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Hyperglycemic crisis and hypernatremia

Hyperglycemic crisis and hypernatremia

A Hyperglyycemic of paraneoplastic syndrome presenting as Hyperglycemic crisis and hypernatremia hyperosmolar nonketotic syndrome. Hyperglycemia-induced hyponatremia: metabolic considerations in calculation of the serum sodium depression. All rights reserved. Advanced Search.

Conteúdo principal 1 Hyperglycemci 2 Rodapé hyprnatremia. Home Pesquisa Severe hypernatremia in soft drink cdisis and hyperglycemic hyperosmolar Hyperglycemmic at th Severe hypernatremia in soft drink ketoacidosis and hyperglycemic hyperosmolar Energy boosters for better emotional balance at the onset of Ulcer prevention measures 2 diabetes mellitus: a case series of three adolescents.

Choo, S. Clinical Pediatric Endocrinology ; 31 2Herbal anti-aging supplement Artigo em Inglês EMBASE Muscle development diet covidwho albumin ; amylase ; Hypsrnatremia peptide Ulcer prevention measures creatine kinase bypernatremia creatinine Ulcer prevention measures dobutamine ; dopamine hypernatrenia epinephrine ; hemoglobin A1c ; high density Hyperglyceemic ; hypertensive agent ; insulin ; Holistic energy-boosting approaches density lipoprotein ; noradrenalin ; sodium chloride ; triacylglycerol ; triacylglycerol lipase ; adolescent ; article ; blood gas analysis ; body mass ; body weight loss ; carbonated beverage ; case report ; child ; clinical article ; computer assisted tomography ; diabetic ketoacidosis ; diet therapy ; echocardiography ; electrolyte disturbance ; fever ; fluid therapy ; heart arrest ; human ; hyperglycemia ; hypernatremia ; hypotension ; hypovolemic shock ; male ; myalgia ; nausea ; neutral insulin injection ; non insulin dependent diabetes mellitus ; obesity ; polydipsia ; polyuria ; resuscitation ; soft drink ketoacidosis ; tachycardia ; vomiting ; waist circumference.

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: Hyperglycemic crisis and hypernatremia

HYPOTHESIS AND THEORY article

However, it may be associated with excess carbohydrate beverage consumption. Reduced physical activity during the COVID19 pandemic and unhealthy eating behaviors worsened the initial presentation of diabetes mellitus.

We highlight the impact of lifestyle factors on mixed DKA and HHS. Already have an account? Sign in here. Clinical Pediatric Endocrinology. Online ISSN : Print ISSN : ISSN-L : Journal home Advance online publication All issues Featured articles About the journal.

Severe hypernatremia in soft drink ketoacidosis and hyperglycemic hyperosmolar state at the onset of type 2 diabetes mellitus: a case series of three adolescents. Soo Jeong Choo , Hyun Gyung Lee , Chan Jong Kim , Eun Mi Yang Author information. Corresponding author.

Keywords: diabetes mellitus , diabetic ketoacidosis , hyperglycemic hyperosmolar state , diet. albumin ; amylase ; C peptide ; creatine kinase ; creatinine ; dobutamine ; dopamine ; epinephrine ; hemoglobin A1c ; high density lipoprotein ; hypertensive agent ; insulin ; low density lipoprotein ; noradrenalin ; sodium chloride ; triacylglycerol ; triacylglycerol lipase ; adolescent ; article ; blood gas analysis ; body mass ; body weight loss ; carbonated beverage ; case report ; child ; clinical article ; computer assisted tomography ; diabetic ketoacidosis ; diet therapy ; echocardiography ; electrolyte disturbance ; fever ; fluid therapy ; heart arrest ; human ; hyperglycemia ; hypernatremia ; hypotension ; hypovolemic shock ; male ; myalgia ; nausea ; neutral insulin injection ; non insulin dependent diabetes mellitus ; obesity ; polydipsia ; polyuria ; resuscitation ; soft drink ketoacidosis ; tachycardia ; vomiting ; waist circumference.

