Saturday, June 27, 2009

The Basic Geriatric Respiratory Examination CME/CE

From MedscapeCME Family Medicine

Mark E. Williams, MD

CME/CE Released: 06/09/2009; Valid for credit through 06/09/2010


The objective of the pulmonary assessment of a geriatric patient is to check for the following:

  • Quality of respiratory efficiency;
  • Gas exchange; and
  • Presence of disease.
Assessing Respiration Efficiency

Of note, if the patient is bedfast, complete evaluation of respiratory efficiency is often less than optimal because chest expansion is not always symmetric and percussion notes may be less resonant.

Respiratory Rate

Although a patient's respiratory rate is often recorded in his or her chart (most often as 20 breaths per minute), cultivate the discipline to obtain it yourself. Count the respirations for a minute and observe the pattern and degree of respiratory effort. Note that moving the diaphragm without moving any air does not count as a breath. Normal respiratory rates for older patients are12 to 18 breaths per minute for those living independently and 16 to 25 breaths per minute for those in long term-care.

Tachypnea. A respiratory rate of 20 breaths per minute (or more than 25 breaths per minute for someone in a nursing home) indicates tachypnea. In such cases, look for the following:

  • Infection (especially pneumonia);
  • Reactive airways disease (eg, in acute exacerbations of chronic obstructive pulmonary disease [COPD], the patient has air trapping and cannot empty the lungs);
  • Congestive heart failure (patient pants in midrespiration);
  • Pulmonary embolus (very few elderly patients with pulmonary embolus have respiratory rates less than 16); and
  • Metabolic acidosis.

A respiratory rate of more than 30 breaths per minute in a patient with suspected abdominal disease suggests primary chest disease with referred symptoms to the abdomen.

Bradypnea. Bradypnea is a form of hypoventilation, in which the patient has a respiratory rate of less than 10 breaths per minute. In such cases, you might suspect severe myxedema, ingestion of central nervous system (CNS) depressants (eg, narcotics, benzodiazepines), or CNS disease (pontine hemorrhage, hypoglycemia, meningitis).

Respiratory Effort

Normal breathing is quiet and unlabored. If it is labored, it is important to note respiratory effort. In patients with pneumonia or acute abdomen, labored breathing prevents airway closure. Patients who have air hunger will often breathe with an open mouth. Pursed lip breathing mainly in expiration is seen in end-stage emphysema and suggests small-airway disease with terminal bronchiole collapse. Expiring with pursed lips increases the end-expiratory pressure, keeping the airways open and reducing the work of breathing. (It takes more work to put the first breath into a balloon than to add a breath to an already half-filled balloon.)

Audible Breath Sounds

Pay attention to the breath sounds. Wheezing, a musical sound, is an important clue to reactive airways or local obstruction. Coughing indicates lower airway irritation. Stridor (a high-pitched shrieking sound) implies partial airway obstruction. Expiratory stridor without inspiratory stridor suggests lower airway obstruction. Stridor on inspiration and expiration implies airway obstruction at the glottis. Of note, inspiratory stridor suggests obstruction in the oral airway or epiglottis and is a medical emergency.

Respiratory Patterns

Check for respiratory patterns and signs that indicate specific conditions. For example, inspiration interrupted by cough suggests pleuritic pain or inflammation. The following are other patterns and signs to look for.

Kussmaul's Respiration. Kussmaul's respiration is deep rapid respiration (an exaggeration of normal) in metabolic acidosis and is classically associated with diabetic ketoacidosis. Patients with Kussmaul's respiration may have an increase in tidal volume. While talking, they need to breathe between phrases, so their speech pattern can seem choppy.

Cheyne-Stokes Respiration. The pattern of Cheyne-Stokes respiration is one of increasingly deep respirations followed by a steady diminution of breathing until an apneic episode occurs, which can signify prolonged circulatory time or primary neurologic disease. Among the differential diagnoses are the following:

  • Primary CNS disease;
  • Chronic heart failure, meningitis;
  • Pneumonia;
  • Carbon monoxide poisoning; and
  • Medications (eg, morphine).

Obesity may be present. Some patients will show pupillary dilation with rapid breathing and pupillary contraction with apnea.

Biot's Breathing. Biot's breathing is characterized by irregular breathing (the "atrial fibrillation" of respiration) with sudden apneas. It suggests CNS disease and can be a sign of increased intracranial pressure or meningitis.

Apneustic Breathing. Apneustic breathing is seen in severely ill patients with coma. The patient holds his or her breath at the end of inspiration until the Hering-Breuer (carotid body) reflex initiates exhalation. This breathing pattern suggests pontine disease.

Chest Movement During Respiration

The next part of the chest inspection is to observe the patient's chest movement during respiration.

Use of Accessory Muscles

Using accessory muscles implies that the forced expiratory volume in 1 second (FEV1) is decreased to 30% of normal, which is usually between 1.0 and 1.5 liters per second. In such cases, a sitting patient may lean forward with hands propped on the knees. Sternocleidomastoid tension is often present, which is indicated by tense neck muscles, with the muscle being thicker than the patient's thumb.

Diaphragm Movement

Diaphragm movement can sometimes be seen with inspiration as a flickering along the lateral chest. A loss of this movement on one side indicates a paralyzed hemidiaphragm (Litten's sign). Diaphragmatic movement is usually not visible in overweight people.

Chest Symmetry

To check chest symmetry, observe the sides of the chest from the patient's back. Symmetric but decreased expansion suggests extreme old age or emphysema. Decreased chest expansion resulting from substernal goiter is Bryson's sign. Symmetric but increased expansion suggests paralysis of the diaphragm with compensatory intercostal contractions. Asymmetric expansion suggests pneumonia, a large pleural effusion, rib fracture, or pneumothorax. With hemiplegia, the affected side moves more than the unaffected side during quiet respiration but becomes more sluggish with forced respiration (Jackson's breathing sign).

Paradoxic Chest Movements

Paradoxic sternal movement suggests trauma or multiple rib fractures. Paradoxical abdominal movement, in which the abdomen moves out with expiration, can be a sign of a paralyzed diaphragm, respiratory failure, or fatigue during an exacerbation of COPD. Intermittent paradoxic abdominal movement may be caused by muscle fatigue from respiratory pump failure (respiratory alternans). Epigastric depression with inspiration suggests large pericardial effusion or a paralyzed diaphragm (Duchenne's sign).

Intercostal Retractions

Intercostal retractions suggest an imbalance between the negative pressure generated and the ability of the lung to expand. Generalized retractions are a sign of significant inspiratory obstruction. Focal retractions suggests bronchial obstruction, flail chest, or constrictive pericarditis (Broadbent's sign) if over the heart. With flail chest, the ribs themselves show paradoxic movement. Unilateral loss of normal retractions suggests pleural effusion, pneumothorax, or consolidation.

