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Hyperglycemia
Introduction
Hyperglycemia is an elevation in blood glucose above the physiologic range. Diabetes mellitus is diagnosed by a fasting plasma glucose of 126 mg/dL (7.0 mmol/L) or higher, a 2-hour plasma glucose of 200 mg/dL (11.1 mmol/L) or higher during a 75-g oral glucose tolerance test, an HbA1c of 6.5% or higher, or a random plasma glucose of 200 mg/dL or higher in a patient with classic symptoms or hyperglycemic crisis. In the absence of unequivocal symptomatic hyperglycemia, abnormal results should be confirmed with repeat testing.
Prediabetes is defined as fasting plasma glucose 100 to 125 mg/dL, 2-hour plasma glucose 140 to 199 mg/dL, or HbA1c 5.7% to 6.4%.[1] The International Diabetes Federation estimated that 589 million adults aged 20 to 79 years were living with diabetes in 2024, with a projected increase to about 853 million by 2050.[2] In the United States, the Centers for Disease Control and Prevention (CDC) estimates that 40.1 million people had diabetes in 2023 and that 115.2 million adults had prediabetes.[CDC. National Diabetes Statistics Report. 2026]
Etiology
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Etiology
Primary Causes
Type 1 diabetes results from autoimmune destruction of pancreatic beta cells. Genetic susceptibility, especially HLA class II haplotypes, interacts with environmental triggers to initiate an immune cascade. Autoantibodies to GAD65, IA-2, ZnT8, and insulin are useful markers of autoimmune diabetes, although T-cell-mediated beta-cell injury is the main pathologic process.[3]
Type 2 diabetes accounts for most diabetes cases. It develops through a combination of insulin resistance, progressive beta-cell dysfunction, excessive hepatic glucose production, impaired incretin effect, increased lipolysis, increased renal glucose reabsorption, altered central appetite regulation, and reduced skeletal muscle glucose uptake. DeFronzo described these mechanisms as the “ominous octet,” a useful framework for matching therapy to pathophysiology.[4][5]
Secondary Causes
Secondary causes of hyperglycemia include:
- Pancreatic disease, eg, chronic pancreatitis, cystic fibrosis, and pancreatic cancer, can cause pancreatogenic diabetes [6]
- Endocrinopathies, including Cushing syndrome, acromegaly, pheochromocytoma, and glucagonoma, can raise glucose through counter-regulatory hormone excess [7]
- Medications, eg, glucocorticoids, thiazides, antipsychotics, statins, beta-blockers, phenytoin, and protease inhibitors, may precipitate or worsen hyperglycemia[8]
- Critical illness (can produce stress hyperglycemia through catecholamines, cortisol, and increased hepatic glucose output) [9]
Important risk factors for type 2 diabetes include obesity, family history, history of gestational diabetes, hypertension, dyslipidemia, polycystic ovary syndrome, sedentary lifestyle, and metabolic syndrome. ADA screening recommendations use these risk factors to determine who should be tested before age 35.[1]
Epidemiology
The IDF Diabetes Atlas, 11th edition, documents 589 million adults aged 20 to 79 with diabetes worldwide as of 2024, equating to a global prevalence of 11.1%. Projections estimate that 853 million individuals (12.96%) aged 20 to 79 years will be affected by 2050. Diabetes-attributable mortality claimed over 3.4 million lives in 2024.[1]
Within the United States, the most recent CDC National Diabetes Statistics Report (January 2026 update) places the total burden at 40.1 million people with diabetes (11.6% of the population). The prediabetes reservoir is even larger, encompassing an estimated 115 million adults aged 18 and older.[CDC. National Diabetes Statistics Report. 2026]
Pathophysiology
Type 1 Diabetes Mellitus
In genetically susceptible individuals (particularly those carrying HLA-DR3, HLA-DR4, or high-risk HLA-DQ haplotypes), environmental exposures, eg, viral infections, may trigger an adaptive immune response against beta-cell antigens. Autoantibodies to glutamic acid decarboxylase 65 (GAD65), insulinoma-associated protein 2 (IA-2), zinc transporter 8 (ZnT8), and insulin itself are serologic markers of this process. CD4+ and CD8+ T lymphocytes infiltrate the islets (insulitis), leading to progressive beta-cell loss. Clinical hyperglycemia generally appears only after 80% to 90% of beta-cell mass is lost, which explains the relatively abrupt onset typical of type 1 diabetes.[3]
Type 2 Diabetes Mellitus
