Nephrology

Pregnancy outcomes were similar for women who underwent kidney transplants in childhood and those who received transplants as adults, according to findings published Feb. 2 in JAMA Pediatrics.

Live births occurred in 76% of pregnancies in women who received kidney transplants as children, compared with 77% of pregnancies among women who received transplants as adults, wrote Melanie L. Wyld and her colleagues from Sydney Medical School in Australia.

©London_England/Thinkstockphotos.com

The study examined a total of 101 pregnancies in 66 women who received transplants before age 18 years, and 626 pregnancies in 401 women who were adults at the time of transplant.

Mean gestational age and prematurity incidence were also similar in the two groups, with child-transplant recipients having a mean gestational age of 35 weeks, and adult-transplant recipients having a mean gestational age of 36 weeks.

Incidence of prematurity was 45% in child-transplant mothers and 53% in adult-transplant mothers, the researchers reported.

“To our knowledge, this study is the first to look at pregnancy outcomes for women who received a kidney transplant as a child,” the researchers wrote. These results should “provide comfort to such mothers and their physicians that their early onset of kidney failure and longer period of posttransplant exposure to immunosuppression do not adversely affect their pregnancy outcomes,” they added.

Read the full article at: JAMA Pediatr. 2015;169(2):e143626. (doi:10.1001/jamapediatrics.2014.3626).

Pregnancy outcomes were similar for women who underwent kidney transplants in childhood and those who received transplants as adults, according to findings published Feb. 2 in JAMA Pediatrics.

Live births occurred in 76% of pregnancies in women who received kidney transplants as children, compared with 77% of pregnancies among women who received transplants as adults, wrote Melanie L. Wyld and her colleagues from Sydney Medical School in Australia.

©London_England/Thinkstockphotos.com

The study examined a total of 101 pregnancies in 66 women who received transplants before age 18 years, and 626 pregnancies in 401 women who were adults at the time of transplant.

Mean gestational age and prematurity incidence were also similar in the two groups, with child-transplant recipients having a mean gestational age of 35 weeks, and adult-transplant recipients having a mean gestational age of 36 weeks.

Incidence of prematurity was 45% in child-transplant mothers and 53% in adult-transplant mothers, the researchers reported.

“To our knowledge, this study is the first to look at pregnancy outcomes for women who received a kidney transplant as a child,” the researchers wrote. These results should “provide comfort to such mothers and their physicians that their early onset of kidney failure and longer period of posttransplant exposure to immunosuppression do not adversely affect their pregnancy outcomes,” they added.

Read the full article at: JAMA Pediatr. 2015;169(2):e143626. (doi:10.1001/jamapediatrics.2014.3626).

Pregnancy outcomes were similar for women who underwent kidney transplants in childhood and those who received transplants as adults, according to findings published Feb. 2 in JAMA Pediatrics.

Live births occurred in 76% of pregnancies in women who received kidney transplants as children, compared with 77% of pregnancies among women who received transplants as adults, wrote Melanie L. Wyld and her colleagues from Sydney Medical School in Australia.

©London_England/Thinkstockphotos.com

The study examined a total of 101 pregnancies in 66 women who received transplants before age 18 years, and 626 pregnancies in 401 women who were adults at the time of transplant.

Mean gestational age and prematurity incidence were also similar in the two groups, with child-transplant recipients having a mean gestational age of 35 weeks, and adult-transplant recipients having a mean gestational age of 36 weeks.

Incidence of prematurity was 45% in child-transplant mothers and 53% in adult-transplant mothers, the researchers reported.

“To our knowledge, this study is the first to look at pregnancy outcomes for women who received a kidney transplant as a child,” the researchers wrote. These results should “provide comfort to such mothers and their physicians that their early onset of kidney failure and longer period of posttransplant exposure to immunosuppression do not adversely affect their pregnancy outcomes,” they added.

Read the full article at: JAMA Pediatr. 2015;169(2):e143626. (doi:10.1001/jamapediatrics.2014.3626).

A 59-year-old man with autosomal dominant polycystic kidney disease (ADPKD), end-stage renal disease on hemodialysis, hypertension, and diverticulosis presented with acute pain in the left lower abdomen. The pain began 4 days previously, was dull and nonradiating, was relieved partially with hydrocodone-acetaminophen, and had no clear exacerbating factors. Two days before presentation, he developed a fever with chills. He reported no recent dysuria, diarrhea, hematuria, hematochezia, or melena. He had not been taking anticoagulants or nonsteroidal anti-inflammatory drugs, and he had no history of heavy lifting or trauma.

His temperature was 38.5˚C (101.3˚F), blood pressure 141/60 mm Hg (normal for this patient). On examination, his left lower quadrant was tender with voluntary guarding. Also present was a reducible ventral hernia, which was not new.

His hemoglobin level was 10.6 g/dL (reference range 13.0–17.0), which had dropped from a previous value of 13.7 g/dL.

Computed tomography of the abdomen and pelvis revealed a ruptured retroperitoneal hemorrhagic cyst (Figure 1) in the inferior aspect of the left kidney extending into the fascia of Gerota.

Since his vital signs were stable, he was managed supportively during his hospitalization with intravenous fluids, serial hemoglobin checks, and analgesia. He was eventually discharged home in good condition.

CYST HEMORRHAGE IN POLYCYSTIC KIDNEY DISEASE

ADPKD is a relatively common, inherited systemic disease that leads to cyst formation,  primarily in the kidneys but also in the liver (94%), seminal vesicles (40%), pancreas (9%), arachnoid membrane (8%), and spinal meningeal area (2%).¹

In addition to cyst formation in multiple organs, ADPKD can have extrarenal manifestations such as connective-tissue abnormalities (including mitral valve prolapse) (25%), abdominal hernia (10%), and intracranial aneurysm (8%).¹ Management of extrarenal complications of ADPKD is discussed in detail elsewhere.²

The estimated prevalence of ADPKD is 1 of every 400 to 1,000 live births. However, given that ADPKD is often clinically silent, it is diagnosed during the lifetime of fewer than half of people who have it.³

Most ADPKD cases are caused by mutations in either the PKD1 or PKD2 gene.^4,5  Although the mechanism of cyst formation in ADPKD is still unclear, it is known that PKD1 and PKD2 encode proteins called polycystin-1 and polycystin-2, respectively. Polycystin-1 is a membrane protein found in renal tubular epithelia, hepatic bile ductules, and pancreatic ducts. Polycystin-2 is involved in cell calcium signaling and has been identified in the renal distal tubules, collecting duct, and thick ascending limb. Mutations in PKD1 and PKD2 are thought to contribute to cyst formation, with PKD1 mutations associated with earlier onset and more severe development of renal and extrarenal cysts.

