The Blog by Ziyad Nazem

The Importance of a History & Physical Exam

I’ve been rather busy with my Internal Medicine clerkship as of late, but I thought I’d write a post on the importance of a History & Physical Exam (H&PE) in medicine. There are several basic pieces of information that can be joined to establish the proper diagnosis by us.

These are:

History (which must be accurate, skillfully elicited, carefully interpreted, and coherently expressed).
Physical Examination (which should build on the existing information and provide clues for obtaining additional history).
Ancillary data (routine and special studies, consultations, etc.).
Observations of the course of the illness (usually less expensive and more rewarding than extensive excursions in the use of ancillary studies, e.g., lab).

Our basic thesis is that the vast majority of clinical problems should and can be resolved by the effective use of the H&PE. In most cases the history should be and is the most productive. You will find this conclusively and objectively demonstrated when dealing with patients about whom no history can be obtained.

To put it another way, the diagnosis should be clear based on the present illness and related points of the history most of the time. In fact, if the diagnosis is not apparent at the end of the history and the physical examination, there is little likelihood that such will emerge by the use of ancillary data/or special studies.

Laboratory studies should be viewed and used primarily to confirm a diagnosis rather than make one. Furthermore, experience has taught us that thoughtful observation of the patient and his or her illness can be the most effective tool of complex, particularly chronic, problems.

Below is a HIPAA friendly copy of a recent complete H&PE that I wrote up regarding one of my patients —

Chief Complaint:

New onset of abdominal pain, and altered mental status.

History of Present Illness:

This is a 37 year old african american female who presents with a past medical history of cirrhosis of the liver, alcohol abuse, and esophageal varices. The patient was brought in to the emergency department, and subsequently admitted after having abdominal pain in the RUQ for one day prior to her admission. The patient developed pain which radiates to the right side. Additionally, she also admits to having dark stools, sore throat, and a non-productive cough. Upon questioning, she denies fever or chills, but admits to binge drinking for the past seven (7) days.

Review of Systems:

Constitutional Symptoms: Patient presents with some generalized fatigue and lethargy, abdominal pain, and is sleepy, but can be awaken.
HEENT: Denies vertigo, rhinorrhea, congestion. Patient has dried blood in nasal passage, and admits to having a sore throat.
Cardiac: Denies racing heart, orthopnea, edema.
Pulmonary: Patient has non-productive cough, and sore throat.
Neurological: Patient has AMS, denies numbness, tingling.
GI: Patient has abdominal Pain in RUQ radiating to the right side. Tender LUQ, around the liver.
GU: Denies polyuria, burning, or pain.
Integumentary: Denies rashes, bruises.
Musculoskeletal: Patient claims of joint pain, but denies swelling.
Psychiatric: Patient denies depressive state or anxious mood, but claims to have been on an ETOH binge for seven days prior to admission.

Past Medical/Surgical History:

Patient was diagnosed with liver cirrhosis secondary to ETOH abuse in June 2008.
Patient has history of esophageal varices.
Patient has mild gastritis, leading to bleeding of the GI.
Patient has history of mild asthma.

Medications:

Aripiprazole 10mg QD PO
Thiamine 100mg QD PO
Folic Acid 1mg QD PO
Esomerprazole 40mg QD PO
Lactulose 30grams TID PO
Moriphine 2mg/ml Q4H PRN
Ipratroprium 0.5mg/2.5 Q4h
Albuterol Inh PRN
Propranolol 10mg Q12H PO
Spironolactone 50 mg BID PO

Allergies/Adverse Drug Reactions:

ASA
Trimethoprim/Sulfamethoxazole (Bactrim)

Social History:

With good reliability, the patient admits to smoking a pack per day for 20 years, as well as drinking 1 pint of alcohol a day, and binge drinking for the past seven (7) days prior to hospital admission. The patient denies any drug usage.

Family History:

With good reliability, the patient reports that her immediate brother, and mother have a PMH of HTN.

Physical Exam:

Vitals — BP: 107/58, Temp: 98.1, Pulse: 90, Resp Rate: 20, Height: 5’6”, Weight: 180 lbs.

