The Journal of Family Practice is a peer-reviewed and indexed journal that provides its 95,000 family physician readers with timely, practical, and evidence-based information that they can immediately put into practice. Research and applied evidence articles, plus patient-oriented departments like Practice Alert, PURLs, and Clinical Inquiries can be found in print and at jfponline.com. The Web site, which logs an average of 125,000 visitors every month, also offers audiocasts by physician specialists and interactive features like Instant Polls and Photo Rounds Friday—a weekly diagnostic puzzle.

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Proclivity ID
18805001
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Citation Name
J Fam Pract
Negative Keywords
gaming
gambling
compulsive behaviors
ammunition
assault rifle
black jack
Boko Haram
bondage
child abuse
cocaine
Daech
drug paraphernalia
explosion
gun
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ISIL
ISIS
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Is colonoscopy indicated if only one of 3 stool samples is positive for occult blood?

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Is colonoscopy indicated if only one of 3 stool samples is positive for occult blood?
EVIDENCE-BASED ANSWER:

Yes. Any occult blood on a fecal occult blood test (FOBT) should be investigated further because colorectal cancer mortality decreases when positive FOBT screenings are evaluated (strength of recommendation: A, systematic review, evidence-based guidelines).

 

Follow-up of positive screening results lowers colorectal cancer mortality

No studies directly compare the need for colonoscopy when various numbers of stool samples are positive for occult blood on an FOBT. However, a Cochrane review of 4 randomized controlled trials (RCTs) with more than 300,000 patients examined the effectiveness of the FOBT for colorectal cancer screening.1 Each study varied in its follow-up approach to a positive FOBT.

Two RCTs offered screening with FOBT or standard care (no screening) and immediately followed up any positive results with a colonoscopy. The screened group had lower colorectal cancer mortality (N=46,551; risk ratio [RR]=0.75; 95% confidence interval [CI], 0.62-0.91) than the unscreened group (N=61,933; RR=0.84; 95% CI, 0.73-0.96).

Another trial screened with FOBT or standard care and offered colonoscopy if 5 or more samples were positive on initial testing or one or more were positive on repeat testing. The screened group showed reduced colorectal cancer mortality (N=152,850; RR=0.87; 95% CI, 0.78-0.97).

The final trial examined screening with FOBT compared with standard care and inconsistently offered repeat FOBT or sigmoidoscopy with double-contrast barium enema if any samples were positive on initial testing, which resulted in decreased colorectal cancer mortality for the screened group (N=68,308; RR=0.84; 95% CI, 0.71-0.99).

 

 

Evidence-based guidelines recommend follow-up colonoscopy

Evidence-based guidelines from the United States Preventive Services Task Force, the European Commission, and the Canadian Task Force on Preventive Health Care state that FOBT should be used for colorectal cancer screening and that any positive screening test should be followed up with colonoscopy to further evaluate for neoplasm.2-4

An evidence- and expert opinion-based guideline from the American Cancer Society, the US Multi-Society Task Force on Colorectal Cancer, and the American College of Radiology clarifies the issue further by emphasizing that any positive FOBT necessitates a colonoscopy and stating that repeat FOBT or other test is inappropriate as follow-up.5

References

1. Hewitson P, Glasziou P, Watson E, et al. Cochrane systematic review of colorectal cancer screening using the fecal occult blood test (hemoccult): an update. Am J Gastroenterol. 2008;103:1541-1549.

2. United States Preventive Services Task Force. Screening for colorectal cancer: US Preventive Services Task Force recommendation statement. Ann Intern Med. 2008;149:627-638.

3. vonKarsa L, Patnick J, Segnan N, eds. European Guidelines for Quality Assurance in Colorectal Cancer Screening and Diagnosis. Luxembourg: Publications Office of the European Union; 2010.

4. McLeod RS; Canadian Task Force on Preventive Health Care. Screening strategies for colorectal cancer: a systematic review of the evidence. Can J Gastroenterol. 2001;15:647-660.

5. Levin B, Lieberman DA, McFarland B, et al. Screening and surveillance for the early detection of colorectal cancer and adenomatous polyps, 2008: a joint guideline from the American Cancer Society, the US Multi-Society Task Force on Colorectal Cancer, and the American College of Radiology. Gastroenterology. 2008;134:1570-1595.

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Christopher Gilchrist, MD
Bachir Tazkarji, MD

University of Toronto, Canada

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Corey Lyon, DO
University of Colorado Family Medicine Residency, Denver

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Christopher Gilchrist, MD; Bachir Tazkarji, MD; colonoscopy; FOBT; fecal occult blood test; colorectal cancer
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Christopher Gilchrist, MD
Bachir Tazkarji, MD

University of Toronto, Canada

EDITOR
Corey Lyon, DO
University of Colorado Family Medicine Residency, Denver

Author and Disclosure Information

Christopher Gilchrist, MD
Bachir Tazkarji, MD

University of Toronto, Canada

EDITOR
Corey Lyon, DO
University of Colorado Family Medicine Residency, Denver

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EVIDENCE-BASED ANSWER:

Yes. Any occult blood on a fecal occult blood test (FOBT) should be investigated further because colorectal cancer mortality decreases when positive FOBT screenings are evaluated (strength of recommendation: A, systematic review, evidence-based guidelines).

 

Follow-up of positive screening results lowers colorectal cancer mortality

No studies directly compare the need for colonoscopy when various numbers of stool samples are positive for occult blood on an FOBT. However, a Cochrane review of 4 randomized controlled trials (RCTs) with more than 300,000 patients examined the effectiveness of the FOBT for colorectal cancer screening.1 Each study varied in its follow-up approach to a positive FOBT.

Two RCTs offered screening with FOBT or standard care (no screening) and immediately followed up any positive results with a colonoscopy. The screened group had lower colorectal cancer mortality (N=46,551; risk ratio [RR]=0.75; 95% confidence interval [CI], 0.62-0.91) than the unscreened group (N=61,933; RR=0.84; 95% CI, 0.73-0.96).

Another trial screened with FOBT or standard care and offered colonoscopy if 5 or more samples were positive on initial testing or one or more were positive on repeat testing. The screened group showed reduced colorectal cancer mortality (N=152,850; RR=0.87; 95% CI, 0.78-0.97).

The final trial examined screening with FOBT compared with standard care and inconsistently offered repeat FOBT or sigmoidoscopy with double-contrast barium enema if any samples were positive on initial testing, which resulted in decreased colorectal cancer mortality for the screened group (N=68,308; RR=0.84; 95% CI, 0.71-0.99).

 

 

Evidence-based guidelines recommend follow-up colonoscopy

Evidence-based guidelines from the United States Preventive Services Task Force, the European Commission, and the Canadian Task Force on Preventive Health Care state that FOBT should be used for colorectal cancer screening and that any positive screening test should be followed up with colonoscopy to further evaluate for neoplasm.2-4

An evidence- and expert opinion-based guideline from the American Cancer Society, the US Multi-Society Task Force on Colorectal Cancer, and the American College of Radiology clarifies the issue further by emphasizing that any positive FOBT necessitates a colonoscopy and stating that repeat FOBT or other test is inappropriate as follow-up.5

EVIDENCE-BASED ANSWER:

Yes. Any occult blood on a fecal occult blood test (FOBT) should be investigated further because colorectal cancer mortality decreases when positive FOBT screenings are evaluated (strength of recommendation: A, systematic review, evidence-based guidelines).

 

Follow-up of positive screening results lowers colorectal cancer mortality

No studies directly compare the need for colonoscopy when various numbers of stool samples are positive for occult blood on an FOBT. However, a Cochrane review of 4 randomized controlled trials (RCTs) with more than 300,000 patients examined the effectiveness of the FOBT for colorectal cancer screening.1 Each study varied in its follow-up approach to a positive FOBT.

Two RCTs offered screening with FOBT or standard care (no screening) and immediately followed up any positive results with a colonoscopy. The screened group had lower colorectal cancer mortality (N=46,551; risk ratio [RR]=0.75; 95% confidence interval [CI], 0.62-0.91) than the unscreened group (N=61,933; RR=0.84; 95% CI, 0.73-0.96).

Another trial screened with FOBT or standard care and offered colonoscopy if 5 or more samples were positive on initial testing or one or more were positive on repeat testing. The screened group showed reduced colorectal cancer mortality (N=152,850; RR=0.87; 95% CI, 0.78-0.97).

The final trial examined screening with FOBT compared with standard care and inconsistently offered repeat FOBT or sigmoidoscopy with double-contrast barium enema if any samples were positive on initial testing, which resulted in decreased colorectal cancer mortality for the screened group (N=68,308; RR=0.84; 95% CI, 0.71-0.99).

 

 

Evidence-based guidelines recommend follow-up colonoscopy

Evidence-based guidelines from the United States Preventive Services Task Force, the European Commission, and the Canadian Task Force on Preventive Health Care state that FOBT should be used for colorectal cancer screening and that any positive screening test should be followed up with colonoscopy to further evaluate for neoplasm.2-4

An evidence- and expert opinion-based guideline from the American Cancer Society, the US Multi-Society Task Force on Colorectal Cancer, and the American College of Radiology clarifies the issue further by emphasizing that any positive FOBT necessitates a colonoscopy and stating that repeat FOBT or other test is inappropriate as follow-up.5

References

1. Hewitson P, Glasziou P, Watson E, et al. Cochrane systematic review of colorectal cancer screening using the fecal occult blood test (hemoccult): an update. Am J Gastroenterol. 2008;103:1541-1549.

2. United States Preventive Services Task Force. Screening for colorectal cancer: US Preventive Services Task Force recommendation statement. Ann Intern Med. 2008;149:627-638.

3. vonKarsa L, Patnick J, Segnan N, eds. European Guidelines for Quality Assurance in Colorectal Cancer Screening and Diagnosis. Luxembourg: Publications Office of the European Union; 2010.

4. McLeod RS; Canadian Task Force on Preventive Health Care. Screening strategies for colorectal cancer: a systematic review of the evidence. Can J Gastroenterol. 2001;15:647-660.

5. Levin B, Lieberman DA, McFarland B, et al. Screening and surveillance for the early detection of colorectal cancer and adenomatous polyps, 2008: a joint guideline from the American Cancer Society, the US Multi-Society Task Force on Colorectal Cancer, and the American College of Radiology. Gastroenterology. 2008;134:1570-1595.

References

1. Hewitson P, Glasziou P, Watson E, et al. Cochrane systematic review of colorectal cancer screening using the fecal occult blood test (hemoccult): an update. Am J Gastroenterol. 2008;103:1541-1549.

2. United States Preventive Services Task Force. Screening for colorectal cancer: US Preventive Services Task Force recommendation statement. Ann Intern Med. 2008;149:627-638.

3. vonKarsa L, Patnick J, Segnan N, eds. European Guidelines for Quality Assurance in Colorectal Cancer Screening and Diagnosis. Luxembourg: Publications Office of the European Union; 2010.

4. McLeod RS; Canadian Task Force on Preventive Health Care. Screening strategies for colorectal cancer: a systematic review of the evidence. Can J Gastroenterol. 2001;15:647-660.

5. Levin B, Lieberman DA, McFarland B, et al. Screening and surveillance for the early detection of colorectal cancer and adenomatous polyps, 2008: a joint guideline from the American Cancer Society, the US Multi-Society Task Force on Colorectal Cancer, and the American College of Radiology. Gastroenterology. 2008;134:1570-1595.

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“Will you pray with me, Doctor?”

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Last week, a patient asked me to pray with her, and I did. That, in itself, made the visit extraordinary. But the time spent getting to know this patient over the course of several visits is the real family medicine story I want to share with you.

I first met 52-year-old Thelma a few months ago as a new patient. She had a 25-year history of chronic back and leg pain stemming from an auto accident. She had made the usual rounds to pain consultants, tried numerous medications, and undergone multiple procedures—but still had daily pain. I was starting to get that uneasy feeling that she would be difficult to manage.

She was taking gabapentin, which provided minimal pain relief, but no narcotics. She also had large fibroids that caused iron deficiency, but the iron tablets she’d been taking made her sick to her stomach.

Her initial hemoglobin was 5.4 g/dL. I switched her to an oral iron supplement she could tolerate. A repeat pelvic ultrasound showed even larger fibroids than 3 years ago, so I thought she was probably headed for surgery, and I asked her to come back to discuss it. I also asked her to try amitriptyline 10 mg/d at bedtime, which might help her pain and improve her poor sleep.

We need to stay open to the possibility that a patient's own treatment plan may be superior to the one we come up with.

I was wrong on both accounts, as I discovered during the “prayer visit.” When I walked into the exam room, I noticed Thelma was reading her pocket bible. I greeted her with, “Hello, Thelma. Good to see you.” Then I added, “I see you are reading a good book.” She said Yes, and put it away as I proceeded with the interview. Yes, she was tolerating the iron supplement just fine and her hemoglobin was up to 9.2 g/dL. No, the amitriptyline was not working and she didn’t like to take drugs anyway.

She explained that God helped her to manage her pain—with help from her daughter and granddaughter. She also told me she didn’t want surgery for the fibroids. “God will shrink them for me,” she said. (And she was right, as she was approaching menopause.)

“Will you pray with me, Dr. Hickner?” she asked.

I was touched that she trusted me enough to ask me to pray with her, and so I agreed. Thelma’s request also reminded me how important it is to get to know our patients in a personal way, and to explore their ideas about treatments rather than sticking to our own narrow medical repertoire.

Thelma’s treatment plan was different than I anticipated. In fact, I am humbled to say that it was far superior to mine.

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Last week, a patient asked me to pray with her, and I did. That, in itself, made the visit extraordinary. But the time spent getting to know this patient over the course of several visits is the real family medicine story I want to share with you.

I first met 52-year-old Thelma a few months ago as a new patient. She had a 25-year history of chronic back and leg pain stemming from an auto accident. She had made the usual rounds to pain consultants, tried numerous medications, and undergone multiple procedures—but still had daily pain. I was starting to get that uneasy feeling that she would be difficult to manage.

She was taking gabapentin, which provided minimal pain relief, but no narcotics. She also had large fibroids that caused iron deficiency, but the iron tablets she’d been taking made her sick to her stomach.

Her initial hemoglobin was 5.4 g/dL. I switched her to an oral iron supplement she could tolerate. A repeat pelvic ultrasound showed even larger fibroids than 3 years ago, so I thought she was probably headed for surgery, and I asked her to come back to discuss it. I also asked her to try amitriptyline 10 mg/d at bedtime, which might help her pain and improve her poor sleep.

We need to stay open to the possibility that a patient's own treatment plan may be superior to the one we come up with.

I was wrong on both accounts, as I discovered during the “prayer visit.” When I walked into the exam room, I noticed Thelma was reading her pocket bible. I greeted her with, “Hello, Thelma. Good to see you.” Then I added, “I see you are reading a good book.” She said Yes, and put it away as I proceeded with the interview. Yes, she was tolerating the iron supplement just fine and her hemoglobin was up to 9.2 g/dL. No, the amitriptyline was not working and she didn’t like to take drugs anyway.

She explained that God helped her to manage her pain—with help from her daughter and granddaughter. She also told me she didn’t want surgery for the fibroids. “God will shrink them for me,” she said. (And she was right, as she was approaching menopause.)

“Will you pray with me, Dr. Hickner?” she asked.

I was touched that she trusted me enough to ask me to pray with her, and so I agreed. Thelma’s request also reminded me how important it is to get to know our patients in a personal way, and to explore their ideas about treatments rather than sticking to our own narrow medical repertoire.

Thelma’s treatment plan was different than I anticipated. In fact, I am humbled to say that it was far superior to mine.

Last week, a patient asked me to pray with her, and I did. That, in itself, made the visit extraordinary. But the time spent getting to know this patient over the course of several visits is the real family medicine story I want to share with you.

I first met 52-year-old Thelma a few months ago as a new patient. She had a 25-year history of chronic back and leg pain stemming from an auto accident. She had made the usual rounds to pain consultants, tried numerous medications, and undergone multiple procedures—but still had daily pain. I was starting to get that uneasy feeling that she would be difficult to manage.

She was taking gabapentin, which provided minimal pain relief, but no narcotics. She also had large fibroids that caused iron deficiency, but the iron tablets she’d been taking made her sick to her stomach.

Her initial hemoglobin was 5.4 g/dL. I switched her to an oral iron supplement she could tolerate. A repeat pelvic ultrasound showed even larger fibroids than 3 years ago, so I thought she was probably headed for surgery, and I asked her to come back to discuss it. I also asked her to try amitriptyline 10 mg/d at bedtime, which might help her pain and improve her poor sleep.

We need to stay open to the possibility that a patient's own treatment plan may be superior to the one we come up with.

I was wrong on both accounts, as I discovered during the “prayer visit.” When I walked into the exam room, I noticed Thelma was reading her pocket bible. I greeted her with, “Hello, Thelma. Good to see you.” Then I added, “I see you are reading a good book.” She said Yes, and put it away as I proceeded with the interview. Yes, she was tolerating the iron supplement just fine and her hemoglobin was up to 9.2 g/dL. No, the amitriptyline was not working and she didn’t like to take drugs anyway.

She explained that God helped her to manage her pain—with help from her daughter and granddaughter. She also told me she didn’t want surgery for the fibroids. “God will shrink them for me,” she said. (And she was right, as she was approaching menopause.)

“Will you pray with me, Dr. Hickner?” she asked.

I was touched that she trusted me enough to ask me to pray with her, and so I agreed. Thelma’s request also reminded me how important it is to get to know our patients in a personal way, and to explore their ideas about treatments rather than sticking to our own narrow medical repertoire.

Thelma’s treatment plan was different than I anticipated. In fact, I am humbled to say that it was far superior to mine.

References

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Abdominal distention • loss of appetite • elevated creatinine • Dx?

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THE CASE

A 21-year-old male college student sought care at our urology clinic for a 2-year history of progressive abdominal distention and loss of appetite due to abdominal pressure. On physical examination, his abdomen was distended and tense, but without any tenderness on palpation or any costovertebral angle tenderness. He had no abdominal or flank pain, and wasn’t in acute distress. His blood pressure was normal.

Initial lab test results were significant for elevated creatinine at 2.7 mg/dL (normal: 0.7-1.3 mg/dL) and blood urea nitrogen (BUN) at 31.1 mg/dL (normal: 6-20 mg/dL). Results of a complete blood count (CBC) were within normal ranges, including a white blood cell (WBC) count of 7900, hemoglobin level of 15.1 g/dL, and platelet count of 217,000/mcL. A urinalysis showed only a mild increase in the WBC count.

