Shan E. Zainab, MBBS

Background

Accurate clinical coding that reflects all diagnoses and problems addressed during a patient encounter is essential for the cancer program’s data quality, research initiatives, and securing VERA (Veterans Equitable Resource Allocation) funding. However, providers often face barriers such as limited time during patient visits and difficulty navigating Electronic health record (EHR) systems. These challenges lead to inaccurate coding, which undermines downstream data integrity. This quality improvement (QI) study aimed to identify these barriers and implement an intervention to improve coding accuracy, while also assessing the financial implications of improved documentation.

Methods

This QI study was conducted at the Albany Stratton VA Medical Center, focusing on hematology/ oncology outpatient encounters. A baseline chart audit of diagnosis codes from June 2023 revealed an accuracy rate of 69.8%. To address this, an intervention was implemented in which dedicated coders were assigned to support attending physicians in coding for over a two-week period. These coders reviewed and corrected diagnosis codes in real-time. A follow-up audit conducted after the intervention showed an improved coding accuracy of 82%.

Discussion/Implications

Coding remains a timeconsuming task for providers, made more difficult by EHR systems that are not user-friendly. This study demonstrated that involving dedicated coders significantly improves documentation accuracy—from 69% to 82%. In addition to data quality, the financial benefits are notable. A projected annual return on investment of $216,094 was calculated, based on an internal analysis showing that in a sample of 124 patients, 10% could have qualified for higher VERA funding based on accurate coding, generating an estimated $17,427 in additional reimbursement per patient. This cost-benefit ratio supports the recommendation to staff dedicated coders. Other interventions were also utilised, such as updating the national encounter form and auto-populating documentation in Dragon software, but had limited impact and did not directly address diagnosis accuracy respectively.

Conclusions

Targeted interventions improved coding accuracy, but sustainability remains a challenge due to time and system limitations. Future efforts should focus on hiring full-time coders. These steps can further enhance coding quality and potentially increase hospital revenue.

Background

Accurate clinical coding that reflects all diagnoses and problems addressed during a patient encounter is essential for the cancer program’s data quality, research initiatives, and securing VERA (Veterans Equitable Resource Allocation) funding. However, providers often face barriers such as limited time during patient visits and difficulty navigating Electronic health record (EHR) systems. These challenges lead to inaccurate coding, which undermines downstream data integrity. This quality improvement (QI) study aimed to identify these barriers and implement an intervention to improve coding accuracy, while also assessing the financial implications of improved documentation.

Methods

This QI study was conducted at the Albany Stratton VA Medical Center, focusing on hematology/ oncology outpatient encounters. A baseline chart audit of diagnosis codes from June 2023 revealed an accuracy rate of 69.8%. To address this, an intervention was implemented in which dedicated coders were assigned to support attending physicians in coding for over a two-week period. These coders reviewed and corrected diagnosis codes in real-time. A follow-up audit conducted after the intervention showed an improved coding accuracy of 82%.

Discussion/Implications

Coding remains a timeconsuming task for providers, made more difficult by EHR systems that are not user-friendly. This study demonstrated that involving dedicated coders significantly improves documentation accuracy—from 69% to 82%. In addition to data quality, the financial benefits are notable. A projected annual return on investment of $216,094 was calculated, based on an internal analysis showing that in a sample of 124 patients, 10% could have qualified for higher VERA funding based on accurate coding, generating an estimated $17,427 in additional reimbursement per patient. This cost-benefit ratio supports the recommendation to staff dedicated coders. Other interventions were also utilised, such as updating the national encounter form and auto-populating documentation in Dragon software, but had limited impact and did not directly address diagnosis accuracy respectively.

Conclusions

Targeted interventions improved coding accuracy, but sustainability remains a challenge due to time and system limitations. Future efforts should focus on hiring full-time coders. These steps can further enhance coding quality and potentially increase hospital revenue.

Background

Accurate clinical coding that reflects all diagnoses and problems addressed during a patient encounter is essential for the cancer program’s data quality, research initiatives, and securing VERA (Veterans Equitable Resource Allocation) funding. However, providers often face barriers such as limited time during patient visits and difficulty navigating Electronic health record (EHR) systems. These challenges lead to inaccurate coding, which undermines downstream data integrity. This quality improvement (QI) study aimed to identify these barriers and implement an intervention to improve coding accuracy, while also assessing the financial implications of improved documentation.

