Hyperglycemic Hyperosmolar Nonketotic Syndrome Research Articles

The effectiveness of booklets on family knowledge of diabetes mellitus patients about the management of hypoglycaemia

The three main acute complications of diabetes mellitus related to an imbalance in glucose levels that lasted in the short term were hypoglycemia, diabetic ketoacidosis (DKA), and hyperglycemic hyperosmolar nonketotic syndrome. The family, as the people closest to and always interacting with the patient, played a significant role in preventing complications. A booklet served as one medium to increase knowledge for families. This study aimed to determine the effectiveness of the booklet on the knowledge of families of DM patients regarding the management of hypoglycemia. A quantitative method with a quasi-experimental design approach involving pre-test and post-test designs was employed. The population in this study comprised families of Diabetes Mellitus patients who were at Puskesmas (Public Health Centre) Batu X and Puskesmas Mekarbaru, Indonesia. The research sample consisted of 70 respondents selected through purposive sampling. The research variables included demographic factors, family knowledge before and after the intervention in the intervention and control groups, and bivariate analysis. The research instrument employed a questionnaire and a booklet regarding the management of hypoglycemia. Independent t-test analysis was conducted (α = 0.05). The booklet proved effective in improving the knowledge of families of diabetes mellitus patients regarding the management of hypoglycemia, with a p-value of 0.028. The booklet can enhance family knowledge about the management of hypoglycemia. Therefore, every internal medicine clinic or health centre should provide booklets as an educational medium.

Differences between hyperglycemic hyperosmolar non-ketotic syndrome and diabetic ketoacidosis

Since high blood glucose levels might result from inadequate insulin levels, diabetic ketoacidosis is more commonin those with insulin-dependent diabetes mellitus. Diabetic ketoacidosis develops only when there is insufficientinsulin in the body to convert blood sugar into energy. The liver then uses the acids created by this process,known as ketones, to breakdown fat for energy. Osmotic diuresis, which results in significant amounts of urineproduction and volume depletion, as well as dehydration, occurs when an excessive amount of glucose entersthe renal tubules of an individual with diabetes. Non-insulin-dependent diabetes mellitus can be more likely tocause hyperglycemic hyperosmolar non-ketotic syndrome. More often than not, people with non-insulin-dependentdiabetes mellitus who do not have their diabetes under control will experience hyperglycemic and hyperosmolarnon-ketotic syndrome. The majority of cases of hyperglycemic hyperosmolar non-ketotic syndrome occur in peoplewith non-insulin-dependent diabetes mellitus who also have another condition that reduces fluid intake.

Differences Between Hyperglycemic Hyperosmolar Non-Ketotic Syndrome and Diabetic Ketoacidosis

Since high blood glucose levels might result from inadequate insulin levels, diabetic ketoacidosis is more common in those with insulin-dependent diabetes mellitus. Diabetic ketoacidosis develops only when there is insufficient insulin in the body to convert blood sugar into energy. The liver then uses the acids created by this process, known as ketones, to breakdown fat for energy. Osmotic diuresis, which results in significant amounts of urine production and volume depletion, as well as dehydration, occurs when an excessive amount of glucose enters the renal tubules of an individual with diabetes. Non-insulin-dependent diabetes mellitus can be more likely to cause hyperglycemic hyperosmolar nonketotic syndrome. More often than not, people with non-insulin-dependent diabetes mellitus who do not have their diabetes under control will experience hyperglycemic and hyperosmolar non-ketotic syndrome. The majority of cases of hyperglycemic hyperosmolar non-ketotic syndrome occur in people with non-insulin-dependent diabetes mellitus who also have another condition that reduces fluid intake.

Outcomes in Hospitalizations for Patients Admitted With Hyperosmolar Hyperglycemic State and Obesity: Analysis of National Inpatient Sample

