Reading and Test Schedule
| |
Readings |
Test |
Core 1 – July
Core 1 – August |
7/10 - #9, 7/17 - #10, 7/24 - # 15
8/7 - #3, 8/14 - #5, 8/21 - #6 |
7/29
8/26 |
Core 2 – September
Core 2 – October |
9/4 - #9, 9/11 - #10, 9/18 - #15
10/2 - #3, 10/9 - #5, 10/16 - #6 |
9/30
10/28 |
Core 3 – November
Core 3 – December |
11/6 - #9, 11/13 - #10 & #15
12/4 - #3, 12/11 - #5, 12/18 - #6 |
11/18
12/23 |
Core 4 – January
Core 4 – February |
1/8 - #9, 1/15 - #10, 1/22 - #15
2/5 - #3, 2/12 - #5, 2/19 - #6 |
1/27
2/24 |
Core 5 – March
Core 5 – April |
3/5 - #9, 3/12 - #10, 3/19 - #15
4/2 - #3, 4/9 - #5, 4/15 - #6 |
3/31
4/28 |
Core 6 – May
Core 6 – June |
5/7 - #9, 5/14 - #10, 5/21 - #15
6/4 - #3, 4/11 - #5, 6/18 - #6 |
5/26
6/30 |
Readings are at 3:00 pm – 5:00 pm in the Doctor’s Conference Room, OSUMC
Tests are at 7:30 am in the Computer Lab, Houston Parke
Core III - Case Presentation 3
Presentation
A 49-year old woman comes to see you because of shortness of breath. Unable to date the onset of her problem exactly, she is certain, nonetheless, that her exercise capacity has been deteriorating over the past few months. She had always prided herself in being an active healthy woman; now she has difficulty walking up a single flight of stairs. She has not had dyspnea at rest or while walking slowly on level ground.
The chief complaint here is dyspnea.
What physiologic abnormality correlates with this symptom?
Discussion
Dyspnea occurs as a subjective sensation when the effort of breathing, or either during exercise or at rest, rises to the point where it is no longer subconscious. It correlates, therefore, with the work of breathing. It does not indicate hypoxia or hypercapnia.
How would you organize the questions asked in the history to elucidate the cause of her dyspnea?
Presentation
She is unaware of any childhood respiratory abnormalities. Before her marriage 22-years ago, she worked as a clerk and secretary. Since her marriage, she has been a full-time housekeeper. She smokes one package of cigarettes per day. She denies wheezing and has not been troubled by a chronic cough. She has had no chest pains or hemoptysis.
The history is negative for rheumatic fever. She has never been told of a heart murmur. She denies palpitations and symptoms of angina. She has no difficulty sleeping on just one pillow and reports no paroxysmal nocturnal dyspnea. There has been no edema. The remainder of the history is negative.
What two general causes of dyspnea have been considered? How do you interpret these data?
Discussion
The history here is well organized. Dyspnea is an extremely common symptom and a feature of innumerable specific diseases. Generally, these can be divided into two categories: pulmonary and cardiac. The line of questioning being employed here seems to follow that system of classification.
Except for the fact that she smokes, the history so far has not been helpful in elucidating the cause of her chief complaint. But, it should be kept in mind that when a patient seeks medical help early in the course of an illness, the diagnosis may be more difficult to recognize. The full-blown syndrome may not yet have developed. Accordingly, congestive heart failure, in an early stage, is not ruled out by the absence of edema or paroxysmal nocturnal dyspnea (PND). At a more advanced stage, however; such as in the patient with dyspnea at rest, the weight of these pertinent negatives becomes far greater in excluding heart failure.
The physical exam should help you decide if her symptoms are cardiac or pulmonary in origin.
What specific findings would you be interested in?
Presentation
Overall, she appears to be in good health. Vital signs are blood pressure (BP) 120/84, pulse 90/min, respirations 19/min, and temperature 37oC. There are no rashes. Head and neck exams are normal. At rest, her respirations appear normal, but expansion seems slightly reduced when she takes a full inspiration. Diaphragmatic excursion is 2 to 3 cm bilaterally. Normal resonance is heard upon chest percussion. There are bibasilar end inspiratory crackles. No rhonchi or wheezes are heard, even on forced expiration. Neck veins are at a normal level. The apical impulse is in the fifth inter-space, midclavicular line. No right ventricular (RV) lift is felt. There is a 1/6 systolic ejection murmur. No diastolic murmurs, gallops or opening snaps are heard. The abdominal and musculoskeletal exam is normal. There is no edema or clubbing. Neurologic exam is normal.
What specific cardiac diagnosis, relevant to a middle-aged female, becomes unlikely, given these data? What diagnosis needs to be considered further?
Discussion
The cardiac exam seems entirely normal. Findings of mitral stenosis should be very carefully sought in a female patient presenting with dyspnea on exertion. There is no evidence for that here. The end inspiratory crackles could represent interstitial pulmonary edema, but there is little else to suggest congestive heart failure (CHF).
Is this obstructive pulmonary disease? In obstructive disease – either asthma or chronic obstructive pulmonary disease (COPD) – the increased work of breathing is caused by high airway resistance. Patients attempt to minimize this resistive work by breathing at a high lung volume, thereby preventing collapse of their small airways. One expects to find, therefore, a hyperexpanded chest and deeper respirations than were observed here. Also, noises originating from the airways – wheezes and rhonchi – are commonly heard in obstructive lung disease. This patient’s exam does not suggest this diagnosis.
There are some important positive findings, however. She has a slight tachypnea, a decrease in lung volumes, and end inspiratory crackling rales. Together, these signs suggest that her dyspnea is related to the other component of the work of breathing: overcoming the lungs’ elastic forces. Patients with restrictive lung disease have stiff lungs, usually due to diffuse infiltration or fibrosis. It is difficult to expand such lung parenchyma; accordingly, respiratory work is minimized by breathing shallowly while maintaining total minute ventilation by increasing the respiratory rate.
Restrictive lung disease seems likely. The next step would be to try to obtain further objective data to support this assessment.
What tests would you order?
Presentation
The chest X-ray is shown.
What is your interpretation?
Discussion
The chest X-ray reveals a diffuse fibrotic appearance in both lung fields, with decrease in lung volumes bilaterally. The overall size of the lungs is somewhat reduced. No hilar or mediastinal adenopathy is present. The cardiac silhouette is normal.
What further tests would you order?
Presentation
Pulmonary function tests show an FEV1 of 60%, an FVC of 58% of predicted normal, and a normal FEV1/FVC ratio. Total lung capacity (TLC) and functional residual capacity (FRC) are reduced. Diffusing capacity is 50% of normal. Arterial blood gases on room air, at rest, are PO2 74 mm Hg, PCO2 37 mm Hg, and pH 7.42.
What is her pathophysiologic diagnosis?
Discussion
The initial hypothesis is confirmed: she has restrictive (interstitial) lung disease of moderate severity. The chest X-ray, blood gases, and pulmonary function tests all support the diagnosis. Moreover, this diagnosis is in keeping with the abnormalities observed on physical exam.
The pathophysiology of her disease now seems well defined, but an etiologic diagnosis is still required. There are many causes of interstitial lung disease. Decisions about prognosis and therapy can be undertaken only after a specific diagnosis is made. Finding the specific cause of a patient’s restrictive lung disease often proves difficult. Many cases – perhaps too many – are ultimately termed idiopathic pulmonary fibrosis.
How would you proceed?
