Increased urinary atrial natriuretic peptide-like immunoreactivity excretion but decreased plasma atrial natriuretic peptide concentration in patients with hyperosmolar-hyperglycemic nonketotic syndrome.
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OBJECTIVE: This study was undertaken to measure urinary atrial natriuretic peptide-like immunoreactivity (ANP-LI) and plasma ANP concentration in patients with hyperosmolar-hyperglycemic nonketotic syndrome (HHNS) to investigate the change of renal ANP-LI and cardiac ANP synthesis in volume-depleted diabetic patients. RESEARCH DESIGN AND METHODS: The urine ANP-LI:creatinine ratio, plasma ANP level, and plasma renin activity (PRA) were measured in 12 patients with HHNS during the acute stage and after recovery, in 28 oral hypoglycemic agent (OHA)-treated type 2 diabetic patients, and in 23 normal subjects. ANP and PRA were measured by radioimmunoassay. RESULTS: These HHNS patients had severe hyperglycemia and hyperosmolality as well as increased blood urea nitrogen, creatinine, and PRA levels, as compared with normal subjects and OHA-treated type 2 diabetic patients. In these patients, the urinary ANP-LI:creatinine ratio (11.69 +/- 2.11 pmol/mmol) was significantly increased in comparison with the normal group (1.78 +/- 0.11 pmol/mmol) and OHA-treated diabetic patients (2.43 +/- 0.45 pmol/mmol), whereas plasma ANP concentration (5.12 +/- 0.72 pmol/l) was significantly lower than the corresponding values of the normal group (7.39 +/- 0.85 pmol/l) and OHA-treated diabetic patients (8.43 +/- 1.05 pmol/l). All of these abnormalities were significantly ameliorated after insulin, fluid, and electrolyte replacement. CONCLUSIONS: Our data show that urinary ANP-LI was significantly increased, whereas plasma ANP concentration was decreased, in the face of raised PRA in HHNS patients. This study indicates that renal ANP-LI substances and cardiac ANP may exhibit different responsiveness in diabetic patients with HHNS. (+info)
Management of the hyperosmolar hyperglycemic syndrome.
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Hyperglycemic hyperosmolarity is part of a clinical spectrum of severe hyperglycemic disorders ranging from pure hyperglycemic hyperosmolarity without ketosis to diabetic ketoacidosis, with significant overlap in the middle. From 50 to 75 percent of hospitalizable patients who have uncontrolled diabetes present with significant hyperosmolarity. An altered state of consciousness attributable to uncontrolled diabetes is virtually always the result of severe hyperosmolar hyperglycemia. The linchpin of therapy is prompt, rapid administration of crystalloid solutions that have tonicity appropriate to the level of hyperosmolarity. A decrease in the plasma glucose concentration indicates the adequacy of therapy, especially rehydration; the goal is for the plasma glucose level to decline by at least 75 to 100 mg per dL (4.2 to 5.6 mmol per L) per hour. Patients with hyperosmolar hyperglycemic syndrome are often chronically ill, and they may have major total body deficits of potassium, phosphate and magnesium, as well as B-complex vitamins (especially thiamine). These deficits also require attention and correction during therapy. (+info)
Hyperosmolar nonketotic syndrome with hypernatremia: how can we monitor treatment?
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We report the case of a 62 year-old symptomatic patient with severe hyperglycemic hyperosmolality associated with hypernatremia. During treatment, the progressive decrease in serum tonicity, which resulted in the amelioration of the neurological symptoms, followed the decrease in serum glucose and mainly the corrected serum sodium levels rather than the decrease in the uncorrected serum sodium levels. The case illustrates the usefulness of glucose - corrected serum sodium levels to monitor treatment in such conditions in order to avoid neurological consequences caused by the decrease in serum osmolality. (+info)
Bilateral putaminal hemorrhage with cerebral edema in hyperglycemic hyperosmolar syndrome.
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Bilateral putaminal hemorrhages rarely occur simultaneously in hypertensive patients. The association of intracerebral hemorrhage with cerebral edema (CE) has been rarely reported in diabetic patients. We present a patient with bilateral putaminal hemorrhage (BPH) and CE during the course of hyperglycemic hyperosmolar syndrome (HHS). A 40-year-old man with a history of diabetes mellitus and chronic alcoholism was admitted with acute impaired mentality. His blood pressure was within the normal range on admission. Laboratory results revealed hyperglycemia and severe metabolic acidosis without ketonuria. After aggressive treatment, plasma sugar fell to 217 mg/dl, but brain CT showed BPH and diffuse CE. Our case demonstrated that HHS should be considered as a cause of BPH with CE. Initial brain imaging study may be recommended for patients with diabetic coma. (+info)
Inpatient management of diabetes: survey in a tertiary care centre.
