CASE STUDY
A case of a patient with hyperosmolar hyperglycemic state: Implications for nurse practitioners in primary care Jennifer Hackel, DNP, GNP-BC (Assistant Clinical Professor) College of Nursing and Health Science, University of Massachusetts, Boston, Massachusetts
Keywords Diabetes; hyperglycemia; hyperosmolar; guidelines. Correspondence Jennifer Hackel, DNP, GNP-BC, College of Nursing and Health Science 30107, University of Massachusetts, Boston, 100 Morrissey Blvd., Boston, MA 02125. Tel: 734-287-7500; Fax 617-287-7527; E-mail: [email protected] Received: 30 August 2011; accepted: 14 June 2012 doi: 10.1002/2327-6924.12098
Abstract Purpose: The purpose of this case study is twofold: first, to present the pathophysiology of hyperosmolar hyperglycemic state (HHS) as it relates to a hospitalized patient with undiagnosed diabetes; the second is to increase awareness among primary care nurse practitioners (NPs) about the complexities of diagnosing less typical forms of diabetes. The case illustrates how HHS can be life threatening, how it is differentiated from diabetic ketoacidosis (DKA), and how it is treated. The importance of closer surveillance of blood glucose in high-risk individuals is highlighted. Data sources: Review of the literature and application to the case. Conclusions: HHS is a potentially lethal and preventable hyperglycemic crisis, which is in a continuum with DKA, occurring frequently in individuals with no prior diagnosis of diabetes. The incidence of HHS is increasing as the epidemic of diabetes continues. It is important for NPs to understand the pathophysiology of HHS, and identify which patients are at risk. Many high-risk patients, when under stress, develop acute hyperglycemic crisis, which begets further cardiovascular complications. Implications for practice: With improved understanding of the phenomena leading to glucose dysregulation, less typical forms of diabetes might be identified earlier and controlled. NPs in primary care are uniquely positioned to reduce the risk of hyperglycemic crises.
Case Report The hospital-based advanced practice registered nurse (APRN) came to the bedside of Mr. J after receiving a referral requesting diabetes education for his new diabetes diagnosis. Mr. J, a 47-year-old African American man, had presented to the emergency room with acute confusion 5 days previously. He and his family had just returned from a trip out of state to see relatives. The patient had only a vague recollection of his prodromal symptoms, which came on insidiously during the last days of his journey. He recalled feeling profoundly weak before he lost the ability to think clearly. As soon as the family returned home, his wife drove him directly to the closest emergency room (ER). On admission to the ER, Mr. J’s serum glucose was found to be 958 mg/dL, or about 10 times the normal concentration; his urine showed infection, but only trace ketones, excluding the diagnosis of diabetic ketoacidosis (DKA). He was admitted, and reJournal of the American Association of Nurse Practitioners 26 (2014) 595–602
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ceived over 10 L of intravenous fluid during his first day, which corrected his dehydration, weakness, and clouded cognition. Mr. J’s diagnosis, hyperosmolar hyperglycemic state, or HHS, is associated with uncontrolled diabetes. Yet he had no known diagnosis of diabetes, and believed he would not need insulin therapy upon discharge. “This problem of high blood sugar happened six months ago,” he said, “and insulin made my glucose too low; I did not need it when I got better at home. My doctor told me I don’t have diabetes; the problem only came from my prednisone pills.” The prior event of hyperglycemia requiring insulin occurred when he was placed on high doses of prednisone for sarcoidosis. Steroid therapy quieted the inflammatory process but is a well-known cause of hyperglycemia. His prednisone dose was tapered back down to 2.5 mg daily, a dose he was prescribed after his kidney transplantation 3 years prior. His antirejection program also included 595
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Table 1 Mr. J’s medication list on day 5 of his hospital admission • Levofloxacin 500 mg po daily • Metoprolol 25 mg po q6h • Fentanyl patch 25 mcg transdermal patch • Oxycodone 15 mg po q 6 h • Tacrolimus 2 mg po q 12 h • Mycophenolic acid (Cellcept) 360 mg a.m., 720 mg po q p.m.
• Prednisone 5 mg 1/2 tablet daily • Ergocalciferol 50,000 units weekly • Esomeprozole 40 mg daily • Sodium potassium phosphate oral suspension ×1 (given) • Insulin aspart sliding scale at meals
mycophenolate (Cellcept) and tacrolimus (Prograf) daily in addition to several other medications for his chronic illness management (see medication list, Table 1). Mr. J had undergone kidney transplantation from renal failure resulting from genetic factors. Past medical history included hypertension, coronary artery disease, hyperlipidemia, and lumbar spine injury resulting in chronic low back pain. Past surgical history included cadaveric renal transplant 3 years prior and coronary artery bypass grafting 4 years prior. Social history included college education, computer programmer currently on disability, and married with two children. In addition to profound hyperglycemia, his admission labs revealed several abnormal chemistries including hyponatremia and hypochloremia, as well as the elevated BUN, creatinine, and BUN: creatinine ratios related to dehydration (see Table 2). His anion gap was 18, consistent with mild acidosis, yet his urine ketone test was only trace-positive, his bicarbonate level was normal at 28 mmol/dL, and his pH was low normal at 7.35. His serum osmolality of 338 mmol/kg gave further indication that his body had lost many liters of water. The clinical picture indicated dehydration and hyperglycemia rather than ketoacidosis. His pH level confirmed he was not in DKA but HHS. His admission and the subsequent 5-day blood chemistries most important to his HHS evaluation and management are noted in Table 2. On urine culture, he was found to have more than 100,000 colonies of Klebsiella pneumoniae, resistant to penicillin, sulfa, and nitrofurantoin. He was placed on levofloxacin (Levaquin). His ECG showed new-onset atrial fibrillation for which he was placed on a beta blocker for rate control. He was also found to have a deep vein thrombosis (DVT) and was anticoagulated. His echocardiogram showed global hypokinesis with an ejection fraction of 40%, thickened left ventricle, and no enlargement of the right ventricle. His admission chest xray showed no sign of granulomas (from sarcoidosis) or active infection, though dehydration can mask infiltrates. 596
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In such a multifaceted case, a number of factors may have tipped the delicate balance of glucose regulation resulting in Mr. J’s hyperglycemia. While being on immunosuppression increased the risk of infection as well as hyperglycemia, the physiological stress of travel, enhanced by emotional stress, immobility, a high carbohydrate diet, and other risk factors also contributed to his evolving diabetes (see Figure 1). The urinary tract infection fueled the vicious cycle of hyperglycemic crisis (see Figure 2). Infection is the most common cause of HHS, and left untreated, the syndrome has a mortality rate between 10% and 50%, depending on when and where patients present in the course of their illness (Stoner, 2005). Reviewing Mr. J’s recent orders, the hospitalist team had been careful to give him adequate fluid resuscitation, yet slowly enough to avoid overwhelming his compromised heart and kidney function. Lowering the glucose level slowly is important to avoid hypoglycemia, as well as overcorrection of electrolyte disturbances (Kitabchi, Umpierrez, Fisher, Murphy, & Stentz, 2008). By the fifth day of hospitalization, Mr. J’s serum creatinine had returned to 0.82 mg/dL, indicating that his transplanted kidney was filtrating well. Kidney injury can occur with severe dehydration, particularly if rhabdomyolysis from muscle injury further complicates the patient’s acute illness, as seen in many cases of HHS (Kitabchi, Umpierrez, Miles, & Fisher, 2009).
