James S. Newman, MD

An 84-year-old white female, a former smoker with a medical history significant for coronary artery disease, chronic renal insufficiency, hypertension, and hyperlipidemia, presented to our hospital with two weeks of progressively worsening lower-back pain.

A detailed review of systems was negative for other symptoms. The patient was normotensive with stable vital signs. A physical examination found a 4 cm nontender, pulsatile mass above umbilicus, but a neurovascular exam of her lower extremities was normal. Laboratory testing revealed an elevated serum creatinine of 4.8 mg/dL (0.8-1.2 mg/dL). An abdominal computed tomography (CT) scan without contrast was performed. (See figure 1, below). TH

What should be your next appropriate

a) Obtain additional imaging studies

b) Initiate intravenous beta-blocker therapy to keep systolic blood pressure < 90 mm Hg

c) Initiate intravenous heparin therapy

d) Observation

e) Perform surgery emergently

Discussion

The answer is “d”: Observation. A CT scan of the abdomen without contrast shows a calcified abdominal aorta with aneurysmal dilatation measuring 4.4 cm in greatest diameter. No dissection or aneurysmal rupture is seen.

The abdominal aorta is the most common site for an arterial aneurysm, occurring below the origin of renal vessels in majority of cases. A diameter greater than 3.0 cm is considered aneurysmal.1 The prevalence increases markedly in individuals older than 60.2 Known risk factors include age, smoking, gender, atherosclerosis, hypertension, and family history of abdominal aneurysm.

The vast majority of the individuals with abdominal aortic aneurysms are asymptomatic. Abdominal or back pain is the most common complain in symptomatic patients. Often, patients have a ruptured aneurysm on presentation, along with pain in the abdomen, back or groin, hypotension with a tender, pulsatile abdominal mass seen on physical examination. In addition to history and examination, several imaging modalities are utilized for diagnosis. Most aneurysms are picked up incidentally on imaging studies performed for other purposes. Abdominal ultrasonography, CT scan, magnetic resonance imaging/magnetic resonance angiography and angiography are all used for diagnosis.

The size of the aneurysm is important when making management decisions. Risk of rupture increases dramatically for aneurysm diameter greater than 5-5.5 cm.3 Elective repair is generally indicated for asymptomatic aneurysms this size because mortality for emergency repair in case of rupture is extremely high. For asymptomatic aneurysms between 3.0-5.5 cm in diameter, the choice between surgery and surveillance depends on the patient’s preference, co-morbidities, presence of risk factors and the risk of surgery. For surveillance, monitor with ultrasound or CT scan every six to 24 months.1 Smoking cessation and treatment of hypertension and hyperlipidemia are important in medical management. Surgical repair is done either by the traditional transabdominal route or retroperitoneal approach. Endovascular stent grafts have also been introduced more recently. Symptomatic aneurysms require repair, regardless of the diameter.

Our patient had several risk factors, including age, smoking, hypertension, and atherosclerosis for developing an abdominal aortic aneurysm. After discussion of findings and management options, patient did not elect to undergo surgical repair. Smoking cessation, continued medical therapy for risk factors and surveillance was advised on discharge. TH

Drs. Aijaz and Newman practice at the Department of Medicine, Mayo Graduate School of Medical Education, Mayo Clinic, Rochester, Minn.

References

1. Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 Practice Guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): a collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease): endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and Vascular Disease Foundation. Circulation 2006 Mar 21;113(11):e463-654.
2. Singh K, Bønaa KH, Jacobsen BK, Bjørk L, Solberg S. Prevalence of and risk factors for abdominal aortic aneurysms in a population-based study: The Tromso Study. Am J Epidemiol. 2001 Aug 1;154(3): 236-244.
3. Powell JT, Greenhalgh RM. Clinical practice. Small abdominal aortic aneurysms. N Engl J Med. 2003 May 8;348(19):1895-1901.

An 84-year-old white female, a former smoker with a medical history significant for coronary artery disease, chronic renal insufficiency, hypertension, and hyperlipidemia, presented to our hospital with two weeks of progressively worsening lower-back pain.

A detailed review of systems was negative for other symptoms. The patient was normotensive with stable vital signs. A physical examination found a 4 cm nontender, pulsatile mass above umbilicus, but a neurovascular exam of her lower extremities was normal. Laboratory testing revealed an elevated serum creatinine of 4.8 mg/dL (0.8-1.2 mg/dL). An abdominal computed tomography (CT) scan without contrast was performed. (See figure 1, below). TH

What should be your next appropriate

a) Obtain additional imaging studies

b) Initiate intravenous beta-blocker therapy to keep systolic blood pressure < 90 mm Hg

c) Initiate intravenous heparin therapy

d) Observation

e) Perform surgery emergently

Discussion

The answer is “d”: Observation. A CT scan of the abdomen without contrast shows a calcified abdominal aorta with aneurysmal dilatation measuring 4.4 cm in greatest diameter. No dissection or aneurysmal rupture is seen.

