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66 CHAPTER 4: Vital Signs, Anthropometric Data, and Pain
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High blood pressure.
Hypertension. The cause of most hypertension is unknown, i.e., essential
hypertension. The primary lesion is suspected to be in the kidney. Increased
stroke volume and decreased aortic compliance increase systolic pressure.
Vasoconstriction and intimal thickening increase peripheral vascular resistance and diastolic pressure.
pressure with normal diastolic pressure, often seen in the elderly. More commonly, both systolic and diastolic pressures are elevated. Mean arterial pressure is largely a function of diastolic pressure, the minimal continuous load
on the vascular tree. Elevated diastolic with normal systolic pressure lowers
the pulse pressure suggesting reduced cardiac output. Hypertension is a major risk factor for stroke, heart failure, left ventricular hypertrophy, and chronic kidney failure. Over age 50, systolic pressure contributes more to risk than
diastolic. With sustained hypertension, search for hypertensive retinopathy,
left ventricular hypertrophy, and renal insufciency.
CLINICAL OCCURRENCE: Essential hypertension is a diagnosis of exclu-
sion, so alternative explanations need to always be considered. Congenital:
Coarctation of the aorta, congenital adrenal hyperplasia (early or late onset),
polycystic kidney disease; Degenerative/Idiopathic: Essential hypertension, toxemia of pregnancy; Endocrine: Pheochromocytoma, aldosteronoma,
adrenal hyperplasia, hypercortisolism (Cushing disease and syndrome),
hyperthyroidism, hypothyroidism, hyperparathyroidism, acromegaly;
Inammatory/Immune: Atherosclerosis, vasculitis; Mechanical/Traumatic:
Obstructive sleep apnea, acute spinal cord injury; Metabolic/Toxic: Renal
insufciency, medications (NSAIDs, estrogens, oral contraceptives, cyclosporine), drug abuse (cocaine, amphetamines, etc.), porphyria, lead poisoning,
hypercalcemia; Neoplastic: Adrenal adenoma, pheochromocytoma, pituitary adenoma, brain tumors;
increased intracranial pressure; Psychosocial: Substance abuse (cocaine,
amphetamines, alcohol); Vascular: Renal artery stenosis (atherosclerosis,
bromuscular dysplasia).
Isolated systolic hypertension is elevated systolic
Neurologic: Stroke, diencephalic syndrome,
Isolated systolic hypertension (ISH).
The increased systolic pressure results
from increased stroke volume and/or decreased compliance of the aorta and
its branches.
Causes of increased stroke volume include hyperthyroidism,
anemia, arteriovenous stulas, aortic regurgitation, and anxiety. Atherosclerosis decreases aortic compliance. ISH increases risk for stroke, left ventricular hypertrophy, and heart failure.
White coat syndrome. BP is elevated in clinical settings but normal at home
and by ambulatory BP monitoring. Cardiovascular risk is less than with sustained hypertension.
Malignant hypertension. Severely elevated BP causes end-organ dys-
function that further elevates the BP. Diastolic pressure is >120 mm Hg
and systolic pressure usually >200 mm Hg. Patients present with headache, confusion, dyspnea, seizures, angina, or rapidly progressive renal
insufciency. Rapid moderation of pressure prevents irreversible brain,
heart, eye, and kidney damage.
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Paroxysmal hypertension: pheochromocytoma. Benign adrenal or sym-
pathetic chain tumors secrete epinephrine or norepinephrine. In onethird of the patients, secretion is intermittent. Episodic hypertension is
associated with pallor, anxiety, sweating, palpitation, nausea, and vomiting. Most patients have sustained hypertension. Intravascular volume
depletion leads to orthostatic hypotension, an early clinical sign. Pheochromocytoma must be distinguished from panic attacks and the whitecoat syndrome.
Low blood pressure.
Hypotension. Hypotension results from blood loss, decreased vascular tone,
and/or decreased cardiac output. Systolic and diastolic pressures are low.
In usually hypertensive patients, normal BPs are concerning. Cool skin, decreased urine output, and decreased alertness are signs of hypoperfusion.
Peripheral vasoconstriction and tachycardia, signs of compensatory cardiovascular responses indicate pathologically low BP.