Background and pathogenesis of hyperglycemic crisis HHS used to be considered the hyperglycemic crisis of Type 2 diabetes, distinct from DKA of Type 1 diabetes. HHS is increasingly being seen as the incidence and prevalence of diabetes increases. HHS and DKA are now seen as extremes of a spectrum of hyperglycemic syndromes, as the features of ketosis, and degrees of hyperosmolality and dehydration, can be present in both types (Nugent, 2005; Ting, 2001). HHS has gone through several diagnostic labels, including Hyperosmolar Nonketotic Coma (HONK), Hyperosmolar Hyperglycemic Nonketotic Coma (HHNC), and Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS), because coma is present in a minority of those presenting (Nugent, 2005). Both HHS and DKA have been reported in patients with either Type 1 or Type 2 diabetes, and up to a third of patients with severe hyperglycemia show an overlap in the diagnostic criteria (Nugent, 2005). However, where patients have some reserve of insulin secretion, there is less tendency toward lipolysis and ketoacidosis, and a greater severity of dehydration (Kitabchi et al., 2009). In both disorders, as glucose levels rise above the renal threshold, where glucose “spills” in to the urine, the
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Table 2 Mr. J’s lab results on admission and at day 5 Lab test
Day of admission
Result day 5
Plasma glucose Sodium Potassium Chloride Bicarbonate BUN Creatinine Calcium Anion gap Magnesium Osmolality Troponin
958 126 4.3 80 28 51 1.88 10.7 18 2.5 338 0.11
214 134 4.1 104 25 7 0.82 10.3 5 1.5
A1C
10.3%
pH
7.35
0.07
Illness induced immobility & reduced lean muscle mass
Emotional stress
Steroids for sarcoidosis
Comments
74–118 mg/dL 136–144 mmol/dL 3.2–5.2 mmol/dL 102–111 mmol/dL 22–32 mmol/dL 8–20 mg/dL 0.64–1.27 8.9–10.3 5–17 1.5–2.1 mEq/dL 280–308 mOsm/kg 0.01–0.04 ng/dL; cutoff for acute MI is 0.5 ng/dL 4.5%–5.6%
7.35–7.45
kidneys’ ability to concentrate urine becomes impaired. Because glucose must be diluted in water to be excreted, the body undergoes osmotic diuresis, and triggers thirst to correct the dehydration, causing the classic symptoms of polyuria and polydipsia. Yet other factors may blunt the thirst response, and the dehydration may blunt the polyuria. In HHS more so than with DKA, the protracted process of glucose toxicity leads to further release of stress hormones, causing a vicious cycle of insulin resistance, worsening glycemia, osmotic diuresis, hemoconcentration, intracellular dehydration, further stress hormone release, and escalating glycemia (see Figure 2). As intra-
Post transplant immunosuppressants
Reference range
Insulin resistance
Metabolic syndrome w/ BMI >25
Improved Corrected Maintained Corrected Corrected Corrected Corrected Corrected Corrected Corrected Resolving troponin leak Equiv. estimated average glucose of 250 mg/dL Low normal
cellular fluid shifts to the contracting vascular compartment, hyponatremia frequently develops. It is the development of intracellular dehydration and hyponatremia that ultimately cause the mental status changes, as well as the more profound loss of water with minimal ketogenesis, that distinguish HHS (Nugent, 2005). In both DKA and HHS, typically a precipitating event starts the upward trend to hyperglycemia. In classic DKA of Type 1 diabetes, the affected person is more severely insulin deficient, and, without it, becomes ill in hours to days. This may be from undiagnosed diabetes or a diagnosed individual missing his or her insulin therapy. It
UTI causing physiologic stress
Relative insulin deficiency
Lifestyle with high carb diet & colas
Aging (> 45)
Type 2 Diabetes African American race
Figure 1 The forces promoting diabetes in Mr. J.
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Triggering event(see Table 3) Convergence of factors causing progressive hyperglycemia and inability to correct it due to progressive dehydration
Insulin deficiency in state of high demand but enough to prevent
Stress response/stress hormone release Increased hepatic glucose production Insulin resistance
Hyperglycemia Osmotic diuresis
ketogenesis
Confusion, weakness, cardiac arrhythmias
Impaired glucose excretion in context of dehydration
Water loss
Secondary intracellular fluid and electrolyte loss to correct contracted intravascular volume
Intravascular volume contraction
Electrolyte loss
Hyperosmolality
Figure 2 The vicious cycle of hyperosmolar hyperglycemic state.