Bulging Interspaces and Apices

Bulging interspaces on inspiration suggests a tension pneumothorax, a large pleural effusion, emphysema, or reactive airways disease. Elevation of the supraclavicular space in an asynchronous manner suggests pleural effusion as the lung floats like a cork on the pleural fluid. The side with the fluid will elevate first.

The Costal Angle (Hoover's sign)

An especially useful observation is to watch the costal angle during respiration (Hoover's sign). Normally this angle should increase as the intercostal muscles open the chest as the diaphragm contracts. Hoover's sign is paradoxic closing of the costal angle with inspiration because of the loss of intercostal contribution secondary to air trapping. This sign indicates chronic obstruction and an FEV1 less than 1 liter per second. Restrictive lung disease by itself does not produce Hoover's sign.

Unilateral Movements

If there are unilateral movements, consider the source of the inequality. One side moving more laterally implies significant atelectasis if it is pulling up from above or subphrenic abscess if pushing up from below.

If one side moves more medially than the other, consider intercostal paralysis, pleural effusion, or tension pneumothorax. Unilateral narrowing of the intercostal spaces suggests pneumothorax or inflammation (Przewalski's sign). If you see decreased medial movement with normal lateral movement, consider cardiac enlargement, severe right heart failure, and pericardial effusion.

Palpate the Lateral Chest Walls

Palpation over the lateral chest wall can provide helpful information on respiratory excursion. Make sure your hands are warm before beginning. Feeling an area of localized warmth in a febrile patient could represent an empyema. Appreciating a mass in the chest wall could represent a rib fracture (there may be an area of point tenderness and possibly ecchymosis), tuberculosis, nocardia, or actinomycosis. A mass felt in an interspace suggests abscess (possibly actinomycosis, tuberculosis, or empyema necessitans) or lymphadenopathy from lymphoma. Detecting crepitus suggests subcutaneous emphysema from a rib fracture, ruptured bleb with pneumothorax, esophageal rupture, or abdominal perforated viscus with retroperitoneal air tracking.

Palpate the Trachea

If you have not already done so, palpate the trachea. Check the lateral tracheal wall with the clavicular heads to determine whether it is midline. Deviation from the midline is significant.

Palpate Rib Expansion

Palpate the rib expansion segmentally. For examining the upper lobes, place your hands on each upper lobe with the thumbs under each clavicular head. Watch for symmetric thumb expansion with each inspiration. To check the middle and lingular segments, place your hands across the lower chest with each thumb at the fifth intercostal space on the sternum. Watch for symmetric thumb expansion with each inspiration. A lack of symmetric movement suggests bronchial stenosis on the side with the reduced movement.

To evaluate the lower lobes, place your hands across the lower chest anteriorly, with each thumb at the costal margin.

It is especially useful to check the costal angle during respiration. Normally the angle increases on inspiration as the intercostal muscles open the chest and the diaphragm contracts. Paradoxic movement with a decrease in the costal angle on inspiration that is caused by severe air trapping in COPD (FEV1 < 1 L) is Hoover's sign (see above). Restrictive lung disease by itself does not produce Hoover's sign. Repeat the lower lobe examination posteriorly at the level of the tenth rib. Normal movement is 1 to 2 centimeters.

Tactile Fremitus

Checking for tactile fremitus requires detecting palpable vibrations. Have the patient say "toy coin" each time you touch the chest with the ulnar side of your hand. The "oy" sound is the key to producing the vibration. (It is sometimes recommended to ask the patient to say "99." However, the origin of this came from the German words for "99," which in that language contains "oy" sounds.). Feeling increased vibration (fremitus) over an area of dullness to percussion suggests consolidation or direct communication between the bronchus and the chest wall. Appreciating decreased fremitus over an area of dullness suggests pleural effusion or pneumonectomy. Use both hands to compare each side simultaneously. Begin at the apices posteriorly and work down the back, then go anteriorly to the apices. Normally the right apex will have slightly more fremitus than the left because of the aortic position. Note the level of the diaphragm.

Pain on Palpation

Localized pain on palpation suggests early herpes zoster, rib fracture, or costochondritis (Tietze's syndrome). Sternal tenderness can be a sign of fracture, leukemia (classically the lower third of the sternum), other blood marrow abnormalities, metastatic prostate cancer, or xiphoidalgia. Pneumonia can produce tenderness and spasm of the insertion of the sternocleidomastoid muscle.

General Points

As with palpation, make sure your hands are warm before you begin percussion. Start at the back and check each side to compare the quality of the sensation. It is key to keep the wrist loose and the hand floppy. As you percuss, consider the characteristic of the structure you are percussing. One trick is to practice over a table percussing from the center toward the legs. Notice how the percussion note feels firm when over the leg of the table. Close your eyes and practice until you can reliably stop over the leg. Sometimes an elderly patient is too ill to sit up and percussion must be accomplished with the patient in the lateral decubitus position. This position can add some artifacts of lung compression, producing dullness in the mid lung fields of both the dependent and upward lungs. Of note, the feel of the resonance may be more sensitive than the sound of the percussion note, especially in a noisy setting such as a crowded emergency room, where subtleties of sound are more difficult to appreciate.

Basic Percussion Techniques

There are 3 basic percussion techniques: the light pat (an excellent general technique for pulmonary examination), the direct percussion, and the indirect percussion (what students are generally taught as percussion).

  1. Light pat. Gently pat the back on each side starting at the apices and moving down to the diaphragm.
  2. Direct percussion. Place your dominant hand on the skin and raise your forefinger and tap on the skin directly.
  3. Indirect percussion Place your non-dominant hand on the skin and with your dominant middle finger tap the middle finger of your nondominant hand at the sistal interphalangeal joint.

Some experts believe that the second and third techniques are best used to define an interface such the cardiac border or the upper border of the liver.

The Sequence of Percussion

The patient should be upright if at all possible. Percuss down the posterior midclavicular line on each side of the chest. Note the diaphragmatic excursion by checking its level during expiration and then during deep inspiration. Normally this excursion is about 4 centimeters. Compare each side.

After percussing the diaphragm, percuss down the midaxillary line on each side. An elevated left hemidiaphragm is clearly abnormal and implies volume loss, paralysis of the left hemidiaphragm, or a left upper quadrant abdominal mass. An elevated right hemidiaphragm is normal but can suggest volume loss, a right upper quadrant mass, and a paralyzed right hemidiaphragm.

Next, percuss across the trapezius from the shoulder to the base of the neck to check Krönig's isthmus (of resonance) on each side. This area is significantly more resonant than the shoulder or the base of the neck. Loss of normal resonance in this area suggests upper lobe disease.

Percuss the clavicles. Dullness on one side suggests upper lobe disease.

Finally, percuss over the right middle lobe in the right midchest and along the left anterior chest.