CLINICAL OCCURRENCE: Loss of Blood Volume: Bleeding, capillary
leak syndrome (anaphylaxis, sepsis, IL-2, idiopathic), third-spacing (ascites,
burns, secretory diarrheas), polyuria (diabetes mellitus, diabetes insipidus,
diuretics), inadequate uid intake, excessive sweating (heat prostration and
heat stroke), adrenal insufciency;
Loss of Vascular Tone: Sepsis, drugs (vaso-
dilators, tricyclic antidepressants, ganglionic blockers), fever, autonomic
insufciency (multisystem atrophy), acute spinal cord injury (spinal shock),
arteriovenous malformations; Decreased Cardiac Output: Acute myocardial
infarction, ischemic cardiomyopathy, idiopathic dilated cardiomyopathy, aortic stenosis, saddle pulmonary embolism, pericardial tamponade, and severe
mitral insufciency.
Orthostatic (postural) hypotension. Causes are hypovolemia, decreased
sympathetic drive to the heart and vasculature, and decreased venous return. Supine BP is normal but falls, within 3 minutes of standing, by ≥20 mm
Hg systolic or ≥10 mm Hg diastolic, and/or the pulse rate rises by ≥15 bpm.
This is an early sign of intravascular volume loss. A BP drop not accompanied by a rise in pulse rate suggests autonomic insufciency. Patients with
chronic orthostatic hypotension frequently have postprandial hypotension
and reversal of the normal circadian BP pattern, i.e., higher BP at night than
during the day.
CLINICAL OCCURRENCE: Loss of Blood Volume: See Hypotension above;
Loss of Vascular Tone: Deconditioning after long illnesses, autonomic insuf-
ciency (multisystem atrophy), peripheral neuropathies (diabetes, tabes dorsalis, alcoholism), drugs (vasodilators, tricyclic antidepressants, ganglionic
blockers); Impaired Venous Return: Ascites, pregnancy, venous insufciency,
inferior vena cava obstruction and hemangiomas in the legs.
Postprandial hypotension. In some individuals, especially older adults on
vasoactive medications, the BP drops by ≥20 mm Hg following meals. The
exact mechanisms are unclear, but the result is increased risk for falls, syncope, dizziness, and fatigue. Question carefully about the relation of symptoms
to meals.
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Anaphylactic shock. IgE-mediated mast cell degranulation releases his-
tamine and other vasoactive substances producing vasodilatation and
opening endothelial tight junctions with loss of plasma volume. This
fulminant life-threatening hypersensitivity reaction occurs on exposure
to specic allergens. Sudden vascular collapse is preceded or accompanied by malaise, pruritus, pallor, stridor, cyanosis, syncope, vomiting,
diarrhea, tachypnea, tachycardia, and distant heart sounds. Angioedema
and urticaria may be present but are often absent.
CLINICAL OCCURRENCE: Hymenoptera stings, drugs (e.g., penicillin and
other antibiotics), peanut ingestion, and many others. Anaphylaxis may occur
with exercise, cold exposure, heat exposure, or without evident cause (idiopathic anaphylaxis). Clinically identical anaphylactoid reactions occur when
mast cell release is stimulated by non-IgE-mediated mechanisms such as
radiographic contrast agents.
Septic shock. This is a complex physiologic reaction to circulating endo-
toxin activating inammatory and thrombotic pathways. Patients pres-
ent with hypotension, often, but not always, accompanied by fever and
prostration. Initially, the skin is warm and ushed, despite the low BP,
followed by peripheral vasoconstriction, decreased urine output, confusion, progressive hypotension and acidosis. Prompt recognition and
treatment are essential.
Toxic shock syndrome. Toxins produced by strains of Staphylococcus
aureus produce hypotension with high cardiac output and generalized
erythroderma. Though initially described in association with highly
absorbent vaginal tampons, surgical wound infections containing foreign bodies (sutures) and sinusitis are now common sites of infection.
The patient suddenly develops high fever, myalgia, nausea, vomiting,
and diarrhea. Diffuse erythroderma is followed by confusion, acute lung
injury, hypotension, and shock. Exfoliation of the palms and soles may
occur in convalescence.
Pulse pressure.