Texto completo. Buscar no Google. Texto completo: Disponível Coleções: Bases de dados de organismos internacionais Base de dados: EMBASE Idioma: Inglês Revista: Clinical Pediatric Endocrinology Ano de publicação: Tipo de documento: Artigo.

Consulta Detalhada ×. Email ×. Keywords: Case repot; Desmopressin; Diabetic ketoacidosis; Hyperglycemia; Hyperglycemic hyperosmolar state; Hypernatremia. Published by Baishideng Publishing Group Inc.

All rights reserved. Abstract Background: Diabetic ketoacidosis DKA and hyperglycemic hyperosmolar state HHS are common acute complications of diabetes mellitus with a high risk of mortality. Publication types Case Reports.

Introduction

Diabetic ketoacidosis DKA and hyperglycemic hyperosmolar state HHS are diabetic emergencies. Some patients with a hyperglycemic crisis can present with an overlap of DKA and HHS.

The coexistence of DKA and HHS is associated with higher mortality than in isolated DKA and HHS. In addition, electrolyte derangements caused by global electrolyte imbalance are associated with potentially life-threatening complications. Here, we describe three cases of mixed DKA and HHS with severe hypernatremia at the onset of type 2 diabetes mellitus.

All patients had extreme hyperglycemia and hyperosmolarity with acidosis at the onset of diabetes mellitus. They showed severe hypernatremia with renal impairment. Two patients recovered completely without any complications, while one died. Severe hypernatremia with mixed DKA and HHS is rare.

However, it may be associated with excess carbohydrate beverage consumption. Reduced physical activity during the COVID19 pandemic and unhealthy eating behaviors worsened the initial presentation of diabetes mellitus.

We highlight the impact of lifestyle factors on mixed DKA and HHS. As a result, a structured and systematic treatment approach is critical. We discuss the therapeutic approach and implications of this uncommon presentation. Case summary: A year-old man with no known past medical history presented to emergency department with altered mental status.

He was admitted to the intensive care unit ICU and was started on insulin drip as per DKA protocol. But his mental status didn't show much improvement.

Management of decompensated diabetes. diabetic ketoacidosis and hyperglycemic hyperosmolar syndrome. Crit Care Clin ;17 1 Gullans SR, Verbalis JG. Control of brain volume during hyperosmolar and hypoosmolar conditions.

Annu Rev Med ; Adrogu� HJ, Mad�as NE. N Engl J Med ; 20 Liamis G, Kalogirou M, Saugos V, Elisaf M. Therapeutic approach in patients with dysnatraemias.

Nephrol Dial Transplant ;21 6 Stoner GD. Hyperosmolar hyperglycemic state. Am Fam Physician ;71 9 Katz MA. Hyperglycemia induced hyponatremia-calculation of expected serum sodium depression.

Publication types The diagnostic features of DKA include low arterial blood pH and serum bicarbonate, presence of ketone bodies in serum and urine, a wide serum anion gap, and variable tonicity 1. Navbar Search Filter Journal of the Endocrine Society This issue Endocrine Society Journals Endocrinology and Diabetes Books Journals Oxford Academic Mobile Enter search term Search. Umpierrez GE, Kelly JP, Navarrette JE, Kaslas MM, Kitabchi AE. Al-Matrafi J, Vethamuthu J, Feber J. Davidson AJG. Indian J Crit Care Med. Khaleeli AA, Wyman AL.

Hyperglycemic crisis and hypernatremia -

In these patients, quantitating the isolated effect of glucose gain is imperative because this effect is predictable with a reasonable degree of certainty, as shown in the previous section, and more importantly, it will disappear with correction of hyperglycemia without requiring additional measures.

Prediction of the quantitative effects of water intake and particularly of osmotic diuresis, which is the dominant effect on tonicity in severe hyperglycemic episodes 2 , 3 , is difficult because the magnitude of these processes varies greatly 2 , The effects of osmotic diuresis on [Na] require correction by fluid infusion.

One report calculated the effects of osmotic diuresis on tonicity-related values in a hypothetical subject with extreme hyperglycemia [Glu] of This finding suggests that the corrected [Na] by the Al-Kudsi formula provides a reasonable prediction of the part of hypertonicity that is due to osmotic diuresis.