Introduction: Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHS) is a highly lethal disease with an estimated mortality rate of up to 20%. Although mortality has decreased in recent years, its incidence has increased in the setting of a higher prevalence of underlying conditions that have been previously well described, such as uncontrolled diabetes, Obesity, and a high-carbohydrate diet. All these comorbidities usually overlap with acute complications such as infections or dehydration, which incite the onset of HHS. Currently, limited literature exists for the role of obesity in mortality, hospital stay, and other adverse outcomes in patients with HHS. It is important to know which underlying conditions truly affect outcomes for patients being treated for this condition so further studies can be done, and treatment optimized. Objective: We aim to prove if obesity plays a role in increasing mortality and secondary adverse outcomes in patients with HHS compared to non-obese patients. Methods: A retrospective cohort study was conducted using the Nationwide Inpatient Sample from 2016 and 2017. 42,740 hospitalizations who had HHS as primary diagnosis were enrolled and further stratified based on the presence or absence of Obesity as a secondary diagnosis using ICD-10 codes. The primary outcome was inpatient mortality and secondary outcomes included length of hospital stay, total hospital charges, Sepsis, Septic Shock, Acute Kidney Injury (AKI), and Acute Respiratory Failure (ARF). Multivariate regression analysis was done to adjust for confounders. Results: Out of the 42 740 hospitalizations with HHS, 9,630 had Obesity. The in-hospital mortality for patients with HHS was 45 overall, out of which 45 patients had Obesity as a secondary diagnosis. Compared with patients without Obesity, non-obese patients had similar in-hospital mortality (OR 0.77, 95% CI 0.39–1.52, p=0.45) when adjusted for patient and hospital characteristics. Patients with HHS and Obesity had similar lengths of hospital stay, total hospital charges, rate of Sepsis, Septic Shock, and ARF in comparison to patients without Obesity; however, non-obese patients had higher odds of developing AKI throughout hospitalization. Conclusion: Although it is known and described that being obese plays a significant role in the onset of diabetes, and consequently HHS, there is no statistically significant difference in mortality or most other adverse outcomes compared to patients that are not obese and develop HHS. Although being obese plays a major role in inciting HHS in the general population, there is no need for a different approach to treatment, and outcomes are similar to non-obese patients with HHS.

Eating and Glycemic Control Among Critically Ill Patients Receiving Continuous Intravenous Insulin

Objective: Consensus guidelines recommend that intensive care unit (ICU) patients with blood glucose (BG) levels >180 mg/dL receive continuous intravenous insulin (CII). The effectiveness of CII at controlling BG levels among patients who are eating relative to those who are eating nothing by mouth (nil per os; NPO) has not been described. Methods: We conducted a retrospective cohort study of 260 adult patients (156 eating, 104 NPO) admitted to an ICU between January 1, 2014, and December 31, 2014, who received CII. Patients were excluded for a diagnosis of diabetic ketoacidosis or hyperglycemic hyperosmolar nonketotic syndrome, admission to an obstetrics service, or receiving continuous enteral or parenteral nutrition. Results: Among 22 baseline characteristics, the proportion of patients receiving glucocorticoid treatment (GCTx) (17.3% eating, 37.5% NPO; P<.001) and APACHE II score (15.0 ± 7.5 eating, 17.9 ± 7.9 NPO; P = .004) were significantly different between eating and NPO patients. There was no significant difference in the primary outcome of patient-day weighted mean BG overall (153 ± 8 mg/dL eating, 156 ± 7 mg/dL NPO; P = .73), or day-by-day BG (P = .37) adjusted for GCTx and APACHE score. Surprisingly, there was a significant difference in the distribution of BG values, with eating patients having a higher percentage of BG readings in the recommended range of 140 to 180 mg/dL. However, eating patients showed greater glucose variability (coefficient of variation 23.1 ± 1.0 eating, 21.2 ± 1.0 NPO; P = .034). Conclusion: Eating may not adversely affect BG levels of ICU patients receiving CII. Whether or not prandial insulin improves glycemic control in this setting should be studied. Abbreviations: BG = blood glucose; CII = continuous insulin infusion; CV = coefficient of variation; HbA1c = hemoglobin A1c; ICU = intensive care unit; NPO = nil per os; PDWMBG = patient day weighted mean blood glucose.

Clinical Activity of CC-90009, a Cereblon E3 Ligase Modulator and First-in-Class GSPT1 Degrader, As a Single Agent in Patients with Relapsed or Refractory Acute Myeloid Leukemia (R/R AML): First Results from a Phase I Dose-Finding Study

Clinical Activity of CC-90009, a Cereblon E3 Ligase Modulator and First-in-Class GSPT1 Degrader, As a Single Agent in Patients with Relapsed or Refractory Acute Myeloid Leukemia (R/R AML): First Results from a Phase I Dose-Finding Study

Left Lower Arm Hemichorea: An Unusual Presentation of New-Onset Type 2 Diabetes.