Wide pulse pressure. Pulse pressure increases with increased systolic pres-
sure (increased stroke volume, increased rate of ventricular contraction,
decreased aortic elasticity) and/or decreased diastolic pressure (decreased
peripheral resistance, arteriovenous shunts, aortic insufciency)
pressure ≥65 mm Hg is abnormal. With large stroke volumes, the pulse is
bounding or, in aortic regurgitation, collapsing. Suggestive signs include
head bobbing with each heartbeat and thrills and audible murmurs over AV
shunts. When vasodilation decreases vascular resistance, the skin is warm
and ushed. Widened pulse pressure is a major risk factor for cardiovascular
morbidity and mortality, including atrial brillation.
CLINICAL OCCURRENCE: Increased Systolic Pressure: Systolic hyperten-
sion, atherosclerosis, increased stroke volume (aortic regurgitation, hyperthyroidism, anxiety, bradycardia, heart block, post-PVC, after a long pause in
atrial brillation, pregnancy, fever, systemic arteriovenous stulas); Increased
Diastolic Runoff: Aortic regurgitation, sepsis, vasodilators, patent ductus
arteriosus, hyperthyroidism, arteriovenous stulas, beriberi.
. Pulse
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Narrow pulse pressure. Pulse pressure narrows with decreased stroke vol-
ume and decreased rate of ventricular ejection.
Pulse pressures less than 30
mm Hg may occur with tachycardia and conditions associated with a low
stroke volume.
CLINICAL OCCURRENCE: Decreased Stroke Volume: Severe aortic steno-
sis, dilated cardiomyopathy, restrictive heart disease, constrictive pericarditis,
pericardial tamponade, intravascular volume depletion, venous vasodilata-
Decreased Rate of Ventricular Contraction: Ischemic and dilated cardio-
tion;
myopathy, aortic stenosis, myocarditis.
ANTHROPOMETRIC DATA
Height: Linear growth occurs throughout infancy, childhood, and adolescence,
ending with closure of the long bone epiphyses. Mature height is determined
by both genetic and environmental factors, especially nutrition. Linear growth
requires growth hormone, adequate nutrition (protein, calories, vitamin D, calcium, and phosphorus) and a skeleton able to respond to these signals. Height
should not change throughout the years of maturity. With aging, there is a
hormone-independent loss of bone mineral density, particularly of trabecular
bone, leading to a slow and gradual loss of height often aggravated decreased
muscle tone and strength affecting posture. Pathology such as osteoporosis
and spinal compression fractures sometimes produce dramatic height loss.
Throughout infancy and childhood height is recorded regularly at wellchild visits. Standardized charts visually display growth over time. Once
stable height is reached, it is measured once every ~5 years until age 60, when
annual measurement resumes.
Measuring height.
without shoes, the head in neutral position (the occiput does not touch the
wall), with heels, buttocks, and scapulae touching the wall. The vertical distance between the oor and the highest point of the scalp is recorded in inches
or centimeters. Compress the hair to avoid overestimating height; separate
especially thick hair.
Height is best measured standing erect against a wall
Short stature. Short stature indicates a failure of growth hormone produc-
tion, decreased tissue receptivity, or impaired nutrition. Expected stature is
estimated from standard tables or by adding 6.5 cm (2.6 in.) for boys and
subtracting 6.5 cm (2.6 in.) for girls from the mid-parental height. Consult
pediatric textbooks for the evaluation of short stature in children.
CLINICAL OCCURRENCE: Congenital: Intrauterine growth retardation,
pseudohypoparathyroidism, vitamin D-resistant rickets, familial short stature,
Turner syndrome, achondroplasia, Noonan syndrome, Prader–Willi syndrome;
Endocrine: Growth hormone deciency, hypothyroidism, hyperthyroidism,
diabetes mellitus, Cushing disease, hypogonadism; Degenerative/Idiopathic:
Constitutional delay in growth; Infectious: Any chronic debilitating infection; Inammatory/Immune: Juvenile rheumatoid arthritis (RA), SLE, chronic
glomerulonephritis; Mechanical/Traumatic: Brain injury; Metabolic/Toxic:
Chronic glucocorticoid use, malnutrition; Neoplastic: suprasellar masses, cancer
treatment during childhood, including brain irradiation; Psychosocial: Chronic
emotional deprivation, mistaken paternity; Vascular: Pituitary infarction.