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AIMS: Good glycaemic control in hospitalised patients with diabetes mellitus improves wellbeing and aids recovery. This survey aimed to: (1) assess glycaemic control in patients with diabetes admitted to hospital for reasons other than diabetes, (2) compare the glycaemic control in patients treated in medical and surgical units, and (3) see the impact of specialists' input on glycaemic control. METHODS: The first 150 patients admitted to hospital were identified; those with acute metabolic complications of diabetes mellitus, acute myocardial infarction, pregestational or gestational diabetes, and patients in different intensive care units were excluded. Case notes were reviewed with particular attention to glycaemic control, frequency of blood monitoring, complications, and the actions taken to improve glycaemic control. RESULTS: Four of the 150 patients died in hospital. When subcutaneous insulin was used glycaemic control was good in 48%, suboptimal in 15%, and poor in 37% of patients. The results were not significantly different with subcutaneous or intravenous insulin. There was also no difference in glycaemic control among medical and surgical patients. Patients managed by designated specialists had better control than those managed by physicians (p<0.001). Hypoglycaemia was documented in 20% and two patients developed non-ketotic hyperosmolar coma while in hospital. In a few cases treatment at discharge was not changed despite poor control while in hospital. CONCLUSION: More attention should be given to improving glycaemic control in patients hospitalised for reasons other than diabetes. Particular care should be taken to modify the dose of insulin needed to get good glycaemic control; control was better with specialists' input. A follow up survey will be conducted. (+info)
Hyperglycaemic crises and lactic acidosis in diabetes mellitus.
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Diabetic ketoacidosis, hyperglycaemic hyperosmolar state, and lactic acidosis represent three of the most serious acute complications of diabetes. There have been some advances in our understanding of the pathogenesis of these conditions over the last three decades, together with more uniform agreement on their treatment and innovations in technology. Accordingly their incidence, morbidity, and mortality are decreasing, but at rates that fall short of our aspirations. Hyperglycaemic crises in particular remain an important cause of morbidity and mortality in diabetic populations around the world. In this article, understanding of these conditions and advances in their management, and the available guidelines for their treatment, are reviewed. As far as is possible, the recommendations are based on clear published evidence; failing that, what is considered to be a common sense synthesis of consensus guidelines and recommendations is provided. (+info)
Hyperosmolar hyperglycemic state.
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Hyperosmolar hyperglycemic state is a life-threatening emergency manifested by marked elevation of blood glucose, hyperosmolarity, and little or no ketosis. With the dramatic increase in the prevalence of type 2 diabetes and the aging population, this condition may be encountered more frequently by family physicians in the future. Although the precipitating causes are numerous, underlying infections are the most common. Other causes include certain medications, non-compliance, undiagnosed diabetes, substance abuse, and coexisting disease. Physical findings of hyperosmolar hyperglycemic state include those associated with profound dehydration and various neurologic symptoms such as coma. The first step of treatment involves careful monitoring of the patient and laboratory values. Vigorous correction of dehydration with the use of normal saline is critical, requiring an average of 9 L in 48 hours. After urine output has been established, potassium replacement should begin. Once fluid replacement has been initiated, insulin should be given as an initial bolus of 0.15 U per kg intravenously, followed by a drip of 0.1 U per kg per hour until the blood glucose level falls to between 250 and 300 mg per dL. Identification and treatment of the underlying and precipitating causes are necessary. It is important to monitor the patient for complications such as vascular occlusions (e.g., mesenteric artery occlusion, myocardial infarction, low-flow syndrome, and disseminated intravascular coagulopathy) and rhabdomyolysis. Finally, physicians should focus on preventing future episodes using patient education and instruction in self-monitoring. (+info)
A case of hyperglycemic hyperosmolar state associated with Graves' hyperthyroidism: a case report.
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Hyperglycemic hyperosmolar state (HHS) is an acute complication mostly occurring in elderly type 2 diabetes mellitus (DM). Thyrotoxicosis causes dramatic increase of glycogen degradation and/or gluconeogenesis and enhances breakdown of triglycerides. Thus, in general, it augments glucose intolerance in diabetic patients. A 23-yr-old female patient with Graves' disease and type 2 DM, complying with methimazole and insulin injection, had symptoms of nausea, polyuria and generalized weakness. Her serum glucose and osmolarity were 32.7 mM/L, and 321 mosm/kg, respectively. Thyroid function tests revealed that she had more aggravated hyperthyroid status; 0.01 mU/L TSH and 2.78 pM/L free T3 (reference range, 0.17-4.05, 0.31-0.62, respectively) than when she was discharged two weeks before (0.12 mU/L TSH and 1.41 pM/L free T3). Being diagnosed as HHS and refractory Graves' hyperthyroidism, she was treated successfully with intravenous fluids, insulin and high doses of methimazole (90 mg daily). Here, we described the case of a woman with Graves' disease and type 2 DM developing to HHS. (+info)