We compared a low dose 0. Leese, G. They can kettoacidosis.

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Acute complications of diabetes - Hyperosmolar hyperglycemic nonketotic state - Khan Academy

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Inpatients who ketoacisosis hypoglycaemia are likely to experience a krtoacidosis duration hyprosmolar hospital stay and Diabetiv mortality. This Hperosmolar describes the clinical presentation, Diabrtic causes, diagnosis and acute management of these diabetic emergencies, including a discussion of practical strategies for their prevention.

This is a preview of subscription content, access via your institution. Kitabchi, A. Hyperglycemic crises in adult patients with diabetes. Diabetes Care 32— Article PubMed PubMed Central CAS Google Scholar.

Centers for Disease Control and Prevention. Fishbein, H. in Diabetes in America 2nd edn Ch. Google Scholar. Pasquel, F. Hyperosmolar hyperglycemic state: a historic review of the clinical presentation, diagnosis, and treatment. Diabetes Care 37— Geller, A. et al.

National estimates of insulin-related hypoglycemia and errors leading to emergency department visits and hospitalizations.

JAMA Int. Article CAS Google Scholar. Krikorian, A. Comparisons of different insulin infusion protocols: a review of recent literature.

Care 13— Article CAS PubMed Google Scholar. Umpierrez, G. Randomized study of basal-bolus insulin therapy in the inpatient management of patients with type 2 diabetes RABBIT 2 trial. Diabetes Care 30— Umpierrez, E. Randomized study of basal bolus insulin therapy in the inpatient management of patients with type 2 diabetes undergoing general surgery RABBIT 2 surgery.

Diabetes Care 34— Basu, A. Persisting mortality in diabetic ketoacidosis. Malone, M. Characteristics of diabetic ketoacidosis in older versus younger adults. Bhowmick, S. Hyperosmolar hyperglycemic crisis: an acute life-threatening event in children and adolescents with type 2 diabetes mellitus.

Article PubMed Google Scholar. Fadini, G. Characteristics and outcomes of the hyperglycemic hyperosmolar non-ketotic syndrome in a cohort of 51 consecutive cases at a single center. Diabetes Res. McCoy, R. Increased mortality of patients with diabetes reporting severe hypoglycemia.

Diabetes Care 35— Article PubMed PubMed Central Google Scholar. Management of hyperglycemic crises in patients with diabetes. Diabetes Care 24— Hyperglycemic crises in urban blacks.

Boucai, L. Hypoglycemia-associated mortality is not drug-associated but linked to comorbidities. Kosiborod, M. Relationship between spontaneous and iatrogenic hypoglycemia and mortality in patients hospitalized with acute myocardial infarction. JAMA— Garg, R. Hypoglycemia, with or without insulin therapy, is associated with increased mortality among hospitalized patients.

Diabetes Care 36— Finfer, S. Hypoglycemia and risk of death in critically ill patients. Carey, M. Impact of hypoglycemia in hospitalized patients. Diabetes Rep.

Article Google Scholar. Rhoads, G. Contribution of hypoglycemia to medical care expenditures and short-term disability in employees with diabetes. Turchin, A. Hypoglycemia and clinical outcomes in patients with diabetes hospitalized in the general ward.

Randall, L. Recurrent diabetic ketoacidosis in inner-city minority patients: behavioral, socioeconomic, and psychosocial factors. Taylor, S. SGLT2 inhibitors may predispose to ketoacidosis.

Peters, A. Euglycemic diabetic ketoacidosis: a potential complication of treatment with sodium-glucose cotransporter 2 inhibition. Diabetes Care 38— Ennis, E. The hyperosmolar hyperglycemic syndrome. Diabetes Rev.

Foster, D. The metabolic derangements and treatment of diabetic ketoacidosis. McGarry, J. Regulation of hepatic fatty acid oxidation and ketone body production.

Regulation of ketogenesis and the renaissance of carnitine palmitoyltransferase. Diabetes Metab. Reichard, G. Jr, Skutches, C. Acetone metabolism in humans during diabetic ketoacidosis.

Diabetes 35— Gerich, J. Clinical and metabolic characteristics of hyperosmolar nonketotic coma. Diabetes 20— Abdominal pain in patients with hyperglycemic crises.