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Accelerated growth: gigantism and acromegaly. A pituitary adenoma
secreting growth hormone accelerates linear growth until the epiphyses close
in late adolescence. Secretion starting or continuing after epiphyseal closure
enlarges hands, feet skull, and mandible disproportionately and thickens soft
tissue. Linear growth normally goes through early and late growth accelera-
tions. Growth charts will readily identify deviations from expected growth.
Excessive growth hormone production beginning after epiphyseal closure
results in acromegaly (enlarged hands, feet, skull, mandible, and soft-tissue
thickening) without increasing height. See Chapter 13, page 581.
Abnormal body proportions: Marfan syndrome.
Chapter 13, page 570.
Affected individuals are tall, extremely slender, and have arm span exceeding height.
Loss of height. Decreasing height after skeletal maturity results from short-
ening of long bones in the legs, cartilage loss in the hips/or and knees,
decreased vertebral and/or intervertebral disc-space height (especially lumbar), or spinal curvature. History and physical exam plus a minimal radio-
graphic investigation quickly identies the cause(s). Measuring regularly
detects slow height loss before disability occurs.
CLINICAL OCCURRENCE: Long Bones: Trauma, surgery, osteomalacia;
Cartilage: osteoarthritis, RA; Intervertebral Discs: Herniated discs, desic-
cated disks, disk infection; Vertebrae: Osteoporosis, osteomalacia, Paget disease, traumatic compression fracture, multiple myeloma; Spinal Curvature:
Scoliosis, pregnancy, abdominal muscle weakness, myositis, polio.
Weight: Body mass is distributed in muscle, bone, adipose tissue, organs,
viscera, and intercellular tissue. Weight loss or gain occurs in one or more
of these compartments. The organs, viscera, and skeleton vary little in mass.
The extracellular uid, skeletal muscle, and fat compartments are more labile.
Inappropriate or unexpected weight changes are the combined changes in
body water, muscle, and fat. Physiologic and etiologic hypotheses vary with
the compartment(s) involved. A two-compartment scheme divides body mass
into water and everything else, water is ~60% of the mass in men, slightly
less in women, and decreases with age in both sexes. Fat is low in water so
higher body fat lowers the proportion of water. Body water is divided into
two compartments, the intracellular water (66%) and the extracellular water
(34%). The extracellular compartment is divided into extravascular (75%)
and intravascular uid (25%). Extracellular water is essentially saline with an
approximate sodium concentration of 140 mEq/L. Intracellular water is rich
in potassium and relatively low in sodium.
Measuring weight.
Weight is measured in pounds or kilograms at each visit
establishing a baseline range.
Body mass index (BMI).
a risk factor for adverse events. The BMI is calculated by dividing the weight
in kilograms by the (height in meters)
The BMI is a function of weight and height and is
2
; the units are kg/m2. The upper limit
of normal is the point at which the risk for adverse health outcomes begins
to rise; the lower limit was similarly determined (Table 4-2). The BMI does
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TABLE 4-2Interpretation of BMI
BMI Description
<18.5 Underweight
18.5–25 Normal
>25–30 Overweight
>30–35 Class I: obese
>35–40 Class II: very obese
>40 Class III: extremely obese
not distinguish increases in lean body mass from increases in fat mass. BMI
growth charts are increasingly used in well-child care. BMI is useful in setting
weight loss goals enabling patients to compare the population risks associated with their current and target BMI.
Waist–hip ratio. Women more than men put more fat stores subcutaneously.
Men, especially with weight gain in mid-life, develop adiposity in the organs
and omentum. Visceral adipose tissue is metabolically distinct from subcutaneous fat and appears to contribute to hyperlipidemia and insulin resistance.
The waist-hip ratio (the ratio of the body circumference at the hip and waist)
is an indicator of visceral adiposity. Waist–hip ratio >0.9 for women and >1.0
for men is abnormal. Waist circumference >40 in. (90 cm) for men or >35 in.
(80 cm) for women is another indicator. Increased waist–hip ratio and waist
circumference are risk factors for adverse health events and appear to be better predictors than BMI.