Cyst hemorrhage

Hemorrhage of renal cysts is a well-known complication, occurring in up to 70% of patients with ADPKD.6 Renal cyst hemorrhage often presents clinically as flank pain with point tenderness or hematuria, or both. Flank pain results from hemorrhage into a cyst with consequent distention of the renal capsule, whereas hematuria results from rupture of a cyst into the collecting system.

Spontaneous nonfatal retroperitoneal cyst hemorrhage, as in our patient, is  rare. Indeed, in one series reviewing the abdominal computed tomographic findings of 66 patients with ADPKD, only 2 patients (3%) had perinephric hematomas in the absence of recent trauma.⁶

Management of cyst hemorrhage is primarily conservative. Pain associated with cyst hemorrhage is managed conservatively with bed rest, intravenous hydration, and analgesics (but not nonsteroidal anti-inflammatory drugs).

Fewer than half of people with ADPKD are diagnosed with it in their lifetime

Hematuria is also managed conservatively with bedrest and intravenous hydration, and most episodes of hematuria are self-limiting and last 2 to 7 days. However, if excessive bleeding occurs, the patient may be at risk of urinary tract obstruction from clot formation. If obstruction occurs and persists beyond 2 weeks, then ureteral stenting may be necessary. In rare cases of prolonged, severe bleeding with extensive subcapsular or retroperitoneal hematomas, patients require hospitalization, transfusion, or percutaneous transcatheter embolization of the renal artery. If such efforts are not successful, surgery, including nephrectomy, may be required to control the hemorrhage.²

Other causes of abdominal pain

In addition to renal cyst hemorrhage, the differential diagnosis of abdominal pain in a patient with ADPKD includes cyst enlargement causing stretching of the renal capsule or traction on the renal pedicle, cyst infection, nephrolithiasis, pyelonephritis, and rarely, tumors including renal cell carcinoma.

Unlike cyst rupture and hemorrhage, which are associated with point tenderness, cyst infection often manifests as diffuse, usually unilateral flank pain with associated fever, nausea, malaise, and leukocytosis. Our patient had none of these except for fever, which can also occur in cyst hemorrhage.

Nephrolithiasis occurs in up to 35% of patients with ADPKD,⁷ but no kidney stones were seen on computed tomography in our patient.

Pyelonephritis was unlikely in our patient, given that he had no significant white blood cells in his urinalysis and no leukocytosis.

Abdominal and pelvic imaging did not reveal any tumors in our patient.

A 59-year-old man with autosomal dominant polycystic kidney disease (ADPKD), end-stage renal disease on hemodialysis, hypertension, and diverticulosis presented with acute pain in the left lower abdomen. The pain began 4 days previously, was dull and nonradiating, was relieved partially with hydrocodone-acetaminophen, and had no clear exacerbating factors. Two days before presentation, he developed a fever with chills. He reported no recent dysuria, diarrhea, hematuria, hematochezia, or melena. He had not been taking anticoagulants or nonsteroidal anti-inflammatory drugs, and he had no history of heavy lifting or trauma.

His temperature was 38.5˚C (101.3˚F), blood pressure 141/60 mm Hg (normal for this patient). On examination, his left lower quadrant was tender with voluntary guarding. Also present was a reducible ventral hernia, which was not new.

His hemoglobin level was 10.6 g/dL (reference range 13.0–17.0), which had dropped from a previous value of 13.7 g/dL.

Computed tomography of the abdomen and pelvis revealed a ruptured retroperitoneal hemorrhagic cyst (Figure 1) in the inferior aspect of the left kidney extending into the fascia of Gerota.

Since his vital signs were stable, he was managed supportively during his hospitalization with intravenous fluids, serial hemoglobin checks, and analgesia. He was eventually discharged home in good condition.

CYST HEMORRHAGE IN POLYCYSTIC KIDNEY DISEASE

ADPKD is a relatively common, inherited systemic disease that leads to cyst formation,  primarily in the kidneys but also in the liver (94%), seminal vesicles (40%), pancreas (9%), arachnoid membrane (8%), and spinal meningeal area (2%).¹

In addition to cyst formation in multiple organs, ADPKD can have extrarenal manifestations such as connective-tissue abnormalities (including mitral valve prolapse) (25%), abdominal hernia (10%), and intracranial aneurysm (8%).¹ Management of extrarenal complications of ADPKD is discussed in detail elsewhere.²

The estimated prevalence of ADPKD is 1 of every 400 to 1,000 live births. However, given that ADPKD is often clinically silent, it is diagnosed during the lifetime of fewer than half of people who have it.³

Most ADPKD cases are caused by mutations in either the PKD1 or PKD2 gene.^4,5  Although the mechanism of cyst formation in ADPKD is still unclear, it is known that PKD1 and PKD2 encode proteins called polycystin-1 and polycystin-2, respectively. Polycystin-1 is a membrane protein found in renal tubular epithelia, hepatic bile ductules, and pancreatic ducts. Polycystin-2 is involved in cell calcium signaling and has been identified in the renal distal tubules, collecting duct, and thick ascending limb. Mutations in PKD1 and PKD2 are thought to contribute to cyst formation, with PKD1 mutations associated with earlier onset and more severe development of renal and extrarenal cysts.

Cyst hemorrhage

Hemorrhage of renal cysts is a well-known complication, occurring in up to 70% of patients with ADPKD.6 Renal cyst hemorrhage often presents clinically as flank pain with point tenderness or hematuria, or both. Flank pain results from hemorrhage into a cyst with consequent distention of the renal capsule, whereas hematuria results from rupture of a cyst into the collecting system.

Spontaneous nonfatal retroperitoneal cyst hemorrhage, as in our patient, is  rare. Indeed, in one series reviewing the abdominal computed tomographic findings of 66 patients with ADPKD, only 2 patients (3%) had perinephric hematomas in the absence of recent trauma.⁶

Management of cyst hemorrhage is primarily conservative. Pain associated with cyst hemorrhage is managed conservatively with bed rest, intravenous hydration, and analgesics (but not nonsteroidal anti-inflammatory drugs).