may be that the individual’s insulin needs rise precipitously with infection, rendering them too ill to comply with glucose testing and treatment before glucose escalates out of control. It is the absolute lack of insulin, which leads to lipolysis for energy, which in turn causes ketoacidosis, the hallmark of DKA. The resulting accumulation of ketoacids causes acute symptoms of illness, such as nausea, vomiting, and abdominal pain. The Kussmaul respirations, deep and rapid, are the telltale sign of compensatory respiratory alkalosis in response to ketoacidosis, and tachypnea is more pronounced in DKA than HHS (Tokuda et al., 2010). By way of comparison, the course of HHS has a less clear onset and insidious progression over days to weeks. The nausea, vomiting, abdominal pain, and tachypnea of DKA are typically absent, because ketosis is mild or nonexistent in HHS (Nugent, 2005). The more prolonged process of osmotic diuresis, without clear symptoms of overt illness, leads to the patient to show a remarkable but ultimately unhelpful adaptation, as he or she does not seek medical attention until it has escalated to a critical level. This is made worse by mental status changes, which prevent rational judgment. An isolated individual, such as an elderly person, may be more likely to reach coma before he or she is found by others. HHS has a higher mortality rate among the elderly (Kitabchi et al., 2008). In HHS, depending on its course, and when the person presents for medical attention, its variable presentation and comorbidities often delays its diagnosis and treatment. There are case reports of pulseless electrical activity from the severe dehydration and hyperkalemia associated with HHS (Ting, 2001). There are also cases 598
of focal neurologic deficits presenting like stroke or seizure that resolve with insulin and hydration (Nugent, 2005). There are cases of neuroleptic drugs such as olanzapine being implicated as the inciting cause, and the patient presents with a fever not from infection but from neuroleptic malignant syndrome (Ahuja, Palanichamy, Mackin, & Lloyd, 2010). While infection is the most common known cause of HHS, a variety of other events can trigger the process, as listed in Table 3. Table 4 lists the drugs that can predispose the person further. In the case of Mr. J, the need for prednisone contributed to the previous episode of acute hyperglycemia, but this time it appeared that the urinary tract infection may have precipitated the cascade to HHS. Further, his previous heart surgery and renal transplant are also clues that his body has been stressed to a degree that significantly increases his vulnerability to develop hyperglycemia and overt diabetes at any time, particularly in the presence of other stressors. Many cardiovascular events have been found to be both precursors and outcomes of HHS including cerebral infarct, pulmonary embolism, and myocardial infarction (Lin, Wang, & Wang, 2010). Research has shown that glucose toxicity progressing to hyperglycemic crisis is associated with release of cytokines, elevated inflammatory markers such as C-reactive protein, and activated clotting factors that resolve with hydration and insulin therapy (Kitabchi et al., 2009). It is unclear if Mr. J had started developing the DVT and elevated troponin levels during the time of his progression into HHS or from it. It is possible the condition was beginning prior to his admission given his recent air travel. The interrelationships of
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Table 3 Precipitating factors for hyperglycemic crisis (adapted from Nugent, 2005) Infection Pneumonia Urinary tract infection Sepsis Wounds or skin infections Acute illness that leads to release of stress hormones, stimulating endogenous glucose release Thromboembolic disease Stroke Deep vein thrombophlebitis or pulmonary embolus Myocardial infarction Acute/metabolic illness Acute pancreatitis Hyper- or hypothermia Intestinal obstruction Renal failure Gastrointestinal bleeding Endocrine disease Undiagnosed diabetes mellitus Cushing’s disease Acromegaly Thyrotoxicosis Major surgery Cardiac surgery Organ transplantation Other Trauma Burns Alcohol abuse Cocaine use Accidental poisoning with Vacor, a rodenticide
Table 4 Medications or other agents shown to contribute to hyperglycemic crisis Antipsychotics Beta blockers Carbemazepine Chlorpromazine Cimetidine Corticosteroids, glucocorticoids Diazoxide Didanosine Gamma interferon Immunosuppressants L-asparaginase Lithium Mannitol Neuroleptics Nicotinic acid Pentamadine Phenytoin Thiazide and loop diuretics Thyroid hormone Total parenteral nutrition
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hyperglycemia, inflammatory cytokines, the hypercoagulable state, and cardiovascular damage are undergoing research, which is confounded by the complexity and diversity of critically ill patients (Kitabchi et al., 2008).
Posthyperglycemic crisis diagnosis and discharge planning By the time the APRN met Mr. J, 5 days post admission, his confusion had entirely cleared. Mental status changes associated with HHS normalize with the correction of dehydration and electrolyte imbalance, usually in hours. Mr. J was then exhibiting no cognitive deficits and was remarkably keen: attentive to teaching, articulate in his questions, and sharp on counterdemonstration of the new skills in glucose testing and insulin administration. Nurses must assess their patients’ abilities to learn and counterdemonstrate new skills, as well as their readiness to accept responsibility for diabetes self-care. Because he expressed skepticism, based on his previous experience, that he would need these skills once he went home, the APRN had to explain that his “tendency to hyperglycemia” was now overt diabetes, a condition to which he had been at risk for years. She addressed his questions about his new diagnosis, reviewed written information on diabetes for him to read and absorb, and trained him in performing self-monitoring of blood glucose. Arming Mr. J with the tools and knowledge to assess his own random blood glucose during this session, and having him teach back its significance, helped him comprehend the importance of his taking charge of his new diagnosis. By using the event of capillary glucose testing as a “teaching moment” the APRN empowered Mr. J in becoming an active decision maker in his care instead of a passive recipient. Diabetes self-care can prevent hyperglycemic crises as well as long-term complications. The APRN offered to return when his wife was visiting so she could participate in the remainder of the teaching on meal planning, sick day management, and diabetes care goals. Mr. J’s A1c level of 10.3%, in less extenuating circumstances, would have been equivalent to an estimated average blood glucose level of about 250 mg/dL (Nathan et al., 2008); however, the HHN renders his previous average uncertain. Nonetheless, it is helpful that diagnosis of diabetes can now be based on the A1c level of 6.5% or greater, reducing the need for the difficulties involved in an oral glucose tolerance test (OGTT; American Diabetes Association, 2012).