Growth retardation—cystic brosis. Several autosomal recessive epithelial
chloride channel gene mutations lead to production of viscous mucus by the
exocrine glands resulting in chronic progressive pulmonary and pancreatic
dysfunction. Though most are diagnosed in childhood, mild mutations may
escape detection until adulthood. Symptoms include bulky, foul-smelling
stools, cough, and dyspnea. Pancreatic obstruction leads to maldigestion and
growth retardation. Lung involvement produces cough and recurrent pulmonary infections, often leading to chronic infection with Pseudomonas aeru-
ginosa and bronchiectasis. Sweat gland involvement increases susceptibility
to salt and water loss in warm environments. Complications include fecal
impaction, intussusception, volvulus, and chronic bronchitis. With advanced
pulmonary disease cardiomegaly and nger clubbing are seen.
Weight loss. Weight is lost when energy utilization or loss exceeds caloric
intake. Decreased effective intake (net of ingestion, emesis and stool losses),
maldigestion, malabsorption, increased metabolic utilization, and increased
losses of calories are all possible. Failure to gain weight and grow appro-
priately in childhood and adolescence has the same signicance as weight
loss in the adult. The history is most useful for hypothesizing a probable
pathophysiology. Have the patient estimate the weight lost over a specic
time; obtain weight records to validate the history. Ask whether the patient’s
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clothes t differently or if family or friends have noted a change in appearance. Review the daily intake of food and drink and identify any change in
physical activity. Examine the patient’s belt for a change in wear pattern.
Search for striae and loose skin over the abdomen and upper arms. Often
more than one mechanism is implicated. DDX: Weight loss with no change
of intake suggests impaired nutrient assimilation (maldigestion, malabsorption), glucosuria (diabetes mellitus), or increased metabolic rate (hyperthyroidism, pheochromocytoma). Cancer and psychosocial problems, especially
depression, are the two most prevalent explanations.
CLINICAL OCCURRENCE: Endocrine: Hyperthyroidism, adrenal insuf-
ciency, diabetes (especially type 1), hypothalamic disorders; Degenerative/
Idiopathic: Advanced age (normal adults lose weight gradually after age 60
years), any debilitating disease; Infectious: Chronic disseminated infection
or advanced local infection, for example, tuberculosis, chronic active hepatitis, AIDS, intestinal parasites; Inammatory/Immune: Any systemic inammatory disease, for example, SLE, RA, vasculitis; Mechanical/Traumatic:
Bowel obstruction, dysphagia, odynophagia, dental and chewing problems,
decreased mobility, paralysis, apraxia; Metabolic/Toxic: Organ failure (uremia, advanced liver disease, emphysema, congestive heart failure), increased
physical activity, maldigestion and malabsorption, dieting, decreased intake
and starvation; Neoplastic: Cancers decrease appetite and increase utilization, especially when disseminated or involving the liver;
Dieting, dementia, depression, anorexia nervosa, bulimia, abuse, isolation,
poverty; Vascular: Vasculitis, multiinfarct dementia.
Psychosocial:
Cachexia.
wasting of muscle protein and increased metabolic demands resulting in profound weight loss and redistribution. Cachexia is physiologically distinct from
starvation and cannot be reversed by refeeding. Cachexia is classically seen in
chronic tuberculosis (“consumption”) and slow growing visceral malignancies
(e.g., advanced pancreatic and colon cancers), but any chronic disease with
persistent activation of the immune system may produce the syndrome.
advanced liver and renal disease, RA, Addison disease, chronic obstructive
pulmonary disease, and advanced age.
Weight gain. Weight increases whenever the intake of calories exceeds meta-
bolic demands or when calorie-free salt and water are retained in advanced
heart, kidney, and liver disease. Weight gain continues after linear growth
stops as skeletal muscle mass increases to adult size, especially in men. After
reaching adult body mass, any further weight increase indicates a pathologic
condition, a decrease in physical exercise, an increase in caloric intake, or an
intense body building program. Fats and alcohol have the highest energy
content, 9 and 7.5 kcal/g, respectively; the energy content of carbohydrates
and protein is 4.5 kcal/g. A careful history with attention to diet, exercise,
appetite, libido, skin, hair, and bowel habits is essential. On physical exam
evaluate possible extracellular uid retention (edema, ascites), adiposity, and
muscle mass.