THE DIAGNOSIS

We performed a computed tomography (CT) scan of the patient’s abdomen, which revealed bilateral hydronephrosis secondary to ureteropelvic junction obstruction (UPJO). The patient’s right kidney was mildly to moderately enlarged, but the left kidney was massive (FIGURE 1A). The hydronephrotic left kidney had extended itself across the midline (FIGURE 1B), pushed the ipsilateral diaphragm upward, and displaced the bladder downward.

The patient underwent right-sided ureteral stent placement for temporary drainage and a complete left-sided nephrectomy. During the surgery, the left kidney was first aspirated, and more than 11,000 cc of clear urine was drained. (Aspiration reduced the kidney size, allowing the surgeon to make a smaller incision.) The removed kidney contained an additional 1200 cc of cloudy residual fluid (FIGURE 2). UPJO was confirmed by the pathological examination of the excised organ.

DISCUSSION

UPJO is the most common etiology for congenital hydronephrosis.1 Because it can cause little to no pain, hydronephrosis secondary to UPJO can be asymptomatic and may not present until later in life. Frequently, an abdominal mass is the initial clinical presentation.

When the hydronephrotic fluid exceeds 1000 cc, the condition is referred to as giant hydronephrosis.2 Although several cases of giant hydronephrosis secondary to UPJO have been reported in the medical literature,3-5 the volume of the hydronephrotic fluid in these cases rarely exceeded 10,000 cc. We believe our patient may be the most severe case of hydronephrosis secondary to bilateral UPJO, with 12,200 cc of fluid. His condition reached this late stage only because his right kidney retained adequate function.

Diagnosis of hydronephrosis is straightforward with an abdominal ultrasound and/or CT scan. Widespread use of abdominal ultrasound as a screening tool has significantly increased the diagnosis of asymptomatic hydronephrosis, and many cases are secondary to UPJO.6 The true incidence of UPJO is unknown, but it is more prevalent in males than in females, and in 10% to 40% of cases, the condition is bilateral.7 Congenital UPJO typically results from intrinsic pathology of the ureter. The diseased segment is often fibrotic, strictured, and aperistaltic.8

Treatment choice depends on whether renal function can be preserved

Treatment of hydronephrosis is straightforward; when there is little or no salvageable renal function (<10%), a simple nephrectomy is indicated, as was the case for our patient. Nephrectomy can be accomplished by either an open or laparoscopic approach.

When there is salvageable renal function, treatment options include pyeloplasty and pyelotomy. Traditionally, open dismembered pyeloplasty has been the gold standard. However, with advances in endoscopic and laparoscopic techniques, there has been a shift toward minimally invasive procedures. Laparoscopic pyeloplasty—with or without robotic assistance—and endoscopic pyelotomy—with either a percutaneous or retrograde approach—are now typically performed. Ureteral stenting should only be used as a temporary measure.

Our patient. Four weeks after the nephrectomy, our patient underwent a right side pyeloplasty, which was successful. He had an uneventful recovery from both procedures. His renal function stabilized and other than routine follow-up, he required no additional treatment.

THE TAKEAWAY

Most cases of hydronephrosis in young people are due to congenital abnormalities, and UPJO is the leading cause. However, the condition can be asymptomatic and may not present until later in life. Whenever a patient presents with an asymptomatic abdominal mass, hydronephrosis should be part of the differential diagnosis. Treatment options include nephrectomy when there is no salvageable kidney function or pyeloplasty and pyelotomy when some kidney function can be preserved.

References

1. Brown T, Mandell J, Lebowitz RL. Neonatal hydronephrosis in the era ultrasonography. AJR Am J Roentgenol. 1987;148:959-963.

2. Stirling WC. Massive hydronephrosis complicated by hydroureter: Report of 3 cases. J Urol. 1939;42:520.

3. Chiang PH, Chen MT, Chou YH, et al. Giant hydronephrosis: report of 4 cases with review of the literature. J Formos Med Assoc. 1990;89:811-817.

4. Aguiar MFM, Oliveira APS, Silva SC, et al. Giant hydronephrosis secondary to ureteropelvic junction obstruction. Gazzetta Medica Italiana-Archivio per le Scienze Mediche. 2009;168:207.

5. Sepulveda L, Rodriguesa F. Giant hydronephrosis - a late diagnosis of ureteropelvic junction obstruction. World J Nephrol Urol. 2013;2:33.

6. Bernstein GT, Mandell J, Lebowitz RL, et al. Ureteropelvic junction obstruction in neonate. J Urol. 1988;140:1216-1221.

7. Johnston JH, Evans JP, Glassberg KI, et al. Pelvic hydronephrosis in children: a review of 219 personal cases. J Urol. 1977;117:97-101.

8. Gosling JA, Dixon JS. Functional obstruction of the ureter and renal pelvis. A histological and electron microscopic study. Br J Urol. 1978;50:145-152.

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shaw.p.wan@hotmail.com

The authors reported no potential conflict of interest relevant to this article.

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shaw.p.wan@hotmail.com

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THE CASE

A 21-year-old male college student sought care at our urology clinic for a 2-year history of progressive abdominal distention and loss of appetite due to abdominal pressure. On physical examination, his abdomen was distended and tense, but without any tenderness on palpation or any costovertebral angle tenderness. He had no abdominal or flank pain, and wasn’t in acute distress. His blood pressure was normal.

Initial lab test results were significant for elevated creatinine at 2.7 mg/dL (normal: 0.7-1.3 mg/dL) and blood urea nitrogen (BUN) at 31.1 mg/dL (normal: 6-20 mg/dL). Results of a complete blood count (CBC) were within normal ranges, including a white blood cell (WBC) count of 7900, hemoglobin level of 15.1 g/dL, and platelet count of 217,000/mcL. A urinalysis showed only a mild increase in the WBC count.

THE DIAGNOSIS

We performed a computed tomography (CT) scan of the patient’s abdomen, which revealed bilateral hydronephrosis secondary to ureteropelvic junction obstruction (UPJO). The patient’s right kidney was mildly to moderately enlarged, but the left kidney was massive (FIGURE 1A). The hydronephrotic left kidney had extended itself across the midline (FIGURE 1B), pushed the ipsilateral diaphragm upward, and displaced the bladder downward.

The patient underwent right-sided ureteral stent placement for temporary drainage and a complete left-sided nephrectomy. During the surgery, the left kidney was first aspirated, and more than 11,000 cc of clear urine was drained. (Aspiration reduced the kidney size, allowing the surgeon to make a smaller incision.) The removed kidney contained an additional 1200 cc of cloudy residual fluid (FIGURE 2). UPJO was confirmed by the pathological examination of the excised organ.

DISCUSSION

UPJO is the most common etiology for congenital hydronephrosis.1 Because it can cause little to no pain, hydronephrosis secondary to UPJO can be asymptomatic and may not present until later in life. Frequently, an abdominal mass is the initial clinical presentation.

When the hydronephrotic fluid exceeds 1000 cc, the condition is referred to as giant hydronephrosis.2 Although several cases of giant hydronephrosis secondary to UPJO have been reported in the medical literature,3-5 the volume of the hydronephrotic fluid in these cases rarely exceeded 10,000 cc. We believe our patient may be the most severe case of hydronephrosis secondary to bilateral UPJO, with 12,200 cc of fluid. His condition reached this late stage only because his right kidney retained adequate function.

Diagnosis of hydronephrosis is straightforward with an abdominal ultrasound and/or CT scan. Widespread use of abdominal ultrasound as a screening tool has significantly increased the diagnosis of asymptomatic hydronephrosis, and many cases are secondary to UPJO.6 The true incidence of UPJO is unknown, but it is more prevalent in males than in females, and in 10% to 40% of cases, the condition is bilateral.7 Congenital UPJO typically results from intrinsic pathology of the ureter. The diseased segment is often fibrotic, strictured, and aperistaltic.8

Treatment choice depends on whether renal function can be preserved

Treatment of hydronephrosis is straightforward; when there is little or no salvageable renal function (<10%), a simple nephrectomy is indicated, as was the case for our patient. Nephrectomy can be accomplished by either an open or laparoscopic approach.

When there is salvageable renal function, treatment options include pyeloplasty and pyelotomy. Traditionally, open dismembered pyeloplasty has been the gold standard. However, with advances in endoscopic and laparoscopic techniques, there has been a shift toward minimally invasive procedures. Laparoscopic pyeloplasty—with or without robotic assistance—and endoscopic pyelotomy—with either a percutaneous or retrograde approach—are now typically performed. Ureteral stenting should only be used as a temporary measure.

Our patient. Four weeks after the nephrectomy, our patient underwent a right side pyeloplasty, which was successful. He had an uneventful recovery from both procedures. His renal function stabilized and other than routine follow-up, he required no additional treatment.

THE TAKEAWAY

Most cases of hydronephrosis in young people are due to congenital abnormalities, and UPJO is the leading cause. However, the condition can be asymptomatic and may not present until later in life. Whenever a patient presents with an asymptomatic abdominal mass, hydronephrosis should be part of the differential diagnosis. Treatment options include nephrectomy when there is no salvageable kidney function or pyeloplasty and pyelotomy when some kidney function can be preserved.

THE CASE

A 21-year-old male college student sought care at our urology clinic for a 2-year history of progressive abdominal distention and loss of appetite due to abdominal pressure. On physical examination, his abdomen was distended and tense, but without any tenderness on palpation or any costovertebral angle tenderness. He had no abdominal or flank pain, and wasn’t in acute distress. His blood pressure was normal.

Initial lab test results were significant for elevated creatinine at 2.7 mg/dL (normal: 0.7-1.3 mg/dL) and blood urea nitrogen (BUN) at 31.1 mg/dL (normal: 6-20 mg/dL). Results of a complete blood count (CBC) were within normal ranges, including a white blood cell (WBC) count of 7900, hemoglobin level of 15.1 g/dL, and platelet count of 217,000/mcL. A urinalysis showed only a mild increase in the WBC count.

THE DIAGNOSIS

We performed a computed tomography (CT) scan of the patient’s abdomen, which revealed bilateral hydronephrosis secondary to ureteropelvic junction obstruction (UPJO). The patient’s right kidney was mildly to moderately enlarged, but the left kidney was massive (FIGURE 1A). The hydronephrotic left kidney had extended itself across the midline (FIGURE 1B), pushed the ipsilateral diaphragm upward, and displaced the bladder downward.

The patient underwent right-sided ureteral stent placement for temporary drainage and a complete left-sided nephrectomy. During the surgery, the left kidney was first aspirated, and more than 11,000 cc of clear urine was drained. (Aspiration reduced the kidney size, allowing the surgeon to make a smaller incision.) The removed kidney contained an additional 1200 cc of cloudy residual fluid (FIGURE 2). UPJO was confirmed by the pathological examination of the excised organ.

DISCUSSION

UPJO is the most common etiology for congenital hydronephrosis.1 Because it can cause little to no pain, hydronephrosis secondary to UPJO can be asymptomatic and may not present until later in life. Frequently, an abdominal mass is the initial clinical presentation.

When the hydronephrotic fluid exceeds 1000 cc, the condition is referred to as giant hydronephrosis.2 Although several cases of giant hydronephrosis secondary to UPJO have been reported in the medical literature,3-5 the volume of the hydronephrotic fluid in these cases rarely exceeded 10,000 cc. We believe our patient may be the most severe case of hydronephrosis secondary to bilateral UPJO, with 12,200 cc of fluid. His condition reached this late stage only because his right kidney retained adequate function.

Diagnosis of hydronephrosis is straightforward with an abdominal ultrasound and/or CT scan. Widespread use of abdominal ultrasound as a screening tool has significantly increased the diagnosis of asymptomatic hydronephrosis, and many cases are secondary to UPJO.6 The true incidence of UPJO is unknown, but it is more prevalent in males than in females, and in 10% to 40% of cases, the condition is bilateral.7 Congenital UPJO typically results from intrinsic pathology of the ureter. The diseased segment is often fibrotic, strictured, and aperistaltic.8

Treatment choice depends on whether renal function can be preserved

Treatment of hydronephrosis is straightforward; when there is little or no salvageable renal function (<10%), a simple nephrectomy is indicated, as was the case for our patient. Nephrectomy can be accomplished by either an open or laparoscopic approach.

When there is salvageable renal function, treatment options include pyeloplasty and pyelotomy. Traditionally, open dismembered pyeloplasty has been the gold standard. However, with advances in endoscopic and laparoscopic techniques, there has been a shift toward minimally invasive procedures. Laparoscopic pyeloplasty—with or without robotic assistance—and endoscopic pyelotomy—with either a percutaneous or retrograde approach—are now typically performed. Ureteral stenting should only be used as a temporary measure.

Our patient. Four weeks after the nephrectomy, our patient underwent a right side pyeloplasty, which was successful. He had an uneventful recovery from both procedures. His renal function stabilized and other than routine follow-up, he required no additional treatment.

THE TAKEAWAY

Most cases of hydronephrosis in young people are due to congenital abnormalities, and UPJO is the leading cause. However, the condition can be asymptomatic and may not present until later in life. Whenever a patient presents with an asymptomatic abdominal mass, hydronephrosis should be part of the differential diagnosis. Treatment options include nephrectomy when there is no salvageable kidney function or pyeloplasty and pyelotomy when some kidney function can be preserved.

References

1. Brown T, Mandell J, Lebowitz RL. Neonatal hydronephrosis in the era ultrasonography. AJR Am J Roentgenol. 1987;148:959-963.

2. Stirling WC. Massive hydronephrosis complicated by hydroureter: Report of 3 cases. J Urol. 1939;42:520.

3. Chiang PH, Chen MT, Chou YH, et al. Giant hydronephrosis: report of 4 cases with review of the literature. J Formos Med Assoc. 1990;89:811-817.

4. Aguiar MFM, Oliveira APS, Silva SC, et al. Giant hydronephrosis secondary to ureteropelvic junction obstruction. Gazzetta Medica Italiana-Archivio per le Scienze Mediche. 2009;168:207.

5. Sepulveda L, Rodriguesa F. Giant hydronephrosis - a late diagnosis of ureteropelvic junction obstruction. World J Nephrol Urol. 2013;2:33.

6. Bernstein GT, Mandell J, Lebowitz RL, et al. Ureteropelvic junction obstruction in neonate. J Urol. 1988;140:1216-1221.

7. Johnston JH, Evans JP, Glassberg KI, et al. Pelvic hydronephrosis in children: a review of 219 personal cases. J Urol. 1977;117:97-101.

8. Gosling JA, Dixon JS. Functional obstruction of the ureter and renal pelvis. A histological and electron microscopic study. Br J Urol. 1978;50:145-152.

References

1. Brown T, Mandell J, Lebowitz RL. Neonatal hydronephrosis in the era ultrasonography. AJR Am J Roentgenol. 1987;148:959-963.

2. Stirling WC. Massive hydronephrosis complicated by hydroureter: Report of 3 cases. J Urol. 1939;42:520.

3. Chiang PH, Chen MT, Chou YH, et al. Giant hydronephrosis: report of 4 cases with review of the literature. J Formos Med Assoc. 1990;89:811-817.

4. Aguiar MFM, Oliveira APS, Silva SC, et al. Giant hydronephrosis secondary to ureteropelvic junction obstruction. Gazzetta Medica Italiana-Archivio per le Scienze Mediche. 2009;168:207.

5. Sepulveda L, Rodriguesa F. Giant hydronephrosis - a late diagnosis of ureteropelvic junction obstruction. World J Nephrol Urol. 2013;2:33.

6. Bernstein GT, Mandell J, Lebowitz RL, et al. Ureteropelvic junction obstruction in neonate. J Urol. 1988;140:1216-1221.

7. Johnston JH, Evans JP, Glassberg KI, et al. Pelvic hydronephrosis in children: a review of 219 personal cases. J Urol. 1977;117:97-101.

8. Gosling JA, Dixon JS. Functional obstruction of the ureter and renal pelvis. A histological and electron microscopic study. Br J Urol. 1978;50:145-152.

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PRACTICE RECOMMENDATIONS

› To increase adherence, give patients treatment options, ensure that they participate in discussions of treatment, and empower them to reach "informed collaboration" as opposed to informed consent. A
› Ask patients to tell you in their own words what they understand about the treatment they have chosen. A
› At each follow-up visit, anticipate nonadherence, ask nonjudgmental questions about missed medication doses and sexual adverse effects, and offer simple solutions. A

Strength of recommendation (SOR)

A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series

Medication nonadherence is a major—and remediable—contributor to poor outcomes, leading to approximately 125,000 preventable deaths,1 worsening of acute and chronic conditions, and billions of dollars in avoidable costs related to increased hospitalizations and emergency visits each year.2,3 Nonadherence rates are 20% to 30% among patients being treated for cancer and acute illness3 and 50% to 60% for chronic conditions, with an average of 50% of all patients taking their medication incorrectly—or not at all.2,4,5

What’s more, nonadherence disrupts the physician-patient relationship6—a serious problem, given that feeling understood is often the most critical component of recovery.7-9

With that in mind, the words used to describe the problem have changed. Compliance and noncompliance, the older labels, were based on the assumptions that patients are passive recipients of medical advice that they should follow without question and that they are to blame for not doing so. Adherence and nonadherence, on the other hand, emphasize mutual agreement and the patient’s freedom to follow the doctor’s recommendations or not, without blame if he or she decides not to do so.10

Many systemic approaches have been tried to maximize adherence, including disease management (eg, Web-based assessment tools, clinical guidelines, and call center-based triage), smart phone apps11 (for reminders and monitoring), and paying for or subsidizing the cost of drugs for those who can’t afford them. All have met with limited success.12 Based on a thorough review of the literature, we suggest a different approach.

Evidence-based efforts by clinicians are the key to effective prescribing and maximal adherence. In the text and table that follow, we summarize physician and patient factors that influence adherence and present optimal prescribing guidelines.

Listen carefully, then respond

Whether patients are seeing a primary care physician or a specialist, they want their doctors to spend more time with them and to give them more comprehensive information about their condition.13-15 The interaction should begin with the physician listening carefully to the patient before responding, but all too often this is not the case.

