A 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||Male Genital/Rectal Exam||The Oral Presentation|
|The Rest of the History||The Upper Extremities||Outpatient Clinics|
|Review of Systems||The Lower Extremities||Inpatient Medicine|
|Vital Signs||Musculo-Skeletal Exam||Clinical Decision Making|
|The Eye Exam||The Mental Status Exam||Physical Exam Lecture Series|
|Head and Neck Exam||The Neurological Exam||A Few Thoughts|
|The Lung Exam||Physical Exam Check Lists||Commonly Used Abbreviations|
|Cardiovascular Exam||Medical Links||References|
|Exam of the Abdomen|
The "daVinci Anatomy Icon" denotes a link to related gross anatomy pictures.
Chief Complaint or Chief Concern (CC):
One sentence that covers the dominant reason(s) for hospitalization. While this has traditionally been referred to as the Chief Complaint, Chief Concern may be a better description as it is perhaps less pejorative/confrontational sounding.
"Mr. Smith is a 70 year old male admitted for evaluation of increasing chest pain."History of Present Illness (HPI):
"Mr. S is a 70 yr old male with known coronary artery disease who is:That's a rather complicated history. However, it is obviously of great importance to include all of the past cardiac information "up front" so that the reader can accurately interpret the patient's new symptom complex. From a purely mechanical standpoint, note that historical information can be presented as a list (in the case of Mr. S, this refers to his cardiac catheterizations and other related data). This format is easy to read and makes bytes of chronological information readily apparent to your audience. While this data is technically part of the patient's "Past Medical History," it would be inappropriate to not feature this prominently in the HPI. Without this knowledge, the reader would be significantly handicapped in their ability to understand the patient's current condition. Knowing which past medical events are relevant to their area of current concern takes experience. In order to gain insight into what to include in the HPI, continually ask yourself, "If I was reading this, what historical information would I like to know?" Note also that the patient's baseline health status is described in some detail so that the level of impairment caused by their current problem is readily apparent to the reader.
-Status Post 3 vessel CABG in 4/82.
-Suffered recurrent chest pain in 12/93 which ultimately lead to catheterization and stent placement in a mid-LAD lesion.
-Recathed in 1/95 for recurrent chest pain at rest; at that time there was no significant change compared to cath of 12/93; patient was therefore continued on medical therapy.
-Known to have an Ejection Fraction of 30% with inferior and lateral akinesis by echo in 2/96
-No prior episodes of heart failure.
-Last Exercise Tolerance Test was performed in 1/97 and showed no ischemia at 10 METS of activity.
Mr. S was well until last week (9/97), when he began to experience recurrent episodes of chest pain, exactly like his past angina, after walking only one block. This represented a significant change in his anginal pattern, which is normally characterized as mild discomfort which occurs after walking vigorously for 8 or 9 blocks. In addition, 1 day prior to admission, the pain briefly occurred while the patient was reading a book. He has also noted swelling in his legs over this same time period and has awakened several times in the middle of the night, gasping for breath. In order to breathe comfortably at night, Mr. S now requires the use of 3 pillows, whereas in the past he was always able to lie flat on his back without difficulty. Mr. S is known to have poorly controlled diabetes and hypertension. He currently smokes 2 packs of cigarettes/day. He denies fevers, chills, cough, wheezing, nausea vomiting or other complaints."
The remainder of the HPI is dedicated to the further description of the presenting complaint. As the story teller you are expected to put your own spin on the write-up. That is, the history is written with some bias. You will be directing the reader towards what you feel is the likely diagnosis by virtue of the way in which you tell the tale. If, for example, you believed that the patient's chest pain was of cardiac origin, you would highlight features that supported this notion (e.g. crushing chest pain with activity, relieved with nitroglycerin, preponderance of coronary risk factors etc.). These are referred to as "pertinent positives." This is not misleading; all of the details written are based on facts and no important features have been omitted. The reader retains the ability to provide an alternative interpretation of the data if he/she so wishes. A brief review of systems related to the current complaint is generally noted at the end of the HPI. This also includes "pertinent negatives" (i.e. symptoms which the patient does not have). If present, these symptoms might lead the reader to entertain alternative diagnoses. Their absence, then, lends support to the candidate diagnosis suggested in the HPI.
