UCSD's Practical Guide to Clinical Medicine
A comprehensive physical examination and clinical education site for medical students and other health care professionals
|Introduction||Breast Exam||Write Ups|
|History of Present Illness||The Pelvic Examination||The Oral Presentation|
|The Rest of the History||Male Genital/Rectal Exam||Outpatient Clinics|
|Review of Systems||The Upper Extremities||Inpatient Medicine|
|Vital Signs||The Lower Extremities||Clinical Decision Making|
|The Eye Exam||Musculo-Skeletal Exam||Physical Exam Lecture Series|
|Head and Neck Exam||The Mental Status Exam||A Few Thoughts|
|The Lung Exam||The Neurological Exam||Commonly Used Abbreviations|
|Cardiovascular Exam||Physical Exam Check Lists||References|
|Exam of the Abdomen||Medical Links|
The "daVinci Anatomy Icon" denotes a link to related gross anatomy pictures.
Note: A test should only be obtained if the result will in some way affect your decision making. That is, if you are going to embark on a particular strategy regardless of the results, why obtain it in the first place? Furthermore, if you don't understand the operating characteristics of a test (e.g. it's sensitivity and specificity and thus how the results will affect your view of the candidate diagnosis), don't order it.
Case 1: A 24 year old otherwise healthy male presents with a 3 day history of cough productive of green sputum, fever, chills and slight shortness of breath associated with right sided chest pain. Exam is remarkable for a temperature of 102 F with otherwise normal vital signs. The patient looks well (i.e. not distressed). A few crackles are noted in the right base on lung exam. No other abnormalities are apparent.
Discussion: Following the above question template, we can reason through the case as follows:
1 & 2: This clinical situation seems most consistent with a well compensated bacterial pneumonia. Other possibilities might include:Example 2, by design, is a bit more murky.viral infectionEach, however, either cannot explain all of the findings present or is not supported by the objective data. A viral infection, for example shouldn't cause a focal lung exam; asthma can cause a cough and shortness of breath, but wheezing should be present; while a pulmonary embolism can cause shortness of breath, cough and chest pain, it should not result in fever, chills or sputum production. Furthermore, P.E.s generally occur in patient's who have risk factors for this illness, none of which were present in this case. "Other" includes the list of unlikely diagnoses (e.g. eosinophilic pneumonitis, histoplasmosis, malignancy etc.) that would only be considered if the patient's course deviated markedly from expected and/or could not be explained on the basis of those things higher on the differential.
pulmonary embolism (P.E.)
3&4: Many clinicians would feel comfortable enough at this point (based on their clinical impression) to proceed without obtaining any additional tests to either support the candidate diagnosis or rule out other possibilities. Other approaches would also be acceptable. For example, another clinician may have seen a similar case in the past, treated the patient for a bacterial process, and found out later that they had actually had a P.E. Because of this experience, they might be uncomfortable proceeding without first obtaining a CXR (to confirm the presence of an infiltrate), CBC (to identify a leukocytosis c/w a bacterial infection), D-Dimer (clot breakdown product elevated in DVTs/PEs), and an EKG (to look for stigmata of a P.E.). This approach would not necessarily be incorrect. It's driven by a particular provider's anecdotal experience, which for obvious reasons has a powerful impact on future decision making. This is generally helpful, as long as it is based on logic and not fear. You might then wonder, "Why not obtain confirmatory tests whenever possible?" Remember, tests come at a cost (in terms of dollars, time and patient discomfort). You need to be able to justify, at least in your own mind if not that of the insurance company, the expense. Furthermore, the expected value of any test is dependent on the situation in which it is being applied. In general, as few tests in medicine have 100% sensitivity and specificity (i.e. correctly identify those with and without disease all of the time), the likelihood that a result is correct is dependent on how strongly you already feel about the candidate diagnosis. That is, if you are certain that someone is suffering from a particular disease (on the basis of history, exam and other findings) and you order an additional test "just to make sure" then the results of the test aren't likely to have a significant impact on your decision making (i.e. if it confirms your suspicions, so what; if it conflicts, you'll ignore it, treating the result as a false negative). The same principles apply in the reverse situation (i.e. if you are certain that someone does not have a particular illness). Tests have their greatest value when applied to situations where you're truly on the fence about a particular diagnosis. An in depth discussion of this subject can be found in any text under Baysean Analysis.