Family physicians have been found to interrupt patients 23 seconds after asking a question.16 To improve communication, listen quietly until the patient finishes presenting his or her complaints and agenda for the visit. Then ask, “Is there anything else that’s important for me to know?”17

Be more forthcoming

It is equally important for physicians to respond fully, but this is often not the case. A study involving internists found that in patient encounters lasting 20 minutes, physicians devoted little more than one minute, on average, to explaining the patient’s medical condition. The research showed that many physicians greatly overestimated the time they spent doing so.13

Studies have also shown that clinicians tell patients the name of the drug they’re prescribing 74% of the time and state its purpose 87% of the time, but discuss potential adverse effects and duration of treatment a mere 34% of the time. More than 4 in 10 patients are not told the frequency or timing of doses or the number of tablets to take.18

To improve communication, take the following steps when it’s your turn to talk:

Avoid medical jargon. Technical language (eg, edema) and medical shorthand (eg, history) is a significant barrier to patient understanding. In one study of more than 800 pediatrician visits, such speech was found to be detrimental more than half of the time. Although many mothers were confused by the terms, they rarely asked for clarification.19

Listen quietly until patients finish presenting their complaints and reason for the visit, then ask whether there is anything else that's important for you to know.

It has been suggested that doctors and patients have engaged in a “communication conspiracy.”20 In one study, even after obstetricians and gynecologists had identified terms that they knew their patients did not understand, they continued to use them, and in only 15% of visits where unfamiliar terms were used did the patients admit that they did not understand them.21 Part of the problem may be that patients believe they must be seen as undemanding and compliant if they are to receive optimal attention from their physicians.22

 

 

Compounding the problem is the fact that clinicians’ use of highly technical language doubles when they are pressured for time,20 suggesting that this behavior could become more widespread as the demand for greater efficiency on the part of physicians increases.

Simplify the treatment regimen. It also helps to keep treatment regimens as straightforward as possible. Prescribing multiple medications simultaneously or giving patients a more complicated regimen decreases adherence. In one study, adherence rates of 84% were achieved when the regimen called for once-a-day dosing, but dropped to 59% when patients were instructed to take their medication 3 times a day.23

Ask the patient to summarize. Using simple terms and clear, succinct explanations promotes understanding, but asking the patient to summarize what you’ve just said is an ideal way to find out just how much he or she grasped. “What will you tell your family about your diagnosis and treatment?” you might ask, or “Tell me what you plan to do to ensure that you follow the prescribed regimen.”

This is particularly important when patients are not native English speakers or when the news is bad. Patients find it particularly tough to understand difficult messages, such as a poor prognosis,24 and are often unaware of their poor comprehension. This was underscored by a study of emergency department (ED) patients, in which 78% demonstrated deficient comprehension in at least one domain (eg, post-ED care, diagnosis, cause) but only 20% recognized their lack of understanding.25

Asking patients if they have any other questions is a crucial step in ensuring complete understanding.21,26

Take steps to maximize patient recall

Even when patients understand what they’ve heard, research suggests they may not retain it. Overall, 40% to 80% of medical information is forgotten immediately, and almost half of what is retained is incorrect.27,28 This is a serious problem, as understanding and accurate recall increase patient satisfaction and the likelihood of adherence to treatment (FIGURE W1).28,29

There are 3 basic explanations for poor recall: factors related to the clinician, such as the use of difficult medical terminology; the mode of communication (eg, spoken vs written); and factors related to the patient, such as a low level of education or learning disability.29-32

Being as specific as possible and spending more time explaining the diagnosis and treatment has been shown to enhance patient recall. In an experiment in which patients read advice on how to develop self-control over their eating, the use of simple language and specific instructions, rather than general rules, increased recall.33 Providing generic information by whatever means does little to improve recall and might even inhibit it.

Linking advice to the patient’s chief complaint, thereby creating a “teachable moment,” is also helpful.34 For example, you might tell a patient with a kidney infection that “Your backache is also because of the kidney infection. Both the backache and the burning during urination should be better about 3 days after you start these pills.”

Watch your affect. How relaxed or worried you appear also influences patient recall. In a recent study, 40 women at risk for breast cancer viewed videotapes of an oncologist presenting mammogram results. Compared to women whose results were conveyed by a physician who appeared relaxed, those who had the same findings presented by a physician who seemed worried perceived their clinical situation to be more severe, developed higher anxiety, and recalled significantly less of what they were told.35

Use multiple means of communication. In a comparison study, patients who received verbal lists of actions for managing fever and sore mouth accompanied by pictographs—images that represented the information presented—had a correct recall rate of 85%; those who received the verbal information alone had a recall rate of only 14%.36,37

Clinicians tell patients the name of the drug they're prescribing 74% of the time and its purpose 87% of the time, but discuss potential adverse effects and duration of treatment a mere 34% of the time.

A review of recall in cancer patients also found that tailoring communication to the individual—providing an audiotape of the consultation, for instance, or having the patient bring a list of questions and addressing them one by one—is most effective.36 Another study assessed the retention of pediatric patients and their parents when they received either a verbal report alone or a verbal report plus written information or visuals. The researchers concluded that children and their parents should receive verbal reports only when such reports are supplemented with written information or visuals.37

The large body of research on learning and memory has proven useful in designing educational materials for those with poor reading skills. When images were used to convey meaning to 21 adults in a job training program—all with less than fifth grade reading skills—they had on average 85% correct recall immediately after the training and 71% recall 4 weeks later. Although the impact on symptom management and patient quality of life has yet to be studied, these findings suggest that pictures can help people with low literacy recall and retain complex information.38

 

 

Overall, while written or recorded instructions appear to improve recall in most situations,39 images have been shown to have the greatest impact.36,37,40

Is the patient ready to adhere to treatment?

No matter how well or by what means you communicate, some patients are not ready for change. Patients in the “precontemplation” stage of change—who may not even recognize the need for change, let alone consider it—can benefit from supportive education and motivational interviewing, while those in the “contemplation” stage need support and convincing to reach the “preparation” stage. It is only in the “action” stage, however, that a patient is ready to collaborate with his or her physician in agreeing on and adhering to treatment.40

Comorbid depression is a common condition, particularly in those with chronic illness, and one of the strongest predictors of nonadherence.1,41 Thus, depression screening for all patients who are chronically or severely ill or nonadherent is strongly recommended, followed by treatment when appropriate.41

“Informed collaboration” is critical

Comorbid depression is particularly common among those with chronic illnesses, and one of the strongest predictors of nonadherence.

Research shows that if both physician and patient agree on the individual’s medical problem, it will be improved or resolved at follow-up in about half of all cases. In contrast, when the physician alone sees the patient’s condition as a problem, just over a quarter of cases improve, regardless of the severity.42 Compounding this difficulty is the finding that patients fail to report up to two-thirds of their most important health problems.43 When physicians identify them, discord and denial typically result.42

Thus, concordance (we prefer the term “informed collaboration”)—an overt agreement reached after a discussion in which the physician shares expert knowledge, then listens to and respects the feelings and beliefs of the patient with regard to how, when, or whether he or she will take the recommended treatment44—is crucial.42,43,45,46

One way to reach informed collaboration is to give patients problem lists or letters summarizing their health problems in simple and specific terms after each visit, in hopes that the written communication will encourage discussion and a physician-patient partnership in addressing them.43 In a recent study of 967 psychiatric outpatients, adherence was significantly higher among those who cited concordance between their preferences and their treatment and felt that they had participated in decision making.47

Problems can arise at any time

Even after a patient starts out fully adhering to his medication regimen, several issues can derail treatment. Inability to afford the medication is one potential problem.48 Adverse effects are another major reason for discontinuation. Sexual dysfunction, caused by a number of drugs, is embarrassing to many patients and frequently goes unaddressed.49 Thus, a patient may stop taking the medication without saying why—seemingly for no apparent reason. The best approach is to ask specifically why it was discontinued, including direct questions about sexual adverse effects.

Prescribing recommendations

Sexual dysfunction, caused by a number of drugs, is embarrassing to many patients and frequently goes unaddressed.

We believe that the outcome of treatment is being determined from the moment a patient steps into your office. Thus, we’ve compiled an evidence-based checklist (TABLE)24,33,40,41,47,49,50 with broad areas for discussion that constitute the art and science of prescribing. These fall into 3 main areas: 1) what to say before you write a prescription; 2) how to get patient buy-in (informed collaboration, rather than informed consent) when you’re ready to write the prescription; and 3) what to address to boost the likelihood of continued adherence at follow-up visits.

It is clear that allowing adequate patient participation and arriving at concordance and overt agreement lead to better clinical outcomes.51 The sequential steps we recommend may take a few extra minutes up front, but without them, nonadherence is highly likely. While physicians are supportive of shared decision making in theory, they are often less confident that this is achieved in practice.52,53

It may help to keep in mind that every step need not be carried out by the physician. Using other members of the health care team, such as a nurse, medical assistant, or health coach, to provide patient education and support and take the patient through a number of the steps that are included in a physician visit has become increasingly necessary—and is easily accommodated in this case.

As the physician, you bear the final responsibility to ensure that the critical elements—particularly the overt agreement—are addressed. Ultimately supporting your patient's decision and reinforcing it will ensure continued adherence.

CORRESPONDENCE
Swati Shivale, MBBS, Department of Psychiatry, SUNY Upstate Medical University, 750 Adams Street, Syracuse, NY 13210; shivalsw@upstate.edu

References

 

1. Martin LR, Summer LW, Haskard KB, et al. The challenge of patient adherence. Ther Clin Risk Manage. 2005;1:189-199.

2. Jha AK, Aubert R, Yao J, et al. Greater adherence to diabetes drugs is linked to less hospital use and could save nearly $5 billion annually. Health Aff. 2012;8:1836-1846.

3. DiMatteo MR. Variations in patients’ adherence to medical recommendations: a quantitative review of 50 years of research. Med Care. 2004;42:200–209.

4. Brown MT, Bussell JK. Medication adherence: WHO cares? Mayo Clin Proc. 2011;86:304-314.

5. Iuga AO, McGuire MJ. Adherence and health care costs. Risk Manage Healthcare Policy. 2014;7:35-44.

6. Ansell B. Not getting to goal: the clinical costs of noncompliance. J Managed Care Pharm. 2008;14(Suppl):6-b.

7. Van Kleef GA, van den Berg H, Heerdink MW. The persuasive power of emotions: effects of emotional expressions on attitude formation and change. J Appl Psychol. 2014. Nov 17 [Epub ahead of print].

8. Wright JM, Lee C, Chambers GK. Real-world effectiveness of antihypertensive drugs. Can Med Assoc J. 2000;162:190–191.

9. Dunbar J, Agras W. Compliance with medical instructions. In: Ferguson J, Taylor C, eds. The Comprehensive Handbook of Behavioral Medicine. New York, NY: Springer; 1980:115–145.

10. Horne R, Weinman J, Barber N, et al. Concordance, adherence and compliance in medicine taking. Report for the National Coordinating Centre for NHS Service Delivery and Organisation R & D (NCCSDO). December 2005. University of Leeds, School of Healthcare. Available at: http://www.netscc.ac.uk/hsdr/files/project/SDO_FR_08-1412-076_V01.pdf. Accessed June 18, 2015.

11. Dayer L, Heldenbrand S, Anderson P, et al. Smartphone medication adherence apps: potential benefits to patients and providers. J Am Pharm Assoc. 2013; 53:172-181.

12. Jaarsma T, van der Wal ML, Lesman-Leegte I, et al. Effect of moderate or intensive disease management program on outcome in patients with heart failure: coordinating study evaluating outcomes of advising and counseling in heart failure (COACH). Arch Intern Med. 2008;168:316-324.

13. Waitzkin H. Doctor-patient communication. Clinical implications of social scientific research. JAMA. 1984;252:2441–2446.

14. Freeman GK, Horder JP, Howie JGR, et al. Evolving general practice consultation in Britain: issues of length and context. BMJ. 2002;324:880-882.

15. Beisecker AE, Beisecker TD. Patient information-seeking behaviors when communicating with doctors. Med Care. 1990;28:19-28.

16. Marvel M, Epstein R, Flowers K, et al. Soliciting the patient’s agenda: have we improved? JAMA. 1999; 281:283-287.

17. Barrier P, Li T, Jensen N. Two words to improve physician-patient communication: what else? Mayo Clin Proc. 2003;78:211-214.

18. Tarn D, Heritage J, Paterniti D, et al. Physician communications when prescribing new medications. Arch Internal Med. 2006;166:1855-1862.

19. Korsch BM, Gozzi EK, Francis V. Gaps in doctor-patient communication, doctor-patient interaction and patient satisfaction. Pediatrics. 1968;42:855-871.

20. Lipton HL, Svarstad BL. Parental expectations of a multi-disciplinary clinic for children with developmental disabilities. J Health Soc Behav. 1974;15:157-166.

21. McKinlay JB. Who is really ignorant--physician or patient? J Health Soc Behav. 1975;16:3-11.

22. Nehring V, Geach B. Patients’ evaluation of their care: why they don’t complain. Nurs Outlook. 1973; 21:317-321.

23. De las Cuevas C, Peñate W, de Rivera L. To what extent is treatment adherence of psychiatric patients influenced by their participation in shared decision making? Patient Preference Adherence. 2014;8:1547–1553.

24. Tuckett D, Boulton M, Olson C, et al. Meetings Between Experts–An Approach to Sharing Ideas in Medical Consultations. London, UK: Tavistock Publications; 1985.

25. Engel K, Heisler M, Smith D, et al. Patient comprehension of emergency department care and instructions: are patients aware of when they do not understand? Ann Emerg Med. 2009;53:454-461.

26. Viswanathan M, Golin CE, Jones CD, et al. Interventions to improve adherence to self-administered medications for chronic diseases in the United States: a systematic review. Ann Intern Med. 2012;157:785-795.

27. McGuire LC. Remembering what the doctor said: organization and older adults’ memory for medical information. Exp Aging Res. 1996;22:403-428.

28. Anderson JL, Dodman S, Kopelman M, et al. Patient information recall in a rheumatology clinic. Rheumatol Rehab. 1979;18:18-22.

29. Ley P. Communicating with Patients. New York, NY: Croom Helm; 1988.

30. Ley P. Primacy, rated importance, and the recall of medical statements. J Health Soc Beh. 1972;13:311-317.

31. Ley P, Bradshaw PW, Eaves D, et al. A method for increasing patients’ recall of information presented by doctors. Psychol Med. 1973;3:217-220.

32. Kessels R. Patients’ memory for medical information. J Royal Soc Med. 2003;96:219-222.

33. Bradshaw PW, Ley P, Kincey JA. Recall of medical advice: comprehensibility and specificity. Br J Clin Psychol. 1975;14:55-82.

34. Flocke S, Stange K. Direct observation and patient recall of health behavior advice. Prev Med. 2004;38:34-349.

35. Shapiro DE, Boggs SR, Melamed BG, et al. The effect of varied physician affect on recall, anxiety, and perceptions in women at risk for breast cancer: an analogue study. Health Psychol. 1992;11:61-66.

36. van der Meulen N, Jansen J, van Dulmen S, et al. Interventions to improve recall of medical information in cancer patients: a systematic review of the literature. Psychooncology. 2008;17:857-868.

37. Houts PS, Bachrach R, Witmer JT, et al. Using pictographs to enhance recall of spoken medical instructions. Patient Educ Couns. 1998;35:83-88.

38. Watson P, McKinstry B. A systematic review of interventions to improve recall of medical advice in healthcare consultations. J Royal Soc Med. 2009;102:235-243.

39. Houts PS, Witmer JT, Egeth HE, et al. Using pictographs to enhance recall of spoken medical instructions II. Patient Educ Couns. 2001;43:231-242.

40. Prochaska J, Norcross J, DiClemente C. Changing for Good. New York, NY: Avon; 1995.

41. DiMatteo M, Lepper H, Croghan T. Depression is a risk factor for non-compliance in medical treatment: a meta-analysis of the effects of anxiety and depression in patient adherence. Arch Int Med. 2000;160: 2101-2107.

42. Starfield B, Wray C, Hess K, et al. The influence of patientpractitioner agreement on outcome of care. Am J Pub Health. 1981;71:127–131.

43. Scheitel SM, Boland BJ, Wollan PC, et al. Patient-physician agreement about medical diagnoses and cardiovascular risk factors in the ambulatory general medical examination. Mayo Clin Proc. 1996;71: 1131-1137.

44. Bell JS, Airaksinen MS, Lyles A, et al. Concordance is not synonymous with compliance or adherence. Br J Clin Pharmacol. 2007;64:710-711.

45. Staiger T, Jarvik J, Deyo R, et al. Patient-physician agreement as a predictor of outcomes in patients with back pain. J Gen Int Med. 2005;20:935-937.

46. Stewart M, Brown J, Donner A, et al. The impact of patient-centered care on outcomes. J Fam Pract. 2000;49:796-804.

47. Saini SD, Schoenfeld P, Kaulback K, et al. Effect of medication dosing frequency on adherence in chronic diseases. Am J Manage Care. 2009;15:e22–e33.

48. Kedenge SV, Kangwana BP, Waweru EW, et al. Understanding the impact of subsidizing artemisinin-based combination therapies (ACTs) in the retail sector–results from focus group discussions in rural Kenya. PLoS One. 2013;8:e54371.

49. Santini I, De Lauretis I, Roncone R, et al. Psychotropic-associated sexual dysfunctions: a survey of clinical pharmacology and medication-associated practice. Clin Ter. 2014;165:e243-e252.

50. Ibrahim S, Hossam M, Belal D. Study of non-compliance among chronic hemodialysis patients and its impact on patients’ outcomes. Saudi J Kidney Dis Transpl. 2015;26:243-249.

51. Légaré F, Stacey D, Turcotte S, et al. Interventions for improving the adoption of shared decision making by healthcare professionals. Cochrane Database Syst Rev. 2014;(9):CD006732.

52. Cox K, Stevenson F, Britten N, et al. A Systematic Review of Communication between Patients and Healthcare Professionals about Medicine Taking and Prescribing. London, UK: GKT Concordance Unit Kings College; 2004.

53. Edwards A, Elwyn G. Involving patients in decision making and communicating risk: a longitudinal evaluation of doctors’ attitudes and confidence during a randomized trial. J Eval Clin Pract. 2004;10:431-437.