Occasionally, patients will present with two (or more) dominant, truly unrelated problems. First, spend some extra time and effort assuring yourself that they are truly unconnected and worthy of addressing in the HPI. That being the case, present them as separate HPIs, each with its own paragraph.
Past Medical History (PMH):
This should include any illness (past or present) for which the patient has received treatment. Items which were noted in the HPI (e.g. the cardiac catheterization history mentioned previously) do not have to be re-stated. You may simply write "See above" in reference to these events. All other historical information should be listed. Detailed descriptions are generally not required. If, for example, the patient has hypertension, it is acceptable to simply write "HTN" without giving an in-depth report on the duration of this problem, medications used to treat it, etc. (unless this has been a dominant problem, requiring extensive evaluation...as might occur in the setting of Secondary Hypertension resulting from Renal Artery Stenosis). Also, get in the habit of looking for the data that supports each diagnosis that the patient is purported to have. It is not uncommon for misinformation to be perpetuated when past write-ups are used as the template for new H&Ps. When this occurs, a patient may be tagged with (and perhaps even treated for) an illness which they do not have! For example, many patients are noted to have Chronic Obstructive Pulmonary Disease (COPD). This is, in fact, a rather common diagnosis but one which can only be made on the basis of Pulmonary Function Tests (PFTs). While a Chest X-Ray and smoking history offer important supporting data, they are not diagnostic. Thus, it is not unusual to see "COPD" repeatedly appear under a patient's PMH on the basis of a suggestive CXR and known smoking history, despite the fact that they have never had PFTs! So, maintain a healthy dose of skepticism when reviewing old records and get in the habit of checking on the primary information yourself.
Past Surgical History (PSH):
All past surgeries should be listed, along with the rough date when they occurred.
Includes all currently prescribed medications as well as over the counter and non-traditional therapies. Dosage and frequency should be noted.
Identify the specific reaction that occurred with each medication.
Social History (SH):
This is a broad category which includes:
Family History (FH):
This includes history of illnesses within the patient's immediate family. In particular, seach for a history of cancer, coronary artery disease or other heritable diseases among first degree relatives.
Obstetrical History (where appropriate):
Review of Systems (ROS): As mentioned previously, the most important ROS questioning (i.e. pertinent positives and negatives related to the chief complaint) is generally noted at the end of the HPI. The responses to a more extensive review which covers all organ systems are placed in this "ROS" area of the write-up. In actual practice, most providers do not document such an inclusive ROS. The ROS questions, however, are the same ones that, in a different setting, are used to unravel the cause of a patient's chief complaint. Thus, at this stage of your careers it is probably a good idea to practice asking all of these questions as well as noting the responses so that you will be better able to use them for obtaining historical information when interviewing future patients.
Generally begins with a one sentence description of the patient's appearance.
HEENT: Includes head, eyes, ears, nose, throat, oro-pharynx, thyroid.
Extremities, Including Pulses:
Lab Results, Radiologic Studies, EKG Interpretation, Etc.:
Assessment and Plan:
It's worth noting that the above format is in no way written in stone. When you're exposed to other styles, think about whether the proposed system is logical and readily comprehensible. Then incorporate those elements that make sense into your future write-ups.
SAMPLE WRITE UP #1
01/27/98 MEDICAL SERVICE STUDENT ADMISSION NOTE
Mr. "B" is a 72 yo man with h/o CHF and CAD, who presented with increasing lower extremity edema and weight gain.