Dullness and Its Indications

Dullness to percussion implies consolidation, pleural fluid, or pleural scarring. Parenchymal consolidation suggests pneumonia or cancer. If you suspect pleural fluid, recheck your percussion with the patient in the lateral decubitus position with the dull side up. Look for any change in dullness caused by fluid shift. No change in dullness with a change in position implies either consolidation or loculated fluid. Dullness to percussion plus absent breath sounds caused by hydatid disease in the lungs is Bird's sign.

Dullness in the medial base of the lung (Grocco's triangle) near the spinous process is contralateral to a pleural effusion (or significant pneumonia) and is ipsilateral to a massive pleural effusion or pericardial effusion (obviously on the left side).

Dullness below the left scapula (Ewart's sign) or below the right scapula (Conner's sign) suggests a large pericardial effusion.

Pleural effusion may be suggested by the following:

  • Increased rib vibration in the anterior chest to percussion posteriorly (Kellock's sign);
  • Change in the percussible dullness with change in position (D'Amato's sign); or
  • Hyperresonance just above an area of dullness (skodaic hyper-resonance).

With small pleural effusion, dullness is in the T9 to T11 interspaces. In pneumothorax, the percussion note is more resonate (Biermer's sign). In this case, check for hyperresonance over the midclavicle. Confirm by appreciating decreased breath sounds over the hyperresonant side and with the coin test (see below).

Noting a band of hyperresonance near the diaphragm suggests subphrenic abscess or lower lobe pneumonia.

General Points

Make sure that the listening area is quiet, and importantly, do not listen through the patient's clothing. Warm your stethoscope either by carrying it in your pants pocket or by vigorously rubbing it. One strategy is to place a rubber membrane on the bell and have the patient breath deeply with the mouth open. Make sure that your stethoscope bell is securely placed flat on the chest and that you are not breathing on your tubing. In fact, breathe on the tubing beforehand to appreciate the low-pitched rustling sound your breath produces. Be sure that your earpieces are securely in your ears to exclude environmental noise.

Listen to at least 2 respiratory cycles at each location. All breath sounds should increase in pitch with inspiration and decrease with expiration. If patient has been intubated, listen for bilateral breath sounds and over the epigastric area to help determine the tube placement.

Begin at the bases and work up the back. Starting at the bases allows you to appreciate any basilar crackles secondary to atelectasis or early congestive heart failure. If you start at the apices and work down, such crackles might disappear by the time you get to the bases. If you hear additional noises make sure they are coming from the patient's chest and not from the skin, muscles, or other extraneous source. For example, body hair can produce a crackling sound that resembles dry cellophane crackles.

Quality of Breath Sounds

Alveolar (vesicular) breath sounds are normal but pathologic processes cause these sounds to disappear. Upper airway or bronchial (tubular) breath sounds are normal over an airway but hearing these sounds in the peripheral lung fields suggests consolidation or lymphadenopathy. They also may be heard at the top of a pleural effusion. Bronchial breath sounds are only heard at the top of the effusion. Pay attention to the inspiratory to expiratory ratio of breath sounds. Chronic obstructive lung disease increases the expiratory phase of respiration. Hearing equal inspiratory and expiratory sounds suggests respiratory obstruction (Grancher's sign). Localized prolongation of expiratory sounds is Jackson's sign, which can sometimes signify a localized obstruction such as an endobronchial mass.

Loudness of Breath Sounds

Increased breath sounds over an area of dullness suggests consolidation. If there is upper lobe consolidation, consider tuberculosis, Pancoast's tumor, or aspiration pneumonia. Signs of middle lobe consolidation suggest pneumonia, malignancy, or conditions producing lymphadenopathy (middle lobe syndrome). Lower lobe consolidation suggests pneumonia, aspiration, or pulmonary infarct. Decreased breath sounds over an area of consolidation suggest pleural effusion or pneumonectomy.

Adventitious Breath Sounds

If there is stridor (see above), listen over the trachea or at the base of the neck to see if loudness is greatest there. Stridor heard on inspiration is a red flag for a medical emergency and you should consider epiglottic obstruction, epiglottitis, vocal cord dysfunction, tracheal obstruction, whooping cough, neoplasm, foreign body, tracheal stenosis, or palatal obstruction. Stridor only in expiration suggests lower airway obstruction, such as from a foreign body.


Wheezes are musical sounds that indicate airway obstruction, which when it occurs during expiration, suggests a source within the chest. Wheezing that occurs on inspiration suggests obstruction in the trachea (outside the chest). Hearing both inspiratory and expiratory wheezes is more concerning than hearing either alone. Focal wheezes help to localize the site of obstruction. End-expiratory wheezes suggest reactive airways (asthma) and imply bronchiolar disease. Peak flow is reduced significantly. Hearing wheezes throughout expiration suggests asynchrony of one lung area with another, such as occurs with organophosphate poisoning. Hearing end-inspiratory wheezes implies a small airway opening in the deflated section of lung. This finding suggests chronic bronchitis, bronchiectasis, or organophosphate poisoning. Hearing wheezes throughout inspiration implies a fixed stenosis or obstruction of the upper tracheal bronchial tree, such as in interstitial fibrosis or hypersensitivity pneumonitis.

Crackles (Rales)

Inspiratory crackles are common in elderly people. Early inspiratory crackles, however, imply significantly decreased FEV1/forced vital capacity caused by broncho-obstructive disease as a result of chronic bronchitis, emphysema, or reactive airways disease. Midinspiratory crackles suggest bronchiectasis, whereas late inspiratory crackles suggest restrictive (alveolar) disease caused by congestive heart failure, idiopathic pulmonary fibrosis, sarcoidosis, or drug toxicity.

Localized midexpiratory crackles can be a sign of bronchiectasis or pneumonia. Note the location of expiratory crackles. If their location changes with the patient's position, consider congestive heart failure because this implies an increased pulmonary capillary wedge pressure (above 25 mm Hg). Fixed crackles suggest fibrosis or pneumonia.

Note the quality of the crackles. Peripheral lesions tend to increase the pitch (fineness) of the crackles. Fine crackles (like crackling cellophane) suggest interstitial fibrosis, sarcoidosis, or asbestosis. Coarse Velcro®-like crackles suggest chronic pulmonary fibrosis. Moist crackles (resembling the sound of the fizz of a carbonated drink) suggest congestive heart failure. Posttussive rales (crackles) suggest parenchymal disease or lung abscess.


Rhonchi are coarse flapping sounds that suggest fluid or mucus in an airway.

Amphoric Breathing

Amphoric breathing is a low-pitched sound resembling blowing over a soft drink bottle (an amphora). To appreciate the nature of this sound, trying listening over the occiput while the patient whispers "wahoo." Amphoric breathing is never heard in the presence of alveoli so hearing it suggests alveolar destruction with air going into and out of a cavity and signifies a large bullae or lung abscess. Disappearance of amphoric breathing suggests that something has occupied the void (aspergillus fungus ball or fluid).