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PRACTICE RECOMMENDATIONS

› To increase adherence, give patients treatment options, ensure that they participate in discussions of treatment, and empower them to reach "informed collaboration" as opposed to informed consent. A
› Ask patients to tell you in their own words what they understand about the treatment they have chosen. A
› At each follow-up visit, anticipate nonadherence, ask nonjudgmental questions about missed medication doses and sexual adverse effects, and offer simple solutions. A

Strength of recommendation (SOR)

A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series

Medication nonadherence is a major—and remediable—contributor to poor outcomes, leading to approximately 125,000 preventable deaths,1 worsening of acute and chronic conditions, and billions of dollars in avoidable costs related to increased hospitalizations and emergency visits each year.2,3 Nonadherence rates are 20% to 30% among patients being treated for cancer and acute illness3 and 50% to 60% for chronic conditions, with an average of 50% of all patients taking their medication incorrectly—or not at all.2,4,5

What’s more, nonadherence disrupts the physician-patient relationship6—a serious problem, given that feeling understood is often the most critical component of recovery.7-9

With that in mind, the words used to describe the problem have changed. Compliance and noncompliance, the older labels, were based on the assumptions that patients are passive recipients of medical advice that they should follow without question and that they are to blame for not doing so. Adherence and nonadherence, on the other hand, emphasize mutual agreement and the patient’s freedom to follow the doctor’s recommendations or not, without blame if he or she decides not to do so.10

Many systemic approaches have been tried to maximize adherence, including disease management (eg, Web-based assessment tools, clinical guidelines, and call center-based triage), smart phone apps11 (for reminders and monitoring), and paying for or subsidizing the cost of drugs for those who can’t afford them. All have met with limited success.12 Based on a thorough review of the literature, we suggest a different approach.

Evidence-based efforts by clinicians are the key to effective prescribing and maximal adherence. In the text and table that follow, we summarize physician and patient factors that influence adherence and present optimal prescribing guidelines.

Listen carefully, then respond

Whether patients are seeing a primary care physician or a specialist, they want their doctors to spend more time with them and to give them more comprehensive information about their condition.13-15 The interaction should begin with the physician listening carefully to the patient before responding, but all too often this is not the case.

Family physicians have been found to interrupt patients 23 seconds after asking a question.16 To improve communication, listen quietly until the patient finishes presenting his or her complaints and agenda for the visit. Then ask, “Is there anything else that’s important for me to know?”17

Be more forthcoming

It is equally important for physicians to respond fully, but this is often not the case. A study involving internists found that in patient encounters lasting 20 minutes, physicians devoted little more than one minute, on average, to explaining the patient’s medical condition. The research showed that many physicians greatly overestimated the time they spent doing so.13

Studies have also shown that clinicians tell patients the name of the drug they’re prescribing 74% of the time and state its purpose 87% of the time, but discuss potential adverse effects and duration of treatment a mere 34% of the time. More than 4 in 10 patients are not told the frequency or timing of doses or the number of tablets to take.18

To improve communication, take the following steps when it’s your turn to talk:

Avoid medical jargon. Technical language (eg, edema) and medical shorthand (eg, history) is a significant barrier to patient understanding. In one study of more than 800 pediatrician visits, such speech was found to be detrimental more than half of the time. Although many mothers were confused by the terms, they rarely asked for clarification.19

Listen quietly until patients finish presenting their complaints and reason for the visit, then ask whether there is anything else that's important for you to know.

It has been suggested that doctors and patients have engaged in a “communication conspiracy.”20 In one study, even after obstetricians and gynecologists had identified terms that they knew their patients did not understand, they continued to use them, and in only 15% of visits where unfamiliar terms were used did the patients admit that they did not understand them.21 Part of the problem may be that patients believe they must be seen as undemanding and compliant if they are to receive optimal attention from their physicians.22

 

 

Compounding the problem is the fact that clinicians’ use of highly technical language doubles when they are pressured for time,20 suggesting that this behavior could become more widespread as the demand for greater efficiency on the part of physicians increases.

Simplify the treatment regimen. It also helps to keep treatment regimens as straightforward as possible. Prescribing multiple medications simultaneously or giving patients a more complicated regimen decreases adherence. In one study, adherence rates of 84% were achieved when the regimen called for once-a-day dosing, but dropped to 59% when patients were instructed to take their medication 3 times a day.23

Ask the patient to summarize. Using simple terms and clear, succinct explanations promotes understanding, but asking the patient to summarize what you’ve just said is an ideal way to find out just how much he or she grasped. “What will you tell your family about your diagnosis and treatment?” you might ask, or “Tell me what you plan to do to ensure that you follow the prescribed regimen.”

This is particularly important when patients are not native English speakers or when the news is bad. Patients find it particularly tough to understand difficult messages, such as a poor prognosis,24 and are often unaware of their poor comprehension. This was underscored by a study of emergency department (ED) patients, in which 78% demonstrated deficient comprehension in at least one domain (eg, post-ED care, diagnosis, cause) but only 20% recognized their lack of understanding.25

Asking patients if they have any other questions is a crucial step in ensuring complete understanding.21,26

Take steps to maximize patient recall

Even when patients understand what they’ve heard, research suggests they may not retain it. Overall, 40% to 80% of medical information is forgotten immediately, and almost half of what is retained is incorrect.27,28 This is a serious problem, as understanding and accurate recall increase patient satisfaction and the likelihood of adherence to treatment (FIGURE W1).28,29

There are 3 basic explanations for poor recall: factors related to the clinician, such as the use of difficult medical terminology; the mode of communication (eg, spoken vs written); and factors related to the patient, such as a low level of education or learning disability.29-32

Being as specific as possible and spending more time explaining the diagnosis and treatment has been shown to enhance patient recall. In an experiment in which patients read advice on how to develop self-control over their eating, the use of simple language and specific instructions, rather than general rules, increased recall.33 Providing generic information by whatever means does little to improve recall and might even inhibit it.

Linking advice to the patient’s chief complaint, thereby creating a “teachable moment,” is also helpful.34 For example, you might tell a patient with a kidney infection that “Your backache is also because of the kidney infection. Both the backache and the burning during urination should be better about 3 days after you start these pills.”

Watch your affect. How relaxed or worried you appear also influences patient recall. In a recent study, 40 women at risk for breast cancer viewed videotapes of an oncologist presenting mammogram results. Compared to women whose results were conveyed by a physician who appeared relaxed, those who had the same findings presented by a physician who seemed worried perceived their clinical situation to be more severe, developed higher anxiety, and recalled significantly less of what they were told.35

Use multiple means of communication. In a comparison study, patients who received verbal lists of actions for managing fever and sore mouth accompanied by pictographs—images that represented the information presented—had a correct recall rate of 85%; those who received the verbal information alone had a recall rate of only 14%.36,37

Clinicians tell patients the name of the drug they're prescribing 74% of the time and its purpose 87% of the time, but discuss potential adverse effects and duration of treatment a mere 34% of the time.

A review of recall in cancer patients also found that tailoring communication to the individual—providing an audiotape of the consultation, for instance, or having the patient bring a list of questions and addressing them one by one—is most effective.36 Another study assessed the retention of pediatric patients and their parents when they received either a verbal report alone or a verbal report plus written information or visuals. The researchers concluded that children and their parents should receive verbal reports only when such reports are supplemented with written information or visuals.37

The large body of research on learning and memory has proven useful in designing educational materials for those with poor reading skills. When images were used to convey meaning to 21 adults in a job training program—all with less than fifth grade reading skills—they had on average 85% correct recall immediately after the training and 71% recall 4 weeks later. Although the impact on symptom management and patient quality of life has yet to be studied, these findings suggest that pictures can help people with low literacy recall and retain complex information.38

 

 

Overall, while written or recorded instructions appear to improve recall in most situations,39 images have been shown to have the greatest impact.36,37,40

Is the patient ready to adhere to treatment?

No matter how well or by what means you communicate, some patients are not ready for change. Patients in the “precontemplation” stage of change—who may not even recognize the need for change, let alone consider it—can benefit from supportive education and motivational interviewing, while those in the “contemplation” stage need support and convincing to reach the “preparation” stage. It is only in the “action” stage, however, that a patient is ready to collaborate with his or her physician in agreeing on and adhering to treatment.40

Comorbid depression is a common condition, particularly in those with chronic illness, and one of the strongest predictors of nonadherence.1,41 Thus, depression screening for all patients who are chronically or severely ill or nonadherent is strongly recommended, followed by treatment when appropriate.41

“Informed collaboration” is critical

Comorbid depression is particularly common among those with chronic illnesses, and one of the strongest predictors of nonadherence.

Research shows that if both physician and patient agree on the individual’s medical problem, it will be improved or resolved at follow-up in about half of all cases. In contrast, when the physician alone sees the patient’s condition as a problem, just over a quarter of cases improve, regardless of the severity.42 Compounding this difficulty is the finding that patients fail to report up to two-thirds of their most important health problems.43 When physicians identify them, discord and denial typically result.42

Thus, concordance (we prefer the term “informed collaboration”)—an overt agreement reached after a discussion in which the physician shares expert knowledge, then listens to and respects the feelings and beliefs of the patient with regard to how, when, or whether he or she will take the recommended treatment44—is crucial.42,43,45,46

One way to reach informed collaboration is to give patients problem lists or letters summarizing their health problems in simple and specific terms after each visit, in hopes that the written communication will encourage discussion and a physician-patient partnership in addressing them.43 In a recent study of 967 psychiatric outpatients, adherence was significantly higher among those who cited concordance between their preferences and their treatment and felt that they had participated in decision making.47

Problems can arise at any time

Even after a patient starts out fully adhering to his medication regimen, several issues can derail treatment. Inability to afford the medication is one potential problem.48 Adverse effects are another major reason for discontinuation. Sexual dysfunction, caused by a number of drugs, is embarrassing to many patients and frequently goes unaddressed.49 Thus, a patient may stop taking the medication without saying why—seemingly for no apparent reason. The best approach is to ask specifically why it was discontinued, including direct questions about sexual adverse effects.

Prescribing recommendations

Sexual dysfunction, caused by a number of drugs, is embarrassing to many patients and frequently goes unaddressed.

We believe that the outcome of treatment is being determined from the moment a patient steps into your office. Thus, we’ve compiled an evidence-based checklist (TABLE)24,33,40,41,47,49,50 with broad areas for discussion that constitute the art and science of prescribing. These fall into 3 main areas: 1) what to say before you write a prescription; 2) how to get patient buy-in (informed collaboration, rather than informed consent) when you’re ready to write the prescription; and 3) what to address to boost the likelihood of continued adherence at follow-up visits.

It is clear that allowing adequate patient participation and arriving at concordance and overt agreement lead to better clinical outcomes.51 The sequential steps we recommend may take a few extra minutes up front, but without them, nonadherence is highly likely. While physicians are supportive of shared decision making in theory, they are often less confident that this is achieved in practice.52,53

It may help to keep in mind that every step need not be carried out by the physician. Using other members of the health care team, such as a nurse, medical assistant, or health coach, to provide patient education and support and take the patient through a number of the steps that are included in a physician visit has become increasingly necessary—and is easily accommodated in this case.

As the physician, you bear the final responsibility to ensure that the critical elements—particularly the overt agreement—are addressed. Ultimately supporting your patient's decision and reinforcing it will ensure continued adherence.

CORRESPONDENCE
Swati Shivale, MBBS, Department of Psychiatry, SUNY Upstate Medical University, 750 Adams Street, Syracuse, NY 13210; shivalsw@upstate.edu

 

PRACTICE RECOMMENDATIONS

› To increase adherence, give patients treatment options, ensure that they participate in discussions of treatment, and empower them to reach "informed collaboration" as opposed to informed consent. A
› Ask patients to tell you in their own words what they understand about the treatment they have chosen. A
› At each follow-up visit, anticipate nonadherence, ask nonjudgmental questions about missed medication doses and sexual adverse effects, and offer simple solutions. A

Strength of recommendation (SOR)

A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series

Medication nonadherence is a major—and remediable—contributor to poor outcomes, leading to approximately 125,000 preventable deaths,1 worsening of acute and chronic conditions, and billions of dollars in avoidable costs related to increased hospitalizations and emergency visits each year.2,3 Nonadherence rates are 20% to 30% among patients being treated for cancer and acute illness3 and 50% to 60% for chronic conditions, with an average of 50% of all patients taking their medication incorrectly—or not at all.2,4,5

What’s more, nonadherence disrupts the physician-patient relationship6—a serious problem, given that feeling understood is often the most critical component of recovery.7-9

With that in mind, the words used to describe the problem have changed. Compliance and noncompliance, the older labels, were based on the assumptions that patients are passive recipients of medical advice that they should follow without question and that they are to blame for not doing so. Adherence and nonadherence, on the other hand, emphasize mutual agreement and the patient’s freedom to follow the doctor’s recommendations or not, without blame if he or she decides not to do so.10

Many systemic approaches have been tried to maximize adherence, including disease management (eg, Web-based assessment tools, clinical guidelines, and call center-based triage), smart phone apps11 (for reminders and monitoring), and paying for or subsidizing the cost of drugs for those who can’t afford them. All have met with limited success.12 Based on a thorough review of the literature, we suggest a different approach.

Evidence-based efforts by clinicians are the key to effective prescribing and maximal adherence. In the text and table that follow, we summarize physician and patient factors that influence adherence and present optimal prescribing guidelines.

Listen carefully, then respond

Whether patients are seeing a primary care physician or a specialist, they want their doctors to spend more time with them and to give them more comprehensive information about their condition.13-15 The interaction should begin with the physician listening carefully to the patient before responding, but all too often this is not the case.

Family physicians have been found to interrupt patients 23 seconds after asking a question.16 To improve communication, listen quietly until the patient finishes presenting his or her complaints and agenda for the visit. Then ask, “Is there anything else that’s important for me to know?”17

Be more forthcoming

It is equally important for physicians to respond fully, but this is often not the case. A study involving internists found that in patient encounters lasting 20 minutes, physicians devoted little more than one minute, on average, to explaining the patient’s medical condition. The research showed that many physicians greatly overestimated the time they spent doing so.13

Studies have also shown that clinicians tell patients the name of the drug they’re prescribing 74% of the time and state its purpose 87% of the time, but discuss potential adverse effects and duration of treatment a mere 34% of the time. More than 4 in 10 patients are not told the frequency or timing of doses or the number of tablets to take.18

To improve communication, take the following steps when it’s your turn to talk:

Avoid medical jargon. Technical language (eg, edema) and medical shorthand (eg, history) is a significant barrier to patient understanding. In one study of more than 800 pediatrician visits, such speech was found to be detrimental more than half of the time. Although many mothers were confused by the terms, they rarely asked for clarification.19

Listen quietly until patients finish presenting their complaints and reason for the visit, then ask whether there is anything else that's important for you to know.

It has been suggested that doctors and patients have engaged in a “communication conspiracy.”20 In one study, even after obstetricians and gynecologists had identified terms that they knew their patients did not understand, they continued to use them, and in only 15% of visits where unfamiliar terms were used did the patients admit that they did not understand them.21 Part of the problem may be that patients believe they must be seen as undemanding and compliant if they are to receive optimal attention from their physicians.22

 

 

Compounding the problem is the fact that clinicians’ use of highly technical language doubles when they are pressured for time,20 suggesting that this behavior could become more widespread as the demand for greater efficiency on the part of physicians increases.

Simplify the treatment regimen. It also helps to keep treatment regimens as straightforward as possible. Prescribing multiple medications simultaneously or giving patients a more complicated regimen decreases adherence. In one study, adherence rates of 84% were achieved when the regimen called for once-a-day dosing, but dropped to 59% when patients were instructed to take their medication 3 times a day.23

Ask the patient to summarize. Using simple terms and clear, succinct explanations promotes understanding, but asking the patient to summarize what you’ve just said is an ideal way to find out just how much he or she grasped. “What will you tell your family about your diagnosis and treatment?” you might ask, or “Tell me what you plan to do to ensure that you follow the prescribed regimen.”

This is particularly important when patients are not native English speakers or when the news is bad. Patients find it particularly tough to understand difficult messages, such as a poor prognosis,24 and are often unaware of their poor comprehension. This was underscored by a study of emergency department (ED) patients, in which 78% demonstrated deficient comprehension in at least one domain (eg, post-ED care, diagnosis, cause) but only 20% recognized their lack of understanding.25

Asking patients if they have any other questions is a crucial step in ensuring complete understanding.21,26

Take steps to maximize patient recall

Even when patients understand what they’ve heard, research suggests they may not retain it. Overall, 40% to 80% of medical information is forgotten immediately, and almost half of what is retained is incorrect.27,28 This is a serious problem, as understanding and accurate recall increase patient satisfaction and the likelihood of adherence to treatment (FIGURE W1).28,29

There are 3 basic explanations for poor recall: factors related to the clinician, such as the use of difficult medical terminology; the mode of communication (eg, spoken vs written); and factors related to the patient, such as a low level of education or learning disability.29-32

Being as specific as possible and spending more time explaining the diagnosis and treatment has been shown to enhance patient recall. In an experiment in which patients read advice on how to develop self-control over their eating, the use of simple language and specific instructions, rather than general rules, increased recall.33 Providing generic information by whatever means does little to improve recall and might even inhibit it.

Linking advice to the patient’s chief complaint, thereby creating a “teachable moment,” is also helpful.34 For example, you might tell a patient with a kidney infection that “Your backache is also because of the kidney infection. Both the backache and the burning during urination should be better about 3 days after you start these pills.”

Watch your affect. How relaxed or worried you appear also influences patient recall. In a recent study, 40 women at risk for breast cancer viewed videotapes of an oncologist presenting mammogram results. Compared to women whose results were conveyed by a physician who appeared relaxed, those who had the same findings presented by a physician who seemed worried perceived their clinical situation to be more severe, developed higher anxiety, and recalled significantly less of what they were told.35

Use multiple means of communication. In a comparison study, patients who received verbal lists of actions for managing fever and sore mouth accompanied by pictographs—images that represented the information presented—had a correct recall rate of 85%; those who received the verbal information alone had a recall rate of only 14%.36,37

Clinicians tell patients the name of the drug they're prescribing 74% of the time and its purpose 87% of the time, but discuss potential adverse effects and duration of treatment a mere 34% of the time.

A review of recall in cancer patients also found that tailoring communication to the individual—providing an audiotape of the consultation, for instance, or having the patient bring a list of questions and addressing them one by one—is most effective.36 Another study assessed the retention of pediatric patients and their parents when they received either a verbal report alone or a verbal report plus written information or visuals. The researchers concluded that children and their parents should receive verbal reports only when such reports are supplemented with written information or visuals.37

The large body of research on learning and memory has proven useful in designing educational materials for those with poor reading skills. When images were used to convey meaning to 21 adults in a job training program—all with less than fifth grade reading skills—they had on average 85% correct recall immediately after the training and 71% recall 4 weeks later. Although the impact on symptom management and patient quality of life has yet to be studied, these findings suggest that pictures can help people with low literacy recall and retain complex information.38

 

 

Overall, while written or recorded instructions appear to improve recall in most situations,39 images have been shown to have the greatest impact.36,37,40

Is the patient ready to adhere to treatment?