Presentation
It is decided that a careful “second look” (systemic review of the initial body data) is needed. A list of the known causes of interstitial lung disease is scanned. First, an occupational history is taken again: it proves negative. Next, her habits are exposures are reviewed. She has no pets and does only a little routine indoor gardening. There has been no exposure to agents associated with extrinsic allergic alveolitis (e.g., farmer’s lung, bird breeder’s lung). Inquiries are made about symptoms that would suggest an underlying illness. She has had no arthralgias, rashes, dysphagia, or pleurisy. Nothing suggests a collagen vascular disease as a cause of her interstitial fibrosis. The past medical history and drug history are reviewed. She now recalls that, in fact, she does take a pill each night to prevent bladder infections. She has been taking it for so long – at least four years – that she no longer considers it medicine. She believes the drug is called nitrofurantoin.
Discussion
Bravo! Physicians sometimes forget that there is often great value in retaking the history. In the case at hand, much more was already known about this woman’s illness when the history was reviewed than when it was originally taken. Accordingly, her doctors were now able to be more specific and detailed in their questions. The same can be said for repeating specific parts of the physical exam when the diagnosis is not apparent. To ignore the usefulness of the careful second look is to assume that both the doctors and patients never omit anything – a fantasy quite far from reality.
Nitrofurantoin has been associated with both an acute pulmonary reaction with cough, fever, and patchy infiltrates, and also with a more indolent fibrotic reaction. This patient’s illness is consistent with the chronic pulmonary toxicity of this drug.
Obviously the nitrofurantoin should be discontinued.
What further studies should be done to insure that she does not have interstitial lung disease from some other cause?
Presentation
Her complete blood cell (CBC) count is normal. No eosinophilia is seen on the blood smear. Sed rate and collagen vascular studies are all normal. The remainder of the routine studies are negative except for the urinalysis where rare white blood cells (WBCs) are present in the spun sediment. A pulmonary consultant is asked about the need for a lung biopsy and about treatment.
In general, what is the rationale for lung biopsy in patients with interstitial lung disease?
Discussion
Excluding populations exposed to an agent known to be toxic to the lungs, in most cases of interstitial lung disease a definite etiologic diagnosis cannot be made from the history and physical alone. Ancillary studies may suggest an associated allergic or collagen vascular problem. Often, however, the only way to make a definite diagnosis is with biopsy.
The biopsy may establish the specific diagnosis in diseases like eosinophilic granuloma or sarcoidosis, thereby leading to more accurate information about prognosis and indications for therapy. In idiopathic pulmonary fibrosis, the biopsy will allow estimation of relative degrees of fibrosis and cellularity. An end-stage fibrotic lesion is believed to be less responsive to steroids than a cellular one.
Would you recommend a lung biopsy for this patient?
Presentation
It is recommended that no biopsy be done. Rather, she will be treated with corticosteroids and followed. Her response to treatment will be determined by both subjective symptoms and objective measurements of pulmonary function.
Discussion
This appears to be a reasonable plan for this patient. It is very likely that her problem is related to the drug exposure. Her pulmonary disability should improve – or at least should get no worse – once the offending agent has been withdrawn and a trial of corticosteroids are given. Hopefully she will not require prolonged treatment with steroids. In the more common idiopathic variety of pulmonary fibrosis, the outlook is variable. Unfortunately, many patients are unresponsive to corticosteroids and go on to develop severe end-state disease.
Core III - Case Presentation 5
Presentation
A 72-year old retired plumber is evaluated because of severe back and hip pain. “I’ve had arthritis for many years,” he laments, “but this is just terrible. Why, I can barely get out of bed in the morning.”
Further history reveals that he has had joint problems for many years. Prior to his retirement seven years ago, he was confined to his bed on a few occasions because of low back pain.
For the past few years he has had pain in his right hip after walking long distances, sometimes accompanied by pain in his right knee. Nonetheless, he remained an active man, at least until recently.
For the past two months he has had progressive pain and stiffness in his back which has spread around to both hips and thighs. More recently, he has begun to have an aching feeling in his neck and shoulders. His symptoms are worse in the morning and, in contrast to his previous symptoms, they are also worse after a long rest. Bending and climbing stairs have become particularly difficult. He has had to curtail most of his activities. In addition, he has noted a poor appetite and a 10-pound weight loss over the past month. There have been no fevers or sweats; he has, however; felt generally weak and tired.
His age and past history suggest degenerative joint pain.
Is that diagnosis compatible with his presentation now?
Discussion
Degenerative joint disease (DJD), the most frequent form of arthritis seen in clinical practice, certainly comes to mind early when evaluating an elderly patient with rheumatic complaints. The clinical importance of this common pathologic entity is highly variable. Severe joint involvement may cause very little difficulty, neither pain nor loss of motion. For example, the distal interphalangeal joints of the fingers, frequently the sites of deforming bony swelling (Heberden’s nodes) in elderly patients with DJD, most often are asymptomatic. However, in other joints, particularly the hips, knees, and spine, DJD may be severely disabling.
When symptoms arise from DJD, they are typically insidious in onset and often localized around one or a few joints. The pain is brought on by motion or weight bearing and typically relieved by resting. Morning stiffness, when present, is very brief. Since this disease primarily affects the articular cartilage and not the synovium, signs of inflammation are few in degenerative joint disease. Systemic signs like fever or elevated sedimentation rate are not found in DJD, no matter how severe. Many features, and indeed the entire “flavor” of this patient’s history suggest that DJD does not fully explain his clinical presentation now. Generalized proximal stiffness leading to severe disability, accompanied by weight loss, weakness, and fatigue suggest some other process.
Presentation
The physical examination of the patient begins as he is observed walking into the examining room: he is stooped, walking slowly, with careful steps. He appears tired but not cachectic. Vital signs are normal. Of the entire examination, only the musculoskeletal system is remarkable. Bony swelling of all the DIP joints is present; there is no heat or tenderness in any of the joints of the hands. No subcutaneous nodules are present. His neck has limited mobility in extension and rotation. No tenderness can be elicited over the lumbosacral vertebrae. While full range of motion is present in both hips, there is obvious pain when the thighs and legs are flexed, extended, or rotated. Bilateral knee crepitus and varus deformities are present; there are no knee effusions. Motor exam is difficult because of generalized pain and stiffness. Neck, trunk, and proximal limb muscles are perhaps diminished in power; distal muscular strength seems normal. The neurologic exam is normal.
What key features of his clinical presentation would you select to serve as the basis for the differential diagnosis? What diagnoses come to mind?
Discussion
He has several symptoms – fatigue, weakness, weight loss, pain, stiffness – all of which are important. As a basis for formulating a differential diagnosis, however; the clinician should select the symptom with the greatest specificity. His proximal muscle stiffness, of all of the symptoms listed, appears to be most specific: it focuses attention on the musculoskeletal system. A symptom like fatigue would have been a poor choice because it may be caused by so many illnesses in so many different organ systems.
What about his other symptoms? By focusing on one symptom, are we overlooking the others? As it turns out, symptoms that derive from the same organ system usually are manifestations of the same disease. It is unlikely that he has one disease causing stiffness, another causing weakness, still a third causing muscle pain. The fatigue and weight loss are not necessarily musculoskeletal symptoms; they should not be prematurely attributed to the same process responsible for his other symptoms.
What laboratory tests would you order to help with the diagnosis of this problem?
Presentation
The following results are obtained: white blood cell count of 7,300/cu mm, Hct 35% with a normal peripheral smear, platelet count 240,000/cu mm. ESR is 110 mm/hr. Tests for rheumatoid factor were negative. ANA titer was less than 1:20 and with a speckled pattern. CPK and liver function studies were normal. Prostatic specific antigen, thyroid function tests, electrolytes, BUN, creatinine, glucose, calcium all are normal. Urinalysis and stool guaiacs were negative. Protein electrophoresis demonstrated evidences of broad band increase in the beta-2 fractions; otherwise was normal. Lumbosacral spine series revealed anterior osteophytes consistent with degenerative joint disease. Chest X-ray was within normal limits.
