Neurological Prognostication After Hypoglycemic Coma: Role of Clinical and EEG Findings

Bouyaknouden, Douaae; Peddada, Teja; Ravishankar, Nidhi; Fatima, Safoora; Fong-Isariyawongse, Joanna; Gilmore, Emily J.; Struck, Aaron F.; Husain, Aatif M.; Fernandez, Andres; Ruiz, Andres Rodriguez; Bagić, Anto; Amin, Assad F.; Foreman, Brandon; Appavu, Brian; Maciel, Carolina B.; Hahn, Cecil D.; Nwankwo, Chinasa; Rubiños, Clio; Wusthoff, Courtney J.; Amorim, Edilberto; Gerard, Elizabeth E.; Ritzl, Eva K.; Drislane, Frank W.; Kapinos, Gregory; Chen, Hai; Britton, Jeffrey W.; Szaflarski, Jerzy P.; Yoo, Ji Yeoun; Lee, Jong Woo; Ding, Kan; Chapman, Kevin; Hirsch, Lawrence J.; Huh, Linda; Westover, M. Brandon; Holmes, Manisha; Ng, Marcus; Mizrahi, Moshe; Abend, Nicholas S.; Gaspard, Nicolas; Selioutski, Olga; Taraschenko, Olga; Mani, Ram S.; Sainju, Rup K.; Hantus, Stephen; Herman, Susan T.; LaRoche, Suzette M.; Gofton, Teneille; Loddenkemper, Tobias; Uysal, Utku; Zutshi, Deepti; Sheikh, Zubeda

doi:10.1007/s12028-022-01495-2

Cited by 4 publications

(5 citation statements)

References 26 publications

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“…Urgent identification of reversible causes of coma is mandatory [86] as several etiologies require timely treatment initiation, e.g., status epilepticus (convulsive and nonconvulsive) [82,87], sepsis [88,89], and meningitis/encephalitis [90][91][92]. Even hypoglycemia, if prolonged, can lead to irreversible brains lesions [93,94]. Thus, prompt initiation of antibiotic or antiepileptics, correction of a metabolic disturbance, withholding of neurotoxic drugs, and reversal of intoxication with antidotes should be considered.…”

Section: Managementmentioning

confidence: 99%

Acute encephalopathy in the ICU: a practical approach

Kurtz,

van den Boogaard,

Girard

et al. 2024

Current Opinion in Critical Care

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Purpose of review Acute encephalopathy (AE) – which frequently develops in critically ill patients with and without primary brain injury – is defined as an acute process that evolves rapidly and leads to changes in baseline cognitive status, ranging from delirium to coma. The diagnosis, monitoring, and management of AE is challenging. Here, we discuss advances in definitions, diagnostic approaches, therapeutic options, and implications to outcomes of the clinical spectrum of AE in ICU patients without primary brain injury. Recent findings Understanding and definitions of delirium and coma have evolved. Delirium is a neurocognitive disorder involving impairment of attention and cognition, usually fluctuating, and developing over hours to days. Coma is a state of unresponsiveness, with absence of command following, intelligible speech, or visual pursuit, with no imaging or neurophysiological evidence of cognitive motor dissociation. The CAM-ICU(−7) and the ICDSC are validated, guideline-recommended tools for clinical delirium assessment, with identification of clinical subtypes and stratification of severity. In comatose patients, the roles of continuous EEG monitoring and neuroimaging have grown for the early detection of secondary brain injury and treatment of reversible causes. Summary Evidence-based pharmacologic treatments for delirium are limited. Dexmedetomidine is effective for mechanically ventilated patients with delirium, while haloperidol has minimal effect of delirium but may have other benefits. Specific treatments for coma in nonprimary brain injury are still lacking.

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Section: Managementmentioning

confidence: 99%

Acute encephalopathy in the ICU: a practical approach

Kurtz,

van den Boogaard,

Girard

et al. 2024

Current Opinion in Critical Care

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show abstract

“…Hypoglycemic cerebral injury is also readily distinguished by clinical history and laboratory confirmation of hypoglycemia 26 . Typically, the event is preceded by unintentional (or intentional) overdose of insulin or other pharmacotherapies used in diabetes mellitus, but can also be related to neuroendocrine disturbances 27,28 . Clinically, patients progress from dizziness and palpitations to coma over a period of minutes as circulating serum glucose is taken up in the pancreatic islet cells.…”

Section: Acute Hypoglycemiamentioning

confidence: 99%

“…The prognosis following severe hypoglycemia with coma is similar to that of anoxic brain injury, with early mortality rates between 40% and 75% 28 . In one of the largest studies to date, the outcomes of 60 patients with hypoglycemic coma were recently reported in a retrospective multicenter cohort by Bouyaknouden et al., with half (31) of patients recovering consciousness 3 months after hospital discharge 27,28,32 .…”

Section: Acute Hypoglycemiamentioning

confidence: 99%

“…26 Typically, the event is preceded by unintentional (or intentional) overdose of insulin or other pharmacotherapies used in diabetes mellitus, but can also be related to neuroendocrine disturbances. 27,28 Clinically, patients progress from dizziness and palpitations to coma over a period of minutes as circulating serum glucose is taken up in the pancreatic islet cells. Heterogeneous distribution of glucose transporters in various brain regions is proposed to explain some of the patterns of injury seen in hypoglycemic encephalopathy.…”

Section: Affected Sequences On Mri Common Distribution Uncommon Distr...mentioning

confidence: 99%

“…31 The prognosis following severe hypoglycemia with coma is similar to that of anoxic brain injury, with early mortality rates between 40% and 75%. 28 In one of the largest studies to date, the outcomes of 60 patients with hypoglycemic coma were recently reported in a retrospective multicenter cohort by Bouyaknouden et al, with half (31) of patients recovering consciousness 3 months after hospital discharge. 27,28,32 Favorable predictors of recovery included preserved pupillary reflexes within 48-72 hours of onset, and lack of suppression (including burst suppression, suppression with periodic discharges, or persistent suppression) on continuous electroencephalography (EEG).…”

Section: Affected Sequences On Mri Common Distribution Uncommon Distr...mentioning

confidence: 99%

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Neuroimaging mimics of anoxic brain injury: A review

Sharma

Birnhak

Sanborn

et al. 2023

Journal of Neuroimaging

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Diffuse cortical diffusion changes on magnetic resonance imaging (MRI) are characteristically ascribed to global cerebral anoxia, typically after cardiac arrest. Far from being pathognomonic, however, this neuroimaging finding is relatively nonspecific, and can manifest in a myriad of disease states including hypoxia, metabolic derangements, infections, seizure, toxic exposures, and neuroinflammation. While these various conditions can all produce a neuroimaging pattern of widespread cortical diffusion restriction, many of these underlying causes do have subtly unique imaging features that are appreciable on MRI and can be of clinical and diagnostic utility. Specific populations of neurons are variably sensitive to certain types of injury, whether due to differences in perfusion, receptor type density, or the unique tropisms of infectious organisms. In this narrative review, we discuss a number of distinct etiologies of diffuse cortical diffusion restriction on MRI, the unique pathophysiologies responsible for tissue injury, and the resulting neuroimaging characteristics that can be of assistance in differentiating them. As widespread cortical injury from any cause often presents with altered mental status or coma, the differential diagnosis can be enhanced with rapid acquisition of MRI when clinical history or detailed physical examination is limited. In such settings, the distinct imaging features discussed in this article are of interest to both the clinician and the radiologist.

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