No matter how well or by what means you communicate, some patients are not ready for change. Patients in the “precontemplation” stage of change—who may not even recognize the need for change, let alone consider it—can benefit from supportive education and motivational interviewing, while those in the “contemplation” stage need support and convincing to reach the “preparation” stage. It is only in the “action” stage, however, that a patient is ready to collaborate with his or her physician in agreeing on and adhering to treatment.40

Comorbid depression is a common condition, particularly in those with chronic illness, and one of the strongest predictors of nonadherence.1,41 Thus, depression screening for all patients who are chronically or severely ill or nonadherent is strongly recommended, followed by treatment when appropriate.41

“Informed collaboration” is critical

Comorbid depression is particularly common among those with chronic illnesses, and one of the strongest predictors of nonadherence.

Research shows that if both physician and patient agree on the individual’s medical problem, it will be improved or resolved at follow-up in about half of all cases. In contrast, when the physician alone sees the patient’s condition as a problem, just over a quarter of cases improve, regardless of the severity.42 Compounding this difficulty is the finding that patients fail to report up to two-thirds of their most important health problems.43 When physicians identify them, discord and denial typically result.42

Thus, concordance (we prefer the term “informed collaboration”)—an overt agreement reached after a discussion in which the physician shares expert knowledge, then listens to and respects the feelings and beliefs of the patient with regard to how, when, or whether he or she will take the recommended treatment44—is crucial.42,43,45,46

One way to reach informed collaboration is to give patients problem lists or letters summarizing their health problems in simple and specific terms after each visit, in hopes that the written communication will encourage discussion and a physician-patient partnership in addressing them.43 In a recent study of 967 psychiatric outpatients, adherence was significantly higher among those who cited concordance between their preferences and their treatment and felt that they had participated in decision making.47

Problems can arise at any time

Even after a patient starts out fully adhering to his medication regimen, several issues can derail treatment. Inability to afford the medication is one potential problem.48 Adverse effects are another major reason for discontinuation. Sexual dysfunction, caused by a number of drugs, is embarrassing to many patients and frequently goes unaddressed.49 Thus, a patient may stop taking the medication without saying why—seemingly for no apparent reason. The best approach is to ask specifically why it was discontinued, including direct questions about sexual adverse effects.

Prescribing recommendations

Sexual dysfunction, caused by a number of drugs, is embarrassing to many patients and frequently goes unaddressed.

We believe that the outcome of treatment is being determined from the moment a patient steps into your office. Thus, we’ve compiled an evidence-based checklist (TABLE)24,33,40,41,47,49,50 with broad areas for discussion that constitute the art and science of prescribing. These fall into 3 main areas: 1) what to say before you write a prescription; 2) how to get patient buy-in (informed collaboration, rather than informed consent) when you’re ready to write the prescription; and 3) what to address to boost the likelihood of continued adherence at follow-up visits.

It is clear that allowing adequate patient participation and arriving at concordance and overt agreement lead to better clinical outcomes.51 The sequential steps we recommend may take a few extra minutes up front, but without them, nonadherence is highly likely. While physicians are supportive of shared decision making in theory, they are often less confident that this is achieved in practice.52,53

It may help to keep in mind that every step need not be carried out by the physician. Using other members of the health care team, such as a nurse, medical assistant, or health coach, to provide patient education and support and take the patient through a number of the steps that are included in a physician visit has become increasingly necessary—and is easily accommodated in this case.

As the physician, you bear the final responsibility to ensure that the critical elements—particularly the overt agreement—are addressed. Ultimately supporting your patient's decision and reinforcing it will ensure continued adherence.

CORRESPONDENCE
Swati Shivale, MBBS, Department of Psychiatry, SUNY Upstate Medical University, 750 Adams Street, Syracuse, NY 13210; shivalsw@upstate.edu

References

 

1. Martin LR, Summer LW, Haskard KB, et al. The challenge of patient adherence. Ther Clin Risk Manage. 2005;1:189-199.

2. Jha AK, Aubert R, Yao J, et al. Greater adherence to diabetes drugs is linked to less hospital use and could save nearly $5 billion annually. Health Aff. 2012;8:1836-1846.

3. DiMatteo MR. Variations in patients’ adherence to medical recommendations: a quantitative review of 50 years of research. Med Care. 2004;42:200–209.

4. Brown MT, Bussell JK. Medication adherence: WHO cares? Mayo Clin Proc. 2011;86:304-314.

5. Iuga AO, McGuire MJ. Adherence and health care costs. Risk Manage Healthcare Policy. 2014;7:35-44.

6. Ansell B. Not getting to goal: the clinical costs of noncompliance. J Managed Care Pharm. 2008;14(Suppl):6-b.

7. Van Kleef GA, van den Berg H, Heerdink MW. The persuasive power of emotions: effects of emotional expressions on attitude formation and change. J Appl Psychol. 2014. Nov 17 [Epub ahead of print].

8. Wright JM, Lee C, Chambers GK. Real-world effectiveness of antihypertensive drugs. Can Med Assoc J. 2000;162:190–191.

9. Dunbar J, Agras W. Compliance with medical instructions. In: Ferguson J, Taylor C, eds. The Comprehensive Handbook of Behavioral Medicine. New York, NY: Springer; 1980:115–145.

10. Horne R, Weinman J, Barber N, et al. Concordance, adherence and compliance in medicine taking. Report for the National Coordinating Centre for NHS Service Delivery and Organisation R & D (NCCSDO). December 2005. University of Leeds, School of Healthcare. Available at: http://www.netscc.ac.uk/hsdr/files/project/SDO_FR_08-1412-076_V01.pdf. Accessed June 18, 2015.

11. Dayer L, Heldenbrand S, Anderson P, et al. Smartphone medication adherence apps: potential benefits to patients and providers. J Am Pharm Assoc. 2013; 53:172-181.

12. Jaarsma T, van der Wal ML, Lesman-Leegte I, et al. Effect of moderate or intensive disease management program on outcome in patients with heart failure: coordinating study evaluating outcomes of advising and counseling in heart failure (COACH). Arch Intern Med. 2008;168:316-324.

13. Waitzkin H. Doctor-patient communication. Clinical implications of social scientific research. JAMA. 1984;252:2441–2446.

14. Freeman GK, Horder JP, Howie JGR, et al. Evolving general practice consultation in Britain: issues of length and context. BMJ. 2002;324:880-882.

15. Beisecker AE, Beisecker TD. Patient information-seeking behaviors when communicating with doctors. Med Care. 1990;28:19-28.

16. Marvel M, Epstein R, Flowers K, et al. Soliciting the patient’s agenda: have we improved? JAMA. 1999; 281:283-287.

17. Barrier P, Li T, Jensen N. Two words to improve physician-patient communication: what else? Mayo Clin Proc. 2003;78:211-214.

18. Tarn D, Heritage J, Paterniti D, et al. Physician communications when prescribing new medications. Arch Internal Med. 2006;166:1855-1862.

19. Korsch BM, Gozzi EK, Francis V. Gaps in doctor-patient communication, doctor-patient interaction and patient satisfaction. Pediatrics. 1968;42:855-871.

20. Lipton HL, Svarstad BL. Parental expectations of a multi-disciplinary clinic for children with developmental disabilities. J Health Soc Behav. 1974;15:157-166.

21. McKinlay JB. Who is really ignorant--physician or patient? J Health Soc Behav. 1975;16:3-11.

22. Nehring V, Geach B. Patients’ evaluation of their care: why they don’t complain. Nurs Outlook. 1973; 21:317-321.

23. De las Cuevas C, Peñate W, de Rivera L. To what extent is treatment adherence of psychiatric patients influenced by their participation in shared decision making? Patient Preference Adherence. 2014;8:1547–1553.

24. Tuckett D, Boulton M, Olson C, et al. Meetings Between Experts–An Approach to Sharing Ideas in Medical Consultations. London, UK: Tavistock Publications; 1985.

25. Engel K, Heisler M, Smith D, et al. Patient comprehension of emergency department care and instructions: are patients aware of when they do not understand? Ann Emerg Med. 2009;53:454-461.

26. Viswanathan M, Golin CE, Jones CD, et al. Interventions to improve adherence to self-administered medications for chronic diseases in the United States: a systematic review. Ann Intern Med. 2012;157:785-795.

27. McGuire LC. Remembering what the doctor said: organization and older adults’ memory for medical information. Exp Aging Res. 1996;22:403-428.

28. Anderson JL, Dodman S, Kopelman M, et al. Patient information recall in a rheumatology clinic. Rheumatol Rehab. 1979;18:18-22.

29. Ley P. Communicating with Patients. New York, NY: Croom Helm; 1988.

30. Ley P. Primacy, rated importance, and the recall of medical statements. J Health Soc Beh. 1972;13:311-317.

31. Ley P, Bradshaw PW, Eaves D, et al. A method for increasing patients’ recall of information presented by doctors. Psychol Med. 1973;3:217-220.

32. Kessels R. Patients’ memory for medical information. J Royal Soc Med. 2003;96:219-222.

33. Bradshaw PW, Ley P, Kincey JA. Recall of medical advice: comprehensibility and specificity. Br J Clin Psychol. 1975;14:55-82.

34. Flocke S, Stange K. Direct observation and patient recall of health behavior advice. Prev Med. 2004;38:34-349.

35. Shapiro DE, Boggs SR, Melamed BG, et al. The effect of varied physician affect on recall, anxiety, and perceptions in women at risk for breast cancer: an analogue study. Health Psychol. 1992;11:61-66.

36. van der Meulen N, Jansen J, van Dulmen S, et al. Interventions to improve recall of medical information in cancer patients: a systematic review of the literature. Psychooncology. 2008;17:857-868.

37. Houts PS, Bachrach R, Witmer JT, et al. Using pictographs to enhance recall of spoken medical instructions. Patient Educ Couns. 1998;35:83-88.

38. Watson P, McKinstry B. A systematic review of interventions to improve recall of medical advice in healthcare consultations. J Royal Soc Med. 2009;102:235-243.

39. Houts PS, Witmer JT, Egeth HE, et al. Using pictographs to enhance recall of spoken medical instructions II. Patient Educ Couns. 2001;43:231-242.

40. Prochaska J, Norcross J, DiClemente C. Changing for Good. New York, NY: Avon; 1995.

41. DiMatteo M, Lepper H, Croghan T. Depression is a risk factor for non-compliance in medical treatment: a meta-analysis of the effects of anxiety and depression in patient adherence. Arch Int Med. 2000;160: 2101-2107.

42. Starfield B, Wray C, Hess K, et al. The influence of patientpractitioner agreement on outcome of care. Am J Pub Health. 1981;71:127–131.

43. Scheitel SM, Boland BJ, Wollan PC, et al. Patient-physician agreement about medical diagnoses and cardiovascular risk factors in the ambulatory general medical examination. Mayo Clin Proc. 1996;71: 1131-1137.

44. Bell JS, Airaksinen MS, Lyles A, et al. Concordance is not synonymous with compliance or adherence. Br J Clin Pharmacol. 2007;64:710-711.

45. Staiger T, Jarvik J, Deyo R, et al. Patient-physician agreement as a predictor of outcomes in patients with back pain. J Gen Int Med. 2005;20:935-937.

46. Stewart M, Brown J, Donner A, et al. The impact of patient-centered care on outcomes. J Fam Pract. 2000;49:796-804.

47. Saini SD, Schoenfeld P, Kaulback K, et al. Effect of medication dosing frequency on adherence in chronic diseases. Am J Manage Care. 2009;15:e22–e33.

48. Kedenge SV, Kangwana BP, Waweru EW, et al. Understanding the impact of subsidizing artemisinin-based combination therapies (ACTs) in the retail sector–results from focus group discussions in rural Kenya. PLoS One. 2013;8:e54371.

49. Santini I, De Lauretis I, Roncone R, et al. Psychotropic-associated sexual dysfunctions: a survey of clinical pharmacology and medication-associated practice. Clin Ter. 2014;165:e243-e252.

50. Ibrahim S, Hossam M, Belal D. Study of non-compliance among chronic hemodialysis patients and its impact on patients’ outcomes. Saudi J Kidney Dis Transpl. 2015;26:243-249.

51. Légaré F, Stacey D, Turcotte S, et al. Interventions for improving the adoption of shared decision making by healthcare professionals. Cochrane Database Syst Rev. 2014;(9):CD006732.

52. Cox K, Stevenson F, Britten N, et al. A Systematic Review of Communication between Patients and Healthcare Professionals about Medicine Taking and Prescribing. London, UK: GKT Concordance Unit Kings College; 2004.

53. Edwards A, Elwyn G. Involving patients in decision making and communicating risk: a longitudinal evaluation of doctors’ attitudes and confidence during a randomized trial. J Eval Clin Pract. 2004;10:431-437.

References

 

1. Martin LR, Summer LW, Haskard KB, et al. The challenge of patient adherence. Ther Clin Risk Manage. 2005;1:189-199.

2. Jha AK, Aubert R, Yao J, et al. Greater adherence to diabetes drugs is linked to less hospital use and could save nearly $5 billion annually. Health Aff. 2012;8:1836-1846.

3. DiMatteo MR. Variations in patients’ adherence to medical recommendations: a quantitative review of 50 years of research. Med Care. 2004;42:200–209.

4. Brown MT, Bussell JK. Medication adherence: WHO cares? Mayo Clin Proc. 2011;86:304-314.

5. Iuga AO, McGuire MJ. Adherence and health care costs. Risk Manage Healthcare Policy. 2014;7:35-44.

6. Ansell B. Not getting to goal: the clinical costs of noncompliance. J Managed Care Pharm. 2008;14(Suppl):6-b.

7. Van Kleef GA, van den Berg H, Heerdink MW. The persuasive power of emotions: effects of emotional expressions on attitude formation and change. J Appl Psychol. 2014. Nov 17 [Epub ahead of print].

8. Wright JM, Lee C, Chambers GK. Real-world effectiveness of antihypertensive drugs. Can Med Assoc J. 2000;162:190–191.

9. Dunbar J, Agras W. Compliance with medical instructions. In: Ferguson J, Taylor C, eds. The Comprehensive Handbook of Behavioral Medicine. New York, NY: Springer; 1980:115–145.

10. Horne R, Weinman J, Barber N, et al. Concordance, adherence and compliance in medicine taking. Report for the National Coordinating Centre for NHS Service Delivery and Organisation R & D (NCCSDO). December 2005. University of Leeds, School of Healthcare. Available at: http://www.netscc.ac.uk/hsdr/files/project/SDO_FR_08-1412-076_V01.pdf. Accessed June 18, 2015.

11. Dayer L, Heldenbrand S, Anderson P, et al. Smartphone medication adherence apps: potential benefits to patients and providers. J Am Pharm Assoc. 2013; 53:172-181.

12. Jaarsma T, van der Wal ML, Lesman-Leegte I, et al. Effect of moderate or intensive disease management program on outcome in patients with heart failure: coordinating study evaluating outcomes of advising and counseling in heart failure (COACH). Arch Intern Med. 2008;168:316-324.

13. Waitzkin H. Doctor-patient communication. Clinical implications of social scientific research. JAMA. 1984;252:2441–2446.

14. Freeman GK, Horder JP, Howie JGR, et al. Evolving general practice consultation in Britain: issues of length and context. BMJ. 2002;324:880-882.

15. Beisecker AE, Beisecker TD. Patient information-seeking behaviors when communicating with doctors. Med Care. 1990;28:19-28.

16. Marvel M, Epstein R, Flowers K, et al. Soliciting the patient’s agenda: have we improved? JAMA. 1999; 281:283-287.

17. Barrier P, Li T, Jensen N. Two words to improve physician-patient communication: what else? Mayo Clin Proc. 2003;78:211-214.

18. Tarn D, Heritage J, Paterniti D, et al. Physician communications when prescribing new medications. Arch Internal Med. 2006;166:1855-1862.

19. Korsch BM, Gozzi EK, Francis V. Gaps in doctor-patient communication, doctor-patient interaction and patient satisfaction. Pediatrics. 1968;42:855-871.

20. Lipton HL, Svarstad BL. Parental expectations of a multi-disciplinary clinic for children with developmental disabilities. J Health Soc Behav. 1974;15:157-166.

21. McKinlay JB. Who is really ignorant--physician or patient? J Health Soc Behav. 1975;16:3-11.

22. Nehring V, Geach B. Patients’ evaluation of their care: why they don’t complain. Nurs Outlook. 1973; 21:317-321.

23. De las Cuevas C, Peñate W, de Rivera L. To what extent is treatment adherence of psychiatric patients influenced by their participation in shared decision making? Patient Preference Adherence. 2014;8:1547–1553.

24. Tuckett D, Boulton M, Olson C, et al. Meetings Between Experts–An Approach to Sharing Ideas in Medical Consultations. London, UK: Tavistock Publications; 1985.

25. Engel K, Heisler M, Smith D, et al. Patient comprehension of emergency department care and instructions: are patients aware of when they do not understand? Ann Emerg Med. 2009;53:454-461.

26. Viswanathan M, Golin CE, Jones CD, et al. Interventions to improve adherence to self-administered medications for chronic diseases in the United States: a systematic review. Ann Intern Med. 2012;157:785-795.

27. McGuire LC. Remembering what the doctor said: organization and older adults’ memory for medical information. Exp Aging Res. 1996;22:403-428.

28. Anderson JL, Dodman S, Kopelman M, et al. Patient information recall in a rheumatology clinic. Rheumatol Rehab. 1979;18:18-22.

29. Ley P. Communicating with Patients. New York, NY: Croom Helm; 1988.

30. Ley P. Primacy, rated importance, and the recall of medical statements. J Health Soc Beh. 1972;13:311-317.

31. Ley P, Bradshaw PW, Eaves D, et al. A method for increasing patients’ recall of information presented by doctors. Psychol Med. 1973;3:217-220.

32. Kessels R. Patients’ memory for medical information. J Royal Soc Med. 2003;96:219-222.

33. Bradshaw PW, Ley P, Kincey JA. Recall of medical advice: comprehensibility and specificity. Br J Clin Psychol. 1975;14:55-82.

34. Flocke S, Stange K. Direct observation and patient recall of health behavior advice. Prev Med. 2004;38:34-349.

35. Shapiro DE, Boggs SR, Melamed BG, et al. The effect of varied physician affect on recall, anxiety, and perceptions in women at risk for breast cancer: an analogue study. Health Psychol. 1992;11:61-66.

36. van der Meulen N, Jansen J, van Dulmen S, et al. Interventions to improve recall of medical information in cancer patients: a systematic review of the literature. Psychooncology. 2008;17:857-868.