What is your diagnosis?
Discussion
The elevation of the sedimentation rate is striking. Also, there is a low-grade anemia and nonspecific increase in the beta-2 fraction of the gamma globulins. In a 72-year old man with an illness characterized by proximal muscle stiffness, these abnormalities support the diagnosis of polymyalgia rheumatic.
To some extent, this is a diagnosis of exclusion. These same laboratory abnormalities would also be consistent with a number of other systemic illnesses. Malignancy (including multiple myeloma), tuberculosis, and endocarditis should all be considered in a patient like this. Nonetheless, the total clinical evidence found here strongly suggests polymyalgia rheumatic.
Other possible diagnoses of his musculoskeletal symptoms become less likely when all the data are considered. Polymyositis can be excluded by the normal muscle enzymes. Metabolic bone disease, multiple myeloma, or carinomatous invasion of the spine may present with a similar picture; none is supported by the data. Rheumatoid arthritis, ankylosing spondylitis, and Reiter’s syndrome would not be expected to develop de novo in a 72-year old man.
You suspect the diagnosis of polymyalgia rheumatic. What additional finds or history or physical exam would support the diagnosis?
Presentation
He is seen again one week later, and some aspects of the history are reviewed. Once again, the most distressing symptom for him is the proximal limb and girdle stiffness, especially in the morning. In addition, he feels terribly weak and tired. He denies visual symptoms, neurologic symptoms, and jaw claudication. There is no history of headache or pain around the temples.
Mydriatic eye drops are instilled to permit more complete funduscopic examination; no abnormalities are seen. There is no scalp tenderness; the temporal arteries are normal.
Why is this additional information important?
Discussion
Polymyalgia rheumatic often coexists with temporal arteritis. Because this association is so common and because of differences in recommended therapy when temporal arteritis is present, many experts recommend routine biopsy of the temporal artery in all patients with polymyalgia rheumatic, even if there are no symptoms or signs of temporal arteritis. The significance of temporal arteritis lies with its ocular complications, including blindness. Treatment is very effective but requires much higher initial doses of corticosteroids than would ordinarily be recommended for polymyalgia rheumatic alone.
How would you proceed?
Presentation
A temporal artery biopsy is performed; no evidence of vasculitis is found. Treatment is begun with prednisone 20 mg/day. Within one day his stiffness is considerably improved, and within one week he is able to resume his usual activities. ESR, checked two weeks after beginning steroids, is 26 mm/hr.
He remains on 20 mg prednisone for an additional two weeks and then careful tapering of the dose is begun, while following his symptoms and ESR. He is feeling extremely well six months after diagnosis, taking just 5 mg of prednisone per day. He has regained his weight and essentially has returned to his previous state of health.
Discussion
Such an impressive response to steroids is expected in polymyalgia; in fact, the absence of such a response should lead one to question the diagnosis. About six months of therapy is usually required, bearing in mind that relapses can occur when steroids are discontinued. The concerns about malignancy in this patient can now be dismissed in view of the favorable outcome.
A fundamental point about the diagnostic process was illustrated by this case. The correct diagnosis was reached by focusing on the symptom with the greatest specificity, and then seeing if the working diagnosis accounted for all the other symptoms. This is a helpful strategy when a patient presents with a collection of symptoms. This is a helpful strategy when a patient presents with a patient presents with a collection of symptoms, none of which is diagnostic. But before one gets the impression that clinical medicine is simple, recall the other components that led to the successful outcome in this case: a detailed history and physical; the clinical wisdom to realize that this man was not suffering from his previously diagnosed illness; recognition of the clinical features of the new diagnosis; and finally, knowledge of the proper treatment.
Core III - Case Presentation 6
Presentation
A renal consultation is requested for a 74-year old man on the surgical service. He has had chronic lymphocytic leukemia treated with chlorambucil and allopurinol for the past three years. Over the past few months he has experienced abdominal pains and his platelet count has been falling – both attributable to his enlarging spleen. Splenectomy was recommended; he agreed and underwent surgery three days ago.
Immediately before surgery, his blood urea nitrogen (BUN) was 22 mg/dl, creatinine was 1.4 mg/dl, and urinalysis was normal. When checked again three days postoperatively, the following values are obtained: BUN 40 mg/dl; creatinine 2.9 mg/dl. Urine output for each of the past two days has been around 300 ml/24 hours.
Based on the information you have so far, how would you classify his renal problem? How would you organize your approach to the differential diagnosis?
Discussion
He is oliguric and progressively becoming azotemic. The term acute renal failure (ARF) best describes his problem. However, ARF is only a descriptive term applied to many specific etiologies, not a diagnosis. The differential diagnosis of acute renal failure is best considered when the causes are divided into three categories: (1) prerenal azotemia, (2) renal (e.g., acute tubular necrosis or acute glomerular injury), and (3) postrenal obstruction.
Both prerenal azotemia and postrenal obstruction should be considered early, when a patient with acute renal failure is first evaluated. Each carries a good prognosis if specific corrective measures are instituted before permanent renal damage occurs.
Consider this man’s specific set of clinical circumstances.
What further data would you gather from the history, hospital record, and physical exam to help you decide whether his acute renal failure has resulted from either prerenal or postrenal factors?
Presentation
You take his history. He denies excessive thirst over the past few days. He has had no symptoms of congestive heart failure. (A urethral catheter has been in place since the surgery, so you need not inquire about symptoms of prostatism.) He has had no flank pain.
The hospital record is reviewed. Serious bleeding during the operation resulted in transient hypotension. Blood pressure (BP) was restored within 10 minutes, and since that time he has been normotensive. His urine output was 700 ml the day of surgery and 200 to 300 ml/day for the last two days. Total fluid balance, despite continued nasogastric suction, has been positive, about 1 liter/day. His weight on admission was 69 kg; present weight is 71.2 kg. His only medication over the past few days has been intramuscular (IM) Demerol.
Your examination begins with the vital signs. BP is 130/92 lying and 140/80 sitting; pulse is 82/min lying and 84/min sitting; respiration is 14/min; temperature is 37.2oC (99oF). Skin turgor is good. Neck veins are 1 cm above the sterna angle. There are no pulmonary rales. The abdomen is soft without flank bruits or masses. As expected, there is slight tenderness around the fresh Splenectomy scar, but there is no costovertebral angle tenderness. The bladder is not distended to percussion. Using aseptic technique, the urethral catheter is irrigated and found to be functioning well.
How do you interpret these date? Are prerenal azotemia and postrenal obstruction likely diagnoses?
Discussion
Neither prerenal azotemia nor postrenal obstruction is compatible with the data gathered. Prerenal azotemia implies that the kidneys are under-perfused because of either hypovolemia or heart failure. In this patient, all evidence indicates that he is euvolemic. He does not complain of thirst (a valuable symptom, unless the patient is obtunded). His vital signs – specifically, the absence of postural change in pulse or blood pressure – and the neck veins indicate normal vascular volume. There is no evidence of heart failure. Finally, his weight confirms that if anything he might be a bit volume-expanded.
Postrenal obstruction, whether complete or partial, can cause acute renal failure. Complete blockage will, of course, cause total anuria. When the obstruction is incomplete, urine volumes may vary. In this patient, because of the catheter, the most common cause of obstructive uropathy, prostatism, is not a consideration. Another common cause of obstructive uropathy is neurogenic bladder. In an elderly patient at bed rest and receiving anticholinergic, narcotic medications, this is a real concern. Once again, the patient’s catheter eliminates this possibility.