Methods

This QI study was conducted at the Albany Stratton VA Medical Center, focusing on hematology/ oncology outpatient encounters. A baseline chart audit of diagnosis codes from June 2023 revealed an accuracy rate of 69.8%. To address this, an intervention was implemented in which dedicated coders were assigned to support attending physicians in coding for over a two-week period. These coders reviewed and corrected diagnosis codes in real-time. A follow-up audit conducted after the intervention showed an improved coding accuracy of 82%.

Discussion/Implications

Coding remains a timeconsuming task for providers, made more difficult by EHR systems that are not user-friendly. This study demonstrated that involving dedicated coders significantly improves documentation accuracy—from 69% to 82%. In addition to data quality, the financial benefits are notable. A projected annual return on investment of $216,094 was calculated, based on an internal analysis showing that in a sample of 124 patients, 10% could have qualified for higher VERA funding based on accurate coding, generating an estimated $17,427 in additional reimbursement per patient. This cost-benefit ratio supports the recommendation to staff dedicated coders. Other interventions were also utilised, such as updating the national encounter form and auto-populating documentation in Dragon software, but had limited impact and did not directly address diagnosis accuracy respectively.

Conclusions

Targeted interventions improved coding accuracy, but sustainability remains a challenge due to time and system limitations. Future efforts should focus on hiring full-time coders. These steps can further enhance coding quality and potentially increase hospital revenue.

Background

Gastrointestinal stromal tumors (GISTs) are rare neoplasms of the gastrointestinal (GI) tract, accounting for approximately 1–2% of GI cancers. Hypoglycemia in patients with GIST is an uncommon and diagnostically challenging presentation, often involving a broad differential diagnosis. This case report explores the diagnostic difficulties encountered in managing persistent hypoglycemia in a patient with a history of advanced GIST.

Case Presentation

An 80-year-old male with a history of stage IV GIST, diagnosed in 2010, presented with persistent symptomatic hypoglycemia. His medical history included extensive abdominal disease, managed with multiple interventions: esophagogastrostomy, left lateral liver resection, a Whipple procedure, and Y-90 radioembolization. He received adjuvant imatinib therapy, which was discontinued in April 2024 due to significant adverse effects, including anasarca. In 2025, the patient developed progressive hypoglycemia, ultimately requiring continuous D10 infusion to maintain euglycemia, prompting an endocrinology evaluation. The initial diagnostic workup included cortisol, insulin, C-peptide levels, and IGF-1/IGF-2 ratio ruling out insulinoma, adrenal insufficiency, and GISTrelated paraneoplastic syndrome. Imaging studies, including PET and CT, showed no radiological evidence of recurrent GIST. Treatment with octreotide infusion resulted in minimal improvement, whereas daily corticosteroid therapy significantly alleviated the patient’s symptoms. The etiology of hypoglycemia remains elusive, with potential causes under consideration including Y-90 radioembolization-induced damage to glucagon-producing cells, immunotherapy-related adverse effects, or radiologically occult GIST. Insulin autoantibody testing is pending, and the case remains under active investigation, highlighting the diagnostic complexity of hypoglycemia in advanced GIST.

Discussion

Hypoglycemia in the context of GIST is a rare and poorly understood phenomenon. Potential mechanisms include paraneoplastic syndromes, such as non-islet cell tumor hypoglycemia (NICTH) mediated by IGF-2, or treatment-related effects, such as radiation-induced pancreatic or hepatic dysfunction. In this case, the absence of detectable IGF-2 abnormalities and negative imaging complicates the diagnosis. The lack of response to octreotide indicates that somatostatin receptor-mediated pathways may not be involved. The discontinuation of imatinib and prior Y-90 radioembolization further broadens the differential, as both could contribute to metabolic dysregulation.

Conclusions

This case illustrates the need for a systematic and multidisciplinary approach to evaluate hypoglycemia in patients with advanced GIST.

Background

Gastrointestinal stromal tumors (GISTs) are rare neoplasms of the gastrointestinal (GI) tract, accounting for approximately 1–2% of GI cancers. Hypoglycemia in patients with GIST is an uncommon and diagnostically challenging presentation, often involving a broad differential diagnosis. This case report explores the diagnostic difficulties encountered in managing persistent hypoglycemia in a patient with a history of advanced GIST.