Fewer than half of people with ADPKD are diagnosed with it in their lifetime

Hematuria is also managed conservatively with bedrest and intravenous hydration, and most episodes of hematuria are self-limiting and last 2 to 7 days. However, if excessive bleeding occurs, the patient may be at risk of urinary tract obstruction from clot formation. If obstruction occurs and persists beyond 2 weeks, then ureteral stenting may be necessary. In rare cases of prolonged, severe bleeding with extensive subcapsular or retroperitoneal hematomas, patients require hospitalization, transfusion, or percutaneous transcatheter embolization of the renal artery. If such efforts are not successful, surgery, including nephrectomy, may be required to control the hemorrhage.²

Other causes of abdominal pain

In addition to renal cyst hemorrhage, the differential diagnosis of abdominal pain in a patient with ADPKD includes cyst enlargement causing stretching of the renal capsule or traction on the renal pedicle, cyst infection, nephrolithiasis, pyelonephritis, and rarely, tumors including renal cell carcinoma.

Unlike cyst rupture and hemorrhage, which are associated with point tenderness, cyst infection often manifests as diffuse, usually unilateral flank pain with associated fever, nausea, malaise, and leukocytosis. Our patient had none of these except for fever, which can also occur in cyst hemorrhage.

Nephrolithiasis occurs in up to 35% of patients with ADPKD,⁷ but no kidney stones were seen on computed tomography in our patient.

Pyelonephritis was unlikely in our patient, given that he had no significant white blood cells in his urinalysis and no leukocytosis.

Abdominal and pelvic imaging did not reveal any tumors in our patient.

A 59-year-old man with autosomal dominant polycystic kidney disease (ADPKD), end-stage renal disease on hemodialysis, hypertension, and diverticulosis presented with acute pain in the left lower abdomen. The pain began 4 days previously, was dull and nonradiating, was relieved partially with hydrocodone-acetaminophen, and had no clear exacerbating factors. Two days before presentation, he developed a fever with chills. He reported no recent dysuria, diarrhea, hematuria, hematochezia, or melena. He had not been taking anticoagulants or nonsteroidal anti-inflammatory drugs, and he had no history of heavy lifting or trauma.

His temperature was 38.5˚C (101.3˚F), blood pressure 141/60 mm Hg (normal for this patient). On examination, his left lower quadrant was tender with voluntary guarding. Also present was a reducible ventral hernia, which was not new.

His hemoglobin level was 10.6 g/dL (reference range 13.0–17.0), which had dropped from a previous value of 13.7 g/dL.

Computed tomography of the abdomen and pelvis revealed a ruptured retroperitoneal hemorrhagic cyst (Figure 1) in the inferior aspect of the left kidney extending into the fascia of Gerota.

Since his vital signs were stable, he was managed supportively during his hospitalization with intravenous fluids, serial hemoglobin checks, and analgesia. He was eventually discharged home in good condition.

CYST HEMORRHAGE IN POLYCYSTIC KIDNEY DISEASE

ADPKD is a relatively common, inherited systemic disease that leads to cyst formation,  primarily in the kidneys but also in the liver (94%), seminal vesicles (40%), pancreas (9%), arachnoid membrane (8%), and spinal meningeal area (2%).¹

In addition to cyst formation in multiple organs, ADPKD can have extrarenal manifestations such as connective-tissue abnormalities (including mitral valve prolapse) (25%), abdominal hernia (10%), and intracranial aneurysm (8%).¹ Management of extrarenal complications of ADPKD is discussed in detail elsewhere.²

The estimated prevalence of ADPKD is 1 of every 400 to 1,000 live births. However, given that ADPKD is often clinically silent, it is diagnosed during the lifetime of fewer than half of people who have it.³

Most ADPKD cases are caused by mutations in either the PKD1 or PKD2 gene.^4,5  Although the mechanism of cyst formation in ADPKD is still unclear, it is known that PKD1 and PKD2 encode proteins called polycystin-1 and polycystin-2, respectively. Polycystin-1 is a membrane protein found in renal tubular epithelia, hepatic bile ductules, and pancreatic ducts. Polycystin-2 is involved in cell calcium signaling and has been identified in the renal distal tubules, collecting duct, and thick ascending limb. Mutations in PKD1 and PKD2 are thought to contribute to cyst formation, with PKD1 mutations associated with earlier onset and more severe development of renal and extrarenal cysts.

Cyst hemorrhage

Hemorrhage of renal cysts is a well-known complication, occurring in up to 70% of patients with ADPKD.6 Renal cyst hemorrhage often presents clinically as flank pain with point tenderness or hematuria, or both. Flank pain results from hemorrhage into a cyst with consequent distention of the renal capsule, whereas hematuria results from rupture of a cyst into the collecting system.

Spontaneous nonfatal retroperitoneal cyst hemorrhage, as in our patient, is  rare. Indeed, in one series reviewing the abdominal computed tomographic findings of 66 patients with ADPKD, only 2 patients (3%) had perinephric hematomas in the absence of recent trauma.⁶

Management of cyst hemorrhage is primarily conservative. Pain associated with cyst hemorrhage is managed conservatively with bed rest, intravenous hydration, and analgesics (but not nonsteroidal anti-inflammatory drugs).

Fewer than half of people with ADPKD are diagnosed with it in their lifetime

Hematuria is also managed conservatively with bedrest and intravenous hydration, and most episodes of hematuria are self-limiting and last 2 to 7 days. However, if excessive bleeding occurs, the patient may be at risk of urinary tract obstruction from clot formation. If obstruction occurs and persists beyond 2 weeks, then ureteral stenting may be necessary. In rare cases of prolonged, severe bleeding with extensive subcapsular or retroperitoneal hematomas, patients require hospitalization, transfusion, or percutaneous transcatheter embolization of the renal artery. If such efforts are not successful, surgery, including nephrectomy, may be required to control the hemorrhage.²

Other causes of abdominal pain

In addition to renal cyst hemorrhage, the differential diagnosis of abdominal pain in a patient with ADPKD includes cyst enlargement causing stretching of the renal capsule or traction on the renal pedicle, cyst infection, nephrolithiasis, pyelonephritis, and rarely, tumors including renal cell carcinoma.