Defects in insulin secretion by beta cells and decreased ability of insulin-sensitive tissues to respond to insulin (insulin resistance) are the primary drivers of the development of type 2 diabetes. In muscle, insulin resistance reduces glucose uptake; in the liver, insulin fails to suppress gluconeogenesis, leading to excessive hepatic glucose output; and in adipose tissue, obesity-related adipocyte enlargement promotes lipolysis, free fatty acid release, macrophage infiltration, and low-grade inflammation. These inflammatory and lipid-mediated signals worsen insulin resistance and create glucotoxicity and lipotoxicity, which further injure β-cells. Initially, β-cells compensate by secreting more insulin, leading to hyperinsulinemia, but over time, they lose function and mass, resulting in inadequate insulin secretion.[10]
Mechanisms of Hyperglycemia-Induced Tissue Injury
Chronic hyperglycemia increases mitochondrial production of reactive oxygen species, especially superoxide. This oxidative stress damages DNA and activates poly (ADP-ribose) polymerase, which inhibits glyceraldehyde-3-phosphate dehydrogenase, causing upstream glycolytic intermediates to accumulate and spill over into 4 major damaging pathways: increased polyol pathway activity, increased advanced glycation end-product formation, activation of protein kinase C, and increased hexosamine pathway activity. Together, these pathways promote inflammation, endothelial dysfunction, and cellular injury.[11]
History and Physical
The classic triad of hyperlycemia includes polyuria, polydipsia, and unintended weight loss. Other complaints include blurred vision, fatigue, and poor wound healing.[1] DKA typically presents with nausea, vomiting, diffuse abdominal pain, and acetone-scented breath. Hyperglycemic hyperosmolar state (HHS), more common in older patients with type 2 diabetes, presents with profound dehydration and altered mental status.[12]
Volume depletion in DKA and HHS may be evident as hypotension, resting tachycardia, dry mucous membranes, and diminished skin turgor. Cutaneous markers of insulin resistance include acanthosis nigricans, skin tags, diabetic dermopathy (shin spots), and necrobiosis lipoidica.[13]
Evaluation
A structured evaluation of hyperglycemia includes confirmation, diabetes classification, and screening for complications.
Diagnostic Criteria
According to ADA 2026 standards of care, a diabetes diagnosis is confirmed when any 1 of the following is present on at least 2 occasions in the absence of unequivocal symptomatic hyperglycemia:
- Fasting plasma glucose at or above 126 mg/dL (7.0 mmol/L), with fasting defined as no caloric intake for a minimum of 8 hours
- 2-hour plasma glucose at or above 200 mg/dL (11.1 mmol/L) during a standardized 75-g OGTT
- HbA1c at or above 6.5
- Random plasma glucose at or above 200 mg/dL (11.1 mmol/L) in the context of classic hyperglycemic symptoms or hyperglycemic crisis, DKA/HHS (single measurement sufficient) [1]
The criteria for a diagnosis of prediabetes are a fasting plasma glucose of 100 to 125 mg/dL, a 2-hour OGTT plasma glucose of 140 to 199 mg/dL, or an HbA1c 5.7% to 6.4%.[1]
Screening Recommendations
The 2026 ADA Standards advise universal screening beginning at age 35 using any of the 3 standard tests (fasting plasma glucose, 2-hour OGTT, or HbA1c). Earlier screening should be pursued in any adult who is overweight or obese and carries at least 1 additional risk factor. Patients with normal results should be retested every 3 years at a minimum, while those with prediabetes warrant annual surveillance. Emerging evidence also supports screening first-degree relatives of patients with type 1 diabetes for islet autoantibodies to enable disease interception strategies.[1]
Hyperglycemic Crisis Workup
Initial testing should include plasma glucose, electrolytes, serum osmolality, serum and urine ketones, complete blood counts with differential, arterial blood gas, ECG, blood cultures, urinalysis and cultures, and chest x-ray.[14]
DKA is defined by the presence of diabetes or hyperglycemia (glucose≥200 mg/dL) or a prior history of diabetes, plus evidence of ketosis, eg, a β-hydroxybutyrate concentration of 3.0 mmol/L or higher or a urine ketone strip result of 2+ or greater. A DKA diagnosis also requires metabolic acidosis, defined as a pH of less than 7.3 or serum bicarbonate less than 18 mmol/L.[15]
HHS is characterized by more severe hyperglycemia, with plasma glucose of 600 mg/dL or higher, and hyperosmolarity, defined as calculated effective serum osmolality greater than 300 mOsm/kg using the formula 2 × sodium + glucose in mmol/L, or total serum osmolality greater than 320 mOsm/kg using 2 × sodium + glucose + urea in mmol/L. HHS also requires the absence of significant ketonemia, defined as β-hydroxybutyrate less than 3.0 mmol/L or urine ketones less than 2+, and the absence of acidosis, defined as a pH of 7.3 or higher and a bicarbonate of 15 mmol/L or higher.[15]
Treatment / Management
Treatment goals are symptom control, prevention or slowing of micro- and macrovascular complications, avoidance of treatment-related harm (especially hypoglycemia and weight gain), and quality of life.