Case Presentation

An 80-year-old male with a history of stage IV GIST, diagnosed in 2010, presented with persistent symptomatic hypoglycemia. His medical history included extensive abdominal disease, managed with multiple interventions: esophagogastrostomy, left lateral liver resection, a Whipple procedure, and Y-90 radioembolization. He received adjuvant imatinib therapy, which was discontinued in April 2024 due to significant adverse effects, including anasarca. In 2025, the patient developed progressive hypoglycemia, ultimately requiring continuous D10 infusion to maintain euglycemia, prompting an endocrinology evaluation. The initial diagnostic workup included cortisol, insulin, C-peptide levels, and IGF-1/IGF-2 ratio ruling out insulinoma, adrenal insufficiency, and GISTrelated paraneoplastic syndrome. Imaging studies, including PET and CT, showed no radiological evidence of recurrent GIST. Treatment with octreotide infusion resulted in minimal improvement, whereas daily corticosteroid therapy significantly alleviated the patient’s symptoms. The etiology of hypoglycemia remains elusive, with potential causes under consideration including Y-90 radioembolization-induced damage to glucagon-producing cells, immunotherapy-related adverse effects, or radiologically occult GIST. Insulin autoantibody testing is pending, and the case remains under active investigation, highlighting the diagnostic complexity of hypoglycemia in advanced GIST.

Discussion

Hypoglycemia in the context of GIST is a rare and poorly understood phenomenon. Potential mechanisms include paraneoplastic syndromes, such as non-islet cell tumor hypoglycemia (NICTH) mediated by IGF-2, or treatment-related effects, such as radiation-induced pancreatic or hepatic dysfunction. In this case, the absence of detectable IGF-2 abnormalities and negative imaging complicates the diagnosis. The lack of response to octreotide indicates that somatostatin receptor-mediated pathways may not be involved. The discontinuation of imatinib and prior Y-90 radioembolization further broadens the differential, as both could contribute to metabolic dysregulation.

Conclusions

This case illustrates the need for a systematic and multidisciplinary approach to evaluate hypoglycemia in patients with advanced GIST.

Background

Gastrointestinal stromal tumors (GISTs) are rare neoplasms of the gastrointestinal (GI) tract, accounting for approximately 1–2% of GI cancers. Hypoglycemia in patients with GIST is an uncommon and diagnostically challenging presentation, often involving a broad differential diagnosis. This case report explores the diagnostic difficulties encountered in managing persistent hypoglycemia in a patient with a history of advanced GIST.

Case Presentation

An 80-year-old male with a history of stage IV GIST, diagnosed in 2010, presented with persistent symptomatic hypoglycemia. His medical history included extensive abdominal disease, managed with multiple interventions: esophagogastrostomy, left lateral liver resection, a Whipple procedure, and Y-90 radioembolization. He received adjuvant imatinib therapy, which was discontinued in April 2024 due to significant adverse effects, including anasarca. In 2025, the patient developed progressive hypoglycemia, ultimately requiring continuous D10 infusion to maintain euglycemia, prompting an endocrinology evaluation. The initial diagnostic workup included cortisol, insulin, C-peptide levels, and IGF-1/IGF-2 ratio ruling out insulinoma, adrenal insufficiency, and GISTrelated paraneoplastic syndrome. Imaging studies, including PET and CT, showed no radiological evidence of recurrent GIST. Treatment with octreotide infusion resulted in minimal improvement, whereas daily corticosteroid therapy significantly alleviated the patient’s symptoms. The etiology of hypoglycemia remains elusive, with potential causes under consideration including Y-90 radioembolization-induced damage to glucagon-producing cells, immunotherapy-related adverse effects, or radiologically occult GIST. Insulin autoantibody testing is pending, and the case remains under active investigation, highlighting the diagnostic complexity of hypoglycemia in advanced GIST.

Discussion

Hypoglycemia in the context of GIST is a rare and poorly understood phenomenon. Potential mechanisms include paraneoplastic syndromes, such as non-islet cell tumor hypoglycemia (NICTH) mediated by IGF-2, or treatment-related effects, such as radiation-induced pancreatic or hepatic dysfunction. In this case, the absence of detectable IGF-2 abnormalities and negative imaging complicates the diagnosis. The lack of response to octreotide indicates that somatostatin receptor-mediated pathways may not be involved. The discontinuation of imatinib and prior Y-90 radioembolization further broadens the differential, as both could contribute to metabolic dysregulation.

Conclusions

This case illustrates the need for a systematic and multidisciplinary approach to evaluate hypoglycemia in patients with advanced GIST.

Background

Genetic testing can reveal inherited or acquired genetic changes that can help with identifying diagnosis, treatment, prognosis, and risk of the malignancy. CDH1 is a gene that prevents cancer by controlling cell growth. Mutated CDH1 gene can lead to specific malignancies including gastric and breast cancer.