37. Houts PS, Bachrach R, Witmer JT, et al. Using pictographs to enhance recall of spoken medical instructions. Patient Educ Couns. 1998;35:83-88.

38. Watson P, McKinstry B. A systematic review of interventions to improve recall of medical advice in healthcare consultations. J Royal Soc Med. 2009;102:235-243.

39. Houts PS, Witmer JT, Egeth HE, et al. Using pictographs to enhance recall of spoken medical instructions II. Patient Educ Couns. 2001;43:231-242.

40. Prochaska J, Norcross J, DiClemente C. Changing for Good. New York, NY: Avon; 1995.

41. DiMatteo M, Lepper H, Croghan T. Depression is a risk factor for non-compliance in medical treatment: a meta-analysis of the effects of anxiety and depression in patient adherence. Arch Int Med. 2000;160: 2101-2107.

42. Starfield B, Wray C, Hess K, et al. The influence of patientpractitioner agreement on outcome of care. Am J Pub Health. 1981;71:127–131.

43. Scheitel SM, Boland BJ, Wollan PC, et al. Patient-physician agreement about medical diagnoses and cardiovascular risk factors in the ambulatory general medical examination. Mayo Clin Proc. 1996;71: 1131-1137.

44. Bell JS, Airaksinen MS, Lyles A, et al. Concordance is not synonymous with compliance or adherence. Br J Clin Pharmacol. 2007;64:710-711.

45. Staiger T, Jarvik J, Deyo R, et al. Patient-physician agreement as a predictor of outcomes in patients with back pain. J Gen Int Med. 2005;20:935-937.

46. Stewart M, Brown J, Donner A, et al. The impact of patient-centered care on outcomes. J Fam Pract. 2000;49:796-804.

47. Saini SD, Schoenfeld P, Kaulback K, et al. Effect of medication dosing frequency on adherence in chronic diseases. Am J Manage Care. 2009;15:e22–e33.

48. Kedenge SV, Kangwana BP, Waweru EW, et al. Understanding the impact of subsidizing artemisinin-based combination therapies (ACTs) in the retail sector–results from focus group discussions in rural Kenya. PLoS One. 2013;8:e54371.

49. Santini I, De Lauretis I, Roncone R, et al. Psychotropic-associated sexual dysfunctions: a survey of clinical pharmacology and medication-associated practice. Clin Ter. 2014;165:e243-e252.

50. Ibrahim S, Hossam M, Belal D. Study of non-compliance among chronic hemodialysis patients and its impact on patients’ outcomes. Saudi J Kidney Dis Transpl. 2015;26:243-249.

51. Légaré F, Stacey D, Turcotte S, et al. Interventions for improving the adoption of shared decision making by healthcare professionals. Cochrane Database Syst Rev. 2014;(9):CD006732.

52. Cox K, Stevenson F, Britten N, et al. A Systematic Review of Communication between Patients and Healthcare Professionals about Medicine Taking and Prescribing. London, UK: GKT Concordance Unit Kings College; 2004.

53. Edwards A, Elwyn G. Involving patients in decision making and communicating risk: a longitudinal evaluation of doctors’ attitudes and confidence during a randomized trial. J Eval Clin Pract. 2004;10:431-437.

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PRACTICE RECOMMENDATIONS

› Perform a biopsy and carefully monitor all potentially malignant oral lesions, including leukoplakia and erythroplakia. A
› Consider evaluation for human immunodeficiency virus infection for any patient who has acute necrotizing ulcerative gingivitis/acute necrotizing ulcerative periodontitis, recurrent candidiasis, or oral hairy leukoplakia. A
› Include melanoma in the differential diagnosis of oral pigmented lesions that have any features of cutaneous melanoma (eg, asymmetry, irregular borders, or variable or changing color). A

Strength of recommendation (SOR)

A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series

Family physicians can play an essential role in managing their patients’ oral health by promptly recognizing and diagnosing conditions that demand further medical attention, including non-odontogenic and odontogenic infections, primary oral mucosal diseases, oral manifestations of systemic disease, and malignancy. Many conditions are amenable to treatment by the family physician, while others will require referral to a specialist.

This article and accompanying photo guide describe the types of lesions you may encounter during examinations of the oral cavity, and the corresponding diagnoses.

Be vigilant for non-odontogenic conditions that may require urgent treatment

There are several uncommon, acute non-odontogenic conditions that affect the oral cavity that, when severe, can require urgent medical attention and possible hospitalization.

Primary herpes simplex virus 1 (HSV-1) infection is generally subclinical, but some patients develop significant oral disease—called primary herpetic gingivostomatitis—that’s characterized by painful diffuse, irregular, crop-like ulcerations throughout the oral cavity and lips1 (FIGURE 1). The gingiva is nearly universally affected, which distinguishes this condition from erythema multiforme and aphthous stomatitis, which are described below. The incidence is highest in children, followed by adolescents and young adults.2

Erythema multiforme. This mucocutaneous hypersensitivity reaction can be limited to the oral cavity and lips, without accompanying skin lesions. Flu-like symptoms, including fever and chills, are followed by acute onset of diffuse oral ulcerations that are generally limited to non-keratinized mucosa, and spare the gingiva (FIGURE 2).3 Ulceration and crusting of the lips is common.

   

Aphthous stomatitis. Recurrent aphthous stomatitis (RAS) is a common immune-mediated inflammatory condition characterized by “canker sores,” or small round/ovoid ulcers with a well-defined erythematous halo (FIGURE 3). Lesions almost exclusively affect non-keratinized mucosa (and never the lip vermilion) and heal within 7 to 10 days, although “major” (>0.5 cm) lesions may persist much longer (FIGURE 4). A herpetiform pattern with multiple coalescing ulcers closely mimics HSV.

   

Small subsets of patients develop “complex” RAS, which is characterized by continuous and often multiple ulcerations that may extend into the esophagus, with associated chronic pain and compromised intake.2 RAS associated with systemic conditions is reviewed below.

How to spot signs of common dental diseases

In 2010 in the United States, close to 1.4 million emergency department visits and about $1 billion in hospital charges were due to dental problems.4 Approximately 40% of these visits were made by individuals without insurance.4 Due to a lack of dental insurance, patients may present to a medical professional rather than a dental professional. Additionally, uninsured individuals may neglect their dental problem until it becomes a medical emergency. Family physicians need to recognize dental disease and be able to provide basic management of emergencies.5

Dental abscess. A dental abscess can arise from pulpal infection (due to progression of caries) or periodontal infection (due to progression of periodontal disease). Pain symptoms are variable; however, intense, spontaneous cyclical pain is generally characteristic of a dental abscess of pulpal etiology, whereas a periodontal abscess can have less obvious symptoms. Swelling intraorally or extraorally indicates the spread of a localized infection (FIGURE 5).

Severe infection and swelling can limit mouth opening and function, and in extreme cases may obstruct swallowing and even breathing (eg, Ludwig’s angina). Affected teeth may or may not demonstrate obvious findings of advanced dental disease, such as gross caries, fracture, heavy calculus deposits, or marked periodontal attachment loss. Oral examination may reveal a parulis (focal erythematous swelling of the adjacent gingiva with a central draining sinus tract) (FIGURE 6) and percussion of the affected tooth is generally painful.

   

Pericoronitis is infection and swelling of the gingival tissues that surround a tooth, typically in association with a partially erupted third molar. Signs and symptoms include pain, discomfort with eating and swallowing, and limited mouth opening. Examination demonstrates gingival inflammation around a tooth, with or without purulence (FIGURE 7).

Acute necrotizing ulcerative gingivitis (ANUG) and periodontitis (ANUP) are severe conditions that are typically associated with psychological stress, severe malnutrition, and immunosuppression in patients with preexisting gingivitis or periodontitis.6 ANUG is associated with intense gingival pain, halitosis, generalized erythema, and destruction of the gingival papilla, often with bleeding.7 ANUP is a more advanced condition associated with damage and loss of the periodontium (including bone), often with loose teeth (FIGURE 8).8

 

 

Trauma. Dental trauma can be limited to the teeth and soft tissues, while more severe injuries can also affect the jaw bone.9 Accidental falls, assault, and motor vehicle traffic accidents are the most common causes of facial fractures in the United States, and are often associated with dentoalveolar trauma (FIGURE 9). The most commonly fractured facial bone is the mandible, characterized by painful opening and closing and an incomplete or altered bite.10

       

Oral symptoms may be the first sign of systemic disease

Inflammatory bowel disease. Crohn’s disease may affect the gastrointestinal tract anywhere from the mouth to the anus and may initially present with oral findings that may not correlate with abdominal symptoms. Oral Crohn’s disease may present as mucosal cobblestoning, mucosal tags, deep linear ulcerations, gingival hyperplasia, lip fissuring, aphthous ulcers, and angular cheilitis (FIGURES 10 AND 11). Other features may include diffuse, painless swelling of the lips and mucosal erythema.

Pyostomatitis vegetans is an uncommon condition typically associated with ulcerative colitis that is characterized by serpentine pustules that coalesce in a “snail track” pattern (FIGURE 12).11

       

Dermatologic/vesiculo-bullous diseases. Vesiculo-bullous lesions in the mouth may be seen in pemphigus vulgaris or bullous pemphigoid. Pemphigus vulgaris is an autoimmune intraepithelial blistering disease that often first presents in the oral cavity as flaccid bullae or painful ulcerations, prior to the onset of skin lesions (FIGURE 13).

Mucous membrane pemphigoid is an autoimmune subepithelial disease that affects mucous membranes and the skin. Characteristic oral mucosal blisters quickly rupture and form ulcerations, which may be present in the absence of other mucosal involvement (eg, anus, genitalia, nose or throat) (FIGURE 14).12 Painful aphthous ulcers are common. When oral ulcerations are diffuse and recurrent, they may be the first sign of Behçet’s disease, a multisystem autoimmune vasculitis.13

Oral lichen planus is a chronic immunemediated mucocutaneous disease that is often limited to the oral cavity. It presents with characteristic radiating white striations of the buccal mucosa and tongue, often with associated erythema and ulcerations (FIGURE 15).14

       

Rheumatologic conditions. Systemic or discoid lupus erythematosus may present with oral findings that largely resemble those of oral lichen planus (FIGURE 16).15 Sjögren’s syndrome is an autoimmune disease with characteristic xerostomia, which can lead to oral discomfort, dysphagia, recurrent candidiasis, and rampant dental caries.

Other conditions to watch for. Erosion of the enamel on the lingual surface of the teeth may be a sign of gastroesophageal reflux disease or bulimia (FIGURE 17). Examination of the oral mucosa can reveal typical white plaques of oral candidiasis (FIGURE 18), which may be associated with systemic immune suppression as well as salivary gland dysfunction.

       

Oral conditions that have been associated with human immunodeficiency virus infection include ANUG/ANUP, recurrent candidiasis, and oral hairy leukoplakia (FIGURE 19). In the absence of known HIV infection, patients who present with any of these oral conditions should be evaluated for HIV infection.13 (For more on recognizing the signs of HIV infection in patients without classic risk factors, see “HIV: 3 cases that hid in plain site” [J Fam Pract. 2015;64:20-26]).

Atrophic glossitis may indicate a vitamin B deficiency. Thrombocytopenia and leukemia may present with oral petechiae, purpura, oral hematomas, or hemorrhagic bullae (FIGURE 20).13 Painless pseudomembranous mucosal erosions may be a presentation for secondary syphilis.16

   

Look for signs that suggest malignancy

In the United States, oral and pharyngeal cancers account for approximately 40,000 cases of cancer and 8000 deaths each year.17 More than 90% of these are squamous cell carcinomas (SCCs); the remainder are mainly salivary gland tumors, lymphoma, and other infrequent cancers.18

SCC of the oral cavity most commonly occurs on the tongue but can develop in any site, presenting as mucosal ulcers, plaques, or masses that do not heal (FIGURE 21). Tobacco and alcohol use are associated with up to 80% of cases of SCC of the head and neck.18 Some oropharyngeal SCCs are associated with human papillomavirus infection type 16.19

Potentially malignant oral lesions include leukoplakia and erythroplakia. Leukoplakia is a white patch or plaque of the oral mucosa that can’t be explained by any other clinical diagnosis (FIGURE 22). These lesions are at risk for malignant transformation and may demonstrate dysplasia or frank SCC on biopsy.20 Proliferative verrucous leukoplakia is a unique form of leukoplakia that’s characterized by a wrinkled appearance that is often multifocal; the condition is associated with a higher risk of malignant transformation.

   

Erythroplakia is a red patch that similarly can’t be explained by another diagnosis. It has a very high risk of malignant transformation over time. All potentially malignant oral lesions, including leukoplakia and erythroplakia, require biopsy and careful monitoring.

 

 

Non-SCC cancers. Salivary gland tumors are rare and most commonly occur in patients ages 55 to 65 years. Most neoplasms (70%-85%) occur in the parotid gland, while 8% to 15% develop in the submandibular salivary gland and less than 1% involve the sublingual gland.21 Minor salivary gland tissue, especially in the lips and palate, may also be affected (FIGURE 23). Patients present with circumscribed, fixed or movable, painless, soft or firm masses in a salivary gland.

Melanoma should be included in the differential diagnosis of oral pigmented lesions that have any features of cutaneous melanoma, such as asymmetry, irregular borders, or variable or changing color.22

Hematologic malignancies may initially present (or demonstrate evidence of relapse) in the oral cavity. Leukemia typically presents with sheet-like overgrowth and swelling of the gingiva with associated erythema and bleeding (FIGURE 24), whereas lymphoma typically presents as a solitary mass or ulceration. Solid tumors that metastasize to the oral cavity may present with localized unexplained soft or hard tissue growths, with or without associated neurologic symptoms (eg, paresthesia).

   

CORRESPONDENCE
William D. Anderson, III, MD, DABFM, FAAFP, University of South Carolina School of Medicine, 15 Medical Park, Suite 300, Columbia, SC 29203; william.anderson@uscmed.sc.edu

References

1. Spruance SL. The natural history of recurrent oral-facial herpes simplex virus infection. Semin Dermatol. 1992;11:200-206.

2. Balasubramaniam R, Kuperstein AS, Stoopler ET. Update on oral herpes virus infections. Dent Clin North Am. 2014;58:265-280.

3. Lozada-Nur F, Gorsky M, Silverman S Jr. Oral erythema multiforme: clinical observations and treatment of 95 patients. Oral Surg Oral Med Oral Pathol. 1989;67:36-40.

4. Allareddy V, Rampa S, Lee MK, et al. Hospital-based emergency department visits involving dental conditions: profile and predictors of poor outcomes and resource utilization. J Am Dent Assoc. 2014;145:331-337.

5. Allareddy V, Lin CY, Shah A, et al. Outcomes in patients hospitalized for periapical abscess in the United States: an analysis involving the use of a nationwide inpatient sample. J Am Dent Assoc. 2010;141:1107-1116.

6. Folayan MO. The epidemiology, etiology, and pathophysiology of acute necrotizing ulcerative gingivitis associated with malnutrition. J Contemp Dent Pract. 2004;5:28-41.

7. Atout RN, Todescan S. Managing patients with necrotizing ulcerative gingivitis. J Can Dent Assoc. 2013;79:d46.

8. Todescan S, Nizar R. Managing patients with necrotizing ulcerative periodontitis. J Can Dent Assoc. 2013;79:d44.

9. Allareddy V, Allareddy V, Nalliah RP. Epidemiology of facial fracture injuries. J Oral Maxillofac Surg. 2011;69:2613-2618.

10. Nalliah RP, Allareddy V, Kim MK, et al. Economics of facial fracture reductions in the United States over 12 months. Dent Traumatol. 2013;29:115-120.

11. Padmavathi B, Sharma S, Astekar M, et al. Oral Crohn’s disease. J Oral Maxillofac Pathol. 2014;18(suppl 1):S139-S142.

12. Xu HH, Werth VP, Parisi E, et al. Mucous membrane pemphigoid. Dent Clin North Am. 2013;57:611-630.

13. Chi AC, Neville BW, Krayer JW, et al. Oral manifestations of systemic disease. Am Fam Physician. 2010;82:1381-1388.

14. Lavanya N, Jayanthi P, Rao UK, et al. Oral lichen planus: An update on pathogenesis and treatment. J Oral Maxillofac Pathol. 2011;15:127-132.

15. Uva L, Miguel D, Pinheiro C, et al. Cutaneous manifestations of systemic lupus erythematosus. Autoimmune Dis. 2012;2012:834291.

16. Ficarra G, Carlos R. Syphilis: The renaissance of an old disease with oral implications. Head Neck Pathol. 2009;3:195-206.

17. Siegel R, Ward E, Brawley O, et al. Cancer statistics, 2011: the impact of eliminating socioeconomic and racial disparities on premature cancer deaths. CA Cancer J Clin. 2011;61:212-236.

18. Licitra L, Locati LD, Bossi P, et al. Head and neck tumors other than squamous cell carcinoma. Curr Opin Oncol. 2004;16:236-241.

19. Gillison ML, Broutian T, Pickard RK, et al. Prevalence of oral HPV infection in the United States, 2009-2010. JAMA. 2012;307:693-703.

20. Silverman S Jr., Gorsky M, Lozada F. Oral leukoplakia and malignant transformation: A follow‐up study of 257 patients. Cancer. 1984;53:563-568.

21. Spiro RH. Salivary neoplasms: overview of a 35-year experience with 2807 patients. Head Neck Surg. 1986;8:177-184.

22. DeMatos P, Tyler DS, Seigler HF. Malignant melanoma of the mucous membranes: a review of 119 cases. Ann Surg Oncol. 1998;5:733-742.

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Nathaniel S. Treister, DMD, DMSc
E.J. Mayeaux, Jr., MD, DABFM, FAAFP
Romesh P. Nalliah, DMD

University of South Carolina School of Medicine, Columbia (Drs. Anderson and Mayeaux); Brigham and Women’s Hospital, Boston (Dr. Treister); Harvard Medical School, Boston (Dr. Nalliah)

william.anderson@uscmed.sc.edu

The authors reported no potential conflict of interest relevant to this article.