Glycemic Targets
The 2026 ADA Standards of Care continue to endorse the following individualized glycemic goal-setting:
- Most nonpregnant adults: HbA1c below 7.0%
- Selected patients with short disease duration, long life expectancy, absence of significant cardiovascular disease, and low hypoglycemia risk: a more ambitious HbA1c below 6.5% may be pursued
- Patients with extensive comorbidities, advanced complications, limited life expectancy, longstanding disease, or high hypoglycemia susceptibility: a relaxed HbA1c target of below 8.0% or even below 8.5% is acceptable
- Older adults: targets should reflect functional and cognitive status; for those with complex or intermediate health, HbA1c below 8.0% is reasonable [16]
Continuous glucose monitoring (CGM) is especially valuable for individuals with diabetes who are prone to hypoglycemia and for those with type 1 diabetes. CGM use in type 2 diabetes and other diabetes subtypes is increasing, particularly among patients treated with insulin.[17][16][18](B3)
Lifestyle and Nonpharmacologic Intervention
In people with type 2 diabetes who are overweight or obese, weight management should be a key treatment goal alongside glycemic control. Any amount of weight loss is beneficial, with 5% to 7% weight loss improving glycemia and cardiovascular risk factors. Weight loss greater than 10% may provide larger benefits, including possible diabetes remission and improved long-term outcomes. Treatment should include nutrition, physical activity, and behavioral strategies, ideally with frequent counseling and a 500 to 750 kcal/day calorie deficit. Screen adults annually for overweight and obesity using BMI. Obesity-related measurements should be monitored at least yearly, and every 3 months during active weight management.[19]
Pharmacologic Management of Type 2 Diabetes
Type 2 diabetes pharmacotherapy has moved from a glucose-centered stepwise approach to a comorbidity-driven, patient-centered model. The 2022 ADA/EASD consensus and the 2026 ADA Standards of Care are the primary frameworks.[20][21](B3)
First-line agents
Metformin remains a preferred initial agent in most patients. It suppresses hepatic glucose output, modestly increases peripheral insulin sensitivity, does not cause hypoglycemia on its own, is weight-neutral, and is inexpensive. The UKPDS showed cardiovascular mortality benefit with metformin in overweight patients.[22] Metformin can be used down to an eGFR of 30 mL/min/1.73 m², with dose reduction between 30 and 45. In patients with established atherosclerotic cardiovascular disease, heart failure, or chronic kidney disease, first-line therapy should include an SGLT2 inhibitor and/or a GLP-1 receptor agonist with proven cardiorenal benefit, regardless of baseline HbA1c or metformin use.[20][21](A1)
Cardiorenal risk-directed therapy
Strong evidence supports SGLT2 inhibitors and GLP-1 RAs in type 2 diabetes complicated by atherosclerotic cardiovascular disease, high atherosclerotic cardiovascular disease risk, heart failure, or chronic kidney disease.[23][24](A1)
For GLP-1 receptor agonists (eg, liraglutide, semaglutide, dulaglutide), cardiovascular outcomes trials (LEADER, SUSTAIN-6, REWIND) showed reductions in major adverse cardiovascular events (MACE). Meta-analyses also show kidney benefits, including slowed progression of albuminuria and reduced risk of kidney failure.[25][26][27][28](A1)
For SGLT2 inhibitors (eg, empagliflozin, canagliflozin, dapagliflozin), EMPA-REG OUTCOME, CANVAS, and DECLARE-TIMI 58 trials showed reductions in MACE and heart failure hospitalization. The dedicated kidney trials (CREDENCE, DAPA-CKD) confirmed a reduction in progression to end-stage kidney disease.[29][30][31][32][33](A1)