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Classification of hyperglycemia and diabetes While it remained unclear exactly what type of diabetes Mr. J had developed and when, the critical point to consider was that he had been at risk for developing diabetes for some years, and a diagnosis of prediabetes would have been helpful in avoiding the crisis. He mistakenly thought, because his previous episode of high blood sugars resolved, he was now “cured” instead of remaining at high risk. Indeed, there are rare cases of hyperglycemic crisis followed by euglycemia. Kitabchi et al. (2009) reviewed data on cases of patients presenting in DKA, who go into remission after the crisis where insulin therapy is no longer needed, sometimes for years, after glycemic correction. This represents atypical diabetes mellitus (ADM), also known as Flatbush diabetes, coined for patients presenting with ketoacidosis consistent with complete insulin deficiency who had return of insulin secretion after glucose normalization (often confirmed by C-peptide testing), and no evidence of beta-cell autoimmunity (Rasouli & Elbein, 2004). These cases with ADM are noted most commonly among Blacks and Hispanics, as well as Native Americans and Asians, more so than Caucasians (Kitabchi et al., 2008), a predominance mirrored in the epidemiology of Type 2 diabetes. However, the caveat is that such patients still have a diagnosis of diabetes, usually Type 2, even if it has reverted to “diet controlled.” Mr. J was under the impression he was at low risk for Type 2 diabetes based on his relatively young age, lack of obesity, and lack of known family history. However his history argues for elevated risk based on age over 45, African American race, and presence of metabolic syndrome factors including hyperlipidemia and hypertension, as well as loss of lean body mass from immobility. The convergence of contributing factors to Mr. J’s diagnosis are noted in Figure 1. Mr. J wondered if he perhaps had “Hospital-related Hyperglycemia,” a syndrome in which a critically ill patient’s glucose is in diabetic ranges in the hospital but converts to normal levels after discharge. This syndrome of acute stress-induced glucose dysregulation is in the center of a large controversy over assessing and managing the glucose levels of ill inpatients regardless of their history of known diabetes (Kosiborod et al., 2009). Prevalence in various studies in intensive care units of academic medical centers find it occurring in 23%–60% of patients (Kovalaske & Gandhi, 2009). There are no definitive epidemiologic data yet available to indicate what percentage of such persons without a known diagnosis of diabetes in fact show normal glucose tolerance thereafter if they remain healthy. It is safest to consider all such persons as remaining at 600
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high risk for diabetes, and order an A1C or OGTT to elucidate their glucose regulation status 6–8 weeks after discharge. The American Diabetes Association recommends use of an A1C level of 5.7%–6.4% to diagnosis prediabetes, and 6.5% or higher to confirm the diagnosis of diabetes (American Diabetes Association, 2012). Meanwhile, the APRN considered the possibility that Mr. J had NODAT, the acronym for new-onset diabetes after transplantation. This diabetes syndrome is an increasingly noted phenomenon with the advent of organ transplantation becoming commonplace in mainstream medical care. In one study of over 21,000 patients receiving renal transplant, more than 19% developed new onset of diabetes within 3 years, and 58% of these individuals already had at least one complication of diabetes at diagnosis (Burroughs et al., 2007). It remains unclear why diabetes mellitus occurs more commonly and complications develop more rapidly in this subgroup, though many hypotheses are being tested. While a genetic predisposition is one theory, the diabetogenic effect of immunosuppressant therapy such as tacrolimus has also been implicated, which would apply to Mr. J. In one study, subjects with impaired oral glucose tolerance prior to transplantation showed an increased risk of developing NODAT after transplantation; repeating an OGTT after transplantation was superior to using fasting glucose levels to identify high-risk patients developing NODAT (Delgado et al., 2008). When using the A1C for diagnosis, care should be taken to be sure there is not significant anemia, common among hospitalized patients with renal disease, which may invalidate the A1c level. Perhaps if Mr. J did have an A1c drawn by his primary care provider (PCP), it was not valid because of previous anemia.
The role of discharge planning and primary care Mr. J was eventually discharged on glipizide (Glucotrol) 5 mg twice daily, metformin (Glucophage) 500 mg twice daily, and 10 units of glargine (Lantus) insulin at bedtime. He was given a referral to an endocrinologist, outpatient diabetes education, and an appointment for followup with his PCP. The APRN educated him in the use of the insulin pen and the glucose meter and made sure he had prescriptions for these supplies at his outpatient pharmacy. Such proactive management after his previous episode of hyperglycemia may have prevented his current life-threatening illness. The critical difference in terms of prevention of severity of illness and hospitalization of persons developing hyperglycemic crisis is the time available to stop the process. Inpatient nurses and PCPs have the opportunity to
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prevent serious illness in their patients with diabetes, or in their patients at high risk to develop it, by empowering them with knowledge. Self-monitoring of glucose and sick day management education should lead patients to hydrate themselves and contact providers early for assistance in management of hyperglycemia before it escalates out of control. The cost cannot be measured when a person such as Mr. J has a lengthy hospitalization rendering him unable to function because of critical illness, let alone the damage his diseased heart and transplanted kidney endured. Patients with this history, particularly those such as Mr. J who remain on diabetogenic medications, should be educated while in the hospital regarding the basics of blood glucose regulation and dietary principles of control. They should not only be trained in home glucose monitoring and provided with a monitor, lancets, and test strips, but be given clear instruction regarding bringing their glucose monitoring meter and log to their PCP for follow-up. A diagnosis such as “Atypical Diabetes” or “Prediabetes” and not just “Hospital Related Hyperglycemia” should be added to the problem summary list in the primary care setting to induce adequate followup in transition of care to the community setting. Knowing the tendency of a person to develop diabetes (and therefore hyperglycemic crisis) and taking preventive action saves many healthcare dollars and improves quality of life. This is a critical piece of the current healthcare reform. If patients are homebound, they can benefit from a visiting nurse for follow-up of home glucose levels. Visiting nurses can offer an important contribution to patients and families’ comprehension of day-to-day glucose control, stress or sick day management, and menu planning. While inpatient diabetes education is important, it is also difficult to achieve, and the discharge orders that include referral to community health nurses and outpatient diabetes education will offer benefit at a fraction of the cost of rehospitalization. If the diagnosis of diabetes is unconfirmed in high-risk patients, PCPs should avoid giving false reassurance. Instead, diligence in educating patients in healthy eating, exercise, and close monitoring of glucose status should be encouraged. Patients with an A1C between 5.7% and 6.4% should be given a diagnosis of prediabetes. An OGTT is rarely needed now with the common use of A1C, but may be helpful to look for abnormal postchallenge glucose levels or further assess anemic patients (Simmons, Echouffo-Tcheugui, & Griffin, 2010). APRNs such as primary care nurse practitioners (NPs), whose practice philosophy emphasizes prevention, patient education, and the therapeutic alliance, can help at-risk individuals to be on alert for worsening glycemia, especially during stress, illness, or trauma.
Conclusion Mr. J’s case demonstrates that individuals who have undergone organ transplantation, and have a history of acute hyperglycemia, particularly those with African American or Hispanic ancestry, are at much greater risk of developing diabetes. The complication of HHS is potentially lethal and increasingly common as individuals undergo organ transplantation, survive stressful complex illnesses and surgeries, and take medications that worsen glucose tolerance. HHS has an insidious onset and may be challenging to promptly diagnose. It requires intensive, careful treatment to rehydrate the patient, correct electrolyte disturbances, normalize blood glucose, and minimize collateral physiologic damage. The crisis might have been prevented if Mr. J had been adequately forewarned of his elevated risk. While patients such as Mr. J may show some remission of hyperglycemia after illness, they remain at high risk for diabetes and this information should be given to them clearly. They deserve the self-care education and glucose monitoring tools to minimize illness from hyperglycemia regardless of whether or not they fit into typical diabetes classifications. Both inpatient and primary care APRNs are well positioned to identify patients at risk, use diagnostic criteria to identify patients without prior history of diabetes, and arm them with knowledge to prevent crisis.