Diabetes mellitus is a growing public health concern and a chronic metabolic disease worldwide. The most common clinical manifestations at the onset of diabetes are blurry vision, weight loss, polyuria, polydipsia, and polyphagia. Neurological symptoms are rare but have been reported to be associated with initial presentation of type 2 diabetes, especially hyperglycemic hyperosmolar nonketotic syndrome (HHNS). Hemichorea-hemiballism (HCHB) is a spectrum of involuntary, continuous, nonpatterned movements involving one side of the body that is usually caused by a variety of hereditary neurological diseases, metabolic disorders, post-rheumatic fever sequelae, strokes, and other vascular diseases. Herein, we report the case of a man with left-side arm hemichorea (HC) who presented with HHNS and had resolution of his symptoms when his blood glucose was back under control. This case report highlights the association between HC and HHNS and reinforces the need to recognize HHNS promptly, especially in elderly patients who present with a neurological complaint. A 72-year-old Caucasian man presented with a 2-week history of progressive writhing movements of his left arm, with occasional sudden amplitude excursions, associated …

Hyperglycemic Hyperosmolar Nonketotic Syndrome with Rhabdomyolysis in a Patient with Newly-Onset Diabetes: One Case Report and Literature Review

Hyperglycemic Hyperosmolar Nonketotic Syndrome with Rhabdomyolysis in a Patient with Newly-Onset Diabetes: One Case Report and Literature Review

Type 2 Diabetes in Children and Adolescents

Type 2 Diabetes in Children and Adolescents

Electrolyte-free water clearance: a clinical utility in managing osmotic urea diuresis-associated polyuria in tube feeding syndrome

Hypernatremia is a common problem in critically ill patients. Part of the reason for the inadequate treatment of hypernatremia may be that we tend to replace only the free water deficit (FWD) and neglect replacing ongoing losses of free water. In most cases, ongoing losses of free water occur in the urine, the quantity of which can be easily calculated using the electrolyte free water clearance (EFWC). We report a case of man presenting with tube feeding syndrome (TFS) and hyperglycemic hyperosmolar nonketotic syndrome (HHNS). He developed life-threatening hypernatremia from an osmotic urea diuresis that was appropriately treated by replacing both the FWD as well as ongoing free water losses calculated from the EFWC. A 37 year-old man in a persistent vegetative state from a left thalamic hemorrhage status post ventriculostomy and PEG tube placement was admitted with sepsis and HHNS. He was receiving large amounts of Jevity 1.2. He had acute kidney injury due to severe volume depletion from an osmotic urea diuresis. BUN was 200 mg/dL, sodium was 165 mEq/L, glucose was 635 mg/dL, and serum osmolality was 449 mOsm/kg. To prevent the development of cerebral edema from overly rapid correction of hyperosmolality, he was started on an insulin drip and hypernatremia was allowed to persist until the hyperglycemia was fully normalized. This was followed by correcting the hypernatremia over 3 days. He was urinating up to about 4 L/day of mostly electrolyte free water. Using the FWD to arrive at the rate of free water administration, he would only have received 2 L of free water per day and hypernatremia would have persisted. Instead, he required about 4.5 L/day of free water as calculated by the FWD and EFWC together, and his hypernatremia resolved as expected. Our patient presented with a triad of TFS including hypernatremia, dehydration, and azotemia. Rapidly increased fluid loss from sepsis and HHNS initially caused severe hypernatremia. Only by using the combination of FWD and EFWC calculations could we have arrived at the appropriate rate of free water administration.

Characteristics and outcomes of the hyperglycemic hyperosmolar non-ketotic syndrome in a cohort of 51 consecutive cases at a single center

Aims The hyperglycemic hyperosmolar syndrome (HHS) is a life-threatening diabetic complication. We aimed to portrait the short and long term outcome after a HHS episode and to describe features associated with increased early mortality. Methods We collected data from consecutive HHS cases, defined based on rigorous glucose and osmolality criteria. We retrieved anthropometric measures, history of diabetes, other cardiovascular risk factors and chronic co-morbidity. Clinical and biochemical parameters were recorded at admission, after 24 h and at discharge. We assessed incidence of complications, as well as short (≤30 days) and long term mortality. Results Patients were about 80-year old. Fifty-one cases were included, characterized by severe hyperglycemia (55.5 mosm/L) and hyperosmolality (385 mosm/L). Thirty-three percent developed at least one complication. Short term mortality was 16%; lower Glasgow Coma Scale, higher plasma glucose and mild acidosis were predictive of short term mortality. The long term mortality (median follow-up 1.27 years) was not significantly different from historical mortality data after hypoglycemic coma. Conclusion In this study, early mortality of HHS was 16% and some clinical features at presentation were predictive of an adverse short term outcome. Long term survival after a HHS episode did not appear to be severely impaired.