: Diabetic ketoacidosis vs hyperglycemic hyperosmolar syndrome

Management of Hyperglycemic Crises: Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar State	Indian J. Learn more. Thank you for visiting nature. Diabetic ketoacidosis and related events in the canagliflozin type 2 diabetes clinical program. Reproduced from Kitabchi et al. See Diabetes physiology review.
The Etiology of DKA Vs HHS	Winter, R. Elevated serum sialic acid concentration in NIDDM and its relationship to blood pressure and retinopathy. Kitabchi AE, Ayyagari V, Guerra SMO, Medical House Staff: The efficacy of low dose versus conventional therapy of insulin for treatment of diabetic ketoacidosis. Article CAS Google Scholar Morris LR, Murphy MB, Kitabchi AE. This Feature Is Available To Subscribers Only Sign In or Create an Account. When insulin production is inhibited, Type 1 or Type 2 diabetes may result. Article CAS PubMed Google Scholar McCoy, R.
DKA and HHS: compare onset, diagnosis, and treatment	DKA typically occurs in patients with Type 1 diabetes, although Ketacidosis in those with Type 2 hyperglycemiv is rising accounting Injury rehabilitation exercises an estimated 1 in 5 Hyperglycemia and hypoglycemia. Download references. Winter, R. An evaluation of recurrent diabetic ketoacidosis, fragmentation of care, and mortality across Chicago, Illinois. DKA occurs when insulin levels are low or nonexistent. Article CAS PubMed Google Scholar Carey, M. As hospital admissions for both conditions continue to increase, early identification and treatment can reduce length of stay and healthcare costs.
Management of Hyperglycemic Crises: Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar State	With DKA clients, the objective is to stabilize the blood sugar. This typically includes administering insulin and fluids, as well as monitoring vitals. With HHS clients, the main objective is treating dehydration and electrolyte imbalances. During my exam, I could literally see and hear him going over different areas as I was answering my questions. This past Friday I retook my Maternity Hesi and this time, I decided for my last week of Holiday break to just watch all of his OB videos. Although they may appear different on lab testing, both conditions can result in an imbalance of acids and bases in the blood. Without it, the body switches to burning fat for energy instead of sugar , resulting in an accumulation of ketones in the blood and urine. One of the main distinctions between DKA and HHS is that DKA usually results in acidosis and HHS usually has higher blood glucose. Need help with your next exam? Our proven system has helped over 1,, nursing students reduce their study time, survive their nursing school lectures and PASS their exams! SimpleNursing membership offers:. DKA vs HHS NCLEX Review Practice Questions. TEST YOUR KNOWLEDGE. Please enable JavaScript play-sharp-fill. Overview Lorem ipsum dolor sit amet, consectetur adipiscing elit. Donec non tellus ut sem commodo blandit. Suspendisse nisi orci, pellentesque faucibus dolor ut, aliquam iaculis est. Learning Outcomes Sed at turpis sit amet urna malesuada fermentum. Nulla convallis vehicula lobortis. The symptoms of DKA can worsen quickly if a person does not get treatment. They can include:. HHS can present very similarly to DKA, meaning that doctors must take care to distinguish between the two syndromes. One distinguishing characteristic is that HHS can cause neurological signs and symptoms, which may include:. Finally, HHS can also present with symptoms related to its cause. Sometimes, a person may develop HHS following an infection or a cardiac event, such as a heart attack or stroke. However, one key difference is the presence of neurological symptoms. HHS can cause a person to experience hallucinations, confusion, drowsiness, loss of vision, or a coma. Both conditions cause an unsafe level of blood sugar. However, DKA is associated with high levels of ketones in the blood, whereas HHS is not. However, DKA can occur due to a missed insulin dose, heavy alcohol use, or a physical injury. Although both conditions can lead to diabetic coma and death, the mortality rate of HHS is 10 times higher than that of DKA. However, a person can survive either condition with proper treatment. The two most common causes of DKA are missing a dose of insulin and an acute illness. Other possible causes include an injury, such as a car accident, and alcohol or drug use. The treatments for DKA and HHS are similar. Doctors will typically recommend the use of an IV line to deliver:. A doctor may discuss ongoing diabetes management with the person, including any necessary changes to their diet and exercise regimen. A person can take steps at home to help prevent the development of either DKA or HHS. These include :. DKA and HHS are emergencies that require immediate medical attention. A person living with diabetes should seek emergency care if they develop symptoms of either condition. It is also advisable for a person to test their blood sugar levels if they start to have early warning signs of hyperglycemia, such as extreme thirst or frequent urination. Both DKA and HHS can be life threatening and require prompt treatment. However, HHS has a fatality rate that is about 10 times that of DKA. HONK stands for hyperglycemic hyperosmolar non-ketotic coma, which is how the medical community previously referred to HHS. Non-ketotic hyperglycemic coma and hyperosmolar hyperglycemic non-ketotic syndrome are two other former names for the condition. DKA and HHS are two complications of diabetes that have similar symptoms, causes, and treatments. Both conditions result from high blood glucose levels and require insulin to help treat them. Evan Dingle, MD Corey Slovis, MD. PDF Download. The Etiology of DKA Vs HHS The fundamental underlying issue in both DKA and HHS is an absolute or relative lack of insulin that results in an increase in counter-regulatory hormones, including glucagon, cortisol, and catecholamines. Recommended Reading FDA already balances safety, access to investigational drugs. Journal of Clinical Outcomes Management. Do free meals to physicians affect opioid prescribing? Trump administration proposes changes to HHS, FDA. Cost led to missed care for 4. Who are the 'high-need, high-cost' patients? Pregnancy and years of reproductive capability linked to dementia risk. CMS proposes site-neutral payments for hospital outpatient setting.