HPI: Mr. "B" has a long history of CHF subsequent to multiple MI's last in 1991. Cardiac cath at that time revealed occlusions in LAD, OMB, and circ with EF of 50%. ECHO in 1996 showed a dilated LV, EF of 20-25%, diffuse regional wall motion abnormalities, 2+MR and trace TR. His CHF has been managed medically with captopril, lasix, metolazone, and digoxin. Over the past 6mos he has required increasing doses of lasix to control his edema. He was seen 2 wks ago by his Cardiologist, at which time he was noted to have leg, scrotal and penile edema. His lasix dose was increaed to 120 bid without relief of his swelling.
Over the past week he and his wife have noticed an increase in his LE edema which then became markedly worse in the past two days. The swelling was accompanied by a weight gain of 10lb in 2 days (175 to 185lb) as well as a decrease in his exercise tolerance. He now becomes dyspneic when rising to get out of bed and has to rest due to SOB when walking on flat ground. He has 2 pillow orthopnea, denies PND. His chronic cough has worsened and is now productive of "transparent" sputum with no hemoptysis. He has occ audible wheeze. Denies CP/pressure/palpitations/diaphoresis. Occ nausea/no vomiting. He eats limited quantities but does not salt or fluid restrict--eating canned soup and drinking 6-8 glasses liquid/day. He has increased urinary freq. but decreased amount. He states he has been taking all prescribed medications.
CHF: as above
Afib: on coumadin
Pacemaker placed in 3/93 for afib/flutter and slow ventricular response
Chronic renal insufficiency: BUN/Cr stable on 1/21/98, 52/1.4
DM: controlled with glyburide. Admitted for hypoglycemia in 9/97.
Lasix 120 mg BID
Metolazone 5 mg gd
Captopril 50 mg TID
Digoxin 0.125 mg qd
coumadin 4mg qd
Glyburide 2.5 mg BID
Colace 100 mg BID
|ALLERGIES:||No Known Drug Allergies|
|OTHER SUBSTANCE USE||None|
|SOCIAL HISTORY:||Married for 45 years, sexual active with wife. Three children, 2 grandchildren, all healthy and well; all live within 50 miles. Retired school teacher. Enjoys model car building. Walks around home, shopping but otherwise not physically active.|
|FAMILY HISTORY||+ sister and mother with DM, father with CAD, age onset 50. Brother with leukemia.|
|ROS||If written, would be present here.|
VS: T 97.1, P65, BP 116/66, O2Sat 98% on 2L NC
GEN: elderly man lying in bed with head up, NAD
HEENT: NCAT, multiple telangiectasias on face and nose, EOMi, PERRL, OP-benign
NECK: thyroid not palpable, no LAD, carotic pulse 2+B, no bruits, no JVD
RESP: +dullness to perc at right base, +ant wheezes, +crackles 1/2 way up chest bilat.
COR: rrr, +2/6 holosystolic murmur at apex radiating to axilla, no gallops
ABD: +BS, distended, nontender, no HSM, liver percussed to 9cm at MCL
PULSES: 2+femoral B, 1+ PT/DP B
EXT: 3+ edema to lower back, abdomen including genitals, hyperemia over ant., legs bilat, warm, non-tender; non clubbing, cyanosis
SKIN: 4 cm ulcer on R buttock with central scabbing, non-tender, no discharge
NEURO: AOX3; difficulty remembering events, dates; remainder of exam nonfocal
Na 138, C1 96, BUn 59, Glu 92, K 4.4, CO2 40.8, CR 1.4, WBC 7.9, PLT 349, HCT 43.9, pulses P73 L16 E3 B0
Alk phos 72, Tot prot 5.6, Alb 2.5 T Bili 0.5, AlT 17, AST 52, LDH 275, CPK 229
CXR: mildly prominent vessels. Minimal interstitial congestion. Cardiomegaly, no infiltrates.
ECHO 1/27: 1. LV mild dilated (ED=6.0 cm) severaly depressed global systolic function with EF 20-25%. Extensive area thinning and akinesis: anterior, anteroseptal, anterolateral c/w old infarct
72 year old man with h/o CHF following MI, chronic renal insufficiency and venous stasis admitted with worsening edema and DOE. His symptoms are most consistent with incrasing CHF-biventricular-which would account for both his pulmonary congestion as well as his peripheral edema. His renal disease is a less likely explanation for his extensive edema as his BUN/Cr have remained stable throughout. However, his low albumin which could contribute to his edema may be due to renal losses.