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A case of a patient with hyperosmolar hyperglycemic state: Implications for nurse practitioners in primary care Jennifer Hackel, DNP, GNP-BC (Assistant Clinical Professor) College of Nursing and Health Science, University of Massachusetts, Boston, Massachusetts
Keywords Diabetes; hyperglycemia; hyperosmolar; guidelines. Correspondence Jennifer Hackel, DNP, GNP-BC, College of Nursing and Health Science 30107, University of Massachusetts, Boston, 100 Morrissey Blvd., Boston, MA 02125. Tel: 734-287-7500; Fax 617-287-7527; E-mail: [email protected] Received: 30 August 2011; accepted: 14 June 2012 doi: 10.1002/2327-6924.12098
Abstract Purpose: The purpose of this case study is twofold: first, to present the pathophysiology of hyperosmolar hyperglycemic state (HHS) as it relates to a hospitalized patient with undiagnosed diabetes; the second is to increase awareness among primary care nurse practitioners (NPs) about the complexities of diagnosing less typical forms of diabetes. The case illustrates how HHS can be life threatening, how it is differentiated from diabetic ketoacidosis (DKA), and how it is treated. The importance of closer surveillance of blood glucose in high-risk individuals is highlighted. Data sources: Review of the literature and application to the case. Conclusions: HHS is a potentially lethal and preventable hyperglycemic crisis, which is in a continuum with DKA, occurring frequently in individuals with no prior diagnosis of diabetes. The incidence of HHS is increasing as the epidemic of diabetes continues. It is important for NPs to understand the pathophysiology of HHS, and identify which patients are at risk. Many high-risk patients, when under stress, develop acute hyperglycemic crisis, which begets further cardiovascular complications. Implications for practice: With improved understanding of the phenomena leading to glucose dysregulation, less typical forms of diabetes might be identified earlier and controlled. NPs in primary care are uniquely positioned to reduce the risk of hyperglycemic crises.
Case Report The hospital-based advanced practice registered nurse (APRN) came to the bedside of Mr. J after receiving a referral requesting diabetes education for his new diabetes diagnosis. Mr. J, a 47-year-old African American man, had presented to the emergency room with acute confusion 5 days previously. He and his family had just returned from a trip out of state to see relatives. The patient had only a vague recollection of his prodromal symptoms, which came on insidiously during the last days of his journey. He recalled feeling profoundly weak before he lost the ability to think clearly. As soon as the family returned home, his wife drove him directly to the closest emergency room (ER). On admission to the ER, Mr. J’s serum glucose was found to be 958 mg/dL, or about 10 times the normal concentration; his urine showed infection, but only trace ketones, excluding the diagnosis of diabetic ketoacidosis (DKA). He was admitted, and reJournal of the American Association of Nurse Practitioners 26 (2014) 595–602
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ceived over 10 L of intravenous fluid during his first day, which corrected his dehydration, weakness, and clouded cognition. Mr. J’s diagnosis, hyperosmolar hyperglycemic state, or HHS, is associated with uncontrolled diabetes. Yet he had no known diagnosis of diabetes, and believed he would not need insulin therapy upon discharge. “This problem of high blood sugar happened six months ago,” he said, “and insulin made my glucose too low; I did not need it when I got better at home. My doctor told me I don’t have diabetes; the problem only came from my prednisone pills.” The prior event of hyperglycemia requiring insulin occurred when he was placed on high doses of prednisone for sarcoidosis. Steroid therapy quieted the inflammatory process but is a well-known cause of hyperglycemia. His prednisone dose was tapered back down to 2.5 mg daily, a dose he was prescribed after his kidney transplantation 3 years prior. His antirejection program also included 595
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Table 1 Mr. J’s medication list on day 5 of his hospital admission • Levofloxacin 500 mg po daily • Metoprolol 25 mg po q6h • Fentanyl patch 25 mcg transdermal patch • Oxycodone 15 mg po q 6 h • Tacrolimus 2 mg po q 12 h • Mycophenolic acid (Cellcept) 360 mg a.m., 720 mg po q p.m.
• Prednisone 5 mg 1/2 tablet daily • Ergocalciferol 50,000 units weekly • Esomeprozole 40 mg daily • Sodium potassium phosphate oral suspension ×1 (given) • Insulin aspart sliding scale at meals
mycophenolate (Cellcept) and tacrolimus (Prograf) daily in addition to several other medications for his chronic illness management (see medication list, Table 1). Mr. J had undergone kidney transplantation from renal failure resulting from genetic factors. Past medical history included hypertension, coronary artery disease, hyperlipidemia, and lumbar spine injury resulting in chronic low back pain. Past surgical history included cadaveric renal transplant 3 years prior and coronary artery bypass grafting 4 years prior. Social history included college education, computer programmer currently on disability, and married with two children. In addition to profound hyperglycemia, his admission labs revealed several abnormal chemistries including hyponatremia and hypochloremia, as well as the elevated BUN, creatinine, and BUN: creatinine ratios related to dehydration (see Table 2). His anion gap was 18, consistent with mild acidosis, yet his urine ketone test was only trace-positive, his bicarbonate level was normal at 28 mmol/dL, and his pH was low normal at 7.35. His serum osmolality of 338 mmol/kg gave further indication that his body had lost many liters of water. The clinical picture indicated dehydration and hyperglycemia rather than ketoacidosis. His pH level confirmed he was not in DKA but HHS. His admission and the subsequent 5-day blood chemistries most important to his HHS evaluation and management are noted in Table 2. On urine culture, he was found to have more than 100,000 colonies of Klebsiella pneumoniae, resistant to penicillin, sulfa, and nitrofurantoin. He was placed on levofloxacin (Levaquin). His ECG showed new-onset atrial fibrillation for which he was placed on a beta blocker for rate control. He was also found to have a deep vein thrombosis (DVT) and was anticoagulated. His echocardiogram showed global hypokinesis with an ejection fraction of 40%, thickened left ventricle, and no enlargement of the right ventricle. His admission chest xray showed no sign of granulomas (from sarcoidosis) or active infection, though dehydration can mask infiltrates. 596
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In such a multifaceted case, a number of factors may have tipped the delicate balance of glucose regulation resulting in Mr. J’s hyperglycemia. While being on immunosuppression increased the risk of infection as well as hyperglycemia, the physiological stress of travel, enhanced by emotional stress, immobility, a high carbohydrate diet, and other risk factors also contributed to his evolving diabetes (see Figure 1). The urinary tract infection fueled the vicious cycle of hyperglycemic crisis (see Figure 2). Infection is the most common cause of HHS, and left untreated, the syndrome has a mortality rate between 10% and 50%, depending on when and where patients present in the course of their illness (Stoner, 2005). Reviewing Mr. J’s recent orders, the hospitalist team had been careful to give him adequate fluid resuscitation, yet slowly enough to avoid overwhelming his compromised heart and kidney function. Lowering the glucose level slowly is important to avoid hypoglycemia, as well as overcorrection of electrolyte disturbances (Kitabchi, Umpierrez, Fisher, Murphy, & Stentz, 2008). By the fifth day of hospitalization, Mr. J’s serum creatinine had returned to 0.82 mg/dL, indicating that his transplanted kidney was filtrating well. Kidney injury can occur with severe dehydration, particularly if rhabdomyolysis from muscle injury further complicates the patient’s acute illness, as seen in many cases of HHS (Kitabchi, Umpierrez, Miles, & Fisher, 2009).