Diabetic ketoacidosis vs hyperglycemic hyperosmolar syndrome -

As a result of this deficiency, the liver starts to break down fats for energy instead of sugar, causing a buildup of ketones in the blood and urine. DKA is more common in type one diabetes clients, and HHS is more common for those with type two diabetes.

Clients in the early stages of DKA and HHS may present with the same manifestations, such as hyperglycemia, excessive thirst, and frequent urination. Although both conditions may share some similarities, there are distinct differences. Nurses must carefully assess their clients, record a thorough history and physical, evaluate, and report findings to differentiate between DKA and HHS.

Both of these complications can be life-threatening. With DKA clients, the objective is to stabilize the blood sugar. This typically includes administering insulin and fluids, as well as monitoring vitals. With HHS clients, the main objective is treating dehydration and electrolyte imbalances.

During my exam, I could literally see and hear him going over different areas as I was answering my questions. This past Friday I retook my Maternity Hesi and this time, I decided for my last week of Holiday break to just watch all of his OB videos.

Although they may appear different on lab testing, both conditions can result in an imbalance of acids and bases in the blood. Without it, the body switches to burning fat for energy instead of sugar , resulting in an accumulation of ketones in the blood and urine.

One of the main distinctions between DKA and HHS is that DKA usually results in acidosis and HHS usually has higher blood glucose.

Need help with your next exam? Our proven system has helped over 1,, nursing students reduce their study time, survive their nursing school lectures and PASS their exams! SimpleNursing membership offers:. DKA vs HHS NCLEX Review Practice Questions. TEST YOUR KNOWLEDGE. Setting: Our earliest studies evaluated the comparative efficacy of low-dose vs.

pharmacological amounts of insulin and the use of low-dose therapy by various routes in adults and later in children.

Subsequent studies evaluated phosphate and bicarbonate therapy, lipid metabolism, ketosis-prone type 2 patients, and use of rapid-acting insulin analogs as well as leptin status, cardiac risk factors, proinflammatory cytokines, and the mechanism of activation of T lymphocytes in hyperglycemic crises.

Main Outcome: The information garnered from these studies resulted in the creation of the American Diabetes Association ADA technical review on DKA and HHS as well as the ADA Position and Consensus Paper on the therapy for hyperglycemic crises. Conclusions: Areas of future research include prospective randomized studies to do the following: 1 establish the efficacy of bicarbonate therapy in DKA for a pH less than 6.

more expensive insulin analogs on the general ward for the treatment of DKA. We had based our method of research on the clinical trial design known as a prospective study that compares the effect and value of intervention against a control human subject 2.