Tirzepatide, the first dual GIP and GLP-1 receptor agonist, produced larger HbA1c reductions (1.24% to 2.58%) and weight losses (5.4 to 11.7 kg) than prior injectable agents in the SURPASS program. SURPASS-2 showed superiority over semaglutide 1 mg weekly for both HbA1c and weight at 40 weeks. Tirzepatide is approved for type 2 diabetes (Mounjaro) and for chronic weight management (Zepbound).[34][35](A1)
GLP-1 receptor agonists increase glucose-dependent insulin secretion, suppress inappropriate glucagon release, slow gastric emptying, and increase satiety through central appetite pathways.[36] SGLT2 inhibitors block sodium-glucose cotransporter 2 in the early proximal renal tubule, reducing renal glucose absorption.[37]
Other glucose-lowering agents
Additional agents that may be utilized to reduce hyperglycemia include:
- Sulfonylureas (glimepiride, glipizide): stimulate pancreatic beta-cell insulin release by closing ATP-sensitive potassium channels (KATP channels)
- DPP-4 inhibitors (sitagliptin, linagliptin): inhibit DPP-4 enzyme activity, increasing endogenous GLP-1 and GIP levels to enhance glucose-dependent insulin secretion and suppress glucagon
- Thiazolidinediones (pioglitazone): activate PPAR-γ nuclear receptors to improve peripheral insulin sensitivity and reduce hepatic insulin resistance
- Alpha-glucosidase inhibitors (acarbose, miglitol): inhibit intestinal alpha-glucosidase enzymes, delaying carbohydrate digestion and reducing postprandial glucose absorption
- Insulin: used in type 2 diabetes when hyperglycemic symptoms are present or HbA1c >10%, regardless of the other glucose-lowering therapies [21][38][21]
Type 1 Diabetes Management
Lifelong insulin replacement is required. Physiologic replacement uses multiple daily injections (basal-bolus) or continuous subcutaneous insulin infusion (pump therapy). Automated insulin delivery (AID) systems, which combine real-time CGM with algorithmic pump control, increase time in range and reduce hypoglycemia in clinical trials.[21][39](A1)
Hospital Management of Hyperglycemia:
DKA treatment
Treatment of diabetic ketoacidosis requires prompt volume resuscitation, correction of electrolyte deficits, intravenous insulin therapy, and treatment of the precipitating cause. Initial management begins with isotonic IV fluids to restore intravascular volume, followed by assessment of potassium. Insulin should generally be delayed if potassium is severely low. Dextrose-containing fluids are added once glucose falls to prevent hypoglycemia, while insulin is continued until ketoacidosis resolves. Before stopping IV insulin, subcutaneous basal insulin should be administered about 2 hours earlier to prevent rebound hyperglycemia.[15] Please see StatPearls' companion resource, "Adult Diabetic Ketoacidosis," for further information on the management of DKA.
Hyperglycemic hyperosmolar state treatment
Treatment of HHS focuses first on aggressive but carefully monitored fluid replacement because profound dehydration and hyperosmolality are the dominant abnormalities. Insulin is used more cautiously than in DKA, because glucose may fall substantially with fluids alone, and rapid osmolar shifts can be harmful. Management also requires identifying and treating the precipitating cause. After hyperosmolality, dehydration, and mental status improve, patients should be transitioned to an appropriate scheduled subcutaneous insulin regimen with overlap from IV insulin when used.[15] Please see StatPearls' companion resource, "Hyperosmolar Hyperglycemic Syndrome," for further information on the management of HHS.