Accounting for changes in external balances of water, sodium, and potassium during development and treatment of hyperglycemia is necessary for any evaluation of the corrected [Na] in patients with renal function.

There is a paucity of studies in this area. These findings were used in the development of several guidelines 30 — Assuming baseline values of 5.

According to these calculations, tonicity, after rising appropriately with [Glu] rising from 5. The guidelines for hyperglycemic crises address diabetic ketoacidosis DKA and hyperosmolar hyperglycemic state HHS 1 , 21 — The diagnostic features of DKA include low arterial blood pH and serum bicarbonate, presence of ketone bodies in serum and urine, a wide serum anion gap, and variable tonicity 1.

However, euglycemic DKA has become more frequent after the introduction of sodium glucose cotransporter 2 SGLT-2 inhibitors in the treatment of diabetes mellitus Hypertonicity may cause coma in hyperglycemic syndromes 60 , At equal levels of hyperglycemic hypertonicity, elevated [Na] indicates severe water deficit 64 , The corrected [Na] illustrates the difference in water deficit between high [Na] and high [Glu] in this case.

Table 2 shows presenting values for [Glu], [Na], tonicity, and corrected [Na] in reports of DKA 66 — , HHS 3 , 9 , 13 , 75 — 78 , , , , — , and hyperglycemia in chronic kidney disease CKD stage V 12 , 16 , 47 — 49 , , , — , which was included in Table 2 as the control group because it causes limited or no water and electrolyte losses through osmotic diuresis.

All but three of the cases in this last group were on maintenance dialysis. To show the range of the tonicity-related values, Table 2 includes studies as well as case reports. Reports of combined DKA and HHS were included in the DKA part of the table. Studies reporting median, instead of mean, tonicity-related values were not included in this table.

The reason for including these cases was explained above. Table 2. Presenting serum glucose, sodium, tonicity, and corrected sodium levels in reported hyperglycemic crises.

In Table 2 , there exists considerable overlap of [Glu], [Na] tonicity, and corrected [Na] ranges in the three categories of hyperglycemia. DKA combined with HHS occurred in many instances. The term Diabetic Hyperosmolar Ketoacidosis DHKA was proposed for DKA combined with HHS Patients on dialysis who presented with hyperglycemia and elevated corrected [Na] have usually lost hypotonic fluids through hemodialysis , or peritoneal dialysis — , , with high glucose concentration in the dialysate.

The second important finding in Table 2 is in the mean corrected [Na] values. Thus, although many patients have water deficits in excess of sodium and potassium deficits, an equal or even larger number of patients do not have excessive water deficits at presentation with DKA.

This finding has important consequences in the choice of the tonicity of replacement solutions. Mean corrected [Na] was in the eunatremic range in hyperglycemia of patients with CKD stage 5. Preventing cerebral edema is a key concern during treatment of hyperglycemic crises.

Tonicity-related parameters have received attention in the studies of the pathogenesis of this complication.

These values do not differ substantially from the mean values of all DKA cases in Table 2. However, factors related to tonicity statistically associated with brain edema during treatment of DKA include decrease in tonicity, large early infusion volumes, very high [Glu] at presentation, rapid decline in [Glu], very low [Na], and administration of large doses of insulin , , The change in corrected [Na] during treatment of DKA was the best discriminator for the development of severe coma in one study Deterioration of neurological manifestations associated with substantial rises of the corrected [Na] has been reported during treatment of both DKA 2 , and HHS , , Other reported factors associated with cerebral edema in DKA include the degree of acidosis 96 , , , , high levels of blood urea at presentation , , and vasogenic factors One study found no effect of the rate of replacement fluid infusion The PECARN study found no significant differences in neurological manifestations during and following treatment of DKA between using 0.

Vascular endothelial changes caused by elevated blood levels of cytokines and chemokines secondary to inflammatory status associated with DKA were proposed by the authors of the PECARN study as the main mechanism for the development of cerebral edema.

High value of corrected [Na] at presentation with DKA is associated with increased incidence and severity of acute kidney injury AKI , Weighed mean values at presentation with DKA and AKI were AKI occurs frequently in HHS 3 , , , , , , Attention to tonicity plays a role in prevention of severe neurological manifestations during treatment of hyperglycemic emergencies.