Pleural Friction Rubs

Pleural friction rubs are leathery, creaky sounds similar to the sound of slowly rubbing your palms together. They do not have a musical quality, like a wheeze does, but suggest 2 inflamed pleural surfaces (the parietal and visceral pleura) rubbing together. They can occur on both inspiration and expiration, but they usually occur with inspiration and tend to be localized. Hearing a pleural friction rub implies neoplasm, pulmonary infarction, pneumonia, tuberculosis, or systemic lupus erythematosus. A sternal friction rub heard when the patient raises and lowers the arms suggests aortic arch aneurysm or fibrotic mediastinal tumor (Perez's sign).

Special Sounds and Signs

d'Espine's Sign. During auscultation, when you reach the level of the midscapula (about T5), check for an important sign of a posterior mediastinal mass (d'Espine's sign). Listen on either side of the vertebral column and compare the quality and intensity of these sounds with those over the spinous process. Normally, the lateral sounds are louder and more distinct. With a positive d'Espine's sign, the vertebral breath sounds are loud and upper airway sounds are of greater intensity than the corresponding lateral lung sounds. This implies continuity between the main stem bronchus and the vertebrae and suggests malignancy, lymphoma, metastatic cancer, tuberculosis, sarcoidosis, and other causes of mediastinal lymphadenopathy. Listen for egophony, bronchophony, and whisper pectoriloquy. These may be more sensitive for posterior mediastinal lymphadenopathy than the change in breath sounds. If d'Espine's sign is present, try also percussing over the spinous processes of T1-T5. The appearance of red spots over the spinous processes of T1-T5 after percussing them suggests bronchial lymphadenopathy (Cattaneo's sign). False positives of d'Espine's sign can occur in severe kyphosis, which should be obvious.

Egophony (Goat Sound). Egophony (or goat sound) is an "e" to "a" change and is considered the most sensitive sign of pulmonary consolidation. Have the patient say "e." A compressed lung will produce a bleat like a goat, changing the "e" to an "a" sound. For practice, listen over the skull or the base of the neck where this "e" to "a" change is normal. Egophony may be present along the top of a pleural effusion. It may also be present over a massive pleural effusion caused by significant lung compression. Extensive pulmonary fibrosis can also produce egophony.

Whisper Pectoriloquy. Whisper pectoriloquy is the second best sign of consolidation. Have patient whisper "66 whiskeys please," which produces hissing sibilant "s" sounds. When bronchial breathing is abnormal, the sounds will be more distinct and you can more easily appreciate the words whispered.

Bronchophony. In bronchophony, spoken sounds seem more distinct when listening over a consolidated or compressed lung. Have the patient say a sentence like "UNC is number one," or repeat a word such as "99" several times. With consolidation or compressed lung, the words will be heard clearly over the involved area.

Expiratory Time. Have the patient take a deep breath and exhale as quickly as possible. Listen over the trachea. Hearing expiratory sounds for more than 6 seconds suggests airway obstruction Another but less accurate method is to listen over the upper posterior chest and use a 3-second threshold.

The Test for Pneumothorax. For this test, the patient must be sitting upright and asked to hold a large silver dollar, flat against the chest just below the midclavicle. Tap the silver dollar with another coin. (Note: A Susan B. Anthony dollar or coins such as quarters or nickels are too small and will not work. It must be a pre-1964 silver dollar.) A pneumothorax or a large bulla will produce a loud ringing bell-like sound rather than the usual metallic tap. Tuning forks can sometimes be used as an alternative.

Shephard's Sign of Sleep Apnea. In some patients with sleep apnea, a sonorous expiratory wheeze will develop at the base of the neck. Listen with the patient supine and breathing through his or her nose.

Identifying Specific Conditions
Differentiating Pleural Effusion From Consolidation

Because both pleural effusion and consolidation produce dullness, percuss just above the dullness, preferably using the light pat technique. The following clues each indicate that the presence of a pleural effusion is more likely:

  • Increased rib vibration in the anterior chest to percussion posteriorly (Kellock's sign);
  • Change in the percussible dullness with change in position (D'Amato's sign);
  • A rim of hyperresonance heard just above the dullness (skodaic hyperresonance);
  • Increased resonance of the thoracic spinous processes (Korányi's sign);
  • An "s"-shaped line of dullness on percussion of the chest (Damoiseau-Ellis line); and
  • Change in the tympanitic note above a pleural effusion when the patient opens and closes his or her mouth.

The following are additional techniques for differentiating between pleural effusion and consolidation:

  • Listen to the quality of breath sounds in the area of dullness. Hearing an increased intensity of sounds suggests consolidation; a decreased intensity suggests pleural effusion;
  • Listen for egophony (see discussion above). A change to a goat-like "a" sound after saying "e" in the area of dullness suggests consolidation (Shibley's sign). Egophony -- either "e" to "a" or "u" to "a" (Karplus' sign) -- just above an area of dullness suggests pleural effusion;
  • Hearing no sound at all over an area of dullness implies resection; and
  • Listen for whisper pectoriloquy by having the patient whisper "66 whiskeys please." Clearly hearing the phrase in an area of dullness suggests consolidation; hearing no sound suggests pleural effusion.

If the signs suggest pleural effusion, gently move the patient while listening over the effusion. Hearing a sloshing sound suggests hydropneumothorax. Note the location of the effusion. A right-sided pleural effusion suggests congestive heart failure. A left-sided effusion suggests pancreatitis, pulmonary infarct, pericarditis, ascites, or a ruptured thoracic duct.

Signs of Cavitary Lung Disease

Pulmonary cavities may be identified in several ways. In patients with pulmonary cavities, the percussion note may change when the patient opens and closes his or her mouth (Wintrich's sign). While listening over a pulmonary cavity, harsh inspiratory sounds that quickly diminish in intensity (Seitz's sign) may be heard. Forced inspiration can lower the pitch of the sound over a cavity (Friedreich's lung sign). Cough following apical percussion producing an area of apical tympany suggests cavitary disease (Ernis' sign).

Signs of Pleural Inflammation

Decreased rib expansion can be caused by an inflammatory process in the lungs (Bethea's sign). Palpable intercostal muscle rigidity suggests pleural inflammation (Pottenger's sign); disappearance of this sign can indicate empyema (Ramond's sign).

Pain offers a clue to possible pleuritic inflammation. With pleuritic inflammation, the patient will lie with the good side down (Andral's decubitus sign). Pleural inflammation can produce sensitivity of the upper back and shoulder muscles to palpation (Sternberg's sign). Pain from pleural irritation may also be referred to the shoulder (Capp's sign). Pain on palpation on the left upper abdominal quadrant (the mirror image of Murphy's point) suggests lower lung pleural inflammation (de Mussey's sign). Chest pain that increases with bending toward the pain suggests intercostal neuralgia; increase in pain bending away from the pain suggests pleuritic pain (Schepelmann's sign).