Unlike cyst rupture and hemorrhage, which are associated with point tenderness, cyst infection often manifests as diffuse, usually unilateral flank pain with associated fever, nausea, malaise, and leukocytosis. Our patient had none of these except for fever, which can also occur in cyst hemorrhage.

Nephrolithiasis occurs in up to 35% of patients with ADPKD,⁷ but no kidney stones were seen on computed tomography in our patient.

Pyelonephritis was unlikely in our patient, given that he had no significant white blood cells in his urinalysis and no leukocytosis.

Abdominal and pelvic imaging did not reveal any tumors in our patient.

After 4 decades of clinical practice in a teaching hospital, I believe that the notes we write to document medical consultations are too long. When I review them for my own patients, the only part I read is the consultant’s assessment and diagnostic and therapeutic recommendations. Many of my colleagues and trainees do the same.

In the old days, when medical records were handwritten, the first three pages of my hospital’s four-page consultation form were for the history, review of systems, physical examination, and test results. The top two-thirds of the last page was for diagnostic impressions and recommendations for additional testing and treatment, to be completed by the trainee performing the consultation.

This left only the bottom third of this page for attestation and additional remarks from the senior consultant. Often, this last (but most used) page was just a bullet list of diagnostic possibilities and suggested tests and treatments, with nothing about the critical reasoning underlying the differential diagnosis and recommendations. This was probably the result of fatigue from having to fill in the first three pages by hand, and then having only limited space on the final page.

Even though the written record has been replaced by the electronic medical record in my hospital, consult notes continue to be at least as long as before, without any change in the length of the assessment and recommendations section. I would guess this is true in most institutions and practices that have switched to an electronic record system.

WHY ARE CONSULT NOTES SO LONG?

The main factor contributing to the lengthy consultation document is that the Center for Medicare and Medicaid Services, with other third-party payers following suit, ties the level of reimbursement to detailed documentation of the history (present, past medical, past surgical, medications, allergies, social, and family), review of systems, and physical examination in the consultation.¹ Physicians are under constant pressure from professional fee-coders to meet these requirements.

Avoid repeating what is already in the record, but include your reasoning and teaching points

Since most of this information is already in the medical record, to require that it be documented again in the consultation note is unnecessary duplication. I believe that consultants comply with this requirement mainly to ensure adequate reimbursement, even though they know that the referring medical team will probably not read the repeated information.

Electronic medical record systems, which focus disproportionately on meeting insurers’ requirements governing reimbursement,^2–5 have made it easier to create a lengthy consult note by checking boxes in templates and copying and pasting from other parts of the electronic record.^2,6–12 Although verbatim copying and pasting may result in punitive audits by insurers, this practice remains common,¹³ including, in my experience, in consultations.

WHAT ARE THE NEGATIVE EFFECTS OF A NEEDLESSLY LONG CONSULT NOTE?

Time spent on repeating information—even if less time is required when using an electronic system—is clearly time wasted, since this part of the consult note is hardly ever read. Equally bad, the assessment and recommendations section in consult notes continues to be very short, probably because long-standing physician practices change slowly.

An ideal consult note has been described as one that, in addition to addressing the patient care issues, is as brief as possible, avoids duplication of already documented information, and has educational value to the person requesting it.^14,15 The educational value of the consultation is especially important in teaching hospitals.

If the only part of the consultation perused in depth consists merely of lists of diagnoses, recommended tests, and therapy and does not include the consultant’s critical reasoning underlying them, the educational value of the consultation is lost.

HOW CAN THE FORMAT BE MADE SHORTER, YET MORE USEFUL?

The note should begin by briefly documenting the reason the consultation was requested. Ideally, institutions should train their staff to state this very specifically. For example, instead of “clearance for surgery,” it is better to ask, “Please identify risks involved in proposed surgery and suggest ways to reduce them.” The former steers the consultant to merely say “cleared for surgery, but with increased risk,” whereas the latter ensures a more specific and detailed response.

The consulting team must review in detail and verify the accuracy of all available information in the patient’s record. Once this is done, instead of repeating it, a statement that all existing information has been thoroughly reviewed should suffice, with mention in a separate paragraph of only the additional relevant positive or negative points in the history related to the issue the consultant has been asked to address.

The consultant shares with all users of the medical record the responsibility of pointing out and correcting any errors in the previously recorded information, thereby decreasing perpetuation of erroneous “chart lore,” an undesirable consequence of copying and pasting. If only previously unrecorded data and corrections to existing information are documented, the referring team is more likely to read the note because it points out relevant information that has been overlooked.

The main part should consist of a detailed assessment and recommendations section

The main part of the document should consist of a detailed assessment and recommendations section, which should include not only a list of diagnoses and recommendations for testing and treatment, but also the consultant’s reasoning behind them, the results of tests already obtained that support the consultant’s conclusions, and information of value for teaching and cost-effective practice. A critically reasoned assessment and recommendation section not only will prove very educational, but by challenging the consultant to justify his or her choices, may discourage unnecessary testing and questionable therapy^4,14 and thereby contribute to cost-saving.

My suggestions would not shorten the time spent by the consulting team in evaluating the patient, but only eliminate redundant documentation. I believe the consultation document will be shorter but adequate for patient care, the referring team will read and use the entire document, its educational value will be enhanced, and the time spent on redundant documentation will be saved.

A CASE VIGNETTE

The following vignette (from my own subspecialty) of a patient with acute kidney injury illustrates how a consult note can be made shorter but more useful and educational.

A 78-year-old man had a history of long-standing insulin-requiring diabetes mellitus, hypertension (treated with lisinopril and amlodipine), and benign prostatic hypertrophy. One month earlier, his blood urea nitrogen level had been 15 mg/dL and his serum creatinine had been 1.2 mg/dL.

He presented with a 3-day history of vomiting, diarrhea, and fever, presumed to be viral gastroenteritis. His blood urea nitrogen level was 100 mg, serum creatinine 2.5 mg, and blood glucose 450 mg/dL. Urinalysis revealed 2+ albuminuria, 3+ glucosuria, and 6 red blood cells per high-power field.

In the emergency department he received 2 L of normal saline and regular insulin intravenously, and an indwelling bladder catheter was inserted. He was admitted after 6 hours.