So if his edema is due to CHF, why has it become gradually and now acutely worse? Possibilities include: 1) worsening LV function, 2) another MI, 3) worsening valvular disease, 4) poor compliance with medications or 5) excess salt and water intake. His ECHO today shows no change in his EF, but there is marked wall motion abnormalities with akinesis. There is no evidence in his history, EKG, or enzymes for current ischemia/infarct. He does have MR and TR and his valvular disease may in part account for his worsening symptoms though his estimated PA pressure is unchanged and his LA is not dilated. The most likely precipitant of his failure is a combination of poor compliance with medication and fluid overload from excessive intake. We will continue to investigate the possibility of a structural precipitant for his deterioration and treat his current symptoms.
SAMPLE WRITE-UP #2
01/19/98, 21:44 MEDICAL SERVICE STUDENT ADMISSION NOTE
Mr. "S" is a 65 year old man with a history of Atrial Fibrillation, S/P Distant stroke, who has been off anticoagulation for 4 mos during evaluation of slow GI Bleed. He presents with 2 complaints:
1. Acute eye pain with difficulty seeing.
2. Several day history of a cough.
HPI: 1. Visual changes: Patient has a known history of atherosclerotic and hypertensive cerebrovascular disease: workup for dizziness/?TIA's in 94/95 revealed critical carotid stenosis and old R basal ganglia and L occipital infarcts on CT. A cerebral angiogram was complicated by a CVA manifested as R arm weakness with resolution. He subsequently had a R CEA in 1995 and no further TIA's.
Patient has had PAF for past 2+ years. ECHO in 1996 showed nl EF and marked LA enlargement (6cm) with mild-mod MR. Hehad been anticoagulated with coumadin until last summer. Developed GIB and chronic iron def. anemia. Coumadin d/c'd prior to colonscopy in Sept. and has not been restarted.
Yesterday morning while eating lunch patient had the sudden onset of sharp, R eye pain accompanied by decrease in vision. Pain was worse with coughing, unchanged by position, unrelieved by tylenol, aspirin or percocet. When the pain started, he "couldn't see the clock." He also had difficulty determining the numbers on the telephone. No blurred vision or diplopia. Vision is the same whether he covers right or left eye. He had nausea and vomiting x2--NB/NB at the onset of the pain. Was unable to give niece directions to hospital--unable to decide whether to make right or left turns. Pain and visual changes persisted through the night. No photophobia. No dizziness, weakness, dysarthria, CP, palpitations.
2. Cough: Patient has history of COPD with 60+ pack year smoking history and most recent PFT's showing mild deficits. Over the past few days he has noted increased dyspnea, wheezing, and sputum production. Sputum still clear, no hemoptysis and no fevers noted. No orthopnea or PND.
? CAD: ETT 7/96 6 min Bruce HR 134 showed 1mm upsloping ST seg depressions and MIBI with lg fixed anteroapical and anterinf defect
Seizure disorder - though patient does not recall last event or details of evaluation
GI Bleed: Intermittent heme + stools. Colonscopy on 9/97 showed 2 cm polyp. Biopsy showed adenoma. Patient declined polypectomy.
Anemia: Extensive workup consistently shows iron deficinecy anemia with last HCT 12/97 at 30.
H/O asbestos exposure
Bilateral shoulder bursitis.