A prospective, randomized clinical trial is the most definitive tool to evaluate the validity of clinical research and to identify research activities with a potential to improve the quality of health care and control costs through careful comparison of alternative treatment 2.

This review describes our journey in the field over the past three decades and summarizes major advances in the pathogenesis and treatment of patients with hyperglycemic crises. DKA is the most serious hyperglycemic emergency in patients with type 1 and type 2 diabetes mellitus and is associated with significant morbidity and mortality 3.

In the early years of insulin therapy, due to limited supply, small amounts of insulin were used to treat DKA.

Although low-dose insulin therapy was found to be effective 7 , high-dose insulin therapy became the standard of care 8 , 9.

Complicated schemes were devised for the selection of initial and subsequent insulin dosage based on the degree of hyperglycemia, ketonemia, and level of consciousness.

These retrospective nonrandomized studies in the s and s were later replaced by prospective randomized studies showing no advantage of high-dose insulin, compared with lower doses 10 , In Alberti et al.

They reported that an initial average bolus dose of 16 U followed by 5—10 U of im regular insulin per hour was effective in correcting hyperglycemia and metabolic acidosis This report, however, was taken with some skepticism because it was not a prospective randomized trial.

Based on these findings, we initiated a series of prospective randomized clinical studies on the management of DKA. Six major issues needed to be considered and properly addressed before the initiation of these studies:. Adequate number of study patients. At our county teaching hospital, the Regional Medical Center, we were able to treat approximately patients with acute hyperglycemic crises per year.

This allowed us to have enough power to undertake our first randomized protocol 1. Approval of simple and scientifically valid treatment protocol, by the University of Tennessee Institutional Review Board and the Scientific Advisory Committee of the General Clinical Research Center GCRC. We were cautious to exclude patients who might have other comorbid conditions that might distract the house staff from focusing on the management of the hyperglycemic state.

Administrative support for treatment protocol. It was critical to efficiently transfer eligible DKA patients from the emergency room to the GCRC to complete the protocol with a high degree of accuracy. This was supported by the Chief of Medicine and Physician-in-Chief at the Regional Medical Center, who endorsed the protocol.

Dissemination of the protocol to the house staff. The house staff were informed of the approved protocol at various conferences, medicine grand rounds, and in-service training and were given 3 × 5 in.

pocket-size index cards imprinted with the protocol. Simplification of procedures in the GCRC and identification of on-call personnel. A critical component to the success of this study was the rapid turnaround of the biochemical profile, which was done in the GCRC, and supported treatment changes on an hour-to-hour basis.

This service increased patient safety and resulted in an excellent educational experience. The results of our first protocol, which took about 2 yr to complete, proved to be gratifying not only to us for providing the scientific community with evidence-based data but also to more than house staff who played a pivotal role in the execution of this program.

We therefore acknowledged them as a fourth author in our first publication 1. The major protocols , which are described in Fig. Treatment protocols for DKA studies The first protocol was designed to clarify the controversy surrounding the use of low-dose insulin treatment, addressing the following three questions: 1 Is low-dose im insulin effective in the treatment of DKA; 2 how does low-dose im insulin treatment compare with conventional high-dose therapy; and 3 how do plasma insulin values compare with the two regimens?

Patients were randomized to receive either a high-dose or low-dose insulin regimen. This was followed by 50 U of insulin sc per hour. The low-dose regimen of insulin was given according to body weight, i. In addition, seven of 24 in the high-dose group but only one of 24 in the low-dose group developed hypokalemia; and 6 no deaths occurred in either group, even though seven patients in the high-dose and five in the low-dose group were stuporous or comatose on admission.

It was of historical interest that during this period of our study, the treatment of patients during resolution of DKA in community hospitals was based on sliding scale insulin using qualitative urine glucose, as blood glucose meters were not widely used. However, later we demonstrated the inaccuracy of urine glucose by dipstick 16 , and, therefore, discouraged the further use of sliding scale based on urine glucose testing.

The efficacy of low-dose vs. conventional therapy of insulin for treatment of DKA. Reproduced from Kitabchi et al. Comparison of high-insulin dosage A with low-insulin dosage group B as well as low-dose insulin dosage by the sc C , iv D , and im E routes in plasma. IRI and its glucose-lowering effect in DKA patients previously untreated with insulin.