Examining the Patient With Respiratory Distress
Demeanor and Posture

Patients in respiratory distress may appear restless, agitated, or drowsy. The patient's eyes may be prominent. Patients in respiratory distress will often sit leaning forward using their accessory muscles. Hypertrophy of the sternocleidomastoid may be present and the patient may have calluses on the extensor surface of the forearm or distal thigh (Dahl's sign) as evidence of the chronicity of their lung disease. Patients who sit leaning forward with their legs dependent (Fowler's position) may have severe heart failure. Patients leaning forward with their head protruding forward as if sniffing flowers may have epiglottitis.

Breathing difficulty when sitting up and relieved when supine is platypnea and implies severe upper lobe disease. Patients lying on one side (lateral decubitus position) tend to place the good lung in the dependent position to maximize ventilation-perfusion matching. However, if a pleural effusion is present, it will tend to be on the dependent side.

Skin Color

Obviously the patient's skin color gives important clues to the level of oxygen saturation. Cyanosis suggests at least 5 grams of deoxyhemoglobin. If only the nail beds are cyanotic, the peripheral circulation is clamped down or slowed.

Clubbing of the Fingernails and Schamroth's Sign

One way to see whether the fingers are clubbed is check for Schamroth's sign. Have the patient place both forefinger nails together. If you can see a small diamond space between the nails, the nails are not clubbed. If the diamond is not visible, Schamroth's sign is positive and clubbing is present. Pulmonary causes of clubbing (not an exhaustive list) include the following:

  • Bronchogenic carcinoma;
  • Alveolar cell carcinoma;
  • Pulmonic abscess;
  • Interstitial pulmonary fibrosis;
  • Sarcoidosis;
  • Beryllium poisoning; and
  • Pulmonary arteriovenous fistula.

Some cardiac and gastrointestinal disorders can also cause clubbing.

Chest Shape and Symmetry

Chest wall deformities can have a significant impact on respiratory dynamics. For example, scoliosis and kyphosis are common in elderly people. The following conditions should also be looked for.

A barrel-shaped chest, indicated by increased anterior-posterior diameter, suggests air trapping caused by chronic lung disease. In some cases of emphysema, the AP diameter may not really be increased but is an optical illusion because of decreased abdominal diameter. Emphysema is also suggested in patients with a thin wiry habitus and distended arm veins.

Pectus excavatum (funnel chest) occurs when the sternum is depressed, creating a funnel-like shape. It is associated with Marfan's syndrome and congenital abnormalities in the respiratory tract and heart.

In pectus carinatum (pigeon chest), the sternum sticks out like a ridge on the chest. It is associated with acromegaly, Marfan's syndrome, and congenital problems of the diaphragm.

Tracheal Location

Normally the trachea is slightly to the right of the midline. Atelectasis and consolidation shifts the trachea toward the involved side. Pleural scarring will cause the trachea to deviate to the involved side during inspiration. Pneumothorax will pull the trachea to the opposite side, whereas massive pleural effusion or goiter will push the trachea to the opposite side

Venous Patterns

Note the venous pattern over the chest, which may indicate specific conditions. Unilateral venous distension suggests an underlying pulmonary neoplasm. Juicy collaterals can be seen in superior vena cava syndrome. Varicosities over the C7-T3 spinous processes is Lombardi's sign of tuberculosis. Fine telangiectasias along the border of the costal margin are commonly seen in elderly men.

Reading List

Maitre B, Similowski T, Derenne J-P. Physical examination of the adult patient with respiratory diseases: inspection and palpation. Eur Respir J. 1995;8:1584-1593. Available at: Accessed May 21, 2009.

Bureau of Medicine and Surgery, Department of the Navy. Hospital Corpsman Sickcall Screener's Handbook. Thorax, Lungs, and Respiratory Disorders. BUMEDINST 6550:9A; 1999. Available at:
CorpsmanSickcall/ThoraxLungsResp.html Accessed May 21, 2009.

Who Named It? Website. Available at Accessed May 21, 2009.

HIV Serosorting in Men Who Have Sex With Men: Is It Safe?

From JAIDS: Journal of Acquired Immune Deficiency Syndromes

Matthew R. Golden, MD, MPH; Joanne Stekler, MD, MPH; James P. Hughes, PhD; Robert W. Wood, MD

Authors and Disclosures

Published: 01/12/2009


Abstract and Introduction

Background: Serosorting is the practice of preferentially having sex with partners of concordant HIV status or of selectively using condoms with HIV-discordant partners.
Methods: We evaluated the epidemiology of serosorting among men who have sex with men (MSM) seen in a sexually transmitted disease clinic, Seattle, WA, 2001-2007, and defined the percentage of visits during which MSM tested HIV positive based on whether they reported nonconcordant unprotected anal intercourse (UAI), UAI only with partners thought to be HIV negative (serosorters), no UAI, or no anal intercourse.
Results: Men reported serosorting during 3295 (26%) of 12,449 visits. From 2001 to 2007, the proportion of visits during which men reported serosorting increased (P = 0.02); this change was greater among HIV-infected MSM than among HIV-uninfected MSM. Among men who tested HIV negative in the preceding year, HIV tests were positive in 49 (3.5%) of 1386 who reported nonconcordant UAI, 40 (2.6%) of 1526 serosorters, 28 (1.5%) of 1827 who had only protected anal intercourse, and 0 of 410 who had no anal intercourse (P < 0.0001); 32% of new HIV infections occurred in serosorters. The prevalence of HIV was higher among serosorters tested during 2004-2007 than among those tested during 2001-2003 (0.85% vs. 3.2%, P = 0.03).
Conclusions: Serosorting offers MSM limited protection from HIV.


Studies conducted in the early 1990s documented that men who have sex with men (MSM) use condoms more often with partners of discordant HIV status than with HIV-concordant partners.[1-3] Subsequent reports compared the sexual mixing patterns of HIV-infected and -uninfected MSM and found that MSM disproportionately have sex with partners of the same HIV status,[4,5] an observation that is consistent with findings from studies restricted to either HIV-infected[6-10] or HIV-uninfected MSM.[11,12] More recently, we observed that among HIV-infected MSM receiving medical care at the largest HIV clinic in Seattle, WA, 24% reported that they had decided not to have sex with another man in the last year because that potential partner was HIV negative and that 31% thought that a potential partner decided not to have sex with them because they were HIV infected.[13] These studies document what is now widely referred to as serosorting.[14]

Serosorting is the practice of preferentially having sex with partners of concordant HIV status or of selectively using condoms with HIV-discordant partners. Reports from San Francisco, London, and Sydney suggest that this practice may be increasing,[15-18] and some investigators have suggested that increased serosorting may be responsible for preventing large increases in HIV acquisition rates even as rates of bacterial sexually transmitted diseases (STDs) among MSM have risen dramatically.[17] Responding to the increased attention focused on serosorting, some US health departments have developed or funded online resources to advise MSM and medical providers about the practice.[19,20]

The extent to which serosorting protects HIV-uninfected MSM from acquiring HIV is uncertain. Prospective studies have associated HIV acquisition with having unprotected anal intercourse (UAI) with partners that study subjects believe are HIV uninfected[21] and with the number of HIV-uninfected partners a participant reports.[22] These findings suggest that serosorting does not eliminate the risk of HIV acquisition. In particular, serosorting may fail if people misreport their HIV status, either because they do not know they are infected or because they knowingly mislead partners.[13] Although the limits of serosorting remain ill defined, a mathematical modeling study evaluating the risk of HIV acquisition associated with serosorting suggested that because of the high risk of HIV transmission during the period after initial HIV acquisition, the practice may be more risky than having sex with persons with known, long-standing HIV infection.[23] We evaluated the epidemiology and protective efficacy of serosorting among MSM tested for HIV in Seattle, WA.