Conceivably, he could have bilateral incomplete, ureteral obstruction, giving rise to acute renal failure with oliguria. His spleen has been enlarging recently; perhaps he has bulky retroperitoneal adenopathy pressing on the ureters. Still another possibility, not yet excluded, is obstructive uropathy from uric acid crystallization in the distal tubes or ureters. This is occasionally an important consideration in patients with malignancies, especially at the onset of chemotherapy or radiotherapy. Invoking either of these diagnoses, however; ignores the important fact that his renal failure occurred in the immediate postoperative period; until proved otherwise, it must be considered as related to the surgery.
What is a more likely diagnosis? How would you proceed?
Presentation
The urine sediment contains rare red blood cells, no white blood cells, numerous epithelial cells, and muddy brown degenerating cellular casts. There are no crystals.
The urine sodium is 40 meq/L; the serum sodium is 138 meq/L. The serum creatinine is 3.5 mg/dL; the urine creatinine is 30 mg/dL. Urine osmolality is 310m osmol/kg. Now, four days after surgery, the BUN is 50 mg/dL, his glucose is 120 mg/dL, calcium is 8.9 mg/dL, and uric acid is 9.2 mg/dL. A renal ultrasound demonstrates normal sized kidneys without pyelocaliectasis.
What is the diagnosis?
Discussion
The most likely diagnosis is acute tubular necrosis (ATN). The cause of ATN in this patient was probably the hypotension during surgery. The oliguria, progressive azotemia, evidence of tubular dysfunction (inability to concentrate the urine or reabsorb sodium), and urine sediment are characteristic. The renal ultrasound study excluded the remote possibility of partial ureteral obstruction presenting as acute renal failure, but probably was unnecessary. The fractional excretion of Na is calculated =
Urine Na Serum Cr
Serum Na Urine Cr
X100
If this patient’s ATN proves to be typical, what might its course be? What are some of the important considerations in managing a patient with ATN?
Presentation
By day five, the BUN is 68 mg/dl; creatinine is 4.1 mg/dl. Urine volume remains between 300 and 500 ml/day. Serum electrolytes are: sodium 142; potassium 4.4; chloride 98; and bicarbonate 23 mEq/L.
Fluid and salt restriction is begun. He remains oliguric, but begins to lose about one-half pound in weight per day. By day eight, the BUN is 84 mg/dl; creatinine is 6.2 mg/dl.
The following day his urine output begins to rise. Total output is 1 liter on day nine, 3 to 4 liters on each of the next two days. On day 11, his BUN and creatinine begin to fall. Urine output decreases to about 1.5 liter/day over the next week. Fluid and salt restriction is discontinued. Three weeks after surgery, his renal function has returned to baseline values.
Discussion
The course of his illness was typical of ATN. He remained oliguric for one-half weeks (anywhere between a few days and a few weeks may be anticipated), during which the BUN and creatinine rose daily. A brief period of dieresis then occurred, and soon thereafter the BUN and creatinine began to fall.
Treatment of ATN is essentially supportive. It is desirable to adjust total intake during the oliguric phase to achieve a small daily weight loss, while also providing adequate nutrition. Infection, electrolyte disturbances, fluid overload, and all the complications of uremia can arise during the oliguric phase. If azotemia becomes excessive of oliguria is prolonged beyond a few days, dialysis is usually instituted.
During the recovery period, the patient is subject to additional problems. Polyuria usually results from excess fluid and solute retained during the oliguric phase; rarely, severe polyuria may result from tubular damage. In this patient, the moderately positive fluid balance during the early part of the oliguric phase probably led to the transient dieresis during the recovery phase.
Core III - Case Presentation 9
Presentation
A 48-year old woman with a history of chronic alcoholism is admitted to the hospital because of abdominal pain, fever, and jaundice. She had been drinking more than one pint of liquor per day before she developed anorexia and nausea about one week ago. Soon thereafter, she began having continuous epigastric and right upper quadrant pain, along with postprandial vomiting. There was no evidence of “coffee grounds” vomitus, hematemesis, or melena. She has felt feverish but denies shaking chills.
Three years ago she was hospitalized for evaluation of hepatomegaly. At that time, she was working as a secretary and, according to the record, had no history of alcoholism. A liver biopsy was done: fatty infiltration, some focal hepatonecrosis, and alcoholic hyaline (Mallory bodies) were seen. The implication of the biopsy – that her liver disease was almost certainly due to alcoholism – was explained to her. At first she continued to deny any drinking problem; with time, however; she dropped all pretenses and admitted to the severity of her problem. Unfortunately, she continued to drink.
She continued to work until one month ago when she became increasingly tired and weak. Her appetite has been poor for the past few weeks; she has lost about 10 pounds. Up until this present hospitalization, she had no significant abdominal pain, distention, or jaundice. There is no history of transfusions, medications, or exposure to hepatitis. Her medical history is otherwise negative.
On physical examination now, she appears quite ill. Temperature is 38.5oC (101.2oF), pulse 96/min, and respirations 18/min. Her face is sunken with temporal wasting. Her sclera is icteric; nail beds are pale, without clubbing. There is a blotchy redness over the hypothenar region that blanches with pressure. Spider angiomata are seen on the upper back. The lung and heart exams are unremarkable. The liver is 18 cm in span, firm, and tender. No spleen is felt. The abdomen is not distended, but there is shifting dullness and bulging flanks. There is vague tenderness over the entire abdomen, most marked in the right upper quadrant. Bowel sounds are present but diminished. Neurological exam is negative. Her mental status seems appropriate for her degree of discomfort; that is, she is less than fully cooperative but obviously alert and oriented. No asterixis is present. Pelvic exam and stool guaiac are negative.
She undoubtedly has alcoholic liver disease.
Which histologic stage – fatty liver, hepatitis, or cirrhosis – best fits her clinical presentation now? Are there other important diagnoses that would explain her pains, fever, and jaundice?
Discussion
The history her-persistence of alcoholism despite significant alcoholic liver disease – is encountered all too frequently. The patient who denies a problem with alcohol is particularly difficult to rehabilitate. It seems that being confronted with the results of the biopsy served only to break down her defenses, not to alter her behavior.
The biopsy three years ago showed mostly fatty liver with mild alcoholic hepatitis. Her lack of symptoms and the absence of extrahepatic physical findings were consistent with that histologic diagnosis. At the present time, fever, jaundice, and ascites, together with tender hepatomegaly, suggest sever alcoholic hepatitis. The other physical findings of alcoholic liver disease observed here – the spiders and palmar erythema – suggest that she may also have some degree of cirrhosis.
All stages of alcoholic liver disease – fatty liver, hepatitis, and cirrhosis – arise as a result of alcoholism; nutritional deficiencies need not be invoked. Fatty liver can be induced in all subjects by administering surprisingly small quantities of ethanol. Alcoholic hepatitis and cirrhosis develop only in patients who have been drinking heavily for years. However; individual susceptibility is important also. Hepatitis and, even more so, cirrhosis occur only in a fraction of heavy drinkers. The reason for this is not understood.
Alcoholic hepatitis can account for the “toxic” features observed in this patient. Prolonged fever, leukocytosis, and even leukemoid reactions are seen. It would be an error, however; to limit the diagnostic possibilities to alcoholic liver disease. Such a hasty conclusion ignores two important principles: (1) alcoholics are subject to the same diseases as are non-alcoholics, and (2) alcoholic liver disease and alcoholism are, in effect, systemic illnesses. Such patients often have extrahepatic problems, arising as a result of cirrhosis or ethanol, which may be of great significance.