ADA 2026 guidelines also emphasize the following principles for the management of hyperglycemia in the hospital:
- Initiate insulin when glucose persistently exceeds 180 mg/dL (confirmed on 2 measurements within 24 hours)
- In critically ill (ICU) patients, continuous intravenous insulin targeting 140 to 180 mg/dL is preferred for its titratable pharmacokinetics
- In noncritically ill patients, scheduled subcutaneous insulin incorporating basal, nutritional (prandial), and correction components is the standard
- Perioperative targets: 140 to 180 mg/dL [15]
Prognosis
In type 1 diabetes, the DCCT/EDIC program showed that intensive treatment (mean HbA1c approximately 7%) reduced retinopathy by 76%, nephropathy by 50%, and neuropathy by 60% relative to conventional control. These benefits persisted as a metabolic memory effect through 9 years of follow-up, with a 42% reduction in cardiovascular events and a 57% reduction in nonfatal myocardial infarction, stroke, or cardiovascular death.[40][41]
In type 2 diabetes, the UKPDS showed that intensive control (median HbA1c 7.0%) reduced microvascular complications by 25% over 10 years. After 10 more years of posttrial monitoring, intensive treatment was associated with sustained reductions in myocardial infarction (15% with sulfonylurea or insulin; 33% with metformin) and all-cause mortality (13% and 27%, respectively).[42][43] The VADT and ADVANCE trials showed a reduction in nephropathy with intensive blood glucose control.[44][45] Another trial, ACCORD, was stopped due to higher mortality in the intensive glycemic control arm.[46]
Complications
Microvascular
Diabetic retinopathy is the leading cause of new-onset blindness in working-age adults in developed countries. The disease ranges from non-proliferative changes (microaneurysms, hemorrhages, hard exudates) to sight-threatening proliferative retinopathy and diabetic macular edema, which can occur at any stage. Screen using dilated fundoscopic examination at type 2 diabetes diagnosis, within 5 years of type 1 diagnosis, then annually or per ophthalmologist guidance.[47]
Diabetic kidney disease develops in 20% to 40% of people with diabetes and is the leading cause of end-stage kidney disease in the United States. Pathology includes glomerular basement membrane thickening, mesangial expansion, and nodular glomerulosclerosis (Kimmelstiel-Wilson lesions); it presents clinically with progressive albuminuria and falling GFR. Check urine albumin creatinine ratio (UACR) and eGFR assessed annually starting at diagnosis in type 2 and after 5 years in type 1 diabetes.[48]
Diabetic neuropathy is the most common chronic complication, affecting up to half of patients over the disease course. Forms include distal symmetric polyneuropathy, cardiovascular autonomic neuropathy, gastrointestinal autonomic neuropathy (gastroparesis), and focal/multifocal neuropathies.[47]
Macrovascular
Cardiovascular disease includes atherosclerotic cardiovascular disease and heart failure. Atherosclerotic cardiovascular disease encompasses a broad range of conditions, eg, hypertension, coronary artery disease, stroke, and peripheral artery disease.[49]
Other Conditions
Metabolic-dysfunction-associated steatotic liver disease (MASLD, formerly NAFLD) affects up to 70% of patients with type 2 diabetes and may progress to steatohepatitis, fibrosis, and hepatocellular carcinoma.[50]
Postoperative and Rehabilitation Care
Perioperative hyperglycemia is a well-established predictor of surgical site infection, wound complications, prolonged hospitalization, and perioperative mortality. A glucose target of 140 to 180 mg/dL is recommended for the majority of surgical patients. Insulin remains the preferred pharmacologic agent in this setting. SGLT2 inhibitors should be discontinued 3 to 4 days preoperatively because of the risk of perioperative euglycemic DKA.[51][52]
Consultations
Initial management of hyperglycemia is within the scope of primary care and internal medicine. An endocrinology referral is warranted when glycemic targets remain unmet and for complex insulin regimen management. The broader interprofessional team may include: endocrinologist, ophthalmologist, nephrologist, cardiologist, podiatrist, vascular surgeon, neurologist, certified diabetes care and education specialist (CDCES), registered dietitian/nutritionist, pharmacist, and behavioral health professional.
Deterrence and Patient Education
Deterrence of hyperglycemia centers on early identification of at-risk individuals and sustained engagement in preventive, evidence-based care to reduce progression to diabetes and its complications. Screening based on age and risk factors, including obesity, metabolic syndrome, history of gestational diabetes, and cardiovascular comorbidities, enables earlier diagnosis of dysglycemia and timely intervention. Reinforcing lifestyle modification, weight reduction, and routine monitoring of glycemic status supports the prevention of progression from prediabetes to overt diabetes and reduces the incidence of acute metabolic crises and long-term microvascular and macrovascular complications.