Decrease in tonicity from extracellular solute loss leads to osmotic entry of fluid into cells and could contribute to the development of cerebral edema For this reason, one report proposed a very slow decrease in tonicity during the early stages of treatment The optimal rate of decline in tonicity, however, has not been clarified.

The change in tonicity due exclusively to correction of hyperglycemia has two components, a fall in [Glu] and a rise in [Na]. Guidelines propose hourly rates of 2. The corrected [Na] predicts the relation between effective body solute and total body water after decrease of [Glu] to its desired level 2 , 17 and should be used as a guide for the composition of replacement solutions in the same fashion as actual [Na] values are used to guide fluid management of dysnatremias 7 , — Evidence presented earlier supports the use of the Al-Kudsi formula for calculation of the corrected [Na].

Two limitations of the corrected [Na] should be addressed during treatment: First, the corrected [Na] using the Al-Kudsi formula is not accurate in some conditions, mainly in advanced extracellular volume disturbances.

Second, and more importantly, the corrected [Na] reflects the relation between effective body solute and body water at the moment of blood sampling 2 , 17 , Correction of the extracellular volume deficit improves renal function and in the face of persistent hyperglycemia leads to large volume osmotic diuresis, which causes further water deficit and rises in the corrected [Na] 2.

We propose the following scheme for use of the corrected [Na] during treatment of hyperglycemic crises: The initial measurement of serum values should include osmolality in addition to basic metabolic panel.

In the absence of an exogenous solute e. In the second case, falsely low [Na] values are reported when this measurement is performed in an autoanalyzer that requires dilution of the samples measured If there is a large osmol gap, [Na] should be measured again in an apparatus that does not require dilution of the measured specimen, e.

The tonicity of replacement solutions should be based on repeated calculations of the corrected [Na]. If the corrected [Na] at presentation is in the eunatremic range, infusion of isotonic saline should be started at a rate dictated by clinical manifestations of hypovolemia.

Prevention of either decline or rise in the corrected [Na] is critical. Patients with corrected [Na] values within the normal range of [Na], like the average patient with DKA Table 2 , do not have relatively larger deficit of water compared to monovalent cations.

In these patients, use of isotonic solutions as initial treatment of DKA and slow decline of [Glu], as proposed in the guidelines 1 , leads to rapid correction of severe extracellular volume deficits and prevents sharp changes in the corrected [Na].

In subjects with initial corrected [Na] in the eunatremic range, tonicity should decline at a low rate. Maintenance of the corrected [Na] at the same level and decrease in [Glu] at the rate proposed in the guidelines 2. In the rare instance of low presenting corrected [Na], or for treatment of cerebral edema, hypertonic saline infusion may be used During treatment, urine volume should be monitored and [Glu], [Na], serum potassium concentration, and other relevant parameters should be measured frequently, initially every 1—2 h.

The corrected [Na] should be calculated after each measurement of [Glu] and [Na] and should guide changes in the tonicity of the infusate. Development of large osmotic diuresis may lead to increases in the corrected [Na] and the need for hypotonic infusions later in the course of treatment.

A corrected [Na] in the hypernatremic range at presentation with hyperglycemia indicates excessive water deficit that must be corrected. Initially, infusion of isotonic fluids will correct rapidly volume deficits and will also decrease the level of hypertonicity.

However, the subsequent development of large volume osmotic diuresis may lead to rise in the corrected [Na]. Monitoring urine volume, frequent measurement of the relevant serum biochemical values, and repeated calculation of the corrected [Na] after each measurement of [Glu] and [Na] is imperative.

The corrected [Na] should not rise further; however, deciding whether it should remain at the same level at least early during the decrease in [Glu] or it should decrease at a slow rate e.

Infusion of hypotonic solutions will eventually be needed regardless of whether the early phase of treatment aims at maintaining or decreasing the corrected [Na]. Addition of potassium salts to the infused saline should be guided by repeated measurements of the serum potassium concentration. In deciding the concentration of sodium in the replacement solutions, it is important to take into account the concentration of potassium salts in the infusate 2.