Reproduced, with permission, from Kitabchi et al. In Protocol II the route of insulin administration was studied to determine whether a bolus dose of insulin administered iv would produce the same effect on glucose, ketone bodies, and other metabolic parameters as an identical amount given im or sc.

We randomized 45 consecutive patients presenting in DKA. Fifteen subjects in each group received insulin by the iv, im, or sc route, all other aspects of their care remaining the same Regardless of their initial plasma glucose, all patients were given 0.

We observed that low-dose insulin was highly effective in treating DKA, but several interesting observations were made: 1 iv insulin resulted in a significant decline in ketone bodies over the first 2 h of treatment, compared with the im or sc groups; 2 the decrement of glucose was significantly more rapid in the iv group over the first 2 h, but the three groups were similar by the eighth hour Fig.

All three groups maintained this plateau over 8 h of observation. Comparison of the effects of iv, sc, and im low-dose insulin regimens on changes of plasma glucose and total ketone bodies in patients with DKA. Reprinted from Fisher et al. Prompted by these observations, protocol III 18 was designed to answer the following three questions: 1 could the delay in decrement in ketone bodies noted in DKA patients treated with im and sc insulin be prevented by giving an initial loading dose of regular insulin, half iv and half im; 2 how would that approach compare with a group given continuous iv treatment; and 3 is the use of albumin necessary with insulin infusion?

In a randomized, prospective study of 30 patients in DKA, 15 patients received a loading dose of 0. Recovery parameters were not significantly different in the two groups, indicating that low doses of insulin administered by the priming dose-intermittent im route are as effective as the constant infusion method.

It was also shown that the use of iv insulin ameliorated the delay for decremental changes in ketone bodies. This improvement was due to a higher level of plasma insulin when administered iv, compared with the im method Fig.

Furthermore, we demonstrated that it was not necessary to add albumin to the insulin infusate, as we had done in previous protocols. We then correlated the admission metabolic profiles Table 1 with the state of consciousness These studies showed that about one third of DKA patients are hyperosmolar and that mental status on admission related to serum osmolality and not to the severity of the acid-base disorder Fig.

Generally, comatose patients were older and had higher glucose, blood urea nitrogen BUN , and osmolality levels but lower levels of bicarbonate, which were significantly different from noncomatose patients. Conversely, plasma pH and ketone bodies were not significantly different between the two groups Table 2 Clinical and biochemical profile of DKA patients on admission a.

Reproduced with permission from Kitabchi et al. Values, when applicable, are mean ± sem after initial hydration in the emergency room prior to any other therapy. Kitabchi et al. Fisher et al. Sacks et al. Admission clinical and biochemical profile and response to therapy of comatose vs.

noncomatose patients with DKA from Ref. Calculated serum osmolarity in ketoacidotic patients with relation to mental status at time of admission. Data from Kitabchi et al. Reproduced by permission from Kitabchi and Fisher 19 in Handbook of Diabetes Mellitus Brownlee M, ed.

and Garland ATPM Press. UTCHS, University of Tennessee Center for Health Sciences. Although our studies and those of others for review see Ref. For that reason we embarked on protocol IV in collaboration with pediatric colleagues In this study we used only the iv route of insulin to avoid possible problems with insulin absorption given im or sc in pediatric patients who might be severely dehydrated, leading to poor tissue perfusion.

We compared a low dose 0. a high dose 1. Thanks to randomized assignment, the treatment groups were comparable in all clinical and biochemical aspects on admission. The data indicated that low-dose insulin, despite a slower rate of glucose decline, was as effective as high dose for the treatment of DKA in children.

Furthermore, there was less incidence of hypokalemia and a decreased potential for hypoglycemia with the use of more physiological rather than pharmacological amounts of insulin The efficacy of low-dose insulin regimens was thus established in a strictly controlled environment, but it was not clear whether similar results could be obtained in a community hospital.