Tests obtained on arrival on the inpatient floor revealed a urinary fractional excretion of sodium of 2.5% and a blood glucose level of 295 mg/dL. His admission history and physical listed his home medications as insulin glargine, amlodipine, lisinopril, and tamsulosin. It also listed the differential diagnosis for acute kidney injury as:

• Prerenal azotemia due to volume depletion
• Rapidly progressive glomerulonephritis to be ruled out in view of proteinuria and microhematuria
• Obstructive uropathy to be ruled out.

Ultrasonography the morning after admission showed normal kidneys and no hydronephrosis. The absence of hydronephrosis was interpreted by the primary team as ruling out obstruction secondary to benign prostatic hypertrophy. The nephrology team saw the patient in consultation the day after admission and discovered the following additional information: urinalysis done 6 months earlier had also shown albuminuria and microhematuria, and the patient had been taking over-the-counter ibuprofen 400 mg three times daily for several days prior to admission.

Table 1 compares consultation documentation in the usual format and in the format I am suggesting. The revised format has much more information of educational value (eg, the importance of reviewing past urinalysis results, asking about over-the-counter medications, factors affecting fractional excretion of sodium, effect of bladder catheterization on hydronephrosis due to benign prostatic hypertrophy, and measuring urine protein only after acute kidney injury resolves). It also encourages cost-effective care (ultrasonography could have been delayed or avoided, and the patient could have been cautioned about ibuprofen-like drugs to decrease the risk of recurrent acute kidney injury).

FINAL THOUGHTS

The modifications I have suggested in consult notes will be accepted only if they are reimbursement-neutral. I hope insurers will not equate a shorter note with an opportunity to lower reimbursement and will see the value in not paying for things almost never read. I hope they will recognize and pay for the effort that went into creating a shorter document that contributes adequately to patient care, provides greater educational value, and may promote cost-effective medical practice. Also, not requiring redundant documentation may reduce or even eliminate undesirable copying and pasting.

Accountable-care organizations are an important part of the Affordable Care Act,¹⁶ which went into effect in 2014. Many organizations had already come into existence in the United States before the act became effective, and their numbers and the number of patients covered by them are projected to grow enormously over the next few years.¹⁷

Since the accountable-care organization model will rely heavily on capitated reimbursement to contain costs, these organizations are likely to scrutinize and curtail the use of consultations. I believe that a shorter consultation note—yet one that is more useful for patient care, education, and cost-containment—is more likely to pass such scrutiny, especially if it decreases time spent on documentation. Furthermore, unlike the fee-for-service model, in a capitated-payment system it may not be necessary to lengthen consultation documentation just to ensure adequate reimbursement.

After 4 decades of clinical practice in a teaching hospital, I believe that the notes we write to document medical consultations are too long. When I review them for my own patients, the only part I read is the consultant’s assessment and diagnostic and therapeutic recommendations. Many of my colleagues and trainees do the same.

In the old days, when medical records were handwritten, the first three pages of my hospital’s four-page consultation form were for the history, review of systems, physical examination, and test results. The top two-thirds of the last page was for diagnostic impressions and recommendations for additional testing and treatment, to be completed by the trainee performing the consultation.

This left only the bottom third of this page for attestation and additional remarks from the senior consultant. Often, this last (but most used) page was just a bullet list of diagnostic possibilities and suggested tests and treatments, with nothing about the critical reasoning underlying the differential diagnosis and recommendations. This was probably the result of fatigue from having to fill in the first three pages by hand, and then having only limited space on the final page.

Even though the written record has been replaced by the electronic medical record in my hospital, consult notes continue to be at least as long as before, without any change in the length of the assessment and recommendations section. I would guess this is true in most institutions and practices that have switched to an electronic record system.

WHY ARE CONSULT NOTES SO LONG?

The main factor contributing to the lengthy consultation document is that the Center for Medicare and Medicaid Services, with other third-party payers following suit, ties the level of reimbursement to detailed documentation of the history (present, past medical, past surgical, medications, allergies, social, and family), review of systems, and physical examination in the consultation.¹ Physicians are under constant pressure from professional fee-coders to meet these requirements.

Avoid repeating what is already in the record, but include your reasoning and teaching points

Since most of this information is already in the medical record, to require that it be documented again in the consultation note is unnecessary duplication. I believe that consultants comply with this requirement mainly to ensure adequate reimbursement, even though they know that the referring medical team will probably not read the repeated information.

Electronic medical record systems, which focus disproportionately on meeting insurers’ requirements governing reimbursement,^2–5 have made it easier to create a lengthy consult note by checking boxes in templates and copying and pasting from other parts of the electronic record.^2,6–12 Although verbatim copying and pasting may result in punitive audits by insurers, this practice remains common,¹³ including, in my experience, in consultations.

WHAT ARE THE NEGATIVE EFFECTS OF A NEEDLESSLY LONG CONSULT NOTE?

Time spent on repeating information—even if less time is required when using an electronic system—is clearly time wasted, since this part of the consult note is hardly ever read. Equally bad, the assessment and recommendations section in consult notes continues to be very short, probably because long-standing physician practices change slowly.

An ideal consult note has been described as one that, in addition to addressing the patient care issues, is as brief as possible, avoids duplication of already documented information, and has educational value to the person requesting it.^14,15 The educational value of the consultation is especially important in teaching hospitals.

If the only part of the consultation perused in depth consists merely of lists of diagnoses, recommended tests, and therapy and does not include the consultant’s critical reasoning underlying them, the educational value of the consultation is lost.

HOW CAN THE FORMAT BE MADE SHORTER, YET MORE USEFUL?

The note should begin by briefly documenting the reason the consultation was requested. Ideally, institutions should train their staff to state this very specifically. For example, instead of “clearance for surgery,” it is better to ask, “Please identify risks involved in proposed surgery and suggest ways to reduce them.” The former steers the consultant to merely say “cleared for surgery, but with increased risk,” whereas the latter ensures a more specific and detailed response.

The consulting team must review in detail and verify the accuracy of all available information in the patient’s record. Once this is done, instead of repeating it, a statement that all existing information has been thoroughly reviewed should suffice, with mention in a separate paragraph of only the additional relevant positive or negative points in the history related to the issue the consultant has been asked to address.

The consultant shares with all users of the medical record the responsibility of pointing out and correcting any errors in the previously recorded information, thereby decreasing perpetuation of erroneous “chart lore,” an undesirable consequence of copying and pasting. If only previously unrecorded data and corrections to existing information are documented, the referring team is more likely to read the note because it points out relevant information that has been overlooked.