The abdominal aorta is the most common site for an arterial aneurysm, occurring below the origin of renal vessels in majority of cases. A diameter greater than 3.0 cm is considered aneurysmal.1 The prevalence increases markedly in individuals older than 60.2 Known risk factors include age, smoking, gender, atherosclerosis, hypertension, and family history of abdominal aneurysm.

The vast majority of the individuals with abdominal aortic aneurysms are asymptomatic. Abdominal or back pain is the most common complain in symptomatic patients. Often, patients have a ruptured aneurysm on presentation, along with pain in the abdomen, back or groin, hypotension with a tender, pulsatile abdominal mass seen on physical examination. In addition to history and examination, several imaging modalities are utilized for diagnosis. Most aneurysms are picked up incidentally on imaging studies performed for other purposes. Abdominal ultrasonography, CT scan, magnetic resonance imaging/magnetic resonance angiography and angiography are all used for diagnosis.

The size of the aneurysm is important when making management decisions. Risk of rupture increases dramatically for aneurysm diameter greater than 5-5.5 cm.3 Elective repair is generally indicated for asymptomatic aneurysms this size because mortality for emergency repair in case of rupture is extremely high. For asymptomatic aneurysms between 3.0-5.5 cm in diameter, the choice between surgery and surveillance depends on the patient’s preference, co-morbidities, presence of risk factors and the risk of surgery. For surveillance, monitor with ultrasound or CT scan every six to 24 months.1 Smoking cessation and treatment of hypertension and hyperlipidemia are important in medical management. Surgical repair is done either by the traditional transabdominal route or retroperitoneal approach. Endovascular stent grafts have also been introduced more recently. Symptomatic aneurysms require repair, regardless of the diameter.

Our patient had several risk factors, including age, smoking, hypertension, and atherosclerosis for developing an abdominal aortic aneurysm. After discussion of findings and management options, patient did not elect to undergo surgical repair. Smoking cessation, continued medical therapy for risk factors and surveillance was advised on discharge. TH

Drs. Aijaz and Newman practice at the Department of Medicine, Mayo Graduate School of Medical Education, Mayo Clinic, Rochester, Minn.

References

1. Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 Practice Guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): a collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease): endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and Vascular Disease Foundation. Circulation 2006 Mar 21;113(11):e463-654.
2. Singh K, Bønaa KH, Jacobsen BK, Bjørk L, Solberg S. Prevalence of and risk factors for abdominal aortic aneurysms in a population-based study: The Tromso Study. Am J Epidemiol. 2001 Aug 1;154(3): 236-244.
3. Powell JT, Greenhalgh RM. Clinical practice. Small abdominal aortic aneurysms. N Engl J Med. 2003 May 8;348(19):1895-1901.

An 84-year-old white female, a former smoker with a medical history significant for coronary artery disease, chronic renal insufficiency, hypertension, and hyperlipidemia, presented to our hospital with two weeks of progressively worsening lower-back pain.

A detailed review of systems was negative for other symptoms. The patient was normotensive with stable vital signs. A physical examination found a 4 cm nontender, pulsatile mass above umbilicus, but a neurovascular exam of her lower extremities was normal. Laboratory testing revealed an elevated serum creatinine of 4.8 mg/dL (0.8-1.2 mg/dL). An abdominal computed tomography (CT) scan without contrast was performed. (See figure 1, below). TH

What should be your next appropriate

a) Obtain additional imaging studies

b) Initiate intravenous beta-blocker therapy to keep systolic blood pressure < 90 mm Hg

c) Initiate intravenous heparin therapy

d) Observation

e) Perform surgery emergently

Discussion

The answer is “d”: Observation. A CT scan of the abdomen without contrast shows a calcified abdominal aorta with aneurysmal dilatation measuring 4.4 cm in greatest diameter. No dissection or aneurysmal rupture is seen.

The abdominal aorta is the most common site for an arterial aneurysm, occurring below the origin of renal vessels in majority of cases. A diameter greater than 3.0 cm is considered aneurysmal.1 The prevalence increases markedly in individuals older than 60.2 Known risk factors include age, smoking, gender, atherosclerosis, hypertension, and family history of abdominal aneurysm.

The vast majority of the individuals with abdominal aortic aneurysms are asymptomatic. Abdominal or back pain is the most common complain in symptomatic patients. Often, patients have a ruptured aneurysm on presentation, along with pain in the abdomen, back or groin, hypotension with a tender, pulsatile abdominal mass seen on physical examination. In addition to history and examination, several imaging modalities are utilized for diagnosis. Most aneurysms are picked up incidentally on imaging studies performed for other purposes. Abdominal ultrasonography, CT scan, magnetic resonance imaging/magnetic resonance angiography and angiography are all used for diagnosis.