In a nonrandomized but prospective study, we evaluated the effectiveness of low-dose insulin in a private community university-affiliated hospital under the care of an established diabetologist, with the help of the medical house staff. This study showed that low-dose insulin in DKA is as effective in a private community hospital as in a more academic and controlled environment with no morbidity or mortality Because there was little known about the renal metabolism of insulin during treatment and after recovery of DKA, we then investigated the urinary clearance of immunoreactive insulin IRI during physiological and pharmacological concentrations of IRI Immunoreactive β 2 -microglubulin Iβ 2 M was measured simultaneously as a marker of proximal tubular function initially and 2—3 wk later.

Ten patients in DKA were randomly assigned to receive either low-dose or high-dose insulin therapy protocol V. Two to three wk after the correction of hyperglycemia, five patients were restudied.

In protocol V we observed the following: 1 an approximately fold increase in urinary and fractional urinary clearance of IRI and a fold increase in Iβ 2 M clearance, suggesting that hyperinsulinuria was secondary to a nonspecific defect in tubular luminal uptake of low-molecular weight proteins; 2 because increased IRI clearance was not changed by pharmacologic IRI plasma levels, residual tubular absorptive capacity is not saturable; 3 Iβ 2 M but not IRI clearance was significantly improved by the time metabolic control was attained, which suggested a defect tubular transport systems; 4 a therapeutically insignificant fraction of infused insulin was lost in the urine during treatment of DKA; and 5 defective renal tubular luminal uptake and possibly degradation of IRI was reversible.

In protocol VI we investigated the long-standing controversy surrounding the use of phosphate therapy in DKA In a prospective, randomized study we evaluated 15 patients with DKA treated with a low-dose insulin protocol who received Another 15 patients were assigned to receive potassium chloride We found that the phosphate-treated patients had higher levels of 2, 3-diphosphoglyceric acid at the end of 48 h, but the difference was not significant and there was no demonstrable effect on tissue oxygenation or clinical response.

Furthermore, phosphate therapy was associated with significantly lower ionized calcium levels. We concluded because of that observation there is reason for caution in the use of phosphate salts in the treatment of DKA, but there are circumstances, as in patients with congestive heart failure, anemia or other conditions associated with hypoxia, when such therapy might be especially indicated.

In protocol VII we addressed the impact of bicarbonate treatment in patients with DKA. This issue had been a contentious subject due to the conflicting results from a small number of clinical trials Proponents of bicarbonate therapy point to the potential deleterious effects of acidosis on cardiac hemodynamics.

Opponents of bicarbonate therapy have been concerned with possible paradoxical cerebrospinal fluid CSF acidosis and a shift in the oxyhemoglobin curve back to the left, resulting in tissue hypoxia. We randomly assigned patients with moderate to severe DKA pH 6.

Lumbar puncture was performed at baseline, 6—8 h, and 12—24 h during therapy with analysis of the CSF for glucose, bicarbonate, pH, total ketone, and osmolality. There were no significant differences in the rate of glucose or ketone body decline or the rate of increase in pH or bicarbonate between the experimental or control groups.

Interestingly, for those patients who had simultaneous measurements of plasma and CSF at baseline, glucose and ketone body levels were significantly lower in the CSF, whereas pH and bicarbonate were significantly higher.

We concluded that bicarbonate therapy did not alter recovery outcomes in adults with moderate DKA pH 6. During the s it was suggested that there was a strong interrelationship among abnormal lipid metabolism, atherosclerosis, and diabetes With the availability of patients in a severe insulin-deficient state such as DKA, we were interested to know whether high triglycerides, cholesterol, and high-density lipoprotein could be reduced by low-dose insulin therapy.

Our results provided evidence that insulin can actively decrease triglycerides but not cholesterol. However, the lowering of apolipoprotein A-1 by low-dose insulin that occurred may be due to decreased secretion of apolipoprotein A-1 into plasma or increased metabolism More than half of newly diagnosed African-Americans with unprovoked DKA are obese.

The majority of such patients display clinical and metabolic features of type 2 diabetes, including a high rate of obesity, a strong family history of diabetes, a measurable pancreatic insulin reserve 29 — 33 , and the ability to discontinue insulin therapy and go through a period of near-normoglycemic remission that may last for a few months to several years This clinical presentation has been reported primarily in Africans and African-Americans but also in other minority ethnic groups This variant of type 2 diabetes has been referred to in the literature as idiopathic type 1 diabetes, atypical diabetes mellitus, type 1.