5: In this setting, I would probably not be comfortable waiting for the process to "play out" any further without initiating therapy. Bacterial processes tend to worsen unless they are treated, even in otherwise healthy 23 year olds.
6: Therapy in this case could be initiated on an outpatient basis with an antibiotic directed against Strep and H. Flu, the pathogens most commonly associated with respiratory infections in this age group. Treatment would last for a total of 7 days (a somewhat arbitrary number) and the patient instructed to return for re-evaluation on the last day of therapy to insure that the infection was completely treated and that the antibiotics could be discontinued. In addition, they would be told to contact me if they felt worse. If this, in fact, occurred I would have to consider why things did not go as I had anticipated. Did the patient have an atypical infection (e.g. Legionellosis)? Were they non-compliant with medications? Had they developed a complication (e.g. empyema)? Were they suffering from a particularly virulent strain of bacterium? Or was the initial diagnosis (e.g. infectious process) correct in the first place? The only way to make this determination (and catch the rare zebra) would be through re-evaluation of the patient, applying additional tests in a logical and ordered fashion.
Case 2: A 55 year old male with history of Chronic Obstructive Pulmonary Disease (COPD), Coronary Artery Disease (CAD), and past Pulmonary Embolism (P.E.) presents with several hours of chest pain radiating to his left arm associated with shortness of breath and diaphoresis. This is somewhat reminiscent of his past myocardial infarction, but is also similar to past admissions for COPD and his P.E. ... he's just not sure. Exam is remarkable for a pale gentleman who looks quite distressed, sweating profusely. Vital signs remarkable for Temp 99 P 110 BP 180/100 RR 30 Sat 91%. JVP is at 8cm. Lung exam is remarkable for diffuse wheezing. Patient has bilateral lower extremity edema (1+ to the mid shin) with the right leg slightly more swollen then the left, which he says has been present since his DVT and subsequent PE several years ago.
Discussion: We will approach this case in the same way as the previous example.
1&2: An exacerbation of any of this patient's underlying conditions could explain his presentation. On the basis of the history and examination, recurrent cardiac ischemia, a flair of his COPD or another P.E. are all possible. Additionally, this could represent new Congestive Heart Failure (CHF), perhaps associated with ongoing cardiac ischemia. Although he has never had this before, I know that CHF tends to occur in patients with CAD (which this patient does have) and can cause a clinical picture similar to that presented above. A bacterial infection (either bronchitis or pneumonia) is usually accompanied by additional symptoms (e.g. fever, chills, sputum production), but remains a possibility, particularly as I know that COPD flairs usually occur in association with such an infection. Bringing up the rear would be "other" which would include, but not be restricted to, the initial presentation of a lung cancer or a pneumothorax. These processes do occur in patients with COPD but tend to present with other exam/historical findings (e.g. malignancy is often associated with weeks-to-months of weakness, fatigue, weight loss and a focal lung exam; pneumothorax causes decreased/absent breath sounds on the affected side). Ordering these possibilities from most to least likely, I would put coronary ischemia/CHF and P.E. 1 and 2, followed by COPD flair, pneumonia and "other." In this case, I am impressed by the acuity of the presentation, which has increased my suspicion for the first 2 processes. The others, however, remain reasonable diagnostic possibilities which cannot be ruled out on a clinical basis.There are a few themes that are common to both cases and help guide decision making in general:
3&4: All of the above conditions carry significant morbidity and/or mortality. In addition, treatment strategies for each are quite different, and may themselves carry risk. Anti-coagulation with heparin, for example, would be useful in patients with PEs but has no role in the treatment of a COPD flair, and would unnecessarily expose the patient to the risk of bleeding. There is also a sense of urgency that surrounds the need to make the diagnosis and begin treatment as:
The following tests, essentially performed simultaneously, are necessary in order to rapidly make a diagnosis:
- the patient appears ill, with clear potential for further deterioration
- some of the treatments are only effective if applied within a narrow window of opportunity (e.g. thrombolytics can open an occluded coronary artery and save downstream myocardium only if they are given soon after the onset of ischemia).