The size of the aneurysm is important when making management decisions. Risk of rupture increases dramatically for aneurysm diameter greater than 5-5.5 cm.3 Elective repair is generally indicated for asymptomatic aneurysms this size because mortality for emergency repair in case of rupture is extremely high. For asymptomatic aneurysms between 3.0-5.5 cm in diameter, the choice between surgery and surveillance depends on the patient’s preference, co-morbidities, presence of risk factors and the risk of surgery. For surveillance, monitor with ultrasound or CT scan every six to 24 months.1 Smoking cessation and treatment of hypertension and hyperlipidemia are important in medical management. Surgical repair is done either by the traditional transabdominal route or retroperitoneal approach. Endovascular stent grafts have also been introduced more recently. Symptomatic aneurysms require repair, regardless of the diameter.

Our patient had several risk factors, including age, smoking, hypertension, and atherosclerosis for developing an abdominal aortic aneurysm. After discussion of findings and management options, patient did not elect to undergo surgical repair. Smoking cessation, continued medical therapy for risk factors and surveillance was advised on discharge. TH

Drs. Aijaz and Newman practice at the Department of Medicine, Mayo Graduate School of Medical Education, Mayo Clinic, Rochester, Minn.

References

1. Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 Practice Guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): a collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease): endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and Vascular Disease Foundation. Circulation 2006 Mar 21;113(11):e463-654.
2. Singh K, Bønaa KH, Jacobsen BK, Bjørk L, Solberg S. Prevalence of and risk factors for abdominal aortic aneurysms in a population-based study: The Tromso Study. Am J Epidemiol. 2001 Aug 1;154(3): 236-244.
3. Powell JT, Greenhalgh RM. Clinical practice. Small abdominal aortic aneurysms. N Engl J Med. 2003 May 8;348(19):1895-1901.

The hospital is the only proper college in which to rear a true disciple of Aesculapius.—John Abernethy (1764-1831), surgeon and teacher

With this quote Sir William Osler began his address, “The Hospital as a College?” to the Academy of Medicine in New York in 1903. His second quote for this report was from the famed physician Oliver Wendell Holmes Sr. in 1867:

“The most essential part of a student’s instruction is obtained, as I believe, not in the lecture room, but at the bedside. Nothing seen there is lost: the rhythms of disease are learned by frequent repetition: its unforeseen occurrence stamp themselves indelibly on the memory. Before the student is aware of what he had acquired he has learned the aspects and causes and probable issue of the disease he has seen with his teacher and the proper mode of dealing with them, as far as his master knows.”

In his report Osler was celebrating a quarter century’s success in education. He demanded a better general education for students, a lengthened period for professional study, and the substitution of theoretical by practical learning. He wanted the student not to learn only from dissecting the sympathetic nervous system but to learn to “take a blood pressure observation” with a kymograph (an instrument used to record the temporal variations of any physiological or muscular process; it consists essentially of a revolving drum, bearing a record sheet on which a stylus travels).

Osler observed that there should be no teaching without a patient for a text: “The whole of medicine is in observation” that the teacher’s art is educating the student’s finger to feel and eyes to see. Give the student good methods and a proper point of view, and experience will do the rest.

Osler expressed confidence that students would keep the hospital physician from slovenliness and improve the care of patients. He was also concerned that “we ask too much of the resident physicians, whose number has not increased in proportion to the enormous amount of work thrust upon them.” Students were the answer, the proto-scut-monkey.

The practicality of working out of a teaching hospital was outlined at length in Osler’s report. The student’s third year should begin with a systematic physical diagnosis course, first in history taking, then in writing reports. Concurrently, a physical examination course should be given several days a week with individual cases assigned to students to follow, and instruction is accessing the literature. Next comes clinical microscopy—an essential in an era where there was often no lab to call upon. In general, medical clinic occurs one day a week when interesting cases are brought from the wards. Of note, committees were appointed to report on every case of pneumonia.

In revamping medical education Osler brought the third-year students to the outpatient clinic and the fourth-year students to the wards. What implication does this have for us as hospitalists?

I have no pretensions about being another Osler (I am barely a Newman on my best days), but still my colleagues and I trudge along in our teaching duties. What education do we really do? I sat down after reading Osler’s paper, stimulated by a tangential question from the esteemed Tom Baudenistel, MD, and decided to see exactly whom we were teaching.

First there are medical students. We are faculty on their first-year selectives, offering a shadow experience. We staff the introduction to physical exam courses in second year. Third-year students rotate on our services, and seniors take our elective as well as taking acting internships on our teaching services. We act as mentors and interest group leaders. There is certainly more to this list. We also spend time teaching NP and PA students.

The internal medicine residents rotate on our hospitalist services, and we staff the general medical services. We interact with them daily when they are on consult services, trying to set a role model. General medicine, geriatric, and hospital medicine fellows rotate through as well.

We also teach the nurses on services and through in-services and daily rounds to cement the working relationship and improve communication. We teach each other. A day rarely goes by without a colleague passing on a tasty medical tidbit. (Of course, for me, a tabla blanca, no shortage of space for pearls). And finally we teach our patients and their families. Every day we do this, and if we don’t then we are missing the point of our profession entirely.