Background and pathogenesis of hyperglycemic crisis HHS used to be considered the hyperglycemic crisis of Type 2 diabetes, distinct from DKA of Type 1 diabetes. HHS is increasingly being seen as the incidence and prevalence of diabetes increases. HHS and DKA are now seen as extremes of a spectrum of hyperglycemic syndromes, as the features of ketosis, and degrees of hyperosmolality and dehydration, can be present in both types (Nugent, 2005; Ting, 2001). HHS has gone through several diagnostic labels, including Hyperosmolar Nonketotic Coma (HONK), Hyperosmolar Hyperglycemic Nonketotic Coma (HHNC), and Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS), because coma is present in a minority of those presenting (Nugent, 2005). Both HHS and DKA have been reported in patients with either Type 1 or Type 2 diabetes, and up to a third of patients with severe hyperglycemia show an overlap in the diagnostic criteria (Nugent, 2005). However, where patients have some reserve of insulin secretion, there is less tendency toward lipolysis and ketoacidosis, and a greater severity of dehydration (Kitabchi et al., 2009). In both disorders, as glucose levels rise above the renal threshold, where glucose “spills” in to the urine, the
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Table 2 Mr. J’s lab results on admission and at day 5 Lab test
Day of admission
Result day 5
Plasma glucose Sodium Potassium Chloride Bicarbonate BUN Creatinine Calcium Anion gap Magnesium Osmolality Troponin
958 126 4.3 80 28 51 1.88 10.7 18 2.5 338 0.11
214 134 4.1 104 25 7 0.82 10.3 5 1.5
A1C
10.3%
pH
7.35
0.07
Illness induced immobility & reduced lean muscle mass
Emotional stress
Steroids for sarcoidosis
Comments
74–118 mg/dL 136–144 mmol/dL 3.2–5.2 mmol/dL 102–111 mmol/dL 22–32 mmol/dL 8–20 mg/dL 0.64–1.27 8.9–10.3 5–17 1.5–2.1 mEq/dL 280–308 mOsm/kg 0.01–0.04 ng/dL; cutoff for acute MI is 0.5 ng/dL 4.5%–5.6%
7.35–7.45
kidneys’ ability to concentrate urine becomes impaired. Because glucose must be diluted in water to be excreted, the body undergoes osmotic diuresis, and triggers thirst to correct the dehydration, causing the classic symptoms of polyuria and polydipsia. Yet other factors may blunt the thirst response, and the dehydration may blunt the polyuria. In HHS more so than with DKA, the protracted process of glucose toxicity leads to further release of stress hormones, causing a vicious cycle of insulin resistance, worsening glycemia, osmotic diuresis, hemoconcentration, intracellular dehydration, further stress hormone release, and escalating glycemia (see Figure 2). As intra-
Post transplant immunosuppressants
Reference range
Insulin resistance
Metabolic syndrome w/ BMI >25
Improved Corrected Maintained Corrected Corrected Corrected Corrected Corrected Corrected Corrected Resolving troponin leak Equiv. estimated average glucose of 250 mg/dL Low normal
cellular fluid shifts to the contracting vascular compartment, hyponatremia frequently develops. It is the development of intracellular dehydration and hyponatremia that ultimately cause the mental status changes, as well as the more profound loss of water with minimal ketogenesis, that distinguish HHS (Nugent, 2005). In both DKA and HHS, typically a precipitating event starts the upward trend to hyperglycemia. In classic DKA of Type 1 diabetes, the affected person is more severely insulin deficient, and, without it, becomes ill in hours to days. This may be from undiagnosed diabetes or a diagnosed individual missing his or her insulin therapy. It
UTI causing physiologic stress
Relative insulin deficiency
Lifestyle with high carb diet & colas
Aging (> 45)
Type 2 Diabetes African American race
Figure 1 The forces promoting diabetes in Mr. J.
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Triggering event(see Table 3) Convergence of factors causing progressive hyperglycemia and inability to correct it due to progressive dehydration
Insulin deficiency in state of high demand but enough to prevent
Stress response/stress hormone release Increased hepatic glucose production Insulin resistance
Hyperglycemia Osmotic diuresis
ketogenesis
Confusion, weakness, cardiac arrhythmias
Impaired glucose excretion in context of dehydration
Water loss
Secondary intracellular fluid and electrolyte loss to correct contracted intravascular volume
Intravascular volume contraction
Electrolyte loss
Hyperosmolality
Figure 2 The vicious cycle of hyperosmolar hyperglycemic state.