The Good Patient


From Academic Medicine

Evan J. Zucker MD
Published: 06/11/2009

Before medical school, I had taken it for granted that doctors treated all patients equally. My experience caring for a patient on my third-year surgical rotation taught me otherwise.
My patient was a young man, just a few years older than myself. He was a good kid-from the suburbs, a law school student, with two devoted parents. He was tall with an athletic build, dark blond hair, light brown eyes, the kind of guy nurses doted over, someone whose path I might have crossed in other circumstances.
He was otherwise healthy, but he had a problem. Some vague fatigue, a hematocrit in the low 20s, and then the CT, which revealed a massive gastric sarcoma. I was there for his debulking surgery; the morale in the OR was high that day. Nurses played Guess how much the tumor weighs as the surgeon scooped out the bowling-ball-sized cancer in record time. And what an interesting case! A brother with Wilms tumor, aunts with early-onset breast cancer-could it be Li-Fraumeni, we wondered?
And then the surgery was done, and he was my patient. I was the first one to see him each morning, to turn on the light just hours after the previous night's blood draw. From the team's perspective, he was one of our healthiest patients and did not require much attention.
Early on, he complained of some throat irritation and pain with swallowing, likely related to his nasogastric tube, which I faithfully reported back to the team. We spent a few minutes with him and gave him some numbing spray for his throat, but he still complained daily. The team teased, We'll just have to make him your personal patient, now won't we? I could take the hint-in bringing up my patient's throat, I was also wasting precious time on rounds, and so I learned to keep quiet about his complaints.
Yet, the following week, in taking signout with my intern, I found there was page after page about my patient's throat but that the nightfloat had decided not to check on him. While I knew this probably wasn't crucial and didn't want anyone to be blamed, I kept thinking-he was so young, my age. If our positions had been reversed, who would speak up for me if no one would hear me? I broke my silence and brought up my patient's throat again on rounds.
This time, the intern was chastised on the spot for not taking care of things sooner. Yet, when we got to my patient's room, the reminder of our 25-patient list soon caught up to us, and the patient was simply handed the stern Okay, yes ... someone will come back to see you line. The next day, nothing had changed-neither his discomfort nor the lack of attention to it-and yet he had no complaints and tried to crack a smile. I remember looking at him that day. He seemed dirty and disheveled; his hair was now matted and frazzled. A good patient today-no complaints, right on schedule. Today he had given up. Just like everyone on the team, he had learned his place, too.
My patient was discharged shortly thereafter, only to return the following weekend with an intraabdominal abscess almost as large as his original tumor. Probably, there was no way our team could have prevented this. At least his throat didn't hurt anymore.
During my clinical years, I learned more and more to think and act like a doctor. In caring for this patient, I also learned that it is important to continue to take a step back and think about what kind of doctor I want to become. Acknowledging and alleviating what seems like a minor complaint may not be as medically necessary as, say, tumor removal, but such acts recognize and dignify patients' humanity. Doctors may not always get good patients, but we must always be good to our patients.
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Saturday, June 13, 2009

Chronic Kidney Disease ( CKD ) Overview


CKD as an Underrecognized Threat to Patient Safety

Jeffrey C. Fink, MD; Jeanine Brown, MS; Van Doren Hsu, PharmD; Stephen L. Seliger, MD; Loreen Walker, BS; Min Zhan, PhD

Chronic kidney disease (CKD) is common, but underrecognized, in patients in the health care system, where improving patient safety is a high priority. Poor disease recognition and several other features of CKD make it a high-risk condition for adverse safety events. In this review, we discuss the unique attributes of CKD that make it a high-risk condition for patient safety mishaps. We point out that adverse safety events in this disease have the potential to contribute to disease progression; namely, accelerated loss of kidney function and increased incidence of end-stage renal disease. We also propose a framework in which to consider patient safety in CKD, highlighting the need for disease-specific safety indicators that reflect unsafe practices in the treatment of this disease. Finally, we discuss the hypothesis that increased recognition of CKD will reduce disease-specific safety events and in this way decrease the likelihood of adverse outcomes, including an accelerated rate of kidney function loss and increased incidence of end-stage renal disease.

From American Journal of Kidney Diseases


Uric Acid and Long-term Outcomes in CKD

Magdalena Madero, MD; Mark J. Sarnak, MD; Xuelei Wang, MS; Tom Greene, PhD; Gerald J. Beck, PhD; John W. Kusek, PhD; Allan J. Collins, MD; Andrew S. Levey, MD; Vandana Menon, MD

Background: Hyperuricemia is prevalent in patients with chronic kidney disease (CKD); however, data are limited about the relationship of uric acid levels with long-term outcomes in this patient population.
Study Design: Cohort study.
Setting & Participants: The Modification of Diet in Renal Disease (MDRD) Study was a randomized controlled trial (N = 840) conducted from 1989 to 1993 to examine the effects of strict blood pressure control and dietary protein restriction on progression of stages 3 to 4 CKD. This analysis included 838 patients.
Predictor: Uric acid level.
Outcomes & Measurements: The study evaluated the association of baseline uric acid levels with all-cause mortality, cardiovascular disease (CVD) mortality, and kidney failure.
Results: Mean age was 52 ± 12 (SD) years, glomerular filtration rate was 33 ± 12 mL/min/1.73 m2, and uric acid level was 7.63 ± 1.66 mg/dL. During a median follow-up of 10 years, 208 (25%) participants died of any cause, 127 (15%) died of CVD, and 553 (66%) reached kidney failure. In multivariate models, the highest tertile of uric acid was associated with increased risk of all-cause mortality (hazard ratio [HR], 1.57; 95% confidence interval [CI], 1.07 to 2.32), a trend toward CVD mortality (HR, 1.47; 95% CI, 0.90 to 2.39), and no association with kidney failure (HR, 1.20; 95% CI, 0.95 to 1.51) compared with the lowest tertile. In continuous analyses, a 1-mg/dL greater uric acid level was associated with 17% increased risk of all-cause mortality (HR, 1.17; 95% CI, 1.05 to 1.30) and 16% increased risk of CVD mortality (HR, 1.16; 95% CI, 1.01 to 1.33), but was not associated with kidney failure (HR, 1.02; 95% CI, 0.97 to 1.07).
Limitations: Primary analyses were based on a single measurement of uric acid. Results are generalizable primarily to relatively young white patients with predominantly nondiabetic CKD.
Conclusions: In patients with stages 3 to 4 CKD, hyperuricemia appears to be an independent risk factor for all-cause and CVD mortality, but not kidney failure.