Each party—patient or student—has something to learn from us, but more importantly we have something to learn from them. Osler wrote that “The stimulus of their presence (the student) neutralizes the clinical apathy certain, sooner or later, to beset the man who makes lonely “rounds” with his house physician.”

One hundred years plus later, much of what was written is still true: Whether in a teaching institution or making “lonely rounds” we must strive to continue to educate ourselves, our colleagues, and our patients. And what better place to do it than the hospital? TH

Dr. Newman is the physician editor of The Hospitalist. He’s also consultant, Hospital Internal Medicine, and assistant professor of internal medicine and medical history, Mayo Clinic College of Medicine, Rochester, Minn.

Bibliography

Osler W (Sir) Aequanimitas. 1945. The Blakiston Company, Philadelphia. p. 311-327.

The hospital is the only proper college in which to rear a true disciple of Aesculapius.—John Abernethy (1764-1831), surgeon and teacher

With this quote Sir William Osler began his address, “The Hospital as a College?” to the Academy of Medicine in New York in 1903. His second quote for this report was from the famed physician Oliver Wendell Holmes Sr. in 1867:

“The most essential part of a student’s instruction is obtained, as I believe, not in the lecture room, but at the bedside. Nothing seen there is lost: the rhythms of disease are learned by frequent repetition: its unforeseen occurrence stamp themselves indelibly on the memory. Before the student is aware of what he had acquired he has learned the aspects and causes and probable issue of the disease he has seen with his teacher and the proper mode of dealing with them, as far as his master knows.”

In his report Osler was celebrating a quarter century’s success in education. He demanded a better general education for students, a lengthened period for professional study, and the substitution of theoretical by practical learning. He wanted the student not to learn only from dissecting the sympathetic nervous system but to learn to “take a blood pressure observation” with a kymograph (an instrument used to record the temporal variations of any physiological or muscular process; it consists essentially of a revolving drum, bearing a record sheet on which a stylus travels).

Osler observed that there should be no teaching without a patient for a text: “The whole of medicine is in observation” that the teacher’s art is educating the student’s finger to feel and eyes to see. Give the student good methods and a proper point of view, and experience will do the rest.

Osler expressed confidence that students would keep the hospital physician from slovenliness and improve the care of patients. He was also concerned that “we ask too much of the resident physicians, whose number has not increased in proportion to the enormous amount of work thrust upon them.” Students were the answer, the proto-scut-monkey.

The practicality of working out of a teaching hospital was outlined at length in Osler’s report. The student’s third year should begin with a systematic physical diagnosis course, first in history taking, then in writing reports. Concurrently, a physical examination course should be given several days a week with individual cases assigned to students to follow, and instruction is accessing the literature. Next comes clinical microscopy—an essential in an era where there was often no lab to call upon. In general, medical clinic occurs one day a week when interesting cases are brought from the wards. Of note, committees were appointed to report on every case of pneumonia.

In revamping medical education Osler brought the third-year students to the outpatient clinic and the fourth-year students to the wards. What implication does this have for us as hospitalists?

I have no pretensions about being another Osler (I am barely a Newman on my best days), but still my colleagues and I trudge along in our teaching duties. What education do we really do? I sat down after reading Osler’s paper, stimulated by a tangential question from the esteemed Tom Baudenistel, MD, and decided to see exactly whom we were teaching.

First there are medical students. We are faculty on their first-year selectives, offering a shadow experience. We staff the introduction to physical exam courses in second year. Third-year students rotate on our services, and seniors take our elective as well as taking acting internships on our teaching services. We act as mentors and interest group leaders. There is certainly more to this list. We also spend time teaching NP and PA students.

The internal medicine residents rotate on our hospitalist services, and we staff the general medical services. We interact with them daily when they are on consult services, trying to set a role model. General medicine, geriatric, and hospital medicine fellows rotate through as well.

We also teach the nurses on services and through in-services and daily rounds to cement the working relationship and improve communication. We teach each other. A day rarely goes by without a colleague passing on a tasty medical tidbit. (Of course, for me, a tabla blanca, no shortage of space for pearls). And finally we teach our patients and their families. Every day we do this, and if we don’t then we are missing the point of our profession entirely.

Each party—patient or student—has something to learn from us, but more importantly we have something to learn from them. Osler wrote that “The stimulus of their presence (the student) neutralizes the clinical apathy certain, sooner or later, to beset the man who makes lonely “rounds” with his house physician.”

One hundred years plus later, much of what was written is still true: Whether in a teaching institution or making “lonely rounds” we must strive to continue to educate ourselves, our colleagues, and our patients. And what better place to do it than the hospital? TH

Dr. Newman is the physician editor of The Hospitalist. He’s also consultant, Hospital Internal Medicine, and assistant professor of internal medicine and medical history, Mayo Clinic College of Medicine, Rochester, Minn.

Bibliography

Osler W (Sir) Aequanimitas. 1945. The Blakiston Company, Philadelphia. p. 311-327.

