Overview of Cerebral Edema During Correction of Hyperglycemic Crises

Varela, Daniel; Held, N.; Linas, Stuart L.

doi:10.12659/ajcr.908465

Cited by 15 publications

(18 citation statements)

References 3 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Hyperosmolarity was common among untreated dogs with non-ketonuric or ketonuric diabetes or the hyperosmolar hyperglycemic syndrome in several studies [6, 15]. Hyperosmolality is important to understand because it is associated with risk for osmotic complications in diabetic patients, including severe neurologic dysfunction, which may be fatal [23, 24, 25]. The frequency and range of osmotic complications due to hyperosmolality and, more specifically, hypertonicity in dogs are currently unknown.…”

Section: Discussionmentioning

confidence: 99%

The mean cell volume difference (dMCV) reflects serum hypertonicity in diabetic dogs

Norris

Schermerhorn

2019

PLoS ONE

View full text Add to dashboard Cite

Serum hypertonicity may develop during diabetes mellitus due to hyperglycemia and other biochemical changes. Hypertonicity may produce detrimental cellular and systemic effects and has been identified as a serum marker for some clinical disorders. In non-diabetic dogs, the mean cell volume difference, a novel erythrocyte measure, is increased by serum hypertonicity. However, it is not known whether hyperglycemic hypertonicity produces a similar change. The hypothesis that the mean cell volume difference could detect serum hypertonicity in diabetes was investigated in a group of thirty-two dogs with naturally-occurring diabetes mellitus that were prospectively recruited over a 1-year period from the outpatient population of a veterinary teaching hospital. The effect of hyperglycemia on the mean cell volume difference and the ability of the mean cell volume difference to predict serum hypertonicity were examined. Serum hyperosmolality and hypertonicity due to hyperglycemia was present in 91% and 94% of dogs, respectively. Hyperglycemia was the principal cause identified for serum hypertonicity and hyperosmolality. Using a cut-off value of ≥ 3 μm 3 for the mean cell volume difference, serum hypertonicity ≥ 320 mmol/kg was identified with 79% sensitivity and 61% specificity. The dMCV correlated with changes in serum glucose, tonicity, and measured osmolality. Dogs with a mean cell volume difference ≥ 3 μm 3 were at risk for serum tonicity ≥ 320 mmol/kg (risk ratio = 2.2) and serum glucose ≥ 13.9 mmol/L (risk ratio = 2.3). In conclusion, the mean cell volume difference is a useful surrogate marker for detecting serum hypertonicity in diabetic dogs and elevated mean cell volume difference is associated with increased risks for clinically relevant serum hypertonicity and hyperglycemia.

show abstract

Section: Discussionmentioning

confidence: 99%

The mean cell volume difference (dMCV) reflects serum hypertonicity in diabetic dogs

Norris

Schermerhorn

2019

PLoS ONE

View full text Add to dashboard Cite

show abstract

“…Brain edema is more common in patients with Type 1 DM, but also can be seen in patients with type 2 DM. 5,32,33 However, in a study on children with Type 1 DM, it was observed that no ONSD alterations occurred in association with disease severity. 3 Similarly, in our study, it was determined that the ONSD measurements in the DKA and HHS patients were not different compared to those in the patients with isolated hyperglycemia.…”

Section: Discussionmentioning

confidence: 96%

The measurement of ultrasonographic optic nerve sheath diameter in patients with hyperglycemia

Dönertaş

Kozacı

Avcı

2022

Hong Kong j. emerg. med.

View full text Add to dashboard Cite

Background: Diabetes mellitus is a disease associated with several complications in its acute and chronic stages. Objective: The aim of the study was to determine the treatment-associated changes in optic nerve sheath diameter in patients admitted to the emergency department due to one of the acute hyperglycemic complications of diabetes mellitus. Materials and method: Diabetic patients with serum glucose levels of 250 mg/dL or higher were included in the study. Healthy volunteers were included in the control group. Optic nerve sheath diameter was measured at 0th hour and at the end of the second hour. Blood samples were collected simultaneously with optic nerve sheath diameter measurements. Results: The study included 100 individuals. Group 1 included 50 patients and Group 2 included 50 healthy adults. Optic nerve sheath diameter was 4.5 ± 0.4 mm in Group 1 and 4.4 ± 0.5 mm in Group 2 in 0th hour, and no statistical difference was found between the groups (p = 0.162). In Group 1, optic nerve sheath diameter increased 0.6 ± 0.4 mm after the treatment. Of the patients in Group 1, 22 (44%) patients with diabetic ketoacidosis or hyperosmolar hyperglycemic state were assigned to Group 1A and 28 (56%) patients with isolated hyperglycemia were assigned to Group 1B. There was not a difference between the pre- and post-treatment optic nerve sheath diameter values of the patients in Group 1A and Group 1B. Optic nerve sheath diameter was observed to enlarge after treatment. The difference in optic nerve sheath diameter was 0.6 ± 0.4 mm in Group 1A and 0.5 ± 0.4 mm in Group 1B (p = 0.294). Conclusion: Pre-treatment optic nerve sheath diameter values of the patients who were diagnosed with one of the acute hyperglycemic complications of diabetes mellitus are not different from healthy adults. Furthermore, optic nerve sheath diameter values do not change with the severity of the disease. However, optic nerve sheath diameter values change with treatment. For this reason, optic nerve sheath diameter can be used to following the development of brain edema.

show abstract

“…Cerebral edema develops when fluid moves from the extracellular to the intracellular compartment faster than the brain cells can adapt to increased intracellular volume [ 8 ]. This can happen when there is rapid correction of hyperglycemia, leading to a sudden drop in serum osmolality.…”

Section: Discussionmentioning

confidence: 99%

“…Another mechanism involves idiogenic osmoles, which are osmotically active substances produced within brain cells during periods of extracellular hyperosmolality to counteract the osmolar imbalance. These idiogenic osmoles have a slow clearance rate, resulting in high intracellular osmoles which can lead to the movement of extracellular fluid into the intracellular space [ 8 ].…”

Section: Discussionmentioning

confidence: 99%

Diabetic Ketoacidosis Complicated by a Brain Death

Kabashneh¹,

Al-Sagri²,

Alkassis³

et al. 2020

Cureus

View full text Add to dashboard Cite

Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes mellitus (DM). Cerebral edema (CE) can complicate DKA management. We report a patient with no significant medical history who presented with DKA and a new-onset DM; she received the standard management with regular insulin and IV fluids, the management resulted in a rapid drop in serum osmolality, the patient`s mental status deteriorated and became nonresponsive, brain imaging confirmed CE, a few days later the patient was declared brain dead by neurology. This case highlights the importance of gradual correction of hyperosmolar conditions including hyperglycemia and urges all healthcare providers to closely trend glucose levels in the management of DKA.

show abstract

Overview of Cerebral Edema During Correction of Hyperglycemic Crises

Cited by 15 publications

References 3 publications

The mean cell volume difference (dMCV) reflects serum hypertonicity in diabetic dogs

The mean cell volume difference (dMCV) reflects serum hypertonicity in diabetic dogs

The measurement of ultrasonographic optic nerve sheath diameter in patients with hyperglycemia

Diabetic Ketoacidosis Complicated by a Brain Death

Contact Info

Product

Resources

About