From American Journal of Kidney Diseases

coffee bean

New Formula Promises More Accurate Estimation of Kidney Function

Lynda A. Szczech, MD, MSCE

Ann Intern Med. 2009;150:604-612
Levey AS, Stevens LA, Schmid CH, et al


Creatinine has been, is now, and will be for the foreseeable future our easiest way to monitor kidney function. However, the inadequacies and limitations of creatinine as such a marker are well described. Due to the nonlinear relationship between creatinine and kidney function, as well as the effect of a patient's muscle mass on the association between absolute value of creatinine and kidney function, formulas to approximate kidney function using serum creatinine and proxies for muscle mass are essential.

The Cockcroft-Gault equation was the first widely used formula.[1] Although creatinine clearance using this equation is relatively simple to calculate, it was recognized to overestimate kidney function, and many have raised concerns on the basis of its limited generalizability. Investigators from the Modification of Diet in Renal Disease (MDRD) study subsequently derived a number of formulas to approximate kidney function using that study that performed better than the Cockcroft-Gault formula.[2,3] The formula has been widely applied in both clinical care and research since its publication, but clinicians continue to discuss whether it can be used for patients with clearance of less than 60 mL/min and without diabetes mellitus.

Given these continued generalizability limitations, Levey and colleagues collaborated with multiple investigators to obtain data from studies in which the glomerular filtration rate (GFR) was measured using exogenous filtration markers and serum creatinine. Ten studies were available and were randomly divided into 2 groups for development of the new estimation equation and the internal validation of the new equation. At the Cleveland Clinical Laboratory, serum creatinine values were recalibrated to standardized creatinine measurements using the Roche enzymatic method. The equation was developed with potential clinical predictor variables of serum creatinine, age, race (black vs white and other), and sex. Additional variables available in some models include diabetes mellitus, previous organ transplantation, and weight.

The dataset used for development of the equation contained 5504 subjects. The mean serum creatinine was 1.65 mg/dL with a mean GFR measured at 68 mL/min, providing a robust representation of patients with milder kidney disease than was possible with the MDRD study. Approximately 29% of participants had diabetes mellitus and 32% were African American. The mean age was 47 years with limited representation of the elderly (9% between 66 and 70 years, and 3% > 71 years).

The Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formula developed is represented as the equation below, in which the values of the constants of a, b, and c vary on the basis of race, sex, and serum creatinine.

GFR = a × (serum creatinine/b) c × (0.993)age

The variable a takes on the following values on the basis of race and sex:

  • Black
    • Women = 166
    • Men = 163
  • White/other
    • Women = 144
    • Men = 141

The variable b takes on the following values on the basis of sex:

  • Women = 0.7
  • Men = 0.9

The variable c takes on the following values on the basis of sex and creatinine measurement:

  • Women
    • Serum creatinine ≤ 0.7 mg/dL = -0.329
    • Serum creatinine > 0.7 mg/dL = -1.209
  • Men
    • Serum creatinine ≤ 0.7 mg/dL = -0.411
    • Serum creatinine > 0.7 mg/dL = -1.209

The investigators compared the abilities to identify patients with various degrees of kidney disease of the new CKD-EPI formula with the MDRD formula. Although both formulas performed similarly well, in which subjects were misclassified in terms of category of kidney disease, the CKD-EPI formula was more often correct (P < .001). In the separate subset of patients designated to validate the new formula, the CKD-EPI formula demonstrated less bias and improved precision and greater accuracy than the MDRD formula (P < .001), particularly for those patients with an estimated GFR > 60 mL/min. The median difference between measured and estimated GFR was 2.5 mL/min for the CKD-EPI formula and 5.5 mL/min for the MDRD formula (P < .001).

Because of the reduced error of overestimation of kidney function, the CKD-EPI equation yielded a lower estimated prevalence of kidney disease in the National Health and Nutrition Examination Survey (NHANES) dataset. Where the MDRD equation estimated the prevalence of kidney disease at 13.1%, the CKD-EPI formula estimated it slightly lower at a prevalence of 11.5%. This limited extent to which the equation overestimates GFR reflects the major advantage of this newer formula.


The use of serum creatinine is a cheap and easy way to estimate kidney function. Although the manner in which to transform serum creatinine into an accurate measure of absolute kidney function remains a problem, this analysis takes use 1 step closer. Researchers anticipate that it will be quickly adopted in the clinical community to allow an even more accurate equation of kidney function.



babu green

Early Detection Aims to Reverse Rising Rate of Kidney Disease

(New York, NY) — The old adage "an ounce of prevention is worth a pound of cure" will take on new meaning this March as kidney experts make plans to help ensure that people at risk don't end up with kidney failure or dying an early death due to complications of the disease. Those with kidney failure require dialysis treatment or a kidney transplant in order to stay alive.

Led by kidney specialists Dr. Andrew S. Levey at Tufts Medical Center in Boston, MA, and Dr. William McClellan at Emory University in Atlanta, GA, the panel of experts designed a comprehensive public health strategy to prevent the development and complications of chronic kidney disease in the U.S.

Commissioned by the U.S. Centers for Disease Control and Prevention (CDC), their report is published in the March issue of the American Journal of Kidney Diseases, the official journal of the National Kidney Foundation, scheduled to coincide with National Kidney Month (March) and World Kidney Day on March 12.

The treachery of chronic kidney disease, which currently affects 26 million Americans, is its silent progression in the early stages when it is most treatable. If left unchecked, the most deadly form of the disease - kidney failure - occurs when the kidneys can no longer function to filter out the body's waste products. Kidney failure is expected to affect a growing number of patients over the next decade, devouring an increasing fraction of available health care dollars.

But according to the authors, the ravages of kidney failure, also known as end stage kidney disease, can be held at bay by preventing the disease to begin with, detecting it in its earliest stages and providing treatment.

Their plan begins by targeting people who may not yet have kidney disease but are at risk, either because of their advancing age, a family history of the condition, or the presence of conditions that damage the kidneys, such as high blood pressure, diabetes, or cardiovascular disease.