- EKG... to assess for evidence of acute myocardial infarction or stigmata of PE
- CXR... to evaluate for signs of CHF, PE, infiltrate... will also identity pneumothorax or evidence of malignancy
- CBC... to asses for anemia which could be a precipitant for cardiac ischemia or shortness of breath; might also suggest a bacterial process if the white blood cell count is elevated.
- Chem 7 (includes electrolytes, BUN, Creatinine, Glucose)... might be helpful in determination of volume status; also useful if patient will need diuretic therapy if diagnosed with CHF.
- Arterial Blood Gas... to define Alveolar-arterial gradient and degree of gas exchange abnormality
- CK-MB, Cardiac Troponins... will be elevated if patient has suffered a myocardial infarction.
- D-Dimer... elevated in cases of DVT/PE
- BNP (B-type naturetic peptide)... elevated in cases of CHF
The test results are as follows:
EKG remarkable for sinus tachycardia at 110, non-specific ST segment changes in the inferior and precordial leads.
CXR consistent with moderate emphysema; no evidence infection, pneumothorax or malignancy; ? upper zone vascular redistribution consistent with CHF
Chem 7 and cardiac enzymes all normal.
CBC... mildly elevated White Blood Cell Count (14 thousand) with normal differential; normal hematocrit
ABG... PO2 50, PCO2 30, PH 7.5... c/w hypoxemia and acute respiratory alkalosis
D-Dimer...600 (moderately elevated)
BNP 300 (mildly elevated)
The diagnosis still remains in doubt. The data does not support an acute myocardial infarction, though unstable angina without myocardial necrosis is still a possibility. There is nothing to suggest a pneumonia, pneumothorax or malignancy, which we thought were unlikely. I would now re-order my differential, placing pulmonary embolism at the top followed by COPD exacerbation, CHF and unstable angina. I still need to press on and make use of additional tests in order to identify the correct diagnosis and institute appropriate therapy. In this case I would obtain a radiologic test known as a CT-angiogram of the chest to assess for evidence of a pulmonary embolism. If this were negative, I would then be left with a diagnosis of COPD, CHF or unstable angina. Further treatment would be based on the clinical course, response to therapy, and if, in fact, there were any additional means of distinguishing between these possibilities.
5&6: Because this patient is rather ill, treatment should occur in concert with the diagnostic evaluation and would include:
Thrombolytics are not indicated. Nor would I initiate therapy with any of the more potent platelet inhibiting agents (the 2a/3b receptor antagonists), as these carry a higher risk of bleeding (at least until that point when unstable angina was more clearly the leading diagnosis). As additional data became available, I would need to continually re-evaluate all of these decisions.
- Oxygen: The patient is hypoxemic and would benefit from oxygen, regardless of the underlying cause.
- Heparin: As it may take some time before the CT scan is performed, I would elect to begin therapy with heparin while waiting to obtain the study. This decision is based on my high clinical suspicion that the patient has had an embolous. Because he already appears pretty sick and compromised, I would be uncomfortable withholding therapy that could prevent additional (and perhaps catastrophic) emboli. Furthermore, anti-coagulation would also be used as first-line treatment for unstable angina, which is #2 on my differential. Only in the setting of COPD flair (#3) would heparin be inappropriate. In this case, I have decided that the potential benefit of heparin out weighs the short term risk of bleeding.
- Aerosolized Albuterol (a beta-2 agonist): I would also give the patient a breathing treatment with nebulized albuterol to see if it relieved any of his bronchospasm.
- Lasix: This would help improve hypoxemia in the event that some component of the patient's illness is caused by CHF. While I have no way of knowing definitively that he does have pulmonary edema and would therefore benefit from diuresis, there are few other therapeutic options that would have a rapid, dramatic impact on his gas exchange. He certainly does not appear intravascularly depleted, a situation where Lasix would be dangerous. By my calculations then, the potential benefits of this treatment outweigh its risks.
- Steroids: Another therapeutic option would be to give him a dose of intravenous steroids for his possible COPD. A single dose of steroids has little downside. I also know that it takes a while (at least several hours) to have an effect. Thus, particularly if it will take some time to get the V/Q scan, I would probably opt to initiate steroid therapy, which could always be discontinued if the results were consistent with a P.E.
- Antibiotics: Since COPD remains high on my list, and COPD flairs are most frequently precipitated by bacterial infections, it's logical to treat for this potential problem as well.
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