Biliary tract disease is certainly an important consideration. Cirrhotics have an increased incidence of pigment gallstones. Pancreatitis is, of course, common in alcoholism; it could certainly account for the clinical picture observed here. Spontaneous bacterial peritonitis should be ruled out in any patient with liver disease, ascites, and evidence of a systemic infection. Peptic ulcer disease is twice as common in patients with alcoholic liver disease as in the general population. While an uncomplicated ulcer would not cause prolonged vomiting, generalized tenderness, or fever, certainly an ulcer giving rise to either gastric outlet obstruction, perforation or penetration could account for some or all of her symptoms. Hepatic abscess, diverticulitis, ischemic bowel disease and gastrointestinal malignancy are less likely diagnoses. Finally, an important metabolic consequence of alcoholism – alcoholic ketoacidosis – should be considered in a patient such as this. Like ketoacidosis in the diabetic, alcoholic ketoacidosis very commonly is associated with abdominal pain; it may even mimic an acute abdomen.
The list of possible diagnoses is length. Priorities must be set. She is febrile with pain and tenderness in the right upper quadrant, vomiting, and jaundice.
What admission orders would you write? What preliminary laboratory tests should be done?
Presentation
The working diagnosis is severe alcoholic hepatitis, but extrahepatic obstruction, pancreatitis, and intestinal obstruction must be ruled out. A nasogastric tube is passed and intermittent suction is begun. The aspirated material is guaiac negative. An intravenous infusion of dextrose, saline, potassium, and vitamins (including thiamine) is started. Abdominal X-rays (upright and flat plates) show a nonspecific gas pattern with no evidence of free air; calcifications in the pancreas are noted. Preliminary laboratory tests include a complete blood cell (CBC) count: 18,200 WBC/cu mm (64 polys, 32 lymphocytes [lymphs], 4 monocytes [monos]); Hct 44% with macrocytic indices; and platelets 112,000/cu mm. Glucose is 88 mg/100 ml, BUN 10 mg/100 ml, and creatinine 1.9 mg/100 ml. Electrolytes show sodium 131 mEq/L, potassium 3.1 mEq/L, chloride 94 mEq/L, and bicarbonate 29 mEq/L. Liver function tests indicate serum glutamic oxaloacetic transaminase (SGOT) 260 international units (IU), serum glutamic pyruvic transaminase (SGPT) 86 IU, alkaline phosphatase 470 IU, and bilirubin 4.7 mg/100 ml. Amylase is 102 units (normal 70-100). Prothrombin time is 15 seconds, (control, 12 seconds). Blood is sent for hepatitis B antigen. Blood cultures are drawn. Urinalysis reveals an inactive sediment but is positive for bilirubin.
What is your interpretation of the lab data?
Discussion
The elevated serum transaminases are indicative of hepatocellular necrosis; the GOT greater than GPT is a feature of alcoholic hepatitis. The surprisingly high alkaline phosphatase indicates cholestasis – either intrahepatic as in hepatitis, or extrahepatic as in choledocholithiasis. As might have been predicted from the physical exam, there is significant hyperbilirubinemia. The presence of bilirubin in the urine indicates an elevation of the direct reacting fraction and obviates the need for fractionating the bilirubin in the serum.
Extrahepatic biliary obstruction is an important consideration. If she does have an obstructed common duct, the fever and leukocytosis are indicative of potentially severe disease, such as a gangrenous gallbladder or ascending cholangitis.
How would you make the distinction between intrahepatic and extrahepatic cholestasis?
Presentation
An abdominal and pancreatic ultrasound study is performed the very next day: the gallbladder is of normal size, multiple gallstones are seen, and the common duct is normal. The pancreas is lightly edematous and gives dense echos consistent with calcific pancreatitis. The presence of ascites is suggested.
Blood cultures, urine culture, and hepatitis B antigen are negative. A liver scan reveals hepatomegaly, with slight inhomogeneity of hepatic uptake and borderline splenomegaly.
By the next day, no significant change has occurred. She remains febrile (37.7-38.4oC; 100-101oF) and tachycardic; blood pressure is stable. Her mental status remains normal, though she is distressed by her symptoms. Her abdomen is slightly tenser than on admission; the tenderness is still centered around the right upper quadrant. Bowel sounds are present. Nasogastric suction and intravenous fluids are continued.
A second abdominal X-ray reveals a normal gas pattern. WBC count is 19,600/cu mm; electrolytes, BUN, creatinine, and glucose are normal. Calcium and serum amylase are normal. A 24-hour urine collection for amylase and creatinine is begun.
A diagnostic paracentesis is performed: 100ml of clear yellow fluid is removed; there are 220 white cells/cu mm (85% lymphs); Gram stain is negative. A sample of the fluid is sent for determination of amylase, protein, and LDH.
What is your interpretation of these data?
Discussion
The ultrasound examination is the best initial imaging procedure for a patient like this. The other test commonly employed to rule out biliary tract disease – the oral cholycystogram – could not have been performed in this patient. She is unable to swallow pills and, as evidenced by the direct hyperbilirubinemia, hepatobiliary function was too impaired to allow for visualization of the gallbladder. The ultrasonogram was positive for gallstones. No evidence of common duct obstruction was present, however; false negatives certainly do occur. Biliary obstruction, though less likely, is still a possibility. The pancreatic ultrasound indicates chronic, recurrent pancreatitis and perhaps some acute inflammation, but not a massive phlegmon. The normal serum amylase is reassuring. A urinary amylase will be even more reliable in excluding acute pancreatitis.
Spontaneous bacterial peritonitis has been ruled out by the paracentesis. Cell counts above 300/cu mm, with a predominance of polys or bacteria or both seen on Gram stain, indicate infection. Causative organisms are commonly Escherichia coli, Klebsiella, or pneumococci, or anaerobic streptococci. Blood cultures are often positive for the same organism found in the ascetic fluid.
Clinically, she seems no better and no worse.
What course of action would you take?
Presentation
A 24-hour urine amylase is normal. Blood cultures and ascetic fluid cultures are negative. Bowel sound return to normal, however; she is unable to take even clear liquid feedings without vomiting. She remains NPO and intravenous alimentation is begun.
Over the next week, the fever and diffuse abdominal tenderness (still most impressive in the right upper quadrant) continue. The liver is 16 cm and tender. No masses can be felt. She is clearly more icteric than on admission. The following blood tests are obtained: WBC 24,4000/c7 mm (44 polys, 42 lymphs, 12 monos, and 2 eosinophils); Hct 34%; prothrombin time 16 seconds (control, 12 seconds); SGOT 180, SGPT 74, alkaline phosphatase 520, bilirubin 7.6. The abdominal ultrasound is repeated: it is unchanged from the admission study.
What would you be concerned about?
Discussion
The situation here is by no means simple. After one week in the hospital, she has not improved. In fact, she is more jaundiced now than on admission. Biliary obstruction from a stone is still a worrisome possibility. It must be appreciated, however; that the mere presence of gallstones (especially in a cirrhotic) does not necessarily mean that they are the cause of a patient’s symptoms; most often, they are silent.
When gallstones do cause problems, the following syndromes can occur: (2) acute cholecystitis, manifested by prolonged epigastric and right upper quadrant pain and tenderness which, if the gallbladder and its contents become infected and rupture, may ultimately give rise to peritonitis or abscess formation, (2) choledocholethiasis manifested by intermittent colicky pain, often radiating to the back, with or without evidence of transient extrahepatic obstruction, and (3) ascending cholangitis manifested by colic, fever and chills, jaundice, and when sever, septicemia and prostration. Many times the observed clinical picture is not easily categorized into one of these typical syndromes.
In this woman there is a real concern that she has an obstructed common duct, giving rise to progressive jaundice with persistent pain and fever. On the other hand, alcoholic hepatitis, uncomplicated by biliary tract disease, can account for the clinical picture observed here – including the progressive jaundice one week after hospitalization. Persistent biliary obstruction with evidence of infection should be treated surgically. Sever alcoholic hepatitis makes her a very poor operative risk.
How would you manage this situation?