The hospital is the only proper college in which to rear a true disciple of Aesculapius.—John Abernethy (1764-1831), surgeon and teacher

With this quote Sir William Osler began his address, “The Hospital as a College?” to the Academy of Medicine in New York in 1903. His second quote for this report was from the famed physician Oliver Wendell Holmes Sr. in 1867:

“The most essential part of a student’s instruction is obtained, as I believe, not in the lecture room, but at the bedside. Nothing seen there is lost: the rhythms of disease are learned by frequent repetition: its unforeseen occurrence stamp themselves indelibly on the memory. Before the student is aware of what he had acquired he has learned the aspects and causes and probable issue of the disease he has seen with his teacher and the proper mode of dealing with them, as far as his master knows.”

In his report Osler was celebrating a quarter century’s success in education. He demanded a better general education for students, a lengthened period for professional study, and the substitution of theoretical by practical learning. He wanted the student not to learn only from dissecting the sympathetic nervous system but to learn to “take a blood pressure observation” with a kymograph (an instrument used to record the temporal variations of any physiological or muscular process; it consists essentially of a revolving drum, bearing a record sheet on which a stylus travels).

Osler observed that there should be no teaching without a patient for a text: “The whole of medicine is in observation” that the teacher’s art is educating the student’s finger to feel and eyes to see. Give the student good methods and a proper point of view, and experience will do the rest.

Osler expressed confidence that students would keep the hospital physician from slovenliness and improve the care of patients. He was also concerned that “we ask too much of the resident physicians, whose number has not increased in proportion to the enormous amount of work thrust upon them.” Students were the answer, the proto-scut-monkey.

The practicality of working out of a teaching hospital was outlined at length in Osler’s report. The student’s third year should begin with a systematic physical diagnosis course, first in history taking, then in writing reports. Concurrently, a physical examination course should be given several days a week with individual cases assigned to students to follow, and instruction is accessing the literature. Next comes clinical microscopy—an essential in an era where there was often no lab to call upon. In general, medical clinic occurs one day a week when interesting cases are brought from the wards. Of note, committees were appointed to report on every case of pneumonia.

In revamping medical education Osler brought the third-year students to the outpatient clinic and the fourth-year students to the wards. What implication does this have for us as hospitalists?

I have no pretensions about being another Osler (I am barely a Newman on my best days), but still my colleagues and I trudge along in our teaching duties. What education do we really do? I sat down after reading Osler’s paper, stimulated by a tangential question from the esteemed Tom Baudenistel, MD, and decided to see exactly whom we were teaching.

First there are medical students. We are faculty on their first-year selectives, offering a shadow experience. We staff the introduction to physical exam courses in second year. Third-year students rotate on our services, and seniors take our elective as well as taking acting internships on our teaching services. We act as mentors and interest group leaders. There is certainly more to this list. We also spend time teaching NP and PA students.

The internal medicine residents rotate on our hospitalist services, and we staff the general medical services. We interact with them daily when they are on consult services, trying to set a role model. General medicine, geriatric, and hospital medicine fellows rotate through as well.

We also teach the nurses on services and through in-services and daily rounds to cement the working relationship and improve communication. We teach each other. A day rarely goes by without a colleague passing on a tasty medical tidbit. (Of course, for me, a tabla blanca, no shortage of space for pearls). And finally we teach our patients and their families. Every day we do this, and if we don’t then we are missing the point of our profession entirely.

Each party—patient or student—has something to learn from us, but more importantly we have something to learn from them. Osler wrote that “The stimulus of their presence (the student) neutralizes the clinical apathy certain, sooner or later, to beset the man who makes lonely “rounds” with his house physician.”

One hundred years plus later, much of what was written is still true: Whether in a teaching institution or making “lonely rounds” we must strive to continue to educate ourselves, our colleagues, and our patients. And what better place to do it than the hospital? TH

Dr. Newman is the physician editor of The Hospitalist. He’s also consultant, Hospital Internal Medicine, and assistant professor of internal medicine and medical history, Mayo Clinic College of Medicine, Rochester, Minn.

Bibliography

Osler W (Sir) Aequanimitas. 1945. The Blakiston Company, Philadelphia. p. 311-327.

An 84-year-old woman with history of coronary artery disease, hypertension, and hyperlipidemia presented with six months of anorexia, nausea, a five-pound weight loss, weakness, and nonbloody diarrhea. Over the past one to two weeks, she noticed decreased urine output despite her use of furosemide.

She was found to have a serum creatinine of 3.5 mg/dL on admission, increased from 1.5 mg/dL five days previously. She had no rash, dyspnea, cough, or abdominal pain. Urinalysis revealed >100 red blood cells (RBC), >100 white blood cells (WBC), occasional hyaline casts, and many gramnegative bacilli. Ciprofloxacin was started for her urinary tract infection. A renal biopsy was performed. The images shown are photomicrographs of light microscopy and immunofluorescence of the renal biopsy specimen. TH

Kidney biopsy: Immunofluorescence

Which of the following would be the most appropriate initial therapy for this condition?