Hyperglycemic Hyperosmolar State: An Emerging Pediatric Problem

n his 1886 Bradshawe lecture on diabetic coma, Dreschfeld described a relatively uncommon form that he and other European authors had noted, in which dyspnea and the acetone smell of the breath were absent, and the urine did not contain acetone or aceto-acetic acid. He described a clinical presentation of shock occurring chiefly, but not exclusively, in older people who had diabetes symptoms for some time and were, ‘‘still stout and well-nourished at the time of attack.’’ Despite this early description and occasional subsequent reports of diabetic coma without significant ketosis/acidosis, the report of Sament and Schwartz in 1957 is widely credited as the original description of what has been variously referred to as hyperosmolar nonketotic coma, hyperglycemic hyperosmolar nonketotic syndrome, hyperosmolar nonacidotic uncontrolled diabetes, diabetic hyperosmolar state, and hyperglycemic hyperosmolar coma or syndrome (HHS). Although the 1957 herald case was a thin young man of 32 years with new-onset diabetes, the usual adult patient with HHS is more consistent with Dreschfeld’s original description, occurring in an elderly, often disabled, person with type 2 diabetes (T2D). The designation HHS has been in general use for more than a decade, recognizing that there can be altered sensorium without true coma and mild to moderate ketosis in the typical syndrome. The term HHS also recognizes that there is a continuum from typical diabetic ketoacidosis (DKA) without substantial hyperosmolality to typical HHS, rather than always a clear distinction between the two diabetes coma syndromes. Proposed criteria for HHS are plasma glucose concentration >600 mg/dL (33.3 mmol/L), serum carbon dioxide concentration [CO2] >15 mmol/L, no or small ketonuria, absent to small ketonemia, effective serum osmolarity >320 mOsm/L, and stupor or coma. However, acidosis with depressed [CO2] may be present in the absence of substantial ketosis in these patients as the result of dehydration and lactic acidosis, and coma is not constant. In adults, approximately one third of hyperglycemic emergencies involve a mixed state of ketoacidosis and hyperosmolarity, with the degree of hyperosmolarity but not acidosis being an independent predictor of mortality. From the first report of HHS in a child in 1966 until 35 years later, 26 pediatric cases had been described, but in only 8 years, from 2001 to 2008, there were 65 cases reported, thought to be related to the increase in frequency of pediatric

Approach to management of malignant hyperthermia-like syndrome in pediatric diabetes mellitus

Hyperglycemic hyperosmolar nonketotic syndrome (HHNS) is usually associated with type 2 diabetes mellitus and is rare in children. However, a fatal malignant hyperthermia-like syndrome (MHLS) with rhabdomyolysis associated with new-onset diabetes mellitus and HHNS in adolescents has been described. Case series. A 16-yr-old obese male (case A) and a 10-yr-old mid-pubertal nonobese female (case B) presented within a 6-month period with emesis, altered mental status, blood glucose >1600 mg/dL, and laboratory evidence of rhabdomyolysis. Case A developed fever after initiation of insulin therapy, along with refractory hypotension and multiorgan failure. He died 14 hrs after admission. Case B developed fever before insulin therapy, was treated with dantrolene, and made a full recovery. Metabolic workup showed evidence of short-chain acyl-CoA dehydrogenase (SCAD) deficiency. We report two cases of malignant hyperthermia-like syndrome associated with HHNS in adolescents. Their respective fluid management and clinical courses are described. Dantrolene therapy should be initiated immediately after this syndrome is recognized. We believe it is unlikely insulin is the sole trigger for MHLS. Case B is unique in that there was evidence of SCAD deficiency, a metabolic defect that we propose could lead to MHLS. We recommend that all patients with HHNS and MHLS be evaluated for an underlying metabolic disorder.