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William D. Anderson, III, MD, DABFM, FAAFP; Nathaniel S. Treister, DMD, DMSc; E.J. Mayeaux, Jr., MD, DABFM, FAAFP; Romesh P. Nalliah, DMD; oral lesions; mouth; HSV-1 infection; erythema multiforme; aphthous stomatitis; ANUG; ANUP; dental abscess; parulis; pericoronitis; ulcerative periodontitis; dentoalveolar trauma; Crohn's disease; pyostomatitis vegetans; pemphigus vulgaris; muscous membrane pemphigoid; lichen planus; systemic lupus erythematosus; enamel erosion; candidiasis; oral hairy leukoplakia; thrombocytopenia purpura; squamous cell carcinoma; leukplakia; mucoepidermoid carcinoma; acute myselogenous leukemia
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University of South Carolina School of Medicine, Columbia (Drs. Anderson and Mayeaux); Brigham and Women’s Hospital, Boston (Dr. Treister); Harvard Medical School, Boston (Dr. Nalliah)

william.anderson@uscmed.sc.edu

The authors reported no potential conflict of interest relevant to this article.

Author and Disclosure Information

William D. Anderson, III, MD, DABFM, FAAFP
Nathaniel S. Treister, DMD, DMSc
E.J. Mayeaux, Jr., MD, DABFM, FAAFP
Romesh P. Nalliah, DMD

University of South Carolina School of Medicine, Columbia (Drs. Anderson and Mayeaux); Brigham and Women’s Hospital, Boston (Dr. Treister); Harvard Medical School, Boston (Dr. Nalliah)

william.anderson@uscmed.sc.edu

The authors reported no potential conflict of interest relevant to this article.

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PRACTICE RECOMMENDATIONS

› Perform a biopsy and carefully monitor all potentially malignant oral lesions, including leukoplakia and erythroplakia. A
› Consider evaluation for human immunodeficiency virus infection for any patient who has acute necrotizing ulcerative gingivitis/acute necrotizing ulcerative periodontitis, recurrent candidiasis, or oral hairy leukoplakia. A
› Include melanoma in the differential diagnosis of oral pigmented lesions that have any features of cutaneous melanoma (eg, asymmetry, irregular borders, or variable or changing color). A

Strength of recommendation (SOR)

A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series

Family physicians can play an essential role in managing their patients’ oral health by promptly recognizing and diagnosing conditions that demand further medical attention, including non-odontogenic and odontogenic infections, primary oral mucosal diseases, oral manifestations of systemic disease, and malignancy. Many conditions are amenable to treatment by the family physician, while others will require referral to a specialist.

This article and accompanying photo guide describe the types of lesions you may encounter during examinations of the oral cavity, and the corresponding diagnoses.

Be vigilant for non-odontogenic conditions that may require urgent treatment

There are several uncommon, acute non-odontogenic conditions that affect the oral cavity that, when severe, can require urgent medical attention and possible hospitalization.

Primary herpes simplex virus 1 (HSV-1) infection is generally subclinical, but some patients develop significant oral disease—called primary herpetic gingivostomatitis—that’s characterized by painful diffuse, irregular, crop-like ulcerations throughout the oral cavity and lips1 (FIGURE 1). The gingiva is nearly universally affected, which distinguishes this condition from erythema multiforme and aphthous stomatitis, which are described below. The incidence is highest in children, followed by adolescents and young adults.2

Erythema multiforme. This mucocutaneous hypersensitivity reaction can be limited to the oral cavity and lips, without accompanying skin lesions. Flu-like symptoms, including fever and chills, are followed by acute onset of diffuse oral ulcerations that are generally limited to non-keratinized mucosa, and spare the gingiva (FIGURE 2).3 Ulceration and crusting of the lips is common.

   

Aphthous stomatitis. Recurrent aphthous stomatitis (RAS) is a common immune-mediated inflammatory condition characterized by “canker sores,” or small round/ovoid ulcers with a well-defined erythematous halo (FIGURE 3). Lesions almost exclusively affect non-keratinized mucosa (and never the lip vermilion) and heal within 7 to 10 days, although “major” (>0.5 cm) lesions may persist much longer (FIGURE 4). A herpetiform pattern with multiple coalescing ulcers closely mimics HSV.

   

Small subsets of patients develop “complex” RAS, which is characterized by continuous and often multiple ulcerations that may extend into the esophagus, with associated chronic pain and compromised intake.2 RAS associated with systemic conditions is reviewed below.

How to spot signs of common dental diseases

In 2010 in the United States, close to 1.4 million emergency department visits and about $1 billion in hospital charges were due to dental problems.4 Approximately 40% of these visits were made by individuals without insurance.4 Due to a lack of dental insurance, patients may present to a medical professional rather than a dental professional. Additionally, uninsured individuals may neglect their dental problem until it becomes a medical emergency. Family physicians need to recognize dental disease and be able to provide basic management of emergencies.5

Dental abscess. A dental abscess can arise from pulpal infection (due to progression of caries) or periodontal infection (due to progression of periodontal disease). Pain symptoms are variable; however, intense, spontaneous cyclical pain is generally characteristic of a dental abscess of pulpal etiology, whereas a periodontal abscess can have less obvious symptoms. Swelling intraorally or extraorally indicates the spread of a localized infection (FIGURE 5).

Severe infection and swelling can limit mouth opening and function, and in extreme cases may obstruct swallowing and even breathing (eg, Ludwig’s angina). Affected teeth may or may not demonstrate obvious findings of advanced dental disease, such as gross caries, fracture, heavy calculus deposits, or marked periodontal attachment loss. Oral examination may reveal a parulis (focal erythematous swelling of the adjacent gingiva with a central draining sinus tract) (FIGURE 6) and percussion of the affected tooth is generally painful.

   

Pericoronitis is infection and swelling of the gingival tissues that surround a tooth, typically in association with a partially erupted third molar. Signs and symptoms include pain, discomfort with eating and swallowing, and limited mouth opening. Examination demonstrates gingival inflammation around a tooth, with or without purulence (FIGURE 7).

Acute necrotizing ulcerative gingivitis (ANUG) and periodontitis (ANUP) are severe conditions that are typically associated with psychological stress, severe malnutrition, and immunosuppression in patients with preexisting gingivitis or periodontitis.6 ANUG is associated with intense gingival pain, halitosis, generalized erythema, and destruction of the gingival papilla, often with bleeding.7 ANUP is a more advanced condition associated with damage and loss of the periodontium (including bone), often with loose teeth (FIGURE 8).8

 

 

Trauma. Dental trauma can be limited to the teeth and soft tissues, while more severe injuries can also affect the jaw bone.9 Accidental falls, assault, and motor vehicle traffic accidents are the most common causes of facial fractures in the United States, and are often associated with dentoalveolar trauma (FIGURE 9). The most commonly fractured facial bone is the mandible, characterized by painful opening and closing and an incomplete or altered bite.10

       

Oral symptoms may be the first sign of systemic disease

Inflammatory bowel disease. Crohn’s disease may affect the gastrointestinal tract anywhere from the mouth to the anus and may initially present with oral findings that may not correlate with abdominal symptoms. Oral Crohn’s disease may present as mucosal cobblestoning, mucosal tags, deep linear ulcerations, gingival hyperplasia, lip fissuring, aphthous ulcers, and angular cheilitis (FIGURES 10 AND 11). Other features may include diffuse, painless swelling of the lips and mucosal erythema.

Pyostomatitis vegetans is an uncommon condition typically associated with ulcerative colitis that is characterized by serpentine pustules that coalesce in a “snail track” pattern (FIGURE 12).11

       

Dermatologic/vesiculo-bullous diseases. Vesiculo-bullous lesions in the mouth may be seen in pemphigus vulgaris or bullous pemphigoid. Pemphigus vulgaris is an autoimmune intraepithelial blistering disease that often first presents in the oral cavity as flaccid bullae or painful ulcerations, prior to the onset of skin lesions (FIGURE 13).

Mucous membrane pemphigoid is an autoimmune subepithelial disease that affects mucous membranes and the skin. Characteristic oral mucosal blisters quickly rupture and form ulcerations, which may be present in the absence of other mucosal involvement (eg, anus, genitalia, nose or throat) (FIGURE 14).12 Painful aphthous ulcers are common. When oral ulcerations are diffuse and recurrent, they may be the first sign of Behçet’s disease, a multisystem autoimmune vasculitis.13

Oral lichen planus is a chronic immunemediated mucocutaneous disease that is often limited to the oral cavity. It presents with characteristic radiating white striations of the buccal mucosa and tongue, often with associated erythema and ulcerations (FIGURE 15).14

       

Rheumatologic conditions. Systemic or discoid lupus erythematosus may present with oral findings that largely resemble those of oral lichen planus (FIGURE 16).15 Sjögren’s syndrome is an autoimmune disease with characteristic xerostomia, which can lead to oral discomfort, dysphagia, recurrent candidiasis, and rampant dental caries.

Other conditions to watch for. Erosion of the enamel on the lingual surface of the teeth may be a sign of gastroesophageal reflux disease or bulimia (FIGURE 17). Examination of the oral mucosa can reveal typical white plaques of oral candidiasis (FIGURE 18), which may be associated with systemic immune suppression as well as salivary gland dysfunction.

       

Oral conditions that have been associated with human immunodeficiency virus infection include ANUG/ANUP, recurrent candidiasis, and oral hairy leukoplakia (FIGURE 19). In the absence of known HIV infection, patients who present with any of these oral conditions should be evaluated for HIV infection.13 (For more on recognizing the signs of HIV infection in patients without classic risk factors, see “HIV: 3 cases that hid in plain site” [J Fam Pract. 2015;64:20-26]).

Atrophic glossitis may indicate a vitamin B deficiency. Thrombocytopenia and leukemia may present with oral petechiae, purpura, oral hematomas, or hemorrhagic bullae (FIGURE 20).13 Painless pseudomembranous mucosal erosions may be a presentation for secondary syphilis.16

   

Look for signs that suggest malignancy

In the United States, oral and pharyngeal cancers account for approximately 40,000 cases of cancer and 8000 deaths each year.17 More than 90% of these are squamous cell carcinomas (SCCs); the remainder are mainly salivary gland tumors, lymphoma, and other infrequent cancers.18

SCC of the oral cavity most commonly occurs on the tongue but can develop in any site, presenting as mucosal ulcers, plaques, or masses that do not heal (FIGURE 21). Tobacco and alcohol use are associated with up to 80% of cases of SCC of the head and neck.18 Some oropharyngeal SCCs are associated with human papillomavirus infection type 16.19

Potentially malignant oral lesions include leukoplakia and erythroplakia. Leukoplakia is a white patch or plaque of the oral mucosa that can’t be explained by any other clinical diagnosis (FIGURE 22). These lesions are at risk for malignant transformation and may demonstrate dysplasia or frank SCC on biopsy.20 Proliferative verrucous leukoplakia is a unique form of leukoplakia that’s characterized by a wrinkled appearance that is often multifocal; the condition is associated with a higher risk of malignant transformation.

   

Erythroplakia is a red patch that similarly can’t be explained by another diagnosis. It has a very high risk of malignant transformation over time. All potentially malignant oral lesions, including leukoplakia and erythroplakia, require biopsy and careful monitoring.

 

 

Non-SCC cancers. Salivary gland tumors are rare and most commonly occur in patients ages 55 to 65 years. Most neoplasms (70%-85%) occur in the parotid gland, while 8% to 15% develop in the submandibular salivary gland and less than 1% involve the sublingual gland.21 Minor salivary gland tissue, especially in the lips and palate, may also be affected (FIGURE 23). Patients present with circumscribed, fixed or movable, painless, soft or firm masses in a salivary gland.

Melanoma should be included in the differential diagnosis of oral pigmented lesions that have any features of cutaneous melanoma, such as asymmetry, irregular borders, or variable or changing color.22

Hematologic malignancies may initially present (or demonstrate evidence of relapse) in the oral cavity. Leukemia typically presents with sheet-like overgrowth and swelling of the gingiva with associated erythema and bleeding (FIGURE 24), whereas lymphoma typically presents as a solitary mass or ulceration. Solid tumors that metastasize to the oral cavity may present with localized unexplained soft or hard tissue growths, with or without associated neurologic symptoms (eg, paresthesia).

   

CORRESPONDENCE
William D. Anderson, III, MD, DABFM, FAAFP, University of South Carolina School of Medicine, 15 Medical Park, Suite 300, Columbia, SC 29203; william.anderson@uscmed.sc.edu

PRACTICE RECOMMENDATIONS

› Perform a biopsy and carefully monitor all potentially malignant oral lesions, including leukoplakia and erythroplakia. A
› Consider evaluation for human immunodeficiency virus infection for any patient who has acute necrotizing ulcerative gingivitis/acute necrotizing ulcerative periodontitis, recurrent candidiasis, or oral hairy leukoplakia. A
› Include melanoma in the differential diagnosis of oral pigmented lesions that have any features of cutaneous melanoma (eg, asymmetry, irregular borders, or variable or changing color). A

Strength of recommendation (SOR)

A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series

Family physicians can play an essential role in managing their patients’ oral health by promptly recognizing and diagnosing conditions that demand further medical attention, including non-odontogenic and odontogenic infections, primary oral mucosal diseases, oral manifestations of systemic disease, and malignancy. Many conditions are amenable to treatment by the family physician, while others will require referral to a specialist.

This article and accompanying photo guide describe the types of lesions you may encounter during examinations of the oral cavity, and the corresponding diagnoses.

Be vigilant for non-odontogenic conditions that may require urgent treatment

There are several uncommon, acute non-odontogenic conditions that affect the oral cavity that, when severe, can require urgent medical attention and possible hospitalization.

Primary herpes simplex virus 1 (HSV-1) infection is generally subclinical, but some patients develop significant oral disease—called primary herpetic gingivostomatitis—that’s characterized by painful diffuse, irregular, crop-like ulcerations throughout the oral cavity and lips1 (FIGURE 1). The gingiva is nearly universally affected, which distinguishes this condition from erythema multiforme and aphthous stomatitis, which are described below. The incidence is highest in children, followed by adolescents and young adults.2

Erythema multiforme. This mucocutaneous hypersensitivity reaction can be limited to the oral cavity and lips, without accompanying skin lesions. Flu-like symptoms, including fever and chills, are followed by acute onset of diffuse oral ulcerations that are generally limited to non-keratinized mucosa, and spare the gingiva (FIGURE 2).3 Ulceration and crusting of the lips is common.

   

Aphthous stomatitis. Recurrent aphthous stomatitis (RAS) is a common immune-mediated inflammatory condition characterized by “canker sores,” or small round/ovoid ulcers with a well-defined erythematous halo (FIGURE 3). Lesions almost exclusively affect non-keratinized mucosa (and never the lip vermilion) and heal within 7 to 10 days, although “major” (>0.5 cm) lesions may persist much longer (FIGURE 4). A herpetiform pattern with multiple coalescing ulcers closely mimics HSV.

   

Small subsets of patients develop “complex” RAS, which is characterized by continuous and often multiple ulcerations that may extend into the esophagus, with associated chronic pain and compromised intake.2 RAS associated with systemic conditions is reviewed below.

How to spot signs of common dental diseases

In 2010 in the United States, close to 1.4 million emergency department visits and about $1 billion in hospital charges were due to dental problems.4 Approximately 40% of these visits were made by individuals without insurance.4 Due to a lack of dental insurance, patients may present to a medical professional rather than a dental professional. Additionally, uninsured individuals may neglect their dental problem until it becomes a medical emergency. Family physicians need to recognize dental disease and be able to provide basic management of emergencies.5

Dental abscess. A dental abscess can arise from pulpal infection (due to progression of caries) or periodontal infection (due to progression of periodontal disease). Pain symptoms are variable; however, intense, spontaneous cyclical pain is generally characteristic of a dental abscess of pulpal etiology, whereas a periodontal abscess can have less obvious symptoms. Swelling intraorally or extraorally indicates the spread of a localized infection (FIGURE 5).

Severe infection and swelling can limit mouth opening and function, and in extreme cases may obstruct swallowing and even breathing (eg, Ludwig’s angina). Affected teeth may or may not demonstrate obvious findings of advanced dental disease, such as gross caries, fracture, heavy calculus deposits, or marked periodontal attachment loss. Oral examination may reveal a parulis (focal erythematous swelling of the adjacent gingiva with a central draining sinus tract) (FIGURE 6) and percussion of the affected tooth is generally painful.

   

Pericoronitis is infection and swelling of the gingival tissues that surround a tooth, typically in association with a partially erupted third molar. Signs and symptoms include pain, discomfort with eating and swallowing, and limited mouth opening. Examination demonstrates gingival inflammation around a tooth, with or without purulence (FIGURE 7).

Acute necrotizing ulcerative gingivitis (ANUG) and periodontitis (ANUP) are severe conditions that are typically associated with psychological stress, severe malnutrition, and immunosuppression in patients with preexisting gingivitis or periodontitis.6 ANUG is associated with intense gingival pain, halitosis, generalized erythema, and destruction of the gingival papilla, often with bleeding.7 ANUP is a more advanced condition associated with damage and loss of the periodontium (including bone), often with loose teeth (FIGURE 8).8

 

 

Trauma. Dental trauma can be limited to the teeth and soft tissues, while more severe injuries can also affect the jaw bone.9 Accidental falls, assault, and motor vehicle traffic accidents are the most common causes of facial fractures in the United States, and are often associated with dentoalveolar trauma (FIGURE 9). The most commonly fractured facial bone is the mandible, characterized by painful opening and closing and an incomplete or altered bite.10

       

Oral symptoms may be the first sign of systemic disease

Inflammatory bowel disease. Crohn’s disease may affect the gastrointestinal tract anywhere from the mouth to the anus and may initially present with oral findings that may not correlate with abdominal symptoms. Oral Crohn’s disease may present as mucosal cobblestoning, mucosal tags, deep linear ulcerations, gingival hyperplasia, lip fissuring, aphthous ulcers, and angular cheilitis (FIGURES 10 AND 11). Other features may include diffuse, painless swelling of the lips and mucosal erythema.

Pyostomatitis vegetans is an uncommon condition typically associated with ulcerative colitis that is characterized by serpentine pustules that coalesce in a “snail track” pattern (FIGURE 12).11

       

Dermatologic/vesiculo-bullous diseases. Vesiculo-bullous lesions in the mouth may be seen in pemphigus vulgaris or bullous pemphigoid. Pemphigus vulgaris is an autoimmune intraepithelial blistering disease that often first presents in the oral cavity as flaccid bullae or painful ulcerations, prior to the onset of skin lesions (FIGURE 13).