1. Increase dose of furosemide;
2. Start fish oil;
3. Initiate Low-dose dopamine;
4. Discontinue ACE inhibitor; or
5. Begin emergent plasmapheresis.

Discussion

The correct answer is e: plasmapheresis. The renal biopsy, as shown in the image at left, reveals crescents involving glomeruli on light microscopy and linear IgG staining on immunofluorescence. This patient has antiglomerular basement membrane (anti-GBM) glomerulonephritis (GN), which accounts for 10% to 20% of crescentic glomerulonephritides. It is characterized by circulating antibodies to the glomerular basement membrane with deposition of IgG or, rarely, IgA along the GBM.

The pulmonary-renal vasculitic syndrome is called Goodpasture’s syndrome, in which pulmonary hemorrhage occurs concurrently with GN. Anti-GBM disease has a bimodal distribution, with peaks in the second to third decades and the sixth to seventh decades of life.

Kidney biopsy: Immunofluorescence

Etiology is usually idiopathic, but hydrocarbon exposure has also been associated with the disease. Clinical presentation of renal anti-GBM disease is characterized by an acute onset of GN with severe oliguria or anuria. Urinalysis typically shows hematuria, dysmorphic red blood cells, and red blood cell casts. The diagnostic laboratory finding is circulating antibodies to GBM, specifically to the alpha-3 chain of type IV collagen; these are detected by radioimmunoassay or enzyme immunoassay in approximately 90% of patients.

The standard treatment for anti-GBM disease includes intensive plasmapheresis combined with corticosteroids and cyclophosphamide or azathioprine. Plasmapheresis consists of removal of two to four liters of plasma and replacement with fresh frozen plasma or a 5% albumin solution on a daily basis until circulating antibody levels become undetectable (usually two to three weeks). Steroids should be administered initially as pulse methylprednisolone (30 mg/kg or 1,000 mg intravenously over 20 minutes) for three doses (daily or every other day) followed by daily oral prednisone (1 mg/kg per day) for at least the first month, followed by a gradual taper. The initial cyclophosphamide dose is 2 mg/kg per day either orally or intravenously (0.5 g/m2 body surface area).

Selecting patients for treatment is based primarily on severity at presentation. Based on a large retrospective review of 71 patients treated with plasma exchange, prednisolone, and cyclophosphamide, those who presented with plasma creatinine (Cr) concentration of less than 5.7 mg/dL or those who had Cr greater than 5.7 mg/dL but did not require immediate dialysis had a favorable long-term patient and renal survival (approximately 70% to 80% at 90 months). Patients who required immediate dialysis had poor survival (approximately 35% at 90 months). Patients who had crescents in all glomeruli on renal biopsy required long-term maintenance dialysis. Therefore, plasma exchange, prednisone, and cyclophosphamide should be administered in the following settings:

1. Pulmonary hemorrhage;
2. Renal failure (Cr above 5-7 mg/dL) but not requiring immediate renal replacement therapy; and
3. Less severe disease on renal biopsy (less than 30% to 50% crescents). Therapy is unlikely to be effective in patients who present with dialysisdependent renal failure without hemoptysis or if 100% of glomeruli have crescents on renal biopsy. In these settings, the risk of therapy may exceed the likelihood of benefit.

Fish oil is a potential therapy for IgA nephropathy, not anti-GBM disease. ACE inhibition may be useful in patients with nephrotic syndrome. IV hydration would be likely to cause volume overload and precipitate the need for acute dialysis. Low-dose dopamine has not proven effective in reversing acute renal failure. TH

REFERENCES

1. Clarkson MR, Brenner BM. Pocket Companion to Brenner & Rector’s The Kidney, 7th ed. Philadelphia, Pa: Elsevier Inc; 2005:198-199.
2. Rose BD, Kaplan AA, Appel GB. Treatment of anti-GBM antibody disease (Goodpasture’s syndrome). UpToDate Online. Available at: www.uptodate.com/physicians/pulmonology_toclist.asp. Last accessed August 18, 2005.
3. Levy JB, Turner AN, Rees AJ, et al. Long-term outcome of anti-glomerular basement membrane antibody disease treated with plasma exchange and immunosuppression. Ann Intern Med. 2001;134:1033.
4. Bolton WK. Goodpasture’s syndrome. Kidney Int. 1996;50:1753.
5. Jennette JC. Rapidly progressive crescentic glomerulonephritis. Kidney Int. 2003;63:1164.

An 84-year-old woman with history of coronary artery disease, hypertension, and hyperlipidemia presented with six months of anorexia, nausea, a five-pound weight loss, weakness, and nonbloody diarrhea. Over the past one to two weeks, she noticed decreased urine output despite her use of furosemide.

She was found to have a serum creatinine of 3.5 mg/dL on admission, increased from 1.5 mg/dL five days previously. She had no rash, dyspnea, cough, or abdominal pain. Urinalysis revealed >100 red blood cells (RBC), >100 white blood cells (WBC), occasional hyaline casts, and many gramnegative bacilli. Ciprofloxacin was started for her urinary tract infection. A renal biopsy was performed. The images shown are photomicrographs of light microscopy and immunofluorescence of the renal biopsy specimen. TH

Kidney biopsy: Immunofluorescence

Which of the following would be the most appropriate initial therapy for this condition?