Hyperglycemic hyperosmolar nonketotic syndrome

Hyperglycemic hyperosmolar nonketotic syndrome (HHNS) was infrequently diagnosed till recently. Now it is being diagnosed with increasing frequency in obese children with type 2 diabetes mellitus (T2 DM) and its incidence is likely to go up, given global increase in incidence of childhood obesity, increased insulin resistance, and T2 DM. The syndrome is characterized by severe hyperglycemia, a marked increase in serum osmolality and dehydration without accumulation of beta -hydroxybutyric or acetoacetic ketoacids. Significant ketogenesis is restrained by the ability of the pancreas to secrete small amount of insulin. Prolonged phase of osmotic diuresis leads to severe depletion of body water, which excees that of sodium, resulting in hypertonic dehydration. These children, usually obese adolescents with T2 DM, present with signs of severe dehydration and depressed mental status but continue to have increased rather than decreased urine output and are at increased risk of developing rhabdomyolysis and malignant hyperthermia. Emergency treatment is directed at restoration of the intravascular volume, followed by correction of deficits of fluid and electrolyte (Na+, K+, Ca++, Mg++, PO4++), hyperglycemia and serum hyperosmolarity, and a thorough search for conditions that may lead to this metabolic decompensation and their treatment. Use of iso-osomolar isotonic fluid (0.9% saline) until hemodynamic stabilization initially, followed by 0.45% saline with insulin infusion at the rate of 0.1 units/kg/hour, addition of 5% dextrose in fluids and reduction of insulin infusion once the blood glucose is 250 to 300 mg/dl is generally recommended. However, evidence-based guidelines about composition and tonicity of fluids and electrolyte solutions for early resuscitation and rehydration, the rate of infusion-rapid vs slow, and insulin dose-low vs normal, in treatment of HHNS in children are awaited. Careful monitoring of glucose levels and ensuring adequate hydration in patients 'at risk' of HHNS, including those receiving medications that interfere with the secretion or effectiveness of insulin should decrease the risk of HHNS.

Metabolic hyperglycemic emergencies with acute pancreatitis in a child with known insulin-dependent diabetes mellitus

The combined clinical and biochemical profile of diabetic ketoacidosis, hyperglycemic hyperosmolar non-ketotic syndrome, complicated by acute pancreatitis, in an 11-year-old with established insulin-dependent diabetes mellitus, is presented. The management requires diligent correction of dehydration and hyperglycemia, while monitoring neurological status and blood chemistry. It is imperative to monitor and avoid potentially fatal complications of the combined entity, namely, cerebral edema, thromboembolism, acute respiratory distress syndrome and rhabdomyolysis. Excluding acute pancreatitis in the face of persistent abdominal pain in this setting is emphasized.

Hyperglycemic hyperosmolar non-ketotic syndrome in children with type 2 diabetes*

Hyperglycemic hyperosmolar non-ketotic (HHNK) syndrome is thought to be a rare entity in the pediatric population, associated with significant mortality based on case reports in the literature. As obesity and type 2 diabetes in childhood grow in prevalence, such related complications may also increase. This study will serve to provide updated information regarding typical clinical course and sequelae of HHNK syndrome in childhood. Patients diagnosed with type 2 diabetes at Children's Hospital of Philadelphia (CHOP) over a period of 5 yr were screened retrospectively for any laboratory evidence of previous episodes of HHNK syndrome. The standard diagnostic criteria of blood glucose >600 mg/dL and serum osmolality >330 mOsm/L with only mild acidosis (serum bicarbonate >15 mmol/L and small ketonuria 15 mg/dL or less) were utilized. The records of all patients with type 2 diabetes mellitus (DM) diagnosed over a 5-yr period were reviewed (n=190). Seven patients were found to have one episode of HHNK syndrome by diagnostic criteria (five males, mean age at presentation 13.3 yr, age range 10.1--16.9 yr), yielding a frequency of 3.7%. All were African-American. HHNK syndrome was the clinical presentation at diagnosis of new onset diabetes for all seven children. Three of seven children had a previously diagnosed developmental delay. The average Glasgow Coma Scale (GCS) score at presentation was 13 (range 9--15). Mean body mass index (BMI) at presentation was 32.7 kg/m(2) (n=6). Mean serum osmolality was 393 mOsm/L (n=7), and mean blood glucose was 1604 mg/dL (n = 7). The average time until mental status returned to baseline among survivors was 3 d (range 1--7 d). The average number of hospital days for survivors was 10 (range 5--24 d). Four of seven patients had an uncomplicated course. One patient developed multisystem organ failure and died on hospital day 4. The case fatality rate was 14.3% (one of seven). Survivors had no appreciable neurodevelopmental sequelae. This retrospective chart review provides updated information regarding the entity of HHNK syndrome in children. This study supports the need for increased awareness of type 2 diabetes in children so that morbidity and mortality related to HHNK syndrome can be prevented.