Case Presentation

42 year old female with past medical history of ovarian cysts presented to the VA Emergency Department for right sided abdominal pain and red colored stool. Further workup showed ileocolonic intussusception with stranding. She underwent a colonoscopy which showed 4 centimeter mass at the ileocecal valve. Biopsy was done which showed invasive adenocarcinoma. She underwent laparoscopic hemicolectomy and was referred to oncology. Referral to genetic testing was positive for CDH1 gene mutation. She was advised that CDH1 mutation has a high risk of developing gastric and breast cancer with recommendations including possible total gastrectomy and bilateral mastectomies. The patient however, decided to decline gastrectomy and mastectomy and instead decided to be followed by frequent EGDs and mammograms.

Discussion

CDH1 mutations are found in only 3.8% of colorectal signet ring cell cancers, with limited data of their presence in typical adenocarcinomas. This case underscores the value of genetic testing in all colorectal adenocarcinomas for its prognostic significance and potential impact on other cancer screenings. CDH1 mutations can lead to an aggressive type of gastric cancer called hereditary diffuse gastric cancer in 56-70% of patients with the mutation. CDH1 mutations also have a 37-55% of having breast cancer compared to the 12% in the general population and patients tend to present with lobular breast cancer. Patients with positive CDH1 mutation should have regular screenings or in some cases, prophylactic surgery.

Background

Genetic testing can reveal inherited or acquired genetic changes that can help with identifying diagnosis, treatment, prognosis, and risk of the malignancy. CDH1 is a gene that prevents cancer by controlling cell growth. Mutated CDH1 gene can lead to specific malignancies including gastric and breast cancer.

Case Presentation

42 year old female with past medical history of ovarian cysts presented to the VA Emergency Department for right sided abdominal pain and red colored stool. Further workup showed ileocolonic intussusception with stranding. She underwent a colonoscopy which showed 4 centimeter mass at the ileocecal valve. Biopsy was done which showed invasive adenocarcinoma. She underwent laparoscopic hemicolectomy and was referred to oncology. Referral to genetic testing was positive for CDH1 gene mutation. She was advised that CDH1 mutation has a high risk of developing gastric and breast cancer with recommendations including possible total gastrectomy and bilateral mastectomies. The patient however, decided to decline gastrectomy and mastectomy and instead decided to be followed by frequent EGDs and mammograms.

Discussion

CDH1 mutations are found in only 3.8% of colorectal signet ring cell cancers, with limited data of their presence in typical adenocarcinomas. This case underscores the value of genetic testing in all colorectal adenocarcinomas for its prognostic significance and potential impact on other cancer screenings. CDH1 mutations can lead to an aggressive type of gastric cancer called hereditary diffuse gastric cancer in 56-70% of patients with the mutation. CDH1 mutations also have a 37-55% of having breast cancer compared to the 12% in the general population and patients tend to present with lobular breast cancer. Patients with positive CDH1 mutation should have regular screenings or in some cases, prophylactic surgery.

Background

Genetic testing can reveal inherited or acquired genetic changes that can help with identifying diagnosis, treatment, prognosis, and risk of the malignancy. CDH1 is a gene that prevents cancer by controlling cell growth. Mutated CDH1 gene can lead to specific malignancies including gastric and breast cancer.

Case Presentation

42 year old female with past medical history of ovarian cysts presented to the VA Emergency Department for right sided abdominal pain and red colored stool. Further workup showed ileocolonic intussusception with stranding. She underwent a colonoscopy which showed 4 centimeter mass at the ileocecal valve. Biopsy was done which showed invasive adenocarcinoma. She underwent laparoscopic hemicolectomy and was referred to oncology. Referral to genetic testing was positive for CDH1 gene mutation. She was advised that CDH1 mutation has a high risk of developing gastric and breast cancer with recommendations including possible total gastrectomy and bilateral mastectomies. The patient however, decided to decline gastrectomy and mastectomy and instead decided to be followed by frequent EGDs and mammograms.

Discussion

CDH1 mutations are found in only 3.8% of colorectal signet ring cell cancers, with limited data of their presence in typical adenocarcinomas. This case underscores the value of genetic testing in all colorectal adenocarcinomas for its prognostic significance and potential impact on other cancer screenings. CDH1 mutations can lead to an aggressive type of gastric cancer called hereditary diffuse gastric cancer in 56-70% of patients with the mutation. CDH1 mutations also have a 37-55% of having breast cancer compared to the 12% in the general population and patients tend to present with lobular breast cancer. Patients with positive CDH1 mutation should have regular screenings or in some cases, prophylactic surgery.