Our studies indicate that at presentation, patients with ketosis-prone type 2 diabetes have markedly decreased pancreatic insulin secretion, which is lower than in obese patients with comparable hyperglycemia but significantly greater reserve than in lean type 1 diabetic patients with DKA The underlying mechanisms for β-cell dysfunction in ketosis-prone diabetes are not known; however, preliminary evidence suggests that patients with ketosis-prone type 2 diabetes display a unique propensity to glucose toxicity Several investigators have consistently reported that subjects with ketosis-prone type 2 diabetes have a nonautoimmune type of diabetes.

Studies in humans and animal models have shown that muscle and adipocyte tissues exposed to sustained hyperglycemia have reduced insulin binding to its receptor, receptor phosphorylation, and tyrosine kinase activity and phosphorylation of insulin receptor substrate These postreceptor defects result in decreased insulin receptor substrateassociated phosphatidylinositol 3-kinase activity and insulin resistance.

To investigate the molecular mechanisms underlying hyperglycemia-induced insulin resistance in skeletal muscle on obese patients with ketosis-prone diabetes, we recently performed muscle biopsies 1 d after follow-up and during near-normoglycemic remission at 8 wk of follow-up We observed that overt hyperglycemia is associated with decreased stimulation of Akt Ser phosphorylation by a physiological concentration of insulin without changes in AktThr phosphorylation.

These results indicate that in ketosis-prone diabetes, improvement of metabolic control with insulin therapy is accompanied by increased expression of key elements of the insulin-regulated signaling cascade in skeletal muscle The availability of a large number of obese and lean DKA patients also provided us the opportunity to evaluate the controversial issues regarding the stimulating effect of insulin on leptin during hyperglycemia 40 , We investigated the effect of low-dose insulin therapy in a group of obese and lean DKA patients.

These studies demonstrated that baseline values of leptin in DKA were low, but low-dose insulin could significantly stimulate serum leptin levels within 12 h. This effect could be seen as early as 4 h after injection of insulin in obese DKA patients The presence of high levels of epinephrine and cortisol, which have negative and positive effect on leptin secretion, respectively 43 , 44 , suggested that the role of insulin as an anabolic hormone along with the role of elevated cortisol played important roles in the overall stimulating effect of insulin on leptin Recently the concept of a chronic inflammatory state in diabetes as part of insulin resistance has received considerable attention 45 , Having a large group of obese and thin DKA patients and obese nonketotic hyperglycemic subjects in whom no evidence of infection or a history of cardiovascular event was noted, we assessed the status of proinflammatory cytokines TNFα, ILβ 1 , IL-6, IL-8 ; various cardiovascular risk factors homocysteine, plasminogen activator inhibitor-1, C-reactive protein, free fatty acids ; levels of lipid peroxidation by measuring thiobarbituric acid TBA -reacting material; the state of reactive oxygen species ROS , measured by dichlorofluorescein DCF ; and counterregulatory hormones cortisol, GH These studies demonstrated that levels of these parameters were increased by at least 2- to 3-fold over normal levels.

Interestingly, however, in DKA patients all these values reached near normal levels except for homocysteine with insulin therapy and resolution of glycemic crises within 24 h see Table 3. Proinflammatory cytokines, cardiovascular risk factors, counterregulatory hormones, lipid peroxidation TBA , and DCF values on admission and resolution of hyperglycemic crises in lean and obese DKA and obese hyperglycemic patients, compared with lean and obese nondiabetic subjects Data are mean ± se.

Resol, resolution; PAI-1, plasminogen activator inhibitor-1; FFA, free fatty acid; CRP, C-reactive protein. To determine whether hyperglycemia or hyperlipidemia could in fact bring about stimulation of cytokines, ROS, and lipid peroxidation, we chose human T lymphocytes T cells 48 or human aortic endothelial cells 49 and incubated them either in the presence of high glucose or high lipid 50 , measuring activation of these cells by assessing lipid peroxidation, ROS, growth factor receptor emergence such as insulin, IL-2 and IGF-I, or elevated proinflammatory cytokines.

The results suggested that high concentrations of glucose 15—30 but not 5 m m and palmitate but not unsaturated fatty acids stimulate production of ROS, lipid peroxidation, and cytokine elevation and convert these insulin nonresponsive cells to insulin-responsive cells.