The main part should consist of a detailed assessment and recommendations section

The main part of the document should consist of a detailed assessment and recommendations section, which should include not only a list of diagnoses and recommendations for testing and treatment, but also the consultant’s reasoning behind them, the results of tests already obtained that support the consultant’s conclusions, and information of value for teaching and cost-effective practice. A critically reasoned assessment and recommendation section not only will prove very educational, but by challenging the consultant to justify his or her choices, may discourage unnecessary testing and questionable therapy^4,14 and thereby contribute to cost-saving.

My suggestions would not shorten the time spent by the consulting team in evaluating the patient, but only eliminate redundant documentation. I believe the consultation document will be shorter but adequate for patient care, the referring team will read and use the entire document, its educational value will be enhanced, and the time spent on redundant documentation will be saved.

A CASE VIGNETTE

The following vignette (from my own subspecialty) of a patient with acute kidney injury illustrates how a consult note can be made shorter but more useful and educational.

A 78-year-old man had a history of long-standing insulin-requiring diabetes mellitus, hypertension (treated with lisinopril and amlodipine), and benign prostatic hypertrophy. One month earlier, his blood urea nitrogen level had been 15 mg/dL and his serum creatinine had been 1.2 mg/dL.

He presented with a 3-day history of vomiting, diarrhea, and fever, presumed to be viral gastroenteritis. His blood urea nitrogen level was 100 mg, serum creatinine 2.5 mg, and blood glucose 450 mg/dL. Urinalysis revealed 2+ albuminuria, 3+ glucosuria, and 6 red blood cells per high-power field.

In the emergency department he received 2 L of normal saline and regular insulin intravenously, and an indwelling bladder catheter was inserted. He was admitted after 6 hours.

Tests obtained on arrival on the inpatient floor revealed a urinary fractional excretion of sodium of 2.5% and a blood glucose level of 295 mg/dL. His admission history and physical listed his home medications as insulin glargine, amlodipine, lisinopril, and tamsulosin. It also listed the differential diagnosis for acute kidney injury as:

• Prerenal azotemia due to volume depletion
• Rapidly progressive glomerulonephritis to be ruled out in view of proteinuria and microhematuria
• Obstructive uropathy to be ruled out.

Ultrasonography the morning after admission showed normal kidneys and no hydronephrosis. The absence of hydronephrosis was interpreted by the primary team as ruling out obstruction secondary to benign prostatic hypertrophy. The nephrology team saw the patient in consultation the day after admission and discovered the following additional information: urinalysis done 6 months earlier had also shown albuminuria and microhematuria, and the patient had been taking over-the-counter ibuprofen 400 mg three times daily for several days prior to admission.

Table 1 compares consultation documentation in the usual format and in the format I am suggesting. The revised format has much more information of educational value (eg, the importance of reviewing past urinalysis results, asking about over-the-counter medications, factors affecting fractional excretion of sodium, effect of bladder catheterization on hydronephrosis due to benign prostatic hypertrophy, and measuring urine protein only after acute kidney injury resolves). It also encourages cost-effective care (ultrasonography could have been delayed or avoided, and the patient could have been cautioned about ibuprofen-like drugs to decrease the risk of recurrent acute kidney injury).

FINAL THOUGHTS

The modifications I have suggested in consult notes will be accepted only if they are reimbursement-neutral. I hope insurers will not equate a shorter note with an opportunity to lower reimbursement and will see the value in not paying for things almost never read. I hope they will recognize and pay for the effort that went into creating a shorter document that contributes adequately to patient care, provides greater educational value, and may promote cost-effective medical practice. Also, not requiring redundant documentation may reduce or even eliminate undesirable copying and pasting.

Accountable-care organizations are an important part of the Affordable Care Act,¹⁶ which went into effect in 2014. Many organizations had already come into existence in the United States before the act became effective, and their numbers and the number of patients covered by them are projected to grow enormously over the next few years.¹⁷

Since the accountable-care organization model will rely heavily on capitated reimbursement to contain costs, these organizations are likely to scrutinize and curtail the use of consultations. I believe that a shorter consultation note—yet one that is more useful for patient care, education, and cost-containment—is more likely to pass such scrutiny, especially if it decreases time spent on documentation. Furthermore, unlike the fee-for-service model, in a capitated-payment system it may not be necessary to lengthen consultation documentation just to ensure adequate reimbursement.

After 4 decades of clinical practice in a teaching hospital, I believe that the notes we write to document medical consultations are too long. When I review them for my own patients, the only part I read is the consultant’s assessment and diagnostic and therapeutic recommendations. Many of my colleagues and trainees do the same.

In the old days, when medical records were handwritten, the first three pages of my hospital’s four-page consultation form were for the history, review of systems, physical examination, and test results. The top two-thirds of the last page was for diagnostic impressions and recommendations for additional testing and treatment, to be completed by the trainee performing the consultation.

This left only the bottom third of this page for attestation and additional remarks from the senior consultant. Often, this last (but most used) page was just a bullet list of diagnostic possibilities and suggested tests and treatments, with nothing about the critical reasoning underlying the differential diagnosis and recommendations. This was probably the result of fatigue from having to fill in the first three pages by hand, and then having only limited space on the final page.

Even though the written record has been replaced by the electronic medical record in my hospital, consult notes continue to be at least as long as before, without any change in the length of the assessment and recommendations section. I would guess this is true in most institutions and practices that have switched to an electronic record system.

WHY ARE CONSULT NOTES SO LONG?

The main factor contributing to the lengthy consultation document is that the Center for Medicare and Medicaid Services, with other third-party payers following suit, ties the level of reimbursement to detailed documentation of the history (present, past medical, past surgical, medications, allergies, social, and family), review of systems, and physical examination in the consultation.¹ Physicians are under constant pressure from professional fee-coders to meet these requirements.

Avoid repeating what is already in the record, but include your reasoning and teaching points

Since most of this information is already in the medical record, to require that it be documented again in the consultation note is unnecessary duplication. I believe that consultants comply with this requirement mainly to ensure adequate reimbursement, even though they know that the referring medical team will probably not read the repeated information.

Electronic medical record systems, which focus disproportionately on meeting insurers’ requirements governing reimbursement,^2–5 have made it easier to create a lengthy consult note by checking boxes in templates and copying and pasting from other parts of the electronic record.^2,6–12 Although verbatim copying and pasting may result in punitive audits by insurers, this practice remains common,¹³ including, in my experience, in consultations.