roidism, insulinoma, hypothalamic injury, treatment of diabetes, anabolic
Cytokines released with chronic infections and malignancies lead to
CLINICAL OCCURRENCE: Common associations are HIV-AIDS, CHF,
CLINICAL OCCURRENCE: Increased Intake: Overeating, mild hyperthy-
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steroids; Decreased Demand: Hypothyroidism, hypogonadism, inactivity,
connement;
Salt and Water Retention: Congestive heart failure, kidney
failure, nephrotic syndrome, hepatic insufciency, hypothyroidism, portal
hypertension with ascites, idiopathic edema, diuretic rebound, venous insufciency with dependent edema.
Obesity. Genetics and lifestyle each are important in the development of
obesity. Calorie intake in excess of expenditures leads to weight gain, but
obesity requires failure of feedback to limit intake; the cause(s) of this failure
are unknown. Obesity is epidemic; a third or more of the adult population is
obese. Obesity causes insulin resistance and increases risk for hypertension,
diabetes, heart disease, cancer, and overall mortality. Obesity is readily recognized and diagnosed, but is very difcult to treat, especially if onset is in
childhood or adolescence. Commonly the exact factors leading to the marked
weight gain, beyond dietary and exercise habits, are obscure.
DDX: The
distribution of adipose tissue assists diagnosis. Truncal obesity with thin limbs,
round faces and a prominent hump of fat over the upper back are characteristic of Cushing disease, iatrogenic steroid use, and use of protease inhibitors
for treatment of HIV-AIDS. Localized accumulations of fat are seen at sites
of repetitive insulin injection (lipodystrophy). Abdominal obesity is common in
men with mid-life weight gain (“beer belly”).
Metabolic syndrome. The metabolic syndrome is the association of several
conditions with increased risk for diabetes and cardiovascular disease. The
cause is unknown, but obesity and insulin resistance play large roles. A consensus denition was published in 2005. Diagnosis is based on increased
waist circumference (ethnically specic, Table 4-3), plus any two of the following: elevated triglycerides (>150 mg/dL) or treatment of hypertriglyceridemia; reduced HDL-cholesterol (men <40 mg/dL, women <50 mg/dL) or
treatment for low HDL; elevated BP (systolic ≥130 mm Hg, diastolic ≥85 mm
Hg) or treatment of hypertension; elevated fasting plasma glucose (≥100 mg/
dL) or previously diagnosed type 2 diabetes.
TABLE 4-3Waist Circumference Norms by Ethnic Group.
Ethnic Group Men Women
European descent ≥94 ≥80
South Asians ≥90 ≥80
Chinese ≥90 ≥80
Japanese ≥85 ≥90
Ethnic South and Central Americans Use South Asian recommendations
Sub-Saharan Africans Use European recommendations
Based upon Alberti KG, Zimmet P, Shaw J. The metabolic syndrome—a new worldwide definition. Lancet. 2005;366:
1059–1062.
Waist Circumference (cm)
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PAIN
Pain is a complex subject beyond the scope of this text. The reader is encouraged to explore pain texts to understand pain pathways and the pathophysiology of acute and chronic pain, which are distinct entities requiring different
diagnostic and management strategies.
Pain can be roughly classied as acute or chronic. Acute pain is an event.
Most acute pain is caused by direct tissue injury, ischemia, or
Adequate treatment of acute pain decreases the likelihood of progression
to chronic pain. Unremitting pain remodels central pain pathways
facilitating persistent pain as a chronic pain syndrome. Chronic pain is a
persistent experience frequently accompanied by functional impairment and
depression.
Diagnostic Attributes of Pain, PQRST: Pain directs attention to a specic ana-
tomic region and often, although not always, indicates tissue injury. Use of
the PQRST mnemonic improves diagnostic precision. The same questioning
strategy is useful for other symptoms.
P: provocative and palliative factors. Pain with movement implicates
mechanical mechanisms involving moving or displaced structures. The location is conrmed by pressure eliciting tenderness. Conversely, if resting a
part relieves pain, those tissues are likely the source of pain. Therapeutic
interventions can be used diagnostically: chest pain relieved by nitroglycerin suggests angina pectoris while relief by antacids suggests acid-peptic
disease.