may be that the individual’s insulin needs rise precipitously with infection, rendering them too ill to comply with glucose testing and treatment before glucose escalates out of control. It is the absolute lack of insulin, which leads to lipolysis for energy, which in turn causes ketoacidosis, the hallmark of DKA. The resulting accumulation of ketoacids causes acute symptoms of illness, such as nausea, vomiting, and abdominal pain. The Kussmaul respirations, deep and rapid, are the telltale sign of compensatory respiratory alkalosis in response to ketoacidosis, and tachypnea is more pronounced in DKA than HHS (Tokuda et al., 2010). By way of comparison, the course of HHS has a less clear onset and insidious progression over days to weeks. The nausea, vomiting, abdominal pain, and tachypnea of DKA are typically absent, because ketosis is mild or nonexistent in HHS (Nugent, 2005). The more prolonged process of osmotic diuresis, without clear symptoms of overt illness, leads to the patient to show a remarkable but ultimately unhelpful adaptation, as he or she does not seek medical attention until it has escalated to a critical level. This is made worse by mental status changes, which prevent rational judgment. An isolated individual, such as an elderly person, may be more likely to reach coma before he or she is found by others. HHS has a higher mortality rate among the elderly (Kitabchi et al., 2008). In HHS, depending on its course, and when the person presents for medical attention, its variable presentation and comorbidities often delays its diagnosis and treatment. There are case reports of pulseless electrical activity from the severe dehydration and hyperkalemia associated with HHS (Ting, 2001). There are also cases 598
of focal neurologic deficits presenting like stroke or seizure that resolve with insulin and hydration (Nugent, 2005). There are cases of neuroleptic drugs such as olanzapine being implicated as the inciting cause, and the patient presents with a fever not from infection but from neuroleptic malignant syndrome (Ahuja, Palanichamy, Mackin, & Lloyd, 2010). While infection is the most common known cause of HHS, a variety of other events can trigger the process, as listed in Table 3. Table 4 lists the drugs that can predispose the person further. In the case of Mr. J, the need for prednisone contributed to the previous episode of acute hyperglycemia, but this time it appeared that the urinary tract infection may have precipitated the cascade to HHS. Further, his previous heart surgery and renal transplant are also clues that his body has been stressed to a degree that significantly increases his vulnerability to develop hyperglycemia and overt diabetes at any time, particularly in the presence of other stressors. Many cardiovascular events have been found to be both precursors and outcomes of HHS including cerebral infarct, pulmonary embolism, and myocardial infarction (Lin, Wang, & Wang, 2010). Research has shown that glucose toxicity progressing to hyperglycemic crisis is associated with release of cytokines, elevated inflammatory markers such as C-reactive protein, and activated clotting factors that resolve with hydration and insulin therapy (Kitabchi et al., 2009). It is unclear if Mr. J had started developing the DVT and elevated troponin levels during the time of his progression into HHS or from it. It is possible the condition was beginning prior to his admission given his recent air travel. The interrelationships of
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Table 3 Precipitating factors for hyperglycemic crisis (adapted from Nugent, 2005) Infection Pneumonia Urinary tract infection Sepsis Wounds or skin infections Acute illness that leads to release of stress hormones, stimulating endogenous glucose release Thromboembolic disease Stroke Deep vein thrombophlebitis or pulmonary embolus Myocardial infarction Acute/metabolic illness Acute pancreatitis Hyper- or hypothermia Intestinal obstruction Renal failure Gastrointestinal bleeding Endocrine disease Undiagnosed diabetes mellitus Cushing’s disease Acromegaly Thyrotoxicosis Major surgery Cardiac surgery Organ transplantation Other Trauma Burns Alcohol abuse Cocaine use Accidental poisoning with Vacor, a rodenticide
Table 4 Medications or other agents shown to contribute to hyperglycemic crisis Antipsychotics Beta blockers Carbemazepine Chlorpromazine Cimetidine Corticosteroids, glucocorticoids Diazoxide Didanosine Gamma interferon Immunosuppressants L-asparaginase Lithium Mannitol Neuroleptics Nicotinic acid Pentamadine Phenytoin Thiazide and loop diuretics Thyroid hormone Total parenteral nutrition
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hyperglycemia, inflammatory cytokines, the hypercoagulable state, and cardiovascular damage are undergoing research, which is confounded by the complexity and diversity of critically ill patients (Kitabchi et al., 2008).
Posthyperglycemic crisis diagnosis and discharge planning By the time the APRN met Mr. J, 5 days post admission, his confusion had entirely cleared. Mental status changes associated with HHS normalize with the correction of dehydration and electrolyte imbalance, usually in hours. Mr. J was then exhibiting no cognitive deficits and was remarkably keen: attentive to teaching, articulate in his questions, and sharp on counterdemonstration of the new skills in glucose testing and insulin administration. Nurses must assess their patients’ abilities to learn and counterdemonstrate new skills, as well as their readiness to accept responsibility for diabetes self-care. Because he expressed skepticism, based on his previous experience, that he would need these skills once he went home, the APRN had to explain that his “tendency to hyperglycemia” was now overt diabetes, a condition to which he had been at risk for years. She addressed his questions about his new diagnosis, reviewed written information on diabetes for him to read and absorb, and trained him in performing self-monitoring of blood glucose. Arming Mr. J with the tools and knowledge to assess his own random blood glucose during this session, and having him teach back its significance, helped him comprehend the importance of his taking charge of his new diagnosis. By using the event of capillary glucose testing as a “teaching moment” the APRN empowered Mr. J in becoming an active decision maker in his care instead of a passive recipient. Diabetes self-care can prevent hyperglycemic crises as well as long-term complications. The APRN offered to return when his wife was visiting so she could participate in the remainder of the teaching on meal planning, sick day management, and diabetes care goals. Mr. J’s A1c level of 10.3%, in less extenuating circumstances, would have been equivalent to an estimated average blood glucose level of about 250 mg/dL (Nathan et al., 2008); however, the HHN renders his previous average uncertain. Nonetheless, it is helpful that diagnosis of diabetes can now be based on the A1c level of 6.5% or greater, reducing the need for the difficulties involved in an oral glucose tolerance test (OGTT; American Diabetes Association, 2012).
