The chronic hyperglycemia of diabetes is associated with long-term damage, dysfunction, and failure of various organs, especially the eyes, kidneys, nerves, heart, and blood vessels. Several pathogenic processes are involved in the development of diabetes. The basis of the abnormalities in carbohydrate, fat, and protein metabolism in diabetes is deficient action of insulin on target tissues. Impairment of insulin secretion and defects in insulin action frequently coexist in the same patient, and it is often unclear which abnormality, if either alone, is the primary cause of the hyperglycemia.
PDF Abstract The hyperosmolar hyperglycemic state HHS is the most serious acute hyperglycemic emergency in patients with type 2 diabetes. Despite the severity of this condition, no prospective, randomized studies have determined best treatment strategies in patients with HHS, and its management has largely been extrapolated from studies of patients with DKA.
There are many unresolved questions that need to be addressed in prospective clinical trials regarding the pathogenesis and treatment of pediatric and adult patients with HHS.
Introduction The hyperosmolar hyperglycemic state HHS is a syndrome characterized by severe hyperglycemia, hyperosmolality, and dehydration in the absence of ketoacidosis. Most cases of HHS are seen in elderly patients with type 2 diabetes; however, it has also been reported in children and young adults 2.
The prognosis is determined by the severity of dehydration, presence of comorbidities, and advanced age 467. Treatment of HHS is directed at replacing volume deficit and correcting hyperosmolality, hyperglycemia, and electrolyte disturbances, as well as management of the underlying illness that precipitated the metabolic decompensation.
Low-dose insulin infusion protocols designed for treating DKA appear to be effective; however, no prospective randomized studies have determined best treatment strategies for the management of patients with HHS. Herein, we present an extensive review of the literature on diabetic coma and HHS to provide a historical perspective on the clinical presentation, diagnosis, and management of this serious complication of diabetes.
Several case reports followed this publication, describing patients with newly diagnosed or previously known diabetes presenting with drowsiness or coma, most of them with a peculiar breath odor resembling acetone 9.
InPetters 10 detected a substance in the urine of a fatal case of diabetic coma that resembled acetone in its reaction with sulfuric acid and caustic alkalis and was later recognized as acetoacetic acid, also called diacetic acid 11 Acetone was then recognized as an important outcome marker warning physicians about serious diseases, including diabetes 13 InKussmaul reported several fatal cases of diabetic coma preceded and accompanied by severe dyspnea 15 Kussmaul breathing, as this condition came to be known, quickly became one of the hallmarks in the diagnosis of diabetic coma, along with the presence of positive urine ketones 14 In the s, they reported patients presenting with an unusual type of diabetic coma characterized by severe hyperglycemia and glycosuria but without Kussmaul breathing, fruity breath odor, or a positive urine acetone test.
In the early s, others reported the presence of two distinct types of patients with diabetic coma, noting that not all cases presented with the characteristic Kussmaul respiration or positive urine acetone or diacetic acid 22 — These reports created confusion and were taken with skepticism, as the source of ketone bodies and the role of acetoacetic acid in the pathogenesis of diabetic coma were not known at the time.
Many physicians were against accepting that adult patients could progress to diabetic coma in the absence of ketonuria. For example, in the s, Elliot P.
Joslin 17 and others 27 stated that the presence of acetone or diacetic acid in the urine was requisite for the diagnosis of diabetic coma.
HHS syndrome received little attention and remained poorly understood until the reports by de Graeff and Lips 29 and Sament and Schwartz 30 in They reported that severe hyperglycemia resulted in osmotic diuresis, polyuria, and progressive water deficit.
They discussed the relevance of measuring sodium and chloride levels to estimate extracellular hypertonicity and cellular dehydration, and they proposed that patients with severe hyperglycemia and diabetic coma should be treated with large quantities of water Sament and Schwartz 30 suggested that some comatose patients with severe hyperglycemia and negative or trace ketonuria could be treated successfully with the administration of fluids and lower amounts of insulin compared with regular acidotic patients with diabetic coma.
Pathophysiology HHS is characterized by extreme elevations in serum glucose concentrations and hyperosmolality without significant ketosis Fig.
These metabolic derangements result from synergistic factors including insulin deficiency and increased levels of counterregulatory hormones glucagon, catecholamines, cortisol, and growth hormone 31 — Hyperglycemia develops because of an increased gluconeogenesis and accelerated conversion of glycogen to glucose glycogenolysis and by inadequate use of glucose by peripheral tissues, primarily muscle.
From the quantitative standpoint, increased hepatic glucose production represents the major pathogenic disturbance responsible for hyperglycemia in DKA As the glucose concentration and osmolality of extracellular fluid increase, an osmolar gradient is created that draws water out of the cells.
Glomerular filtration is initially increased, which leads to glucosuria and osmotic diuresis. The initial glucosuria prevents the development of severe hyperglycemia as long as the glomerular filtration rate is normal. However, with continued osmotic diuresis, hypovolemia eventually occurs, which leads to a progressive decline in glomerular filtration rate and worsening hyperglycemia.Type 1 diabetes is a chronic illness characterized by the body’s inability to produce insulin due to the autoimmune destruction of the beta cells in the pancreas.
Onset most often occurs in childhood, but the disease can also develop in adults in their late 30s and early 40s. The American Diabetes Association (ADA) criteria for diagnosis of diabetes are the same for children, adolescents, and adults.
According to these guidelines, E.J.'s diabetes could be diagnosed by the presence of polydipsia along with a random plasma glucose level > mg/dl.
Herein, we present an extensive review of the literature on diabetic coma and HHS to provide a historical perspective on the clinical presentation, diagnosis, and management of this serious complication of diabetes. The hyperosmolar hyperglycemic state (HHS) is the most serious acute hyperglycemic emergency in patients with type 2 diabetes.
von Frerichs and Dreschfeld described the first cases of HHS in the s in patients with an “unusual diabetic coma” characterized by severe hyperglycemia and. The Cardiovascular Autonomic Neuropathy (CAN) Subcommittee of the Toronto Consensus Panel on Diabetic Neuropathy worked to update CAN guidelines, with regard to epidemiology, clinical impact, diagnosis, usefulness of CAN testing, and management.
DEFINITION AND DESCRIPTION OF DIABETES MELLITUS. The information that follows is based largely on the reports of the Expert Committee on the Diagnosis and Classification of Diabetes (Diabetes Care References ↵ The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus: Report of the Expert Committee on the.