Presentation
Observation and medical management continues. Over the second week of her hospitalization there seems to be a partial resolution in the right upper quadrant pain. Nasogastric suction is discontinued. The liver size decreases to about 14 cm. She has gained about 12 pounds; an increase in abdominal girth is noted. The hyperalimentation fluid is adjusted to limit NaCl to500 mg/day.
By the third week of her hospitalization her jaundice has diminished. Temperature varies between 37.4 and 37.8oC (99 and 100oF). WBC falls to 12,900. Liver function tests include SGOT 134 IU, SGPT 66 IU, alkaline phosphatase 225 IU, and bilirubin 3.9 mg/dL.
Given her clinical course, what is the likely diagnosis?
Discussion
She is better. Her physicians displayed a good deal of patience, wisdom, and courage in holding to conservative medical management. An appreciation of the natural history and diverse manifestations of her disease allowed such good clinical judgment. Had there been any further deterioration in her condition, or had there been less assurance in the diagnosis, the issue of extrahepatic cholestasis could have been fully resolved with either a transhepatic “skinny needle” cholangiogram or endoscopic retrograde cholangiopancreaticogram (ERCP). Both would have provided definitive information, but incurred the risks inherent in any invasive procedure.
What other issues need to be addressed?
Presentation
She continues to improve, and begins taking oral feedings without any discomfort or vomiting. The intravenous lines are removed and spironolactone, 26 mg qid, is started. Her urine output improves and she begins to lose about ½ pound each day.
By the fourth week she is afebrile, nonicteric, and fully ambulatory. Her liver is now 12 cm in size and only minimally tender. WBC is 8,800/cu mm with a normal differential. Prothrombin time is two seconds above control. Serum albumin is 2.9 gm/100 ml; total protein is 8.8 gm/100 ml. Liver function tests include SGOT 75 IU, SGPT 32 IU, alkaline phosphatase 180 IU, and bilirubin 1.9 mg/100 ml.
She begins attending a weekly support group designed to address the problems of alcoholics. Having abstained from alcohol for one month, she gives assurances that she will remain abstinent. She is discharged from the hospital on spironolactone, 25 mg qid, and vitamin supplements. She will be seen frequently7 as an outpatient, while also attending the weekly support group sessions that she joined in the hospital.
Discussion
We have observed in this patient the transition from alcoholic fatty liver, with minimal symptoms three years ago, to very sever alcoholic hepatitis. In her case, features of inflammation and cholestasis were quite impressive and, when combined with the observed right upper quadrant tenderness and nonspecific ileus, closely mimicked biliary obstruction. By the time of discharge, most of these features were resolving.
It is difficult to predict her future course. Ascites is present in about one-half of patients with alcoholic hepatitis and, while it does not necessarily imply that she has developed cirrhosis, it is nonetheless a poor prognostic sign. Actually, whether or not she has already developed some cirrhosis is a moot point. Whatever her histologic diagnosis, it is obvious that she must avoid alcohol.
Ultimately, about 10 to 15% of alcoholic patients develop cirrhosis, usually after heavy drinking for more than 10 years. Hepatic insufficiency, portal hypertension, and encephalopathy then become major causes of morbidity and mortality for these patients. There is well-founded concern that this woman could fall within that group.
Core III - Case Presentation 10
Presentation
A new patient presents to your office. He is a 54-year old truck driver. For the past few weeks he has experienced chest pain, sometimes accompanied by lightheadedness. His last attack occurred yesterday afternoon. He described the discomfort as a “pressure-like” feeling below his sternum, often accompanied by a dizzy, swimming sensation. He was unable to relate absolutely a relationship between the chest pain and dizziness. However, he relates that the dizziness can occur independent of his chest pain. He notices it the majority of the time with major exertion. His symptoms of chest pain are worse when he exerts such as unloading his truck or spading in his garden. Recently, the past few days, very moderate efforts such as walking up a flight of stairs have caused these same symptoms. He related that often times the pain was associated with dyspnea. It is not accompanied with diaphoresis. He denies radiation of the pain into his neck or his back. The pain symptoms are brief, occurring approximately two to five minutes in duration and resolving when he rests or sits down. He denies exacerbations of dyspnea or pain while at rest.
What sort of questions should be used to begin a history of chest pain? Do we have a working hypothesis? What are the pertinent portions of the history contributing to your hypothesis?
Discussion
A simple, open-ended invitation resulted in extremely useful information. Had the first question been more restrictive, the history might not have been so valuable. The time for specific questions – “What makes it better?” “Does the pain radiate?” “How long does it last?” – is after the patient has had a chance to tell his own story.
This is a very typical description of angina pectoris. Less classic symptoms such as arm pain, abdominal pain, jaw pain, or merely an ill-defined heaviness, should still suggest angina if the symptoms arise during exertion and are relieved by rest. Cold weather, stress, or a heavy meal may bring on an attack. The duration of symptoms varies but is most often between one minute to one-half hour. The chest discomfort may be accompanied by shortness of breath or sweating. Dizziness can occur with angina and may represent a transient drop in cardiac output during the angina attack; such a response often indicates sever disease.
Non-cardiac diseases may mimic angina.
The patient denies dysphagia, heartburn, or abdominal pain. There is no antecedent history of chest trauma. He denies pain on turning or twisting or with deep breathing. There is no history of a cough and no previous past medical history of pneumonia. He denied hemoptysis. His father died of a myocardial infarction at the age of 86. He was unaware if that was his first heart attack. His mother and siblings are well. There is no other history of heart disease and/or vascular disease in the family. He personally smoked a pack of cigarettes a day throughout his adult life. He has approximately a 40-pack year history of cigarettes. He has never been told that he had hyper-tension, diabetes, or hyperlipidemia, although his medical examinations have been few and far between. He denied previous hospitalization. He was unable to relate a history of chronic disease and denied taking medications on a regular basis. He was told he had a heart murmur during a military physical, however; he was inducted into the service. He was unsure of its significance and studies were not performed at that time. There is no history of palpitations, orthopnea, paroxysmal nocturnal dyspnea or edema. Recently, he noticed some dark black stools occurring intermittently over the past month. He denied any other change in his bowel habit. There was no history of dyspeptic symptoms. He denied a history of a food, pain, relief sequence. He did state that he had been fatigued in recent days to weeks but he attributed this to his chest discomfort and periodic problems of lightheadedness.
How could his symptoms of fatigue be related to his chest pain? Could the heart murmur be of any significance?
Discussion
Smoking is an important risk factor for ischemic heart disease in this patient. Even after coronary atherosclerosis is well established, the patient with angina will benefit if he stops smoking. (We know little about his personality type and behavior patterns – not unimportant traits in a patient with possible coronary artery disease.)
His angina symptoms and symptom complex has accelerated over the past one month.
Presentation
He appears slightly sallow with pale conjunctivae and nail beds. BP is 118/90 lying, and 120/88 sitting. Pulse is 92/min, respirations are 16/min, and temperature is 37.2oC (99.0oF). The pulse is regular but small and slowly rising in the carotids; neck veins are at the level of the sterna angle; lungs are clear. The PMI is located in the fifth interspace at the midclavicular line; the impulse is sustained and forceful. There is no parasternal lift. An S4 and a 4/6 mid-to-late peaking harsh crescendo-decrescendo (diamond-shaped) systolic murmur is heard at the apex. At the base, the same murmur is heard, accompanied by a thrill and radiating up to the carotids; S2 is soft; there is no S3; no diastolic murmurs are heard. Valsalva maneuver fails to alter the murmur. No edema is present. The abdomen is normal. Rectal exam is negative but stool is 2+ guaiac positive. A finger-stick hematocrit (Hct) is 24%.
What diagnosis is suggested by these data?
