosis (p. 298), drugs (L-dopa, contraceptive steroids). Early stages of chorea ma y be detected by feeling fluctuations in muscle tension while the patient grips your finger . Treat the underlying cause; reserve drugs (i.e., dopamine receptor blockers) for severe c ases. Ask a neurologist for help. Chvostek \200\231s sign Tapping on the facial nerve cause s a facial twitch in hypocalcemia; caused by nerve hyperexcitability. Clubbing Fingernails have exaggerated longitudinal curvature with loss of angle between nail and nail-fold, and the nail-fold feels boggy. GI causes Thoracic causes \212 \212 Cardiac causes \212 Bronchial carci- noma (usually not small cell) Chronic lung suppuration Empyema, abscess Br onchiectasis Cystic fibrosis Fibrosing alveolitis Mesothelioma Inflammatory bowel (especially Crohn \200\231s disease) Cyanotic congenital heart disease Endocarditis \212 \212 \212 \212 \212 \212 \212 \212 \212 \212 Rare: \212 \212 \212 Cirrhosis GI lymphoma Malabsorption, e.g., celiac \212 Atrial myxoma 72 Familial Thyroid acropachy Unilateral clubbing, from: \212 axillary artery aneurysm \212 brachial arteriovenous malformations Constipation (see p. 213) Cough p. 54; see also Hemoptysis (p. 76) Cramp (painful muscle sp asm) Cramp in the legs is common, especially at night. It may also occur after exercise. It only occasionally indicates a disease, in particular salt depletion, muscle ischemia, or m yopathy. Forearm cramps suggest motor neuron disease. Quinine is no longer recommended for leg cramps due to potential for serious side effects. Writer \200\231s cramp is a focal dys tonia causing difficulty with the motor act of writing. The pen is gripped firmly, with exc essive flexion of the thumb and index finger ( tremor). There is normally no CNS deficit. Oral drugs or psychotherapy rarely help, but botulinum toxin can help \200\224sometimes dr amatically \200\224but it has side effects. Similar specific dystonias may apply to other t asks. Cyanosis Dusky blue skin ( peripheral , e.g., of the fingers) or mucosa ( cen- tral , e.g., of the tongue; occurs more readily in polycythemia than anemia). Causes: 1 Lung dise ase resulting in inadequate oxygen transfer (e.g., COPD, severe pneumonia); often correctable by increasing inspired O2. 2 Shunting from pulmonary to systemic circulation (e.g., R \200\223L shunting VSD, patent d uctus arteriosus, transposition of the great arteries); cyanosis is not reversed by increas ing inspired O2. 3 Inadequate oxygen uptake (e.g., met-, or sulf-hemoglobinemia). Cyanosis \200\223Dyspepsia and indigestion s n g i s Figure 4.1 How to test for finger clubbing The dorsal aspect of 2 fingers, side by side with the nails touching. Normally, you should see a kite-shaped gap. If not, there is clubbing. d n a s m o t p m y S Fig. 1a No dip \200\224therefore clubbing Fig. 1b Fig. 1c Acute cyanosis is a sign of impending emergency. Is there asthma, an inhaled foreign body, a pneumothorax (X-RAY PLATE 6), or left ventricular failure (LVF) (p. 128)? Peripheral cyan osis will occur in causes of central cyanosis, but may also be induced by changes in the pe ripheral and cutaneous vascular systems in patients with normal oxygen saturations. It occu rs in the cold, in hypov- olemia, and in arterial disease and is therefore not a specific s ign. Deafness (p. 357) Dehydration (p. 458) Diarrhea (p. 210) Dizziness is a trinity: (1) V ertigo (p. 355) is the illusion of rotation, as if one just stepped off a merry-go-round. ( 2) Imbalance (i.e., difficulty in walk- ing straight) e.g., from peripheral nerve, posterio r column, cerebellum, or other central pathway failure. (3) Faintness (sense of collapse) e .g., seen in anemia, BP, hypoglycemia, carotid sinus hypersensitivity, and epilepsy. 1 \200\2233 may coexist. Dysarthria (p. 66) Dyspepsia and indigestion These are broad terms, used by patients to signify epigastric or retrosternal pain (or discomfort) that is usually related to meals. Find out exactly what your patient means. Thirty percent have no real ab normality on endoscopy. Of positive findings: Esophagitis alone Duodenal ulcer (DU) Hiatal hernia 73 24% Gastritis 17% Duodenitis 15% Gastric ulcer 23% 9% \211 2 lesions 6% Bile reflux 0.7% 5% Gastric cancer 0.2% Endoscopic or nonendoscopic testing can be used to diagnose Helicobacter pylori infection. Noninvasive tests include the 13 C-urea breath test, serologi- cal tests, and stool antigen tests. Antibody testing identifies an immuno- logic reaction to the disease, whereas the b reath test and