R orchiectomy at age 5 for traumatic injury
Cataract s/p removal and implant placement on right
Ecotrin 325 mg po qd
Verapamil SA 180 po qd
Lansoprazole 15 po qd
Dilantin 300 po qhs
Atrovent 4 puffs QID
Vanceril 4 puffs BID
Colace 100 mg po BID
|ALLERGIES:||No Known Drug Allergies|
|SMOKING||60 pack year hx, now 1 pack per day.|
|ALCOHOL||Heavy use in past, quit 5 years ago. None current.|
|OTHER SUBSTANCE USE||None|
|SOCIAL HISTORY:||Lives with roommate in Rockland, MA. Heterosexual, not currently active. Never married, no children. Worked in past as architect, though currently on disability. Enjoys walking and reading.|
|FAMILY HISTORY||Brother and father with CAD. Brother with CABG at age 55. Father with multiple strokes. Mother with DM.|
VS: T 100.2, P89, irreg irreg BP 139/63, RR 35 O2 Sat 98% RA
GEN: Obese, pale man turning his head side to side to see us with labored breathing.
HEENT: NCAT, pupils L larger than R. Both reactive to light. Discs sharp. EOMI. Left Homonymous hemianopia. Temporal arteries nontender. Conjunctiva clear. Decreased hearing of high freq on left. OP-benign
NECK: CEA scar on right. No LAD. No JVD. Carotic pulse 2+ on right, 1+ on left.
RESP: CTP. + audible wheeze. Good aearation. Occ. Wheezes on ausc throughout. Coarse insp crackles at bases
CAR: PMI at L lower sternal border. nl s1/s2. II/VI systolic crescendo-decrescendo murmur at LUSB.
ABD: Obese + nl BS. Soft. Nontender. Liver nonpalpable. Liver 10cm at MCL.
RECTAL: OV neg in ER
MS: Decreased ROM at shoulders
PULSES: Fem R 2+ L +1. DP 2+ B. PT 1+ B
EXT: ? clubbing, no cyanosis. No edema. Warm, well-perfused.
NEURO: AOX3; Able to see clock, unable to tell time. Unable to give directions from home to grocery store. Speech intact. Naming intact. Drawing clockface required prompting to put in numbers on left side. Min neglect for left side.
CN: II: as above
III, IV, VI: as above
V: decreased light touch on right, MM 5/5 B
VII: muscles of facila expression intact
IX, X: palate symmetric
XI: SCM, Trap 5/5
XII: Tongue midline
Motor: Strength 5/5:biceps, triceps, grip, quad, hamstring, plantarflex, dorsiflex. F-N slight int. tremor on left. RAM: slowed on left. ? pronator drift on left. Gait: unsteady. Able to walk on heels not toes.
Sensory: Slightly decreased light touch on right. Romberg neg.
Reflexes: Biceps/triceps/brachio: 1+ B. Knee/ankle: 0 Toes equivocal.
Labs 1/19. Na 138, C1 106, BUn 13, Glu 99, K 4.5, CO2 25.4, CR 0.7, WBC 12.2, PLT 597, HCT 22.4, MCV 72.5, pulses P73 L16 E3 B0
Alk phos 72, T prot 7.2, Alb 3.1, ALT 9, AST 14, Alk phos 75, LDH 123, TB 0.5, Dilantin Less than 2.5, PT 13.5, INR 1.3, PTT 21.1
Head CT: new well-demarcated infarct in R occipitoparietal region. Old lacunar infarcts and L occipital infarct. No evidence hemorrhage. No shift in midline.
65 year old man with h/o PAF, HTN, CVA now presents with visual field deficits and spatial perception difficulty. Story of the sudden onset of neurologic deficits while awake, eating lunch in the setting of chronic intermittent atrial fibrillation is most consistent with embolic stroke. Infarction was confirmed with CT showing lesion in R PCA distribution. Patient has multiple risk factors for cardiogenic embolization from afib: h/o previous stroke, hypertension, age over 65, increased LV size, and valvular disease. Given his carotid disease artery-artery embolization is possibility but less likely becasue 1) less common than cardiac embolization and 2) his current infarct is in the posterior curculation.
Visual disturbances could also be caused by temporal arteritis: though he does have a temporal headache, he has no tenderness and his visual defect is a bilateral loss of the left visual fields which is consistent with a cortical as opposed to a retinal injury.
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