Structured diabetes self-management education and support (DSMES) serves as a foundational strategy for patient education and should be delivered at diagnosis, annually, when complications develop, and at transitions of care. DSMES improves patient competence in blood glucose self-monitoring, continuous glucose monitoring (CGM) use, and interpretation of glycemic trends. Education also emphasizes proper insulin administration techniques, medication adherence, and the recognition and immediate treatment of hypoglycemia and hyperglycemia, which are critical to preventing avoidable emergency department visits and hospitalizations.
Patient education further focuses on lifestyle modification strategies that directly influence insulin sensitivity and glycemic control. These include individualized medical nutrition therapy, carbohydrate awareness, structured physical activity, weight management, and behavioral strategies for stress reduction and sustained adherence. Education on the warning signs of DKA and hyperglycemic hyperosmolar state, such as polyuria, polydipsia, dehydration, and altered mental status, enables earlier presentation for care and reduces morbidity.
Effective deterrence and patient education rely on interprofessional reinforcement and continuous follow-up. Clinicians, nurses, pharmacists, dietitians, and diabetes care and education specialists collaborate to ensure consistent messaging, address barriers to adherence, and adjust education based on patient literacy and clinical status. This coordinated approach improves long-term glycemic outcomes, reduces complications, and strengthens patient autonomy in chronic disease self-management.
| Pause and Reflect |
A 52-year-old patient has newly diagnosed type 2 diabetes with an HbA1c of 8.4% and is preparing for discharge after hospitalization for severe hyperglycemia. The patient expresses uncertainty about using a glucose meter, administering prescribed insulin, recognizing hypoglycemia, and making dietary changes.
|
Pearls and Other Issues
Key factors that should be kept in mind when managing hyperglycemia include:
- Any patient with glucose exceeding 600 mg/dL warrants immediate evaluation for HHS or mixed DKA-HHS.
- Stress hyperglycemia in a hospitalized patient without a history of diabetes should prompt an HbA1c measurement.
- Cancer treatment-associated hyperglycemia is an emerging concern warranting heightened vigilance. Close glucose monitoring at every oncology visit is now endorsed by the ADA 2026 Standards.
- HbA1c can be misleading in the presence of hemoglobin variants, iron-deficiency anemia, chronic kidney disease, recent blood transfusion, and pregnancy; in such cases, fructosamine or CGM provides more reliable assessments.
- Glycemic variability, defined as wide amplitude oscillations in glucose concentration, is emerging as an independent contributor to vascular complications.
Enhancing Healthcare Team Outcomes
Hyperglycemia and diabetes mellitus represent a spectrum of metabolic disease characterized by chronic elevation of blood glucose due to insulin resistance, β-cell dysfunction, or autoimmune β-cell destruction. Diagnostic criteria include fasting plasma glucose of 126 mg/dL or higher, 2-hour oral glucose tolerance test of 200 mg/dL or higher, HbA1c of 6.5% or higher, or random glucose of 200 mg/dL or higher with symptoms. Prediabetes reflects intermediate dysglycemia and signals increased cardiometabolic risk. Patients may present with polyuria, polydipsia, weight loss, or acute decompensation, including diabetic ketoacidosis or hyperglycemic hyperosmolar state. Evaluation requires confirmation of diagnosis, classification of diabetes type, assessment of complications, and risk stratification. Management integrates lifestyle modification, individualized glycemic targets, and pharmacotherapy, including metformin, SGLT2 inhibitors, GLP-1 receptor agonists, and insulin, with an emphasis on the prevention of microvascular and macrovascular complications and acute metabolic crises.
Optimal outcomes require interprofessional collaboration. Physicians and advanced practitioners guide diagnosis, treatment selection, complication screening, and referral. Primary care clinicians ensure early identification, longitudinal monitoring, and guideline-based risk management. Nurses coordinate care, triage glycemic events, and support transitions of care. Pharmacists optimize medication selection, adherence, safety, and cost-effectiveness. Registered dietitians provide individualized nutrition therapy, while certified diabetes care and education specialists deliver structured self-management education and device training. Behavioral health professionals address psychological comorbidities affecting adherence. Coordinated communication and shared decision-making across disciplines improve glycemic control, reduce hospitalizations, and enhance patient safety and quality of life.
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