WHAT ARE THE NEGATIVE EFFECTS OF A NEEDLESSLY LONG CONSULT NOTE?

Time spent on repeating information—even if less time is required when using an electronic system—is clearly time wasted, since this part of the consult note is hardly ever read. Equally bad, the assessment and recommendations section in consult notes continues to be very short, probably because long-standing physician practices change slowly.

An ideal consult note has been described as one that, in addition to addressing the patient care issues, is as brief as possible, avoids duplication of already documented information, and has educational value to the person requesting it.^14,15 The educational value of the consultation is especially important in teaching hospitals.

If the only part of the consultation perused in depth consists merely of lists of diagnoses, recommended tests, and therapy and does not include the consultant’s critical reasoning underlying them, the educational value of the consultation is lost.

HOW CAN THE FORMAT BE MADE SHORTER, YET MORE USEFUL?

The note should begin by briefly documenting the reason the consultation was requested. Ideally, institutions should train their staff to state this very specifically. For example, instead of “clearance for surgery,” it is better to ask, “Please identify risks involved in proposed surgery and suggest ways to reduce them.” The former steers the consultant to merely say “cleared for surgery, but with increased risk,” whereas the latter ensures a more specific and detailed response.

The consulting team must review in detail and verify the accuracy of all available information in the patient’s record. Once this is done, instead of repeating it, a statement that all existing information has been thoroughly reviewed should suffice, with mention in a separate paragraph of only the additional relevant positive or negative points in the history related to the issue the consultant has been asked to address.

The consultant shares with all users of the medical record the responsibility of pointing out and correcting any errors in the previously recorded information, thereby decreasing perpetuation of erroneous “chart lore,” an undesirable consequence of copying and pasting. If only previously unrecorded data and corrections to existing information are documented, the referring team is more likely to read the note because it points out relevant information that has been overlooked.

The main part should consist of a detailed assessment and recommendations section

The main part of the document should consist of a detailed assessment and recommendations section, which should include not only a list of diagnoses and recommendations for testing and treatment, but also the consultant’s reasoning behind them, the results of tests already obtained that support the consultant’s conclusions, and information of value for teaching and cost-effective practice. A critically reasoned assessment and recommendation section not only will prove very educational, but by challenging the consultant to justify his or her choices, may discourage unnecessary testing and questionable therapy^4,14 and thereby contribute to cost-saving.

My suggestions would not shorten the time spent by the consulting team in evaluating the patient, but only eliminate redundant documentation. I believe the consultation document will be shorter but adequate for patient care, the referring team will read and use the entire document, its educational value will be enhanced, and the time spent on redundant documentation will be saved.

A CASE VIGNETTE

The following vignette (from my own subspecialty) of a patient with acute kidney injury illustrates how a consult note can be made shorter but more useful and educational.

A 78-year-old man had a history of long-standing insulin-requiring diabetes mellitus, hypertension (treated with lisinopril and amlodipine), and benign prostatic hypertrophy. One month earlier, his blood urea nitrogen level had been 15 mg/dL and his serum creatinine had been 1.2 mg/dL.

He presented with a 3-day history of vomiting, diarrhea, and fever, presumed to be viral gastroenteritis. His blood urea nitrogen level was 100 mg, serum creatinine 2.5 mg, and blood glucose 450 mg/dL. Urinalysis revealed 2+ albuminuria, 3+ glucosuria, and 6 red blood cells per high-power field.

In the emergency department he received 2 L of normal saline and regular insulin intravenously, and an indwelling bladder catheter was inserted. He was admitted after 6 hours.

Tests obtained on arrival on the inpatient floor revealed a urinary fractional excretion of sodium of 2.5% and a blood glucose level of 295 mg/dL. His admission history and physical listed his home medications as insulin glargine, amlodipine, lisinopril, and tamsulosin. It also listed the differential diagnosis for acute kidney injury as:

• Prerenal azotemia due to volume depletion
• Rapidly progressive glomerulonephritis to be ruled out in view of proteinuria and microhematuria
• Obstructive uropathy to be ruled out.

Ultrasonography the morning after admission showed normal kidneys and no hydronephrosis. The absence of hydronephrosis was interpreted by the primary team as ruling out obstruction secondary to benign prostatic hypertrophy. The nephrology team saw the patient in consultation the day after admission and discovered the following additional information: urinalysis done 6 months earlier had also shown albuminuria and microhematuria, and the patient had been taking over-the-counter ibuprofen 400 mg three times daily for several days prior to admission.

Table 1 compares consultation documentation in the usual format and in the format I am suggesting. The revised format has much more information of educational value (eg, the importance of reviewing past urinalysis results, asking about over-the-counter medications, factors affecting fractional excretion of sodium, effect of bladder catheterization on hydronephrosis due to benign prostatic hypertrophy, and measuring urine protein only after acute kidney injury resolves). It also encourages cost-effective care (ultrasonography could have been delayed or avoided, and the patient could have been cautioned about ibuprofen-like drugs to decrease the risk of recurrent acute kidney injury).

FINAL THOUGHTS

The modifications I have suggested in consult notes will be accepted only if they are reimbursement-neutral. I hope insurers will not equate a shorter note with an opportunity to lower reimbursement and will see the value in not paying for things almost never read. I hope they will recognize and pay for the effort that went into creating a shorter document that contributes adequately to patient care, provides greater educational value, and may promote cost-effective medical practice. Also, not requiring redundant documentation may reduce or even eliminate undesirable copying and pasting.

Accountable-care organizations are an important part of the Affordable Care Act,¹⁶ which went into effect in 2014. Many organizations had already come into existence in the United States before the act became effective, and their numbers and the number of patients covered by them are projected to grow enormously over the next few years.¹⁷

Since the accountable-care organization model will rely heavily on capitated reimbursement to contain costs, these organizations are likely to scrutinize and curtail the use of consultations. I believe that a shorter consultation note—yet one that is more useful for patient care, education, and cost-containment—is more likely to pass such scrutiny, especially if it decreases time spent on documentation. Furthermore, unlike the fee-for-service model, in a capitated-payment system it may not be necessary to lengthen consultation documentation just to ensure adequate reimbursement.