Discussion
This man’s physical examination revealed some important findings. He is anemic and appears to have a significant heart murmur. In coronary artery disease alone one may hear an S4 gallop and if the ischemia is active, a transient murmur of mitral insufficiency resulting from papillary muscle dysfunction. Less common are findings of LV dysfunction and paradoxical splitting of the second heart sound during an angina attack. Any other findings indicate that there has been permanent damage to the heart from chronic ischemia (ischemic cardiomyopathy) or as seems likely in this man, another cardiac disease is present.
The cause of his systolic murmur is obviously aortic stenosis (AS). Furthermore, the slow and delayed carotid pulse, sustained LV impulse, the late peaking crescendo-decrescendo systolic murmur with a thrill, and the soft second should all indicate hemodynamic significance. The lack of augmentation with Valsalva maneuver suggests that the murmur is not caused by idiopathic hypertrophic subaortic stenosis (IHSS). It may be difficult, however; to assess the severity of a murmur in an anemic patient. Anemia alone may be associated with hyperdynamic cardiac impulse and flow murmur.
What would you do now?
Presentation
Routine laboratory studies are obtained including a cross-match for blood transfusion. You admit him to the hospital where he is to receive three units of packed red cells. The blood studies are normal except for the CBC, which shows white blood cell count 7,200 cells/cu mm, Hct 24%, and platelet count 477,000/cu mm. The smear reveals microcytosis and poikilocytosis.
Given the above data, should the initial formulation of chest pain due to coronary artery disease be reconsidered? Why should he be helped by transfusion? What is your interpretation of the ECG?
Discussion
Transfusion to restore oxygen-carrying capacity is the appropriate first step for this patient. While it is still unclear whether his chest pain is due to increased O2 delivery caused by coronary atherosclerosis, anemia can certainly exacerbate any tendency toward angina.
The chest X-ray reveals a cardiac silhouette at the upper limits of normal with a slightly prominent left ventricle. There is mild poststenotic dilation of the ascending aorta. This illustrates the interesting point that in aortic stenosis, the overall cardiac size is normal or only slightly enlarged until late in the disease when dilatation finally occurs. The X-ray changes may therefore be quite subtle. The ECG in this patient shows a pattern that is common in significant AS. He has left ventricular hypertrophy (LVH) with anterolateral repolarization abnormalities suggesting strain. In the adult with sever AS, LVH is invariably found.
How would you proceed during his first days in the hospital?
Presentation
He remains at bed rest. After transfusion the Hct is 34%. The murmur is unchanged except that a thrill can no longer be felt. The ECG remains stable. Serial cardiac enzymes are normal over a 48-hour period. Antacids after each meal and at bedtime are begun.
Three days after admission to the hospital he is up and walking and no further chest pain has occurred. An upper gastrointestinal endoscopy reveals a large duodenal ulcer with an adherent clot. There is an antral deformity, a CLO test is positive. Prilosec is continued and iron supplements are started. Stool guaiacs become negative, Hb and Hct remain stable.
An echocardiogram shows increased thickness of the LV and decreased ventricular cavity size. Dense echoes suggestive of calcifications are noted on what appears to be a bicuspid aortic valve.
Given the above data, should the initial formulation of chest pain due to coronary artery disease be reconsidered?
Discussion
The original presentation – chest pain and lightheadedness during exertion – is also compatible with AS. In patients with AS, LVH caused by significant, longstanding outflow obstruction may increase O2demand enough to result in ischemic chest pain, even when the coronary arteries are normal. (Older patients with AS and chest pain commonly have coronary disease in addition to valvular pathology.) Another important symptom of AS is dizziness or syncope with effort. This is due to reflex vasodilatation and inability to augment cardiac output during exertion. The third classic symptoms of AS is congestive heart failure. Any of these three symptoms – angina, syncope, or presyncope, or congestive heart failure – indicate significant stenosis.
With and Hct of 34% and a low level of activity, the patient is asymptomatic. Some important questions still need answers: (1) How severe is the aortic stenosis? (2) Does he have significant coronary disease? (3) What therapy, either medical or surgical, is necessary?
The echocardiogram is compatible with significant AS and rules out significant IHSS. There is no surprise in view of the findings on physical examination.
How can these questions be answered? How would you proceed during his first days in the hospital? Is a cardiac catheterization necessary?
Presentation
A cardiologist is consulted. He recommends catechization to measure the gradient across the aortic valve and to determine the presence or absence of coronary artery disease. True, the patient is asymptomatic, the cardiologist explains, but the evidence for severe aortic stenosis is considerable. Even without symptoms, catheterization is indicated. Furthermore, the patient is asymptomatic in the hospital; his clinical status at home may be quite different. If chest pain does reoccur, it will be important to know whether it is related to AS or coronary disease. The medical treatment for coronary artery disease – nitrates and beta-blocking drugs – might be dangerous in a patient with fixed LV outflow obstruction.
Why the concerns about the use of these drugs in a patient like this?
Discussion
Nitrates, acting as vasodilators, are often hazardous in patients with AS. The left heart cannot increase output to compensate for the decrease in peripheral resistance that results from nitrate therapy. Serous hypotension can result. Beta-blockers may precipitate congestive heart failure in an otherwise well-compensated patient because they have a negative inotropic action.
Predict the results of the cardiac catheterization.
Presentation
Cardiac catheterization is performed. The intraventricular systolic pressure is 190 mm Hg, and the aortic systolic pressure is 125 mm Hg (gradient of 65 mm Hg). The valve area is 0.6 sq cm (normal 3 sq cm). There is a 60% stenosis of the right coronary artery, but the remaining coronary vessels are normal.
What is your interpretation of these data?
Discussion
Clearly, his AS is severe, and surgery with valve replacement is indicated. A 60% coronary artery stenosis is significant as well; coronary artery bypass graft can be done at the time of valve replacement.
Presentation
The results are explained to the patient. Surgery is recommended and he agrees. The operation is scheduled in three weeks to allow time for his ulcer to heal before surgery.
Discussion
Most patients with angina do not have significant anemia and aortic stenosis; most have only coronary artery disease. This patient serves as a reminder that thorough and thoughtful evaluation is necessary even when the problem seems straightforward.
Core III - Case Presentation 15
Presentation
A 52-year old man is evaluated in the emergency room because of a persistent cough and fever. He has been hospitalized many times because of alcoholism. Acute intoxication, delirium tremors, and alcohol withdrawal seizures – each has been treated on multiple occasions. Despite attempts to stop drinking, he continues to consume about a pint of liquor per day. That, however; is not his present problem.
His chief complaint now is a chronic cough accompanied by fever for at least one month. He is sent for a chest X-ray. Chest X-ray reveals a cavitary infiltrate 4 cm in size located in the posterior segment of the left lower lobe.
What categories of disease could account for such a chest film?
Discussion
The X-ray is quite interesting. He appears to have a cavitating infiltrate, 4 cm in size, located in the posterior segment of the left lower lobe. Before considering diagnoses, some definitions are in order.
As it is used radiologically, the term cavity implies an air-filled or fluid-filled space surrounded by a variable thick zone of increased parenchymal density. An abscess is a homogeneous area of necrotic lung tissue, which can be referred to as a cavity only when it erodes into a bronchus and partially or completely drains its contents.
Many diseases can cause pulmonary cavitation; infections and neoplasm are the two major categories. Of the infectious etiologies, certain bacterial, fungal, and mycobacterial pneumonia can progress to cavitation. The history and physical exam should help you to focus on the correct diagnosis.
Presentation
Approximately one month ago he developed a dry cough. At that same time he began to feel feverish but reported no chills or drenching night sweats. Within a week, the cough became productive. He noted at least one-half cup of yellow-green sputum, occasionally blood tinged, per day. He did not notice a foul odor to the sputum. He had no chest pain, pleurisy, or shortness of breath. Although a chronic smoker (about one pack of cigarettes per day for all of his adult life), he does not have any chronic respiratory problems.