The corrected [Na] calculated by the Al-Kudsi formula should guide the tonicity of replacement solutions. This use should be tempered by the knowledge that rarely encountered extreme volume disturbances can cause [Na] changes substantially different from those predicted by the corrected [Na] and, more importantly, that the corrected [Na] can vary greatly during treatment depending on changes in the external balances of water, sodium and potassium.

For these reasons, frequent measurements of [Glu] and [Na], repeated calculation of the corrected [Na] after each measurement, and changes in the tonicity of replacement solutions based on the corrected [Na] are critical steps in the management of tonicity issues in hyperglycemia.

Publicly available datasets were analyzed in this study. This data came from tables of publications cited in the text.

TI: conceptualization. TI, KG, GB, CA, and AT: literature review. TI, GB, SL, and AT: methodology. SL, CA, and AT: visualization.

TI and AT: writing-original draft preparation. KG, GB, SL, EA, and CA: writing-review and editing. All authors contributed to the article and approved the submitted version.

GB was supported by a Burrows Wellcome Fund Career Award for Medical Scientists and NIH grant RO1 DK The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

The reviewer DM declared a past co-authorship with several of the authors TI, AT, and CA to the handling editor. The authors acknowledge Dialysis Clinic Inc. for supporting this work by covering publication expenses [DCI C].

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Risk factors for developing brain herniation during diabetic ketoacidosis. Pediatr Neurol. Vanelli M, Chiari G, Ghizzoni L, Capuano C, Bonetti L, Costi G, et al. Ketoacidosis and hyperosmolarity as first symptoms of type 1 diabetes mellitus following ingestion of high-carbohydrate-containing fluids.

J Pediatr Endocrinol Metab. Wagner A, Risse A, Brill HL, Wienhausen-Wilke V, Rottmann M, Sondern K, et al. Therapy of severe diabetic ketoacidosis. Zero-mortality under very-low-dose insulin application. Azzopardi J, Gatt A, Zammit A, Alberti G.

Lack of evidence of cerebral oedema in adults treated for diabetic ketoacidosis with fluids of different tonicity. Hollander AS, Olney RC, Blackett PR, Marshall BA. Fatal malignant hyperthermia-like syndrome with rhabdomyolysis complicating the presentation of diabetes mellitus in adolescent males.

Kamat P, Vats A, Gross M, Checchia PA. Use of hypertonic saline for the treatment of altered mental status associated with diabetic ketoacidosis. Pediatr Crit Care Med. Glaser NS, Wooton-Gorges SL, Marcin JP, Buonocore MH, Dicarlo J, Neely EK, et al. Mechanism of cerebral edema in children with diabetic ketoacidosis.

Newton CA, Raskin P. Diabetic ketoacidosis in type 1 and type 2 diabetes mellitus: clinical and biochemical differences. McDonnell CM, Pedreira CC, Vadamalayan B, Cameron FJ, Werther GA. Diabetic ketoacidosis, hyperosmolarity and hypernatremia: are high-carbohydrate drinks worsening initial presentation?

Murthy K, Harrington JT, Siegel RD. Profound hypokalemia in diabetic ketoacidosis: a therapeutic challenge. Endocr Pract. Yordam N, Gönç EN, Kandemir N, Alikaşifoglu A, Ozön A. Ten-year experience in management of diabetic ketoacidosis and ketosis: episodes at pediatric age. Turk J Pediatr. Dixon AN, Jude EB, Banerjee AK, Bain SC.

Simultaneous pulmonary and cerebral oedema, and multiple CNS infarctions as complications of diabetic ketoacidosis: a case report. Edge JA, Jakes RW, Roy Y, Hawkins M, Winters D, Ford-Adams ME, et al. The UK case-control study of cerebral oedema complicating diabetic ketoacidosis in children.

Bhowmick SK, Hundley OT, Rettiq KR. Severe hypernatremia and hyperosmolality exacerbated by an herbal preparation in a patient with diabetic ketoacidosis.