stool antigen test detect the presence of active infection. Prior to perform ing a urea breath test, patients must be off antibiotics for 4 wks and off proton pump inhi bi- tors for 2 wks to avoid false negatives. Do endoscopy if there are \200\234alarm \200 \235 Dyspepsia and indigestion \200\223Facial pain symptoms (>45 yrs, weight, vomiting, hemat emesis, anemia, dysphagia, family history of upper GI malignancy). Dysphasia (p. 84) Dyspho nia (p. 66) Dyspnea (p. 90) is the subjective sensation of shortness of breath, often exace rbated by exertion. Try to quantify exercise tolerance (e.g., dressing, distance walked, cl imbing stairs, New York Heart Association [NYHA] clas- sification [p. 129]). Causes: \212C ardiac : E.g., mitral stenosis or left ventricular failure of any cause; LVF is associated with orthopnea (dyspnea worse on lying; \200\234how many pillows? \200\235) and paroxysmal nocturnal dyspnea (PND; dyspnea waking with the sensa- tion of air hunger). There may also be ankle edema. Any patient who is in shock may also be dyspneic: This may be shock \200 \231s presenting feature. \212Lung : Both airway and interstitial disease. May be hard to separate from cardiac caus es; asthma may wake the patient as well as cause early morn- ing dyspnea and wheeze. Focus on the circumstances in which dyspnea occurs (e.g., on exposure to an occupational allergen ). \212Anatomical : I.e., diseases of the chest wall, muscles, or pleura. \212Others : Thyro toxicosis, ketoacidosis, aspirin poisoning, anemia, psycho- genic. Look for other clues: Dy spnea at rest, not associated with exertion may be psychogenic; look for respiratory alkale mia (peripheral perioral paresthesia carpopedal spasm). Speed of onset helps diagnosi s: Acute Foreign body Pneumothorax (PLATE 6) Acute asthma Pulmonary embolus Acute pulmonary ed ema Subacute Asthma Parenchymal disease (e.g., alveolitis) Chronic COPD and chronic parenchymal diseases 74 Nonrespiratory causes (e.g., cardiac failure) Effusions Pneumonia Anemia Dyspraxia (p. 358) Dysuria is painful micturition (from urethral or bladder inflammation, t ypi- cally from infection; also urethral syndrome [p.257]). Edema Causes: ^ Venous pressure (e.g., DVT or right-heart failure) or low- ered intravascular oncotic pressure ( plasma proteins; e.g., cirrhosis, nephro- sis, malnutrition, or protein-losing enteropathy; here, water moves down the osmotic gradient into the interstitium to dilute the solutes there). On standing, venous pressure at the ankle rises due to the height of blood from the heart ( 100 mm Hg). This is short-lived if leg movement pumps blood through valved veins; but if v enous pressure rises or valves fail, capillary pressure rises, fluid is forced out (edema), PCV rises locally, and micro- vascular stasis occurs. Pitting edema , nonpitting (i.e., no nindentible)edema; caused by poor lymph drainage (lymphedema), either primary (Milroy \200 \231s syndrome) or secondary (radiotherapy, malignant infiltration, infection, filariasis). The mechanism is complex. Epigastric pain Acute causes: Peritonitis, pancreatitis, GI obst ruction, gall bladder disease, peptic ulcer, ruptured aortic aneurysm, irritable bowel synd rome. Referred pain: Myocardial infarct, pleural pathology; psychologi- cal causes are also important. Chronic causes: Peptic ulcer, gastric cancer, chronic pancreatitis, aortic aneu rysm, nerve root pain. Facial pain This can be neurological (e.g., trigeminal neuralgia) or from any other pain-sensitive structure in the head or neck (see Table 4.1). Postherpetic neuralgia: This nasty burning-and-stabbing pain (e.g., ophthalmic division of V) all too of ten becomes chronic and intractable. Skin previously affected Facial pain \200\223Fatigue s n g i s Table 4.1 Non-neurological causes of facial pain Cervical disc pathology Sinusitis, neoplasia Glaucoma, iritis, eye strain Arthritis Caries, abscess, malocclusion Otitis media, otitis externa Giant cell arteritis Neck Sinuses Eye Temporomandibular joint Teeth Ear Vascular When all causes are excluded, a group that is mostly young and female remains ( \200\234atypical facial pain \200\235) who complain of unilateral pain deep in the face or at the angle of cheek and nose, which is c onstant, severe, and unresponsive to analgesia. Do not dismiss this as psychological. Do no t expose these patients to the risks of destructive surgery; few meet the criteria of depre ssion. Although many are prescribed antidepressants, some neurologists advocate no treatmen t. d n a s m o t p m y S