On physical examination, he appears pale, tired, and thin. His BP is 110/70, pulse 100/min, respirations 18/min, and temperature 38.0oC. There are no skin lesions. Some small, rubbery, cervical nodes are felt, but none larger than 1 cm. There are many carious teeth; gums are red and tender in several areas. Lung exam reveals symmetric expansion without splinting. There is dullness and egophony over the left midzone posteriorly; bronchial breath sounds are heard over that same area. The heart is normal in size. Neck veins are flat. A soft 1/6 systolic ejection murmur is heard. The liver is 14 cm in span, smooth, non-tender. There is no evidence of edema. Early clubbing appears to be present. Neurologic exam is normal.
Which category of diseases is suggested? What specific diagnosis should be considered early on?
Discussion
The physical exam is notable for findings of lung consolidation in the area of involvement on chest X-ray and for clubbing. The hepatomegaly is consistent with fatty liver. Both the fever and character of his sputum suggest an infectious process. The chronicity of his illness – one month duration – helps limit the kind of infections to consider.
Obviously, this is not a simple pneumococcal pneumonia. That disease is characterized by an acute onset of fever, a single shaking chill, pleuritic chest pain, and often, rusty-colored sputum. An indolent course, even untreated, is not a feature of pneumococcal pneumonia and cavitation is highly unusual. Viral pneumonias and mycoplasma infections are similarly unlikely here, given the long course and appearance of the X-ray.
While perhaps not the leading diagnosis in this case, tuberculosis (TB) should be ruled out in a patient like this man. The chronicity of his symptoms is consistent with this diagnosis. Furthermore, TB is a communicable disease; one would not want to delay making this diagnosis. By far, the most common form of TB seen in a patient of his age and socioeconomic background is not primary TB, but reactivation of an old dormant focus. Accordingly, we can be helped by information from his past medical record.
What data would you look for?
Presentation
During his first admission to the hospital six years ago, he was found to have a positive purified protein derivative (PPD) skin test. Chest X-rays prior to the present admission showed no infiltrates or hilar node enlargement.
A Ziehl-Nielson-stained sputum sample is inspected. No acid fast organisms are seen.
Given these data, is active tuberculosis still a likely diagnosis in this man?
Discussion
The positive skin test indicates infection, not necessarily disease. This distinction is important. We can conclude that he was exposed to tubercle bacilli prior to six years ago. The route of the primary infection is via the bronchial tree, from organisms which are inhaled. Soon thereafter, hematogenous and lymphatic seeding occurs with spread of tubercle bacilli to many parts of the body. Within six weeks cellular immunity develops and macrophages are activated to kill the bacilli. The skin test typically becomes positive at this point. Generally, the primary infection heals, occasionally leaving some calcifications in the lung and mediastinal or hilar lymph nodes. While most of the distant sites of infection heal completely, certain foci continue to harbor viable organisms which can become reactivated at some future date. The most common location for reactivation is foci located in the posterior segments of the upper lobes of the lungs. Chronic cavitary tuberculosis results when such lesions undergo caseous necrosis, liquefy, and drain into a bronchus.
Returning to the patient, it is unlikely that he has active tuberculosis. The location of the infiltrate would be atypical, but more important, in cavitating TB; the sputum almost always contains acid-fast bacilli. The negative microscopic exam in this case almost certainly excludes the diagnosis.
What diagnosis would you consider next? How can the history be helpful? What do you think the sputum Gram stain will show?
Presentation
His alcoholism, he admits, is as much a problem as it ever was. He has been stuporous on many occasions recently, often waking up with no memory of the preceding few hours. He may, in fact, have had a seizure during one such episode.
The sputum is Gram stained and a specimen sent for culture. It is greenish-yellow with a slightly putrid odor. The gram stain shows numerous polymorphonuclear leukocytes (polys) and countless gram-positive cocci, along with various forms of gram-negative rods.
Further laboratory studies include WBC 18,300 cells/cu mm with 64 polys, 4 bands, 20 lymphocytes (lymphs), 10 mononuclear cells (monos), and 2 eosinophils. Hematocrit (Hct) is 31%, platelets 450 thousand/cu mm, and sedimentation rate (ESR) 84 mm/hr. Liver function tests are consistent with fatty liver: transaminases are twice normal; bilirubin and alkaline phosphatase are normal.
What diagnosis is most likely?
Discussion
The evidence that he has an anaerobic lung abscess, caused by aspiration of infected nasopharyngeal contents, is very convincing. His poor oral hygiene and frequent periods of unconsciousness, seizures, or both make him a likely candidate for this problem. His presentation is quite typical also. Most patients with anaerobic lung abscess are ill for weeks or months with low-grade fever, cough, weight low, and generalized fatigue and malaise. This is quite distinct from the other bacterial causes of lung abscess (Klebsiella, Pseudomonas, and Staphylococcus) where the onset is acute and fulminant. The sputum fits this diagnosis as well. Not all cases have foul smelling sputum, however; when present, this finding is very suggestive of anaerobes. The numerous polys and multitude of gram-positive and gram-negative organisms observed here are expected. Most often such abscesses result from a mixture of anaerobic bacteria (e.g., Bacteroides, Fusobacteria, and microaerophilic streptococci).
The diagnosis of anaerobic lung abscess seems quite probable in this patient.\
What other diagnoses would you feel obligated to exclude? What treatment would you order?
Presentation
He assures you that he has not been outside the northeastern United States over the past year. Three sputum samples are sent to confirm the absence of acid-fast bacilli. An additional three samples are ordered; one collected each of three consecutive mornings, and sent for cytologic examination to look for malignant cells. Blood cultures are taken and he is begun on intravenous penicillin, 6 million units/day. Postural drainage is given two times per day.
Discussion
Bear in mind that a culture of expectorated sputum in an anaerobic abscess may not be diagnostic. Unless a transtracheal aspiration is done, the diagnosis will be a clinical one, not confirmed by bacteriologic data. That is entirely appropriate, especially when the clinical picture is as characteristic as this patient’s. The physician should take care, however; to exclude other conditions that might mimic an anaerobic lung abscess.
Tuberculosis can be excluded by the more sensitive fluorescent staining technique done by the laboratory, along with three negative cultures. Neoplasms can produce cavitations either by bronchial obstruction with infection distally and lung necrosis, or by excavation of the tumor itself. Sputum cytologic examination is indicated for a patient like this. If the suspicion of malignancy was greater, bronchoscopy could be done. Fungal infections, specifically histoplasmosis and coccidiomycosis, can cavitate and give rise to a clinical picture not unlike this man’s. A careful travel history is warranted. In the immunocompromised patient, opportunistic pathogens such as Nocardia or invasive aspergillosis need to be ruled out. And finally, an unusual but important cause of lung abscess is septic embolism from right-sided endocarditis or other focus of infection. Negative blood cultures, before antibiotics, will exclude this.
What parameters should be followed to ascertain if the treatment, and therefore the diagnosis, is correct?
Presentation
One week after beginning treatment his temperature returns to normal. By the third week he has begun to gain weight and is coughing less. The X-ray begins to show improvement. Intravenous penicillin is changed to PO therapy. It is planned that he receives two months of antibiotics with careful follow-up.
Discussion
He has had good responses to penicillin. The importance of the postural drainage in such patients should not be minimized either. Had he not responded to therapy, after a few weeks, bronchoscopy would be indicated. Bronchoscopy would be helpful in ruling out the possibility of bronchial obstruction from tumor and would allow for better cytologic and culture specimens.
This patient appears to be getting better. If his present illness in any way convinces him of the need to stop drinking, that would be an added – and most important – benefit.