Clin Pediatr. Hoorn EJ, Carlotti AP, Costa LA, MacMahon B, Bohn G, Zietse R, et al. Preventing a drop in effective plasma osmolality to minimize the likelihood of cerebral edema during treatment of children with diabetic ketoacidosis.

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Deeter KH, Roberts JS, Bradford H, Richards T, Shaw K, Marro K, et al. Hypertension despite dehydration during severe pediatric diabetic ketoacidosis. Durward A, Ferguson LP, Taylor IA, Tibby SM. The temporal relationship between glucose-corrected serum sodium and neurological status in severe diabetic ketoacidosis.

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J Intensive Care Med. Kim HJ, Kim DH, Jun YH, Lee JE. A rare diabetes ketoacidosis in combined severe hypernatremic hyperosmolarity in a new onset Asian adolescent with type 1 diabetes.

Li W, Gong C, Wu D, Liu M. Hypernatremia is an uncommon electrolyte abnormality in this setting, with unclear exact etiology. We present a year-old gentleman who was found to have severe hypernatremia in the setting of combined DKA and HHS.

A year-old male with class III obesity presented to the emergency department with altered sensorium and lethargy. Patient was having nausea and vomiting, along with polyuria, polydipsia and nocturia, prior to worsening encephalopathy. Physical exam showed rapid shallow breathing and lethargy.

No focal neurologic deficits noted. Hemoglobin A1C was 9. Ketonuria and ketonemia were present. Given the high osmolality, he was diagnosed with DKA and HHS.

Free water deficit was Insulin drip was started, along with 5 liters of intravenous Lactated Ringer's boluses. Encephalopathy improved approximately 48 hours after admission. His glucose stabilized, renal function improved, acidosis resolved, and sodium returned to normal. He was transitioned to general wards and started on an oral carbohydrate-restricted diet and subcutaneous insulin regimen containing long- and short-acting insulin analogs.

During severe hyperglycemia, glucose increases extracellular osmolality, creating a gradient for water to move from intracellular to extracellular compartments, leading to hyponatremia. As the renal threshold is reached, glucosuria ensues, causing osmotic diuresis and water loss.

If this process continues, excess water loss can cause dehydration, further increase serum osmolality, and lead to hypernatremia. A previous study evaluated patients who present with hypernatremia during DKA.

It was found that patients with new-onset diabetes are more likely to present with hypernatremia 1. Several etiologies contribute to altered sensorium in such patients, including cerebral hypoperfusion in the setting of dehydration and excess water loss, acidosis, and direct effect of ketone bodies on brain cells 2.

As electrolyte abnormalities are corrected with adequate fluid selection, patients return to baseline mentation. KW Monroe, WD King, MH Nichols, JA Atchinson. Hypernatremia in diabetic ketoacidosis. Practical Diabetes Int ;14 6 : Elias Estifan, Sushant M.

Nanavati, Vinod Kumar, et al. Salty diabetes: a case series of hypernatremia presenting with diabetic ketoacidosis.

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Journal Article. PSUN Severe Hypernatremia in a patient with combined Hyperosmolar Hyperglycemic State and Diabetic Ketoacidosis. Jennifer Batch, MD , Jennifer Batch, MD. Oxford Academic. Google Scholar.

Language: Spanish References: 15 Page: Ceisis size: Key words:. Kugler JP, Hustead T. Hyponatremia and hypernatremia in the elderly. Am Fam Physician ;61 12 Diabetic Ulcer prevention measures DKA and hyperosmolar hyperglycemic state HHS Hypergpycemic the hyperhatremia of Hyperglycemic crisis and hypernatremia with highest hypeernatremia. In both, there are fluid shifts and osmotic diuresis with electrolyte hypernartemia that result in hyponatremia. With high glucose levels, sodium become falsely decreased due to dilutional effects of water shifting from intracellular to extracellular space. Hypernatremia is an uncommon electrolyte abnormality in this setting, with unclear exact etiology. We present a year-old gentleman who was found to have severe hypernatremia in the setting of combined DKA and HHS.

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Diabetic Ketoacidosis (DKA) \u0026 Hyperglycemic Hyperosmolar Syndrome (HHS)

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