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Classification of hyperglycemia and diabetes While it remained unclear exactly what type of diabetes Mr. J had developed and when, the critical point to consider was that he had been at risk for developing diabetes for some years, and a diagnosis of prediabetes would have been helpful in avoiding the crisis. He mistakenly thought, because his previous episode of high blood sugars resolved, he was now “cured” instead of remaining at high risk. Indeed, there are rare cases of hyperglycemic crisis followed by euglycemia. Kitabchi et al. (2009) reviewed data on cases of patients presenting in DKA, who go into remission after the crisis where insulin therapy is no longer needed, sometimes for years, after glycemic correction. This represents atypical diabetes mellitus (ADM), also known as Flatbush diabetes, coined for patients presenting with ketoacidosis consistent with complete insulin deficiency who had return of insulin secretion after glucose normalization (often confirmed by C-peptide testing), and no evidence of beta-cell autoimmunity (Rasouli & Elbein, 2004). These cases with ADM are noted most commonly among Blacks and Hispanics, as well as Native Americans and Asians, more so than Caucasians (Kitabchi et al., 2008), a predominance mirrored in the epidemiology of Type 2 diabetes. However, the caveat is that such patients still have a diagnosis of diabetes, usually Type 2, even if it has reverted to “diet controlled.” Mr. J was under the impression he was at low risk for Type 2 diabetes based on his relatively young age, lack of obesity, and lack of known family history. However his history argues for elevated risk based on age over 45, African American race, and presence of metabolic syndrome factors including hyperlipidemia and hypertension, as well as loss of lean body mass from immobility. The convergence of contributing factors to Mr. J’s diagnosis are noted in Figure 1. Mr. J wondered if he perhaps had “Hospital-related Hyperglycemia,” a syndrome in which a critically ill patient’s glucose is in diabetic ranges in the hospital but converts to normal levels after discharge. This syndrome of acute stress-induced glucose dysregulation is in the center of a large controversy over assessing and managing the glucose levels of ill inpatients regardless of their history of known diabetes (Kosiborod et al., 2009). Prevalence in various studies in intensive care units of academic medical centers find it occurring in 23%–60% of patients (Kovalaske & Gandhi, 2009). There are no definitive epidemiologic data yet available to indicate what percentage of such persons without a known diagnosis of diabetes in fact show normal glucose tolerance thereafter if they remain healthy. It is safest to consider all such persons as remaining at 600
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high risk for diabetes, and order an A1C or OGTT to elucidate their glucose regulation status 6–8 weeks after discharge. The American Diabetes Association recommends use of an A1C level of 5.7%–6.4% to diagnosis prediabetes, and 6.5% or higher to confirm the diagnosis of diabetes (American Diabetes Association, 2012). Meanwhile, the APRN considered the possibility that Mr. J had NODAT, the acronym for new-onset diabetes after transplantation. This diabetes syndrome is an increasingly noted phenomenon with the advent of organ transplantation becoming commonplace in mainstream medical care. In one study of over 21,000 patients receiving renal transplant, more than 19% developed new onset of diabetes within 3 years, and 58% of these individuals already had at least one complication of diabetes at diagnosis (Burroughs et al., 2007). It remains unclear why diabetes mellitus occurs more commonly and complications develop more rapidly in this subgroup, though many hypotheses are being tested. While a genetic predisposition is one theory, the diabetogenic effect of immunosuppressant therapy such as tacrolimus has also been implicated, which would apply to Mr. J. In one study, subjects with impaired oral glucose tolerance prior to transplantation showed an increased risk of developing NODAT after transplantation; repeating an OGTT after transplantation was superior to using fasting glucose levels to identify high-risk patients developing NODAT (Delgado et al., 2008). When using the A1C for diagnosis, care should be taken to be sure there is not significant anemia, common among hospitalized patients with renal disease, which may invalidate the A1c level. Perhaps if Mr. J did have an A1c drawn by his primary care provider (PCP), it was not valid because of previous anemia.
The role of discharge planning and primary care Mr. J was eventually discharged on glipizide (Glucotrol) 5 mg twice daily, metformin (Glucophage) 500 mg twice daily, and 10 units of glargine (Lantus) insulin at bedtime. He was given a referral to an endocrinologist, outpatient diabetes education, and an appointment for followup with his PCP. The APRN educated him in the use of the insulin pen and the glucose meter and made sure he had prescriptions for these supplies at his outpatient pharmacy. Such proactive management after his previous episode of hyperglycemia may have prevented his current life-threatening illness. The critical difference in terms of prevention of severity of illness and hospitalization of persons developing hyperglycemic crisis is the time available to stop the process. Inpatient nurses and PCPs have the opportunity to
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prevent serious illness in their patients with diabetes, or in their patients at high risk to develop it, by empowering them with knowledge. Self-monitoring of glucose and sick day management education should lead patients to hydrate themselves and contact providers early for assistance in management of hyperglycemia before it escalates out of control. The cost cannot be measured when a person such as Mr. J has a lengthy hospitalization rendering him unable to function because of critical illness, let alone the damage his diseased heart and transplanted kidney endured. Patients with this history, particularly those such as Mr. J who remain on diabetogenic medications, should be educated while in the hospital regarding the basics of blood glucose regulation and dietary principles of control. They should not only be trained in home glucose monitoring and provided with a monitor, lancets, and test strips, but be given clear instruction regarding bringing their glucose monitoring meter and log to their PCP for follow-up. A diagnosis such as “Atypical Diabetes” or “Prediabetes” and not just “Hospital Related Hyperglycemia” should be added to the problem summary list in the primary care setting to induce adequate followup in transition of care to the community setting. Knowing the tendency of a person to develop diabetes (and therefore hyperglycemic crisis) and taking preventive action saves many healthcare dollars and improves quality of life. This is a critical piece of the current healthcare reform. If patients are homebound, they can benefit from a visiting nurse for follow-up of home glucose levels. Visiting nurses can offer an important contribution to patients and families’ comprehension of day-to-day glucose control, stress or sick day management, and menu planning. While inpatient diabetes education is important, it is also difficult to achieve, and the discharge orders that include referral to community health nurses and outpatient diabetes education will offer benefit at a fraction of the cost of rehospitalization. If the diagnosis of diabetes is unconfirmed in high-risk patients, PCPs should avoid giving false reassurance. Instead, diligence in educating patients in healthy eating, exercise, and close monitoring of glucose status should be encouraged. Patients with an A1C between 5.7% and 6.4% should be given a diagnosis of prediabetes. An OGTT is rarely needed now with the common use of A1C, but may be helpful to look for abnormal postchallenge glucose levels or further assess anemic patients (Simmons, Echouffo-Tcheugui, & Griffin, 2010). APRNs such as primary care nurse practitioners (NPs), whose practice philosophy emphasizes prevention, patient education, and the therapeutic alliance, can help at-risk individuals to be on alert for worsening glycemia, especially during stress, illness, or trauma.
Conclusion Mr. J’s case demonstrates that individuals who have undergone organ transplantation, and have a history of acute hyperglycemia, particularly those with African American or Hispanic ancestry, are at much greater risk of developing diabetes. The complication of HHS is potentially lethal and increasingly common as individuals undergo organ transplantation, survive stressful complex illnesses and surgeries, and take medications that worsen glucose tolerance. HHS has an insidious onset and may be challenging to promptly diagnose. It requires intensive, careful treatment to rehydrate the patient, correct electrolyte disturbances, normalize blood glucose, and minimize collateral physiologic damage. The crisis might have been prevented if Mr. J had been adequately forewarned of his elevated risk. While patients such as Mr. J may show some remission of hyperglycemia after illness, they remain at high risk for diabetes and this information should be given to them clearly. They deserve the self-care education and glucose monitoring tools to minimize illness from hyperglycemia regardless of whether or not they fit into typical diabetes classifications. Both inpatient and primary care APRNs are well positioned to identify patients at risk, use diagnostic criteria to identify patients without prior history of diabetes, and arm them with knowledge to prevent crisis.
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