Q: quality. Pain quality also assists diagnosis. Somatic pain, arising from
the skin, skeletal muscles, bones, ligaments, tendons, and soft tissues, is
described as sharp or stabbing and is well localized; the patient can point
with one nger to the site of maximal pain. Visceral pain, arising from isch-
emia; inammation; or other injury to the body cavities is poorly localized; the patient can only indicate a general area or areas of pain, often
described as deep or inside. It is aching, pressing, or squeezing in quality,
and often accompanied by autonomic symptoms such as nausea, vomiting,
diaphoresis, and intestinal ileus. Neuropathic pain arises from damage to the
nerve cells themselves; it is described as burning in the distribution of the
affected nerve or nerves. These distinctions are far from exact but are clinically useful. Shooting pain usually results from irritation of a nerve trunk.
Displacement of inamed tissues surrounding a pulsating artery causes
throbbing pain.
inammation.
R: region and referral. Pain is usually located in the anatomic region indicated by the patient. Pain is also referred following developmental and neurological organizational principles. Nerve injury will refer pain, and often
cause paresthesias, in the dermatomal distribution subserved by the sensory
components of the nerve (Chapter 14, page 643). Muscular pain is referred
toward muscles innervated by or derived from the same spinal segments
(the myotome). Similarly, skeletal pain radiates to structures innervated by or
derived from the same spinal segments (the sclerotome).
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S: severity. Individuals have remarkably similar thresholds for pain.
However, they vary greatly in their reactions to pain, and fear may aggravate pain. Assessment of pain severity is mandated by Medicare at each visit.
Pain is a subjective sensation, so the patient’s statement should be accepted
without debate. It is useful to calibrate pain on a 0 to 10 scale: with 0 being
no pain and 10 being the worst possible pain. Pain scores are used to follow
progression and response to management. Always communicate the goals for
pain relief: “We should be able to reduce your pain to a 3/10.” Intense pain
is usually accompanied by physiologic signs such as apprehension, postures
(protecting a limb, abdominal guarding), sweating, pallor, pupil dilatation,
hypertension, tachycardia, nausea, and vomiting.
T: timing.
is insidious in onset and relentlessly progressive without palliative features suggests cancer pain or increasing pressure in a closed space (e.g.,
intracranial pressure, toothache). Intermittent episodic pain suggests a
predisposition to specic episodic events, e.g., kidney stones, intermittent
intestinal obstruction. A single episode may be short or prolonged, steady,
worsening, or relenting in waves. Daytime pain is common when movement causes pain; daytime relief suggests muscle or joint stiffening improving with motion. Nighttime pain occurs when muscle relaxation stops
splinting tender tissues or the absence of competing sensory inputs allows
the
typical of bonepain.
Pain Syndromes:. Site-specic pain is discussed in the chapters dealing with
each body region.
Complex regional pain syndrome (CRPS)—reex sympathetic dystrophy, causalgia.
responses resulting in altered autonomic function and pain perception.
occurs after surgery or injury to an extremity, especially the hands or feet. The
pain may involve an entire anatomic region and can occur days to weeks after
the injury. The pain is disproportionate to the injury and usually described as
constant, burning, aching, and/or throbbing. Examination may reveal hyperalgesia, hyperesthesia, edema, erythema, and skin temperature changes.
Progression leads to vascular changes (cyanosis and mottling), altered sweating, atrophic skin, muscle and subcutaneous tissue, and contractures. Two
forms are recognized: CRPS type 1 occurs without nerve injury and CRPS
type 2 (causalgia) is associated with major nerve injury. Early recognition and
treatment is necessary.
Timing and duration of pain often indicate its cause. Pain that
persistent pain of an unremitting process to become predominant,
Minor injury initiates a complex series of spinal and CNS
CRPS
Postherpetic neuralgia.
dorsal root ganglia produces clinical herpes zoster and can result in a subacute or chronic painful neuropathy. Most patients with acute herpes zoster
have intense pain which abates over a period of weeks to months. The pain
is burning in quality, sometimes very severe, and associated with allodynia
where the slightest skin disturbance induces lancinating pain. Older adults
are at increased risk for persistent postherpetic neuralgia.
Reactivation of latent varicella-zoster virus in the
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