1. Increase dose of furosemide;
2. Start fish oil;
3. Initiate Low-dose dopamine;
4. Discontinue ACE inhibitor; or
5. Begin emergent plasmapheresis.

Discussion

The correct answer is e: plasmapheresis. The renal biopsy, as shown in the image at left, reveals crescents involving glomeruli on light microscopy and linear IgG staining on immunofluorescence. This patient has antiglomerular basement membrane (anti-GBM) glomerulonephritis (GN), which accounts for 10% to 20% of crescentic glomerulonephritides. It is characterized by circulating antibodies to the glomerular basement membrane with deposition of IgG or, rarely, IgA along the GBM.

The pulmonary-renal vasculitic syndrome is called Goodpasture’s syndrome, in which pulmonary hemorrhage occurs concurrently with GN. Anti-GBM disease has a bimodal distribution, with peaks in the second to third decades and the sixth to seventh decades of life.

Kidney biopsy: Immunofluorescence

Etiology is usually idiopathic, but hydrocarbon exposure has also been associated with the disease. Clinical presentation of renal anti-GBM disease is characterized by an acute onset of GN with severe oliguria or anuria. Urinalysis typically shows hematuria, dysmorphic red blood cells, and red blood cell casts. The diagnostic laboratory finding is circulating antibodies to GBM, specifically to the alpha-3 chain of type IV collagen; these are detected by radioimmunoassay or enzyme immunoassay in approximately 90% of patients.

The standard treatment for anti-GBM disease includes intensive plasmapheresis combined with corticosteroids and cyclophosphamide or azathioprine. Plasmapheresis consists of removal of two to four liters of plasma and replacement with fresh frozen plasma or a 5% albumin solution on a daily basis until circulating antibody levels become undetectable (usually two to three weeks). Steroids should be administered initially as pulse methylprednisolone (30 mg/kg or 1,000 mg intravenously over 20 minutes) for three doses (daily or every other day) followed by daily oral prednisone (1 mg/kg per day) for at least the first month, followed by a gradual taper. The initial cyclophosphamide dose is 2 mg/kg per day either orally or intravenously (0.5 g/m2 body surface area).

Selecting patients for treatment is based primarily on severity at presentation. Based on a large retrospective review of 71 patients treated with plasma exchange, prednisolone, and cyclophosphamide, those who presented with plasma creatinine (Cr) concentration of less than 5.7 mg/dL or those who had Cr greater than 5.7 mg/dL but did not require immediate dialysis had a favorable long-term patient and renal survival (approximately 70% to 80% at 90 months). Patients who required immediate dialysis had poor survival (approximately 35% at 90 months). Patients who had crescents in all glomeruli on renal biopsy required long-term maintenance dialysis. Therefore, plasma exchange, prednisone, and cyclophosphamide should be administered in the following settings:

1. Pulmonary hemorrhage;
2. Renal failure (Cr above 5-7 mg/dL) but not requiring immediate renal replacement therapy; and
3. Less severe disease on renal biopsy (less than 30% to 50% crescents). Therapy is unlikely to be effective in patients who present with dialysisdependent renal failure without hemoptysis or if 100% of glomeruli have crescents on renal biopsy. In these settings, the risk of therapy may exceed the likelihood of benefit.

Fish oil is a potential therapy for IgA nephropathy, not anti-GBM disease. ACE inhibition may be useful in patients with nephrotic syndrome. IV hydration would be likely to cause volume overload and precipitate the need for acute dialysis. Low-dose dopamine has not proven effective in reversing acute renal failure. TH

REFERENCES

1. Clarkson MR, Brenner BM. Pocket Companion to Brenner & Rector’s The Kidney, 7th ed. Philadelphia, Pa: Elsevier Inc; 2005:198-199.
2. Rose BD, Kaplan AA, Appel GB. Treatment of anti-GBM antibody disease (Goodpasture’s syndrome). UpToDate Online. Available at: www.uptodate.com/physicians/pulmonology_toclist.asp. Last accessed August 18, 2005.
3. Levy JB, Turner AN, Rees AJ, et al. Long-term outcome of anti-glomerular basement membrane antibody disease treated with plasma exchange and immunosuppression. Ann Intern Med. 2001;134:1033.
4. Bolton WK. Goodpasture’s syndrome. Kidney Int. 1996;50:1753.
5. Jennette JC. Rapidly progressive crescentic glomerulonephritis. Kidney Int. 2003;63:1164.

An 84-year-old woman with history of coronary artery disease, hypertension, and hyperlipidemia presented with six months of anorexia, nausea, a five-pound weight loss, weakness, and nonbloody diarrhea. Over the past one to two weeks, she noticed decreased urine output despite her use of furosemide.