We were also able to demonstrate in vivo activation of T cells in DKA with production of ROS, lipid peroxidation, and cytokine stimulation Further studies are in progress to assess the mechanism of these phenomena using other models of stress besides hyperglycemia and hyperlipidemia.

We had earlier noted that use of illicit drugs may be a contributing factor in DKA presentation In a recent retrospective study in a large metropolitan university-affiliated hospital, we were able to demonstrate that the use of cocaine was also a significant independent risk factor for recurrent DKA In June , the first of two rapid-acting analogs of human insulin lispro or Humalog became commercially available.

We asked whether this new formulation could be used as an alternative route to the use of iv regular insulin in patients with DKA.

In a prospective and randomized study, we compared the efficacy and safety of sc insulin lispro every hour with that of a standard low-dose iv infusion protocol of regular insulin in adult patients with DKA Patients treated with sc lispro were treated in the emergency department or regular medicine wards and because of hospital regulations iv-treated patients were managed in the intensive care units.

Patients treated with sc lispro received an initial injection of 0. Patients treated with iv regular insulin received an initial sc bolus of 0. Treatment with sc insulin injections on an hourly schedule, however, may be difficult due to the intensity of treatment and shortage of nursing staff on regular wards.

To facilitate the management of patients with DKA, we studied whether treatment with sc rapid-acting insulin analogs, given at different time intervals 1 and 2 h , is equally effective as the use of iv regular insulin in patients with DKA.

A total of 45 consecutive patients admitted with DKA were randomly assigned to receive sc aspart Novolog, Novo-Nondisk, Bagsvaerd, Denmark every hour or every 2 h or iv infusion of regular insulin.

Patients treated with aspart sc every hour received an initial injection of 0. Those treated with sc aspart every 2 h received an initial injection of 0.

Patients treated with iv regular insulin received an initial bolus of 0. Response to medical therapy was evaluated by assessing the duration of treatment until resolution of hyperglycemia and ketoacidosis. Similar to our experience with lispro, we observed no mortality, and there were no differences in the length of hospital stay, total amount of insulin administration until resolution of hyperglycemia or ketoacidosis, or the number of hypoglycemic events among treatment groups Table 4 summarizes results of hourly sc injection of lispro vs.

two hourly sc injection of aspart, compared with continuous infusion of regular insulin given iv, showing no significant difference among the three regimens. Based on these studies, we concluded that the use of sc rapid-acting insulin analogs every 1 or 2 h represents a safe and effective alternative to the use of iv regular insulin in the management of patients with uncomplicated DKA.

As the glucose levels increase, patients with HHS become increasingly hyperosmolar and dehydrated, resulting in further elevation of glucose levels, causing a perpetual cycle of increasing glucose and resultant hyperosmolarity and dehydration.

Skip to main content. Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic Syndrome Management. Emergency Medicine. Author s : H. Evan Dingle, MD Corey Slovis, MD. PDF Download. The Etiology of DKA Vs HHS The fundamental underlying issue in both DKA and HHS is an absolute or relative lack of insulin that results in an increase in counter-regulatory hormones, including glucagon, cortisol, and catecholamines.

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Diabetic ketoacidosis Insulin sensitivity and PCOS and hyperglycemic Diabbetic state HHS ktoacidosis the most serious and life-threatening hyperglycemic emergencies Injury rehabilitation exercises diabetes. DKA is more common in young people with type 1 diabetes and HHS in adult and elderly patients with type 2 diabetes. Features of the 2 disorders with ketoacidosis and hyperosmolality may coexist. Both are characterized by insulinopenia and severe hyperglycemia. Early diagnosis and management are paramount. Guillermo E. UmpierrezMary Beth MurphyAbbas Hypsrosmolar. Kitabchi; Diabetic Ketoacidosis and Injury rehabilitation exercises Hyperosmolar Syndrome. DDiabetic Spectr 1 January ; 15 1 : 28— Diabetic ketoacidosis DKA and hyperosmolar hyperglycemic syndrome HHS are two acute complications of diabetes that can result in increased morbidity and mortality if not efficiently and effectively treated.