Mucous membrane pemphigoid is an autoimmune subepithelial disease that affects mucous membranes and the skin. Characteristic oral mucosal blisters quickly rupture and form ulcerations, which may be present in the absence of other mucosal involvement (eg, anus, genitalia, nose or throat) (FIGURE 14).12 Painful aphthous ulcers are common. When oral ulcerations are diffuse and recurrent, they may be the first sign of Behçet’s disease, a multisystem autoimmune vasculitis.13

Oral lichen planus is a chronic immunemediated mucocutaneous disease that is often limited to the oral cavity. It presents with characteristic radiating white striations of the buccal mucosa and tongue, often with associated erythema and ulcerations (FIGURE 15).14

       

Rheumatologic conditions. Systemic or discoid lupus erythematosus may present with oral findings that largely resemble those of oral lichen planus (FIGURE 16).15 Sjögren’s syndrome is an autoimmune disease with characteristic xerostomia, which can lead to oral discomfort, dysphagia, recurrent candidiasis, and rampant dental caries.

Other conditions to watch for. Erosion of the enamel on the lingual surface of the teeth may be a sign of gastroesophageal reflux disease or bulimia (FIGURE 17). Examination of the oral mucosa can reveal typical white plaques of oral candidiasis (FIGURE 18), which may be associated with systemic immune suppression as well as salivary gland dysfunction.

       

Oral conditions that have been associated with human immunodeficiency virus infection include ANUG/ANUP, recurrent candidiasis, and oral hairy leukoplakia (FIGURE 19). In the absence of known HIV infection, patients who present with any of these oral conditions should be evaluated for HIV infection.13 (For more on recognizing the signs of HIV infection in patients without classic risk factors, see “HIV: 3 cases that hid in plain site” [J Fam Pract. 2015;64:20-26]).

Atrophic glossitis may indicate a vitamin B deficiency. Thrombocytopenia and leukemia may present with oral petechiae, purpura, oral hematomas, or hemorrhagic bullae (FIGURE 20).13 Painless pseudomembranous mucosal erosions may be a presentation for secondary syphilis.16

   

Look for signs that suggest malignancy

In the United States, oral and pharyngeal cancers account for approximately 40,000 cases of cancer and 8000 deaths each year.17 More than 90% of these are squamous cell carcinomas (SCCs); the remainder are mainly salivary gland tumors, lymphoma, and other infrequent cancers.18

SCC of the oral cavity most commonly occurs on the tongue but can develop in any site, presenting as mucosal ulcers, plaques, or masses that do not heal (FIGURE 21). Tobacco and alcohol use are associated with up to 80% of cases of SCC of the head and neck.18 Some oropharyngeal SCCs are associated with human papillomavirus infection type 16.19

Potentially malignant oral lesions include leukoplakia and erythroplakia. Leukoplakia is a white patch or plaque of the oral mucosa that can’t be explained by any other clinical diagnosis (FIGURE 22). These lesions are at risk for malignant transformation and may demonstrate dysplasia or frank SCC on biopsy.20 Proliferative verrucous leukoplakia is a unique form of leukoplakia that’s characterized by a wrinkled appearance that is often multifocal; the condition is associated with a higher risk of malignant transformation.

   

Erythroplakia is a red patch that similarly can’t be explained by another diagnosis. It has a very high risk of malignant transformation over time. All potentially malignant oral lesions, including leukoplakia and erythroplakia, require biopsy and careful monitoring.

 

 

Non-SCC cancers. Salivary gland tumors are rare and most commonly occur in patients ages 55 to 65 years. Most neoplasms (70%-85%) occur in the parotid gland, while 8% to 15% develop in the submandibular salivary gland and less than 1% involve the sublingual gland.21 Minor salivary gland tissue, especially in the lips and palate, may also be affected (FIGURE 23). Patients present with circumscribed, fixed or movable, painless, soft or firm masses in a salivary gland.

Melanoma should be included in the differential diagnosis of oral pigmented lesions that have any features of cutaneous melanoma, such as asymmetry, irregular borders, or variable or changing color.22

Hematologic malignancies may initially present (or demonstrate evidence of relapse) in the oral cavity. Leukemia typically presents with sheet-like overgrowth and swelling of the gingiva with associated erythema and bleeding (FIGURE 24), whereas lymphoma typically presents as a solitary mass or ulceration. Solid tumors that metastasize to the oral cavity may present with localized unexplained soft or hard tissue growths, with or without associated neurologic symptoms (eg, paresthesia).

   

CORRESPONDENCE
William D. Anderson, III, MD, DABFM, FAAFP, University of South Carolina School of Medicine, 15 Medical Park, Suite 300, Columbia, SC 29203; william.anderson@uscmed.sc.edu

References

1. Spruance SL. The natural history of recurrent oral-facial herpes simplex virus infection. Semin Dermatol. 1992;11:200-206.

2. Balasubramaniam R, Kuperstein AS, Stoopler ET. Update on oral herpes virus infections. Dent Clin North Am. 2014;58:265-280.

3. Lozada-Nur F, Gorsky M, Silverman S Jr. Oral erythema multiforme: clinical observations and treatment of 95 patients. Oral Surg Oral Med Oral Pathol. 1989;67:36-40.

4. Allareddy V, Rampa S, Lee MK, et al. Hospital-based emergency department visits involving dental conditions: profile and predictors of poor outcomes and resource utilization. J Am Dent Assoc. 2014;145:331-337.

5. Allareddy V, Lin CY, Shah A, et al. Outcomes in patients hospitalized for periapical abscess in the United States: an analysis involving the use of a nationwide inpatient sample. J Am Dent Assoc. 2010;141:1107-1116.

6. Folayan MO. The epidemiology, etiology, and pathophysiology of acute necrotizing ulcerative gingivitis associated with malnutrition. J Contemp Dent Pract. 2004;5:28-41.

7. Atout RN, Todescan S. Managing patients with necrotizing ulcerative gingivitis. J Can Dent Assoc. 2013;79:d46.

8. Todescan S, Nizar R. Managing patients with necrotizing ulcerative periodontitis. J Can Dent Assoc. 2013;79:d44.

9. Allareddy V, Allareddy V, Nalliah RP. Epidemiology of facial fracture injuries. J Oral Maxillofac Surg. 2011;69:2613-2618.

10. Nalliah RP, Allareddy V, Kim MK, et al. Economics of facial fracture reductions in the United States over 12 months. Dent Traumatol. 2013;29:115-120.

11. Padmavathi B, Sharma S, Astekar M, et al. Oral Crohn’s disease. J Oral Maxillofac Pathol. 2014;18(suppl 1):S139-S142.

12. Xu HH, Werth VP, Parisi E, et al. Mucous membrane pemphigoid. Dent Clin North Am. 2013;57:611-630.

13. Chi AC, Neville BW, Krayer JW, et al. Oral manifestations of systemic disease. Am Fam Physician. 2010;82:1381-1388.

14. Lavanya N, Jayanthi P, Rao UK, et al. Oral lichen planus: An update on pathogenesis and treatment. J Oral Maxillofac Pathol. 2011;15:127-132.

15. Uva L, Miguel D, Pinheiro C, et al. Cutaneous manifestations of systemic lupus erythematosus. Autoimmune Dis. 2012;2012:834291.

16. Ficarra G, Carlos R. Syphilis: The renaissance of an old disease with oral implications. Head Neck Pathol. 2009;3:195-206.

17. Siegel R, Ward E, Brawley O, et al. Cancer statistics, 2011: the impact of eliminating socioeconomic and racial disparities on premature cancer deaths. CA Cancer J Clin. 2011;61:212-236.

18. Licitra L, Locati LD, Bossi P, et al. Head and neck tumors other than squamous cell carcinoma. Curr Opin Oncol. 2004;16:236-241.

19. Gillison ML, Broutian T, Pickard RK, et al. Prevalence of oral HPV infection in the United States, 2009-2010. JAMA. 2012;307:693-703.

20. Silverman S Jr., Gorsky M, Lozada F. Oral leukoplakia and malignant transformation: A follow‐up study of 257 patients. Cancer. 1984;53:563-568.

21. Spiro RH. Salivary neoplasms: overview of a 35-year experience with 2807 patients. Head Neck Surg. 1986;8:177-184.

22. DeMatos P, Tyler DS, Seigler HF. Malignant melanoma of the mucous membranes: a review of 119 cases. Ann Surg Oncol. 1998;5:733-742.

References

1. Spruance SL. The natural history of recurrent oral-facial herpes simplex virus infection. Semin Dermatol. 1992;11:200-206.

2. Balasubramaniam R, Kuperstein AS, Stoopler ET. Update on oral herpes virus infections. Dent Clin North Am. 2014;58:265-280.

3. Lozada-Nur F, Gorsky M, Silverman S Jr. Oral erythema multiforme: clinical observations and treatment of 95 patients. Oral Surg Oral Med Oral Pathol. 1989;67:36-40.

4. Allareddy V, Rampa S, Lee MK, et al. Hospital-based emergency department visits involving dental conditions: profile and predictors of poor outcomes and resource utilization. J Am Dent Assoc. 2014;145:331-337.

5. Allareddy V, Lin CY, Shah A, et al. Outcomes in patients hospitalized for periapical abscess in the United States: an analysis involving the use of a nationwide inpatient sample. J Am Dent Assoc. 2010;141:1107-1116.

6. Folayan MO. The epidemiology, etiology, and pathophysiology of acute necrotizing ulcerative gingivitis associated with malnutrition. J Contemp Dent Pract. 2004;5:28-41.

7. Atout RN, Todescan S. Managing patients with necrotizing ulcerative gingivitis. J Can Dent Assoc. 2013;79:d46.

8. Todescan S, Nizar R. Managing patients with necrotizing ulcerative periodontitis. J Can Dent Assoc. 2013;79:d44.

9. Allareddy V, Allareddy V, Nalliah RP. Epidemiology of facial fracture injuries. J Oral Maxillofac Surg. 2011;69:2613-2618.

10. Nalliah RP, Allareddy V, Kim MK, et al. Economics of facial fracture reductions in the United States over 12 months. Dent Traumatol. 2013;29:115-120.

11. Padmavathi B, Sharma S, Astekar M, et al. Oral Crohn’s disease. J Oral Maxillofac Pathol. 2014;18(suppl 1):S139-S142.

12. Xu HH, Werth VP, Parisi E, et al. Mucous membrane pemphigoid. Dent Clin North Am. 2013;57:611-630.

13. Chi AC, Neville BW, Krayer JW, et al. Oral manifestations of systemic disease. Am Fam Physician. 2010;82:1381-1388.

14. Lavanya N, Jayanthi P, Rao UK, et al. Oral lichen planus: An update on pathogenesis and treatment. J Oral Maxillofac Pathol. 2011;15:127-132.

15. Uva L, Miguel D, Pinheiro C, et al. Cutaneous manifestations of systemic lupus erythematosus. Autoimmune Dis. 2012;2012:834291.

16. Ficarra G, Carlos R. Syphilis: The renaissance of an old disease with oral implications. Head Neck Pathol. 2009;3:195-206.

17. Siegel R, Ward E, Brawley O, et al. Cancer statistics, 2011: the impact of eliminating socioeconomic and racial disparities on premature cancer deaths. CA Cancer J Clin. 2011;61:212-236.

18. Licitra L, Locati LD, Bossi P, et al. Head and neck tumors other than squamous cell carcinoma. Curr Opin Oncol. 2004;16:236-241.

19. Gillison ML, Broutian T, Pickard RK, et al. Prevalence of oral HPV infection in the United States, 2009-2010. JAMA. 2012;307:693-703.

20. Silverman S Jr., Gorsky M, Lozada F. Oral leukoplakia and malignant transformation: A follow‐up study of 257 patients. Cancer. 1984;53:563-568.

21. Spiro RH. Salivary neoplasms: overview of a 35-year experience with 2807 patients. Head Neck Surg. 1986;8:177-184.

22. DeMatos P, Tyler DS, Seigler HF. Malignant melanoma of the mucous membranes: a review of 119 cases. Ann Surg Oncol. 1998;5:733-742.

Issue
The Journal of Family Practice - 64(7)
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Oral lesions you can’t afford to miss
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William D. Anderson, III, MD, DABFM, FAAFP; Nathaniel S. Treister, DMD, DMSc; E.J. Mayeaux, Jr., MD, DABFM, FAAFP; Romesh P. Nalliah, DMD; oral lesions; mouth; HSV-1 infection; erythema multiforme; aphthous stomatitis; ANUG; ANUP; dental abscess; parulis; pericoronitis; ulcerative periodontitis; dentoalveolar trauma; Crohn's disease; pyostomatitis vegetans; pemphigus vulgaris; muscous membrane pemphigoid; lichen planus; systemic lupus erythematosus; enamel erosion; candidiasis; oral hairy leukoplakia; thrombocytopenia purpura; squamous cell carcinoma; leukplakia; mucoepidermoid carcinoma; acute myselogenous leukemia
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William D. Anderson, III, MD, DABFM, FAAFP; Nathaniel S. Treister, DMD, DMSc; E.J. Mayeaux, Jr., MD, DABFM, FAAFP; Romesh P. Nalliah, DMD; oral lesions; mouth; HSV-1 infection; erythema multiforme; aphthous stomatitis; ANUG; ANUP; dental abscess; parulis; pericoronitis; ulcerative periodontitis; dentoalveolar trauma; Crohn's disease; pyostomatitis vegetans; pemphigus vulgaris; muscous membrane pemphigoid; lichen planus; systemic lupus erythematosus; enamel erosion; candidiasis; oral hairy leukoplakia; thrombocytopenia purpura; squamous cell carcinoma; leukplakia; mucoepidermoid carcinoma; acute myselogenous leukemia
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A patient handout from the health services department of the University of California, Berkley titled “Insomnia Self-Care Guide” teaches patients how their behaviors might be contributing to their sleep difficulties. In addition to providing general information about sleep, the handout, which is available at http://www.uhs.berkeley.edu/home/healthtopics/PDF%20Handouts/Insomnia.pdf, also includes a checklist of questions about behaviors tied to insomnia, such as “Do you drink alcohol in the evenings?” and suggestions for inducing sleep, such as exercising daily.

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A patient handout from the health services department of the University of California, Berkley titled “Insomnia Self-Care Guide” teaches patients how their behaviors might be contributing to their sleep difficulties. In addition to providing general information about sleep, the handout, which is available at http://www.uhs.berkeley.edu/home/healthtopics/PDF%20Handouts/Insomnia.pdf, also includes a checklist of questions about behaviors tied to insomnia, such as “Do you drink alcohol in the evenings?” and suggestions for inducing sleep, such as exercising daily.

A patient handout from the health services department of the University of California, Berkley titled “Insomnia Self-Care Guide” teaches patients how their behaviors might be contributing to their sleep difficulties. In addition to providing general information about sleep, the handout, which is available at http://www.uhs.berkeley.edu/home/healthtopics/PDF%20Handouts/Insomnia.pdf, also includes a checklist of questions about behaviors tied to insomnia, such as “Do you drink alcohol in the evenings?” and suggestions for inducing sleep, such as exercising daily.

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What is the cause of this young woman’s persistent back pain?

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The back pain this patient from northern India had was initially blamed on small, nonobstructive renal calculi. The real culprit was spinal tuberculosis, a common cause of back pain in parts of the world where the infection is rampant. To read the full article, go to the Cleveland Clinic Journal of Medicine: http://www.ccjm.org/topics/infectious-diseases/single-article-page/persistent-back-pain-in-a-young-woman/5dd03a44eed9e20a5d01df4d7bd85328.html.

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The back pain this patient from northern India had was initially blamed on small, nonobstructive renal calculi. The real culprit was spinal tuberculosis, a common cause of back pain in parts of the world where the infection is rampant. To read the full article, go to the Cleveland Clinic Journal of Medicine: http://www.ccjm.org/topics/infectious-diseases/single-article-page/persistent-back-pain-in-a-young-woman/5dd03a44eed9e20a5d01df4d7bd85328.html.

The back pain this patient from northern India had was initially blamed on small, nonobstructive renal calculi. The real culprit was spinal tuberculosis, a common cause of back pain in parts of the world where the infection is rampant. To read the full article, go to the Cleveland Clinic Journal of Medicine: http://www.ccjm.org/topics/infectious-diseases/single-article-page/persistent-back-pain-in-a-young-woman/5dd03a44eed9e20a5d01df4d7bd85328.html.

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The Liver Foundation offers a brief educational guide that teaches patients about the hepatitis C virus. The brochure, which is available at http://www.liverfoundation.org/downloads/alf_download_24.pdf, uses a Q&A format to explain what hepatitis C is, how it is spread, who is at risk, and how it is diagnosed and treated.

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The Liver Foundation offers a brief educational guide that teaches patients about the hepatitis C virus. The brochure, which is available at http://www.liverfoundation.org/downloads/alf_download_24.pdf, uses a Q&A format to explain what hepatitis C is, how it is spread, who is at risk, and how it is diagnosed and treated.

The Liver Foundation offers a brief educational guide that teaches patients about the hepatitis C virus. The brochure, which is available at http://www.liverfoundation.org/downloads/alf_download_24.pdf, uses a Q&A format to explain what hepatitis C is, how it is spread, who is at risk, and how it is diagnosed and treated.

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PTSD increases risk of heart failure

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PTSD increases risk of heart failure

Researchers who reviewed the medical records of 8248 veterans found that those with posttraumatic stress disorder (PTSD) were nearly 50% more likely to develop heart failure than veterans without PTSD. The increased risk remained even after researchers controlled for known clinical risk factors and military-specific factors, such as combat service.

To read the full article, go to Federal Practitioner: http://www.fedprac.com/the-publication/past-issues-single-view/ptsd-increases-chance-of-heart-failure/f40e2d20b2f4d6193925c8a1884c1746/ocregister.html.

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Researchers who reviewed the medical records of 8248 veterans found that those with posttraumatic stress disorder (PTSD) were nearly 50% more likely to develop heart failure than veterans without PTSD. The increased risk remained even after researchers controlled for known clinical risk factors and military-specific factors, such as combat service.

To read the full article, go to Federal Practitioner: http://www.fedprac.com/the-publication/past-issues-single-view/ptsd-increases-chance-of-heart-failure/f40e2d20b2f4d6193925c8a1884c1746/ocregister.html.

Researchers who reviewed the medical records of 8248 veterans found that those with posttraumatic stress disorder (PTSD) were nearly 50% more likely to develop heart failure than veterans without PTSD. The increased risk remained even after researchers controlled for known clinical risk factors and military-specific factors, such as combat service.

To read the full article, go to Federal Practitioner: http://www.fedprac.com/the-publication/past-issues-single-view/ptsd-increases-chance-of-heart-failure/f40e2d20b2f4d6193925c8a1884c1746/ocregister.html.

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PTSD increases risk of heart failure
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PTSD increases risk of heart failure
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