GENERAL APPEARANCE: Well developed, well nourished, alert and uncooperative, and appears to be in no acute distress. Patient is sleepy, but can be awaken on command.
HEAD: Normocephalic.
EYES: PERRL, EOMI. Fundi normal, vision is grossly intact.
EARS: External auditory canals and tympanic membranes clear, hearing grossly intact.
NOSE: No nasal discharge. Dried blood found within nasal cavity.
THROAT: Oral cavity has some redness in the back of the throat, with a normal pharynx. No signs of inflammation, swelling, exudate, or lesions. Teeth and gingiva in good general condition.
CARDIAC: Normal S1 and S2. No S3, S4 or murmurs. Rhythm is regular. There is no peripheral edema, cyanosis or pallor. Extremities are warm and well perfused. Capillary refill is less than 2 seconds. No carotid bruits.
LUNGS: Clear to auscultation and percussion without rales, rhonchi. Patient has minor wheezing and diminished breath sounds.
GASTROINTESTINAL: Abdominal pain in RUQ, with tenderness. Patient is presenting with new increased pain in LUQ. Patient is positive for hepatomegaly. Patient is having dark stools.
MUSCULOSKELETAL: Adequately aligned spine. ROM intact spine and extremities. No joint erythema or tenderness. Normal muscular development. Normal gait.
NECK: Neck supple, non-tender without lymphadenopathy, masses or thyromegaly.
BACK: Examination of the spine reveals normal gait and posture, no spinal deformity, symmetry of spinal muscles, without tenderness, decreased range of motion or muscular spasm.
EXTREMITIES: No significant deformity or joint abnormality. No edema. Peripheral pulses intact. No varicosities.
LOWER EXTREMITY: Examination of both feet reveals all toes to be normal in size and symmetry, normal range of motion, normal sensation with distal capillary filling of less than 2 seconds without tenderness, swelling, discoloration, nodules, weakness or deformity; examination of both ankles, knees, legs, and hips reveals normal range of motion, normal sensation without tenderness, swelling, discoloration, crepitus, weakness or deformity.
NEUROLOGICAL: CN II-XII intact. Strength and sensation symmetric and intact throughout. Reflexes 2+ throughout. Cerebellar testing normal.
SKIN: Skin normal color, texture and turgor with no lesions or eruptions.
PSYCHIATRIC: The mental examination revealed the patient was oriented to person, place, and time. The patient was drowsy, but was awake-able with stimuli. The patient was able to demonstrate good judgement and reason, without hallucinations, abnormal affect or abnormal behaviors during the examination. Patient is not suicidal.
Patient reports her LMP on 09/30/2011, no mammograms preformed, and last pap smear in 2010.

Diagnostic Tests:

CBC: WBC = 7.2, Hgb = 9.6, Hct = 28.5, Plts = 116, RDW = 18.5, PT = 22.3, INR = 3.3.
CMP: Na = 138, K = 3.7, Cl = 108, Bicarb = 22, BUN = 1, Cr = 0.71, Glu = 52, Ca = 7.9, Alb = 2.0, Bili = 5.2, Alk(Ph) = 159, AST = 103, ALT = 24, Lipase = 27, Ammonia = 68.
UA/Umicro: WBC = >50, Bile = negative, Nitrate = positive, Leukocytes = moderate.

Imaging:

CT of abdomen WO contrast: Cholelithiasis with gallbladder distention. Increased ascites, NS stranding around pancreas, pyelonephritis.

Assessment & Plan of Care:

This is a 37 year old african american female with a PMH of liver cirrhosis secondary to ETOH abuse, esophageal varices, mild gastritis, asthma, and medication non-compliance who presents with both right sided pain, left sided pain. The patient also presents with hepatomegaly primarily due to liver cirrhosis due to alcoholic liver disease, along with ETOH abuse and dark stools.

Abdominal pain:
1. DDx: Acute cholelithiasis (due to gallstones causing biliary colic obstruction), alcoholic liver disease (hepatocyte injury -> liver fibrosis), alcoholic gastritis (inflammation of stomach lining), pyelonephritis (inflammation of the kidney from bacterial infection).
  1. Patient was given Levaquin and Flagyl.
Lethargy: Hepatic encephalopathy (confusion as a result from liver failure)
1. Patient was given laxative Lactulose 30G TID.
Alcoholic Liver Disease: Alcoholic liver disease is caused by chronic ETOH abuse where the body in return ends up having excess NADH, and acetyldehye which causes hepatocyte injury and liver fibrosis. Reasons for Dx are patient has low albumin, increased INR, and AST > ALT.
UTI: Patient has WBCs in urine = >50, nitrate positive with leukocytes, confirming Dx for UTI.
Black stools: Secondary to esophageal varices, most likely causing GI bleeding.
ETOH abuse: Watch for increased ETOH withdrawal signs and symptoms and treat patient accordingly. Patient currently shows mild to moderate signs. Suggest AA/12 step to patient to help quit and provide support.

Discussion:

Alcoholic liver disease is a major cause of cirrhosis. Cirrhosis can be classified as late stage liver disease, marked by inflammation, fibrosis and damaged membranes which prevent the body from detoxifying itself from harmful chemicals such as alcohol. Acetyldehyde is mainly responsible for fibrosis due to stimulating collagen deposition by stellate cells. The production of oxidants and these proteins move towards the middle of the liver and subsequently damage the cell membrane. Symptoms of alcoholic liver disease include jaundice, hepatomegaly, pain and tenderness, ascites. Other complications of alcoholic liver disease are esophageal varices and hepatic encephalopathy.

First and foremost the most important part of treatment is for the patient to stop using alcohol, if need be a patient can be given disulfram to help stop. After the cessation of drinking, a patient with signs of alcoholic liver disease can be given corticosteroids for treatment, as well as colchicine to inhibit hepatic fibrosis, but as the patient above already has cirrhosis trying to heal the liver will not help. In cases of cirrhosis, one must manage the symptoms, and possibly opt for a liver transplant.