The authors propose concrete measures to reduce this public health threat, such as:

  • Raising awareness of the danger among those at risk
  • Routine testing to detect the condition in its earliest stages, with a urine test to detect albumin and a blood test for creatinine to estimate the glomerular filtration rate (a measure of how well the kidneys are functioning)
  • Reducing risk by improving blood pressure control among those with hypertension
  • Reducing risk by improving blood sugar control among those with diabetes

"Equally as important is preventing progression in patients who already have chronic kidney disease," said Dr. Levey, who is a member of the National Kidney Foundation's Scientific Advisory Board. "One important measure is treating hypertension with drugs called ACE inhibitors and angiotensin-receptor blockers (ARBs) that protect the kidneys while keeping blood pressure in check."

For patients with more advanced stages of chronic kidney disease, and those with kidney failure, the panel urges continuing education for health care providers as to best treatment practices. Proper interventions for complications of reduced kidney function, such as anemia, malnutrition, and bone and mineral disorders, are necessary to prolong survival, enhance quality of life, and reduce the cost of care.

"While all the proposed measures are important, as a physician, I stress routine testing of patients at increased risk for chronic kidney disease," Dr. Levey said. "Given the high prevalence of hypertension and diabetes in the elderly, this would include testing most older individuals with a chronic medical condition."

"Routine reporting of glomerular filtration rate estimates by clinical laboratories whenever serum creatinine is measured has been a big help, and should receive continued emphasis," adds Dr. Kerry Willis, Senior VP for Scientific Activities, National Kidney Foundation.

Of paramount importance to the success of this initiative, the specialists say, is their final recommendation to increase public awareness of chronic kidney disease in order to improve health-related decisionecommendation to increase public awareness of chronic kidney disease in order to improve health-related decision-making.

In order to enact these recommendations, "Cooperation among federal, state and local governmental and private organizations will be necessary," noted Dr. Levey.

As a first step towards increasing public awareness of and making early detection as easy as possible, the National Kidney Foundation is offering 50 free screenings in locations around the U.S. on World Kidney Day, March 12 through the Kidney Early Evaluation Program (KEEP). KEEP is offered to those at risk -anyone with diabetes, high blood pressure or a family history- with the goal of preventing kidney disease from becoming kidney failure. For locations and schedules, visit

The National Kidney Foundation is dedicated to preventing and treating kidney and urinary tract diseases, improving the health and well being of individuals and families affected by these diseases, and increasing availability of all organs for transplantation.

To learn more about CKD risk factors, prevention and treatment, contact the National Kidney Foundation at or (800)622-9010.


Treatment of Chronic Kidney Disease After Solid Organ Transplantation

Robert J. Stratta, MD

Kidney Transplantation in Previous Heart or Lung Recipients
Lonze BE, Warren DS, Stewart ZA, et al
Am J Transplant. 2009;9:578-585

Should Heart, Lung, and Liver Transplant Recipients Receive Immunosuppression Induction for Kidney Transplantation?
Ranney DN, Englesbe MJ, Muhammad W, et al
Clin Transplant. 2009 Feb 17. [Epub ahead of print]


Using national data from the United Network for Organ Sharing (UNOS), Lonze and colleagues evaluated outcomes in 568 kidney after heart (KAH) and 210 kidney after lung (KAL) transplants performed between 1995 and 2008. Median time to kidney transplant was 100.3 months after heart and 90.2 months after lung transplant.

Renal failure was attributed to calcineurin inhibitor toxicity in 69% of KAH and 82% of KAL transplants. In a smaller proportion of cases, renal failure was attributed to hypertensive nephrosclerosis (7% KAH, 5% KAL) or diabetic nephropathy (6% KAH, 1.4% KAL). Outcomes were compared to matched controls to account for numerous pertinent characteristics.

Although 5-year renal graft survival rates were lower than those in primary kidney recipients in matched controls (61% KAH vs 73.8% controls, 63% KAL vs 83% controls, both P < .001), 5-year death-censored-graft survival rates were comparable (85% KAH vs 88% controls, 88% KAL vs 90% controls, both P = NS). Graft survival rates were higher in all populations (KAH, KAH, controls) of live donor compared to deceased donor kidney recipients.

Kidney transplantation reduced the risk for mortality compared with dialysis by 43% for KAH and 54% for KAL recipients. The authors concluded that renal grafts function well and provide survival benefit in KAH and KAL recipients, but are limited in longevity by the general life expectancy of these recipients.

In the second single center study of 42 kidney recipients following heart (n = 11), lung (n = 2), or liver (n = 29) transplantation, 21 patients received antibody induction (14 Thymoglobulin®, 5 ATGAM®, 2 Simulect®) and 21 were managed without antibody induction.

Patients receiving antibody induction had more delayed graft function (48% vs 9.5% without induction, P = .004) and trends toward more infections (47% vs 29% without induction), fewer acute rejection episodes (9.5% vs 14.3% without induction), more readmissions (65% vs 45% without induction), and lower 1-year patient and graft survival rates (both 81% vs 95% without induction, all P = NS).

Based on these results, Ranney and colleagues concluded that there is a trend toward lower patient and graft survival rates and greater morbidity among patients receiving antibody induction vs no induction following KAH, KAL, or kidney after liver transplantation.


Chronic renal failure is an increasingly recognized long-term complication of solid organ transplantation. Chronic kidney disease in the transplant population is associated with a 4- to 5-fold increased risk of death. The 5-year risk of chronic renal failure after transplantation of a nonrenal organ ranges from 7% to 21%, depending on the type of organ transplanted.

Treatment of end-stage renal disease with kidney transplantation in the nonrenal organ transplant population has been associated with a nearly 50% reduction in mortality compared to other renal replacement therapy options. Calcineurin inhibitor therapy, which remains the mainstay of contemporary immunosuppressive regimens, has been implicated as the major cause of posttransplant renal dysfunction due to nephrotoxicity.

Multiple other factors contribute to the development of chronic kidney disease following nonrenal organ transplantation. These include acute tubular necrosis/perioperative renal failure, sepsis, use of diuretics, exposure to radiographic contrast agents, atheroembolism, acute interstitial nephritis, anemia, ventricular dysfunction, increasing recipient age, female recipient gender, diabetes, hypertension, dyslipidemia, hepatitis B or C infection, or administration of other nephrotoxic drugs.

Ironically, the development of chronic kidney disease has become an unexpected measure of success following nonrenal solid organ transplantation because it correlates with longevity and in some respects may be inevitable until safe and efficacious nonnephrotoxic chronic immunosuppression is introduced into clinical transplantation. It is important to note that kidney transplantation in the setting of chronic immunosuppression because of a previous nonrenal organ transplant may pose unique challenges because these patients are considered "high risk" not only from a medical and immunological standpoint, but also "medically urgent" from a transplant perspective.

In the presence of delayed graft function following kidney transplantation, the complexities of patient outcomes underscore the need to carefully weigh the risks for and benefits of antibody induction immunosuppression in these chronically immunosuppressed, chronically ill, and usually elderly patients. Moreover, these patients may not tolerate kidney delayed graft function, which further highlights the role for living donor kidney transplantation in this patient population.