She was found to have a serum creatinine of 3.5 mg/dL on admission, increased from 1.5 mg/dL five days previously. She had no rash, dyspnea, cough, or abdominal pain. Urinalysis revealed >100 red blood cells (RBC), >100 white blood cells (WBC), occasional hyaline casts, and many gramnegative bacilli. Ciprofloxacin was started for her urinary tract infection. A renal biopsy was performed. The images shown are photomicrographs of light microscopy and immunofluorescence of the renal biopsy specimen. TH

Kidney biopsy: Immunofluorescence

Which of the following would be the most appropriate initial therapy for this condition?

1. Increase dose of furosemide;
2. Start fish oil;
3. Initiate Low-dose dopamine;
4. Discontinue ACE inhibitor; or
5. Begin emergent plasmapheresis.

Discussion

The correct answer is e: plasmapheresis. The renal biopsy, as shown in the image at left, reveals crescents involving glomeruli on light microscopy and linear IgG staining on immunofluorescence. This patient has antiglomerular basement membrane (anti-GBM) glomerulonephritis (GN), which accounts for 10% to 20% of crescentic glomerulonephritides. It is characterized by circulating antibodies to the glomerular basement membrane with deposition of IgG or, rarely, IgA along the GBM.

The pulmonary-renal vasculitic syndrome is called Goodpasture’s syndrome, in which pulmonary hemorrhage occurs concurrently with GN. Anti-GBM disease has a bimodal distribution, with peaks in the second to third decades and the sixth to seventh decades of life.

Kidney biopsy: Immunofluorescence

Etiology is usually idiopathic, but hydrocarbon exposure has also been associated with the disease. Clinical presentation of renal anti-GBM disease is characterized by an acute onset of GN with severe oliguria or anuria. Urinalysis typically shows hematuria, dysmorphic red blood cells, and red blood cell casts. The diagnostic laboratory finding is circulating antibodies to GBM, specifically to the alpha-3 chain of type IV collagen; these are detected by radioimmunoassay or enzyme immunoassay in approximately 90% of patients.

The standard treatment for anti-GBM disease includes intensive plasmapheresis combined with corticosteroids and cyclophosphamide or azathioprine. Plasmapheresis consists of removal of two to four liters of plasma and replacement with fresh frozen plasma or a 5% albumin solution on a daily basis until circulating antibody levels become undetectable (usually two to three weeks). Steroids should be administered initially as pulse methylprednisolone (30 mg/kg or 1,000 mg intravenously over 20 minutes) for three doses (daily or every other day) followed by daily oral prednisone (1 mg/kg per day) for at least the first month, followed by a gradual taper. The initial cyclophosphamide dose is 2 mg/kg per day either orally or intravenously (0.5 g/m2 body surface area).

Selecting patients for treatment is based primarily on severity at presentation. Based on a large retrospective review of 71 patients treated with plasma exchange, prednisolone, and cyclophosphamide, those who presented with plasma creatinine (Cr) concentration of less than 5.7 mg/dL or those who had Cr greater than 5.7 mg/dL but did not require immediate dialysis had a favorable long-term patient and renal survival (approximately 70% to 80% at 90 months). Patients who required immediate dialysis had poor survival (approximately 35% at 90 months). Patients who had crescents in all glomeruli on renal biopsy required long-term maintenance dialysis. Therefore, plasma exchange, prednisone, and cyclophosphamide should be administered in the following settings:

1. Pulmonary hemorrhage;
2. Renal failure (Cr above 5-7 mg/dL) but not requiring immediate renal replacement therapy; and
3. Less severe disease on renal biopsy (less than 30% to 50% crescents). Therapy is unlikely to be effective in patients who present with dialysisdependent renal failure without hemoptysis or if 100% of glomeruli have crescents on renal biopsy. In these settings, the risk of therapy may exceed the likelihood of benefit.

Fish oil is a potential therapy for IgA nephropathy, not anti-GBM disease. ACE inhibition may be useful in patients with nephrotic syndrome. IV hydration would be likely to cause volume overload and precipitate the need for acute dialysis. Low-dose dopamine has not proven effective in reversing acute renal failure. TH

REFERENCES

1. Clarkson MR, Brenner BM. Pocket Companion to Brenner & Rector’s The Kidney, 7th ed. Philadelphia, Pa: Elsevier Inc; 2005:198-199.
2. Rose BD, Kaplan AA, Appel GB. Treatment of anti-GBM antibody disease (Goodpasture’s syndrome). UpToDate Online. Available at: www.uptodate.com/physicians/pulmonology_toclist.asp. Last accessed August 18, 2005.
3. Levy JB, Turner AN, Rees AJ, et al. Long-term outcome of anti-glomerular basement membrane antibody disease treated with plasma exchange and immunosuppression. Ann Intern Med. 2001;134:1033.
4. Bolton WK. Goodpasture’s syndrome. Kidney Int. 1996;50:1753.
5. Jennette JC. Rapidly progressive crescentic glomerulonephritis. Kidney Int. 2003;63:1164.