Hyperglycemic Hyperosmolar Nonketotic Syndrome in a Child With Acute Lymphoblastic Leukemia Undergoing Induction Chemotherapy

Hyperglycemic hyperosmolar nonketotic syndrome, a life-threatening complication commonly associated with uncontrolled type 2 diabetes mellitus in adults, is characterized by severe hyperglycemia, a marked increase in serum osmolality, and clinical evidence of dehydration without the accumulation of beta-hydroxybutyric or acetoacetic ketoacids. There is a variable alteration in sensorium. The syndrome has been rarely reported in children with leukemia undergoing induction therapy. The authors' aim is to sensitize physicians to this life-threatening illness, which can be treated effectively if diagnosed early.

DIABETES EMERGENCIES IN THE PATIENT WITH TYPE 2 DIABETES

Type 2 diabetes has traditionally been associated with the development of hyperglycemic hyperosmolar nonketotic syndrome (HHNKS), yet evidence suggests that diabetic ketoacidosis (DKA) is increasing among this population. Patients with type 2 diabetes may develop DKA or HHNKS and require hospitalization. In addition, patients with type 2 diabetes, hospitalized for other medical or surgical conditions, are clearly at risk for the development of metabolic decompensation during hospitalization. This article explores the acute complications of type 2 diabetes and some of the issues associated with managing these patients in the hospital setting.

DIABETIC KETOACIDOSIS AND HYPERGLYCEMIC HYPEROSMOLAR NONKETOTIC SYNDROME

Diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar nonketotic syndrome (HHNS) are life-threatening acute metabolic complications of diabetes mellitus. Although there are some important differences, the pathophysiology, the presenting clinical challenge, and the treatment of these metabolic derangements are similar. Each of these complications can be seen in type 1 or type 2 diabetes, although DKA is usually seen in patients with type 1 diabetes and HHNS in patients with type 2 disease. The clinical management of these syndromes involves careful evaluation and correction of the metabolic and volume status of the patient, identification and treatment of precipitating and comorbid conditions, a smooth transition to a long-term treatment regimen, and a plan to prevent recurrence.

Hyperglycemic Crises in Urban Blacks

The hospital admission and mortality rates of patients with diabetic emergencies, such as diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar nonketotic syndrome (HHNS), are higher in black patients than in white patients with diabetes. However, there is limited data describing the precipitating events and response to treatment in black patients. Analysis of their clinical characteristics and response to medical therapy is needed to evaluate the impact of programs designed to reduce the development of these acute metabolic complications. A prospective evaluation was conducted of 144 consecutive patients with DKA and 23 patients with HHNS admitted to a large inner-city hospital between July 1993 and October 1994. In patients previously diagnosed as having diabetes, poor compliance with insulin therapy was the major precipitating cause for DKA (49%) and HHNS (42%). Alcohol or cocaine abuse was a contributing factor for noncompliance and was present in 35% and 13% of patients with DKA and in 44% and 9% of patients with HHNS, respectively. Newly diagnosed diabetes accounted for 17% of patients with DKA and HHNS. Obesity (body mass index > 28 kg/m2 [the weight in kilograms divided by the square of the height in meters]) was present in 29% of patients with DKA and in 17% with HHNS and was most common in patients with DKA who were newly diagnosed as having diabetes (56%). Patients were treated by residents, who used a low-dose insulin protocol with an algorithm for insulin adjustment in 88 of 144 patients with DKA and 14 of 23 patients with HHNS. Although there was no difference in mortality rates or time needed to correct hyperglycemia or ketoacidosis, the use of the protocol significantly reduced the risk of hypoglycemia (5%) compared with patients treated without a protocol (23%) (P < .01). In urban black patients, poor compliance with insulin therapy was the main precipitating cause of acute metabolic decompensation, and substance abuse was a significant contributing factor for noncompliance. Obesity is common in black patients with DKA; it was present in more than half of those with newly diagnosed diabetes. Improved patient education and better access to medical care might reduce the development of these hyperglycemic emergencies.