Q) When I see a patient for an annual physical or gynecologic exam (or even just to give a flu shot), I try to encourage healthy living. Are there any CKD statistics I can use to “encourage” my hypertensive or overweight patients to follow a better plan of care?

According to a recent study by McMahon et al, risk factors for chronic kidney disease (CKD)—including hypertension, dyslipidemia, and diabetes—may be present up to 30 years prior to diagnosis of CKD.¹ Since these risk factors are modifiable, the researchers concluded that early intervention could lead to a reduction in new CKD cases.¹

Using data from the Framingham Offspring Study, the researchers identified 441 patients with incident CKD and then matched them with a control group of 882 patients who did not develop CKD during the 30-year study period. Subjects who eventually developed CKD were more likely than their counterparts to have hypertension (odds ratio [OR], 1.76), obesity (OR, 1.71), and elevated triglyceride levels (OR, 1.43) 30 years prior to CKD diagnosis. Having diabetes nearly tripled a patient’s likelihood of developing CKD within 20 years (OR, 2.90).¹

Early identification of these risk factors and treatment of affected patients is imperative to help prevent kidney disease. Regular screening of young and middle-aged adult patients, as well as early intervention when risk factors are identified, should slow not only the progression of these detrimental conditions but also the development of CKD.

Joanne Hindlet, ACNP, CNN-NP
Houston Nephrology Group

REFERENCES
1. McMahon GM, Preis SR, Hwang S-J, Fox CS. Mid-adulthood risk factor profiles for CKD. J Am Soc Nephrol. 2014 Jun 26; [Epub ahead of print].
2. Byham-Gray L, Stover J, Wiesen K. A Clinical Guide to Nutrition Care in Kidney Disease. 2nd ed. The Academy of Nutrition and Dietetics; 2013.
3. Crews DC. Chronic kidney disease and access to healthful foods. ASN Kidney News. 2014;6(5):11.
4. Moe SM. Phosphate additives in food: you are what you eat—but shouldn’t you know that? ASN Kidney News. 2014;6(5):8.
5. Narva A, Norton J. Medical nutrition therapy for CKD. ASN Kidney News. 2014;6(5):7.

Q) When I see a patient for an annual physical or gynecologic exam (or even just to give a flu shot), I try to encourage healthy living. Are there any CKD statistics I can use to “encourage” my hypertensive or overweight patients to follow a better plan of care?

According to a recent study by McMahon et al, risk factors for chronic kidney disease (CKD)—including hypertension, dyslipidemia, and diabetes—may be present up to 30 years prior to diagnosis of CKD.¹ Since these risk factors are modifiable, the researchers concluded that early intervention could lead to a reduction in new CKD cases.¹

Using data from the Framingham Offspring Study, the researchers identified 441 patients with incident CKD and then matched them with a control group of 882 patients who did not develop CKD during the 30-year study period. Subjects who eventually developed CKD were more likely than their counterparts to have hypertension (odds ratio [OR], 1.76), obesity (OR, 1.71), and elevated triglyceride levels (OR, 1.43) 30 years prior to CKD diagnosis. Having diabetes nearly tripled a patient’s likelihood of developing CKD within 20 years (OR, 2.90).¹

Early identification of these risk factors and treatment of affected patients is imperative to help prevent kidney disease. Regular screening of young and middle-aged adult patients, as well as early intervention when risk factors are identified, should slow not only the progression of these detrimental conditions but also the development of CKD.

Joanne Hindlet, ACNP, CNN-NP
Houston Nephrology Group

REFERENCES
1. McMahon GM, Preis SR, Hwang S-J, Fox CS. Mid-adulthood risk factor profiles for CKD. J Am Soc Nephrol. 2014 Jun 26; [Epub ahead of print].
2. Byham-Gray L, Stover J, Wiesen K. A Clinical Guide to Nutrition Care in Kidney Disease. 2nd ed. The Academy of Nutrition and Dietetics; 2013.
3. Crews DC. Chronic kidney disease and access to healthful foods. ASN Kidney News. 2014;6(5):11.
4. Moe SM. Phosphate additives in food: you are what you eat—but shouldn’t you know that? ASN Kidney News. 2014;6(5):8.
5. Narva A, Norton J. Medical nutrition therapy for CKD. ASN Kidney News. 2014;6(5):7.

Q) When I see a patient for an annual physical or gynecologic exam (or even just to give a flu shot), I try to encourage healthy living. Are there any CKD statistics I can use to “encourage” my hypertensive or overweight patients to follow a better plan of care?

According to a recent study by McMahon et al, risk factors for chronic kidney disease (CKD)—including hypertension, dyslipidemia, and diabetes—may be present up to 30 years prior to diagnosis of CKD.¹ Since these risk factors are modifiable, the researchers concluded that early intervention could lead to a reduction in new CKD cases.¹

Using data from the Framingham Offspring Study, the researchers identified 441 patients with incident CKD and then matched them with a control group of 882 patients who did not develop CKD during the 30-year study period. Subjects who eventually developed CKD were more likely than their counterparts to have hypertension (odds ratio [OR], 1.76), obesity (OR, 1.71), and elevated triglyceride levels (OR, 1.43) 30 years prior to CKD diagnosis. Having diabetes nearly tripled a patient’s likelihood of developing CKD within 20 years (OR, 2.90).¹

Early identification of these risk factors and treatment of affected patients is imperative to help prevent kidney disease. Regular screening of young and middle-aged adult patients, as well as early intervention when risk factors are identified, should slow not only the progression of these detrimental conditions but also the development of CKD.

Joanne Hindlet, ACNP, CNN-NP
Houston Nephrology Group

REFERENCES
1. McMahon GM, Preis SR, Hwang S-J, Fox CS. Mid-adulthood risk factor profiles for CKD. J Am Soc Nephrol. 2014 Jun 26; [Epub ahead of print].
2. Byham-Gray L, Stover J, Wiesen K. A Clinical Guide to Nutrition Care in Kidney Disease. 2nd ed. The Academy of Nutrition and Dietetics; 2013.
3. Crews DC. Chronic kidney disease and access to healthful foods. ASN Kidney News. 2014;6(5):11.
4. Moe SM. Phosphate additives in food: you are what you eat—but shouldn’t you know that? ASN Kidney News. 2014;6(5):8.
5. Narva A, Norton J. Medical nutrition therapy for CKD. ASN Kidney News. 2014;6(5):7.